2005 With Explanations (2005 AK No Answers) Flashcards

Question

20. Which of the following causes of polyuria is associated with a high urine specific gravity? A. Diabetes Mellitus B. SIADH C. Acute non-oliguric renal failure D. ATN

Answer 1

A. DM A. Diabetes Mellitus – High urine specific gravity and polyuria B. SIADH – I don’t think they have polyuria C. Acute non-oliguric renal failure – usually decreased specific gravity D. ATN – Also decreased specific gravity

Answer 2

B. Weak wrist extension

Answer 3

C. IFN-gamma Inhibits collagen synthesis. Remaining choices promote wound healing.

Answer 4

A. VII PT/INR measures: extrinsic pathway (VII) and common pathway factors including , V, X, prothrombin/thrombin (II), and fibrinogen/fibrin. PTT measures: intrinsic pathway factors (HMWK, prekallikrein, VIII, IX, XI, XII) and common pathwayfactors (II/thrombin, V, X and fibrinogen/fibrin)

Answer 5

B. Tremor Clinical Manifestations of Mg - Cardiac manifestations (7): 1. Prolonged PR interval 2. Prolonged QT 3. T-wave flattening 4. Tachyarrhythmias (unstable VT) 5. A. fib 6. Torsades de pointes 7. Digitalis toxicity enhanced as both inhibit the membrane pump -Neurologic manifestations: • Changes in mental status, seizures, Tremors, Hyperreflexia • All uncommon, non-specific and have little clinical value • Tremor is the MOST CHARACTERISTIC finding with hypomagnesemia but tetany is first sign.

Answer 6

A. Lefort I LEFORT I: Through maxilla (separates maxilla from rest of skull) LEFORT II: Maxilla inferior orbit lacrimal bone (bridge of nose) LEFORT III: Zygomatic arch lateral orbit inferior orbit lacrimal bone

Answer 7

C. 2cm Wide resection down to fascia. 2mm -trial French Cooperative Group consisted of 362 patients with melanomas ≤2 mm in thickness, who were randomly assigned to 2 cm versus 5 cm margins. There was no difference between the groups in the risk of local recurrence or in overall survival.

Answer 8

B. Primary Lung Cancer Small cell lung cancer is most common cause ~50 of SVC syndrome cases. (UptoDate)

Answer 9

C. Langerhans Cell Antigen presenting cells mediating skin immunity.

Answer 10

D. Multiple Fractures **of note, paget's doesn't normally cause elevated Ca2+, but can with periods of immobility. ``` Causes of hypercalcemia 1. Parathyroid mediated -Primary hyperparathyroidism (sporadic) Inherited variants -Multiple endocrine neoplasia (MEN) syndromes -Familial isolated hyperparathyroidism -Hyperparathyroidism-jaw tumor syndrome -Familial hypocalciuric hypercalcemia -Tertiary hyperparathyroidism (renal failure) ``` 2.Non-parathyroid mediated -Hypercalcemia of malignancy PTHrp -Activation of extrarenal 1 alpha-hydroxylase (increased calcitriol) -Osteolytic bone metastases and local cytokines -Vitamin D intoxication -Chronic granulomatous disorders -Activation of extrarenal 1 alpha-hydroxylase (increased calcitriol) 3. Medications - Thiazide diuretics - Lithium - Teriparatide - Excessive vitamin A - Theophylline toxicity 4. Miscellaneous - Hyperthyroidism - Acromegaly - Pheochromocytoma - Adrenal insufficiency - Immobilization - Parenteral nutrition - Milk alkali syndrome

Answer 11

A. Hyperkalemia ``` LABS • Hypo Na • Hypo Cl • Hypo Bicarb • Hypoglycaemia • Hyper K • +/- Hypercalcemia ```

Answer 12

D. Cross 1st and 2nd Fingers (Adduction) ``` Ulnar nerve innervates Below wrist: -Interossei - 3rd and 4th lumbricle -Hypothenars -Adductor Pollicis -Deep head of flexor pollicis braves ``` Above Wrist: - FCU - 4th and 5th FDS

Answer 13

B. Catecholamines Effects of EPI and NE (7) = mobilize glucose & run your ass off 1. Tachycardia 2. Ionotropy 3. Peripheral vasoconstriciton 4. METABOLIC RATE 5. Glycogenolysis 6. gluconeogenesis 7. Inhibition of insulin secretion

Answer 14

A. Basic Fibroblast Growth Factor C5a/C3a promote vasodilation Decreased wound O2 causes dehiscence IL-1 promotes and aggregates inflammatory response.

Answer 15

D. Antiemetics to counteract nausea Most common side effect.

Answer 16

C. Decreases thromboxane A2 production Mechanism of Heparin: 1. Accelerates the reaction between thrombin and anti-thrombin III, accelerating the inhibition of thrombin (II) and other serine proteases (VII, IX, X, XI, and Kallikreinin) by antithrombin III. It is not consumed by this reaciton 2. Directly binds and inhibits coagulation proteases and is important for the selective inhibitor of thrombin, heparin cofactor II. 3. Decreases platelet aggregability.

Answer 17

E. Greenstick fractures occur in children, but not in adults They can occur in adults, just much more uncommon. A &B are salter Harris 1&2, lowest potential for growth disturbance - potential for arrest increases as you go up the classification.

Answer 18

D. 2-point discrimination Pain is the first to return.

Answer 19

D. Elbow flexion C5-C6 responsible for elbow flexion. C7/C8- elbow extension/wrist extension/finger extension/finger flexion T1- Finger abduction

Answer 20

C. Odds Ratio The odds ratio equals the odds that an individual with a specific condition has been exposed to a risk factor divided by the odds that a control has been exposed. The odds ratio is used in case-control studies and is often generated in multivariate analyses. The odds ratio provides a reasonable estimate of the relative risk for uncommon conditions. (UptoDate) PPV - represents the likelihood that a patient with a positive test has the disease Sensitivity- the number of patients with a positive test who have a disease divided by all patients who have the disease. T-Test- test used to terming if two data sets are significantly different from each other, if both follow normal distribution.

Answer 21

C. Split Cast Supracondylars - associated with Volkmann's Ischemic Contractures (comparment syndrome causing decreased vascularity and schema). Want to decrease pressure, split the cast and monitor.

Answer 22

A. Irrigate, close, and send urgently to appropriate surgical specialist Nerve repair isn't an A-case, but is relatively urgent. Should irrigate the wound, can close because it's clean, and urgent referral (24 hrs or less) to plastics.

Answer 23

B. L5 nerve root injury at time of accident. Sensation of first dorsal webspace innervated by L5 nerve root.

Answer 24

B. Obtain an aortogram. Widened mediastinum is the most common signs of aortic dissection on radiographs- emergency, needs to be ruled out

Answer 25

A. Infection is the #1 cause of late death causes of death post transplant: 1. graft failure- first 30 days 2. infection - 6mos-1 year 3. Acute rejection 1 - 3 years 4. Cardiac Alograft Vasculopathy - after 1 year 5. Malignancy and Lymphoma - after 5 years (UptoDate) half of pts have ischemic disease, but better prognosis for those without

Answer 26

D. osteoclast inhibition

Answer 27

C. Ectopic gastric mucosa - Meckel's diverticulum is a true diverticulum, containing all layers of the small bowel wall. They arise from the antimesenteric surface of the middle-to-distal ileum. The diverticulum represents a persistent remnant of the omphalomesenteric duct, which connects the midgut to the yolk sac in the fetus. - Case series have found that 12 to 21 percent of patients with Meckel's diverticula have ectopic tissue within the diverticulum [5,10,25,26]. Gastric heterotopia is more common in patients with symptomatic versus asymptomatic Meckel’s diverticula [6,10,11].

Answer 28

A. Metformin Metformin is contraindicated in patients with factors predisposing to lactic acidosis. These predisposing factors/contraindications are: ●Impaired renal function ●Concurrent liver disease or alcohol abuse ●Unstable or acute heart failure at risk of hypoperfusion and hypoxemia ●Past history of lactic acidosis ●Decreased tissue perfusion or hemodynamic instability due to infection or other causes In clinical practice, some experts use an estimated glomerular filtration rate (eGFR) of >30 mL/min as a threshold for the safe use of metformin.

Answer 29

A. Confines tissue damage to between the tines. Bipolar advantages (5): 1. Less thermal injury to surrounding tissue 2. Less risk of patient burn 3. No interference with ECG 4. No interference with pacemakers 5. Can be used in wet fields

Answer 30

B FFP has all factors but VII has shortest half life It is used mostly for Vit K factors and is the only replacement that has Factor V (as per schwarz)

Answer 31

B. Restrict fluid to less than daily urine output Uptodate Water restriction to below the level of output is the primary therapy for hyponatremia in edematous states (such as heart failure and cirrhosis), the syndrome of inappropriate antidiuretic hormone secretion (SIADH), primary polydipsia, and advanced renal failure. Hyponatremia develops gradually in these settings and is not usually associated with overt symptoms. Restriction to 50 to 60 percent of daily fluid requirements may be required to achieve the goal of inducing negative water balance

Answer 32

C. Decreased urinary output Up to Date • Mild dehydration (3 to 5 percent volume loss) – A history of fluid losses may be the sole finding, as clinical signs may be absent or minimal. Such patients may have a reduction in urine output, but this may not be appreciated. • ●Moderate dehydration (6 to 9 percent volume loss) – Signs and symptoms are now apparent and can include the following: tachycardia, orthostatic falls in blood pressure, decreased skin turgor, dry mucous membranes, irritability, decreased peripheral perfusion with a delay in capillary refill between two and three seconds, and deep respirations with or without an increase in respiratory rate. There may be a history of reduction in urine output and decreased tearing, and, in infants, an open fontanelle will be sunken on physical examination. • ●Severe dehydration (≥10 percent volume loss) – Such children typically have a near-shock presentation as manifested by hypotension, decreased peripheral perfusion with a capillary refill of greater than three seconds, cool and mottled extremities, lethargy, and deep respirations with an increase in rate. Severe hypovolemia requires immediate aggressive isotonic fluid resuscitation to restore the effective circulating volume (ECV) and prevent ischemic tissue injury. • • They also say that decreased cap refill is one of the first signs of dehydration.

Answer 33

A. But very unlcear A. Impaired calcium metabolism B. Impaired renal bicarb reabsorption C. Impaired oxalate metabolism – Often diagnosed in kids. Nephrolithiasis, joint pain D. Medullary sponge kidney – Usually asymptomatic but can present renal calculi, UTIs, and hematuria

Answer 34

B. 70% ``` A=true positive=350 B = False positive= C=False negative=150 D=True negative=1200 Sensitivity = 350/(350+150) = 70% ``` Medbullets ``` 1. Sensitivity (SN) o % with disease who test positive o = a/(a+c) = TP/(TP+FN) 2. Specificity (SP) o % without disease who test negative o = d/(b+d) = TN/(FP+TN) 3. Positive predictive value (PPV) o % positive test results that are true positives o = a/(a+b) = TP/(TP+FP) 4. Negative predictive value (NPV) o % negative test results that are true negatives o = d/(c+d) = TN/(FN+TN) ```

Answer 35

B. IV antibiotics and chest tube drainage

Answer 36

D. Urinary metabolites of catecholamines Measuring plasma fractionated metanephrines is a first-line test when there is a high index of suspicion for pheochromocytoma. VHL is high suspicion

Answer 37

B Mono filament, non absorbable Prolene is less reactive than dexon (least reactive of absorbable) but more reactive than steel – steel is least reactive of all.

Answer 38

A. Salicylate poisoning * M-Methanol * U-Uremia (chronic kidney failure) * D-Diabetic ketoacidosis * P-Propylene glycol ("P" used to stand for Paraldehyde but this substance is not commonly used today) * I-Infection, Iron, Isoniazid, Inborn errors of metabolism * L-Lactic acidosis * E-Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.) * S-Salicylates

Answer 39

A. At end expiraton For positive pressure ventilation, this is when you read it.

Answer 40

A. Sciatic

Answer 41

C. Number of asthma attacks per month

Answer 42

D. Simultaneous administration of Tenanus toxoid and immunoglobulin • Tetanus • Check status with any wound • All TBSA burns > 10% require ppx • For clean wounds ○ If no reliable record of three prior toxoid injections or no booster for 10 yrs, give Td (tetanus diptheria) toxoid -- 0.5 cc tetanus toxoid IM ○ No further immunization necessary ○ If that injection is not third, pt should be scheduled to complete entire series ○ TIG not necessary • Dirty wounds ○ Td given if given > 5 yrs since previous booster ○ No TIG if complete immunization received ○ If status of series unclear: give TIG (250-500U IM, higher dose for long latency time and severity of injury) at same time as Td but diff locations ○ TIG inactivates toxin § Debridement is best way to prevent infection

Answer 43

A. It is associated with CMV Cardiac transplant • Can store for 6 hrs • Need ABO compatibility and cross match • For pts with life This is a duplicate question. I think the answer is actually C. They get diffuse atherosclerotic changes

Answer 44

D. Surgical Excision Preauricular tumors All lumps near ear are parotid gland tumors until proven otherwise Diagnosis usually made after superficial lobectomy

Answer 45

C. MI within last 6 months • Clinical Predictors of increased Perioperative Cardiovascular Risk • Major ○ Unstable coronary syndromes § Recent MI (w/I 30 d) with evidence of important ischemic risk by clinical sxs and non-invasive study § Unstable or severe angina (Canadian class III or IV) ○ Decompensated CHF ○ Significant arrhythmias § High grade AV block § Symptomatic ventricular arrhythmia in presence of underlying heart disease § Supraventricular arrhythmias with uncontrolled ventricular rate ○ Severe valve disease • Intermediate ○ Mild angina (Class I or II) ○ Prior MI with history of pathologic Q waves ○ Compensated or prior CHF ○ DM • Minor ○ Advanced age ○ Abnormal ECG (LBBB, ST-T abnormalities, left ventricular hypertrophy) ○ Rhythm other than sinus ○ Low functional capacity ○ History of CVA ○ Uncontrolled HTN

Answer 46

B. Perioperative blood transfusion

Answer 47

D. The dose of acetaminophen would exceed the recommended level Max tylenol 4g/day. Currently taking 325x2=650 q4h or 3.9g/day. If he increases, he will exceed tylenol max dose.

Answer 48

B. The lungs have a double blood supply Pulmonary and bronchial arteries

Answer 49

C. Sutures ○ Immediately after wound creation: i. Transient vasoconstriction (10 min) ii. Release of tissue thromboplastic factors iii. Vasodilation iv. Coagulation activation v. Complement activation vi. Hemostasis with platelet involvement that degranulate alpha and dense granules □ Alpha: contain PDGF and PF4, B-thrombomodulin, TGF-B; most notable effect is chemotaxis and inflammation □ Dense: vasoactive amines (vasodilation and increased permeability), ADP, serotonin, Ca vii. Platelet plug → fibrin mesh → clot (via intrinsic and extrinsic pathway acitvation) → vasoconstriction (via catecholamines, local smooth muscle response, thromboxane, PGF2A) → platelet degranulation (PDGF, TGF-B) causes chemotaxis → vasodilation after 10-15 min → endothelium becomes leaky allowing cells and materials to migrate (mediated by PGI2, PGE2, histamine, EGF) □ Clot of fibrin provides strength until collagen laid down (starts around 3-4 d) ® Epithelialization is most imp factor for early wound strength viii. Leukocytes chemo attracted immediately (by IL-1 and TNF-a from local monocytes, inh by steroids) and activated □ Resulting neutrophils/PMNs scavenge, debride, and kill bacteria ix. Lymphocytes proliferate and release cytokines (inh by steroids) □ Minor role except when there is heavy contamination x. Monocytes chemoattracted (inh by steroids) at same time as lymphocytes and reach peak number in 2-3 d (replace neutrophils) □ Activated into macros that phagocytose necrotic tissue and bacteria □ Macros also release ® IL-1, IL-6 -- further inflammation ® TNFa -- further inflammation and angiogenesis ® TGFa -- stims epidermal growth and angiogenesis ® TGFb -- chemoattracts and stims fibroblasts prodn of collagen and fibronectin, and angiogenesis [macrophages must be present for this to occur] □ Macros dominant cell type in this phase □ Mast cells and injured endothelial cells release histamine and PGs increase vascular permeability and vasodilate (like dense granules) § Days 0-2: PMNs § Days 3-4: macrophages § Days 5+: fibroblasts

Answer 50

A. Medication induced * Abnormal test repeated with mix of 50:50 pooled and pt plasma * If normal then deficiency of XI, IX, or VIII isolated. * If pooled abnormal then inhibitor present, or antiphospholipid. * If she had F8 or F9 (hemophilia) then she would likely have a history of bleeding. * Medication induced (at home) include LMWH

Answer 51

C. It maintains a high diastolic pressure Balloon pumps lead to: • A decrease in systolic pressure by 20 percent • An increase in diastolic pressure by 30 percent, which may raise coronary blood flow to territory perfused by a vessel with a critical stenosis • A reduction of the heart rate by less than 20 percent • A decrease in the mean pulmonary capillary wedge pressure by 20 percent • An elevation in the cardiac output by 20 percent

Answer 52

A. Intravascular sodium content

Answer 53

A. Delayed repair of facial fractures Nasoethmoidal orbital fractures - 70% have CSF leak Conservative tx for 2 weeks Can try epidural catheter to decease CSF pressure and help it close

Answer 54

B. Cellular response decreases tumour growth NK Cells • Not restricted to MHC, do no require previous exposure, do not require ag presentation • Not considered T/B cells • Recognize cells lacking self-MHC Part of body's natural immunosurveillance for cancer

Answer 55

C. Apical Bleb

Answer 56

B. Femoral embolectomy • Best given as one dose prior to case start ( 70 y.o. which acute cholecystitis and/or requiring choledochostomy (cephalosporins best) ○ Small/large bowel resections ○ Appendectomy for gangrenous or perforated appendix ○ Hysterectomy ○ Abdominal and LE revascularization ○ Clean OR with implant of high-risk prostheses (knee, hip, valve) ○ Sternotomy ○ Ischemic ulcer amputation ○ C-section (emergent) ○ Craniotomy ○ Known gross contamination ○ Dirty wounds ○ Injuries prone to clostridial infections (devitalized, heavy contamination, impaired blood supply) Procedures > 8 hrs

Answer 57

A. Emergency angioplasty

Answer 58

A. Thrombocytosis

Answer 59

A. Intact proprioception in feet

Answer 60

B. Staph aureus toxin Toxic shock syndrome ○ Inflammatory response to toxin resulting in fever, hypotension, shock and MODS ○ Staph endotoxin A prodn ○ Strep endotoxin A and B produced by beta hemolytic S pyogenes ○ Stimulate TNF, IL-1, and IFNy ○ Strep TSS has much higher mortality ○ Occur occurs in young healthy individuals ○ Patchy erythematous rash which desquamates 1-2 weeks later Starts on trunk

Answer 61

C. Associated with a monoclonal spike on protein electropheresis NOTE: lesions in MM are lytic, high ca, incr alk phos

Answer 62

D. Increased urinary calcium

Answer 63

B. Autosomal dominant transmission Defect in Ca metabolism Ca released from SR causes muscle excitation-contraction syndrome Side effects: 1st sign is increased end-tidal CO2, then fever, tachycardia, rigidity, acidosis, hyperK Tx: dantrolene inhibits Ca release and decouples excitation complex, cooling blankets, HCO3, glucose, supportive care

Answer 64

B. Electrical cardioversion Unstable patient with atrial fibrillation must be cardioverted

Answer 65

B. TGF-β Chemotactic factors: For inflammatory cells: TFG-b, PDGF, IL-8, LTB-4, C5a and C3a, PAF For fibroblasts: TGF-b, PDGF, EGF, FGF Angiogenesis factors: TGF-b, EGF, FGF, TGF-a, IL-8, hpyoxia Epithelialization factors: TGF-b, PDGF, EGF, FGF, TGF-a

Answer 66

A. Binds available Ca2+ resulting in a deleterious effect on myocardium Massive transfusion complications • Hypothermia (next most common when dilution thrombocytopenia isnt on list) causing: decreased plt function/clotting, hypoCa from increased citrate (liver cant convert it to HCO3), reduced citrate clearance, arrhythmias • Alkalosis bc citrate converted to HCO3 (except when liver is hypothermic) • Acidosis can occur b/c blood is acidic • Low 2-3 DPG in transfused pRBCs (decreased O2 release in periphery) • Citrate load: can cause hypoCa (hypotension, narrower PP, inc LVEDP, inc PAP, inc CVP, prolonged QT) • HypoCa: normally body can metabolize citrate readily • When in shock, decreased metabolism by liver causes it to bind Ca and Mg -- hypotension and arrhythmias ○ Give 1 amp of CaCl if this happens • K changes • Theoretic risk of hyperK but most are in shock with aldosterone, ADH, permissive steroids to they get hypoK • Dilutional TCP (most common complication) -- requires plt transfusion if microvasc bleeding unrelated to hypothermia develops • DIC • Dilutional coagulopathy • One of most common complications • 50% ofppl have INR > 2 and 33% have plt

Answer 67

C. TPN Normal AG acidosis usually due to loss of Na/HCO3 (ileostomies, small bowel fistula, RTA, diarrhea)

Answer 68

B. Detecting a cancer early when it is more amenable to successful therapy Primary - prevent disease occurence (i.e., HPV vaccination) Secondary - early disease detection (i.e., Pap smear) Tertiary - reduce disability from disease (i.e., Chemo) PDR (Prevent, Detect, Reduce Disability)

Answer 69

A. Renal Failure Primary hyperparathyroidism - solitary adenoma - expect increased Ca and PTH Secondary hyperparathyroidism - usually secondary to renal failure. Expect high PO4 / low Ca and resulting high PTH Tertiary hyperparathyroidism - after a long time develop hyperplasia of the parathyroid.

Answer 70

B. Bupivicaine

Answer 71

C. Insert an LMA

Answer 72

C. Acidosis and hypothermia

Answer 73

E: None of above HypoK: flattened T wave, U wave, low lying S-T segment

Answer 74

Answer – none – should be ST depression, increased PR, prolonged QRS, inverted T waves Explanation: Similar to hyperkalemia, hypokalemia produces changes on the ECG that are not necessarily related to the serum potassium level. There is depression of the ST segment, decrease in the amplitude of the T wave, and an increase in the amplitude of the U wave, best seen in leads V4 to V6. U waves are often seen in the lateral precordial leads V4 to V6. Other findings associated with hypokalemia include the following: ●The U wave and T wave merge in some cases to form a T-U wave, which may be misdiagnosed as a prolonged QT interval. ●The P wave can become larger and wider and the PR interval may prolong slightly ●The QRS duration may increase when the hypokalemia is more severe; in addition, the ST segment becomes markedly depressed, and T waves are inverted.

Answer 75

Answer - A - hypoglycemia 1. After head injury, BP goes up to try to achieve adequate cerebral perfusion pressure in the context of elevated ICP. 2. If CPP inadequate, you get pontine ischemia. 3. This results in Cushing’s reflex (brady + hypertensive) 4. Next, massive catecholamine release resulting in : Hypertension, tachycardia, peripheral vasoconstriction, increased O2 demands 5. Next, hypotension secondary to sympathetic outflow loss from brainstem damage and catecholamine depletion, fluid loss (most people go into diabetes insipidus at this point), cardiac dysfunction and ischemia (from autonomic storm, increased Calcium intake, hypothermia, hypoxia, decreased T3) 6. After brain death: hypothalamic + pituitary abnormal function, results in decreased T3/T4, diabetes insipidus, decreased ACTH production and cortisol production. Also, found an article that says 24-50% incidence of DIC post head-injury Hypoglycemia can commonly cause brain failure. Rarely, profound and prolonged hypoglycemia can cause brain death

Answer 76

Answer – B or C? Explanation – Signs of classical cardiac tamponade include 3 signs = Beck’s traid 1. Hypotension due to decreased stroke volume, 2. jugular venous distension due to impaired venous return to the heart, and 3. muffled heart stounds due to fluid buildup inside inside the pericardium Other signs of cardiac tamponade include: - Chest pain - Syncope or presyncope - Dyspnea and tachypnea - Tachycardia - Peripheral edema - Elevated jugular venous pressure - Pulsus paradoxus = drop of at least 10 mmHg in arterial blood pressure with inspiration Pulsus alternans = variation in pulse amplitude occurring with alternate beats due to changing systolic pressure; most commonly associated with left ventricular failure In cardiac tamponade there is equalization of the right atrial pressure, right and left ventricular diastolic pressure and pulmonary arterial diastolic pressures In cardiac tamponade, systemic venous return increases with inspiration, enlarging the right heart and encroaching on the left

Answer 77

Answer – B | Explanation – Hepatits B is the most common infectious disease transmitted through work- related exposure to blood

Answer 78

Answer – B Explanation – Antimetabolites interfere with the synthesis of nucleic acids and exert their immunosuppressive effects by inhibiting the proliferation of both T and B lymphocytes. Antimetabolite drugs were among the first effective chemotherapeutic agents discovered and are folic acid, pyrimidine or purine analogues. They are characterized by low molecular weights. They have similar structures as naturally occurring molecules used in nucleic acid (DNA and RNA) synthesis. Antimetabolites are similar to chemicals needed for normal biochemical activity, but differ enough so that they interfere with normal cell function. Generally, antimetabolites induce cell death during the S phase of cell growth when incorporated into RNA and DNA or inhibit enzymes needed for nucleic acid production. These agents are used for a variety of cancer therapies including leukemia, breast, ovarian and gastro-intestinal cancers Chlorambucil = alkylating agent Alkylating Agent Gemcitabine = antimetabolite Vinblastine =antimicrotubular Bleomycin = antineoplastic agent/antibiotic

Answer 79

Answer – B Explanation – Plasma renin levels can be used to classify hypertension. A significant proportion of hypertensive individuals display a low-renin profile and thus low-renin hypertension (LRH). LRH includes essential, secondary and genetic forms, the most common of which are low-renin essential hypertension and primary hyperaldosteronism. Suppressed renin release is one of the hallmarks of hypertension, induced by excess mineralcorticoid activity as with primary hyperaldosteronism. The role of mineralocorticoid excess in LRPH is supported by the observation that such patients derive greater blood pressure reduction with mineralcortiocoid antagonism than with other antihypertensive drugs.

Answer 80

Answer – B Explanation – While evidence favors aspirin for the prevention of thrombotic events in atherosclerotic disease, its efficacy for the prevention of VTE in medical and surgical patients is unclear. An older meta-analysis suggested that, compared with placebo, aspirin reduced the incidence of VTE by approximately 20 percent. However, other studies suggest that it is less efficacious when compared with LMW heparin. Renewed interest in aspirin, as a prophylactic agent in at-risk patients led to a multicenter randomized, controlled trial of aspirin in 778 surgical patients after total hip replacement (THR). All patients received 10 days of LMW heparin prior to randomization. Compared to LMW heparin, aspirin was associated with a lower rate of VTE that did not reach statistical significance for superiority (0.3 versus 1.3 percent). This trial was stopped early due to slow enrollment and event numbers were small which may explain why a four-fold difference in event rates between the groups was not reported as superior. The 2012 ACCP Guidelines included aspirin among the list of thromboprophylactic agents that can be considered for use in patients undergoing total hip or total knee arthroplasty or hip fracture surgery. However, its use was not unanimously supported. We also suggest that it can be considered, but is not the preferred agent, for extended VTE prophylaxis in this population of surgical patients.

Answer 81

Answer – B Explanation – Accepted methods of management of ICP and CPP are: - Sedation, analgesia and mild to moderate hyperventi~atien (PaCO2 4-4.5 kPa, 30-35 mmHg) - Volume expansion and inotropes or vasopressors when arterial blood pressure is insufficient to maintain CPP in a normovolaemic patient. - Osmotic therapy: preferably mannitol given repeatedly in bolus infusions, or as indicated by monitoring. Serum osmolarity should be maintained

Answer 82

Answer – B | Explanation – Half-life of factor VIII is 8-12 hours.

Answer 83

``` Answer – D Explanation – Major causes of hypokalemia – 1. Decrease potassium intake 2. Increased entry into cells o Elevation in extracellular pH o Increased availability of insulin o Elevated beta-adrenergic activity – stress administration of beta agonists o Hypokalemic periodic paralysis o Marked increase in blood cell production o Hypothermia o Chloroquine intoxication 3. Increased gastrointestinal losses o Vomiting o Diarrhea o Tube drainage o Laxative abuse 4. Increased urinary losses o Diuretics o Primary mineralocorticoid excess o Loss of gastric secretions o Non-reabsorbable anions o Renal tubular acidosis o Hypomagnesemia o Amphotericin B o Salt wasting nephropathies – including Bartter’s or Gitelman’s syndrome o polyuria 5. Increase sweat losses 6. Dialysis 7. Plasmapheresis A. Increased Excretion - Non-renal losses: Diarrhea, laxative abuse, vomiting - Renal losses: loop diuretics (furosemide, bumetanide, torsemide), thiazide diuretics (hydrochlorothiazide), osmotic diuresis (uncontrolled diabetes) - With hypertension: mineralcorticoid excess, primary hyperaldosteronism, glucocorticoid, apparent mineralcortiocid excess (11 beta hydroxysteroid dehydrogenase deficiency – genetic, drug induced (chewing tobacco, licorice)) - With normal blood pressure – Barterr’s syndrome, Gitelman’s syndrome, Magnesium depletion (cis-platinum, alcoholism), renal tubular acidosis (type 1 and 2) B. Transcellular shifts - Drugs – insulin administration - Beta-adrenergic agnoists – bronchodilators, decongestants, tocolyic agents, theophylline, caffine - Acyte catecholamine surger from stress eg acute myocardial infarction - Delirium tremens - Thyrotoxic hypokalemic paralysis - Familial hypokalemic periodic paralysis - Barium poisoning – metabolic alkalosis Hypokalemia can cause digoxin toxicity ```

Answer 84

Answer – B Explanation – PCWP = pulmonary capillary wedge pressure, or cross-sectional pressure (also called the pulmonary wedge pressure or pulmonary arterial wedge pressure or PAWP, pulmonary capillary wedge pressure or PCWP, pulmonary venous wedge pressure or PVWP, or pulmonary artery occlusion pressure or PAOP), is the pressure measured by wedging a pulmonary catheter with an inflated balloon into a small pulmonary arterial branch CVP = Central venous pressure also known as mean venous pressure (MVP) is the pressure of blood in the thoracic vena cava, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system Berlin Definition of ARDS requires that all of the following criteria be present to diagnose ARDS: ●Respiratory symptoms must have begun within one week of a known clinical insult, or the patient must have new or worsening symptoms during the past week. ●Bilateral opacities consistent with pulmonary edema must be present on a chest radiograph or computed tomographic (CT) scan. These opacities must not be fully explained by pleural effusions, lobar collapse, lung collapse, or pulmonary nodules. ●The patient’s respiratory failure must not be fully explained by cardiac failure or fluid overload. An objective assessment (eg, echocardiography) to exclude hydrostatic pulmonary edema is required if no risk factors for ARDS are present. ●A moderate to severe impairment of oxygenation must be present, as defined by the ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2). The severity of the hypoxemia defines the severity of the ARDS: •Mild ARDS – The PaO2/FiO2 is >200 mmHg, but ≤300 mmHg, on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H2O. •Moderate ARDS – The PaO2/FiO2 is >100 mmHg, but ≤200 mmHg, on ventilator settings that include PEEP ≥5 cm H2O. •Severe ARDS – The PaO2/FiO2 is ≤100 mmHg on ventilators setting that include PEEP ≥5 cm H2O. To determine the PaO2/FiO2 ratio, the PaO2 is measured in mmHg and the FiO2 is expressed as a decimal between 0.21 and 1. As an example, if a patient has a PaO2 of 60 mmHg while receiving 80 percent oxygen, then the PaO2/FiO2 is 60 mmHg/0.8 = 75 mmHg The above characteristics are the "Berlin criteria" of 2012 by the European Society of Intensive Care Medicine, endorsed by the American Thoracic Society and theSociety of Critical Care Medicine. They are a modification of the previously used criteria: • Acute onset • Bilateral infiltrates on chest radiograph sparing costophrenic angles • Pulmonary artery wedge pressure

Answer 85

Answer: D Explanation – Confirming the adequacy of resuscitation is more important than strict adherence to Parkland or any fluid resuscitation formula. Monitoring urine output using an indwelling bladder catheter (eg, Foley catheter) is a readily available means of assessing fluid resuscitation. Hourly urine output should be maintained at 0.5 mL/kg in adults. Patients with minimal or no urine output after sustaining severe burns, despite appropriate fluid resuscitation, generally do not survive. Clinical signs of volume status, such as heart rate, blood pressure, pulse pressure, distal pulses, capillary refill, and color and turgor of uninjured skin are monitored every hour for the first 24 hours. Inadequate fluid resuscitation is the most common cause of diminished distal pulses in the newly burned patient. Specific laboratory measurements such as mixed venous blood gas and serum lactate concentration are additional important guides to the adequacy of resuscitation. A decrease in mixed venous oxygen saturation and an increase in serum lactate suggest inadequate end-organ perfusion (elevated serum lactate can also occur with carbon monoxide or cyanide poisoning). If available, invasive monitoring, such as central venous pressure, may be useful for monitoring fluid resuscitation, but it is generally not used in acute burn management

Answer 86

Answer – A Explanation – Despite promising initial data, recombinant human activated protein C (rhAPC) has not been confirmed to improve survival in patients with severe sepsis or septic shock, prompting withdrawal of this drug from the market [60]. Recombinant human activated protein C (also called drotrecogin alfa) promotes fibrinolysis and inhibits thrombosis. It was hypothesized that rhAPC may benefit patients with sepsis because it modulates the procoagulant response that is believed to contribute to multisystem organ dysfunction. This hypothesis was initially tested in the PROWESS trial, which reported that rhAPC improved 28-day mortality in patients with severe sepsis or septic shock, with its greatest benefit among patients with a high risk of death (ie, APACHE II score ≥25) [61]. However, conflicting data from subsequent studies eventually led to a new trial, the PROWESS-SHOCK trial. In this trial, 1696 patients with vasopressor-dependent septic shock were randomly assigned to receive rhAPC or placebo [62]. Preliminary analyses done by the maker of the drug indicated that rhAPC did not improve 28-day mortality (26.4 versus 24.2 percent for placebo, RR 1.09, 95% CI 0.92-1.28). No evidence suggesting that activated protein C (APC) reduced the risk of death in adults or children with severe sepsis or septic shock. On the contrary, APC increased the risk of serious bleeding.

Answer 87

Answer - D | Explanation -

Answer 88

Answer – D Explanation – Children with Congenital Adrenal Hyperplasia are at risk for early puberty and adult short stature. Exposure to high levels of sex hormones can induce early puberty and premature epiphyseal closure. Excess glucocorticoid exposure secondary to treatment may also suppress growth and contribute to adult short stature.

Answer 89

Answer – C Note that afferent vasodilation and efferent vasoconstriction is not a mechanism of POD. Mechanisms include: volume overload, renal insensitivity to ADH, urea osmotic diuresis (most important in physiologic POD), elevated ANP.

Answer 90

Answer – C Explanation – Synthesis of Collagen - First, a three-dimensional stranded structure is assembled, with the amino acids glycine and proline as its principal components. This is not yet collagen but its precursor, procollagen. Procollagen is then modified by the addition of hydroxyl groups to the amino acids proline and lysine. This step is important for later glycosylation and the formation of the triple helix structure of collagen. The hydroxylase enzymes that perform these reactions require Vitamin C as a cofactor, and a deficiency in this vitamin results in impaired collagen synthesis and the resulting disease scurvy. These hydroxylation reactions are catalyzed by two different enzymes: prolyl-4-hydroxylase and lysyl-hydroxylase. Vitamin C also serves with them in inducing these reactions. In this service, one molecule of vitamin C is destroyed for each H replaced by OH.

Answer 91

Answer – A Explanation - Normal values: pH 7.35.7.45 paO2 75-100 pCO2 35-45 HCO3 22-26 BE -2 to 2 ABG Interpretation - 1. What is the pH? Is it alkolotic (57.45) or acidotic (67.35)? 2. What’s happening with the respiratory system (CO2) and the metabolic systems (HCO3- )? • If the problem is in the lungs (respiratory) the CO2 will be heading in the opposite direction of the pH. For example: respiratory acidosis: The pH will be low - pH 7.22 and the CO2 will be high - CO2 55mmhg • If the problem is metabolic the HCO3 will head in the same direction as the pH For example: metabolic alkalosis: The pH will be high – pH 7.55 and the HCO3- will also be high HCO3- 35mmol/L. Note: an easy way to remember for a “M”etabolic problem, think “M” as in the pH will head in the sa”M”e direction as the HCO3- . For respiratory the pH will head in the “O”pposite direction as the C”O”2. 3. Is there any (if any) compensation occurring? • No compensation: pH remains abnormal, and the ‘other’ value (where the problem isn’t occurring, i.e. CO2 or HCO3- ) will remain normal or has made no attempt to help normalise the pH. For example: in uncompensated metabolic acidosis: pH 7.23, HCO3- 15mmol/L, and the CO2 will be normal at 40mmHg. • Partial compensation pH is still abnormal, and the ‘other’ value is abnormal in an attempt to help normalise the pH. For example: in partially compensated respiratory alkolosis: pH 7.62, pCO2 27 and the HCO3- will be abnormal at 17mmol/L • Full compensation The pH is normal, as the ‘other’ value is abnormal and has been successful in normalising the pH. For example: Fully compensated metabolic acidosis pH 7.38, HCO3- 15mmol/L and the CO2 30mmHg

Answer 92

Answer – A Explanation – Both O2 and CO2 bind reversibly to hemoglobin, but certain other molecules, like carbon monoxide, are small enough to fit into the protein crevice, but form such strong bonds with the iron that the process is irreversible. Thus high concentrations of CO rapidly use up the body's limited supply of hemoglobin molecules, and prevent them from binding to oxygen. This is why CO is poisonous - the affected person rapidly dies of asphyxiation because his blood is no longer able to carry enough oxygen to keep the tissues and brain supplied. Hemoglobin binding affinity for CO is 200 times greater than its affinity for oxygen, meaning that small amounts of CO dramatically reduces hemoglobin’s ability to transport oxygen. When hemoglobin combines with CO, it forms a very bright red compound called carboxyhemoglobin. When inspired air contains CO levels as low as 0.02%, headache and nausea occur. If the CO concentration is increased to 0.1%, unconsciousness will follow. Hemoglobin binds with carbon monoxide 200–250 times more readily than with oxygen. The reaction: HbO2 + CO ↔ HbCO + O2, completely dissociates the oxygen molecules for the more favorable carbon monoxide, yielding Carboxyhemoglobin. Moreover, because of hemoglobin's affinity for carbon monoxide over oxygen, carbon monoxide is a highly successful competitor. Even at minuscule partial pressures, carbon monoxide can displace oxygen. When carbon monoxide binds to haemoglobin, it increases the strength of the haemoglobin-oxygen bond. This increased affinity for oxygen means that it cannot be given up to the tissues as readily and results in a shift of the oxygen dissociation curve to the left. The affinity of carbon monoxide for myoglobin is even greater than for haemoglobin1. Binding to cardiac myoglobin causes myocardial depression, hypotension and arrhythmias. Cardiac decompensation results in further tissue hypoxia and is ultimately the cause of death

Answer 93

Answer – B Explanation – From Wheeless’ Textbook of Orthopedics - the flexed view is usually most helpful in detecting ligamentous injury that is not apparent on the neutral view - determines the integrity of the supporting soft tissues and ligaments, as well as the stability of a known injury - subluxations may be the sequelae of ligamentous tears w/o frxs; - this malalignment may only be apparent w/ the dynamic study; - typically, this view is ordered at 7 to 10 days post injury when C-spine is less tender - Contraindications to flexion/extension views: - altered state of consciousness (closed head injury, intoxication, or combativeness); - documented neurologic deficit; - inability of patient to flex and extend the neck w/o assistance

Answer 94

Answer – C Explanation – Fusobacterium = anerobic gram negative bacilli (thin tapered ends). Part of the commensal flora of the oropharynx. It is an important pathogen for odontogenic infection. It has been associated with anaerobic pleuropulmonary infection (aspiration pneumonia, lung abscesses, nectrotizing pneumonia, empyema), brain abscesses, chronic sinusitis, liver abscesses, intraabdominal infections, skin infections (human bite wounds) and bacteremia. Typically susceptible to metronidazole, beta lactam/beta-lactamase inhibitor combinations and carbapenems. There is some resistance to penicillin and significant resistance to clindamycin and linezolid. Cephalosporins and moxifloxiacin do not have reliable activity.

Answer 95

Answer – B Explanation – Edrophonium (by the so-called Tensilon test) is used to differentiate myasthenia gravis from cholinergic crisis and Lamber-Eaton myasthenic syndrome. Myasthenia gravis (MG) is an autoimmune disorder and neuromuscular disease with characteristic symptoms of unpredictable and irregular bouts of muscle weakness and fatigability. MG is mediated by circulating anti-acetylcholine receptor antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction. A characteristic finding associated with MG is a bimodal peak incidence that usually occurs in females between the ages of 20 to 30 years and males greater than 60 years. The onset of this disorder is often sudden with reports of intermittent symptoms that become worse during periods of activity and improve after periods of rest. Feature signs and symptoms include weakness in the muscles that control eye and eyelid movements (ocular myasthenia), facial expression, chewing, swallowing (dysphagia), slurred speech (dysarthria) that is often associated with a nasal tone (dystonia) due to weakness of the velar muscles, and generalized muscle weakness that may involve the extremities and trunk. Ocular myasthenia symptoms vary in severity but usually include asymmetrical drooping of one or both eyelids (ptosis) and double vision (diplopia). In fact it is these two symptoms that are usually first reported by patients with MG. It is also worth mentioning that the occurrence of dysphonia and dysphagia are found to be the first symptoms related to late-onset MG. In severe cases, the muscles that control respiration can be affected (myasthenia crisis), and when this happens assisted ventilation is often required to sustain life. In patients whose respiratory muscles are already weak crisis may be triggered by infection, fever, or by an adverse reaction to a medication.Diagnosis of MG is based on a thorough physical examination, clinical testing, serologic testing, and imaging studies to rule out the commonly associated thymoma. In addition to the signs and symptoms as described above, other examinations that may facilitate the diagnosis of MG include applying ice to fatigued muscles to observe a characteristic increase in strength, and by performing and monitoring the following tests to observe the muscle fatigability. Clinical testing may involve the Edrophonium test, electromyography, and/or in severe cases, pulmonary function tests. The Edrophonium test is valuable when the diagnosis of MG is unconfirmed. This test is positive if there is increased muscle strength (especially observed in the eyes) after the administration of intravenous edrophonium chloride or neostigmine, drugs that temporarily increase the amount of acetycholine at the neuromuscular junction. Side effects associated with this test are usually mild (such as urinary or fecal incontinence and excessive salivation). Severe bradycardia and bronchoconstiction are rare risks associated with this test but can happen if parasympathetic supply of the cardiopulmonary system becomes over active. It is because of these effects closer cardiac monitoring is advised while performing this test. Also Edrophonium administration should be performed in a setting where immediate ventilatory support can be provided if needed. On the other hand, electromyography is considered to be one of the most sensitive tests in diagnosis of MG. Electromyography measures muscle fatigability by stimulating repetitive electrical impulses to muscle fibers Imaging studies are usually taken in patients with MG because studies have found the association of MG with thymoma to be about 15%, and 35% in older patients (Brachmann K, 1). A thymoma is considered a rare tumor of the thymus gland that is usually benign but when it becomes malignant it is extremely invasive. Thymomas represent about 50% of tumors in the anterior mediastinum and may grow in size and eventually squeeze blood vessels, the heart and/or lungs. The connection between the thymus gland and MG has led to the medical recommendation of a thymectomy. However, a thymectomy does not cure MG but may significantly decrease the symptoms of MG in 90% of patient

Answer 96

Answer – D Explanation – Most patients with acute pancreatitis have acute onset of persistent, severe epigastric abdominal pain. In some patients, the pain may be in the right upper quadrant or, rarely, confined to the left side.In patients with gallstone pancreatitis, the pain is well localized and the onset of pain is rapid, reaching maximum intensity in 10 to 20 minutes. In contrast, in patients with pancreatitis due to hereditary or metabolic causes or alcohol, the onset of pain may be less abrupt and the pain may be poorly localized. In approximately 50 percent of patients, the pain radiates to the back. The pain persists for several hours to days and may be partially relieved by sitting up or bending forward.Approximately 90 percent of patients have associated nausea and vomiting which may persist for several hours.Patients with severe acute pancreatitis may have dyspnea due to diaphragmatic inflammation secondary to pancreatitis, pleural effusions, or adult respiratory distress syndrome. Approximately 5 to 10 percent of patients with acute severe pancreatitis may have painless disease and have unexplained hypotension (eg, postoperative and critically ill patients, patients on dialysis, organophosphate poisoning, and Legionnaire's disease). Physical findings vary depending upon the severity of acute pancreatitis. In patients with mild acute pancreatitis, the epigastrium may be minimally tender to palpation. In contrast, in patients with severe pancreatitis, there may be significant tenderness to palpation in the epigastrium or more diffusely over the abdomen. Patients may have abdominal distention and hypoactive bowel sounds due to an ileus secondary to inflammation. Patients may have scleral icterus due to obstructive jaundice due to choledocholithiasis or edema of the head of the pancreas. Patients with severe pancreatitis may have fever, tachypnea, hypoxemia, and hypotension. In 3 percent of patients with acute pancreatitis, ecchymotic discoloration may be observed in the periumbilical region (Cullen's sign) or along the flank (Grey Turner sign). These findings, although nonspecific, suggest the presence of retroperitoneal bleeding in the setting of pancreatic necrosis. In rare cases, patients may have subcutaneous nodular fat necrosis or panniculitis. These lesions are tender red nodules that frequently occur on the distal extremities but may occur elsewhere. Fat necrosis is a form of necrosis characterized by the action upon fat by digestive enzymes. In fat necrosis the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to formsoaps. These soaps appear as white chalky deposits. It is usually associated with trauma of the pancreas or acute pancreatitis.

Answer 97

Answer – C Explanation – Warfarin inhibits the vitamin K-dependent synthesis of biologically active forms of the calcium-dependent clotting factors II, VII, IX and X, as well as the regulatory factors protein C, protein S, and protein Z. Other proteins not involved in blood clotting, such as osteocalcin, or matrix Gla protein, may also be affected. Pneumonic to remember: Canada vs Soviet Union 1972 (C S X IX VII II)

Answer 98

Answer – D Explanation – This is - Respiratory acidosis: pH decreased, PaCO2 increased, HCO3 normal Examples of causes of ABG changes: METABOLIC ACIDOSIS Can be caused by either an increase in circulating acids and or a loss of base (HCO3- ). These include: • Renal failure (unable to excrete acids or H+) • Lactic acidosis (increase in circulating acids) • Keto - acidosis (increase in circulating acids) • Diarrhoea (HCO3- loss) METABOLIC ALKOLOSIS Can be caused by an increase in HCO3- or loss of metabolic acids. These include: • Prolonged vomiting (acid loss) • GI suctioning (acid loss) • Hypokalaemia (H+ (an acid) excreted to maintain electrolyte balance) RESPIRATORY ACIDOSIS Caused by increased CO2 levels which is then converted to an acid (H+) as the body tries compensate by excreting acids via the kidneys. These include: • Hypoventilation: - sedatives/sedation/opiates • Depression of respiratory centre in brain stem via trauma • Pneumonia • Pulmonary oedema • Asthma RESPIRATORY ALKALOSIS Caused by a hyperventilation, the body getting rid of too much CO2, for example: • Anxiety • Hypoxaemia (caused by heart failure)

Answer 99

Answer – B Explanation – A branched-chain amino acid (BCAA) is an amino acid having aliphatic side-chains with a branch (a central carbon atom bound to three or more carbon atoms). Among the proteinogenic amino acids, there are three BCAAs: leucine, isoleucine and valine. Non-proteinogenic BCAAs include norvaline and 2-aminoisobutyric acid. Alanine can be manufactured in the body from pyruvate and branched chain amino acids such as valine, leucine, and isoleucine. Alanine is most commonly produced by reductive amination of pyruvate Branched-chain amino acids stimulate the building of protein in muscle and possibly reduce muscle breakdown. Branched-chain amino acids seem to prevent faulty message transmission in the brain cells of people with advanced liver disease, mania, tardive dyskinesia, and anorexia Most metabolic and catabolic activities of amino acids occur in the liver. However, a subgroup of essential amino acids, the branched-chain amino acids (BCAAs), including leucine, isoleucine, and valine, are catabolized in non-hepatic tissues, mostly cardiac muscle, neuron, andkidney BCAAs may be beneficial for use in : ♣ Alcohol abuse, anorexia nervosa, athletes. ♣ Heavy exercise, hepatic failure, hyper catabolic states. ♣ Low birth weights in infants, renal failure, stress, surgery and uremia Branched-chain amino acids are contraindicated in those with the rare inborn errors of metabolism maple syrup urine disease and isovaleric acidemia. BCAA’s are also contraindicated in those with hypersensitivity to any component of a BCAA-containing supplement.

Answer 100

Answer – A Explanation – The great saphenous vein (also referred to as the greater or long saphenous vein), which is the longest vein in the body, originates at the ankle as a continuation of the medial marginal vein of the foot and ends at the femoral vein within the femoral triangle. At the ankle, it crosses 1 cm anterior to the medial malleolus and continues up the anteromedial aspect of the lower leg. It continues its superficial course and lies on the posteromedial aspect at the level of the knee. In the thigh, the great saphenous vein courses anterolaterally through the fossa ovalis, where it joins the femoral vein approximately 4 cm below the inguinal ligament. Procedure – Saphenous vein cutdown Prepare the skin of the ankle with antiseptic solution (eg, povidone-iodine or chlorhexidine), and drape the area. Locate the vein 1 cm anterior and 1 cm superior to the medial malleolus. Anesthetize the skin over the area by infiltrating 1% lidocaine with or without epinephrine through a 25-gauge needle. Make a 2.5-cm full-thickness transverse skin incision over the site. With the curved hemostat, bluntly dissect the subcutaneous tissue parallel to the course of the great saphenous vein. Free the vein from its bed for a length of 2 cm. With the curved hemostat, pass the ties underneath the exposed vein proximally and distally. Ligate the distal exposed vein, and leave the free ends of the tie in place for traction. Place traction on the proximal tie to further expose the vessel from its bed. With the scalpel, perform a small transverse venotomy through no more than 50% of the total diameter of the vessel. Be extremely careful not to transect the vein fully. Introduce the plastic catheter through the venotomy opening, and secure it with the proximal tie. The opening of the venotomy site may be difficult to access; if so, try using a 20-gauge needle bent at a right angle as a vein elevator or dilator.Attach intravenous (IV) tubing to the catheter. Alternatively, the IV tubing can be inserted directly into the venotomy site for more rapid flow rates. The distal tubing can be cut on a bevel for easier insertion into the opened vein.Close the incision with simple interrupted sutures. Apply sterile dressing.

Answer 101

Answer – C Explanation – Nociceptive Pain: Nociceptive pain is believed to be caused by the ongoing activation of pain receptors in either the surface or deep tissues of the body. There are two types: "somatic" pain and " visceral" pain. "Somatic" pain is caused by injury to skin, muscles, bone, joint, and connective tissues. Deep somatic pain is usually described as dull or aching, and localized in one area. Somatic pain from injury to the skin or the tissues just below it often is sharper and may have a burning or pricking quality. Somatic pain often involves inflammation of injured tissue. Although inflammation is a normal response of the body to injury, and is essential for healing, inflammation that does not disappear with time can result in a chronically painful disease. The joint pain caused by rheumatoid arthritis may be considered an example of this type of somatic nociceptive pain.

Answer 102

Answer – C Explanation – Necrotising pneumonia (NP) is a severe complication of community-acquired pneumonia characterised by liquefaction and cavitation of lung tissue.

Answer 103

Answer – A Explanation– Long-term manifestations of injury caused by pelvic radiotherapy include abscess and fistula formation, stricture, mucus discharge, urgency, tenesmus, diarrhea, increased risk of cancer, and most commonly, bleeding. Most patients present with several symptoms; however, usually one symptom dominates

Answer 104

Answer – C | Explanation -

Answer 105

Answer – C | Explanation – ACLS algorithm

Answer 106

Answer - C Explanation - The use of leeches in modern medicine made a small-scale comeback in the 1980s after years of decline, with the advent of microsurgeries, such as plastic and reconstructive surgeries. In operations such as these, problematic venous congestion can arise due to inefficient venous drainage. Sometimes, because of the technical difficulties in forming an anastomosis of a vein, no attempt is made to reattach a venous supply to a flap at all. This condition is known as venous insufficiency. If this congestion is not cleared up quickly, the blood will clot, arteries that bring the tissues their necessary nourishment will become plugged, and the tissues will die. To prevent this, leeches are applied to a congested flap, and a certain amount of excess blood is consumed before the leech falls away. The wound will also continue to bleed for a while due to the anticoagulant hirudin in the leech's saliva. The combined effect is to reduce the swelling in the tissues and to promote healing by allowing fresh, oxygenated blood to reach the area.

Answer 107

A. FEV1 less than 50% predicted value Indicators of significant risk of postoperative ventilatory failure: - Resp rate greater than 40/min - PaCO2 greater than 50mmHg - PaO2 less than 60 mmHg - gradient greater than 300mmHg on 100% O2 - Vd/Vt ratio 0.6 - FVC less than 15 ml/kg - FEV1 less than 50% predicted value (Fundamentals of Surgical Practice)