module 2

What is Reactive RA / Reiter syndrome?

A sterile joint inflammation (aseptic arthritis) that develops after an anatomically distant infection Systemic The triggering infection is usually in the throat, urogenital or GI tracts May be no preceding infection ** Reiter's Syndrome • Collection of symptoms i.e. arthritis, urethritis and conjunctivitis in a patient with dysentery

What psychosocial problems can be the result of chronic disability?

Anxiety Depression Anger Social withdrawal Social isolation Poor quality of life

What is a Full agonist?

Binds to and maximally activates receptor E.g. Morphine, Epinephrine

What are partial agonists?

Binds to but only sub-maximally activates receptor E.g. Buprenorphine, Pentazocine, Pindolol, Partial agonist functions as an antagonist in presence of a full agonist

What is drug potency?

Determined by strength of binding to the receptor - receptor affinity Greater the drug potency, the lower the concentration required to bind to the receptor and to produce a response for an agonist or to block a response for an antagonist. Potency is the concentration needed to give 50% of maximal response

What is the management for AS?

Diagnosis MDT & Patient Phys.The. NSAIDS, biologic DMARDs for peripheral joints only

How can Dr's help avoiders to become copers?

Elicit ICE Avoid unnecessary, excessive or inappropriate investigations Avoid inconsistent care Provide adequate amount and type of information

How is AS diagnosed?

FBC, ESR/CR X-ray SIJ (sacroiliac joints) & spine MRI FBC may show anaemia of chronic disease ESR & CRP are often raised during active phases of the disease X-rays - sclerosis and erosions seen on lumbar spine

How can the MDT help in people with disabilities?

GP Physiotherapist use a wide range of techniques and approaches, including: - massage and manipulation, using the hands to relieve muscle pain and stiffness and encourage blood flow to an injured part of the body to help recovery - heat, cold, electric current, light and water - remedial exercise (exercise that takes into account a person's current level of health and any specific requirements they may have) - providing support to help patients manage chronic conditions Physiotherapy techniques and approaches can improve a person's ability to use parts of their body that are affected by a health condition or injury. For example, arthritis is a chronic condition that causes painful, stiff joints and is often associated with ageing. Physiotherapists can help keep the joints mobile and strengthen the surrounding muscles. Social Services Understandably day to day activities will be affected with a disability. Some individuals may practical require support in order to preserve their independence. A disable individual may be eligible for state-funded support from health and social care services. More precisely, assistance might encompass adaptations to the home (i.e. support railings in the shower) or home care visits to assist with activities such as shopping, cleaning and personal hygiene. In order to determine whether an individual is eligible or not, they must be assessed by the social services department of their local council. The assessment is known as the "assessment of need" and is conducted by an occupational therapist. The report written by the OT will prioritize the needs as well as indicate the associated risks if assistance is not provided. A care package will then be drafted by the OT and the local health and social services team with the input of the patient. If an individual is eligible for assistance, they may be able purchase the services themselves via a scheme known as direct payment, meaning a patient will pick and choose the services themselves with funds provided by the council. If not, the council will provide the necessary services. One final note, care will be reassessed given that an individual's circumstances and needs will change with time Psychologist Living with a disability will evidently require life adjustments both for the individual and their family. In some instances, a patient might feel confused, depressed and anxious regarding their diminishing independence. Mental health can clearly be affected and thus should be referred and encouraged to seek counseling. Occupational therapist Once again let's use a child with a disability as an example: An OT will aim to enable the child to be as physically, psychologically and socially independent as possible. Assessment may include information gathering from parents, families and others involved in the child's life and building on what is already known about the child from other agencies such as education and social work. Assessment will include: Functional difficulties such as dressing, play skills, sensory abilities such as balance, gross motor and movement abilities. This may include formal and informal assessment such as observation. The decision whether to offer further support from Occupational Therapy is based on the outcome of assessment, the impact of the difficulty on the child's life and the likelihood of effecting change at this time. Following assessment the outcome will be discussed with the parent and a written report will be sent to the parent and the referrer. The therapist may need to share this information with other people for the child's benefit. This will be discussed with the parents and referrer. Orthotist provide a range of splints, braces and special footwear to aid movement, correct deformity and relieve discomfort Charities The NHS websites provides links to organisations such as RADAR and National Centre for Independent living (NCIL) organisations which provide assistance to those living with a disability. More precisely, both organisations campaign for the rights of the disabled as well provide information regarding their rights in terms of employment. Furthermore, these organisations link individuals with support groups specific to certain disabilities, allowing families and individuals to meet others in similar circumstances.

What is Septic Arthritis, what are the signs and symptoms and what is the treatment?

Generally unwell Very wary - very painful to move 'cries as you approach the bed' Raised inflammatory markers Raised white cell count Septic arthritis is an infection of the synovium and joint space, commonly caused by the organism Staphylococcus Aureus (also in osteomyelitis) and Group B Streptococcus (more commonly in neonates). Prior to the advent of the Hib vaccine, Haemophilus influenza was also a common cause of septic arthritis in infants from 2 months to 5 years. Seeding of the infection usually begins through haematogenous bacterial spread, with joints in which there is an intra-articular metaphysis (e.g. hip, shoulder, ankle and elbow) being particularly vulnerable. In children under 18 months, the physis does not prevent blood from entering the epiphysis, making the joints more vulnerable to infection. Left untreated, septic arthritis may cause destruction of the joint and arrested growth. Presentation: Children typically present with fever > 38o, swelling, erythema, warmth, rapid onset of pain and limitation of movement in the affected joint, with minimal to no weight-bearing. They may present with an antalgic posture, holding their joint in a position which offers maximum pain relief. Investigations: - An aspiration of the affected joint is usually performed, with subsequent gram stain and culture of the fluid collected from the joint. - Full blood count with inflammatory markers shows a raised white blood cell count, elevated neutrophils, raised ESR and CRP. -Ultrasound may be helpful in showing joint effusion. Treatment: • intravenous antibiotics, analgesia • Aspiration of the joint. • Care must be taken to ensure that infection is fully treated to prevent recurrence.

What is the thick filament of muscle made of?

Many myosin molecules arranged like 2 golf clubs intertwined Myosin head contains an actin binding site and a myosin ATPase site.

What are antagonists?

Opposing end result Acting via a different receptor

How is depression diagnosed by NICE?

Persistent sadness or low mood almost every day Loss of interest in most activities. This can generally be accompanied by these symptoms: Fatigue or loss of energy Worthlessness or the patient suffering from excessive or inappropriate guilt Frequent thoughts of death, suicide or actual attempts to commit suicide Decreasing ability to concentrate or increased indecision Psychomotor agitation or retardation Insomnia or hypersomnia Changes in appetite or weight loss

Describe a sarcome and its components

Sarcomere - 1 functional units connected by Z disk Sarcomere - thick & thin filaments Myosin - thick filament - tethered to Z disk by titin Actin - thin filament - tethered to Z disk A band - myosin filaments (note the overlap of myosin & actin) I band - actin filaments H band - myosin filaments M line - central line - myosin bound Titin: - Extends from the M line in both directions along the length of the thick filaments and stabilises position of thick filament in relation to thin filaments. - Acts as a spring helping the muscle to spring back to its resting position as it is a highly elastic protein. Muscle contraction: - A band stays the same size - I band shortens in length. Picture

Discuss the organisation of muscle

whole muscle is made up of a series of fibres each fibre made up of elements called myofibrils each myofibril made up of repeating units (sarcomeres) consisting of interdigitating filaments (myofilaments) Picture

What is indirect cost?

"what society loses out on" i.e. productivity loss when the sick person not working or their partner not working as they after looking after them. Includes loss of earnings. Also hospitals beds that are full of fracture patients can not be used for anything else.

what are PROMs

(Patient Reported Outcome Measures) - take into account the patients ideas or feelings about their condition. There are many types of PROMs, (e.g. Health Assessment questionnaire (HAQ ))and EQ5D:

What is reiters syndrome characterised by?

** Reiter's Syndrome • Collection of symptoms i.e. arthritis, urethritis and conjunctivitis in a patient with dysentery

Name soft tissue injuries?

- DVT - Cellulitis - Sprains - Strains - Gas gangrene - Bursitis - Necrotising Fascitis - Lymphodema - Phlebitis - Varicose veins - Tendonitis

What is the transmission process in a neuromuscular junction i.e. action potential?

- AP reaches the NMJ - This triggers the voltage gated Ca2+ channels - The Ca2+ attracts the synaptic vesicles to the active zone and they empty their contents into the synaptic cleft - The ACh passes across the cleft and binds to the AChRecptor and this causes channel proteins in the postsynaptic cleft side to open - This allows Na+ ions into the cell which creates a potential change in the muscle membrane and causes muscle contraction - Finally, ACh is cleared out of the receptors by Acetylcholineesterase and breaks it down to acetic acid anmd choline http://www.youtube.com/watch?v=CYnASKJJoSY

what is peripheral tolerance in t cells?

- Anergy (functional inactivation) - Deletion (apoptosis) - Immunological ignorance - Suppression

What types of conservtive treatment are there for fractures?

- Cast and splints - Traction

What are the causes of limping in a child?

- Congenital hip dislocation / Developm ental dysplasia of the hip - Transient Synovitis (also toxic synovitis / irritable hip) - Septic Arthritis - Slipped Capital Femoral Epiphysis. - Perthes' Disease (also known as Legg-Calve-Perthes' Disease) - Juvenile idiopathic arthritis

Name the 2 types of bone?

- Corticol / Compact - Cancellous or trabecular or spongy bones

What physiological affects does the Parasympathetic system have on the body?

- Dilates blood vessels leading to the GI tract, increasing blood flow. This is important following the consumption of food, due to the greater metabolic demands placed on the body by the gut. - Constricts the bronchiolar diameter when the need for oxygen has diminished. - Dedicated cardiac branches of the vagus and thoracic Spinal Accessory nerves impart Parasympathetic control of the Heart or Myocardium. - Causes constriction of the pupil and contraction of the ciliary muscle to the lens, allowing for closer vision. - Stimulates salivary gland secretion, and accelerates peristalsis, so, in keeping with the rest and digest functions, appropriate PNS activity mediates digestion of food and indirectly, the absorption of nutrients. - Is also involved in erection of genitals, via the pelvic splanchnic nerves

What physiological affects does the sympathetic system have on the body?

- Diverts blood flow away from the gastro-intestinal (GI) tract and skin via vasoconstriction. - Blood flow to skeletal muscles and the lungs is enhanced - Dilates bronchioles of the lung, which allows for greater alveolar oxygen exchange. - Increases heart rate and the contractility of cardiac cells myocytes, thereby providing a mechanism for the enhanced blood flow to skeletal muscles. - Dilates pupils and relaxes the ciliary muscle to the lens, allowing more light to enter the eye and far vision. - Provides vasodilation for the coronary vessels of the heart. - Constricts all the intestinal sphincters and the urinary sphincter. Inhibits peristalsis.

Anti histone is associted with?

- Drug induced lupus

Name the 2 types of bone infection

- Haematogenous Osteomyelitis - Contiguous Osteomyelitis.

The perception of a disability can depend on?

- How severe they see their condition/ disability as, - How they feel about their disability: Many disabled people live very active and fulfilling lives and consider themselves to be just as healthy as a non- disabled individual and vice versa. - Their personality type - Gender and Disabilities:

Where can fincial help be provided by?

- Ill health payments - Disabilities facilities grant - The family fund - Disability living allowance - Attendance allownace

Define impairment

- Impairment: any loss or abnormality of psychological, physiological and anatomical structure of function

Name some biologics?

- Infliximab, - Adalimumab - Etanercept.

What is the social impact of being disabled in children?

- Less opportunity to participate in normal activites - Child and the parents can't relate to other people who have less in common with normal families. - Prejudices and a negative attitude from the community - Social exclusion of the whole family including siblings - Stigmatizing beliefs about the cause of disabilty - Affect culture they live in -

Name some DMARDs?

- Methotrexate • Sulphasalazine • Hydroxychloroquine • Leflunomide • Gold • Penicillamine • Azathioprine • Cyclosporin • Minocycline

What are the divisions of the nervous system?

- Nervous system CNS - PNS The CNS branches into the brain and spinal cord. The peripheral nervous system branches into the autonomic nervous system and somatic nervous system. The autonomic nervous system branches into the sympathetic nervous system and parasympathetic system and the enteric nervous system.

What medications can be used for chronic pain?

- PAracetamol - NSAIDs - Opioids - Antidepressants - Anticonvulsants

Anti Scl70 is associated with?

- PSS - Scleroderma

What types of fractures are associated with children?

- Plastic bowing - Torus / buckle - Greenstick Childhood fractures include torus fractures (buckling of the bone cortex) and greenstick fractures (cracks in only 1 side of the cortex). Because a child's bones are much more pliable than adult bone, an incomplete, or 'greenstick,' fracture may occur. A "greenstick fracture" means that one side of the fracture has broken and one side is bent; therefore it is classified as an incomplete break. The most common fractures that occur are Fractures that travel through physis but part of the metaphysis is involved. This is called a type II fracture in Salter-Harris classification. (picture)

Name some common fractures?

- Radial fracture (Colles) - Fractured neck of femur - Scaphoid fracture

Anti RNP is associated with?

- SLE - MCTD

Name some connective tissue diseases

- Systemic lupus erythematosis (SLE) - Sjogren's syndrome - Systemic sclerosis - Polymyositis/ dermatomyositis - Antiphos-pholipid syndrome - Vasculitis

Name some non pharmalogical treatments for muscoluskeletal pain?

- TENS machine (Transcutanous Electrical Nerve Stimulation) - Spinal cord stimulation (SCS) - Acupunture - Biofeedback - Progressive muscle relaxation (PMR) - Psychological preparation and information giving.

What cells produce collagen type I and elastin in tendons?

- Tenoblasts - Tenocytes

Describe some fractures?

- Transverse (straight across) - Oblique (at an angle) - Spiral (bone has been twisted) - Longitudinal

Tendons consist of what element?

- Type I collagen - Elastin

What is a TENs Machine?

- Used for acute and chronic pain. It consists of a small electrical pulse generator with 2 to 4 electrodes are placed on the skin. - It is thought to work by sending a weak electrical current though the skin to stimulate the sensory nerve endings, causing a prickly, buzzing sensation. TENS is thought to work by gate theory, by closing the gate. It also may stimulate the release of endorphins within the brain and spinal cord. -

what is antigen LA associated with?

- sjogrens - SLe

What is the function of synovial fluid?

-Acts as a lubricant of articulating surfaces in a joint. -Nourishes the chondrocytes (the only cells present in cartilage). Remember that cartilage is not vascular so synovial fluid plays an essential role in delivering vital nutrients and oxygen to the cartilage in order to maintain proper function. -Removal of waste and debris from the joint , the synovial fluid achieves this by acting as a medium for white blood cells (macrophages) to circulate within the joint an phagocytose debris. - Acts as a shock absorber within the joint. Synovial fluid achieves this due to its property of becoming more viscous under stresses. The term given to substances that do this is dilatant.

What is antigen Ro associated with?

-Sjogrens - SLE - SSc

How does muscle contraction occur?

1) Acetylcholine (Ach) is released at the neuromuscular junctions between motor neuron terminal button and muscle fibres. 2) This changes the permeability in the muscle fibre resulting in an action potential that is conducted over the entire surface of the muscle cell membrane. 3) The action potential spreads down the transverse tubules that are on the surface membrane. 4) Ca2+ to be released from its stores in the sarcoplasmic reticulum to the cell cystol. 5) Ca2 + binds to troponin (heterotrimer i.e. TI, TT, TC) moving molecule exposing the binding site on the actin molecule. 6) The myosin then binds to the actin molecule binding site forming a cross bridge. 7) The cross bridge then bends pulling the actin filament forward (known as the POWER STROKE). It then releases the s tored up ADP and Pi. 8) Detachment- ATP binds to the myosin head releasing it from the actin molecule. This can sometimes be known as the rigor complex as if there is no ATP to detach the binding the cross bridge remains and the muscle becomes stiff. Hence when we die our body goes stiff as there is no ATP to release the myosin so causes rigor mortis. 9) Myosin then returns to its relaxed position. The fresh ATP molecule that released it is then hydrolysed. Splitting the molecule into ADP and Pi by myosin ATPase. 10) Binding then occurs to a more distal actin molecule and the energy from the hydrolysis reaction is then stored in the cross bridge (like a cocked gun) for the next power stroke. The cycle then repeats N.B. Muscle cells control cycle by regulating step 3 i.e. preventing cross-bridge cycling until tropomyosin moves out of way as a result of an increase in intracellular Calcium concentration The cycle then stops when the action potential stops and Ca2 + is then taken back into the sarcoplasmic reticulum. Tropomyosin then returns to its original position blocking the actin binding sites. This stops any further contraction and the thin filaments slide passively back to the original relaxed positions. http://www.khanacademy.org/vide/tropomyosin-and-troponin-and-their-role-in-regulating-muscle-contraction?topic=biology

Name the 10 red flag symptoms

1) Age under 20 or new symptoms over 55 2) Non-mechanical pain 3) Thoracic pain 4) History of cancer, steroid use HIV or other Significant PMH 5) Fever and weight loss 6) Widespread deformity, e.g., bilateral leg signs. 7) Structural deformity 8) Persistent night pain (with or without night sweats) 9) Saddle anaesthesia/sphincter disturbance 10) Recent bacterial infection

Name some monoarticular joint problems?

1) Gout a) Acute gout b) Chronic gout 2) Pseudogout

Describe the anatomy of a neuron?

1. A cell body (soma) containing the nucleus and other intracellular organelles (particularly concerned with protein synthesis and secretory process) 2. The dendrites and the cell body are the main areas for receiving information. The chemical message is translated by the membrane receptors into an electrical or biochemical event that influences the state of excitability of the receiving neuron 3. A single axon extending from the cell body to the target cell. Axons can be as long as a few millimeters to several meters (Motor neurons supplying muscles distant from the spinal cord). At the beginning of the axon is the axon hillock or trigger zone where actions potentials can be generated

NAme the 6 phases in the gait cycle?

1. Heel strike 2. Midstance 3. Heel off 4. Acceleration 5. Mid swing 6. Deceleration

What are the 3 ways of inhibiting COX enzymes?

1. Irreversible inhibition - The NSAID causes acetylation of the active site. Aspirin binds in this way 2. Competitive inhibition -The NSAID acts as a competitive substrate, ibuprofen bind in this way 3. Reversible, non-competitive inhibition -free radical action interferes with the production of certain chemicals, which play an essential role in the activity of Cox enzyme. Paracetamol is thought to works in this way.

Name the 5 types of receptors?

1. Ligand gated channels 2. G-protein receptors 3. Nuclear receptors for steroid hormones 4. Tyrosine-kinase receptors 5. Voltage-gated ion channels

What are the 3 components that contribute to joint movement?

1. Muscle work 2. Motor Control 3. Joint anatomy

What is the pahtophysiology of RA?

1. The first change that occurs in the synovium is an increase in the number cells of the synovial lining. The first cells to increase are the mononuclear cells which are a type of white blood cells. 2. An increase in the cells also leads to an increase in the other substances in the tissue. This results in the synovium becoming thick and swollen. The synovium now protrudes into the joint cavity in the form of small finger like projections called villi. 3. Symptoms of the disease begin to manifest when the mononuclear cells are replaced by T lymphocytes. 4. As the disease progresses the synovium develops a characteristic picture of chronic (long standing) inflammatory arthritis. 5. The following changes also occur: increased number of blood vessels in the synovium which are leakier and at places they develop blood clots. Mast cells contribute to rheumatoid arthritis pathology by release of histamine and fibroblast cells release enzymes that cause destruction of cartilage. The various cells present in the synovium release certain substances called cytokines and chemokines that are responsible for mediating the inflammatory process that leads to destruction of bone and cartilage. 6. T cells release certain cytokines that cause the B cells to produce more antibodies against the synovium. These antibodies result in the activation of the complement system (a group of proteins present in the blood that are activated sequentially and lead to cell destruction). 7. Cytokines cause the cells of the pannus to release a large amount of destructive enzymes. They also stimulate the cells of the cartilage (chondrocytes) and bone (osteocytes) to release destructive enzymes.

What factors can affect the rate of healing a fracture?

1. Type of bone 2. Patient age 3. Mobility at the fracture site 4. Separation of bone ends 5. Bone loss 6. Infection 7. Disturbance of blood supply 8. Other factors 1. Type of bone Cancellous (spongy) bone: This applies to bones which are composed mainly of cancellous tissue, and also to fractures involving the cancellous bone found at the ends of long bones. Cancellous bone heals in the 6 weeks after the time of injury, and protection of the fracture can be abandoned in almost all cases. For example: 1. Weight bearing after a fracture of calcaneus may be permitted after about 6 weeks 2. Patient with a traumatic compression fracture of a vertebral body may begin full mobilization after 6 weeks 3. Bed rest for 6 weeks is usually advised for any fracture of the pelvis involving those parts through which weight transmission is mediated. Cortical (compact) bone: Endosteal callus may take many months to become reasonably well established, and many uncomplicated long bone fractures may take 9-18 weeks to unite. In some cases, abundant external bridging callus may allow an earlier return of function. For example: 1) Average time to union of a fracture of the tibial shaft treated conservatively is 16 weeks 2) Fractures of the humeral shaft can often be left unsupported after 10 weeks 3) Fractures of the metatarsals, metacarpals and phalanges, where external bridging callus is usually substantial, are usually quite firm in 4-5 weeks. 2. Patient Age The speed of union decreases as age increases until skeletal maturity is reached. Then there is not a great difference in the rate between young adults and the elderly. Apart from great speed of union in children, they also have remarkable powers of remodeling fractures. This is great as far as displacement is concerned, but poor in the case of axial rotation in both adults and children. The power of remodel decreases rapidly once adolescence is reached. 3. Mobility at the fracture site Excessive mobility persisting at the fracture site for example due to poor fixation may interfere with vascularisation of the fracture haematoma; may disrupt early bridging callus and may prevent endosteal new bone growth. 4. Separation of bone ends If bone ends are separated, the union will be delayed or prevented; and this will interferes with the normal mechanisms of healing. Separation may occur under several circumstances: 1) Interposition of soft tissue between the bone ends. E.g. in fractures of the femoral shaft, one of the bone ends may become isolated from the other by herniating through some of the surrounding muscle mass, thereby delaying or preventing union. 2) Excessive traction. 3) Following internal fixation. The fixation device may continue to hold the bone fragments in the way that may prevent bones to reunite. The internal fixation device may interfere with the local blood supply and the fracture haematoma. 5. Bone loss This is comparatively rare. The main causes are bone extrusion in open fracture at the site of the causal incident, bone removal during debridement procedures, and injuries due to gunshots or explosions. Because of the mechanism of injury is often accompanied by skin loss, tissue contamination, and neural and vascular damage, the loss is usually substantial and treatment becomes prolonged and difficult. The first decision that must be made is therefore whether amputation is the best approach. If decided not to amputate, an appropriate method of fixation of the fracture must be chosen depending on the site, extend of bone loss and other local factors. 6. Infection Infection at region of fracture may delay or prevent union. Infection at fracture site is extremely rare, usually occurs by an open injury or treated with internal fixation. 7. Disturbance of blood supply Reduction of blood supply to site will interfere with the healing process. Interference with the blood supply to one fragment at the time of injury leads to immediate bone death. On the other hand, reduction of blood supply to one fragment, especially if cancellous bone is involved, may not interfere with union; in some situations may apparently stimulate it. Also, bulky internal fixation may interfere with local blood supply too as previously mentioned. 8. Other factors 1) Smoking, slows down rate and reduce quality of union 2) Joint involvement, occasionally delayed if involves a joint due to dilution of the fracture haematoma by synovial fluid 3) Bone pathology, some primary and secondary malignant bone tumours may delay or prevent union 4) HIV/AIDS, HIV patients have retroviral therapy causes derangement in the levels of those cytokines involved in

What will appear on an x-ray if a patient has gout?

1a) Acute Gout - inflammatory arthritis AG distribution: first MTP joint - most commonly affected, ankle, elbow, wrist and hand can also be involved. Distribution is usually asymmetrical X-rays *Radiological changes do not appear until years of recurrent gout attacks have elapsed 1b) Chronic Gout - inflammatory arthritis Patients with uncontrolled hyperuricaemia who have had recurrent attacks of gout for years X-rays tophus formations - soft tissue deposits of urate - tophi will appear opaque on the x-ray "punched out" erosions +/- gross bone and joint destruction soft tissue swelling overhanging edges sclerotic bone

What will appear on an x-ray with a patient with pseudo gout?

2) Calcium Pyrophosphate dehydrate (Pseudo Gout) CPPD crystals are deposited mainly in cartilage but also in the synovium, joint capsule and tendons. Distribution: knees, hip, shoulders, elbows, wrists and MCPs (2nd and 3rd) X-rays Chondrocalcinosis (calcification of cartilage) - often noted in the menisci of the knee, triangular cartilage of the wrist and the symphysis pubis. OA - like changes (i.e. cartilage loss, sclerosis, cysts and osteophytes)

Discuss acute inflammation?

3 main parts: 1. Vasodilation (hyperaemia) a. Involves increased blood flow to the injured area and increased hydrostatic pressure, by mediator-induced relaxation of arterioles and precapillary sphincters. b. Associated with the first two components of Lewis' triple response- flush and flare, which explains signs of redness and heat. 2. Increased vascular permeability and oedema Under the influence of inflammatory mediators, endothelial intracellular proteins contract which results in: a. Increased fenestration (gaps) between endothelial cells1 b. Increased permeability of vessels to plasma proteins c. Protein leaks out of the plasma into the interstitial spaces, which reduces the intravascular osmotic pressure and increases the osmotic pressure of the interstitial fluid. Together with the increased hydrostatic pressure from hyperaemia, this leads to an outflow of fluid from plasma and its accumulation in the interstitial tissue. The net increase of extravascular fluid results in oedema. As a result, blood flow rate is decreased and blood viscosity increases. d. The protein-rich leaking fluid is an exudate. e. Explains the last component of Lewis' triple response- 'weal'. 3. Leucocyte emigration - The cellular events: 5 stages: a. Margination - Occurs as fluid leaves the vessel (due to vascular permeability) causing leucocytes to settle out of the central flow column and 'marginate' along the endothelial surface. b. Rolling of leucocytes along the endothelium due to repeated formation and destruction of transient adhesions with the endothelium. c. Adhesion - Leucocytes firmly adhere to the vascular endothelium. d. Transmigration (diapedesis) - Leucocytes pass between endothelial cells into tissue spaces. e. Chemotaxis - Once outside the blood vessel, neutrophils are guided towards the injury by various diffusing chemotactic factors. Examples include the chemokines and the complement peptide C5a, which is released when the complement system is activated.

How long does a fracture take to heal in an adult?

6 weeks

Define acute inflammation?

A rapid response to an injurious agent that serves to deliver mediators of host defense to the site of injury.

What is the vestibular system and how does it help in standing upright?

A cavity situated at the entrance to a hollow part of the ear. The vestibule of the ear is the cavity of the bony labyrinth that contains the saccule & urticle - the organs if equilibrium. Split into Otolith organs and semicircular vessels Semicircular canals: Receptors here are responsible for monitoring dynamic equilibrium. Here, dispersion of fluid upon movement of the head causes impulses to be generated & subsequently be transmitted to the brain via the vestibulocochlear nerve. There are 3 canals in both ears. At the base of each canal lies the ampulla, containing the crista (a structure containing hair-like projections) which is inserted into the jelly-like covering of the cupula. NB. For detecting angular acceleration Otolith organs: Consist of the utricle & saccule, which contain a otithilic membrane lined with masses of small crystals of calcium carbonate. In the accule/utricle there is a fluid called endolymph & this moves in accordance with the position of the head. Receptor hairs detect this movement and it passes to brain via vestibulocochlear nerve. NB. For detecting linear acceleration.

Define subluxation?

A partial loss of congruity between articular surfaces

What is the treatment for reactive arthritis?

ACUTE • Analgesia • NSAIDs • Steroid* • Antibiotics - if organism is isolated • Rest • Splinting • Rehab *Septic A. must be excluded before use of corticosterioid CHRONIC • Arthralgia NSAIDS • Physio • DMARDs (used for severe & persistent disease)

Invuntary Smooth muscle and cardiac muscle is controlled by?

AUTONOMIC SYSTEM of the PERIPHERAL NERVOUS SYSTEM.

What is drug efficacy?

Ability to produce the maximal response possible, For example, agonists can be divided into full agonists, which give an increase in response with increase in concentration until the maximum possible response is obtained, whereas partial agonists also give an increase in response with increase in concentration but cannot produce the maximum possible response.

What are the risk factors for falling in the elderly?

Accidents: • Some accidents can't be avoided, but through keeping active, and engaging in strength and balance training, research has shown that the risk can be lessened. Disease and ageing: • Eye - MD, glaucoma, cataracts etc. • Middle ear - reduced hairs and nerve fibres in vestibular system makes relexes slower and less accurate • Brain - reduced integration of sensory information coming from the body means person is slower and less responsive • Less muscles mass and reduced strength, and slower contraction affects speed and accuracy of movements, and stamina. • Diseases like Parkinson's • Replacement joints and joint disorders like osteoarthritis affect stability. • 10% of falls are associated with acute illlness, e.g. stroke, MI etc. Poision and polypharmacy: • The risk of falls increases if the individual is on >4 medications • Some medications have an added risk of associated fallls: Psychotropics (like diazepam) • Agents for lowering BP (like statins) e.g. for hypertension; Treatments for heart failure and angina; Narcoleptic • Alcohol considerably increases risk. Environmental factors: • Slippery surfaces, trailing wires, loose or frayed carpets, poor lighting, climbing on ladders or stools, or wearing loose fitting trailing clothes are just some of the 'environmental factors' that can cause falls.

What is Lymphodema, presentation, causative organism and treatment?

Accumulation of lymph in tissue, causing swelling. Presentation: Usually occurs in legs, so patient presents with swollen legs CO: Accumulation of lymph in tissues. causes such as breast cancer surgery/treatment and bacterial or fungal infections. Tx: Elastic support with bandages and diuretics.

What is the thin filament of muscle made of?

Actin: Each actin molecule has a binding site for the attachment of the myosin head Tropomyosin- threadlike in shape and twist around the actin concealing the myosin binding sites. Troponin complex Troponin I - binds to actin and inhibits contraction Troponin T - helps to stabilise tropomyosin Troponin C - binds to calcium ions.

What are the symptoms of gout?

Acute Gout: • Acute onset of symptoms e.g. overnight • Severe pain and swelling • Skin overlaying the joint is shiny, warm and red • Joint is tender • 1st Metatarsophalangeal joint is most common (big toe) • Less common- ankle, knee, wrist, elbow and hand joint (often mimics RA) Chronic Gout: • Musculoskeletal- tophus formation (soft tissue deposits of urate. E.g. in helix of ear) and joint destruction. (cartilage destruction and bony erosions causing deformities) • Renal disease- urate deposition causing uric acid stones in urinary tract.

What are acute phase proteins?

Acute-phase proteins - Proteins that are produced by the liver and induced by circulating levels of IL-1; the serum levels of these proteins increase significantly during infection, e.g. C-reactive protein

What are the side effects of aspirin?

Adverse side effects • GI ulceration and erosions - Local effects - Impaired mucosal prostaglandins • Bleeding - Anti-platelet effects - Displacement of warfarin • Complex acid-base effects in overdose - Respiratory alkalosis - Reye's syndrome (as a result no longer give it to <12 yrs) Aspirin and Reye's syndrome - Usually <5 years old • Associated with viral illnesses - Influenza epidemics - Varicella (chickenpox)

What are the likely causes of limping in adolescents aged 11> years?

Adolescents 11> Infectious: - Septic arthritis (gonococcal) - Osteomyelitis Trauma: - Fractures - Sprains and strains Rheumatologic: - Juvenile rheumatoid arthritis Degenerative: - Slipped capital femoral epiphysis

What is autonomy?

Adult patients have the right to refuse treatment at any time, unless deemed medically incompetent. This is regardless of whether the doctor agrees, or disagrees with the decision. Doctor should not make assumptions about patient when relaying treatment options to them (e.g. not telling a 'poorer' patient about a treatment that is only available privately) However, where a patient wishes to have a treatment that - in the doctor's view - is not clinically indicated, there is no ethical or legal obligation on the doctor to provide it.

What is SLE?

Aetiology is unknown however there is a genetic link, hormone link (pre-menopausal women most affected), drug induced An inflammatory multisystem disease of unknown aetiology with diverse clinical and laboratory manifestations and a variable course and prognosis

Describe what is gout, its symptoms, investigations and treatment / management?

Aetiology: • Drinking too much alcohol • Lack of Vitamin C in your diet • If you drink sugar-sweetened soft drinks high in fructose (A recent research study found that having two drinks a day of a sugar-sweetened soft drink increased the risk of developing gout by 85%) • Fructose-rich fruits and fruit juices may also increase the risk. • Eating a lot of heart, herring, sardines, yeast extracts, or mussels may increase the level of uric acid • However, eating a normal balanced diet should not have much effect on the uric acid level. • Some medicines: Diuretics, aspirin and some chemotherapy medicines. • More uric acid is made than usual in illnesses where the cells of the body have a rapid turnover (severe psoriasis and some blood disorders). • Obesity, high blood pressure, kidney damage, diabetes mellitus, bone marrow disorders, lipid disorders, vascular disease. Pathophysiology: Gout occurs in people who have a higher-than-normal level of urate in the bloodstream. About two thirds of the urate in our bodies comes from the breakdown of purines that are present in the cells of our bodies. The other third comes from the breakdown of purines in some of the foods we eat. When urate levels start to build up, your body normally gets rid of any excess through your kidneys into your urine. If your body is making too much urate, or if your kidneys aren't able to remove excess urate effectively, then urate levels start to rise. If the level goes above a certain point, urate can form crystals of sodium urate. These crystals mainly form in and around joint tissues, especially your finger and toe joints. The crystals gradually build up in your cartilage and after some years can spill out into the joint cavity. This is known as crystal shedding. The hard, needle-shaped crystals come into contact with the synovium and make it very inflamed very quickly. The inflammation process dissolves the crystals in your joint, and the attack gradually settles over a few days or weeks, depending on how many crystals were shed. A build-up of crystals can eventually lead to the formation of tophi in and around your joints. Tophi can grow and cause pressure damage to your joint cartilage and bone. This is just like the damage caused by osteoarthritis, but tophi can cause more regular, daily pain. At this stage the condition is often called chronic tophaceous gout. By the time tophi are visible from the outside, the parts below the skin may be quite extensive. Triggers of gout attacks: • a knock or injury to the joint • an illness, such as pneumonia or flu, that makes you feverish • an operation, which puts your temperature up a little • excessive eating • excessive drinking of alcohol • dehydration Symptoms: Acute Gout: • Acute onset of symptoms e.g. overnight • Severe pain and swelling • Skin overlaying the joint is shiny, warm and red • Joint is tender • 1st Metatarsophalangeal joint is most common (big toe) • Less common- ankle, knee, wrist, elbow and hand joint (often mimics RA) Chronic Gout: • Musculoskeletal- tophus formation (soft tissue deposits of urate. E.g. in helix of ear) and joint destruction. (cartilage destruction and bony erosions causing deformities) • Renal disease- urate deposition causing uric acid stones in urinary tract. Investigations: • Synovial fluid analysis Needle aspiration of symptomatic joints and examined under a microscope under polarised light. If Sodium urate crystals are present they will be needle shaped and show strong negative birefringence (meaning crystals appear yellow if parallel to plane of light and blue if at right angles to plane of light). Blood test • Serum uric acid measured but is NOT diagnostic of gout. • Raised ESR and CRP • Full blood count- may show polymorphonuclear leucocytosis (These are a type of neutrophil found in inflammatory conditions). Treatment: • Synovial fluid analysis Needle aspiration of symptomatic joints and examined under a microscope under polarised light. If Sodium urate crystals are present they will be needle shaped and show strong negative birefringence (meaning crystals appear yellow if parallel to plane of light and blue if at right angles to plane of light). Blood test • Serum uric acid measured but is NOT diagnostic of gout. • Raised ESR and CRP • Full blood count- may show polymorphonuclear leucocytosis (These are a type of neutrophil found in inflammatory conditions). Patient education- exercise and low purine diet e.g. less oily fish and red meat. Pharmacological NSAIDS- to reduce pain and inflammation Colchicine- 500mcg 2-3 x a day Corticosteriods-for patients who can't tolerate the two above but should only be used short term. Prophylactic therapy- allopurinol- decreases uric acid synthesis. (But should not be used until 2-3 weeks after gouty attacks otherwise can make gout worse).

What are the clinical features of PM / DM?

Age of onset is 40 - 60 years. DM is often seen in children but PM is unusual in this age group. Myositis: • PM and DM are characterised by symmetrical proximal muscle weakness - It develops over weeks to months. • Patient find certain tasks increasingly difficult: o Rising from chair o Climbing stairs o Reaching for things above head height. • There is intercostal muscle and diaphragm involvement - This can lead to type 2 respiratory failure. • Dysphagia and regurgitation of food - due to weakness of the pharyngeal muscles and upper third of oesophagus. • Muscle pain • Muscle bulk and tendon reflexes often remain normal. Cutaneous Features: • DM - Skin rashes: o Gottrons papules - scaly papules or plaques over MCP and PIP joints. o Heliotrope rash - rash over eyelids (lilac discoloration with periorbital oedema). o Macular erythematous - Rash on neck, chest, shoulders and hands o Calcinosis - seen in juvenile DM o Cutaneous vasculitis - Can cause ulceration There are many systemic features of PM and DM: • Non specific: o Fatigue o Malaise o Weight loss o Fever Skeletal features: • Polyarthralgia • Myalgia Pulmonary features • Interstitial lung disease • Aspiration pneumonia - due to dysphagia Cardiovascular features • Myocarditis - can cause cardiac failure or arrhythmias • Reynaud's phenomenon • Vasculitis Gastrointestinal Features: • Vasculitis can result in intestinal haemorrhage or perforation. Malignancy: 5 - 15 % of adults with inflammatory muscle disease have an underlying malignancy. There is stronger association between DM than PM. Malignancies associated with DM are: • Lung • Oesophagus • Breast • Colon • Ovary

What is the mechanism of action of antidepressants in pain and what type of pain is it used for and name some types?

Amitriptyline, Fluoxetine, despramine, venlafaxine. The action and mechanism as an analgesic is not well understood. The current theory as to their mechanism of action is inhibitory effect on nociceptors pathways by blocking the reuptake of serotonin and norepinephrine. Rapid re-uptake limits the time that both serotonin and norepinephrine are available for receptor binding and thereby to inhibit transmission of nociceptive signals. The drugs also, to varying degrees, block a number of other receptor types involved in pain processing including α-adrenergic, H1-histaminergic and N-methyl-D-aspartate (NMDA) receptors. They may also have blocking effects on calcium and sodium channels and be weakly stimulatory at μ-opioid receptors. - Neuropathic pain

What is Externalities?

An externality is when an external party to a transaction is directly affected by it and not compensated. The use of vaccination programmes in healthcare is an example of a positive externality. People who are vaccinated against a disease are less likely to spread the infection and infect others. Positive externalities are where social benefit of the consumption of a commodity exceeds the private benefit. Private benefit - benefit to consumers who buy and consume goods Social benefit - benefit to all in society, including those who do not consume it An example of a negative externality is pollution caused by pharmaceutical company making medicines.

Define pain?

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

What do prostaglandins act on and what effect do they have on the body?

Analgesic action: - Inhibiting the actions of prostaglandins. Normally, prostaglandins act to: • Make nociceptive fibre endings more sensitive to inflammatory mediators, e.g. histamine and bradykinin. • This makes their pain message stronger Anti-inflammatory action: - Inhibiting the actions of prostaglandins Normally, prostaglandins act to: • Cause vasodilation, vascular permeability and oedema during inflammation. Antipyretic action - Inhibiting the actions of prostaglandins Normally, prostaglandins act to: • Increase temperature set-point by acting on the hypothalamus. Ordinarily this is done by cascade, by leucocytes releasing pyrogens such as interleukin-1 which affect the hypothalamus, and are thought to produce Prostaglandins E's. The NSAID's affect the COX which produces PGE. The importance of prostaglandin It enhances pain by potentiating (enhancing) the effects of inflammatory markers such as bradykinin and histamine on nociceptive nerve endings, causeing the sensation of pain. Other functions of prostaglandins, which explain NSAID's side effects: • GI mucosal protection • GI fluid secretion • Inhibits gastric acid

What terms are used to describe a position of a fracture / bone?

Angulation Displacement Distraction Impaction Foreshortening

What is angulation?

Angulation - this is the angle of the distal fragment of the bone measured from the proximal fragment.

Define chronic inflammation?

Inflammation of prolonged duration (weeks or months) in which active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously. Can start following acute inflammation if the causative agent is not removed or as an asymptomatic response.

Sjogrens is associated with which autoantibody?

Anti Ro Anti La

Sle is assocaited with which antibody?

Anti dsDNA Anti Sm

What antobodies are significant in sjogrens syndrome?

Antibodies Antinuclear Antibodies Anti La (35-85%) Anti-Ro (40-60%) Increased levels of gamma globulin Rheumatoid factor (90%)

What antibodies are significant in SLE investigations?

Antibodies Antinuclear Antibodies Anti ds DNA (70%) Anti-Ro (40-60%) Anti-Sm (Caucasian: 10-25%) (Black Af.: 30-505) Anti-La (15%) Rhuematoid Factor (25%)

What antibodies are significant in systemic sclerosis?

Antibodies Rheumatoid factor (30%) ANA (90%) In limited sclerosis, anti-centromere antibodies occur In diffuse sclerosis, anti-topoisomerase-1 antibodies

What antibodies are significant in PM/DM?

Antibodies Rheumatoid factor (50%) - Anti JO (30%)

Define disability

Anyone who has a physical or mental impairment that has a substantial and long-term adverse effect on his or her ability to carry out day-to-day activities" (The Equality act of 2010)

What is prostaglandin and what does it cause?

Arachidonic acid, prostaglandins and leukotrienes - Prostaglandins - Derived from mast cells and leucocytes; causes vasodilation, permeability and pain.

what is Asymmetric Information?

Asymmetric information is where one person has more information than another. This creates a power imbalance which can lead to market failure. In healthcare GPs often act as agents for their patients and tend to have more information and knowledge.

What factors can cause lost of tolerance?

Autoimmune diseases/disorders which are multifactorial and can in many cases lead to chronic debilitating disorders. They are caused by failure of the tolerance processes to protect the host from the action of self-reactive lymphocytes. Some factors that play a part are: • Certain HLA haplotypes predispose to autoimmunity • Hormonal influences in autoimmunity • Environmental factors: o Molecular mimicry: sequence homology between microbial and human proteins as potential cross-reacting T-cell epitopes o Microbes may act as adjuvants: self-antigen is associated with microbial antigens (altered self-antigen) and induces autoimmunity o Microbes may activate lymphocytes polyclonally: the activation of B cells occurs without T help8

What is organ specific autoimmunity?

Autoimmune response primarily directed against a single organ or gland so the manifestation is largely limited to that organ. Can be caused by cell-mediated or humoral effector mechanisms9: • Cellular damage where lymphocytes or autoantibodies bind to cell membrane antigens causing cellular lysis and/or inflammatory response in the affected organ. Gradually the damaged cells/tissue are replaced by connective tissue (fibrosis) and the organs function is declined. E.g. Hashimoto's thyroiditis, autoimmune anaemias, Goodpasture's syndrome, Insulin-dependent diabetes mellitus. • Stimulating/blocking Abs where auto-Abs act as agonists. Binding to hormone receptors and stimulate inappropriate activity. Leading to an overproduction of mediators or increase in cell growth. Or auto-Abs act as antagonists, binding to hormone receptors and blocking the function causing decreased secretion of mediators and atrophy of the affected organ. E.g. Grave's disease, Myasthenia gravis.

what is autoimmunity?

Autoimmunity is the term used to describe specific immunological reactions against components of the individual own body. These may occur in a wide range of clinical situations and are not always associated with harmful effects or diseases. There are, however a distinct group of autoimmune diseases which may be organ specific or non-organ specific. A most obvious example would be rheumatoid arthritis. Rheumatoid Arthritis (RA) is an autoimmune disorder and the most common cause of chronic inflammatory symmetrical polyarthritis affecting small and large joints of upper and lower limbs

What is tendonitis, presentation, causative organism and treatment?

Inflammation of the tendon. Commonly occurs after excessive overuse, but can sometimes be bacterial. Presentation: Pain in joint. Tennis elbow, jumpers knee etc. CO: Excessive overuse Tx: NSAIDs and rest

Discuss peripheral tolerance in B cells?

B cells require interaction with T helper cells to be activated; if this does not occur then the B cell will enter a state of anergy.

What are the ethics of treatment disclosure?

Before any treatment is given to the patient, guidelines state that the patient must be fully informed about the treatment in order to give informed consent. The ethical guidelines on the GMC website state that the only occasion where information can be withheld from a patient is when the information would cause them serious harm. This does not mean that information can be withheld if it will cause the patient to become upset. If the doctor decides to withhold information from the patient this should be recorded in the notes and the doctor should be prepared to justify and answer questions about why they withheld the information.

What is Ankylosing Spondylitis (AS) and who does it effect?

Belongs to the group "spondyloarthropathy" - group of related and overlapping inflammatory joint disorders AS is part of the Spondyloarthropathy (SPA) group which includes reactive A., psoriatic A., and Reiter's syndrome (list not exhaustive) SPAs genetically associated with HLA-B27 Distinct from RA, SPA which includes AS is characterized by enthesitis* & synovitis Patients are seronegative for RF *enthesis is the insertion of a tendon, ligament or capsule into bone Epidemiology: Prevalence: 0.5-1% of amongst Caucasians 3 times more common in men than women, more severe in men Presents in early adulthood, peak age is mid-20s

What is Imperfect information?

Better information and patient education would make healthcare interventions more efficient, and less chance of market failure. Consumers would understand the health benefits of a therapy and at what cost. However, the information patients have may not be perfect because: 1. Patients don't know they need the information 2. They do not know where to get the information 3. They don't know the information exists 4. They cannot interpret and use the information 5. The information is incomplete and uncertain We need good, reliable data and information available to be able to use when making healthcare decisions to achieve efficient use of resources.

What are biologics?

Biologics are very expensive drugs that cost about £10,000 per year per patient. They are very effective at modifying the progression of RA by inhibiting Tumour Necrosis Factor (TNF). This is one of the key cytokines in inflammation. If 2 DMARDs aren't effective in a patient then a biologic may be tried. If patients don't show a measurable response they should be stopped. Biologics include: Infliximab, Adalimumab and Etanercept.

What blood tests may you order is you suspect an inflammatory disease?

Blood tests you might order: WBC: White Blood Count, elevated in infection, reference range = 4.0-11.0 x 109/L. ESR: Erthrocyte Sedimentation Rate, elevated in inflammation, reference range varies with age but normal average ranges are 3 mm for men and 7 mm for females, a raised ESR may indicate infection, rheumatoid arthritis, malignancy, myocardial infarction, anaemia or marcocytosis. CRP: C-Reactive Protein, raised in inflammation, reference range = Normal range of CRP in serum is <10 mg/L, associated with wide range of acute and chronic inflammatory conditions like bacterial, viral, or fungal infections; rheumatic and other inflammatory diseases; malignancy; and tissue injury or necrosis. ANA Testing (e.g. Immunofluorescence): Antinuclear antibodies (ANAs) are antibodies that target the contents of the nucleus of normal cells. Different subtypes of ANA target different proteins in the nucleus. Their presence indicates an auto-immune response, but this test alone isn't specific enough to show which connective tissue disease it is. Outcome of test is either positive or negative. Positive ANA tests can be found in the following conditions: • SLE • Drug induced lupus • Scleroderma • Dermatomyositis • Sjögren's Syndrome • Mixed connective tissue disease • Long standing RA • Some conditions that aren't connective tissue diseases: certain infectious diseases, certain endocrine diseases, some cancers, liver disease, haematological disease, juvenile arthritis and as a result of some drugs. ENA Testing (e.g. ELISA): extractable nuclear antigen (ENA) test. Outcome is a specific autoantibody. See table below.

what is central tolerance in B cells?

Bone marrow (B cell death when they encounter antigen they recognise)

Discuss fracture healing?

Bone repair can be divided into four stages: - haematoma formation, - callus formation, - callus ossification - bone remodelling. • Bone growth in length happens at the epiphyseal plates The steps that happen after a bone is fractured: 1. First of all a haematoma is formed. A haematoma is 'an accumulation of blood within the tissues that clots to form a solid swelling' In the case of bone fracture, it occurs because the blood and vessels in both the bone and periosteum are damaged. The clot stops the bleeding thanks to the fibrous proteins it contains. However, due to the damage to the blood vessels the osteocytes in the bone do not receive enough blood and the bone tissues by the fracture will die. 2. Next the callus is formed. The callus is 'the composite mass of tissue that forms between bone ends when the fracture is healing.' This can be divided into the internal and external callus, with internal callus being the callus between the two parts of bone and in the marrow cavity, and external callus being being outside this, around the bone. The following sequence of events occurs to form the callus: • Cytokines from the macrophages also recruit fibroblasts and osteoblasts. As the clot begins to break down, macrophages clean up cell debris, osteoclasts break down dead bone debris and fibroblasts produce granulation tissue made up of collagen, connective tissue cells , blood vessels, histiocytes and extracellular materials. • The collagen fibres from the fibroblasts form a dense network that holds the bone together • Chondroblasts produce cartilage in the fibrous network. • New osteoblasts are formed to produce new bone. • The external callus is there to stabilize the ends of the bone and is formed of cartilage, which takes less time to form than bone. 3. The callus is now ossified. This happens through the cartilage in the external being replaced by woven, cancellous bone (this is known as endochondral ossification). Firbroblasts do this job. 4. The bone now has to be remodelled, because woven bone is not as strong as lamellar/compact bone. This process takes a long time, even longer than a year in some cases. What happens is that the osteons from both sides of the fracture must extend across the fracture line. Meanwhile osteoclasts get rid of the external callus.

Define inflammation?

Inflammation: the protective response of living tissue to cellular injury intended to localise and eliminate the initial cause of injury, limit tissue injury and restore tissue to normality.

What is the reality of supply and demand in healthcare?

But the reality is slightly different. In practice demand of healthcare provisions is always outstripped by the supply and the demand for healthcare is ever increasing. SUPPLY < DEMAND

What is peripheral tolerance in T - cells?

CLONAL ANERGY: Auto-reactive T cells when exposed to antigenic peptides that do not possess co-stimulatory molecules (B7-1 or B7-2) become anergic (nonresponsive) to the antigen. I.e. if only 1 of the 2 signals is recognised then anergy occurs but if both are present the cell is activated. To understand anergy it is important to known that a naïve CD4+ T cell requires 2 signals to proliferate and differentiate into effector cells. If the T cell does not receive this second signal it becomes inactivated. In the case of anergy, a T cell will recognise the antigen via the MHC - TCR interaction however it does not receive a second signal. Normally the second signal is from a co-stimulator which are ligands that are expressed on professional antigen presenting cells (APCs) found on macrophages, B lymphocytes or dendritic cells. Usually it is CD28 found on the T cell binding to one of the B7 family (a type of receptor). This reaction would then cause the cell to activate and proliferate producing cytokines. So if no co-stimulatory molecule appears then the cell undergoes longstanding unresponsiveness or the cell undergoes apoptosis. 2. CLONAL IGNORANCE: T cells reactive to self-antigen not represented in the thymus will mature and migrate to the periphery, but may never encounter the appropriate antigen because it is sequestered in inaccessible tissues. Such cells may die out for lack of stimulus. 3. IMMUNE SUPPRESSION: self-reactive T lymphocytes that encounter self-antigens may develop into regulatory cells. These cells function is preventing or suppressing the activation of other, potentially harmful, self-reactive lymphocytes. 4. CLONAL DELETION: Repeated activation of mature T cells by self-antigen or recognition of self-antigens without the second signal as stated before can induce apoptosis.

What doe COX-2 action and where is it mainly found?

COX- 2 is produced at the site of inflammation and is involved in the inflammatory response. NSAID's action on it can reduce Bone Pain, by suppressing its pain-increasing and inflammatory effect.

Describe what is pseudo gout, its symptoms, investigations and treatment / management?

Calcium pyrophosphate dehydrate (CPPD) crystal deposition disease involves intra-articular and or extra-articular deposition of CPPD crystals. Etiology: The cause is unknown. Frequent association with other conditions such as: - trauma (including surgery) - amyloidosis, - hypothyroidism, - hypomagnesemia, - hyperparathyroidism, - gout, - Hemochromatosis (too much iron being absorbed from the gastrointestinal tract) - old age, all these suggest that CPPD crystals deposits are secondary to degenerative or metabolic changes in the affected tissues. Some cases are familial, unusually transmitted in an autosomal dominant pattern. Both symptomatic and asymptomatic CPPD crystal deposition (chondrocalcinosis) is common with aging. The incidence of asymptomatic chondrocalcinosis in patients aged 70 is about 3% reaching nearly 50% in patients aged 90. Asymptomatic chondrocalcinosis is common in the knee, hip. Women and men are affected equally. Pathophysiology • chemical imbalances, which can trigger an increase in crystal production and cause deposits • changes in cartilage due to osteoarthritis encouraging calcium crystal formation • crystals being shaken loose into joints or tendons by injuries to the joint or tendon, or by having a fever (for example flu or a chest infection) or a stress to your body (such as an operation or heart attack) • the way crystals are made - the hard, sharp angles of the crystals rub and grind things down that are in contact with them. Their rough surface also has a strong electrical charge, which can injure cells and trigger your immune system • metabolic diseases - which affect the regulation of calcium or polyphosphate levels, including hyperparathyroidism (overactivity of the parathyroid glands), haemochromatosis (also known as iron-storage disease) and hypomagnesaemia (magnesium deficiency) • genetic factors - recent research has found that an abnormality of the ANKH gene may lead to the production of too much pyrophosphate, which can result in widespread calcium crystal depositing. This can cause recurrent attacks of acute CPP crystal arthritis at an unusually young age (20s or 30s) Symptoms: • sudden pain and stiffness in affected joint (most commonly knee) • swelling and tenderness • red, inflamed skin over the joint • raised temperature • generally feeling unwell • These symptoms tend to last several days to 2 weeks before completely settling • On investigation the crystals appear to be rhomboid shaped Investigations: • Pseudogout is suggested when abnormal calcifications chondrocalcinosis. are seen in the cartilage of joints on x-ray testing. • The arthritis of pseudogout is common in older adults, particularly in the context of dehydration such as occurs with hospitalization or surgery. • The diagnosis of pseudogout is ultimately made when fluid from a joint is examined under a special microscope called a polarizing microscope. With this microscope, the calcium pyrophosphate crystals are identified. Treatment: Treatments for acute attacks of calcium crystal diseases are aimed at relieving pain, reducing inflammation and shortening the length of the attack) • Paracetamol, co-codamol and non-steroidal anti-inflammatory drugs (NSAIDs) for pain • Colchicine is sometimes used, which can reduce the symptoms and severity of acute CPP crystal arthritis. • Joint aspiration and injection This is to quickly reduce the high pressure in the joint that is causing the extreme pain. It is common after this to inject a small volume (1-2 ml) of a long-acting steroid back into the joint through the same needle. This helps to reduce inflammation in the lining of your joint and prevent the build-up of more fluid. • Lavage - You may need to have your knee joint washed out in hospital, especially if an infection is a possible cause. However, this is very rarely needed.

What is displacement?

Can be lateral or medial. Lateral displacement is the degree to which the two ends of the fractured bone are out of alignment with each other. The same example goes for medial too.

What are the structures of the nervous system for controlling movement?

Cerebral cortex is the main centre for the control of voluntary movement. It uses the information it receives from the cerebellum, basal ganglia and other centres in the CNS, as well as the feedback from the periphery, to bring movements under voluntary control. The cerebral cortex provides the transition from perception to action since it is able to perceive, understand and integrate all various sensations. Its function is to plan and execute motor activities. Basal ganglia is predominantly for the provision of internal cues for the smooth running of learned movements. This includes the selection of initiation of most activities of the body as well as the selective suppression of unwanted movements. The basal ganglia is also responsible for controlling highly practiced behaviors such as driving a car, skilled movements that you carry out with little thought. Cerebellum does not initiate motor activities but plays a important role in planning, mediating, correcting, coordinating and predicting motor activities especially for rapid movements. Loss of cerebellum will lead to incoordination of rapid movements such that the actions are still available but no longer rapid or coordinated. This is caused by the loss of the planning function. The cerebellum makes comparisons between the movement plan and output and can change movement signal if there is a discrepancy. The cerebellum smooths muscle contractions, maintains muscle tone and posture, coordinate the motions of different joints with each other Brainstem connects the spinal cord to the cerebral cortex. The principle role of the brainstem is to provide background contractions of the postural muscles of the body, so provide support for body against gravity. Spinal cord's grey matter is for spinal reflexes and other automatic motor functions in addition to transmitting information to the brain and sending commands to the body.

What is carpal tunnel syndrome?

Carpal tunnel syndrome = compression of the median nerve inside the carpal tunnel.

What do Chondroblasts produce?

Cartilage

What are the characteristics, receptor type, pain quality of A delta fibres?

Characteristics: • Primary afferent fibres • Large diameter • Myelinated • Fast conducting Receptor type: • High-threshold mechanoreceptors respond mechanical stimuli over a certain intensity. Pain quality: • Well-localised • Sharp • Stinging • Pricking • Referred to as 'fast' or 'first' pain

What are the characteristics, receptor type, pain quality of C fibres?

Characteristics: • Primary afferent fibres • Small diameter • Unmyelinated • Slow conducting Receptor type: • Polymodal respond to more than one type of noxious stimuli: • Mechanical • Thermal • Chemical Pain quality: • Diffuse • Dull • Burning • Aching • Referred to as 'slow' or second' pain

What are the likely causes of limping in children aged 4 - 11 years?

Children 4 - 11 years Infectious: - Spetic arthritis - Transient synovitis - Osteomyelitis Trauma: - Fractures - Sprains and strains Rheumatologic: - Juvinile rheumatoid arthritis Degenerative: - Perthes

Discuss chronic inflammation?

Chronic inflammation - all you need to know!!! 3 main parts 1. Mononuclear cell infiltration These cells predominate after 24 hours, and include: a. Macrophages: Activated by T cell derived cytokines and other products of inflammation. Reach site of injury within 24-48 hours. Remove damaged tissue by phagocytosis and produce growth factors to aid repair through fibrosis. This results in the replacement of damaged tissue with granulation tissue. b. Lymphocytes: B and T lymphocytes are antigen-activated via macrophages and dendritic cells. They release macrophage-activating cytokines (in turn, macrophages release lymphocyte-activating cytokines until inflammatory stimulus is removed). c. Plasma cells: Terminally differentiated B lymphocytes. d. Eosinophils: Found at sites of parasitic infection or allergic (IgE mediated) sites. e. Mast cells 2. Tissue destruction Occurs due to inflammatory cells and persistent infecting material 3. Healing Occurs by connective tissue replacement of damaged tissue, which is accomplished by proliferation of small blood vessel (angiogenesis) and fibrosis.

What is chronic pain and what are its pathways?

Chronic pain can be neuropathic in origin, nociceptive or mixed. A key mechanism in chronic pain is central sensitization ('wind up'). Central sensitization describes changes that occur in the brain in response to repeated nerve stimulation. Following repeated stimulation, levels of neurotransmitters and brain electrical signals change as neurons develop a "memory' for responding to those signals. Frequent stimulation results in a stronger brain memory, so that the brain will respond more rapidly and effectively when experiencing the same stimulation in the future. The changes of central sensitization occur after repeated experiences with pain. Research in animals show that repeated exposure to a painful stimulus will change the animal's pain threshold and result in a stronger pain response. Researchers believe that these changes may explain the persistent pain that occurs in chronic pain. The NMDA receptors, in particular, are thought to play a key role in the development and maintenance of central sensitization. Several other neuromodulators enhance central sensitization, including neuropeptides, prostaglandins, pro-inflammatory cytokines and second messengers. Normally, spinal hyper excitability is counteracted by descending inhibitory systems in the central nervous system. A number of endogenous substances, including opioids, cannabinoids, norepinephrine and adenosine, are released to counteract the development of the central sensitization process. Dysfunction in these inhibitory systems may also contribute to increased spinal hyper excitability in some chronic conditions.

What are the clinical features of SLE?

Clinical features are diverse and the severity of the disease will vary over time. Initial symptoms may be mild and vague but the exacerbations of SLE and the resultant tissue damage can cause significant health problems. Severe lupus flare ups can cause life threatening problems such as renal failure or cerebral vasculitis. There are factors that can cause these flare ups: • Overexposure to sunlight • Oestrogen containing contraceptive therapy • Infection • Stress SLE affects multisystems, the following describes the common symptoms of SLE on these systems: Non specific symptoms: • Fatigue • Malaise • Fever • Weight loss Musculoskeletal • Arthalgia or arthritis - usually polyarticular and does not usually cause erosion and the symptoms are usually worse than the signs. • Myalgia - this is a common feature of SLE. • Avascualr necrosis of bone and osteoporosis can occur but these are often due to corticosteroid treatment. • Septic arthritis - Rare. Dermatological features: • Photosensitivity is common • Malar flush / butterfly rash • Discoid lupus - patchy redness that can cause scarring • Hair loss - this reflects disease activity and alopecia can develop. • Mucosal ulceration - Affects nose, mouth and vagina. • Cutaneous vasculitis - this can present with urticarial (hive) lesions, Livedo reticularis (A mottled purplish discoloration of the skin), palpable pupura (Visible non-blanching haemorrhages), splinter haemorrhages (tiny lines that run vertically under nails) Cardiovascular features: • Serositis (inflammation of the serous tissues of the body, the tissues lining the lungs (pleura), heart (pericardium). • Pericarditis - commonest cardiac feature • Myocarditis - may present with arrhythmias or cardiac failure. • Libman - Sacks Endocarditis (inflammation of the inside lining of the heart chambers and heart valves) - Is due to non-infective vegetations and seldom causes clinical problems. • Reynaud's phenomenon - At least one third of patients with SLE will present with this. It is provoked by the cold, cause's peripheral ischemia. This can be seen in the digits of the fingers , tips of nose and ear lobes which become pale and numb before turning blue. The final phase is of redness and flushing due to eventual vasodilation. • Vasculitis - Presents with skin rashes or ulcers. Pulmonary Feature: • Pleurisy and pleural effusions - are common • Acute pneumonitis (Inflammation of the walls of the alveoli in the lung) - Can mimic pneumonia. Chronic pneumonitis can cause pulmonary fibrosis and presents with gradual shortening of breath. Renal features: • Glomerulonephritis (Acute inflammation of the kidney, characterized by inflammation of the glomeruli, or small blood vessels in the kidneys) - Is the commonest cause of lupus related death in patients. This does not cause clinical feature until there is significant renal damage. It is important that BP and urine protein, red cells are checked so that renal disease can be detected early. Neurological features: • Headaches - migranious • Psychiatric problems • Seizures • Neuropathies • Chorea (jerky involuntary movements affecting esp. the shoulders, hips, and face) Haematological features: • Lymphopenia - Is common • Anaemia - Caused by chronic inflammation or autoimmune haemolysis. • Other cytopenias

Describe a comminuted fracture?

Comminuted or multi-fragmentary fractures tend to occur as a result of direct trauma. They are breaks in which the bone is splintered into multiple different fragments, making anatomical reconstitution very difficult, and at times, impossible.

What is valid consent?

Components of valid concent: • Fully informed; • Capacity; • Voluntarily.

For consent to be valid?

Consent: Before any treatment can be carried out consent should be obtained, in order to make it legal. For the consent to be valid: • The patient must have the capacity to give consent • It must be voluntary • The patient must understand what treatment they are receiving and the risks involved

What is CRUSH syndrome?

Crush injury can follow prolonged continuous pressure on muscle tissue. Crush injury can lead to crush syndrome. Ischaemia reperfusion (when the pressure is released from the crushed limb) is the main mechanism of muscle injury in crush syndrome. There is traumatic rhabdomyolysis. Muscle injury causes large quantities of potassium, phosphate, myoglobin, creatine kinase and urate to leak into the circulation. Myoglobin levels in the plasma are normally very low. If a significant amount of skeletal muscle is damaged (>100 g),excess myoglobin is filtered by the kidneys and can cause renal tubular obstruction and renal damage: the excess myoglobin is nephrotoxic. Intravascular volume depletion and renal hypoperfusion, combined with myoglobinuria, result in renal dysfunction. Crush syndrome is characterised by: Hypovolaemic shock (due to sequestration of water in the injured muscle cells). Hyperkalaemia (release of cellular potassium by the injured muscle cells). This can also lead to: Metabolic acidosis (release of cellular phosphate and sulphate by the injured muscle cells).Acute kidney injury. Disseminated intravascular coagulation (DIC).

What are cytokines?

Cytokines - A family of chemical messengers that bind to specific sites on target cell surfaces. - Lymphokines - cytokines produced by lymphocytes. - Monokines - cytokines produced by monocytes/macrophages. - Interleukins - cytokines that act between leucocytes. - IL-1 activates macrophages and fever. - Interferons - activate macrophages and NK cells and inhibit replication of viruses within cells. - Growth factors - Tumour necrosis factors - kill tumour cells and stimulates muscle catabolism leading to weight loss. - TNFα activates macrophages. The major cytokines that mediate inflammation are Il-1 and TNF (α and beta).

Describe compact and cancellous bone structure.

Picture

How does vision aid in standing up?

Enables us to monitor the positioning of the body within our spatial surroundings

What are the 3 principles decisions on treatments should be based on? But what does the GMC say?

Decisions on treatments can be based on 3 principles: • Facts - This is something which is true beyond a doubt • Hypothesis - This is something which is believed to be true but has the potential to be proved or disproved by empirical data • Value Judgments - This is something that is purely based on personal interpretation However, the GMC states that it is a doctor's role to: 'Identify appropriate treatment options based on: up to date clinical evidence about efficacy, side effects and other risks, referring to any relevant clinical guidelines on the treatment and management of the patient's condition, or of patients with similar underlying risk factors'

What is the the treatment for vasculitis?

Depends on which type of vessels the vasculitis is affecting. But according to the Oxford of Clinical Medicine large vessel vasculitis is treated with steroids and medium/small vasculitis is treated with immunosuppressants and steroids.

Define depression?

Depression is defined as both the presence of a negative/low mood and/or the absence of positive affect, in a patient this would present as a loss of interest and pleasure in most activities. Depression usually comes with many emotional, cognitive, physical and behavioral symptoms.

Appearance of synovial fluid that may be significant discuss?

Less viscous = inflammation cloudy = Presence of microorganisms, wbc's, crystals Reddish tinge = blood

How is a nerve entrapment problem diagnosed?

Diagnosis will centre around history, examination, nerve conduction studies and trial steroid injection. X-rays can be used for any of the nerve entrapment syndromes but rarely used in practice.

Define disability, impairment and handicap

Disability: "Anyone who has a physical or mental impairment that has a substantial and long-term adverse effect on his or her ability to carry out day-to-day activities" (The Equality act of 2010) • These impairments include and range from severe conditions such as MS, to congenital problems (Down's syndrome) , learning difficulties, mental health problems to loss of limbs and deformation. • More than 10 million people in the UK are disabled ( of which just under 10 % are children) - Impairment: any loss or abnormality of psychological, physiological and anatomical structure of function - Handicap: is a disadvantage for a given individual, resulting from impairment or a disability that limits or prevents the fulfilment of a role that is normal for the individual."

What are the clinical features of systemic sclerosis?

Disease is divided into Limited cutaneous SSc and diffuse cutaneous SSc. Limited is 2x as common as diffuse and is referred to as CREST syndrome. Limited / CREST: Calcinosis (formation of calcium deposits in any soft tissue) Raynauds oEsophageal disease Sclerodactyly (Localized thickening and tightness of the skin of the fingers or toes) Telangiectasia (A dilatation of small blood vessels (arterioles, capillaries, venules), often multiple in character. Telangiectasias create small red lesions, sometimes spidery in appearance, usually in the skin or mucous membranes, which blanch on pressure.) Diffuse: • skin thickening over proximal sites and / or trunk (more aggressive form and more likely to develop organ involvement) Skin features: • Sclerodactyly • Microstomia (micro- a combining form meaning small stomia a combining form meaning mouth = (abnormally) "small mouth) • Furrowing of skin around the lips • Loss of normal skin creases • Flexion contractures of joints Other Systems and SSc: Cardiovascular features: • Raynauds phenomenon • Cardiac disease - Myocardial fibrosis Pulmonary features: • Fibrosing alveolitis • Pulmonary hypertension Renal features: • Scleroderma renal crisis - Causes rapid renal failure with accelerated hypertension. This is a life threatening medical emergency. Gastrointestinal features: • Reflux oesophagitis - causes gastric reflux (heartburn) and dysphagia. Musculoskeletal features: • Arthalgia and joint stiffness • Flexor contractures of interphalangeal joints are common.

What does drug specificity mean?

Drug acts only act on one type of receptor

what is central tolerance in t cells?

Elimination of self-reactive cells during lymphocyte development (positive/negative selection) (Thymus)

What are the investigations for sjogrens syndrome?

Examination of eyes - lesions, dilation of vessels Examination of mouth - may look dry; wooden tongue depressor may stick; Schirmer test positive (filter paper inserted in lower conjuctiva. After five minutes, a positive result = <5mm) Bloods FBC Anaemia Raised ESR Normal CRP Antibodies Antinuclear Antibodies Anti La (35-85%) Anti-Ro (40-60%) Increased levels of gamma globulin Rheumatoid factor (90%) Imaging Ultrasound or X-ray of salivary gland (sialogram); CT may be useful for detecting a developing lymphoma.

What is a strain, presentation, causative organism and treatment?

Excessive stretching or working of a muscle Presentation: Pain and swelling of muscle CO: Excessive stretching or working Tx: Protect + RICE; NSAIDs for pain; Corticosteroids for swelling

What is the function of the enteric nervous system?

Found in the GIT, regulates glands and smooth muscles.

What are the side effects of steroids?

General: • Cushingoid Appearance o Cushing syndrome is a condition where too much cortisol hormone is produced by the adrenal glands. It can occur naturally but it can also be a side effect of long term use of corticosteroids, which are a synthetic cortisol o Cortisol has many functions in the body. It helps regulates blood pressure and the immune system, it is involved in the balance of insulin and it helps the body to respond to stress. o Cushing syndrome has many symptoms which are non-specific which can make it hard to diagnose. These include obesity (especially around the trunk), facial puffiness and redness, high blood pressure, tiredness, muscle weakness and diabetes. The most indicative symptoms are easy bruising skin, proximal muscle weakness, striae (stretch marks) and facial plethora (redness) Infection: • People being treated with steroids are more likely to pick up infections due to the immunosuppressant action of the steroids this is as follows: o Steroids firstly weaken the collagen in the skin which means it can be easily damaged allowing pathogenic micro-organisms to enter the body more easily. It also slows down the healing process of the skin o Steroids raise the neutrophil levels in the blood (neutrophil leukocytosis) however they decrease the neutrophils ability to migrate to the site of inflammation. They also inhibit phagocytosis so micro-organisms are more likely to survive o They also cause lymphocytopenia and monocytopenia. These are conditions where there are lymphocyte and monocyte deficiencies in the blood (Klien, Go, & Cunha) Metabolic effects • Glucose o Steroids increase gluconeogenesis (generation of glucose from non-carbohydrate sources). They also damage tissue uptake and utilisation of glucose. These actions lead to hyperglycaemia • Protein o Muscle is catabolised to allow synthesis of glucose and increase amount of amino acids available Musculoskeletal • Myopathy • Osteoporosis o This occurs because steroids inhibit osteoblast formation, increase apoptosis of mature osteoblasts and increase action of osteoclasts which leads to bone demineralisation o This is one of the more serious side effects of steroid use o Steroids are now given with bisphosphonates to reduce the effect of the steroids on the bone • Osteonecrosis • Tendon rupture Ophthalmic • Cataracts o This is where the lens of the eye becomes cloudy allowing less light to enter the eye causeing vision to be reduced. • Glaucoma o Steroids increase the intraocular pressure which can lead to damage to the optical nerve Central Nervous System - these symptoms are caused by abnormally high levels of glucocorticoid in the blood • Psychosis • Depression • Mood & sleep disturbance • Benign Intra-cranial hypertension Dermatological - These result of using topical steroids which thin the epidermis and alter the connective tissues within the skin. • Acne • Striae • Alopecia • Bruising • Skin atrophy Growth Retardation - this occurs mainly in children • Linear growth bone growth is reduced • The epiphyseal plate closes prematurely Sudden withdrawal after long term use can lead to acute adrenal crisis as the hypothalamic-pituitary-adrenal axis has been suppressed and needs time to recover slowly. This recovery can take several months

What bacteria is most likely to cause septic arthritis?

Most cases of acute septic arthritis are caused by bacteria such as staphylococcus or streptococcus and Neisseria gonorrhoeae. Chronic septic arthritis (which is less common) is caused by organisms such as Mycobacterium tuberculosis and Candida albicans

What is the pathophysiology of gout?

Gout occurs in people who have a higher-than-normal level of urate in the bloodstream. About two thirds of the urate in our bodies comes from the breakdown of purines that are present in the cells of our bodies. The other third comes from the breakdown of purines in some of the foods we eat. When urate levels start to build up, your body normally gets rid of any excess through your kidneys into your urine. If your body is making too much urate, or if your kidneys aren't able to remove excess urate effectively, then urate levels start to rise. If the level goes above a certain point, urate can form crystals of sodium urate. These crystals mainly form in and around joint tissues, especially your finger and toe joints. The crystals gradually build up in your cartilage and after some years can spill out into the joint cavity. This is known as crystal shedding. The hard, needle-shaped crystals come into contact with the synovium and make it very inflamed very quickly. The inflammation process dissolves the crystals in your joint, and the attack gradually settles over a few days or weeks, depending on how many crystals were shed. A build-up of crystals can eventually lead to the formation of tophi in and around your joints. Tophi can grow and cause pressure damage to your joint cartilage and bone. This is just like the damage caused by osteoarthritis, but tophi can cause more regular, daily pain. At this stage the condition is often called chronic tophaceous gout. By the time tophi are visible from the outside, the parts below the skin may be quite extensive.

Define handicap

Handicap: is a disadvantage for a given individual, resulting from impairment or a disability that limits or prevents the fulfilment of a role that is normal for the individual."

What are the side effects of Ibruprofen?

Ibuprofen side-effects • GI ulceration and dyspepsia (disorder of digestion) • Bleeding • Nephropathy (kidney disease as above) • Asthma • It is better tolerated and causes fewer gastrointestinal disturbances than the majority of its class.

discuss central tolerance of a b cell and it development?

Immature surface IgM molecules undergo negative selection by recognizing self-molecules present in the bone marrow B cells expressing only. When immature B cells express surface IgM that recognizes ubiquitous self-cell-surface antigens (such as those of the MHC) they are eliminated by a process known as clonal deletion. Only B cells that do not encounter antigen whilst they are maturing in the bone marrow can be activated after they enter the periphery. These cells bear both IgM and IgD receptors and constitute the repertoire of B cells that recognize foreign antigen Immature B cells that bind soluble self-antigens do not die but their ability to express IgM on their surfaces is lost

David is a 4-yr.-old who has a form of cerebral palsy (CP) called spastic diplegia. David's CP causes his legs to be stiff, tight, and difficult to move. He cannot stand or walk. What are his impairments, disabilities and handicap?

Impairment: The inability to move the legs easily at the joints and inability to bear weight on the feet is an impairment. Without orthotics and surgery to release abnormally contracted muscles, David's level of impairment may increase as imbalanced muscle contraction over a period of time can cause hip dislocation and deformed bone growth. No treatment may be currently available to lessen David's impairment. Disability: David's inability to walk is a disability. His level of disability can be improved with physical therapy and special equipment. For example, if he learns to use a walker, with braces, his level of disability will improve considerably. Handicap: David's cerebral palsy is handicapping to the extent that it prevents him from fulfilling a normal role at home, in preschool, and in the community. His level of handicap has been only very mild in the early years as he has been well-supported to be able to play with other children, interact normally with family members and participate fully in family and community activities. As he gets older, his handicap will increase where certain sports and physical activities are considered "normal" activities for children of the same age. He has little handicap in his preschool classroom, though he needs some assistance to move about the classroom and from one activity to another outside the classroom. Appropriate services and equipment can reduce the extent to which cerebral palsy prevents David from fulfilling a normal role in the home, school and community as he grows.

What is an impaction fracture?

In impacted fractures, bone fragments are driven into each other, shortening the bone; these fractures may be visible as a focal abnormal density in trabeculae or irregularities in bone cortex.

What investigations are used for diagnosisng systemic sclerosis?

In limited sclerosis, tight skin may produce flexion deformities of the fingers or a beak like nose and small mouth Diffuse sclerosis can cause swelling and stiffening of the fingers. Calcinosis; Proteinuria. Bloods FBC Normochromatic, normocytic anaemia Acute renal disease causes high urea and creatinine¹ Antibodies Rheumatoid factor (30%) ANA (90%) In limited sclerosis, anti-centromere antibodies occur In diffuse sclerosis, anti-topoisomerase-1 antibodies Imaging CT can determine if there is fibrotic involvement of the lungs

What is mixed pain?

In some patients components of continued nociceptive pain may coexist with a component of neuropathic pain. Patients with persistent back and leg pain after lumbar spine surgery (failed low back surgery syndrome) represent a common example.

Discuss a simple relflex / reflex arc?

In this type of reflex, the brain is not involved. The receptor is stimulated which is conducted to the spinal cord by the effector. The effector neuron from the spinal cord conducts a response to the muscle or the gland. This causes an immediate reaction. It does not involve any thinking or reasoning. It is a natural response and will occur even in new-born babies. For example, blinking of eyes when strong light falls on the eyes.

What are the main side effects associated with COX - 2 selective inhibitors?

Increased atherosclerosis, which can lead to increased cardio-vascular mortality, due to the effect on thrombosis.

What is gas gangrene, presentation, causative organism and treatment?

Infection in the muscle usually due to deep penetrating injury, e.g. compound fracture; surgical wounds (especially in the bowel) Presentation: Compound fracture or surgical wounds etc. not healing properly, pain, sepsis and gas production CO: Clostridium perfringens (which is present is faeces), but can also be caused by C. novyi and C.septicum. pathogens release exotoxins which damage cell membranes and are destructive to neutrophils Tx: High doses of antibiotics, usually of Benzylpenicillin, and sometimes clindamycin. Surgical debridement

What is informed consent?

Informed consent in a nutshell: 'The concent given by a patient to a surgical or medical procedure or participation in a clinical study after achieving an understand of the relevant medical facts and the risks involved (i.e. after being informed)'

What is a sprain, presentation, causative organism and treatment?

Injury to a ligament caused by suddent over stretching Presentation: Inflammation; Pain in that one area (localised); Swelling; Hard to walk or stay upright CO: Overstretching Tx: Protect + RICE; NSAIDs for pain; Corticosteroids for swelling

what term is used to describe joint involvement in fractures

Intra-articular: fractures which involve joint surfaces

What doe COX-1 action and where is it mainly found?

Is involved in the physiological cell signaling, and is found in most tissues, but especially in the gastric mucosa and platelets.

What is necrotising fasciatus, presentation, causative organism and treatment?

It destroys widespread tissue & is associated with a high mortality rate due to multiple organ failure, with a high incidence after abdominal surgery, in diabetics and IV drug users. Presentation: Excruciating pain at the affected site which subsequently undergoes necrosis rapidly afterwards, grey wash water pus. CO: Streptococcal or E.coli. Mortality is very high, 30%. Tx: Extensive surgical debridement, and strong doses of Benzylpenicillin, metronidazole and gentamycin

Describe what is septic arthritis, its symptoms, investigations and treatment / management?

It is a rather rare but important disease characterized by inflammation of a synovial membrane with purulent effusion into the joint capsule, usually due to bacterial infection. It typically affects monoarticular joints. The infection resides in the synovial or periarticular tissues and evolves over hours or days. Despite advances in diagnostic studies, powerful antibiotics, and early drainage, significant joint destruction commonly occurs. Septic arthritis can also cause many complications, including osteomyelitis, bony erosions, fibrous ankylosis, sepsis, and even death. Age: The age range of those affected is broad, extending from the neonatal period to advanced age. In adults, septic arthritis most commonly affects the knee In children, infection into the hip joint predominates. Etiology: Infections reach joints by direct penetration (e.g. trauma, surgery, bites), extensions from an adjacent infection (e.g. osteomyelitis, a soft tissue abscess, an infected wound), or by heamtogenous spread from a remote site of infection. Most cases of acute septic arthritis are caused by bacteria such as staphylococcus or streptococcus and Neisseria gonorrhoeae. Chronic septic arthritis (which is less common) is caused by organisms such as Mycobacterium tuberculosis and Candida albicans. Pathophysiology: Infecting organisms multiply in the synovial fluid and synovial lining. Some bacteria (e.g. staphylococcus aureus) produce virulence factors (adhesions) which allow bacteria to penetrate, remain within and infect joint tisues. Other bacterial products (e.g. endotoxin from gram negative organism, immune complexes fromed by bacterial antigens and host antibodies) augement the inflammatory reaction. Symptoms: Systemic symptoms may be absent. Children may present with limited spontaneous movement of the limb, irritability, feeding disturbances and high or low grade or no fever. Usually a rapid onset of symptoms. Pain from the affected joint. The pain tends to be severe and usually develops quite quickly. Any movement of the joint is usually very painful. Restricted active and passive motion Swelling usually develops over the affected joint and usually very tender. Redness of the overlying skin. Feeling generally unwell with fever (high temperature) is common. Investigations: • Aspirate-MC & S to determine if fluid is puss of reactive fluid. The fluid is sent for microscopy gram staining and culturing • Blood culture (FBC, ESR, CRP-these are often positive (raised) • Leucocytosis-this is usual unless the patient is immunosuppressed • Skin wound swabs, sputum and throat swab or urine (surgical) • X-rays, these may not change for some time in children until chronic changes in weeks' time. After 48 hours a joint can look a little osteoporotic. • Ultrasound (increased amount of fluid in the hip? could be reactive fluid or pus) Treatment: Septic arthritis is a medical emergency and needs treatment immediately. Antibiotics are used to treat the infection. Antibiotics-IV for 2 weeks then orally for a further 4 weeks (Normally IV flucloxacillin 1-2 g is given 6 hourly + fusidic acid 500 mg orally 8 hourly). Resting, keeping the joint still, raising the joint, and using cool compresses may help relieve pain. Exercising the affected joint helps the recovery process. If joint (synovial) fluid builds up quickly due to the infection, a needle may be inserted into the joint often to aspirate the fluid. Severe cases may need surgery to drain the infected joint fluid.

What is the appearance of an x-ray for a patient with OA?

Joint Distribution Asymmetrical and distal knee, hip, hands (often the first carpometacarpal joint), fingers (distal interphalangeal DIP joints), spine, shoulder, elbow and wrist X-ray Focal joint space loss Sclerosis Cysts Osteophytes

What are the investigations for SLE?

Joint Involvement- symmetrical small joint arthralgia, but joints will probably appear clinically normal; deformity is rare. Skin Involvement - look for rashes in less obvious areas e.g. vasculitic lesions on the nail folds and finger tips, alopecia on the scalp GI involvement - ulcers are common in the mouth Optical involvement - vasculitis can cause haemorrhage and conjunctivitis Bloods FBC Leucopenia Lymphopenia Thrombocytopenia Anaemia Raised ESR, in proportion to disease activity CRP usually normal C3 and C4 often reduced during active disease Antibodies Antinuclear Antibodies Anti ds DNA (70%) Anti-Ro (40-60%) Anti-Sm (Caucasian: 10-25%) (Black Af.: 30-505) Anti-La (15%) Rhuematoid Factor (25%) Imaging MRI and CT may be able to show structural damage to the brain e.g. haemorrhage

What is the appearance of an x-ray for a patient with acute gout?

Joint distribution Asymmetrical First MTP joint - most commonly affected Ankle, elbow, wrist and hand. *Radiological changes do not appear until years of recurrent gout attacks have elapsed

What is the appearance of an x-ray for a patient with chronic gout?

Joint distribution Asymmetrical First MTP joint - most commonly affected Ankle, elbow, wrist and hand. X-ray: tophus formations - soft tissue deposits of urate - tophi will appear opaque on the x-ray "punched out" erosions +/- gross bone and joint destruction Cartilage destruction soft tissue swelling overhanging edges sclerotic bone

What is the appearance of an x-ray for a patient with pseudo gout?

Joint distribution: knees, hip, shoulders, elbows, wrists MCPs (2nd and 3rd) X-ray: Chondrocalcinosis (calcification of cartilage) - noted in the menisci of the knee, triangular cartilage of the wrist and the symphysis pubis. OA - like changes (i.e. cartilage loss, sclerosis, cysts and osteophytes)

What is Juvenile idiopathic arthritis , what are the signs and symptoms and what is the treatment?

Juvenile idiopathic arthritis (JIA) (aka Juvenile Rheumatoid Arthritis JRA) is the most common form of persistent arthritis in children. (Juvenile in this context refers to an onset before age 16. JIA is a subset of arthritis seen in childhood, which may be transient and self-limited or chronic. It differs significantly from arthritis commonly seen in adults (osteoarthritis, rheumatoid arthritis), and other types of arthritis that can present in childhood which are chronic conditions (e.g. psoriatic arthritis and ankylosing spondylitis). It is an autoimmune disorder. Presentation • The diagnosis is based on the presence of arthritis that persists for at least 6 weeks, with all other causes excluded. The onset can be gradual or abrupt, with morning stiffness and joint pain. • Joint pain is variable but may be severe and there may be a marked limp. • Fatigue and weight loss may occur and uveitis may cause photophobia. • Systemic-onset juvenile chronic arthritis (JCA): o Is characterized by spiking fevers and may be accompanied by a salmon-pink rash, which affects the trunk and extremities. o Some children may have a generalised myalgia. Hepatosplenomegaly is often present and there may also be lymphadenopathy. o Arthralgia is often present but joint swelling is unusual and a definite diagnosis of systemic-onset JIA cannot be made until the development of arthritis, which may not occur for months following the onset. Investigations • Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP): always elevated in children with systemic-onset, usually elevated in polyarticular disease, but is often normal in those with pauciarticular disease. • FBC may show anaemia (often microcytic), lymphopenia and thrombocytopenia. • X-rays, CT scan, MRI and bone scans are often important in establishing the diagnosis and ruling out other possible diagnoses. Treatment: The major emphasis of treatment for JIA is to help the child regain normal level of physical and social activities. This is accomplished with the use of physical therapy, pain management strategies and social support.

What are kinins?

Kinins - Are small, vasoactive peptides. Bradykinin - Increases vascular permeability and produces pain •

What is varicose veins, presentation, causative organism and treatment?

Leaky valves of the veins (most commonly in the superficial veins of the legs) Presentation: Veins are distended, lengthened and torturous due to pooling of blood. CO: Inherited tendancy, job involving standing for hours Tx: Elastic stockings; slerotherapy; and sometimes avulsion (stripping)

What are leukotrienes?

Leukotrienes- A chemotaxin to neutrophils that increases vascular permeability.

How do spiral fractues occur?

Like an oblique fracture, a spiral fracture causes a break in the bone which is at an angle. However, the key differential here is that a spiral fracture traverses both planes of the bone. A helpful way to understand the difference between an oblique and spiral fracture is to use the analogy of a breaking twig: suppose you slice a twig in half at an angle, this is a break similar to an oblique fracture. However, if you were to twist the twig to break it, it would result in a break pattern which would start from one point, moving obliquely in one direction and, on reaching the other end, would continue on the other side of the stick until it met the original point. Such a fracture may arise as a result of a sharp twist to the leg, whilst the foot is stuck in one position. Unlike transverse fractures, the fragments of a spiral fracture are more difficult to balance against each other, and are thus very unstable. The spikes of bone created by the break can also damage blood vessels, nerves and skin, or the tips of the spikes can actually break off to produce a triangular fragment known as a "butterfly fragment".

How does carpal tunnel present?

Main presentation is pain, numbness and tingling of the fingers. Patients may also describe the pain as burning and itching. • There may be weakness and clumsiness of the hand. • Mainly affects the thumb, middle fingers and ring finger. Sometimes affects the index finger.

How do you manage OA?

Management The aim is to relieve pain, improve joint function, and minimise disability and handicap Education: about self-help such as reducing weight, wearing appropriate footwear, using heat or cool packs etc. A progressive exercise regime is used to improve function. Low-impact continuous exercise is recommended 3 times a week for 15-30 minutes. Surgery: Osteotomy: A wedge of bone is cut and pinned to realign the weight-bearing surfaces of the knee. This redistributes weight bearing more evenly on the joint. Useful in knee OA in patients under 55. Arthroscopy: This is done particularly if the joint is locking such as when there is a problem with the menisci in the knee. Debridement can also be done. Arthroplasty: Diseased surfaces are cut away and replaced with metal and plastic. is very expensive, but are cost-effective for those with significant symptoms despite conservative therapy. Approximately 90% of patients have a pain-free hip after recovery from hip arthroplasty. Hip, Knee replacements etc

What is drug selectivity

Many drugs act preferentially on particular receptor types or subtypes. The expression of selectivity is dependent on the dose and on the concentration of receptors, as high concentrations will give a maximal blockade at both receptor subtypes

What are the most common dislocations?

Most common in the glenohumeral joint, due to the small are of articulation between glenoid fossa and head of humerus. • 95% are anterior dislocations ((head of humerus moves anterior to scapula) • 5% posterior dislocations (head off numerous moves posterior to scapula) - usually as a result of extremely vigorous muscle contractions during, for example, an epileptic seizure

What members of the MDT are involved in rehabilitation for pt's with musculoskeletal injuries

Medical (doctors, nurses): Initial assessment of injury, clinical examination and investigations. Medication / surgery Physiotherapy: Promotion of mobility through strengthening exercises, walking aids and graded exercise Rehabilitation Assistant / Carers: Support with personal care and activities of daily living. Assisting patient in carrying out tasks within community. Social Care: Assessment of eligibility for homecare or other support at home. Funding towards specialist equipment. Occupational Therapy: Assessment and intervention aimed at supporting patient to achieve independence with all activities of daily living, including personal care, banking, shopping, and writing. Provision (or recommendation) of specialist equipment to support around the home e.g. raised toilet seat, splints etc. Speech and Language Therapist: Assessment and intervention aimed at restoring social and communication ability, including specific language impairments, articulation difficulties and poor social confidence. Psychologist / Neuropsychologist (brain injury): Assessment and intervention aimed at reconciling pre-and post-injury state, and understanding the emotional impact of any long-lasting disability on the self, family and the patient's place within society. Dietician: A dietician is particularly important if, as a result of injury, the patient is likely to spend a long time on bed-rest. The dietician can advise on the right foods to eat to promote recovery ,regain strength and minimise any weight concerns. Podiatrist / Chiropodist: A podiatrist assesses, diagnoses and treats problems of the lower leg and foot. They can be particularly helpful in providing preventative treatment and advice around nail and foot conditions. Orthotist: Assessment and measurement of patient and subsequent design of orthoses e.g. splints, to support injured limbs and promote recovery. Design and fitting of special footwear and insoles to treat deformity.

How do oblique fractures occur?

Most fractures of the long bone are caused by a violent twisting movement about the long axis of the bone rather than a sideways bending. Oblique fractures are essentially breaks which are at an angle which is oblique to the long axis of the bone (instead of being at a right angle, as in transverse fractures). These fractures are confined to one plane and tend to be relatively uncommon.

What is the medical model and how does it differ from the Social model?

Medical Model: Sees disability as an individual deficit. Social Model: Sees people are made disabled by society. The way in which Society stigmatises Disability and the way in which we as a society increase the limitation of activities for disabled people - for example failure to provide a disability ramp to certain areas hence making those who are disabled an wheel chair bound unable to go certain places hence limiting their activities. The social model emphasises the fact that Disabled people are different from non-disabled people and the fact that they want legislation , civil rights and developmental action would be far more beneficial than charity or pity for the disabled that society seems to focus on.

What is moral hazard?

Moral Hazard is when having some form of insurance cover makes you less careful. The NHS is funded by taxes. People may go and see their GP for minor symptoms because they feel they have paid for NHS cover. This leads to excess demand & resource loss.

Describe motor control in joint movment?

Motor control is information processing related activities carried out by the central nervous system that organize the musculoskeletal system to create coordinated movements and skilled actions. Motor control must be performed in order to achieve movement. 1. The cortical association areas' function is to design and plan of voluntary movements. Action potentials from the cortical association areas project to the basal ganglia for refinement and selective activation of movements and/ or to inhibit unwanted movements. 2/3. The thalamus here is part of the basal ganglia loops and sends impulses to the motor cortex, which is seen as the final common pathway. 4. Impulses from the motor cortex are almost simultaneously sent to the cerebellum, the brainstem and the spinal cord. The cerebellum use this information to compare it with the movement sensory information received from the periphery. The brainstem helps maintaining background postural control, while impulses to the spinal cord are more of a crucial for the activation of individual muscles or groups of muscles. 5. Alpha motor neurons cause muscle contraction. 6. The sensation of movement, together with other relevant feedback information, is sent towards the CNS. The spinal cord uses the feedback in its integration of spinal reflexes. The brainstem utilizes sensory feedback mostly for postural control and balance. Sensory feedback is also sent to the thalamus. The cerebellum compares the movement as it occurs with the original movement instruction sent by the motor cortex. 7. If there is a inconsistency between the intended movement and the actual movement, correcting signals will be sent directly to the execution centres. 8. The thalamus distributes sensory feedback to its appropriate location on the sensory cortex. 9. Sensory experiences are interpreted by the cortical association areas, and memorizes movements are stored for future use in the design and planning movements.

What neurones are involved in muscle innervation?

Motor neurones

Describe muscle work and joint movment?

Muscle Work The central nervous system (CNS) needs sensory feedback for movement control provided by receptors inside the muscle and between muscle and tendon. The receptors are the muscle spindle and the Golgi tendon organ. Muscle spindles detect the rate and changes in length of muscle, whereas Golgi tendon organs detect degree and rate of change of tension. These signals assist in the control of muscle contraction.

What are the investigations for PM / DM?

Muscle wasting and weakness, especially in the shoulder and pelvic girdle; Purple rash affecting eyelids and fingers (Gottron's pauples) Bloods ESR not normally raised Serum creatine kinase is raised, indicating muscle damage¹ Antibodies Rheumatoid factor (50%) Anti JO (30%) Histology Biopsy of areas surrounding blood vessels and myofibrils will show chronic inflammatory cells Imaging MRI can detect inflammation of muscles; Electromyography (for evaluating electrical activity of skeletal muscle) shows disorders of contraction¹

What are the symptoms of reative arthritis?

Musculoskeltal • Acute onset with high fever and fatigue • symptoms start a few days to a few weeks after the infection • Arthritis is asymmetric and oligoarticular • Usually in the lower extremities; targets large weight-bearing joints, fingers and toes • Creation of 'sausage digit' i.e. dactylitis • Enthesitis is common and pain in the sacroiliac region • Joints will be red and warm • Knee effusion Extraskeletal • Conjunctivitis • Urethritis • Skin & muscoal lesion e.g. Circinate balantis, erythema nodosum

What is the clinical feature of AS?

New York classification criteria : bilateral sacroiliitis & 4/5 of the following: 1) low back pain > 3 months 2) thoracic pain + stiffness 3) iritis 4) decrease in movement lumber spine 5) decrease in chest expansion N.B. peripheral joints less commonly involved than the axial skeleton in AS. Inflammation tends to target medium/large joints such as the shoulders hip or knees. In severe disease lumbar lordosis is lost and spine thoracic and cervic becomes kyphotic "question mark posture" Musculoskeletal features: gradual onset of lower back pain and stiffness. Symptoms are worse early in the morning and after long periods of rest however usually improve with exercise. Extraskeletal features - anorexia, fever, fatigue, pulmonary fibrosis, cardiovascular disease, iritis and rarely amyloidosis

What is nitric oxide?

Nitric oxide - A vasodilator that is released by macrophages and endothelial cells. It actively reduces the effect of other pro-inflammatory mediators.

What is nociceptor pain? And what are the two types?

Nociception: the term for pain that is detected by specialized sensory nerves called nociceptors. These nerves are located throughout the soft tissues, such as muscles and skin, as well as the internal organs. There are two types of nociceptive pain: somatic pain and visceral pain. Somatic pain comes from the joints, bones, muscles and other soft tissues, while visceral pain comes from the internal organs.

What are the differences between nociceptive pain, neuropathic pain and psychogenic pain?

Nociceptive pain is associated with, or secondary to, a noxious (peripheral) stimulus (e.g. following bone fracture, surgery, inflammation, and muscle spasm). Neuropathic pain is a result of a lesion or dysfunction in the peripheral nervous system or central nervous system (e.g. post-herpetic neuralgia, painful diabetic neuropathy, central post-stroke pain, pain following spinal cord injury). Psychogenic Pain is the term for pain that is primarily caused by psychological factors, such as depression and anxiety. While psychogenic pain is primarily psychological, it is a very real type of chronic pain.

Decsribe differences of nociceptive pain and neuropathic pain?

Nociceptive pain: - Somatic pain: Arises from bone, joint, muscle, skin, or connective tissue. It is usually aching or throbbing in quality and is well localised. - Visceral pain: Arises from visceral organs such as the GI tract and pancreas. This may be subdivided: - Tumour involvement of the organ capsule that causes aching and fairly well localised. - Obstruction of hollow viscus which causes intermittent cramping and poorly localised pain. Neuropathic pain: - Centrally generated pain: Deafferentation of pain: injury to either the peripheral or central nervous system. Examples: phantom pain may reflect injury to the peripheral nervous sytem, burning pain below the level of the spinal cord lesion reflects injury to the CNS. Sympathetically maintained pain: Associated with dysregulation of the sutonomic nervous system. Examples: May include some of pain associated with reflect symptomatic dystrophy - Peripherally Generated Pain: Painful polyneuropathies: pain is felt along the distribution of may peripheral nerves. Examples: diabetic neuropathy, alcohol nutritional neuropathy and those associated with Guillian barrie syndrome. Painful mononeuropathies: Usually associated with a known peripheral nerve injury, the pain is felt at least partly alnog the distribution of the damged nerve. Example: nerve root compression, nerve entrapment etc.

What must always be considered when examining a child with injuries / limping?

Non accidental injuries should always be considered when examining a child. Recognizing red flags of NAI is vitally important: Keep the child safe

what are the clinical features of vasculitis?

Non specific symptoms: • Fatigue • Anorexia • Weight loss • Fever Vasculitis can affect any system in the body: Manifestations of vasculitis Rashes Palpable pupura Ulceration Ischaemia Arthalgia Arthritis Glomerulonephritis Ischaemia Neuropathies Stroke Pulmonary haemorrhage

Name the two phases in a normal gait cycle?

Normal Gait Is broken down in to Two Phases - It is important to know and understand these two phasesl. These two phases are the STANCE PHASE and the SWING PHASE.

What are the normal limitations of range of movement brought about by?

Normal limitation of range of movement is brought about by: Articular surface contact Limit of ligament extensibility Limit of tendon and muscle extensibility Apposition of soft tissue The two main factors that normally limit joint mobility are the shape of the joints and the type of structure that run over them. Articular surface contact could mean that the joint is in the close-packed position, as in the elbow, where the joint is actually prevented from extending beyond approximately 180o by the olecranon of the ulna impinging on the humerus.

What is a deep vein thrombosis, risk factors and how does it present, common organism and treatment?

Obstrustion of a vein by a blood clot , without preceding inflammation of its walls. DVTs occur in the deep veins of the leg. Risk factors: include prolonged immobility; heart failure; pregnancy and injury. Presentation: Affected leg may be swollen and tender. Swelling has been described as a woody firmness CO: Blood clot Tx: Compression socks; Regular exercise; Anticoagulants such as herapin and warfarin

What are the differences between OA and RA?

Osteoarthritis Associated symptoms: Symptoms occur in isolation, with no systemic symptoms such as fatigue, fever, organ involvement; can develop Heberden's or Bouchard's nodes - Severity: Less severe than RA Disease process: Normal wear and tear Gender: Common in both men and women Diagnosis: x-ray Treatment: NSAIDs Pain in movement: movement increases pain Pattern of joints that are affected: Asymmetrical & may spread to the other side. Symptoms begin gradually and are often limited to one set of joints, usually the finger joints closest to the fingernails or the thumbs, large weight-bearing joints. Cause: wear and tear associated w/ aging or injury Age of onset: usually in old age Speed of onset: slow, over years Joint symptoms: Joints painful but without swelling; affects joints asymmetrically; affects bigger joints such as hips & knees Duration: Morning stiffness lasts less than 30 mins; tends to get worse later throughout day Presence of symptoms affecting the whole body (systemic): Whole-body symptoms are not present. Rheumatoid arthritis: Associated symptoms: Frequent feelings of "being sick inside," with fevers, weight loss, or involvement of other organ systems - nodules may develop on sclera or lungs; may develop Sjogren's or Felty syndrome Severity: More severe than OA Disease process: Autoimmune Gender: Affects more women than men Diagnosis: Blood tests--RA, ESR, CRP Treatment: NSAIDs,Steroids, Immunosuppresants pain w/ movement: movement decreases pain Pattern of joints that are affected: Symmetrical - often affects small and large joints on both sides of the body, such as both hands, both wrists or elbows, or the balls of both feet. Cause: disease in which own immune system mistakenly attacks healthy tissue, causing inflammation that damages your joints Age of onset: at any time in life speed of onset: Relatively rapid, over weeks to months Joint symptoms: Joints are painful, swollen, and stiff; affects joints symmetrically; affects smaller joints such as hands & ankles Duration of morning stiffness: Morning stiffness lasts longer than 1 hour; worse in AM; stiffness occurs in AM & periods of rest Presence of symptoms affecting the whole body (systemic): Frequent fatigue and a general feeling of being ill are present

What is joint space swelling?

Osteoarthritis causes deterioration of the joint structures. Wearing away or deterioration of articular cartilage leads to narrowing of the joint space (i.e., the space between the end of bones in a joint). Progressively smaller joint space suggests worsening of osteoarthritis. Joint space loss is usually not uniform within the joint. "Bone-on-bone" suggests there is no joint space left.

Name the 3 cells in bone remodelling and their function?

Osteoblasts produce type 1 collagen and form bone. Osteocytes actually make up 90% of the cells of the skeleton once it has matured. These cells are responsible for the maintenance of bone. Derived from local mesenchymal stem cells, these cells synthesize matrix (osteoid) and regulate its mineralization. After bone formation, the majority of osteoblasts are removed by apoptosis, others remaining at the bone/marrow interface as lining cells or within the bone as osteocytes. Osteocytes are former osteoblasts that have been trapped in the matrix. They play a vital role in controlling the extracellular concentration of calcium and phosphorus. These are generally small cells that are interconnected with each other and with bone lining cells through cytoplasmic processes. They respond to mechanical strain by undergoing apoptosis or through altered cell signaling. Osteoclasts are multinucleated giant cells, they have a ruffled border/membrane to increase surface area. Osteoclasts actively break down bone. These are cells with the unique capacity to resorb bone and are derived from haematopoietic precursors of the macrophage lineage.

What are Osteophytes?

Osteophytes, also called bone spurs, are protrusions of bone and cartilage. The bony projections are commonly seen in areas of a degenerating joint and can be seen on x-rays. Osteophytes, which typically develop as a reparative response by remaining cartilage, cause pain and limited range of motion in the affected joint.

What non invasive treatments/managements can be given to patients with RA?

Other types of Management include: • Education • Physiotherapy - Exercises, walking aids and splints etc • Occupation therapy - Home assessment • Dietician - Diet advice • Support groups

Anti jo is associated with?

PM / DM

What is the aetiology of tendinitis and what is its clinical features and treatments?

Pain arises from the strain or injury to tendons and their insertions to bone. The term enthesopathy refers to a disorder of entheses (bone attachments) is used to describe cases with peristeal component such as epicondylitis (tennis elbow) Aetiology is poorly understood: - a systemic inflammatory condition - injury from overuse - Idiopathic Clinical features: Most frequent sites of tendinitis are: - Shoulder - Elbow - Achillies tendon Pts complain of pain that is worsened by active movement. Examination findings include: - Tenderness of the tendon and its insertion. - An increase pain when active movement is performed against resistance. - Soft tissue swelling. Treatment: - Rest and avoidance of precipitating cause - NSAIDs - Local corticosteroid injections - US therapy - Surgery

What is the biopsychosocial model of pain?

Pain is a complex phenomenon involving interactions between physical or biological, psychological and psychosocial aspects. Other factors (such as litigation and compensation issues) can influence pain symptoms or disability. Effective pain management therefore requires a multidimensional assessment of the pain problem that goes beyond the physiological cause. The "bio-psycho-social" model of pain includes a biological, psychological and psychosocial assessment of pain. Picture

When will synovial fluid be aspirated?

Removal of synovial fluid (Athrocentesis) may be done by a doctor for the following joint problems: - If the Patient is experiencing Joint pain / Redness around the joint - If the joint appears to be Swollen or inflamed - Removed to monitor the progress of a patient with a known joint condition.

What is the treatment for gout?

Patient education- exercise and low purine diet e.g. less oily fish and red meat. Pharmacological NSAIDS- to reduce pain and inflammation Colchicine- 500mcg 2-3 x a day Corticosteriods-for patients who can't tolerate the two above but should only be used short term. Prophylactic therapy- allopurinol- decreases uric acid synthesis. (But should not be used until 2-3 weeks after gouty attacks otherwise can make gout worse).

What are the clinical features of polymyalgia?

Patients with PMR will present with: • Symmetrical pain and stiffness in the shoulder and pelvic girdles. • Proximal muscles are weak and may be tender. • Peripheral synovitis affecting medium sized joints may be present.

Discuss perception of pain?

Perception of pain is the end result of the neuronal activity of pain transmission and where pain becomes a conscious experience. The experience of pain has affective-motivational, sensory-discriminative, emotional and behavioural components. When the painful stimuli are transmitted to the brain stem and thalamus, multiple cortical areas are activated and responses are elicited. These areas are: 1. Somatosensory cortex: This is involved with the perception and interpretation of sensations. It identifies the intensity, type and location of the pain sensation and relates the sensation to past experiences, memory and cognitive activities. It identifies the nature of the stimulus before it triggers a response, for example, where the pain is, how strong it is and what it feels like. 2. Limbic system: This is responsible for the emotional and behavioural responses to pain for example, attention, mood, and motivation, and also with processing pain and past experiences of pain.

What is Perthes' Disease (also known as Legg-Calve-Perthes' Disease). , what are the signs and symptoms and what is the treatment?

Perthes' disease is a degenerative childhood disease in which the developing femoral head gradually softens and breaks down (idiopathic avascular osteonecrosis), becoming deformed, as a result of inadequate blood supply to the growth plate (epiphysis) of the bone. This process typically happens over several weeks. Over the course of several months, the blood vessels regrow and the blood supply returns to the 'dead' bone tissue. New bone tissue is then laid down and the femoral head regrows and remodels over several years. Presentation: present with pain in the groin, thigh or knee, which worsens on activity. They may limp and have a restricted range of movement of the hip joint. These symptoms may persist on and off for many months, and the disease itself lasts for a few years. Affected children are usually shorter than their peers and tend to present as hyperactive. Investigations: The condition can be diagnosed via radiography of the pelvis, which shows sclerosis, fragmentation and eventual flattening of the proximal femoral epiphysis. However, radiographic changes may not be detectable in the early stages of the disease, and so the condition can often be misdiagnosed as synovitis. The differential here is that, whilst synovitis will generally settle within around two weeks, the symptoms of Perthes' disease will persist. If symptoms do persist, a bone scan or MRI can help to identify the pathology, which is seen as an area of reduced perfusion on a bone scan or signal change on MRI. Treatment: Heals spontaneously (18-36 months) but may leave a damaged and arthritic joint Treatment - wheelchair? Age 5 - 12 years, boys>girls Avascular necrosis of the capital femoral epiphysis

What colour is synovial fluid and what may different colours and thickness identify?

Physical characteristics - the normal appearance of a sample of synovial fluid is usually: • Straw coloured • Clear • Moderately viscous - drops of it from a syringe needle will form a "string" a few inches long. Changes in the physical characteristics may provide clues to the disease present such as: • Less viscous fluid may be seen with inflammation. • Cloudy synovial fluid may indicate the presence of microorganisms, white blood cells, or crystals. • Reddish synovial fluid may indicate the presence of blood, but an increased number of red blood cells may also be present in cloudy synovial fluid.

Describe bone structure

Pic

What are platelet activation factors and what do they do?

Platelet activation factors - Released from mast cells and neutrophils during degranulation. They have the following effects: - Encourage platelet aggregation and degranulation. - Increase vascular permeability. - Induce leucocyte adhesion to the endothelium. •

What is polymyositis / dermatomyositis?

Polymyositis (PM) and Dermatomyositis (DM) are autoimmune, inflammatory muscle diseases. DM can also affect the skin. Pathologic changes in both disorders include cellular damage and atrophy, with variable degrees of inflammation. Muscles in the hands, feet, and face are affected less than other skeletal muscles. Involvement of visceral muscles in the pharynx and upper esophagus and occasionally the heart, stomach, or intestines can impair the functions of those organs. High blood levels of myoglobin from rhabdomyolysis can damage the kidneys. Inflammation may occur in joints and lungs, especially in patients with antisynthetase antibodies.

What is the function of the sympathetic nervous system?

Prepares the body for fight/flight/frolic

What is the mechanism of action of opioids and what type of pain is it used for?

Produce effects on neurons by acting on receptors located on neuronal cell membranes. Three major types of opioid receptor, m or µ, d and k (mu, delta and kappa). Opioids have actions at two sites, the presynaptic nerve terminal and the postsynaptic neuron. The postsynaptic actions of opioids are usually inhibitory. The presynaptic action of opioids is to inhibit neurotransmitter release, and this is considered to be their major effect in the nervous system. However, the final effect of an opioid in the brain is the result, not only of its action at multiple presynaptic sites on both inhibitory and excitatory neurons, but also of its postsynaptic effects. For example, presynaptic inhibition of neurotransmitter release may result in excitatory effects in a target neuron if the neurotransmitter normally produces an inhibitory effect. However, if the opioid also has a postsynaptic inhibitory effect on the target neuron, the excitatory effects may not occur. Opioids also inhibit the release of neurotransmitters:. Morphine, by an action on µ receptors, inhibits release of several different neurotransmitters including noradrenaline, acetylcholine and the neuropeptide, substance P - Nociceptive pain

What is Supplier- Induced Demands?

Providers of healthcare have superior knowledge about health and health services and are therefore in a position to influence demand for them. This is known as supplier induced demand. It can result in greater or lesser use of a service than would have potentially been the case if the patient had decided on the treatment they required for themselves.

What are the investigations of pseudo gout?

Pseudogout is suggested when abnormal calcifications chondrocalcinosis. are seen in the cartilage of joints on x-ray testing. • The arthritis of pseudogout is common in older adults, particularly in the context of dehydration such as occurs with hospitalization or surgery. • The diagnosis of pseudogout is ultimately made when fluid from a joint is examined under a special microscope called a polarizing microscope. With this microscope, the calcium pyrophosphate crystals are identified.

How is psoriatic arthritis diagnosed on an X-ray?

Psoriatic arthritis: • Mild bony erosion at the edge of cartilage. • Asymmetric erosive changes in the small joints of the hands and feet. • Distal interphalangeal (DIP) or proximal interphalangeal (PIP) involvement - more common than metatarsophalangeal (MTP) or metacarpophalangeal (MCP) changes. • Pencil in cup deformity • Swelling of soft tissue around joint Distribution: • asymmetrical and distal with erosion

What are the psychological consequences of a chronic illness?

Psycho-social consiquences As well as these physical features there are further psychosocial consequences of IP: • Frustration: at being unable to do things as previous, not being able to partake in leisure activities etc. • Fear and anger: Anger at being unable to do things as previous and its relation with loss's of independence and role etc. • Loss of independence and sense of inadequacy: Having to have help, not being able to look after children etc. • Self consciousness: especially if there is altered bodily image • Restriction or loss of role • Change in relationships: Partner changing from partner to carer. • Loss of confidence • Uncertainty of future

What is the function of the autonomic nervous system?

Regualtes visceral organs and blood vessels

What is non organ autoimmunity?

Response is directed towards a range of target antigens and involves a variety of organs resulting from cell-mediated responses and cellular damage caused by auto-Abs or immune deposits complexes. These diseases typically reflect a general defect in immune regulation that results in hyperactive T cells and B cells11. Some examples include: • SLE-Auto-Ab's to DNA, histones, RBCs, platelets, leukocytes, clotting factors. • MS-Auto-reactive T cells induce inflammation along the myelin in nerve fibres. • RA-Auto-Abs (Rheumatoid factors): IgM-IgG complex in joints and activate complement cascade causing chronic inflammation of the joint.

What is the pahtophysiology of RA?

Rheumatoid arthritis causes inflammation in the synovium. The synovium is a membrane that covers joints. When antibodies attack the synovium, they leave it sore and inflamed. This inflammation causes chemicals to be released, causing the synovium to thicken. These chemicals can also damage bones, cartilage, tendons and ligaments. The chemicals gradually cause the joint to lose its shape and alignment and, eventually, can destroy the joint completely. The joint hurts for 2 reasons: • Nerve endings are irritated by the chemicals produced by the inflammation. • The capsule is stretched by the swelling in the joint. When the inflammation goes down, the capsule stays stretched and can't hold your joint in its proper position. This can make your joint unstable, and it can move into unusual or deformed positions.

What is a rombergs test?

Romberg's test is used by doctors in neurological examinations (and is also a test for drunk driving!) to look for loss of motor co-ordination (ataxia) The patient is asked to stand with hands to their sides and close their eyes. A loss of balance (swaying or toppling over) is interpreted as Positive Romberg's Sign Romberg's test for: • Proprioception (special awareness of your body) • Vestibular function (Where your head is in space) • Vision

What are key rules when interpreting an X-ray not in regards to the bone?

Rules for interpretation • Always check patient details of that on the image e.g. name, age, date. • Orientation: Right - left - right, anterior - posterior and scale markers.

What are the diagnostic findings of OA on an X-ray?

Rules of interpretation: • Patient Name • Age / DOB • What view (Anterior - Posterior AP, Lateral, Skyline) • What is the X- Ray of? (Right or Left, Which bones, Which joints, is there a joint replacement?) Bone: • Is the bone regular, or is there a gross abnormality? If so describe it. • Is the cortex intact? Follow the entire cortex and look for any discontinuity. • Fractures: - Location (Epiphysis/ Metaphysis/ Diaphysis ; Proximal, Mid or distal third) Joints • Is the joint in the correct position? Is it dislocated- which direction? • Does a fracture involve the joint? • Are there any features of joint damage or degeneration? Soft tissues • Is there any evidence to suggest this is an open fracture? • Can you see any localised swelling?

What are the rules of interpretation?

Rules of interpretation: • Patient Name • Age / DOB • What view (Anterior - Posterior AP, Lateral, Skyline) • What is the X- Ray of? (Right or Left, Which bones, Which joints, is there a joint replacement?) Bone: • Is the bone regular, or is there a gross abnormality? If so describe it. • Is the cortex intact? Follow the entire cortex and look for any discontinuity. • Fractures: - Location (Epiphysis/ Metaphysis/ Diaphysis ; Proximal, Mid or distal third) Joints • Is the joint in the correct position? Is it dislocated- which direction? • Does a fracture involve the joint? • Are there any features of joint damage or degeneration? Soft tissues • Is there any evidence to suggest this is an open fracture? • Can you see any localised swelling?

Anti dsDNA is associated with?

SLE

What is antigen Sm associated with?

SLE

what is skeletal voluntary muscle controlled by?

SOMATIC SYSTEM of the PERIPHERAL NERVOUS SYSTEM

What is systemic sclerosis?

Scleroderma means hardening of the skin. There are many conditions where this is a feature. Systemic sclerosis (SSc) involves internal organs as well. Excessive collagen deposition causes skin and internal organ changes. Many factors, including environmental factors, can lead to immunologic system disturbances and vascular changes. Endothelial alterations may lead to a cascade of stimulatory changes that involve many cells, including fibroblasts, T lymphocytes, macrophages, and mast cells. In turn, the activated cells secrete a variety of substances, including cytokines and their soluble receptors and enzymes and their inhibitors. These substances lead to changes in the extracellular matrix compounds, including fibronectin; proteoglycans; and collagen types I, III, V, and VII. Increased collagen deposition in tissues is a characteristic feature of systemic sclerosis. Increased collagen production or disturbances in its degradation can cause excessive collagen deposition in tissues

What is the treatment for septic arthritis?

Septic arthritis is a medical emergency and needs treatment immediately. Antibiotics are used to treat the infection. Antibiotics-IV for 2 weeks then orally for a further 4 weeks (Normally IV flucloxacillin 1-2 g is given 6 hourly + fusidic acid 500 mg orally 8 hourly). Resting, keeping the joint still, raising the joint, and using cool compresses may help relieve pain. Exercising the affected joint helps the recovery process. If joint (synovial) fluid builds up quickly due to the infection, a needle may be inserted into the joint often to aspirate the fluid. Severe cases may need surgery to drain the infected joint fluid.

What does the term shorterning mean in regards to fractures?

Shortening: In fractures in which the two broken ends have been displaced (see green box above), there may also be bone shortening (also known as overriding), where the two ends of the bone have crossed over into a side-by-side position, shortening the overall length of the bone. This type of fracture is very unstable.

What is Congenital hip dislocation / Developm ental dysplasia of the hip, what are the signs and symptoms and what is the treatment?

Signs and Symptoms: Well child Normal growth Abnormal gait (trendelenburg positive) Asymmetric skin creases - groin and buttock Limited abduction - Left leg Short Left leg Congenital diseases cause significant morbidity in children Many congenital problems can be ameliorated if detected and treated early From birth Treatment: Early diagnosis - pavlik harness Late diagnosis surgery

What is phlebitis, presentation, causative organism and treatment?

Similar to DVT but occur in the superficial leg veins. Presentation: Superficial veins of legs may be tender CO: Clot blocks superficial veins Tx: Keeping active; support stockings; NSAIDs for pain.

What is bursitis, presentation, causative organism and treatment?

Similar to cellulitis but it affects joints. Inflammation of the bursa Presentation: Joint may be inflammed, turning red in colour rapidly, hot but also painful. CO: Stept.pyogenes or Staph. aureus. Tx: Benzylpenicillin and Flucloxacillin. If swelling is superGicial, clinician may aspirate out some of the puss.

What is sjogrens syndrome?

Sjogrens syndrome is a chronic autoimmune disease and is characterised by inflammation of exocrine glands (mainly salivary and lacrimal glands) resulting in xerophthalmia (dry eyes), xerostomia (dry mouth). Sjogrens syndrome can be primary or secondary.

What 3 types of mucles are there?

Skeletal cardiac smooth

What types of surgery can be offered to a pateint with RA?

Surgery is an option if conservative treatment fails. It is more to relieve persistent pain than restore function, and will only be used if nonsurgery options have failed. Options include - arthroplasty - synovectomy.

What is the function of the parasympathetic system?

Slows down the regulations, secretions from glands and GI motility.

Describe smooth muscle

Smooth Involuntary Controls movement of contents through hollow tubes and organs. E.g. Food down the digestive tract

what is immunological tolerance?

So, how does the body prevent autoimmunity from happening in us all? The immune system has a powerful in-built regulatory system in which T- and B-cells with self-reactive receptors capable of binding to self-molecules are eliminated or down-regulated so that the immune system is made unreactive or "tolerant" to self-antigens. Since T-cells (particularly CD4+ cells) are needed for both the T-cell and B-cell mediated response (they help B-cells to produce antibodies), the process of T-cell tolerance is more important in avoiding autoimmunity than B-cell tolerance.

What is propreception and how is this important in standing upright?

Specialized sensory nerves located in the muscles and tendons. They relay information to the brain on the body's spatial positioning & posture. It also helps in identification of the relative positions of different body parts. The information is used to coordinate muscle activity. Stretch receptors - muscles + tendons Mechanoreceptors - joints

Describe cardiac muscle

Striated Involuntary Pumps blood out of the heart

Describe skeletal muscle

Striated Voluntary Moves the skeleton

What is Subchondral Sclerosis?

Subchondral bone is the layer of bone just below the cartilage. Sclerosis means that there is hardening of tissue. Subchondral sclerosis is seen on x-ray as increased bone density, frequently found adjacent to joint space narrowing. The degeneration of bone which occurs in osteoarthritis causes bone to turn into a dense mass at the articular surfaces of bone.

What is a Subchondral Cyst Formation?

Subchondral cysts are fluid-filled sacs which extrude from the joint. The cysts contain thickened joint material, mostly hyaluronic acid. Traumatized subchondral bone undergoes cystic degeneration.

What is subluxation of a joint?

Subluxation can also be seen on x-ray as a possible consequence of osteoarthritis. Subluxation is a partial dislocation of a bone.

What mediators influence the degree of nerve activity and hence the insensity of pain?

Substance Source Potassium Damaged cells Serotonin Platelets Bradykinin Plasma Histamine Mast cells Prostaglandins Damaged cells Leukotrienes Damaged cells Substance P Primary nerve afferents Release of chemicals such as substance P causes vasodilation and swelling, protecting the injured area by producing behaviours that keep that area away from mechanical or other stimuli.

Discuss what supplt is in regards to healthcare?

Suppliers of healthcare include hospitals, GP's and pharmacists. The doctor will demand a medicine from the NHS trust to supply to a patient. The NHS trust may use a committee, such as a Medicines Management Committee, to decide whether the medicine should be available for use in practice, subject to the available budget.

What is the function of the somatic nervous system?

Supplies the skin, muscles and joints

What are the symptoms of SLE?

Symptoms are diverse and can include non-specific features such as malaise, fever, weight loss and fatigue (2). Symptoms can present in the following systems: Musculoskeletal, Dermatological Hematological Pulmonary Renal Neurological Cardiovascular Musculoskeletal: ~90% of patients with arthralgia or arthritis, usually polyart. The arthritis is NOT erosive. Myalgia is common Freq. of Symptoms Constitutional 41-77% Arthritis 63-91% Skin 55-78% Mucous membranes 19-52% Pleurisy 30-36% Lung 7-14% Pericarditis 12-23% Myocarditis 3% Raynauds 24-60% Vasculitis 56% Renal 28-74% CNS 11-53% Spectrum of SLE - Late-stage - Drug-induced - Anti-phospholipid syndrome - Latent lupus - Classic lupus

What is synovial fluid?

Synovial fluid lines the joints of the body. It is secreted by the synovial cells (mostly by the fibroblast-like B-cells) in the synovial membrane, or synovium. The fluid is vital in allowing the joints of the body to move smoothly and in supplying the cartilage with nutrients.

What are the symptoms of septic arthritis?

Systemic symptoms may be absent. Children may present with limited spontaneous movement of the limb, irritability, feeding disturbances and high or low grade or no fever. - Usually a rapid onset of symptoms. Pain from the affected joint. - The pain tends to be severe and usually develops quite quickly. - Any movement of the joint is usually very painful. - Restricted active and passive motion Swelling usually develops over the affected joint and usually very tender. - Redness of the overlying skin. - Feeling generally unwell with fever (high temperature) is common.

How does central tolerance work in T-cell development, discuss positive and negative selection?

T cell development: Progenitor T cells arise in the bone marrow and migrate to the thymus gland for maturation by rearrangement of their TCRs genes. During this stage they will develop into 2 subclasses: T helper (TH) or cytotoxic T cells (TC). 'These can be distinguished by the presence of either CD4 or CD8 glycoproteins on their surface respectively' Positive or negative selection is undertaken to either delete T cells unable to recognise self MHC molecules in the thymus or delete T cells with high affinity for self MHC molecules or self-antigen + self MHC molecules respectively. Negative selection generates self-tolerance.

What is shared care?

The Overarching Principles of shared care • Treatment must be based on shared decisions by patients and rheumatologist. • The primary goal is maximization of long-term health-related quality of life through symptom control, prevention of structural damage, and normalization of function. • The most important way to reach these goals is through avoidance and abrogation of inflammation. • Treatment to target requires measuring disease activity and adjusting therapy accordingly. Shared care is the basis of holistic care of the patient in collaboration of all members of the MDT.

What is the aetiology of Tendon rupture and what is its clinical features, investigations and treatments?

Tendon rupture may result from chronic inflammation and degeneration or trauma. For example rupture of extensor tendons of the fingers is often seen in RA. - Loss of movement at the joint where the tendon provides power - Deformity - Swelling Examples: After rupture of the biceps tendon a bulge formed by the lateral muscle belly is seen in the upper arm. Extensors tendon rupture at the distal end of the finger can occur when catching a cricket ball, it results in flexion of the distal interphalangeal joint (DIP). Called mallet finger. Treatment: - Surgery

What are tenoblasts and tenocytes?

Tenoblasts are immature tendon cells. They are spindle-shaped, with numerous cytoplasmic organelles reflecting their high metabolic activity5. As they age, tenoblasts become elongated and transform into tenocytes. The tenocytes produce the collagen molecules, which aggregate end-to-end and side-to-side to produce collagen fibrils. Fibril bundles are organized to form fibres with the elongated tenocytes closely packed between them. There is a three-dimensional network of cell processes associated with collagen in the tendon. The cells communicate with each other through gap junctions and this signalling gives them the ability to detect and respond to mechanical loading. Tenocytes in the tendon actively synthesize ECM components

What is the aetiology of Tenosynovitis and what is its clinical features and treatments?

Tenosynovitis is inflammation of the synovial lining of a tendon sheath. Aetiology: - Inflammatory arthritis - Trauma Trauma usually results from repetitive or unaccustomed movement. Clincal features: - Pain in the region of the affected tendon - O/E: the tendon is swollen and tender - O/E: Crepitus may be felt on palpation - A trigger finger or thumb may result from tenosynovitis of the flexor tendons. A nodule can develop on the tendon in response to contriction of the tendon sheath. The nodule catches as it enters or leaves the flexor tunnel and a snapping or flicking movement of the digit occurs on flexion or extension. Common sites include: Abductor pollis longus and extensor pollis brevis tendons and finger flexors. Treatment: - Rest - Splinting - Local corticosteroid injections - Surgical decompression of the tendon sheath

Discuss the afferent leg of muscle innervation?

The afferent leg of the peripheral nervous system is responsible for conveying sensory information to the brain, primarily from the sense organs like the skin. In the muscles, the muscle spindles convey information about the degree of muscle length and stretch to the central nervous system to assist in maintaining posture and joint position. The sense of where our bodies are in space is called proprioception, the perception of body awareness. More easily demonstrated than explained, proprioception is the "unconscious" awareness of where the various regions of the body are located at any one time. This can be demonstrated by anyone closing their eyes and waving their hand around. Assuming proper proprioceptive function, at no time will the person lose awareness of where the hand actually is, even though it is not being detected by any of the other senses. Several areas in the brain coordinate movement and position with the feedback information gained from proprioception. The cerebellum and red nucleus in particular continuously sample position against movement and make minor corrections to assure smooth motion.

What is assessed in home assessments?

The aim of a home assessment is for the healthcare and social care services to be able to assess an individual's needs and provide the appropriate support and guidance they may need. Each individual's case is different and decisions made are on a case by case basis. A specialist - most often a occupational therapist or possibly a social worker - will look at a patients individual needs and discuss with them what help they need and are entitled to. Often the patient coming out of hospital or other rehabilitation What is assessed? Disability is typically assessed by something known as activities of daily living or ADL's. These assess the person's ability to perform everyday tasks such as: • Feeding themselves • Washing themselves • Using the bathroom • Dressing • Using stairs • Ability to navigate around the home These are just a few. Other services that may be needed can include: • Ongoing healthcare needs • Home care help with things like cleaning and shopping • Disability equipment and adaptations to your home • Day centre's to give you or the person who cares for you a break • Day care for your child if either you or they are disabled • Care homes/residential homes

What is the anatomy of the carpal tunnel?

The carpel tunnel is a narrow passageway on the wrist and hand formed anteriorly by the flexor retinaculum and posteriorly by the carpal bones. Through this tunnel passes the median nerve (the most superficial structure) and the tendons of the long flexors for the digits.

What are the causes of pseudo gout?

The cause is unknown. Frequent association with other conditions such as: - trauma (including surgery) - amyloidosis, - hypothyroidism, - hypomagnesemia, - hyperparathyroidism, - gout, - Hemochromatosis (too much iron being absorbed from the gastrointestinal tract) - old age,

Discuss what demand is in healthcare?

The demand of healthcare relates to the users of the NHS (& users of private healthcare) services; the greater the number of patients, the greater the demand for healthcare. As well as patients acting as consumers so do GP's and local health authorities. This is because they act as agents for the patient and both demand and supply medicines, treatments and services. They have what is termed a "duality of roles". A GP will supply a drug, via an NHS prescription, to a patient who has gone to the clinic. The same doctor will demand a medicine from the NHS trust.

What is disability allownace, what are the requirements to recieve allowance and what are the rates?

The disability allowance is split into 2 parts: the care and mobility components. Care is for people who need help to look after themselves Mobility is for people who cannot walk or have difficulty in moving around Requirements for the allowance: • Need help with daily activities such as washing, dressing, eating, getting to and using the toilet, communicating • Need supervision to avoid putting yourself or others in substantial danger • Need someone with you when you are on dialysis • Unable to prepare a cooked main meal for yourself (if you have the ingredients), if you are aged 16 or over. There are 3 rates of care component depending on how the disability affects you: Lowest rate = £19.55 per week If you need help for some of the day or you are unable to prepare a cooked main meal Middle rate = £49.30 per week If you need help with personal care frequently or supervision continually throughout the day only, oe help with personal care or someone to wacth over you during the night, or someone with you while you are on dialysis Highest rate = £73.60 per week If you meet both a day and night condition for the middle rate, or if you are terminally ill and claiming under special rules Mobility component: High = £51.40 per week or Low = £19.55 per weel

Discuss the efferent leg of muscle innervation?

The efferent leg of the peripheral nervous system is responsible for conveying commands to the muscles and glands, and is ultimately responsible for voluntary movement. Nerves move muscles in response to voluntary and autonomic (involuntary) signals from the brain. Deep muscles, superficial muscles, muscles of the face and internal muscles all correspond with dedicated regions in the primary motor cortex of the brain, directly anterior to the central sulcus that divides the frontal and parietal lobes. In addition, muscles react to reflexive nerve stimuli that do not always send signals all the way to the brain. In this case, the signal from the afferent fiber does not reach the brain, but produces the reflexive movement by direct connections with the efferent nerves in the spine. However, the majority of muscle activity is volitional, and the result of complex interactions between various areas of the brain. Nerves that control skeletal muscles in mammals correspond with neuron groups along the primary motor cortex of the brain's cerebral cortex. Commands are routed though the basal ganglia and are modified by input from the cerebellum before being relayed through the pyramidal tract to the spinal cord and from there to the motor end plate at the muscles. Along the way, feedback, such as that of the extrapyramidal system contribute signals to influence muscle tone and response. Deeper muscles such as those involved in posture often are controlled from nuclei in the brain stem and basal ganglia.

What is the name of the connective tissue sheath that surrounds a tendon?

The entire tendon is surrounded by a fine connective tissue sheath called epitenon.

Why is it important to know what type of femur fracture it is?

The femoral head is supplied with blood by ligamentum teres(decreasingly as you age), through the retinacular blood vessels capsule and through the intramedullary veins. If you have an intracapsular fracture the link between the retinacular blood vessels will be cut off and you could end up with Avascular necrosis (the blood supply from the ligamentum teres may either be not enough or nonexistent in an adult)

How do you manage a dislocation?

The following must be considered when treating a dislocation: • Specific treatment would be based on the patient's age, health and medical history, the extent of the injury, tolerance for certain medications, etc. • All dislocations require immediate treatment as left untouched they can lead to fractures. • Initial treatment = RICE (rest, ice, compression and elevation). • Some dislocations will go back into place on their own accord (if the ligaments pull them back into place). • Dislocations which do not reduce themselves will require the doctor to manipulate them back into place physically so it can heal. This is done under sedation. • Split/cast may be required to immobilize the area to promote alignment and protect the injured area from movement until it has healed, • Medication for pain relief • Traction (application of force to stretch certain parts of the body in a specific direction) which aims to stretch the muscle and tendons around the bone ends to help reduce the injury, • Surgery may be required if a ligament or tendon has been badly damaged and needs to be repaired.

What is the gait cycle?

The gait cycle is a step by step break down which describes the manner in which we as human beings walk. It is defined as the "rhythmic movements of the lower two extremities which result in the forward movement of the body." And as the "time interval between two successive occurrences of one of the repetitive events of walking. Measured from heel contact of one foot to the next heel contact of the same foot.

What treatment is required for an displaced intracapsular fracture?

The main worry is avascular necrosis Normally it would be a arthroplasty- either hemi-arthroplasty or total hip replacement. NICE guidelines say: Offer total hip replacements to patients with a displaced intracapsular fracture who: • were able to walk independently out of doors with no more than the use of a stick and • are not cognitively impaired and • are medically fit for anaesthesia and the procedure.

What are the market failures in healthcare?

The market for healthcare provision and the perfect situation of supply matching demand is almost never reached. There are a number of reasons for market failure in relation to healthcare in the UK. These include: • Imperfect information • Moral Hazard • Asymmetric Information • Supplier- Induced Demands • Externalities Imperfect information Better information and patient education would make healthcare interventions more efficient, and less chance of market failure. Consumers would understand the health benefits of a therapy and at what cost. However, the information patients have may not be perfect because: 1. Patients don't know they need the information 2. They do not know where to get the information 3. They don't know the information exists 4. They cannot interpret and use the information 5. The information is incomplete and uncertain We need good, reliable data and information available to be able to use when making healthcare decisions to achieve efficient use of resources. Moral Hazard Moral Hazard is when having some form of insurance cover makes you less careful. The NHS is funded by taxes. People may go and see their GP for minor symptoms because they feel they have paid for NHS cover. This leads to excess demand & resource loss. Asymmetric Information Asymmetric information is where one person has more information than another. This creates a power imbalance which can lead to market failure. In healthcare GPs often act as agents for their patients and tend to have more information and knowledge. Supplier- Induced Demands Providers of healthcare have superior knowledge about health and health services and are therefore in a position to influence demand for them. This is known as supplier induced demand. It can result in greater or lesser use of a service than would have potentially been the case if the patient had decided on the treatment they required for themselves. Externalities An externality is when an external party to a transaction is directly affected by it and not compensated. The use of vaccination programmes in healthcare is an example of a positive externality. People who are vaccinated against a disease are less likely to spread the infection and infect others. Positive externalities are where social benefit of the consumption of a commodity exceeds the private benefit. Private benefit - benefit to consumers who buy and consume goods Social benefit - benefit to all in society, including those who do not consume it An example of a negative externality is pollution caused by pharmaceutical company making medicines.

What are the secondary causes of OA?

The possibility that it is secondary OA needs to be considered. It might develop due to: • trauma • mechanical factors like obesity, hypermobility, varus-valgus deformities. • Bone dysplasia • Calcium deposition disease • Avascular necrosis • Paget's disease • Rheumatoid arthritis • Neuropathic disease • Some metabolic/endocrine diseases(hyperparathyroid, haemachromatosis etc) • Gout, Pseudogout etc

Describe Bone Growth

The process of remodelling of bones is called Ossification. During growth specialised areas at the ends of each long bone (epiphyses) are separated from the shaft of the bone by a plate of active proliferating cartilage called the epiphysial plate. The bone increases in length at this plate laying down new bone on the end of the shaft. The width of the epiphysial plate is proportionate to the rate of growth. The width is affected by a numbers of hormones but most markedly by the pituitary growth hormone and IGF - I (insulin growth factor 1) Linear bone growth occurs as long as the epiphyses are separated from the shaft of the bone, but linear growth will stop once the epiphyses unite with the shaft. The cartilage cells stop proliferating and become hypertrophic and secrete vascular endothelial growth factor (VEDF) leading to vacuolisation and ossification. The last epiphyses close after puberty.

What is the psychological model?

The psychological model of disability emphasises that 'activities performed by someone with health condition are influenced by the same psychological processes that affect the performance of these behaviours by non-disabled people'. People are motivated by the belief that their family and friends would be happy if they participated in an activity. Someone who is emotionally depressed or anxious will suffer more with their disability as they have a loss in cognitive ability whereas those that are happy and determined get along with their disability and it does not stop them from doing anything and living a 'normal' independent life.

Discuss the supply and demand curve?

The supply curve is vertical because in the short-term there is only a fixed amount of healthcare that the government can supply. The demand curve is a normal downward-sloping one, but because the price is zero, there is a lot of excess demand (A to B). This results in queues and waiting lists. The demand curve is continually shifting to the right, and at a faster rate than the government can force the supply curve to the right

Describe joint activity in joint movement?

The reciprocal convex and concave shapes of the joint surfaces - combined with the movements of roll, spin and glide - provide a greater surface area over which the two bone ends can move. Hyaline cartilage, present on the articulating surfaces of the bone ends, has the dual function of providing a smooth surface over which the bone ends can glide and affording the joint protection from wear and tear. Both the functions of the hyaline cartilage are enhanced by the presence of synovial fluid within the joint. The fluid layer over the two joint surfaces will reduce the amount of friction between the bone ends when movements occur and act as a form of shock absorber to reduce the trauma of constant impact, particularly in weight-bearing joints. Synovial fluid produced by the synovial membrane also provides the joint with some of its nutrition. Most of the capsule surrounding joints is lax, thus permitting a large Range of movement by the joint. Most ligaments and all tendons are primarily composed of white fibrous collagen. One of the properties of collagen is that it is fairly inelastic and stretching achieved by deformation requires strong forces. Therefore within normal activities, if the ligaments or tendons are at their maximum length, no more movement is possible at that joint. Movements at synovial joints are produced by the contraction of the skeletal muscles that span the joints and attach to or near the bones forming the articulations. In these actions, the bones act as levers, the muscles provide the force, and the joints are the pivots.

How are prices influenced by supply and demand?

The relationship between supply and demand determines the price of a commodity. As demand for an item or service increases, so does the cost. As more healthcare services are desired by the patient, more supply is required. If more supply is not available generally the price goes up. If there are not enough doctors in an area, doctors could potentially charge more to work there to fulfil the demand. If there's a shortage of drugs, pharmaceutical companies could potentially charge more as the demand is there.

what is Central Processing what parts of the brain are involved and how does it help in standing upright?

The spinal chord: Stretch reflex automatically contracts a muscle when a muscle is stretched. This can be seen during a knee jerk reaction. It also controls rossed extensor reflex when a person automatically lifts up their leg if they stand on something sharp. Cerebral cortex: Primary Motor cortex is responsible for simple voluntary movements. Supplementary Motor Area -voluntary actions being carried out that had to be learned e.g. walking and so requires some memory Premotor cortex - linked to the sensory cortex, it's involved in coupling external stimuli to motor actions such as turning towards sound or moving out the way of a tennis ball. Basal Ganglia: filled with nerve nuclei deep in the cerebrum. They supply time ques when carrying out different 'learned automatic movements) e.g. walking. It is closely linked to the Supplementary Motor Area. Cerebellum: Controls slow voluntary movements like changing your posture however it is also plays a very important role in extreme rapid movements

What is a DMARD?

Therapy with these drugs should begin as soon as possible, as joint damage happens rapidly in RA. What do they do? They slow down or stop damage to the joints, thus reducing swollen joints and decreasing acute-phase response. It is possible for the disease to go into remission with these drugs. The main DMARD used is methotrexate. Methotrexate is a type of antimetabolite: a folate antagonist. Folates are used to make purine nucleotides which are essential for DNA synthesis, which is why methotrexate is useful for treating cancer. However, it is thought that the success of methotrexate in treating RA is not due to its action as a folate antagonist. It is given weekly and the patient is given folic acid supplements as well. Regular blood monitoring is needed to check for potential side effects such as cytopenias( a decrease in the number of blood cells). It is usually started at 7.5mg/week and increased to 15-25mg/week. Other DMARDs include: • Sulphasalazine • Hydroxychloroquine • Leflunomide • Gold • Penicillamine • Azathioprine • Cyclosporin • Minocycline Combinations of DMARDs- Giving the patient two or three DMARDs together has been successful in trials and are thought to be more effective than taking single DMARDs one after the other. So if a an 'incomplete' response is seen with one DMARD, the patient may have another added to their prescription.

What are the pharmacological treatments for RA?

There are 4 main drugs used to treat RA and can be used in combination: • Analgesics Paracetamol, codeine • NSAIDs Reduce pain & swelling, may be prescribed with a proton pump inhibitor (PPI) to protect the stomach • Disease-modifying anti-rheumatic drugs (DMARDs) Aims to treat underlying condition. There are 2 types: - Conventional DMARDs - e.g. methotrexate - Biological therapy - some anti-TNF drugs, e.g. infliximab Side effects include: - GI disturbances - Rashes - Headaches - Sore throat & fever • Steroids Powerful anti-inflammatory drugs. Can be injected or taken as tablets. Side effects can include: -Thinning of the skin at the injection site -Interference with menstrual cycle

Name 9 ways self tolerance can be broken?

There are 9 ways that the autoimmune process can bypass self tolerance and lead to autoimmunity: Alteration of self-antigens Molecular mimicry (self antigens that are structurally similar to nonself antigens) Release of sequestered antigen Breakdown of T-cell suppression Enhanced T helper cell function Inappropriate MHC molecule expression on non antigen presenting cell Dysfunction in cytokine production Abnormality in the thymic selection process Polyclonal activation (A substance that will activate T-cells, B-cells, or both regardless of their specificities.) NB: Release of sequestered antigen: The hypothesis holds that certain sequestered antigens in the brain, the lenses of the eye, and spermatozoa are isolated from the circulation of the blood and the lymph and therefore do not contact the cells of the immune system. When body tissues are damaged, the sequestered antigens are suddenly exposed to the immune system, which treats them as foreign, triggering an autoimmune reaction.

How can the side effects of steroids be reduced?

There are a few ways that you can reduce the adverse side effects of steroids • Use the minimum does of steroid possible for the shortest amount of time • Try to alternate the days on which the steroids are administered o Instead of giving 10mg every day give 20mg every two days • Give in conjunction with other drugs in order to reduce the effects o Corticosteroid sparing agents

What are the 3 mechanisms involved in autoimmunity?

There are three mechanisms involved in autoimmunity these are: 1. BREAKDOWN IN SELF-TOLERANCE: • Regulatory abnormalities • Cross-reactive antigens • Polyclonal activation • Release of sequestered antigens 2. CENTRAL TOLERANCE BREAKDOWN • Self-reactive antigens escape negative selection 3. PERIPHERAL TOLERANCE BREAKDOWN • Release of sequestered antigens. • Molecular mimicry and cross reactivity between self/non-self • Regulatory abnormalities which include cytokine deregulation or tissue cells that acquire the ability to present self-peptides e.g. up-regulation of HLA-DR in Graves' disease. • Polyclonal B-cell activation i.e. B-cell activation occurs without T help.

What are the likely causes of limping in a toddler aged 1 - 3 years?

Toddlers 1 - 3 years: Infectious: - Septic arthritis - Transient synovitis - Ostemyelitis Trauma: - Toddlers fracture - Stress fracture - Child abuse Congenital: - Developmental dysplasia of hip Neuromuscular: - Cerebral palsy

How is RA diagnosed?

There is no single test can give a definite diagnosis of rheumatoid arthritis in the early stages of the condition. A detailed history and physical exam to look at pain and movement will be undertaken. • Blood tests Blood tests can measure inflammation. • Erythrocyte sedimentation rate (ESR) • C-reactive protein (CRP) Both of these may show a high value when inflammation is present. - Can be used to detect rheumatoid factor, which is antibody produced by a reaction in your immune system. • Antinuclear antibody(ANA) (This antibody has a high prevalence in systemic lupus erythematosus. You test for this to see if there is evidence to support a diagnosis of connective tissue disease. By checking levels in people you think may have RA you are checking that it isn't a connective tissue disease instead.) • Consider testing for anti-CCP(anti-cyclic citryllinated peptide) antibodies. This is NOT routinely used. NICE guidelines say it should be used if the patient is negative for RF ANS there 'is a need to inform decision-making about starting combination therapy.' Citrullinated proteins are found in inflamed synovium and a positive test is highly suggestive of RA. Once RA is established testing for anti-CCP antivodies has a specificity of more than 90%. This test may replace testing for RF in the future. • X-rays X-rays will show any damage caused to your joints by the inflammation in rheumatoid arthritis. The changes often show up in x-rays of your feet before they appear in other joints, so may want to x-ray your feet even if they're not causing you any problems. Joint deformities and erosions tend to be symmetrical on x-rays (but not always!) • MRI & Ultrasound May look at the damage around the joints and soft tissue.

What treatment is required for an extracapsular fracture?

These are fractures in the trochanteric region. With these fractures we aren't so worried about blood supply. The main two options are: Extramedullary: This is a sliding hip screw and is the most commonly used device. Intramedullary fixation: These nails are used particularly for subtrochanteric fractures

What is tactile sense and how does it help in stading upright?

These are the stimulation of the pressure sensors that lie deep within the foot used for balance. The tactile sense fluctuates depending on the surface you walk on.

What is direct cost?

This is "what you have to spend", the direct cost to society i.e. the cost of the operation or the after care on the tax payer/NHS

What is cellulitis, presentation, causative organism and treatment?

This is an acute infection of the skin & subcutaneous layers of soft tissue Presentation: Presents with an affected area of inflammation, turning red in colour rapidly, hot but also painful. CO: Mainly group A Streptococcus (including Strep. pyogenes), it can also be Staph. aureus Tx: 7 day course (or longer) of Benzylpenicillin & Flucloxacillin

What is spastic gait and what can cause it?

This is can be split into two types • Hemiplegia o pelvis may be tilted on one side with the elbow flexed and the leg extended o This can be congenital (cerebral palsy) of acquired (Stroke etc.) • Paraplegia o Feet may be inverted and/or cross, the steps will be slow and awkward. Sometimes known as a scissoring gait o This is usually a result of spinal cord compression maybe as a result of trauma

What is Slipped Capital Femoral Epiphysis. , what are the signs and symptoms and what is the treatment?

This occurs when the ball part of the hip joint slips off the upper thighbone due to a weakened growth plate. A slipped capital femoral epiphysis is caused by dislocation of the femoral head from its neck and shaft at the level of the upper epiphyseal plate. • typically affects obese adolescent boys. • Black children are more predisposed to slipped capital femoral epiphysis than are Caucasian children. • The characteristic pain occurs in the affected hip and/or the medial aspect of the ipsilateral knee • Limping is the most common symptom. • Leg held in external rotation and 10 degrees flexion. Reduced range. Treatment: Early diagnosis and treatment prevents disability Treatment - fix femoral epiphysis - do both sides. Puberty a critical time physiologically Can be associated with onset of disease Can be associated with worsening / instability of known disease • This occurs just before puberty between ages 9 and 15.

Age and its relation to common eitiolgoes of a limping child?

Toddlers 1 - 3 years: Infectious: - Septic arthritis - Transient synovitis - Ostemyelitis Trauma: - Toddlers fracture - Stress fracture - Child abuse Congenital: - Developmental dysplasia of hip Neuromuscular: - Cerebral palsy Children 4 - 11 years Infectious: - Spetic arthritis - Transient synovitis - Osteomyelitis Trauma: - Fractures - Sprains and strains Rheumatologic: - Juvinile rheumatoid arthritis Degenerative: - Perthes Adolescents 11> Infectious: - Septic arthritis (gonococcal) - Osteomyelitis Trauma: - Fractures - Sprains and strains Rheumatologic: - Juvenile rheumatoid arthritis Degenerative: - Slipped capital femoral epiphysis

What is tolerance?

Tolerance refers to the specific immunological non-reactivity to an antigen resulting from a previous exposure to the same antigen. While the most important form of tolerance is non-reactivity to self-antigens, it is possible to induce tolerance to non-self antigens. When an antigen induces tolerance, it is termed tolerogen.

How is RA diagnosed on an X-ray?

To diagnose osteoarthritis the following findings on an X-ray include: • Loss of joint space • Articular erosions • Periarticular osteopenia • Soft tissue swelling Rheumatoid distribution: • symmetrical and proximal (MCP's / PIPs)

Define dislocation?

Total loss of congruity between articular surfaces

Discuss transduction of pain

Transduction begins when the free nerve endings (nociceptors) of C fibres and Aδ- (delta) fibres of primary afferent neurones respond to noxious stimuli. Nociceptors are exposed to noxious stimuli when tissue damage and inflammation occurs as a result of, for example, trauma, surgery, inflammation, infection, and ischemia. Nociceptors are unspecialised, free, unmyelinated nerve endings that convert (transduce) a variety of stimuli into nerve impulses, which the brain interprets to produce the sensation of pain.

What is Transient Synovitis (also toxic synovitis / irritable hip), what are the signs and symptoms and what is the treatment?

Transient synovitis of the hip occurs as a result of inflammation of the inner lining (synovium) of the capsule of the hip joint. A childhood limp which develops in the absence of any trauma is very likely to be caused by attributable to this self-limiting condition, which presents in children (more commonly in boys) between 3 and 10 years of age. Although there is no confirmed cause, there is some evidence to suggest that it follows a viral illness. Presentation: Typically the child will awaken with intense groin pain that causes him to limp and / or refuse to walk. The leg is often held in a flexed and externally rotated position. On clinical examination, the range of movement in one hip is limited but examination is otherwise normal. Crucially, the child does not show any signs of systemic illness (fever etc), or possible trauma - thus ruling out septic arthritis (which presents with systemic symptoms) or a fracture (trauma or hip dislocation). Investigations: A blood test may reveal raised inflammatory markers. An ultrasound scan of the hip joint area will tend to show effusion (fluid collection). Treatment: If mild - paracetamol If severe - ultrasound scan and aspiration of an effusion Differential diagnosis is septic arthritis 3-10 years

How does a transverse fracture occur?

Transverse Fractures are usually the result of a direct blow or angular force applied to the bone. The fracture line is across the bone, at a right angle to the long axis of the bone. The shape of the bone ends in transverse fractures helps these breaks to stay aligned more easily than fractures which do not fit together so neatly.

What is the treatment for a dislocation?

Treatment and Management • Reduction - Easiest to achieve as soon as possible after injury, as muscles have not yet gone into spasm. • Arm is placed in sling (stabilization) • Physiotherapist gives gentle exercises to reduce stiffness, relieve some pain and build up shoulder muscle strength (rehabilitation). • 12-16 weeks to completely recover. • Heavy lifting/sports that use shoulder should be avoided for 6 weeks to 3 months.

What is the treatment for systemic sclerosis?

Treatment is organ based • Oral or parental vasodilators e.g. ACE inhibitors, calcium-channel blockers to treat pulmonary hypertension and Raynaud's symptoms and to manage renal involvement • Proton-pump inhibitors to manage symptoms of oesophageal involvement e.g. heartburn, acid reflux, dysphagia • Nutritional supplements as systemic sclerosis can cause malabsoprtion • Antibiotics to prevent small intestine bacterial overgrowth. Antibiotics are given rotationally to prevent resistance. • Warfarin or prostacyclin therapy to treat pulmonary hypertension • Immunosuppression ( e.g. cyclophosphamide /azaithropine) and low dose oral prednisolone to treat pulmonary fibrosis1

What is the treatment for pseudo gout?

Treatments for acute attacks of calcium crystal diseases are aimed at relieving pain, reducing inflammation and shortening the length of the attack) • Paracetamol, co-codamol and non-steroidal anti-inflammatory drugs (NSAIDs) for pain • Colchicine is sometimes used, which can reduce the symptoms and severity of acute CPP crystal arthritis. • Joint aspiration and injection This is to quickly reduce the high pressure in the joint that is causing the extreme pain. It is common after this to inject a small volume (1-2 ml) of a long-acting steroid back into the joint through the same needle. This helps to reduce inflammation in the lining of your joint and prevent the build-up of more fluid. • Lavage - You may need to have your knee joint washed out in hospital, especially if an infection is a possible cause. However, this is very rarely needed.

What is vasculitis?

Vasculitis is inflammation and necrosis of the blood vessels. It can be primary and secondary. Primary vasculitis is rare. Secondary vasculitis complicates other diseases such as Rheumatoid arthritis, SLE or HIV infection. The primary systemic vasculitides are autoimmune disorders of unknown aetiology. One explanation is that exposure to an unidentified antigen, such as a virus or toxin, leads to activation of the immune response. In some cases this immune response is not down-regulated, leading to production of immune complexes that deposit in blood vessel walls and lead to vasculitis. This causes inflammation or leads to necrosis of the blood vessel. Vascular inflammation can have severe consequences: • Aneurysm formation can lead to rupture of vessels. • Vessel stenosis or occlusion leading to distal infarction.

What treatment is required for an undisplaced intracapsular fracture?

Undisplaced intracapsular fractures are treated by internal fixation using screws. Why: Because the fracture isn't displaced, the retinacular blood vessels are probably still intact Avascular necrosis occurs in 5% of cases

When would an MRI scan be used when looking at fractures?

Used for internal derangements of joints and staging of musculoskeletal tumours Uses the magnetic properties of spinning hydrogen atoms to produce images. Common indications • The shoulder and knee are the most common parts imaged using MRI but can be used on any joint within the body. Joint derangements are disruption of supporting structures such as ligaments, cartilages and menisci. • MRI images allow physicians to clearly see very small tears and injuries to tendons, ligaments and muscles, and even some fractures that cannot be seen on x-rays3 • Widely used to diagnose sports-related injuries and work disorders5 e.g. RSI

What is histamine and what does it cause?

Vasoactive amines - Histamine: - Released following the degranulation of mast cells and is stimulated to release by IL-1. - Causes dilation of arterioles and increased vascular permeability.

What are the causes of carpal tunnel syndrome?

Volume of the canal decreases: - Fracture (trauma) - Ganglion - Arthritis - Hypertrophy of the flexor retinaculum Volume of the canal increases: - Tendosynovitis - Bleeding - Abherrant structures: muscle, artery Other causes include: inflammation of the digital tendon sheaths, fluid retention, excessive exercise, infection and/or repetitive activities that involve flexion of the wrist e.g. keyboard typing, piano playing and cutting hair.

What is external fixation?

Used when a cast or splint would not allow proper realignment but internal fixation is not required. Involves putting holes into uninjured parts of the bone. Wires or bolts are then put into the holes through the skin. They attach to a curved rod or piece of metal which sits outside of the body with ball and socket joints which can be altered to realign the fractured bone to its correct anatomical position. As the device sticks out of the skin there is risk of infection.

what are the investigations for vasculitis?

Vasculitis can be primary or secondary. It is secondary if it is due to underlying connective tissue disease. It is not a connective tissue disease itself. Investigations: • CRP, ESR • Anti-neutrophil cytoplasm antibodies (ANCA)- these are antibodies that target enzymes in neutrophils and monocytes. The presence of ANCAs is detected using indirect immunofluorescence. • Urine: proteinuria, haematuria • Angiography and possibly biopsy.

What are the causes of acute inflammation?

What causes acute inflammation: Acute inflammatory reactions are triggered by: • Infection- bacterial, viral • Trauma- penetrating, blunt • Physical and chemical agents- thermal injury, irradiation • Foreign bodies- sutures, splinters • Tissue necrosis • Immune reactions- hypersensitivity, autoimmunity

What are the causes of chronic inflammation?

What causes chronic inflammation: Chronic inflammatory reactions are caused by: • Persistent infections- micro organisms, TB, fungi • Prolonged exposure to toxic agents (can be endogenous or exogenous)- atherosclerosis • Autoimmunity- Rheumatoid Arthritis

What is the haversian system?

What gives this bone type its compact structure is the tightly packed osteons otherwise known as the haversian system. Haversian canals connect the osteons. These canals contain nerves, arterioles, venules, capillaries and lymphatic channels. The Haversian canals are a system designed to distribute the blood vessels carrying nutrients to supply the cells trapped within the dense calcified matrix. Interstitial lamellae lie between osteons and there are 'cement lines' that define the outer border of an osteon.

What does the term elastic mean in economics?

When an industry becomes more competitive - either by too much supply or too little demand - market equilibrium tends to become, what is known in economics, as elastic. Price elasticity is a measure used in economics to show the responsiveness of the quantity demanded of a good or service to a change in its price.

When can consent be taken without permission?

When we can contravene these: • If patient is unconscious • If testing for a notifiable disease • If patient is not competent (mentally disabled, child etc.)

Why do we measure PROMs?

Why measure PROMs? Clinically there are many reasons: o Screening for hidden problems o Identifying & prioritising problems o Communication o Identifying preferences, shared decision-making o Monitoring change/response o Aid in treatment & resource allocation decisions There are also many emotional impacts of a disease and these measures allow the clinician to understand the psychosocial needs of the patient: o Emotional impact key feature of some conditions (e.g. depression) o Emotional effects of many chronic physical conditions increasingly recognised o Fear, anxiety, depression common emotions o May relate to stages of adjustment: o e.g. shock (fear), encounter reaction (anxiety, depression), retreat (denial), re-orientation

Define acute pain?

a complex constellation of unpleasant sensory, perceptual, and emotional experiences and certain associated autonomic, psychological, emotional and behavioural responses.

The sequence of cellular infiltrates in acute and chronic inflammation can be explained simply with the following:

a) Acute Inflammation- Neutrophils appear first, followed by macrophages. b) Chronic Inflammation- Lymphocytes in greater numbers, followed by plasma cells and macrophages. c) Granulomatous Chronic Inflammation- Macrophages clusters, followed by peripheral lymphocytes in small numbers.

What are ligands?

are small molecules which interact with larger targets - Endogenous: ACh, epinephrine, insulin, endorphins - Exogenous (drugs): nicotine, propranolol, morphine, naloxone

What is opportunity cost?

can't be spent on other problems as money as already been spent.

What is NSAIDs main mode of action?

inhibition of cyclooxygenase enzymes, which convert Aracidonic acid to Prostanoids such as prostaglandins and thromboxanes.

What is internal fixation?

involves the use of pins, plates or nails directly into the bone or on the bone surface, inside the body. Can be open reduction internal fixation (open surgery) or closed reduction internal fixation (reduction achieved without surgery, but followed up with open reduction later. Common in condylar fractures).

How is osteomyelitis managed?

o Depends on the extent of the disease, host factors and the infection causing organism. o Antibiotics long term (first line antibiotics are flucloxacillin and fusidic acid) o Surgery is essential to remove dead tissue or contaminated material.

Define chronic pain?

pain that persists a month beyond the usual course of an acute disease or a reasonable time for an injury to heal or that is associated with a chronic pathologic process that causes continuous pain or the pain recurs at intervals for months or years.

What is the mechanism of action of anticonvulsants in pain and what type of pain is it used for and name some types?

phenytoin, carbamazepine, sodium valproate clonazepam, and baclofen, Gabapentin, pregabalin Gabapentin and pregabalin have become the gold standard treatment of neuropathic pain, the mechanism of action is not fully understood but it is believed that it works through binding the alpha-2 delta receptors in the central nervous system. When bound by gabapentin or pregabalin they decrease the influx of calcium into the presynaptic terminal thereby decreasing the release of excitatory neurotransmitters. Gabapentin and pregabalin work by increasing GABA and reducing the release of glutamate thereby suppressing the sensitivity of N-metyl-D-asparate (NMDA) receptor. Reducing neuronal hyper excitability recorded at the spinal dorsal horn near the level of injury. Neuropathic pain

Anti centromere is associated with?

scleroderma

What are the symptoms of pseudo gout?

sudden pain and stiffness in affected joint (most commonly knee) • swelling and tenderness • red, inflamed skin over the joint • raised temperature • generally feeling unwell • These symptoms tend to last several days to 2 weeks before completely settling • On investigation the crystals appear to be rhomboid shaped

What is intangible cost?

the cost that can not be measured i.e. the worry, pain, suffering, anxiety

What is distraction without displacement?

this is where the two ends of a bone are pulled apart but essentially within the same axis, such that if they were reduced, the bone would fit back together well

Describe a simple fracture?

• Simple or Comminuted Simple fractures generally occur along one line, splitting the bone into two pieces, with the skin remaining intact (i.e. there is no bone protrusion).

What is the treatment for sjogrens syndrome?

• Eye drops to replace the tears • Saliva substitutes, available as sprays, lozenges, gum, gel • Pilocarpine stimulates the tear ducts and saliva glands • Antimalarial drugs e.g. chloroquine, hydroxychloroquine can be used to treat the symptoms of fatigue and arthralgia, and also to slow the immune system attack on the tear ducts and saliva glands • Corticosteroids used to treat persistent salivary gland swelling and neuropathy

What is the basic unit of a tendon?

• A bunch of collagen fibrils forms a collagen fibre which is the basic unit of a tendon.

What are G protein couple receptors?

• A family of receptors which have 7 membrane spanning helices • Examples of G-Proteins are mAChR (muscarinic acetyecholine receptor, amine receptors, 5-HT receptors, opiate receptors.... Many more.... • Usually linked to physiological response by second messengers • Function of G-Protein is to recognize activate G-Protein Coupled Receptors (GPCR) and 'pass on' the message to the effector systems which will generate a cellular response • The stimulation of adenyl cyclase and phosphokinase following receptor activation is mediated by a family of regulatory guanosine triphosphate (GTP) binding proteins • The occupatiuon of the ligand binding site results in conformation change in the cytoplasmic domain of receptor • Ligand-receptor complex has enhanced affinity for the G-Protein complex -> binding is achieved • Binding induces the release of GDP bound to the alpha subunit; GDP is replaced by GTP • GTP dissociates from the and subunits. GTP is the activated form of the G-Protein • GTP diffuses through membrane and activates target (i.e. adenyl cyclase) • Activation targets for G-Proteins include adenyl cyclase as already mentioned to generate camp (see section below on second messengers),targets also include the phosphoinositide system and ion channels. • The GTP complex dissociates from the G-Protein and activates (or inhibits) the enzyme • The signal to the enzyme ends because GTP has intrinsic GTPase activity and turns itself off by hydrolyzing the GTP to GDP. GDP then reassociates with the G-Protein subunits. Second Messengers = are chemicals whose intracellular concentration increases or decreases in response to receptor activation by agonists, and which trigger processes that eventually result in a cellular response. An example is cAMP. cAMP is formed from ATP by the enzyme adenyl cyclase when adrenooceptors are activated or stimulated (this is how asthma inhalers work). The cAMP activcates an enzyme (protein kinase A) which phosphorylates a protein (enzyme or ion channel) and leads to a physiological effect.

How can osetomylitis be aquired?

• A haematogenous route (via the blood supply to the bone by blood borne bacteria) • Direct inoculation (from adjoining tissue from trauma, surgery or direct spread) - the skin is broken allowing direct access to the bony surfaces.

What are the clinical features of sjogrens syndrome?

• Affects people in 40 - 50 ages. Ocular symptoms: • Reduced tear production - resulting in destruction of corneal and conjunctival epithelium (keratoconjunctivitis sicca). Patients will complain that eyes are sore and gritty and usually red. • Bacterial conjunctivitis - is common Oral synptoms: • Xerostomia (dryness of the mouth) - this causes difficulty in swallowing; patients often take frequent sips of water. • Mucosa is dry - there is little saliva and tongue may appear very dry. • Oral candidiasis is common (Thrush) • Intermittent parotid swelling - this affects 50% of patients Other symptoms • Secretions from other exocrine glands may also be diminished. - may give clinical effects: vaginal dryness can cause dyspareunia. Lack of GI mucus secretion can result in oesophagitis or gastritis. Sjogren syndrome has many systemic feature too: (1) • Fatigue • Weight loss • Fever • Arthritis - episodic, non erosive and similar to joint disease seen in SLE • Reynaud's phenomenon • Interstitial lung disease • Interstitial nephritis - can lead to diabetes insipidus • Vasculitis - causes cuntaneous lesions: purpura and ulcers. • Neurological features: peripheral neuropathies result due to small vessel vasculitis. • Cranial neuropathies - hemiparesis, seizures and movement disorders. • Lymphomas - Develop in salivary glands, reticulebdotheial system, GI tract, lungs or kidneys.

What are lignad gated channels?

• Agonists • Involved in fast synaptic transmission • Made up of protein subunits which form a central pore (this is the "proline hinge") -> 5 subunits: 2 x alpha, beta, gamma and delta. • Has 4 transmembrane regions (M1 to M4) • Receptor is linked directly to ion channel • A ligand will bind to the N terminus of the alpha subuit, this will create a conformational change which will open the pore and allow entry. • Examples include nicotinic receptor, GABA and 5-HT3 receptors.

What are the 3 main clinical actions of NSAIDs?

• Analgesic • Anti-inflammatory action, • Antipyretic action

How is the stimulation spread (myelin)?

• Around each neuron is an insulating layer called the myelin sheath. It is made fatty cells collectively called Schwann cells. • Between each Schwann cell is a small exposed space - the node of Ranvier. • An AP can jump from node to node. • This speeds up the transmission, and means less energy is needed to depolarize whole cell.

What is an action potential and how is it fired?

• At rest there is a greater concentration of K+ inside the cell, which diffuse outward (because the cell membrane is selectively permeable to K+). • This exodus of K+ causes a potential of -70mV to develop. Action Potentials: • Stimulation of the nerve causes depolarization (i.e. voltage to become >-70mV). • If this stimulation is large enough, and the membrane is depolarized above the threshold value (~-55mV) then selective voltage controlled ion channels open, and an avalanche of Na+ ions enter the cell, and the PD spikes up to ~+50mV in less than a few tenths of a second. • This "All or Nothing" concept means if a stimulant does not exceed the threshold then no signal is fired. • While an AP is being stimulated it is virtually impossible to stimulate further AP before such time as a return to close to the resting membrane potential of ~-70mV. This return to normal is called the "refractory period". Just before the refractory period ends an AP can be produced, but it requires a larger stimulus than was the case for the initial AP. • Once the AP has been initiated it automatically spreads up along the nerve. This is called self-propagation.

What is peripheral tolerance in B cells?

• B cell activation depends on antigen and T cell help • B-cells reactive with self-antigens in the periphery become anergic or are deleted

Describe the route of infection of haematogenous osteomylitis

• Bacteria travel in blood supply into bone blood supply (bacteraemia) and start to seed in the medulla. • An abscess forms in the medulla which raises the periosteum as it pushes into its space. • The dead bone within the abscess is called sequestrum. • The new bone formation under periosteum is called involucrum. • Periosteum is eroded which leads to sinus formation and communication with exterior. • Affects the vertebrae and the long bones. Most common in the tibia and femur.

What do the colours on an X-ray indicate?

• Black = Air • Dark grey = Fat • Grey = Soft tissue • White = Bone

Describe the long term musculoskeletal & systemic complications in patients with rheumatoid arthritis

• Carpel Tunnel Syndrome: Rheumatoid Arhtiris commonly affects the hands and with inflammation of the wrist, the chance of contracting carpal tunnel syndrome is dramatically increased. • Septic Arthritis • Ruptured tendons: The inflammation of the joints can cause inflammation in the tendons surrounding that joint. If this inflammation is severe enough the tendon can actually rupture, leading to loss of function in that muscle. This may have drastic impacts upon the individuals quality of life and is therefore treated with surgical repair. • Bakers cyst: Baker's Cysts are fluid filled and effect the knee. Essentially when inflammation occurs in the knee, there is an increase in the production of synovial fluid. This increase can lead to a swelling at the back of the knee as the joint lining is stretched. This leads to further inflammation and can be quite painful for the patient. • Spine: Involvement of the cervical spine in rheumatoid arthritis is common following the involvement of joints in the hand. In fact the progression of the disease in the cervical spine tends to mirror that in the hands. With the inflammation occurring here, there is an increased chance of compression on the spinal cord, which can lead to several neurologic complications • Amyloidosis: Although quite rare and only really found in severe cases of RA, Rheumatoid Arthritis is the leading cause of something called Secondary AA Amyloidosis. Amyloidosis itself is a disorder of protein metabolism. Essentially protein gets deposited externally to cells around the body and these proteins are insoluble. • Cardiac problems: Pericariditis / effusion • CVS: vasculitis • Eyes: Iritis, Scleramalacia, sicca (scare of tear ducts, Dry eye) • Mouth: Xerostoma (drymouth) • Skin: Nodules • Pulmonary: Pulmonary fibrosis • Kidney: Amyloidosis can lead to renal failure • GUT: amyloid in gut • Blood: Bone marrow changes, Aneamia - normochronic, Iron levels, splenomegaly (enlargement causing RBC too many being removed), Lymphodenopathy • CNS: Peripheral neuropathy • Psychosocial: There are many psychosocial impacts of rheumatoid arthritis which I have outlined in my other PBL in more detail. Very briefly these are depression (40% of RA patients seen in hospital), social isolation and unemployment. These are severe

Name examples of COX-2 selective inhibitors?

• Celecoxib • Meloxicam • Rofecoxib • Etodolac + other Coxib drugs

name the 2 types of tollerance are there and describe both.

• Central tolerance is the deletion of self-reactive cells during lymphocyte development in primary lymphoid organs i.e. thymus (T cells) or bone marrow (B cells). • Peripheral tolerance is the unresponsiveness of self-reactive cells outside in the peripheral tissue (i.e. secondary lymphoid tissues). T cells will recognise antigen + co-stimulation and B cells will recognise antigen + T cell helper.

What are chemokines?

• Chemokines - Produced by leucocytes and act as activators and chemoattractants for more leucocytes.

What would you examine in a patient you suspect has carpal tunnel syndrome?

• Examination will focus on looking for numbness, weakness of thumb abduction (which will indicate a problem with the muscle abductor polllicis brevis and not with the median nerve), - Tinel's test (tap down on the forearm in the area of the median nerve and monitor the nerve activity) and also the doctor should examine the rest of the limb and spine to rule out other conditions.

What are the finacial implications of a disability?

• Reducing your income • Increasing your living expenses • Requiring you to purchase expensive items • Increasing your travel costs

What is the difference between a closed and open fracture?

• Closed or Open (Compound) In medicine, fractures are classified as closed or open (compound), and simple or multi-fragmentary (also known as comminuted). Closed fractures are those in which the skin remains intact. Open (or "compound") fracture is one in which there is soft tissue damage, and an open wound, often communicating with the bone. Open injuries carry an elevated risk of infection, which can impede bone healing and cause significant complications. They require antibiotic treatment and, in most cases, urgent surgical debridement to remove debris, damaged and infected tissue. Where the skin has been penetrated by a bone fragment from inside the leg, the fracture is sometimes referred to as "compound from within", to distinguish it from a true open fracture and to emphasise the potential seriousness of the injury.

What are the early complications of fractures?

• Compartment syndrome, • Infection (oseteomylitis) • Complex regional pain syndrome (CRPS) • Deep vein thrombosis (DVT), • Fat embolus Compartment syndrome is an important complication that you are not allowed to miss as a doctor. It is the result of excessive pressure development in closed fascial muscle. Fascial muscle is muscle covered in a layer of deep fascia that strongly binds groups of muscles together while allowing the muscles to slide past each other and other structures. After a fracture, blood supply to the muscle can be blocked as a result of swelling, this occurs in small vessels. 'The patient will complain of excessive pain (more than normal) and pain on passive movement of the digits is demonstrated. Paraesthesia develops early as a result of ischaemia of the nerves. The diagnosis is clinical (sometimes confirmed with pressure monitoring), and if present requires urgent surgical fasciotomy (release of compartments)'. Infection can result from operation or open fracture, to can present early or late. gas gangrene or tetanus! Complex regional pain syndrome (CRPS). The cause of this condition is not known, but it is thought to relate to the sympathetic nervous system. It is an unusual condition but has been shown to occur after operation or injury. Usually affecting the upper limb, the patient has red, swollen shiny fingers with excessive joint stiffness; atypical pain is also a feature. Physiotherapy is the most effective treatment method for this complication. Deep vein thrombosis (DVT) afflicts the lower limb. It occurs after a lower limb injury. It is prevented using mechanical or chemical means. The mechanical means are foot pumps, graduated compression stockings. The chemical means are heparin and aspirin. There are many differential diagnoses for DVT and it is often difficult to diagnose because the limb may just be swollen and painful directly because of the injury. If a doctor is unsure they will carry out a duplex scan or venogram on the patient. At-risk patients are prophylactically treated with warfarin. Venography (phlebography) n. imaging of the anatomy of veins in a particular region of the body. Fat embolus is another important condition that must be detected and is common after long bone fractures, particularly the femur. It occurs because fat enters the circulation and embolizing to the lungs. The medullary canal of long bones contains fat, so when broken the fat is released into circulation, saying this early stabilization of fractures reduces the risk of fat embolus. This complication can be very serious and lead onto the development of acute adult respiratory failure that can be fatal. If this occurs then the patient should be transferred to a high-dependency unit and treated with supportive oxygen and fluids.

How is the compliment system activated?

• Complement System - A cascading sequence of serum proteins made up of more than 20 components. During an acute inflammatory response, the system can be activated in four ways: 1) Necrotic cells release enzymes that are capable of activating complement. 2) Antibody-antigen complexes activate complement through the classical pathway. 3) Gram -ve bacterial endotoxins activate complement through alternative pathway. 4) Products of the kinin and fibronolytic systems activate complement. e.g. C3a and C5a- vasodilation and permeability C3b- opsonin •

What are voltage gated ion channels?

• Consist of 1 large glycoprotein -subunit which has 4 identical domains each containing 6 membrane spanning helices (24 helices!). These stack together to form a central pore. • The exact mechanism of action of these channels is unknown but though that it depends on their conductance and the membrane potential. • Contain m-gates and h-gates. • At resting potential most h-gates are open and m-gates are closed (closed channel) • Depolarisation cause the m-gates to open (open channel) but the intense depolrisation of the action potential causes the h-gates to close (inactivation). • Examples include local anesthetics (such as lidocaine, bupivacaine) which bind to the h-gates are stop them from opening (blocks receptor) -> when too many channels are blocked then there are not enough for depolarization to occur and nerve block occurs.

How is SLE diagnosed?

• Cytopenias (i.e. anemia, thrombocytopenia, leucopenia) • Low C3, C4 (consumption) • ANA • Anti Sm • False positive test for syphilis • Renal / liver

What are the late complications of a fracture?

• Delayed Union / Non-union • Malunion • Avascular necrosis • Contracture • Stiffness • Osteoarthritis • Growth disturbances These are the complications you need to look out for further down the line regarding fractures. Delayed union/non-union refers to bone that is extremely slow in coming together and healing or bone that fails to unite completely despite medical treatment. There are certain fractures that are more prone to delayed union/non-union for example fracture of the tibia. This complication is more likely if the injury was high impact or complicated by compartment syndrome. This is usually treated by further surgery to encourage the bone to heal. Malunion is the abnormal positioning of bone after a fracture; this comes from inadequate stabilization of the fracture. Malunion of bone can reduce movement in a joint and predispose to arthritis in later life. Avascular necrosis (AVN): Avascular necrosis is an occasional complication after fracture. This is the cellular death of bone components due to the interruption of blood supply. The bone structures then collapse, resulting in bone destruction, pain, and loss of joint function. AVN tends to occur in bones where the blood supply to one major fragment crosses the plane of the fracture and is disrupted, especially if the fracture is displaced. Significant displacement will almost invariably damage the blood supply and late AVN is therefore a risk after reduction. The manifestations of AVN may develop very slowly over 18-24 months, and the timing and duration of fallow up must take this into consideration. Contracture. Untreated compartment syndrome or vascular complication can result in contracture. Volkmann's ischaemic contracture is an example. Contracture n. fibrosis of skeletal muscle or connective tissue producing shortening and resulting in deformity of joint. Volkmann's contracture fibrosis and shortening of muscles due to inadequate blood supply that may arise from arterial injuries or compartment syndrome. Stiffness. While a fracture is healing the patient may be immobilized and prolonged immobilization can lead to severe joint stiffness. Osteoarthritis is common in intra-articular fractures. Growth disturbances are present in fractures going through the growth plate, it can cause deformity by partial arrest of growth or shortness of limb and treatment of this complication is complex.

What are the causes of gout?

• Drinking too much alcohol • Lack of Vitamin C in your diet • If you drink sugar-sweetened soft drinks high in fructose (A recent research study found that having two drinks a day of a sugar-sweetened soft drink increased the risk of developing gout by 85%) • Diet high purine. • Some medicines: Diuretics, aspirin and some chemotherapy medicines. • More uric acid is made than usual in illnesses where the cells of the body have a rapid turnover (severe psoriasis and some blood disorders). • Obesity, high blood pressure, kidney damage, diabetes mellitus, bone marrow disorders, lipid disorders, vascular disease,

What is the treatment for PM/ DM?

• Early intervention with steroid-sparing agents e.g. methotrexate, is common, especially in cases of relapse1 • Prednisolone (0.5-1.0mg/kg bodyweight) is prescribed until at least one month after the disease has become inactive.

How is psoriatic arthritis diagnosed?

• FBC • ESR • CRP Once again these will show similar picture to AS X-ray • Erosions with proliferation of adjacent bone • Reabsorb of terminal phalange • Ankylosis • New bone formation at entheses

How is Reactive arthritis diagnosed?

• FBC • ESR • CRP The above three present similarly to AS • Serology for Ab against Salmonella, Campylo-bacter, Chlamydia & Neisseria • Synovial fluid from affected joints & Gram stain culture N.B. cultures are negative in RA BUT must exclude septic arthritis

What are the physical effects of a chronic illness?

• Functional loss / disability • Fatigue • Altered body image • Pain

What may synovial fluid be analysed for?

• Glucose - usually slightly lower than levels in the blood. Significantly lower levels are seen in joint inflammation and infection. • Protein - this is increased with bacterial infection • Lactate dehydrogenase (LDH) - increased levels are seen in rheumatoid arthritis, infectious arthritis and gout. • Uric acid - increased levels in gout (crystals present in synovial fluid)

What are the investigations used if osteomyelitis is suspected

• Imaging: look for signs of bone destruction, abscess formation or new bone formation. o Plain x-ray, o MRI o isotope studies. • Laboratory Investigations: o microscopy and blood culture (direct plating to look for growth of organisms), o FBC looking for inflammatory markers WCC o CRP (C-reactive protein: inflammatory marker)

What are the risk factors for OA?

• Increasing age. • Female sex (for knee disease). • Family history (several chromosomal loci and gene variations have been identified as putting someone at increased risk for OA). • Previous joint injury including infection, intra-articular fracture and ligament tear causing joint instability. • Joint malalignment problems such as Perthes' disease, slipped upper femoral epiphysis, and congenital dislocation of the hip. • Obesity. • Occupational (knee OA in elite athletes, elbow OA in people working with pneumatic drills).9 • Ethnic origin (more common in white Europeans).

What musculoskeletal causes are there of limping?

• Infection o Septic Arthritis o Transient synovitis o Oesteomyelitis o Lymes disease • Mechanical o Trauma: Fracture, soft tissue injury, contusion o Slipped femoral epiphysis o Congential hip dislocation / Developmental dysplasia of the hip • Inflammatory o Transient synovitis o Juvenile rheumatoid arthritis • Vascualr o Perthes disease • Neoplastic o Leukemia o Oesteosarcoma o Ewings Sarcoma

What is psoriatic arthritis?

• Inflammatory Arthritis. associated with psoriasis

What types of neck of femur fractures are there?

• Intracapsular • Extracapsular

What are the immediate complications of fractures?

• Ischaemia, • Nerve Palsy • Haemorrhage, • Hypovolaemic shock Local An open fracture can be caused by the displacement of bone tearing the skin open. From this the fragments of bone may press on nerves, producing a nerve palsy. Nerve palsy is common in the humerus and causes radial nerve palsy. Also fracture fragments may press on blood vessels causing ischaemia in that area, for example fracture of femur to popliteal vessels. Quite often the blood vessels and nerves are torn completely and need to be repaired immediately. General Femoral, pelvis, open or multiple fractures can cause serious haemorrhage and in some cases it can be excessive resulting in hypovolaemic shock.

What are the presenting symptoms of RA?

• Joint pain and swelling • Stiffness, especially in the morning or after sitting for long periods • Fatigue • Joint deformity • Poor sleep • Loss of weight • Flu like symptoms • Unpredictable flares of inflammation • Psychological effects: anxiety and depression

What are the symptoms of psoriatic arthritis?

• Joint pain, stiffness and occasional swelling • Dactylitis & enthesitis are common features • DIP with pitting or oncholysis of the nail • Bone reabsorption at metacarpals and phalanges => telescoping of digits Pattern of joint disease • asymmetrical oligoarthritis 30-40% • symmetrical polyarthritis 30% • DIP joint predominant (small joints of hands and feet) 10-15% • spondarthritis 10-20% • mutilans <10%

Why do some patients heal more slowly than others?

• Local: patient's age, type and site of fracture, nutritional status of the patient, type of bone (is it composed mainly of lamellar bone or is it flat?) • Systemic: cigarette smoking, nutritional status of the patient or other underlying medical conditions (Diabetes Mellitus, RA, Osteoporosis) • Generally bone takes 6-8 weeks to heal and adequate strength is returned within 3-6 months. Children's bones tend to heal faster than adults.

What is the treatment for SLE?

• Monitor for end organ disease / disease activity • Hydroxychloroquine for skin / mucous membrane involvement • Treat organ involvement with appropriate immunosuppression • Control cardiovascular risk factors

What are the clinical features of giant cell ateritis?

• Most symptoms are due to carotid artery inflammation although arteries can be involved. • Onset of symptoms is quick - often appearing overnight • Initial symptoms: o Headache o Scalp tenderness o Pain on chewing • Most feared complications are: o Blindness - due to ischaemic optic neuritis caused by arteritis of the ophthalmic arteries. o Vision may be disturbed o Stroke Early recognition and treatment can prevent blindness and other complications due to occlusion or rupture of arteries

What is the treatment for Psoriatic arthritis?

• NSAID • DMARDs ciclosporin, azathioprine and sulfasalazine, methatrexate. • biologics • physio/OT/education N.B. treated the same way as AS and Reactive A.

How do you describe a fracture?

• Name of the fractured bone(s) + specific part that is fractured e.g. proximal shaft/mid-shaft/distal shaft. • Whether the fracture is simple/comminuted (2 fracture fragments only or more than two fragments respectively). • A closed or open fracture. • Joint involvement (e.g. intrarticular) • Type of deformity/path of fracture line.1 What else to look for in an x-ray: o Black lines (bones have separated) o White lines (compression of bones .g. stress fracture) o Joint effusion (intra-articular fracture) - fat is seen darker on the film then soft tissue. o Ring fractures: Fracturing a ring structure means there must always be a break in 2 places. (pelvis, paired long bones etc.

Describe contigous osteomyelitis (from direct inoculation)

• Organisms enter the body from the outside e.g. open fracture, infection spreading from skin or soft tissue. • Create non-healing fractures, sinus formation and sequestrum - this is the same as the route of infection for haematogenous osteomyelitis (see previous section). • Organisms may create a biofilm. This is an organised layer of microorganisms that form a surface, it is this organised surface which prevents attack from the immune system. It may have a surface of "slime" which protects it from antibiotics. • Leads to chronic pain, bone loss, sinus formation and discharge from sinus.

How can the fracure be stabilised surgically?

• Percutaneous wiring(usually at the wrist and removed 4-6 weeks later) • Internal fixation (plate and screws) • Intramedullary nail (commonly used in tibia and fibula) • External fixation: pins or wires are inserted into bone and fixed to an external frame

What are the specific protein targets in the body? (4 of them)

• Receptors • Ion channels • Enzymes • Carrier Molecules

What are the 3 main goals in managing fractures and disolocations?

• Reduce • Stabilise / Immobilise • Rehabilitate

What is the treatment for carpal tunnel syndrome?

• Splintage: place the hand into a splint (non-invasive technique) • Steroid Injections (reduce inflammation) and NSAIDs. • Surgery - make a skin incision above the carpel tunnel and cut the flexor retinaculum. • Results of treatment (surgery): generally very good and will • reduce the pain and tingling effects but the numbness and weakness may become worse. Grip strength should return within 3 months and the patient can usually return to work within 3-6 weeks. There is a chance of reoccurrence.

Describe the types of surgery that can be used when treating a fracture?

• Surgery is used when conservative treatment fails or the fracture is open. • Carried out under local or general anesthetic. • Surgeon will make an incision over the fractured bone and place the bone into it's normal position. • Screws, pins or plates are then attached to or placed inside the fractured bone. Long bones (e.g. femur) may have nails used instead to fix the bone in place. • Any disruptive blood vessels are tied off or cauterized (burned). • If there has been a large loss of bone then the surgeon may do a bone graft.

What is the treatment for SLE?

• Symptoms of arthralgia, arthritis, fever and serositis can be managed by NSAIDs1 Commonly prescribed: ibuprofen, naproxen, diclofenac, piroxicam2 • Topical corticosteroids are used to treat cutaneous lupus e.g. erythema across the skin on the face1 (see below for dosage) • Antimalarial drugs e.g. chloroquine, hydroxychloroquine can be used to treat cutaneous symptoms, fatigue and arthralgias1 • Oral corticosteroids can be used to treat severe flares of the disease, as well as serious renal and cerebral complication, anaemia and thromobcytopoenia • Immunosupressants limit the damage caused by the immune system: • Cyclophosphamide, Mycophenolate mofetil, Azathioprine, Rituximab

What are the investigations for gout?

• Synovial fluid analysis Needle aspiration of symptomatic joints and examined under a microscope under polarised light. If Sodium urate crystals are present they will be needle shaped and show strong negative birefringence (meaning crystals appear yellow if parallel to plane of light and blue if at right angles to plane of light). Blood test • Serum uric acid measured but is NOT diagnostic of gout. • Raised ESR and CRP • Full blood count- may show polymorphonuclear leucocytosis (These are a type of neutrophil found in inflammatory conditions).

What is synovial fluid made up of?

• Synovial fluid is excreted from the synovial membrane (also known as the synovium) which is a thin inner layer that constitutes part of the articular capsule of a synovial joint. • Hyaluronic acid - essentially the component which enhances the viscosity and elasticity of synovial fluid • Lubricin - essential in lubrication between layers of cartilage • White blood cells - (monocytes, macrophages, lymphocytes and neutrophils) - essential in the "removal of debris" in the joint discussed above

What are some of the rules when interpreting a fracture?

• Take a minimum of 2 views (lateral & AP) • At 90o to each other • X-ray the joint above and below when paired bones are injured • Supplementary signs e.g. soft tissue swelling and joint effusion. • Elevated anterior fat pad. • Any posterior fat pad. • Elbow effusion. • For suspected ankle trauma three standard views are performed: AP, lateral and oblique.

What are the 4 transitional tissues from tendon to bone?

• Tendon • Fibrocartilage • Mineralised fibrocartilage (Sharpey's fibres) • Bone

What is the commenest infective agent for osteomyelitis

• The most infecting organism is Staphylococcus aureus. • Steptococcal infections are common in neonates due to the mother's birth canal being colonizied by this organism. • Gram negative infections e.g. Pseudomonas can also occur and also Mycobacterium tubercuolosis.

What is cerebellar gait or ataxia and what can cause it?

• The patient will lurch from side to side and the stance will be unsteady and wide • The patient may also have difficulty walking in a straight line and turning • There are many causes of this gait including strokes, genetic diseases, alcohol, multiples sclerosis and neurodegenerative conditions

What are Tyrosine kinase linked receptors?

• These are surface receptors that possess intrinsic tyrosine kinase activity. • On activation, they will mediate an effect through activation of other enzymes. This is different to Steroid hormone receptors which participate directly in regulation of gene transcription by binding to DNA.

What are nuclear receptors for steroid hormones?

• These receptors are present in the cell nucleus and regulate transcription and protein synthesis • The are soluble cytosolic or nuclear proteins with ligand and DNA binding domains, which contain a "zinc finger" motif which is characterisitic of proteins which regulate transcription. • After binding of steroid to receptor and before the interaction with DNA, there is a dimer formation (the linking of 2 steroid-receptor complexes). • Hormone must cross the cell membrane to elicit response. • Hormone binds to receptor in the cytosol or nucleus. • Hormone binding results in accessibility or activation of DNA-binding domain. • Receptor-hormone complex binds to defined regions of the genome (known as "hormone responsive elements"). • DNA binding domain recognizes specific base sequences and therefore affects particular genes. • The pattern of gene activation depends on both cell type and the nature of the hormone so the effects are highly diverse. • Effect of receptor activation: causes an increase in RNA polymerase activity and increase mRNA production - but the effects are not noticed until the protein is synthesized.

What is parkinsonian gait and what can cause it?

• This gait will be short paced, shuffling and on a narrow base • Presents as a result of Parkinson's disease

What is sensory ataxic gait and what can cause it?

• This is a wide based, stamping gait as the patient has to overcompensate for the loss of peripheral sensation • This can be caused by peripheral neuropathies such as in diabetes mellitus, spinal dorsal column dysfunction and complex neurodegenerative disorders

What is a high stepping gait and what can cause it?

• This is where the patient lifts their leg higher than normal in order to lift their foot off of the floor • Usually occurs when the dorsiflexion of the foot is lost maybe as a result of injury to peroneal nerve or wasting of the muscles of the outer leg • Can also be caused by neuropathies as well such as in diabetes mellitus or leprosy

What are the features of anti phospholipid antibody syndrome?

• Venous Thrombosis - Deep vein thrombosis and pulmonary embolism are most common. Other veins can be affected: Inferior vena cava, pelvic, renal, portal and hepatic. • Arterial thrombosis - Cerebral ischaemia: stroke, transient ischemic attacks, peripheral ischaemia. • Fetal complications - Spontaneous abortions - often in the 3rd trimester • Thrombocytopenia - Not severe enough to cause haemorrhage. Associated features: • Livedo reticularis • Leg ulcers • Cardiac valve abnormalities (mitral and aortic regurgitation) • Chorea • Epilepsy • Migraine • Haemolytic anaemia

What is apraxic gait and what can cause it?

• Wide based, shuffling gait • All individual neurological elements are normal however the patient is not able to function normally • Due to loss of cerebral cortical function as a result of diffuse cerebrovascular disease

Discuss dorsal horn sensitisation

• Within hours of an injury, changes take place in the dorsal horn of the spinal cord which alters the way that sensory impulses are processed. When these changes have occurred the dorsal horn is said to have become sensitised. This means that sensory and painful signals are more likely to be transmitted up the spinal cord to the brain, rather than being blocked at the dorsal horn level. Sensitisation is said to be dependent on N-methyl-D-aspartate (NMDA) receptor activation. NMDA receptor antagonists (blockers) like ketamine can help prevent sensitisation occurring. • Normally after an injury dorsal horn sensitisation reduces in line with tissue healing. However, in some people the sensitisation seems to go on for much longer, and may explain why some go on to develop chronic pain. • There is also a connection between emotions and dorsal horn sensitisation. In severe anxiety and depression states, lack of descending inhibition is enough to maintain the dorsal horn in its sensitised state.

How is pain transmitted?

• from the site of transduction along the nociceptor fibres to the dorsal horn in the spinal cord; • from the spinal cord to the brain stem; • through connections between the thalamus, cortex and higher levels of the brain. The C fibre and Aδ fibres terminate in the dorsal horn of the spinal cord. There is a synaptic cleft between the terminal ends of the C fibre and Aδ fibres and the nociceptive dorsal horn neurones (NDHN). In order for the pain impulses to be transmitted across the synaptic cleft to the NDHN, excitatory neurotransmitters are released, which bind to specific receptors in the NDHN. The pain impulse is then transmitted from the spinal cord to the brain stem and thalamus via two main nociceptive ascending pathways. These are the spinothalamic pathway and the spinoparabrachial pathway. Picture

How does osteomyelitis present?

• localised pain • tenderness, • progressive pain over 1-3 months. • Symptoms such as fever or other normal signs of infection may be absent in bone infections. • In chronic haematogenous myelitis the presentation is the same but with a longer duration of the symptoms.