CP3Medicine and Surgery

OESOPHAGUS - Name three typical symptoms of gastro-oesophageal reflux disease (GORD). Describe the investigations used to confirm a diagnosis of GORD. Discuss general measures and medical therapy. Outline the surgical measures used to treat GORD. Outline the possible long-term complications of GORD.

A chronic symptom of mucosal damage due to reflux of stomach acid. It is associated with hiatus hernias and weakened lower oesophageal sphincter (smoking). Investigations:typically clinical, occasionally endoscopy. Manometry. Management: avoiding spicy foods, weight loss, smoking cessation, proton pump inhibitors, alginate, antacids and h2 receptor antagonists. Complications: barrats oesophagus....metaplasia that is a precursor to cancer.

CNS INFECTION - Describe the clinical presentation of an epidural spinal abscess

A collection of pus outside of the dura, But inside the vertebral column. Typically these occur in the rack: bar region because The region is larger and contains more fat. Presentation: pain, weakness and paralysis (think of an abscess compressing the spinal cord). There may also be associated signs of infection (fever) and meningism. Risk factors: increasing age, intravenous drug use, spinal instrumentation, Diabetes, immunosuppression.

PANCREATIC PSEUDOCYST - Define pseudocyst and discuss mechanisms of their formation. List and discuss the symptoms and signs and natural history of an untreated pseudocyst. Discuss the indications for and sequence of investigations for suspected pseodocyst. Describe the treatment of pancreatic pseudocyst.

A common side effect of acute pancreatitis. The pseudocystic is when fluids containing pancreatic enzymes and necrotic tissue collected in the lesser sac. they account for 75% of pancreatic masses. as they do not have an epithelial lining they are technically not real cysts. Cause: Post pancreatis, post-abdominal trauma, pancreatic neoplasm. Presentation: abdominal discomfort, digestion difficulty - post pancreatitis. Investigations: blood tests include amylase (raised), carcinoembryonic Antigen (low in pseudocyst but raised in cancer), fluid viscosity (low in pseudocyst raising cancer). CT is the gold standard. Complications: one in 10 pancreatic pseudocyst become infected, making them more likely to rupture. Management: drain the cyst into the stomach, duodenum or jejunum with a cystogastrostomy/Cystjejunostomy/Cystduodenostomy.

HERNIA - Define an umbilical hernia and relate it to the embryological origin of the umbilicus. List the factors that predispose to the development of umbilical and para-umbilical hernia. Describe the symptoms of patients with umbilical hernia. Perform a physical examination of patients with umbilical hernia, differentiating reducible and non-reducible hernia; recognise the signs of strangulation. Outline the principles on management of patients with umbilical hernia, including distinguishing those needing operative repair from those who do not.

A congenital malformation of the umbilicus (A TRUE UMBILICAL HERNIA) or an acquired protrusion (A PARAUMBILICAL HERNIA) as a result of raised intra-abdominal pressure. (Children and adults respectively). Typically adults have a mass adjacent to the umbilicus termed parumbilical associated with cirrhosis/ascites, obesity, chronic cough and multiple pregnancies. Embryologically: children are prone to umbilical hernias as embryologically the gastrointestinal system formed outside of the body and regresses back into the body via the umbilicus. Presentation: an umbilical mass (in children it will typically disappear into the three years), true umbilical hernias very rarely obstruct or cause any symptoms. Parumbilical hernias in adults may strangulate or obstruct and can grow to large sizes. Management: childhood umbilical hernias can be left alone and less symptomatic. surgical repair is typically indicated for symptomatic parumbilical hernias in adults if they are fit for general anaesthetic.

MOTOR NEURONE DISEASE - Describe the clinical presentation of MND Describe the 2 commonest manifestations of MND leading to death

A disease that causes progressive degeneration of motor neurones in the motor cortex and anterior horns of the spinal cord. There is also degeneration of cells in the motor nuclei of cranial nerves in the brain stem. Typically, progression leads to death within 1 to 5 years. Diagnosis: clinical with the support of an EMG which shows denervation in the muscles. Nerve conduction studies show reduced motor nerve conduction. There is no cure, treats symptomatically with speech and language therapy, assistive technology, altered food consistency, Analgesia, physiotherapy etc. Conditions under the Aegis of motor neurone disease include: AMYOTROPHIC LATERAL SCLEROSIS: (Synonymous with MND, typically a man in his 60s who dies three years after onset. There is a mixture of upper and lower motor neurone signs causing increased tone, weakness, increased reflexes, the densities and muscle cramps, fasciculations, wasting weakness. Presentationis asymmetrical with segmental progression from one limb to another and 50% of patients have cognitive impairments including frontotemporal dementia.) PROGRESSIVE MUSCULAR ATROPHY: (lower motor neurone disease causing wasting, weakness and fasciculation starting in the small muscles of the hands and feet then progressing to eventually include upper motor neurone signs. PROGRESSIVE BULBAR AND PSEUDOBULBAR PALSY: bulbar means the lower brainstem motor nuclei, typically lower motor neurone involvement of the time with wasting, and the palate with regurgitation. Pseudo-bulbar is an upper motor neurone condition causing dysarthria, dysphagy, hypersalivation, laryngospasm and emotional lability. There is an increased risk of aspiration and speeches often lost. PRIMARY LATERAL SCLEROSIS: solely upper motor neurone signs, typically in the legs before progressing to involve the arms and bulb muscles. This is a diagnosis of exclusion as signs must remain upper motor neurone for a least three years. Patients have slower progression and better prognosis. Patients may have sensory symptoms such as cramps at night and can often present in respiratory failure.

SKILLS IN PALLIATIVE CARE - Take a pain history, including the use of a pain chart and pain scores.

A full history should be taken to establish the causes and any underlying diagnoses. Patients can honestly have multiple pains. Methods for assessing pain include: verbal rating scale (no pain, mild pain, moderate, severe), visual analogue scale (zero - 10), behavioural rating scale (if a patient has cognitive impairments observing agitation and other markers of pain). Also assess symptoms of anxiety and depression as these can exacerbate pain. Examination should look for signs of neuropathic pain (sensory loss, allodynia, hyperalgesia, poor relief from opioids) and bony tenderness seen in metastasis. Investigations: do not assume that all pain is due to the underlying terminal diagnosis, imaging may be required to determine the courts.

TEMPORAL ARTERITIS - Describe the pertinent epidemiological features of temporal arteritis, including age at presentation and association with other inflammatory conditions Describe the pathological process involved in temporal arteritis Describe the clinical features of a headache arising from temporal arteritis List the clinical investigations employed to confirm a clinical suspicion of temporal arteritis Describe the management of temporal arteritis Outline the main complication that arises from untreated or missed temporal arteritis

A granulomatous inflammation of branches of the external carotid (Particularly the ophthalmic artery) Presentation: A woman over the age of 55 is the technical patient. Presenting with: raised ESR, visual loss/anaerosis fugax, headache, jaw claudication, scalp tenderness. 50% also have polymyalgia rheumatica (proximal muscle weakness). Associated conditions: Lupus, Rheumatoid arthritis, polymyalgia rheumatica. Pathological process: A large and medium vessel vasculitis whereby branches of the external carotid become inflamed. This may occur in skip lesions (hence a temp oral artery biopsy requiring a minimum length of 1 cm). Investigations: Measure ESR, CRP, LFT's (Alkaline phosphatase is raised). Ultrasound of the TEMP oral artery may show a halos sign Due to inflammation. The gold standard is a biopsy of the temp or artery although a negative biopsy does not necessarily mean that the disease is excluded. Management: Immediate high-dose steroids such as 60 mg of prednisolone. Complications if untreated: Permanent visual loss which can spread to the other eye, brainstem ischaemia, cranial nerve palsies and involvement of other vessels such as the aorta, coronary and mesenteric arteries.

NEUROPATHY - List the common causes of peripheral nerve damage and classify peripheral neuropathy into demyelinating and axonal types Outline the main clinical patterns of peripheral nerve damage, and describe typical findings on examination. Discuss the diagnosis of the likely cause of peripheral neuropathy using relevant aspects of history, examination, electrophysiological and laboratory investigation. Discuss the clinical presentation, diagnosis and management of GuillainBarre syndrome. Discuss the clinical features and management of shingles

A neuropathy is a pathological process affecting peripheral nerves either by demyelination or axonal degeneration (wallerian degeneration - commonly from alcohol toxicity and associated vitamin defiiencies). Causes: MONONEUROPATHIES: compression (acutely is reversible) or entrapment (chronically leads to demyelination - includes carpel tunnel, ulnar compression, radial, common peroneal from cross legged, meralgia paraesthetics). MULTIFOCAL NEUROPATHY (multiple mononneuropathies) such as in: diabetes, connective tissue disorders, sarcoidosis, amyloidosis, NF, HIV, leprosy. POLYNEUROPATHIES: As seen in diabetes (distal LOS or distal painful neuropathy due to involvement of small nmyelinated nerve damage or proximal motor neuropathy, autonomic neuropathy), Renal failure (give progressive sensorymotor neuropathy). Paraneoplastic (pure sensory neuropathy). Connective tissue diseases and Vasculitis (usually painful and sensorimotor). TOXIN/DRUG INDUCED: Lead, alcohol, medication. VITAMIN DEFICIENCY NEUROPATHIES: Thiamine (beriberi/wenike korsakoffs), B6 deficiency, B12 deficiency, VitE. INFECTION INDUCED HEREDITARY Demyelinating v. Axonal: Depending on what part of the nerve is affeted there is reduced electrical impulse amplitude (axonal degeneration) or reduced velocity of electrical transmission (demyelination). Differentiate with nerve conduction studies. Presentation: Consider symptoms as negative (loss of sensation (difficulty discriminating textures, hands feel like cotton wool, loss of proprioception, charott joints) Or as positive: (seen more when smaller, unmyelinated nerves are damaged) burning, pain, hyperalgesia, allodynia. Examination: loss of sensation, poor joint position sense, abnormal gait (if proprioception is lost), rhomburg positive, trauma/damage/neuropathic ulcers. There may be muscle wasting and weakness. Remember there may be autonomic symptoms (postural hypotension, impotence, constipation, diarrhoea, loss of bladder control, sweating), motor symptoms (usually distal muscle weakness), and skeletal symptoms include deformities (clawing, pes cavus, kyphoscoliosis). Investigations: nerve conduction studies, EMG (to localise lesions), nerve biopsies (identifies vasculitis or inflammation), CSF examination can identify Gullian-Barre. GULLIANBARRE: An inflammatory, demyelinating neuropathy seen a few weeks after a respiratory infection, with: distal paraesthesia, minimal sensory loss, proximal weakness that progressive and may lead to complete paralysis. If respiratory muscle are involved there may be respiratory failure. Autonomic dysfunction can cause arhythmias, constipation and urinary dysfunction. (proximal GB with occular muscle involvement, areflexia and ataxia is miller fisher). Monitoring and IV immunoglobulins with ventilation until improvement are needed. SHINGLES: Herpes zoster infection causing a painful dermatomal eruption. Tingling may preceed the rash and it will self resolve in 2-4weeks. There may be postherpeti neuralgia.

MECKELS DIVERTICULUM - Describe the nature of a Meckel's diverticulum and its possible pathological effects. Describe the variable clinical presentations of a patient with a Meckel's diverticulum.

A remnant of the vitellointestinal duct which normally disappears during the embryological period. Think of the rules of 2 - seen in 2% of the population, 2feet proximal to the ileocaecal valve and typically 2inches long. Presentation: Usually asymptomatic but can cause an appendicitis like picture, bleeding, volvulus or intussuception. Rarely the meckels contains gastric mucosa which causes bleeding (the most common cause of major GI bleed in teens). Diagnosis is on technetium scan or laparotomy. Treatment is surgical excision.

EVIDENCE BASED MEDICINE - Describe the benefits, and outline the steps involved, in a systematic review and meta-analysis.

A systematic review is when a researcher collates multiple studies on a single issue, collects the data, assesses their quality, collates all the study data and determines the overall findings. Benefits to a systematic review: Good because they collate multiple studies and have a large sample size but are still prone to bias. A meta-analysis is a statistical analysis of the results from a systematic review.

BRAIN BLEEDS - Describe the clinical presentation of an extradural haemorrhage Describe the acute investigation and management of a suspected extradural haemorrhage Explain how an extradural haemorrhage arises, including the artery involved.

A traumatic brain injury whereby bloods fills the space between the dura and the skull. As the spinal-cord is also covered in dura this can also happen in the spinal canal. Presentation: There may be an initial post-traumatic lucid period. Cranial nerve three lesion can develop (dilated, down and out pupil). There will be an intense headache and larger bleeds can show signs of raised intracranial pressure. Cause: Typically, traumatic rupture of the middle meningeal artery. Investigations: CT scan. Management: If pressure is raised then maybe requirement for by holes or craniotomy.

HEPATITIS -Describe the infective causes of acute hepatitis. Describe the causes of chronic hepatitis. Describe the morphology and pathological consequences of acute and chronic hepatitis. Outline the clinical presentation of acute and chronic hepatitis including relevant features in the medical history. Outline the treatment options for hepatitis due to autoimmunity, hepatitis B or C and paracetamol overdose. Outline the indications for and discuss the contraindications of liver biopsy in hepatitis

ACUTE HEPATITIS: less than six months inflammation of the liver which may cause no symptoms or jaundice, malaise and poor appetite. it can be self-limiting or can progress to chronic hepatitis. CHRONIC HEPATITIS: more than six months inflammation of the liver which may cause no symptoms or can progress to cirrhosis (cirrhosis itself increases the risk of hepatocellular carcinoma). Causes: viral hepatitis, toxins, alcohol, autoimmune, non-alcoholic fatty liver, metabolic disorders (haemochromatoses, Wilsons). Viral hepatitis: these are five unrelated viruses that happen to be hepatotoxic. HEPATITIS A: self-limiting acute infective jaundice spread fico orally. HEPATITIS B: mostly acute, but chronic in 15%. Spread by bodily fluids there is likely to be an element of immune response. Complications include cirrhosis and Hepatocellular carcinoma, although in curable hepatitis B can be managed with interferon. HEPATITIS C: a blood-borne chronic hepatitis that, after a number of years, results in cirrhosis. Those infected are more susceptible to other types of hepatitis and so should be A and B vaccinated. HEPATITIS D: only present alongside hepatitis B. HEPATITIS E: typically acute like hepatitis a, but can be fulminant (rapidly progressing and lethal). Management: cause specific, for example interferon for hepatitis B, liver transplant in severe paracetamol overdose when N-acetyl-L-cysteine has failed, treatment of complications. AUTOIMMUNE HEPATITIS: Chronic auto destruction of liver cells managed by steroids with or without azothioprine. Biopsy: the test is performed diagnostically or to assess the response to treatment. Risks include pneumothorax, damage to the gallbladder or bile ducts, peritonitis, seeding of cancer. biopsies required to confirm cirrhosis or fibrosis but unnecessary if the clinical diagnosis is already obvious unless you need to determine severity.

RESPIRATORY FAILURE - Outline the treatment for acute ventilatory failure.

ACUTELY Prompt diagnosis and management of the underlying cause of respiratory failure is vital. Type 1:40 to 60% oxygen will relieve hypoxia acutely. Mechanical ventilation may be required and if oxygen is given for more than a few hours it needs to be humidified. Type II: acutely this is an emergency remove any obstruction, Treat any respiratory distress, relieve any tension pneumothorax, controlled oxygen delivery For exacerbations of COPD and in severe cases intubation. Non-invasive ventilation via bipap is possible. In acute asthma argues nebulae salbutamol with oxygen. Blood gases are indicated in all situations to determine the pH etc. Aim for 88 to 92% saturation and regularly monitor. Patients with acute type to respiratory failure may begin to lose consciousness because of carbon dioxide narcosis. This may be due to CNS depressing drugs for which they could be antidotes (Naloxone). ................................... CHRONICALLY Here the most common cause is COPD and metabolic compensation is usually complete. Again and aim for lower oxygen saturations is to avoid depressing the respiratory drive.(Severe hypoxia can cause fatal arrhythmias and Sarid will complications). Assessed for an acute on chronic picture with an ABG. Patients may benefit from at home non-invasive ventilation and eventually lung transplantation. A single lung may be appropriate except in cystic fibrosis or chronic bilateral infection where infection will spread. Transplantation gives a 50% ten-year survival but patients will require lifelong immunosuppression.

BASE OF SKULL FRACTURE - Describe the clinical signs present in a fracture of the base of the skull List the complications of a fracture of the base of the skull

Also called a basillar skull fracture, This usually involves the temporal, occipital, sphenoid and/or ethmoid Bones. Is a rare but serious fracture as it can tear the meninges resulting in CSF rhinorhorhoea/otorhoea and possible Secondary infection. Presentation: usually after a traumatic incident, with a headache, CSF rhinorrhoea/otorhoea, haemotympanum and Possible cranial nerve palsys (Facial nerve, oculomotor, vestibulocochlear). After about one day a battle sign (Bruising over the mastoid) and raccoon eyes (Periorbital ecchimosis) may appear. Management: antibiotics are required to prevent Meningitis. Fortunately, undisplaced fractures tend to heal quite well. Acute injury to the internal carotid artery can cause Life-threatening bleeding. Possible surgical interventions are to stop persistent cerebrospinal fluid leak or to surgically correct a significantly depressed bacilar skull fracture.

GALLBLADDER DISEASE - List the common types of gallstones and describe their pathophysiology Describe the natural history of asymptomatic gallstones. List the common tests used in the diagnosis of gallstones. Discuss the management of gallbladder disease. List the complications of gallstones and describe the history, physical examination and laboratory findings for each (see also OBSTRUCTIVE JAUNDICE)

Also called a cholelith, stones are made up of cholesterol or pigment (bilirubin breakdown products) or a mixture. Pure pigment stones are rare and seen in haemolytic anaemia, most stones (75%) are predominantly cholesterol. This means that 90% of gallstones do not show up on a plain x-ray (unlike kidney stones which are predominantly calcium). Risk factors: fair, fat, female, 40 and fertile (premenopausal). Presentation: most gallstones are asymptomatic found incidentally. They only present if complications occur. Complications: chronic cholecystitis (inflammation of the gallbladder), biliary colic (constant, not colicky pain as the gallbladder contracts against a stone), acute cholecystitis (inflammation of the gallbladder which may also give an empyema, peritonitis by an abscess), mucocoele, gallbladder cancer, obstructive jaundice, cholangitis (inflammation of the biliary tract), acute pancreatitis or a gallstone ileus. Examination: is dependent upon the complications. For example obstruction causes jaundice, colicystitis causes pain, mucocoele causes a mass. Remember that painless jaundice and a palpable gallbladder are unlikely to be gallstones as chronic gallstones cause fibrosis of the gallbladder mean it cannot distend. Laboratory findings: jaundice rises bilirubin, inflammation rises CRP/ESR, Ultrasound identifies stones and may show a fistula as with gallstone ileus. Management: if asymptomatic this requires no treatment. If not, laparoscopic cholecystotomy is indicated using carbon dioxide distension of the peritoneal cavity and removal of the gallbladder through an incision at the umbilicus. Previous surgery/adhesions are a relative contraindication, suspected cancer and bleeding disorders/portal hypertension are indications for open cholecystotomy.

PERIANAL INFECCTION - Define fistula in ano. Outline the principles of management of patients with perianal infections including management of fistula in ano.

An abnormal connection opening internally to the anal canal and externally to the skin. Typically starting as a perianal abscess or because of Crohn's disease/carcinoma/radiotherapy/TB they are classified as low (not crossing the sphincter muscles above the dentate line) or high (crossing the sphincter muscles above the dentate line) Presentation: pain, bloody or purulent discharge and itching. Management: low fistulates can be treated by being laid open so that the wound can heal from the depths of upwards and not form an abscess. Doing this with high fistulates would damage the sphincters so a seaton is inserted - as the Reds through the fistulates track which is gradually tightened allowing the fistula to slowly heal behind it. Goodsalls rule states that this still anterior to the anus have an opening in a straight line, those posterior have curving tract opening in the midline posteriorly.

KIDNEYS AKI - Describe the clinical features of ARF and the concept and causes of Acute Kidney Injury (AKI) leading to ARF

An abrupt and sustained decrease in kidney function.... Compared to a baseline STAGE ONE is 1.5 to 2 times creatinine increase, STAGE TWO is 2 to 3fold and STAGE THREE is greater than 3fold increase in creatinine. Also considered is the degree of oligurea (<0.5ml/kg/hr for six, twelve or greater hours). Features of the underlying cause will of course be present (hyovolaemia, shock, hypotension, poor perfusion of other organs). As urea accumulates the patient gets nausea, vomiting, fatigue, headaches and loss of appetite. As potassium increases there can be arrhythmias. Fluid retention can cause hypertension but hypotension is an AKI cause. See above for causes.

NEUROMUSCULAR JUNCTION DISORDERS - Describe the clinical presentation of myasthenia gravis and outline the immunological basis of disease

An acquired autoimmune condition in which antibodies are directed against ACh receptors. The result is a weakness and fatigue ability of skeletal muscle groups particularly in the proximal limbs, ocular muscles and bulbar (throat) muscles. There is often associated with thymic hyperplasia or a thymoma. Typical patients are either young women with an acute, severely fluctuating condition HLA associated. Or, older man with an occulobulbar presentation. Symptoms/signs: ptosis, Ophthalmoplegia, weakening of movements if repetitive, Weakening of the face and jaw, dysarthria, dysphonia, dysphagia and possibly, shortness of breath. Investigations: giving a fast acting anticholinesterase allows more ACh to be active in the cleft and will provide a couple of minutes of relief from symptoms. ACh receptor antibodies are present in the serum for 80% of patients. Electromyography will confirm progressive fatigue. As there may be a thymoma, CT or MRI of the chest is required so that abnormalities can be exercised. Remember to perform spirometry because a patient's respiratory muscles may become fatigued. Management: education so that acute worsening of the disease causing respiratory involvement is identified early. It is possible for patients to have permanent remission, treatments available for those not in remission include: thymectomy, oral anticholinesterases (.... Stigmine) and immunosuppression with corticosteroids (start low end go slow, prefer be in hospital as symptoms temporarily worsen). For serious cases plasmapheresis or intravenous immunoglobulin may be required to stop the respiratory depression and azathioprine/Methotrexate/cyclosporine may be used to immunosupress.

ASTHMA - Describe the morphology and pathological consequences of asthma.

An acute attack can cause significant disress and may ause death. More chronically, if poorly controlled, airway remodelling will occur causing fibrosis and fixed narrowing of the bronchioles and a COPD picture. Remember that asthma medications also cause adverse effects.

CYSTIC FIBROSIS - Describe pathological changes in the lungs and the natural history of disease in a typical patient

An autosomal recessive disease with a carrier rate of 1 in 25, with an incidence of 1 inn 2500. A mutation (commonly F508) of a gene on chromosome seven coding for CF transmembrane conductance regulator that allows chlorine to freely flow across a cell membrane. In CF the channel is broken so chloride cannot be pumped out of cells (into the airways). Low chloride in the airways is associated with low water leading to a mucus heavy state that destroys the lungs eventually giving bronchiectasis via prolonged ciliary dysfunction. Sweat has more salt than normal hence the sweat test. Most present at birth with a positive heel prick detecting immunoreactive trypsin. Prior to this test presentation was with bowel obstruction, steatorrhoea and respiratory symptoms. Genetic testing is available but there are thousands of associated mutations. Upper lobes are affected before lower lobes. Life expectancy is currently 41years with aggressive use of antibiotics and nutritional support. Death is usually by respiratory failure secondary to bronchiectasis.

CYSTIC FIBROSIS - Describe the clinical presentation of a patient with cystic fibrosis with respect to disease of the lung and pancreas; and describe its inheritance

An autosomal recessive disease with a carrier rate of 1 in 25, with an incidence of 1 inn 2500. A mutation (commonly F508) of a gene on chromosome seven coding for CF transmembrane conductance regulator that allows chlorine to freely flow across a cell membrane. In CF the channel is broken so chloride cannot be pumped out of cells (into the airways). Low chloride in the airways is associated with low water leading to a mucus heavy state. LUNG - Bronchiolar inflammation and infections turn initially healthy lungs into bronchectatic. Phlegm production is excessive and exercise tolerance is decreased. Haemoptysis, pulmonary hypertension and bheart failure can occur. PANCREAS - Presentation may be with a muconium ileus (failure to pass muconium as it is thickened and congested). Pancreatic secretions are excessivly thick and cause poor digestion of food, bowel obstruction and malnutrition. Pancreatic ducts can be completely blocked causing pancreaic fibrosis therefore insufficiency and diabetes.

NEUROLOGY - Assess a patient's level of consciousness using Glasgow Coma Scale

An objective measure of a person's conscious state using the following three headings: Eyes: Maximum score four. One equals no movement, two equals movement pain, three equals movement to voice, for equals spontaneous movement. Speech: Maximum score 5. One equals no speech, two equals Incomprehensible sounds, three equals inappropriate words, for equals disorientated, five equals normal speech. Motor: Maximum score 6. One equals no movement, to equals extension to pain, three equals flexion to pain, four equals flexion and withdrawal from pain, five equals localises pain, six equals obeys commands. The lowest possible score is three, the highest 15.

PNEUMOTHORAX - Distinguish between simple and tension Pneumothorax including features that aid in recognition of critically ill patients presenting with a tension Pneumothorax

An open pneumothorax still communicates with the airway Such as fistula which can facilitate the transmission of infection (examples include rupture of an emphysematous bulla). A close pneumothorax is when the pleural space seals off and doesn't reopen - Air will eventually reabsorb and the long will re-expand. These are both examples of a simple pneumothorax. A tension pneumothorax is when the pleural space acts as a one-way valve allowing air to enter but not escape. Large amounts of air rapidly accumulate crushing the lung, deviating the trachea, impairing venous return and causing cardiovascular compromise.

VENOUS SINUS THROMBOSIS - List the risk factors for the development of venous sinus thromboses Outline the clinical presentation of venous sinus thrombosis and how it differs from the presentation of arterial stroke

An unusual type of stroke whereby of thrombus blocks off a part of the venous sinuses. The presentation is typically with a few days history of worsening headache, some patients may develop/symptoms (motor deficits, speech and language difficulties). 40% of patients develop seizures. There may be raised intracranial pressure causing papilloedema and visual disturbances. Considering the difference between this and an arterial stroke, Venus blockage is a slower process Allowing for collaterals to be used and is far less likely to stick to common territories (Affecting only one side of the body is therefore less common). Risk factors for venous sinus thrombosis: Thrombophilia (patients more likely to clot because of the protein C/S or antithrombin deficiency), Nephrotic syndrome (thickens blood), dehydration, Inflammatory diseases, pregnancy, oestrogen containing medications, Meningitis and sickle cell anaemia. Essentially this translates to anything that thickens the blood aures procoagulant causing an increase risk of venous sinus thrombosis. Confirm the diagnosis with CT/MRI and give anticoagulation (Warfarin or heparin). Venous sinus thrombosis can cause raised intracranial pressure which may need surgical decompression.

PREOPERATIVE ASSESSMENT - Discuss the principles of general, regional and local anaesthesia. Describe the common and major risks associated with general and spinal anaesthesia

Anesthesia is a temporary state in which one or more of the following: unconciousness, analgesia, paralysis or amnesia. General: An infusion or gaseous drug to induce paralysis, unconciousness and blunting of the stress response (avoiding extremes of blood pressure/pulse etc.) Examples include sevoflurane gas throughout the procedure with propofol to induce fentanyl to blunt the stress response and midazolam for amnesia. High ASA patients have a greater risk of death, coma, heart attack. They may revert into atrial fibrilation. Common side effects include nausea and vomiting (ondansetron, dexamethasone and droperidol). Sedation: Used in combination with analgesia, these cause sleepiness, amnesia and muscle relaxation. Examples include benzos, propofol and ketamine. Regional: Blocking pain to a specific body part - centrally ((epidural/spinal) or peripherally. Local: Infiltrative is when local is injected at a certain site. When injected around a nerve this is a nerve block. SPINAL:Central injection of a local anaesthetic into the subarachnoid space also causing loss of muscle control (epidural = outside the dura, needing larger doses but does not affect muscle control). Central neuraxial blockade causes vasodilation so blood pressure can drop significantly. Blocks may be ineffective due to inadequate anxiolysis or sedation instead of an inadequate block itself. Risks of a spinal include: post spinal headache, cauda equina damage, spinal haematoma, epidural abscess and heart attack. Hypotension may be severe enough to cause spinal shock.

HERNIA - Discuss the incidence of incisional hernia according to risk factors of patient comorbidity and previous surgery. Describe the symptoms of patients with incisional hernia. Describe the potential complications of incisional hernia including bowel obstruction and strangulation. Perform a physical examination of patients with incisional hernia and assess the risk of obstruction or strangulation. Outline the risk factors for recurrence after repair, including the size of the defect, obesity and chronic cough.

Incidence: it is estimated that 12 - 15% of abdominal surgeries result in incisional hernias.this is a hernia which protrudes through a faschial defect created surgically. The most common incision is midline abdominal and large. Causative factors:raised intra-abdominal pressure, surgical technique (length, location, direction), weakened abdominal wall. Therefore obesity, chronic coughs, constipation, urinary obstruction (prostatsm), pregnancy or ascites or increase the risk of developing an incisional hernia. Presentation: a bulge near an area of surgical incision. Complications: as previously described, obstruction and strangulation presenting with acute pain, redness and distention associated with constipation or blood per rectum and possible vomiting. Management: open repair is difficult because the abdominal wall is already weak and prone to infection. Surgical repair often involves insertion of a mesh (prone to infection again and linked to increased post-operative pain). reported recurrence rates up to 20%. Laparoscopic repair and mesh insertion is therefore favoured. Remember that the original wound is never reincised. in high-risk patients even large incisional hernia is managed conservatively with an elastic support corset as repair is difficult without causing further attention.

THE SPLEEN - Outline the haematological abnormalities correctable by splenectomy. Discuss the potential adverse consequences associated with splenectomy and recommendations for preventing overwhelming post-splenectomy sepsis

Indications for a splenectomy: gross splenomegaly,lymphoma, wandering spleen (weekend splenic ligaments), autoimmune conditions (Immune thrombocytopaenia), trauma, spontaneous rupture, haemolytic anaemia, malignancy, to harvest the splenic artery for renal revascularisation. Remember also leukaemia is and lymphomas. Haematological abnormalities correctable by splenectomy: chronic idiopathic thrombocytopenic purpura (low platelets and the purpurate rash), polycythaemia vera (neoplastic excessive red blood cell production in the bone marrow resulting in thick blood and symptoms such as itching and gouty arthritis), thalassaemia (this often has associated splenomegaly which worsens the anaemia) and sickle cell disease (splenic crisis). Adverse complications of splenectomy: without the spleen patients are more prone to infection by encapsulated organisms such as strep pneumoniae and H influenzae. these organisms would ordinarily just cause pharyngitis but in patients without spleens the infection is more severe. after splenectomy the white blood cell and platelet levels rise making a blood clot more likely. Oddly, there also seems to be an increased rate of diabetes and ischaemic heart disease. Protection of patients postsplenectomy: pneumococcal vaccine, meningococcal vaccine

IMAGING CT and MRI - Outline clinical situations where a CT scan of the head is indicated Explain how the results of a CT scan of the head would influence the management of an acute stroke Explain the advantages of MRI over CT scan of the head List the important contra-indications to an MRI scan

Indications: In trauma when GCS <13, more than one episode of vomiting, a focal neurological deficit, posttraumatic seizures or evidence of a skull fracture. Any head trauma to a Warfarin patient regardless of clinical features. Signs/symptoms of a stroke whereby a haemorrhage must be excluded in order to permit thrombolysis. Also CT any ? subarachnoid haemorrhage. Other indications include: space occupying lesions, hydrocephalus, Intracranial infection, Sinus pathologies etc. Implications: CT head does not necessarily confirm an ischaemic stroke, but can exclude a bleed that would be a contraindication to thrombolysis. Advantages: CT is far superior to the MRI in determining trauma, but MRI Is better at viewing the posterior fossa, parasellar Region and for conditions such as multiple sclerosis, epilepsy and tumours. Contraindications to MRI: Metal implants such as cochlear implants and pacemakers. Acute situations whereby patients cannot feasibly be maintained stable throughout the procedure. A relative contraindication is movement such as in Parkinson's which will ruin the image and claustrophobia if severe.

TRAUMA - Describe the main causes, pathophysiological mechanisms and effects of increased intracranial pressure.

Intracranial pressure is said to be raised over 20 mmHg. The Monro Kelly hypothesis suggests that blood, cerebrospinal fluid and brain tissue reach a volume equilibrium so that an increase in one will be balanced by a decrease in one or more of the other. Cause: consider the following categories: Mass effect, decreased venous return, generalised swelling, cerebrospinal fluid obstruction. Examples include: venous sinus thrombosis, ruptured aneurysm, encephalitis, traumatic haematoma, cerebral oedema, STATus epilepticus, brain bleeds, stroke, meningitis etc. Pathophysiology: the vertebral canal, cranium and relatively inelastic dura form a fixed volume space. this means that once CSS has been displaced into the spinal canal and the falx/tentorium has stretched as much as possible then small increases in brain volume lead to marked rises in intracranial pressure. Midline shift can lead to compression that results in hydrencephalus. Brainstem compression can suppress the respiratory drive causing death by coning. Effect: injury occurs both at the primary time of injury and also secondary to ischaemia. Patients initially present with nausea, vomiting,Headache and ocular policies. pupils may become violated and Cushing's Triad of bradycardia, increased systolic blood pressure and a widened pulse pressure may occur. respiration will become altered's and cerebral infarcts can result in coma and death.

PNEUMONIA - Describe the investigation of a patient presenting with a community acquired pneumonia and interpret investigations List the common pathogens causing community-acquired and hospital-acquired pneumonia and outline predisposing factors

Investigations: FBC (WBCs may be either extreme, haemolytic anaemia if mycoplasma), U&E (urea raised), LFTs (lower lobe pneumonia can irritate the liver), ESR?CRP, blood culture, lycoplasma/legionella/chlamydia serology, ABG if severely unwel. Think septic six if appropriate. Urinary antigens for legionella/pneumococcal, sputum for gram stain and culture, chest Xray and a pleural fluid aspirate if present. Common pathogens in CAP: Most commonly strep pneumoniae (causes rust coloured sputum), mycoplasma pneumoniae (in the young), legionella, chlamydia pneumonaie, haemophylis influenze, staph aureus (post flu). Note also viruses (influenza, measles, herpes, varicella). Common pathogens in HAP: seen in the immuno-compromised and immobile 48 hours after admission. Gives higher rates of staph aureus, MRSA, as well as gram negatives escerischia, pseudomonas, klebsiella. Pneumonia DDX: Pulmonary infarction, pulmonary TB, pulmonary oedema, malignancy. Risk factors: Smoking, URTI, alcohol, steroid use, old age, recent flu, HIV, preexisting lung disease, air pollution.

DIABETES VASCULAR COMPLICATIONS - Discuss the macrovascular complications of diabetes; compare and contrast the distribution and severity of macrovascular disease in patients with and without diabetes (see also the section on Vascular Medicine and Surgery). Discuss additional cardiovascular risk factors in diabetic patients and outline their assessment and management.

Ishaemic heart disease is the most common cause of death in diabetics. (there may be glycosylation of the cardiac muscle causing IHD) Hyperglycaemia over decades causes damage to large blood vessels by thickening their membranes and narrowing their lumens. Remember the ateroma process (from fatty streak to a growing plaque that enlarges and can ulcerate causing thrombus or embolism). This increases the risk of cardiovascular disease, stroke and peripheral vascular disease. The result is a significantly increased risk of heart attacks, strokes and amputations. It is therefore much more important to control blood pressure, cholesterol, (vascular risk factors are magnified by diabetes) maintain a healthy diet and exercise alongside avoiding hypoglycaemia.

OCCUPATIONAL LUNG DISEASE - Discuss the effect of inhalation of coal dust on lung function and its relation to pneumoconiosis. Describe the pathology of simple and complicated coal workers pneumoconiosis. Demonstrate awareness that patients exposed to coal and asbestos can obtain industrial compensation

Any permanent alteration of lung structure due to inhalation of mineral dust and the reactions of the tissues to it's presence. Examples include: coal workers pneumoconiosis, silicosis (silicone in stone/metal workers), asbestosis, siderosis (iron), stannosis (tin), berylliosis (from beryllium). COAL WORKERS PNEUMOCONIOSIS: Long term acccumulation of coal dust in the lungs leads to aggregates of coal containing macrophages forming macules. The result is a fibrotic reaction at the site of macules so the patient has multiple scattered discrete fibrotic lesions. >Simple CWP is Xray nodules without symptoms - it seldom progresses if exposure isn't persistant. >Progressive massive fibrosis is the formation of large masses associated with cough, black sputum (melanoptysis) and breathlessness. Often the Xray looks like lung cancer. Can progress to respiratory failure. The workers compensation act 1979 means that employment induced pneumoconiosis causng disability. A sum can also be claimed by a dependent following the death of a sufferer.

MISCELLANEOUS HAEMATOLOGY - Outline the clinical features of aplastic anaemia and describe the laboratory diagnosis and principles of treatment.

Aplastic anaemia is a rare stem cell disorder leading to pancytopenia and hypoplastic bone marrow whereby the bone marrow stops making cells. Cause: autoimmune, drug/virus/irradiation induced or inherited such as Fanconi anaemia. Laboratory: anaemia, infection with low white blood cell counts and low platelets (exactly what you would expect if the bone marrow stopped working). Management: support the blood count with a red blood cell transfusion, platelet transfusion. Consider immunosuppression with cyclosporine although this tends to be only a temporary solution. Young patients may be cured with allergenic bone marrow transplant.

EMERGENCY MEDICINE - Describe the immediate assessment and management of acute presentations of Anaphylaxis

Approach with an ABCDE algorithm. Stop the offending medication/sedating agent/food if possible if possible. Remember that anaphylaxis is most likely when the three criteria are met: 1. sudden onset, rapid progression 2. life-threatening airway, breathing or circulation problems. 3. Skin or mucosal symptoms (flushing, urticarious, angioedema). Unlike in cardiac arrest when the adrenaline dosing is one in 10,000 1mg (or 10ml) IV, anaphylaxis requires one in 1000 1 mg (or 1 mL) intramuscular administration.

Spirometry explained? Asthma diagnosis?

Approach: Look first at FEV1/FVC. If <70% there is an obstructive component. The FEV1 predicted - 50-80 is mild, 30-50 is moderate, <30 is severe obstruction. Then FVC predicted % - if >80% there is no restriction, if <80% there is restriction. Peak flow measured in the morning and evening show a >20% diurnal variation in asthma. Spirometry indicates a reversible airway obstruction. Spirometry graphs show the tidal volume, total lung capacity, reserve volumes, functional residual capacity etc Spirometry loops read from right to left show expiration then inspiration at a flow volume. An obstructive picture has a normal volume but flow is reduced and never reaches maximum so FEV1/FVC is less than 70% predicted because there is a lowered FEV1 dispite a normal FVC. Think COPD/asthma. A restrictive pattern has a lower volume with the curve starting further left but flow is normal. So FVX and FEV1 aare lowered but equally giving near 100% FEV1/FVC. Think lung fibrosis, flail chest, MSK weakness. For lung volumes use heluim dilution or nitrogen washout (by inhailing 100% oxygen).

ACUTE CORONARY DISEASE - Describe the complications of AMI and describe their presentation:

Arrhythmias: often these are only transient and have no clinical significance corrected by pain relief, rest, treatment of electrolyte imbalance. However, ventricular fibrillation is the major cause of death in heart attacks and requires defibrillation. Atrial fibrillation is common but often transienct but if it causes low blood pressure or circulatory collapse then shock. Ischaemia: this is treated with PCI or CABG. Post in Fat angina can occur and many patients have stenosis of the infarct-related vessel. Acute circulatory failure: scene with an extensive STEMI. Pericarditis: pain at the same site that is positional and worse on inspiration. There may be a pericardial Rob and NSAIDs are needed. Remember post-myocardial infarction syndrome (Dressler's) is characterised by fever, pericarditis and pleurisy - probably due to an autoimmune problem, requiring NSAIDs or steroids. Rupture of papillary muscles. This causes acute pulmonary oedema and shock due to the sudden onset mitral regurgitation. Rupture of the interventions in the septum: causing a right-to-left shunt. Rupture of the ventricle: leading to cardiac camp in it which is usually fatal. Embolism. Remodelling of the ventricle is: the infarcted segment usually bins and stretches causing progressive dilation and hypertrophy of the remaining ventricle. The heart becomes less efficient and heart failure in stews. ACE inhibitor can reduce remodelling and prevent the onset of heart failure. Aneurysms can occur (which can cause heart failure, arrhythmias, thrombus and embolisation).

BRONCHIECTASIS - Outline the investigations of a patient with suspected bronchiectasis and discuss treatment with postural drainage and physiotherapy and antibiotics for infective exacerbation

As infections and resistant organisms are common sputum cultures should be frequent. Chest Xray only helps if disease is severe (you may see tram tracking where there is thickening along bronchioles) but CT will show thickened dilated airways, cystic bronchiectatic spaces and consolidation or collapse (honeycombing of large airways and thickened bronchioles). Xray is often persormed because an acute presentation is often mistaken for pneumonia. Cilliary dysfunction can be identified with a saccharin pellet - timing the time taken for a pellet to be moved from the anterior nose to the pharynx where it is tasted. A normal person takes <20minutes. Nasal biopsies also identify cilliary dysmotility and structural abnormalities by electron microscopy. TREATMENT: Inhaled bronchodilators, twice 5-10mins daily physio to assist secretion drainage (lie in a position where the lobe to be drained is uppermost, deep breathing with forced expiration then vigorous coughing), prophylactic and acute antibiotics (large doses, long courses). Bronchiectatic areas are occasionally removed if focal and severe aacute exacerbations with haemoptysis that persists may need percutaineous embolisation. Smoking cessation is vital. PREVENTION: Adequate prophylaxis and treatment of TB, measles/pertussus pnumonia. Vaccinations need to be up to date (pneumococcal and seasonal flu).

KIDNEYS AKI - Discuss the associated electrolyte abnormalities and describe the management of life threatening hyperkalaemia.

As it is the kidneys role to remove potassium in AKI hyperkalaemia (normal K is 3.-5mmol/l) can occur causing arhythmias and tented T waves. A metabolic acidosis often results - so te patient hyperventilates to compensate. Remember that pseudohyperkalaemia may be due to haemolysis (such as rough venepuncture and syringing through a fine needle into blood bottles). Protect the heart with 10ml calcium gluconate. Move potassium into the cells with 10units IV insulin (with dextrose to prevent a hypo) and 10mg nebulised salbutamol. This buys time to correct the cause by treating it and encouraging urine production (fluids in, diuretics). If this is not possible dialysis may need to be planned.

OPERATIVE AND POSTOPERATIVE MANAGEMENT - Demonstrate an understanding of a surgical procedure by being able to describe the following: > preoperative and postoperative diagnosis > important anatomical and physiological observations about the patient > operative procedure performed and incision used type and method of anaesthetic used and any anaesthetic sequelae > estimated blood loss and type and amount of fluid given during the procedure. > results of any intra-operative examinations or tests (eg, operative cholangiogram, portal venous pressure) > complications or unusual events > tubes, drains, prosthetic material used and relevant information about these devices > disposition and condition of the patient at the end of surgery

As procedures may be diagnostic or change based on findings the pre and post op diagnosis may differ. Obs:HR = 60-100, RR = 12-20, Temp = 37, BP <140/90 Classic incisions include: HEAD/NECK: Wilde's incision (behind the ear to drain the mastoids). EYE: Keratotomy (through cornea). CHEST: sternotomy (over sternum), thoracotomy (between the ribs). ABDO/PELVIS: Laparotomy (midline incision), pfannenstein (bakini line for C section/gynae), chevron inscision (upsidedown V below the midline), kocher/subcostal (for gallbladder/biliary tract/spleen), if bilateral kocher is a chevron (for liver, gastric, stomach, kidneys), Mercedes extends a chevron. Also note McBurneys for appendectomy (this is diagonal, Lanz is transverse) Blood loss - weighing is ideal, measuring losses in containers and knowing how much blood will soak each sponge/gauze/swab. Also consider the patients clinical picture. Complications are variable, remember A to E. Types of drain: JAXON PRATT - negative pressure drain. BLAKE - negative pressure drain. PENROSE - A soft rubber tube. PIGTAIL - Curved end with multiple draining holes. DAVOL - Suction balloon drain. Remember that surgery induces eb and flow stages. Initially in the eb phase the patient is shocked, hypothermic and cold. The flow stage is at first catabolic (negative nitrogen balance with proteins broken down) then anabolic (positive nitrogen balance, weight gain).

OCCUPATIONAL LUNG DISEASE - Describe the clinical features of the main conditions associated with asbestos inhalation. Describe the natural history of pleural plaques, mesothelioma and asbestosis

Asbestos are naturally occuring salicylate fibres (most commonly white asbestos - chrysotile) that are fantastic at thermal and chemical insulation so were used extensively in the 20th century as the pleural and pulmonary disease were unknown. PLEURAL PLAQUES: These are the most common asbestos exposure manifestation but fortunately are usually asymptomatic. Fibrosis of focal areas of parietal pleura occurs and may be seen calcified on chest Xray. PLEURISY: An episodic condition. May or may not be symptomatic with mild fever and pleuritic chest pain as the pleura are inflamed. Repeated episoded of pleuriy can cause diffuse pleural thickening. DIFFUSE PLEURAL THICKENING: Scarring of the lung with thickening of the visceral pleura. Costophrenic angles are lost on Xray but a biopsy may be needed to exclude mesothelioma. This is irreversible causing breathlessness, chest pain and a restrictive picture. ASBESTOSIS: Chronic inflammatory and fibrotic parenchymal lung disease after substantial asbestos exposure (with retention of fibres causing lung scarring). Giving exertional breathlessness and the classic end expiratory crackles of fibrosis as well as finger clubbing. MESOTHELIOMA: A malignant tumor of pleura many years after asbestos exposure. Presenting with increasing breathlessness, pleural effusion, unremitting chest pain, and possible metastatic disease. It is almost always fatal and few patients are suitable for radical resection. Chemo, radio, pleurodesis/pleural effusion draining are used with analgesia too palliate.

THE PLATELET - Describe the mechanism of action of aspirin and outline its role in cardiovascular disease prevention

Aspirin alters the balance between thromboxane A2 which promotes platelet aggregation and prostaglandin2 which inhibits it. It is a cyclo-oxygenase inhibitor that reduces both thromboxane on the platelets and prostaglandin in the endothelium. Because the endothelial cells have nuclei they can synthesise new prostaglandin by regenerating cyclo-oxygenase and are relatively unaffected. Where is the platelets cannot replace the inhibited cyclo-oxygenase and therefore thromboxane is markedly reduced preventing its prothrombotic state. platelet recovery will occur in 7 to 10 days so low doses of aspirin given every one - two days will decrease thromboxane without drastically reducing prostaglandin production. Remember the adverse effects on the gastrointestinal tract (Cyclo-oxygenase one inhibition).

GALLBLADDER DISEASE - Describe the symptoms and signs of biliary colic and contrast with acute cholecystitis.

Biliary colic: the pain caused by a gallbladder contracting against a stone stuck in Hartman's pouch or the cystic duct. Is not colicky, but continuous making the patient ride around in pain. It is in the epigastrium or right upper quadrant and can radiate around the costal margins to the back. Patients can be pale, sweaty and tachycardic with vomiting. An attack lasts less than six hours but important differentials include a perforated ulcer, pancreatis or a ruptured aneurysm. managed biliary colic with Analgesia, Ultrasound to confirm gallstones and elective cholecystotomy. Acute cholecystitis: inflammation of the gallbladder which may begin with biliary colic but progresses because of the chemical inflammation behind the obstruction. Often bacterial infection occurs giving severe right upper quadrant or epigastric pain radiating around the costal margins to the back. Unlike biliary colic, patients lie still because of the peritonitis. they have temperature, tachycardic, Murphys sign and a possible mass due to adherent onemtum (phlegmon). Manage with resuscitation, fluids and antibiotics. Keep the patient nil by mouth and consider important differentials such as pancreatis (amylase). Ultrasound confirms gallstones and a thick oedematous gallbladder which needs treating with Analgesia and fluids. If severe, treat sepsis and remove the gallbladder.

THE BLADDER AND PROSTATE - Discuss the management of trauma to the bladder (both accidental and surgical). Describe the diagnosis and management of bladder calculi.

Bladder trauma: most bladder trauma is because of blunt injury especially in road traffic collisions. Pelvic fractures are heavily associated with bladder injury and the bladder can even be ruptured (intraperitoneal or extraperitoneal - a full bladder is much more likely to be damaged). Iatrogenic bladder trauma typically occurs during obstetric or gynaecological investigations (may also occur in urological or general surgeries). Bladder trauma presents with a history of trauma or surgery, haematuria (gross), abdominal pain and possible suprapubic bruising and voiding problems. Cystoscopy is indicated in almost all cases and management is often is surgical ensuring that any extraperitoneal leakage from rupture is drained. Bladder stones: these may be formed from many different metabolites (calcium, magnesium, ammonium, urate) and so may or may not appear on x-ray. Most stones occur because of dehydration so patients may be showing signs of this as well as abdominal or back pain, urinary frequency, fever and dysuria (remember many stones can be asymptomatic). As with renal stones the pain is colicky (coming in waves) and associated with nausea vomiting and chills. Risk factors for the formation of bladder stones include: dehydration, prostatic enlargement, neurological problems (and anything else that facilitates the stasis of urine), anything that causes inflammation (catheter use). Diagnosis: with ultrasound or intravenous pylogram. Treatment: prevent further stones with good hydration, increase fluid intake to facilitate the passage of small stones, ultrasound or laser fragmentation during cystoscopy or open removal of large stones through an incision.

ANAEMIA - Describe the pathophysiology and diagnosis of B12/folate deficiency causing a macrocytic anaemia

Both B12 and folate deficiency cause a macrocytic anaemia. VITAMIN B12: cause: low dietary intake in vegans, impaired binding (pernicious anaemia, stomach removal, congenital deficiency of intrinsic factor), ileal disease, congenital transcobalam deficiency or nitrous oxide (which inactivates B12). Pathophysiology: without B12 you cannot synthesise DNA. Diagnosis:Macrocytic anaemia with megaloblasts in the bone marrow, low B12 levels. The deoxyuridine supression test is performed on the patient's bone marrow in vitro - add thymidine to the bone marrow, if B12 corrects the abnormality then B12 deficiency is the cause. FOLATE: cause: poor dietary intake (few vegetables, starvation or alcoholism), poor intake in anorexia/Crohn's disease/coeliac's/gastrectomy, anti-folate drugs (methotrexate), excess use (pregnancy and lactation), immoral assists, malignant disease, malabsorption in the jejunum. Pathophysiology: without folate you cannot synthesise DNA. Diagnosis: Microsoft can anaemia with megaloblasts the bone marrow, low serum folate. The deoxyuridine suppression test is performed on the patient's bone marrow in vitro - as thymidine to the bone marrow, if folate correct the abnormality then the problem is either folate or B12 deficiency.

BREAST CYST (Identify and describe the major types of breast lump (fibroadenoma, fibroadenosis, cyst, carcinoma). Outline the natural history of benign and malignant breast neoplasms. Present a classification of the main types of carcinoma of the breast.) Describe the principles of management of a breast cyst.

Breast cysts are benign fluid filled sacs palpable as round or oval lumps with distinct edges. They are more common in premenopausal women in their 30s-40s and can cause pain (that may be cyclical and associated with a fluctuation in lump size). They are likely to regress, especially postmenopausally. After diagnosis is confirmed by ultrasound and aspiration, treatment is unnecessary unless symptomatic. Treatment for painful lumps is aspiration (although they often reccur) or excision.

Describe the diagnosis of a breast lump and the concept of triple assessment - including mammography, ultrasound and cytology/biopsy (core and open).

Breast lumps present with symptoms (lump, bloody nipple discharge, pain) or on routine screening (3yearly for 50-70year olds). Investigations for carcinoma include: full clinical examination, mammography (if older as the breast is less fibrous and more fatty), ultrasound (younger patients have less fat), biopsy (fine needle aspirate for cytology or core biopsy for histology). Histology can be used to assess whether the tumor has oestrogen and progesterone receptors and its HER2 status. If metastasis are suspected then CT the thorax. Remember that triple assessment = clinical examination, mammography and biopsy.

ASTHMA - Define the classical features of asthma and outline common precipitants.

Bronchial asthma (not cardiac where wheezing is due to heart failure). Recurrent wheezy episodes of chest tightness, breathlessness and cough commonly mistaken for a chest infection. Cough variant asthma may present with only a cough - particularly nocturnal. There will be an early morning worsening of symptoms corresponding to an early morning dip in peak flow. Precipitants: exercise (particularly in cold weather), allergens, pollutants, viral URTIs. Beta blockers (even as eye drops), asprin, alcohol (contains salicylates), NSAIDs or other drugs can trigger symptoms. Remember samters triad: Asthma, asprin insensitivity and nasel polyps. A rare differential of asthma is churg straus (vasculitis).

LUNG CANCER - Outline the treatment options for a patient with confirmed lung cancer.

Bronchial carcinoma - Surgical resection carries the best survival chance if not radical radio and chemo. Unfortunately >75% of bronchial cancers are not appropriate for curative treatment due to stage or co-morbidities therefore palliation and best supportive care is appropriate (Eg radio for vena cava obstrution, haemoptysis, pain. Lasering or stenting bronchial obstruction). Chemotherapy for small cell carcinoma can help to prevent metastasis which are common. Chemo is pretty useless for non small cell. Remember 5HT antagonists to treat the nausea and vomiting. Treat any malignant pleural effusion with drainage. If recurrence a talc pleurodesis will treat. BRONCHIAL CARCINOMA HAS A 30% SURVIVAL RATE. MEDIASTEINAL masses need surgical excision as they always cause early symptoms.

BRONCHIECTASIS - Describe the typical history of a patient with bronchiectasis and describe how it differs from COPD

Bronchiectasis is when there is abnormal dilatation of the bronchi resulting in chronic suppurative airway infection. Causes: Cystic fibrosis or non cystic fibrosis (idiopathc, reccurrent infections, foreign body, immunodeficiency). Smoking tends not to be a cause although COPD causing reccurrent infections is. Presentation is with a chronic, persistant cough, copius amounts of sputum, haemoptysis, halitosis, weightloss and breathlessness. There are often many acute exacerbations - especially when patients become colanised with Pseudomonas. Examination reveals loads of sputum and crackles due to mucus in the lungs. There may be lobar collapse. Similarly to COPD there is dyspnoea, chronic cough, sputum and an obstructive picture but in bronchectasis you get classic honeycombing on CT, much more sputum.

PNEUMONIA - Create a treatment plan including specification of observations, general supportive measures, appropriate antibiotic regimens, analgesia and physiotherapy Outline clinical management during recovery, emphasising the need for radiological follow-up until the consolidation has cleared.

CAP = oxygenation to sats above 92% with CPAP if patients do not improve, fluid balance, antibiotics, nutritional support if illness is prolonged. ANalgesia to relieve pleural pain can help promote chest movement (paracetamol, co-codamol, NSAIDs - opiates often avoided as they supress the respiratory drive). Physio again helps move fluid. Antibiotics for CAP? Mild/moderate = amoxicillin. Severe = Coamoxiclav Antibiotics for HAP? Mild/moderate = levofloxacin Severe = pipericillin plus taobactam. Recovery usually takes several days but Xraychanges can persist for weeks or months and it may have been an underlying pathology causing the pneumonia in the first place. Review at six weeks for a repeat chest Xray and if resolution is not seen onsider an underlying malignancy.

EXTRINSIC ALLERGIC ALVEOLITIS - Describe the typical clinical presentation and list common causes

CAUSES: Farmers lung: mouldey hay/straw sensitise the body to aspergillus. Bird fancier's lung: avian excretions, proteins and feathers sensitize the body to avian serum proteins. Malt workers lung: Mouldy malt sensitise to aspergillus. Cheese workers lung: Mouldy cheese sensitizes to penicillium and aspergillus. PRESENTATION: This may be acute or more chronic depending on antigen exposure. Acutely there may be influenza like symptoms, cough, breathlessness, wheeze within hours of a large amount of exposure. Low grade long term exposure will present as slowly progressive breathlessness. There may be fibrosis already on diagnosis and end expiratory crackles. INVESTIGATIONS: Xray shows patchy shadowing that can be mistaken for pneumonia (so a history of birds//farming etc. is important). Chronic disease shows: volume loss, restrictive spirometry, type 1 resp failure if severe. Serological testing can identify hypersensitivities but can be present in farmers etc without disease. Biopsy can confirm but is often not needed.

COPD - Describe a management plan for patients with stable COPD and those who present with an acute complication of COPD

CHRONIC MANAGEMENT: reduce exposure (smoking cessation, avoiding burning biomass fuels indoors), bronchodilators (beta agonists or anticholinergics (so inhibits parasympathetic drive)/ipatropium bromide), oral agents (theophyline, phosphodiesterase inhibitors). Inhailed steroids reduce the frequency of attacks and should be used if a patient has two or more exacerbations needing oral steroids a year. Do not use oral steroids except in exacerbations as they worsen osteoporosis. Encourage exercise, good nutrition. Oxygen can be given aimig for sats no higher than 90%. Bulla can be removed if large and comressing normal tissue and other measures include up to date vaccination and the consideration of end of life care when relevant. ACUTE COMPLICATION: Needs increased bronchodilator, short course of corticosteroids, antibiotics for infections. Give 25% O2 aiming for 88-92% sats and nebulisors may be driven with air. Oral steroids may be useful. If these do not help commence non invasive ventilation.Any peripheral oedema should respond to diuretics.

ANAEMIA - Discuss appropriate investigations to confirm that a patient has iron deficiency. Outline appropriate investigations for a patient with confirmed iron deficiency anaemia

CONFIRM: Full blood count and film will identify a microcephalic anaemia with hypo-chromic/pale red blood. Serum iron levels will be low with an increased total iron binding capacity. Serum ferritin will be low, meaning iron stores are low. There will be an increased number of serum soluble transferrin receptors. Bone marrow will be normal. INVESTIGATE: in the absence of a convincing history of menorrhagia investigate the GI tract for blood loss (endoscopy, colonoscopy and stool microscopy if history of recent foreign travel)

HEART VALVE DISEASE - Outline the reasons for performing right and left heart catheterisation. Outline the indications for medical or surgical treatment of valvular heart disease affecting the aortic and mitral valves.

CORONARY CATHETERISATION is part of percutaineous intervention for a STEMI. Access to the coronary arteries is via the LEFT heart. The right heart may be catheterised to calculate pulmonary pressures - the right heart does not provide access to the coronary arteries. For VALVULAR HEART DISEASE management is generally only surgical for severe or symptomatic problems. Medical management involves treating AF, diuretics for pulmonary oedema and hypertension control. Surgery for stenosis involves balloon valvuloplasty or replacement. For regurgitation use valve repair or replacement.

EVIDENCE BASED - Define the terms cost-benefit analysis, cost-effectiveness analysis, cost utility analysis, QALY, efficiency and effectiveness. Discuss the difference between wants, demands and needs for health care.

COST-BENEFIT ANALYSIS: balancing the positives and negatives of a situation COST-EFFECTIVENESS ANALYSIS: comparing the financial implications of a situation to the positives COST UTILITY ANALYSIS: comparing the financial benefits of two different drugs or procedures whose benefits may be different. QALY: a measure of disease burden whereby one QALY equals one year of perfect health. EFFICIENCY: minimizing waste EFFECTIVENESS: a measurement of success Clearly a patient's wants and demands are not the same as their needs for health care. A patient can refuse treatment but not demand it.

INFLAMMATORY BOWEL DISEASE - Describe the morphology and pathological consequences of Crohn's disease and ulcerative colitis. Describe common presenting symptoms. Discuss the investigation of a patient with suspected inflammatory bowel disease. Describe the medical therapy available. Discuss complications of Crohn's disease and ulcerative colitis and indications for surgery. List the extra-colonic manifestations of inflammatory bowel disease and discuss the response to each to surgery. Outline the risk of colonic malignancy in inflammatory bowel disease

CROHN'S Chronic, relapsing, transmural (unlike uc which only affects the mucosa) granulomatus disorder anywhere from mouth to anus, commonly the terminal ileum. Skip lesions are common resulting in fibrosis and strictures causing fistulas. Presentation: colicky central abdominal pain, change in bowel habit, usually diarrhoea, right iliac fossa, tender abdomen. Also, fever, anorexia, weight loss and malaise. Investigations: there is raised crp because of the inflammatory reaction. Endoscope may show strictures and fibrosis as well as ulceration in a cobblestone pattern. Biopsy is helpful. Complications (fistulas, abscesses) can be identified by ct/mri. Cause: Due to the impact of bacteria, environment and immune factors on a genetically susceptible individual. It is more common in smokers and after gastroenteritis. Management: mesalazine (anti inflammatory), steroids and surgery (for complications). This can include stricturoplasties, resect. The result may be short gut syndrome and nutritional deficiencies. Remember also the increased risk of erythema nodosum, pyoderma Gangrenosum, arthritis, ocular diseases. Differential: Bechets, IBS. Difference between uc/crohns: typically the ilium in crohns (rectum in Uc), skip lesions in crohns (continuous in uc) , transmural in crohns (more superficial in uc). Also stenosis is more common in crohns. Diagnosis: Appearance of the bowel wall, biopsy ULCERATIVE COLITIS Only affects the colon, only the colon, typically affecting the rectum spreading proximally in a continuous pattern. Presentation: blood stained diarrhoea and abdominal pain eased by defication. Severe cases may present with nausea, vomiting and distension.....this may be toxic mega colon which is acute colonic distension. Investigations: biopsy and sigmoidoscopy. No....uc has a definite malignant potential.....10% for every ten years therefore screen regularly. Management: resection leaving an ileostomy or j pouch. Medication includes...antidiarrhoeals, steroids, mesalazine. Surgery is usually only for toxic mega colon or significant cancer risk. Note, on barium enema uc typically give apple core strictures.

IMMUNOLOGY - Describe the indications for and interpretation of the following investigations: C-reactive protein, serum immunoglobulins, serum and urine electrophoresis, complement levels, autoantibodies (including autoimmune screen), total and specific IgE levels, lymphocyte phenotyping, skin prick and patch testing

CRP - and acute-phase protein elevated in inflammation. it can therefore monitor inflammatory conditions (Crohn's, rheumatoid arthritis). It is more sensitive and more specific than ESRwith the normal value less than five. Serum immunoglobulin - used to detect general immune function or autoimmune disease. Serum and urine electrophoresis - this checks for para proteins such as Spence Jones proteins in myeloma. Remember there may be a benign paraprooteinaemia to exclude before confirming malignant disease. Complement levels - can be low in hereditary angioedema, nephritis and paroxysmal nocturnal haemoglobinurea. Autoantibodies - these vary by sensitivity and specificity. Sensitivity is when the test to correctly identifies those who are positive, specificity is when the test correctly identifies people who are negative. For example, antinuclear antibodies in lupus are 98% sensitive but only 79% specific therefore non-diagnostic. Anti-mitochondrial antibodies found in primary biliary cirrhosis are 94% sensitive and 99% specific. Other also antibodies may be diagnostic such as anti-glomerular basement membrane antibodies in good passages disease. Others are prognostic such as anti-CCP and rheumatoid factor in rheumatoid disease. To detect autoantibodies we use ELISA - autoantigens in the well bind to auto antibodies in the patient's serum, then wash, then add animal antibodies against the human antibodies, then wash, then add a substrate that will change the colour of an enzyme attached to the animal antibodies. Colour changes positive. Eliza has been superseded by immunofluorescent probing. patch testingis used to identify antigens causing allergic reactions, the results can be read on day five. Skin prick tests look for a wheel and flare reaction after 15 minutes but there is a small risk of anaphylaxis and a negative and positive control must be used.

CARDIAC SURGERY - Describe the main incisions for cardiac surgery and outline the difference between open and closed heart surgery and outline the principles involved in cardio-pulmonary bypass.

Cardiac incisions include a MEDIAN STERNOTOMY (Most common for heart and aortic arch), ANTERIOLATERAL THORACOTOMY (particularly on the right to expose the mitral and tricuspid valves by incising along the plane of the ribs), POSTERIOLATERAL THORACOTOMY (to access the distal aortic arch Open heart surgery - requires pulmonary bypass, whether or not this involves opening the heart. Eg. CABG is open. Closed heart surgery - does not require pulmonary bypass. Cardio-pulmonary bypass - a machine taking over the function of the heart and lungs enabling a motionless heart for the operation duration. The aorta is clamped proximal to a cannula returning oxygenate blood from the machine. Venous blood is removed from the right atria. The blood can be warmed or cooled by the machine and blood returning to the body must be filtered for potential micro-emboli. The myocardium will become anoxic and at risk of infarction so the following is done to reduce the risk: cooling the myocardium (4-12degrees) and arresting the electrical and mechanical activities of the heart by giving a high potassium cardioplegic solution. Problems with cardio-pulmonary bypass are as follows: the process activates clotting (so the patient needs high dose intra-operative heparin to prevent thrombosis), clotting factors are consumed (so there is a bleeding risk) and complement is activated by the procedure.

ACUTE ARTERIAL OCCLUSIVE DISEASE - Describe the causes, symptoms, signs and initial management of acute arterial occlusion. Differentiate symptoms and signs of acute arterial from acute venous occlusion. Differentiate embolic and thrombotic occlusion. Describe the natural history of treated and untreated acute arterial occlusion. Contrast the indications for surgical and medical treatment of acute arterial occlusion

Cause: Typically thrombus. Rupture of an atherosclerotic plaque. Or an embolism (AF/anyerism). Symptoms/signs: pain, pallor, pulseless, paraesthesia, perishingly cold and paralysis. In particular paralysis and paraesthesis are the most limb threatening. Management and its indications: Remember DVT thromboprophylaxis with enoxaparin for all patients. Acute ischaemia needs revascularisation in 4-6hours if the limb is to be saved. If an embolism is suspected then use a fogarty thrombectomy catheter which is inserted and pushed passed the resistance prior to inflation of a balloon. Balloon removal pulls the embolus with it. Send a sample for histology to exclude subacute endocarditis and atrial myxoma (rare atrial tumor). Then place the patient on warfarin. If a thrombus is suspected, post CT/MRI arterography, the patient may require grafting for chronic changes. After successfully restoring flow, many patients need a fasciotomy to prevent compartment syndrome and monitoring from kidney failure because myoglobin is leaked from dead muscle and is nehrotoxic. Difference between acute arterial and acute venous: Cause (arthrosclerosis versus thrombosis), Risk factors (hypertension, hyperlipidaemia, diabetes, hypertension versus venous hypertension, Varicose veins), Pain (intermittent claudication and rest pain versus Moderate aching worst on prolonged standing), Features (diminish pulses And pallor versus Oedema And varicosities). More acutely arterial problems have the five P's, but venous problems may be asymptomatic or cause aching and oedema. Embolic or thrombotic: The main causes of acute ischaemia are embolism (a substance - thrombus/air/fat/amniotic fluid etc - that is distal from its site of origin) and thrombus (solid mass of platelets and fibrin that form locally in a vessel). With a thrombus there is usually a history of claudication.With an embolus there is usually no history, contralateral intact pulses and AF. Treated v. untreated: Classically, untreated disease leads to loss of limb. If treated prognosis Improved that monitoring is required and atherosclerotic risk factors should be strictly controlled.

THE URETHRA, PENIS AND SCROTUM - Outline the causes of male erectile dysfunction, list screening investigations, and list the available treatments

Causes (The most common are vascular, neuropathic or psychological): If there is reduced libido as well think depression or hypogonadism, without reduced libido think anxiety, vascular insufficiency (Arthroderma), neuropathic causes (diabetes, alcohol access, multiple sclerosis) or medication (beta-blockers, thiazide diuretics). Over 50% of men with advanced CK D or on dialysis have erectile dysfunction. Investigations: Bloods for glucose (diabetes), prolactin, testosterone, LH, FSH (hypogonadism). Other tests includes nocturnal monitoring directions (rarely performed as it does not change management), cavernosal injections (of prostaglandin to test the blood supply), nerve conduction studies or internal pudendal angiography. The history should include questions about hypogonadism - loss of libido, the Sergey, muscle weakness, decreased frequency of shaving, gynaecomastia, infertility, delayed puberty, anaemia of chronic disease. Psychological problems may mean that erections on awakening still occur. Treatments: This depends upon the cause, psychotherapy may help psychological problems but neuropathy and vascular disease are unlikely to improve. First-line therapy is with an oral phosphodiesterase inhibitor (sildenafil Aka Viagra). Inhibition of phosphodiesterase results in vasodilation using cGMP. Other treatments include self injection of prostaglandins or urethral gel prostaglandins, vacuum devices and prosthetic implants. Obviously any hypogonadism should be treated.

RAISED INTRACRANIAL PRESSURE - List the main causes of raised intracranial pressure List the features in a headache which reflect a raised intracranial pressure (with reference to variation with posture, coughing, visual symptoms and diurnal variation) List the pertinent examination findings in raised intracranial pressure List the potential complications of Acutely raised intracrianial pressure and Chronically raised intracranial pressure

Causes: Mass effect (tumour, haematoma), Generalised brain swelling (liver failure, Hypertensive encephalopathy), Increased venous pressure (venous sinus thrombosis, heart failure), CSF obstruction (Hydrocephalus) Or increased CS F production (meningitis). Features: Generalised headache aggravated by bending, coughing or straining which all raise intracranial pressure. The headache is worse in the morning or after prolonged lying down, may awaken patients from sleep and is gradually progresses. Other features include vomiting, visual obscuration is, focal neurological signs. Examination: There may be focal neurological signs, papiloedema. Cushing's reflex/triad is hypertension, bradycardia and irregular breathing - it may indicate imminent coning.Remember that in infants the fontanels bolds and the sutures separate. Treatment: oral corticosteroids such as dexamethasone can reduce Sarid will deem. Rapid reduction can also be performed with intravenous mannitol. If the cause is hydrocephalus than a shunt may be required, Seizures need treating and any tumours may require surgery/radiotherapy/chemotherapy. Complications acutely: Death, stroke, Seizures, neurological deficits. Complications chronically: Visual impairments, chronic headaches, neurological deficits.

CHEST PAIN - Given a history of chest pain and its features, describe and interpret appropriate investigations and list a differential diagnosis in order of probability

Chest pain is not cardiac specific - it may indicate MSK (often pain associated with a specific movement), respiratory, gastrointestinal (non exercise related) or psychological (post activity or emotional event) problems. Consider chest pain as cardiac - typical or atypical, versus non-cardiac. Characteristics: Classic cardiac pain is in the central chest, radiating to the neck, jaw and left arm. The pain is likely to be dull, consrticting or choking in character although patients may describe it as a discomfort or sensation of breathlessness. With angina, pain is provoked on exertion and relieved by rest. Whereas PE/dissection/pneumothorax cause sudden onset pain an MI or angina related pain builds over a few minutes. Associated autonomic disturbance (sweating, nausea, vomiting) is ommon with MI, PE or dissection. Differential: Anxiety, angina, MI, pericarditis (retrosternal pain, worse on movement), mitral valve prolapse (sharp left sided pain), aortic dissection, aortic anyerism, oesophagitis, bronchospasm, PE, pneumonia, pneumothorax, costochondritis, rib fracture/injury, prolapsed disc, thoracic outlet. With such a vast differential suspected cardiac chest pain needs the following INVESTIGATIONS: history, ECG, echo, troponin etc (Ie, confirm or exclude your most likely and most serious differentials).

THE WHITE CELL - Describe the clinical features and laboratory diagnosis of chronic myeloid leukaemia and outline the principles of management.

Chronic Myeloid Leukaemia: uncontrolled proliferation of myeloid cells, this accounts for 15% of leukaemias. > Most sufferers are age 40 to 60 and male, the disease is rare in childhood. Chronic myeloid leukaemia is associated (in more than 80%) with the PHILADELPHIA CHROMOSOME (translocation between the long arms of chromosome 9 and 22 forming a fusion of the BCR and ABL genes. The presence of the Philadelphia chromosome in chronic myeloid anaemia improves prognosis. The new gene has tyrosine kinase activity. Features of chronic myeloid leukaemia: many are found by chance. Symptoms include tiredness, weight loss, fever, sweat, doubts, bleeding and abdominal discomfort (due to enlargement of the spleen). Examination: large spleen, large liver, anaemia and bruising. Laboratory findings: raised myeloid cells (neutrophils, Baeza fails, yes and fills), reduced haemoglobin, raised you rates, raised B12, hyper cellular bone marrow and the Philadelphia chromosome. Management of chronic myeloid leukaemia: chemotherapy, imatinib (tyrosine kinase inhibitor if they have the Philadelphia chromosome). The only treatment that will achieve remission and offer long-term survival is stem cell transplants but this has significant morbidity and mortality. Used stem cell transplant in young patients, otherwise offer imatinib. Prognosis of chronic myeloid leukaemia: most patients last 5 to 6 years. The three phases are chronic (months to years with few symptoms), then they accelerated phase (increasing symptoms, enlarged spleen) then the blast transformation phase whereby the patient presents much like acute leukaemia and will die without stem cell transplantation.

THE WHITE CELL - Describe the clinical features and laboratory diagnosis of chronic lymphatic leukaemia and outline the principles of treatment

Chronic lymphocytic leukaemia: the accumulation of mature B cells that have escaped programmed cell death. Chronic lymphoblastic leukaemia is the most common leukaemia, typically elderly men when pneumonia can be a triggering event. Features of chronic lymphocytic leukaemia: may be presentation on routine SBC, anaemia, recurrent infections and (if severe) weight loss and sweats. Examination: a large spleen, enlarged liver, enlarged rubbery tender notes. Investigations: raised white blood cells (lymphocytes), autoimmune remorseless if later stage, bone marrow infiltration (low haemoglobin, low neutrophils, low platelets) Management of chronic lymphocytic leukaemia: only if the patient is symptomatic give chemotherapy (cylophosphamide), steroids to reduce autoimmune haemolysis, supportive care (including transfusions and immunoglobulins) and radiotherapy (to relieve spleen and liver problems). Stem cell transplant can be tried. Chronic lymphocytic leukaemia prognosis can be considered by the rule of threes. One third never progress, one third progress in time, one third actively progress. Debt is due to infection or transformation of chronic lymphocytic leukaemia into an aggressive lymphoma (termed RICHTER'sSYNDROME).

CHRONIC LIVER DISEASE - Define cirrhosis in pathological terms. Describe the morphology and pathological consequences of cirrhosis. Describe the investigation of a patient with suspected cirrhosis. Discuss how to establish the diagnosis of the cause of cirrhosis. Outline the pathophysiology underlying the clinical features of cirrhosis. Describe the clinical features of complications of cirrhosis and portal hypertension (see next section) and outline their management.

Cirrhosis: chronic liver damage leading to failure. The normal architecture of the liver is replaced by scar tissue resulting in a shrunken, nonfunctioning liver. Typically there is a preceding period of hepatitis. Investigations: gold standard is a liver biopsy (percutaneous, jugular or laparoscopic). Blood tests show low platelets, abnormal liver function tests, increased prothrombin time. Serology may detect hepatitis virus, (B, C), autoantibodies. Ferrin and transferrin may be raised in haemochromatosis. Ultrasound may show a shrunken and nodular liver and splenomegaly (portal hypertension). Elastography can be used to indicate how elastic the liver is, with cirrhosis reducing this figure. Cause: most commonly: alcohol (acetaldehyde itself is damaging and causes the buildup of byproducts in the liver), hepatitis B (chronic inflammation, worse if hepatitis D is also present), hepatitis C (chronic inflammation triggers scarring), and non-alcoholic fatty liver disease (lipid buildup triggers scar tissue). Less common causes are autoimmune hepatitis, haemochromatosis, wilsons, primary biliary cirrhosis (autoimmune destruction of the livers bile ducts), and gallstones. Presentation: tired, weak, itchy, yellow, peripheral oedema. Presentation may also be with the complications such as varices. Typically symptoms are late stage indications. reduced oestrogen clearance in liver failure leads to Palmer erythema, hypogonadism, gynaecomastia and spider naevi. Ascites and oedema are because of low albumin and jaundice is because of raised bilirubin. really an advanced stage disease gives acute renal failure (liver failure alters blood supply to the kidneys), encephalopathy and clotting abnormalities. Management: treat the cause, avoid alcohol, hepatitis vaccinations can prevent cirrhosis, steroids can treat autoimmune conditions, but if severe the patient should be on the transplant list. Complications: portal hypertension (the other objective), hepatic encephalopathy (confusion and loss of consciousness as toxins build up in the bloodstream, the mainstay of treatment is lactulose)

OBSTRUCTIVE SLEEP APNOEA - Outline the clinical presentation of a patient with OSA, describe the use of sleep studies in its investigation and outline the principles of treatment.

Clinical Presentation: remember that central sleep apnoea is an abnormality of ventilation. Obstructive sleep apnoea is when the upper airway (Usually at the level of the soft palate)is blocked and is much more common. This may coexist with COPD resulting in severe respiratory failure. Seen in 2 - 4% of the middle-aged population the presentation is with daytime sleepiness, Irritability, poor concentration, poor cognitive function, waking feeling unrefreshed and loud snoring. There is an increased risk of traffic accidents. Risk factors: male gender, obesity (fat deposits narrow the pharynx), nasal obstruction, small mandible, acromegaly and family history. Alcohol and sedatives will also relax the upper airways causing narrowing. Investigations: Assess sleep patterns (deleted sleep too late, shift work?) Then send for sleep assessment. The Epworth sleepiness Scale Predominantly assesses the situations in which a person would fall asleep. Overnight oximetry and other investigations are diagnostic but expensive. The current threshold for diagnosing apnoea is 15 episodes per hour with each episode lasting for 10 seconds. Differential: narcolepsy, hypersomnia. Treatment: Driving should not be undertaken until treatment has relieved daytime sleepiness due to the risk of accidents. If mild, relief of nasal obstruction and cessation of alcohol consumption can prevent obstruction. Weight loss is advised but the majority of patients require continuous positive airway pressure at night to splint open the upper airways. 30 to 50% of patients will not tolerate this even though it is highly effective. Some mouth guards can advance the mandible thus opening the pharynx. There is no evidence that surgery is beneficial.

THE BLADDER AND PROSTATE - Discuss the diagnosis of bladder infection outlining the importance of confirming significant bacteriuria (>100,000 organisms/ml) and the importance of white cells in the urine. Discuss the management of bladder infections.

Cystitis is inflammation of the bladder which can be due to infection. Very similar to a UTI, is caused by bacteria which usually tracks up from the urethra (therefore is far more likely in those with catheters, poor hydration and poor immune systems). Other risk factors include being female, older, obstructions to urine flow, urinary tract abnormalities, urinary retention, bowel incontinence, pregnancy and diabetes. Symptoms are cloudy or bloody urine with a foul smell, dysuria, frequency, lower abdominal or back pain. Diagnosis: urinalysis to check for nitrites (bacteria convert nitrates to nitrites) and blood. Treatment: appropriate antibiotics and hydration. The white cell count found in urine is often mildly raised because of contamination so only significant levels of bacteria confirm an infection. Of course, a suprapubic aspirate should be entirely sterile.

DEMENTIA - Provide a definition of dementia List the main clinical features of dementia including memory loss and global intellectual deterioration and relate these to different lobes of the cerebral hemisphere. Classify dementia according to cause Describe the difference between dementia and delirium List the potentially treatable causes of cognitive decline. Outline an investigation plan to exclude a treatable cause of dementia Perform and interpret a mini-mental state examination on a patient Describe the management of dementia, with particular reference to the multi-disciplinary approach and (where appropriate) control of risk factors Describe the pharmacological management of Alzheimer disease

Definition: Dementia is a syndrome of progressive impairment of higher cortical functions including memory, orientation, comprehension, calculation, learning, language, judgement. Features: These depend upon the area of the brain involved.Remember that dementia with Lewy bodies often gets symmetrical signs and respond to the less well to the asymmetrical signs and picture of Parkinson's dementia. Classification: Primary neurodegenerative diseases such as: Alzheimer's, dementia with Lewy bodies (Early visual hallucinations), Parkinson Dementia, frontotemporal (including picks disease -- Young onset), Huntington's disease. Vascular dementia (Common and and presenting with stepwise deterioration beginning with behavioural changes). Metabolic disorders (hypothyroidism, vitamin B12, folate deficiency, Wilson's disease, mitochondrial defects. Infections: HIV, prion diseases, syphilis, subacute sclerosing panencehalitis.Neoplastic/paraneoplastic: primary or secondary tumour. Other causes include normal pressure Hydrocare for less, epilepsy, head injury, repeated toxin exposure and depression causing pseudodementia. Delirium: This is an acute, fluctuating, potentially reversible, confusional states whereby there is an alteration of consciousness (Hypo or hyper-Active). Typically as a response to infection or other illnesses management is synonymous with good nursing care. Treatable causes of cognitive decline: Trauma, infections, hydrocephalous, Normal pressure hydrocephalous, brain tumours, Toxin exposure,Thyroid diseases, hypoxia, vitamin B12 or folate deficiency. Often, treatment of the cause stops further progression but existing damage remains. Investigations: Take a thorough history - This will often identify delirium. Blood tests should exclude low thyroid, B12/folate deficiency, and syphilis. Specific tests may include those for metabolic disorders (Wilsons), HIV, vasculitis, and enephalitis. CT or MRI are obligatory in a patient with dementia to exclude space occupying lesions and normal pressure hydrocephalous - In dementia the CT is likely to reveal cerebral atrophy. Younger patients should also has a lumbar puncture to identify encephalitis, infections or inflammatory disorders. Remember that dementia can give widespread delta waves on an EEG, particularly in Alzheimer's. CJD shows a characteristic EEG With generalised abnormalities over the whole brain. Remember also that genetic testing can identify Huntington's career, the presinalin genes seen in Alzheimer's And some other mutations associated with CJD or frontotemporal dementia. Mini mental State examination: A screening test for altered cognitive function involving 30 questions. Questions include:Time, place, word recall, serial sevens, Naming objects, copying two Pentagon's. Management: Treat any treatable causes (This includes vasculitis). Antipsychotics may be required for behavioural disturbance (but can worsen Parkinson pictures). The general approach should be with a multidisciplinary team with the understanding that the disease is progressive and long-term care will eventually be required. The vascular dementia it is vital to control cardiovascular risk factors. Death tends to occur around seven years after diagnosis.

INGUINAL HERNIA - Define indirect and direct inguinal hernia. List the factors that predispose to the development of inguinal hernia. Discuss the relative frequency of indirect, direct and femoral hernia in children, women, young men and elderly men. Perform a physical examination of patients with inguinal hernia and describe signs of incarceration, obstruction and strangulation. Outline the principles of management of reducible inguinal hernia in patients with obstructed or strangulated inguinal hernia.

Direct: pushes directly through the weakness in the transversalis fascha before exiting via the superficial ring. (above and medial to the pubic tubercle). Unlike indirect hernias, these rarely extends down to the scrotum. Indirect:because of failure of the embryonic closure of the deep inguinal ring this hernia goes through the deep inguinal ring before exiting via the superficial ring. (above and medial to the pubic tubercle) Typically, a little hernias are seen in men because of the patented processes vaginalis - a supposedly temporary connection that helps with the detention of the testes. Whereas men are much more likely to get this inguinal hernias, femoral hernias are more common in women because of their wider pelvis. Femoral hernia is also much more common in adults than children. Presentation: a lump in the groin becomes more apparent on coughing/straining/standing up and may or may not be reducible. Obstruction will cause absolute constipation and abdominal distension alongside pain. Incarceration may not cause obstruction, but can resulting in vomiting, constipation, pain. Strangulation causes intense pain acutely, vomiting, constipation, blood PR. Management: Those causing few symptoms may be treated conservatively. If not excise the sac (herniotomy) and surgically repaired the defect (herniorrhaphy). This can be done elective league for a reducible hernia. Those with obstruction or strangulation signs required emergency surgery -remember that morphine post operatively will cause constipation which constrain the wound. bowel resection may be required in strangulation.

EVIDENCE BASED MEDICINE - Define and discuss explanatory/management trial, different trial designs, randomisation and its effects, types of blinding, "intention to treat" versus "per protocol" analyses, and Type I and Type II errors.

EXPLANATORY TRIAL - a trial which aims to determine how effective an intervention is in a well controlled environment. MANAGEMENT TRIAL - Also known as a pragmatic trail determines how effective an intervention is in an actual clinical setting. BLINDING: Open, single blind (participant), double blind (participant and data collector), triple blind (participant and data collector including not telling anyone what the variables being measured are). INTENTION TO TREAT: everybody in the study population is randomized and the groups remain as such even if patients drop out. PER PROTOCOL: only patients who complete the trail are included in the results TYPE 1 ERRORS are when an error results in the alternative hypothesis being accepted, whereas TYPE 2 ERRORS are when the error occurs and results in the null hypothesis being accepted. RANDOMISED CONTROL TRIAL is when participants are allocated to one of two groups and are followed up over time.

DIABETES VASCULAR COMPLICATIONS - Discuss the microvascular complications of diabetes affecting the eyes, kidney and nerves and outline their relationship to diabetic control and disease duration. Describe the features of diabetic sensorimotor neuropathy and associated risks. Describe the musculoskeletal conditions associated with diabetes Describe the appearances of background retinopathy, proliferative retinopathy and maculopathy and recognise the appearance these and cataract on direct ophthalmoscopy. Outline the treatment of proliferative retinopathy and maculopathy Outline the pathology of renal complications of diabetes mellitus Outline the natural history of diabetic nephropathy emphasising the importance of blood pressure control. Outline the treatment of painful diabetic neuropathy. Describe the clinical presentation and natural history of other neurological complications including ocular nerve palsies, diabetic amyotrophy, foot drop, impotence and autonomic neuropathy

EYES: changes such as hypoglycaemia can cause transient visual disturbances, cataracts develop early in diabetic patients, glaucoma can be secondary to diabetic retinopathy, iritis is associated with type I diabetes and retinopathy occurs in all diabetics after around eight years. Diabetic retinopathy: this is more likely if there is poor glycaemic control, hypertension, a longer duration of diabetes, proteinuria, high cholesterol, anaemia, pregnancy, smoking. The condition occurs because arterioles are destroyed in diabetes leading to ischaemia of the retina. Micro-aneurysms form because there is a reduced number of endothelial cells and pericytes in the capillaries. Intraretinal haemorrhages cause dot, blot and flame shaped bleeds on the retina, Nerve cell death causes cotton wool spots. Hard exudates are because of the deposition of lipids. The condition is either pre-proliferative/background or proliferative (less common, more likely in type I and gives neovascularisation causing vitreous haemorrhage and retinal detachment). If the condition involves the macula it is called diabetic maculopathy - this threatens vision. Treat retinopathy with laser photocoagulation and proliferative retinopathy with intravitreal Triamcinalone and injections of anti-VEGF. KIDNEY: Diabetic nephropathy is classified on the basis of urinary protein that can be micro-albuminurea (an early indication, Less than 300 mg a day ), or nephropathy. Diabetic nephropathy is when urinary albumin is produced in excess of 300 mg a day. This can mean a patient with or without raised serum creatinine. Glomerular filtration will be reduced Progressively requiring good diabetic control, a low protein diet, and modification of cardiovascular risk factors. MSK: With diabetes, hands can become sick and waxy as in scleroderma Because collagen is glycosylated. Flexion contractures, Carpal tunnel and trigger finger can also occur. Adhesive capsulitis and calcific periarthritis more common in diabetics. Charot foot can occur whereby there is bone Reabsorption and deformity secondary to neuropathy. Diabetic muscle infarction is rare That can occur with acute pain of the muscle groups. NEUROPATHY: This is more commonly seen in older men with type II diabetes and may affect sensory nerves, motor nerves and the autonomic nervous system (affecting organ systems such as the heart, skin, eyes, GI tract and genitourinary system). The risk is raised with other factors such as high cholesterol, high blood pressure, smoking and alcohol intake. Polyneuropathy is maybe symmetrical or asymmetrical. Hypoglycaemia will damage nerves causing an inability to feel damage (leading to ulceration) or burning/prickling sensations and pins and needles. Loss of most sensation in the fee can lead to contraction of the digits giving hammertoes. Management includes tight glucose control, pain relief (tricyclic antidepressants and neuroleptics), Topical capsaicin, cognitive therapy, prescribed exercise, acupuncture and eventually opiates. Neuropathy can cause foot drop, Impotence and incontinence as well as ocular palsies. Diabetic autonomic neuropathy can be of many of the body systems. Cardiovascular - giving Arrythmias and orthostatic hypotension, gastrointestinal - giving delayed emptying and abdominal discomfort, urogenital - hesitancy, poor stream, poor emptying, overflow incontinence, pseudomotor - sweating problems. Treatment may be symptomatic of the presentation and involves good glycaemic control.

CONGENITAL HEART DISEASE - Define the Eisenmenger syndrome including the clinical features and underlying pathophysiology

Eisenmenger syndrome, a cyanotic heart disease when in the fetal heart there is a left to right shunt (Through a large Atrial or ventricular septal defect, Sometimes in patent ductus arteriosus). This results in increased pulmonary resistance Reversing the shunt into right to left. Signs and symptoms: A blue baby! Cyanosis, clubbing, raised red blood cell count (polycythaemia),Fainting,Heart failure, arrhythmias, stroke (And other clots because of the raised viscosity of the blood). The pulmonary resistance causes damage to the pulmonary vasculature and scarring (fibrotic lung tissue does not contribute to oxygen transfer). As the condition progresses there will be right ventricular hypertrophy. Later signs actually becoming more rare because of prenatal screening. Treatment: if identified before Pulmonary hypertension the whole can simply be repaired. If not there must be a heart-lung or lung transplants (with heart repair).

CNS INFECTION - Outline the clinical features of encephalitis and list the common causes

Encephalitis is inflammation of the brain parenchyma with associated neurological dysfunction. This may be combined with managers. Remember that encephalopathy is a disturbance in brain function in the absence of an inflammatory process and is therefore different (caused by metabolic disturbances, hypoxia, drugs, organ failure or systemic infections but not brain inflammation). Cause: infection of the central nervous system, postinfection, paraneoplastic. Typical infections from herpes or enterovirus, these are more common than bacteria. Features: similar to meningitis, patients often have fever, headache, altered consciousness. There may be focal neurological signs, seizures, confusion and even coma. Diagnosis: cerebrospinal fluid may show polite, lymphocytes and raised protein. Polymerase chain reaction is often positive for herpes simplex or enteroviruses. HIV testing may be positive and MRI imaging of the brain can show changes if caught late. EEG shows cerebral dysfunction. Treatment: intravenous acyclovir as the cause is likely to be herpes simplex one, herpes simplex two or enteroviruses (echovirus, poliovirus, coxsackievirus), influenza, measles, mumps etc. There is a 10% mortality rates and many sufferers have physical, cognitive, emotional, behavioural and social difficulties after the disease. Herpes simplex viruses are the most fatal.

Describe the aetiology, morphology and pathological consequences of carcinoma of the breast

Epidemiology: Breast cancer is second only to lung cancer among female cancer related deaths. 70% of breast cancers are invasive ductal carcinomas. The remaining cases are mostly invasive lobular carcinomas. Ductal carcinoma in situ is also common and is often multifocal with a high risk of becoming invasive (still as high as 10%. Less commonly is lobular carcinoma in situ, again a risk for later malignancy. Aetiology: 5-10% are genetic involving BRAA1/2 genes etc. Unopposed oestrogen is a known association (obesity, HRT, long term oral contraceptives (in theory), low parity, early menarche, late menopause - oestrogens start and puberty and end at menopause. Breast cancer presents 1. mamographic screening 2. palpable mass (with bloody nipple discharge) 3. pain The breast may metastasize to bone, lung, liver, pleura, adrenals, skin and brain.

ANALGESIA - Describe the principles, risk and benefits of epidural analgesia Describe methods of non-drug analgesia (eg heat/cold, TENS, splinting)

Epidural anaesthesia administers local anaesthetic into the epidural space via a catheter. It can be topped up as the catheter is left in situ but has a slower onset than a spinal taking up to 45 minutes. Patient must be closely monitored with respect to ECG, blood pressure, respiratory rate and oxygen saturations. Remember the epidurals cause hypotension by vasodilation, postspinal headache, respiratory depression, itching and may fail or the procedure can cause accidental damage to the dura. Nondrug analgesia: splinting, cognitive behavioural therapy, acupuncture, TENS, aromatherapy, hypnotherapy.

ASTHMA - Describe the clinical features of acute asthma and the blood gas abnormalities associated with acute severe asthma

Features of an acute severe attack: PEF is <50% expected. Resp rate >25/min. Heart rate >110/min. Inability to complete sentences in one breath. Features of life threatening asthma: PEF<30%, raised PaCO2 (body is no longer able to get rid of CO2), silent chestm cyanosis, poor respiratory effort, bradycardia, arhythmias, hypotension, exhaustion, confusion, coma. At the start of an attack PaO2 and PaCO2 both fall as oxygen cannot get in and hyperventilation is blowing off carbon dioxide. The pH rizes slightly becoming more alkaline. As the asthma attack worsens the body is less able to blow off CO2 and the PaCO2 rizes with a corresponding fall in pH. PaO2 continues to fall.

HYPERTENSION - Describe the features of 'accelerated phase' or 'malignant' hypertension, discuss differential diagnosis of hypertension and causes of secondary hypertension. Describe pathological consequences of hypertension as they affect the cardiovascular, cerebrovascular and renal systems.

Features: (180 Systolic or 110 Diastolic minimum). This is when BP is so high (Cerebral autoregulation is lost) that it causes acute damage to one or more organ systems (Central nervous system, cardiovascular, renal system). This is a medical emergency as organ damage can be permanent. Typically the cause or the malignant hypertension is trauma, glomerular nephritis, Eclampsia, abrupt cessation of antihypertensive treatment or stimulants (cocaine, amphetamines). Symptoms/signs: retinal haemorrhages, papiloedema, raised intracranial pressure (often due to cerebral haemorrhage). The kidneys are affected causing haematuria, proteinuria and acute renal failure. Other signs include chest pain, epistaxis, anxiety, Headaches, fainting, vertigo etc. Differential diagnosis: Coartion of the aorta, Acute kidney failure, eclampsia, Aortic dissection, pheochromocytoma, renal artery stenosis, Subarachnoid haemorrhage. Causes of secondary hypertension: Unlike primary hypertension which is idiopathic, secondary hypertension is caused by problems such as tumours, kidney problems and endocrina disorders. Specific examples include: Chronic kidney failure, renovascular stenosis, conn's syndrome, pheochromocytoma, Cushing's, acromegaly, High or low thyroid Etc. Consequences: Death, Ischaemic heart disease, stroke, renal failure.

FIBROADENOSIS (Identify and describe the major types of breast lump (fibroadenoma, fibroadenosis, cyst, carcinoma). Outline the natural history of benign and malignant breast neoplasms. Present a classification of the main types of carcinoma of the breast.)

Fibroadenosis is also known as fibrocystic breast disease, a group of benign breast conditions. Presentation: Fibrous tissue n the breast causes a lumpy texture. Individual lumps are smooth, well defined and mobile, often in the armpit and upper outer quadrant. Breasts may become periodically tender and nipples may itch. Cause: The condition is likely to be hormonally related and it regresses postmenopausally. Investigations: Assess to exclude carcinoma. Treatment: May not be required,

BURNS - Outline the fluid resuscitation of burns patients, including composition, volume and timing of fluid. List the other management steps in the initial 24 hours following a burn injury, including general support, wound management and antibiotics. Discuss the management of a burns patient after the first 24 hours including fluids, wound management, metabolic needs and rehabilitation.

Fluid resuscitation: initiate in children with more than 10% burns and adults with more than 15% burns. Replace half the fluid in the first eight hours, and the other half in the first 16 hours. use the parkland formula to estimate the volume. The Formula States that the volume needing to be replaced is 4 X mass in kilograms X %Burns. As always, crystalloid is best. Management: remove the source, assess ABCDE, intubate early if inhalation is suspected. Burn wounds are susceptible to infection so give a tetanus booster. Keep wounds clean due to the risk of infection, cool early with prolonged cold water, topical antibiotics and a clean non stick dressing. replace fluids, children may also require glucose and severe burns benefit from early NG feeding. Analgesia is vital. Management after 24 hours: continue fluid resuscitation, managed other injuries, continu wound closure. Consider grafting and reconstruction so that future rehabilitation can achieve the desirable outcome of optimising function and reducing the lack of mobility associated with wound contracture.

ASTHMA - Describe the stepped approach to treatment of an acute asthma attack and create a management plan for a patient presenting with acute asthma.

For a mild/moderate exacerbation remember that a short course of oral pred may be helpful. If given for less than three weeks dose tapering for withdrawal is not needed. Indications for a short 'rescue' course are: peak flow <60%, persistent morning symptoms, worsening night-time waking. For acute severe asthma an immediate ABC approach is needed. PEF is <50% expected. Resp rate >25/min. Heart rate >110/min. Inability to complete sentences in one breath. Give high flow oxygen, nebulised salbutamol with or without ipatropium bromide (an anticholinergic that reduces bronchospasm), systemic corticosteroids (s oral pred or IV hydrocortisone). If this fails then ventilation is the next step.

DIABETES MELLITIS - Classify the different types of oral hypoglycaemic drugs used in Type 2 diabetes and outline their indications and contraindications.

For treating T2DM when lifestyle measures have failed. BIGUANIDES - Metformin. Works by decreasing the production of glucose by the liver and increasing glucose uptake by tissues. Beware in kidney or liver damage, use in obesity as it helps weight loss by supressing apetite and has a lower risk of hypos. GLITAZONES - .....glitazone. Work by binding to PPAR gamma (a protein involved in the transcription of genes responsible for glucose and fat metabolism) resulting in increased use of glucose by the cells. SULFONYLUREAS - tolbutamine. Works by encouraging insulin release therefore can cause hypos. MEGLITANIDES - ..........glinide. Work by encouraging insulin release therefore can cause hypos.

KIDNEYS Describe the normal functions of the kidneys. Classify renal failure into pre-renal, renal and post-renal causes, outlining the pathology of the common diseases that may cause each type

Functions: > Acid base balance (HCO3 retention, H+ excretion). < Excretion of urea, uric acid and other metabolities. > Reabsorbttion of glucose, water, amino aids and electrolytes. < Osmolality regulation (high osmolality/dehydration causes the hypothalamus to trigger ADH release from the posterior pituitary so that more water is retained/reabsorbed by the kidneys). > BP control via RAAS (Aldosterone from the adrenals causes the nephrons collecting ducts to retain water thus increasing BP). < EPO production. Considering Acute failure causes can be prerenal, renal or post renal. PRE: Decreased bloodflow to the kidney (Low BP, heart failure, liver cirrhosis, renal artery stenosis). RENAL: Glomerulonephritis, tubular necrosis, rhabdomylysis as well as prerenal causes or medications (NSAIDs, ACEi, angiotensin II antagonists) severe enough to damage the kidneys themselves. POSTRENAL: Obstruction (prostatic, cancer, stones, fibrosis, strictures, surgery, blocked catheter).

GALLBLADDER DISEASE - Outline carcinoma of the gallbladder, bile duct and ampulla of Vater with regard to presenting symptoms and survival.

GALLBLADDER: A Rare cancer that usually presents after metastasis to the liver and lymph nodes with abdominal pain, jaundice and vomiting. By this point, it is too late to cure by simple cholecystectomy. Typically the causes chronic gallstones leading the calcification of the gallbladder which is termed porcelain gallbladder. other risk factors include being overweight, older, female or having gallbladder polyps. Management: remove the gallbladder and lymph nodes. Prognosis is poor due to early diagnosis being challenging. BILE DUCT CANCER aka cholangiocarcinoma this is rare but aggressive giving jaundice, weight loss and abdominal pain. Again, prognosis is poor and treatment is surgical. The main risk factor is primary sclerosing cholangitis (progressive scarring of the bile duct). AMPULLA OF VATER - also known as the hepaticopancreatic duct, this is where the common bile duct and pancreatic duct meet halfway along the second part of the duodenum. cancer here is another rare malignancy but because of obstruction this tends to present early with jaundice and abdominal pain. Surgery is the only hope of cure but prognosis is poor.

PREOPERATIVE ASSESSMENT - Describe the effects of general and spinal anaesthesia on normal cardiac and respiratory physiology.

General: decreased myocardial contractility, reduced cardiac output, hypotension (secondary to vasodilation) Arrythmias, increased myocardial sensitivity to catecholamines, depressed ventilation, laryngospasm (ventilation may initially be difficult and the patient may be hiccupping), airway obstruction, hypoxia and hypercapnia (due to depressed ventilatory effort) and bronchodilation. Spinal: respiratory depression (if opiates), slowed heart rate, hypotension (due to vasodilation as the anaesthetic blocks sympathetic nerves). complications of general anaesthesia: post-op nausea and vomiting, acid aspiration syndrome (aspiration of gastric contents) allergies, fluid and electrolyte imbalance, awareness under anaesthetic (identify unconsciousness by an EEG score less than 60, 100 is fully alert), respiratory arrest: slow recovery from anaesthesia, suxamethonium apnoea (rare due to inability to break down of the drug, Complications of spinal anaesthesia: failure, neurological trauma, localised bruising and pain, respiratory depression with opiates, post-operative nausea and vomiting, bladder distention, slow heart rate, infection, postspinal headache and hypotension (blocking sympathetic nerves leads to vasodilation)

ANAEMIA - Describe the laboratory features of haemolysis. Outline the causes of haemolytic anaemia and their treatment

HAEMOLYSIS is the breakdown of red blood cells before the normal lifespan of 120 days this may be intravascular or extravascular (liver, spleen and bone marrow). Haemolysis itself is asymptomatic but the result will be anaemia. Investigations may show raised bilirubin, raised lactic dehydrogenase. The body may compensate by increasing reticulocytes. The spleen or liver can enlarge if extravascular whereas intravascular haemolysis may rise plasma haemoglobin, haemoglobinurea (redbrown urine) and possible methaemaglobinurea (ferric not ferrous iron in the haemoglobin molecule resulting in difficulty releasing oxygen). Causes include: malaria, thalassaemia, sickle cell, microangiopathic haemolytic anaemia, haematological malignancy, spherocytosis, elptocytosis, G6PD deficiency. Membrane red blood cell abnormalities can be identified with osmotic fragility testing, electrophoresis can identify haemoglobinopathies and the red blood cell lifespan can be determined by chromium labelling. Haemolysis is made worse by infection and parvovirus (which induces an aplastic anaemia by stopping red blood cell production in the bone marrow temporarily). Causes and Management: haemolysis may be immune or nonimmune mediated. Immune causes are drug induced (triggering red blood cell autoantibodies - penicillin or immune complexes - quinine), Autoimmune Haemolytic Anaemia (needs immunosuppression if binding occurs at body temperature or chemotherapy of binding occurs in the cold/Raynauds related), paroxysmal cold haemoglobinurea (with viruses or syphilis - self-limiting haemolysis) or acute transfusion reactions/haemolytic disease of the newborn. Non-immune-mediated causes include: microangiopathic haemolytic anaemia, infection (malaria) or paroxysmal nocturnal haemaglobinurea (needs anticoagulation and stem cell treatment).

Classify heart block and identify the ECG features of each type of heart block, describe ECG features of left and right bundle branch block and atrial and ventricular arrhythmias.

HEART BLOCK Here the PR interval is more than 3-5small squares/0.12-0.2 seconds. First degree: Prolonged PR as the electrical activity is a delay through the AV node. Second degree: MOBITZ 1/wenkeback - progressive PR lengthening until a beat is dropped due to AV node malfunction. MOBITZ 2: Fixed pattern of dropped beats. Third degree: Complete so P waves are dissociated. BUNDLE BRANCH BLOCK A defect in the conection from the AV node to the bottom of the ventricles. RIGHT is caused by an atrial septal defect, right ventricular hypertrophy, coronary artery disease but left is more likely to be aortic stenosis or an acute MI. Here looking at V1 and V6 use WiLLiaM and MaRRoW whereby a right BBB has a V1 Q wave so looks like a W but V6 does not so looks like an M. (Visa versa for left). ATRIAL FIBRILATION - irregularly irregular ATRIAL FLUTTER -Saw tooth P waves VENTRICTULAR FIBRILATION - uncoordinated contraction, ventricles quiver. VENTRICULAR TACHYCARDIA - Rapid contriction, wide QRS, no P waves.

HAEMOSTASIS - outline a plan of investigation for a patient complaining of easy bruising

HISTORY Muscle and joint bleeding indicates a coagulation defects (haemophilia a equals factor seven deficiency, haemophilia B equals factor 9 deficiency)whereas mucocutaneous bleeding may indicate a platelet disorder, thrombocytopenia or von Willebrand's. remember that systemic diseases such as level or kidney failure or connective tissue diseases can cause bleeding disorders. EXAMINATION telangiectasia, Kmart process, stigma of liver disease, splenomegaly (causes thrombocytopaenia). INVESTIGATIONS full blood count, coagulation tests.

HAEMOSTASIS - Discuss the clinical features, diagnosis and management of inherited bleeding disorder including haemophilia and von Willebrands disease.Discuss the clinical features, diagnosis and management of inherited bleeding disorder including haemophilia and von Willebrands disease.

Haemophilia A: factor seven deficiency inherited in an X linked recessive pattern (30% have no family history due to high rate of new mutations). Haemophilia B/Christmas disease: factor nine deficiency inherited in an X linked recessive manner. Haemophilia: presenting early in life or after surgery/trauma with bleeding into joints and muscle haematomas. Arthropathy can be crippling and raised pressure in compartments containing blood can cause compartment syndrome or nerve palsies. diagnosis is with raised APTT (indicating a prolonged intrinsic pathway) and low factor seven or factor nine on assay. Manage haemophilia by avoiding intramuscular injections and NSAIDs, compress and elevate minor bleeding, Desmopressin/recombinant ADH to raise factor seven levels. If more severe give infusions of the missing clotting factor. VON WILEBRANDS DISEASE: deficient von Willebrand factor leading to increased bleeding (at this access, menorrhagia, mucosal bleeding) that may vary in severity. investigations show arranged bleeding time but normal prothrombin time although activated partial thromboplastin time may be increased because von Willebrand factor binds to factor seven. Management is with desmopressin/recombinant ADH which increases von Willebrand factor and factor seven. the pill can be used to control menorrhagia and factor seven given in times of major bleeding or surgery. Other causes of clotting factor deficiency include liver disease, vitamin K deficiency, anticoagulant drugs and disseminated intravascular coagulation.

EVIDENCE BASED MEDICINE - Describe the main components of the health needs assessment process. Discuss the various ways of measuring ill health Describe how population characteristics may be measured and the effects of these on local outcome measures.

Health needs assessment is a systematic method for reviewing the health issues facing a population, leading to agreed priorities and resource allocation that will improve health and reduce inequalities. Methods: Surveys, Audits, Quality of life measurements etc.

HERNIA - HERNIA - Define hernia and the descriptive terms reducible, irreducible, obstructed, strangulated and sliding. Outline the principles of management of patients with hernia

Hernia: the protrusion of the Viscous or part of the Viscous through the walls of its containing cavity into an abnormal position. Reducible: its contents can return to the abdominal cavity spontaneously or with manipulation. Irreducible: its contents cannot return despite manipulation. Incarcerated: irreducible due to the presence of adhesions but in the absence of obstruction. Obstructed: the bowel within the hernia is blocked giving signs of pain, vomiting, distention an absolute constipation. Strangulated: vasculature is occluded by pressure on the neck of the hernia therefore the viability of the bowel is impaired. Usually veins are occluded first then the swelling results in arterial occlusion and eventually gangrene. Sliding: a hernia that contains a partially extraperitoneal structure (examples include the cecum other sigmoid colon). The SAC will not completely surround the hernia. Richter's hernia: only part of the bowel wall is caught and may become strangulated but not typically obstructed. Herniotomy: excision of the hernial sac. Herniorraphy: actual repair of the hernial defect.

CEREVROVASCULAR DISEASE - List the irreversible and reversible risk factors leading toward the development of ischemic stroke Describe the risk factors, clinical presenting features and pathological causes and consequences of ischaemic and haemorrhagic stroke.

ISCHAEMIC STROKE: Irreversible risk factors: Increasing age, diabetes, Familial hyperlipidaemia, Family history, personal history, Sickle cell disease. Reversible risk factors: Hypertension, atrial fibrillation, Poor diabetic control, smoking, obesity, high cholesterol, Inactivity, Excess alcohol (i.e. The risk factors for atherosclerosis). HAEMORRHAGIC STROKE: Irreversible risk factors: As above and also including clotting disorders such as lack of protein C and protein S. Reversible risk factors: As above and also including warfarin, anticoagulants Typically strokes present As described in the Bamford classification with hemianopia (Visual disturbances), hemiparesis, higher cerebral dysfunction (dysphasia, dysarthria, inattention. I.e. comprehension and language difficulties) and/or brainstem symptoms such as locked in syndrome. Consequences: death, Coma, Disability (poor motor function, poor higher cerebral function), contractures, Pressure sores, pneumonia, incontinence, emotional difficulties, Cognitive deficits. Many patients suffer with activities of daily living, swallowing and up to 10% can suffer seizures after a stroke. Haemorrhagic stroke or haemorrhagic transformation of a stroke can cause intracranial pressure to rise.

THE WHITE CELL - Describe the clinical features of lymphoma. Classify lymphomas into Hodgkin's and Non-Hodgkin's disease and to high-and low-grade groups. Outline the principles of treatment

Lymphomas are the malignant proliferation of lymphocytes. they accumulates in peripheral lymph nodes causing lymphadenopathy but may also be found in the blood or infiltrate organs. Most are derived from the lymphocytes. HODJKINS: Hodgkin's lymphoma is characterised by two mirror imaged nuclei turned Reed Sternberg cells. it is much more likely to occur in men and there are two peak incidences in the 20 - 30 and 50 - 70-year-old group. Risk increases if siblings affected, with EBV, with lupus, post transplantation, in the West and obesity. Hodgkin's lymphoma is slow growing, localised and rarely fatal. Hodgkin's lymphoma presents within large painless, non-tender, rubbery superficial lymph nodes. The size fluctuates spontaneously and nodes can become matted. 25% of people have fever, weight loss, night sweats, itching and lethargic. Lymph nodes may become painful with alcohol and mediastinal lymph node involvement can cause SVC or bronchial obstruction or pleural effusions. Patients presents with a large lymph nodes, cachexia, anaemia and enlarged spleen or liver. Hodgkin's lymphoma investigations include lymph node excision biopsy, bloods and then the ANN ARBOR system to stage lymphoma. NON-HODGKIN'S LYMPHOMA: this includes all lymphomas without Reed Sternberg cells. This includes Burkitt's lymphoma and classically presents in the 60 to 70 years age group. Non-Hodgkin's lymphoma may be associated with HIV, EBV, human herpesvirus eight, H. pylori (if gastric lymphoma). Can also occur post transplantation and in congenital immunodeficiency. Classification of non-Hodgkin's lymphoma: high-grade (rapidly dividing, present acutely and can be life-threatening - symptoms of rapid lymphadenopathy with systemic symptoms, aggressive bit curable) or low-grade tumours (divide slowly, months before diagnosis, widely disseminated at diagnosis and often incurable). Non-Hodgkin's lymphoma presents as superficial lymphadenopathy although 25% have extra nodal disease at presentation (throat, skin, bone, guts, lung symptoms). Patients may have fever, night sweats, weight loss, itching, anaemia, neutropenia and thrombocytopenia (bone marrow involvement). Investigations in non-Hodgkin's lymphomathe same as in Hodgkin's lymphoma with lymph node excision biopsy, bloods and then the use of the Ann Arbor staging system. non-Hodgkin's lymphoma has a worse prognosis than Hodgkin's lymphoma with a 30% five-year survival for high-grade and 50% five-year survival for low-grade. The management of all types of lymphoma is as follows: chemotherapy or radiotherapy or both. Consider stem cell transplantation in relapsed disease. Radiotherapy will increase the risk of secondary malignancy, heart and lung disease and hypothyroidism where is chemotherapy causes suppression of the immune system and acute myeloid leukaemia as well as infertility. Consider a acute lymphoma in SVC obstruction, facial oedema, shortness of breath and blackouts.

THE URETHRA, PENIS AND SCROTUM - Outline the cause of non-descent and mal-descent of the testis, the risks of this condition and its management. Discuss the pathology, clinical presenting features, diagnosis and management of torsion of the testis and epididymo-orchitis.

MAL DESCENT OF THE TESTES/Cryptorchidism: Cause: often this is found in Newborn babies (30% if premature, 3% if not) and will correct itself (80% within the first year of life). The testes itself can be along the line of descent, in the inguinal canal (most), ectopic, Hypoplastic, or not present at all. It is also more heavily associated with maternal obesity, diabetes and alcohol use during pregnancy as well as genetic conditions such as Down's syndrome and Prada Willi. Risks: an undescended testicle is more likely to be associated with infertility (even when relocated), inguinal hernias, testicular torsion and psychological morbidity. There is also an increased risk of testicular cancer especially a seminoma. Management: the primary treatment is watchful waiting but if the testes is not descended within six months an orchiopexy May be used to relocate and permanently fixed to the scrotum. This may involve endoscopy to find an ectopic testicle. Hormone therapy with injected hCG is thought to be an alternative with lower success rates. EPIDIDYMO-ORCHITIS: Inflammation of the testicle and epididymitis (more subacute than torsion). Cause: This is particularly seen with STI's such as chlamydia but is also an associated with mumps and brucellosis infection. Ischaemic epididymoorchitis can occur from vascular damage during a hernia repair. Features: Blood and semen, blood in the urine, severe testicular pain, swelling of the testes and possible lymphadenopathy in that area. Diagnosis: It is important to consider testicular torsion which presents in a similar manner. Other than that search for the infective cause (this usually involves a urinary STI screen). Management: NSAIDs and is an appropriate antibiotic. In some cases opiates are appropriate to relieve pain. TESTICULAR TORSION: Acute pain and tender to palpate in a young male, examination may be normal (can be high riding). Surgical untwist and tethering must be within 6hours - acute pain is torsion until proven otherwize. Remove if necrotic.

Outline the principles of management or local recurrence and metastatic breast cancer

METASTASIS - management is palliative Radiotherapy can help bone pain from boney mets. If oestrogen receptor positive hormaonal therapy can be helpful if negative consider combination chemotherapy. Remember the prognosis is poor and symptom relief is the main focus. RECURRENCE -This may be local, regional or distant/mets. Local recurrence is managed with a mastectomy (if the previous treatment was a lumpectomy) or radiotherapy. There must also be a thorough investigation to determine if mets are present.

HYPERTENSION - Discuss common investigations to exclude a secondary cause of hypertension and outline the common groups of drugs used to treat hypertension including indications, contraindications, side effects and rational combinations of drugs

Identify end organ damage: urine dipstick, EGFR, ECG and fundoscopy. Cynically hypertension that is essential is easy to control with blood pressure medication, secondary hypertension is far more difficult to control. Consider their current medications (things like steroids can cause hypertension), Measure levels of thyroid hormone, consider Dexamethasone suppression to diagnose acromegally, 24 hour urinary cortisol for Cushing's, Measure aldosterone to renin ratio when considering Conn's. You should listen for renal brewies And ultrasound the renal tract. Treating hypertension: always remember lifestyle advice around diet, exercise and smoking/alcohol. Cholesterol should also be controlled. Remember the following rule: Given ace inhibitor is less than 55 years old and nonblack. Give a calcium channel blocker for anyone over 55 or anyone who is black. If this does not completely control the problem then add a thiazide like diuretic. If this still does not control the problem add on a beta blocker, alpha blocker or spironolactone.

KIDNEYS AKI - Describe the assessment of a patient with renal failure including fluid balance. Outline the investigation of a patient with acute renal failure. Outline the principles of treatment. Outline the indications for referral for a specialist opinion/renal replacement therapy.

If acutely unwell think ABC. Assess kidney function (U&Es, creatinine). Perform and ECG and manage any hyperkalaemia. Check for renal, pre and post renal causes (BP, haemorrhage, glomerulonephritis, vasculitis, rhabdomylysis, BPH, blocked catheter). Fluid balance is vital.... First ask if they are dehydrated - input? output? low BP?dry mucus membranes, dec cap refil, diuretic medications. They need a 500ml crystaloid (saline) bowlus stat if theeir BP is <100 systolic, cap refil is extended, resp rate >20 or heart rate over 90. Once resus is complete give maintenance of 25-30/ml/kg/day plus replacement of any additional losses (stoma). Coninue monitoring weight, fluid balance, U&E, creatanine). Send for a specialist if resus is not working, stage 4/5 chronic kidney disease and if you think dialysis may be required.

LUNG CANCER - List relevant investigation for lung cancer and interpret results

Imaging: Xray (lobar collapse secondary to tumor mass, malignant bone erosion, pleural effusions). CT can identify mediasteinal spread or metastasis and can help to plan a biopsy. Biopsy: Brushing at bronchoscopy if by the bronchus. If more peripheral use a percutaneous needle biopsy under CT or USS guidance. If there s a pleural effusion then take a washout. If not surgery can obtain a directly visualised sample. Lymph node biopsies are important. PET scans are used for metabolically active cancers. If the cancer needs aggressive treatment consider the general health of the patient and their ability to tolerate. For a mediasteinal mass needs a CT/MRI as on Xray the mediasteinum just looks widened. Mediastinoscopy helps visualise the anterior mediasteinum or go via thee oesophagus for the posterior mediasteinum.

THE WHITE CELL - Interpret a blood count showing a leucocytosis and listcommon causes for neutrophilia and neutropaenia, lymphocytosis and lymphopaenia

The white blood cells are as follows: > Neutrophils ingest and kill bacteria/fungi/damage cells. >Lymphocytes are either T cell mediated immunity or antibody production. > Eosinophils are involved in allergic reactions and parasite infection. > Monocytes are macrophage precursors. > Basophils are involved in histamine release. LEUCOCYTOSIS = increased numbers of white blood cells in the blood. NEUTROPHILIA = increased circulating neutrophils, seen in bacterial infections, inflammation (MI, polyarthritis nodosa), myeloproliferative disorders, drugs (steroids), malignancy and stress (trauma, surgery, Burns, bleeds, seizures). NEUTROPENIA = decreased numbers of circulating neutrophils. seen in infections, chemotherapy, severe sepsis, antibodies against neutrophils (lupus, haemolytic anaemia), hypersplenism and bone marrow failure. AGRANULOCYTOSIS = an absence of neutrophils. LYMPHOCYTOSIS = increased numbers of circulating lymphocytes seen in viral infections, chronic infections, leukaemia and lymphomas. LYMPHOPENIA = decreased numbers of circulating lymphocytes seen with steroids, SLE, legionnaires disease, HIV, bone marrow infiltration, chemotherapy and radiotherapy.

TRANSFUSION - Outline the management of a transfusion reaction

There are several different types of transfusion reaction managed as follows: An acute haemolytic reaction: presenting with agitation, increased temperature, lowered blood pressure, flushing, abdominal or chest pain, oozing venipuncture sites or disseminated intravascular coagulation. Management involves stopping the transfusion, rechecking the identity of who the blood is intended for, inform haematologist, take blood to assess clotting, cultures and full blood count. Keep the intravenous line open with a line and treat the disseminated intravascular coagulation. In anaphylaxis slow or stop the transfusion, maintain the airway, give oxygen and calling anaesthetists whilst you administer anaphylaxis medication. In bacterial contamination presenting with a temperature, lowered blood pressure and right cause again stopped the transfusion and check the identity. Inform haematologist, send bloods and start broad-spectrum antibiotics In TRALI (transfusion related acute lung injury, a form of acute respiratory distress because of antibodies in the donor plasma) the patient presents with shortness of breath, cough and a pleural effusion. Again stopped the transfusion, give oxygen and treat for acute respiratory distress. In non-haemolytic febrile transfusion reaction the patient develops a fever and shiverring and our after transfusion has begun. Stop the transfusion and give an antipyretic. In allergic reactions stop the transfusion and give Chlorphenamine 10mg. In fluid overload leads presenting with shortness of breath, hypoxaemia, raced heart rate, raised the JVP and basal crepitations stop or slow the transfusion and consider a diuretic alongside oxygen.

HAEMORRHOIDS - Discuss the anatomy of haemorrhoids. Describe the role of the anal sphincters in maintaining faecal continence. State the aetiological factors of haemorrhoids. Describe the symptoms and complications of haemorrhoids. Discuss the differential diagnosis of rectal bleeding. Describe the physical examination of a patient with haemorrhoids, including proctosigmoidoscopy. Outline the principles of management of patients with symptomatic haemorrhoids including investigation and differential diagnosis appropriate to patient factors including history and age.

These are a vascular cushion, covered by mucosa containing a branch of the superior rectal artery and tributaries of the superior rectal vein. therefore, they are not simply dilator drains. They occur where the superior rectal artery and vein enter the muscle. Classification: first degree do not prolapse from the anus, second-degree prolapse on defication return spontaneously, third-degree prolapse and remained so unless manually repositioned. also remember that internal haemorrhoids are above the pectinate line (typically painless) and external haemorrhoids are below. Anal sphincters: the external sphincter is in a state of tonic contraction and can be voluntarily tightened such as during coughing or sneezing. The internal sphincter is entirely involuntary. These are the main keys to maintaining faecal continence. Cause of haemorrhoids: although not 100% certain, they are associated with diarrhoea or constipation, straining and a low fibre diet. they are also associated with obesity and prolonged periods of sitting. Presentation of haemorrhoids: may be asymptomatic although the most common presentation is with fresh blood, minor pain and itching. Rectal bleeding differential: Investigations: typically grades two and three haemorrhoids can be visualised and internal grade one haemorrhoids can be palpated on PR. Endoscopy with an anus scope can be helpful. Management: injection with alcohol will cause scar formation thus shrinking the Hemorrhoid. Other methods to shrink include rubber band ligation or coagulation with infrared devices. If these fail formally excise the haemorrhoids. Complications: presenting with more severe pain, prolapsed haemorrhoids can thrombose. This is known as a perianal haematoma.

PLEURAL EFFUSION - Obtain a relevant history from a patient with a pleural effusion. Discuss the investigation of a unilateral pleural effusion.

Think of the causes: exudate (infection - fever, weight loss, malaise, known TB/TB risk factors), transudate (liver/kidney/heart function?) Expect SOB, a dull to percuss area of the chest, tachypnoea, reduced chest expansion, tracheal deviation away (towards a white out is atelectasis) if large and asymetric, absent breath sounds over a large efustion, Pleural rub as well as signs of the cause such as pneumonia. On Xray the costophrenic angles blunten with a curved line as a fluid level. Fluid appears to trak up the lateral chest wall. Remember that to be spotted on x-ray pleural effusion must be at least 200 mL. Ultrasound will confirm that the fluid is not inside the lung. Only use CT scan if you suspect malignancy. Pleural aspiration may be required to determine if the fluid is pus or lymph. If blood is presents consider pulmonary infarction or malignancy but remember that the procedure itself may be traumatic causing bleeding. Biochemical analysis of an aspiration allows you to differentiate between transudate and exudate, gram staining and culture can help determine suitable antibiotics. Pleural biopsy can be ultrasound or CT guided to enable microbiological analysis of tissue.

ACUTE CORONARY DISEASE Describe the causes, morphology, pathological consequences, typical history, examination features, differential diagnosis, management of the acute coronary syndromes ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation (NSTEMI) and unstable angina (UA).

This encompasses both myocardial infarction and unstable or crescendo angina. Angina is explained previously. Causes: Unstable angina:An artheromatous plaque that fissures within an adherent platelet rich Thrombus and local coronary artery spasm. Myocardial infarction: an occlusive thrombus usually where a plaque has ruptured. (It may spontaneously lyse every few days by this time the myocardium has become necrotic. History: infarction progresses over several hours so often it is possible to salvage some myocardium. There is pain, breathlessness, vomiting, collapse. The patient goes pale however, M I can be silent or simply present as breathlessness. (Atypical presentation is more common with diabetics and elderly patients). Anything to be is usually due to an arrhythmia or low blood pressure. There may be sudden death from ventricular fibrillation or asystole. Heart failure may follow. Examination: pale, sweaty, in obvious pain. There may be an arrhythmia and signs of atheroma risk factors (obesity). Troponin and creatinine kinase (non specific) are raised within 6 hours indicating myocardial damage. ECG (unless normal as seen in 1/3rd initially - repeat ECG is important) shows ST elevation or non-ST elevation and there may be a new bundle branch block. Without ST elevation then maybe persistent T wave inversion. Biochemical markers: creatinine kinase, troponin, Raised ESR, raised CRP. Differential diagnosis: this is why including all the causes of central chest pain (respiratory, gastrointestinal, anxiety, musculoskeletal). Management: ST elevation (Complete blockage)= MONA (Morphine, oxygen, nitrates, Aspirin. For non-ST elevation (Incomplete blockage) = BROMANCE (Beta-blockers, reassure, oxygen, morphine, aspirin, nitrates, clopidogrel, enoxaparin).

THE PLATELET - Outline the clinical features, investigation and treatment of immune thrombocytopaenia

This has many names, for example ITP or idiopathic thrombocytopenic purpura. Cause of thrombocytopenic in general: reduced platelet production in the bone marrow or excessive destruction (in the spleen). Impaired production may be because of aplastic anaemia, megaloblastic anaemia, bone marrow malignancy or bone marrow suppression (drugs and radiotherapy). Excess destruction may be because of immune thrombocytopenic purpura, other autoimmune diseases, haemolytic uraemic syndrome or hyper splenism. The specific cause of ITP is unknown but bone marrow is normal. Platelets become oxidised by antibodies and are removed by binding to macrophages. presentation: usually in children this is a cute and self-limiting after a viral infection and requires no treatment. In adults the presentation is more chronic and associated with other autoimmune disorders. Patients have increased bleeding and bruising. The spleen will not be enlarged and major bleeding is rare. Investigations: full blood count shows an isolated low platelets, bone marrow examination will show normal or increased levels of megakaryocytes (platelet precursors) and platelet autoantibodies may or may not be found. Treatment: none for children (avoid contact sports). In adults the first-line therapy is oral steroids or intravenous immunoglobulin (if correction is needed quickly for something like surgery). Second line is the next to me and if this fails attempt further high-dose corticosteroids. Some require platelet transfusions in the cases of extreme haemorrhage.

SUB DURAL HAEMORRHAGE - List the predisposing factors which make a patient vulnerable to developing subdural haemorrhage Describe the clinical presentation of a chronic subdural haemorrhage Describe the CT scan appearance of a subdural haemorrhage, and how it would change with time. Describe the management of a patient once a subdural haemorrhage is detected, with specific reference to who's advice should be sought.

This is a Venous bleeds whereby cortical veins bridging between the dura and brain rupture due to trauma. Risk factors: Subgerminal haemorrhage classically occurs in patients with a shrunken brain after a fall. This means alcoholics and the elderly. Other risk factors includes a predisposed to bleeding such as being on warfarin. Shaken babies are predisposed this condition due to the trauma. Presentation: This may be acute (Often fatal), sub acute or chronic. As it is Venous typically onset is chronic - Gradually increasing headache and confusion. There may be fluctuating levels of consciousness, irritability and seizures. CT scans: Haematoma appears as a crescent Around the brain. Initially the blood shows up as white and hyperdense, Around one months it becomes isodensity and difficult to see but in three months this old haematoma can be seen as a hypodense dark crescent. Management: Small subdural haematomas can be managed conservativly (monitoring). Other small haematomas can be removed with a Small catheter. Larger haematomas require neurosurgery (craniotomy for evacuation).

EPIGASTRIC HERNIA - List common presenting features, including epigastric pain and/or a lump in the epigastrium. Distinguish on examination between an epigastric hernia and a divarication of the rectus abdominus muscle, and describe why one requires surgical treatment whereas the other doesn't.

This is a fat herniation that arises in the midline through the linea alba and is typically small and difficult to feel. It rarely contains any bowels but often contains extraperitoneal facts and causes symptoms out of proportion to its size. Presentation: usually an obese or pregnant person causing epigastric pain (but often no discernable mass therefore there are often multiple unnecessary investigations). Divercation of the rectus abdominus: also termed diastasis recti, when there is a gap greater than 2.7 cm (benign, unlike epigastric hernia, this will not trap tissues/give significant symptoms) between the rectus abdominus muscles. there is no associated morbidity or mortality and the cause is stretching of the linea alba seen in newborns and pregnant women. a ridge is seen from xiphoid process to the umbilicus. Surgery is only required in extreme cases and never whilst the mother is still pregnant.

HAEMOSTASIS - Outline the clinical management of over-anticoagulation with warfarin

This is dependent upon the INR. 4.5-6 = reduce the warfarin dose or omits and restart when INR <5. 6-8 = stop the warfarin and restart when INR<5 >8 with no significant leads = stop the warfarin and give up to 2 mg vitamin K orally with daily INR. Any INR with a major bleed = stop the warfarin, give prothrombin or fresh frozen plasma plus up to 10 mg vitamin K intravenously. Monitor INR. Remember that giving vitamin K will not work immediately.

HYPOCALCAEMIA - List the causes of acute and chronic hypocalcaemia Describe the symptoms and signs, investigation and treatment of hypocalcaemia.

This is much less common than high calcium. Remember that calcium will go down if there is low albumin (calcium bound albumin or free and physiologically active), low vitamin D (which is needed for the absorption of calcium), renal failure, hypoparathyroidism, acute pancreatitis (calcium stones form in the pancreas) or low magnesium (Mg usually keeps Ca in the cells). Acute causes: Alkaloses, as in hyperventilation, can cause ionised calcium to be low despite normal serum calcium. This is because alkalosis alters the affinity of albumin for calcium meaning that more calcium is bound to albumin and less is available in its physiologically active state. Chronic causes: Magnesium depletion in patients with malabsorption causes low-calcium because it is ordinarily magnesium's job to keep calcium in the cells Hands low magnesium decreases parathyroid hormone secretion. Hypoparathyroidism is the most common cause of low calcium which may be due to thyroid or parathyroid surgery, Immune mediated causes or rarer causes (iron deposition in haemosiderosis, copper in Wilson's). Symptoms and signs: The patient will be weak with petichiae, Tetani, bone pain and layngospasm. Signs include Chvosteks (facial twitching on tapping the Masseter) and trousseau (Spasm of the hand when a blood pressure cuff is applied for several minutes). Investigations: Hypocalcaemia can cause papilloedema and prolonged QT (so perform an ECG). Measure for lowered potassium and alkalosis. And consider that it can cause Ricketts in children and osteomalacia in adults. Treatment: Chronic treatment involves oral calcium and vitamin D, Recombinant parathyroid hormone if there is Hypoparathyroidism and consider alandronic acid for osteoporosis. More acutely: gives an immediate calcium gluconate with cardiac monitoring. If there is associated low magnesium also give magnesium chloride. Remember pseudo hypoparathyroidism whereby high levels of PTH are produced but the tissues are resistant to its action resulting in low calcium (and often other associations such as short fingers, rounded face, obesity and subcutaneus calcification as seen in Albright's osteodystrophy).

KIDNEY TRANSPLANTATION - Outline the indications for transplantation in patients with chronic renal failure. Outline the complications of this procedure and the need for immunosuppressive therapy following surgery. Outline the moral and ethical issues associated with renal transplantation.

This is when a cadaveric or living donor Donates their kidney to a patient with end-stage renal failure (Regardless of cause, When EGFR is less than 15). The main causes are malignant hypertension, infection, diabetes, Glomerulosclerosis and polycystic kidney disease. Renal tumours such as Wilms' tumour in children and renal cell carcinoma and adults can also be treated with transplantation. Contraindications: HLA and blood group matching donor, current smoker, obesity, poor pulmonary and cardiac function. Remember that in most cases the old kidney is not removed so the new one is transported into the groin connected to the iliac veins and arteries. Complications: Death, rejection (Acute or chronic- Acute cellular rejection by T lymphocytes, hyperacute rejection by pre-existing antibodies from previous exposure, acute vascular rejection where antibodies formed after the transplants or chronic failure as the transplants fibroses), Bleeding, infection, Electrolyte imbalance, Proteinuria and all of the side-effects of the immunosuppressive medication.The average kidney Survives 10 to 15 years. The mainstay of immunosuppressive therapy is prednisolone. Long-term use (as is required) is associated with opportunistic infections, cancer, cataracts, Glucose intolerance, diabetes, Muscle weakness and osteoporosis. To further reduce the risk of transplant rejection and to lower the doses of prednisolone used other immunosuppressive agents are added in conjunction. Other immunosuppressants include azathioprine and cyclosporin. Ethics: There is a black market for kidneys in which donors are exploited by salespersons, Hepatitis and HIV are often spreadAnd there is a raised risk from the surgery to both the donor and recipient.

PORTAL VENOUS HYPERTENSION - Describe portal venous anatomy. Define portal hypertension and classify its causes. Describe the clinical manifestations of portal hypertension.

This is when there is raised blood pressure in the portal vein and its tributaries. The hepatic portal vein drains the gastrointestinal tract, spleen and liver - it is formed from the superior mesenteric vein and splenic vein (which meets blood from the inferior mesenteric vein) converging. The hepatic portal vein is technically not a true vein because it drains into the capillary network of the liver after splitting into the right and left hepatic portal veins. This capillary network then drains via the hepatic veins into the inferior vena cava. Portal hypertension: a hepatic venous pressure gradient greater than 5 mmHg. Presentation: because of the reins's portal venous pressure blood is shunted elsewhere causing ascites, splenomegaly, hepatic encephaliitis (blood needs to get from the portal vein to the liver to be filtered) and portocaval anastomoses (oesophageal varices, caput medusa, gastric varices, anorectal varices). Therefore patients complain of the distended abdomen with possible visible abdominal veins or present with a major bleed from ruptured oesophageal varices. Causes: consider the causes of portal venous hypertension as prehepatic, post-hepatic or intrahepatic. PREHEPATIC: congenital atresia of the portal vein or portal venous thrombosis. INTRAHEPATIC: liver cirrhosis (alcoholic, non-alcoholic fatty liver disease), liver fibrosis (Wilson's disease, haemochromatosis), granulomatous disease (TB). POST HEPATIC: any obstructions such as hepatic vein thrombosis, inferior vena cava from basis, congenital atresia or constrictive pericarditis. Management: treat the cause, portosystemic shunts can make some of the blood bypass the liver (these are termed selective if they only bypass non-mesenteric blood, meaning the liver still filters intestinal flow), prevent bleeding medically or with banding of varices, salt restriction and diuretics for ascites, antibiotics and lactalose enemas to prevents encephalopathy.

THE SPLEEN - Discuss the potential causes of splenic rupture

This may be spontaneous, traumatic (blunt force - sports, road traffic collisions, domestic violence etc). gunshots and knife wounds are a lot less likely.

ASTHMA - Discuss the importance of identifying occupational asthma.

This should be considered in any working age individual who develops new onset asthma. Especially when work holidays cause improved symptoms and there is a latency period of up to a year from starting the job. Skin prick testing for allergins will be positive. As with all asthma, identifying and avoiding precipitants is important. Prevention may involve better education of workers, respiratory protection and exposure limits. The patient may require different work tasks or even a new job and compensation may be paid by the employer as well as funds to alter the workplace. At risk occupations include veterinarians (animal proteins), miners, adhesive handlers, cleaning staff, seafood processors, plastics and textile workers etc.

OPERATIVE AND POSTOPERATIVE MANAGEMENT - Describe the immediate postoperative care of the surgical patient by proposing a concise management plan.

This varies, think.... diagnosis, condition; disposition of the patient (eg ward, home, ITU); frequency of vital signs; requirements for analgesia; activity restrictions; wound care; tube and drain care; diet orders; intake and output orders; special nursing care orders; pulmonary physiotherapy orders; required fluids and medications; the indications for prophylactic antibiotics; necessary laboratory or radiological procedures; special monitoring support and instructions for use of equipment; special circumstances under which the physician is to be notified

CEREVROVASCULAR DISEASE - Outline the commonest causes of disability in people with impaired mobility.

Those with impaired mobility can have significant psychological problems such as depression as they are far more likely to be isolated and integrated into society. Other problems include blood clots. Consider deep-vein thrombosis, pulmonary embolism as well as an increased risk for strokes and cardiovascular disease.

HAEMOSTASIS - Discuss the clinical use of thrombolysis, including monitoring and complications

Thrombolysis is achieved using fibrinolytic agents such as streptokinase (because this is derived from cultures of Streptococcus antigens develop preventing repeated use). Side-effects include bleeding, nausea, vomiting and arrhythmias. Plasminogen activators such as alteplase may also be used for thrombolysis - these have a higher risk of intra cerebral haemorrhage but do not have antigens and do not give rise allergic reactions. Give alteplase if the patient has previously had streptokinase. Indications:STEMI, /without contraindications. always perform a CT head 24 hours after thrombolysis to identify any bleeding. Contraindications: bleeding, prolonged or traumatic CPR, pancreatitis, recent surgery, previous allergy, pregnancy, varices, peptic ulcer etc.

THE PLATELET - Discuss the role of platelets in the pathophysiology of vascular disease including vascular thrombosis and platelet emboli

Thrombosis: ordinarily endothelial cells prevent activation of the coagulation cascade by..... > Intact endothelium preventing platelets from coming into contact with collagen and von Willebrand factor that trigger platelet aggregation. > Prostacyclin and nitric oxides prevents platelet adhesion and aggregation to the endothelium > Thrombomodulin on the endothelial surface binds to any form then and initiates the anticoagulant effects of protein C and S. > The Endothelium produces heparin like modules to inhibit the coagulation cascade. > The endothelium produces plasminogen activator is to produce plasmin which lyses fibrin > antithrombin three inhibits coagulation. > blood flow itself is such that platelets are at the centre of a vessel. However, endothelial damage will expose collagen and von Willebrand factor resulting in platelet adhesion via surface glycoproteins. Once attached, platelets stimulate further platelet aggregation to form a plug. Prostaglandin thromboxane is produced by platelets causing vasoconstriction and further platelet aggregation. Fibrin is produced. Embolism: occlusion of the vessel by material that has been transported in the bloodstream. For example, strokes, pulmonary emboli, ischaemic limbs.

PERIANAL INFECTION - Discuss the role of anal crypts in perianal infection. Outline the symptoms of patients with perianal infections. Describe the various types of perianal infections. Describe the physical examination of patients with perianal infections.

Typically an abscess because of blockage of the anal crypts whose role is to lubricate motions before they are past. ANORECTAL ABSCESS: Abscesses are commonly seen as emergencies that may have developed from anal gland infections (anal crypts) infected by intestinal organisms such as E. coli, or from skin infections such as staphylococcus. Symptoms: severe throbbing pain worse on sitting, fever, tachycardia. Management: surgical drainage, packing and healing by secondary intention. There may be an underlying fistula the requires laying open or a seton. PILONIDAL ABSCESS: meaning nest of hair, typically in the inter-gluteale cleft hairs have worked their way into the skin resulting in an abscess. More common in teenagers and young adults whose occupations involve prolonged sitting. The sinuses asymptomatic until it becomes infected and requires incision and drainage followed by packing and healing by secondary intention. Later on, surgically remove the tract. Recurrences common.

PLEURAL EFFUSION - Discuss the management of pleural effusion and empyema.

Typically aspiration is therapeutic relieving breathlessness. Remember that removing more than one and a half litres at a time may cause re-expansion pulmonary oedema. An effusion should never be drained to dryness before establishing a diagnosis as biopsy is impossible without fluid present. Most important is treating the underlying cause. For example, heart failure, pneumonia, pulmonary embolism. Otherwise diffusion will simply redevelop. An empyema will only heal if infection is eradicated and the empyema removed with drain insertion. Sometimes regular flushing via a chest drain is required. Surgical intervention is required for the pass and to break down any delusions that are formed. Empyema gives a significant morbidity and mortality as the damage it causes prevents movement of the lung.

HYPERTENSION - Outline the difficulties of defining hypertension and outline the levels of blood pressure defined as normal, borderline or raised including the need to confirm with a minimum of three measurements.

Typically greater than 140/90 although there is considerable variation in the population and those with additional risk factors such as diabetes should be aiming for lower blood pressures Of 130/80. It is an asymptomatic disease that significantly increases the chances of cardiovascular disease, stroke, aneurysms and peripheral vascular disease. At least three measurements are required to diagnose hypertension as blood pressure goes up with a whitecoat effect, stress, exercise etc. Misdiagnosis can also lead to dangerous postural hypotension with over medication that increases the risk of falls and their associated morbidity. Remember normal blood pressure is arranged between 100-140/60 - 90. Stage one hypertension is greater than 140/90, stage II hypertension is greater than 160/100 And severe hypertension is greater than 180 Systolic or 110 Diastolic.

Describe the characteristic, and contrasting, features of chest pain resulting from AORTIC DISSECTION. ANEURYSMS - Describe the pathophysiology of arterial dissection and outline clinical presentation, medical and surgical treatment, complications and causes of death.

When a breach in the integrity of the aortic wall allows arterial blood to enter the media which splits forming a true and false lumen. This can damage the aortic valves or compromise the branches off the aorta. Usually the false lumen rejoins he true lumen (double barrel aorta) but the lumen may also open to te pleural space or pericardium. Cause: Hypertension, aortic atheroslerosis, aortic anyerism, marfans, ehlers danlos, pregnancy, trauma, iatrogenic. Type A = Ascending aorta involved. Type B = Ascending aorta not involved. Presentation: Anterior chest pain if the ascending aorta is involved, intrascapular chest pain if the descending aorta is involved. Pain is abrupt in onset, tearing and seen in a hypertensive patient (unless there is a haemorhage). If the aortic branches are occluded a dissection can present with: MI, stroke, paraplegia, an acute abdomen,renal failure or acute limb ishaemia. Investigations: Chest Xray shows a widened mediasteinum and distorted aortic knuckle. CT shows a double lumen. ECG may show LVH (linked to long standing hypertension). Echo may show aortic regurg and the dilated aorta (possibly also the dissection flap). Management: Mortality rate is 1-5% per hour so this is an emergency. If type A operate to replace the ascending aorta. Type B is more likely to be treated medically (get MAP 60-75mmHg using beta blockers, or calcium channel blockers. Percutaineous repair is a lower risk surgery involving stenting or fenestrating the lumen (allowing the false and true to freely connect).

HERNIA - Define femoral hernia. Describe the symptoms and signs of patients with femoral hernia. Perform the physical examination of patients with femoral hernia.

When a hernia protrudes having emerged through the femoral canal (which normally contains only fat and lymph nodes). The medial border of the femoral ring is the sharp edged lacunar ligament making femoral hernia is much more likely to strangulate than inguinal hernias. considering the landmarks: anteriorly will be the inguinal ligament, posteriorally the pectinatee ligament and latterly the femoral vein. This means that these hernias appear below and lateral to the pubic tubercle (whereas an inguinal hernia is above and medial to the pubic tubercle). Presentation:a lump in the groin that is more prominent on standing, coughing. there may may not be paying depending upon whether or not there is a complication and, unlike in inguinal hernias, the cough reflex is absent. Management: Herniotomy plus herniorraphy.

ACUTE HYDROCEPHALUS - Describe the clinical presentation of an acute hydrocephalus List 3 patient groups most at risk of developing an acute hydrocephalus. Describe the immediate investigation and management of suspected acute hydrocephalus

When there is abnormal accumulation of cerebrospinal fluid in the brain that raises intracranial pressure. Congenital causes include spina bifida and venous malformations words acquired causes include meningitis, trauma, Tumours and cysts. Hydroephalus can be obstructive (noncommunicating) Or communicating (but with improper reabsorption Through the arachnoid granulations). Presentation: Acutely, there will be signs of raised intracranial pressure (Headache, nausea, vomiting, coma, confusion). In infants the fontanel will bulge And sutures will separate. Young infants may be irritable and sleepy. Learning difficulties and epilepsy are more common. Risk factors: Developmental abnormalities of the brain or brain vasculature, Premature birth, Uterine infection, Brain tumours, trauma. Investigations: For infants and ultrasound may be sufficient. For adults using MRI/CT, Confirm the presence of hydrencephalus and look for a cause (such as stenosis of the aqueduct of Sylvius). Management: This involves syrigmus shunting to permit drainage into the peritonaeum, pleura or atrium. Remember that shunts may become infected, blocked or disconnected and can be outgrown.

HYDROCEPHALOUS- Describe the clinical triad reflective of normal pressure hydrocephalus

When there is decreased reabsorption of cerebrospinal fluid causing ventriculomegally which may be idiopathic or secondary (to trauma, bleeding, infection, tumour). It is turned normal pressure because on LP there is Normal/hi normal CSF pressure despite the increased volume of fluid - Meaning few patients present with raised intracranial pressure symptoms such as nausea, vomiting and altered consciousness. The clinical presentation is with the triad of incontinence, Ataxic Gait and Frontal dementia sometimes described as wet, wobbly and wacky. It is therefore a differential for Parkinson's, dementia and Alzheimer's. Gait: because the lateral ventricles enlarge and put pressure on the corticospinal motor fibres. Frontal dementia: because the lateral ventricle is i enlarge and put pressure on the Frontal and limbic fibres. Incontinence: detrusor instability is a late symptom, Perhaps because of the dementia. Confirm by relieving symptoms on draining and treat with a shunt.

OBSTRUCTIVE JAUNDICE - Describe the clinical features of obstructive jaundice and outline their pathophysiology.

Yellowing (greater than 50 mm/l) of the skin and mucus membranes, especially the sclera, itching, pale stools, dark urine (urine becomes darker because conjugated bilirubin enters the urine, stool becomes pale becaause no bilirubin can access the bowel because it is the other side of the obstruction). Remember that itching is not because of the bilirubin, but because bile salts deposit in the skin. Pain is variable and more often due to the cause, such as gallstones. Examination may also find enlarged lymph nodes or signs of alcoholism (chronic pancreatitis, the main risk factor for pancreatic cancer). Remember cancer red flags and signs of chronic liver disease (for example, raised estrogen causes spider naevi, testicular atrophy, gynaecomastia. Other signs of liver disease include liver flap, palmer erythema, dupuytren's contracture, ascites, Courvoisier's law)

OBSTRUCTIVE JAUNDICE - Classify intrahepatic and extrahepatic causes of obstructive jaundice and outline underlying pathology.

Yellowish discolouration of the skin caused by high bilirubin. Consider obstructive jaundice as pre/intra/post hepatic Prehepatic-haemolytic anaemia. Hepatic-hepatitis, see above, or drug induced (chlorpromazine) Post-hepatic - typically due to obstruction. The main 2 causes are gallstones and cancer at the head of the pancreas.

IMMUNOLOGY - Describe the ways in which the immune system may be manipulated therapeutically

the immune system can be manipulated to increase its activity, decrease its activity water remembering new antigen. Drugs can stimulate proliferation of the bone marrow (cytokines) or immunosuppress (azathioprine). Vaccination will add a new antigen. In patients with antibody deficiencies donor antibodies can be given regularly. Specific preparations can be made by vaccinating the donors prior to sample donation (this is the basis of postexposure prophylaxis of advertisers, rabies, tetanus etc). Monoclonal antibodies can be artificially produced from a single B-cell clone (....zumab or herceptin) but are very expensive. Desensitisation: subcutaneous injection of allergens weekly for 15 weeks with maintenance doses every six weeks. Interferon alpha is an anti-viral agents using the treatment of hepatitis. interferon gamma enhances Phaedo site function, used in primary immunodeficiency. granulocyte stimulating factors can be used to enhance neutrophil levels and reduce neutropenia during bone marrow transplantation for malignancy.

CONGESTIVE CARDIAC FAILURE - Outline the drugs used in the long-term management of CCF

Management of acute pulmonary oedema: a medical emergency, sit the patient up, give high flow oxygen, nitrites To control blood pressure and an intravenous loop diuretic. Management of chronic heart failure: General measures: education, daily weighing to determine fluid load and adjust diuretic treatments and treatment of the underlying cause. Improving cardiac function: this can be done by increasing contractility, optimizing preload or decreasing afterload. Diuretics: this reduces preload and reduces congestion (systemic and pulmonary). A fall in preload will reduce the cardiac output (Starling curve) which is not desirable but getting rid of excess fluid treats the symptoms. Excessive therapy causes hypotension, lethargic and renal failure (hence daily weighing in some patients). Loop diuretics include furozemide. Spironolactone and potassium sparing diuretics may be used in heart failure with left ventricular dysfunction but can cause high potassium. ACE inhibitors: these prevent the production of ace in the lung which converts angiotensin 1 to angiotensin two. Without it there is less Aldosterone and so lower blood pressure/Less water retention (but higher potassium -Sodium is spared at the expense of potassium). Angiotensin receptor blockers: these block angiotensin twos action on the heart giving much the same effect as ACE inhibitors. Useful in patients who cannot tolerate ACE inhibitors. They are more likely to cause high potassium and renal dysfunction than ACE inhibitors. Vasodilators: nitrates can be used to venodilate and reduce preload. Arterial dilators will reduce afterload. They tend to be badly tolerated and cause low blood pressure. Beta-blockers: reduce the sympathetic drive to the heart slowing it down. Digoxin: controls the rate in patients with heart failure and atrial fibrillation. Amiodarone: an antiarrhythmic for the treatment of symptomatic arrhythmias and not prevention. Remember also that there are implantable defibrillators (for symptomatic arrhythmias), coronary revascularisation (PCI/CABG), transplants (in coronary artery disease or dilated cardiomyopathy with cyclosporin, Azathioprine and steroids for immunosuppression lifelong) Also used whilst waiting for heart transplants are ventricular assist devices - a pulsatile pump that is either external or implanted to act in place of a failing heart (i.e. it unloads the ventricles and loads back into the pulmonary and systemic circulations. Complication rates are high - bleeds, embolism, infection).

CHRONIC PERIPHERAL ARTERIAL DISEASE -Describe the radiological and surgical treatment choices for patients with occlusive arterial disease according to affected vessel. Describe the symptoms, signs, investigations, differential diagnosis and treatment of chronic mesenteric vascular occlusive disease

Management: Conservative management: stop smoking and keep walking. Manage any comorbidities such as anaemia, hypertension, hyperlipidaemia, diabetes and heart failure. Encourage weight loss and add aspirin and statin. More severe claudication warrants an angiogram to see if angioplasty is viable. If gangrene has set in an amputation may be necessary. Angioplasty: typically radiological intervention with a balloon at the end of the catheter which can then be stented. This doesn't even require a general anaesthetic and carries minimal risk to the patient. Usually, we only consider surgery if critical ischaemia or severe claudication is making the patient's life intolerable. This involves bypass grafting using artificial Dacron grafts, the exhilarating arteries or the long saphenous vein. MESENTERIC Vascular disease: Lack of blood supply to the small Intestine which may occur acutely or chronically. Typically there is abdominal pain after a meal, unintentional weight loss, vomiting and a fear of eating. Investigate with angiography or CT. There may be evidence of lactic acidosis. Treatment again involves risk modification, smoking cessation, heparin as medical management or interventional radiology (Stenting)/bypass grafting. If severe, bowel resection may be required.

PNEUMOTHORAX - Describe treatment options including chest aspiration or intercostal underwater chest drain. Outline the indications for surgical pleurectomy and pleurodesis. Describe the emergency treatment of a tension pneumothorax.

Management: a primary pneumothorax with the long edge less than 2 cm from the chest wall without significant symptoms will resolve without intervention. A young patient with a moderate or large spontaneous pneumothorax may require needle aspiration. Patients with a significant underlying lung disease (secondary pneumothorax) the resulting respiratory distress necessitates the insertion of an intercostal chest drain and inpatient observation - typically these patients are over 50 with respiratory compromise. Tension pneumothorax: this is an emergency requiring immediate release of the positive pressure by insertion of a blunt cannula into the pleural space. A chest drain follows, Inserted at the fourth fifth or sixth intercostal spaces in the mid-axillary line. An underwater seal is used and wants the drain is stopped bubbling it can be removed. Bubbling after 5 to 7 days necessitates surgery. Close pneumothorax means that the patient cannot fly is gas will expand at higher altitudes. Patients should stop smoking and diving is dangerous. PLEURODESIS - this is recommended following a second pneumothorax or in a first episode pneumothorax if respiratory reserve makes recurrence hazardous as well as if a drain previously inserted has been bubbling for more than a week. The procedure artificially a bitter rates the pleural space Chemically with talc or surgically by irritating the pleura. PLEURECTOMY - Removal of the pleura to prevent further fluid accumulation, This can be performed prior to pleurodesis adhering the parietal pleura to the chest wall. It is used more commonly for a mesothelioma.

VENOUS THROMBO-EMBOLIC DISEASE - Discuss the treatment of a deep vein thrombosis, the methods of administering and monitoring appropriate anticoagulants. Outline the indications for primary thrombo-prophylaxis. Administer a VTE risk assessment using a recognized risk scoring system.

Management: elevation, Analgesia and a low molecular weight heparin anticoagulated. (Stop propagation of the clot but allow the body to thrombolyse itself in less cluttered limb threatening). Follow-up the five days of heparin with warfarin a coumarin (INR 2-3 - first signs of too high are oral bleeding and haematurea). Treat for three months if there is a known cause that you can remove, six months otherwise.) or one of the new anticoagulants (riveroxiban). Remember that DVT recurs in about 3% a year if provoked, 8% unprovoked.With a 40% risk at five years. Use the wells score to determine the need for hrombopropylaxis in hospital (clexane aka enoxaparin). Consider current features of DVT, previous clots, pregnancy, malignancy, Surgery etc.

INFECTIVE ENDOCARDITIS - Define bacterial endocarditis and who is at risk. Describe the morphology and histological changes seen and the pathological complications of infective endocarditis.

Microbial infection of the heart valves typically bacterial (commonly staph epidermidis, staph aureus from IVDU - may even cause abscesses, strep viridens/normal commensals of the mouth, enterococci/gut commensals). Damaged valves attract platelets and fibrin that can be colonised by bacteria. Typically someone with pre-existing endocardial damage gets infection and vegetations from opportunistic organisms although highly virulent organisms can infect normal valves. Infections grow well on the valves as they are avascular and platelet/fibrin aggregates protect bacteria from the host defences. Aggregates can grow large enouugh to obstruct. Risk factors: IVDU, dental surgery, congenital defects (Septal defects - cause high pressure jets of blood), cardiac surgery, prosthetic valves. Complications of endocarditis.......20%mortality, emboli (stroke, MI, PE), kidney failure, abscess formation, subacute infection, anyerisms, valve regurgitation, valve prolapse.

GALLBLADDER DISEASE - Define the following: Murphy's sign, Courvoisier's sign, T-tube (including purpose and circumstances of use), gallstone ileus.

Murphy sign: use to differentiate cholecystitis (inflamed gallbladder) from bile duct stones, pyelonephritis and ascending cholangitis (infection in the bile duct). wrap your fingers under the right costal margin, mid clavicle and get the patient to take a deep breath in. Pain is a positive sign implying that as your fingers rub over the gallbladder it is inflamed as in coleocystitis. Courvoisier's law: painless jaundice and a palpable gallbladder is unlikely to be gallstones because chronic gallstones cause fibrosis of the bladder stopping it from enlarging. Gallstone ileus: a misnomer, when a large gallstone slowly worked its way through the gallbladder wall and into the duodenum leaving behind a fistula and eventually causing small-bowel obstruction around the terminal ileum where its narrowest. Remember that an ilius is actually an absence of peristalsis. Treatment is stone removal whilst leaving the gallbladder well alone as its removal will leave a hole in the duodenum. T-tube: A T shaped stent put into the common duct surgically to temporarily drain any secretions from infection/inflammation to the skin. T-tubes can also be used to insert dye to demonstrate residual stones. However some studies suggest that this increases the risk of bile leaking into the abdomen. Obviously another procedure is required for removal.

THE WHITE CELL - Describe the clinical features and laboratory diagnosis of multiple myeloma. Outline the associated laboratory abnormalities including changes in blood viscosity, renal function and serum calcium

Myeloma is a cancerous proliferation of plasma cells which come from B lymphocytes. Ordinarily, plasma cells are polyclonal body and myeloma a single clone of plasma cells produces identical immunoglobulins termed para proteins (bence Jones proteins in the urine). Patients are typically in their 70s, male more than female. Afro-Caribbean is more commonly than Caucasians. Classification: this is based upon the type of para protein produced. IgG is more common than IgA. Bence Jones proteins are seen in the urine in only two thirds of cases whereby free para proteins have been filtered out by the kidney. Features: bone lesions (Lytic), bone pain/backache, vertebral collapse, pathological fractures, hypercalcaemia (bones, stones, moans, groans), anaemia/neutropenia/thrombocytopenia (because the bone marrow has been infiltrated by plasma cells). There is also renal impairment because plasma cell chains deposit in the kidneys and induce glomerular changes. Investigations: Sarah protein electrophoresis identifies para proteins, irritable sedimentation rates/plasma viscosity are raised, the rear and creat and a raised, calcium is raised and patients may be anaemic with low neutrophils and low platelets due to bone marrow infiltration. X-ray shows punched out lytic lesions such as the pepperpot skull, vertebral collapse. Diagnosis: monoclonal proteins in serum or urine electrophoresis, plasma cells increased on bone marrow biopsy and evidence of end organ damage from myeloma (bone lesions, renal damage, raise calcium or anaemia). Management: chemotherapy and supportive treatment. Prognosis: three - four years with complications from raised calcium, spinal cord compression, hyper viscosity of blood (alters vision and cognition) and acute renal failure. Death is typically from kidney failure or infection.

NEPHROTIC SYNDROME - Define the nephrotic syndrome and describe its relationship to conditions causing abnormal proteinuria List the three main primary renal causes and outline briefly the key pathological features. List secondary causes and outline investigations necessary to confirm the diagnosis Outline the investigation necessary to confirm the diagnosis. Outline the treatment including the need for diuretics and a low-salt diet

Nephrotic syndrome: a type of glomerulopathy associated with massive proteinuria, hypoalbuminaemia and hyperlipidaemia. Albuminaemia, oedema and hyperlipidaemia. Other glomerulopathies includes acute nephritic syndrome (acute glomerular nephritis), rapidly progressive glomerular nephritis (essentially acute glomerular nephritis with necrosis) and diseases of the kidney that cause asymptomatic haematuria (RBC casts), proteinuria or both. A good way to identify nephrotic diseases is that they can have membrane in the name (membranous glomerulonephritis as they involve thickening of the memberane). Other examples include IgG nephropathy and minimal change. Cause: albumin is catabolised in the proximal convoluted tubules, the glomerular basement membrane is damaged so that protein enters the urine, LDL is increased and triglycerides are poorly cleared... Therefore hypoalbuminaemia, proteinuria and hyperlipidaemia. Features: this varies depending upon the type of nephrotic syndrome. Minimal change nephropathy (the glomeruli appear normal on light microscopy but on electronmicroscopy the foot processes/podocytes are fused) presents with a child with facial oedema and proteinuria. Requiring high-dose corticosteroids for 4 to 6 weeks with lower doses carried on for up to 12 weeks. In congenital nephrotic syndrome, and autosomal recessive disorder, newborn babies have an enlarged placenta gross proteinuria, raised alpha-fetoprotein in utero progressing relentlessly to end-stage renal failure. Investigations: for all glomerular diseases urine microscopy is needed (haematuria), urinary protein (nephrotic if high), serum urea (indicates poorly functioning kidneys), creatic in, culture (for any kidney damaging organisms), antibody testing (conditions such as lupus or vasculitis - Anca or good pastures disease - anti-GBM), renal imaging (usually normal and renal biopsy which will help definitive diagnosis. Treatment: general management for nephrotic syndrome includes restricting dietary sodium and giving diuretics to reduce the oedema. Ensure that they do not eat high-protein diets as this increases proteinuria. If the patient is hypercoagulable (high levels of lipids and low-volume because of gross oedema) then ensure venous thrombus prophylaxis. Treat hyperlipidaemia to reduce cardiovascular risk and give ace inhibitors to protect the kidneys. Regular monitoring of blood pressure and renal functioning is important. Other treatment is more specific, for example in minimal change nephropathy high-dose steroids are required, in diabetic nephropathy lifestyle changes and diabetic control are important. Dietary requirements: use good lifestyle choices to reduce the risk of cardiovascular disease predisposed to by high lipids, have low-sodium diets to reduce oedema.

NEUROMUSCULAR EMERGENCIES - Describe the clinical signs which point to neuromuscular ventilatory compromise Name the bedside respiratory test of most use in monitoring neuromuscular ventilatory function Describe the findings on arterial blood gas which reflect type II respiratory failure

Neuromuscular ventilatory compromise may occur acutely or chronically requiring ventilatory support. Think the progression of muscular dystophies etc. The patient will be unable to ventilate without extreme effort, use of respiritory accessory muscles. They may be cyanotic and tired with a raised respiratory rate. ONe of the commonest causes of death in neuromuscular disorders is resp failure. CPAP (initially nocternally) may be appropriate for some patients with desaturations. Has the patient got orthopnoea? IT important to do an ABG (respiratory acidosis and hypercapnia). Bedside respiratory test: Spirometry (if FEV1/FVC is <70% thats obstructive. If FVC is <80% that's restrictive). T2RF: Hypercapnia, hypoxia, acidosis and high bicarbonate if this is a chronic picture.

VENOUS DISEASE - Outline normal venous physiology and describe the roles of superficial, deep and perforating veins and venous valves. Recognise varicose veins and describe their anatomical distribution and potential complications. Describe the use of different investigations in diagnosing venous disease and be aware that the Trendelenburg test is no longer a recognised method. Outline the management of a venous ulcer. Outline the management of varicose veins including indications for surgery. Describe the treatments available to patients with venous disease

Normal: The deep venous system is at a higher pressure than the superficial venous system but has valves were two systems joined to prevent pressure entering the superficial system. Varicose veins: incompetent valves between the superficial and deep systems result in dilatation of superficial veins termed varicosities. -Common sites include the long saphenous femoral vein junction, the popliteal fossa and the perforating veins (the past from superficial to deep). - Patients may complain of the cosmetic issue, aching pains, ankle swelling, cramps and non-specific leg pains. Watch out for deep vein thrombosis and pulmonary embolism. -Examination must include an abdominal examination because pelvic masses (pregnancy and malignancies) can cause varicose veins because of pressure on the inferior Vena Cava or iliac veins. Skin changes in venous disease includes haemosiderin deposition and lipoedematosclerosis. Is important to palpate as any visible lumps in the groin could be saphena varix or hernia. The tap test identifies incompetent valves is a real will not be transmitted through valves. Check pulses and consider tourniquet and Trendelenburg. - Management may be conservative (regular elevation, reassurance) but surgery is indicated for significant symptoms, skin changes or ulceration. Surgery includes ligation of the saphenofemoral junction and stripping of the long saphenous vein. Other options include laser and microwave catheters to ablate or the injection of sclerosing foam. Venous investigations: Doppler ultrasound in combination with tourniquet test. Duplex scanning of the veins. Trendelenburg test: An outdated method of determining Venous valve competency. With the patient supine raised the leg and use squeezing and gravity to drain the veins. Occlude the superficial veins with a tourniquet around the mid thigh then ask the patient to stand. A normal response would be for the superficial saphenous vein to fill in 30 seconds. Very slow filling means that the superficial veins are incompetent So the veins will rapidly fill on removal of the tourniquet. Fast filling means The deep veins are incompetent. This test is no longer recognised method. Venous ulcers:Venous ulcers account for 80% of ulcers (arterial due to atherosclerosus, vasculitis and connective tissue diseases, Traumatic ulcers, systemic disease ulcers such as pyoderma gangrenosum, neoplastic ulcerating skin lesions and neuropathic ulcer is seen with alcoholism and diabetes are other causes). Venous ulceration is because of superficial venous incompetence or deep vein incompetence and is typically found in the gator area with haemosiderin deposition and lipodermatosclerosis. Remember that neuropathic ulcer is seen on a warm foot with a good blood supply but significant loss of sensation. Treatment: reduce the underlying causative factors, elevate, compressed and dress a venous ulcer. Antibiotics are reserved for patients with cellulitis (all ulcers will have some form of colonising organisms, don't encourage resistance). Keep the ulcer moist in order to promote regrowth of epithelium and, if ABPI indicates, Use compression stockings even after healing. Surgical approach can be used for superficial venous incompetence (stripping/sclerosing foam/ablation) when the deep valves are incompetent there is no good surgical procedure. Skin grafting may provide extremely useful in helping the venous ulcer heal.

OPERATIVE AND POSTOPERATIVE MANAGEMENT - Understand principles of day care or ambulatory surgery.

Outpatient surgery, also known as ambulatory surgery, same-day surgery, day case, or day surgery, is surgery that does not require an overnight hospital stay. The term "outpatient" arises from the fact that surgery patients may go home and do not need an overnight hospital bed. The purpose of outpatient surgery is to keep hospital costs down, as well as saving the patient time that would otherwise be wasted in the hospital. Outpatient surgery has grown in popularity due to the rise in outpatient surgery centers and improved technology. Outpatient surgery centers often allow patients to get medical surgery and cosmetic surgery done in much more luxurious settings than a state hospital and are often preferred by patients for minor surgical procedures. Improved technology has also increased the frequency of outpatient surgery procedures. With shorter medical procedure duration and fewer complications it makes sense to let patients go home sooner. About 65% of all surgical procedures are done on an outpatient basis.[1] Patients should check with their doctor for all information covering preparation for outpatient procedures. Complications related to surgery occur less than 1% of the time in outpatient settings.[2] However, in terms of patient safety, non-hospital settings are not as regulated as hospitals are. Patients should inquire about all ambulatory clinics, surgical centers, and physicians' offices to make sure they meet state guidelines.

CARDIAC SURGERY - Outline the clinical presentation and constrictive pericarditis.

PERICARDITIS is CONSTRICTIVE when the pericardium rogressivly thickens, fibroses and calcifies. This is seen in trauma, TB, RA and other autoimmune causes of pericarditis an d mediasteinal radiotherapy. Symptoms of congestive pericarditis are those of venous congestion (hepatomegally, ascites). Pulmonary congestion is not as prominent a sign. Echo and CT establish the diagnosis. Treatment is surgical resection of the entire pericardium, a risky operation that has a high morbidity and poor results in up to 50% of patients.

CYSTIC FIBROSIS - Describe the main principles of treatment including physiotherapy, antibiotics, pancreatic enzymes, DNAse, and lung transplantation.

PHYSIO - Regular and more frequently during exacerbations if sputum is produced. ANTIBIOTICS - Usually oral for Staph but intravenous for Pseudomonas (may be injected a home through an implanted subcutaneous vascular port). Regular nebulised antibiotics can be used to suppress chronic pseudomonas infection. PANCREATIC ENZYMES - Often derived from pig enzymes these replace the enzymes that are not being produced by the failing pancreas. An example is creon, to be sprinkled over food. DNAse - Brand name Pulmozyme is a human recombinant DNA used to thin the mucus by selectivly cleaving the DNA in the sputummucus of patients. Other options include mucolytics (acetylcystine). For advanced disease home oxygen and non invasive ventilation are necessary and eventually... LUNG TRANSPLANTATION which is limited by donor availability and requires lifelong immunosupression. Both lungs must be replaced as a single transplant would simly become infected by the remaining lung. Pancreatic and liver transplants are also available. Non pulmonary problems are managed with: microsurgical sperm aspiration for infertility, high calorie diet/supplementary NG feeding or PEG, insulin and other diabetic control

EVIDENCE BASED MEDICINE - Define placebo, nocebo and contextual responses to treatment and describe possible mechanisms that explain these effects Discuss the relevance of contextual responses in clinical practice and ways of optimising these effects for patient benefit.

PLACEBO - a medicine or procedure prescribed for the psychological benefit to the patient rather than for any physiological effect. NOCEBO - a detrimental effect on health produced by psychological or psychosomatic factors such as negative expectations of treatment or prognosis. CONTEXTUAL RESPONSES TO TREATMENT - A patient's response to treatment which is dependent on multiple factors such as environment, social and psychological. The most popular theory for placebos working is down to expectations and conditioning.

PERI-OPERATIVE CARE - Describe causes of postoperative nausea and vomiting (PONV) Describe indications, contra-indications and doses for commonly used drugs for PONV: antihistamines (e.g. cyclizine), 5HT3 antagonists (e.g. ondansetron), Dopamine antagonists (e.g. droperidol), Dexamethasone

PONV is seen in 25-30% causing delayed discharge and recovery (electrolyte imbalance, wound dehissance and dehydration). Pathophysiology of vomiting: 1. Pains/smell/sites and memories/fear/anticipation can trigger higher cortical centres. 2. Chemotherapy is anaesthetics and opiates trigger the chemo receptor trigger zone in area postrema in the fourth ventricle. 3. Chemotherapy, surgery and radiotherapy trigger the stomach and small intestines. 4. Surgery can trigger the labyrinth. All of these will trigger the vomiting centre in the dollar leading to the vomiting reflex. More susceptible patients are female, children, obese, nonsmokers (smoking appears to be protective), laparoscopic/abdominal/gynaecological/ear nose and throat surgery, longer surgeries, nitric oxide, Inhalants, opiates etc. Medication: ANTIHISTAMINES - useful for motion sickness and ear surgery, cyclizine 50 mg. 5-HT3 ANTAGONISTS - useful for prophylaxis in surgery or before chemotherapy. Four - 8 mg slow IM/RAV ondansetron. These are very good antiemetics acting by blocking the vagal afferents in the gut and chemoreceptor trigger zone but are very expensive. DOPAMINE ANTAGONISTS - Act by antagonising agents that stimulate the chemoreceptor trigger zone (oiates, chemtherapy). Metaclopramide is no longer used, use 12.55mg droperidol or prochlorperizine. DEXAMETHAZONE - used to augment other antiemetics. ANTICHOLINERGICS - like hyoscine or atropine block stimulation of the vomiting centre.

PREOPERATIVE ASSESSMENT - Describe the indications for common pre-operative tests and their potential impact on peri-operative care

PREOPERATIVE TESTS - little evidence in a healthy individual, consider investigation depending on the extent of the surgery, age of patient in ASA 1 or greater. FBC: Anaemia, infections. All patients. U&E: Electrolyte imbalance, consider in patients taking steroids, diuretics, digoxin, or those with diabetes, kidney failure, vomiting and diarrhoea. BLOOD SUGAR: For diabetics or patients on long term steroids LFTs: Liver disease, alcoholics, cancer or malnourished patients. Coagulation: Those on anticoagulants, liver disease. CXR: In cardio-respiratory disease, expected malignancy, ECG: If hypertensive, older than 40, signs of ischemia or arrhythmias ECHO: In heart failure (symptomatic) LUNG FUNCTION: SOB, chronic lung conditions (also consider ABG)

ANALGESIA - Define pain Describe the adverse effects of pain Describe the WHO pain ladder

Pain is an unpleasant sensation associated with real or potential tissue damage, it is subjective. Acute = less than three months, chronic = greater than three months. Pain is perceived by free nerve endings either directly stimulated or stimulated by chemicals released post injury. A-delta fibres = sharp immediate pain C-delta fibres = prolonged, slower onset diffuse pain. Adverse Effects: hypoventilation (can lead to collapse or consolidation), atonic gastrointestinal tract (ileus, nausea/vomiting), bladder atony (urinary retention), catecholamine release (vasoconstriction, increased clotting and reduced wound perfusion delaying healing) as well as psychological effects. see image for pain ladder. Remember you can move up and down.

PALLIATIVE MEDICINE - Define supportive palliative care and specialist palliative care. Describe the role and contributions of the individual members of the multidisciplinary team. Describe services commonly available in the UK. Discuss the importance of communication skills in palliative care. Discuss the various psychological responses of patients and their relatives to illness and bereavement. Reflect upon their own and other professionals' attitudes and responses to death and dying. Discuss the aetiology of pain in patients with cancer. Discuss an approach to relieving cancer pain that takes into account diagnosis, different types of pain and range of treatments available, monitoring response and psychological factors that influence pain.

Palliative care centres around improving quality-of-life rather think you're for ultimately fatal diseases. Diseases are focused on balancing comfort and the individual's wishes with treatments might prolong life. multidisciplinary team: clearly important, remember the pain management team and involvement of friends and family. UK services:193 specialist in-patient units providing 2,774 beds, of which 20% were NHS beds. 295 home care services 314 hospital based services. 234 day care services. 314 bereavement support services. Aetiology of pain in cancer: remember that not all patients with pain and cancer have all their pain due to cancer. Pain experienced may be due to destruction of cells, the tumour compressing structures, reaction to drugs etc. often there is a significant neuropathic element. Relieving pain:broadly the two types of pain are nociceptive (in response to a stimulus) or neuropathic (dysfunction of pain perception, challenging to treat). Remember that chronic pain will also the pain perception system leading to increased pain perception. Therefore early pain reduction reduces the potential for chronic changes. Management: use the world health organisation Analgesia ladder (non-opioids, then non-opioids plus mild opioids/codeine 60mg, then add a strong opiate) Oral morphine takes 20 minutes to have an effect with relief for four hours. Therefore prescribed immediate release oral morphine every four hours for continuous relief. Controlled relief lasts 12 or 24 hours but takes longer to kick in. once at the top of the ladder, breakthrough pain can be managed with PR and immediate release oral morphine. Transdermal preparations of strong opioids (fentanyl) may be appropriate and diamorphine is available as subcutaneus. Remember that opiates cause nausea and vomiting and confusion and drowsiness at high doses. High doses also give the risk of respiratory depression. Manage constipation with a laxative, encourage good hydration for dry mouth, give metoclopramide for nausea/vomiting and explain that sedation will settle within a few days. Opiate toxicity: early side-effects include visual hallucinations and myoclonus so regular assessments is important to enable dose changing. Remember that fentanyl is not really excreted so is useful in patients with renal failure. Complimentary treatments: these may be helpful in palliative care and include: stimulation therapies (acupuncture or transcutaneous electrical nerve stimulation to release endorphins), psychological techniques (relaxation, hypnosis, CBT and biofeedback). Nonpharmacological management includes radiotherapy and physiotherapy. Other palliative problems include breathlessness (may benefit from steroids, nebulised salbutamol, talking through specific anxieties, lorazepam during breathlessness attack), cough (manage the underlying cause, codeine linctus), nausea and vomiting (from medication, hypercalcaemia), gastrointestinal obstruction , weight loss, weakness (nutrition), anxiety and depression, delirium and agitation (haloperidol for delirium, and that I has been the agitation)

DIAGNOSTIC STUDIES IN BILIARY TRACT DISEASE - Outline the place of radiological and endoscopic investigation in the diagnosis of obstructive jaundice and in staging of pancreatic cancer. Describe the indications for, and risk of, ultrasound scanning, transhepatic cholangiography and endoscopic retrograde cholangiopancreatography (ERCP).

Panreatic cancer staging: TNM after staging CT. Staging may change post surgery. ULTRASOUND: No risk, used to identify obstruction, pre obstructive distension, free fluid etc. Less effective in obesity. TRANSHEPATIC CHOLANGIOGRAPHY: Percutaineous contrast injection into the bile dut and subsequent Xrays. It has been superseded by non invasive contrast imaging but can be used for temporary biliary drainage or to insert a palliative stent. Complications (infection, bleeding, bile leaks) are more common than in ERCP but it is used when ERCP fails. ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY: Endoscopic examination under general of the pancreatic and bile ducts. A cannula can then be sent into the ampulla of vater to insert contrast and take Xrays. The main indication is obstructive jaundice and it can diagnose gallstones, strictures, proximal cancer and leaks from prior surgery. Theraputically it can perform a sphyncterotomy (cutting the sphyncter to release a stricture), stone removal, stent insertion or dilation of strictures. Contraindications include acute pancreatitis, severe cardiopulmonary disease, coagulation disorders and recent MIs. Risks: 5% get pancreatitis which may be life threatening, perforating the GI tract, bleeding and contrast allergies.

ANALGESIA - Describe indications, contra-indications, complications, routes and doses for commonly used drugs for acute pain: Paracetamol, Non-steroidal antiinflammatory drugs, Weak and strong opioids, Local anaesthetics

Paracetamol: Indicated in lid/moderate pain and/or pyrexia, caution in renal or liver failure and chronic alcoholism. Hepatotoxic in overdose. Take up to 1g PO x4daily. IV and PR doses are also up to 4g daily at 4hour intervals. Ibuprofen: For use in pain, inflammation and migranes. Contraindicated in asprin or NSAID induced angioedema asthma or urticaria. Caution in known heart disease and peptic ulcer disease as will as kidney failure. Take 400mg four times daily with a maximum dose of 2.4grams (up to six times a day). Codeine phosphate: INdicated for mild/moderate pain, diarrhoea and cough suppression. contra-indicated in ultra rapid codeine metabolisers, respiratory depression, paralytic ileus risk, raised intracranial pressure and comatosed patients. Give 60mg four hourly up to 240mg. Morphine: Indicated in pain and cough supression in terminal disease. Contraindicated in respiratory depression, risk of paralytic ileus, raised ICP, coma. Dose varies by preparation, there is no maximum dose but start with 10mg 4hourly. Lidocaine: For topical analgesia there are few contraindications. DO not apply to damaged skin.

ANALGESIA -Describe the principles, risk and benefits of patient controlled analgesia (PCAS)

Patient controlled analgesia is indicated post-operatively, in oncology, sickle cell crisis and in Burns. The principle is to initially control the pain and allow the patient to administer their own maintenance dose PRN. it reduces anxiety and increases patient satisfaction resulting in a lower overall requirement for analgesia. Delivered through a syringe pump intravenously with the patient triggered bolus (1 mg morphine) whereby the machine will lock out for a set time preventing overdose. Bolus triggers can be set alongside a continuous background. Advantages: available on demands, patient control, dose directly adjusted in response to pain, avoids repeated injections, reduces demands on nursing staff. Disadvantages: limited mobility as patient is connected to syringe driver, intravenous access required, needs education, possible misuse. Side effects: nausea vomiting (area prostrema where the chemo receptor trigger zone is), itchiness (opiates cause histamine release), respiratory depression, constipation, pupil constriction.

PERI-OPERATIVE CARE - Describe the principles of intravenous fluid therapy in the postoperative period. Describe the indications for oxygen therapy in the postoperative period Describe the methods of providing increased inspired oxygen. Describe the benefits and limitations of pulse oximetry.

Patients exit theatre oliguric (surgery caused increased ADH secretion) with low sodium excretion and high potassium excretion. Patients have also been fasted. For minor surgery with patients rapidly resuming normal intake no routine fluids are needed. If the surgery is prolonged or the pt cannot drink within 4-6hrs then give 1.5mls/kg/hr with 1mmol K+ and Na+. Dextrose saline is best. For major surgery replace fluids lost, give maintainance, consider pyrexia as a loss alongside drains etc. Remember that epidurals cause vasodilation. You need roughly: 1.5mls/kg, 1mmol/l/kg of Na and K+. OXYGEN: Anaesthesia depresses the sensitivity to CO2 so supplementary oxygen is needed (up to 72hrs postop). Remember patients reliant on the hypoxic drive (88-92%). Oxygen can be humidified to aid physio and sputum clearance. Pulse Ox: Non invasive but harder if peripherally shut down and cannot work through nail varnish.

CONGENITAL HEART DISEASE - Outline the pathophysiological complications that may occur as a result of adult cyanotic congenital heart disease.

Persistent ductus arteriosus: connecting the aorta to the pulmonary artery this should close soon after birth but can fail to do so. There will be an arterio-venous shunt into the pulmonary artery. If small, the shunt can go unnoticed but will eventually cause heart failure Presenting initially with shortness of breath. A large shunt in infancy can damage the POM only vasculature. As resistance increases the shunt can reverse leading to eisenmenger's syndrome. Initially, prostaglandin synthatase inhibitors Can induce closing. Co-arction of the aorta: this can be congenital or acquired post-traumatic (takayasu's arteritis). This causes heart failure in the newborn but can be asymptomatic until adult hood giving headaches from hypertension proximal to the coarction, weak legs and a radio radial delay. Eventually the left ventricle will fail and the aorta is more prone to dissection. Surgically correct even the mildest of cases those repaired in adulthood often remain hypertensive. Atrial septal defect:One of the most common congenital heart defects, primarily osteum secundum (At the site of the foramen ovale). Ostium primun = at the atrioventricular septum. Blood shunts left-to-right causing right heart Hyper trophy and pulmonary hypertension. Often the presentation is later in life with heart failure, shortness of breath or on routine examination. Most signs relate to the volume overload of right ventricular failure. Ventricular septal defect: again causing a left-to-right shunts, right sided heart failure and pulmonary hypertension. The condition can also be secondary to damage post-myocardial infarction or trauma. Again presentation is with heart failure. Tetralogy of fallow: Childhood congenital heart defects involving: pulmonary artery stenosis, large ventricular septal defect giving a right-to-left shunt, overarching aorta and Hypertrophy of the right ventricle. More adult causes of heart disease are as follows: hypertension in adult hood after childhood Coarction of the aorta. Tricuspid atresia (narrowing of the valve leading to An underdeveloped right ventricle), pulmonary atresia, Ebstein's abnormality (Displaced tricuspid valves).

PLEURAL EFFUSION - Classify causes of a pleural effusion including infective, neoplastic, metabolic, and cardiac causes.

Pleural effusion is a collection of serous fluid within the pleural space. If it is pus is called an empyema, blood a haemothorax and chyle a chylothorax. The fluid typically accumulates because of an increased hydrostatic pressure or decreased osmotic pressure (transudate) or because of pleural injury (exudate). Causes: These can be split into transudate (due to altered osmotic forces- Seen in cardiac, liver or renal failure), exudate (due to Inflammation- Seen in pleural disease or injury) and other. Infection: Pneumonia, tuberculosis Neoplastic:Lung cancer or cancer that seeds into the pleura. Meigs syndrome where a varying cancer is seen with a pleural effusion. Metabolic:Low proteins seen in liver or kidney disease as well as malnutrition causes transudates. Cardiac: Post Myocardial infarction.

PNEUMONIA -Describe the typical presentation of a patient with a community-acquired pneumonia and the features that identify severe pneumonia. Describe the role of CURB-65 as a risk prediction tool.

Pneumonia is an acute respiratory illness, primarily spread by droplet infection, with recent pulmonary shadowing. Presentation: Typically acute onset of fevers, rigors, shivering, malaise, and possible delerium on a background of cough (becomes mucopurulent after initial dryness), rust coloured sputum in strep pneumoniae, pleuritic chest pain. The elderly and young may present atypically. On examination: Raised resp rate and pulse, lowered BP, possible delerium, pyrexia, low O2 sats. If consolidated the lung is dull to percuss, bronchial breathing (harsh poor quality sounds because of turbulant flow), whispering pectoriloquy ((louder transmission of whisering as liquid/solid is easier to pass sound through), crackles. CURB 65: Assessing the severity of CAP C=onfusion U=rea >7mmol//l R=esp rate >30 B=P >90/<60 systolic 65= years or more Te risk of death is heavilty correlated to the score. Curb 1 or less is treated at home, curb 2 depends but >curb 3 is admitted.

PNEUMOTHORAX - Describe its typical clinical presentation and the recognised risk factors together with the underlying pathology and investigations.

Pneumothorax is when enters the pleural space either spontaneously (primary) or secondary to a pre-existing lung disease (COPD, TB, asthma, lung abscess, pulmonary infarct, carcinoma, fibrotic or cystic lung disease). Clinical presentation: sudden onset unilateral pleuritic chest pain or breathlessness. If this is a small pneumothorax (such as in a tall young man) examination can be normal. In a large pneumothorax there is de creased breath sounds, resonant percussion and they're ready signs of an underlying lung disease. Investigations: a chest x-ray shows a deflated lung with absent long markings between this and the chest wall. There may be evidence of an emphysema bulla and other underlying lung conditions. If this is a tension pneumothorax there is rapidly progressive breathlessness, marked tachycardia, hypotension, cyanosis and tracheal displacement away from the pneumothorax. If malignancy has scarred the mediastinum this may prevent tracheal deviation. If this is found there is no time for investigations, drainage must be immediate. Risk factors: Male, smoker, Tall and underweight 20 to 40 rolled male, Family history, pre-existing lung disease (particularly COPD), Personal history and use of assisted ventilation.

ANYERISMS - Describe the presentation, complications and treatment of popliteal aneurysm. Describe the pathophysiology of arterial dissection and outline clinical presentation, medical and surgical treatment, complications and causes of death. Differentiate true and false aneurysm

Popliteal: Presentation - These are less common than abdominal aortic aneurysms although 50% of patients with a popliteal aneurysm also have an aortic aneurysm. They present with an easy to palpate popliteal pulse or in acute thrombosis causing ischaemia. Complications - Unlike AAA's popliteal aneurysm is rarely rupture but can cause acute thrombosis resulting in acute ischaemia (six Ps). Treatment - If identified prior to you acute thrombosis the popliteal aneurysm should be tied off electively. True or false aneurysm? A false aneurysm is when there is a hole in the wall of the artery allowing haematoma to form Outside the arterial wall. Where is a true aneurysm is dioxation of all three layers of the vessel wall.

THEATRE ROUTINE - Demonstrate an understanding of operating theatre routine through adherence to the prescribed rules of conduct and dress. Demonstrate an understanding of the role of the surgeon in relation to that of other members of the theatre team. Demonstrate an understanding of the principles of safety in theatre (for patients and staff), including the place of pre-theatre team briefing and various safety checks. Demonstrate the proper technique for surgical scrubbing, gowning and gloving in the operating room, assisted and unassisted. Demonstrate knowledge of aseptic technique and discuss themicrobiological principles involved. Identify areas that are considered part of the sterile operative field. Demonstrate the ability to function as an assistant in the operating theatre. Define the classifications of operative procedures with reference to their potential for infectious complications (clean, potentially contaminated,contaminated and dirty); discuss the importance of this classification system

Predominantly common sense..... The WHO checklist is split into three: BEFORE ANAESTHESIA: patient self identifies, indicates the procedure and any allergies. Blood loss and expected complications are noted and the anesthetists do a check. TIME OUT before any excision is a time for introducing the team, discussing potential complications, reconfirming the patient and procedure, checking imaging and equipment. SIGN OUT is for instrument check and discussion of recovery plan. CLEAN PROCEDURE = does not enter a normally colonised viscus of the body. Eg... elective hernia repair does not open the bowel. CLEAN-CONTAMINATED PROCEDURE = enters a normally colonised viscus but under controlled conditions. Eg... elective intestinal procedures, head and neck surgery, gynae procedures. CONTAMINATED = exposed to a foreign body (bullet, knife wound) or gross GI spillage. DIRTY = Procedure performed when infection is already present. Eg.....peritonitis laparotomy, abscess drainage.

BURNS - Discuss the methods used to prepare a full thickness burn for grafting and the factors relevant to the successful take if the graft on the wound surface. Identify patients who require specialised burns centre management. Define the maximum extent to which a patient can be burned and still be managed on an outpatient basis. Describe a type of burn of < 10% that would require hospitalisation.

Preparing a burn for grafting: Debridlement is first required. Then choose the type of graft: thin (layer stripped) or full thickness (donor skin excised - more likely to be rejected). The norm is self tissue. Grafting success: The intention of a graft is to promote healing and improve function and aesthetics. Risks include: bleeding, infection, denervation, graft rejection. To reduce risks choose the donor carefully to get the closest match and use aseptic techniques and good wound care. Those requiring specialised management: inhalation problems, ocular involvement, full thickness, significant comorbidities. remember the psychiatric morbidity is associated with severe burns and facial burns. The man Outpatient burns: superficial burns can be managed with topical treatment especially in patients without significant comorbidities. Inpatient care may be required for complications such as infections, respiratory failure, compartment syndrome, rhabdomylysis, blood clots. <10% burns needing hospitalisation: consider comorbidities and whether or not the Burns facial and indicative of inhalation. Also be wary of ocular damage which can lead to blindness.

PANCREATIC NEOPLASMS - Describe the symptoms and signs of pancreatic cancer depending on location of the tumour within the gland. Outline investigations indicated. List common pancreatic neoplasms; describe the pathology of each with reference to cell type and function. Discuss non-surgical management, indications for surgery and list common operations. Discuss the prognosis of pancreatic neoplasms with regard to histology

Presentation: Courvoisiers law states that painless enlarged gallbladder in the presence of mild jaundice is unlikely to be gall stones and is therefore more likely to be pancreatic cancer. patients complain of back pain, yellow skin, pale stools, dark urine, weight loss and loss of appetite. These are all late symptoms, often occurring after metastasis. constipation is common because compression impedes digestion. 50% of sufferers have diabetes at the time of diagnosis. Classic Patient: 40-year-old obese, diabetic tobacco smoker. Investigations: Ultrasound excludes gallstones but may show an enlarged gallbladder, endoscopic ultrasound can visualise the pancreas, CT scan is ideal, carcinoembryonic antigen may be raised. liver function tests can show an obstructive picture. Types: 85% are adenocarcinomas typically arising in the ducts of the pancreas at the head end - tumours at the head and tend to cause more jaundice and are thought to be less aggressive than those found in the tail (Whipple's is only suitable for head of the pancreas tumours). Other tumours include neuroendocrine tumours (secreting insulin, glucagon, gastrin) which tend to be less aggressive and presenting earlier because they're secretory in nature. Acinar cell tumours secrete lipase therefore causing arthritis and fat necrosis. Nonsurgical management: chemotherapy and radiotherapy can shrink a nonresectable tumour for palliation. Surgical management: The only cure is surgical, less than 20% of patients are eligible for surgery. The tumour should be in the head of the pancreas without the prior metastasis/or spread to vasculature. Whipples procedure is a pancreaticoduodenectomy (remove the distal stomach, approximal two thirds of the duodenum, common bile duct, gallbladder and head of the pancreas. The duodenum has to be removed because of its shared blood supply with the head of the pancreas. then reconnect the bile duct, stomach, pancreatic tail to the remaining small intestine.) otherwise, surgery can be palliative to remove an obstruction and relieve symptomatic jaundice. Prognosis: Adenocarcinoma has a 25% survival rate one year but only 5% survive five years. Neuroendocrine cancers have far better prognosis, 65% at five years.

CHRONIC PERIPHERAL ARTERIAL DISEASE - List the clinical manifestations of chronic peripheral arterial occlusive disease and describe its investigation and management.

Presentation: Minor narrowing of major arteries can be completely asymptomatic, but as occlusions occur symptoms depend upon the anatomical level of the blockage in the presence of collaterals. Typical presentation is Intermittent claudication (muscle ischaemia with the buildup of metabolites of anaerobic metabolism - lactic acid induced by a particular walking distance, relieved by rest). The pain is very well localised to the calf area And the walking distance becomes gradually shorter until there is pain at rest. Whereas claudication brought on by exercise causes calf pain, rest pain is in the foot or toes and typically occurs at night (waking the patient because of the lack of gravity helping blood flow to the feet, Reduce cardiac output and vasodilation Of the skin from the warm of the the bedclothes, diverting blood flow from soft tissues). They may hang of out of bed or walk on a cold floor (To vasoconstrict) to relieve the pain. Differential: lumbaris spinal canal stenosis: a.k.a. spinal claudication (although these patients have numbness, weakness and pins and needles after a particular walking distance instead of pain. Investigations: A BPI (<0.3 or symptoms of rest pain is critical ischaemia). Management: Conservative management: stop smoking and keep walking. Manage any comorbidities such as anaemia, hypertension, hyperlipidaemia, diabetes and heart failure. Encourage weight loss and add aspirin and statin. More severe claudication warrants an angiogram to see if angioplasty is viable. Angioplasty: typically radiological intervention with a balloon at the end of the catheter which can then be stented. This doesn't even require a general anaesthetic and carries minimal risk to the patient. Usually, we only consider surgery if critical ischaemia or severe claudication is making the patient's life intolerable. This involves bypass grafting using artificial Dacron grafts, the exhilarating arteries or the long saphenous vein.

INTESTINAL OBSTRUCTION - Describe the symptoms and signs in a patient with intestinal obstruction. List the common causes and the associated pathology of intestinal obstruction. Discuss the complications of small bowel obstruction and their recognistion List the appropriate laboratory and X-ray tests to be employed in a patient with suspected small intestinal obstruction. Differentiate between mechanical small bowel obstruction and paralytic ileus. List the symptoms and signs suggestive of strangulation. Compare and contrast a large bowel obstruction and a small bowel obstruction. Outline a plan of treatment in a patient with small bowel obstruction including a consideration of fluid and electrolyte therapy, antibiotic therapy, intestinal intubation and operative therapy.

Presentation: Severe, central, colicy pain (every few minutes for a few seconds), abdominal distention, vomiting (more proximal obstruction means earlier vomiting) and absolute constipation (not even flatus!) Causes: Most commonly: adhesions (secondary to surgery) and hernias. In the lumen: faeces, foreign body, large polyps, intussusception. In the wall: tumours, infarction, crohn's, benign stricture. Outside: adhesions, hernias, volvulus or external compression. Examination: Distension, hyperactive bowel sounds, tenderness implies strangulation (also supported by peritonitis - ridgidity, temp and high white cell count this will progress to gangrene). Groin examination may reveal hernias and abdo exam may show scars (?adhesions). Complications: Peritonitis, perforation, gangrene if volvulus, sepsis. Investigations: Abdo Xray (distended bowel loops with a diameter <4cm, central with valvulae conniventes all across). Paralytic ileus: Intestinal obstruction due to paralysis of the intestinal muscles typically post surgery. There will be absent bowel sounds. Treat with NG aspiration and bowel rest. Strangulation: Typically a hernia stuck in the bowel wall. Occlusion of the vasculature leads to venous engorgement and eventually gangrene. Large or small bowel: Think central, <4cm, valvulae conniventes all around for small bowel. And non central, larger diameter, taenia colie and circular muscles forming haustra. Large bowel obstruction is typically due to cancer, volvulus or diverticulitis and presents with distention, colicy abdo pain, vomiting (later onset) and constipation. Perforation is more likely if the iileocaecal valve is competent - it occurs at the caecum which is thinnest. Operate if there is peritonitis (indicating perforation) if not IV fluid rescuss, NG aspirate and bowel rest. Palliative treatment involves endoscopic stenting for patients unfit for theatre. Management: Conservative management is bowel rest (NG aspiration, nil by mouth) Repair any hernia, inspect bowel and resect if non-viable. Adhesions can be divided at surgery.

PARKINSONS - Describe and recognize the clinical triad of parkinsonism Outline the pathological basis of classical Parkinson's disease and describe the common clinical features List non-motor features of Parkinson disease, with specific reference to disorders of sleep, mood and cognition Outline less common causes of Parkinsonism including drugs and the Parkinson-plus syndromes Outline commonly used drugs to treat Parkinson's disease and their common adverse effects

Presentation: This is an akinetic rigid syndrome Seen more commonly in men, typically on setting around the age of 60 and progressing slowly primarily involving the basal ganglia. Remember that Parkinson's typically presents in an asymmetrical manner. Death is usually after 10 to 15 years with bronchopneumonia. Symptoms/signs: There is a classic triad of: Resting tremor, Rigidity (often cog wheeling) and dyskinesia (Powerful but delayed initiation and slow movements - Facial movements are reduced in amplitude giving an expressionless face known as hypomimia). Other symptoms include: shuffling gait, impaired balance, Insomnia, Monoterminal speech, micrographia, stooping posture, is constipation, urinary difficulties, depression, loss of smell, dec concentration and eventually dementia. Pathology: Progressive degeneration of cells within the substantia nigra (Whose job is to release those mean for motor control). These cells retain dopamine which is toxic to them the overall result is a loss of dopamine in the substantia nigra. The remaining cells of the substantia nigra may contain Lewy bodies - aggregates of alpha synuclein. The actual cause is unknown although there are some familial Parkinson's disease associations, links between MPTP contaminated recreational drugs and pesticides/herbicides. Less common causes of parkinsonism: Features of Parkinson's disease can also be caused by dopamine antagonists (antipsychotics), trauma (boxing), Wilson's disease, cerebrovascular disease (infarcts in the basal ganglia), hydrocehalis, brain tumours, infections and progressive supranuclear palsy (parkinsonism, early falls, cognitive decline, dysphagy, dysarthria). Management: Parkinson's is a clinical diagnosis but if you were to perform dopamine transporter scams they would show decreased binding in the basal ganglia. The aim of treatment is to restore dopamine levels. LDOPA (a precursor to dopamine production) Is the mainstay of treatment in combination with a decarboxylase inhibitor to prevent peripheral conversion of inactive drug to the active form (decarboxylase inhibitor will not cross the blood brain barrier meaning that the drug can activate in the brain). LDOPA Will improve rigidity and bradykinin easier but does not improve the tremor and will become progressively ineffective and can even induce dyskineasias. For this reason, the drug is often held back in younger patients. (It also causes drowsiness, pot hypertension, vivid dreams, delusions and hallucinations as well as impulse control disorders). Anti-cholinergic drugs (procyclidine) may reduce the tremor will not affect the rigidity and bradycinesia and have anti-muscarinic side-effects. Anti-cholinergic's tend to be used for younger patients to help them stay at work. Monoamine oxydase B inhibitors (...giline) may block the degradation of dopamine so when used early can delay the need for L-dopa. Dopamine agonists activate dopamine receptors. COMT (catechol o-Methyltransferase) Inhibitors prevent dopamine breakdown (dopamine is ordinary broken down by DOPA decarboxylase or catechol-O-methyltransferase). These are used in conjunction with L-dopa. Medication is often withdrawn as it can cause hallucinations and psychosis. If antipsychotics are required go for quetiapine, olanzapine or clozapine (Remembering that they worsen parkinsonism). Surgery can involve deep brain stimulation of the subthalamic nucleus to reduce tremor and dyskinesia.

PSYCHIATRY AND MENTAL HEALTH Discuss the backgrounds to and presentation of patients who self harm Describe the main aspects of a mental state examination in the setting of acute self harm Describe the general approach to the management of patients who have taken an overdose (including main agents of overdose and antidotes etc)

Presentation: any deliberate behaviour with the intention of damaging one's own tissues. there may be a background of substance abuse, history of traumatic incidents, underlying personality disorders (borderline). Mental state examination: this assesses your patient under the following headings: appearance and behaviour, speech, mood and affect, thoughts, perceptions, cognition and insight. Management: initially treat the wound with adequate analgesia, securing, infection prevention etc. then consider the underlying problem with potential referral to psychiatric services. Overdoses: assess using the ABCDE approach, fluid resuscitate and consider using the antidote. Paracetamol = Nacetylcystine morphine = naloxone antifreeze = ethanol anticholinergic = physostigmine anticholinesterase = atropine

THYROID CANCER - Classify thyroid cancer and outline the clinical presentation, diagnosis and principles of treatment Outline the investigation and management of a patient presenting with a thyroid nodule/swelling

Presentation: typically a solitary nodule of the thyroid gland. Classification: most are benign although these may be toxic adenomas (secreting excess thyroid hormones). Primary malignancy of the thyroid is rare. Classified thyroid cancer with respect to the type of cell: follicular cells (papillary or follicular or anaplastic), Parafollicular cells/medullary (Secrete calcitonin - Lowers blood calcium), Lymphocytes (lymphoma). Most (except for lymphoma) have 70 to 90% survival rate. MAIN THYROID CANCERS Toxic adenoma: a solitary benign but toxic nodule causing hyperthyroidism giving high T3 but lowered TSH causing atrophy of the remaining thyroid gland. Most patients are over 40 with a palpable nodule diagnosed through scintography. Patients complain of hyperthyroidism symptoms and the ideal treatment is radioactive iodine (the normal thyroid is naturally preserved because it is so atrophic). Papillary carcinoma: The most common malignant thyroid tumour, spread by lymph nodes, so presents with lymphadenopathy But no apparent thyroid enlargement. Total thyroidectomy followed by radioactive iodine. As growth is thought to be TS H dependent levothyroxine is used to suppress TS H lifelong to prevent recurrence. Follicular carcinoma: a single thyroid lesion, spread will be blood-borne to the bone, lungs and brain. Total thyroidectomy followed by radioactive iodine. As growth is thought to be TS H dependent levothyroxine is used to suppress TS H lifelong to prevent recurrence. Follow-up can involve measuring thyroglobulin which should be undetectable except in tumour recurrence. Anaplastic carcinoma and lymphoma: difficult to distinguish clinically, patients greater than 60-year-old present with rapid thyroid enlargement over a couple of months. The goitre is hard and there may be stridor from tracheal compression and hoarseness from invasion of the recurrent laryngeal nerve. For anaplastic carcinoma survival rates are poor (Seven months) and treatment is ineffective. For lymphoma the average survival is nine years using chemotherapy and radiotherapy. MEDULLARY/PARAFOLLICULAR CELL CANCERS Medullary carcinoma is that which has arisen from parafollicular calcitonin secreting cells that ordinarily LOWER calcium in the blood. Medullary carcinomas can secrete serotonin, ACTH and prostaglandins. They can therefore cause carcinoid (Neuro endochrine) syndrome and Cushing's. Patients usually present in middle age with a firm thyroid mass and lymph node involvement. Calcitonin levels will be raised which can cause diarrhoea. Treat with total thyroidectomy, iodine will obviously not work. Radiotherapy can be considered if there is a high risk of recurrence. Prognosis is good but less than that of papillary and follicular cancer.

Inerpreting CSF?

Pressure: Low pressure can indicate a blockage, severe hypotension or circulatory collapse or dehydration. Raised pressure can indicates cerebral oedema, Hydrocehalus, subarachnoid haemorrhage. Cell count: This is usually very low although there must be some monocytes. The present agranulocytes is always abnormal, and if very high indicates bacterial meningitis. Microbiology: culture of any organism is abnormal, PCR is also useful. Remember TB requires a zeal neilson stain. Glucose: should be 60% of that in blood, Decreased by bacteria, fungi or TB. Lactate: maybe raised in multiple sclerosis or tumours of the central nervous system. Protein: Seen raised in bacterial infection as Bacteria produce proteins. Blood: Xanthochromia, a byproduct of blood is that is yellow because he is high in bilirubin, may imply a subarachnoid haemorrhage or simply be a byproduct of the procedure. In summary, Bacterial: high granulocytes/white blood cells, low glucose, High-protein, Positive gram stain and a turbid fluid. Viral: Some white blood cells, Normal glucose, a slight raising protein, no gram staining and clear fluid. TB: Culture will reveal nothing but protein will be raised, glucose will be slightly lowered and there will be some cells.

TRAUMA - Describe the following potentially life threatening injuries and outline their initial management: pulmonary contusion, aortic disruption, tracheobronchial disruption, oesophageal disruption, diaphragmatic disruption, myocardial contusion

Pulmonary contusion: bruising of the long as a direct result of trauma whereby blood and other fluids collected in the lung obstructing gas exchange. Patients present with chest pain, haemoptysis and possible cyanosis after blunt trauma. provide supplementary oxygen and consider the need for mechanical ventilation and fluids whilst avoiding fluid overload. heavily associated with acute respiratory distress syndrome and pneumonia, mortality can be as high as 40%. Aortic disruption: when the aorta is torn or ruptured often leading to exsanguination. Causes may be traumatic as in a road traffic collision or through a ruptured aneurysm and often will cause severe hypovolaemic shock. Patient may have hypertension on the right-hand side severe hypotension the left-hand side depending upon the location of the tear. After resuscitation management is surgical. in the meantime, keep blood pressure as low as possible to prevent further bleeding which involves adequate pain management as well as anti-hypertensives. Tracheobronchial disruption: a rare complication of trauma or smoke inhalation they can cause and airflow obstruction resulting in respiratory failure. Mortality rate is high and pneumonia is commonly is that survive initially. After diagnosis, management and requires an adequate airway. Invasive ventilation can cause a pneumothorax. Oseophageal disruption: rupture of the oesophagus that can cause gross intrathoracic contamination. This may be spontaneous (especially in Alcoholics) with chest pain, vomiting, haematemasis and back pain. patients should be managed on intensive care, nil by mouth, NG tube fed and surgery should be considered in any deteriorating patient or any patient with gross contamination (washout). Diaphragmatic disruption: typically from trauma, giving chest and abdominal pain and difficulty breathing. repairers obviously surgical (even a small tear will never heal bitches of the constant diaphragmatic movement) but remember that gross abdominal trauma may be associated with a traumatic hiatus hernia which may be a more pressing issue. Myocardial contusion: bruising of the heart after blunt trauma. Often associated with chest injuries are located on the right-hand side of the heart because its anatomical location. bruising can cause arrhythmias up to 72 hours later. the only real management is treating other associated problems and monitoring the echocardiogram for disarhythmias.

CHRONIC KIDNEY DISEASE - Describe the morphology and pathological consequences of pyelonephritis, interstitial nephritis, polycystic kidney disease, hypertensive renal damage and obstructive uropathy to the kidney.

Pyelonephritis: Inflammation of the kidney typically from an ascending bacterial infection. It may result in pyonephritis Whereby pus accumulates. Sepsis, kidney failure and even death can result. Patients present with fever, tachycardia, dysuria and loin pain requiring urgent antibiotics. Interstitial nephritis: Inflammation of the tissues of the kidney that can be acute or chronic and is typically seen with An infection (Pyelonephritis) or toxic damage to the kidney (disease or drugs- NSAIDs or penicillin). Patients present with symptoms of pyelonephritis or drug allergy alongside Hyperkalaemia, metabolic acidosis And kidney failure. Treat the cause. Polycystic kidney disease: A genetic disease of multiple kidney cysts there may be autosomal dominant (More common, progresses to end stage renal failure requiring dialysis) or autosomal recessive (Rarer and more commonly fatal). Hypertensive renal damage:Damage to the kidney that is secondary to general hypertension (not Reno vascular disease). In hypertension the arterial walls gain deposits of hylan which gradually thickens them (arthrosclerosis). The resulting ischaemia causes tubular atrophy and Interstitial fibrosis. Glomerular damage may result in protein and/or blood in the urine. Eventually chronic kidney disease will progress and it is important to control hypertension to prevent this. Obstructive uropathy:Any obstruction to urine flow.This can cause acute pain such as that seen with stones.Treatment commonly involves prompt drainage and removal of the blockage. If left long-term chronic kidney disease will develop.

EVIDENCE BASED MEDICINE - Define relative risk, absolute risk, attributable risk fraction and population attributable risk.

RELATIVE RISK is also known as the risk ratio, it is the prevalence of the disease in the exposed group compared to (divided by) the prevalence of the disease in the unexposed group. ABSOLUTE RISK is the risk of developing the disease over a time period ATTRIBUTABLE RISK FRACTION is the contribution a risk factor makes to a disease POPULATION ATTRIBUTABLE RISK is the contribution a risk factor makes to the prevalence of disease in a population

ABG - Obtain an arterial blood sample and interpret arterial blood gas results.

REMEMBER NORMAL: pH7.35-7.45, O2 11, CO2 4-7, HCO3- 22-26. These vary by machine. 1. The first step in analyzing ABGs is to look at the pH. Normal blood pH is 7.35-7.45. Is the blood acidotic or alkalotic? 2. The second step is to examine the pCO2. Normal pCO2 levels are 35-45mmHg. Below 35 is alkalotic, above 45 is acidic. Label it. 3. The third step is to look at the HCO3 level. A normal HCO3 level is 22-26 mEq/L. If the HCO3 is below 22, the patient is acidotic. If the HCO3 is above 26, the patient is alkalotic. Label it. 4. Next match either the pCO2 or the HCO3 with the pH to determine the acid-base disorder. For example, if the pH is acidotic, and the CO2 is acidotic, then the acid-base disturbance is being caused by the respiratory system. Therefore, we call it a respiratory acidosis. However, if the pH is alkalotic and the HCO3 is alkalotic, the acid-base disturbance is being caused by the metabolic (or renal) system. Therefore, it will be a metabolic alkalosis. 5. Fifth, does either the CO2 or HCO3 go in the opposite direction of the pH? If so, there is compensation by that system. For example, the pH is acidotic, the CO2 is acidotic, and the HCO3 is alkalotic. The CO2 matches the pH making the primary acid-base disorder respiratory acidosis. The HCO3 is opposite of the pH and would be evidence of compensation from the metabolic system. 6. Finally, evaluate the PaO2 and O2 sat. If they are below limits there is evidence of hypoxemia. SO.....acidotic or alkalotic? Resp (CO2) or metabolic (HCO3)?

TRAUMA - specify the indications for tetanus prophylaxis

Regardless of vaccination status any person with a tetanus prone wound at high risk of infection should be sent to hospital for tetanus immunoglobulin. Note that tetanus prone wounds include any wound or burn whose closure is delayed by more than six hours, compound fractures, significant puncture wounds in contact with soil and foreign bodies. For less high risk lacerations consider the patient's vaccination status. Give boosters or start the vaccination schedule as required.

ACUTE CORONARY DISEASE - Discuss the indications and contraindications for thrombolysis. Describe pharmacological methods of secondary prevention Outline the principles of cardiac rehabilitation including advice given regarding driving and employment.

Remember Mona and bromance. Indications for thrombolysis: Immediate reperfusion is indicated in ST elevation but not in non-ST elevation where from the lysis may even be harmful (bleeding into a plaque). Give aspirin for any myocardial infarction, add clopidogrel in NSTEMI. The new anticoagulants (....mab) are particularly useful in PCI and those with recurrent ischaemia. Antiplatelet therapy is particularly important in diabetes and markedly raised troponin. Consider warfarin in AF. Contraindications: Risk of bleeds. Pre-existing anticoagulation therapy. Particular risks include those of stroke and intracranial haemorrhage. Secondary prevention: Anticoagulants (Aspirin or clopidogrel) to reduce the risk of thromboembolic complications and prevent reinfarction (particularly useful if PCI or CABG have not been used -nstemi). Beta-blockers slow the heart improving flow which occurs during diastole. ACE inhibitors to prevent ventricular moulding. Implantable cardiac defibrillators can be used in patients prone to arrhythmias. Cardiac rehabilitation: you cannot drive for FOUR weeks after a heart attack And rehabilitation involves exercise, smoking cessation, healthy diet.

HEADACHE - Outline the features and management of headaches disorders including Tension Headaches, medication overuse headache, migraine and cluster headaches

Remember that a headache may be primary (described below) or second aerie (usually the result of more sinister pathology). Tension headache: Typically presenting as a band like, dull headache with scalp tenderness that is aggravated by noise and light but NOT associated with nausea, vomiting, photophobia etc.Treatment should be with massage, relaxation therapy and simple analgesia is episodic, but if chronic then amitriptyline may be useful. Medication overuse headache: These may be solely medication induced or Tension headaches that are exacerbated by analgesia overuse such as the chronic use of paracetamol. Treatment is therefore slow weaning off their Analgesia to commence a small dose of amitriptyline. After this patient should avoid either profane, paracetamol etc except for acute exacerbations. Migraine: Are common, often for medial, episodic throbbing headache from 4 to 72 hours associated with photophobia, Osmophobia (odours), phonophobia (sounds) nausea and sometimes vomiting. There may be a preceding aura and the headache is thought to have neurovascular basis such that levels of Serotonin rise during the aura and fall throughout the headache. A migraine is described as classical if it has an aura. A common migraine does not have an aura. A basilar migraine Has an aura arising from the posterior cerebral circulation meaning visual, a tax year, dysarthria, vertigo can be included in the aura and consciousness can be lost in the headache. A hemiplegic migraine is one that is lateralised and may be mistaken for a stroke. Management includes avoiding any precipitants, avoiding smoking and oral contraceptives because of the increased risk of stroke, prophylaxis with propranolol or amitriptyline and treating any attack with aspirin, paracetamol, antiemetics etc. More severe attacks may require serotonin agonists such as the tryptans. Cluster headache: A rare syndrome more common in middle-aged men who get severe unilateral pain around the I with ipsilateral autonomic features such as redeye, tearing, rhinorrhoea and sometimes a transient one is syndrome. Symptoms occur in clusters of up to 8 times a day for weeks at a time with each attack lasting 2:45 hours. There may be features similar to a migraine but there is no movement sensitivity and patients with cluster headaches often paced the room rather than lying still in bed. New imaging is required is is there may be an underlying Pituitrin pathology. After excluding pathology treats as early as possible in an attack with oxygen and Tryptan injections or nasal sprays.

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY - Draw and label a cross section of the spinal cord, with specific reference to spinothalamic pathways, corticospinal tracts and dorsal columns - SEE NEURO NOTES Describe the clinical syndrome that would arise from; Cord transaction at C3 and at T10; Cord hemisection; Posterior cord lesion Describe the clinical difference between upper and lower motor neuron limb weakness, with specific reference to findings on inspection, tone, deep tendon reflexes and pattern of weakness - SEE NEURO NOTES Describe the clinical syndrome that would arise from S1 root lesion; C5 root lesion; Median nerve compression at the carpal tunnel; Ulnar nerve palsy; Peripheral neuropathy; Neuromuscular junction disorders; myopathy

Remember that a transection is a complete tear. Partial tears and contusions are also possible (giving variable loss of motor and sensory control). A complete lesion results in total loss of motor and sensory function below the cut. C3 lesion = bowel and bladder dysfunction, sexual dysfunction, difficulty with HR/BP/sweating/temp control, spasticity, muscle atrophy, osteoporosis and gallstones. They are likely to require ventilatory support for C1-c3 lesions if complete. C5 lesion = Typically giving quadraplegia, bowel and bladder dysfunction, sexual dysfunction, difficulty with HR/BP/sweating/temp control, spasticity, muscle atrophy, osteoporosis and gallstones. Patients are less likely to need a trachy and ventilatory support than higher lesions. C7/T1 = gross arm movement is generally preserved with limited fine motor control at the hands. T10 lesion = As above the lesion is spared the patient has paraplegia not tetraplegia. Symptoms include: Bowel and bladder dysfunction, Sexual dysfunction, Difficulty regulating heart rate, blood pressure, sweating, and body temperature, Spasticity , Neuropathic pain, Muscle atrophy, Osteoporosis, Gallbladder and renal stones. S1 lesion = Depending on the level some hip, knee and foot movement may be preserved. Cord hemisection = damage to half the cord causes an ipsilateral loss of function that is usually contralateral (may be ipsilateral if high enough) ALso known as a brown sequard lesion. May be trauma or tumour. Posterior cord syndrome = when the posterior spinal artery is occluded or another problem (trauma/tumour) damages the posterior cord. There is isolated loss of proprioception and vibration due to dorsal column damage. Median nerve compression = roots C5, C6, C8, T1. Carpel tunnel gives weakness, numbness and tingling in the radial 3 1/2 digits. If severe a lesion here can give the hand of benediction (flexion problems as the lateral two lumbricles and flexor digitorum profundus are supplied by the median nerve). Ulnar nerve palsy = from entrapment in the thoracic outlet, cubital tunnel or goyons canal (where the ulna nerve and artery run above the carpel tunnel). Presents with altered sensation in the median two digits, ulnar claw (cannot extend the medial two digits because the medial lumbricles are supplied by the ulna nerve). Peripheral neuropathy = numbness, tremor, tingling, pain, itching, burning, loss o function. Seen with diabetes, vitamin deficiencies, drugs, chemo. Neuromuscular junction disorders = Classically myaesthenia gravis where antibodies attach AcH receptors causing fatiguability of the muscles affected. Swallowing or breathing issues may be encountered. Myopathy = a generic term for muscle disease - may be neuromuscular or musculoskeletal in nature. Common symptoms are cramps, weakness, stiffness and tetany. Proximal muscle weakness results in a positive gowers sign.

HYPOTHYROIDISM - Describe the classical symptoms, examination findings and treatment of hypothyroidism. Classify the causes of hypothyroidism and outline the pathological features of Hashimoto's thyroiditis.

Remember that the role of the thyroid is: calorigenesis (producing heat), carbohydrate and fat metabolism (lipolysis). Thyroid hormone is esential for normal growth hormone production. Symptoms: Cold, weight gain, depression, lethargy, constipation, aches and pains, heavy menstrual flow Examination: bradycardia, SOB on exertion, dry skin, anaemia. Cause: Primary = hashimotos, drug induced (lithium), congenital abnormalities. Secondary (low TSH) = hypothalamic-pituitary axis disorders. (Hypothalamus should release thyrotropin releasing hormone so the pituitary releases TSH so the thyroid produces T3(acitve)/T4. Hashimotos: Autoantibodies against thyroid peroxidase (that converts iodine for the production of thyroid hormones). Treatment of hypothyroidism: Hormone replacement (levothyroxine).

IMMUNOLOGY - Describe the main clinical features, immunopathology, investigation and principles of management of the following conditions: asthma, eczma, anaphylaxis, urticaria and angioedema

Remember the four types of immune reaction: type I (immunoglobulin E cross-linking leading to mast cell degranulation as in anaphylaxis's), type II (immunoglobulin mediated cytotoxic action and complement activation as in hypersensitivity good pastures and is myaesthenia gravis), type III (immune complex formation as in lupus and extrinsic allergic alveolitis) and type for (T-cell mediated delayed response as in dermatitis). In type I hypersensitivity cross-linking of mast cells gives an immediate's response followed by a late phase reaction due to the introduction of prostaglandins and cytokines. Both reactions involve wheeze, pitch, low blood pressure, stomach cramps although the second bout of symptoms is seen 8 to 12 hours later. ANAPHYLAXIS: urticaria, angioedema,, wheeze, abdominal cramps, low blood pressure and collapse (triggers includes blood products and maybe idiopathic). 0.5 mg one in 1000 intramuscular adrenaline, 300 mg intravenous hydrocortisone, 10 mg intravenous chlorphenamine. Confirm anaphylaxis with tryptase. URTICARIA: hives, wheel and flare reaction that may be acute or chronic depending on whether it lasts more than six weeks. If chronic this is rarely due to an allergy and more likely to be due to vasculitis, physical triggers or idiopathic. Three minutes primarily with antihistamines. If patients present with angioedema without urticaria consider ace inhibitor, C1 deficiency or idiopathic as causes. ALLERGIC RHINITIS: hayfever, its management will improve the management of asthma. Classification is as intermittent or assistance, mild or moderate/severe, seasonal or perennial. If mild and intermittent use allergen avoidance, H2 blocker and a short course of nasal D congestion. Step up the ladder by adding intranasal steroids then immunotherapy. ECZEMA: remember that acutely this gives vesicles, and eczema is always itchy. Treatment is with emoliants and possible steroids alongside avoiding triggers (contact eczema). FOOD ALLERGY: although 50% of people think they have a food allergy, it is only actually present in 3% of adults and 4% of children. The food intolerance is related to the amount of food you send and has no immune cause. Food aversion is simple this line. CHINESE RESTAURANT SYNDROME: monosodium glutamate can cause sweating, vomiting and headache in susceptible individuals. VASOACTIVE AMINES: mono amines present in chocolate, cheese and wine whereby susceptible individuals get headaches, flushing, rhinitis and palpitations. ORAL ALLERGY SYNDROME: itching and swelling in the mouth after surfacing food is consumed. WHEAT: throat swelling and abdominal pain if a true allergy, bloating variable with quantity if intolerance.

PREOPERATIVE ASSESSMENT - Describe the principles of management of the diabetic patient presenting for surgery

Remember to not only note if a patient is diabetic but also if they are high risk - eg, poorly controlled or with diabetic complications. Patients should have the shortest possible starvation time and given adequate antiemetics to return to eating asap after the operation. Any patient missing more than one meal should be put on a variable rate IV insulin infusion (previously a sliding scale). Monitor BMs hourly during and immediately after the procedure. Aim for 6-10mmol/l. If possible optimise HBA1C and co-morbidities before referral. BM >10mmol//l consider an insulin glucose regime. Consider regional anaesthesia if possible. Rapid sequence induction may be better due to diabetis increased risk of aspiration. Newer generation sulfonylureas, such as glyburide (Micronase) and glipizide (Glucotrol), can be withheld the morning of the surgery. Metformin (Glucophage) should be stopped 24 h before the procedure. This is done to prevent the possibility of lactic acidosis if the patient's renal function is compromised because of the surgery or its complications. Insulin can be continued.

CEREVROVASCULAR DISEASE - Outline medical and surgical management for TIA.

Remember to use the ABCD2 score To determine the risk of a stroke in the future. (Age greater than 60, blood pressure greater than 120 systolic/greater than 90 diastolic, clinical picture - weakness/slurred speech, diabetes, duration - greater than 60 minutes or 10 to 59 minutes.) Medical management of a TIA: Remember lifestyle measures (smoking cessation, low-salt diet, exercise, Avoiding alcohol access). Drugs used to reduce the cardiovascular risk include: Optimal management of AF, diabetes and hypertension, an antiplatelet (75 mg of clopidogrel or aspirin daily) and a statin. As common causes of TIA//RH or fibrillation and carotid stenosis perform an ECG and ultrasound of the carotid artery. Remember the four-week ban on driving. Surgical management of a TIA: If carotid artery stenosis is greater than 75% perform a carotid endarterectomy.

OBSTRUCTIVE AND NEOPLASTIC CONDITIONS OF THE KIDNEY AND URETER - Discuss the aetiology and presentation of calculi in the kidney and ureter. Describe how renal stones are treated including use of non-operative methods of treatment.

Renal calculi typically present with renal colic, acute loin pain radiating to the groin in combination with haematuria. The pain may also radiate to the testes or labia and will Last hours to days depending on how long it takes to pass the stone. The patient seems unable to stay still trying to gain relief by changing position or pacing. They are sweaty, pale and often vomiting with possible urinary symptoms. Remember that line to groin pain simply implies an obstruction of the year it which could be because of a sloughed renal papilla, tumour or blood clot. Investigations: there are red cells in the urine and the stone can be identified on abdominal x-ray if it contains calcium or IV urogram (showing delayed excretion of contrast and a dilated ureter prior to the stone). Ultrasound can also show a dilated ureter. Management: most stones pass spontaneously (90% if less than 4 mm)so the immediate treatment is bedrest and the application of warmth to the site of pain. The patient may require morphine or diclofenac. Stone is greater than 6 mm need endoscopic surgical intervention. If there is an urari or severe infection this requires urgent surgery. Stones can also be fragmented by waves to make them smaller and easier to pass.

CHRONIC KIDNEY DISEASE - Outline the different forms of renal replacement therapy. Describe the effect of declining renal function on drug clearance and discuss the need to adjust doses according to British National Formulary (BNF) guidelines.

Renal replacement therapy: This may be temporarily in acute kidney failure or permanent in CKD - this involves dialysis or transplantation. Replacement therapy should be prepared well in advance to improve outcomes (a year in advance). EGFR for beginning dialysis (haem or peritoneal) around 8 mL (when symptoms have started to appear that serious complications have not yet occurred). Haemodialysis: efficient, four hours three times a week, in hospital, requires fistula, significant diet and fluid restrictions. There is a risk of confusion and convulsions because of cerebral oedema if haemodialysis is performed to rapidly, Anticoagulation is required. Patients should be screened for hepatitis and HIV and given vaccinations prior to haemodialysis. Those positive can be managed with machine segregation and standard infection control measures. The aim is to reduce your rear and most patients feel the difference within six weeks. There is the option for at home haemodialysis during the night. Conservative: if there is significant comorbidities and a higher age conservative treatment is palliative, treating the symptoms. Haemofiltration: used to treat acute kidney injury, water and solutus filtered from the blood across the membrane under pressure. Replacement fluids and electrolytes added to the Blood prior to its return to the body. The aim is to replace one to 2 L of filtrates an hour. Anticoagulation is required. Note that haemofiltration and haemodialysis can be combined. Peritoneal dialysis: a catheter into the peritoneal cavity uses 2 L of sterile dialysis fluid each for 4 to 6 hours so that waste products diffused from capillaries into the fluid to then be drained. Use 4 L four times a day. Again this can be performed by an automated machine at night. It is particularly useful in children. Dose adjustment for renal failure: Renally metabolised drugs Will not be metabolised correctly in renal failure, renally Excreted drugs will stick around for longer therefore doses need to be adjusted according to the BNF.

Renin angiotensin aldosterone system

Renin is produced by the juxtaglomerular apparatus And converts angiotensinogen into angiotensin one Which is converted by ACE (Which is actually produced in the lung) into angiotensin II Therefore resulting in aldosterone production. This will increase blood pressure but also increase potassium. He goes to say that low aldosterone (scene with low cortisol and Addison's) will raise potassium.

TRANSFUSION - Describe the procedures that should be followed when prescribing blood or blood products for transfusion

Requesting blood products: ensure the sample is then taken, gain consent from the patient (the HIV risk is one in 3 million, hepatitis B is one in 50,000, more common is the risk of transfusion reaction), request the blood and blood products using a form (you should indicate the patient's current haemoglobin knowing that one unit of blood will rise the haemoglobin by 1 g/dL.) Prescribing blood products: use the intravenous infusion section of the chart, remember the slowest rate is four hours per unit, give 100 mL of saline before and after transfusion to keep the line open and gives 40 mg of furozemide with every unit to stop fluid overload.

RESPIRATORY FAILURE - Distinguish type-2 from type-1 respiratory failure and describe the implications of having a high arterial pCO2. Distinguish between acute and chronic type II respiratory failure and respiratory and metabolic causes of acidosis. Describe the causes of ventilatory failure and outline the effect of chest wall and spinal deformity on respiratory function. Outline the conditions that may cause ventillatory failure due to neuromuscular disease.

Respiratory failure is when pulmonary gas exchange fails to maintain normal arterial oxygen and carbon dioxide levels. Type I: hypoxia. This occurs when there is impaired ventilation to part of the lung (asthma, pneumonia) but increased ventilation to the remaining healthy lung maintains carbon dioxide excretion. As mentioned, this occurs with ventilatory impairments - acute asthma, pulmonary oedema, pneumonia, lobar collapse, pneumothorax, PE, acute respiratory distress, some COPD, localised fibrosis. Type II: hypoxia with hypercapnia. This is when there is generalised severe ventilation perfusion mismatch meaning that carbon dioxide builds in the bloodstream this occurs in any disorder affecting the mobility of the chest. Acute type II respiratory failure Leaves no time for metabolic compensation so the pH may be deranged. Causes include acute asthma, acute exacerbation of COPD, acute upper airway obstruction, paralysis, respiratory depressant drugs, hyperventilation and flail chest. Chronic type II respiratory failure allows time for metabolic compensation by retaining bicarbonate at the kidneys. The pH may be normal. Causes include: COPD, chronic apnoea, Kaifu scoliosis, myopathy, ankylosing spondylitis. Ordinarily, we rely upon the hypercapnic state to trigger breathing. With type II respiratory failure chronic hypercapnia desensitises this mechanism so patients rely upon low oxygen to trigger breathing (breathing will stop if put on high oxygen therapy).

GASTRIC CANCER - List risk factors for the symptoms suggestive of and investigations for gastric cancers. Describe the epidemiology, classification, morphology and natural history of gastric cancers. Outline the general principles of curative and palliative surgical procedures for gastric cancers and discuss the role of adjuvant and palliative therapy Quantify the prognosis for gastric cancer

Risk factors: Helicobacter pylori, blood group A, smoking, a high salt diet, Pernicious anaemia and previous stomach surgery. Vitamin C consumption is protective. Epidemiology/natural history: Gastric cancer is one of the most common cancers in the world's because it is common in East Asia and South America, although less common in the UK it is still the sixth commonest cancer here. It used to be more common distally but is now more common proximally in the cardia. As the stomach lining is columnar, most cancers are adenocarcinomas - Rare causes include lymphomas, stromal tumours and neuroendocrine tumours. Classification: early gastric cancer is confined to the mucosa or submucosa but late gastric cancer is when the muscularis propria is breached. A leather bottle stomach or linitis plastica is when diffuse gastric cancer affects the whole stomach completely stopping its distention and often spreading throughout the peritoneal cavity, particularly to the ovaries. Presentation: Late gastric cancer is more common in the West and includes Weight loss, anorexia, epigastric pain, nausea and vomiting. More rarely patients may have a gastrointestinal bleeding or gastric perforation. Examination can reveal a succession splash (Auscultation reveals fluids splashing on movement because of an antral obstruction), hepatomegally, ascites, virchows node, acanthosis nigricans. Treatment: After endoscopy, biopsies and staging CT treatment can be determined. The greatest possibility of cure is with surgery (like oesophageal cancer). Palliative surgery includes bypass procedures but curative surgery may be as drastic as a gastrectomy or subtotal gastrectomy. Chemotherapy is used less than in oesophageal cancer, its current role is predominantly in palliation. Other palliative treatment includes stenting, proton pump inhibitors to reduce bleeding from ulcerations and argon plasma coagulation to stop Leeds. Radiotherapy is useless in stomach cancer. Prognosis: Five year survival is 10%. Tumours spread locally, via lymphatics (virchovs node), across the peritonaeum/transcoelomic or by blood (particularly to the lungs). GASTROINTESTINAL STROMAL TUMOURS: Rare tumours originating within the bowel wall including things like leiomyosarcomas, and neurofibromas. Typically benign, only one third on malignin's and most have found incidentally with abdominal pain, GI bleeding and obstruction. Treatment is with surgical resection and possible kit selective tyrosine kinase inhibitors.

LUNG CANCER - Describe the common clinical presentation and risk factors. Outline the epidemiology of lung cancer in developed countries. Outline local metastatic manifestations of lung cancer and describe systemic non-metastatic manifestations.

Risk factors: Smoking (smoking is directly related to 90% of lung cancers and heavy smokers are more likely to die), radon exposure, atmospheric pollution, occupation and urban dwelling. Presentation: Lung cancers may be very large before giving symptoms (if peripherally located) - dry cough (may have a secondary infection), change in smokers cough, haemoptysis, bronchial obstruction (SOB, possible atelectasis), breathlessnesss (from collapse, secondary infection/pneeumonia, phrenic nerve compression paralsing the diaphragm), pleuritic chest pain (if locally invasive), horners syndrome (if apical), dermatomal pain (if intercostal nerves are invaded), hand weakness (brachial plexus erosion). If there is mediasteinal spread : dysphagia, pericardial effusion, voice alteration (recc larengeal nerve erosion). With metastasis think bone, brain, liver, adrenals and skin........headaches, seizures, personality change, jaundice, skin nodules, bone pain (hypercalcaemia). Alongside the usual red flags of weight loss and anorexia. Finger clubbing can be seen. Small cell lung cancers can cause SIADH.

EVIDENCE BASED MEDICINE - Define screening and distinguish between mass proactive screening and opportunistic case finding. Describe the circumstances in which preliminary consideration of screening would be reasonable and how screening should then be evaluated. Describe how lead time bias, duration bias and selection bias affect the assessment of screening Discuss examples of the major screening programmes currently operating in the UK.

Screening is about identifying patients with an increased risk of having a condition, therefore flags them up as potentially benefiting from further tests. Mass screening is testing a wider population whereas opportunistic is picking a specific population. In order for a screening test to be viable it should be: >The condition should be an important health problem. >There should be a treatment for the condition. >Facilities for diagnosis and treatment should be available. >There should be a latent stage of the disease. >There should be a test or examination for the condition. >The test should be acceptable to the population. >The natural history of the disease should be adequately understood. >There should be an agreed policy on whom to treat. >The total cost of finding a case should be economically balanced in relation to medical expenditure as a whole. >Case-finding should be a continuous process, not just a "once and for all" project. LEAD TIME BIAS: Lead time is the time between screening identifying a disease and the time it would actually clinically present. Bias here is when survival time is perceived to be longer because of earlier diagnosis but is not actually longer. SELECTION BIAS: Selecting participants in a non randomised manner. CURRENT UK SCREENING PROGRAMMES: > AAA: ultrasound for men 65 and over > BCSP: Faecal occult blood bi-annually aged 60 to 74 > BSP: Mamograms for women aged 50 to 70 every 3 years > CSP: Every 3 years for women aged 25 to 49 > Diabetic Eye Screening: annual > Fetal anomaly screening, newborn baby check, sickle cell and thalassaemia screening.

ELECTROCARDIOGRAM - Describe the normal ECG and how the electrical changes of the cardiac cycle relate to the ECG.

See diagram - remember that PR is to the start of the Q wave and QT is to the end of the T wave. An electrocardiogram is a recording of the elecctrical activity of the heart used to identify and locate pathologies. A positive deflection implies electrical activity running towards the lead, a negative away. P = atrial depolarisation. PR = movement of electricity from atria to ventricles. 3-5small sq/0.12ms. QRS = depolarisation of the ventricles. <3small sq/<0.12ms ST = when the ventricles are depolarised prior to repolarisation. Elevation is >1small sq, depression is >0.small sq. T = Ventricular repolarisation. Ten electrodes give a twelve lead ECG. Right arm = red Left arm = yellow Left leg = green Right leg = black (Ride your green bike) V1 = 4ics right sternal edge V2 = 4ics left sternal edge V3 = 5th rib V4 = 5ics mid clavicular V5 = 5ics mid axillary V6 = 5ics mid axillary Septal view = V1, V2 Anterior view = V3, V4 Lateral view = V5, V6, aVL, I Inferior = II, III, aVF

CEREVROVASCULAR DISEASE - List the clinical differences between a stroke which arises from anterior circulation territory and one which arises from posterior circulation territory Explain the Bamford classification of stroke, describing the prognostic difference between each stroke type.

See image. The middle Cerebral artery provides the blood supply to most of the brain. TACS - Total anterior circulation stroke meaning the anterior and middle cerebral Artery territories are both involved and symptoms of hemiplegia, hemianopia and highest readable dysfunction (problems with comprehension and language) are seen. This has the worst prognosis as 60% die in one year, although there is a low recurrence risk. PACS - Partial anterior Circulation stroke meaning that either the anterior or middle cerebral artery territories are involved giving symptoms of two of the following three are seen: hemiplegia, hemianopia and higher cerebral dysfunction (comprehension and language). Here 16 % of people die within a year, but the recurrence rate is low. LACS - lacuna anterior circulation stroke of deeper penetrating arteries meaning that there will be focal deficits (sensory or motor or sensorimotor or ataxic hemiparesis). 11% die within a year, but recurrence rate is low. POCS - posterior circulation/meaning it there will be/In the region of the posterior cerebral artery or the vertebrobasilar artery. This gives symptoms of visual disturbance, cranial nerve palsys, motor deficits and cerebellar dysfunction. 19% die within a year, but recurrence rate is low.

CEREVROVASCULAR DISEASE - Explain the following terms, with specific reference to time course; Stroke; Transient Ischaemic Attack; Amaurosis Fugax

Stroke: A neurological deficit of cerebrovascular cause That persists beyond 24 hours or causes death within the first 24 hours. TIA: An episode of neurological dysfunction whose side-effects reversed completely within 24 hours. This significantly increases the chance of a further stroke - Use ABCD2 score to determine the risk of a stroke in the next 90 days (Age greater than 60, blood pressure greater than 140/greater then 60 diastolic, clinical features - weakness/slurred speech, diabetes, duration of TIA >60 or 10-59mins). Remember the TIA could be focal brain/retinal/spinal cord But does not cause acute infarction is. Amaurosis Fugax: Transient monoauricular visual loss That comes down like a curtain That lasts a few seconds (maybe minutes). Typically, this is because of an obstruction in the retinal or ophthalmic artery (Arthrosclerosis, embolism, Giant cell arteritis, Lupus, malignant hypertension etc).

LYMPHATIC DISORDERS - Define lymphoedema. Differentiate primary from secondary lymphoedema and explain the pathophysiology and treatment of lymphoedema

Swelling of the tissues as a result of lymphatic drainage failure. Over time fluid becomes fibrosis and depositioned adipose. Primary: due to abnormal development of the lymphatic system. Secondary: from extrinsic processes which damage previously normal lymphatic system (trauma, radiotherapy, surgery, infection). In clinical practice pure lymphoedema is actually uncommon in many patients there is chronic (Greater than three months) oedema with lymphatic components Alongside increased venous pressure, and reduced plasma oncotic pressure because of low protein. Presentation: swelling (Initially pitting as there is fluid, then no pitting because of fibrosis and fat) , second, dry skin, lymph blisters, skin creases. Patients tend to get a heavy aching pain in the limb as well as joint pain because of having to support the weight of the limb. Their mobility can be reduced and there can be lymphorhoea and psychological difficulties because of the image. Complications: cellulitis, increased chance of malignancies (Both due to poor local immune response), deep vein thrombosis and lymphorhoea. Diagnosis: exclude heart failure, nephrotic syndrome (therefore low-protein), medications, venous disease and tumours before making the clinical diagnosis. Lymphoscintigraphy is rarely performs but can show the distribution of lymphatics and ultrasounds can help distinguish between Venous and lymphatic causes. Treatment: Compression bandaging for two weeks followed by general use of compression stockings alongside moisturiser on a daily basis. Remember that lymphoedema will not respond to loop diuretics and any overlying cellulitis must be treated. Typically, lymphoedema is chronic and incurable.

PLEURAL EFFUSION - Describe the typical examination features of a pleural effusion and describe the aetiology and clinical features of an EMPYEMA.

Symptoms: pain on inspiration and coughing. Signs: Tachypnoea, reduced chest expansion, tracheal deviation away (towards a white out is atelectasis) if large and asymetric, dull to percuss, absent breath sounds over a large efustion, Pleural rub as well as signs of the cause such as pneumonia. On Xray the costophrenic angles blunten. EMPYEMA: Pus in the pleural cavity. Typically with pneumonia it presents With severe pleuritic chest pain Alongside symptoms of Pulmonary infection (fever, malaise alongside cough, SOB and chest pain worse on cough or inspiration). Systemic features are prominent. Plurals surfaces become covered in a thick inflammatory exudate and because the pass is often creating a high-pressure space it can rupture into the bronchus causing a fistula and track through the chest wall forming abscesses. Empyema investigations: chest x-ray will be indistinguishable from a pleural effusion other you may see pleural adhesions. Ultrasound confirms the presence of a fluid, and Ultrasound or CT can identify the optimal site to attempt aspiration.

HAEMOSTASIS - Outline the clinical indications for screening for thrombophilia and how this is done

THrombophillia is an inherited or acquired coagulopathy predisposing to thrombosis. Those affected requires special precautions in surgery, pregnancy and any immobility (risk factor for DVT). Inherited: protein C and S deficiency, factor five Leiden (a mutated form of factor five), prothrombin gene mutation, antithrombin deficiency. Acquired: progesterone in the oral contraceptives pill or antiphospholipid syndrome. Indications for screening: an arterial thrombus in someone younger than 50 or venous thrombus in someone less than 40, family history of DVT, unexplained recurrent VTE, unusual sites for thrombus, three or more fetal losses. Investigations: full blood count, Blood film, clotting tests, lupus anticoagulant and anti-cardiolipin antibodies, antithrombin and protein C/S assays, factor five liedin mutation PCR and PCR for prothrombin gene mutation.

ADRENAL DISEASE - Discuss the possible clinical presentation of a phaeochromocytoma and list the syndromes of which it is a component.

The adrenal medulla secretes catecholamides (Dopamine and adrenaline), the next layer is the zona reticularis (androgens), next out is the zona fasciculata (Glucocorticoids), Then the zona glomerulosa (mineralocorticoid - aldosterone). Phaeochromocytoma: rare neurondocrine tumour that secrete catecholamides (Adrenalin, noradrenaline) typically occurring in the adrenal medulla although 20% rise elsewhere in the body in sympathetic ganglia (known as a paraganglioma). Most are benign, 15% share malignancy and 30% are associated with inherited disorders (M EN two, von hippel Lindau). Patients present hypertensive with abdominal pain, vomiting, constipation, weight loss, glucose in tolerance and paradoxes is of pallor, flushing, palpitations, sweating, headache and anxiety. They may also present with a complication of hypertension (stroke, MRI, left ventricular failure, hypertensive retinopathy). Investigations should include: serum and urinary Metabolites of adrenaline/noradrenaline. Remember that these levels will be falsely high if the patient is stressed, acutely unwell or following vigourous exercise. Serum chromagranin A is a tumour marker and genetic testing should be considered if there is a family history. Identify the tumor wth CT/MRI. Management: six weeks of an alpha blocker (phenoxybenamine) with the addition of the beta-blocker if this is not working. The medical therapy helps prepare the patient for surgery where the tumour is removed. Metastatic cancer may require additional chemotherapy.

BRONCHIECTASIS - List recognised risk factors and outline the morphology and pathological consequences of Bronchiectasis

The cause is variable - from congenital ion transport deficiencies (cystic fibrosis, cilliary dysfunction, hypogammaglobuminaemia) too damage from inhaled toxins or foreign bodies (TB, severe pneumonia, aspergillosis, bronchial tumors - in these pus distal to the obstruction may cause localised bronchiectasis). Risk factors are anything that causes reccurrennt infections such as impaired immunity. Bronchiectasis is progressive if associated with genetic conditions (cystic fibrosis, cilliary dysfunction) and will eventually cause respiratory failure. In other patients prognosis is good if physio is regular and antibiotics use is aggressive.

HAEMOSTASIS - describe the role of the liver in normal clotting, including the part played by vitamin K in the synthesis of some clotting factors

The coagulation cascade: a series of enzyme reactions leading to the conversion of soluble plasma fibrinogen to a fibre and clot. consider it as the combination of the extrinsic, intrinsic and common pathways. Remember that von Willebrand factor is meant to stabilise factor X, thus enabling the extrinsic pathway to - it is produced by endothelial cells and megakaryocytes and stored in platelet granules as well as endothelial cells. Vitamin C is found in green leaves, dairy products and may also be synthesised by intestinal flora in the terminal ileum and colon. It is stored in the liver as a cofactor needed to produce blood clotting factors and the formation of proteins required to make bone. Without vitamin K prothrombin time increases. newborns have low stores in their liver and a lack of intestinal bacteria so often given an injection to prevent haemorrhagic disease of the newborn. This link a deficiency also occurs when there is cholestatic jaundice as bile salts and needed for intestinal absorption. Limiters of coagulation: antithrombin (potentiated by heparin), protein C (from vitamin K dependent precursor, activated by thrombin, destroys factor five and 7 to stop the coagulation cascade), protein S (a cofactor for protein C). Fibrinolysis: also response to vascular damage, plasminogen is converted to plasmin which breaks down fibrinogen and fibre in into fibrin degradation products including D dimer. Plasminogen itself is activated by tissue plasminogen activator from the endothelium (it is triggered by mediators including thrombin). Other plasminogen activator are urokinase from the kidney, factor 12 and pre-kallekrein. protein C also induces fibrin lysis. Recombinant tissue plasminogen activator is now used clinically in scenarios such as myocardial infarction.

HAEMORRHOIDS - Describe symptoms and signs of perianal haematoma and outline management

The complication of an external haemorrhoid. Thrombosis leads to subcutaneus bleeding at the anal margin, particularly after constipated stool. It causes acute perianal pain worsened by desiccation and examination reveals a tense, tender, blue lump at the anal margin. Simply inscise under a local analgesia if presentation is within 1 to 2 days. If later, excise.

DIABETES MELLITUS - Describe the diagnostic criteria for diabetes mellitus and glucose intolerance. Classify major types of diabetes mellitus and describe clinical features suggesting Type 1 diabetes. Compare and contrast the typical presentations of Type 1 and Type 2 diabetes.

The diagnostic criteria for diabetes is greater than 7 mmol per litre fasting or greater than 11.1 mmol per litre two hours after glucose challenge. These values indicates people whose hyperglycaemia carries significant risk of retinopathy, nephropathy, Heart disease, stroke, neuropathy etc. Impaired glucose tolerance (Prediabetic state associated with increased risk of macro vascular disease) Is when Two-hour glucose challenge values are between 7.8 and 11 mmol per litre. Remember that it is Insulin's job to promote glucose uptake and in his absence the fasting state promotes lippolysis eventually producing ketone bodies. Hence DKA. Type I: T-cell autoimmune destruction of insulin secreting beta cells in the pancreatic islets. Symptoms only occur when 80 to 90% of functional capacity is lost: prior to this point insulitis is a pancreas infiltrated with T and B cells and macrophages. Type I diabetics and more likely to suffer from other autoimmune diseases such as thyroid disease, Addison's, vitiligo, coeliac disease and pernicious anaemia. Presentation is with: metabolic acidosis (because of ketogenesis), Hyperglycaemia because of glycogenolysis therefore dehydration (which promotes aldosterone release causing low potassium. Clinically this means a few weeks history of: Fatigue, polyuria, nocturea, thirst and polyurea. Patients may have repeated infections and lipolysis leads to weight loss. They also may present in DKA. Type II: Insulin resistance initially leads to elevated insulin secretion but in susceptible individuals the pancreatic beta cells are unable to sustain this and slow progressive insulin deficiency develops (over years). Typically the patient is older than in T1DM, obese and sedentary with high cholesterol, fatty liver disease, polycystic ovaries (i.e. metabolic syndrome). The insulin that is produced is sufficient enough to prevent weight loss and ketoacidosis, symptoms are: fatigue, polyuria, infections or asymptomatically on screening Or through discovery of the complications of diabetes. Rarer types: Gestation all, pancreatic disease, drug induced, acromegaly, Cushing's, glucagonoma, phaeochromocytoma, tyrotoxicosis etc.

EVIDENCE BASED MEDICINE - Define evidence based clinical practice and the actions involved in its execution Describe the sources of variation in clinical measurement including regression to the mean and the importance of observer variation. Discuss the different approaches to defining abnormality and the arguments for and against them

The integration of clinical expertise, patient values, and the best research evidence into the decision making process for patient care. Regression: the relationship between one dependent variable and many independent variables (the mean) Mean: the average of numbers Observer variation: Differing results by multiple researchers as the method is subjective Dependent variable: what you measure Independent variable: what you change Abnormal can be considered as outside the WHO definition of health which encompasses physical, psychological and social well being. Or consider statistically values outside of a set range, two standard deviations from the mean etc.

IMMUNOLOGY - Outline the main immunological barrier to successful transplantation and how this may be overcome by tissue typing and immunosuppressive therapy

The main problem is organ rejection. Host teeth cells recognise Oren HLA molecules triggering the rejection process. The rejection process itself involves cytotoxic T cells, B cells and macrophages developed to attack foreign tissue. This is modified by HLA typing and matching, graphed preparation (relatives make better donors, removal of dendritic cells contain lots of HLA, removal of T cells), strict cross matching between the patient's blood in the donors lymphocyte, monitoring the response (needle aspiration biopsy), immunosuppression. Additionally, an immunological tolerance may be enhanced by introducing small amounts of the donor tissue prior to transplant (example pre-renal transplant blood transfusion is shown to reduce rejection).

PITUITARY DISEASE - Describe the local symptoms that result from a large pituitary adenoma and outline the clinical consequences of pituitary adenoma producing prolactin, growth hormone or ACTH. Classify pituitary adenomas according to size and function Outline other causes of hypothalamic-pituitary disturbance. Describe the laboratory assessment of pituitary function and outline the radiological techniques used to investigate pituitary disease Outline the treatment and treatment options of a prolactinoma, including the use of dopamine agonists as first line therapy.

The pituitary gland Posterior produces ADH and oxytocin. The anterior section produces Growth hormone, ACTH, LH/FSH, TSH, prolactin. PITUITARY ADENOMA: Local compression can cause bitemporal hemianopia, Signs of raised intracranial pressure (papiloedema, headaches), As well as psychiatric complications and hormonal complications through secretion of prolactin (galactorhoea), ACTH (Cushing's), growth hormone (acromegaly). Classification: And adenoma is micro-if less than 10 mm, macro is greater than 10 mm. They are then subdivided depending upon their secretion. Null cell (no secretion), corticotrophic (ACTH secretion), prolactinoma, Somatotrophic (growth hormone), Gonadotrophic, thyrotrophic. SHEEHAN SYNDOME: Postpartum hypopituitarism because hypovolaemia during childbirth leads ischaemic necrosis of the pituitary gland. Typical presentation is with a lack of breastmilk and hypothyroidism. Treatment is with lifelong hormone replacement. ACROMEGALLY: The adult form of gigantism, when excess growth hormone is secreted, usually by the pituitary adenoma. Features include: Enlargement, Course facial features, Enlarged internal organs (especially heart), thickened of vocal chords (deeper voice), Frontal bossing, macroglossia, prognathism (lower jaw protruding), Carpal tunnel And teeth spacing. They develope kidney failure, heart failure, Hypertension, diabetes, Field defects (compression of the occupiers). Confirm the diagnosis with a glucose tolerance test. In a normal individual two hours after glucose is given growth Hormone should be suppressed. Medically, dopamine agonists or somatostatin are used to suppress growth hormone production. All the adenoma can be removed Surgically/blastid with radiation. CUSHINGS DISEASE: An ACTH secreting tumour of the pituitary giving Cushing's syndrome. DIABETES INSIPIDUS: Excessive diuresis and thirst because of inadequate ADH secretion. On water deprivation the patient still produces excessive urine amounts. This is commonly because of a problem with the posterior pituitary but may also be nephrogenic (the kidneys failed to respond to ADH). Unlike in diabetes melitus there will be no glucose in the urine. Because of excessive dehydration there are high concentrations of sodium and low concentrations of potassium (Nausea, vomiting, constipation). To distinguish between ADH levels being low and nephrogenic diabetes insipidus give Desmopressin (Synthetic ADH). If the body responds to ADH with decreased urine output then there is not enough ADH in the first place (i.e. a pituitary problem). If the body does not respond to the ADH/Desmopressin then the kidneys are able to respond (i.e. nephrogenic). Pituitary diabetes insipidus can be treated with synthetic ADH/Desmopressin. Nephrogenic diabetes insipidus requires removal of the cause And treating the water deficit. GROWTH HORMONE DEFICIENCY: A child with growth deficiency, or more rarely, and adult with low mass and poor bone density. Typically because of a pituitary tumour/autoimmune damage/Surgical damage. They also have depression and poor memory. Diagnosis can be performed by provoking growth hormone (or trying to) with arginine/levoDOPA/Propranolol. Treat with daily injections of growth hormone if they are symptomatic. SIADH: Excessive production of ADH which may be from a pituitary tumour (posterior), ectopic (small-cell lung tumour), Meningitis, pituitary trauma/bleediatrogenic. Patients are hypervolemic, hypertensive with low sodium and need fluid restriction to prevent cerebrum oedema. In acute situations intravenous hyper tonic say line can be given to correct the low sodium. In chronic poor control, ADH inhibitors (demeclocyclone) Can be given. PROLACTINOMA: A benign tumour of the anterior pituitary secreting prolactin. This may cause compression (homonomus hemianopia, Vertigo, vomiting), Galacturia, amenorrhoea, Loss of pubic hair, erectile dysfunction. Remember to check thyroid levels because hypothyroidism is linked to high prolactin. Dopamine agonists (bromocriptine) will shrink the prolactinoma by inhibiting its secretion. GENERAL PITUITARY INVESTIGATIONS: Remember to assess visual fields (Pituitary tumours can compress the optic nerve) and perform imaging. In ACTH deficiency Try to stimulate release with ACTH. Also do a glucose tolerance test. In LH/FSH deficiency random serum testosterone, LH and FSH levels should be tested. Regular menstruation implies normal androgens. In TSH deficiency measure random serum T4 (inactive). In growth hormone deficiency measure growth hormone levels after exercise. In diabetes insipidus (lack of ADH - Because the pituitary cells to produce it all the kidneys failed to respond) use water deprivation tests to see if there is normal retention of water in dehydration.

THE SPLEEN - List the common causes of splenomegaly including portal hypertension, lympho-reticular disease and chronic infection.

The role of the spleen is to synthesise antibodies, phagocytose old red blood cells and hold a reserve of red blood cells. Splenomegaly is a spleen greater than 11 cm and is one of the signs of hypersplenism including reduced circulating red blood cells, compensatory increased proliferation in bone marrow and correction of these abnormalities by splenectomy. Causes: portal hypertension, chronic infection (most commonly infectious mononucleosis but also syphilis and endocarditis), lymphoreticular diseases (excessive overproduction of lymphocytes), haematological malignancy. A better way to consider the causes of a large spleen: INCREASED FUNCTION - chronic infection, sickle cell disease, thalassaemia, haemoglobinopathy's. ABNORMAL BLOOD FLOW -cirrhosis, portal vein obstruction/hypertension. INFILTRATION - haematological malignancies or metabolic diseases. Presentation: abdominal pain, pleuritic chest pain, signs anaemia

TUBERCULOSIS - Describe the global picture of TB, its relation to the AIDS epidemic and the causes and consequences of multidrug resistant tuberculosi

The second most common death due to a single infectious disease (2nd to HIV), leading killer of those with HIV and more prevalent and life threatening in lower income countries. It is closely linked to HIV/AIDs therefore all TB patients should be HIV tested. Multidrug resistance has emerged as TB is resistant to rifampicin and Isoniazid - this is rising. (hence the emergence of directly observed therapy for alcoholics, drug abusers, homeless, those with a poor compliance Hx). It is more common in those with prior TB (especially if inadequatly treated) or HIV. Treat with prolonged (12m) treatment and more toxic therapies. Prognosis: <5% risk of relapse with treatment most occuring within 5months. Mortality is higher if smear positive in treatment, HIV positive and smoking.

DIAGNOSTIC STUDIES IN BILIARY TRACT DISEASE - Contrast changes in liver function tests in obstructive and hepatocellular jaundice.

The six LFTs: biliruben, gamma GT, alkaline phosphatase, albumin, aspatrate transaminase and alanine transaminase. A coagulation screen is also important. ALT/AST occur in hepatic damage as hepatocytes spill out transaminases. Remember ALT is specific but Aspartate transaminase is also released by muscles. ASPARTATE TRANSAMINASE = muscles ALKALINE PHOSPHATASE = bone Alkaline phosphatase is a marker of obstruction but is also released from bone. Gamma GT also shows obstruction but may be markedly rised in alcoholism. Obstruction also rizes conjugated biliruben which is absent in faeces and raised in urine

MISCELLANEOUS SKILLS/TOPICS - Describe the indications for proctoscopy and sigmoidoscopy

1. A PROCTOSCOPY examines the anal canal whereas a RIDGID SIGMOIDOSCOPY examines the rectum up to the recto-sigmoid junction. These can be diagnostic, for biopsy and can enable treatment of haemorrhoids (proctoscopy). As outpatient procedures, they do not need sedation and are indicated in ?rectal cancer, IBD, biopsies up to the rectosigmoid junction, haemarhoid banding and prior to rectal surgery. A FLEXIBLE SIGMOIDOSCOPY is more invasive, needing bowel prep. Again a low risk outpatient procedure, it visualises up to the descending colon. Indications include: ?colorectal cancer, preop evaluation, surveillance of malignancy, removal of rectal foreign body, stent insertion (strictures, decompression, balloon dilatation) and haematochezia (fresh blood PR).

CARDIAC SURGERY - Classify cardiac trauma (penetrating and non-penetrating).

1. BLUNT chest injury tends to have a simpler management once CT has confirmed the pathology. This may involve ventilation and drains. Trauma means that first thing patients will get a supine chest Xray to determine any spinal pathology. PENETRATING wounds often require surgery and complex investigations. Patients tend to be more likely to deteriorate but also more likely to recover quicker. Again, chest Xray is vital, although the patient should be upright if possible so that a haemothorax, pneumothorax or diaphragm injury is easier to detect. Remember ATOM FC (airway damage, tension pneumo, open pneumo (connection remains patent so can track infection into the chest), massive haemothorax, flail chest, cardiac tamponade. >CARDIAC TAMPONADE may give a raised JVP, rounded heart shadow on CXR, pulsus paradoxus, muffled heart sounds and low blood pressure. >CARDIAC CONTUSION needs only conservative management but can give ECG changes indicative of an MI.

CARDIAC SURGERY - Outline the surgical principles and operative risks involved in the treatment of coronary artery disease and valvular disease including types of prosthetic valve and anticoagulation.

1. Indications for coronary artery disease: chronic or unstable angina, asymptmatic patients with a severe lesion, atypical angina with easily provoked symptoms. PCI or CABG? Both are safe and effective with little mortality. PCI has fewer short term complications but is more likely to need repeating. CABG is more invasive but will last longer and helps patients with multi-vessel disease. Technique: CABG uses a midline sternotomy with cardiopulmonary bypass (therefore an open heart surgery). Commonly the left internal mammary artery (aka internal thoracic) or saphenous veins are used as grafts. The internal thoracic can remain in situ, still attached to the subclavian artery, giving better results. Prognosis: fantastic, 98% relief of angina, 5year survival of CABG is >90%. Complications: MI, bleeding, stroke, arrhythmias, tamponade, infection, aortic dissection, pneumonia, respiratory failure, renal failure, GI complications, multi-organ failure.

MISCELLANEOUS SKILLS/TOPICS - List the indications and contraindications for peritoneal lavage; describe the characteristics of a positive or negative lavage in a patient who has sustained trauma.

1. PERITONEAL LAVAGE: This has now been superceeded by the FAST ultrasound scan in trauma to identify free fluid/blood. If free fluid is found on FAST a CT scan is performed. For patients too unstable for CT, use peritoneal Lavage (use a dialysis catheter in the abdomen under local anaesthetic to insert a litre of saline. Once removed the fluid can be inspected for WCC, amylase, bacteria and bile).

MISCELLANEOUS SKILLS/TOPICS - Watch or under supervision, perform the routine care of an 'ostomy' including cleaning, preparing the site and applying an appropriate external appliance.

1. STOMA CARE: It is important to care for a stoma to prevent tissue breakdown, dermatitis around the stoma, infections etc. A stoma is any external opening in a laminated organ. (ureters included). ILEOSTOMY - from small bowel, spouted (contents are irritant), loop or end, prominent mucosal folds, usually right sided, dark pinkred colour and liquid containing. COLOSTOMY - from large bowel, flushed, flat mucosal folds, light pint, solid contents. UROSTOMY - from a length of disconnected ileum through which the ureters are diverted. Typically spouted prominent mucosal folds, dark redpink and right sided with clear liquid contents. GASTROSTOMY - For stomach drainage or feeds. Narrow calibre, flush to the skin, left upper quadrant. JEJUNOSTOMY - For feeds. Narrow calibre, flush to the skin, left upper quadrant.

MISCELLANEOUS SKILLS/TOPICS - Indicate the sites for central venous access.

1. Sites for central venous access include: internal jugular vein, (which is in the caroted sheath posteriolateral to the carotid artery, near the vagus nerve - use USS guidance). If this fails try the subclavian vein at the junction of the middle and outer 1/3rd of the clavicle.1. Sites for central venous access include: internal jugular vein, (which is in the caroted sheath posteriolateral to the carotid artery, near the vagus nerve - use USS guidance). If this fails try the subclavian vein at the junction of the middle and outer 1/3rd of the clavicle.

MISCELLANEOUS SKILLS/TOPICS - Describe the indications for tube thoracotomy and list the necessary steps in performing this procedure.

1. THORACOSTOMY - a tube thoracostomy is a chest drain, required for pneumothorax, haemothorax, hydrothorax, chylothorax, empyema (may be the result of an open pneumothorax), pleural effusion. It is inserted under local anaesthetic via a 2cm incision near to the upper border of the lower rib (Avoids the VAN bundle below the upper rib). After bluntly dissecting the intercostal muscles, free adhesions with your finger and insert the drain. It must then be attached to an underwater seal and its position checked with a CXR. Remove in a pneumothorax 24hours after the drain stops bubbling.

CARDIAC SURGERY - Outline the surgical principles and operative risks involved in the treatment of coronary artery disease and valvular disease including types of prosthetic valve and anticoagulation.

1. Valvular heart disease may result in valve replacement with one for two valves. Manmade mechanical valves (ball in cage tilting discs, bi-leaflets). Modern valves are durable but thrombogenic, needing lifelong anticoagulation. Tissue valves (homographs if human, xenographs if pig), are less thrombogenic so anticoagulation is short term. They are more likely to degrade than manmade grafts, especially if pig, so we favour homographs for the young. Complications: infection of a prosthetic valve is rare but devastating needing extensive treatment and often valve replacement. Homographs have the lowest infection risk. Homographs and xenographs may degrade in time and fail. Indications: symptomatic aortic or mitral stenosis or a patient with left ventricular dysfunction alongside mitral or aortic regurg. Typically a prosthetic valve is mitral, aortic or both. Anticoagulation of a patient with a prosthetic valve: in the absence of contra-indications (bleeding disorders, pregnancy, severe hypertension, peptic ulcer disease) warfarin is used, aiming for a higher INR of 3-4 (not the standard 2-3). Whilst titrating up to this cover with Heparin

THE BLADDER AND PROSTATE - Discuss the clinical presenting features, staging, pathology, natural history and clinical management of carcinoma of the prostate including a description of hormonal manipulation.

7% of all cancers in men are prostate, particularly associated with increasing age, typically adenocarcinoma. Presentation: typically symptoms of lower urinary tract obstruction or prostate cancer presents with signs of metastatic spread (particularly bone disease). Prostate cancer may also be found incidentally is a hard irregular gland on PR or on histological results post TURP for benign prostatic hypertrophy. Staging/diagnosis: investigations must include a transrectal ultrasound of the prostate and a biopsy. Histology is vital prior to treatment and the Gleason scoring system is used. Measure blood levels of PSA (prostate specific antigen) and x-ray can help identify osteosclerotic lesions corresponding to metastases. Treatment relies primarily on the PSA and Gleason score. Management: if disease is confined to the gland then perform a radical prostatectomy or radiotherapy. Manage locally extensive disease with radiotherapy with or without androgen ablation therapy. Hormone ablation therapy/androgen ablation therapy uses the fact that most prostate cancers are hormone sensitive requiring testosterone/dihydrotestosterone/androgen to grow. This means that finasteride and other such drugs can help treat prostate cancer. Metastatic disease requires orchidectomy. Remember that in elderly men with slow growing, low grade cancers treatment may be inappropriate because the person is more likely to die with the disease than of it and treatment carries a high risk of erectile dysfunction and incontinence.

TRANSFUSION - Describe the principles of cross matching blood.

> ABO grouping > Antibody screening for atypical antibodies > Selection of donor and crossmatching (physically mixing samples an looking for agglutination) This takes 45mins-1hr > Additional tests for patients at high risk of atypical antibodies (previous transfusion) If blood is need rapidly give ORh-, if you have 15mins then ABO and Rh match.

INFECTIVE ENDOCARDITIS - Outline important investigations.

> Blood cultures (three to six sets). > Echo to detect vegetations and any abscesses (may need to be trans-thoracic or even trans-oesophageal to detect smaller vegetationa). > CRP and ESR are raised as are leucoytes. > Chest Xray can show cardiomegally due to heart failure. Also do an ECG.

EXTRINSIC ALLERGIC ALVEOLITIS - Outline the treatment options and monitoring of treatment response

> Cease exposure to the offending antigen or dust masks to minimize exposure. >Methods to reduce levels of the antigen such as dying hay more thoroughly. >Give prednisolone for an acute attack for 3-4weeks. >Oxygen for acutely unwell patients. >Treat the symptoms of resulting fibrosis (steroids, oxygen, education, breathing exercises).

CYSTIC FIBROSIS - Outline the non-respiratory manifestations of cystic fibrosis

> Infertility due to failure of the development of the Vas deferens. > Sinuses can fill with mucus causing headaches and infection results in faial pain, sinusitis and fever. > Pulmonary hypertension causes left sided heart failure. > Bowel obstruction from thickened pancreatic secretions as well as constipation and intussiseption. > The same can happen to the liver causing cirrhosis. > Pancreatic fibrosis and failure as mucus plugs ducts. > Diabetes > Malnutrition > Poor vitamin D uptake leads to osteoporosis.

OPERATIVE AND POSTOPERATIVE MANAGEMENT - Describe the typical arrangements for a cancer centre MDT meeting

A Multidisciplinary Team Meeting is a meeting of the group of professionals from one or more clinical disciplines who together make decisions regarding recommended treatment of individual PATIENTS. Multidisciplinary Teams may specialise in certain conditions, such as Cancer.

EPILEPSY Describe the classical features of a generalized seizure. Outline the clinical types of syncope Outline the features that distinguish seizures from syncope Outline a classification of epilepsy and describe the differential diagnosis of epilepsy Outline the immediate 'first aid' treatment of a patient having a generalised seizure plus the drugs used to control an acute seizure Describe an appropriate investigation plan for a patient with recurrent syncope Outline the commonly used anti-epileptic drugs. Describe the current laws dictating epilepsy and driving.

A generalised seizure (tonic clonic, myoclonic, abscence, atonic) occurs without aura/warning. There is loss of consciousness, altered breathing and post ictal confusion. The patient may lose their continence. Immediate management: Move objects they may harm themselves on. Move gently into the recovery position when muscles allow. Time the seizure (call an ambulance if >5mins) and be vigilant for post seizure aspiration of vomit. The common epilepsy deaths are in the first 2mins after seizure with aspiration or an arhythmia. Medication: Epilepsy requires specialist management. Do not start treatments after a single attack.Never use carbamezapine in absence or myoclonus. Aim for monotherapy. Patients with a history of prolonged seizures will require rectal diazepam or buccal medazelam. Valproate should always be first line in generalised seizures, followed by lamotrogene. Valproate or carbamezapine may be used first line for focal seizures. Investigations: Try and exclude non epileptic causes (metabolic imbalance, alcohol, trauma, medications, thyroid imbalance, eclampsia, renal failure). Perform an ECG (cardiac syncope). ABG (post ictal hypoxia, electrolyte imbalance). Monitoring on a video ward to visualise a seizure (with EEG to monitor electrical activity) or at home filming aids diagnosis as does eyewitness accounts. To diagnose epilepsy there must be at least two unprovoked seizures at least 24hours apart. Differential for epilepsy: Non epileptic seizures are by for the most common. These may be psychological, hypoglycaemic, syncope, cardiac etc in origin. Examples of NES's include panic attacks, syncope, ficticious (for personal gain). They tend to last >2mins (longer than epilepsy), with back arching, pelvic thrusting, head movements, more crying and talking than in epilepsy. Movements are much less ridgid and rhythmic, face distortion is rarer and patients are less likely to have post ictal confusion (they respond quicker to questions post ictally). Syncope: A brief LOC that is usually vasovagal bt may be cardiac. Difference between syncope and epilepsy: As above. Syncope often has a history of feeling faint on rizing. Or a cardiac cause (ECG abnormal, known arhythmia). There is no post ictal confusion and twitching can occur but is less common and the patient tends not to be ridgid. Driving laws: All epileptic seizures must be notified to the DVLA. Drivers must be one year free of seizures, one year of only night seizures. The ban is for six months for a one off seizure.

Speiglian hernia?

A hernia that is rare and pushes through the posterior rectus sheath at the arcruate line of Douglas.

COPD - Define the term chronic obstructive pulmonary disease (COPD) and describe the pathology underlying COPD, list recognised risk factors

A preventable and treatable disease characterised by persistent airflow limitation that is progressive. As airways close prematurely there is chronic hyperinflation triggering barrel chest (horizontal ribs). There is an enhanced chronic inflammatory response mostly in the alveoli to noxious stimuli. Emphysema = alveoli walls disintegrate without obvious fibrosis making airspaces larger and less effective. This is because of proteases that have an increased activity because of smoking. Bronchitis = inflamed bronchioles diagnosed b cough or sputum for most days for at least three months in two consecutive years. Also seen: Mucus secreting glands enlarge so secretions increase, vascular remodelling impairs cardiac function (cardiovascular disease is a common co-morbidity). RISK FACTORS: Smoking (1pack year = 20/day/year. Smoking inc. proteases), air pollution, occupational exposure, low birth weight, maternal smoking, recurrent infectioons, low socioeconomic status, cannabis use and Alpha1antitrypsin deficiency (usually the enzyme decreases protease activity).

FISSURE IN ANO - Define anal fissure. Describe the symptoms and physical examination of patients with fissurein-ano. Discuss current theories of the aetiology of anal fissure and describe the principles of management

A tear in the anal canal from trauma (usually after the passage of constipated stool). In some cases it fails to heal and the information produced results in spasm of the sphincter muscle so that further trauma occurs when motion is passed and the Fisher becomes chronic. Symptoms: a small amount of fresh blood, Sharp pain on opening bowels and a burning pain thereafter. There will be very reluctant to permit examination. Examination: often incredibly painful, may show external skin tags or haemorrhoids but otherwise fishes are hard to see. Management: conservative management involves avoiding straining and the use of topical anaesthetic gels. Other medications can promote relaxation of the internal anal sphincter (GTN, calcium channel blockers or botulinum injections). last line is partial division of the internal anal sphincter so they cannot spasm causing further trauma and increases blood supply to the wound promoting healing. This is called a lateral subcutaneus sphincterotomy. treatment can result in minor faecal incontinence and surgery can result in abscesses and bleeding.

TRANSFUSION - Describe the ABO blood group and outline its significance in blood transfusion.

ABO are the most clinically significant blood types. A means A antigens on the surface of RBCs and anti B antibodies in serum. B means B antigens on the surface of RBCs and anti A antibodies in serum. AB means A and B antigens on the surface of RBCs and no A or B antibodies in serum therefor the universal recipient. O means no A or B antigens on the surface of RBCs but both anti A and B antibodies in serum meaning it is the universal donor as it has no trigger antigens on the RBC surface. Remember that the antibodies in serum are IgM and capable of triggering rapid and severe intravascular hemolysis of their corresponding RBCs. Without ABO matching there is a hemolytic transfusion reaction. Rhesus positive means rhesus D IgG antibodies in serum. On second pregnancy a Rh- mother sensitized by a Rh+ first born my have her antibodies attack the next child if Rh+.

PREOPERATIVE ASSESSMENT - Describe the ASA classification and methods used to classify urgency of operation.

ASA CLASSIFICATION: A surgical physical status assessment (1= Healthy, 2= Mild systemic disease, 3= Severe systemic disease, 4= Severe systemic disease threatening to life, 5= Patient would die without the surgery, 6= Brain dead for donation) Classification of operative urgency according to the National confidential enquiry: 1. Immediate - resuscitation at the same time, surgery within minutes of decision to save life, limb or organ. 2. Urgent - Post resuscitation to save life and limb or organ within six or 12 hours. 3. Expedited - a stable patient requiring early intervention, operate within days but note that the condition is not an immediate threat to life and limb or organ. 4. Elective - everything else, nonurgent.

TRAUMA - Identify each of the following common life threatening chest injuries

ATOMFC Airway injury, tension pneumothorax, open pneumothorax, massive haemothorax, flail chest, cardiac tampanard.

DYSPHAGIA - Outline the pathology, presentation and management of achalasia

Achalasia is the failure of relaxation of smooth muscle at the lower end of the oesophagus secondary to an abnormality of its nerve supply. I.e. a neuronal problem meaning that relaxation of the oesophagus is disco-ordinated and the sphynter often remains closed. Achalasia is a risk factor for squamous carcinoma of the oesophagus Cause: the cause is unknown but there is a link to chagas disease where the nerve supply to the oesophageal muscle is deficient. Presentation: a middle-aged person presents with intermittent dysphagia of a gradual progression. There may be fluid regurgitation, worse at night and aspiration pneumonia. Investigations: barium swallow shows a dilated oesophagus of rat and tail/birds beak appearance. Manometry will reveal that the sphincter will not relax. Treatment: endoscopic dilation of the lower oesophageal sphincter or Heller's cardiomyototomy procedure Which involves cutting the muscle layer at the lower oesophagus and cardia via keyhole dilating the area.

THE WHITE CELL - Describe the clinical features of acute leukaemia and discuss the laboratory diagnosis. Outline the general principles of treatment of acute leukaemias

Acute lymphoblastic leukaemia: <15yo. immature B or T-cell lines are affected's leading to uncontrolled proliferation of blast cells (abnormal immature white blood cells) in the bone marrow. it is thought to arise from environmental trigger plus a genetic susceptibility and is linked to radiation in pregnancy and Down's syndrome. Acute lymphoblastic leukaemia is the most common malignancy of childhood but has a good prognosis of up to 90% - is responsive to chemo. If in an elderly person cure rates are less than 5%. Acute myeloid leukaemia: 15-19yo. blast cells proliferate having derived from myeloid elements (red blood cell precursors, platelet precursors, granulocyte precursors). This may arise spontaneously or in a background of myelodysplasia or chemotherapy. Again associated with down syndrome. Unlike acute lymphoblastic leukaemia, acute myeloid leukaemia is a disease of patients over 65 years old. It is rapidly progressing with only 20% surviving three years. Tree with chemotherapy. Clinical features: anaemia (shortness of breath on exertion, tiredness, weakness), leucopenia (recurrent infections), thrombocytopenia (bleeding and bruising if MYELOID), bone pain (from bone marrow infiltration, children may have a limp). On examination: pallor, fever (infection), bruises/petichiae (myeloid), testicular enlargement (ALL), lymphadenopathy and hepatic splenomegaly (ALL). Investigations: full blood count (anaemia, low white blood cell counts, low platelets), blast cells on blood film (abnormal, immature white blood cells), bone marrow aspiration (blast cells and other abnormalities). Chest x-ray vision widening of the mediastinum in ALL. you also need to assess liver, kidney and cardiac function prior to management. Acute lymphoblastic leukaemia Management: supportive care involves blood platelet transfusions, fluid, allopurinol (Reduces the side-effects of chemotherapy mainly tumour lysis syndrome), Hickman line for venous access. Managing infections involves barrier nursing, avoiding unnecessary injections, regular observations and a high calorie diet. Antibiotics should be used if there are two separate temperatures. Consider fungal and atypical infections. typical treatment involves chemotherapy to induce remission with maintenance chemotherapy (vincristine) and central nervous system prophylaxis (intrathecal methotrexate). bone marrow transplant is needed for relapses and as the only way to cure patients with a Philadelphia chromosome. Acute myeloid leukaemia Management: give supportive care as with acute lymphoblastic leukaemia. Chemotherapy has to be very intensive and uses daunorubicin the five cycles in one week block to achieve remission. Give allopurinol to prevent tumour lysis syndrome (High potassium, high uric acid, low calcium etc due to chemo). Bone marrow transplant can be from HLA matched donors or an autologous transplant. Bone marrow transplant is indicated earlier than for acute lymphoblastic leukaemia.

DIAGNOSTIC STUDIES IN BILIARY TRACT DISEASE - List the most common bacteria cultured in acute cholecystitis.

Acute cholecystitis - enterococci/enterobacter (think e. coli) so use penicillins.

SPINAL AND ROOT EMERGENCIES - Describe the clinical presentation of; Acute compression of the cauda equine; Acute lesion of the thoracic cord; L5/S1 root impingement due to disc prolapsed Describe the management of a suspected cord syndrome

Acute compression of the corda equine: This syndrome presents with back pain, urinary retention (therefore overflow incontinence) and saddle Area anaesthesia with progression to faecal incontinence. It is when the cord equine is compressed By a central disc herniation. Within around six hours the incontinence may become permanent. This is a lower motor neurone lesion that requires rapid surgical decompression. Acute lesion of the thoracic cord: This will affect the muscles of the trunk and power and sensation to the lower limbs. If complete it will result in paralysis Although breeding will be unaffected. L4/S1 root impingement: When the nerve roots are compressed, typically because of an L4, L5 or L5, S1 herniated nucleus polyposis causing sciatica picture. Cord syndrome: When the spinal cord is compressed - Seen in elderly people with spondylosis (osteoarthritis of the neck) or in trauma. As this is an incomplete injury, some nerve signals continue but the patient suffers from: Motor impairment, sensory loss and urinary retention. The deficit will be worse in the upper limbs. Management in some cases can be conservative with spine immobilisation and rehabilitation. Surgery may include decompression of the spinal cord and fixation of the vertebrae.

CEREVROVASCULAR DISEASE - Describe the acute management of stroke, with particular attention to Examination; Investigations; Consideration or initiation of Antiplatelet therapy, Anticoagulation, Thrombolysis, Blood pressure control, Statin therapy List Immediate non- pharmacological measures in management of stroke such as assessment of swallow, rehabilitative and nursing care. Outline measures undertaken in secondary stroke prevention Outline methods of evaluating and managing patients with carotid stenosis

Acute management: The immediate issue is to determine whether or not the stroke is a bleed or ischaemia, And whether there are any contraindications to thrombo-lysis. Approach with an ABC structure and perform a CT head. If ischaemic and within 4 1/2 hours of onset (without any contraindications) then give thrombolysis (tissue plasminogen activator). If haemorrhagic, stop any offending drugs And consider neurosurgery. Acute intracranial swelling may be an indication for decompression (Burr hole). Nonpharmacological measures: Rehabilitation whereby a patient re-learns the skills that they have lost or learns to adapt to their new level of functioning Is vital for all stroke sufferers. Adaptive technology in the home and orthotic devices (stop contractures) are vital. SALT Teams are required to assess whether or not the patient can swallow safely and advised on appropriate methods of feeding and encouraging the relearning of speech in a stroke patient. Secondary stroke prevention: After acute management, give two weeks of aspirin and then switch to clopidogrel lifelong (75 mg). Control blood pressure, cholesterol, weight and encourage smoking cessation. Look out fatal fibrillation which may require Warfarin and assess the degree of carotid artery stenosis. Carotid stenosis: The two most common causes of a stroke/TIA Our atrial fibrillation and carotid artery stenosis. Anyone with greater than 75% stenosis should be considered for a carotid endarterectomy. Remember that although initial evaluation is with an ultrasound of the neck, prior to surgery CT or MRI angiography is required. Remember that stroke mimics include: migraine, Todd's paresis, Bell's palsy, TIA, hypoglycaemia, space occupying lesions and can be functional/psychogenic.

CHRONIC KIDNEY DISEASE - Discuss the effect of chronic renal failure on blood and bone based on disturbance of normal renal function. Outline the treatment options and discuss the indications for dialysis. Outline the options for anaemia management and the principles of managing renal bone disease

Adverse effects of renal failure: Hypertension (increase raining), metabolic acidosis, bone disease (no conversion of vitamin D precursors), anaemia (low EPO), poor immune function, insulin resistance and prolonged half life of insulin. Treatment of renal failure:The aim is to prevent or slow further renal damage. Antihypertensives are required to lower blood pressure and the risk of heart failure/strokes/vascular disease. Reduced proteinuria with an ace inhibitor and angiotensin II receptor blocker (this reduces blood pressure and is particularly useful in diabetic nephropathy), lifestyle interventions (limiting potassium and phosphate intake, stop smoking, exercise, weight loss), lowering lipids, treating anaemia (recumbent EPO). Also important is maintaining fluid and electrolyte balance to any patients with fluid retention should have limited dietary sodium intake and should watch out for hyperkalaemia. Fluid overload can be treated with diuretics. Anaemia management: Recombigen EPO is effective as long as there is an significant iron deficiency. This does not influence mortality but will reduce some of the non-specific symptoms of chronic kidney disease. Remember that correcting haemoglobin to normal levels can cause hypertension and thrombosis. Bone disease management: Given active vitamin de metabolites, maintain serum phosphates (with supplements or reducing dietary intake depending upon levels). The parathyroid may need to be removed to help maintain calcium levels.

FIBROADENOMA (Identify and describe the major types of breast lump (fibroadenoma, fibroadenosis, cyst, carcinoma). Outline the natural history of benign and malignant breast neoplasms. Present a classification of the main types of carcinoma of the breast.) Describe the principles of management of fibroadenoma.

Also known as a breast mouse, a benign, common breast tumor of mixed fibrous or glandular tissue. Presentation: painless, firm lump in people of childbearing age. Cause: Fibroadenomas are hormone related and frequently regress postmenapausally. Investigations: examination, ultrasound (as young breasts lack the fat needed for mammography) and possible biopsy if the diagnosis is uncertain. Treatment: Most are left in situ although removal with a cuff of normal tissue can be performed.

ANYERISMS - Describe the common sites and relative incidence of atherosclerotic arterial aneurysms; list the symptoms, signs and differential diagnosis of a ruptured abdominal aortic aneurysm and outline an emergency management plan. ANYERISMS - Discuss the methods available for treating abdominal and thoracic aortic aneurysms and discuss the indications, contraindications and risk factors for surgery in patients with an abdominal aortic aneurysm

An aneurysm is an abnormal widening of an artery found at sites such as the aorta, femoral, popliteal and circle of Willis). Most aneurysms are secondary to arthrosclerosis, rarer causes include connective tissue disorders or syphilis (previously common cause of thoracic aneurysms). Risk factors are those related after a sclerosus as well as a genetic tendency. Aneurysms are more common in men and rarely found before the age of 50 so we screened men over the age of 60 for AAA Site: Aneurysms can be Venous but are much more likely to be arterial. The most common sites are: Aortic, Cerebral, popliteal, mesenteric then splenic. Rare aneurysms include those of renal, splenic and femoral vessels but unlike litre rupture or require surgery. (Except in acute thrombosis) Signs/symptoms: Anyerisms may be asymptomatic, Found on x-ray incidentally or on routine screening. Patients may present post-rupture in hypovolaemic shock. Other signs and symptoms vary by site. Differential diagnosis: The differential diagnosis ruptured AAA is a GI bleed, nephrolithiasis, Ischaemic bowel, perforated peptic ulcer, pyelonephritis. Additionally, any mass in front of an artery is often felt as a pulsatile maths. For example, you may suspect a triple a when there is a pancreatic cancer in front of the aorta causing a pulsatile mass - is important to feel for an expand style mass and confirm with ultrasound. Complications: rupture, thrombosis, embolisation, Pressure and adjacent structures, fistula (into Vina Carver/intestinum) or infection. Ruptured abdominal aortic aneurysm: (Unknown aneurysm that is tender to palpate is at an increased risk of rupture)Sudden onset back pain, syncope and hypovolaemic shock. Treatment is fluid resuscitation and surgical repair.Prior to rupture medical management may be appropriate (antihypertensives, control risk factors). Remember that 90% of abdominal aortic aneurysms affect the aorta below the renal arteries and have an elective mortality of 5% but a ruptured mortality of 50%. Elective surgery is done where in an aneurysm is greater than 5.5 cm In men, 5 cm and women (Ultrasound). . This can be open although endovascular repair is more popular (Even in an emergency) to stent the area. EVAR may need to be avoided If their anatomy is not conducive to stenting (such as if An adequate length of stenting would occlude the renal artery). Clearly, for an open repair the patient must be physically fit for surgery (As with EVAR their renal, respiratory and cardiac function should be carefully assessed). Risks include rupture, embolism, infection, thrombosis and graft failure as well as other general risks of surgery.

HEAD INJURY - After the assessment of airway, breathing, circulation, describe the assessment of a patient with head injury List the features which reflect severe head injury

As with all acute injuries, start with an ABC approach. Be concerned about injury to the C-spine, Glasgow coma score (less than a eight implies that they may not be able to maintain their own airway). Consider whether or not there are any fractures or intracranial bleeds and when stable perform CT. Remember the indications first CT include: G-CSF than 13, p post-traumatic seizure, query fracture, More than one episode of vomiting or focal neurological deficit. A severe head injury may have: lowered Glasgow coma score, vomiting, battle sign, altered consciousness, papiloedema and other signs of raised intracranial pressure, Neurological deficits, CSF rhinorrhoea.

ASTHMA - Classify asthma and discuss the characteristics of a typical patient who is likely to present with each type.

Asthma is a chronic, reversible inflammatory condition of the airways that episodically narrows the airways. The recurrent episodes of symptoms re associated with airway hyperresponsiveness to a specific antigen. Atopy and asthma are closely related. Inhalation of an allergin in a hypersensitive individual triggers an early phase response (where preformed inflammatory mediators are released and narrow the airways via smooth muscle contraction in the bronchioles - not the alveoli which are affected by emphysema) and a late phase response around 8-12 hours later (where the products of the early phase such as cytokines activate leucocytes causing a late phase attack). Most common is ATOPIC/EXTRINSIC - whereby there is a family or personal history of atopy (asthma//eczema//hayfever) Others include..... 1. EXERCISE INDUCED - hyperventilation causes water loss from the respiratory mucosa and triggers an inflammatory response. Airway narrowing peaks 5-20mins after exercise giving an acute attack. 2. COUGH VARIANT - the main presentation is with coughing (which is often triggered by a viral URTI or exercise). It is heavily under or mis-diagnosed. 3. OCCUPATIONAL - may have a latency period of up to a year after starting the job and improves on holidays. 4. NOCTURNAL - asthma shows a marked diurnal variation (perhaps because of exposure to house dust mites, lower temps, reclining position). 5 DRUG INDUCED - think asprin, beta blockers, NSAIDs. Another classification uses: intermittent and mild/moderate/severe persistent.

GALLBLADDER DISEASE - Outline the medical management of a patient with biliary colic and acute cholecystitis including appropriate antibiotic regimen.

Biliary Colic: medical management involves fluid and electrolyte resuscitation because of vomiting, NSAIDs and antiemetics. Infection is less of the concerns antibiotics are not indicated as first line. Acute cholecystitis: again fluid and electrolyte resuscitation is important, prior to cholecystectomy give antibiotics (against gram negative such as E. coli - for example penicillin/Tazocin) and analgesia.

DIABETES METABOLIC COMPLICATIONS - Describe the typical symptoms of hypoglycaemia and outline the difference between autonomic and neuro-glycopaenic symptoms. Outline the major counter-regulatory hormone responses to hypoglycaemia and describe why hypoglycaemia may develop. Describe the treatment of hypoglycaemia

Blood glucose <3.9mm/mol. Symptoms: Consider these as AUTONOMIC (triggered by adrenaline and glucagon which rize when glucose is low). These include shaking, anxiety, nervousness, palpitations, clamminess, sweating, dilated pupils, hunger, nausea, abdo pain, headache. Or as NEURO-GLYCOPAENIC (because of low glucose) symptoms including: impaired judgement, pins and needles/paraesthesia, fatigue, personality change, memory los, confusion, ataxia. Causes: excess insulin, sulphonylureas or (more rarely) metformin. Especially alongside low food consumption, excess exercise and excess alcohol. Other causes include kidney failure and insulin secreting tumors/insulinoma. Treatment: Consumption of sugary foods, dextrose tablets, glucose gel etc. If unconscious IV dextrose or a glucagon injection can help.

BURNS - List and differentiate the categories of burn injury. Describe the pathophysiology of each burn category. Classify the depth of burn injury. Describe and apply the rule of nines.

Burn injuries include: thermal, chemical, electrical, cold and irradiation. Differentiation is obvious based upon history - remember the risk of inhalation injuries. First-degree burn: superficial, affecting only the epidermis. Red. Second-degree burn: superficial affecting the epidermis and dermis - often presents with a blister. Third degree burn: full thickness extending through the epidermis and all of the dermis often resulting in scarring, contractures and skin grafts. These often appear stiff and white/brown. Fourth degree burn: Full thickness also involving muscle, tissue or bone. Often appears black or charred and needs amputation. The Rule of Nines: used to estimate the surface area of the body that has been burnt, consider the head/arm/chest/abdomen as 9% of the body, consider the back/leg as 18% of the body and consider the Palm/groin as 1%.

EVIDENCE BASED MEDICINE - Define clinical audit and describe its purpose and what it involves (the audit loop). Describe the common measures of health care used (structure process, outcome and quality measures).

CLINICAL AUDIT: a quality improvement process that seeks to improve patient care and outcomes through systematic review of care against explicit criteria and the implementation of change An audit involves identifying a problem, defining standards and criteria, collecting data retrospectively, identifying areas for improvement, introducing change and re-auditing.

ACUTE APPENDICITIS List the symptoms and signs of acute appendicitis. Formulate a differential diagnosis and outline appropriate investigations. List the common situations in which appendicitis is difficult to diagnose or manage. List the complications of a perforated appendix. List and discuss the common complications following appendicectomy and explain how each can be prevented. List causes of a mass in the right iliac fossa and outline the assessment, investigation and management.

Cause: Obstruction of the appendix by faecolith/inflammed nodes/foreign body/tumour of the caecum resulting in inflammation and infection. Presentation: Initially poorly localised central abdominal pain (Central because t this point only the appendix is inflamed and this corresponds to the T1 nerve root/midgut referred pain) - Pain is typically colicy (appendicular muscle contracts). The pain progresses to a constant right iliac fossa pain when the peritoneum becomes involved. The pain is worse on movement (typical peritonitis) and associated with anorexia, mild pyrexia and N&V. Examination: RIF tenderness, rebound or percussion tenderness. There may be rectal tenderness if inflammatory fluids have tracked down to the pouch of Douglas. RIF mass: Appendi mass, gynae (ovarian cyst), caecal tumour, soft tissue tumour (sarcoma), lymh nodes, TB, actinomycosis inection, transplanted kidney, iliac anyerism. Management: Appendectomy. NB Mcburneys point 2/3rds from the umbilicus towards the ASIS marks the base of the appendix and retrocaecal appendix's are common. Give IV metranidazole cover. DDx: MESENTERIC ADENITIS (self limiting viral inflammation of mesenteric nodes, photophobia and headache are more common than in appendicitis and fever is higher. Give analgesia) Also: PID, endometriosis, ovarian cyst, ovarian torsion, diverticulitis, crohns, colonic cancer, omental torsion, UTI, gastroenteritis, panreatitis. Essentially any acute abdomen. Challenging diagnosis: >72hours after the onset of pain the omentum can have walled off the appendix giving an appendicular mass that may be treated sucessfully with antibiotics (Although an abscess can form and elective surgery is indicated). In the elderly patients symptoms may be atypical such as pain in the lower back or rectum or absent . Complications: Rupture, peritonitis, abscess, sepsis, death.

VASOSPASTIC DISORDERS - Describe anatomical mechanisms responsible for producing thoracic outlet compression syndromes and list the investigations for thoracic outlet syndrome. Describe the surgical principles for its correction.

Cause: compression at the thoracic inlet Which is bordered by T1, rib one and its costal cartilage. Specific causes may be congenital (cervical rib, elongated transverse process, abnormal scalene muscles), repetitive strain, trauma (whiplash) or an acquired abnormality (tumor, Including Pancoast). Problem: the neurovascular bundle becomes compressed as it passes between anterior and middle scalene. The brachial plexus and subclavian artery (sometimes the subclavian vein are involved). Sign/symptoms: Sharp pain and decolouration of the arms and hands (may be described as an aching or burning). Arms and hands become weak and thoracic outlet syndrome can also be the cause of frozen shoulder and couple tunnel. If there is claimed in vain compression the arm will become swollen, blue and painful, particularly after activity (There is potential for thrombosis). Examination: Adson's test: Straight in the affected arm, Hold it backwards feeling for the radial pulse. A positive test is loss of the pulse or symptoms brought on by the patient extending their neck and looking towards you. Investigations: Doppler With probes on the fingertips can assess diminished blood flow associated with particular movements and symptoms. X-ray may identify a cervical rib. CT angiogram or venogram will identify and occlusion. Also useful are nerve conduction studies and a possible MRI. Management: Conservative measures include rest, physiotherapy, Cortisone or Botox injections. Surgery often involves removal of the first rib or a cervical rib and the scalene muscles. Complications include pneumothorax, infection, nerve damage, loss of sensation, damage to the arteries or veins. Physiotherapy is likely to be required both before and after surgery.

TUBERCULOSIS - Describe the process of infection by the tubercle bacillus together with the route of spread and discuss the presentation of post-primary tuberculosis from reactivation of infection.

Caused by microbacterium tuberculosis - aerosolised droplets entering the alveoli and recruiting macrophages and leucocytes forming a granuloma, Mycobacterium bovis - cattle resovoir spreading from non sterilised milk from infected cows, Mycobacterium africanum - human resovoir. It is heavily associated with HIV and immunosupression. Numerous granulomas aggregate to form a primary lesion known as a ghon focus which is usually peripheral. There is hilar lymphadenopathy. Usually the ghon focus is walled off in a fibrous capsule and TB becomes latent but visible as the focus calcifies (Xray). If lymphatic or haematogenous spread occurs before latency there may be secondary foci in the nodes, liver, kidney, bones, lungs. The only way of knowing there has been infection is by a hypersensitivity to tuberculin (skin prick test). If these reparative processes fail then the patient presents with PRIMARY pulmonary TB giving pleural pain and effusion and blood borne spread (bones, kidney, gut spread or milliary TB with fever, night sweats, anorexia, weight loss, dry cough). Reactivation of infection is when there is TB post previous exposure. Usually the presentation is a pulmonary upper lung lesion (as TB is a strict aerobe) causing an insidious onset of: fever, night sweats, malaise, weight loss, chronic dry cough, haemoptysis, pleural effusion, spontaneous pneumothorax and possible consolidation or collapse.

DIABETES MELLITIS - Outline the secondary causes of diabetes. Describe the principles of the dietary treatment. Describe the methods of evaluating diabetic control. Describe the principles of insulin therapy.

Causes: type I diabetes is immune-mediated (Autoimmune destruction of beta cells in the pancreas)or idiopathic. - Type I is absolute insulin deficiency wearers type to is insulin resistance. Type II diabetes may be gestational, due to a defect in beta-cell function (maturity onset diabetes of the young), genetic insulin defects, pancreatic disease (pancreatis, removal, cancer, cystic fibrosis, haemochromatoses), excess production of hormones that antagonise insulin (acromegaly, Cushing's, glucagonoma, thyrotoxicosis, pheochromocytoma), drug induced (steroids, thiazide diuretics). There is also an association with genetic syndromes such as Down's syndrome, Klinefelter syndrome, Turner syndrome. Diet: Initially T2DM may be managed with diet and exercise. For both types a healthy diet and regular exercise mean reduced cardiovascular complications. A diet low in carbs and with low glycaemic index foods (fruit, beans, whole grain) can reduce HBA1c and decrease insulin resistance (which could reverse T2DM). Evaluating control: Glucose urinary dipstick is a screening diagnostic procedure and if present warrants blood testing. Detection of ketone bodies in the urine with a dipstick Or in blood Are useful in altering insulin levels during intercurrent illness and can identify DKA. Protein on the dipstick in the absence of a UTI indicates diabetic nephropathy. Blood glucose using a portable electronic meter and fingerprint can help with self-monitoring to tailor insulin therapy. Glycosylated haemoglobin/HBA 1C indicates glycaemic control over the previous 120 days. This is because glucose becomes attached to haemoglobin in higher levels in poorly controlled diabetes. Although lowered in an email or pregnancy diabetics should aim for an HBA 1C of 48 mmol per litre or less. Insulin: In T1DM, or severe T2DM insulin is given to replace the absence (T1) or relative lack (T2). It promotes the absorbtion of glucose from blood into muscles and fat and inhibits glucose production by the liver (Ie. reduces available glucose and deposits fat). In T2DM, ONCE DAILY long acting insulin for those who stuggle with hyperglycaemia or an intermediate active insulin given before bed for people who struggle with nightime or morninng hyperglycaemia. TWICE DAILY regims may be used for T1 or T2 but those using this method must eat three regular meals a day. Give a mix of short and intermediate acting insulin morning and before dinner (for children this avoids an at school injection). INSULIN PUMPS are generally offered to T1DM sufferers who struggle to control. It gives a continuous stream of subcut insulin based on your typed in blood glucose levels and can give a larger dose at meals. BASEL-BOLUS is commonly used in T1DM as it allows flexibility of meal times. The basel part is a long/intermediate acting insulin at the begining of the day. Boluses of short/rapid acting insulin are given after a meal. Brands of insulin include: glargine is long acting, novorapid is short acting, actrapid is rapid and suspensions tend to be intermediate.

GALLBLADDER DISEASE - Describe the symptoms and signs and management of bile duct stones.

Choledocholelithiasis/Bile duct stones are either cholesterol or pigment and can be asymptomatic or cause: acute epigastric or right upper quadrant pain, fever, jaundice, nausea and vomiting. They can lead to coleocystitis (an inflamed gallbladder or cholangitis (an inflamed biliary duct) both resulting in infection and acute pain. Risk factors: fair, fat, fertile, female, 40. Examination: Murphys sign negative. Confirmation of the diagnosis is with ultrasound. Management: conservative management with analgesia and nil by mouth. Otherwise consider ERCP, biliary stenting or cholecystectomy

PRE-OPERATIVE EVALUATION - Describe the optimal preoperative evaluation of a patient including clear documentation

Clear documentation should include: > Multiple identifying factors > Diagnosis and proposed procedure > Cardio-respiratory assessment > Medical problems list > Laboratory results/bloodwork > Indication of informed consent > Indication that the patienthas been informed of potential risks and benifits

PRE-OPERATIVE EVALUATION - Describe the optimal preoperative evaluation of a patient including clear documentation

Clear documentation should include: > Multiple identifying factors > Diagnosis and proposed procedure > Cardio-respiratory assessment > Medical problems list > Laboratory results/bloodwork > Indication of informed consent > Indication that the patienthas been informed of potential risks and benifits > Anticipation for HDU/ICU admission > Discharge planning

INFECTIVE ENDOCARDITIS - Describe typical clinical examination features and list common infecting bacteria.

Commonly caused by staph epidermidis, staph aureus from IVDU - may even cause abscesses, strep viridens/normal commensals of the mouth, enterococci/gut commensals. Features.... SUBACUTE (may present due to improperly treated acute BE. May develop acute complications) = persistant fever, fatigue, night sweats, weight loss, heart failure, valve dysfunction. There may be splinter haemorhages, purpura, oslers nodes (painful swellings at the finger tips), clubbing (late sign), hepatosplenomegally. ACUTE = severe febrile illness, new onset or changed heart murmer, petichiae. Cardiac or renal failure can develop rapidly from emboli. POST OPERATIVE = unexplained fever post heart valve surgery. Often resembles subacute BE. Mortality is high and more surgery is often needed to re-replace valves.

IMMUNOLOGY - List the organs that are commonly transplanted and outline the main indications for transplantation

Commonly transplanted organs are: cornea, Heart (cardiomyopathy), lungs (cystic fibrosis), liver (end-stage failure, metabolic disease, cancer), kidney (end-stage renal failure), skin (Burns, bone marrow (haematological cancer, inherited immune deficiency) and bloods (bleeding, anaemia). Transplants require lifelong medication and are only generally performed when there is irepairable damage and the patients life expectancy is short.

TUBERCULOSIS - Outline the investigation of a patient with suspected TB

Confirm diagnosis in a patient with a chronic unexplained cough by sputum culture (can take 4-6weeks!), ziehl neelson or rhodamine- auramine staining. Chest Xray may show a ghon focus in latent TB. Or hilar lymphadenopathy with an initial primary focus area. Post primary/reactivation TB tends to give a mass in thye superior zones (never say loves on Xray as they overlap). Miliary TB shows multiple small lesions and indicates bad haematogenous spread. Drug sensitivity testing is vital in those with a personal Hx of TB. HIV testing may be required.

Describe the principles of management of nipple discharge and breast pain.

Consider the differential. Most worryingly (with bloody discharge +/- a lump) is breast cancer therefore use the triple assessment. Is the breast pain cyclical or non cyclical? Cyclical pain is usually benign. Non cyclical pain may be due to an infection (mastitis in a breast feeding woman), fibroadenoma, cysts or cancer (commonly ductal carcinoma).

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY - Label the constituent portions of the cerebral cortex, (frontal, parietal, temporal, occipital.) Draw and label the circle of Willis and its branches List the cranial nerve nuclei in each constituent part of the brainstem (midbrain, pons, medulla) Describe the syndromes that would arise from a lesion in; Cerebral hemisphere; Brainstem; Cerebellum; Basal ganglia Name the location of the causative lesion in; Homonymous hemianopia; Homonymous quadrantanopia; Bitemporal hemianopia; Monocular visual field defect Describe the location of Broca's and Wernicke's areas and explain their function in language List the causes of dysarthria Explain the difference between a bulbar and pseudobulbar palsy List the causes of Horner Syndrome Describe the clinical difference between upper and lower motor neuron facial weakness

Cranial nerve nuclei: The first four cranial nerve nuclei emerge from the midbrain, the next four from the ponds, the next four from the medulla. Syndromes: this coincides with the Bamford classification. A lesion in the cerebral hemisphere will give hemiparesis, Hemianopia, higher cerebral dysfunction (problems with language and communication). A lesion in the cerebellum will give DANISH. Brainstem lesions will give Problems with specific cranial nerves, visual defects, locked in syndrome. Basal ganglia lesions such as lacunar strokes cause focal sensory, motor, sensory motor or ataxic hemiparesis problems. Field defects: monoccular vision is lost if you cut the optic nerve or destroy the retina. If you destroy the optic chiasms you get bitemporal hemianopia. If you destroy the optic tract you get a homonomous hemianopia. If you destroy the optic radiation you get a quadrantanopia (the lesion is the opposite side to the defects and if the defect is in the parietal zone the lesion will be inferior, if the defect is in the temporal zone The lesion will be superior). Broca: An Expressive aphasia. Wernike: a receptive aphasia. Dysarthria causes: stroke, tumor, Parkinson's disease, multiple sclerosis, Brain injury etc. The difference between a bulbar and a pseudobulbar palsy: A bulbar palsy is abnormal functions of CN 9, 10, 11, 12 because of a LMN lesion in the medulla. Whereas a pseudobulbar palsy is damage in the mid pons (corticobulbar tracts) givin an UMN lesion. Patients have dysphagia, dysarthria, speech problems And, if Pseudo bulbar, brisk jaw jerk , altered gag reflex. Horner syndrome: A lesion to the sympathetic trunk causing anhydrosis, miosis and ptosis. Causes include: Congenital, Pancoast tumour, surgery, Multiple sclerosis, brain tumours, encephalitis, Cervical rib, trauma etc. UMN v. LMN: An upper motor neurone lesion will spare the forehead muscles Because there is bilateral innovation. Lesions are separated by the level of the anterior horn of the spinal cord or the motor neurone in the ventral horn.

ADRENAL DISEASE - List the major clinical and biochemical features of Cushing's disease, Addison's disease, Conn's syndrome and congenital adrenal hyperplasia.

Cushing's disease: When Cushing's syndrome is caused by a tumour of the Pituitary secreting excess ACTH or a tumour of the adrenals secreting excess cortisol/Glucocorticoids. The most common cause of Cushing's syndrome is exogenous steroids. Other causes include ectopic ACTH (from a small cell lung cancer), or an adrenal cancer. The clinical picture may also be mimicked by alcohol excess, major depressive illness and obesity. The typical presentation is with her shooters, hair thinning, acne, moon face, psychosis, central obesity, striatae, hypertension, osteoporosis and hyperglycaemia. Investigations include testing late night serum or salivary cortisol (should be lower), urinary cortisol over 24hr and measure ACTH (raised if there is a pituitary adenoma/Cushing's disease, suppressed if the steroids are coming from and adrenal lesion or lung cancer). Then attempt to supress cortisol with the dexomethasone supression test (normal is supression) Management is usually surgical but there are drugs that inhibit corticosteroid synthesis. Addison's disease: A rare cause of adrenal (Adrenocorticoid and mineralocorticoid) insufficiency (more common causes include withdrawal of steroids. In addisons the adrenal gland is destroyed by autoantibodies). Patients may present in acute circulatory shock (Severe hypotension, hyponitraemia, hyperkalemia, Hypoglycaemia, muscle cramps, nausea, vomiting, diarrhoea and unexplained explained fever often precipitated by intercurrent illness/surgery) or chronically with: fatigue, depression, low sodium, Hyperpigmentation of the mucous membranes/skin, muscle weakness, Low blood sugar, low blood pressure and cravings for salt. Although Addison's disease may be misdiagnosed as chronic fatigue or depression. Diagnosis is confirmed with an ACTH stimulation/short synacthen test (normal patients respond by producing cortisol). Adrenal imaging and is antibody tests are also relevant. Treatment is with lifelong Hydrocortisone, increased at times of acute illness. In addisons patients struggle from low sodium because of aldosterone deficiency and high potassium is common. Some patients also need mineralocortisone replacement with fludrocortisone if BP and Na are uncontrolled. Women may occasionally need androgen replacement, men do not. Conns syndrome: A rare type of hyperaldosteronism because of an adrenal adenoma (more common causes of high aldosterone are idiopathic or secondary to low blood pressure/renal vascular stenosis). Features include: (after initial asymptomatic phase) sodium retention (oedema), low potassium (muscle weakness and paralysis) polyuria (kidney damage) and high blood pressure. Investigations show low potassium, alkalosis and sodium at the high end of normal (unless secondary hyperaldosterone has triggered diabetes insipidus). Aldosterone will be high and renin will be low. The high blood pressure will be difficult to control with conventional treatments and CT or MRI will identify adrenal adenomas and incidentalomas. Management is with mineralocorticoid receptor antagonists such as spironolactone to block the action of aldosterone. With Cons disease after a few weeks of medical therapy the adrenal gland affected can be removed which is curative (although many patients suffer from continued hypertension because of the irreversible damage to blood vessels). Congenital adrenal hyperplasia: A rare cause of adrenal insufficiency (more common causes include withdrawal of glucocorticoid therapy). Autosomal recessive inheritance of enzymatic defects result in insufficient cortisol and aldosterone production leading to excessive ACTH secretion and enlargement of the adrenal glands. The most common defect is 21 hydroxylase deficiency. The result is low cortisol, low aldosterone but increased progesterone. Patients present in infancy with glucocorticoid deficiency and mineralocorticoid deficiency (Addison's picture, weight loss, malaise, diarrhoea, constipation, low blood pressure, shock, low blood sugar, low sodium, high potassium) Alongside signs of androgen excess (ambiguous genitalia in women) some patients may have adequate mineralocorticoid secretion. Some may present late with hirsutism and amenorrhoea but this is not classical. Investigations show raised progesterone levels, low sodium and a possible 21 hydroxylase deficiency. Management is important to prevent salt losing crisis - replace steroids (monitor growth in children) or (if late onset and relatively asymptomatic) only gave antiandrogen therapy for symptom relief (hirsutism, amenorhoea).

DIVERTICULAR DISEASE - Outline the theories on the aetiology of diverticulosis of the colon including age, diet and vascular anatomy of the colon. Describe the morphology and pathological consequences of diverticulosis of the colon. # Describe the clinical features, symptoms and signs of diverticulitis. Outline the complications of diverticulosis. Describe the management of asymptomatic diverticulae of the colon. Discuss the presentation, differential diagnosis, investigations and management of complications of colonic diverticulae including diverticulitis, perforation, bleeding, stricture, abscess and fistula. Discuss indications for elective and emergency surgery.

DIVERTICULOSIS Cause: Middle/Old age, Western country, patient with low fibre diet (diet low in fibre leads to muscle spasm and the increased intraluminal pressure leads to buldging of the mucosa). Pretty much found in anyone with a history of constipation, although most are asystematic, What: Divertiular are outpouches of a tubular structure, they occur when the colon is weak (where blood vessels enter the colonic muscle). Presentation: Symptoms include painless blood per rectum, cramps and tenderness. DDx: acute gastritis, appendicitis, lower GI bleed Management; High fibre diet, avoiding foods that trigger constipation, avoiding spasmodics Complications and their management: Infection, perforation, bleeding. their management is essentially that of acute diverticulitis DIVERTICULITIS Cause: Inflammation of a diverticulum, because of a faecolith (much like acute appendicitis) What: Presentation: Much like left-sided appendicitis, an elderly patient with a history of constipation presents with pain and tenderness in the LIF, fever, localised peritonitis, raised white blood cell count DDx: Gastritis, bowel obstruction, ischemic bowel, gynaecological causes, mesenteric adenitis Management; Typically conservative with bowel rest (NG tube, nil by mouth) IV fluids and antibiotics. If this fails or there are complications, surgery is indicated. Complications: Perforation (sudden onset pain, generalised peritonitis and free gas on a CXR. Give laparotomy and wash out prior to resection of the sigmoid with a hartmanns. Diverticular abscess (after a perforation which doesn't cause peritonitis but is instead walled off by surrounding bowel loops. Mass felt of examination and confirmed by CT. Drain percutaneously with IV antibiotics). Haemorrhage (usually stops spontaneously but embolisation is required if persisting). Stricture (after resolution of acute diveticulitis, maybe severe enough to require resection. Other causes of a stricture include cancer, UC, Crohns, ischemic colitis and post-radiotherapy).

PNEUMONIA - Describe the complications of pneumonia including systemic sepsis, lung abscess and empyema.

Death. Pleural effusion (here termed parapneumonic effusion). Empyema (a collection of pus in the pleural cavity). Lobar collapse. Lung abscess (apears as a ring of cavitation with a fluid level on Xray) or suppurative pneumonia. ARDs. Renal failure. Multi organ failure. Ectopic abscess. Sepsis.

DIABETES METABOLIC COMPLICATIONS - List the two major hyperglycaemic complications of diabetes - diabetic ketoacidosis (DKA) and hyperosmolar non-ketotic (HONK) diabetic coma. Outline the metabolic pathways that underlie diabetic ketoacidosis and outline the common reasons for the development of DKA. Discuss the management principles underlying the treatment of DKA (fluid, insulin and potassium replacement) and HONK.

DKA: When a severe lack of insulin (T1DM omitting insulin. Ketosis prone T2DM) causes the body to metabolise free fatty acids leading to ketone body production. Without insulin the liver produces glucose causing glucoseurea and osmotic diuresis (hence polyurea and dehydration) then there is lipolysis causing ketone bodies (acetoacitate and hydroxybutarate). The HCO3- buffering system is overwhelmed and acidosis ensues. Symptoms - nausea and vomiting, thirst and dehydration, kussmal deep gasping breathing, polyurea, severe abdominal pain, confusion and eventually come/death. Investigations - blood and urine are positive for glucose and ketones. ABG shows metabolic acidosis with attempted resp compromise. Because of dehydration there may be low BP and tachycardia. Small children are prone to cerebral oedema with DKA (pupil reflexes lost, headache, coma) Treatment - IV fluids, insulin (with cardiac monitoring due to low K+ risk) and treating the underlying cause (often an infection which causes insulin demands to rize but people often omit insulin as they have not been eating). IV mannitol is given if cerebral oedema is present. HONK/HHS: A hyperosmolar, hyperglycaemic state seen usually in T2DM when high blood sugars due to poor control cause dehydration. There will be no or only mild acidosis as no ketones are produced (there is enough insulin to suppress lipolysis). Symptoms: Polyurea, polydipsia, disorientation, confusion. Typically triggered by medication ommition or intercurrent illness. Treatment: IV fluids, possible potassium replacement, insulin (with cardiac monitoring for risk of low K+).

INTRACEREBRAL HAEMORRHAGE - List the structural lesions and predisposing factors which may predispose toward Deep intracerebral haemorrhage and Lobar cerebral haemorrhage Describe the clinical presentation of intracerbral haemorrhage, initial investigations and immediate patient management

Deep intracerebral haemorrhage: Type of stroke whereby there is bleeding into areas such as the founder, basal ganglia, Pons and cerebellum. Causes include trauma, vascular malformations, bleeding into brain tumours and clotting abnormalities. Risk factors therefore include clotting disorders, anticoagulant medication, liver disease And hypertension. Symptoms are sudden onset headache with problems with language and communication, ataxia, weakness, loss of consciousness. Anticonvulsants may be required to control seizures. Investigations should include a neurological exam to identify any possible raised intracranial pressure and CT angiogram to identify the bleed. Treatment typically involves surgery if you need to relieve pressure, intravenous mannitol/steroids to reduce the swelling, Anticonvulsants for seizures And analgesia. Lobar cerebral haemorrhage: And intracranial haemorrhage of a single load that presents with a headache and progressively worsening Glasgow coma score. CT scan will confirm. Although surgical evacuation of raised pressure is possible typically the treatment is medical (palliation if the bleeders large, clotting factors are the usual medical treatment).

ACUTE ABDOMEN - Define the acute abdomen. Identify the symptoms and signs of common causes of the acute abdomen. Discuss differential diagnosis, relating these to the pathology of the conditions. Select appropriate investigations to aid diagnosis and interpret these Outline initial management and identify the patient needing urgent resuscitation and operative intervention on the basis of their clinical presentation

Definition: A case of abdominal pain with a short history of presenting as an emergency with no history of trauma. Presentation: Abdominal pain (Socrates). Visceral pain is from the stimulation of the visceral peritonaeum or by obstruction of a viscera - It is poorly localised. Parietal pain is from inflammation of the parietal peritonaeum. Referred pain often comes from nerve root compression. Pain may be colicky in nature From obstruction (coming and going. Remember Biliary colic is not actually typically colicky pain). There may be guarding and rigidity as well as absent bowel sounds. Examination: look for signs of shock, dehydration, proliferal shutdown, hypotension. Remember the six causes of distention: fat, fluid, Flatus, foetus, faeces or tumour. Referral of pain: Foregut structures (oesophagus to the ampulla of vater) Referred to the epigastrium. Midgut structures (second by the duodenum to 2/3 along the transverse colon) referred to the umbilicus and hindgut structures (from the distal third of the transverse colon) referred to the suprapubic region. Differential diagnosis:Grouping causes by the area they cause pain... Epigastrium: peptic ulcer, pancreatis, coleocystitis, cardiac pain, gastritis. Left upper quadrant: peptic ulcer, spleen injury/infarct, pancreatis. Right upper quadrant: coleocystitis, peptic ulcer, hepatitis, cholangitis, Right lower lobe pneumonia, biliary colic. Central: early appendicitis, mesenteric adenitis, Small-bowel obstruction, pancreatis, ischaemic bowel. Left iliac fossa: diverticulitis, ureteric colic, ectopic pregnancy, ovarian cyst, pelvic inflammatory disease. Right iliac fossa: appendicitis, mesenterica colonitis, Crohns, meckels diverticulum, pelvic inflammatory disease, ovarian cysts, ectopic pregnancy, ureteric colic. Suprapubic: urinary tract infection, retention, gynaecological Investigations:Always perform a pregnancy test and urine dipstick (urinary causes).Abdominal ultrasound (Identifies free fluid) or CT can be performed although some specific diagnoses require exploratory laparotomy to confirm (for example generalised peritonitis query cause). Plain x-rays may be helpful for renal stones or bowel obstruction. Management: Fluid and oxygen resuscitation, Analgesia and observation are a great start. Then treat the specific conditions. For example, appendicectomy.

DYSPHAGIA - List the common causes and discuss investigations of dysphagia.

Difficulty in swallowing. (Pain on swallowing is odynophasia). Consider the causes in the following categories: - INTRALUMINAL: foreign body, polyps, oesophagitis, infection (Candida, herpes). - EXTRA LUMINAL: In the wall (benign or malignant strictures, achalasia, oesophageal web/plumber - Vincent syndrome, Nutcracker suffer oesophagus/high-pressure contractions, Scleroderma, presbyoesophagus). Outside the wall (Laryngeal pouch, hiatus hernia, malignancy of the lung or mediastinum, retrosternal goitre, aneurysms or abnormal vessels). -SYSTEMIC: Myasthenia Gravis, multiple sclerosis, Parkinson's disease, pseudobulbar palsy or psychological causes. Investigations: endoscopy is the mainstay as it gives full visual assessment and enables a biopsy with options for therapeutic intervention. Other investigations which may be useful include: barium swallow (for mobility disorders), manometry (pressure and peristalsis assessment in aclasia).

DIABETES MELLITIS - Prescribe insulin therapy for a patient with diabetes who is an in-patient having routine medical or surgical care Describe the essential components of the annual review in diabetes care.

Do prescribing practice questions. AN annual review checks blood glucose control, urine dip (identifies ketonurea or glucosurea - seen with poor control), weight, cholesterol, BP (Ie risk factors for cardiovascular disease). Medication dosing and timing and self monitoring is discussed. It is important to ask about recognition of hypos. Smokers should be encouraged to stop. Injection sites are examined (check they are alternating and for any lipohypertrophy lumps). Other important things to monitor are: diabetic retinopathy, foot care (encourage moisturising, feel pulses, check sensation, encourage daily foot checks for cracks/ulcers/fungi).

The differential for causes of pulmonary fibrosis?

Drug induced: amiodarone, nitrofurantoin, radiation or methotrexate. Occupational: miners, Factory workers etc. Idiopathic Connective tissue diseases: Lupus, sjogrens, rheumatoid arthritis, scleroderma, dermatomyositis, polymyositis. Immunological: Hypersensitivity pneumonitis/extrinsic allergic alveolitis (bird fanciers, pigeon fanciers), sarcoidosis.

INFECTIVE ENDOCARDITIS - Outline the common antibiotic regimen used to treat endocarditis and describe the indications and role of antibiotic prophylaxis in patients with pre-existing valve diseas

Endocarditis has a 20% mortality rate, higher if the patient has a prosthetic valve. >MDT approach. >Remove any source of infection (Eg, tooth with abscess). >Fluclox and gentamycin empirical if there is an acute resentation. >Benzylpenicillin and gentamycin if subacute. >USe gent, vanc and rifampycin if prosthetic valve, ?MRSA or penicillin allergic. (All minimum 2weeks IV) >Surgery may be needed to de-bridle valves. Antibiotic prophyllaxis is now no longer offered to those with prosthetic valves (except for dental procedures etc).

OBSTRUCTIVE JAUNDICE - Describe the aetiology, morphology and pathological consequences of cholelithiasis (see under BILIARY DISEASE for more detail).

Essentially gallstones, most are from cholesterol although some are from pigment (a bilirubin breakdown product seen more commonly in hemolytic anaemia. These may be asymptomatic, cause an obstruction (Cholecystitis) or form a mucocele. The result of obstruction is right upper quadrant or epigastric pain and jaundice. Cholelithiasis = Gallstone Choledocholithiasis = Bile stones Chronic gallstones can lead to gall bladder cancer. The ideal management is gallbladder removal. Although medical dissolving of cholesterol stones and ERCP may be effective.

BURNS - List the causes, symptoms and signs of inhalation injury.

Exposure to hot gaseous products of combustion resulting in respiratory failure thought to contribute to up to 80% of fire related deaths. Death occurs by a combination of thermal damage, poisoning and irritation (causing subsequent swelling). presentation is with coughing, nausea, vomiting, sleepiness and confusion. Often there are visible facial burns. Management is with close monitoring, humidified oxygen, bronchodilators, suction and possible invasive ventilation and intubation.

EXTRINSIC ALLERGIC ALVEOLITIS - Outline the nature of the allergic reaction underlying EAA and how this is used to establish the diagnosis. Outline the pathological consequences of repeated allergen exposure.

Extrinsic allergic alveolitis is also known as hyersensitivity pneumonitis - a local immune response to inhalation of organic antigens which trigger an immune complex reaction in the alveoli and bronhioles. Examples: Farmers lung: mouldey hay/straw sensitise the body to aspergillus. Bird fancier's lung: avian excretions, proteins and feathers sensitize the body to avian serum proteins. Malt workers lung: Mouldy malt sensities to aspergillus. Cheese workers lung: Mouldy cheese sensitizes to penicillium and aspergillus. They are likely to be due to both TIII (immune complexes where antigens are detected and activate complement and inflammatory responses) and TIV (T cell activation which causes non caeseating granulomas in the alveolar walls) hypersensitivity activation. Remember that hypersensitivity pneumonitis/Extrinsic allergic alveolitis is not exclusivly environmental/occupational and may be drug induced. Chronically HP/EAA may progress to pulmonary fibrosis.

UPPER URINARY TRACT INFECTION - Describe the pathological features and complications of acute and chronic pyelonephritis Describe the symptoms and signs of urinary tract infection including the factors that may predispose to urinary tract infection. Describe the investigation of a patient with a suspected infection Discuss the general treatment measures and suitable antibiotic regimens for treatment.

Features of pyelonephritis: A classic triad of fever, loin pain and tenderness over the kidneys indicating acute infection. Possible signs of cystitis/urethritis and systemic symptoms of fever, rigors, vomiting, and hypotension. (Typically acute onset with a differential including an acute abdomen). Complications of acute pyelonephritis: Acute kidney failure, kidney abscess, sepsis, papillary necrosis (may cause ureteric obstruction). Complications of chronic pyelonephritis: Fibrosis of the kidney. Chronic renal failure. Features of a urinary tract infection: Abrupt onset of frequency and urgency, dysuria, suprapubic pain, strangury (Intense desire to pass more urine after micturition because of spasm of the bladder wall), cloudy foul smelling urine, haematuria. If the infection spreads to pyelonephritis there will be systemic symptoms as above. Predisposing factors for UTI: Factors that prevent bladder emptying (outflow obstruction, neurological problems such as MS or diabetes, prolapse or other gynaecological abnormalities and vesico-ureteric Reflux), foreign bodies (catheter, stent), loss of host defences (diabetes, atrophic urethritis in postmenopausal women). Obviously because the shorter urethra and lack of prostatic bacteriocidal secretions women are much more prone to UTIs than men. Investigation of the UTI: Urine dipstick (Positive for Leukocytes and nitrites as bacteria reduces nitrate to nitrite) and urine microscopy/culture, FBC, creatinine (If the infection is complicated). For pyelonephritis you may need a renal tract ultrasound or CT, pelvic examination in man, rectal examination in women. For continuing haematuria perform a cystoscopy. Treatment of the UTI: Typical organisms are E. coli, proteus, pseudomonas, staphylococcus epidermidis and streptococci so antibiotics are recommended in all cases of the proven UTI. Typically this is really day course of trimethoprim or nitrofurantoin if uncomplicated and 7 to 14 days if the infection is more severe. Recommend a fluid intake of at least 2 L a day and investigate any persistent or recurrent urinary tract infections appropriately.

CHRONIC KIDNEY DISEASE - Describe the clinical features associated with chronic renal failure. Discuss the possible physical signs and investigation of a patient with chronic renal failure. List and outline the pathology of the common causes of chronic renal failure. Describe the assessment of CKD using estimated glomerular filtration rate (eGFR) and the five stages of CKD.

Features:This is a gradual process which initially presents as a biochemical abnormality then progresses to give symptoms of excretory, metabolic and endocrine failure of the kidney leading to symptoms collectively referred to as uraemia. This is primarily a disease of the over 65's and is associated with hypertension, diabetes and vascular disease. Symptoms/signs: typically a patient presents with raised urea creatinine known, with hypertension, proteinuria or anaemia. Typically asymptomatic until GFR is below 30, early symptoms knocked urorrhoea, fatigue, breathlessness (because of renal anaemia-low EPO), eventually, deep respiration, muscular twitching, fits, drowsiness and coma. Immune function is impaired leaving patients susceptible to infections, most die by cardiovascular disease (excessive green in production). Increased bleeding, anaemia, electrolyte abnormalities (metabolic acidosis), fluid retention, Diabetes (Insulin is ordinarily metabolised in the tubules so it's half life is prolonged in CKD), Myopathy, hyperparathyroidism, this and indeed efficiency, neuropathy. Calcium and Vitamin D (which the kidney produces from hydroxyvitamin D) disturbances lead to osteoporosis. The result of low calcium is hyperparathyroidism. Investigation: Renal biopsies rarely undertaken as it often doesn't change treatments. Investigations includes you really are, Crasnitin, urinalysis, electrolytes, albumin, FBC, lipids, Ultrasound of the kidney, hepatitis and HIV serology (if dialysis or Trans-Planter planned) and an ECG. It is important to identify reversible factors such as hypertension, obstruction, nephrotoxic drugs and to screen for cardiovascular risk factors. Causes: Congenital/inherited (polycystic kidneys, Alport syndrome), Renovascular disease (Arthroderma), hypertension, glomerular diseases (nephropathia), interstitial diseases (often drug induced), lupus, vasculitis, diabetes (most common!). In many cases the underlying cause is unknown, but a definitive biopsy often does not change treatment. Stages: Based on EGFR greater than 90's stage I, 60 - 89 is stage II, 30 - 59 is stage III, 15 - 29 is stage IV, anyone on dialysis or EGFR less than 15 is stage V.

TRAUMA - Outline diagnostic and supportive therapeutic actions for abdominal trauma including the indications and contra-indications for FAST (focused assessment with sonography for trauma).

Focused Assessment with Sonography in Trauma Rapid utrasound screening test for pericardial effusion, and hemoperitoneum. Look specifically around the heart, at the hepatorenal recess, around the spleen and in the pelvis.

GORD - List the symptoms of GORD Describe and interpret relevantinvestigations to confirm the presence of GORD Outline indications for surgery in this condition.

GORD = Acid reflux sing into the oesophagus. Symptoms: This may be asymptomatic patients complain of heartburn. Less common symptoms include water brash, coughing, nausea and difficulty swallowing. Investigations: 24 hour ambulatory oesophageal pH and manometry studies will confirm reflux - Usually the diagnosis is clinical, only perform investigations if you're considering surgery. Treatment: Nissen's fundoplication will mobilise the fundus of the stomach and wrap it around the lower oesophagus. This tightens the lower oesophageal area preventing reflux. However, this is a serious surgery that will prevent the patient from burping or vomiting, May cause dumping and carries all the general risks of surgery so should be used as last line. Hiatus hernia: Typicall 2 - 4 cm of the oesophagus is within the abdomen. A hiatus hernia moves the oesophagogastric junction up into the thorax and maybe sliding (85% - Oesophagogastric junction moves into the thorax) or rolling (10% - fundus roles beside the oesophagus). Presentationis with retrosternal learning pains, whirs unbending/lying flat. Patients complain of heartburn and GORD symptoms, particularly after meals. Treatment is with weight loss, smoking cessation, smaller meals earlier in the evening and raising the head of the bed. Patients benefit from antiacid and proton pump inhibitors.

PULMONARY FIBROSIS - Describe the clinical and pathological features of interstitial lung disease. Outline the common causes and list the differential diagnosis in patients who present with established pulmonary interstitial fibrosis

Gradual change of the lung parenchyma to fibrous connective tissue leading to lung wall thickening and irreversible reduced oxygen transfer. Because compliance is reduced it is a restrictive lung disease. Features: SOB especially on exertion, chronic, hacking dry cough, fatigue and weakness, chest pain, loss of appetite and weight loss. Fibrosis causes end expiratory crackles, reduced chest expansion and clubbing. Causes: Interstitial lung diseases such as those that are autoimmune, viral, bacterial, TB. Or, idiopathic pulmonary fibrosis. It may also be secondary to: aspestosis, silicosis, smoking, connective tissue diseases (rheumatoid, SLE, scleroderma), sarcoid. Also iatrogenic (medication, chest irradiation). Differential: Pneumonia, hypersensitivity pneumonitis (Eg, farmers lung), granulomatous disease.

Types of shock? (five)

HYPOVOLEMIC - this may be seen with haemorrhage or a systemic inflammatory response which shunts all the fluids into the third space. Patients are tachycardic, hypotensive with a poor urinary output. CARDIOGENIC - patients will be tachycardic, hypotensive with a weakened thready pulse and possible ECG changes. Often venous congestion leads to distended jugular veins. NEUROGENIC - Autonomic dysfunction causes hypotension with bradycardia. ANAPHALAXIS - hypotension, tachycardia, rash, airways obstruction. SEPSIS - hypotension, tachycardia, tachypnoea, temperature.

ANAEMIA - Outline the features and causes of inherited red cell membrane defects and of red cell enzymopathies

Haemoglobinopathies: Sickle cell disease and thalassaemia, discussed previously. Enzymopathies: > Glucose-6-phosphate dehydrogenase deficiency is the most common red blood cell enzyme defects. X linked recessive inheritance, most patients are asymptomatic but susceptible to oxidative crisis (jaundice) during reduced glutathione production precipitated by drugs (antimalarials and aspirin) or illness.Avoid any precipitant such as drugs and transfused if severe. >pyruvate kinase deficiency is an autosomal recessive condition where is there is reduced production of ATP causing a short and red blood cell lifespan. If homozygote there will be neonatal jaundice and chronic jaundice with splenomegaly and jaundice. Splenectomy may help but there is no specific treatment. Membrane defects: > Spherocytosis is an autosomal dominant condition whereby RBCs are less flexible due to a protein (spectrin defect). RBCs are spherical and haemolysed by the liver and spleen. Most patienst are healthy with only mild anaemia. > Eleptocytosis is a similar disease with oval RBCs again autosomal dominant causing asymptomatic mild anaemia.

CONGESTIVE CARDIAC FAILURE - Define heart failure and classify common causes. Describe the typical history and clinical examination findings, investigations and management together with morphology and histological changes in the lungs and liver.

Heart failure is when the heart cannot maintain adequate output or can only do so at the expense of elevated ventricular filling pressure. Cardiac output will be normal until heart failure becomes severe or when metabolic demand increases (exercise). Therefore symptoms only show with significant disease. (Signs of venous congestion) Cause: any form of heart disease (heart attack, myocarditis, hypertension, valve stenosis, Septal defect, arrhythmias (atrial fibrillation, heart block), pericarditis, cardiac tamponade etc.) Remember that the most common causes are coronary artery disease and heart attacks. Findings: If the left side of the highs failing then backflow into the lungs will cause shortness of breath, if the right side of the heart is failing then backflow into the peripheries will cause venous congestion (ankle oedema, congested liver and signs of fluid overload). There's often signs of hyperlipidaemia, hypertension etc that are risk factors for heart disease. JVP is raised with Either side of the heart and pitting oedema is common with both. Investigations: Serum urea, creatinase and, electrolytes, haemoglobin, thyroid function, ECG and chest x-ray help to determine the severity. BNP is elevated in heart failure and Echo will determine the cause. Chest x-ray can show pulmonary oedema (left sided heart failure) (curly beelines are pathognomonic of pulmonary oedema.) Lung and liver changes:Advanced heart failure causes renal failure (poor renal perfusion), low potassium (because of diuretic use) or high potassium because of ACE inhibitors or angiotensin receptor blockers, low sodium (because of diuretics) hepatic venous congestion means that liver function is poor causing jaundice, altered LFTs and reduced synthesis of clotting factors (bleeding), Thromboembolism is more common because blood stasis occurs more frequently and arrhythmias are common because of electrolyte disturbances and atrial damage (AF). As with the liver and lung becomes congested and oedematous.

PULMONARY OEDEMA - Describe the typical history, clinical features, common causes, differential diagnosis, investigations and management of pulmonary oedema together with the morphology and histological changes of the lungs.

History: This is when fluid accumulates within the parenchyma of the lung Leading to impaired gas exchange and possible respiratory failure. It therefore presents with difficulty breathing, haemoptysis, sweating and anxiety. There may be orthonea or paroxysmal nocturnal dyspnoea (Episodes of severe sudden breathlessness at night). Causes: Pulmonary oedema is either cardiogenic or non-cardiogenic. Meaning that is either due to left ventricular failure (with a backflow of fluid causing Fluid overload) or due to Acute respiratory distress, Kidney failure, Seizures. Alternatively think of the pneumonic non-cardiac (Near drowning, oxygen therapy/Post intubation, Trauma/transfusion, CNS, allergic alveolitis, reading all,Drug induced, inhaled toxins, Altitude, contusion. Differential diagnosis: This is complicated by the fact that most causes of shortness of breath are multifactorial. Main differentials include pulmonary haemorrhage And pneumonia. Investigations: Echocardiogram may show left ventricular failure or there may be evidence of non-cardiac causesX-ray will show fluid within the alveolar space and curly B lines (Thin white less than 2 cm lines indicating thickened interlobular septa). Morphology and histological changes: Alveoli become oedematous. The lung becomes heavy and wet and the capillaries become engorged. If chronic this leads to fibrosis. Management: Acutely this is a medical emergency. Sit the patient up to reduce pulmonary congestion, give high flow oxygen (consider CPAP), intravenous nitrates (improves cardiac function), intravenous loop diuretic. Continuously monitor the heart rhythm, blood pressure and oximetry and avoid intravenous opiates or other drugs that suppress the respiratory drive.

PERI-OPERATIVE CARE - Recognize and manage a patient with an obstructed airway (also covered in critical illness attachment): Undertake appropriate head / neck positioning, sizes and insert an appropriate oropharyngeal (Guedel) airway Safely set-up an intravenous fluid (MACCS in critical illness attachment) Recognize and manage a patient with suspected anaphylaxis

ILS TRAINING MANUAL Anaphylaxis: presenting with rash, itching, slid muscle constriction, vasodilation and capillary leakage, bronchospasm, nausea, diarrhoea, angioedema and shock. Comments surgical triggers include latex, antibiotics, muscle relaxants, induction agents, colloid infusions, blood products and the egg found in propofol. Management is as follows... 1. Secure the airway, 100% oxygen, intubate early. 2. Remove the cause. 3. Raise the seat to help restore circulation. 4. Adrenalin 0.5 mg of 1:1000 intramuscular repeating every five minutes if needed. 5. Secure IV access. 6. Chlorphenamine 10 mg IV and hydrocortisone 200 mg IV. 7. normal saline 500 mL. 8. treat any wheeze with nebulised salbutamol. 9. Consider intensive care admission. 10. Confirm anaphylaxis with serum tryptase and mast cell histamine. 11. Further investigations into the trigger, Medic alert bracelet, consider epipen.

What anaesthetics are used for induction? Maintenance?

INDUCTION: Propofol (also used for maintenance), Thiopental, Etomidate MAINTENANCE: Oxygen therapy, muscle relaxants and analgesia in combination with ISO/SEVO/DES/flurane.

ANAEMIA - list the typical symptoms of a patient with anaemia

If slowly falling haemoglobin occurs then there is time for haemodynamic compensation and enhancement of the oxygen carrying capacity of blood. This means that patients may be asymptomatic. Patients may complain of non-specific symptoms such as tiredness, headaches, faintness, breathlessness. They may have angina, intermittent claudication or palpitations. Signs include pallor, tachycardia, systolic flow murmur, heart failure. Koilonychia/spoon shaped nails = iron deficiency anaemia Jaundice = haemolytic anaemia Bone Deformities = thalassaemia major Leg Ulcers = sickle cell anaemia. Anaemia is not a diagnosis so find the cause.

COPD. Discuss the importance of monitored oxygen therapy in treatment and the indications for assisted ventilation, outlining how this is undertaken.

In COPD patients rely on hypoxia (not hypercapnia as is normal). The slow build in CO2 has meant that the brain has learnt to ignore high CO2 so giving high flow oxygen to a COPD patient means they will stop breathing. Therefore use 25% oxygen to maintain sats of 88-92%. CPAP - continuous positive airways pressure essentially keeping the airways open constantly for conditions such as apnoea or other resiratory depressants, will over oxygenate those with COPD so is not used. Long term use in neonates may cause broncopulmonary dysplasia. BiPAP - bilevel positive airway pressure delivers a positive air flow intermittantly to correspond to inspiration wither using time-cycle or flow-cycle. It is effective management of respiratory failure or COPD. Use when patients are not adequately oxygenating on 25% O2 via a nasal cannula.

LUMBAR PUNCTURE - List the acute clinical situations where a lumbar puncture would be indicated. Explain the term CSF xanthochromia. Explain the significance of CSF xanthochromia in a sudden onset headache. List the CSF findings that accompany multiple sclerosis

Indications: Therapeutically, this may be for spinal anaesthesia or intrathecal chemotherapy (not vincristine). Diagnostically, this can confirm meningitis (and differentiate between TV, viral and bacterial), Subarachnoid haemorrhage, hydrocephalus, benign intracranial hypertension and neoplasms (by the presence of neoplastic cells). Xanthochromia: A yellow discolouration of the cerebrospinal fluids as it contains the blood byproduct heme (which degrades into bilirubin). A bleed into the cerebrospinal fluid is often because of subarachnoid haemorrhage which presents with a sudden thunderclap headache due to rupture of a berry aneurysm. Multiple sclerosis CSF: Immunoglobulin levels are markedly raised and if the patient is having an acute attack such as optic neuritis and protein can also be raised, If not it's only slightly raised. Most cells identified RT lymphocyte. As it is a chronic inflammatory condition, inflammatory markers will be markedly raised.

NEURO-ONCOLOGY - Describe the clinical presentation of an intracerebral space occupying neoplastic lesion List the three most common adult primary brain tumours and outline their prognosis List the common somatic tumours which metastasise to the brain

Intracranial tumours are benign or malignant, primary (10% of all cancers, 60% of all intracranial cancers) or secondary (Lung, breast, lymphoma etc). Presentation: Presentation is usually with the effects of raised intracranial pressure From mass effects, haemorrhage into a tumour or obstruction of fluid drainage(headache, vomiting, papilloedema, focal neurological signs and possibly seizures and cognitive impairment). You're more likely to see the early symptoms of an early morning headache worse on coughing and Lying down. Coning maybe the initial presentation With respiratory depression, loss of consciousness and death. Uncal herniation Of the temporal lobe can compress the third nerve giving a dilator down and out pupil. Remember also false localising signs such as nerve palsy presentation secondary to compression at a more distant sites. The most common intracranial tumours are: metastases (lung, breast, skin), gliomas, meningiomas and could shoot Re adenomas. Less common are schwanomas and haemangioblastomatas. Treatment: treat any oedema with dexamathasone (corticosteroid) and or intravenous mannitol. If there is hydrencephalus a shunt may be appropriate. Seizures need to be controlled with anticonvulsants but surgery, radiotherapy and chemotherapy are the definitive treatments. Surgery for meningiomas but radiotherapy for gliomas and metastasis in combination with chemotherapy. Prognosis: this is highly dependent upon the type and grades, location and size as well as patient factors. Overall when you survival is less than 50% if high-grade and malignant. Benign tumours (meningioma, neurofibromin and Pituitary tumours are often cured). Glioma: Consider four types of glioma: astrocytoma (most common, variable malignancy), oligodendroma (slow-growing), ependymoma (from ependymal cells and courage plexus, reasonable prognosis) and lastly glioblastoma multiform a (highly malignant). Meningioma: Benign, slow-growing from the arachnoid membrane peaking in the sixth decade, commonly with calcification and presenting late. Lymphoma of the CNS: Rare, seen more commonly in the immunosuppressed responding to a chemotherapy and radiotherapy. Surgery has no role in the removal of lymphomas. Steroid treatment should be avoided private biopsy as it can shrink the tumour. Pituitary tumours: discussed elsewhere, includes prolactinoma is, nonfunctioning adenomas, growth hormone secretion, ACTH secreting etc.

CHRONIC PERIPHERAL ARTERIAL DISEASE - Differentiate symptoms of ischaemic rest pain and neuropathy as a cause of foot pain and contrast gangrene in diabetic and non-diabetic patients. Describe the pathophysiology of intermittent claudication; differentiate claudication from other causes of leg pain. List criteria to help differentiate leg ulcers.

Ischaemic rest pain versus neuropathy: Ischaemic rest pain is worsened by things that reduce blood flow (one bed clothes causing vasodilation of the skin at nights, losses the effect of gravity when lying down, lowered cardiac output when sleeping). It is typically cost pain with intermittent claudication butts tile and foot pain relieved by walking on a cold surface with rest pain. In contrast, neuropathy (Nerve damage) Maybe motor, sensory or autonomic. There will be painful cramps with muscle twitching, loss of muscle and possible foot deformities (Charcott). The typical pattern is pins and needles. Gangrene: There is a significantly increased risk of gangrene in diabetic patients Due to neuropathy Making injury more likely and vascular disease causing blood flow insufficiency. Intermittent claudication: (see above, as the oxygen requirement of the tissues increases in the presence of a stenosis that does not allow increased blood flow pain results as a particular distance, relieved by rest). Is differentiated primarily on the history which is classic although be aware of its main differential (spinal claudication - more numbness and pins and needles than pain). Leg ulcers: Consider arterial, Venous, neuropathic As discussed previously.

LIVER - Compare and contrast the pathology and natural histories of liver neoplasia, abscesses and cysts. Describe the symptoms and signs associated with liver abscess. List the investigations that differentiate neoplasia, abscesses and cysts and outline their treatment options. Describe the aetiology and pathology of primary and secondary liver neoplasms.

LIVER CANCER - typically liver tumours are metastasised from primary tumours of the gastrointestinal tract. If primary, they tend to be in a patient with underlying liver disease (cirrhosis). Liver cancer is a single solid mass that may be found incidentally. Think hepatocellular carinoma (hepatitis B, C or cirrhosis associated) or hepatic adenoma (link to the pill - benign! Easily resectable.). Liver function tests are deranged, tumour markers may be raised (alpha-fetoprotein), and CT of the chest, abdomen and pelvis may look for primaries. Resection should be considered but if cirrhosis is involved then prognosis is poor. If you find multiple solid liver lesions then this implies disseminated malignancy. Multiple liver metastases are typically unsuitable for resection. LIVER ABSCESS - pus filled cyst in the liver often associated with appendicitis or diverticulitis or other intra-abdominal infections that will haematogenously spread to the liver. fungal or amoebic abscess is also possible. Thlink Streptococcus, Klebciella, pseudomonas etc. management is was the antibiotics, treating the original infection and possible surgical or percutaneous drainage. LIVER CYST -fluid filled sac within the liver. Simple liver cysts are usually asymptomatic although large ones cause RUQ pain. More serious cysts: Hydatid cysts from echinococcosis parasites. Largest this may be biliary cystadenomas (cystic benign tumour). Polycystic liver is an inherited disorder causing abdominal pain and bloating. Potential complications include bleeding, infection and bile duct - may need resection or transplant.

HAEMOSTASIS - Discuss the pharmacokinetics and clinical use of heparin including laboratory tests used in monitoring heparin therapy. Outline the clinical management of over-anticoagulation with heparin

LOW MOLECULAR WEIGHT Heparin inactivates factor Xa, for example in Oxford Parliament which is adequate DVT/PE prophylaxis. UNFRACTIONATED heparin can be given intravenously or subcutaneously and will inhibit thrombin as well as factor 10a and factor 9a. it has a rapid onset and short half life. Monitor with activated partial thromboplastin time. Dose according to wait and remember the side-effects are an increased bleeding risk, high potassium and heparin induced thrombocytopenia. Long-term use of heparin can cause osteoporosis. Contraindications include bleeding disorders, neurosurgery, previous heparin induced thrombocytopenia, peptic ulcer, brain bleed. Antidotes: for unfractionated heparin stop the infusion and give protamine sulphates if there is bleeding.

LUMBAR PUNCTURE -Name the main anatomical landmark(s) used in guiding a lumbar puncture, and the coincident level in the spine. Describe the two different positions a patient may adopt to undergo a lumbar puncture, and advantages of each with respect to ease of success and measuring opening pressure List the potential complications of a lumbar puncture List the contraindications to a lumbar puncture

Landmarks/Positions: Left (or right) lateral position with head blacks and needs Curled up. This flexion of the spine opens up the intervertebral space. An alternative position is that the patient leaning forwards hugging the front of the chair With shoulders forward and head down (Used in obese patients whereby lying on their side would distort the anatomy). Insert the needle at the level of the iliac crest at L4 - L5. A give will indicate you're past the ligamentum flavum, A second give indicates your past the dura. After the procedure as the patient to lie down for six hours on their back and monitor the neurological signs. Complications: Usually, the procedure is relatively safe although post-dural-Puncture headache is common. The most serious complication is coning where the Cerebellar tonsillas have herniated through the foramen magnum. A minor complication is paresthesia because the needle can irritate spinal nerve root. Severe but very rare conditions include arachnoiditis, haemorrhages and trauma to the spinal-cord. Contraindications: Raised intracranial pressure (risk of coning, a CT brain may be needed in advance), Bleeding disorders, Skin infection at the puncture site and Vertebral deformities.

THE WHITE CELL - Distinguish between myeloid and lymphoid cell lineages in the classification ofacute leukaemia; highlight differences between childhood and adult-onset leukaemia.

Leukaemia is a rare disease affecting 1000 thousand per year with an unknown cause although viruses/radiation/poisons/immunosuppression have been associated. MYELOID v LYMPHOID: myeloid refers to erythrocyte, monocyte, granulocytes pre-cursors whereas lymphoid refers to B and T-cell precursors. ACUTE v CHRONIC: more than 50% of leukaemias are acute. Chronic tend to happen more slowly because they affect mature cell lines. PRE-LEUKAEMIAS: myelofibrosis, myelodysplasia, polycythaemia vera. children are more likely to be affected by acute lymphoblastic leukaemia whereas adults are more likely to be affected by acute myeloid leukaemia.

MULTIPLE SCLEROSIS - Describe the pathological lesions of multiple sclerosis, the common sites of involvement in the nervous system and outline the pathogenesis of the disease. Describe the epidemiological features of MS, with specific reference to gender, age of onset and geographic distribution List the different clinical patterns of MS and describe the different courses that MS can take. Describe commonly encountered clinical features of MS relapses List the investigations used in ascertaining a diagnosis in MS. Outline the diagnostic utility of magnetic resonance imaging (MRI), evoked potentials and CSF examination List the differential diagnoses of MS Describe the investigation and management of an acute MS relapse Outline the principles of treatment of: immuno-suppression; symptomatic management and rehabilitation of spasticity, bladder problems, pain, sensory symptoms, weakness, fatigue and depression Outline the disease modifying therapies available in MS, and their effect on relapse rate and long term disability.

Lesions: Inflammatory, demyelinating lesions in the white matter of the brain and spinal-cord termed plaques. The most common sites and involvement are: periventricular region of the cerebral hemispheres, corpus callosum, brainstem, cervical cord and optic nerves. Accidents are preserved until the later stages of the disease. Features: Typically a young Caucasian Female between 20 and 30 years old presenting with the relapsing and remitting form that can convert to secondary progressive multiple sclerosis between 40 and 45 years. Clinical patterns: There is no single presentation. The most common pattern is a RELAPSING - REMITTING picture whereby early relapses result in full recovery or with minimal residual deficit. The SECONDARY PROGRESSIVE lecture is when the disease starts as relapsing remitting but recovery from each successive relapse becomes less complaints and the disease gradually progresses between relapses to cause long-term disability. (40% of relapsing remitting after 10 years). The third pattern is PRIMARY PROGRESSIVE, rare but with disability worsening gradually from the onset without any true relapses and omissions. Once a progressive stage has begun patients tend to need a walking aid after six years. Multiple sclerosis patients have a life expectancy Six - seven years less than the general population, good prognostic factors include Caucasian ethnic origin, relaxing and remitting form, complete recovery from first attack, low relapse rates, long intervals and minimal lesion load on MRI. Symptoms: These are variable but may include: optic neuritis (subacute visual loss, a unilateral central scatoma and pain on eye movement), brainstem demyelination (dysarthria, dysphagy, diplopia, vertigo, facial numbness, trigeminal neuralgia, deafness, a tax year, nystagmus), spinal cord lesions (motor and sensory weakness, urinary incontinence, constipation and erectile dysfunction). Other symptoms include seizures, fatigue and depression. Investigations: There is no diagnostic test but is MRI can pick up areas of demyelination, cerebrospinal fluid Will show raised lymphocytes particularly in relapses and oligoclonal bands corresponding to IgG. Visual evoked potentials will be delayed regardless of symptoms if there is demyelination along the optic nerve, the same can be performed for brainstem auditorii evoked potentials and somatosensory evoked potentials. Differential diagnosis: Lupus, sarcoid, bechets, neurosyphilis, Lyme disease, vitamin B12 deficiency, paranee plastic syndrome and hereditary disorders (ataxias). There are also other demyelinating diseases. Diagnosis: the McDonald criteria Determines the diagnosis of multiple sclerosis and involves the clinical picture, MRI lesions and cerebrospinal fluid oligoclonal bands. Management Of an acute relapse: Steroid therapy intravenously as ethyl prednisolone for severe acute relapses. This shortens the course of relapse is is not affect clinical outcome. Management: interferon is used to modulate or suppress the immune system therefore reduing relapses in patients with relapsing remitting MS Or secondary progressive MS whereby disabilities due to relapses. Multiple interferon drugs can be given as injections with the risk of site reactions. In patients with progressive MS or the failed use of interferon more powerful immunomodulatory agents such as monoclonal antibodies are used. Remember that drugs such as natalizumab are associated with opportunistic infections.

OBSTRUCTIVE JAUNDICE - Describe the laboratory and radiological investigation of a patient presenting with obstructive jaundice.

Liver function tests will reveal raised alkaline phosphatase (also raised in bone problems) and raised gamma GT (grossly so if alcohol related). Transaminases will be less significantly abnormal. Check the base line clotting in all jaundice patients. Most important is al ultrasound scan which will identify gallstones, obstruction and any dilation of the biliary tree. Normal maximum dilation of the common bile duct is 7mm, 1.1mm if previous obstruction. The lower end of the common bile duct and head of the pancreas are often obscured on ultrasound because of overlying bile gas, especially if obese.

VENOUS THROMBO-EMBOLIC DISEASE - Identify the usual initial anatomic location of deep venous thrombosis. Describe the risk factors, clinical features and investigations for this condition.

Location: Primarily the lower extremities (Remember that the deep veins are ephemeral, posterior tibial and anterior tibial as well as the peroneal). Presentation: typically minimal, unilateral or bilateral hot red swollen calf. Especially alongside risk factors: active cancer, inability, swelling of the leg, recent surgery, age, obesity, varicose veins, family or personal history, pregnancy, oestrogen, IVDU, lupus. Investigations: probability screening using the well score (determines PE risk), D dimer, Ultrasound. An alternative to compression ultrasound is venography but this is rarely used.

LUNG CANCER - Outline the major pathological classification of lung cancers and their prognosis

Lung cancer is the most common cancer death worldwide. They are small (propensity to metastasize early)cell or non-small cell (rare) bronchial carcinomas. SMALL = Triggered by smoking, metastasizes early. Chemo is aropriate. NON SMALL = The most common. - Adenocarcinoma, most common, from mucus secreting glands. - Squamous, linked to smoking, often near to the bronchi. - Large cell carcinoma, rapidly growing MESOTHELIOMA = pleural cancer linked to asbestosis. BRONCHIAL CARCINOMA: Smoking associated, (Adenocarinoma 35%, SCC, 30%, small cell 20%, large cell 15%). Symptoms present early if in a large bronchus but late if in the periphery. Nodal spread at diagnosis is common as is local spread causing pleuritic chest pain. Blood bourne mets go to the bone, liver, brain, adrenals and skin. Small cell carcinoma often causes wide spread metastasis despite a small primary. SECONDARY: Breast, kidney, uterus, ovary, testes and thyroid primary tumours may spread haematogenously to the lungs. They are usually asymptomatic unles large (therefore breathlessness). Remember cancer in the hilar lymph nodes can cause haemoptysis and SOB. MEDIASTEINAL CANCER: May be incidentalomas on Xray. Malignant masses invade and compress causing early symptoms of SOB, dysphagia, vocal changes, horners, pericarditis - depending on the location.

ANAEMIA - Classify anaemia in terms of red cell indices and list common causes of each type of anaemia

MICRO: low mean corpuscular volume (<80) as seen with iron deficiency, anaemia of chronic disease, consider aplastic anaemia and thalassaemia. NORMO: normal mean corpuscular volume seen in acute blood loss, anaemia of chronic disease, kidney failure, bone marrow infiltration and haemolytic anaemias. MACRO: high mean corpuscular volume this is either megaloblastic (vitamin B12 and folate deficiency) or normoblastic (alcohol, liver disease).

CARDIAC SURGERY - Outline the clinical presentation and treatment of myxoma

MYXOMA is a rare benign tumor of cardiac muscle. Heart tumors are rare, primary tumors even more so but if seen they will be myxomas. Classically a polypoid gelatinous mass in the left atria that can prolapse through the mitral valve causing a tumor "plop", sound like a mitral murmur or even present like endocarditis (with a fever and raised ESR). Also found incidentally on echo, they simply need excision and fewer than 5% reccur.

VASCULAR DIAGNOSTIC RADIOLOGY - Describe the indications for Magnetic resonance angiography, Duplex ultrasound, CT angiography and invasive investigations of the arterial and venous system and list the common insertion sites for arterial catheter studies. List the risks and complications of angiographic studies and describe their management. Define and discuss transluminal angioplasty as used in coronary, visceral and peripheral vascular arterial beds. List the indications for pulmonary arteriography.

MRI: MRI angiography allows a pulse sequence selected images of arteries/veins can be produced without exposure to ionising radiation. It can also be enhanced with contrast (gadolinium). Its purpose is to evaluate stenosis, occlusions and aneurysms. Ultrasound: This includes hand held Doppler pens whereby the vessel is made audible. Use ultrasound as a non-invasive method of determining blood flow through vessels such as in a suspected clot, Valvular dysfunction, aneurysms Or stenosis. Doppler pens are also used to determine ankle brachial pressure index to see if it's safe to use Venous compression. Normal is greater than one, <0.8 Is arterial disease With <0.3 being critical limb ischaemia. CT angiography: A semi-invasive technique for examining blood vessels By injecting a contrast such as iodine then performing a CT scan. For problems such as ?Pulmonary embolism, Inspecting bloodflow to the kidneys, Aortic aneurysms/dissections/atherosclerosis And for coronary artery disease. Catheter studies: Typically used in intensive care for real-time measurement of blood pressure. Common insertion sites include radial, brachial, ulnar and femoral. Transluminal angioplasty: Using a catheter and/or a balloon to widen a stenosed vessel. Performs primarily for atherosclerosis the risks include: Embolisation, aneurism, rupture of the vessel wall, infection and sequelae of radiation. Pulmonary arteriography: A pulmonary artery catheter can be diagnostic, determining pressures in the right atrium, right ventricle and pulmonary artery which can be diagnostic of heart failure And can assess pulmonary hypertension. The procedure can cause arrhythmias, thrombosis, Infection, bleeding And possible pneumothorax.

OBSTRUCTIVE JAUNDICE - Discuss the methods relieving common bile duct obstruction.

Management: Remove stones with ERCP, consider palliative care or whipples. See specific sections.

CNS INFECTION - Outline the clinical presentation of bacterial meningitis and describe the appearance of the typical rash of meningococcal septicaemia Describe the common bacterial and viral organisms causing meningitis in adult life Describe the pathological changes and complications seen in purulent leptomeningitis, lymphocytic meningitis and granulomatous meningitis. Discuss the aetiology, diagnosis and management of herpes simplex encephalitis. List the risk factors which may predispose a patient to TB or fungal meningitis. Discuss the investigation of a patient with suspected meningitis including indications and contraindications for lumbar puncture. Descrbe the normal CSF constituents and CSF dynamics. Compare the CSF findings in bacterial, fungal and viral meningitis/encephalitis Discuss an appropriate antibiotic regimen for treatment of bacterial meningitis Suggest additional agents which may be added in Suspected viral meningo-encephalitis Outline the long-term complications of bacterial meningitis

Meningitis: any information of the meninges is classified as meningitis so technically this could include sarcoid, malignancy, infection, subarachnoid haemorrhage etc. Infective agents usually reach the meninges directly from the sinuses, native pharynx or inner ear, via blood or through fractures. Remember viral meningitis which will be aseptic but presenting in a similar manner to bacterial meningitis, Despite being self-limiting (Think enteroviruses, herpes and mumps). TB will cause a chronic picture (Presenting similarly to fungal meningitis). Organisms: bacteria tend to be haemophylis influenza A, Neisseria meningitidis and Streptococcus pneumoniae. In children consider E. coli and group B strep. Presentation: Meningism (headache, photophobia, neck stiffness, Kernig signs positive), fever, confusion, decreased consciousness. Presentation is over a few days or hours and neck stiffness may be subtle or marked.Severe infection can cause cerebral oedema and raised intracranial pressure. (Meaning seizures, altered consciousness and cranial nerve palsy's) Diagnosis/investigations: Lumbar puncture with a CT initially to rule out the risk of coning. Gram stain CSF, zeal Nilsson for TB and Indian ink stain for cryptococcal. Take cerebrospinal fluid at the same time as blood glucose and perform blood cultures. Cerebrospinal fluid: Normal cerebrospinal fluid is clear with no neutrophils, few lymphocytes, 60% of blood glucose and nought .2-0 .4 g/L protein In bacterial infection CSF is turbid with high neutrophils, high lymphocytes, high-protein and lowered glucose. In viral infection CSF is usually clear with few neutrophils, markedly raised lymphocytes, increase protein and reduced glucose although not as much as bacterial. In TB infection CSS The fluid is turbid with a couple of neutrophils, markedly raised lymphocytes, high-protein and low glucose. (Glucose can get up to 3 g!). Management: Give cefotaxime or ceftriaxone immediately IV. Add ampicillin or gentamicin if listeria is suspected. Dexamathasone, a steroid is given if you suspect pneumococcal meningitis to decrease the chance of neurological problems. Remember that this is a notifiable disease and contacts must be treated with patient is kept in respiratory isolation. Management additions in meningo-encephalitis: When both the brain and the meninges are inflamed Corticosteroids are required to reduce brain swelling alongside antibiotics. Anticonvulsants may also be required to treat seizures. Purulent leptomeningitis: A purulent meningitis with lots of pass and necrotic debris. Lymphocytic meningitis: Also known as aseptic Meningitis (no bacterial cause) Granulomatous meningitis: A more chronic picture thought to be immune-mediated. Long-term complications of bacterial meningitis: Neurological defects, epilepsy, hearing loss, cerebral palsy, Visual loss, behaviour difficulties, learning disabilities. Gangrene can also result in limb loss.

PULMONARY FIBROSIS - Outline the investigations and treatment options for a patient with suspected interstitial lung disease

NB. INterstitial l;ung disease is an umbrella term for diseases of the lung interstitium - most commonly interstitial pulmonary fibrosis. Investigations: Chest Xray (scar tissue), CT (for extent of fibrosis), echo (determine extent of damage to right heart), spirometry (restrictive deficit - normal FEV1/FVC ratio), oximetry, exercise stress test, bronchoscopy or surgical biopsy. Treatment:Scarring is permanent so treatment is to slow progression by: Steroids/methotrexate/cyclosporin (for any autoimmune trigger), oxygen, avoiding any known causative agents (esp for hypersensitivity pneumonitis induced fibrosis), breathing exercises, education, councelling, nutrition.

GLOMERULONEPHRITIS - Describe the clinical presentation of glomerulonephritis. Outline the main pathological processes affecting the glomerulus. Outline the investigation necessary to confirm the diagnosis and outline the treatment options including the role of immunosuppressive therapy for some forms of GN.

NEPHRITIC haematurea, hypertenion and only minimal proteinurea all due to increased cellularity of the glomerulus (Ie...Proliferative). Examples include post infectionus/strep, IgA nephropathy and crescenteric glomrerulonephritiss seen in goodpastures. Nehritic syndromes are PROLIFERATIVE (as opposed to membranous/nephrotic) All diseases of the glomerulus tend to be autoimmune. Considering two forms of glomerular nephritis: acute glomerular nephritis (known as acute nephritic syndrome) and rapidly progressive glomerular nephritis the two are associated with haematuria (macro or microscopic), proteinuria, hypertension, oedema and temporary oliguria. Acute glomerular nephritis..... Presentation: haematuria, proteinuria, hypertension, oedema and temporary oliguria. Cause: there are many different causes for glomerular nephritis, vasculitis, goodpastures, post-streptococcal glomerular nephritis onsets Within three weeks, Focal segmental glomerulosclerosis, membranous glomerular nephritis, IgA nephropathy (including Henoch Schonlein purpura). Investigation: Bloods, often a renal biopsy is required. Treatment: Often this is with high-dose corticosteroids or other immunosuppressive agents. Rapidly progressive glomerular nephritis....... Presentation: Rapid loss of renal function over days to weeks. Proteinuria may be relatively small. Cause: Typically, rapidly progressive glomerular nephritis is seen with good passages disease because of antibodies against GBM, and in small vessel vasculitis or lupus. Investigation: Renal biopsy identifies crescentic lesions associated with necrotising lesions within the glomerulus making it a focal segmental necrotising glomerular nephritis. Treatment:This is dependent upon the underlying cause but immunosuppressive drugs are often required. In good pastures disease plasma exchange, corticosteroids and immunosuppressants are required. Any anchor associated vasculitis or lupus should be treated with steroids and immunosuppressants.

TUBERCULOSIS - List the common sites of non-pulmonary TB infection and outline the pathological features Describe in broad outline treatment changes between 1930 and 1970 and the implications of this for current treatment. Outline common predisposing factors and outline the principles of treatment of confirmed cases and the principles of contact tracing

Non pulmonary TB: lymphadenitis (initially painless and mobile but in time nodes become matted together and caseated with possible skin discharge), gastrointestinal (fever, night sweats, anorexia and a palpable abdominal mass. The bowel shortens, narrows and distorts and can present like crohns), pericardial (presenting as pericardial effusion or constrictive pericarditis - there is insideous breathlessness and abdominal swelling) ADD STEROIDS TO TREATMENT, central nervous system (meningitis - rare but often devastating), bone/joint (spine = potts disease giving chronic back painamd eventual kyphosis - unlike malignancy which leaves the disk alone TB gives bone disease with discitis. Commonly hip or knee infection with insideous arthritis) genitourinary (haematurea, dysurea, frequency with sterile pyurea). Predisposition to TB: age extremes, immigrants from high prevelant countries, close contacts (Contract tracing is legally required - BCG any known close contacts who are tuberculin negative, chemoprophylax any that are positive but asymptomatic and treat those symptomatic), smoking, personal history. Previous treatment: Open air sanitariums year round, bed rest, high meat diets, lobectomies and isolation to prevent them from infecting others. Current treatment: Chemotherapy (six months of rifampicin and Isoniazid with the first two months accompanied by ethambutol or pyrazinamide). The infection is presumed to be non contagious after 2weeks of therapy. Give a longer course for meningeal TB (12months) - for which ethambutol can be substituted for streptomycin. RIFAMPICIN - orange urine and tears, pill reduced efficacy, hepatitis. ETHABUTOL - beware in renal failure, drug reactions common. CORTICOSTEROIIDs are used in cardiac or meningeal involvement. Treatment failure is positive sputum at 5months.

HYPERCALCAEMIA - Discuss the normal control of serum calcium and outline the actions of PTH, vitamin D and calcitonin. List the causes of a raised serum calcium concentration including hyperparathyroidism and malignancy. Describe the classification and pathology of parathyroid disorders. Discuss the clinical presentation, laboratory features and complications of primary hyperparathyroidism. Outline the important clinical associations of hyperparathyroidism. Describe the investigation and early clinical management of a patient presenting with acute hypercalcaemia.

Normal calcium control:The parathyroid gland has calcium sensing receptors so that when calcium gets low parathyroid hormone secretion is increased. Parathyroid hormone promotes reabsorption of calcium at the expense of potassium in the kidney, increases absorption of calcium from the gut and, with prolonged exposure, Osteoclastic breakdown of bone to mobilise calcium. (Note that pulsatile parathyroid hormone at the right levels actually promotes bone growth). In contrast, calcitonin from the parafollicular cells of the thyroid will de crease the amount of calcium in blood by stopping calcium being ridden reabsorbed in the kidney, promoting osteoblast activity to lay down bone and decreasing absorption in the guts. Causes of high calcium: If parathyroid hormone is elevated this is normally because of hyperparathyroidism, lithium induced hyperparathyroidism or familial hypercalcaemia. If parathyroid hormone levels are low, think malignancy, thyrotoxicosis, Paget's disease, milk alkali syndrome, thiazide diuretics or glucocorticoid deficiency. Hyperparathyroidism (Usually autonomous secretion of parathyroid hormone by a parathyroid adenoma= primary, hyperparathyroidism. Secondary to low calcium= secondary) - presentation: Acutely with severe dehydration and high calcium (Bones, stones, moans, groans). The patient may have polyuria, polydipsia, renal colic, anorexia, nausea, peptic ulceration, constipation, depression, drowsiness and impaired cognition. If late, patients can present with pathological fractures secondary to bone reabsorption. Most present early one routine bloods. - Investigations: Biochemical blood testing (Raised parathyroid hormone in the presence of high calcium), ultrasound and scintography as the parathyroid (prior to surgery to remove the adenoma). Also relevant: investigations into renal caliculi, blood pressure (hypertension is a common feature of hyperparathyroidism. Perform renal tests as renal impairment suggests tertiary hyperparathyroidism. If parathyroid hormone is low and there is no other obvious cause then consider a malignancy. (Suspect myeloma). - Complications: Teritary hyperparathyroidism, parathyroid bone disease (may cause lytic lesions as in myeloma), renal impairment. Severe life-threatening high calcium may occur, precipitated by dehydration and requiring intravenous fluids, and bisphosphonates. Associations of hyperparathyroidism: Pancreatis, Lytic bone lesions. Investigations and acute management of hypercalcaemia: High calcium presents with bones, stones, moans, groans. It can shorten the QT interval and even mimic an MRI on ECG and promotes gastric ulcer formation. Severe hypercalcaemia Is a medical emergency because it can cause coma, heart attacks and death. Management is with fluids and forced diuresis (diuretics) along side Bisphosphonates and calcitonin.

HYPERLIPIDAEMIA - Outline epidemiological links between cholesterol and cardiovascular risk. Discuss the evidence and indications for using lipid-lowering drugs in the prevention of cardiovascular disease, together with their side effects

Normal cholesterol equals 5 mmol per litre, aim for 4 mmol per litre if a person has significant cardiovascular risk such as hypertension, diabetes. First remember the difference between LDL and HDL Low-density lipoprotein is bad because it deposits in the arteries, high-density lipoprotein is good because it keeps cholesterol in solution. High cholesterol is classified as primary (familial), secondary (Usually from diabetes, renal failure or excess alcohol) or idiopathic. High LDL is a significant but modifiable risk factor for cardiovascular disease As low-density lipoprotein deposits in arterial walls causing atherosclerosis. Once any underlying conditions have been treated and diabetes control optimised the management is as follows: Statins: HMG Co-A reductase inhibitors - They increase the uptake of LDL in the liver and reduce cholesterol synthesis. Their most serious side-effect is rare (rhabdomlysis) although more common side effects include muscle aches and pains, Increased liver enzymes (Therefore test within six weeks of starting a statin) and an increased risk of diabetes. High-dose statins require monitoring of kidney and liver function. Nice guidelines recommend the prescription of the statin to prevent cardiovascular disease when Lifestyle measures have been implemented and any secondary causes have been addressed.

THE BLADDER AND PROSTATE - Discuss outlet obstruction of the bladder and list the main causes including mechanical and neurological causes. Describe the clinical presenting features, diagnosis and management of benign prostatic hyperplasia and outline possible complications.

OUTFLOW OBSTRUCTION. Cause: urinary caliculi, Benign or malignant prostatic enlargement, pelvic or retroperitoneale cancers, Neurogenic bladder (Particularly seen diabetes by the bladder can become flaccid or spastic), urethral strictures (history of instrumental isolation), trauma, infection, urethral valves, phimoses, meatal stenosis. Obviously, this causes urinary retention, lower pelvic pain, overflow incontinence. BENIGN PROSTATIC HYPERPLASIA: Features: with age the prostate's continues to increase particularly at the periurethral zone. This means that With increasing age men are more likely to suffer from symptoms from obstruction of the urethra (hesitancy, poor flow, sensation of incomplete emptying) as well as secondary symptoms because of the retained urine (frequency, urgency of micturition, urge incontinence). Patients may present acutely in retention with a painful distended bladder (often precipitated by alcohol excess, constipation or prostatic infection). This is an emergency. In more chronic setting the bladder wall distends over time in a pain-free manner which will eventually dilate the kidneys and cause renal failure. Investigations: assess the severity of symptoms, assess kidney function, measure flow rates, estimate the prostate volume during PR then more accurately with a transrectal ultrasound. Management: mild symptoms can be treated with alpha blockers (Alfuzosin - To relax the smooth muscle of the prostate and bladder neck) or five alpha reductase inhibitors (Finasteride - stops the conversion of testosterone to dihydrotestosterone causing the prostate to shrink). Surgical treatment of severe symptoms is TURP (often using a laser or thermotherapy), But there is a risk of post-operative incontinence.

DYSPHAGIA - List the symptoms suggestive of oesophageal malignancy. Describe the pathology and natural history of oesophageal malignancy. List the treatment options for an oesophageal malignancy. Discuss staging and assessment of fitness for operation for oesophageal malignancy.

Oesophageal cancer is increasing in incidents in the Western world and is now the eighth most common malignancy in the UK. Symptoms: Progressive dysphasia, Weight loss, persistent cough, hoarse voice, Indigestion, haemoptysis. Difficulty in swallowing leads to a higher risk of aspiration pneumonia, particularly at night. Metastasis may cause swollen lymph nodes, hepatomegally and ascites. Typically the squamous epithelium Of the normal oesophagus becomes columnar (Barrett's oesophagus) in response to chronic inflammation (gourds, smoking, alcohol abuse). Typical patients are middle-aged and mail with a history of Barrett's oesophagus/GOR D therefore developing oesophageal adeno-carcinoma. Other risk factors include obesity, high dietary fat, smoking (weakens the oesophagogastric sphincter), alcohol, male Caucasian. Investigations: upper GI endoscopy and biopsy alongside a staging CT. And endoscopic ultrasound can assess the invasion of adjacent structures predicting resectability. Staging is by the TNM system. Treatment: Treatment may be to cure or for palliation. Surgery offers the greatest opportunity for cure Removing all macroscopic tumour and bringing the stomach proximally to bridge the gap - but only one third of patients have a resectable tumour at presentation (presentation is often late with metastases). There is no role for palliative surgery. Chemotherapy alongside surgery is the standard for patients with advanced but potentially curable cancer when I chemotherapy is used to shrink the mass to enable resection. Palliative treatment: repeated dilatations, oesophageal stenting, tumour ablation with laser or argon beam, chemotherapy, radiotherapy - the aim is to relieve dysphasia. Radiotherapy can be performed externally or using brachytherapy within the lumen of the oesophagus. Prognosis: palliative patients die in an average of four months, prognosis even for treatable cancers is poor.

PORTAL VENOUS HYPERTENSION - Outline the treatment methods available for bleeding oesophageal varices

Oesophageal varices are dilating submucosal veins in the lower third of the oesophagus as a result of portal venous hypertension. The oesophagus drains Its Blood in Part to the Superior Vena Cava, with the rest draining to the hepatic portal vein via the gastric venous system - it is congestion here that leads to varices. Diagnosed with endoscopy, medical prevention with reduction of portal hypertension is ideal. prior to bleeding medical management combined with endoscopic banding and regular endoscopic monitoring is required. Management:if ruptured emergency management involves ABCDE assessment, fluid resuscitation, balloon tamponade and endoscopic banding or sclerotherapy to stop the bleeding.

Interpret the ECG in suspected acute coronary syndromes and integrate interpretation with other relevant investigations

One small square = 0.04seconds One large square = 0.2seconds Five large squares = 1second 1. RATE = 300/number big squares R-R. Or, as a standard strip is 10secs, the number of complexes x6. Think tachy v bradycardia. 2. RHYTHM = are there P waves? does every P have a qrs? R-R intervals (regular?). Think fibrilation if irreular. 3. AXIS = compair lead I and III. A normal axis has the overall waveform as positive in both. If I is negative then the electrical activity is flowing to III and there is a right axis deviation. If III is negative then the electrical activity is flowing to the left and there is left axis deviation. 4. WAVEFORM (a) P WAVES = sinus rhythm? (b) PR interval = heart block if long, Wolf parkinson white if short and upsloaping. A normal interval is 3-5 small squares. (c) QRS = >3small squares means the complex is ventricular (not supra-ventricular) (d) ST = elevated more than one square or depressed more than 1/2 indicating MI or previous MI. (e) T = may be tented with hyperkalaemia or inverted with smoking/anxiety/BBB/WPW.

IMMUMOLOGY - Outline the principles, benefits and risks of immunisation

PASSIVE IMMUNISATION: injecting preformed antibodies to provide rapids protection for a short period of time (hepatitis, varicella-zoster, tetanus rabies). ACTIVE IMMUNISATION: triggering the body's own immune response with alive or dead vaccines. Live vaccines (measles, mumps, rubella, BCG) have reduced virulence and give a long-lasting immunity with a single dose although cannot be given to immune compromised patients. Dead vaccines (rabies, hepatitis) have no risk of causing disease but more doses are required. Vaccine contraindications include acute illness, allergic reactions. Live vaccines cannot be given to pregnant or immunodeficient patients. Vaccines may not work in patients on antibiotics or other medications and must be correctly spaced several weeks apart or administer the same time.

Describe the characteristic, and contrasting, features of chest pain resulting from PLEURAL DISEASE, OESOPHAGEAL DISEASE Describe the characteristic, and contrasting, features of chest pain resulting from MSK DISEASE

PLEURAL: This is often heavily related to respiration. There may be end expiratory crackles characteristic of fibrosis. OESOPHAGEAL: This can closely mimic anginaand may even be induced by exercise. Chest pain is also related to posture and eating (unlike in angina) and may be present with dysphagia and interscapular radiation. MSK: This is common and variable in site and intensity. Pain often varies with posture or movement and there may be localised tenderness. Think arthritis, chostochondritis, soft tissue injury, muscle strain.

NEURO-ONCOLOGY - Explain the term paraneoplastic syndrome, and describe two paraneoplastic syndromes involving the nervous system

Paraneoplastic disorders are a rare Set of symptoms or signs that, instead of being because of the Mass effect of a tumour, are because of hormonal, Cytokine or immune responses to the cancer. Consider paraneoplastic disorders in four categories: ENDOCRINE (SIADH, Cushing's, hypoglycaemia, hypercalcaemia etc) NEUROLOGICAL: Paraneoplastic syndrome can cause autoimmune muscle weakness (Lambert Eaton myasthenia), Cerebellar degeneration, encephalitis, ataxia, polymyositis. HAEMATOLOGICAL (Polycythaemia, granulocytosis) MUCOCUTAINEOUS (acanthosis nigricans, dermatomyositis)

VASCULAR TRAUMA - In a patient with recent trauma, outline the physical findings and diagnostic plan for suspected arterial injury together with indications for radiological investigation in the extremities. Differentiate the pathophysiology, findings and treatment in common types of arterial injury.

Penetrating or blunt trauma can risk life and limb or result in permenant neuroascular trauma. Particularly high risk areas are the anterior upper arm where the axillary and brachial vessels are superficial and there are fewer collaterals to the arm. In the lower limb the inguinal and poplyteal areas are high risk for similar reasons. Findings: A history of trauma (gunshot, fraacture etc - usually not hand guns or knives). The patient may be at risk of exanguinating and may be shocked. BP at the site may be lowered, CT angiography can be used to plan a surgery, doppler identifies pulses, Management: ABC approach, tourniquet the limb, apply pressure, reduce any fractures. Typically patients with the following signs require surgical intervention (suturin, ebolisation): pulsatile haemorrhage/haematoma, absent distal pulses or signs of limb ischaemia (pain, pulseless, palour, paraesthesia, Poikilothermia, paralysis). If there is an adequate collateral supply ligation of a severed artery may be sufficient to treat. If not revascularisation by a vascular surgeon may involve grafting.

Discuss smoking cessation methods

Placebo/will alone has a 2% chance of abstinence at 6months. This percentage is increased by 1% with self help materials, 2% with opportunistic advice, 4-7% with face to face specialist advice, 5-12% nicotine replacement therapy with behavioural support, 9 with buproprion. NICOTINE REPLACEMENT THERAPY - nicotine acts on the CNS to cause unpleasant cravings when cessation is attempted. BUPROPRION - An atypical antidepressant that reduces cravings. VARENICLINE - nicotine receptor partial agonist therefore stimulating nicotine receptors to reduce cravings.

VENOUS THROMBO-EMBOLIC DISEASE - Describe the pathophysiology of chronic venous insufficiency and the post-phlebitic syndrome. Describe the range of clinical presentation and associated pathology of pulmonary embolic disease.

Post-thrombotic syndrome: damage of the venous valves after thrombus causing persistent leg swelling, heaviness, discolouration. It can even result in ulceration around the medial Malleolus. Chronic venous insufficiency:Whereby the veins are inadequately pumping blood back to the heart. This results in oedema, ulceration, varicose veins (If reflux is superficial). Unlike post-thrombotic syndrome the veins had not previously been damaged by a clot.Legs become itchy and pigmented, More prone to eczema and ulcers. Pulmonary embolic disease: Arterial blockage in the lung typically from a deep vein thrombosis(Other causes include air, nitrogen, amniotic fluid, fat from marrow, And drugs). 90% of patients have risk factor (surgery, pregnancy, COPD, fracture, varicose veins, malignancy, inability, trauma). Investigate with x-ray (excludes pneumonia pneumothorax) but maybe normal, oxygen saturation (low), ECG (exclude to tackle pericarditis), blood gas reveals type on respiratory failure and metabolic acidosis if massive. D dimer is markedly raised (this is not specific). The definitive test is CT pulmonary angiography (avoid in renal failure), ventilation perfusion scan may be used if you wish to avoid excessive exposure. If there is a massive PE there will be acute dilatation of the right heart. Management of the PE: oxygen, fluids to treat any shock, pain relief, anticoagulation (heparin, minimum five days) then put them on warfarin for the next 3 months If there is a cause but possible lifelong treatment for those with repeated emboli. Do not discontinue the heparin until INR is two or more. D dimer may a remain elevated, especially with post thrombotic syndrome. Thrombolysis (streptokinase) is only indicated in a massive PE Accompanied by cardiogenic shock. Screen patients for bleeding risk and risk of intracranial haemorrhage. Surgical pulmonary embolectomy can be considered in massive PE but mortality rates are high. In patients who cannot take heparin or warfarin vena cava filters can be considered.

HEPATITIS - Describe the features of liver damage resulting from drug therapy and paracetamol overdose.

Presentation: initially patients may be asymptomatic or present with abdominal pain and vomiting. in time, liver failure will develop with acidosis, hypoglycaemia, enephalopathy and coagulation problems. Liver damage does not occur because of paraseptal itself but because of one of its metabolites NAPQI. NAPQI is fine in small doses because glutathione simply clears it. However, the glutathione pathway (a natural antioxidant) becomes saturated meaning the NAPQI becomes directly hepatotoxic. Management therefore relies upon removing the parasexual (activated charcoal) and replacing glutathione (N-acetyl-L-cysteine is a precursor for glutathione). Often liver transplant is required.

MYOPATHIES - Describe the nature of primary diseases of muscle Outline the pathology and causation of the main muscular diseases Outline basic investigations that may be performed in the investigation of a suspected myopathy. Outline the assessment investigation and differential diagnosis of a patient with muscle weakness distinguishing between neurogenic and myopathic causes Outline the management of a patient with impaired motor function.

Primary diseases of muscle and their management: HEREDITARY myopathies: Duchenne muscular dystrophy is an ex-linked recessive absence of dystrophen so patients progressively weaken, Presenting around four years old, wheelchair-bound by 10 years, dead by 20 of respiratory failure. There may be seen hypertrophy of the calves due to lipidique position. Dower's sign positive, diagnosis made by grossly elevated creatinine kinase and DNA examination. Steroids provide short-term improvements. Becker's muscular dystrophy is similar but less severe as the X linked mutation leads to altered but not absent dystrophen. Symptoms begin in the first decades or later, walking continues till early adult life, death is often by cardiomyopathy and arrhythmias. MYOTONIC DISORDERS: myotonic dystrophy is the commonest adult muscle disease, showing anticipation it is a triplet repeat. METABOLIC MYOTONIAS : if they affect ATP. Or periodic myopathies seen with potassium fluctuations (high or low can cause paralysis). Polymyositis/dermatomyositis: INFLAMMATORY myopathies associated with connective tissue disease and possible underlying cancer (dermatomyositis in adults). Patients in their fourth or fifth decades develop proximal muscle weaknessAnd possible skin changes (heliotrope rash, nail fold haemorrhages, photosensitivity and gottrons papules). As this is an inflammatory myopathy ESR and creatinine kinase are raised and biopsy shows necrosis and inflammatory infiltrate. You must investigate for an underlying cancer and treatment involves immunosuppression and corticosteroids. Inclusion polymyositis:The commonest cause of muscle disease over the age of 50, typically a man with weakness and wasting of the flexors in the fore arm so he struggles to grasp objects. Oesophagus can become involved. Muscle biopsy shows inclusions in the muscle fibres enter the name. There is no definitive treatment and death from respiratory compromise occurs. Electrolyte/endocrine myopathies: Thyrotoxicosis, Cushing's, low potassium, vitamin D deficiency can all cause proximal muscle weakness. Drug induced myopathies: Statins may cause rhabdomyolysis, steroids can induce myopathy as can antimalarial is and HIV treatment. Management is to stop the drug. Paraneoplastic myopathy: Widespread malignancy can cause myopathy. Critical illness myopathy:Ventilated patients can develop myopathy presenting as an inability to wean off the ventilator possibly because of prolonged use of paralysing agents. General features: weakness (the distribution may indicate the pathology), Changes in tone (usually hypotonia), wasting of the muscle (enlargement can also occur as a result over activity or as an early sign prior to wasting because of the infiltration of muscle by fats - Pseudo hypertrophy), Myotonia (contraction during attempted relaxation - seen with myotonic dystrophy, hyperkalemic paralysis and congenital myotonia) (remember that fasciculations are typically due to a neuronal problem and not myopathy). Pain is a rare complaint of primary muscle disease except if there is a severe inflammatory problem (for example rhabdomyolysis which can change the colour of urine). Investigations: Consider milestones in childhood, creatinine kinase (raised in muscular dystrophy is), electrodynogram, muscle biopsy, MRI and genetic testing. Differential diagnosis: Lower motor neurone diseases can cause wasting and fasciculations.

HAEMOSTASIS - Describe the laboratory tests to assess the clotting system and recognise and interpret patterns of abnormality

Prothrombin time is the time it takes for blood to clot after adding calcium and thromboplastin as an indication of the extrinsic pathway. It is normally 17 seconds but is prolonged with abnormalities with factor one, two, five, seven or 10, liver disease or on warfarin (1972). International normalised ratio is the ratio of the patient's prothrombin time compares to a normal control. It should be one, aim for two - three in warfarin dosing. Bleeding time is the time taken to clocked in vivo, rarely used. Thrombin time is the time taken to clot after adding thrombin. Normal is 12 seconds, prolonged in fibrinogen deficiency or with heparin. Activated partial thromboplastin time is performed by adding a surface activator, phospholipid and calcium to test the intrinsic pathway. Normal activated partial thromboplastin time is 40 seconds and tests for deficiencies in the inhibitors of clotting factors (but not factor seven).

CHRONIC PERIPHERAL ARTERIAL DISEASE - Describe the clinical presentation, investigation and management of renal artery stenosis. List the surgically or radiologically curable causes of hypertension.

RENAL Artery stenosis: (Low blood supply to the kidney activates the Renee and angiotensin aldosterone system causing severe hypertension) Presentation - Hypertension (Therefore likely asymptomatic), Decreased kidney function and possible flash (rapid) pulmonary oedema. Investigations - Doppler of the renal arteries (narrowed, possible audible bruit). The gold standard is of course an angiogram. Captopril challenge test Involves giving captopril/ACE inhibitor and measuring its effect on renin (The ace inhibitor will lower blood pressure, kidneys become severely hyperoperfused and the result is an excessive increase in renin If there is a renal artery stenosis. Cause/Management - The cause is typically Atherosclerosis so look for the risk factors and modify them (Fibromuscular dysplasia is a rarer cause, a Non-atherosclerotic, non-inflammatory disease of blood vessels that causes overgrowth In the artery walls - If found, it needs stenting). In general though, Medical management is with aggressive blood pressure control Until angioplasty and stenting is indicated. Curable causes of hypertension: Renal artery stenosis, phaeochromocytoma, Cushing's disease, coarction of the aorta, Hyperthyroidism, hyperparathyroidism, Hyperaldosteronism.

MISCELLANEOUS HAEMATOLOGY - Describe the management of a splenectomised patient.

Reasons: trauma, hypersplenism, autoimmune haemolysis. The spleen filters out red blood cells and is a reservoir for lymphocytes. Without it the main problem is a lifelong increased risk of infection. The spleen contains macrophages to phagocytose and filter bacteria especially encapsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis). Management: mobilise soon after the operation as patients will have a transient increase in platelets increasing the risk of thrombus, immunise (pneumococcal, haemophylus influenza, meningococcus and influenza). Patients need lifelong prophylactic oral antibiotics such as erythromycin or penicillin, alert cards, urgent hospital admission if infections develop, warnings of increased risk of malaria and advice to seek medical attention in any sign of infection.

OBSTRUCTIVE AND NEOPLASTIC CONDITIONS OF THE KIDNEY AND URETER - Describe the presenting clinical features of renal cell carcinoma, Wilm's tumour, transitional cell carcinoma or the renal pelvis and renal cysts. Outline the natural history of each together with the main options used in management.

Renal cell carcinoma: Responsible for 90% of kidney cancers in adults-An adeno-carcinoma originating in the proximal convoluted tubule. Patients typically present with advanced disease complaining of symptoms such as blood in the urine, loin pain, Weight loss, fever, feeling generally unwell, night sweats and high blood pressure (Increased renin) with an abdominal mass noticed by the doctor. As it is relatively resistant to radio and chemotherapy excision is the best option. Cancer can metastasise to the lymph nodes, lungs, liver, brain, bone may cause paraneoplastic symptoms such as anaemia/thrombocytopaenia from low/high EPO or high serum calcium (Is the kidney's job to excrete calcium). Renal cell carcinoma is associated with smoking, occupational exposure, hypertension And NSAIDs with some people having a genetic link. Wilms' tumour: a childhood nephroblastomata with a 90% survival rate usually presenting as an abdominal mass. The mass may or may not be painful and associated with hypertension (increased renamed secretion), haematuria, fever and vomiting. It is a highly vascular tumour that is typically unilateral and if it metastasises it will go to the lungs. In the event of rupture the patient is at risk of exsanguination into the abdomen. CT is used to stage a nephroblastomata/Wilms' tumour. Stage one is confined to the kidney therefore easily resected, stage II is not confined to the kidney and has locally spreads, stage III is spread via lymph nodes, stage IV has spread via blood and stage V is bilateral. Treatment is primarily by surgical removal. Transitional cell carcinoma: the most common type bladder cancer, second most common type of ureter cancer and a common type of kidney cancer. It comes from transitional cells and is often described as a creeping tumour as it moves both distally and proximally. The symptoms depend upon the location - with bladder cancer they include haematuria, frequency and dysuria. The most significant causes are smoking and chemical/radiation exposure. Transitional cell carcinoma is difficult to treat requiring accurate staging. Chemotherapy is common as is transurethral resection of the bladder, early tumours may be treated with BCG infusions (risk of TB) to reduce recurrence and muscular invasion necessitate radical excision. Bowel loops can be used to recreate the bladder. Renal cysts: fluid filled pouches within the kidney caused when the services of the kidney forms a diverticulum. Most are simple and do not cause symptoms although if kidney cysts grow large enough they may cause loin pain, fever and backache. Cysts can become infected, burst or cause urinary obstruction leaving to hydronephrosis. If the cyst is causing symptoms or altering kidney function treatments available include: drainage (then refilling the cyst with an alcohol to prevent re-formation), surgical removal endoscopically. However, many cysts are best left alone.

CARCINOMA OF THE COLON, RECTUM AND ANUS - Describe the aetiology, morphology and pathology of carcinoma of the large bowel. Describe the natural history of carcinomas affecting the large bowel. Describe Dukes and TNM staging systems. Discuss the frequency of each according to location of the carcinoma, particularly with rectal and carcinoma of the caecum. Identify the pathological differences between colorectal and anal cancer. Identify the common symptoms and signs of carcinoma of the colon, rectum and anus. List the clinical features that would raise suspicion of a carcinoma and indicate urgent patient referral. Discuss appropriate laboratory tests, radiological studies and endoscopic investigations to investigate a patient with a suspected colonic or rectal carcinoma. Outline the treatment of carcinoma of the colon, rectum and anus and define appropriate resection levels according to lymphatic drainage. Outline the management of carcinoma of the anus and contrast it to management of colorectal carcinoma. Discuss follow up recurrence and metachronous tumours. Outline management of an obstructing colonic cancer.

Risk Factors: Age, African-american, Adenometous polyps, IBD, family history, sedentary lifestyle, low fibre/high fat diet, diabetes, obesity, smoking, alcohol, previous radiation. Cause: Typically unknown ADENOCARCINOMAS, although there may be genetic or pre-cancerous conditions such as certain types of polyps TNM: T = Depth of invasion N = Nodes M = Metastisis Dukes: The staging of colon cancer. Stage A = confined to the mucosa and sub-mucosa, 90% 5 year survival. Stage B = Invasion through the bowel wall into the surrounding tissues but with no nodal spread, 60% 5 year survival Stage C = Lymph node spread, 30% 5 year survival. Stage D = distant spread - 5/10% 5 year survival Location: Right sided present later with a mass or anaemia and a less likely to cause obstruction because the contents is still liquid. On the Left hand side there is early presentation with obstruction and a change in bowel habit. Rectal tumours present with tenesmus (constant need to take a shit). Investigations: PR, sigmoidoscopy, FBC, U&E, LFTs, Carcinoembyronic antigen. Barium enema shows an applecore stricture (IBD or colon cancer) and CT to stage and screen for metastasises (liver) Presentation: The following features necessitate urgent referral - Change in bowel habit, Blood PR, Mucus PR, Weight loss, Anorexia, Abdominal pain COLON - Change in bowel habit, abdominal cramps, fatigue, weight loss, PR bleed. RECTUM - Tenesmus ANUS - Pain or pressure in the anus, change in bowel habits, lump near the anus, rectal bleeding (can be severe), itching, discharge. Management: Right sided = right hemicolectomy Transverse = extended right hemicolectomy Descending = left hemicolectomy Particular attention is played to the blood supply of the tumour so that the bowel can only really be removed if the 2 anastamosis. Rectum = anterior resection connecting the colon to the rectal stump. Systemic chemotheray by 5-fluorouracil and levamisole decreases the reoccurance. Never use radiotherapy in colon cancer. Resection must also include the corresponding lymphatic basin. Lymphatic drainage from the entire colon and proximal two-thirds of the rectum is to the paraaortic lymph nodes that then drain into the cisterna chyli. The lymph from the remaining rectum and anus can either follow the same route, or drain to the internal iliac and superficial inguinal nodes. The pectinate line only roughly marks this transition Obstruction is managed: Resection, palliative stenting. Metachronus tumours: With colon cancer you may find lesions separate to the original tumour occurring synchronously.

EVIDENCE BASED MEDICINE - Describe the sources of bias that can arise in studies of disease prevalence, incidence and prognosis Describe the different types of bias that can influence trial results and their interpretation, and the problems of small trials and publication bias.

SELECTION bias is a bias when choosing participants DETECTION bias is when you're more likely to look for a disease in a certain population FUNDING bias is having results that favour a financial sponsor REPORTING bias is when you do not report all the statistics ATTRITION bias is loss to follow up RECALL bias - variable ability of participants to remember what you're asking them OBSERVER bias is unconscious influences by the researcher

EVIDENCE BASED MEDICINE - Define sensitivity, specificity, predictive value and likelihood ratio, and discuss their inter-relationships, the effect of changes in disease prevalence, and the effects of combining tests in series or in parallel

SENSITIVITY - the number of tests that come back positive and are truly positive. Meaning that if the test is negative you are highly likely to not have the disease. SNOUT - sensitivity rules things out. SPECIFICITY - the number of tests that come back negative that are actually negative. Meaning if the test is positive you are likely to have the disease. SPIN - specificity rules things in. POSITIVE PREDICTIVE VALUE - Number of positive test results that are true positives, high results mean that the statistic is accurate. The result depends on both the test and the population disease prevalence. NEGATIVE PREDICTIVE VALUE - Number of negative test results that are true negatives , high results mean that the statistic is accurate. The result depends on both the test and the population disease prevalence.

SIRS? Sepsis? Septic shock?

SIRS (systemic inflamatory response syndrome (two or more of...) = Resp rate >20, Heart rate > 90, WBC >12/<4 x10^9, temp >38 <36. SEPSIS = SIRS plus signs of infection. Septic shock = sepsis with evidence of organ failure or hypotension. Soooo.....start the septic six. 3in: IV antibiotics, oxygen, fluids. 3out: Catheter, blood cultures, lactate/ABG.

PREOPERATIVE ASSESSMENT - Specify appropriate starvation times for food and clear fluids

STARVATION: Previously 12 or more hours to reduce the risk of aspiration pneumonitis at induction, it is now acceptable to use the 2-6 and 2-4-6 rules. In adults, 2 hours for water, 6 hours for food and other fluids. In children, 2 hours for water, 4 hours for breast milk, 6 hours for everything else

EMERGENCY MEDICINE

See immediate life-support book and re-read. Reread guidelines within book.

VASOSPASTIC DISORDERS - List the underlying diseases or disorders associated with vasospastic changes in the extremities. Specify and explain the defining clinical characteristics of Raynaud's disease or phenomenon. List the clinical and investigational features that may distinguish primary from secondary Raynaud's disease. List the laboratory investigations used to assess vasospastic disorders and describe the medical and surgical approaches.

Spasmodic tonic contractions of blood vessels without disease of the vessel wall itself (although late stage chronic disease can lead to thickening and fibrosis of the arteries and ischaemia of the digits). Diseases include: scleroderma/CREST, raynauds, levido reticularis (spasm of venules), arocyanosis (cosmetic blue discoloration of the hands and feet due to arteriolar spasm and sweating due to venous dilation. May become an emergency acutely in the cold leading to frostbite). Raynauds: Vasospasm from hyperactivation of the sympathetic nervous system causing dec bloodflow due to triggers (cold, emotion). Raynauds phenomenom is a symptom (discomfort) plus a sign (discolouration) but raynauds disease is a diagnosis. Raynauds disease is primary (idiopathic, young woman, worsened by caffeine and smoking) or secondary (to connective tissue disorders - lupus/CREST/RA/Sjogrens/dermatomyositis, trauma/jackhammer!, drugs - beta blockers). Features: On exposure to cold extremities become pale, cold ad numb. When O2 is depleted they become cyanotic/blue. On rewarming they become hyperaemic, red and painful with swelling and pins and needles. Investigations: A digital artery pressure decrease of 15mmHg is diagnostic. Doppler ultrasound confirms reduced flow. FBC may reveal anaemia of chronic disease, exclude hypothyroidism, check lupus and RA antibodies/factors. Management: Trigger avoidance, avoiding sympathomimetics, smoking cessation. Drugs include vasodilators (Ca2+ channel blockers), topical nitrates (losartan), symatholytics (alpha blocker prazosin). Surgical options include botox or sympathectomy.

SUBARACHNOID HAEMORRHAGE -Describe the clinical presentation of a subarachnoid haemorrhage, with specific reference to features in the history and examination including the rate of onset of symptoms, and signs arising from the event Describe the vascular abnormalities which may predispose a patient to developing a subarachnoid haemorrhage. Explain how one may investigate a suspected subarachnoid haemorrhage within the acute setting. Describe the acute management of the subarachnoid haemorrhage, including referral to the appropriate specialty, and management of electrolytes, glucose and blood pressure. List the potential complications of a subarachnoid haemorrhage.

Spontaneous arterial bleeding into the subarachnoid space. Remember that family history, smoking and hypertension are important risk factors to be controlled. Subarachnoid haemorrhage has a prognosis of 50% with 30% of survivors having major neurological deficits and a significant risk of rebleeding in the next two weeks. Presentation: Severe thunderclap headache (there may be minor warning headaches), transient or prolonged loss of consciousness, seizures can occur, nausea and vomiting due to raised intracranial pressure, drowsiness, coma, many injured and after 3 to 12 hours, papilloedema and other signs of raised intracranial pressure. Vascular abnormalities:The cause is typically an intracranial/berry aneurysm although arteriovenous malformations and bleeding into the basal cisterns (Where the arachnoid crosses to lobes) Is also possible. Investigations: CT scan the head and perform a lumbar puncture which will confirm a bleed if there is evidence of xanthochromia (remember that raised intracranial pressure is contraindication for LP). Angiograms can localise any aneurysms or arteriovenous malformations. Management: Immediate supportive care, observations, fluid replacement and calcium channel blockers to reduce the risk of delayed ischaemia secondary to vasospasm. After angiography clipping or coiling of an aneurysm or surgery of an arteriovenous malformation is definitive treatment. Complications: Rebleeds within two weeks are common, 50% die and there is a significant risk from raised intracranial pressure. 30% of survivors are left with neurological deficits.

Describe the clinical staging of breast carcinoma. Outline the current results (survival and recurrence rates) of treated breast cancer according to clinical stage.

Stage I: Tumor <2cm, no nodes therefore 96% survival. Stage 2. Tumor 2-5cm, mobile axillary nodes. 81% survival. Stage 3. Fixation to chest wall and/or fixed axillary lymph nodes. 52% survival. Stage 4. Metastasis. 18% survival. Reccurence rates are higher for higher stages, larger tumors and oestrogen receptor negative tumors (as we have lots of therapies that target the oestrogen receptor)

STATUS EPILEPTICUS - Define status epilepticus and describe initial investigations and components of Management, including airway protection; use of anticonvulsants

Status epilepticus: A seizure that lasts more than five minutes or more than one seizure within five minutes without the patient returning to normal state. The seizure cannot be an absence or complex partial seizure. Typically it is tonic clonic - a convulsive status epilepticus. This may occur with a history of epilepsy or alongside trauma/infection/stroke. Investigations/Management: Immediate management is with an ABC approach to secure the airway,Hi flow oxygen, cardio and respiratory assessment, blood glucose cheque and insertion of a wide bore cannula. FOR CONVULSIVE/TONIC CLONIC: Give IV lorazepam or bucal Medazolam - Up to a maximum of two doses. If seizures continue gave intravenous Phenytoin. It is also possible to give IV valproate. FOR NON CONVULSIVE: This is less severe, more often requiring treatment of the underlying condition (Pabirinex/thiamine for alcohol withdrawal or glucose).

HEADACHE - Describe features of the clinical presentation of a headache that might raise concern about a more sinister pathology, listing, in each case the relevant differentials and appropriate investigations including headache of Subarachnoid haemorrhage (see stroke/ cerebrovascular disease), Meningitis/Encephalitis (see CNS infection), and Raised Intracranial Pressure

Subarachnoid haemorrhage: Sudden, thunder clap headache that may be rapidly fatal due to rupture of a berry aneurysm.This requires a lumbar puncture (xanthochromia) after a CT head Has excluded raised intracranial pressure and indicated a possible bleed. Meningitis/Encephalitis: Associated with signs of meningism including photophobia and symptoms indicative of infection. This requires a lumbar puncture And empirical antibiotic treatment (ceftriaxone/cefutaxime). Raised ICP: This particular headache is a generalised ache that is aggravated by bending, coughing, straining/anything That raises intracranial pressure. Typically the headache is worse in the morning and may wake the patient up. It gradually progresses and is often accompanied by vomiting, visual disturbances, neurological signs, papilloedema. There is a risk of herniation of the tonsils through the foramen magnum referred to as coning. Urgent imaging of the brain with CT is essential as this may identify a space occupying lesion.

List and discuss the treatment options for breast cancer. Describe the rationale for adjuvant radiotherapy, chemotherapy, hormonal therapy and biological therapy in the treatment of breast cancer.

Surgery is the mainstay of treatment. Lumpectomy = only tumor removed. Masectomy = Breast removed Often lymph node sampling is standard. Adjunct radiotherapy helps reduce the risk of local recurrence. Adjunct chemotherapy reduces the overall recurrence rate - used if the risk of recurrence is high as in large oestrogen receptor negative tumors. Adjunct hormonal therapy (Eg. tamoxifen is an oestrogen receptor blocker) improves overall survical but is only relevant in patients whose cancer has oestrogen receptors. Those who are premenopausal with a large oetrogen receptor positive cancer may require tamoxifen plus a leutinizing hormone receptor blocker (useless if postmenopausal). NB. stopping oestrogen stops growth of the tumor but is not likely to shrink like biologicals do. Aromataze inhibitors (aromataze produces all the oestrogen in post menopausal women but a negligable amount in premenopausal). Aromatze inhibitors are therefore used in postmenopausal women with oestrogen receptor positive tumors. Also available are biological treatments such as Herceptin used as a monoclonal antibody against HER2 (therefore only used if HER2 positive). HER receptors ordinarily stimulate uncntrollable growth so their blockade stops cancer growing and has a proteolytic effect that may cause tumor shrinkage.

HYPERTHYROIDISM - Describe the classical symptoms of hyperthyroidism and the typical examination findings. Classify the causes of hyperthyroidism and outline the pathological features of Graves' disease, toxic adenoma and toxic multinodular goiter Discuss medical therapy for hyperthyroidism. Discuss the indications for surgical treatment and the risks of post-operative complications. Discuss the indications for and complications of radioactive iodine therapy.

Symptoms: Weight loss, insomnia, heat intolerance, sweating, nervousness, palpitations, increased frequency of bowel movements and lighter periods. Examination: Tachycardia, tremor, irritability, weight loss, hair loss, hyperglycaemia. Thyroid synctigraphy can show the uptake of iodine - identifying hot spots such as a toxic adenoma. Cause: Typically Graves Graves' disease: TSH receptor activating autoantibodies. Toxic adenoma: A thyroid hormone producing tumor of the thyroid gland. Toxic multinodular goitre: Multinodular expansion of the thyroid gland secreting excess thyroid hormone independent of TSH. Treatment of hyperthyroidism: Propranalol provides initial symptomatic relief. Carbimazole or propylthiouracil are tablets to suppress thyroxine. Other options are radioactive iodine-131 or surgical removal. Complications of treatment: Hypothyroidism is common requiring life long thyroid replacement.

IRRITABLE BOWEL SYNDROME - Describe symptoms that may suggest a diagnosis of IBS. Outline current theories regarding the pathophysiology of IBS. Discuss possible investigations and outline therapeutic approaches.

Symptoms: chronic abdominal pain, bloating, discomfort and altered bowel habits. Diarrhoea or constipation can predominate or alternate. Oncet should be less than 50 years old in the absence of b bloody stool and weight loss. Theories on cause: it is a functional disorder with no known cause of a theories include: a disorder of the gut - brain axis leading to excessive mast cell activation. it may be postinfectious or after a stressful life event and can represent an alteration in bowel flora which causes inflammation. Investigations: all come back negative, but it is important to rule out key differentials such as coeliac disease, lactose intolerance and parasitic infections. the former stool microscopy, blood tests, abdominal ultrasound (looking for gallstones), H. pylori testing and possible endoscopy/biopsy (2 excludes irritable bowel disease, celiac's and/or malignancy). Management: education, diet high in soluble fibres, antidepressant therapy, Antispasmodic agents, laxatives and antidiarrhoeals, avoiding trigger foods, avoiding proton pump inhibitors which can alter the gut flora, psychological therapies and stress relief techniques. Some may find probiotics useful. Ultimately, reassurance is required that this is not the most serious conditions such as irritable bowel disease or malignancy.

HAEMOSTASIS -Outline the clinical features of disseminated intravascular coagulation including laboratory tests used in diagnosis

Systemic activation of the coagulation pathways resulting in widespread fibrin clots causing organ failure and simultaneous depletion of clotting factors and platelets resulting in bleeding. Causes include infection, sepsis, trauma, malignancy, severe liver failure, pancreatitis, Burns, vascular abnormalities, toxins, transfusion reactions, obstetric (amniotic fluid embolism, pre-eclampsia). Features: bruising, bleeding and renal failure (as well as other organ failure due to clots). Investigations: platelets, fibrinogen, clotting studies, indeed I'm a and a blood film which shows broken red blood cells. Treatment: treat the cause, replace the platelets, cryoprecipitate, fresh frozen plasma to replace coagulation factors and give proteins C. Heparin is controversial.

PREOPERATIVE ASSESSMENT - Describe the role of the anaesthetist in: the theatre team; labour suite; the pain team; the critical care (ITU/HDU/outreach) team; the cardiac arrest and trauma team

THEATRE - Inducing anaesthesia, maintaining the airway, monitoring vitals. LABOUR SUITE - Epidurals, general anaesthetic if required. Other pain relief discussions. PAIN TEAM - Discusses options for stronger analgesia CRITICAL CARE/CARDIAC ARREST/TRAUMA TEAM - maintains the airway

THE URETHRA, PENIS AND SCROTUM - Outline the pathological classification of the common tumours of the testis and their biological behaviour. Outline the investigation and management of seminoma and teratoma of the testis.

Testicular caners are rare. If they occur they occur in young men (20-40) and produce beta HCG or alpha fetoprotein that can be used as tumor markers. The main tumors are seminomas and teratomas. More rarely there are leydig cell tumors (these are usually small and benign but secrete oestrogen so present with gynaecomastia). SEMINOMA: from the seminiferous tubules, low grade, if mets occur they are via the lymphatics to the lungs. TERATOMA: from primative germ cells, contain bone/cartilage/hair etc., variable malignancy (high/low grade). Presentation: Painless lump or testicular ache. Leydig cell tumors present with gynaecomastia. Investigations: Testicular ultrasound, alpha fetoprotein, beta HCG, oestradiol levels. Tho adequatly stage the Lungs, luver and retroperitoneal area must be CT'd. Management: Surgical orchidopexy with radiotherapy for seminomas and chemo (cisplatin) for teratomas. Lymph nodes may need to be removed.

CARDIAC SURGERY - Describe the anatomy of the cardiac chambers, valves, coronary arteries, the great arteries and the cardiac conduction system.

The cardiac conduction system: In early diastole the aortic and pulmonary valves close. Mid diastole the aorto-ventricular valves (mitral and tricusped) open and the ventricles fill. End diastole the atria begin to contract. Systole the aorto-ventricular valves close early on then the ventricles contract forcing the aortic and pulmonary valves open to eject the blood from the ventricles. The conduction is lead ny the sinoatrial node from the right atria, then the atrioventricular node which delays the ventricular contraction and the bundle of his which carries the signals to the apex so that the ventricles contract from the bottom up. CARDIAC VASCULATURE: right coronary artery gives the right marginal and posterior descending. It supplies the right atria and ventricle, some of the IV septum and the SA node in 60%. Left coronary artery gives the circumflex, anterior descending and left marginal. It supplies the left atria and ventricle, the SA node in 40% and the AV node.

ASTHMA - Describe the mechanisms of actions of the main drugs used to treat asthma.

The aim of asthma treatment is to maintain good control. Bad control is defined as >2 attacks a week, any limitation of activity, nocturnal wakening or lung function <80% predicted. The stepwise approach to management is as follows (after education, smoking cessation and the avoidance of precipitants. Review technique, adherence and precipitants at each step up): 1. PRN beta-adrenoreceptor agonist bronchodilator (sympathomimetcs that relax the smooth musle of the lungs but contract the cardiac muscle). For patients with symptoms less than one a week and less than two nocturnal episodes per month. Use salbutamol/terbutaline. INHALATOR TECHNIQUE: Remove cap, shake, breath out, tight seal on mouthpiece, simultaneously press and slowly inhail. Hold breath for ten seconds. 2. Add a regular preventer such as an inhaled corticosteroid (beclametasone, budesonide, fluticasone, ciclesonide - supress the inflammatory response) for any patient who needs their reliever more than twice a week, is woken at night by symptoms or has more than two attacks a week. Smoking makes the airways more resistant to steroids so higher doses are needed. 3. Long acting beta2agonist such as salmeterol or formoterol should be added. To make life easier the steroid and LABA can be given in combination inhalers. 4. Increase the dose of steroid or add a fourth drug (leukotriene receptor antagonist, montelukast - blocks leukotrienes resulting in smooth muscle relaxation) or (theophylline - a phosphodiesterase inhibitor that raises cAMP resulting in leukotriene inhibition therefore smooth muscle relaxation). 5. Oral steroid such as regular prednisolone. For long courses consider the risk of osteoporosis (therefore give bisphosphanates). Atopic patients may benifit from omalizumab, a monoclanal antibody against IgE. STEP DOWN once control is established and titrate all steroids to the lowest possible effectiive dose slowly.

HEART VALVE DISEASE - Classify the causes of valvular heart disease and outline the common symptoms and non-invasive assessment.

The disease may cause stenosis or regurgitation best diagnosed on echocardiography. Many patients require review every one to 2 years to ensure that valve disease deterioration is detected before complications (heart failure). The susceptibility to bacterial endocarditis can be reduced by good dental hygiene without the use of routine antibiotics (even during dental procedures). RHEUMATIC HEART DISEASE Acute rheumatic fever: children pick up a strain of group a streptococci to which they developed antigens and have an immune response. The immune mediated response is delayed and the antigens cross-react with cardiac myosin and cause inflammation of the endocardium, myocardium and pericardium as well as joints and skin. Acutely the fever causes anorexia, fever, lethargic and joint pain 2 to 3 weeks after streptococcal pharyngitis. (Think Jones: joints, heart, nodules, erythema marginatum/Red rings, sydenhams chorea). Acute treatment is bedrest, supportive therapy, penicillin to get rid of the Streptococcus, treatment of any heart failure (mitral regurgitation and aortic regurgitation are common), aspirin for the arthritis and steroids for any carditis. Chronic rheumatic fever: half affected by rheumatic fever with carditis will go on to develop mitral Stenosis because of fibrosis.This is a diastolic murmur. PULMONARY VALVE DISEASE Pulmonary stenosis: typically congenital, tetralogy of fallow, ejectione systolic murmur loudest in the left's upper sternum. Loudest on leaning forward and exploration. There may be a right ventricular heave, right ventricular hypertrophy and if severe there should be a balloon valvuloplasty or replacement. Pulmonary regurgitation: a rare diastolic murmur associated with pulmonary hypertension. Had loudest at the left sternal edge and often clinically insignificant. TRICUSPID VALVE DISEASE Tricuspid stenosis: typically from rheumatic fever, a rare diastolic murmur at the right sternal edge associated with a raised JVP and hepatomegally because of right heart failure. Again treats if severe with balloon valvuloplasty Or replacement. Tricuspid regurgitation: seen with right ventricular dilatation, a systolic murmur and signs of right heart failure. Remember ebsteins anomaly Where there is a displaced tricuspid valve that often regurgitates. MITRAL VALVE DISEASE Mitral stenosis: Almost always due to rheumatic fever, causing progressive fibrosis, calcification of the valves, fusion of the cusps and hypertrophy of the left atrium. The murmur is diastolic and there will be significant venous congestion at late stages. Progressive die location of the atrium can also cause atrial fibrillation. Manage with balloon valvuloplasty or valve replacement and treat any pulmonary hypertension. There needs to be anticoagulation if atrial fibrillation as presents. Mitral regurgitation:A pansystolic murmur radiating to the axilla, often due to rheumatic disease, Endocarditis or after valve replacement. Chronic regurgitation causes left atrial dilation. The valve can prolapse because of congenital abnormalities (Marfan's) and may or may not remain competent. This may also happen after myocardial infarction or something else that damages the chordaetendineae. If the onset of mitral regurgitation is acute patients will present with pulmonary oedema, more slowly than regurgitation causes pulmonary hypertension And atrial fibrillation. If mild treat medical a (diuretics, ace inhibitors, atrial fibrillation treatment), if severe, repair the valve or replace it. AORTIC VALVE DISEASE Aortic stenosis:This can be congenital with bicuspid valve that becomes more easily fibrotic in calcified, rheumatic fever or age-related fibrosis and calcification. There is an ejection systolic murmur And left ventricular hypertrophy (patients often develop angina and reduce exercise tolerance). The murmur radiates to the neck and most management is conservative (monitor for heart failure and replace the valve when symptomatic. Aortic regurgitation: Causing left ventricular hypertrophy, breathlessness is often the only symptom. The murmur is diastolic on the left sternal edge during expiration. Treat the underlying condition (endocarditis, syphilis) and replace the valve if the patient is symptomatic. They aortica route may also need replacement with coronary bypass.

ANAEMIA - Discuss the common causes of iron deficiency anaemia

The most common anaemia because of the bodies limited ability to absorb iron and frequent loss in Leeds. Iron itself is abundant but we require it in its Ferrous state (Fe2+). Iron is required for haemoglobin synthesis but there is a latent period whereby normal haemoglobin is maintained for as long as possible after iron stores are depleted. >blood loss (menorrhagia, GI, renal) > Increased demand in growth and pregnancy > Decreased absorption (post gastrectomy) > Poor intake, rare! Symptoms of iron deficiency anaemia: brittle hair, brittle nails, species nails, angular chelitis, glossitis and general symptoms of anaemia.

COPD - Describe the typical history of a patient with COPD including complications and clinical features of acute presentations

The patient, usually a smoker >40yo, initially presents with an increased work of breathing on exercise which progresses to on rest. The breathlessness is progressive and associated with; cough, sputum (haemoptysis in acute exacerbations). Hypercapnia gives morning headaches, CO2 retention flap if severe. Pitting oedema may be present because of cor pulmonalae in late stage COPD, but because of impaired salt and water excretion in early stages. Finger clubbing NEVER happens in COPD. PINK PUFFERS - maintain normal PaCO2 but hyperventilation, BLUE BLOATERS - become hypercapnic early and develop polycythaemia early to compensate. The systemic problems in COPD include: muscle weakness, increased circulatory inflammatory markers, impaired kidney function, weight loss and osteoporosis. Acute exacerbations: increased symptoms often triggered by a viral infection. They may get fluid retention or respiratory failure resulting in death.

TRAUMA - Discuss the basic principles of emergency treatment of haemorrhagic shock; outline steps to be taken in fluid therapy of victims of haemorrhagic shock.

There are 4 categories of haemorrhagic shock (hypovolemic). Think of them as tennis - 15%, 15-30%, 30-40%, >40% blood loss. Managment is good resuscitation with high flow oxygen, crystalloid fluids and clotting factors. Consider the use of blood products.

MISCELLANEOUS HAEMATOLOGY - Outline the clinical features and differential diagnoses of myelofibrosis, polycythaemia rubra vera and essential thrombocythaemia

These are myeloproliferative disorders as a result of proliferation of haemopoietic stem cells in the bone marrow. These cells have the ability to differentiate into platelets, white blood cells or red blood cells. MYELOFIBROSIS is hyperplasia of megakaryocytes (haematopoetic stem cell precursors) leading to fibrosis in the bone marrow, haematopoesis (making blood) in the liver and spleen causing massive hepatiosplenomegaly. Patients with this cancer, a type of chronic leaukaemia present with night sweats, fever, weight loss, abdominal pain (due to a large spleen) and symptoms of bone marrow failure. POLYCYTHAEMIA RUBRA VERA is another cancer whereby there is access proliferation of red blood cell precursor is in the bone marrow. White blood cells and platelets can also accumulate leading to hyper viscosity. Patients are typically older than 60 and asymptomatic or with vague signs of increased viscosity (headache, dizziness, to assess, visual disturbance, itching), splenomegaly, gout and possible deep vein thrombosis. ESSENTIAL THROMBOCYTHAEMIA: another malignancy in which excessive proliferation of precursor cells leads to persistently raised platelets that function abnormally. Patients therefore have bleeding or thrombosis and microvascular occlusion problems. They present with headaches, chest pain, lightheadedness and hypovolaemic inflamed limbs (erythromelalgia).

OESOPHAGUS - List the anatomical and physiological factors predisposing to gastrooesophageal disease. Define hiatus hernia with regard to anatomical type (sliding and paraoesophageal).

Think: smoking cessation, weight loss, avoiding spicy foods. Reflux causes barrats/metaplasia. Hiatus hernia: protrusion of a viscus or part of one through the walls of its containing cavity into an abnormal position. It causes good and is a great mimic......sob due to irritated diaphragm, dysphasia, heart palpitations due to irritation of the vagus nerve. In most it is asymptomatic. Risk factors include raised intraabdominal pressure (stress and straining). Diagnosis: endoscopy and manometry. Types: sliding, rolling/paraoesophageal, mixed. Management: lifestyle changes, raised head at night and after meals. Stress reduction techniques, ppis, h2 receptor blockers. Surgery: nissen fumdoplicatin - wrapping the fungus around the lower oesophagus. When the stomach contracts it prevents reflux but the patient is unable to vomit or burp. Complications Include gas bloating, dysphasia, dumping syndrome.

MALABSORBTION - Describe the clinical presentation of malabsorption and outline appropriate investigations. Outline the pathology of malabsorption of key nutrients and consequent presentation and management for each.

This is abnormal uptake of food from the GI tract and can include obesity. Key intake should include fat, carbohydrates, proteins, fluids and the following electrolytes: sodium, chloride, potassium, calcium, vitamins. Malabsorption may be generalised (as in coeliac disease) specific (two particular nutrients). Symptoms vary but can include diarrhoea, weight loss, bloating, flatulence and abdominal cramps. Steatorrhoea is seen with fat malabsorption whereby oily floaty stools are found. non-gastrointestinal side effects may include anaemia, secondary hyperparathyroidism, oedema from low-protein, dermatitis, amenorrhoea, infertility and impotence. Remember muscle cramps from vitamin D/calcium deficiency and bleeding from low vitamin K. Intestinal malabsorption may be due to:mucosal damage, reduced absorption, hydrolysis defects, iron transport defects, pancreatic insufficiency,impaired enterohepatic circulation. 1. Calcium: giving muscle cramps, fatigue, loss of appetite and arrhythmias. Encourage drinking milk and eating yoghurt. 2. Vitamin D: giving fatigue and weakness. Encourage eating milk and fish. 3. Potassium: giving muscle weakness, constipation and Arrythmias. Encourage bananas, treat any excessive loss through diarrhoea and vomiting. 4.Iron: causing anaemia. Encourage beef, or oyasters, beans, lentils and spinach. 5. B12: causing macrocytic anaemia and glossitis. associated with loss of intrinsic factor made by the gastric mucosa or low intake of milk, eggs and meat. 6. Folate: causing macrocytic anaemia, glossitis, angular chelitis. supplements can be taken to reduce the instance of neural tube defects in pregnancy. 7. Magnesium:required for energy production, causing nausea, vomiting, fatigue, Arrythmias and personality changes. Encourage nuts and spinach.

CHEST PAIN - Describe the characteristic, and contrasting, features of chest pain resulting from MYOCARDIAL ISCHAEMIA (angina). ANGINA - Define stable and unstable angina and describe the typical history, risk factors, underlying causes/pathology, relevant investigations and treatments, including their side effects. Outline treatment options of angioplasty or coronary artery bypass grafting. Outline the employment and driving limitations of a diagnosis of angina (and other cardiac disease).

Transient myocardial ischaemia without infarction is angina. It usually represents >50% occlusion from atherosclerosis although it can be due to cardiomyopathy or valve disease. STABLE ANGINA: > Symptoms: central chest pain/discomfort/breathlessness onevertion (or heavy meals, cold, intense emotion, lying flat/decubitus, vivid dreams/nocturnal). > Examination: is often unremarkable although risk factors (hypertension, diabetes, bruits, peripheral vascular disease). >ECG is often normal or shows a previous MI but on exercise there is ST depression showing ischaemia. >Coronary arterography (usually prior to CABG or PCI) <Management: Education, lifestyle interventions (exercise up to not beyond pain to promote collaterals). Identify high risk patients for CABG/PCI with stress testing or arterography as symptoms are a pore indicator of severity. < Asprin 75mg to reduce the risk of MI (or clopidogrel 74mg) Risk of dyspepsia and bleeds. < ANTIANGINA DRUGS: nitrates (slow the heart and dilate vessels but cause headache, hypotension, syncope - use as treatment and exercise prophylaxis), beta blockers (dec heart rate so reduce O2 demand. Cause bronchospasm), calcium channel antagonists (dec heart contractility so slow it and dec oxygen demand but may precipitate heart failure), Potassium channel activators (dilate vessels but do not show tolerance like nitrates. Nicorandal) or If channel antagonists (induced bradycardia). < Convention is GTN plus asprin, statin (to stabilise the plaque) and beta blocker with the later addition of a calcium antagonist or long acting nitrate). Two or more antianginals and still poor control then consider PCI. DRIVING LAWS: DVLA only need to be notified of angina if unstable, a lorry driver, symptoms at rest/emotion/with driving. Do not drive for one week after an angioplasty or four weeks after an MI or CABG. UNSTABLE ANGINA: When angina symptoms are irregular and unpredictable. It is a type of acute coronary syndrome but there is still no myocardial damage. It is usually due to a complex, fissured artheromatous plaque (and can present with or without previous stable angina). > Presents like a nonSTEMI without raised cardiac troponins >Nitrates and aniplatelets needed prior to PCI/CABG.

AMPUTATION - List the types of amputation of the lower limb and contrast their rehabilitation potential List the indications for amputation and discuss the selection of amputation site. Outline the rehabilitation of a patient with a below- or above-knee amputation.

Types: Consider amputations as minor (digits, midfoot) or major. Lower limb amputations can be classified by location: midfoot, ankle disarticulation, below knee, through knee, above knee, hip disarticulation. The ideal is to amputate at the lowest realistic level (if the knee joint is maintained there is better functioning and less energy expenditure)......for vasccular patients this means assessing the extent of ischaemia realistically. Remember the most common cause of amputation is diabetes. Rehabilitation: Prior to the prosthesis a Pneumatic post amputation mobility aid (ppam) may be used to reduce swelling and help with initial rehabilitation. A femurett is an adjustable prosthesis used for training and rehabilitation particularly whilst a personalized prosthesis is being developed. Also remember occupational therapy, home adaptations, psychological support.

CYSTIC FIBROSIS - List the usual organisms causing lung infection.

Typically in childhood infections are due to Staph aureus and haemophylis influenzae, but in adulthood Pseudomonas becomes a big problem and resistant strains begin to dominate making management harder. The main resistant organisms are pseudomonas, stenotrophomonas and burkholderia.

GI HAEMORRHAGE - Specify the symptoms and common causes of acute upper gastrointestinal bleeding. List the common causes of acute lower gastrointestinal bleeding. List the commonest presentations of chronic GI blood loss. Discuss the initial management of a patient with gastrointestinal haemorrhage. List the criteria for surgical intervention.

UPPER GI BLEED Presentation: Upper GI bleeds present as haematemasis, coffee ground vomiting (As Stomach acid alters the blood) or Melina. Causes: Duodenal ulcers, gastric ulcers, acute erosions/gastritis, Mallory weiss tear, oesophageal varices, oesophagitis or cancer of the stomach/oesophagus. Management: Assess shock and look first big master of liver disease. Insert 2 large bore IV canulae, Fluid resuscitates, crossmatched bloods and test urea level (urea level is elevated if there is intestinal absorption of blood). Consider giving a proton pump inhibitor and testing gastric pH. Surgical intervention: Endoscopy is the mainstay of treatment after initial resuscitation. This both establishes the diagnosis and treats it (adrenaline injections stop bleeding, thermal quite elation, laser ablation, fibrin gllue, Endo clips). If endoscopic procedures fail surgical intervention involves opening the stomach or duodenum and under running the bleeding vessel. Remember to treat the cause and if oesophageal varices remain uncontrolled endoscopically proceed to a Sengstaken tube Which inflates balloon to taponade the bleeding sites in the oesophagus. LOWER GI BLEEDs are typically due to diverticular disease, colon cancer, polyps or crohns. CHRONIC BLOOD LOSS causes an iron deficiency anaemia. The causes are the same as above.

PEPTIC ULCER - List the main causes, symptoms and investigation of peptic ulcer disease. Discuss differences between gastric and duodenal ulcer. Describe the relationship between H.pylori, smoking and non-steroidal anti-inflammatory drugs and peptic ulcer disease and the mechanisms by which they cause peptic ulceration. Outline a regimen for H. pylori eradication and discuss its implications for ulcer recurrence. Discuss the symptomatic management of peptic ulcer disease. List the complications of peptic ulcer disease and describe subsequent treatment. Outline broadly how and why the indications for peptic ulcer disease have changed over time.

Ulcer formation more commonly in the duodenum than the stomach/oesophagus/jejunum (jejunal ulcers are associated with Zollinger-Ellison syndrome, a gastrinoma in the pancreas seen with MEN type I - treat with PPI and tumour excision). Remember the acid is produced primarily in the antrum of the stomach by parietal cells and is stimulated by gastrin or vagal nerve stimulation. Cause: Often due to H. pylori or NSAIDs, other causes include Zollinger-Ellison syndrome, meckels diverticulum containing ectopic gastric mucosa. Presentation: Pain, indigestion, possible bleeding, fistulates into adjacent structures, perforation, obstruction. Investigations: Endoscopy whereby gastric ulcers can be biopsied to Exclude cancer. Important is the test for H. pylori (urea breath test - Bacteria will utilise labelled carbon-14, Antibody blood test Or histological examination post biopsy) Management: H. pylori eradication, smoking cessation, stopping NSAIDs and aspirin. A proton pump inhibitor is vital. Few patients progress to surgery. (Prior to effective medical treatment surgery would involve Trunk call vagotomy/cutting the vagus nerve - also causes inadequate stomach emptying or removal of the stomachs antrum Where most acid is secreted. Complications of peptic ulcer surgery includes the general risks of surgery, stump leakage, failure of the stomach to empty (damage of the vagal nerve), dumping syndrome, diarrhoea, alkaline gastritis, anaemia (lack of intrinsic factor), osteomalacia (poor vitamin d/calcium) And recurrent ulceration/malignancy. Differences between gastric and duodenal ulcers: Duodenal ulcers are used by food, gastric ulcers are worsened by it. Duodenal ulcers are much more likely to cause Melina wearers gastric ulcers cause haematemasis. H. pylori: 10% of patients with helicobacter will develop an ulcer. This is thought to be because of toxins released by the bacteria and the body is inflammatory response to the toxins which both cause injury to the protective gastric mucosa. Helicobacter also increases gastrin production and inflammation it causes reduces somatostatin (An inhibitor of parietal cells). H. pylori treatment: A proton pump inhibitor plus Clarithromycin and amoxicillin - Known as triple therapy. NSAIDs: The second most common factor implicated in ulcers. They inhibit prostaglandin synthesis in the gastrointestinal tract resulting in increased gastrin secretion. Smoking: increases acid secretion as does coffee.

List the risk factors for carcinoma of the breast.

Unopposed oestrogen is a known association (obesity, HRT, long term oral contraceptives (in theory), low parity, early menarche, late menopause - oestrogens start and puberty and end at menopause. Genetics: BRACA1, BRACA2. Family history. Personal history. Ductal or lobular carcinoma in situ.

THE URETHRA, PENIS AND SCROTUM - Discuss the clinical presenting features, diagnosis and management of urethritis and the urethral syndrome. Discuss clinical implications for those causes which can be sexually transmitted

Urethritis is either gonococcal or non-gonococcal (Chlamydia, E. coli etc) Inflammation of the urethra typically presenting with dysuria. Diagnosis involves examination of the urethra With a cotton swab to determine the causative organism. Treatment involves the appropriate antibiotic and education about Perineal hygiene including avoiding any Vagina or cosmetics and avoiding sex until symptoms are gone. As with most STI's contact tracing is important. Commonly in women urethritis is associated with pelvic inflammatory disease Which can scar the pelvic cavity resulting in ectopic pregnancies, chronic pain and infertility. Fitzhugh Curtis syndrome is when pelvic inflammatory disease spreads causing inflammation of the liver Resulting in liver fibrosis.

COPD - Describe and interpret relevant investigations in a patient with suspected COPD

Use a chest Xray to exclude other differentials (heart failure, lung cancer) and identify bulla from emphysema. FBC excludes anaemia and polycythaemia (seen in blue bloaters to compensate). Test for alpha1antitrysin deficiency in young patients or non smokers. Spirometry to identify obstructive changes with FEV1/FVC <70%. Low peak flow is present but non specific. Lung volume measurement shows hyperinflation using helium dilution. Exercise tolerence is decreased. Pulse oximetry may be lowered. Also consider quality of life.

THE URETHRA, PENIS AND SCROTUM - Outline the management of trauma to the urethra. Describe the aetiology, clinical presenting features and management of a urethral stricture. Describe the pathology, presentation and management of: phimosis, paraphimosis; priapism; Peyronie's disease; carcinoma of the penis; varicocoele, hydrocoele, epididymal cyst

Urethral stricture: narrowing as part of the urethra that causes blocked or reduced flow of urine. The long-standing irritation can cause urethral cancer and the stasis of urine can cause recurrent infections. Cause: trauma causes fibrosis which narrows the urethra, infection (STI, UTI) and other forms of inflammation can also cause strictures. Features: reduced flow, spraying of urine, dribbling, urinary frequency, recurrent UTIs, reduced force of ejaculation. Management: the aim is to widen the urethra with balloon dilation (usually not a permanent solution), urethrotomy (cutting a longer stricture to widen it, urethra plasty (removing the area of fibrosis). Antibiotics are indicated for infections. Phimosis: When the foreskin is unable to retract passed the glans and causes symptoms including difficulty with sexual functions And difficulty urinating. It can be normal up to adolescence as a baby has the foreskin fused. Management options include surgery, stretching exercises and steroid creams. Paraphimosis: When the foreskin is trapped retracted because of Oedema of the penis Typically after a medical procedure (catheter, cleaning, examination) were by the medical professional has forgotten to retract the foreskin back over the glands. As this can result in gangrene it is a medical emergency. Treatment is by manual manipulation with aids such as a cold compress an anaesthetic. If this is unsuccessful surgery is required to make a dorsal slit or circumcise. Phimosis is a risk factor for paraphimosis. Remember FOURNIER's GANGRENE is necrotisine fasciitis of the penis - seen more commonly in the immunesupressed. Management is surgical debridlement. Priapism: When, without physical or psychological stimulation, and the penis is erect for greater than four hours. This can be low flow with impairment of venous return, or high flow with Vascular abnormality to the penis. Priapism is associated with haematological disorders such as leukaemia or sickle cell but is usually precipitated by medications (Viagra a phosphodiesterase inhibitor, Antihypertensives, antidepressants, Alcohol, heroin, cocaine). Ischaemic priapism can damage the erectile tissue leading to erectile dysfunction and deformity of the penis. In extreme cases gangrene can occur. The sickle cell sufferers a blood exchange transfusion is required. Other patients should be given an alpha agonist which constricts the smooth-muscle facilitating a venous outflow. If this fails, aspirate blood from the corpus cavernosorum and consider an intra-cavernosal injection of alpha agonist. Next step is to introduce a shunt to send the blood to the corpus spongiosum. Last resort is shunting into the saphenous vein. If mild conservative treatment involves a brisk walk. Peyronie's disease: When the growth of fibrous plaques In the tunica albugenia cause pain, erectile dysfunction and a bend. Patients present with a bend and make pain of in satisfactory intercourse. The cause is often trauma in the diagnosis is the finding of fibrotic bands on ultrasound. Drugs or injections to break down fibrosis may be used. Surgery as a last resort and results in shortening. A better solution appears to be counselling and education. Cancer of the penis: Delivery is when a cell carcinoma that may present with pain, redness,Foul discharge Or a growth. Is associated with HIV, HPV and genital warts. Trimen depends upon the stage and but typically involves a wide local excision with or without radiotherapy. Amputation is possible. Varicocoele: An enlargement of the pampiniforme venous plexus, often due to defective valves causing a dragging pain and heaviness feeling. (New onset and left sided raises the possibility of a renal tumor) Although typically idiopathic the process may be secondary to compression by the mesenteric artery or renal carcinoma. On palpation it feels like a bag of worms and treatment involves Embolectomy is certain veins or surgical removal. Hydroceles: An accumulation of fluid in the tunica vaginalis of the testes usually because there is a patent processus vaginalis (Or Excess fluid secondary to a cancer or information) resulting in a painful swollen testicle. The fluid will make the testes non palpable and will be transluminal - if not think haematocele (post trauma). The main treatment is surgery to exercise the hydroceles sack. Remember if you can't get above the swelling it is a hernia. Epididymal cyst: A Rare fist the epididymus where free fluid filled with spermatozoa aaccumulates. They're typically painless and should be left alone although it is large and causing discomfort they can be exercised. Penile fracture: Snap sound and sudden loss of erection as the tunica albuginea (connective tissue around the corpus cavernosa) ruptures. There can also be a urethral tear and will always be significant swelling. Treatment is surgery. Remember any lump that is not separable from the testes is a tumor until proven otherwie. If the lump is seperate.....(transluminates = epydidamal cyst) (non transluminating = spermatocele)

ANAEMIA - Outline the physiological absorption of vitamin B12 and folate

Vitamin B12: found in meat, fish, eggs and milk but not in plants. > For the Methylation of homocysteine to sistine to methionine. > dietary requirement is similar to the maximum absorptive capacity. > The liver contains large stores of vitamin B12, it is secreted in bile then reabsorbed. > Stores last from 3 to 6 years. > ordinarily vitamin B12 is bound to Rprotein in saliva and gastric juice. Its connection to Rprotein is degraded by pancreatic enzymes and the free B12 that is released can be bound to intrinsic factor. > This complex can be absorbed in the terminal ileum. > B12 then goes via the portal bloodstream bound to trancobalamin II. Therefore without intrinsic factor the person has pernicious anaemia. folate: also known as folic acid, occurs in green vegetables & offal and is required for amino acid metabolism and DNA synthesis. >unlike vitamin B12, the body's reserves of folate are low and deficiency can occur in less than 4months. >absorption is in the jejunum

HAEMOSTASIS - Discuss the pharmacokinetics and clinical use of warfarin and the new oral anticoagulants including laboratory tests used to monitor clinical effect

WARFARIN: indicated for anticoagulation (DVT, PE, prophylaxis, stroke prevention etc). Warfarin inhibits the reductase enzyme responsible for regenerating vitamin K (need it to develop clotting factors, takes up to 5 days for factors to become depleted). There is an initial prothrombotic effect so cover with heparin until INR is in range. Tablets 0.5 mg his white, 1 mg is brown, 3 mg is blue and 5 mg pink. aim for an INR of 2-3 less in recurrent PE/DVT or prosthetic heart valves (then aim for 3-4). if you know the cause and to remove it, and strikingly to 6 weeks, six months if no cause is found and indefinitely if the cause is irremovable. Novel oral anticoagulants/NOACs: these are a new alternative to warfarin with fewer side effects but are not immediately reversible. (....ban).

Obesity hypo-ventilation syndrome?/Pickwickian?

When a severely overweight person fails to breath rapidly or deeply enough resulting in hypoxia and hypercapnia frequently seen alongside sleep apnoea. The disease eventually leads to cardiac failure and requires NIV.

PNEUMONIA - Describe the pathology of acute lobar pneumonia and bronchopneumonia.

When classifying pneumonia it can be considered based on anatomical location..... Acute lobar pneumonia is when the infection affects a large and continuous area of the lobe of a lung. The stages of acute lobar pneumonia are as follows: >CONGESTION where exudate, neutrophhils, bacteria and red cells accumulate in the alveoli. The lung becomes heavy and hyperaemic. >RED HEPATIZATION whereby vascular engorgement persists and copious RBCs extravasate and fibrin forms on the cut surface of the affected lobe this appears like a liver. >GREY HEPATIATION as red cells disintergrate so the lobe becomes greyer and drier. >RESOLUTION as the exuudate is digested by enzymes, engulfed by macrophages and oughed up. Bronchopneumonia is a more patchy consolidation of alveoli associated with bronchial inflammation. The multiple foci of acute inflammation are due to bacteria and are often in both lower lobes.

PANCREATITIS - Describe the clinical presentation of acute pancreatitis. Describe the aetiology and pathology of pancreatitis. Classify pancreatitis on the basis of the severity of organ injury. Discuss the management of acute pancreatitis and potential early complications of acute pancreatitis. Outline the investigation of suspected acute pancreatitis, emphasising the timing, interpretation and reliability of currently available tests. Discuss the criteria used to predict the prognosis for acute pancreatitis. Outline the metabolic complications of pancreatitis.

When pancreatic enzymes are released and activated causing autodigestion of the pancreas in four stages whereby resolution can occur at any point. 1. fat necrosis because oedema into the peritoneal cavity contains autodigesting enzymes. the gross oedema is associated with hypovolaemic shock, compounded by vomiting. 2. Autodigestion of blood vessels causes haemorrhage into the retro peritoneal space hence grey turner sign and Cullens sign - if the attacker severe enough. 3. pancreatic necrosis is the inflammation is destroying the pancreas itself. 4. If the necrosis of the pancreas becomes infected there will be further deterioration in a high mortality rate. Presentation: Acute upper abdominal pain or epigastric pain that is very severe and radiates through to the back. Associated with nausea, vomiting and shock. The abdomen is diffusely tender but soft with normal bowel sounds. (Unless the presentation is severe enough to cause peritonitis). Causes: GET SMASHD (gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion bites, hyperlipidaemia, drugs) or GET SMASH'N (gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion bite, hyperlipidaemia and neoplasms). Clearly the most common gallstones and alcohol. Management: obviously treat the cause (ERCP to remove stones) after resuscitation with IV fluids, oxygen and analgesia. Keep the patient now by mouth and given nasogastric tube to decompress. Keep a strict fluid balance chart because the risk of hypovolaemia. if infection is likely consider antibiotic use. Reduce gastric acid secretion with a proton pump inhibitor or H2 receptor antagonist. if the patient has infected pancreatic necrosis confirmed by CT guided aspiration then open excision of the necrotic areas is required. Complications and metabolic complications: renal failure (as a result of severe hypovolaemia), acute respiratory distress syndrome, infected pancreatic necrosis, instead of getting infected necrosis can also cause pseudocyst's (collections of fluid in the lesser peritoneal sac). Investigations: raised amylase, consideration of other acute abdomen presentations, raised lipase, raised CRP, CT scan shows inflammation and fluid around the pancreas. Ultrasound may show gallstones is a cause. Predicting prognosis: Think APACHE II >8 (For ITU atients generally) or ranson >3.

TRANSFUSION - List the blood products available for transfusion and outline the rationale for using fresh frozen plasma, cryoprecipitate and platelets

Whole blood is rarely used - it is a waste and increases the risk of a transfusion reaction. Red blood cell concentrates, used in anaemia or blood loss. Washed red cell concentrates, washed in saline used in anaphylactic reactions. Platelet concentrates used in thrombocytopenia and bone marrow failure. Granulocyte concentrations used in patients with neutropenia. This fresh frozen plasma containing, like elation factors used to replace coagulation factors in acquired deficiencies, liver disease, warfarin overdose where vitamin K would be too slow. Cryoprecipitate is fresh frozen plasma without Any precipitates/solids. Specific clotting factors can be given for haemophilia and von Willebrand's disease. Albumin can be given in patients with liver disease or in nephrotic syndrome where patients fluid overloaded and resistance to diuretics. Immunoglobulin can be given in ITT and hypogammaglobuminaemia.

TOXICOLOGY - Outline the general principles in the assessment and treatment of a patient who has taken an overdose. Describe the clinical features, investigation and treatment of alcohol intoxication. Describe the clinical features, investigation and treatment of paracetamol overdose including the importance of monitoring of hepatic and renal function. Describe the clinical features and management principles of other overdoses that present commonly to the Emergency Department, including tricyclic antidepressants, benzodiazepines, opiates, cocaine and aspirin. List the antidotes available to treat specific poisons Describe the function of the National Poisons Information Services Describe the features suggesting a high risk of suicide in a patients presenting with self harm or overdose.

assessment: admit patients if they are symptomatic, asymptomatic with an unknown drug will have suicidal intent. Contact toxbase for advice on the poison, physically and psychologically assessed and administer any antidote in line with local guidelines. Alcohol intoxication: dangerously high acute alcohol intoxication sufficient enough to potentially comatose, respiratory depress or kill the patient. Patients present confused, semiconscious, vomiting, with possible seizures/respiratory depression. investigate with a blood alcohol test. Also monitor for hypoglycaemia (alcohol inhibits gluconeogenesis), and acute renal failure. In liver failure patients are more prone to adverse affects. Paracetamol overdose: the alcohol metabolite NAPQI overwhelms the glutathione pathway and accumulates as a hepatotoxic substance. N-acetyl-L-cysteine is the antidote, essentially synthetic glutathione. symptoms include jaundice, hypoglycaemia (sweating, irritability), vomiting. Trycyclic antidepressant overdose: this particular affects the central nervous system, autonomic nervous system and heart. presentationis with tachycardia, dry mouth, nausea, vomiting, drowsiness, urinary retention and other anti-muscarinic side-effects. more serious side-effects include hypotension, Arrythmias, hallucinations and seizures. Worry particularly about the length of the QRS complex. They work by blocking noradrenaline reuptake in the synapses. manage with activated charcoal, nasogastric aspiration, cardiac monitoring and sodium bicarbonate. Benzodiazepine overdose:Presentation is with central nervous system depression, ataxia and slurred speech. Death is rare and management is primarily supportive although the antidote flumazenil is available and activated charcoal is considered. Opiate overdose: presentation is with decreased consciousness and pinpoint pupils. As heart rate and breathing slow the patient becomes cyanotic as they have seizures and muscle spasms. give the antidote naloxone. Cocaine overdose: patients present anxious, teeth grinding, hydrothermic and paranoid. They may have hallucinations and paranoid delusions. lethal side-effects include tachycardia, stroke, tremors, convulsions, heart attack or heart failure.it is the hypertension and tacky Arrythmias that are most often fatal. the slowdown the heart rate use benzodiazepines, avoid beta-blockers as they constrict cardiac vessels. consider cooling techniques. Aspirin overdose: presents with nausea, vomiting, sweating, tinitus, hearing loss and hyperventilation. large enough and overdoses cause seizures and cerebral oedema. Monitor level, ABG, urine PH. There is no specific antidotes, manage with activated charcoal, fluids and dialysis. They may need bicarbonate for respiratory alkalosis secondary to hyperventilation - note that after initial respiratory alkalosis there is metabolic acidosis. Manage with: activated charcoal, fluid resuscitation and possible dialysis. You can also alkalinise the urine to enhance the excretion of aspirin into urine. Replce lost glucose and potassium. National poisons information services: United Kingdom Department of Health independent expert advice on all forms of acute and chronic poisoning - understanding its effects and management. the backbone of the poisons information service is toxbase an index of almost all toxins potentially presenting the healthcare professionals. Features suggestive of suicide risk: when considering a person's risk of suicide think about there: history, adverse events recently, protective factors, access the means, intention, cognitive state etc. There's also peaked demographics such as middle age lesbian females. ANTIDOTES: nacetylcysteine for paracetamol, naloxone for opiates, flumazenil for benzodiazepines, glucagons for beta-blockers, sodium bicarbonate for tricyclic antidepressants

IMMUNOLOGY - Describe the main clinical features, immunopathology, investigation and principles of management of the following conditions; organ specific autoimmune disease including autoimmune thyroid disease, insulin dependent diabetes mellitus, pernicious anaemia, Addison's disease, autoimmune liver disease and bullous skin diseases; Lymphoproliferative disorders including myeloma; Connective tissue disease including systemic lupus erythematosus and scleroderma vasculitis, glomerulonephritis and coeliac disease

lymphoproliferative disorders: MULTIPLE MYELOMA: the cancer seen in older people whereby plasma cells excessively proliferate and cause lytic lesions in bone associated with high calcium and fractures. Excessive monoclonal immunoglobulin is produced which can enter you in detected as bence Jones proteins. these immunoglobulins also destroy renal function. Autoimmune disease: these can be considered as organ specific or multisystem. Think Hashimoto's thyroiditis, Graves' disease, pernicious anaemia, Addison's, diabetes, myaesthenia Gravis, multiple sclerosis etc. Systemic diseases include lupus, rheumatoid arthritis, dermatomyositis and other connective tissue diseases. the bulk of these are covered elsewhere. There is an overlap between autoimmune conditions that is as follows pancreatic, thyroid, stomach, adrenal, parathyroid, ovaries and testes. PERNICIOUS ANAEMIA: also antibodies against parietal cells leading to decreased production of intrinsic factor. Antibodies may also block the binding of intrinsic factor to vitamins B12 or block the absorption of B12 and intrinsic factor in the ileum. ADDISON'S DISEASE: destruction of the adrenal cortex by antibodies typically because of 21 hydroxylase, diagnose ways ACTH/short synacthen test. AUTOIMMUNE LIVER DISEASE: in a genetically predisposed person and environmental agents can trigger fibrosis and cirrhosis through a necroinflammatory process. Bullous skin disease: these primary blistering diseases of the skin are rare and immune mediated requiring biopsy for diagnosis (immunoflourescence and microscopy). You are more likely to see secondary causes such as chickenpox, herpes, impetigo, eczema and insect bites. PHEMPHIGUS VULGARIS: autoimmune and potentially fatal. Treat with high-dose steroids. BULLOUS PHEMPHIGOID: blisters on the hands, limbs and feet treated with prednisolone. DERMATITIS HERPETIFORMIS: seen with coeliac disease, treat with a gluten-free diet. Coeliac disease: immune response to wheat gluten whereby autoantibodies are mage against tissue transglutaminase. Complexes form between tissue transglutaminase and gluten resulting in a T-cell response that causes lymphocytic infilktrate and villous atrophy.

ANAEMIA - Outline the laboratory features of microangiopathic anaemia and list the common causes

microangiopathic = small Lascelles This is a mechanical subtype of haemolytic anaemia caused by physical trauma in the small vessels. Causes include: malignant hypertension, eclampsia/pre-eclampsia, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, vasculitis and disseminated intravascular coagulation. This may also occur with prosthetic heart valves and March haemoglobinurea ( soldiers crush the red blood cells in their feet). In the laboratory there will beSCHISTOCYTES on the blood film (irregularly shaped, jagged and asymmetrical fragments of red blood cells). also referred to as Helmet cells.

ANAEMIA - Outline the clinical features and laboratory diagnosis of sickle cell anaemia. Outline the clinical management of sickle cell crisis and the importance of sickle cell

sickle cell anaemia is an autosomal recessive disorder whereby abnormal beta globulin chains are produced resulting in HbS rather than HbA. Sickle cell anaemia = HbSS sickle cell trait = HbAS (no disability, protects from malaria, may have some hypoxia ) remember that sickle cell can occur alongside other variants such as beta thalassaemia. The presence of HbS causes red blood cells to deform when deoxygenated resulting in fragile cells that are prone to haemolysis and can block small vessels. Symptoms are highly variable, typically an African patient with chronic haemolytic anaemia exacerbated during a crisis. Crisis: 1. vaso-occlusive (painful due to microvascular obstruction, precipitated by cold/infection/dehydration/hypoxaemia. May also cause strokes, seizures and priapism) 2. aplastic crisis (seen with parvovirus infection, usually self limiting but may need transfusion). 3. Sequestration crisis (pool of blood in the spleen with severe anaemia, splenomegaly, hepatomegally and shock requiring immediate transfusion). Full blood count shows high bilirubin and high reticulocytes (red blood cell precursors), blood film shows sickle cells and haemoglobin electrophoresis will confirm the diagnosis and distinguish sickle-cell anaemia from trait. The aim is to diagnose from cord blood to aid early pneumococcal prophylaxis. Management acutely: analgesia, crossmatch, FBC and reticulocytes, infection screen, rehydrate, oxygen, antibiotics, measure spleen and liver size. give blood transfusions if haemoglobin or reticulocytes falls sharply and give exchange transfusion if there is rapid deterioration (remove blood and give donor blood in stages). Complications: infarction of the spleen, gross impairments, bone necrosis (especially avascular necrosis of the femoral head), chronic renal failure, chronic leg ulcers, gallstones, retinal disease, iron overload or blood-borne infection from transfusions and the long-term damage of hypoxaemia/fibrosis/pulmonary hypertension. Management chronically: chemotherapy (hydroxycarbimide/hydroxyurea) will increase the levels acetyl haemoglobin. Splenectomy with antibiotic prophylaxis and immunisation. Bone marrow transplantation can be curative but remains controversial. Prevention: genetic counselling, prenatal tests. If not, early identification with the Guthrie test/heel prick helps management planning and early pneumococcal prophylaxis. Education into the causes of crisis is vital. Prognosis: most deaths occur within six months of life but the life expectancy for someone with sickle cell is 50 years, 70 of they only have trait.

ANAEMIA Outline the clinical features and laboratory diagnosis of thalassaemia Screening prior to surgery

thalassaemia is earned by autosomal recessive genetic disease whereby the haemoglobin produced is abnormal (due to under production of a globin chain). This damages the red blood cell membranes resulting in haemolysis in the bone marrow. Normal haemoglobin, termed HbA is made up of two alpha and two beta chains. beta thalassaemia is caused by a mutation in the beta globin gene leading to reduced beta chain production (beta +) or absent beta chain production (beta0). This means that haemoglobin have excessive alpha globin molecules. BETA THALLASAEMIA > Called minor or traits if the patient is a carrier with only one beta chain affected (beta,beta +). They will be asymptomatic. > Intermedia if the patient has two beta chains with only reduced production (beta +, beta +). Patients are also thalassaemia intermedia if they have one beta + haemoglobin and one other (such as HbS/Sickle). > Beta thalassaemia major has the abnormality in both globin genes resulting in severe anaemia and failure to thrive. Red blood cells will be produced outside of the bone marrow causing skull bossing and hepatosplenomegaly (spleen also enlarged due to haemolysis). The patient needs lifelong transfusions and collation to stop iron overload. Iron overload can cause and crying failure, liver disease and cardiac toxicity. Patients may raise their feet haemoglobin to adapt. ALPHA THALLASAEMIA > Barts hydrops is when all four alpha genes are deleted resulting in death in utero. Termed HbBarts. > HbH is the deletion of three genes leaving only one alpha chain and causing moderate anaemia, hepatosplenomegaly, leg ulcers and jaundice. > If only two genes are deleted, there will be two alpha chains with reduced production but an asymptomatic patient/carrier. > If one gene is deleted the patient is clinically normal. SCREENING prior to surgery we screen for anaemia, coagulopathies (if there is a family history) or hypercoagulable states (VTE risk assessment). Anaemia is a particular concern in patients with heart disease because patients without significant cardiac risk can tolerate blood loss better.