1st take 2022

risk factor for pancreatic cancer is not: A.hereditary pancreatitis B.smoking C.diabetes mellitus D.obesity E.annular pancreas

E.annular pancreas אמבוס- Pancreatic cancer: is the fourth leading cause of cancer deaths in the US and typically affects older individuals in the sixth to eighth decades of life. Underlying risk factors include smoking, obesity, heavy alcohol consumption, and chronic pancreatitis. Pancreatic carcinomas are mostly ductal adenocarcinomas and frequently located in the pancreatic head. The disease is commonly diagnosed at an advanced stage because of the late onset of clinical features (e.g., epigastric pain, painless jaundice, and weight loss). In many cases, the tumor has already spread to other organs (mainly the liver) when it is diagnosed. Treatment is often palliative as surgical resection is only possible in approx. 20% of cases. The most commonly used surgical technique is the pancreaticoduodenectomy (Whipple procedure). Five-year survival rates range from 3-40% depending on the extent, spread, and resectability of the tumor. Occasionally, small, potentially resectable pancreatic lesions can be discovered on imaging. These can represent benign, precancerous, or malignant lesions. Management varies by lesion type, e.g., pancreatic cystic lesions, pancreatic neuroendocrine tumors. Screening is not routinely performed but is recommended for select high-risk individuals. Exogenous risk factor: Smoking (strongest risk factor) Chronic pancreatitis (especially when present for more than 20 years) High alcohol consumption Type 2 diabetes mellitus Obesity Occupational exposure to chemicals used in the dry cleaning and metalworking industries Possibly infections with: H. pylori (and excess stomach acid)Hepatitis B Endogenous risk factor: Age > 50 years Inherited genetic syndromes (10% of pancreatic cancers) Familial atypical multiple mole melanoma (FAMMM) syndrome Hereditary breast and ovarian cancer syndrome (BRCA1 and BRCA2 mutations) HNPCCVon-Hippel-Lindau syndromeNeurofibromatosis type 1Multiple endocrine neoplasia type 1Familial pancreatic carcinomaHereditary pancreatitis (mutations in the PRSS1 gene)Peutz-Jeghers syndrome

The management of pneumothorax includes: A. Coronary artery bypass grafting B. Diuretic medication C. Chest tube insertion D. Intra-aortic balloon pump insertion E. Dialysis

C. Chest tube insertion ספר- Pneumothorax Pneumothorax occurs when air enters the potential space between the visceral and parietal pleura through either an external chest wound or an internal air leak. External air entry occurs with a traumatic chest wall defect, and the resulting open pneumothorax is often associated with a 'sucking wound', where air moves in and out of a chest wound with respiration. Internal air leakage may follow oesophageal perforation or anastomotic breakdown, as air can enter the pleural cavity via the mouth. However, the most common cause of pneumothorax is leakage of air from the lung, due either to a traumatic puncture wound or to spontaneous leakage from a large (bulla) or small (<1 cm, 'bleb') air sac on the lung surface. Occasionally, the pulmonary leak point may have a flap valve mechanism that allows air out of, but not back into, the lung, causing a rapid build-up of pressure within the pleural cavity (tension pneumothorax). This can be fatal, as the high intrapleural pressure completely flattens the ipsilateral lung while deviating the mediastinum to the opposite side, impeding venous return. Spontaneous pneumothorax is described as primary or secondary. Primary pneumothorax typically occurs in young (15-35 years) individuals with essentially normal lungs apart from a few apical bullae or blebs. Secondary pneumothorax develops in elderly patients (55-75 years) with a background of emphysema and chronic obstructive pulmonary disease. It is caused by rupture of a large bulla. Other common causes of secondary pneumothorax include iatrogenic (following subclavian vein catheterisation, pleural biopsy, tracheostomy, transbronchial biopsy etc.), pulmonary tuberulosis, bronchogenic carcinoma and lung abscesses. Management: Initial management is aspiration or by insertion of a chest drain connected to an underwater seal into the pleural space. This allows the lung to re-expand. In most cases of primary pneumothorax, air leakage stops within 48 hours or so, after which the drain can be removed. If the pneumothorax recurs or the air leakage does not stop, thoracoscopic surgery is indicated. The lung is inspected and any blebs or bullae are stapled. These are usually found at the apices of the upper or lower lobes. Pleurodesis is then performed either by using an abrasion technique to scarify the parietal pleura or a pleural strip (pleurectomy), or by insufflation of kaolin. Bullectomy and abrasion or pleurectomy carry about an 8% risk of further recurrent pneumothorax. This is reduced to 1-2% with kaolin insufflation, but as this technique involves leaving foreign material in the chest of a young person, it is usually kept in reserve for recurrent pneumothorax or for patients with no obvious culprit bulla or bleb. Secondary pneumothorax may not settle rapidly, owing to the poor quality of the underlying lung tissue. It typically occurs in individuals who are poor candidates for general anaesthesia and major thoracic surgery. It is customary, therefore, to wait for 1-2 weeks to see if the air leak will stop spontaneously. If not, videothoracoscopy is undertaken in better-risk patients to inspect the lung for a leaking bulla, which can be closed by stapling. Alternatively, kaolin mixed with local anaesthetic can be introduced as a slurry via the intercostal drain. This option avoids general anaesthesia but results in significant pain. Either treatment is associated with an appreciable mortality of 2-5%, owing to respiratory and cardiovascular complications.

Extracorporeal Shock Wave Lithotripsy (ESWL) Is useful in management of: A.urethral stricture B.prostate cancer C. acute pyelonephritis D. small renalI stones E. benign prostatic hyperplasia

D. small renalI stones מהספר- Urinary tract calculi- Management: Symptomatic treatment should be instituted as soon as the diagnosis is confirmed. Intramuscular diclofenac, a nonsteroidal antiinflammatory, is the most effective analgesic; pethidine is an alternative. The likelihood of spontaneous passage of a renal or ureteric calculus depends on the size of the stone and on its smoothness. A stone less than 5 mm in diameter should pass easily. The location of the stone in the ureter also determines the ease with which it will pass: small lower ureteric stones having a higher likelihood compared with larger upper or mid-ureteric calculus. Immediate treatment should be considered in cases of ongoing pain, renal obstruction or, more importantly, where there are signs of sepsis (infected obstructed kidney). Extracorporeal shockwave lithotripsy (ESWL), the technique of focusing external shock waves to break up stones, has revolutionised the treatment of renal and ureteric stones. Stones visualised on x-ray or US can be treated by ESWL, especially those that are single and up to 2 cm in size. Other stones can be visualised directly by ureterorenoscopy (URS), and the stones broken up using a holmium laser or removed intact using a Dormia wire basket. Some stones in the kidney that are unlikely to pass, even if broken up, are best treated by direct puncture of the kidney, insertion of a sheath and removal under vision with a nephroscope with or without ultrasonic disaggregation (percutaneous nephrolithotomy). It is now very rare to perform open surgery to remove renal or ureteric stones. Even large staghorn calculi filling the entire renal collecting system can be treated by percutaneous nephrolithotomy (PCNL) with our without ESWL (multiple sessions may be required). In developing countries in Asia and Africa, where the expertise for the latest noninvasive techniques is not available, large kidney stones continue to be treated by conventional open surgery. In patients with acute obstruction and sepsis (infected obstructed kidney) or renal impairment, decompression of the kidney either via insertion of a ureteric stent or percutaneous nephrostomy is required. Stones and infection within a kidney can be the cause of renal destruction and if the kidney contributes less than 15% of total renal function, then nephrectomy is recommended. Vesical calculi can be treated endoscopically like ureteric calculi, using a stone-crushing device, pneumatic lithotrite or holmium laser. Alternatively, large stones can be dealt with through an open suprapubic cystolithotomy, or by suprapubic insertion of a nephroscope and the use of ultrasonic shattering. Primary urethral calculi are treated along with the inciting cause. Secondary calculi impacted in the urethra may be removed intact endoscopically if small, or may have to be crushed and removed.

Indication for surgical evacuation of subdural hematoma is mid-line shift more than: A.1mm B.5mm C.10mm D.15mm E.25mm

B.5mm subdural hematoma: This is more common than extradural haematoma and results from laceration of vessels (especially small cerebral veins) on the brain surface, or 'bursting' of the brain. CT shows a haematoma that is concave on its inner surface and whose extent is not limited between the cranial sutures, unlike extradural haematomas. Morbidity and mortality are often high, because of the severity of the primary brain injury. An increasingly common problem in the ageing population is chronic subdural haematoma (CSDH). The initial acute bleed, which can occur apparently spontaneously or after relatively very minor head trauma, is rarely symptomatic. Patients with cerebral atrophy, or who are on antiplatelets or anticoagulants, are at greater risk of CSDH. The acute haematoma dissolves and the CSDH collection varies in viscosity from dissolving clot to blood-stained fluid. As the acute haematoma dissolves it draws in water, increasing in size. This process can evolve slowly, so there may be significant midline shift with few signs and symptoms. CSDHs can mimic most neurological syndromes in their presentation. Treatment involves drainage of the subdural collection through burr holes or minicraniotomy. Evidence from an RCT suggests that placement of a drain in the subdural space for 24-48 hours after surgery significantly reduces CSDH recurrence. Patients with mild symptoms may be offered a short course of steroids (without surgery) for symptom management; there is not yet any quality evidence for this strategy, but clinical trials are ongoing. Neurosurgical interventions- Indications: Hematoma size ≥ 10 mm Midline shift ≥ 5 mm Signs of cerebral herniation syndromes (e.g., extensor posturing, anisocoria) Rapid neurological deterioration (e.g., ≥ 2-point decrease in GCS score from the time of injury or symptom onset to ER transfer) Unilateral or bilateral fixed dilated pupils ICP > 20 mm Hg Failure of conservative management

Acute myocardial infarction will not cause: A.Cardiogenic shock B.Chronic mitral stenosis C.Papillary muscle rupture D.Post-myocardial infarction ventricular septal defect E.Acute mitral regurgitation

B.Chronic mitral stenosis 0-24 hours --> Ventricular arrhythmia, HF, cardiogenic shock 1-3 days --> Postinfarction fibrinous pericarditis 3-14 days --> Free wall rupture --> tamponade; papillary muscle rupture --> mitral regurgitation; interventricular septal rupture due to macrophage-mediated structural degradation ---> leftto-right shunt LV pseudoaneurysm (risk of rupture) 2 weeks to several months--> Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus

Patients with acute renal obstruction and sepsis require decompression via: A.nephrectomy B. insertion of a double-J stent C. Anderson-Hynes pyeloplasty D. percutaneous nephrolithotomy E. shockwave lithotripsy

D. percutaneous nephrolithotomy מהספר- Urinary tract calculi- Management: Symptomatic treatment should be instituted as soon as the diagnosis is confirmed. Intramuscular diclofenac, a nonsteroidal antiinflammatory, is the most effective analgesic; pethidine is an alternative. The likelihood of spontaneous passage of a renal or ureteric calculus depends on the size of the stone and on its smoothness. A stone less than 5 mm in diameter should pass easily. The location of the stone in the ureter also determines the ease with which it will pass: small lower ureteric stones having a higher likelihood compared with larger upper or mid-ureteric calculus. Immediate treatment should be considered in cases of ongoing pain, renal obstruction or, more importantly, where there are signs of sepsis (infected obstructed kidney). Extracorporeal shockwave lithotripsy (ESWL), the technique of focusing external shock waves to break up stones, has revolutionised the treatment of renal and ureteric stones. Stones visualised on x-ray or US can be treated by ESWL, especially those that are single and up to 2 cm in size. Other stones can be visualised directly by ureterorenoscopy (URS), and the stones broken up using a holmium laser or removed intact using a Dormia wire basket. Some stones in the kidney that are unlikely to pass, even if broken up, are best treated by direct puncture of the kidney, insertion of a sheath and removal under vision with a nephroscope with or without ultrasonic disaggregation (percutaneous nephrolithotomy). It is now very rare to perform open surgery to remove renal or ureteric stones. Even large staghorn calculi filling the entire renal collecting system can be treated by percutaneous nephrolithotomy (PCNL) with our without ESWL (multiple sessions may be required). In developing countries in Asia and Africa, where the expertise for the latest noninvasive techniques is not available, large kidney stones continue to be treated by conventional open surgery. In patients with acute obstruction and sepsis (infected obstructed kidney) or renal impairment, decompression of the kidney either via insertion of a ureteric stent or percutaneous nephrostomy is required. Stones and infection within a kidney can be the cause of renal destruction and if the kidney contributes less than 15% of total renal function, then nephrectomy is recommended. Vesical calculi can be treated endoscopically like ureteric calculi, using a stone-crushing device, pneumatic lithotrite or holmium laser. Alternatively, large stones can be dealt with through an open suprapubic cystolithotomy, or by suprapubic insertion of a nephroscope and the use of ultrasonic shattering. Primary urethral calculi are treated along with the inciting cause. Secondary calculi impacted in the urethra may be removed intact endoscopically if small, or may have to be crushed and removed.

What will be the most appropriate option in a patient with positive Digital Rectal Examination (DRE) and elevated PSA level? A.uroflowmetry B. IPSS assessment C.prostatectomy D.transrectal biopsy E.antibiotics

D.transrectal biopsy מהספר- Benign prostatic hyperplasia: Investigations- A good history and examination are paramount. A urinary frequency volume chart should be completed over 3 days. International Prostate Symptom Score (IPSS) provides n objective measurement of symptoms and also helps in monitoring response to treatment. Other mandatory assessment includes blood for renal function, electrolytes and following counselling PSA. Prostate cancer can occur with normal PSA values (0-4 ng/mL), while BPH can cause elevated values, so careful interpretation is required. If digital rectal examination (DRE) raises suspicion, TRUS-guided biopsy is indicated. Urine flow rate assessed by uroflowmetry and US assessment of postvoid residual will quantify a reduction in urinary stream and the need for intervention. In some patients, especially the elderly, neurological or pharmacological causes for changes in micturition must be considered. A pressure-flow urodynamic assessment may be necessary for equivocal symptoms or investigations. הרחבה- מאמבוס- Benign prostatic hyperplasia (BPH) is a nonneoplastic glandular and stromal hyperplasia of the transition zone of the prostate. It is a common disorder, affecting ∼ 40% of the male population by the age of 50 years. Although the underlying etiology of BPH has not been conclusively established, sex hormones likely play a key role. BPH typically manifests as lower urinary tract symptoms (LUTS), which includes features of bladder irritation (urinary frequency, urgency, urge incontinence), features of bladder outlet obstruction (urinary hesitancy, straining to urinate, sensation of incomplete voiding), and hematuria. The initial workup comprises standardized questionnaires to assess symptom severity, physical examination including digital rectal examination (DRE), urinalysis, a voiding diary, and, in select patients, serum prostate-specific antigen (PSA) analysis. DRE may reveal a smooth, enlarged, nontender, and firm prostate. Imaging and urodynamic studies are indicated in patients with features of complicated LUTS and to guide management. Behavioral modifications (e.g., fluid restriction at night, bladder training) are advised in all patients with LUTS caused by BPH and may be the only management required in patients with minimal symptoms. Pharmacotherapy, such as alpha blockers, 5-alpha reductase inhibitors (5-ARIs), and parasympatholytics, for BPH is indicated in patients with bothersome symptoms; the choice of agent depends on the size of the prostate and the predominant symptoms. Surgery, e.g., transurethral resection of the prostate (TURP), is indicated in patients with severely symptomatic BPH, those with complications due to BPH (e.g., urinary retention, recurrent UTIs, hydroureteronephrosis), and those who experience intolerable adverse effects with pharmacotherapy. In patients with BPH, the risk of developing prostate cancer is not higher than that of the general male population; therefore, standard PSA screening protocol can be followed. TURP does not reduce the risk of developing prostate cancer and, following the procedure, BPH recurs in ∼ 7% of men.

60 year old patient is scheduled to colon cancer surgery. The properly conducted venous thromboembolism (VTE) prophylaxis should be based in this case on: A. aaspirin 1x150mg B. rivaroxaban or apixaban in therapeutic doses C. low molecular heparin adjusted to the patient body weight(eg,enoxaparin 1mg/kg) D. warfarin E. low molecular heparin in the fixed doses (eg. Enoxaparin 40 mg once daily)

E. low molecular heparin in the fixed doses (eg. Enoxaparin 40 mg once daily) טיפולי זה לפי משקל גוף ופרופילקטי זה קבוע. אמבוס- Prevention of VTE: 1. GENERAL/ABDOMINAL SURGERY 40 mg once daily initiated 2 hours prior to surgery. Usual duration of therapy is 7-10 days, although up to 12 days of treatment has been well tolerated in clinical trials. Extended VTE prophylaxis (generally considered as >3 weeks) may be considered in selected patients undergoing major general surgery. Extended prophylaxis (for up to 4 weeks) recommended by ACCP in patients undergoing abdominal or pelvic surgery for cancer. 2. HIP-REPLACEMENT SURGERY 30 mg every 12 hours initiated 12-24 hours after surgery, provided hemostasis has been established. [ref] Alternatively, may consider dosage of 40 mg once daily, initiated approximately 12 hours before surgery. Because of risk of bleeding, ACCP recommends that LMWHs be initiated at least 12 hours preoperatively or at least 12 hours postoperatively in patients undergoing major orthopedic surgery. Continue prophylaxis throughout the postoperative period, generally for 7-10 days, until risk of DVT has diminished; manufacturer states that up to 14 days of thromboprophylaxis was well tolerated in clinical trials. Following the initial phase of thromboprophylaxis during the acute postoperative period, manufacturer recommends continued prophylaxis with 40 mg once daily for 3 weeks. ACCP recommends a minimum of 10-14 days of thromboprophylaxis, and suggests extending prophylaxis for up to 35 days on an outpatient basis. [ref] ASH guidelines state that extended VTE prophylaxis (generally considered as >3 weeks) may be considered in selected patients undergoing major surgery. 3. KNEE-REPLACEMENT SURGERY 30 mg every 12 hours initiated 12-24 hours after surgery, provided hemostasis has been established. Because of risk of bleeding, ACCP recommends that LMWHs be initiated at least 12 hours preoperatively or 12 hours postoperatively in patients undergoing major orthopedic surgery. Continue prophylaxis throughout the postoperative period, generally for 7-10 days, until risk of DVT has diminished; manufacturer states that up to 14 days of thromboprophylaxis was well tolerated in clinical trials. ACCP recommends a minimum of 10-14 days of thromboprophylaxis, and suggests extending prophylaxis for up to 35 days on an outpatient basis. ASH guidelines state that extended VTE prophylaxis (generally considered as >3 weeks) may be considered in selected patients undergoing major surgery. 4. ACUTELY ILL MEDICAL PATIENTS 40 mg once daily. [ref] Usual duration of therapy is 6-11 days; well tolerated for up to 14 days in clinical trials. ACCP suggests against the use of extended thromboprophylaxis beyond the period of patient immobilization or acute hospital stay in acutely ill medical patients. However, extended thromboprophylaxis has been used in selected patients after hospital discharge. Treatment of VTE Outpatient treatment in patients with uncomplicated DVT without PE: 1 mg/kg every 12 hours. Inpatient (hospital) treatment in patients with DVT with or without PE: 1 mg/kg every 12 hours or 1.5 mg/kg once daily at the same time every day. Manufacturer states average duration of therapy is 7 days. In patients with VTE, ACCP recommends that anticoagulant therapy be continued beyond the acute treatment period for at least 3 months, and possibly longer depending on whether the VTE event was unprovoked or provoked (by a transient risk factor (e.g., surgery), presence of cancer, and patient's risk of bleeding. משוחזר

Which of the proximal femoral fractures are extracapsular? A. Femoral neck fractures B. Pertrochanteric fractures C.Intertrochanteric fractures D.Subtrochanteric fractures E.B+C+D

E.B+C+D Hip fractures are divided into: Intracapsular: Femoral head Femoral neck Extracapsular: Trochanteric Intertrochanteric Subtrochanteric

Which statement regarding lung cancer patients is true: A.Small cell lung cancer is a systemic disease at presentation and patients with this type of cancer are not usually referred for surgery.Chemotherapy and radiotherapy are recommended for those patients. B.Patient presented with non-small cell carcinoma should not be considered for surgery C.Lobectomy is not the procedure of choice for fit patients with lung cancer.Only pneumonectomy should be considered as the procedure of choice. D. Patients with an FEV below 50 predicted prior to resection are the best candidates for resection E.All of the above are wrong

A.Small cell lung cancer is a systemic disease at presentation and patients with this type of cancer are not usually referred for surgery. Chemotherapy and radiotherapy are recommended for those patients. ספר- Small-cell lung cancer is regarded as a systemic disease at presentation and patients are not usually referredforsurgery buttreated with chemotherapy and radiotherapy.All other varieties are resected if possible. Therefore, for surgical treatment purposes, bronchogenic carcinoma is categorised into small cell and nonsmall cell. However, cell type is important as recent advances in pathology and genetics have identifiedmutationsthatmarktumours that may be sensitive to some chemotherapeutic agents and allow tailoring of chemotherapy regimens to specific cell subtypes הרחבה-אמבוס: Lung cancer is the leading cause of cancer death in the US, accounting for almost a quarter of all cancer-related fatalities; 80-90% of cases can be attributed to smoking. Lung cancer is generally divided into two types: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). SCLC is a single histological category and is characterized by its central location, rapid tumor growth, early metastasis, and association with numerous paraneoplastic syndromes. NSCLC accounts for ∼ 85% of all lung cancers and has multiple histological subtypes including adenocarcinoma and central squamous cell carcinoma. Patients with lung cancer are usually asymptomatic during the early stages of the disease. Lung cancer may be diagnosed after the incidental discovery of a pulmonary nodule on imaging. Late-stage disease can manifest with pulmonary symptoms, extrapulmonary symptoms, paraneoplastic syndromes (e.g., syndrome of inappropriate antidiuretic hormone secretion, hypercalcemia), and/or signs of metastatic disease. Patients with lung cancer frequently present with metastasis to the brain, liver, adrenal glands, and/or bones. Evaluation generally begins with CT imaging of the chest and the diagnosis is confirmed with a bronchoscopic or CT-guided biopsy. Patients with no evidence of distant metastases may be eligible for curative surgical resection (with or without adjunct chemotherapy) or radiation therapy. Unfortunately, most patients present with metastatic disease and are, therefore, not eligible for curative resection. These patients often receive palliative chemoradiotherapy. Prognosis is generally poor, with a 5-year survival rate below 20%.

which anatomical description is true: A. there are two coronary arteries (left and right) which originate in the left (posterior) and the right (anterior) sinus. B. the left main coronary artery divides into 3 branches - Left anterior descending artery, Circumflex coronary and azygos posterior coronary artery C. posterior descending artery supplies anterior part of left ventricle and anterior two-thirds of the interventricular septum D. circumflex artery supplies anterior part of right ventricle and acute marginal branches. E. only circumflex coronary artery may terminate as the posteriori descending artery

A. there are two coronary arteries (left and right) which originate in the left (posterior) and the right (anterior) sinus. ספר- Summary Coronary anatomy: • There are two coronary arteries (left and right), which have origin in the coronary sinuses: left or posterior sinus, right or anterior sinus. • The left main coronary artery passes behind the pulmonary trunk and divides into two large branches: the left anterior interventricular artery or left anterior descending (LAD), which supplies the anterior left ventricle and anterior two-thirds of the interventricular septum, and the circumflex coronary, which supplies the posterior and lateral walls of the left ventricle. • The right coronary artery passes down anteriorly in the right atrioventricular groove supplying the anterior right ventricle and acute marginal branches. • Either the right or circumflex may terminate as the posterior descending artery, which supplies the inferior surface of both ventricles and the lower septum. This artery is then considered to be dominant. • The right, LAD and circumflex are each considered to be a 'vessel system'. Disease within any one of these three vessels or its branches is termed single-vessel disease. Similarly, two- and three-vessel disease indicates involvement of two and three systems, respectively.

Which sentence about cardioplegia solution is not true: A.The essential component of a cardioplegie solution is a high potassium concentration, which causes the heart to arrest in systole. B.Cardioplegia is delivered as either a crystalloid solution or using the patient's own blood as a vehicle C. Cardioplegia solutions minimize myocardial energy requirements by abolishing the energy expenditure of contraction and by reducing basal cellular metabolism. D. Cardioplegia is typically delivered at 4-6°C. E.Cardioplegia combined with mild systemic hypothermia (32°C) provides the surgeon with a safe period of cardiac arrest of up to 120 minutes.

A.The essential component of a cardioplegie solution is a high potassium concentration, which causes the heart to arrest in systole. Cardioplegia זה נוזל שמכניסים ללב שהוא קר והיפרקלמי שגורם למטבוליזם של תאי הלב לרדת וכך יש פחות תזוזה של הלב ופחות דם בלב ואז המנתח יכול לעבוד על הלב הסבר מורחב מהספר: Cardioplegia Cardioplegic arrest achieves a still bloodless heart. A cross-clamp is applied across the ascending aorta proximal to insertion of the arterial inflow cannula. This prevents blood flow into the coronary arteries. The heart is arrested by perfusing the coronary circulation with a cardioplegic solution, delivered either antegradely via the aortic root or coronary artery ostia utilising the native coronary arteries, or retrogradely via a catheter placed in the coronary sinus, which is accessed through the right atrium. The essential component of a cardioplegic solution is a high potassium concentration (circa 18 mmol/L), which causes the heart to arrest in diastole. Cardioplegia is delivered as either a crystalloid solution or using the patient's own blood as a vehicle. Blood-based solutions are believed to contain abundant oxygen derived free radical scavengers, and the blood's buffering characteristics may be helpful in reducing the deleterious effects of ischaemic metabolites generated by the arrested myocardium. Cardioplegia solutions minimise myocardial energy requirements by abolishing the energy expenditure of contraction and by reducing basal cellular metabolism. This is enhanced with local tissue cooling, as cardioplegia is typically delivered at 4-6°C. Reducing core temperature on bypass to 26-34°C may further enhance cardiac cooling. Cardioplegia combined with mild systemic hypothermia (32°C) provides the surgeon with a safe period of cardiac arrest of up to 120 minutes, permitting surgery while minimising the risk of myocardial and critical organ damage. Coronary artery bypass surgery (CABG) can be performed using a technique in which an aortic clamp is intermittently applied to cut coronary flow while the heart is electrically fibrillated so as to reduce movement. The resulting brief ischaemic episodes are tolerated. This cross-clamp fibrillation technique activates mechanisms within the myocardial cells that reduce damage caused by subsequent ischaemia (preconditioning). In some circumstances, the surgeon may elect to leave the coronary arteries perfused while on bypass and to operate on a beating heart. Recently, there has been considerable interest in performing CABG on suitable patients without the use of CPB. Proponents of 'off-pump' surgery claim that the risks of artificial perfusion (particularly transient cognitive impairment) are avoided and that recovery may be quicker. Many surgeons, however, feel that the bloodless, still operative field resulting from cardioplegic arrest provides the optimum conditions for high-quality accurate anastomoses.

The most common reason for pericardial constriction is: A.Tuberculosis B.Pericardiectomy C.Infective bacterial endocarditis D.Prior cardiac surgery E.Pericardial effusion

A.Tuberculosis ספר- Pericardial constriction Chronic pericardial inflammation, often from tuberculosis, may heal by intense fibrosis and calcification. This leads to chronic tamponade and investigations should include echocardiography, right heart catheterisation with record of chamber pressures, and CT or preferably MRI. Surgery is undertaken via a median sternotomy to remove the parietal pericardium and any fibrotic visceral pericardium, and can be performed without CPB. Such surgery is difficult and can be accompanied by significant blood loss. Results can occasionally be disappointing because the patient may have already developed irreversible hepatic cirrhosis and myocardial function is poor.

In patients with pheochromocytoma the tumour is malignant in: A. 1%cases B. 10%cases C. 50% cases D. 90% cases E. 100%cases

B. 10% cases מהספר- Phaeochromocytomas- Pathology: Phaeochromocytomas are tumours either of the adrenal medulla (80%), which secrete large amounts of adrenaline (epinephrine) and noradrenaline (norepinephrine), or of the extraadrenal paraganglionic tissue (20%), which secrete only noradrenaline. Virtually all (99%) arise within the abdomen; 10% are multiple and 10% are malignant. Benign tumours are usually chocolate brown and highly vascular. Associated conditions are medullary carcinoma of the thyroid (as part of MEN type II), von Hippel-Lindau disease (VHL) and neurofibromatosis. If it presents in pregnancy, phaeochromocytoma can be mistaken for hypertension of pregnancy, and may cause maternal and foetal mortality. Genetic testing for predisposition syndromes such as succinate dehydrogenase (SDH) B, C and D should be done in all patients under 50 years of age. Phaeochromocytoma- Summary: • Usually benign tumours of the adrenal medulla (80%), but 20% arise in extra-adrenal paraganglionic tissue; 10% are multiple and 10% are malignant • May be associated with medullary carcinoma of the thyroid (MEN II), von Hippel-Lindau disease and neurofibromatosis • Usually presents clinically with hypertension, which is often paroxysmal, and with metabolic effects such as diabetes mellitus • All hypertensive patients <40 years old should be screened for phaeochromocytoma; overnight or 24-hour urinary and plasma metadrenaline and normetadrenaline levels are reliable methods of diagnosis • Location is best defined by CT and radiolabelled metaiodobenzylguanidine scanning • Treatment consists of adrenalectomy after careful preparation to control blood pressure and heart rate, and to re-expand blood volume (by α-adrenergic blockade with β-blockade).

Which of the thoracic pathologies listed below is a life-threatening emergency? A. Thoracic empyema B. Tension pneumothorax C. Closed pneumothorax D. Pleural effusion E. Chylothorax

B. Tension pneumothorax ספר- Early deaths: occur within minutes to hours after injury. They are often the consequence of potentially survivable shock physiology including tension pneumothorax, cardiac tamponade and massive haemorrhage from thoracic or abdominal vascular injury. Trauma systems, which limit time from injury to definitive care through rapid transport, assessment and intervention, dramatically improve survival and reduce subsequent morbidity in this cohort. אמבוס- Tension pneumothorax A life-threatening variant of a pneumothorax in which a one-way valve mechanism (e.g., from a puncture wound) allows air into the pleural space while the chest wall expands during inspiration but does not allow it to escape during expiration. Air progressively accumulates in the pleural space and builds up pressure that causes collapse of the ipsilateral lung and compression of the contralateral lung, heart, and superior vena cava. This culminates in hypoxia and hemodynamic compromise. Chylothorax = Lymphatic fluid from the thoracic duct (chyle) in the pleural cavity. Chyle is a cloudy milky fluid with high concentrations of lipids (↑ triglycerides, cholesterol, chylomicrons, and fat-soluble vitamins).

The healthcare provider is preparing to administer indomethacin to an infant with a persistent patent ductus arteriosus (PDA). The mother of the baby asks why the medication is being given to her baby. What is the healthcare provider's best response? A.Your baby needs help clearing the extra fluid from the lungs B. Your baby needs this drug because it interferes with substances that keep the PDA open C. This drug is a non-steroidal anti-inflammatory drug, so it will help control your baby's pain. D. This drug will help your baby's heart contract stronger E.This is what the guidelines recommend to be given in this situation

B. Your baby needs this drug because it interferes with substances that keep the PDA open אמבוס Treatment of PDA: Observation: regular heart and pulmonary vasculature evaluation in patients with small PDAs and no evidence of left-sided heart volume overload. Elective ductal closure: Indications for closure: Symptomatic PDAs, Left heart enlargement, Mild to moderate pulmonary hypertension. Pharmacological closure (in premature infants)- infusion of indomethacin or ibuprofen- Inhibiting the prostaglandin synthesis with indomethacin or ibuprofen induces the closure of the ductus in preterm infants. Contraindicated in active intraventricular hemorrhage Percutaneous catheter occlusion or surgical ligation in infants > 5 kg Special considerations: Administer prostaglandin (PGE1) to keep the PDA open if needed for survival (e.g., in transposition of the great vessels, tetralogy of Fallot, hypoplastic left heart). משוחזר

During an examination of an infant with a patent ductus arteriosus (PDA),the healthcare provider should expect to observe: A.Clubbing of fingers and toes B.Machine like murmur C.Profound cyanosis D.Squatting down syndrome E.Diastolic murmur

B.Machine like murmur מהספר- If the ductus arteriosus fails to close after birth, pulmonary blood flow is abnormally high, producing pulmonary congestion and hypertension. Infants have retarded growth and a continuous 'machinery' murmur is audible over the precordium and back. The chest x-ray shows pulmonary congestion, and echocardiography can exclude concurrent intracardiac defect(s). In premature children, the duct may close with an indomethacin infusion (prostaglandin E1 inhibition), but clipping or division at left thoracotomy is definitive. Endovascular closure is an option in older children. The operative mortality is low in older children (<1%) but high (25%) in preterm infants, who are generally very unwell. הסבר תמונה- In patent ductus arteriosus, there is a left-to-right shunt, with blood flowing from the aorta to the pulmonary arteries during both systole and diastole (1). This shunt leads to volume overload (recirculation) of the blood within the pulmonary vessels, the left atrium, and left ventricle (2). Eventually, because of the increased blood flow to the pulmonary circulation, pulmonary hypertension may develop as well as Eisenmenger syndrome, which involves a shunt reversal. The left-to-right-shunt without cyanosis becomes a right-to-left shunt with cyanosis (3). משוחזר

Which of the conditions represents a complication of myocardial infarction: A.Aortic valve stenosis B.Ventricular septal defect C.Pneumothorax D.Cardiac myxoma E.Atrial septal defect

B.Ventricular septal defect 0-24 hours --> Ventricular arrhythmia, HF, cardiogenic shock 1-3 days --> Postinfarction fibrinous pericarditis 3-14 days --> Free wall rupture --> tamponade; papillary muscle rupture --> mitral regurgitation; interventricular septal rupture due to macrophage-mediated structural degradation ---> leftto-right shunt LV pseudoaneurysm (risk of rupture) 2 weeks to several months--> Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus

The 5-year survival in the stage I lung cancer patient can be estimated at: A.approx.20% B.approx.60% C.approx.5% D.It depends if the lobectomy was performed or not E-Not enough information is provided to estimate

B.approx.60% אמבוס- Lung cancer is the leading cause of cancer death in the US, accounting for almost a quarter of all cancer-related fatalities; 80-90% of cases can be attributed to smoking. Lung cancer is generally divided into two types: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). SCLC is a single histological category and is characterized by its central location, rapid tumor growth, early metastasis, and association with numerous paraneoplastic syndromes. NSCLC accounts for ∼ 85% of all lung cancers and has multiple histological subtypes including adenocarcinoma and central squamous cell carcinoma. Patients with lung cancer are usually asymptomatic during the early stages of the disease. Lung cancer may be diagnosed after the incidental discovery of a pulmonary nodule on imaging. Late-stage disease can manifest with pulmonary symptoms, extrapulmonary symptoms, paraneoplastic syndromes (e.g., syndrome of inappropriate antidiuretic hormone secretion, hypercalcemia), and/or signs of metastatic disease. Patients with lung cancer frequently present with metastasis to the brain, liver, adrenal glands, and/or bones. Evaluation generally begins with CT imaging of the chest and the diagnosis is confirmed with a bronchoscopic or CT-guided biopsy. Patients with no evidence of distant metastases may be eligible for curative surgical resection (with or without adjunct chemotherapy) or radiation therapy. Unfortunately, most patients present with metastatic disease and are, therefore, not eligible for curative resection. These patients often receive palliative chemoradiotherapy. Prognosis is generally poor, with a 5-year survival rate below 20%. ספר- Survival- Reported 5-year survival data are approximately 60% for stage I, 35% for stage II and <20% for stage IIIa disease. Relatively few patients (<20%) with non-small-cell bronchogenic carcinoma are suitable for resection at presentation. One strategy to address this problem is the use of neoadjuvant preoperative induction chemotherapy to downstage tumours, although there are as yet no data to support the widespread use of this approach. The ot her obvious possibility for improving resection rates would be to detect lung cancers at an earlier stage. Previous mass chest x-ray screening studies did not appear to show an improvement in long-term survival, but there is currently renewed interest in screening high-risk individuals (smoking history, >50 years old) using CT as a more sensitive test

During bedside report, the health care provider learns that the cardiac circulation of an infant with Eisenmenger is shunting from right to left. the infant may have impaired gas exchange related to: A.Decreased pulmonary vascular pressure B. Decreased ventilation in relation to perfusion C.Decreased pulmonary blood flow D.Dilated pulmonary capillaries E.Increased respiratory rate

C. Decreased pulmonary blood flow לא בטוחה אבל נראה לי שזה מה שקורה כאשר יש היפוך של השאנט. אמבוס- הסבר תמונה- In patent ductus arteriosus, there is a left-to-right shunt, with blood flowing from the aorta to the pulmonary arteries during both systole and diastole (1). This shunt leads to volume overload (recirculation) of the blood within the pulmonary vessels, the left atrium, and left ventricle (2). Eventually, because of the increased blood flow to the pulmonary circulation, pulmonary hypertension may develop as well as Eisenmenger syndrome, which involves a shunt reversal. The left-to-right-shunt without cyanosis becomes a right-to-left shunt with cyanosis (3). למרות שאחרי הירידה בזרימה יהיה גם ירידה בלחץ ולכן יש גם את הסעיף הזה- A.Decreased pulmonary vascular pressure משוחזר

Euro score is the scale that is used to assess the risk of: A.Surgical wound infection (SSIRS) C.30-day mortality after non congenital cardiac surgery C.Morbidity after vascular surgery D.In hospital mortality after congenital cardiac surgery E.Valve thrombosis after aortic valve replacement

C.30-day mortality after non congenital cardiac surgery ספר- Mortality- Risk stratification is important in cardiac surgery and Euroscore is a valuable tool for quantifying operative risk across all types of noncongenital cardiac surgery. Patient, condition and procedure-related factors contribute to a score that predicts 30-day mortality. Predicted operative mortality ranges from <1% for routine elective procedures to >50% for complex emergency operations.

in young women with severe aortic stenosis intending to have children it is recommended to insert a biological valve. Choose the proper explanation: A.Mechanical valve would be not durable enough during pregnancy B.Young women are to fit to have prosthetic valve C.Anticoagulation treatment during pregnancy can cause teratogenicity,abortion D.Use of mechanical valve is contraindicated in young women E.Mechanical valve would be too noisy

C.Anticoagulation treatment during pregnancy can cause teratogenicity,abortion ספר- Cardiac valvular disease Valve disease may obstruct forward flow (stenosis) or permit reverse flow (incompetence/regurgitation), or both. The aortic and/or mitral valves are primarily affected; primary tricuspid pathology is rare and pulmonary valve disease is virtually unknown. Formerly, rheumatic fever following streptococcal infection was the most common aetiological factor. This remains the case in many developing countries, but is now rare in the Western world. Surgical management- Options include valve replacement or repair. Replacement utilises either a mechanical or a biological prosthesis. Mechanical valves have developed from the original ball-in-cage design through single disc designs to the current range of carbon bi-leaflet devices (Fig. 22.8). These should last indefinitely, but patients require lifelong warfarin to prevent thrombotic occlusion or embolism. Embolism risk is about 1-6% per year and is influenced by how closely the anticoagulant medication is controlled. Mechanical valves produce audible clicks. Biological valves are derived from: • Glutaraldehyde-preserved porcine aortic and mitral valves mounted on a frame (stent) • Glutaraldehyde-preserved bovine pericardium formed into a three-leaflet valve and mounted on a stent • Glutaraldehyde-preserved porcine aortic unstented valves • Human aortic root homografts removed from cadaveric hearts and preserved in antibiotic solution Unstented valves and homografts offer the advantage of a larger effective orifice area minimising the residual pressure gradient. Warfarin is not required after 3 months with biological valves provided the patient remains in sinus rhythm. However, such valves deteriorate over time and after 15-20 years may need replacement with an increased operative risk. Unless there is a contraindication to anticoagulation, mechanical valves are commonly used in a younger age group (<60 years). In young women intending to have children it is usual to advise a biological valve, with the intention of replacing it with a mechanical device when the valve fails. This avoids problems with warfarin during pregnancy (placental separation, abortion and teratogenicity). Repair is the preferred surgical option in regurgitation and is largely restricted to the mitral and tricuspid valves, but recently has also been applied to the aortic valve. It is superior to valve replacement, as the problems associated with a prosthesis are avoided. The techniques utilised for mitral incompetence include excision of portions of redundant leaflet, repositioning of the chordae and reduction in the size of the annulus (annuloplasty). Generally, only annuloplasty is applicable to the tricuspid valve. Rarely, isolated mitral stenosis without calcification may be found, in which case division of the fused leaflets under direct vision on bypass (commisurotomy) is performed.

Mark the false sentence about aortic dissection: A.This is caused when blood enters the wall of the aorta through a tear in the intima,creating a false lumen that spirals along the vessel within the medial layer B.The false lumen may rupture through the adventitia into the mediastinum or pleural cavity, causing massive and frequently fatal hemorrhage C.Aortic dissection that involves the aortic root (type A) tends to lift the aortic valve leaflets away from the wall, leading to aortic stenosis. D.Aortic dissection may present with severe interscapular pain, collapse, shock,aortic incompetence, unequal peripheral pulses, features of a left hemothorax, stroke, paraplegia, abdominal discomfort and lower limb ischemia. E.Acute dissection is often fatal prior to arrival at hospital.

C.Aortic dissection that involves the aortic root (type A) tends to lift the aortic valve leaflets away from the wall, leading to aortic stenosis. ספר- Aortic dissection This is caused when blood enters into the wall of the aorta through a tear in the intima, creating a false lumen that spirals along the vessel within the medial layer but contained by the adventitia. The entry point is usually either just above the aortic valve or immediately beyond the left subclavian artery. However, the dissection process may extend along the einto the iliac vessels. The false lumen may rupture through the adventitia into the mediastinum or pleural cavity, causing massive and frequently fatal haemorrhage, or into the pericardium, causing fatal tamponade. The origins of aortic side branches, which are encountered by the false lumen, tend to be encircled and occluded. This process can lead to widespread ischaemic damage to the heart (coronaries), brain (branches of the aortic arch), spinal cord (spinal arteries), kidneys (renal arteries), abdominal viscera (coeliac and mesenteric arteries) and the limbs. A dissection that involves the aortic root (type A) tends to lift the aortic valve leaflets away from the wall, leading to regurgitation. Finally, a dissected aorta may dilate over months to years, causing a progressive aneurysmal process. Acute dissection is often fatal prior to arrival at hospital. There may be severe interscapular pain, collapse, shock, aortic incompetence, unequal peripheral pulses, features of a left haemothorax, stroke, paraplegia, abdominal discomfort and lower limb ischaemia. Dissections that originate distal to the left subclavian (Fig. 22.13; type B), do not spread retrogradely to involve the aortic arch or ascending aorta, and are clinically stable are usually managed conservatively by control of blood pressure, as the results of medical and surgical treatment are not different. Endovascular stent placement via the femoral artery under radiological control has an emerging role in this difficult situation, and the decision to intervene on such patients is based on the development of rupture and organ/limb ischaemia. In contrast, most patients with dissections that involve the ascending aorta or arch (type A) are offered emergency surgery to prevent rupture, stroke, MI and aortic valve incompetence. Surgery involves excising and replacing the portion of the aorta containing the entry point. This prevents more blood entering the false lumen and reapposes the layers of the aortic wall. Additional surgery to repair the aortic valve or to replace the aortic arch or descending aorta will be determined by individual circumstance סטאפ1- Aortic dissection: Longitudinal intimal tear forming a false lumen. Associated with hypertension, bicuspid aortic valve, inherited connective tissue disorders (eg, Marfan syndrome). Can present with tearing, sudden-onset chest pain radiating to the back +/− markedly unequal BP in arms. CXR can show mediastinal widening. Can result in organ ischemia, aortic rupture, death. Stanford type A (proximal): involves Ascending aorta. May extend to aortic arch or descending aorta. May result in acute aortic regurgitation or cardiac tamponade. Treatment: surgery. Stanford type B (distal): involves only descending aorta (Below left subclavian artery). Treatment: β-blockers, then vasodilators.

Mark the true sentence about aortic stenosis: A.Aortic stenosis is the most common indication for valvular surgery in patients below 50 years. B.The most frequent etiology in the Western world is rheumatic disease. C.Aortic stenosis causes LV hypertrophy,effort angina,syncope and dyspnea D.Clinically,the patient has a slow rising pulse,a forceful apex beat and an ejection diastolic murmur in the right upper parasternal area that may radiate to the root of the neck. E.The onset of symptoms combined with LV dysfunction (ejection fraction<40%) should initiate referral for surgery.

C.Aortic stenosis causes LV hypertrophy,effort angina,syncope and dyspnea ספר- Aortic valve disease- Stenosis: Aortic stenosis is the most common indication for valvular surgery in the UK. Although rheumatic disease remains a common problem in underdeveloped countries, the most frequent aetiology in the Western world is calcific aortic stenosis, which develops in the older population, typically in patients over 70 years. The normal aortic valve has three cusps, but a congenital bicuspid valve calcifies at an earlier age. Aortic stenosis causes LV hypertrophy, effort angina, episodes of arrhythmia with syncope or even sudden death, and LV failure. Clinically, the patient has a slow rising pulse (pulsus parvus and tardus), a forceful apex beat and an ejection systolic murmur in the right upper parasternal area that may radiate to the root of the neck. Echocardiography will confirm a valvular gradient, which is considered severe aortic stenosis when this exceeds 60 mmHg. However, measurement of orifice area is independent of cardiac output and may be a more reliable measure. The onset of symptoms or LV dysfunction (ejection fraction <50%) should initiate referral for surgery. In the asymptomatic patient, a high transvalvular gradient (mean >40 mmHg), a low valve orifice area (<1 cm2 ), or an abnormal response to exercise (development of symptoms or asymptomatic hypotension) may indicate the need for surgery. Patients with cardiac failure have a low output and consequently a low gradient. In these cases, the decision to operate may be a difficult judgement, based on the absence of any ther likely cause of poor LV function and echocardiographic evidence of severe aortic valve disease. In some patients, e.g., the elderly, those with patent coronary grafts or significant other comorbidities, percutaneous replacement may be considered. TAVI (transcatheter aortic valve insertion) is the procedure where a biological valve on a holder is introduced percutaneously. Vascular access is achieved via the femoral artery or LV apex, or directly to the proximal aortic root via a right parasternal mini-thoracotomy.

Which statement regarding valvular heart diseases is true: A.auscultation of a patient with aortic regurgitation we will normally hear a systolic crescendo-decrescendo murmur B.Patients with aortic stenosis characteristically have big difference between systolic and diastolic blood pressure C.Patients with mechanical prostheses used to be treated with warfarin or coumadin which has been replaced nowadays with safer and easier to use NOACs (new oral anticoagulants) D.Bicuspid aortic valve is the most frequent congenital problem and may lead to aortic valve dysfunction E.Target INR for patients with valvular bioprostheses is 2.0-3.5

D.Bicuspid aortic valve is the most frequent congenital problem and may lead to aortic valve dysfunction ספר- Aortic valve disease Stenosis Aortic stenosis is the most common indication for valvular surgery in the UK. Although rheumatic disease remains a common problem in underdeveloped countries, the most frequent aetiology in the Western world is calcific aortic stenosis, which develops in the older population, typically in patients over 70 years. The normal aortic valve has three cusps, but a congenital bicuspid valve calcifies at an earlier age. Aortic stenosis causes LV hypertrophy, effort angina, episodes of arrhythmia with syncope or even sudden death, and LV failure. Clinically, the patient has a slow rising pulse (pulsus parvus and tardus), a forceful apex beat and an ejection systolic murmur in the right upper parasternal area that may radiate to the root of the neck. Echocardiography will confirm a valvular gradient, which is considered severe aortic stenosis when this exceeds 60 mmHg. However, measurement of orifice area is independent of cardiac output and may be a more reliable measure. The onset of symptoms or LV dysfunction (ejection fraction <50%) should initiate referral for surgery. In the asymptomatic patient, a high transvalvular gradient (mean >40 mmHg), a low valve orifice area (<1 cm2 ), or an abnormal response to exercise (development of symptoms or asymptomatic hypotension) may indicate the need for surgery. Patients with cardiac failure have a low output and consequently a low gradient. In these cases, the decision to operate may be a difficult judgement, based on the absence of any ther likely cause of poor LV function and echocardiographic evidence of severe aortic valve disease. In some patients, e.g., the elderly, those with patent coronary grafts or significant other comorbidities, percutaneous replacement may be considered. TAVI (transcatheter aortic valve insertion) is the procedure where a biological valve on a holder is introduced percutaneously. Vascular access is achieved via the femoral artery or LV apex, or directly to the proximal aortic root via a right parasternal mini-thoracotomy.

To perform cardiopulmonary bypass,you will need all the following except: A. Venous cannula in inferior vena cava B.Arterial cannula in ascending aorta C.Venous cannula in superior vena cava D.Arterial cannula in left appendage E.Venous cannula in right appendage

D.Arterial cannula in left appendage Cardiopulmonary bypass: Modern cardiac and great vessel surgery became feasible with the development of cardiopulmonary bypass (CBP). Venous blood is drained via cannulae inserted into the right atrium or venae cavae and passes to a reservoir. It is then pumped through a heat exchanger coil so that its temperature can be varied and an oxygenator,which adds O2 and removes CO2, and filters it. Finally, the blood is returned to the arterial circulation via a cannula in the ascending aorta or other suitable artery (femoral, axillary). Full anticoagulation with intravenous heparin is required to prevent blood clotting in the bypass circuit. Roller or centrifugal pumps are used, as these minimise red cell trauma. Semipermeable membranes, or more commonly hollow fibres, form the blood-gas interface within the oxygenator. A trained perfusion technician controls the bypass machine. CPB stimulates a systemic inflammatory response mediated by cytokine release, complement activation and white cell activation. These changes do not generally cause clinical problems but may be implicated in postbypass pulmonary, renal and cerebral dysfunction. Cerebral damage occurs in about 1% of cases due to intracerebral bleeding, embolisation of microbubbles or arterial debris, or inadequate cerebral perfusion. Subtle deterioration in cerebral function, as detected by psychological testing, is more frequent. Coagulopathy and haemolysis are associated with prolonged bypass.

Horner's syndrome in the context of the bronchogenic carcinoma suggests: A. The size of the lesion B.Bone metastases C.Nodal spread D. Involvement of superior vena cava E. Involvement of upper sympathetic chain

E. Involvement of upper sympathetic chain אמבוס- Horner syndrome (HS) is a neurological disorder characterized by a symptom triad of miosis (an abnormally small pupil), partial ptosis (drooping of the upper eyelid), and facial anhidrosis (absence of sweating). This condition results from lesions that interrupt the ipsilateral sympathetic nervous supply to the head, eye, and neck. Most cases of HS are idiopathic, but conditions such as brainstem stroke, carotid dissection, and neoplasm are occasionally identified as the cause of HS. Because of the wide array of possible causes, diagnosis of the underlying disorder frequently poses a challenge and requires a systematic approach. Once the lesion has been identified, treatment should be tailored to the specific cause.

Coarctation of the aorta is the narrowing of the thoracic aorta usually at the level of: A.Aortic valve. B. Brachiocephalic trunk C.Sino-tubular junction D.Aortic root E.Ligamentum arteriosum

E.Ligamentum arteriosum אמבוס- Coarctation of the aorta A congenital heart defect that involves the narrowing of the aorta at the aortic isthmus. Frequently associated with other congenital heart defects (e.g., bicuspid aortic valve, VSD and/or PDA) and Turner syndrome. ספר- Coarctation of the aorta This condition is caused by a narrowing ofthe thoracic aorta, usually at the level of the ligamentum arteriosum. The lower body is perfused via extensive chest wall collaterals. Upper body hypertension develops and may lead to heart failure in infancy. Untreated adults develop hypertensive cerebrovascular and renal problems, and accelerated coronary atheroma. Most children and young adults are asymptomatic and present with high blood pressure or an abnormal chest x-ray. The femoral pulses may be impalpable or weak and delayed, and a systolic murmur may be audible over the back. Left ventricular hypertrophy (LVH) is seen on ECG and chest x-ray shows an enlarged heart, reduced aortic knuckle and characteristic rib 'notching', caused by enlarged and tortuous intercostal arteries eroding the ribs nearthe posterior angles (Fig. 22.16). Balloon angioplasty has been used to dilate some coarctations in infants, but surgical correction is usually required. At operation, the left subclavian artery may be used as an onlay patch. Older children and adults are usually managed with a resection and end-toend anastomosis or a Dacron bypass graft. Surgical correction tends to reduce upper body hypertension in children. It is less effective in adults but pharmacological control of hypertension becomes more reliable. The operative risk is approximately 5%

Oliguria in adults is urinary output: A. <400mL/day B.<200mL/day C.<50mL/day D.>200mL/day E.>400mL/day

A. <400mL/day אמבוס- Oliguria The production of an abnormally small amount of urine that is quantitatively defined as urine output of < 400 mL per 24 hours in adults (less than 0.5 mL/kg/h in children). לשנן טבלה!

The most frequent complications of TPN (total parenteral nutrition) are: A. Catheter related sepsis and blood stream infections B.Thrombophlebitis C.Overhydration D. Hypokalaemia E. None of the above

A. Catheter related sepsis and blood stream infections אמבוס- Total parenteral nutrition (TPN): the intravenous provision of all nutritional requirements ספר Parenteral nutrition: • Parenteral feeding is indicated if the patient cannot be fed adequately by the oral or enteral route • The need to restrict volume when using total parenteral nutrition (TPN) means that concentrated solutions are used, which may be an irritant and thrombogenic. TPN is therefore infused through a catheter in a high-flow vein (e.g., superior vena cava) • TPN is usually given in an 'all-in-one' bag with a mixture of glucose, fat and L-amino acids combined with fluid, electrolytes, vitamins, minerals and trace elements • The major complications with TPN can be classed as catheterrelated, septic or metabolic. A multidisciplinary approach to the management of TPN patients by a nutrition team will minimise such complications Infection- Catheter related sepsis and blood stream infection (CRBSI) are the most frequent complications of TPN. The usual offending organisms are skin bacteria; coagulase-negative staphylococci, Staphylococcus aureus and coliforms, but the incidence of fungal infection is increasing, possibly because many of the patients requiring TPN are immunocompromised or receiving broadspectrum antibiotics. Catheter infections are entirely avoidable and are almost always the result of poor line care, with infection usually introduced via the catheter hub as a result of deficient aseptic technique. Although CRBSI rates of 1-5 episodes per 1000 catheter days are regarded as acceptable, it is entirely possible to provide TPN for decades without a single episode, given rigorous attention to asepsis. The insertion site must be protected with an occlusive dressing and should be cleansed on alternate days with an antiseptic agent. The line must only be used for infusion of nutrients and never for taking or giving blood, or administering drugs.

The best and easy tissue approximation method in laparoscopic surgery after suturing is: A. Clipping or stapling. B.Laser welding. C.Tissue glue. D. There is no correct answer. E.All answers are correct.

A. Clipping or stapling. אמבוס Laparoscopic surgery: is a minimally invasive technique used to perform surgical procedures within the abdominal cavity, utilizing specialized instruments introduced through small incisions made on the abdominal wall. The abdominal cavity is first accessed using a trocar or a Veress needle, most commonly in the midline (peri-umbilical region). The peritoneal cavity is then insufflated with carbon dioxide (CO2). A fiber-optic instrument (laparoscope) is inserted into the first trocar to visualize the abdominal cavity and to allow for other ports to be created under direct vision. Laparoscopy is often the preferred diagnostic procedure for most elective gastrointestinal and gynecological surgeries. It is contraindicated in patients with shock, cardiac/pulmonary failure, and in cases of dilated bowel loops/perforation peritonitis. There are several advantages of laparoscopy over laparotomy as the incisions used are much smaller (e.g., less postoperative pain, fewer respiratory complications). However, the surgery is technically more challenging and complications (e.g., hemorrhage, bowel injury) are difficult to control laparoscopically. Complications unique to laparoscopy (secondary to CO2 insufflation of the peritoneal cavity) include hypercarbia, pneumothorax, pneumomediastinum, venous air embolism, and postoperative shoulder pain. Proper patient selection and good surgical technique minimize the risks and complications of laparoscopy. Procedure/application: 1. Anesthesia: general anesthesia (most common), spinal anesthesia with/without epidural anesthesia may be used in some cases. 2. Access to the peritoneal cavity (laparoscopic entry): A trocar/Veress needle is inserted through the abdominal wall (generally midline) into the peritoneal cavity. Trocar: An instrument with a sharp conical end that is used to establish a portal of entry into a body cavity. 3. Creating a pneumoperitoneum: The peritoneal cavity is insufflated with carbon dioxide (CO2). Allows visualization of abdominal contents and creation of operative space Raises intra-abdominal pressure due to the insufflation of gas within a closed cavity 4. Creation of other port sites 5. Removal of instruments and trocars 6. Evacuation of pneumoperitoneum 7. Closure of the port sites: Fascia of port sites > 5 mm must be sutured at the end of the surgery. To minimize the risk of port-site incisional hernia.

A 22 year old woman presented in the emergency room with a two day history of abdominal pain. On physical examination she had tenderness in both lower quadrants, more on the right than the left. Lab tests were unremarkable.. What should be the plan of treatment? A. Diagnostic Laparoscopy. B.Laparoscopic Appendicectomy. C. Open Appendicectomy. D.Only Conservative Treatment. E. There is no correct answer.

A. Diagnostic Laparoscopy. Diagnostic laparoscopy Allows direct visualization of the abdominal cavity, as well as biopsy of suspicious areas (lymphadenopathy) or collection of peritoneal fluid (for culture or cytology) through small incisions in the abdominal wall. Commonly used to avoid laparotomy in the following situations: Evaluation of acute abdominal pain with negative imaging Abdominal trauma with negative imaging when an intra-abdominal injury is suspected (e.g., diaphragmatic tear) Staging of cancers To determine resectability of cancers: gastric cancer, pancreatic/biliary tract cancer, etc. לבדוק אם קשור- The treatment of appendicitis is almost always surgical and now invariably using the laparoscopic technique, especially if a diagostic laparoscopy has been performed first to establish

Intraductal papillary mucinous neoplasm (IPMN): A. Differ from cystic mucinous neoplasms because of a direct communication with the Wirsung duct B. Is Frantz tumour of the pancreas C. Secretes peptides like neurotensin or chromogranin A D. Is a malignant tumor of the liver E. Is a type of ductal adenocarcinoma of the pancreas

A. Differ from cystic mucinous neoplasms because of a direct communication with the Wirsung duct מהספר- Adenocarcinoma of the pancreas: Intraductal papillary mucinous neoplasm (IPMN) Intraductal papillary mucinous neoplasm (IPMN) is a relatively recently recognised entity, and comprises a group of lesions characterised by a papillary growth of the ductal epithelium with rich mucin production and cystic expansion of the affected duct. The widespread availability of cross-sectional imaging has resulted in many being detected incidentally. There is a broad separation into two types; main duct and branch duct. Both subtypes have malignant potential but malignancy or high grade dysplasia is seen more commonly in main duct (70%) than branch duct (15%) IPMN. Resection is recommended for main duct IPMN where clinically appropriate, whereas many branch duct lesions may be observed unless high-risk stigmata are identified. These include nodules within the cyst wall and large cyst size (>4 cm). When malignancy occurs in main duct IPMN, the natural history is different from PDAC in that the majority are resectable, with survival reaching 80-90% for in situ carcinoma, and 50-70% in the presence of invasive carcinoma. Other primary malignant tumours • Angiosarcoma - This rare tumour of the liver may arise after industrial exposure to vinyl chloride or exposure to the previously used radiological contrast medium, Thorotrast. • Haemangioendothelioma- This presents as a diffuse multifocal tumour and is rarely resectable at presentation. • Hepatic mucinous cystic neoplasm- This rare condition of the liver has a marked female predominance. It usually presents as a large complex cystic lesion within the liver detected on ultrasound. It does not communicate with the biliary tree. It has a high rate of malignant transformation and should be resected. These can be mistaken for biliary intraductal papillary mucinous neoplasms (B-IPMN). Unlike hepatic mucinous cystic neoplasms B-IPMN involve the biliary tree and can occur in both genders.

You examine a 36 years old man 2 hours after motor vehicle accident. Heart Rate=99/min, Blood pressure = 155/92 mmllg, respiratory rate 12/minutes. He didn't respond to the voice, but with pain stimulation he opens the eyes,makes simple sounds (not words),and has extensions in extremities. On Glasgow Coma Scale(GCS) he bad: A.6 B.7 C.8 D.9 E. Not enough information to assess GCS

A.6 Glasgow Coma Scale- A standardized scale used to assess level of consciousness and neurological status. The scale scores the patient's eye response (1-4 points), verbal response (1-5 points), and motor response (1-6 points). A maximum score of 15 points indicates full consciousness, while a minimum score of 3 points can indicate deep coma or brain death. Commonly used to classify traumatic brain injury severity.

Rovsing's sign occurs: A. In acute appendicitis B. In patients with severe acute pancreatitis C. In acute cholecystitis D. In acute gastroenteritis E. In urinary tract infection

A. In acute appendicitis ספר- acute appendicitis- Examination: The patient with established acute appendicitis looks unwell, is flushed and has a dry, furred tongue with a foetor. The temperature is usually only mildly elevated (37.3-38.5°C) and there is often a tachycardia. Classically, the area of maximal tenderness is over McBurney's point, with guarding and rebound (percussion) tenderness. Palpation in the left iliac fossa may reproduce the pain in the right iliac fossa (Rovsing's sign) and the patient may find it painful to extend the right hip owing to irritation of the psoas muscle (psoas stretch sign). Although rectal and vaginal examinations are frequently normal, they can be useful when the abdominal signs are vague, particularly if the acutely inflamed appendix lies within the pelvis, when tenderness may be elicited with the examining finger. In women a vaginal examination is extremely useful in helping to differentiate acute appendicitis from acute gynaecological disorders. Specific clinical signs in acute abdominal pain: 1. Murphy's sign - In acute cholecystitis, a deep breath taken by the patient elicits acute pain when the examiner presses downwards into the right upper quadrant. This is caused by the movement of the inflamed gallbladder striking the examining hand. 2. Boas's sign- In acute cholecystitis, pain radiates to the tip of the scapula and there is a tender area of skin just below the scapula, which is hyperaesthetic. 3. Grey Turner's and Cullen's signs- In patients with severe acute pancreatitis, bruising and discoloration may be seen around the umbilicus (Cullen's sign) and in the left flank (Grey Turner's sign). Cullen's sign was actually first described in relation to ruptured ectopic pregnancy, but is now often also associated with acute pancreatitis. 4. Rovsing's sign- In acute appendicitis, palpation in the left iliac fossa produces pain in the right iliac fossa.

Normal adult patient in supine position (physiologie condition) has: A. Intracranial pressure(ICP) is the same as the (cerebrospinal fuid) CSF pressure obtained at lumbar puncture (LP: 5-15cm H2O) B. ICP is different than the CSF pressure obtained at lumbar puncture (L.P: 15-20mmll) C. ICP is differenthan the CSF pressure obtained at lumbar puncture(LP:5-15cm ll0) D. ICP is the same as the CS pressure obtained at lumbar puncture (LP:15-20manlt)

A. Intracranial pressure(ICP) is the same as the (cerebrospinal fuid) CSF pressure obtained at lumbar puncture (LP: 5-15cm H2O) supine position= An anatomical descriptor for horizontal positioning of the body with face and torso facing upward (i.e., lying on the back). Intracranial pressure: Once the skull's sutures fuse, the brain is enclosed within a rigid bony container. Intracranial pressure (ICP) therefore depends on the relative volumes of intracranial blood, CSF and brain parenchyma; if one constituent increases then another must decrease, or else the ICP will increase; this is the essence of the Munro-Kellie doctrine. ICP fluctuates in response to normal variation in intrathoracic pressure (e.g., increased by coughing, defaecation) and cardiac pulsation. These transient increases do no harm. In a normal supine adult, ICP is the same as the CSF pressure obtained at lumbar puncture (LP; 5-15 cm H2O, 4-10 mmHg). Symptoms of raised ICP may include headache, vomiting and visual disturbance (blurring of vision). Papilloedema may be apparent on examination. Neurological deficits may facilitate localisation of a causative lesion. If the raised ICP is chronic then there may be few clinical signs or symptoms. A rapid increase in ICP may precipitate acute reduction in conscious level.

The most common cause of non-traumatic subarachnoid hemorrhage is: A. Ruptured intracranial aneurysm B. Ruptured brain cavernomas C.Ruptured arteriovenous malformation D.Subdural hematoma E.Brain tumors (especially metastatic)

A. Ruptured intracranial aneurysm Subarachnoid haemorrhage: Spontaneous SAH affects 100 persons per million per year and most frequently (70%) results from the rupture of an intracranial 'berry' aneurysm. Other causes include small vessel rupture, arteriovenous malformation (AVM), cavernoma, tumour, infection an trauma. Typically, the patient complains of a sudden onset of severe headache that rapidly peaks in intensity (within 1 minute). Patients often describe it as like being 'hit on the head with a hammer' or as 'the worst headache they have ever had'. There is usually associated neck stiffness and photophobia. A positive Kernig's sign denotes meningism. In some cases, a small 'herald' bleed a few days earlier may have gone unnoticed. Nausea and vomiting are common. Conscious level is variably affected, ranging from mild disorientation to coma to rapid death. Grading of SAH depends on the coma score of the patient at time of presentation. The most widely used system is the World Federation of Neurosurgical Societies' (WFNS) grading, graded 1-5 . Sudden death is not uncommon when an aneurysm ruptures into the brain substance rather than the subarachnoid space. However, when the syndrome is of a grade 1 haemorrhage, a high degree of suspicion for SAH is required. SAH can mimic atypical migraines, thunderclap headache, coital cephalgia, pituitary apoplexy and meningitic-like syndromes. Focal signs depend upon the vessel affected. An unrecognised aneurysmal bleed may recur acutely and be devastating.

Patients who sustain a knee dislocation that spontaneously reduces may have a relatively normal-appearing knee. Subtle signs of Injury such as mild abrasions, or a minimal effusion, or complaints of knee pain may be the only abnormalities. A. both statements are true and causally related B. both statements are true but not causally related C. the first statement is true and second is false D. the first statement is false and second is true E. both statements are false

A. both statements are true and causally related צילום של התשובה מהספר של אורטופדיה מידע כללי מאמבוס- Tibiofemoral joint dislocation Location: knee joint (tibiofemoral articulation) Mechanism of injury: usually caused by high-energy trauma, e.g., dashboard injury, fall from a height; low-energy trauma possible (especially in obese individuals) Anterior dislocation (tibia is anterior to the femur condyles): hyperextension of the knee joint driving the femur posterior to the tibia. Posterior dislocation (tibia is posterior to the femur condyles): direct impact to the proximal tibia displacing the tibia posterior to the femur. Medial/lateral dislocation (tibia is medial or lateral to the femur condyles): due to varus or valgus force Clinical features : Abnormal position of the knee joint Swelling of the knee Ecchymosis Dimple sign (in posterolateral dislocation): indentation of the skin at the medial femoral condyle provoked by the invagination of soft tissue into the intercondylar notch Diagnostics: Immediate evaluation (due to potential severe neurovascular injuries), which includes: Assessment of the popliteal and distal pulses Assessment of the sensory and motor function of the knee, lower leg, and foot Reevaluation after immediate treatment, which includes:Ankle-brachial index X-ray of the knee joint and the lower leg Duplex ultrasound Treatment Isolated anterior or posterior dislocation: immediate closed reduction Posterolateral dislocation: immediate open reduction Complications Injury of ACL, MCL, LCL, PCL, or PLC Popliteal artery injury Common peroneal or tibial nerve injury Compartment syndrome Deep vein thrombosis Knee dislocations are frequently associated with severe neurovascular injuries and should be treated immediately.

In the world most cases of pancreatitis are caused by: A. gallstones and alcohol B. gallstones and metabolic disease(hypertriglyceridemia) C. alcohol and drugs (thiazides and other) D. idiopathic E.trauma and ERCP (endoscopic retrograde cholangiopancreatography)

A. gallstones and alcohol ספר- Acute pancreatitis Acute pancreatitis is a common cause of emergency admission to hospital. The incidence continues to rise, possibly because of an increase in gallstone disease, alcohol misuse and obesity in the population. The disease is relatively rare in children, but all adult age groups may be affected. Gallstone pancreatitis - Gallstones are responsible for nearly three-quarters (75%) of cases of acute pancreatitis in tropical countries in contrast to some 40% of patients in the UK. Tiny gallstones or even microscopic crystals (so-called microlithiasis) are thought to account for the majority of 'idiopathic' cases. Transient impaction of a gallstone within the common channel between the common bile and pancreatic ducts causes obstruction of the pancreatic duct and a sequence of events within the pancreatic acinar cells resulting in intracellular activation of pancreatic enzymes, acinar cell damage and pancreatic inflammation. Alcohol-associated pancreatitis - The proportion of cases linked to alcohol varies in different parts of the world. In Scotland, the figure is around 30%, whereas in some parts of France and North America it may be as high as 50-90%. The mechanism responsible is uncertain. Although there is no direct relationship between the quantity of alcohol consumed and the risk of pancreatitis (in contrast with alcoholic liver disease) alcohol consumption normally exceeds 50 g day (or five standard drinks). אמבוס הרחבה- Acute pancreatitis- is an inflammatory condition of the pancreas most commonly caused by gallstones and alcohol use. The typical manifestation includes sudden, severe epigastric pain that radiates to the back, nausea and vomiting, and epigastric tenderness on palpation. Elevation of serum lipase or amylase ≥ 3× ULN and/or characteristic findings of acute pancreatitis on cross-sectional imaging (e.g., contrast-enhanced CT abdomen) confirm the diagnosis. Clinical scores (e.g., Ranson criteria, APACHE II) are used to predict the severity and prognosis of pancreatitis. Initial management is primarily supportive and includes fluid resuscitation, analgesia, antiemetics, and early enteral nutrition as tolerated. The underlying cause should be identified and managed to prevent recurrence (e.g., cholecystectomy for biliary pancreatitis, long-term lipid-lowering therapy for hypertriglyceridemia-induced pancreatitis). Localized complications of pancreatitis include necrosis (necrotizing pancreatitis), which may become infected, pancreatic pseudocysts, and walled-off necrosis. Systemic complications include sepsis, ARDS, organ failure, and shock. Complications of pancreatitis are associated with significant morbidity and mortality. Etiology # Most common causes: -Biliary pancreatitis (∼ 40% of cases; mostly caused by gallstones) - Alcohol-induced (∼ 20% of cases)Idiopathic (∼ 25% of cases) # Other causes: Hypertriglyceridemia-induced pancreatitis: caused by severe hypertriglyceridemia (> 1,000 mg/dL) Hypercalcemia Post-ERCP Drug-induced pancreatitis Steroids Azathioprine Sulfonamides Loop and thiazide diuretics Estrogen Protease inhibitors NRTIs Anticonvulsants (e.g., valproate) Scorpion stings Viral infections (e.g., coxsackievirus B, mumps) Trauma (especially in children) Autoimmune and rheumatological disorders (e.g., Sjögren syndrome) Pancreas divisum Hereditary (e.g., mutation of PRSS1 gene, cystic fibrosis) I GET SMASHED: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion poison, Hypercalcemia and hypertriglyceridemia, ERCP, and Drugs are the most common causes of acute pancreatitis.

Klatskin tumour A. involving the confluence of the hepatic ducts B. is carcinoma of the rectum C. is associated with MEN type I D. is benign tumour of the stomach E. is small benign fibrous lesion that is often situated beneath the capsule of the liver

A. involving the confluence of the hepatic ducts ספר Carcinoma of the bile ducts Cholangiocarcinoma is a relatively uncommon cancer that affects the elderly and which is increasing in frequency. Such lesions may arise at any site within the biliary tree and can be multifocal. Tumours can be classified based on the level of involvement of the biliary tree and are most common at the hilus. Polypoidal tumours are uncommon but carry a more favourable outlook. Sclerotic lesions involving the confluence of the hepatic ducts (Klatskin tumour) pose considerable problems in management. The lesions are said to be slow-growing, but this has been over-emphasised. Cholangiocarcinoma may develop in patients with underlying primary sclerosing cholangitis or choledochal cyst. אמבוס- Biliary cancer Biliary tract cancers include cholangiocarcinoma and gallbladder carcinoma, which are both rare diseases with very poor prognoses. Cholangiocarcinoma is classified as either intrahepatic or extrahepatic according to the anatomical site of the tumor. Extrahepatic carcinoma, which is the more common form, can be further classified as perihilar (Klatskin tumor; occurs at the bifurcation of the hepatic duct) and distal extrahepatic carcinoma. Risk factors for cholangiocarcinoma include primary sclerosing cholangitis and chronic biliary tract inflammation. The greatest risk factor for gallbladder carcinoma is cholelithiasis. Patients are often initially asymptomatic or only present with nonspecific symptoms (e.g., abdominal pain, fever, weight loss) until late stages of disease, meaning that most tumors are already advanced at the time of diagnosis. Extrahepatic cholangiocarcinoma may manifest with signs of cholestasis (e.g., jaundice, dark urine, pruritus) and a painless, enlarged gallbladder (Courvoisier sign). If liver transaminases and tumor markers are raised and/or ultrasound imaging suggests bile duct or gallbladder carcinoma, MRCP or MDCT are recommended for diagnosis. Although surgical resection of early-stage tumors is curative, approximately 90% of patients have more advanced, unresectable tumors at the time of diagnosis. Cholangiocarcinomas: originate in the bile ducts and are classified based on their anatomical site of origin Extrahepatic cholangiocarcinoma is the most common form (90% of cases). - Perihilar (Klatskin tumor): junction of the right and left hepatic ducts (50% of cases) - Distal extrahepatic: common bile duct (40% of cases)Intrahepatic cholangiocarcinoma: intrahepatic bile ducts (10% of cases) Gallbladder carcinomas: originate within the mucosal lining of the gallbladder

A Plummer-Vinson syndrome: A. is characterized by a post-cricoid web that results in dysphagia. B. is thought to be due to a partial or complete degeneration of the myenteric plexus of Auerbach C. affects the whole oesophagus D. is caused by repetitive forceful peristalsis E. is most commonly caused by streptococcal and gonococcal infection.

A. is characterized by a post-cricoid web that results in dysphagia. אמבוס- Plummer-Vinson syndrome A condition characterized by the triad of dysphagia, upper esophageal webs, and iron deficiency anemia. Associated with glossitis and increased risk of esophageal squamous cell carcinoma. Most commonly presents in white women 40-70 years of age. ספר גרסה 6- Plummer-Vinson syndrome This syndrome, first described by Paterson and Brown Kelly, is characterized by a post-cricoid web that results in dysphagia. The web is related to iron deficiency anaemia, but may be congenital or traumatic in origin. The squamous epithelium becomes hyperplastic and there is hyperkeratosis and desquamation, which leads to web formation. Clinical features Patients are commonly middle-aged women. Dysphagia is the main presenting complaint, but there may also be symptoms and signs of anaemia, including koilonychia, smooth tongue and angular stomatitis. Investigations A full blood count will show hypochromic microcytic anaemia and serum ferritin levels will be low. Barium swallow demonstrates a narrowing of the upper oesophagus with a web in the anterior wall; this is confirmed by endoscopy, during which a friable web can be seen across the lumen of the oesophagus. Management The web is dilated endoscopically and biopsies should also be taken, as there is an association with post-cricoid carcinoma. The iron deficiency status is corrected by oral iron therapy.

The patient with internal carotid artery stenosis of 40% and ipsilateral stroke 2 months ago should be treated: A. with medical treatment only B. with surgical endarterectomy of the carotid artery C. with surgical by-pass D. with stent placement E. with surgery or stent implantation according to the vessel anatomy and the plaque morphology

A. with medical treatment only Endarterectomy This involves the direct removal of atherosclerotic plaque and thrombus, and is a relatively uncommon operation in modern vascular surgical practice except at the carotid and femoral bifurcations Carotid endarterectomy Patients with completed major stroke and little in the way of recovery are not candidates for carotid intervention; nor are those with an occluded internal carotid artery. However, carotid endarterectomy (CEA) combined with BMT is associated with a significant reduction in recurrent stroke, compared with BMT alone in patients with amaurosis, TIA and stroke with good recovery, provided that: • There is a high degree of internal carotid artery stenosis (usually taken as a greater than 60-70% diameter reduction) • The patient is expected to survive at least 2 years • The intervention can be undertaken with a stroke and/or death rate of less than 3-5% • The intervention can be performed soon after the index event. The exact timing remains controversial and is a matter of judgment for each patient but, in general, the sooner the better. Patients who do not fulfil these criteria should, in most cases, be treated medically. The operation can be equally well performed under general or local anaesthetic. The carotid bifurcation is dissected, heparin is given and the arteries are clamped. If this leads to cerebral ischaemia, a shunt is inserted. The plaque is shelled out (the endarterectomy) and the artery repaired with direct suture or a patch graft (patch angioplasty). משוחזר פחות או יותר ככה

What are the disorders in gasometry In children with hypetrophie pyloric stenosis? A.Alkalosis,hypokalicmia,hypochloremia B.Acidosis,hypokalicmia,hypochloremia C.Alkalosis,hyperkaliemia,hyperchloremia D.Acidosis,hyperkalicmia,hypochloremia E.Alkalosis,hypokaliemia,hyperchloremia

A.Alkalosis,hypokalicmia,hypochloremia Hypertrophic pyloric stenosis: Hypertrophic pyloric stenosis, the most common cause of gastric outlet obstruction in infants, is characterized by hypertrophy and hyperplasia of the pyloric sphincter in the first months of life. Clinical manifestations usually appear between three and five weeks of age. The primary symptom is regurgitation progressing to nonbilious, projectile vomiting, which occurs intermittently or after feeding. The infant is irritable and demonstrates a strong rooting and sucking reflex because of hunger. Constant vomiting leads to hypokalemic and hypochloremic metabolic alkalosis. The diagnosis is usually clinical and involves the detection of a palpable, olive-shaped structure in the epigastrium (a sign of marked hypertrophy of the pylorus) and visible gastric peristalsis proximal to the site of obstruction. The condition may also be diagnosed on ultrasound in the absence of a palpable, olive-shaped structure. Initial management involves adequate rehydration and correction of electrolyte imbalances. The definitive treatment is Ramstedt pyloromyotomy.

Which antibiotics could be used in antibiotic prophylaxis? A.Cefazolin B.Penicillin C.Vancomycin D.A and B E.B and C

A.Cefazolin אמבוס- Antibiotic prophylaxis Antibiotics are commonly used for prophylaxis against infections in the following situations: - Immunocompromised patients (e.g., HIV, immunosupression, neutropenia) -Infective endocarditis -Before and/or after surgical procedures (e.g., perioperative cefazolin to prevent surgical site infection) -Post-exposure prophylaxis (e.g., doxycycline against malaria, rifampin against bacterial meningitis)

Treatment of the esophageal atresia A.First minimizing complications from aspiration:(continuous suction from blind pouch, upright position of child with head bended towards chest,Prophylactic antibiotics and then surgical correction via thoracotomy/thoracoscopy B.First minimazing complications from aspiration: (continuous suction from blind pouch, upright position of child with head bended towards chest,Prophylactic antibiotics and then surgical correction via laparotomy/laparoscopy C.You need to treat only C type with Gross classification - the other ones are to difficult to treat D.There is always possibility to connect the blindly ended pouches and perform end to end anastomosis-the other actions are unnecessary E.When you operate the neonate quick enough there are no complications like gastroesophageal reflux disease (GERD) or narrowing the esophageus.

A.First minimizing complications from aspiration:(continuous suction from blind pouch, upright position of child with head bended towards chest,Prophylactic antibiotics and then surgical correction via thoracotomy/thoracoscopy Esophageal atresia: Esophageal atresia is a congenital defect in which the upper esophagus is not connected to the lower esophagus, ending blindly instead. It is caused by the abnormal development of the tracheoesophageal septum. Esophageal atresia with a fistula connected distally to the trachea is the most common kind of esophageal malformation (classified as Gross type C). It manifests immediately after birth with cyanotic attacks, foaming at the mouth, and coughing, and prevents any attempts to pass a feeding tube into the stomach. X‑ray is mandatory for classifying the atresia and should show an air‑filled pouch situated at the level of the third thoracic vertebra. Preoperative: - Placement of an oroesophageal or nasoesophageal tube for continuous suction of secretions to prevent aspiration and facilitate breathing. - Upper body elevated, left lateral decubitus position - Antibiotics in case of aspiration pneumonia - Infants who potentially have esophageal atresia should not be fed orally under any circumstances! Surgery: Surgical treatment should be performed within the first 24 hours of birth. The goal is to reconnect the upper esophageal pouch and the lower esophagus. A long gap between both ends of the esophagus may not allow primary repair. In this case, a gastrostomy tube is necessary to allow enteral feeding. Treatment options include promoting elongation of the esophagus (via the Foker technique) and colon interposition Surgical repair is technically difficult surgery that uses a cervicotomy, cervicosternotomy, or thoracotomy approach; thus, expertise in both esophageal and tracheal surgery are critical for success. The surgical approach for TEF depends upon the size of the fistula Overall good prognosis, but surgical complications occur frequently: Dysphagia, Gastroesophageal reflux disease, Anastomotic stenosis, Wheezing, Infections of the respiratory tract, Anastomotic insufficiency, Recurrence of esophageal, tracheal fistula and Esophageal stricture. פסילת תשובות: B.First minimazing complications from aspiration: (continuous suction from blind pouch, upright position of child with head bended towards chest,Prophylactic antibiotics and then surgical correction via laparotomy/laparoscopy C.You need to treat only C type with Gross classification - the other ones are to difficult to treat- את כולם ננתח D.There is always possibility to connect the blindly ended pouches and perform end to end anastomosis-the other actions are unnecessary- לא תמיד אפשר לחבר קצה לקצה ולפעמים צריך טיוב E.When you operate the neonate quick enough there are no complications like gastroesophageal reflux disease (GERD) or narrowing the esophageus.- סיבוכים מאוד נפוצים

What is granulation tissue? A.Soft,pink,fleshy projections consisting of capillaries surrounded by fibrous collagen. B. The tissue that remains after a scar is healed. C. A group of cells that form a grain. D. Composed of small microscopic grains of epithelial cells. E. Impaired form of scarring.

A.Soft,pink,fleshy projections consisting of capillaries surrounded by fibrous collagen. אמבוס: Granulation tissue Wound healing → Phases of wound healing: A type of connective tissue generated by fibroblasts during wound healing. Initially, it is composed of type III collagen, which is then replaced by type I collagen to create a stronger extracellular matrix. Formation of granulation tissue: Fibroplasia → synthesis and deposition of type III collagen. Growth factors (FGF, EGF, VEGF, PDGF, and TGF-β) from fibroblasts and epithelial cells promote angiogenesis.PDGF stimulates smooth muscle cell migration and fibroblast growth → collagen synthesis. Wound contraction occurs as collagen synthesis increases and pulls the wound edges together. This process is facilitated by myofibroblasts.

What is VACTERL association? A.VACTERL association refers to group of birth defect contain vertebral anomalies, anorectal anomalies, cardiac diseases, tracheoesophageal fistula, renal anomalies and limb defects B.VACTERL association refers to group of birth defect contain variety of eyes anomalies, anorectal anomalies,cardiac diseases, tracheoesophageal fistula, renal anomalies and limb defects C.VACTERL association refers to group of birth defect contain variety of eyes anomalies, anorectal anomalies,cardiac diseases,tracheoesophageal fistula, radius anomalies and other limb defects D.VACTERL association refers to group of birth defect contain vertebral anomalies, anorectal anomalies,cartilage disorders,tracheoesophageal fistula,renal anomalies and limb defects E. VACTERL association refers to group of birth defect contain variety of eyes anomalies, aniridia,cardiac diseases, tracheoesophageal fistula,renal anomalies and limb defects

A.VACTERL association refers to group of birth defect contain vertebral anomalies, anorectal anomalies, cardiac diseases, tracheoesophageal fistula, renal anomalies and limb defects Teratogen: an environmental factor that causes a permanent structural or functional abnormality, growth restriction, or death of the embryo or fetus. Effects depend on multiple factors The pharmacological properties, dose, and regimen of drug exposure determine the risk of developing teratogenic birth defects. Stage of pregnancy in which exposure occurs The physical effects of teratogens are widely varied: VACTERL association : Vertebral, anal, cardiac, tracheoesophageal fistula, renal, and limb abnormalities. Due to a defect during the development of embryonic mesoderm.

What kind of diseases can cause short bowel syndrome A.necrotizing enterocolitis, midgut volvulus, intestinal atresia,gastroschisis or Crohn's disease B.Necrotizing enterocolitis,appendicitis,oncological/hematological diseases C.gastroenterocolits,necrotizing enterocolitis D.Esphageal atresia with tracheoesphageal fistula E.Myelomeningocele

A.necrotizing enterocolitis, midgut volvulus, intestinal atresia, gastroschisis or Crohn's disease Small intestine resection (short bowel syndrome): Definition: a condition in which the small intestine is unable to adequately absorb nutrients, water, and electrolytes Etiologies: surgical resection (e.g., for Crohn disease or trauma), congenital abnormalities In infants and small children- necrotizing enterocolitis and congenital intestinal anomalies, such as mid-gut volvulus, atresias, or gastroschisis, are the most common causes of SBS. SBS in adults- usually results from surgical resection of the small intestine for Crohn disease, trauma, malignancy, radiation, or mesenteric ischemia. Complications: intestinal failure that requires intravenous supplementation necrotizing enterocolitis= A dangerous hemorrhagic inflammation of the intestinal wall that is caused by impaired bowel perfusion and defective immunity. It most often affects premature infants. The pathognomonic finding on abdominal x-ray is pneumatosis intestinalis. midgut volvulus= torsion of a malrotated midgut causing mechanical bowel obstruction, mostly in neonates and infants Torsion of bowel on its axis intestinal atresia= a congenital defect that can occur at any point along the gastrointestinal tract leading to complete (atresia) or incomplete (stenosis) occlusion of the affected lumen gastroschisis= A congenital visceral malformation with paraumbilical herniation of the intestine through the abdominal wall, most commonly on the right side. The herniated organs are not covered by a sac. Seen especially in premature infants and associated with bowel abnormalities (e.g., atresia, malrotation, or stenosis from vascular compromise). Extra-gastrointestinal comorbidities are uncommon (unlike in omphalocele).

The diagnostic tool to exclude deep venous thrombosis (DVT) in patients with the low clinical probability of the deep vein thrombosis occurrence is: A. Clinical examination including leg circumference measurement B.D-dimer assessment C.Angio CT D. Phlebography E. Termography

B. D-dimer assessment Diagnostic approach for suspected lower-extremity DVT : This approach is valid for evaluating a first-episode or recurrent lower extremity DVT. Calculate the pretest probability (PTP) using Wells criteria for DVT. Check D-dimer first for low PTP (initial D-dimer is not diagnostically helpful for intermediate and high PTP). Negative (< 500 ng/mL): DVT ruled out Positive (≥ 500 ng/mL): Possible DVT; Proceed to venous US. Obtain venous ultrasound (US) for intermediate or high PTP, or low PTP with positive D-Dimer Negative US Intermediate and low PTP: DVT ruled out High PTP: Repeat venous US within a week if no alternate diagnosis. Positive US: DVT confirmed; Screen for an underlying cause if no risk factors for DVT are identified on initial evaluation. Inconclusive US: Consider venography, CT venography, or MR venography. A negative D-dimer can help rule out DVT without venous ultrasound in patients with low pretest probability. It is not helpful for patients with intermediate or high pretest probability. Initial evaluation of DVT Based on the patient's pretest probability, the initial test to evaluate for DVT may be either D-dimer or compression ultrasound. D-dimer Indication: preferred initial test for nonpregnant patients with a low PTP of DVT (Wells score = 0) Accuracy: High sensitivity (∼ 96%) Low specificity (∼ 36%) Not reliable for ruling out DVT in patients with intermediate or high PTP In patients with a low pretest probability of DVT, a negative D-dimer (< 500 ng/mL) rules out DVT. A positive D-dimer alone does not confirm DVT.

Cullen's sign may be seen in: A. Acute gastroenteritis B. Patients with severe acute pancreatitis C. Choledocholithiasis D. Meckel's diverticulitis E. Patients with femoral hernia

B. Patients with severe acute pancreatitis ספר- Specific clinical signs in acute abdominal pain: 1. Murphy's sign - In acute cholecystitis, a deep breath taken by the patient elicits acute pain when the examiner presses downwards into the right upper quadrant. This is caused by the movement of the inflamed gallbladder striking the examining hand. 2. Boas's sign- In acute cholecystitis, pain radiates to the tip of the scapula and there is a tender area of skin just below the scapula, which is hyperaesthetic. 3. Grey Turner's and Cullen's signs- In patients with severe acute pancreatitis, bruising and discoloration may be seen around the umbilicus (Cullen's sign) and in the left flank (Grey Turner's sign). Cullen's sign was actually first described in relation to ruptured ectopic pregnancy, but is now often also associated with acute pancreatitis. 4. Rovsing's sign- In acute appendicitis, palpation in the left iliac fossa produces pain in the right iliac fossa.

"Physeal crush injury; difficult diagnosis, made retrospectively after growth arrest; narrowing of physis possible." Which pediatric physeal fractures classiñication system and type is mentioned above? A. Salter-Harris,type 1 B. Salter-Harris,type V C.Wrisberg,type V D.Lachmann,type I E.Kellgren-Lawrence,type V

B. Salter-Harris,type V Pediatric fractures often have distinct fracture patterns due to the unique properties of growing bones. The periosteum in growing bones is thicker and stronger than in adult bones, which is why children are more prone to more incomplete fractures, such as the greenstick fracture or torus fracture. In addition, the periosteum is metabolically active. This feature also explains why childhood fractures heal faster than fractures in adults. Salter-Harris fractures are fractures of the epiphyseal plate, also known as the growth plate or the physis of long bones. These fractures only arise in children and adolescents, whose skeletal growth is not yet complete. Salter-Harris fractures are classified into 5 types according to the extent of damage to the growth plate and joint involvement. Salter-Harris fracture classification: Type I: transverse fractures of the physis, separating the epiphysis from the metaphysis Type II: transverse fractures of the metaphysis and physis, which often involve separation of a triangular section of the metaphysis; most common type of Salter-Harris fracture Type III: transverse fractures of the physis and epiphysis; may extend to the joint and affect the articular surface Type IV: fractures through the metaphysis, physis, and epiphysis, that enter the joint Type V: fractures characterized by impaction and disruption of the physis; occur due to a crush or compression injury

CEAP classification concerns: A.Severity of intermittent claudication B. Severity of chronic venous disease C. Severity of critical leg ischemia D.Severity of metabolic syndrome E.Severity of post-thrombotic syndrome

B. Severity of chronic venous disease EAP classification of chronic venous disorders A standardized system used to classify features of chronic venous disorders. The categories are: Clinical (e.g., manifestations of venous disease), Etiological (e.g., congenital, primary, secondary), Anatomical (e.g., superficial, perforating, deep veins), and Pathophysiological (e.g., due to reflux, obstruction). CVD is classified using the CEAP classification system: C: clinical signs, ranked in severity from C0-C6 E: etiology; may be congenital (Ec), primary (Ep), or secondary (Es) , or ranked as unidentified (En) A: anatomy; involves the superficial veins (As), perforators (Ap), or deep veins (Ad), or is ranked as unidentified (An) P: pathophysiology; caused by reflux (Pr), obstruction (Po), or both (Pr,o), or is ranked as unidentified (Pn) The clinical component of CEAP is often used alone in primary care as it does not require venous studies.

The anisocoria is one of the signs of uncal herniation and: A. Usually is contralateral to hemiation and is due to III nerve compression B. Usually is ipsilateral to hemiation and is due to III nerve compression C. Usually is contralateral to hemiation and is due to optic nerve palsy D.Usually is ipsilateral to hemiation and is due to optie nerve palsy E. Usually is contralateral to hemiation and is due to II and III cranial nerve injury

B. Usually is ipsilateral to hemiation and is due to III nerve compression Transtentorial (uncal) herniation: With large lesions, the medial part of the ipsilateral temporal lobe is pushed down through the tentorial notch to become wedged between the tentorial edge and the midbrain. The opposite cerebral peduncle is also pushed against the sharp tentorial edge. The aqueduct is compressed, obstructing CSF flow. Venous obstruction leads to midbrain haemorrhage. The clinical features of an uncal herniation are: • Glasgow Coma Score (GCS) falls and the motor component may become asymmetrical • Ipsilateral pupil dilates and becomes nonreactive to light • Blood pressure rises, the pulse slows, the respiratory rate falls (Cushing's response) • The patient becomes apnoeic. anisocoria= A condition of having pupils of unequal diameter. oculomotor nerve= III nerve- responsible for constriction of the pupil

The most common type of renal cancer is: A. papillary RCC B. clear cell RCC C.chromophobe RCC D. collecting duct RCC E.TCC

B. clear cell RCC RCC-Renal Cell Carcinoma TCC-Transitional Cell Carcinoma ספר- renal cell carcinoma There are numerous histological subtypes of RCC. The most common is clear cell RCC (85%), followed by papillary RCC (comprised of type 1 and type 2). Chromophobe and collecting duct RCC are less common. RCC may develop in a range of inherited syndromes, i.e., von Hippel-Lindau syndrome and Birt-Hogg- Dube syndrome. אמבוס- לא להתבלבל עם- Nephroblastoma (Wilms tumor) is the most common renal malignancy in children, typically affecting children between 2 and 5 years of age. A minority of cases are associated with specific syndromes (e.g., WAGR, Beckwith-Wiedemann) and gene mutations (e.g., WT1). Nephroblastoma is typically an incidental finding that manifests as a large abdominal mass. Other signs and symptoms may occur, such as hematuria and abdominal pain, especially in tumors that are large, ruptured, or metastasized. Treatment consists of tumor resection and chemotherapy for all stages (except for very low-risk tumors), while radiation is predominantly used in advanced disease. In contrast, renal cell carcinoma (RCC) is more common in the 15- to 19-year-old age group.

Pancreas is usually transplanted with a portion of: A. stomach B. duodenum C. ileum D. colon E. urinary bladder

B. duodenum ספר- Pancreas transplantation: • Combined kidney and pancreas transplantation is an excellent treatment for a carefully selected group of patients with type 1 diabetes mellitus • Patients must undergo rigorous medical evaluation prior to being listed, as they have complicated diabetic disease • Pancreas rejection is difficult to diagnose and this may lead to delay in initiating therapy for such episodes • Despite this, combined kidney-pancreas transplant is associated with a 5-year survival of 70%. The operative procedure Back-table preparation • The pancreas is retrieved en bloc with the spleen, and this is carefully excised on the back table, paying careful attention to the ligation and division of vessels • The 'C' of duodenum is carefully reduced and the ends both stapled and oversewn to avoid leakage • A Y graft (arterial conduit) isformed using donor iliac vessels onto the donor splenic and superior mesenteric vessels • illustrates a pancreas graft just before implantation and shows the vascular reconstruction performed on the back table

Mark the correct answer: A. gluteus medius inserts on the lesser trochanter B. iliopsoas inserts on the lesser trochanter C.iliopsoas is attached to the external trochanter D. gluteus minimus inserts on the adductor tubercule E. gluteus maximus inserts on the lesser trochanter

B. iliopsoas inserts on the lesser trochanter ראה תמונה. פסילת סעיפים: A. gluteus medius inserts on the lesser trochanter- gluteus medius inserts on the greater trochanter D. gluteus minimus inserts on the adductor tubercule- gluteus minimus inserts on the greater trochanter E. gluteus maximus inserts on the lesser trochanter- gluteus maximus inserts on Iliotibial tract, gluteal tuberosity of femur

Which of the following is true,regarding to femoral neck fractures? A. occur in the region between the greater and lesser trochanters of the proximal femur B. nonunion and osteonecrosis are the major problems C. femoral neck fractures are extracapsular fractures D. are common in elderly as a result of high energy trauma E. clinical symptoms are completely different than in intertrochanteric fractures

B. nonunion and osteonecrosis are the major problems ספר- Fractures of the femoral neck These are generally seen in the elderly with osteoporotic bone, as a result of low-energy falls and can often result from an underlying medical condition. They are extremely common and utilise very considerable health-service resources. Such fractures are divided into: • Extracapsular-occurring outside the margins of the joint capsule, particularly the metaphyseal trochanteric area of the femur • Intracapsular- involving the femoral neck within the capsule. This differentiation is important because blood reaches the femoral head via the capsule and runs along the femoral neck. Extracapsular fractures are normally reduced and stabilised using a pin and plate system, commonly known as a dynamic hip screw (DHS), which allows sliding and impaction of the fracture site as the patient walks. Undisplaced intracapsular fractures are pinned in the hope that the blood supply to the femoral head has been preserved and avascular necrosis of the femoral head will not develop. Treatment of displaced intracapsular fractures is a challenge and it still remains 'an unsolved fracture'. Attempt is made to retain the femoral head in a young patient since hip replacement may wear out, requiring revision surgery. Accurate reduction of a displaced intracapsular fracture may require opening the capsule for visualisation of the fracture, further jeopardising the blood supply. In the older patient the preferred treatment is to perform either a emiarthroplasty or a total hip replacement. These allow immediate weight bearing and a more predictable recovery. Clinical features of femoral neck fractures: Groin pain Shortened and externally rotated leg Minimal bruising פסילת סעיף- Clinical features of intertrochanteric fractures: Hip pain and swelling Shortened and externally rotated leg Significant ecchymosis Often associated with other injuries (e.g. other extremity fractures)

Estimation of protein requirements in adult surgical patient with complications amounts: A.0.5-0.7g/kg/day B.1.3-1.5g/kg/day C.2.0-2.3 g/kg/day D.2.3-2.5g/kg/day E.3.0-3.5g/kg/day**

B.1.3-1.5g/kg/day ספר- Assessment of nutritional status The main energy reserves are found in subcutaneous and intraabdominal fat depots, but loss of fat reserves does not usually impair function. In contrast, there are no true protein reserves in the body. In response to starvation or stress, structural tissues such as skeletal muscle and even the gut are broken down (catabolism) to liberate amino acids for the generation of glucose precursors and results in functional impairmentthat can impede recovery. The key elements of nutritional assessment include current food intake, levels of energy and protein reserves, and the patients' likely clinical course. Patients who have not had an adequate dietary intake for 5 days or more require nutritional support, and those with symptoms such as anorexia, nausea, vomiting or early satiety are at risk of a reduced food intake and hence undernutrition. Energy reserves are most easily assessed by examining for loss of subcutaneous fat (skinfolds); whereas protein depletion is most commonly manifest as skeletal muscle wasting (Fig. 3.3). A history of weight loss of more than 10-15% is highly significant, because this level of nutritional depletion is associated with impaired outcome of treatment. Patients can also be assessed according to their body mass index (BMI), which is calculated as weight (in kg) divided by height (in m2 ). Normal BMI is between 18.5 and 24.9 kg/m2 . A BMI of less than 18 suggests significant protein-calorie undernutrition. Finally, it is important to recognise that in assessing the nutritional status of patients, knowledge of their likely clinical course is vital (Fig. 3.4). For example, if patients are well nourished,they should be ableto withstandthe brief period of reduced food intake associated with major surgery. However, if patients are already severely malnourished (e.g., weight loss of 15%, BMI 17), then even a short period of starvation or catabolism may result in further life-threatening nutritional depletion. Taken together, a patient's food intake, level of reserve and likely clinical course should indicate the need for nutritional support and these assessments should form part ofthe routine daily appraisal of every patient during a surgical ward round.

What is the peak incidence of appendicitis: A. 0-10 y.o. B. 10-30 y.o. C. Newborn up to 1 y.o. D. 30-60 y.o. E. The same prevalence in every age group.

B.10-30 y.o. מהספר- In the UK, appendicitis is the most common cause of acute abdominal pain requiring surgery, and it has been estimated that 16% of the population of developed countries will undergo appendicectomy for presumed appendicitis during their lifetime. There has been a decline in the incidence of appendicitis over the last 20 years for unknown reasons. There is an equal incidence in males and females. Appendicitis is uncommon in patients below the age of 2 and above the age of 65, and is most common in the under 40s, with a peak incidence between 8 and 14 years of age. There is a geographical variation in the incidence, being rare in Asia and Central Africa, which is thought to be due to environmental factors. In Western countries, it is seen more frequently in cities than in rural areas

Choose radiolucent stone types (not visible on a plain X-ray film): 1-calciumoxalate II-uricacid III-xanthine IV-magnesium ammonium phosphate A.II,IV B.II,III C.I,II,III D.II,III,IV E.I,II,III,IV

B.II,III מהספר- Radiolucent calculi Uric acid, xanthine, indinavir, triamterene and matrix calculi are the common radiolucent varieties, and are not visualised on a plain film. A noncontrast CT KUB is the modality of choice for these, except indinavir calculi, which appear radiolucent even on a noncontrast CT. מצורפת טבלה מפורטת מאמבוס מידע להרחבה על הנושא הזה מאמבוס- Nephrolithiasis (Urolithiasis) Nephrolithiasis encompasses the formation of all types of urinary calculi in the kidney, which may be deposited along the entire urogenital tract, from the renal pelvis to the urethra. Risk factors include low fluid intake and high-sodium, high-purine, low-potassium diets, which can raise the calcium, uric acid, and oxalate levels in the urine and thereby promote stone formation. Urinary stones are most commonly composed of calcium oxalate. Less common stones are composed of uric acid, struvite (due to infection with urease-producing bacteria), calcium phosphate, or cystine. Nephrolithiasis manifests as sudden-onset colicky flank pain that may radiate to the groin, testes, or labia, commonly called renal or ureteric colic, and it is usually associated with hematuria. Diagnostics include spiral CT without contrast and/or ultrasound of the abdomen and pelvis to detect the stone, as well as urinalysis to assess for concomitant urinary tract infection (UTI) and serum BUN and creatinine to evaluate kidney function. Small stones that do not require urgent urological intervention can be managed with symptomatic treatment and a trial of medical expulsive therapy to promote spontaneous passage. If spontaneous passage appears unlikely or fails because of the size or location of the stone, first-line urological interventions include shock wave lithotripsy, ureterorenoscopy, and, in patients with large kidney stones, percutaneous nephrolithotomy. The most important preventive measure is adequate hydration. In addition, the analysis of passed stones may provide information to guide dietary changes and/or medical therapy (e.g., thiazide diuretics, urine alkalinization) that can prevent future stone formation.

The basic method of treatment of bleeding from esophageal varices is: A.administration of antihemorhagie drugs (vitamin K) B.endoscopic rubber banding ligations (hemonhoid banding)or sclerotherapy C.tamponade with the Sengstaken and Blakemore probe D.transjugular intrahepatic portosystemic shunt(TIPS) E.surgery-esophageal transection and a removal of the spleen

B.endoscopic rubber banding ligations (hemonhoid banding) or sclerotherapy אמבוס- Esophageal varices are dilated collateral veins resulting from increased blood flow due to portal hypertension, often caused by cirrhosis. Nonbleeding varices are typically asymptomatic. Screening for varices with esophagogastroduodenoscopy (EGD) is recommended at the time of cirrhosis diagnosis. Management of nonbleeding esophageal varices focuses on the prevention of bleeding and involves regular surveillance and, in some cases, primary prophylaxis of bleeding using nonselective beta blockers or eradication of varices using endoscopic variceal ligation (EVL). Acute variceal hemorrhage is a potentially life-threatening condition. Patients present with clinical features of gastrointestinal bleeding, e.g., sudden hematemesis and melena, and, in some cases, hypovolemic shock. In addition to stabilizing the patient, management involves administration of vasoactive medication and antibiotic prophylaxis in combination with endoscopic treatment. If the hemorrhage persists, balloon tamponade of the bleeding and/or an emergent transjugular intrahepatic portosystemic shunt (TIPS) may be necessary. Secondary prophylaxis of variceal bleeding involves nonselective beta blockers, EVL, and/or TIPS placement. ספר- Priorities in the management of bleeding oesophageal varices Active resuscitation: • Ensure safe and protected airway • Group and cross-match blood • Establish IV infusion line(s) and resuscitate to haemoglobin of 8g/L • Monitor patient in appropriate high care environment with timely access to appropriately trained staff and interventional therapies • Commence antibiotic prophylaxis and pharmacological treatments to reduce portal pressures (somatostatin analogues or terlipressin) Assessment of coagulation status • Prothrombin time • Platelet count • Physiological coagulation screen • Correct coagulopathies with assistance of haematologist Urgent endoscopy- Control of bleeding: • Endoscopic banding or injection sclerotherapy • Tamponade (Minnesota tube) if bleeding uncontrolled • Pharmacological measures (e.g., vasopressin/octreotide) Treatment of hepatocellular decompensation- Treatment/prevention of portosystemic encephalopathy Prevention of further bleeding from varices • Endoscopic banding or injection sclerotherapy • Stapled oesophagogastric junction • Portosystemic shunting/transjugular intrahepatic portosystemic stent shunting (TIPSS) • Liver transplantation

Which statements about duodenal diverticula are true: 1. The duodenum is the second most common site for diverticulum formation in the gastrointestinal tract 2. The diverticula rarely develop before the age of 40 years 3. The diverticula are offen found at the point of entry of the common bile duct. 4. The diverticula are frequently discovered incidentally at endoscopy or on barium meal examination A. 1,2 B. 2,3,4 C. 1,2,3,4 D. 3,4 E. 1,3,4

C. 1,2,3,4 ספר גרסה 6- Duodenal diverticula The duodenum is the second most common site for diverticulum formation in the gastrointestinal tract. The diverticula rarely develop before the age of 40 years, and are often found at the point of entry of the common bile duct. They are frequently discovered incidentally at endoscopy or on barium meal examination, but can cause obstruction, bleeding and inflammation (diverticulitis). Symptomatic diverticula should be excised if it is certain that they are the cause of problems.

Choose correct answers. The surgical complications after liver transplantation are: 1.Portal vein thrombosis 2.Acute rejection 3.Inferior vena cava syndrome גם לזה יש עדויות אגב.. 4.Hepatic artery thrombosis 5.Cholecystitis A. 1,2,5. B. 1,3,5. C. 1,4. D. 1,4,5. E. 2 ,4

C. 1,4. ספר- Postoperative management and complications: • The patient is managed in an intensive care setting. Evidence of a functioning graft is based on the blood biochemistry of the recipient with falling blood lactate levels and return of clotting and blood glucose towards normal • Primary nonfunction can occur in approximately 2% of patients who require urgent transplantation • Re-exploration can be indicated, and there should be a low threshold for this • Vessel thrombosis, most commonly in the hepatic artery, can be detected on colour Doppler and confirmed by computed tomography angiography. Suspicion of this serious complication necessitates re-exploration and it is possible that the patient may need a second transplant • Rejection in the liver is much less common than with other organs for reasons which are not completely clear. Diagnosis of rejection is often made around day 7 with rising transaminases in the liver function tests. Biopsy may be performed to confirm the diagnosis and the rejection can be treated with daily boluses of methylprednisolone given over 3 days. It is rare, with modern immunosuppression, for acute rejection to cause complete failure of the graft.

The size of abdominal aortic aneurysm being an indication to surgical or endovascular treatment in 70 year old men is: A. 4 cm B. 7 cm C. 5.5 cm D. 6.5 cm E. 3 cm

C. 5.5 cm ספר Abdominal aortic aneurysm (AAA)- is a focal dilatation of the abdominal aorta to more than 1.5 times its normal diameter. AAAs are classified by location as either suprarenal or infrarenal aneurysms. Men of advanced age are at increased risk for their formation; smoking and hypertension are also major risk factors. AAAs are frequently asymptomatic and therefore detected incidentally. Symptomatic AAAs can manifest with lower back pain, a pulsatile abdominal mass, and a bruit on auscultation. Abdominal ultrasound is the best initial and confirmatory test to diagnose AAAs and determine their extent. Observation, close follow-up, and reduction of cardiovascular risk factors are indicated for small aneurysms, whereas pronounced (> 5.5 cm) or rapidly expanding aneurysms require surgery. Surgical treatment involves open resection of the aneurysm with graft placement or, increasingly, endovascular stent placement. The prognosis is markedly worse if dissection or aneurysm rupture occurs. AAA rupture typically presents with sudden onset of severe tearing back or abdominal pain, a painful pulsatile mass, and hypovolemic shock, and should be managed with emergent surgery. All men between 65 and 75 years of age with a history of smoking should be screened once with an ultrasound to exclude an AAA. See also thoracic aortic aneurysm for more information. משוחזר

What are the symptoms of duodenal obstruction A.Jelly-like stool B.Haemorghagic emesis C. Bilious vomits if distal to ampulla of Vater (which is more common type) D. A lot of Levels of fluids on x-ray E.Constipations

C. Bilious vomits if distal to ampulla of Vater (which is more common type) לחסימת מעיים יש הרבה תסמינים אבל זה תלוי איפה החסימה. אם יש חסימה מלאה מתחת לצינור שמוציא מרה לתוך הדואדנום אז המרה לא תוכל להמשיך במורד המעי ולכן יהיה הקאה שכוללת מרה וזה נקרא- Bilious vomits

Choose the right answer about cerebral perfusion pressure (CPP) and cerebral blood flow(CBF): A. CPP=MAP-ICP.optimal CBF-(40-60mmHg) B. CPP=ICP - MAP, optimal CBF = (60 -140 mmllg) C. CPP=MAP-ICP,eptimal CBF=(60-140 mmHg) D. CPP=ICP-MAP.optimal CBF=(40-60 mmHg) E. CPP = ICP - MAP, optimal CBF = (40 - 140mmHg)

C. CPP=MAP-ICP ,eptimal CBF=(60-140 mmHg) The consequence of changes in ICP can be understood in terms of the effect on cerebral perfusion pressure (CPP): CPP is the difference between mean arterial pressure (MAP; pushing blood into the brain) and ICP (effectively resisting blood flow into the brain) (CPP= MAP- ICP). So, if ICP increases, CPP will reduce unless the MAP increases. Simply speaking, a reduction in CPP will reduce CBF unless the heart rate increases. There is, however, also a system of vascular autoregulation to maintain optimal CBF (60-140 mmHg) over a range of CPP. For example, as MAP increases, the cerebral blood vessels vasoconstrict, reducing blood flow, and vice versa. Blood vessel diameter is also controlled by arteriolar carbon dioxide concentration (PaCO2); increased PaCO2 causes vasodilation and increased CBF. Other compounds, such as nitric oxide and endothelin, also regulate local CBF. These different physiological mechanisms work in parallel to compensate for initial changes in ICP. However, if there is a severe and sustained elevation of ICP the compensatory mechanisms become ineffective and cerebral perfusion may be focally or generally compromised, leading to cerebral ischaemia and infarction. The ability of blood vessels to autoregulate can also be impaired by brain injury itself. A CPP of >60 mmHg is generally required to sustain adequate cerebral perfusion, although children and young adults can tolerate lower levels.

In patients requiring nutritional support the standard estimation of energy and proteins is based on body weight. Estimated demand in adult female patient, weighing 50 kg would be: A.Energy-1000 kcal/'day,proteins-40g/day B. Energy-1300kcal/day,proteins-45g/day C. Energy-1500 kcal/day,proteins-50g/day D.Energy-1800 kcal/day,proteins-55g/day E.Energy-2000 kcal/day,proteins-60g/da

C. Energy-1500 kcal/day,proteins-50g/day ר- Assessment of nutritional status The main energy reserves are found in subcutaneous and intraabdominal fat depots, but loss of fat reserves does not usually impair function. In contrast, there are no true protein reserves in the body. In response to starvation or stress, structural tissues such as skeletal muscle and even the gut are broken down (catabolism) to liberate amino acids for the generation of glucose precursors and results in functional impairmentthat can impede recovery. The key elements of nutritional assessment include current food intake, levels of energy and protein reserves, and the patients' likely clinical course. Patients who have not had an adequate dietary intake for 5 days or more require nutritional support, and those with symptoms such as anorexia, nausea, vomiting or early satiety are at risk of a reduced food intake and hence undernutrition. Energy reserves are most easily assessed by examining for loss of subcutaneous fat (skinfolds); whereas protein depletion is most commonly manifest as skeletal muscle wasting (Fig. 3.3). A history of weight loss of more than 10-15% is highly significant, because this level of nutritional depletion is associated with impaired outcome of treatment. Patients can also be assessed according to their body mass index (BMI), which is calculated as weight (in kg) divided by height (in m2 ). Normal BMI is between 18.5 and 24.9 kg/m2 . A BMI of less than 18 suggests significant protein-calorie undernutrition. Finally, it is important to recognise that in assessing the nutritional status of patients, knowledge of their likely clinical course is vital (Fig. 3.4). For example, if patients are well nourished,they should be ableto withstandthe brief period of reduced food intake associated with major surgery. However, if patients are already severely malnourished (e.g., weight loss of 15%, BMI 17), then even a short period of starvation or catabolism may result in further life-threatening nutritional depletion. Taken together, a patient's food intake, level of reserve and likely clinical course should indicate the need for nutritional support and these assessments should form part ofthe routine daily appraisal of every patient during a surgical ward round. Assessment of nutritional requirements Energy and protein/nitrogen requirements vary, depending on weight, body composition, clinical status, level of physical activity and dietary intake. For most patients, an approximation based on weight and clinical status is sufficient. Few adult patients require more than 25-30 kcal/kg/day (approximately 1800-2200 kcal in an adult of average body mass; Table 3.1). Additional calories are unlikely to be used effectively and may even constitute a metabolic stress, leading to excessive activation of the sympathetic nervous system (diet induced thermogenesis), that may result in fever and difficulty weaning from mechanical ventilation as a consequence of the excessive carbon dioxide load. Particular caution should be exercised when 'refeeding' the chronically starved patient because of the dangers of potentially fatal cardiac dysrhythmias due to hypokalaemia and hypophosphataemia (refeeding syndrome). The most common method for assessing protein/nitrogen requirement is based on body weight (Table 3.1). Although more accurate assessment for patients receiving nutritional support can be derived from measurement of 24-hour urinary urea excretion, which can be converted to an estimate of 24-hour urinary nitrogen loss, this is seldom necessary in routine clinical practice. Enteral diets normally provide protein whereas parenteral nutrition delivers nitrogen (N) in the form of amino acids. The nitrogen equivalent of protein is calculated by multiplying protein content (in grams) by a conversion factor of 6.25. In practice, nitrogen requirements are usually estimated based upon predicted calorie intake and the level of metabolic stress. Most patients require 1 g N per 200 kcal of energy daily (typically 10 g N) in the absence of catabolism, but nitrogen requirements increase significantly with the catabolic response to stress and may rise to as much as 18-20 g N/day in critically ill or septic patients. Even if losses exceed this, more than 18 g N/day (equivalent to 112 g protein) is seldom given, however, because it is unlikely to be used effectively because protein is diverted to generate energy precursors associated with the stress response. It is thus impossible to prevent substantial loss of protein reserves and lean body mass in critically ill patients and the aim of meeting requirements under these circumstances is primarily to limit the losses resulting from catabolism. 50X1=50 50X25=1250

Necrolytic migratory erythema, weight loss, diabetes mellitus, stomatitis, diarrhea are characteristic clinical findings of: A. Insulinoma B. VIPoma C. Glucagonoma D.Somatostatinoma E.Gastrinoma

C. Glucagonoma אמבוס- Glucagonoma A rare neuroendocrine tumor of the pancreas that secretes glucagon. In >50% of cases, metastasis is present at diagnosis. Clinical findings include impaired glucose tolerance or diabetes mellitus, weight loss, necrolytic migratory erythema, chronic diarrhea, deep vein thrombosis, and depression. May be associated with multiple endocrine neoplasia type 1. ספר- Pancreatic neuroendocrine tumours (pNET): Pancreatic neuroendocrine tumours are rare tumours (approximately 1/100,000 population/year) of which 60% are nonfunctioning or secrete peptides with low biological impact such as PP or neurotensin. In contrast to insulinoma, the majority of which are benign, approximately 50% of gastrinomas and the majority of nonfunctioning pancreatic neuroendocrine tumours are malignant (Table 15.6). They are usually sporadic but they may also appear among other features of genetic syndromes like multiple endocrine neoplasia type I or von Hippel-Lindau disease. In multiple endocrine neoplasia (MEN1), pancreatic neuroendocrine tumours occur in 40-80% of patients and are mostly nonfunctioning tumours or gastrinomas. Pancreatic neuroendocrine tumours occur in 10-15% of patients with von Hippel-Lindau (VHL) and are frequently multiple (>30%). Functioning pNET : The functioning tumours and syndromes are named according to the hormones they produce: insulinoma, gastrinoma (most gastrinomas are found in the duodenum), VIPoma, glucagonoma and somatostatinoma. The first two (insulinomas and gastrinomas) are the most frequent functioning pancreatic tumours. Presentation of functional pNET is specific and related to the secretion of biologically active peptides like insulin, gastrin, glucagon, somatostatin and vasoactive intestinal polypeptide (VIP)

The Milan criteria for liver transplantation are: A. Single tumor ≤6 cm B. 3 tumors each ≤2cm C. Single tumor ≤5 cm D. Sum of the diameter of the tumors ≤8 cm E. Sum of the diameter of the tumors ≤7 cm

C. Single tumor ≤5 cm אמבוס- Liver transplantation: Indications: -Early stage HCC with significant concomitant liver disease - AND tumor(s) meet Milan criteria (a set of criteria used to assess HCC patients for transplant) **1 tumor measuring ≥ 2 cm and ≤ 5 cm **OR 2-3 tumors measuring ≥ 1 cm and ≤ 3 cm Bridge to transplant: Consider using ablative therapy or locoregional therapy to prevent tumor progression beyond the Milan criteria. Recurrence risk : 11-18%; most commonly extrahepatic Monitor with abdominal and chest CT (surveillance frequency and benefit is uncertain). ספר- Primary malignant tumours of the liver -Hepatocellular carcinoma (hepatoma): The disease is usually advanced at presentation and the 5-year survival rate is less than 10%. Liver transplantation has been used in the treatment of this tumour, but the best results have been reported in cirrhotic patients in whom an incidental hepatoma has been found on examination of the resected specimen following the transplant. If transplantation is not otherwise contraindicated, eligibility criteria have been extended for cirrhotic patients. Traditionally the 'Milan' criteria (single tumour of 5 cm or less in diameter, or with no more than three tumour nodules each one 3 cm or less in size) were employed but these have now been extended in several countries. Transplantation is normally contraindicated if there has been tumour rupture or AFP exceeds 1000 iu/mL

The superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus (so-called Cullen's sign) is a symptom of: A.perforation of the dodenal ulcer B. embolism of the superior mesenteric artery C. acute pancreatitis D.small intestine inflammation(Crohn's disease) E.appendicitis

C. acute pancreatitis- אמבוס- Cullen sign- A physical examination characterized by periumbilical ecchymosis and bluish-red discoloration. Can be seen in any disease that causes retroperitoneal hemorrhage (e.g., ruptured abdominal aortic aneurysm). Classically associated with pancreatitis. הרחבה- Acute pancreatitis- is an inflammatory condition of the pancreas most commonly caused by gallstones and alcohol use. The typical manifestation includes sudden, severe epigastric pain that radiates to the back, nausea and vomiting, and epigastric tenderness on palpation. Elevation of serum lipase or amylase ≥ 3× ULN and/or characteristic findings of acute pancreatitis on cross-sectional imaging (e.g., contrast-enhanced CT abdomen) confirm the diagnosis. Clinical scores (e.g., Ranson criteria, APACHE II) are used to predict the severity and prognosis of pancreatitis. Initial management is primarily supportive and includes fluid resuscitation, analgesia, antiemetics, and early enteral nutrition as tolerated. The underlying cause should be identified and managed to prevent recurrence (e.g., cholecystectomy for biliary pancreatitis, long-term lipid-lowering therapy for hypertriglyceridemia-induced pancreatitis). Localized complications of pancreatitis include necrosis (necrotizing pancreatitis), which may become infected, pancreatic pseudocysts, and walled-off necrosis. Systemic complications include sepsis, ARDS, organ failure, and shock. Complications of pancreatitis are associated with significant morbidity and mortality. ספר- Specific clinical signs in acute abdominal pain: 1. Murphy's sign - In acute cholecystitis, a deep breath taken by the patient elicits acute pain when the examiner presses downwards into the right upper quadrant. This is caused by the movement of the inflamed gallbladder striking the examining hand. 2. Boas's sign- In acute cholecystitis, pain radiates to the tip of the scapula and there is a tender area of skin just below the scapula, which is hyperaesthetic. 3. Grey Turner's and Cullen's signs- In patients with severe acute pancreatitis, bruising and discoloration may be seen around the umbilicus (Cullen's sign) and in the left flank (Grey Turner's sign). Cullen's sign was actually first described in relation to ruptured ectopic pregnancy, but is now often also associated with acute pancreatitis. 4. Rovsing's sign- In acute appendicitis, palpation in the left iliac fossa produces pain in the right iliac fossa.

70 year old patient with chronic circulatory and respiratory insufficiency after 2 heart infarctions with 7 cm asymptomatic subrenal aortic aneurysm should be treated: A. with the surgery and aortic vascular prosthesis placement as the aneurysm size is significant B. conservatively with lipid lowering therapy, smoking cessation and hypertension control C. optimally with aortic stent-graft placement(if anatomically suitable) D. conservatively with aspirin, smoking cessation,statins and hypertension control E.conservatively aspirin, smoking cessation, statins,hypertension control and anti-inflammatory treatmemt

C. optimally with aortic stent-graft placement (if anatomically suitable) Abdominal aortic aneurysm (AAA)- is a focal dilatation of the abdominal aorta to more than 1.5 times its normal diameter. AAAs are classified by location as either suprarenal or infrarenal aneurysms. Men of advanced age are at increased risk for their formation; smoking and hypertension are also major risk factors. AAAs are frequently asymptomatic and therefore detected incidentally. Symptomatic AAAs can manifest with lower back pain, a pulsatile abdominal mass, and a bruit on auscultation. Abdominal ultrasound is the best initial and confirmatory test to diagnose AAAs and determine their extent. Observation, close follow-up, and reduction of cardiovascular risk factors are indicated for small aneurysms, whereas pronounced (> 5.5 cm) or rapidly expanding aneurysms require surgery. Surgical treatment involves open resection of the aneurysm with graft placement or, increasingly, endovascular stent placement. The prognosis is markedly worse if dissection or aneurysm rupture occurs. AAA rupture typically presents with sudden onset of severe tearing back or abdominal pain, a painful pulsatile mass, and hypovolemic shock, and should be managed with emergent surgery. All men between 65 and 75 years of age with a history of smoking should be screened once with an ultrasound to exclude an AAA. See also thoracic aortic aneurysm for more information. Approach: Patients with any symptoms- immediate vascular surgery consult Suspected or known rupture (regardless of patient stability) : emergency repair within 90 minutes Patients with signs or symptoms of impending rupture : urgent aneurysm repair, ideally within normal working hours, as this is associated with better outcomes Maintain BP strictly within normal parameters. Consult anesthesia. Asymptomatic patients: elective aneurysm repair or aneurysm surveillance All patients: reduction of cardiovascular risk factors Appropriate medical management of other atherosclerotic risk factors (e.g., hypertension, diabetes, hyperlipidemia) Smoking cessation Elective repair: Fusiform aneurysm with maximum diameter ≥ 5.5 cm and low or acceptable surgical risk Small fusiform aneurysm expanding ≥ 1 cm per year Saccular aneurysm Aneurysm with maximum diameter 5.0-5.4 cm in women Small aneurysm (4.0-5.4 cm) in patients requiring chemotherapy, radiotherapy, solid organ transplantation: individual approach Procedures: 1. Endovascular aneurysm repair (EVAR)- Indications: minimally invasive procedure that is preferred over open surgical repair for most aneurysms, especially in patients with a high operative risk Procedure: Under fluoroscopic guidance, an expandable stent graft is placed via the femoral or iliac arteries intraluminally at the site of the aneurysm. 2. Open surgical repair (OSR)- Indications: Mycotic aneurysm or infected graft Persistent endoleak and aneurysm sac growth following EVAR Anatomical contraindications for EVAR Procedure: A laparotomy is performed and the dilated segment of the aorta is replaced with a tube graft or Y-prosthesis (bifurcated synthetic stent graft). משוחזר

Critical leg ischemia is the term referring to: A. very severe acute leg ischemia with high risk of amputation B. the presence of limb necrosis in chronic leg ischemia patients C. rest pain longer than 2 weeks or necrosis presence in the patients with chronic leg ischemia D. the presence of the rest pain related to the chronic leg ischemia E. the presence of acute or chronic leg ischemia related to the acute and chronic leg ischemia

C. rest pain longer than 2 weeks or necrosis presence in the patients with chronic leg ischemia אמבוס Acute limb ischemia (ALI): Acute limb ischemia (ALI) is a vascular emergency in which the arterial blood supply to one or more extremities is critically reduced. Arterial thrombosis and cardiac emboli are responsible for the majority of cases. The typical signs and symptoms of ALI include pain, pallor, pulselessness, poikilothermia, paralysis, and paresthesia of the limb distal to the site of vascular occlusion (the 6 Ps). Diagnosis relies on examination and arterial Doppler studies. Clinical findings in combination with Doppler studies are then used to categorize the limb as viable, threatened, or nonviable. Further imaging studies, e.g., digital subtraction angiography, should only be performed if they do not result in treatment delays. Management of viable and threatened limb ischemia begins with intravenous heparin followed by revascularization. Irreversible limb ischemia will inevitably progress to gangrene and requires amputation of the nonviable parts of the limb. Whether long-term anticoagulation and/or further diagnostic studies are required depends on the suspected etiology (e.g., echocardiography in suspected left atrial thrombus formation). אפ טו דייט- Chronic limb-threatening ischemia — is a clinical syndrome defined by the presence of PAD (peripheral artery disease) in combination with rest pain, gangrene, or a lower limb ulceration >2 weeks duration. CLTI is the preferred term replacing the terms critical limb ischemia (CLI) or severe limb ischemia.

40 year old patient admitted to the hospital with aortic dissection, back pain and pressure 200/100 mm Hg should be treated initially with: A.Angiotensin-converting enzyme inhibitors - like captopril B.diuretics(i.v.) C. selective beta blockers(i-v.) D. aortic stent graft placement E. calcium chanel blockers(i.v.)

C. selective beta blockers(i-v.) אמבוס- Approach: Stanford A dissection: immediate surgery. Stanford B dissection: treat conservatively (watchful waiting and ongoing medical therapy) unless complications occur. Blood pressure control: essential in all patients to prevent progression of the dissection Supportive care Medical therapy for Hypertensive patients: Control hypertension and heart rate: target SBP 100-120 mm Hg and HR ≤ 60 beats per minute. Start with an IV beta blocker: to avoid reflex tachycardia. like: Esmolol or Labetalol. Followed by vasodilator (e.g., IV sodium nitroprusside) Contraindications to beta blockers: Start a calcium channel blocker. like Verapamil or Diltiazem Patients with dissection of the descending aorta who remain stable on IV treatment can be transitioned to oral medications and discharged with outpatient imaging surveillance. סטאפ1- Aortic dissection: Longitudinal intimal tear forming a false lumen. Associated with hypertension, bicuspid aortic valve, inherited connective tissue disorders (eg, Marfan syndrome). Can present with tearing, sudden-onset chest pain radiating to the back +/− markedly unequal BP in arms. CXR can show mediastinal widening. Can result in organ ischemia, aortic rupture, death. Stanford type A (proximal): involves Ascending aorta. May extend to aortic arch or descending aorta. May result in acute aortic regurgitation or cardiac tamponade. Treatment: surgery. Stanford type B (distal): involves only descending aorta (Below left subclavian artery). Treatment: β-blockers, then vasodilators.

The patients with pulmonary embolism (PE) at high risk of death needs the aggressive thrombolytic treatment. This situation concerns PE patients with: A. dyspnoe and chest pain B. dyspnoe,chest pain,tachycardia C. shock or hypotension D. shock or hypertension E. shock or ventricular fibrillation

C. shock or hypotension אמבוס- Features of massive PE: (e.g., due to a saddle thrombus): Presyncope or syncope Jugular venous distension and Kussmaul sign Hypotension and obstructive shock Circulatory collapse בנוסף לזכור שיש אמבוליזם בריאות שהוא מסיבי אז זה יכול להוביל לכשל לבבי ימיני ויהיה סימפטומים של כשל לבבי ימני כמו בצקות בגוף וכו'. לגבי הסעיף הזה- B. dyspnoe,chest pain,tachycardia זה נכון בכללי לפולמונרי אמבוליזם, אבל בשאלה נשמע שלבן אדם יש אמבוליזם מסיבי. Common features of PE: Acute onset of symptoms Dyspnea (> 75% of cases) Tachycardia and tachypnea (up to 50% of cases) Sudden pleuritic chest pain (∼ 20% of cases) Cough and hemoptysis Associated features of DVT: e.g., unilaterally painful leg swelling משוחזר

Most of the femoral head atricular surface is involved in load transfer, but damage to this surface will never lead to the development of posttraumatic arthritis. Mark the correct answear. A. both statements are true and causally related B. both statements are true but not causally related C. the first statement is true and second is false D. the first statement is false and second is true E. both statements are false

C. the first statement is true and second is false Osteoarthritis (OA) of a joint may occur as a primary idiopathic condition or secondary to problems such as malalignment, intra-articular fractures or over-stressing (obesity, overuse). In some patients, there is a strong genetic component. OA may occur in any joint (shoulder, elbow, wrist and hands) but predominantly affects those that are weight-bearing (hip and knee). Idiopathic OA is generally of slow onset and affects the elderly. Secondary OA can affect the young and may develop quite rapidly when a joint injury leads to loss of articular cartilage. On plain x-ray , OA is associated with: • Joint space loss due to thinning of articular cartilage • Sclerosis of the joint surface, with the development of increased density of the bone just under the joint space • Osteophytes • Cystic change.

Possible causes of acute abdominal pain are: I. Hypercalcaemia 2. Meckel's diverticulitis 3. Myocardial ischaemia A.1 B.1,2 C.1,2,3 D.2,3 E. 2

C.1,2,3

Hiatus hernias are often asymptomatic, but can produce some of or all the following symptoms: 1.Palpitations and hiccups 2.Oesophagitis 3.Epigastric and lower chest pain 4.Heartburn and regurgitation A.1,3,4 B.2,3 C.1,2,3,4 D.1 E.1,2,3

C.1,2,3,4 אמבוס- Hiatal hernia: A hiatal (or hiatus) hernia is the abnormal protrusion of any abdominal structure/organ, most often a portion of the stomach, into the thoracic cavity through a lax diaphragmatic esophageal hiatus. It may be congenital or secondary to aging, obesity, and/or smoking. There are four types of hiatal hernia: sliding, paraesophageal, mixed, and complex. Sliding hiatal hernias, where the gastroesophageal junction (GEJ) and the gastric cardia migrate into the thorax, account for 95% of hiatal hernias. In paraesophageal hernias (PEH), only the gastric fundus herniates into the thorax, whereas in mixed hiatal hernias, the GEJ as well as the gastric fundus herniate. Complex hiatal hernias are rare and characterized by protrusion of any abdominal organ other than the stomach. Nearly half of all patients with hiatal hernia are asymptomatic and require no medical or surgical intervention. Symptomatic patients with sliding hiatal hernia present with features of gastroesophageal reflux disease (GERD), which are usually managed with lifestyle modification and proton pump inhibitors. Patients with PEH or mixed hiatal hernias typically present with intermittent dysphagia, substernal discomfort, or abdominal pain, and in rare cases present acutely with gastric volvulus and strangulation. All symptomatic PEH, mixed, and complex hiatal hernias require operative intervention to avoid life-threatening complications. ספר- Hiatus hernia A hiatus hernia is an abnormal protrusion of the stomach through the oesophageal diaphragmatic hiatus into the thorax and may be sliding (90%) or rolling (10%). A sliding hernia occurs when the stomach slides through the diaphragmatic hiatus, so that the gastrooesophageal junction lies within the chest cavity. It is covered anteriorly by peritoneum, and posteriorly is extraperitoneal. A rolling or paraoesophageal hernia is formed when the stomach rolls up anteriorly through the hiatus; the cardia remains in its normal position and therefore the cardiooesophageal sphincter remains intact. Rolling and sliding hernias are caused by weakness of the muscles around the hiatus. They tend to occur in middle-aged and elderly patients. Women are affected more frequently than men and there is a higher incidence in the obese. Clinical features: Hiatus hernias are often asymptomatic, but can produce some of or all the following symptoms: • Heartburn and regurgitation owing to an incompetent lower oesophageal sphincter, which is aggravated by stooping and lying flat at night, and can be relieved by antacids. • Oesophagitis resulting from persistent acid reflux, which leads to ulceration, bleeding with anaemia, fibrosis and stricture formation. • Epigastric and lower chest pain, especially in paraoesophageal hernias, as the herniated part of the stomach (usually the fundus) becomes trapped in the hiatus. This can be a surgical emergency owing to the obstruction and strangulation of the stomach. • Palpitations and hiccups, symptoms caused by the mass effect of the hernia in the thoracic cavity irritating the pericardium and the diaphragm. In patients with a large rolling hiatus hernia, displacement of the whole stomach may result in a volvulus into the chest, producing symptoms of vomiting from gastric outflow obstruction Management: Treatment is as for GORD, although patients with obstructive symptoms such as vomiting and regurgitation or breathlessness due to reduced lung capacity should be considered for surgical repair. Patients who present as an emergency with an obstructed hiatus hernia should have it decompressed with a nasogastric tube or endoscopically to prevent strangulation. Emergency surgery is occasionally necessary except if conservative therapy fails or gastric necrosis is suspected. Even large hiatus hernias can be repaired laparoscopically although the risk of conversion to open surgery is higher.

Which of these statements incorrectly describes the hernias in the inguinal region? A. The most common type of inguinal hernia is indirect inguinal hernia. B. A femoral hernia occurs more often in females. C.Direct inguinal hernia enters the inguinal canal through the deep inguinal ring. D. The most common type of surgical hernia repair is the Lichtenstein open tension-free procedure. E. The posterior wall of the inguinal canal is formed by transversalis fascia.

C.Direct inguinal hernia enters the inguinal canal through the deep inguinal ring. אמבוס- inguinal hernia An inguinal hernia is an abnormal protrusion of intraabdominal contents (most commonly fat) through the inguinal canal. Inguinal hernias are the most common type of groin hernia, and can be further subdivided based on anatomic location: an indirect inguinal hernia protrudes lateral to the inferior epigastric vessels through the deep inguinal ring, whereas a direct inguinal hernia protrudes medial to the inferior epigastric vessels through a defect in the posterior wall of the inguinal canal. An uncomplicated inguinal hernia typically manifests as a mass in the groin with or without pain (inguinodynia). Incarceration, obstruction, and strangulation of hernial contents are collectively referred to as complicated inguinal hernia. Inguinal hernia is a clinical diagnosis. Imaging, preferably with ultrasound, is indicated if the clinical diagnosis is uncertain. Surgery is the only definitive management of inguinal hernia and can be performed as an open surgery or laparoscopically. A strangulated inguinal hernia is a surgical emergency. In patients with an incarcerated hernia with or without bowel obstruction, manual reduction of the hernia may be considered as a temporizing measure before surgery. Conservative management may be considered in select patients with a small, uncomplicated inguinal hernia. Direct inguinal hernia: protrusion of abdominal and/or pelvic contents directly through the posterior wall of the inguinal canal Indirect inguinal hernia: protrusion of abdominal and/or pelvic contents into the inguinal canal through the deep inguinal ring Uncomplicated inguinal hernia: an inguinal hernia that is completely reducible and not associated with signs of bowel obstruction or strangulation Complicated inguinal hernia: an inguinal hernia that is either irreducible (incarcerated) or associated with mechanical bowel obstruction and/or strangulation Occult inguinal hernia: an inguinal hernia that is not identifiable on physical examination ספר- Groin hernias account for three-quarters of all abdominal wall hernias, and inguinal herniorrhaphy is one of the most frequently performed general surgical procedures. The most common types of groin hernia are indirect inguinal (60%), direct inguinal (25%) and femoral (15%). Most (85%) groin hernias occur in males. Inguinal hernias occur in 1-3% of all newborn males, and in early life an indirect inguinal hernia is by far the most common. After middle age, weakness of the abdominal musculature eads to an increasing incidence of direct inguinal hernias. Femoral hernias are relatively more common in females (possibly because of stretching of ligaments and widening of the femoral ring in pregnancy), but an indirect inguinal hernia is still the most common type of groin hernia in women. Summary- Groin hernias: • Indirect inguinal hernias comprise 60% of all groin hernias and commence at the deep inguinal ring, lateral to the inferior epigastric vessels • Direct inguinal hernias account for 25% of all groin hernias and bulge through a weakness in the back wall of the inguinal canal, medial to the inferior epigastric vessels. They rarely obstruct or strangulate • Indirect inguinal hernias may pass down within the coverings of the spermatic cord to the scrotum; direct hernias do not descend into the scrotum • Asymptomatic inguinal hernias do not have to be repaired, especially in the elderly • Femoral hernias account for 15% of all groin hernias and pass through the femoral canal, emerging below and lateral to the pubic tubercle (in contrast to inguinal hernias, which pass medially to the tubercle and may descend to the scrotum) • Femoral hernias are often small and easy to miss on clinical examination, but are prone to obstruct and strangulate

.Which of the following groups are not that could impair wound healing? A. Obesity, malnutrition and age. B. Impaired oxygenation,radiation and smoking. C.Height,weight and race. D. Drugs,diabetes mellitus and wound stress. E. Senility

C.Height,weight and race. Principles of wound healing: The essential features of wound healing are common to almost all soft tissues and result in the formation of a scar. 'Primary healing' is achieved when the wound edges are approximated shortly after injury. Epithelial cover is quickly achieved and healing produces a relatively fine scar. 'Delayed primary' healing refers to sharp debridement and direct closure of an old wound, whereas 'secondary healing' occurs when a wound is left to heal spontaneously usually resulting in excessive fibrosis and an unsightly scar. Conceptually, there are three phases of wound healing mediated by several growth factors including fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), epidermal growth factor (EGF) and transforming growth factor beta (TGF-β) Classification of wound healing: • Healing by primary intent is most efficient and rapid resulting in minimal scarring. It is achieved through early debridement and direct closure of a wound • Healing by secondary intent occurs when a wound is left open Healing is delayed and often results in hypertrophic scarring and contracture • Delayed primary healing occurs when an old wound is debrided and closed. The wound will heal more rapidly and with better scarring. Principles of management of contaminated traumatic wounds: • Contaminated wounds should be debrided under general anaesthesia: the margins must be cleansed or sharply excised, and grit, soil and foreign bodies removed. Devitalised tissue is formally excised until viable bleeding tissue is encountered • Primary closure is best avoided if there has been gross contamination or when treatment has been delayed for many hours. In such circumstances, attempts at primary closure increase the risk of wound infection, especially with anaerobes • Wounds may be suitable for delayed primary closure after 24-48 hours or later • Appropriate protection against tetanus and the use of antibiotic prophylaxis should be considered.

The most common primary tumors responsible for brain metastasis are: A.Pancreatic,Kidncy,Bone B.Pancreatic,Liver,Ovary C.Lung,Breast,Kidney D.Colon,Liver,Urinary Bladder E.Liver,Bone,Ovary

C.Lung,Breast,Kidney Brain metastasis: Metastatic tumours are present at postmortem in 20% of patients dying of cancer, and in 50% they are multiple. The most common primary lesions are lung, breast, kidney, melanoma and colon. Brain metastases may be the presenting feature or appear only late in the course of a previously diagnosed primary cancer. Prostate cancer classically spreads to the cranium rather than the brain parenchyma. Gliomas rarely spread beyond the CNS

What is important in diagnosis of imperforate anus A.CT of the abdomen and anal region B.NMR of the abdomen and anal region C.Physical examination,x-ray,perineal US D.Prenatal diagnosis E.CT of perineal region

C.Physical examination,x-ray,perineal US Anorectal malformation (anal atresia) Definition: sporadically occurring malformation of the rectum with absent anal opening Etiology: associated with a number of conditions Mesodermal defects (e.g., VACTERL association) Down syndrome Maternal diabetes Other malformations (e.g., vaginal or uterine anomalies, renal anomalies, spinal cord or cardiovascular malformations) Pathophysiology: failure of the urorectal septum to descend caudally to the cloacal membrane Clinical features: Absence of anal opening Thin anal membrane in place of anal opening through which meconium is visible Obstipation, ileus Fistulas that complicate defecation (e.g., rectovestibular, rectourethral, rectovaginal) Small or missing anal dimple In some cases, bucket-handle malformation Flat bottom (absent or poorly developed midline groove between buttocks) Diagnostics: Clinical diagnosis- Lateral pelvic radiography or invertogram to determine position of the rectal pouch Investigation of additional malformations (e.g., spinal ultrasonography, sacral x-ray) Fistula screening Examination of the genital area and the urethra (e.g., abdominal ultrasound) Urinalysis: meconium detectable in case of a rectourinary fistula Augmented-pressure distal colostography to assess for fistulas Treatment: IV hydration, no oral feedingAnal reconstructive surgery (primary anoplasty) or temporary colostomy in more complex malformations

What is the best treatment option for congenital diaphragmatic hernia: A.Just surgery-immediately after birth B.Surgery-it's not important the time of performing the procedure,but the best and now only option is closing the diaphragmatic defect via laparoscopy C.Stabilization of the respiratory-circulatory system and when patient is stable surgery D.Every child should be put on (Extra Corporeal Membrane Oxygenation) ECMO and then proceed the surgery E Nowadays every child should have prenatal surgical correction of the defect-procedure called FETO(Fetoscopie endoluminal tracheal occlusion).

C.Stabilization of the respiratory-circulatory system and when patient is stable surgery Congenital diaphragmatic hernias (CDH): A diaphragmatic hernia is the protrusion of intra-abdominal contents through an abnormal opening in the diaphragm. Congenital diaphragmatic hernias (CDH) are a common developmental defect, resulting from an incomplete fusion of embryonic components of the diaphragm. Bochdalek hernias= Left-sided postero-lateral diaphragmatic defects are the most common Morgagni hernias= anterior defects. About 50% of babies with CDH have additional congenital malformations. CDH are often diagnosed prenatally on routine antenatal ultrasound. Neonates with CDH present postnatally with respiratory distress and a characteristic absence of breath sounds in the ipsilateral chest. The respiratory distress is due to severe pulmonary hypoplasia, persistent pulmonary hypertension of the newborn (PPHN), and poor surfactant production, all of which are typical characteristics of CDH. Postnatal diagnosis is confirmed on a chest x-ray which reveals abdominal contents in the thorax. Neonates with CDH should be medically stabilized (mechanical ventilation, inotropic support, gastric decompression) before surgical repair, which is then done within the first week of life. Surgical repair (thoracotomy or laparotomy)- Indicated in all cases of CDH Timing: after the infant is stabilized, often after 24-48 hours Procedure: reduction of the hernial contents and primary closure of the defect פסילת תשובות: A.Just surgery-immediately after birth- חייב לייצב קודם B.Surgery-it's not important the time of performing the procedure,but the best and now only option is closing the diaphragmatic defect via laparoscopy- thoracotomy or laparotomy D.Every child should be put on (Extra Corporeal Membrane Oxygenation) ECMO and then proceed the surgery - Intubation and mechanical ventilation- indicated in all infants with CDH ?? E. Nowadays every child should have prenatal surgical correction of the defect-procedure called FETO (Fetoscopie endoluminal tracheal occlusion).- surgical procedure to treat the most severe cases of congenital diaphragmatic hernia (CDH) that are diagnosed in utero

Severity of cirrhosis of the liver Is best described using: A. The Glasgow Prognostic Score B. The Gleeson score C. The Child-Pugh score D. APACHE II score E. The Glasgow Coma Score

C.The Child-Pugh score ספר- Variceal bleeding in cirrhosis: assessment and prophylaxis 'Severity of cirrhosis is best assessed by Child Pugh score. Risk of varices increases with Child Pugh score. Assessment of varices is best done by endoscopy and should be performed for all patients with cirrhosis. Varices should be graded by size (5 mm). For patients with large varices (>5 mm) or small varices and high risk stigmata of bleeding or severe liver disease prophylactic non selective β-blockers should be prescribed. Endoscopic variceal ligation (EVL) can also be used for high risk patients as an alternative to β-blockers. The two treatments have different side effect profiles that should be considered.' אמבוס- Child-Pugh score: A prognostic grading scale for cirrhosis. Scored on the basis of bilirubin, albumin, prothrombin time, and degree of ascites and encephalopathy. Graded A (mild), B (moderate), and C (severe). A prognostic grading scale that assesses survival rate and predicts the likelihood of developing complications based on bilirubin and albumin levels, prothrombin time, and the presence of ascites and encephalopathy Can be used as a prognostic scoring system Child‑Pugh class A: one-year survival rate of ∼ 100% Child‑Pugh class B: one-year survival rate of ∼ 80% Child‑Pugh class C: one-year survival rate of ∼ 45%

What is the most common cause of mortality and morbidity following aneurysm rupture A. Infection B. Thrombosis C. Cushing's ulcer D. Rebleeding E.Cardiac infarction

D. Rebleeding Management of aneurysmal SAH (Subarachnoid hemorrhage): The medical management of SAH includes intravenous fluids, the calcium antagonist nimodipine, analgesia and antiemetics. Patients in coma will usually be intubated and managed in a neurointensive care unit. Clinical deterioration may occur because of rebleeding, vasospasm, hydrocephalus, seizures, metabolic abnormalities and infections. Rebleeding is a major cause of morbidity and mortality following aneurysm rupture. Rebleeding rates are maximum in the first 24 hours and subsequently fall off over the next few weeks, reaching a rate of 4% per annum. Thus, the initial focus of treatment is to prevent rebleeding. Until recently, standard management was occlusion of the aneurysm from the cerebral circulation by surgically clipping its neck. However, it is now standard to place detachable coils within the aneurysm via a catheter passed from the femoral artery into the cerebral circulation. The coils unwind in the aneurysm and induce thrombosis. Coiling is a less invasive procedure than open surgery, and a prospective RCT demonstrated that when an aneurysm can be treated by surgery or coiling, the latter is safer. Improvements in coil, stent and basket technology mean most aneurysms can now be coiled.

What are the most common primary brain tumors: A.Piruitary adenomas B.Metastatic tumors C.Schwannomas D.Gliomas E. Symptomatic meningiomas

D. Gliomas Gliomas: Gliomas are the most common (60%) primary intracranial tumour presenting clinically. They are named because the constituent cells resemble the brain's supporting cells known as glia and are thought to arise from cells with stem-like characteristics, so-called glioma stem-like cells. Gliomas include glioblastoma, astrocytoma, oligodendroglioma and ependymoma. Tumour cells infiltrate among normal brain cells and are graded using a WHO four-point scale based on features such as vascular endothelial proliferation, nuclear pleomorphism and mitotic rate. Grade I tumours (e.g., pilocytic astrocytoma, dysembryoplastic neuroepithelial, ganglioglioma) are on the borderline between hamartomas and extremely low-grade tumours. They are often cured by surgery. Grade II tumours (astrocytoma, oligodendroglioma and ependymoma) have variable intrinsic malignancy and survival periods are usually long (median 8.5 years after surgery, radiotherapy and chemotherapy). Often transform into higher grade lesions. Grade III tumours are anaplastic (e.g., anaplastic astrocytoma, anaplastic oligodendroglioma) and frequently have median survival periods of approximately 3 years after multimodality treatment. As with grade II tumours, oligodendrogliomas tend to be more responsive to therapies than astrocytomas. Grade IV tumours are highly malignant and comprise glioblastoma and gliosarcomas. Despite surgery, adjuvant radiotherapy and chemotherapy, median survival for patients with a glioblastoma is 14 months. Younger age and better function predict improved outcome.

Serum alpha fetoprotein (AFP) is the most widely used tumor marker in detecting patients with: A. Biliary cystadenoma B. Angiosarcoma C. Adenomyomatosis D. Hepatocellular carcinoma E. Ductal adenocarcinoma of the pancreas

D. Hepatocellular carcinoma אמבוס- Alpha feto protein- marker that associated with: Hepatocellular carcinoma (HCC) Hepatoblastoma Yolk sac tumor (endodermal sinus tumor) Mixed germ cell tumor Ataxia-telangiectasia AFP is normally produced by the fetus → transient elevation of maternal AFP levels ↑ AFP: abdominal wall defects, neural tube defects ↓ AFP: associated with trisomy 21, 18, and 13 (see prenatal diagnostics for details) ספר- Primary malignant tumours of the liver - Hepatocellular carcinoma (hepatoma): investigations- LFTs are generally deranged. Although early detection of hepatocellular carcinoma in susceptible individuals can be pursued by a policy of 6-monthly measurement of alpha-fetoprotein (AFP) and ultrasound scanning, this tumour marker is elevated in only onethird of the white population with hepatocellular carcinoma, compared to 80% of African patients with this disease

The patient with critical leg Ischemia related to the atherosclerosis should be treated with: A. Thrombolysis-e.g rt-PA(plasminogen activator) B. Aspirin,pain killers and statins C. Unfractionated heparin followed by Warfarin D. Hospitalization in vascular center and revascularisation E. Low molecular weight heparin in the therapeutic doses and then warfarin if required

D. Hospitalization in vascular center and revascularisation אמבוס Acute limb ischemia (ALI): Acute limb ischemia (ALI) is a vascular emergency in which the arterial blood supply to one or more extremities is critically reduced. Arterial thrombosis and cardiac emboli are responsible for the majority of cases. The typical signs and symptoms of ALI include pain, pallor, pulselessness, poikilothermia, paralysis, and paresthesia of the limb distal to the site of vascular occlusion (the 6 Ps). Diagnosis relies on examination and arterial Doppler studies. Clinical findings in combination with Doppler studies are then used to categorize the limb as viable, threatened, or nonviable. Further imaging studies, e.g., digital subtraction angiography, should only be performed if they do not result in treatment delays. Management of viable and threatened limb ischemia begins with intravenous heparin followed by revascularization. Irreversible limb ischemia will inevitably progress to gangrene and requires amputation of the nonviable parts of the limb. Whether long-term anticoagulation and/or further diagnostic studies are required depends on the suspected etiology (e.g., echocardiography in suspected left atrial thrombus formation). Acute limb ischemia due to thromboembolism: Systemic anticoagulation with an IV heparin bolus followed by continuous infusion unless a contraindication is present. Further management depends on the severity of acute limb ischemia. Viable, non-threatened limb: 1. Urgent angiography to localize the site of the occlusion 2. Revascularization procedure (open or catheter-directed thrombectomy or thrombolysis) within 6-24 hours Threatened limb: emergent revascularization procedure within 6 hours First-line: catheter-directed thrombolysis and/or percutaneous mechanical thromboembolectomy (e.g., balloon catheter embolectomy) Second-line: open thromboembolectomyNon-viable limb: limb amputation ספר Acute limb ischaemia: Management All suspected acutely ischaemic limbs must be discussed immediately with a vascular surgeon; a few hours can make the difference between amputation or death, and complete recovery of limb function. • If there are no contraindications (e.g., trauma/suspected aortic dissection), an intravenous bolus of heparin (3000- 5000 U) is administered to limit propagation of thrombus and protect the collateral circulation • If ischaemia is complete, the patient proceeds for embolectomy (preferably under local anaesthesia) • If ischaemia is incomplete, preoperative imaging is obtained wherever possible, as simple embolectomy or thrombectomy is unlikely to be successful; a 'road-map' for distal bypass is helpful; and it is often possible, at least initially, to manage the patient medically depending on the results of imaging. אפ טו דייט- Chronic limb-threatening ischemia — is a clinical syndrome defined by the presence of PAD (peripheral artery disease) in combination with rest pain, gangrene, or a lower limb ulceration >2 weeks duration. CLTI is the preferred term replacing the terms critical limb ischemia (CLI) or severe limb ischemia. משוחזר

T-Tube: A. Is left after prostatectomy B. Placement of a drain or packing the abscess cavity after incision and drainage is unnecessary C. Is left after open thoracotomy with decortication D. Is a draining tube placed in the common bile duct after common bile duct exploration E. Is used to drain a large pneumothorax, haemothorax or pleural effusion

D. Is a draining tube placed in the common bile duct after common bile duct exploration הם כותבים שלפי מפתח תשובות זה E אבל זה לא הגיוני T-tube drain Kehr tube A T-shaped drain used to provide external biliary drainage (e.g., to treat bile duct injury), decompress the biliary tree (e.g., to treat acute cholangitis), and rarely, to extract common bile duct stones. The short arms of the T-tube are placed within the common bile duct; the long arm is brought out percutaneously through the abdominal wall.

Diffuse axional injury is: A. Mainly caused by medial meningeal arterydisruption B.Correlated with III cranial nerve palsy C.Usually correlated with pathologically low intracranial pressure (ICP) D. Mainly caused by rotational head injury E.Symptoms are mainly correlated with cranial bone injury

D. Mainly caused by rotational head injury Diffuse axional injury- Multifocal shearing tears and disruption of the axons of the brain due to rotational acceleration-deceleration trauma of the head; typically seen in high-impact road traffic accidents. White and gray matter have different densities. Sudden high-impact rotational force of the head causes a difference in rotational motion of the white matter and gray matter tracts, resulting in stretching and shearing tears of multiple axons across the brain. Commonly results in severe neurological injury (e.g., coma, persistent vegetative state)

The hyperacute rejection Is depending on: A. Presence of active T-cells in recipient's circulation B. Presence of active B-cells in recipient's circulation C. Presenting the antigens of the grant D. Presence of preformed antibodies against donor HLA antigens E. Presence of active T and B-cells in recipient's circulation

D. Presence of preformed antibodies against donor HLA antigens אמבוס- Hyperacute rejection Transplantation: Graft-related complications A rejection of transplanted tissue that occurs within 48 hours after transplantation (usually within minutes to hours). Typically manifests with intraoperative swelling of the graft as soon as perfusion is restored. It is due to preformed cytotoxic antibodies against class I HLA molecules that trigger the activation of the complement system, leading to thrombosis and graft ischemia. מהספר- Patterns of allograft rejection 1. Hyperacute rejection: • Results from the presence of preformed cytotoxic antibodies directed against donor HLA or AB antigens • Avoidable through blood group and tissue matching • Apparent following removal of the vascular clamps as the donor organ becomes swollen and discoloured • Leads to graft destruction within 24 hours. 2. Acute rejection: • Occurs in up to 50% of grafts, usually in the first 6 months • Diagnosed on renal transplant biopsy and classified according to Banff 07 diagnostic criteria • Cell-mediated rejection is the more common type; primarily involving T cells, it is treated with high-dose intravenous methylprednisolone • Antibody-mediated rejection is characterised by specific histological findings along with elevated serum donor specific antibody. Treatment is more challenging, and usually involves plasma exchange and intravenous immunoglobulin. 3. Chronic allograft damage: • Occurs after 6 months and often leads to a progressive decline in, and eventual loss of, organ function • Multifactorial aetiology: immune-mediated injury, IRI, toxicity from immunosuppressive agents and viral infections • Characterised histologically by cellular atrophy and fibrosis, there are currently no therapeutic strategies to combat it.

The typical symptoms related to the symptomatic carotid artery stenosis are: A.vertigo,paresis B. headache,vertigo,dizziness C. vertigo,paresis,aphasia D. aphasia, paresis,visual disturbances E. paresis,vertigo, aphasia, virtual disturbances

D. aphasia, paresis,visual disturbances אמבוס- Carotid artery stenosis (CAS) is an atherosclerotic, degenerative disease of the common carotid artery and internal carotid artery. Risk factors include advanced age, tobacco use, arterial hypertension, and diabetes mellitus. Depending on the extent of stenosis, ischemia in the carotid perfusion territory can result in amaurosis fugax, transient ischemic attack (TIA), or stroke. Carotid duplex ultrasonography is the initial test of choice for evaluating the carotid artery and measuring the degree of stenosis. Management depends on the degree of stenosis and patient factors (e.g., life-expectancy, comorbidities). Lifestyle modifications, antiplatelet and statin therapy, and risk factor modifications (e.g., with antihypertensive therapy) are recommended for all patients and should be continued indefinitely. Carotid revascularization is recommended for severe carotid stenosis and may be considered for moderate carotid stenosis if the periprocedural risks are acceptable. Screening for asymptomatic carotid stenosis is controversial. Symptomatic patients may present with: Transient ischemic attacks Symptoms of ischemia of the common carotid artery territory, such as:Ipsilateral amaurosis fugax Contralateral weakness, contralateral sensory deficits (ischemic stroke) Carotid artery stenosis does not typically cause vertigo, lightheadedness, or syncope. משוחזר

65 year old patent with deep vein thrombosis related to the transient (reversible) risk factor (eg.hernia surgery procedure and postprocedure immobilisation), should be treated pharmacologically (specify the shortest possible period of pharmacological treatment): A. 3 weeks B.4 weeks C. at least 2 months D. at least 3-6 months E. one year or more

D. at least 3-6 months אמבוס- Approach: Evaluate and treat concomitant pulmonary embolism and stabilize the patient as needed. Assess bleeding risk on anticoagulation for VTE. Initiate anticoagulation therapy based on the extent and etiology of DVT Expectant management: serial venous ultrasound without anticoagulation Primary treatment: anticoagulation for 3-6 months in patients not being managed expectantly Secondary prevention (of recurrent DVT): extended anticoagulation after completion of primary treatment; should be individualized (e.g., patients with chronic risk factors) Treat the underlying cause, if feasible. משוחזר לא אחד לאחד אבל בול אותו רעיון

Venous leg ulcer is the pathology which is in the majority of the cases related to: A. atherosclerosis and leg ischemia B. decubitus presence C. deep vein thrombosis D. chronic venous disease E.diabetes

D. chronic venous disease אמבוס- Venous ulcers: Definition: an open skin lesion of the leg or foot in an area affected by venous hypertension. Etiology: usually caused by CVI (Chronic venous insufficiency) with or without complications (e.g., untreated stasis dermatitis). CVA= A term used to describe the edema, characteristic skin changes (hyperpigmentation, stasis dermatitis), and ulcers secondary to chronic venous hypertension. Varicose veins may or may not be present. Clinical features: Most frequently occurs just above the ankle (gaiter region) Manifests as a shallow ulcer with irregular borders Typically mild pain and pruritus Additional clinical features of CVI are usually present, e.g., edema, varicose veins. Diagnostics: Perform diagnostic studies for CVI. Perform ABI (Ankle-brachial index) to rule out concurrent PAD (Peripheral artery disease). Work up as needed for important differential diagnoses of leg ulcers (e.g., with diabetes screening). Obtain aerobic and anaerobic wound cultures for suspected infections. Tissue biopsy is indicated for ulcers with any of the following: -No signs of healing after being open continuously for 3 months or after 4-6 weeks of standard treatment - Worsening despite treatment (e.g., worsening pain, increase in size) -Atypical features Treatment: Initiate treatment of CVI, including compression therapy and referral for interventional treatment. Provide topical wound care. Treat underlying stasis dermatitis. Consult wound care for debridement and dressing application. Start systemic antibiotics if there is evidence of infection (e.g., cellulitis, erysipelas) Consider skin graft in large or refractory ulcers. Prognosis: Recurrence rate is as high as 70%. משוחזר

Serum levels of AFP, β-hCG and LDH are markers for: A. prostate cancer B.nephrolithiasis C.urosepsis D.testicular cancer E.congenital urinary tract abnormalities

D. testicular cancer מהספר- Testicular tumours - Investigations: All suspicious scrotal lumps should be imaged by US, which provides a high degree of accuracy. As soon as a tumour is suspected, and before orchiectomy, serum levels of AFP, β-HCG and lactate dehydrogenase (LDH) should be determined. The levels of these 'tumour markers' are increased in extensive disease. Accurate staging is based on CT of the lungs, liver and retroperitoneal area, and an assessment of renal and pulmonary function. Summary- Testicular tumours: • In the UK, there are about 2200 new cases of testicular tumour per year and the 20-40-year age group is predominantly affected • Germ cell tumours account for 95% of all testicular tumours • Seminomas arise from the seminiferous tubules, are of relatively low-grade malignancy, spread mainly via the lymphatic system and are very sensitive to radiotherapy • Nonseminomatous germ cell tumours arise from germinal cells, their differentiation reflects their aggressiveness (well-differentiated tumours being the least aggressive) and they are not radiosensitive • Treatment consists of radical or chiectomy (with division of the spermatic cord at the level of the deep inguinal ring). Radiotherapy is used if the tumour proves to be a seminoma, whereas chemotherapy (bleomycin, etoposide and cisplatin) is used for teratomas that are advanced or recurrent • Seminomas have a 5-year survival rate of 90-95%, whereas teratomas have a more varied prognosis (60-95% 5-year survival rate). אמבוס- Alpha-fetoprotein- A globulin normally produced by fetal endodermal tissues with unclear function (possibly similar to albumin). AFP levels can be used for prenatal testing and as a tumor marker for some germ cell and liver tumors Human chorionic gonadotropin- A hormone produced by the placenta after implantation. Its β subunit is measured to detect pregnancy. Also measured as a tumor marker in seminomas, choriocarcinomas, germ cell tumors, hydatidiform moles, and teratomas. Lactate dehydrogenase- An intracytoplasmic enzyme that catalyzes the reversible conversion of lactate to pyruvate. Five isoenzymes exist that are found in higher concentrations in specific organs: LDH 1 and 2 (heart, kidneys, erythrocytes), LDH 3 (lungs), LDH 4 and 5 (liver and skeletal muscle). LDH levels are elevated in patients with an injury to any of the aforementioned organs and in conditions with an increased cell turnover (e.g., cancer)

Which statements about portal hypertension are true: 1. Portal hypertension is almost always due to obstruction to portal flow (rather than increased inflow), and may be prehepatic,hepatic or posthepatic 2.Portal hypertension rarely develops before the age of 70 years 3.Portal hypertension has a 1:4 risk of malignant transformation and should be resected A. 2 B. 2,3 C.1,2,3 D.1 E. 1,2

D.1 ??? ספר גרסה 7- Portal hypertension: Portal hypertension results from increased resistance to portal venous blood flow. Rarely, it results primarily from an increase in portal blood flow. The normal pressure of 5-15 cmH2O in the portal vein is consistently exceeded (above 25 cmH2O). Portal vein thrombosis is a rare cause and is most commonly due to neonatal umbilical sepsis. The most common cause of portal hypertension is cirrhosis resulting from chronic liver disease and is characterised by liver cell damage, fibrosis and nodular regeneration. The fibrosis obstructs portal venous return and portal hypertension develops. Arteriovenous shunts within the liver also contribute to the hypertension. Alcohol and steatohepatitis associated with obesity are the most common aetiological factor in developed countries, whereas in North Africa, the Middle East and China, schistosomiasis due to Schistosoma mansoni is a common cause. Chronic active hepatitis and primary and secondary biliary cirrhosis may result in portal hypertension, but in a large number of patients the cause remains obscure (cryptogenic cirrhosis). Posthepatic portal hypertension is rare. It is most frequently due to spontaneous thrombosis of the hepatic veins and this has been associated with neoplasia, oral contraceptive agents, polycythaemia and the presence of abnormal coagulants in the blood. Inferior vena caval obstruction above the level at which the hepatic veins open into the cava is more common in South and South East Asia. The resulting Budd-Chiari syndrome is characterised by portal hypertension, caudate hypertrophy, liver failure and gross ascites. ספר גרסה 6- Portal hypertension Portal hypertension is caused by increased resistance to portal venous blood flow, the obstruction being prehepatic, hepatic or posthepatic. Rarely, it results primarily from an increase in portal blood flow. The normal pressure of 5-15 cmH2 O in the portal vein is consistently exceeded (above 25 cmH2 O). Portal vein thrombosis is a rare cause and is most commonly due to neonatal umbilical sepsis. The most common cause of portal hypertension is cirrhosis resulting from chronic liver disease and is characterized by liver cell damage, fibrosis and nodular regeneration

Femoral neck fractures risk factors include: 1.male sex 2.increasing age 3.poor health 4.tobacco and alcohol use 5.previous fracture 6.fall history 7. high estrogen level A.1,3,5,7 B.2,4,6,7 C.3,4,5,6 D.2,3,4,5,6 E.1,2,3,4,5,6,7

D.2,3,4,5,6 Fractures of the femoral neck These are generally seen in the elderly with osteoporotic bone, as a result of low-energy falls and can often result from an underlying medical condition. They are extremely common and utilise very considerable health-service resources. Such fractures are divided into: • Extracapsular, occurring outside the margins of the joint capsule, particularly the metaphyseal trochanteric area of the femur • Intracapsular, involving the femoral neck within the capsule. • This differentiation is important because blood reaches the femoral head via the capsule and runs along the femoral neck. Extracapsular fractures are normally reduced and stabilised using a pin and plate system, commonly known as a dynamic hip screw (DHS), which allows sliding and impaction of the fracture site as the patient walks. Undisplaced intracapsular fractures are pinned in the hope that the blood supply to the femoral head has been preserved and avascular necrosis of the femoral head will not develop. Treatment of displaced intracapsular fractures is a challenge and it still remains 'an unsolved fracture'. Attempt is made to retain the femoral head in a young patient since hip replacement may wear out, requiring revision surgery. Accurate reduction of a displaced intracapsular fracture may require opening the capsule for visualisation of the fracture, further jeopardising the blood supply. In the older patient the preferred treatment is to perform either a arthroplasty or a total hip replacement. These allow immediate weight bearing and a more predictable recovery.

The patient after arterial embolectomy should receive life - long therapy with: A.Aspirin B. Low molecular weight heparin C.Unfractionated heparin D.Warfarin or rivaroxaban E. Cilostazol or rivaroxaban

D.Warfarin or rivaroxaban ספר- Acute embolus: Embolic occlusion of the brachial artery is not usually limbthreatening and, in an elderly patient, nonoperative treatment is reasonable. Younger patients should undergo embolectomy to prevent subsequent claudication, especially where the dominant arm is affected. A leg affected by embolus is nearly always threatened and requires immediate surgical revascularisation. Femoral embolus is usually associated with profound ischaemia to the level of the upper thigh because the deep femoral artery is also affected. Acute embolic occlusion of the aortic bifurcation (saddle embolus) leads to absent femoral pulses and a patient who is 'marble' white or mottled to the waist. Such patients may also present with paraplegia due to ischaemia of the cauda equina, which may be irreversible. Embolectomy can be performed under local, regional or general anaesthesia. Postoperatively, the patient should continue on heparin. Warfarin reduces the risk of recurrent embolism but is associated with an annual risk of significant bleeding of 1-2%. The in-hospital mortality from cardiac death and/or recurrent embolism, particularly stroke, is 10-20%. אמבוס- Embolectomy for PE : Indications- Contraindications to thrombolysis for PE in patients with massive PE or high-risk submassive PE Failure of thrombolysis for PE Options- Surgical embolectomy: removal of the embolus through an incision in the pulmonary artery Endovascular embolectomy: catheter-based thrombus removal אפ טו דייט- Embolectomy — Embolectomy is indicated in patients with hemodynamically unstable PE in whom thrombolytic therapy is contraindicated. It is also a therapeutic option in those who fail thrombolysis. Emboli can be removed surgically or using a catheter. The choice between these options depends upon available expertise, the presence or absence of a known diagnosis of PE, underlying comorbidities, and the anticipated response to such therapies. As an example, when a patient has severe hemodynamic instability and standard dose thrombolysis is contraindicated, catheter-directed techniques may be preferred if the expertise is available. One advantage of this approach is that both diagnostic and therapeutic interventions can be applied simultaneously. While unfractionated heparin may be preferred by most experts in patients who are hemodynamically unstable in anticipation of a potential need for thrombolysis or embolectomy, some trials with catheter-based treatments (lysis and embolectomy) allowed patients on background LMW heparin. Direct thrombin and factor Xa inhibitors should not be used in hemodynamically unstable patients.

What is the most common tumor of the kidney in children A.Angiolipoma tumour of the kidney B.Sarcoma of the kidney C.Clarocellulare tumour of the kidney D.Wilms tumour E.Small round cell tumour

D.Wilms tumour Nephroblastoma (Wilms tumor) is the most common renal malignancy in children, typically affecting children between 2 and 5 years of age. A minority of cases are associated with specific syndromes (e.g., WAGR, Beckwith-Wiedemann) and gene mutations (e.g., WT1). Nephroblastoma is typically an incidental finding that manifests as a large abdominal mass. Other signs and symptoms may occur, such as hematuria and abdominal pain, especially in tumors that are large, ruptured, or metastasized. Treatment consists of tumor resection and chemotherapy for all stages (except for very low-risk tumors), while radiation is predominantly used in advanced disease. In contrast, renal cell carcinoma (RCC) is more common in the 15- to 19-year-old age group.

Superficial low grade Ta and Tl bladder tumours are usually treated by: A.radical cystectomy B. intravesical BCG instillations C.radical radiotherapy D.transurethral resection E.immunotherapy

D.transurethral resection ספר- Management Superficial bladder tumours (Ta, T1): Superficial bladder tumours (Ta, T1) These lesions are treated by TURBT (trans-urethral resection of bladder tumour) down to and including detrusor muscle. A single intravesical dose of intravesical chemotherapy (mitomycin C) reduces the risk of recurrence of superficial bladder cancer. A 6-week course of mitomycin C is also useful to treat multiple low-grade bladder tumours and to reduce recurrence. Regular check cystoscopies are required. Recurrences are mostly treated by repeat diathermy or resection, but, if they become very frequent and excessive, cystectomy may be advisable. Carcinoma in situ (Cis) may be present in mucosa that appears normal or in association with a proliferative tumour. Cis can also exist as a separate entity, when there may be only a generalised redness of the bladder mucosa. Cis should be considered in patients with ongoing torage urinary symptoms associated with pain or symptoms suggestive of ongoing UTI, in the absence of a positive urine culture. Untreated patients with Cis have a high risk of progression to invasive cancer. Cis responds well to intravesical bacillus Calmette- Guerin (BCG) treatment. However, if there is any doubt about the response, and especially ifthere is any pathological evidence of progression, cystectomy is warranted. מהספר- Bladder tumours: • The urothelium or transitional cell epithelial lining of the urinary tract extends from the renal pelvis to the distal urethra • The incidence of urothelial cancer is increasing, possibly because of increasing exposure to occupational carcinogens, smoking and analgesic abuse • Almost all bladder cancers are urothelial cell cancers. Squamous cancers are rarer and are associated with chronic irritation or inflammation (e.g., calculi and schistosomiasis). Adenocarcinomas are extremely rare • Visible haematuria is present in 80% of cases • Urothelial cell cancers of the bladder are treated as follows: • Carcinoma in situ may respond to intravesical bacillus Calmette- Guerin (BCG) but is unpredictable and may require more aggressive treatment • Superficial tumours (Ta, T1) are usually treated by trans-urethral resection with or without intravesical chemotherapy • Invasive tumours (T2, T3) may be best dealt with by radical cystectomy (or by radical radiotherapy) • Invasive T4 tumours with fixation to the pelvis or surrounding organs are dealt with by palliative radiotherapy.

Causes of free subdiaphragmatic gas on abdominal X-ray are: 1. Perforation of an intra-abdominal viscus 2. Gas-forming infection 3. Pleuroperitoneal fistula 4. Gas introduced per vaginam: post-partum A. 1 B. 2,3 C. 1,2,3 D. 1,3,4 E. 1,2,3,4

E. 1,2,3,4 ספר- Radiological investigations of THE ACUTE ABDOMEN: Plain x-rays: The erect chest x-ray (CXR) is the most appropriate first investigation for the detection of free intraperitoneal gas (Fig. 12.6) and should be carried out in any patient who might have a perforation. If the condition of the patient prevents an erect film being taken, then a left lateral abdominal decubitus film might be helpful. Although a visceral perforation is the most common cause of free intraperitoneal gas, other causes exist and should be considered where appropriate. An erect CXR is also useful in identifying a respiratory condition that may present with upper abdominal pain. These patients are usually tachypnoeic. Increasingly computed tomography (CT; see later) is replacing erect CXR in patients with a suspected perforation, particularly if they are unwell and a definitive diagnosis is required urgently to decide immediate management. The role of plain abdominal radiographs remains controversial, despite many studies that have demonstrated that, with the exception of suspected intestinal obstruction, they rarely help in the diagnosis and have even less of a role in altering the clinical decision. However, the supine abdominal x-ray (AXR) can be of use in patients whose diagnosis is unclear and in whom the presence of calcification (e.g., ureteric colic) and abnormal gas shadows (e.g., possible intestinal ischaemia) may be helpful. They should, however, not be performed routinely, and have no role in the investigation of patients with suspected appendicitis. An erect AXR is only of value in patients with intestinal obstruction, although it is well known that even then the information obtained over and above that from the supine film is small. A good-quality supine AXR can indicate the level of obstruction (concertina jejunal loops or characterless ileal loops, caecal distension, or absence of gas in the rectum), whereas the erect film proves the diagnosis of obstruction by showing air fluid levels.

Which of the following can be seen In the Ophthalmopathy of Grave's disease? 1. Bulging eyes 2. Redness 3. Retracting eyelids 4. Strabismus 5. Aniridia A. 1,2,4. B. 1,3.4. C. 1.4,5. D. 2,3,4. E. 1,2,3.

E. 1,2,3. אמבוס- Graves disease is the most common cause of hyperthyroidism and often affects women. It is an autoimmune condition that is associated with circulating TSH receptor autoantibodies leading to overstimulation of the thyroid gland with excess thyroid hormone production. The classic clinical triad of Graves disease involves a diffuse vascular goiter, ophthalmopathy, and pretibial myxedema, although not all features may be present in a patient. The clinical diagnosis of Graves disease is confirmed via assessment of TSH and T3/T4 levels as well as through detection of thyroid antibodies (TRAb, TPOAb, TgAb). In addition, a diffuse uptake of 123I may be seen on thyroid scintigraphy. Treatment includes beta blockers to quickly alleviate symptoms, antithyroid drugs to achieve euthyroid status, and radioiodine ablation or, less commonly, near-total thyroidectomy for definitive control of the disease. Clinical features Symptoms of hyperthyroidism- Triad of Graves disease 1. Diffuse goiter: -Smooth, uniformly enlarged goiter -Bruit may be heard at the superior poles of the lobes 2.Ophthalmopathy : -Exophthalmos -Ocular motility disturbances -Lid retraction and conjunctival conditions 3. Dermopathy (pretibial myxedema): non-pitting edema and firm plaques on the anterior/lateral aspects of both legs ספר- Primary thyrotoxicosis (Graves' disease): Pathophysiology: This condition accounts for 75% of cases. It is an autoimmune disease in which TSH receptors in the thyroid are stimulated by circulating thyroid receptor antibodies (TRAbs). The gland is uniformly hyperactive, very vascular and usually symmetrically enlarged. Histologically, there is marked epithelial proliferation, with papillary projections into follicles devoid of colloid. TRAbs can cross the placental barrier, so that neonatal thyrotoxicosis can occur. Clinical features : The patient is usually a young female (female/male ratio 8:1) and the condition can be familial. The thyroid is usually moderately and diffusely enlarged and soft, and because of its vascularity a bruit may be audible. In addition to the symptoms seen with hyperthyroidism of any cause, some clinical manifestations are more specific to Graves' disease. These include Graves' ophthalmopathy and pretibial myxoedema. In Graves' ophthalmopathy, inflammation of the extraocular muscles and connective tissue leads to proptosis (exophthalmos) and impaired function of the eye muscles. Pretibial myxoedema presents commonly as raised pigmented lesions typically on the shins. Strabismus = Strabismus is a disorder in which both eyes do not line up in the same direction. Aniridia = Aniridia is an eye disorder characterized by a complete or partial absence of the colored part of the eye (the iris).

In patients receiving unfractionted heparin iv infusion, the following should be controled: A.APTT B. INR C.Platelets D. No control required E. APTT and platelets

E. APTT and platelets Unfractionated heparin (UFH) Drug: heparin Administration: Prophylaxis: subcutaneous Therapeutic: continuous intravenous infusion Monitoring during therapy: activated partial thromboplastin time (aPTT) , platelet count (including baseline before treatment is started) Clearance: hepatic (preferred agent for patients with renal insufficiency) Antidote: protamine sulfate (a positively-charged protein that can neutralize negatively-charged heparin by forming inactive complexes) משוחזר

In patients with intermittent claudication related to the chronic leg ischemia, the following therapy should be implemented as the first line treatment: A.Angioplasty always if short stenosis or occlusion is recognized B. Surgery-if short claudication present and angiography documented long distance occlusion C. Low molecular weight heparin, statin,risk factors reduction D. Aspirin, statin, risk factor elimination,cilostazol E. Aspirin,statin,risk factor elimination,walking exercise

E. Aspirin,statin,risk factor elimination,walking exercise אמבוס- Claudication- A pain of vascular origin that is reliably induced by exercise and relieved or reduced by rest. The pain is typically cramping in nature and is most commonly described in the lower extremities (in lower limb peripheral arterial disease). Claudication is caused by tissue ischemia secondary to arterial insufficiency. אפ טו דייט- Chronic limb-threatening ischemia — is a clinical syndrome defined by the presence of PAD (peripheral artery disease) in combination with rest pain, gangrene, or a lower limb ulceration >2 weeks duration. CLTI is the preferred term replacing the terms critical limb ischemia (CLI) or severe limb ischemia. אמבוס- Peripheral arterial disease (PAD): is a condition characterized by the atherosclerotic narrowing of peripheral arteries, most commonly of the lower extremities. Lower extremity PAD may be asymptomatic or manifest with intermittent claudication, critical limb ischemia (CLI), or acute limb ischemia (ALI), which is a surgical emergency that is described in a separate article. In the absence of acute ischemia, the first-line diagnostic test for PAD is the ankle-brachial index (ABI). Imaging, preferably via MR angiography, is indicated if revascularization is planned or if the diagnosis remains uncertain. Structured exercise therapy and modification of cardiovascular risk factors may improve intermittent claudication significantly; cilostazol, a vasodilator, may be considered for symptomatic relief. Revascularization is indicated in patients with limb ischemia and those with life-limiting claudication despite exercise therapy. Additionally, secondary prevention strategies for ASCVD should be initiated in all patients to minimize the risk of atherosclerotic cardiovascular disease. Carotid artery stenosis and chronic mesenteric ischemia are less common types of peripheral arterial disease and are covered separately. Intermittent claudication: # First-line therapy: - Structured exercise therapy: **Patients repeatedly walk or exercise until the onset of claudication and then rest until the pain subsides **This cycle is repeated for 30-45 minutes, three times a week, for a minimum of 12 weeks. Structured exercise therapy has been shown to improve patients' functional status and quality of life. - Cardiovascular risk factor modification. # Persistent claudication despite first-line measures: Consider cilostazol (for symptomatic improvement) OR revascularization. CLI: Consider revascularization in addition to structured exercise therapy and cardiovascular risk factor modification. Risk modification As patients with PAD are at an increased risk of atherosclerotic cardiovascular disease (ASCVD) events such as MI or stroke, secondary prevention strategies for ASCVD should be initiated in all patients. Smoking cessation Treatment of dyslipidemia- Consider high-intensity statin therapy in all patients with PAD. Glycemic control (in patients with type 2 diabetes)- Consider metformin as a first-line oral hypoglycemic agent. Antihypertensive treatment Single-agent antiplatelet therapy : aspirin OR clopidogrel (ticagrelor may also be considered) Recommended in all patients with symptomatic PAD (reduces morbidity and mortality from cardiovascular events)

Tetriary hyperparathyroidism is caused by: A. Parathyroid Carcinoma B. Parathyroid hyperplasia C.Parathyroid Adenoma D.Low serum calcium level E. Development of autonomous secretion of PTH.

E. Development of autonomous secretion of PTH. ספר- Secondary and tertiary hyperparathyroidism: In secondary hyperparathyroidism, there is over-secretion of PTH in response to low plasma levels of ionised calcium, usually because of renal disease or malabsorption. This is an increasing problem in patients with chronic renal failure. It is managed initially by dietary phosphate restriction and by giving 1-α-hydroxyvitamin D3 (alfacalcidol) to increase calcium absorption and provide negative feedback on the parathyroids. Excessive PTH secretion in secondary hyperparathyroidism may become autonomous; it is then termedtertiary hyperparathyroidism. This may occur after renal transplantation. Total parathyroidectomy may be needed, with calcium and vitamin D replacement therapy, subtotalparathyroidectomy leaving half-equivalent of a normal gland in situ or autotransplantation of parathyroid tissue (equivalent in size to one normal gland) into an arm muscle (where it can be readily located if problems persist). Postoperatively, alfacalcidol and calcium are continued to heal bone disease and reduce the risk of recurrent hyperparathyroidism. Calcimimetics (e.g., cinacalcet) may also be used in patients with refractory hyperparathyroidism on dialysis if operative intervention is not possible. אמבוס- Tertiary hyperparathyroidism (tHPT) Definition- Hypercalcemia caused by autonomous and refractory secretion of PTH secondary to untreated sHPT. Causes- Persistent sHPT Laboratory studies: 1. Calcium (ionized calcium or corrected calcium)- high 2. PTH- very high 3. Phosphate- high Treatment: Surgical therapy- Usually first-line treatment . May be curative Medical management- Similar to pHPT

A femoral shaft fracture is a fracture of the femoral diaphysis occurring between 5 cm distal to the lesser trochanter and 5 cm proximal to the adductor tubercle. Mark the correct answer: A. Standard of care for most femoral shaft fractures is nonoperative treatment. B. Because of the small volume of the fascial compartments of the thigh.compartment syndromes are much more common than in the lower leg. C.Ligamentous and meniscal injuries of the ipsilateral knee are never presentin patients with closed femoral shaft fractures. D. The plain radiographs (X-rays) of the femur should no longer be obtained, especially when MRI or ultrasonography are available. E. Skeletal traction is usually used as a temporizing measure before surgery to stabilize the fracture and prevent fracture shortening.

E. Skeletal traction is usually used as a temporizing measure before surgery to stabilize the fracture and prevent fracture shortening. אמבוס- femoral shaft fracture- is a fracture anywhere along the shaft or diaphysis of the femur. These fractures commonly occur in young males as a result of high-impact injuries (e.g., motor vehicle accidents). Low-impact shaft fractures tend to occur in older patients with pre-existing osteopenia, who have fallen from a standing position. Femoral fractures typically present as a painfully swollen, tense thigh with restricted range of motion and signs of fracture (e.g., shortening). Diagnosis is based on clinical examination findings and visualization of the fracture on plain radiographs. Definitive treatment following splinting and traction is usually surgical but depends on the patient's condition. Vascular compromise and fat embolism are common complications. Treatment: Stabilization, analgesia, and open fracture management Splinting and traction Surgery (definitive treatment): 1. Intramedullary rod via an interlocking nail (antegrade nailing): treatment of choice 2. External fixation with conversion to intramedullary nail within 2-3 weeks Compartment syndrome A condition caused by tissue ischemia due to increased pressure within a fascial compartment. Acute compartment syndrome of the extremities is a surgical emergency that can lead to tissue necrosis if untreated, while chronic compartment syndrome is associated with exercise or exertion and can often be managed conservatively. Abdominal compartment syndrome is caused by increased pressure within the abdominal cavity and can lead to organ failure.

Subclavian steal syndrome concerns the patients with: A. Stenosis or occlusion of the vertebral artery B. Stenosis or occlusion of the axillary artery C. Stenosis or occlusion of distal part of the subclavian artery D. Stenosis or occlusion of thoracic aorta E. Stenosis or occlusion ofthe proximal part of the subclavian artery

E. Stenosis or occlusion ofthe proximal part of the subclavian artery אמבוס- Subclavian steal syndrome (SSS)- is a condition in which the subclavian artery proximal to the origin of the vertebral artery narrows or becomes occluded, usually due to atherosclerosis. This blockage results in a lack of blood reaching the ipsilateral arm through the subclavian artery, which can lead to a reversal of blood flow in the affected vertebral artery so that blood from the contralateral side can flow through the circle of Willis to supply the affected arm. The condition is mostly asymptomatic. If symptoms occur, they are mainly caused by ischemia of the affected arm and include limb pain, fatigue, paresthesia, and cold skin. Neurological symptoms such as dizziness or even syncope are rare and usually only occur in the presence of cerebrovascular lesions. A characteristic diagnostic sign is a discrepancy in blood pressure between the arms of > 15 mm Hg. Imaging (e.g., ultrasonography) can identify a reversal of blood flow and/or atherosclerosis that confirms the diagnosis. Endovascular intervention or surgery are used to treat symptomatic SSS. סטאפ 1- Stenosis of subclavian artery proximal to origin of vertebral artery --> hypoperfusion distal to stenosis --> reversed blood flow in ipsilateral vertebral artery --> reduced cerebral perfusion on exertion of affected arm. Causes arm ischemia, pain, paresthesia, vertebrobasilar insufficiency (dizziness, vertigo). >15 mm Hg difference in systolic BP between arms. Associated with arteriosclerosis, Takayasu arteritis, heart surgery משוחזר

The Carpal Tunnel Syndrome results from compression of: A. radial nerve at wrist level B. ulnar nerve at wrist level C. median nerve at elbow D. ulnar nerve at elbow E. none of the above

E. none of the above אמבוס- Carpal tunnel syndrome (CTS)- is a peripheral neuropathy caused by chronic or acute compression of the median nerve under the transverse carpal ligament. CTS is the most common form of entrapment neuropathy, a group that includes cubital tunnel syndrome, radiculopathies, and tarsal tunnel syndrome. It is characterized by both sensory disturbances (pain, tingling, and numbness) and motor symptoms (weakened thenar muscles leading to weakened pinch and grip of the thumb) in the area innervated by the median nerve distal to the carpal tunnel. Several occupational and nonoccupational risk factors (e.g., manual labor, age, sex, diabetes) have been associated with CTS. Diagnosis is usually clinical, supported by symptoms and results of provocative tests for CTS (e.g., hand elevation test, carpal compression test, and Phalen test). Additional testing (e.g., electrodiagnostic studies) is indicated if there is diagnostic uncertainty. Patients with mild to moderate symptoms are generally managed conservatively (e.g., immobilization with a splint, local steroid injections). Surgical release of the transverse carpal ligament with decompression of the median nerve may be indicated for patients with severe disease (e.g., atrophy of the thenar eminence) or symptoms refractory to conservative treatment. מהספר- Symptoms of pain and numbness in the distribution of the median nerve in the hand - More common in patients with diabetes, hypothyroidism, acromegaly, pregnancy - May be intermittent, usually worst at night, may be provoked by wrist flexion - May be relieved by shaking hand while holding it in a dependent position. The symptoms are often characteristic and the history can be key to diagnosis. The differential diagnosis includes cervical radiculopathy. On examination there are usually no signs, but there may be wasting of the thenar eminence, weakness of the abductor pollicis brevis, and diminished or altered sensation in the median nerve distribution. Tapping over the nerve in the carpal tunnel may elicit paraesthesia in the median nerve distribution (Tinel's sign). Phalen's test involves acutely flexing the wrist and holding it in this position. This may precipitate paraesthesia or numbness. This is abnormal if it occurs within 1 minute. Diagnosis can be confirmed with electrophysiology to measure nerve conduction velocity and distal motor latency. Treatment depends on symptom severity. Splinting the wrist or steroid injection into the carpal tunnel relieves a third of cases. The transverse carpal ligament can also be divided surgically, usually under local anaesthetic; risks include injury to the motor branch of the median nerve.

Which of the knee ligaments is tested by the "anterior drawer test" A. posterior cruciate ligament(PCL) B. medial collateral ligament(MCL) C. lateral collateral ligament(LCL) D. posterior oblique ligament(POL) E. none of the above

E. none of the above מהספר- There are specific provocative tests for most joints that are performed depending on the initial findings. Examples include testing for shoulder impingement (Hawkin's test), asking the patient to stand on one leg to test the power of the abductor muscles of the hip (Trendelenburg test) and stressing the ACL of the knee to look for a rupture (anterior drawer test). אמבוס- Anterior drawer test A physical exam test that assesses anterior cruciate ligament (ACL) integrity. The patient is to lie down in the supine position and flex the knee to 90°. The foot of the knee being tested is fixed in place by the examiner and the patient is asked to relax. The proximal end of the tibia is then pulled anteriorly. A firm endpoint along with the absence of anterior tibial movement implies that the ACL is intact. If there is a lax endpoint (especially in comparison to the contralateral leg), the test is positive, suggestive of ACL injury. הסבר לתמונה- Drawer tests- The patient is in supine position, the leg to be examined is erect, and the knee is flexed at approximately 90°. The examiner puts both hands around the lower leg (with the thumbs placed on the tibial tuberosity). To examine the anterior cruciate ligament, the tibia is pulled ventrally. To examine the posterior cruciate ligament, the tibia is pushed dorsally. If the movability of the tibia is increased (particularly compared to the other leg) or if there is a lax endpoint, the drawer test is said to be positive and may indicate an injury to the respective ligament. סרטון- https://next.amboss.com/us/search?q=anterior+drawer+test&v=overview&m=nwb7jD

Which urological investigation allows assessment of differential kidney function, renal obstruction and nonfunctioning areas of renal parenchyma? A. retrograde pyelography B. ultrasonography C. computed tomography scanning D. intravenous urography E. scintigraphic renography

E. scintigraphic renography ספר Nuclear imaging Radiolabelled substances are used for two main purposes: 1. Detecting bony metastases from carcinoma of the prostate (bone scan). 99m-Tc-labelled methylene diphosphonate (MDP) is the most reliable method. 2. Measurement of renal function (scintigraphic renography). Occasionally 'how a kidney looks' does not correlate with 'how it behaves', e.g., hydronephrosis does not always mean the presence of obstruction. Nuclear scintigraphy allows assessment of obstruction to a kidney (e.g., from pelviureteric obstruction), differential kidney function (i.e., how much each kidney is contributing to overall function), assessment for nonfunctioning areas of renal parenchyma (e.g., scarring) and accurate assessment of GFR. Radiolabelled mercaptoacetyltriglycine (MAG-3) has largely superseded technetium-labelled diethylenetriamine pentaacetic acid (Tc-DTPA) for dynamic scanning. It is secreted from the renal tubules and is used in the identification of obstructed kidneys and to assess differential function. Dimercaptosuccinic acid (DMSA) is concentrated in the renal tubules and static imaging can be carried out some 2-3 hours after injection. Parenchymal defects such as scars, haematomas, lacerations or ischaemia may be demonstrated. Differential renal function can be quantified by measuring the dimercaptosuccinic acid (DMSA) concentration/density in each kidney

In the initial treatment of deep vein thrombosis (immediately after diagnosis confirmation) the following drugs can used except: A.unfractionated heparin B. low molecular heparin C.apixaban D.rivaroxaban E. warfarin

E. warfarin

Current options of operations for obesity include: 1.Gastric banding 2.Vertical banded gastroplasty 3.Gastric bypass and duodenal switch 4.Total gastrectomy A. 1,4 B. 2,3,4 C. 1,2,3,4 D.1,3 E.1,2,3

E.1,2,3 ספר- Operations for obesity and related comorbidities : Surgical procedures are offered to patients with very high BMI or with lower BMI up to 35 (32 in Asian population) with severe medical comorbid conditions such as diabetes, hypertension, obstructive sleep apnoea, etc. Their resolution and the potential to 'cure' diabetes is referred to as 'metabolic surgery'. Current options include restrictive procedures like gastric banding and sleeve gastrectomy, a purely malabsorptive procedure such as a duodenal switch procedure, or a combination of a restrictive and malabsorptive procedure such as a gastric bypass procedure. Increased acceptance of these operations has been seen in the last two decades as they can be performed laparoscopically. However, the technical difficulty of such surgery increases in the order that these operations are listed above. The more complex operations are more likely to lead to better excess weight loss in the short term. However, there is increasing evidence to show that although gastric banding is the safest procedure, it accomplishes lower weight loss and slower resolution of comorbidities in comparison to gastric bypass. Sleeve gastrectomy is presently being compared for its long-term efficacy with the gold standard procedure of gastric bypass. The procedures can be combined; for example, gastric banding is technically easier to perform in the very obese patient who has a BMI greater than 55. Once excess weight loss has plateaued, removing the band and performing a gastric bypass may allow further excess weight loss. The gastric band is a ring with an inflatable inner cuff, which is placed laparoscopically a short distance below the oesophagogastric junction, creating a small (approximately 50 mL) gastric pouch (Fig. 13.31A). The cuff can be inflated or deflated via injections into a port site located in the subcutaneous tissues, in order to tighten or relax the cuff around the stomach. The tighter the cuff, the longer foodstuffs entering the gastric pouch will take to exit through the ring into the remainder of the stomach and intestinal tract, prolonging the feeling of satiety. Gastric bypass involves stapling the stomach closed a short distance below the oesophagogastric junction (Fig. 13.31B). A Roux limb is brought up and anastomosed to the small proximal gastric remnant. Depending on the size of the pouch and calibre of the anastomosis, there will be a degree of restrictive activity, as well as a major malabsorptive element, as food will enter the distal jejunum and proximal ileum without exposure to bile or pancreatic and other digestive enzymes. Sleeve gastrectomy has become extremely popular in the last 5 years and involves excision of the fundus and body of the stomach while retaining the pyloric antrum, thereby converting the stomach into a narrow tube with a volume of 100-150 mL (Fig 13.31C). The popularity stems from the ease of this procedure as a restrictive procedure that has shown weight loss comparable to gastric bypass. Most importantly, resolution of comorbidities occurs and there is always a possibility to combine it with a malabsorptive procedure like gastric bypass should the weight loss become static. Vertical banded gastroplasty is rarely performed. Duodenal switch is a complex operation reserved for a minority of obese patients. Most patients with restrictive-type surgery find that they can eat more with time as the gastric remnant dilates. Hopefully, however, the target weight loss will have been achieved and improved eating habits established to allow maintenance of a healthier weight Complications of obesity surgery Obesity increases the risk of all types of surgery: in particular, chest infection, deep venous thrombosis and wound infection. All procedures involving intestinal anastomoses, are prone to leakage, with resultant sepsis and peritonitis that can be life threatening. Such patients need a high index of suspicion for early recognition, drainage of the collection and relook if required together with intensive care management if necessary. Stricture of the anastomosis is managed with endoscopic dilatation and the use of stents. Careful follow-up of patients by the multidisciplinary team is necessary, not only to monitor weight loss, but also to ensure that malnutrition of vitamins, trace elements, essential fatty acids and other important constituents of the diet does not occur. Patients who continue to eat chocolate and ice-cream to excess may not lose weight with the restrictive-type operations. Most patients who lose significant weight will develop gallstones and, in some, cholecystectomy may be indicated at the same time as obesity surgery. Following significant weight loss, plastic surgery procedures may be necessary to remove excess skin, especially from the abdomen, thighs and arms.

Complement-dependent lymphocytotoxicity crossmatch test: A.Is mandatory before an allogenic renal transplantation B. Is an assay between recipient's lymphocytes and donor's serum C. Positive result excludes transplantation within tested pair of donor and recipient D.A and B E.A and C

E.A and C ספר Testing for histocompatibility: Cross-match A cross-match is undertaken in some transplant patients immediately prior to renal transplantation to ensure that there is no reactivity between donor and recipient cells. Common cross-match techniques are: • Complement-dependent cytotoxicity cross-match (CDC-XM), which, when positive in the presence of IgG antibodies, is likely to result in rapid rejection of the transplanted kidney • Flow cytometry cross-match (FC-XM) is a more sensitive test, which, if positive, may represent an increased risk of rejection • Virtual crossmatch: in patients with a known antibody profile who are at low immunological risk, it is possible to predict a negative crossmatch, and thus to proceed without waiting for the tests to be performed. This saves approximately 4 hours of cold ischaemia.

Contraindication(s) to surgical treatment of breast cancer is(are): A.Tumour>5cm B. Infiltration of the skin or chest wall C. Fixed axillary nodes D. Involvement of supraclavicular nodes E.All mentioned above

E.All mentioned above אמבוס- Approach: - Depends on the histopathologic classification and cancer stage. - Involves a combination of surgical management and systemic therapy (chemotherapy, hormone therapy, targeted therapy) - Patient preference for more or less aggressive management plays a significant role in selecting the treatment approach. Surgical tumor removal: Breast-conserving surgery (BCT) Definition: a type of surgery that focuses on the removal of cancerous breast tissue only, in contrast to full-breast mastectomy Contraindications: 1. Large tumor-to-breast volume ratio 2. Multifocal tumors 3. Fixation to the chest wall 4. Involvement of the skin or nipple 5. Subareolar location History of chest radiation 6. Excision with negative tumor margins (> 2 mm) not guaranteed 7. Clustered microcalcifications on imaging הרחבה- אמבוס: Breast cancer is the second most common malignancy in women. The lifetime risk of developing breast cancer for women in the US is approximately 13%. The most important risk factors are increased estrogen exposure, advanced age, and genetic predisposition (e.g., BRCA1/BRCA2 mutations). The majority of tumors are adenocarcinomas. The two most common types of breast cancer are invasive ductal carcinoma and the less aggressive invasive lobular carcinoma. In most cases, breast cancer is detected during routine mammography screening, which is recommended in women starting at 50 years of age. Mammographic abnormalities and breast masses require further radiographic evaluation, and, if there are signs of malignancy or the results are inconclusive, biopsy and subsequent histopathologic analysis. Axillary lymph node status is determined through clinical examination and biopsy of suspicious lymph nodes. Treatment primarily depends on the histopathologic classification and the cancer stage. It involves a combination of surgical resection, radiation, and systemic therapy. Surgery is either breast-conserving or involves the removal of all breast tissue on the affected side (mastectomy), or even both sides. If the tumor is positive for estrogen (ER) or progesterone (PR) receptors, it can be treated systemically with hormone therapy (e.g., tamoxifen). If the tumor is positive for HER2 receptors, it should receive targeted therapy (e.g., trastuzumab). The most important prognostic factors are cancer stage, tumor receptor status, and DNA aneuploidy. Women with a high risk of developing breast cancer (e.g., positive BRCA mutation status) should be offered risk-reducing prophylactic measures (e.g., bilateral prophylactic mastectomy).

In order to prevent surgical site infections in surgical practice, it is crucial to obey some rules. Choose the correct answer- A. Appropriate antibiotic prophylaxis. B. Careful surgical technique to minimize tissue damage and bleeding. C. Avoidance of infective surgical complications such as anastomotic leakage. D. Good patient preparation for surgery, i.e. smoking cessation or adequate nutrition. E.All of the answers are correct.

E.All of the answers are correct. ספר- Surgical site infection (SSI) All surgical wounds are contaminated by microbes but in most cases infection does not develop because of innate host defences. A complex interplay between host, microbial and surgical factors ultimately determines whether infection takes hold and how it progresses. Prevention- The risks of SSI can be reduced by: • Careful surgical technique to minimise tissue damage, bleeding, anastomotic leaks and haematoma • Appropriate antibiotic prophylaxis

In Congenital esophageal atresia the most important in initial treatment is: A.Immediate surgery B.Continous suction from blind pouch C.Upright position of child with head bended towards chest D.Prophylactic antibiotics E.B,C,D are the right answers-minimazing complications from aspiration

E.B,C,D are the right answers-minimazing complications from aspiration Esophageal atresia: Esophageal atresia is a congenital defect in which the upper esophagus is not connected to the lower esophagus, ending blindly instead. It is caused by the abnormal development of the tracheoesophageal septum. Esophageal atresia with a fistula connected distally to the trachea is the most common kind of esophageal malformation (classified as Gross type C). It manifests immediately after birth with cyanotic attacks, foaming at the mouth, and coughing, and prevents any attempts to pass a feeding tube into the stomach. X‑ray is mandatory for classifying the atresia and should show an air‑filled pouch situated at the level of the third thoracic vertebra. Preoperative: - Placement of an oroesophageal or nasoesophageal tube for continuous suction of secretions to prevent aspiration and facilitate breathing. - Upper body elevated, left lateral decubitus position - Antibiotics in case of aspiration pneumonia - Infants who potentially have esophageal atresia should not be fed orally under any circumstances! Surgery: Surgical treatment should be performed within the first 24 hours of birth. The goal is to reconnect the upper esophageal pouch and the lower esophagus. A long gap between both ends of the esophagus may not allow primary repair. In this case, a gastrostomy tube is necessary to allow enteral feeding. Treatment options include promoting elongation of the esophagus (via the Foker technique) and colon interposition Surgical repair is technically difficult surgery that uses a cervicotomy, cervicosternotomy, or thoracotomy approach; thus, expertise in both esophageal and tracheal surgery are critical for success. The surgical approach for TEF depends upon the size of the fistula

The occurrence of the acute mesenteric ischemia can be recognized in the following cases except: A.Aortic dissecton B. Messenteric artery embolia C. Afer resuscitation because of cardiac arrests and hypotension D. Messenteric vein thrombosis E.Splenic artery aneurysm

E.Splenic artery aneurysm אמבוס- Acute decrease in intestinal blood flow, usually due to thromboembolic occlusion of a mesenteric artery. A less common cause is vasospasm (non-occlusive mesenteric ischemia) in critically ill patients on vasopressors. The classic presentation is abdominal pain out of proportion to abdominal examination. Bowel infarction develops within 6 hours, resulting in bloody diarrhea, abdominal distention, and peritonitis. Etiology: AMI has various etiologies, which manifest with similar clinical features despite having different underlying risk factors and pathology. 1. Acute mesenteric artery embolism- Most common cause of AMI (causes 50% of all cases), Risk factors include atrial fibrillation, myocardial infarction, valvular heart disease, and arterial interventions involving the aorta. Most commonly involves the SMA. 2. Acute mesenteric artery thrombosis- Causes ∼ 25% of cases, Risk factors include visceral atherosclerosis, arteritis, aortic aneurysm, and aortic dissection. 3. Nonocclusive mesenteric ischemia- Causes ∼ 20% of cases, Most commonly occurs in critically ill patients with low cardiac output, Risk factors include hypotension and the use of vasopressors, digitalis, ergotamines, or cocaine. 4. Mesenteric venous thrombosis- Least common cause of AMI (causes < 10% of all cases), Risk factors include infection, malignancy, portal hypertension, estrogen therapy, and hypercoagulability disorders. סטאפ 1- Critical blockage of intestinal blood flow (often embolic occlusion of SMA) --> small bowel necrosis A --> abdominal pain out of proportion to physical findings. May see red "currant jelly" stools

Risk factors for acute pancreatitis include: A.male gender B.increasing age C.obesity D.smoking E.all of the above

E.all of the above אינטרנט- Factors that increase your risk of pancreatitis include: - Excessive alcohol consumption- Research shows that heavy alcohol users (people who consume four to five drinks a day) are at increased risk of pancreatitis. - Cigarette smoking- Smokers are on average three times more likely to develop chronic pancreatitis, compared with nonsmokers. The good news is quitting smoking decreases your risk by about half. - Obesity-You're more likely to get pancreatitis if you're obese. - Diabetes- Having diabetes increases your risk of pancreatitis. - Family history of pancreatitis- The role of genetics is becoming increasingly recognized in chronic pancreatitis. If you have family members with the condition, your odds increase — especially when combined with other risk factors.

The most frequent clinical presentation of bladder cancer is: A.dysuria B.nocturia C.urgency D.frequency E.haematuria

E.haematuria מהספר- Bladder tumours-Clinical features: More than 80% of patients have haematuria, which is usually painless. It should be assumed that such bleeding is from a tumour until proven otherwise. In women, symptoms of cystitis are so common that occasional bleeding may be thought to be part of an infective problem. Therefore, in cases of haematuria, an MSSU is mandatory with further investigation required if no growth is found. A tumour at the lower end of a ureter or a bladder tumour involving the ureteric orifice may cause obstructive symptoms. However, visible haematuria may be the only presenting symptom Bladder tumours: • The urothelium or transitional cell epithelial lining of the urinary tract extends from the renal pelvis to the distal urethra • The incidence of urothelial cancer is increasing, possibly because of increasing exposure to occupational carcinogens, smoking and analgesic abuse • Almost all bladder cancers are urothelial cell cancers. Squamous cancers are rarer and are associated with chronic irritation or inflammation (e.g., calculi and schistosomiasis). Adenocarcinomas are extremely rare • Visible haematuria is present in 80% of cases • Urothelial cell cancers of the bladder are treated as follows: • Carcinoma in situ may respond to intravesical bacillus Calmette- Guerin (BCG) but is unpredictable and may require more aggressive treatment • Superficial tumours (Ta, T1) are usually treated by transurethral resection with or without intravesical chemotherapy • Invasive tumours (T2, T3) may be best dealt with by radical cystectomy (or by radical radiotherapy) • Invasive T4 tumours with fixation to the pelvis or surrounding organs are dealt with by palliative radiotherapy. אמבוס-

80 year old patient with acute leg ischemia should be treated initially with: A. aspirin (dose 75-150mg) B. fibrinolytic treatment (thrombolysis) C. low molecular weight heparin (e.g. enoxaparin lmg/kg 2x) D. warfarin-starting dose 10mg E.heparin (with i.v.bolus)

E.heparin (with i.v.bolus) Acute limb ischemia (ALI): Acute limb ischemia (ALI) is a vascular emergency in which the arterial blood supply to one or more extremities is critically reduced. Arterial thrombosis and cardiac emboli are responsible for the majority of cases. The typical signs and symptoms of ALI include pain, pallor, pulselessness, poikilothermia, paralysis, and paresthesia of the limb distal to the site of vascular occlusion (the 6 Ps). Diagnosis relies on examination and arterial Doppler studies. Clinical findings in combination with Doppler studies are then used to categorize the limb as viable, threatened, or nonviable. Further imaging studies, e.g., digital subtraction angiography, should only be performed if they do not result in treatment delays. Management of viable and threatened limb ischemia begins with intravenous heparin followed by revascularization. Irreversible limb ischemia will inevitably progress to gangrene and requires amputation of the nonviable parts of the limb. Whether long-term anticoagulation and/or further diagnostic studies are required depends on the suspected etiology (e.g., echocardiography in suspected left atrial thrombus formation). Treatment: Acute limb ischemia due to thromboembolism Systemic anticoagulation with an IV heparin bolus followed by continuous infusion unless a contraindication is present Further management depends on the severity of acute limb ischemia. # Viable, non-threatened limb- 1. Urgent angiography to localize the site of the occlusion 2. Revascularization procedure (open or catheter-directed thrombectomy or thrombolysis) within 6-24 hours # Threatened limb: emergent revascularization procedure within 6 hours. 1. First-line: catheter-directed thrombolysis and/or percutaneous mechanical thromboembolectomy (e.g., balloon catheter embolectomy) 2. Second-line: open thromboembolectomy # Non-viable limb: limb amputation - Acute limb ischemia due to compartment syndrome: fasciotomy (see compartment syndrome) - Acute limb ischemia due to a dissecting aneurysm: stenting and/or surgical repair אפ טו דייט- Chronic limb-threatening ischemia — is a clinical syndrome defined by the presence of PAD (peripheral artery disease) in combination with rest pain, gangrene, or a lower limb ulceration >2 weeks duration. CLTI is the preferred term replacing the terms critical limb ischemia (CLI) or severe limb ischemia.

Late vascular complication after renal transplantation presents with: A. lymphocele B. anuria C. fever D.INR>1.5 E.hypertension

E.hypertension ספר- Complications after renal transplantation: Early complications following renal transplantation may be general complications of major surgery, technical or immunological. The main immunological complications have been dealt with elsewhere in the chapter. Technical complications: • Acute renal artery thrombosis is rare (approximately 1%) • Venous thrombosis (approximately 6%). Both must be recognised rapidly, using Doppler ultrasound, and require that the patient is returned to theatre immediately if there is to be any chance of salvaging the transplant. • Late vascular complications include renal artery stenosis, which occurs in about 3-5% of patients and usually presents several months posttransplantation with hypertension, and deteriorating graft function. The diagnosis is confirmed by angiography and the treatment of choice is angioplasty • Urinary leaks occur less commonly now that ureteric stenting is adopted more widely: they present with falling urine output and increasing pain. They may be managed conservatively with prolonged urinary catheterisation, but may require surgical intervention • Urinary tract obstruction can occur early or late. The diagnosis is confirmed by a percutaneous antegrade nephrostogram, during which a nephrostomy tube may be placed for temporary decompression. Subsequent percutaneous dilatation and insertion of a double J stent will often treat the stricture, with open surgery reserved for cases in which percutaneous management has failed • Fluid collections (lymphocoeles) around the transplant are a common finding on ultrasound scan but are only relevant if they become symptomatic or cause urinary obstruction. Percutaneous drainage gives temporary symptomatic relief. Definitive management involves drainage of the lymphocele into the peritoneal cavity and this fenestration can be performed laparoscopically.