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1. a. b. c. d. e. Pure mitral stenosis: tends to cause a loud first heart sound T produces displacement of the apex beat F Produces a diastolic murmur, the duration of which, rather then the intensity, determines degree of stenosis T Is better heard with the diaphragm than F the bell of the stethoscope Is louder on inspiration F Mitral stenosis causes a low volume pulse and is commonly linked to Atrial fibrillation. There may be a palpable S1 as it tends to be quite loud, but UNDISPLACED “tapping” apex beat. However, the left atrium may be enlarged to compensate for the defective valve, causing cardiomegaly on CXR. The murmur starts with the rigid valve opening, causing a “snap”, followed by mid-diastolic, lowpitched murmur, best heard with the bell in left lateral position. Although on a world-wide basis quite common, Mitral stenosis has become rare in the developed world as a result of a decline in rheumatic heart disease. In practice, all MS relates to prior RF. Typical presentation is progressive exertional dyspnea in 40-50 year olds. Other presentations may include A.Fib and thromboembolic disease. Mitral facies (malar flush) may also be seen. The severity of MS is established by duration of the diastolic murmur, and the closer the opening snap is to S2. The severity of MR is established by the size of the left ventricle. AS is determined by signs of left ventricular hypertrophy. Murmurs louder on inspiration tend to be right heart while those louder on expiration tend to be left heart… 2. a. b. c. d. e. The following may cause sinus tachycardia Anemia T Atropine T atrial flutter F thyrotoxicosis T carotid sinus massage F Common causes of sinus tachycardia include - pain, fever, hypovolemia, hypoxia, anemia, anxiety, beta-agonists Thyrotoxicosis increased sympathetic drive and thus leads to sinus tachycardia (and is also linked to A.fib) Carotid sinus massage causes vagal stimulation, which decreases heart rate (sinus BRADYcardia) Atrial flutter is a circular re-entrant arrhythmia that bypasses the sinus node. Atropine is a parasympathetic antagonist, acting via acetylcholine receptor antagonism. It causes sinus tachycardia by blocking the heart-slowing effects of the parasympathetic nervous system (via vagus nerve). 3. a. b. c. d. e. Signs of aortic regurgitation include anacrotic pulse wide pulse pressure corrigans neck pulsation durozier’s sign Austin-flint murmur T T T T T Classic eponymous signs of Aortic insufficiency/regurg include Corrigan’s pulse: “Water-hammer” pulse (rapid rise and fall/collapsing) Hill’s sign: (Popliteal SBP-Brachial SBP)> 60 mm Hg Duroziez’s sign: Gradual pressure over femoral artery causes systolic and diastolic bruits Traube’s sound: double sound heard at femoral artery when compressed distally deMusset’s sign: head bobbing with each heartbeat Muller’s sign: systolic pulsations of the uvula Quinke’s pulses: subungual capillary pulsations Austin-Flint murmur: diastolic rumble at apex (AI jet interferes with mitral inflow). Diastolic decrescendo murmur at left upper sternal base, increased by sitting forward, expiration and handgrip. 4. a. b. c. d. e. A third heart sound may be heard in: cardiac failure mitral incompetence systemic HTN with normal ECG pure mitral stenosis contrictive pericarditis T T F F T Heart failure can cause a “gallop rhythm” which is associated with an S3 (third heart sound). This gallop rhythm is specific for Left heart failure. It’s easy to remember what causes S3 cause they all appear to cause heart failure (MR, Constrictive pericarditis, AR etc). HTN doesn’t necessarily cause heart failure nor would MS. In mitral regurgitation, the murmur is at the apex, pansystolic and loud. It may NOT be pansystolic in functional MR. The murmur radiates up the left ventricular outflow tract. An S3 may be heard due to volume overload. Systemic HTN is not sufficient to cause an S3, unless associated with abnormality. Normal ECG and systemic HTN are not by themselves or together associated with S3. Mitral stenosis does not cause an S3. An opening snap, followed by a middiastolic murmur, is more characteristic. Constrictive pericarditis is caused by TB or radiotherapy, and leads to an acute, chronic or relapsing course. Pericardial fibrosis sufficient to constrict the heart leads to impaired cardiac filling and decreased cardiac output. Progressive exertional dyspnea, peripheral edema and ascites can occur. The increase in intravascular volume cause increased JVP-a pericardial knock also occurs in diastole (loud diastolic heart sound). Diuretics relieve symptoms and surgery may be needed. S3 is present (just think it causes heart failure). 5. a. b. c. d. e. Recognized features of acromegaly include loss of libido T reduced fields of vision T arterial HTN T hydronephrosis F enlargement of the tongue T Acromegaly usually results from a GH secreting tumor of the pituitary (pituitary adenoma). Signs and symptoms include: - increased soft tissue, arthralgias, jaw enlargement (“lantern jaw”) - carpal tunnel syndrome, headache, macroglossia, hoarseness - sleep apnea, amenorrhea, impotence, DM, acanthosis, sweating, HTN - glucose intolerance, cardiomyopathy Since acromegaly typically results from pituitary adenoma, which can cause visual field disturbance (classically bitemporal hemianopia), reduced fields of vision may feature in acromegaly. 6. a. b. c. d. e. Nephrotic syndrome is a well recognized feature of chronic pyelonephritis F renal papillary necrosis F thrombosis of renal veins F proliferative glomerulonephritis T disseminated lupus erythematosis T Nephrotic syndrome is the triad of proteinuria (>3g/day), hypoalbuminemia (albumin <30g/L) and edema. Causes of nephrotic syndrome can be categorized into primary glomerular disease or Systemic disease. PRIMARY glomerular diseases causing nephrotic syndrome include: - focal segmental glomerulosclerosis - membranous nephropathy: includes HBV/HCV/syphilis/SLE/RA/Sjogrens/breast,lung,colonCa/ Drugs (gold/penicillamine/ACEi/NSAIDs) - minimal change disease - membranoproliferative glomerulonephritis - glomerulopathy - IgA nephropathy - Mesangial proliferative GN SYSTEMIC diseases include: - Diabetes mellitus (Kimmelsteil-Wilson lesion in kidney reflects nodular glomerulosclerosis large kidneysmicroalbuminurianephrotic range in 10-15 years. - Amyloidosis/SLE/Cryoglobinemia Incidentally, nephritic syndrome comprises hematuria and proteinuria. It is usually associated with hypertension, pulmonary edema, oliguria and rising plasma urea and creatinine. Nephritic syndrome causes include ANCA vasculitis, anti-GBM disease, and immune complex disease (both renal-limited and systemic). ANCA vasculitis includes Churg-Strauss syndrome, Microscopic polyangiitis and Wegener’s granulomatosis. Anti-GBM disease includes both anti-GBM disease (limited to linear staining of kidneys ONLY) and Goodpastures (includes linear staining of renal and pulmonary areas). Immune complex disease can be renal-limited (post-streptococcal GN, membranoproliferative GN, fibrillary GN, IgA nephropathy) or systemic (SLE, endocarditis, Henoch-Schonlein purpura, cryoglobinemia). 7. a. b. c. d. e. Excretion urography can be diagnostic in chronic pyelonephritis F acute glomerulonephritis F renal artery stenosis F polycystic kidney disease F nephritic syndrome F Excretion urography is a study for defining anatomy and detecting pathology distorting the collecting system. Abdominal films are taken before and after IV contrast, which is filtered goes from renal artery to kidney, reaching the glomeruli, then renal tubules, then collecting ducts, then minor then major calyces, then renal pelvis, then ureters, then bladder. Xrays are taken (KUB) to radiologically visualize. Nephritic syndrome is diagnosed by proteinuria and hematuria, both of which can be diagnostically established my urine sample Polycystic kidney disease can not be detected by urography, since the cysts are on the outside of the kidney and not part of the collecting system. While renal artery stenosis can be detected by excretion urography, it is usually at the glomeruli that the initial part of the study is considered. Moreover, a renal arteriogram is considered diagnostic. The cause of acute glomerulonephritis can not be determined by excretion urogram. Usually the diagnosis is made by FBC, U+E, LFTs, ESR/CRP, Ig, complement (C3,C4) and autoantibodies, blood culture, ASOT, and detection of protein or blood in the urine (for nephrotic or nephritic syndrome) is commonly done. A renal biopsy or ultrasound may also be needed. 8. a. b. c. d. e. Hemolytic anemia is a feature of Malaria T tropical sprue F hookworm disease F thalassemia T brucellosis F Hemolytic anemia is classified into congenital or acquired causes. Congenital hemolytic anemias are classified into cell wall defects, metabolic defects and hemoglobin defects. CONGENITAL Cell wall defects: Hereditary spherocytosis, hereditary elliptocytosis Metabolic defects: G6PDH or pyruvate kinase deficiency Hemoglobin defects: Thallessemias and sickle cell disease ACQUIRED Drugs Penicillin, Cephalothin, Ampicillin Methicillin, Quinine, Quinidine Autoimmune Cold or warm antibody mediated Warm-antibody: SLE, IBD, CLL, Non-Hodgkins Cold-antibody: Mycoplasma pneumoniae, EBV/CMV Infection Hep C, EBV Cardiac: Prosthetic valve Hemolytic transfusion reaction Microangiopathic TTP, HUS, Paroxysmal nocturnal hemoglobinuria rbc GPI-anchored protein that normally binds (and thus inactivates) complement 9. a. b. c. d. e. Peripheral neuropathy is a recognized complication of Diphtheria T Leprosy T snake bite ? weil’s disease F typhus F Typhus is causes by Salmonella typhi and causes headache, dry cough and constipation. Fever and bradycardia occur and precede a erythematous maculopapular rash. Splenomegaly, lymphadenopathy and hepatomegaly occur, and complications may include pneumonia, meningitis, acute cholecystitis, osteomyelitis, intestinal perforation and hemorrhage. Peripheral neuropathy is the medical term for damage to nerves of the peripheral nervous system, which may be caused either by diseases of the nerve or from the sideeffects of systemic illness. Peripheral neuropathies vary in their presentation and origin, and may affect the nerve or the neuromuscular junction. Neuropathies can be classified into polyneuropathies or mononeuropathies. Causes of polyneuropathies can be diabetes, amyloidosis, renal failure, alcohol, vasculitis, cancer, alcohol. Mononeuropathies can be caused by diabetes, vasculitis, leprosy, sarcoid, cancer and HIV. Infective causes include leprosy, Lyme disease, HIV and diphtheria. Agent Orange defoliants used by the US armed forces during the Vietnam War is also a major cause of peripheral neuropathy. Mechanical pressure from staying in one position for too long, a tumor, intraneural hemorrhage, exposing the body to extreme conditions such as radiation, cold temperatures, or toxic substances (including some chemotherapy drugs such as vincristine) can also cause peripheral neuropathy. Many of the diseases of the peripheral nervous system may present similarly to muscle problems (myopathies), and so it is important to develop approaches for assessing sensory and motor disturbances in patients so that a physician may make an accurate diagnosis. Peripheral neuropathies may either be symmetrical and generalized or focal and multifocal, which is usually a good indicator of the cause of the peripheral nerve disease. Generalized peripheral neuropathy Generalized peripheral neuropathies are symmetrical, and usually due to various systematic illnesses and disease processes that affect the peripheral nervous system in its entirety. They are further subdivided into several categories: Distal axonopathies are the result of some metabolic or toxic derangement of neurons. They may be caused by metabolic diseases such as diabetes, renal failure, deficiency syndromes such as malnutrition and alcoholism, or the effects of toxins or drugs. Myelinopathies are due to a primary attack on myelin causing an acute failure of impulse conduction. The most common cause is acute inflammatory demyelinating polyneuropathy (AIDP; aka Guillain-Barré syndrome), though other causes include chronic inflammatory demyelinating syndrome (CIDP), genetic metabolic disorders (e.g., leukodystrophy), or toxins. Neuronopathies are the result of destruction of peripheral nervous system (PNS) neurons. They may be caused by motor neurone diseases, sensory neuronopathies (e.g., Herpes zoster), toxins or autonomic dysfunction. Neurotoxins may cause neuronopathies, such as the chemotherapy agent vincristine. Signs and symptoms Those with diseases or dysfunctions of their peripheral nerves can present with problems in any of the normal peripheral nerve functions. In terms of sensory function, there are commonly loss of function (negative) symptoms, which include numbness, tremor, and gait imbalance. Gain of function (positive) symptoms include tingling, pain, itching, crawling, and pins and needles. Pain can become intense enough to require use of opiate drugs (i.e., morphine, oxycontin). Weil’s disease is caused by leptospira interrogans, and is characterized by hepatosplenomegaly, jaundice, hemolytic anemia, myocarditis and renal failure with hematuria. 10. The following associations are correct a. Early morning waking and depression b. Morning headache and depression c. SLE and psychosis d. Late pregnancy and Down’s syndrome e. Right sided endocarditis and drug addiction T F T T T Depression causes, classically, early morning waking, poor sleep, and early REM onset. Morning headache is not associated with depression. It may related to increased intracranial pressure, SLE can cause effects on the: Brain: fits/psychosis/anxiety/headaches Lungs PE from antiphospholipid syndrome, pulmonary fibrosis Hands Arthralgia, Raynauds Legs Peripheral neuropathy, Myositis Skin Malar rash, livedo reticularis (antiphospholipid antibody) HTN End stage renal disease Fetal loss Drug addiction classically causes endocarditits of the valves on the right side of the heart (tricuspid or pulmonary). The incidence of Down’s syndrome increases as maternal age increases. At age 20, the risk is 1 in 1500. At age 40, the risk is 1 in 40. Nuchal tranluscency test takes the sum of the thickness of the fold of skin over the back of the fetal nack and size of baby, between 11 and 14 weeks. A greater translucency is associated with greater risk of Down’s syndrome. A high NT is also associated with trisomy 18, trisomy 13 and Turner’s syndrome. 11. Regarding pernicious anemia: a. Hypersegmentation of neutrophils is a common finding b. Glossitis may be seen c. Platelets are usually normal d. Low serum B12 levels are diagnostic e. Histamine-fast achlorhydia is usual T T T F T Pernicious anemia involves autoantibodies against parietal cells, causing lack of acid and intrinsic factor. The lack of acid causes chronic fundal gastritis, achlorhydia and hypergastrinemia. The lack of intrinsic factor causes insufficient B12 absorption in the terminal ileum and thus B12 deficiency, associated with megaloblastic anemia, peripheral neuropathy in posterior and lateral columns (decrease vibration and position sense, ataxia), glossitis (red sore tongue), angular stomatitis, mild jaundice. Leucopenia and thrombocytopenia may be present in severe cases of B12 deficiency. Megaloblastic anemia is associated with neutrophil hypersegmentation (B12 also needed in development of wbc), increased LDH and indirect bilirubin. The macrocytotic anemia develops because the cytoplasm develops faster than the nucleus, which (as we all remember from histology) is extruded from the rbc during development. For diagnosis to be made in pernicious anemia, serum autoantibodies must be present. 12. In rheumatoid arthritis a. ESR is good index of disease activity T b. Renal lesions commonly occur F c. Amyloidosis may develop T d. Nodules may occur over bony prominences T e. Osteoporosis is a common radiological finding adjacent to the affected joint T Rheumatoid arthritis is a chronic symmetrical polyarthritis of unknown cause. RA affects 1-3% of population worldwide. Women are affected 3x more commonly than men. RA is a disease of the synovium, causing infiltration of chronic inflammatory cells (lymphocytes, plasma cells and macrophages) with secretion of proinflammatory cytokines. Presentation is with pain, stiffness and swelling in small joints of hands and feet, marked on waking (early morning stiffness). Ulnar deviation, Boutonniere deformity and Swan neck deformity are common and swelling in metacarpophalangeal and proximal interphalangeal joints are common. The DIP joints are SPARED. Rheumatoid nodules are present in 20% of cases, usually on the ulnar surface of the forearm just below the elbow (may be over the bony part of the elbow). ESR and CRP are raised in proportion to the activity of the inflammatory process. Serum antibodies are positive in 70% of cases and antinuclear factor in 30%. Radiology shows joint space narrowing, erosions of margins of joints and porosis of periarticular bone and cysts. Extraarticular manifestations of RA include: Systemic: Fever, fatigue, weight loss Eyes: Sjogrens, scleritis, scleromalacia perforans (eye perforation) Neurological Carpal tunnel syndrome, Atlanto-axial subluxation, cord compression, polyneuropathy, mononeuritis multiplex Reticuloendothelial Lymphadenopathy, Felty’s (RA, splenomegaly, neutropenia) Blood Anemia (chronic disease, hypersplenism, NSAIDs, hemolysis) Thrombocytosis Pulmonary rheumatoid nodules, small airway disease, diffuse fibrosing alveolitis, Caplans (rheumatoid pneumoconiosis) Heart Pericarditis, pericardial effusion Kidneys Amyloidosis, analgesic nephropathy Vasculitis While renal amyloidosis CAN occur, it tends not to be terribly common. Osteoporosis is a reduction in bone mass causing thin bone. It includes all bone components, not just calcium. Increased risk of fracture is common. 13. Gynecomastia may occur with a. Adrenal tumors b. Renal tumors c. Cirrhosis of liver d. Myxoedema e. Digitalis treatment T F T F T Gynecomastia is the development of benign breast tissue in the male and is the result of an increase in the estrogen:androgen ratio. Causes include: - liver disease - neonatal (from maternal hormones) - early puberty/old age - hypogonadism - estrogen producing tumors of the testis or adrenal gland - HCG tumors of the testis or lung - PRL secreting tumors of the pituitary - Hyperthyroidism (not hyPOthyroidism aka myxoedema) Drugs: spironolactone, digitalis, cyproterone, cimetidine, estrogens, heroin, cannabis 14. Sacro-iliac involvement is commonly found in the arthropathy of: a. ankylosing spondylitis T b. Reiter’s syndrome T c. Gout F d. Rheumatoid arthritis F e. Ulcerative colitis T Seronegative spondyloarthropathies include: AnkSpon Reactive Sex M>F M>F Age <30 <30 Peripheral joints 40% >90% Axial spine (sacroiliitis) 100% 20% IBD M=F any >90% 30% Psoriasis M=F any >90% 30% Extra-articular Uveitis Conjunctivitis Skin Mucous membrane Aortic incompetence Urethritis Prostatitis + + + 0 0 0 0 + ++ +++ 0 0 0 0 +++ 0 0 0 + 0 ++ ++ +++ ++ + (balanitis) + ++ ++ 15. Hypokalemia can be associated with a. Administration of insulin T b. Conn’s disease T c. Addison’s F d. Diarrhea T e. Terminal stages renal failure F Hypokalemia can be caused by: Gastrointestinal loss: vomiting or diarrhea Urinary tract loss: Diuretic therapy, mineralicorticoid excess (Cushing’s, Conn’s, ectopic ACTH tumors, secondary hyperaldosteronism [RAS, HTN, heart failure] all excessive aldosteroneinc Na+/K+ ATPase activity increased Na+ absorption+ increased K+ excretion Poor intake: Beta stimulation: renal tubular acidosisinc activity H+/K+ exchanger increased H+ reabsorption and increased K+ excretion eating disorders Causes increased potassium into cells Hyperkalemia can be caused by: Hypoaldosteronism: Addison’s, spironolactone/amiloride, ACE inhibitors Cell destruction hemolysis, cytotoxic therapy, rhabdomyolysis Renal failure The ECG changes for altered potassium levels are fairly classic HyPOkalemia: Increased P wave, short QRS, short ST interval, flat/inverted T wave, U waves HyPERkalemia: Decreased P wave, wide QRS (+sine wave), prolonged ST interval, peaked T wave 16. A 75 year old male patient with gross painless hematuria a. Should have a rectal examination T b. May have TB T c. Should be reassured if JVP normal F d. Should be given Vitamin K F e. Is likely to have renal stones F Hematuria can be caused by intrarenal or extrarenal causes. Extrarenal causes are much more common. EXTRArenal: Nephrolithiasis neoplasm (prostate/bladder) infection (urethra/bladder/prostate) Trauma from foley catheter INTRArenal Nephrolithiasis or crystalluria Neoplasm Infection Trauma Vascular (renal infarct, renal vein thrombosis) Glomerulonephritis “Blood In Urine Goes To Nephrotic Syndrome” = Blood clot (vascular), Infection, urine, Glomerulonephritis, Trauma, Neoplasms, Stones Rectal examination may confirm the presence of a prostate neoplasm, or texture consistent with prostatitis. TB may cause infection of the bladder, prostate or urethra. JVP being normal means absolutely nothing as far as reassuring this patient. Vitamin K is given only if the source of the bleeding is related to vitamin K deficiency. As noted above, none of these causes relate to vitamin K deficiency While renal stones do commonly cause hematuria, and men are affected three times more often than women, the peak age is 30-40. Similar pain presentation in a 75 year old male should raise suspicion of AAA. Incidentally, renal stones can be composed of calcium oxalate, urate, cystine, xanthine, calcium phosphate. 17. Fibrosis of the left upper lobe a. TB is likely cause b. Trachea is deviated to the right c. Tactile vocal fremitus increased in the left apex d. Apex displaced left e. Hamman’s sign F F F T F Spontaneous pneumomediastinum may be defined as the presence of free air in the mediastinal structures without an apparent precipitating cause. Pneumomediastinum was first reported by Laennac[2] in 1819, when he described an entity termed interlobular emphysema, which consisted of free air in the tissues of the body. In 1927, Gordon[3] described 127 cases of subcutaneous emphysema and dyspnea in women following childbirth. Spontaneous pneumomediastinum remained a poorly recognized problem, however, until 1939, when Hamman[4] described a precordial crunching noise synchronous with the heart beat - Hamman's sign - in seven patients, and recognized that it was related to free air within the mediastinal compartment. Disorder Mediastinal Chest wall Displacement Movement Consolidation NONE decreased Collapse I/L decreased Pneumothorax C/L (tension) decreased Pleural effusion C/L decreased Percussion Dull Dull Resonant Stony dull Breath Sounds bronchial decreased decreased absent Resonance Fremitus increased decreased decreased decreased Pulmonary Fibrosis involves scarring of the lung. Gradually, the air sacs of the lungs become replaced by fibrotic tissue. When the scar forms, the tissue becomes thicker causing an irreversible loss of the tissue’s ability to transfer oxygen into the bloodstream. Symptoms of pulmonary fibrosis include: Shortness of breath, particularly with exertion Chronic dry, hacking cough, Fatigue and weakness, Discomfort in the chest, Loss of appetite, Rapid weight loss There are five million people worldwide that are affected by this disease. In the United States there are over 200,000 patients with Pulmonary Fibrosis. As a consequence of misdiagnosis the actual numbers may be significantly higher. Of these more than 40,000 expire annually. Traditional theories have postulated that it might be an autoimmune disorder, or the after effects of an infection, viral in nature. There is a growing body of evidence which points to a genetic predisposition. A mutation in the SP-C protein has been found to exist in families with a history of Pulmonary Fibrosis. The most current thinking is that the fibrotic process is a reaction to microscopic injury to the lung. While the exact cause remains unknown, associations have been made with the following: Inhaled environmental and occupational pollutants Cigarette smoking Diseases such as Scleroderma, Rheumatoid Arthritis, Lupus and Sarcoidosis Certain medications Therapeutic radiation Current treatments are relatively ineffective. Corticosteroids have been tried, and recent trials of interferon may be promising. Lung transplant is effective, but all too often not available. I could find nothing specific to the clinical examination findings in interstitial fibrosis…so my answers above are based on the assumption that fibrosis, being scarring, causes pseudo-contraction of the tissues in the area and thus deviation ipsilaterally, and bronchial breath sounds… 18. Clinical features of acute hepatitis include a. Dislike of cigarettes T b. Splenomegaly T c. Glycosuria F d. Anorexia T e. Bilirubinemia T Hep C affected smokers may find a sudden dislike for cigarettes. Acute hepatitis causes malaise, anorexia, jaundice, splenomegaly (10% HepA), arthralgia, and abnormal LFTs. Abnormal LFTs tend to be a predominant hepatocellular derangement of transaminases (AST/ALT). There is a less marked rise in bilirubin and alkaline phosphatase. 19. Following statements are correct a. Carpal tunnel syndrome is commonest in middle aged women b. Pretibial myxoedema is seen in thyrotoxicosis c. Cushing’s syndrome in females usually gives rise to amenorrhea d. Acromegaly may give rise to HTN e. Calcified ascending aorta on Xray suggests syphilis T T T T F Women are three times more likely than men to develop carpal tunnel syndrome, perhaps because the carpal tunnel itself may be smaller in women than in men. The dominant hand is usually affected first and produces the most severe pain. Persons with diabetes or other metabolic disorders that directly affect the body's nerves and make them more susceptible to compression are also at high risk. Carpal tunnel syndrome usually occurs only in adults. The risk of developing carpal tunnel syndrome is not confined to people in a single industry or job, but is especially common in those performing assembly line work - manufacturing, sewing, finishing, cleaning, and meat, poultry, or fish packing. In fact, carpal tunnel syndrome is three times more common among assemblers than among data-entry personnel. A 2001 study by the Mayo Clinic found heavy computer use (up to 7 hours a day) did not increase a person's risk of developing carpal tunnel syndrome. Carpal tunnel syndrome can occur in people of any age, but it most often occurs in people 50 or older (OK, “middle age” should refer to the middle of average life expectancy, say about 35-40…Is 50 “middle aged”? My dad is 63 and says he’s “middle aged.” I’m going with true.) Pretibial myxoedema is seen in thyrotoxicosis, though hypothyroidism is also known as myxoedema Syphilis may affect the aorta, but does so on the descending portion. Thus, when it causes aortic dissection, it is type 2. Acromegaly gives rise to lantern jaw, macroglossia, enlargement of soft tissues, enlargement of feet and hands, hypothyroidism, impotence, hypertension, glucose intolerance… Cushing’s disease affects women 4x more often than men. It can cause depression, psychosis, thinned hair, “moon face” and “buffalo hump,” acne, hirsutism, HTN, obesity, peptic ulcers, striae, impotence, thin skin and easy bruising, proximal myopathy. 20. Diuretic therapy a. May precipitate hepatic encephalopathy b. may cause secondary gout c. May cause collapse in elderly patients d. Should not be prescribed for patients with diabetes mellitus T T T F Diuretic therapy includes thiazides, loops and potassium-sparers. Any agent that can aid in blood pressure decrease can cause collapse, so diuretics can cause collapse. Diabetics may have blood pressure INCREASE on diuretic therapy. This simply requires a change in drug, diet, insulin or oral antidiabetic dosage. Diuretics are commonly prescribed to diabetics Diuretics (thiazides especially) may cause hyperuricemia and thus gout. In patients with cirrhosis, dehydration induced by diuretics is a common precipitant of hepatic encephalopathy (HE), which may respond to volume expansion. 21. Erythema multiforme a. May have associated oral lesions b. Is a vasculitic eruption seen in rheumatic fever c. May be very toxic and require steroid therapy d. Is frequently seen in amyloidosis e. May be fatal T F T F T Erythema multiforme (EM) is a hypersensitivity rash of acute onset frequently caused by infection or drugs. A cell-mediated T cell hypersensitivity response occurs in the skin, causing epidermal cell death. The cause is often idiopathic, but KNOWN causes include: Infection: HSV, EBV, orf, mycoplasma, HIV, Drugs: Sulphonamides, anticonvulsants Neoplasms: Carcinoma and lymphoma CT disease (SLE, polyarteritis nodosa, Wegeners) Lesions can be erythema multiforme (erythematous, polycyclic with “target lesions.” Extensive mucosal involvement can occur in a variant calles Stevens-Johnson syndrome. The difference between EM minor and EM major is that in EM major, mucosal surfaces are involved. Treatment is usually symptomatic; however, some advocate oral steroid therapy in severe disease (this is controversial). Prophylactic oral acyclovir may be helpful. Resistant cases sometimes respond to azathioprine. EM major can (rarely) be fatal. Amyloidosis is rare and may result from a primary amyloidosis, but is more often secondary to CT diseases such as RA, MM, Non-Hodgkin’s Lymphoma, IBD). Rarely, EM can occur with a cause of amyloidosis. Thus I’d say this is false. 22. Acute myocarditis a. Is usually viral in origin T b. May be produced by steroid therapy F c. Produces T-wave abnormality on ECG T d. May result in ventricular dysrhythmias T e. Frequently exhibits Bell’s sign F Bell, who described CN VII palsy in conjunction with the Ramsay Hunt Syndrome, noticed that when patients with a dense facial palsy are asked to close their eyes tightly, the eye on the affected side will roll upwards. This is a positive Bell's sign. Myocarditis is inflammation of the heart muscle caused by: Infections: VIRUSES: Coxsackie/Mumps/Influenza BACTERIA Septicemia Radiation Autoimmune Rheumatic fever Toxin Diphtheria Tachycardia in acute myocarditis is out of proportion with the severity of the heart failure. Tachypnea may also be present A widely inflamed heart shows the classic signs of ventricular dysfunction including Jugular venous distention, Bibasilar crackles, Ascites, Peripheral edema. S3 or a summation gallop may be noted with significant biventricular involvement. Intensity of S1 may be diminished. Cyanosis may occur. Hypotension caused by left ventricular dysfunction is uncommon in the acute setting and indicates a poor prognosis when present. Murmurs of mitral or tricuspid regurgitation may be present due to ventricular dilation. In cases where a dilated cardiomyopathy has developed (chronic myocarditis causes dilatated cardiomyopathy), signs of peripheral or pulmonary thromboembolism may be found. Diffuse inflammation may develop leading to pericardial effusion, without tamponade, and pericardial and pleural friction rub as the inflammatory process involves surrounding structures. Toxic myocarditis has a number of etiologies including both medical agents and environmental agents. Among the most common drugs that cause hypersensitivity reactions are penicillin, ampicillin, hydrochlorothiazide, methyldopa, and sulfonamide drugs. This syndrome is associated with peripheral eosinophilia, fever, and rash in patients who have biopsy findings of an eosinophilic infiltrate of the myocardium. Numerous medications (eg, lithium, doxorubicin, cocaine, numerous catecholamines, acetaminophen) may exert a direct cytotoxic effect on the heart. Zidovudine (AZT) has been associated with myocarditis. Environmental toxins include lead, arsenic, and carbon monoxide, Wasp, scorpion, and spider stings (they don’t just cause pancreatitis holy crap). Echocardiography in ACUTE Impaired contractile function CHRONIC dilatation of left ventricle and atrium Cardiac enzymes: Elevated for many days or weeks CRP and ESR raised Serology for responsible organism (usually viral) ECG findings include: a. Sinus tachycardia is the most frequent finding. b. ST-segment elevation without reciprocal depression, particularly when diffuse, is helpful in differentiating myocarditis from acute myocardial infarction. c. Decreased QRS amplitude and transitory Q-wave development is very suggestive of myocarditis. d. As many as 20% of patients will have a conduction delay, including Mobitz I, Mobitz II, or complete heart block. e. Left or right bundle-branch block is observed in approximately 20% of abnormal ECG findings and may persist for months. 23. Rheumatoid disease a. May lead to impotence b. Usually requires steroid therapy c. May involve temporomandibular joint d. Occasionally causes hypersplenism e. May affect the lungs T T T T Rheumatoid arthritis is a systemic autoimmune disorder characterized by chronic, symmetric and erosive arthritis of synovial joints resulting in disability and handicap. It is associated with extra-articular and circulating autoantibodies to immunoglobulin known as rheumatoid factor (RF). Joints involved include: Metacarpophalangeal joints 85% Carpus 80% Knee 80% Metatarsophalangeal joints 80% Elbow 70% Proximal interphalangeal joints 65% Glenohumeral joint 60% Angle 40% C-spine 35% Temporomandibular joint 25% Extra-articular manifestations of RA include: ON EXAMINATION: Hands splinter hemorage + periungal erythema Carpal tunnel syndrome Elbow nodules Episcleritis, scleritis, kerato-conjunctivitis. Pericarditis + AV block (nodule in conducting system) Lungs effusion and pleuritis and alveolitis Splenomegaly (1% RA get Felty’s = “Felty’s Needs Large Spleen!” Neutropenia, Lymphadenopathy, Splenomegaly) Renal disease (drugs or amyloidosis) Legs: ulcers and distal sensorimotor symmetrical neuropathy. Popular places for nodules include: elbows, Achilles tendon, hands/feet. 24. Acute nephritis is a recognized feature of: a. Brucellosis T b. Ankylosing spondylitis T c. Polyarteritis nodosa T d. Polyposis coli F e. Bacterial endocarditis T Causes of nephritis include postinfectious, renal, and systemic etiologies. Postinfectious etiologies The most common cause is postinfectious Streptococcus species (ie, group A, betahemolytic). Other specific agents include viruses and parasites, systemic and renal disease, visceral abscesses, endocarditis, infected grafts or shunts, and pneumonia. Bacterial : diplococcal, streptococcal, staphylococcal, mycobacterial, and Salmonella typhosa, Brucella suis, Treponema pallidum, Corynebacterium bovis, and actinobacilli Viral: CMV, EBV, coxsackievirus, HepB, rubella, rickettsial scrub typhus, and mumps are accepted as causes only if group A beta-hemolytic strept infection can be excluded. Fungal and parasitic: Attributing glomerulonephritis to a parasitic or fungal etiology requires the exclusion of a streptococcal infection. Identified organisms include Coccidioides immitis and the parasites: Plasmodium malariae, Plasmodium falciparum, Schistosoma mansoni, Toxoplasma gondii, filariasis, trichinosis, and trypanosomes. Systemic causes Wegener granulomatosis Hypersensitivity vasculitis Cryoglobulinemia Systemic lupus erythematosus Polyarteritis nodosa Henoch-Schönlein purpura Goodpasture syndrome While this list does not include Ankylosing spondylitis or IBD (both of which are included in seronegative arthritides, a pubmed search revealed numerous case reports of nephritis and seronegative arthritides coexisting in a disproportionately high amount. Most recently (2004), the journal Rheumatology has published a paper entitled “Increased incidence of recurrent hematuria in ankylosing spondylitis: a possible association with IgA nephropathy” in which nephritis is confirmed… Renal diseases Any cause of glomerulonephritis can cause acute nephritis. 25. In sarcoidosis a. Pleural effusions are common b. Hypocalcemia can occur c. Liver biopsy is often helpful in diagnosis d. Spontaneous remission commonly occurs e. Treatment with steroids or ACTH is mandatory F F T T F Sarcoidosis is a multi-system disease of unknown etiology characterized by presence of non-caseating granulomas in affected organs. It may relate to dust inhalation and a significant genetic contribution is suggested with HLA-B8. Genetic linkage is especially likely if arthritis and erythema nodisum are also present. Sarcoidosis does NOT result from TB. Sarcoid is 15x more common in African-Carribeans, and affects women more often than men. Pathological lesion is the non-caseating granuloma. A syndrome clinically and histologically indistinguishable from sarcoidosis is found occasionally in malignancies. This is an especially important consideration in elderly patients. Two clinical patterns are typical: 1. ACUTE: Bilateral hilar lymphadenopathy + erythema nodosum + arthralgia. This is most common and has a good prognosis (80% resolve within a year). 2. CHRONIC: slowly progressing breathlessness caused by pulmonary fibrosis. This has a worse prognosis FBC lymphopenia + thrombocytopenia ESR raised in active disease 10% have hypercalcemia caused by abnormal Vitamin D metabolism, MORE COMMON in summer months! Serum ACE is raised 2/3 cases The Kveim test involved injecting splenic tissue from someone with sarcoidosis and subsequent skin collection to establish presence of non-caseating granuloma. Concerns about infection meant this is no longer done. Instead, a tissue diagnosis by transbronchial biopsy is preferred, and is positive in 80%. Liver biopsy is diagnostic in 70% of cases, but liver biopsy is not standardly used (but can be helpful and thus “true”). Pleural effusions are relatively uncommon (<5%) Classification of sarcoidosis: Grade Abnormality 0 Normal 1 BHL 2 BHL+ pulmonary infiltrate 3 Pulmonary infiltrate ONLY % resolution all 80% 50% 25% Extrathoracic symptoms are MORE common in cases of sarcoid with a BETTER prognosis (the more extrathoracic symptoms you have the better prognosis you have). No treatment is given in good prognosis sarcoid (BHL, erythema nodosum) If radiological changes persist for 6 months, oral steroids are given. Neurological or cardiac disease can also be treated by steroids. Topical steroids for uveitis Prognosis is worse with age and African-Carribean ancestry. Fewer than 3% of patients die from sarcoidosis. 26. Tetanus a. Is caused by an anaerobic spore-forming organism, which produces tissue destroying enzymes b. Is commoner in underdeveloped countries c. Does not cause sequelae in those who recover d. Confers a high degree of immunity against a second attack e. May resemble strychnine poisoning F T F F T Strychnine is a strong poison; only a small amount is needed to produce severe effects in people. Strychnine poisoning can cause extremely serious adverse health effects, including death. The primary natural source of strychnine is the plant Strychnos nux vomica. This plant is found in southern Asia (India, Sri Lanka, and East Indies) and Australia. In the past, strychnine was available in a pill form and was used to treat many human ailments. Today, strychnine is used primarily as a pesticide, particularly to kill rats. Uncommonly, strychnine is found mixed with “street” drugs such as LSD, heroin, and cocaine. Strychnine prevents the proper operation of the chemical that controls nerve signals to the muscles. The chemical controlling nerve signals works like the body’s “off switch” for muscles. When this “off switch” does not work correctly, muscles throughout the body have severe, painful spasms. Even though the person’s consciousness or thinking are not affected at first (except that the person is very excitable and in pain), eventually the muscles tire and the person can’t breathe. Given strychnine’s ability to target muscle contractions and cause severe and painful spasms, it could quite easily be confused with tetanus. Tetanus can be neonatal, and the anoxia caused by neonatal tetanus commonly causes long term sequelae such as cerebral palsy, mental deficit and behavioral disturbance. Tetanus is a medical term indicating a prolonged contraction of skeletal muscle fibers. Tetanus is the primary symptom caused by the neurotoxin, tetanospasmin, produced by the Gram-positive, obligate anaerobic bacterium Clostridium tetani (which does, incidentally, form spores). Infection usually originates from a contaminated wound, often a cut or deep puncture wound. Common symptoms are muscle spasms in the jaw (hence the common name lockjaw), followed by difficulty swallowing and general muscle stiffness of other parts of the body. The term tetany refers to a state of muscle tension. Whether tetanospasmin qualifies as a “tissue-destroying enzyme” is debatable. It is a neurotoxin but it’s effect is indirect (it doesn’t digest the tissue as implied in the statement-rather it paralyzes it). Thus I would say this is false, although the rest of the statement is true. Incidentally, tetanospasmin works by: 1. Taken up by neuromuscular junction 2. Transported to CNS 3. Acts on Renshaw interneurons by preventing GABA and glycine release 4. Since GABA and gylcine are inhibitory neurotransmitters, the inhibition of inhibitory NTs causes high frequency impulses to muscle cellstetany. The wound must be cleaned; dead and infected tissue should be removed by surgical debridement. Metronidazole treatment decreases the amount of bacteria but has no effect on the bacterial toxin. Penicillin has been used in the past to treat tetanus, but is no longer the treatment of choice because of a theoretical risk that it increases spasms; however, if metronidazole is not available penicillin should still be used. Passive immunization with human anti-tetanospasmin immunoglobulin (or tetanus immune globulin) is a crucial part of treatment; if specific anti-tetanospasmin immunoglobulin is not available then human normal immunoglobulin may be given instead. All tetanus victims should be vaccinated against tetanus or offered a booster vaccine if they have been previously vaccinated. In the most severe of cases, it may be necessary to paralyze the patient using a naturally occurring substance, and engage a machine to continue breathing. It takes 2-14 days for symptoms to develop after infection. Symptoms peak 17 days after infection. Tetanus can be prevented by vaccination. The CDC recommends that adults receive a booster vaccine every ten years, and standard care in many places is to give the booster to any patient with a puncture wound who is uncertain of when he or she was last vaccinated. This booster cannot prevent a potentially fatal case of tetanus from the current wound as it takes 2 weeks for antibodies to form. For children under the age of seven, the tetanus vaccine is often administered as a combined vaccine, TDap or DTaP, which include vaccines against diphtheria and pertussis as well. For adults and children over seven, the Td vaccine (tetanus and diphtheria) is commonly used. 27. Neoplasms of the esophagus a. Are usually adenocarcinomas b. Are commoner in males c. Are more prevalent in patients with achalasia d. Usually present with retrosternal pain e. If resectable, have a good prognosis T T T F F The epidemiology of esophageal carcinoma has changed markedly over the past several decades in the United States. Until the 1970s, squamous cell carcinoma was the most common type of esophageal cancer (90-95%). It was located in the thoracic esophagus and affected mostly African American men who had a long history of smoking and alcohol consumption. Over the last 2 decades, the incidence of adenocarcinoma of the distal esophagus and gastroesophageal junction has progressively increased. Currently, it accounts for more than 50% of all new cases of esophageal cancer. Unlike squamous cell carcinoma, it affects mostly white men, and its pathogenesis is linked to gastroesophageal reflux disease (GERD) and the development of Barrett epithelium Esophageal carcinoma now represents 1% of all malignant lesions, with a male to female preponderance of 3:1. The upper, middle and lower 1/3 of esophagus are affected 20, 30 and 50% of the time. Risk factors include exposure (smoking, alcohol, nitrosamines, radiation) and anatomical deficits (diverticula/hiatus hernia/achalasia/GERD/Barret’s). Plummer-Vinson syndrome also increases risk. The most common presentation is with dysphagia, first for solids then with liquids. Weight loss and weakness are also common. Hematemesis, anemia, tracheoesophageal and bronchoesophageal fistulae can also occur. Odynophagia and then constant pain may occur but are not the most common presentation. Esophageal cancer is a treatable disease that is rarely curable. The overall 5-year survival rate in patients amenable to surgery ranges from 5% to 20%. The occasional patient with very early disease has a better chance of survival. Patients with severe dysplasia in distal esophageal Barrett's mucosa often have in situ or even invasive cancer within the dysplastic area. Following resection, these patients usually have an excellent prognosis. Reading this question is difficult-surgical resection of primary tumor is linked (above) to a dismal prognosis of 5-20%, while the “resection” of in situ lesions has “excellent prognosis.” Since it must be assumed that this answer stem refers to ALL resections done in esophageal cancer, I answer false. Incidentally (I’m starting to love that word), the staging of esophageal cancer is by TNM system T0 Tis T1 T2 T3 T4 No evidence of tumor In situ lesion only (usually found in biopsy of Barrett’s esophagus) Invades submucosa Invades muscularis propria Invades adventitia Invades surrounding structures (eg. Aorta, recurrent laryngeal nerves). N0 N1 M0 M1 No lymph node involvement Lymph node involvement No mets Mets 28. Complications of Ulcerative colitis include: a. cirrhosis T b. colon cancer T c. arthritis T d. thyroiditis F e. pleural effusion F Extra-articular manifestations of IBD (UC and CD) include Erythema nodosum Pyoderma gangrenosum Seronegative arthritides (sacro-iliitis and monoarthritis) Ankylosing spondylitis (esp. HLA-B27) Hepatitis, gallstones, renal stones, primary biliary cirrhosis IT should be noted that ankylosing spondylitis and sacroiliitis occur independently of disease flares and thus are not good indicators of disease activity. There is an increased risk of colon cancer in ulcerative colitis and CD (higher risk in UC). 29. Patients suffering from regional enteritis have a tendency to develop a. fistulae T b. low serum iron T c. vitamin B12 insufficiency T d. cholelithiasis T e. recurrence of disease after surgery T Regional enteritis is also known as Crohn’s disease. Distinguishing Features of CD Versus UC Features Crohn Disease Skip areas Common Cobblestone mucosa Common Transmural involvement Common Rectal sparing Common Perianal involvement Common Fistulas Common Strictures Common Granulomas Common Ulcerative Colitis Never Rare Occasional Never Never Never Occasional Occasional Vitamin B12 is bound by intrinsic factor (secreted by parietal cells in stomach), and absorbed in the terminal ileum. Crohn’s disease commonly involves this portion and thus may limit absorption. Iron absorption may also be affected. The increased incidence of kidney stones has a curious physiology. Usually fat is absorbed in the small intestine, but chronic inflammation in Crohn’s decreases fat absorption. Simultaneously, calcium is usually bound to oxalate, which is poorly soluble and thus mostly excreted. However, in CD, the malabsorbed fatty acids bind calcium, so that the oxalate is bound instead to sodium, which is easily absorbed. The excessive amounts of body oxalate cause them to precipitate in the renal system as calcium oxalate stones. 30. The following are causes of hypercalcemia: a. Milk-alkali syndrome b. Paget’s disease of bone c. Sarcoidosis d. Multiple myeloma e. Rickets The causes of hypercalcemia include: Neoplastic Multiple myeloma, malignancy and metastasis Bone Increased osteoclast activity (Paget’s disease) Increased VitD action Sarcoidosis (10%), excessive intake (“Vit D intoxication”) Endocrine Addison’s, Phaeochromocytoma, inc T4. Drugs Thiazides, Lithium, Milk-alkali syndrome Increased dietary Ca++ Increased PTH Primary or tertiary, ectopic 31. The following drugs are know to give rise to lesions of the eighth cranial nerve a. chloramphenicol b. kanamycin c. cyclophosphamide d. salicylates e. streptomycin The CN VIII is the acoustic (aka vestibulocochlear) nerve. Anything that is ototoxic can affect this nerve… Antibiotics amikacin, streptomycin, neomycin, gentamicin, erythromycin, Kanamycin, Tobramycin, netilmycin, vancomycin Aminoglycosides, Vancomycin and the macrolide erythromycin… Anti-cancer drugs cisplatin, bleomycin, vincristine Anti-malarial drugs quinine and chloroquine Diuretics acetazolamide, furosemide, bumetanide, ethacrynic acid Salicylates can cause ringing in the ears (salicylism). 32. Gout a. Is characterized by deposits of sodium urate in joints and other structures b. Causes symmetrical arthritis c. May lead to renal dysfunction d. May be exacerbated by diuretics T F T T e. An acute attack usually responds to allopurinol F Gout is the deposition of monosodium urate crystals into joint. The resulting synovotis may be limited to a single joint (monoarticular) or become more widespread (polyarticular). Pseudogout is similar except it is calcium pyrophosphate dehydrate that is deposited. Gout is 6x more common in men and almost never found in premenopausal women. Disorders that increase uric acid (severe psoriasis, myeloproliferative disorders, rich diet, alcohol), drugs (thiazides, furosemide, low dose aspirin), renal disease, age, dehydration may all increase risk of gout. Therapy to lower uric acid formation includes allopurinol, and probenecid can be used to increase excretion. Most presentations of gout are monoarticular. Attacks are agonizing and last 7-10 days. Acute episodes can be triggered by alcohol, exercise, starvation or trauma. Gouty nephropathy and renal stones are common. Chronic gout requires uric acid lowering therapy and NSAIDs. Colchicine is used in acute attacks since allopurinol prolongs acute attacks. Uric acid levels may be normal in 20% of attacks. Gout causes punched out cortical erosions, usually away from the joint margin. 33. CO2 retention is a feature of a. status asthmaticus b. coma associated with barbiturate intoxication c. Acute PE d. Bronchopneumonia e. Respiratory muscle involvement in myasthenia gravis T T F F T Asthma triad is asthma+ ASA/NSAID hypersensitivity + nasal polyps. IN any acute attack of asthma, an ABG and CXR must be done. Airway obstruction V/Q mismatch hypoxemia increased ventilation decreasing PaCO2 Inc. pH and fatigue dec. ventilation increased PaCO2 and acidosis. So…as the severity of asthma attack increases, CO2 retention occurs. Other causes of CO2 retention include defective control of breathing or hypoventiliation (drug OD, ALS, Myasthenia gravis, Guillain-Barre, kyphoscoliosis) or structural problems (COPD). While bronchopneumonia can cause hypoxemia, it rarely causes hypercapnia cause it causes tachypnea, thus clearing the lungs of CO2. PE can cause hypoxemia but not hypercapnia. 34. In bronchiectasis a. Hemoptysis is common b. Clubbing of fingers is rare c. CXR commonly confirms the diagnosis T F F d. Coarse crepitations may be heard over the involved area e. Surgery is eventually necessary in most patients T F Bronchial wall dilatation, aka bronchiectasis, is often accompanied by super-added pulmonary infection. Prevalence is about 1:1000, but this is falling because of the decreases in TB and whooping cough. Bronchiectasis can be localized or generalized. LOCALIZED: post-severe pneumonia, distal to obstruction caused by endobronchial (foreign body/tumor) or extrabronchial (Brocks syndrome=TB hilar lymphadenopathy) GENERALIZED: CF, Kartagener’s syndrome, immune defects Immune complex in IBD, RA Marfan’s, Alpha-1 antitrypsin deficiency, yellow nail syndrome Presentation usually includes chronic cough and mucopurulent sputum Other symptoms include: - unpleasant breath - Hemoptysis (50%) - Chronic sinusitis (40%) - anemia (chronic illness) or polycythemia (from respiratory failure) Cyanosis and other signs or cor pulmonale are present in late stages. Crackles are present over affected areas, but airways obstruction and wheeze may also occur. Look for other signs of underlying disorder (Kartagener’s infertility, sinusitis, dextrocardia) Amyloidosis may occur in longstanding severe bronchiectasis. Common findings in bronchiectasis in the clinical exam include: anemia, cyanosis, increased JVP, coarse crackles over affected area, chronic cough with mucopurulent sputum, finger clubbing, and cor pulmonale (right heart failure due to lung disease leg edema and RV heave). The diagnosis of bronchiectasis can only be confirmed by HRCT (high resolution CT), which shows the “signet ring” sign (thick-walled bronchus, larger than adjacent blood vessel. Sputum culture for Pseudomonas should be undertaken. 35. Characteristic features of subacute bacterial endocarditis include a. Heberden’s nodes F b. Proteinuria T c. Osler’s nodes T d. Thrombocytopenia T e. Conjunctival hemorrhages T Osteoarthritis causes the formation of hard bony enlargements of the small joints of the fingers. Classic bony enlargement of the small joint at the end of the fingers is called a Heberden's node, named after a very famous British doctor. The bony deformity is a result of the bone spurs from the osteoarthritis in that joint. Another common bony knob (node) occurs at the middle joint of the fingers in many patients with osteoarthritis and is called a Bouchard's node. Dr. Bouchard was a famous French doctor who also studied arthritis patients in the late 1800s. The Heberden's and Bouchard's nodes may not be painful, but they are often associated with limitation of motion of the joint. Osler's nodes: These are small (the size of split peas), tender, transient nodules in the pads of fingers and toes and the palms and soles. They are a highly diagnostic sign of bacterial infection of the heart (subacute bacterial endocarditis). Named for the Canadian-born physician Sir William Osler (1849-1919). Infective endocarditis can cause splinter hemorrhages, Osler’s nodes and clubbing in the hands. Conjunctival hemorrhages and Roth spots (fundal infarcts). A tachycardia and collapsing pulse may be found (from Aortic regurg). Murmurs may change with time. Splenomegaly and hypersplenism can cause thrombocytopenia and anemia to occur. Abscesses can be found intracranially, intrasplenically…and renal problems may include glomerulonephritis leading to hematuria or renal failure. 36. Recognized causes of amyloid disease include: a. Osteoarthritis F b. Cirrhosis of the liver F c. Osteomyelitis T d. TB T e. Rheumatic valvular disease F Amyloids are insoluble fibrous protein aggregations sharing specific structural traits. The classical, histopathological definition of amyloid is an extracellular, proteinaceous deposit exhibiting cross-beta structure. Common to most cross-beta type structures they are generally identified by apple-green birefringence when stained with congo red and seen under polarized light. Diseases featuring amyloid The phenotypes of genetically transmitted amyloid diseases are often inherited in an autosomal dominant fashion. Sometimes, the difference between aggressive amyloid diseases and senescent amyloid diseases is due to a mutation that makes the protein more prone to aggregation. Most commonly seen are point mutations, which affect the cohesiveness of the protein and promote misfolding; other mutations cause aggregation-prone pieces of the protein to be cleaved off from the rest of the protein. In almost all of the organ-specific pathologies, there is significant debate as to whether the amyloid plaques are the causal agent of the disease or instead a symptom downstream of a common idiopathic agent. The associated proteins are indicated in parentheses. Note that amyloidosis by default usually refers to AA amyloidosis, but any disease which presents amyloid deposition is an amyloidosis. CJD, Alzheimer's and diabetes are almost never referred to as amyloidoses. AL amyloidosis (Ig light chains): MM, Waldenstrom’s, or non-Hodgkins lymphoma Secondary amyloidosis aka reactive systemic amyloidosis: from serum amyloid A (SAA) IBD, RA, TB, osteomyelitis, bronchiectasis. Often presents with hepatosplenomegaly. (Chronic inflammation or chronic infection ) Familial or Hereditary amyloidosis COMMON: transthyretin protein mutations RARE: apolipoprotein A1, gelsolin, fibrinogen, and lysozyme mutations. Importantly, dialysis can cause amyloidosis. This is because dialysis machines (older ones) could not filter out large proteins (esp. beta-2 microglobulin), and thus they precipitate out. Organ-specific amyloidosis Diabetes mellitus type 2 (amylin, also known as IAPP) Alzheimer's disease (Aβ 39-42) Parkinson's disease (alpha-synuclein) Huntington's disease (huntingtin) Transmissible spongiform encephalopathies (prion protein, PrP) Creutzfeldt-Jakob disease (PrP in cerebrum) Kuru (diffuse PrP deposits in brain) Fatal Familial Insomnia (PrP in thalamus) Bovine spongiform encephalopathy (PrP in cerebrum) Congophilic angiopathy (Amyloid beta) Cardiac amyloidosis congestive heart failure; some instances (PrP or transthyretin in heart) Inclusion body myositis Iatrogenic conditions insulin amyloidosis (injection-administered insulin) Excessive calcitonin can also form amyloid but no known disease results 37. In CLL: a. Children are affected more commonly than adults b. Immune response is enhanced c. Spleen is characteristically extremely large d. Sternal marrow biopsy reveals an excess of myelocytes e. Cyclophosphamide is the drug of choice F F F T F The incidence of CLL increases with advancing age, and males are affected more commonly than females. CLL is a malignant illness of B-cells whereby cells look mature but functionally are immature (CLL is the Ben of Cancers! B-cell for Ben, LOOKS mature but actually quite immature!). Half of CLL patients are diagnosed by chance, while the others may present with painless palpable lymphadenopathy, recurrent sepsis (from hypogammaglobinemia), and anemia. Hepatosplenomegaly may occur but is more common in more advanced disease. By definition, the lymphocyte count must be >5x109/L in absence of viral infection. Usually Hb and platelets are normal although thrombocytopenia and anemia may occur. LDH and alkaline phosphatase may be raised. CLL is a chronic and incurable disease-while it may be asymptomatic for years, symptoms may prompt the use of chlorambucil (“ChLorambuciL for CLL”). CML classically presents in middle age, and benzene and ionizing radiation may be causally linked. CML is a clonal disorder of a pluripotent stem cell that contains Philadelphia chromosome (remember the 9:22 translocation, thus producing the BCRABL tyrosine kinase-not targeted pharmacologically by Glevec (Imitanib the monoclonal antibody), which can also be used in ALL). Splenomegaly is characteristically extremely large! While hydroxyurea can be used to decrease the cell counts, eventually an acute phase occurs which is resistant to intensive chemotherapy. Recently however, Glivec has been shown to improve long-term survival in CML. Marrow transplantation can be curative in both CML and CLL, but is usually reserved for younger patients. 38. In pneumonic consolidation the following statements are correct: a. The percussion note is characteristically stony dull F b. Breath sounds are bronchial T c. Kerley’s lines are seen on CXR during resolution T d. Sputum contains Curschmann’s spirals F e. Cavitation suggests staphylococcal aetiology T Condition Percussion Mediastinum Vocal fremitus Auscultation Consolidation Dull None increased Bronchial breathing Alveoli filled with fluid Pleural effusion Stony dull C/L decreased reduced/absent Fluid in pleural space Pneumothorax Hyperresonant C/L (tension) decreased reduced/absent Air in pleural space Collapse Dull I/L decreased reduced/absent Chest wall movement decreased over area in pleural effusion, pneumothorax, collapse or consolidation. Curschmann's spirals are spirally twisted masses of mucus occurring in the sputum in bronchial asthma. In chest radiology, Kerley B lines are a sign seen with interstitial pulmonary edema. Often, they suggest the diagnosis of congestive heart failure, but are also seen in various non-cardiac conditions such as carcinomatous of the lung. Kerley B lines are short horizontal lines at the lung periphery. These lines represent interlobular septal lines, which are usually less than 1 cm in length and parallel to one another at right angles to the pleura. They are located peripherally in contact with the pleura, but are generally absent along fissural surface. They may be seen in any zone but are most frequently observed at the lung bases. In most cases, heart problems are the cause of pulmonary edema. But fluid can accumulate in your lungs for other reasons, including lung problems such as pneumonia, exposure to certain toxins and medications, and exercising or living at high elevations. Thus, pneumonia can cause pulmonary edema which can cause Kerley B lines. Is this in resolution however? I’ve no clue…I’m saying true to this… The differential diagnosis for cavitating lung lesion is “CAVITEY.” Cancer: Bronchogenic carcinoma and Café-au-lait spots as in NFT-1 Autoimmune RA, Takayasu’s arteritis Vascular PE Infective Parasites: Alveolar hydatid disease Fungi: Pneumocystis carinii, Histoplasmosis Bacteria: Staph aureus, TB, Klebsiella Trauma Emphysema Youth (congenital) 39. Characteristic features of aortic incompetence include: a. Atrial fibrillation F b. Heaving apex impulse T c. Right ventricular hypertrophy F d. BP 145/110 F e. Diastolic murmur heard in carotid arteries F Aortic incompetence is also known as aortic regurgitation. It involves backflow/leaking of aortic blood back into the left ventricle during diastole. Collapsing pulse with volume-overloaded left ventricle (hyperdynamic apex beat);chronic AR causes left ventricular hypertrophy. There is a wide pulse pressure (145/110 is not wide pulse pressure), and the diastolic BP is a good guide to the severity of chronic AR (low diastolic BP=severe AR). Atrial fibrillation is not a common feature, as it would be in mitral stenosis. There is an early diastolic murmur heard along left sternal edge. A murmur heard in the carotid arteries would raise suspicion for AS, which typically radiates to the carotids, in systole! Wide pulse pressure causes: Corrigan’s sign: visible carotid pulsations De Musset’s sign head bobbing Quinke’s sign nail-bed pulsations Traube’s phenomemon pistol shot femorals Austin-Flint murmur mid-diastolic, low-pitched rumbling heard at the apex, caused by blood from aorta mixing with entering blood across mitral valve Duroziez’s murmur To and fro murmur over femoral artery. 40. Recognized causes of hypokalemia include: a. Conn’s syndrome T b. Diuretic therapy T c. purgatives T d. metabolic acidosis F e. Cushing’s syndrome T Hypokalemia can be caused by: HyPERadrenalism Conns syndrome, Cushing’s syndrome Diuretics Thiazides or loop diuretics Loss from GIT Diarrhea or vomiting Shift into cells Insulin therapy, beta-agonists (salbutamol), catecholamines Hyperkalemia can be caused by: HyPOadrenalism Addison’s Renal failure Drugs Spironolactone, amiloride, ACE inhibitors Cell destruction Chemotherapy, tumor lysis syndrome, rhabdomyolysis Acidosis Acidosis (high [H+] in plasma) causes hydrogen to be taken up by muscle cells out of the blood in an exchange mechanism involving the transfer of potassium ions into the bloodstream (H+/K+ exchanger). This abnormally elevates the plasma's concentration of potassium ions. Hypokalemia Hyperkalemia peaking. ↑p wave, ↓PR interval, ↓QRS width, T wave flattening, U wave “You (“U”) wave cause the potassium has gone” ↓p wave, ↑PR interval, ↑QRS width (sine wave), T wave 41. Hemolytic anemia a. Excess urobilinogen is present in the urine b. Itching is a feature c. Coombs test may be positive d. Red cell fragility may be increased e. Feces are pale T F T T F Hemolytic anemia causes the red cell life span to be markedly reduced. Hemolysis can be categorized into congenital or acquired causes. Congenital causes: Membrane Congenital spherocytosis, congenital elliptocytosis Enzyme G6P DH deficiency, pyruvate kinase deficiency Hemoglobin Thallesemias, sickle cell anemias Acquired causes: Infection EBV/CMV MAHA TTP/HUS Cardiac Prosthetic valve replacement Autoimmune Warm antibody: IgG binds to cells, from: SLE, IBD, CLL, Non-Hodgkins lymphoma Coombs test positive (detects antibody and complement on rbc surface) Cold antibody: Ig M binds to cells, from: Infection: CMV, EBV, mycoplasma pneumoniae. Cold hemagluttinin disease: acrocyanosis and Coombs test positive for complement but NOT antibody, as IgM falls off in vitro. Paroxysmal nocturnal hemoglobinuria (defective GPI-anchored proteinusually binds complement preventing breakdown-when defective, complement binds and causes hemolysis) Hemolysis is considered a cause of pre-hepatic jaundice as the outflow of excessive hemoglobin metabolites causes hyperbilirubinemia and thus jaundice. Clinical findings: Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed). Serum: increased unconjugated bilirubin. Stools become darker (deep brown) Hepatic jaundice: Urine: bilirubin present, Urobilirubin > 2 units but variable (Except in children) Post-hepatic jaundice: The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal faeces get their colour from bile pigments. Patients sometimes also complain of itching. 42. Right homonymous hemianopia found in a. Retinal detachment F b. Pituitary neoplasms F c. Optic nerve glioma T d. Left cerebral infarct T e. Right occipital tumour F In homonymous hemianopia - literally, a loss of vision on the same side in both eyes the field loss is usually the result of a lesion in the optic radiation or tract on one side. The visual defect is dependent on the site of the lesion: right-hand sided lesions lead to left temporal and right nasal field loss left-hand sided lesions lead to right temporal and left nasal field loss Macular vision is usually lost in lesions arising in the optic tract; it is usually spared in lesions arising in the more posterior optic radiation. Causes of homonymous hemianopia include vascular disease, head injury or cerebral tumours. 43. The findings of weakness, spasticity, and impairment of sensations are compatible with: a. Polymyositis b. Spinal cord compression ??? 44. Manifestations of ankylosing spondylitis include a. Aortic incompetence T b. Proteinuria T c. Blood uric acid level of 9mg/100mL F d. Narrowing of sacroiliac joint space T e. Punched out lesions in vertebral bodies F Aortic incompetence is seen in Ank Spon and Reiter’s, but not in IBD or Psoriatic arthritides, when considering seronegative arthritides. Since ankylosing spondylitis is chronic inflammation, and chronic inflammation can cause amyloidosis which can cause proteinuria, proteinuria may be a manifestation of Ank Spon. Also, IgA nephropathy is more common in Ank Spon than the non-Ank Spon population. The term “Punched out lesions” is reserved for gout and multiple myeloma only. 45. In rheumatoid arthritis a. There is an association with HLA-B27 b. Bony erosions occurring early in the disease imply an adverse prognosis c. Gold therapy may cause fatal pancytopenia d. Carpel tunnel syndrome may be a complication e. Rheumatoid factor is usually negative if subcutaneous nodules are present F T T T F Rheumatoid arthritis is a chronic inflammatory disease affecting synovial joints. It commonly affects proximal interphalangeal, metacarpophalangeal, metatarsophalangeal, elbow, knees, ankles, hips, wrist, TMJ, glenohumeral and cspine. It is linked to HLA-DR4. Poor prognosis factors in RA include: - generalized polyarthritis (>20 joints involved) - High ESR and CRP despite therapy - Extra-articular features (also a sign of disease in IBD, except sacroiliitis) - RF positive - Erosions on plain radiograph within 2 years onset - HLA-DR4 Extra-articular features include: Spinter hemorrhages, elbow nodules, carpal tunnel disorder, Felty’s (“Need Large Spleen!” = neutropenia, lymphadenopathy, splenomegaly), vasculitic ulcers, eyes (scleritis, episcleritis, keratoconjunctivitis), pericarditis, AV block (nodule in conducting system), alveolitis, pleuritis and effusion, renal disease (amyloidosis or secondary to NSAIDs, penicillamine). Common side effects to commonly prescribed medications in RA include: NSAIDs GI ulceration and hemorrhage, renal impairment, fluid retention DMARDs Methotrexate myelosuppresion, hepatotoxicity, pneumonitis, Alopecia, diarrhea/nausea/mucositis Sulfasalazine Rash, myelosuppression, hepatotoxicity, dizziness Gold IM myelosuppression, rash, proteinuria, stomatitis Azathioprine myelosuppression, hepatotoxicity Anti-TNFalpha Reactivation of TB, increased infection risk, lupus like reaction 46. Red cells may be found in the urine of patients with: a. Acute pyelonephritis T b. Post streptococcal acute glomerulonephritis T c. Acute tubular necrosis T d. Subacute bacterial endocarditis T e. prerenal uremia F Hematuria can be caused by pathology at any site in the urinary tract, including renal, ureteric, bladder and urethra Renal: - pyelonephritis Ureter: - stone - renal calculi - carcinoma - trauma - renal cysts including PCKD Bladder: - cystitis - renal carcinoma - trauma - glomerulonephritis - stone - papillary necrosis - carcinoma - TB - AV malformation Urethra: - Prostate Ca - stone/trauma - BPH Glomerulonephritis red cell casts, dysmorphic red cells, abnormal renal function and Proteinuria Structural lesions pain and hematuria terminal or initial! Glomerulonephritis can be caused by infective endocarditis. 47. Postural hypotension occurs in a. Hemolytic anemia T b. Addison’s disease T c. Autonomic neuropathy T d. Salt depletion T e. Hypercalcemia F Orthostatic hypotension (also known as postural hypotension and, colloquially, as head rush) is a sudden fall in blood pressure, typically greater than 20/10 mm Hg, that occurs when a person assumes a standing position. Symptoms, which generally occur after sudden standing, include dizziness, lightheadedness, headache, blurred or dimmed vision (possibly to the point of momentary blindness), and syncope (temporary loss of consciousness). Causes Orthostatic hypotension is substantially more common in tall patients. It may be caused by: - hypovolemia - dehydration - prolonged bed rest - anemia - drugs (diuretics, beta-blockers, calcium channel blockers, vasodilators, ACE inhibitors, tricyclics, antipsychotics, Parkinson’s drugs) - autonomic neuropathy (esp. diabetes) - Addison’s - atherosclerosis - Shy-dragar syndrome (causes damage to autonomic nervous system) Salt depletion can be accompanied by hypovolemia and thus postural hypotension. 48. AIDS: a. Occurs exclusively in homosexuals b. Is uniformly fatal in less than two years c. Is commonly complicated by pneumocystis carini pneumonia d. The latent period after exposure is short, usually less than two months e. Responds to treatment with interferon F F T F F AIDS develops from HIV, and is contracted by sharing of bodily fluids (blood and semen especially). Transmission occurs by homosexual/heterosexual intercourse, IV drug use, blood product transfusion and maternal-child transmission. Once transmitted, HIV enters lymphoid tissue where it infects CD4-T lymphocytes and monocyte/macrophages. The virus enters the cells by binding to the CD4 or chemokine receptors, then replicates itself into host DNA. Progressive loss of CD4+ cells and a number of other mechanisms cause immune function impairment. Clinical patterns: Primary HIV infection: Asymptomatic HIV: Symptomatic HIV: acute clinical syndrome when viral replication occurs. Includes: fever, malaise, maculopapular rash. During this phase, seroconversion occurs MOST patients have prolonged asymptomatic period (median 10 years without treatment) before clinical features develop. As HIV infection progresses, symptoms occur (weight loss, diarrhea and fever) Opportunistic infections include: CD4 count Infection . >500 200-500 50-200 <100 Rare Herpes zoster, oral candidiasis, TB Pneumocystic carinii pneumonia, Mucocutaneous herpes CMV, toxoplasmosis, Cryptococcus, MAC (mycobacterium avium intercellulare) PML (progressive multifocal leukoencephalopathy) It should be mentioned that the incidence of Kaposis sarcoma and NonHodgkin’s lymphoma is also significantly increased in AIDS. PML= progressive multifocal leukoencephalopathy =uncommon demyelinating disease caused by polyoma JC virus. Diagnosis is by imaging (white matter lesions) and PCR of CSF for polyoma JC virus. Treatment is with HAART. Treatment in HIV is with a number of drugs in combination (HAART=highly active antiretroviral therapy), which has led to a significant decrease in mortality and delay in progression to AIDS. Classes of drugs exist including: - nucleoside RT inhibitors ddI=didanosine AZT=azidothymidine aka Zidovudine 3TC=lamivudine - non-nucleoside RT inhibitors nevirapine, efavirenz - protease inhibitors ritonavir, indinavir, nelfinavir, HAART= 2 nucleoside RT inhibitors + either non-nucleoside RT inhibitor Or 1 or 2 protease inhibitors 49. Hookworm disease a. Causes iron deficiency anemia T b. Causes megaloblastic anemia F c. Causes liver abscess F d. Is treated with penicillin F e. Is common in Africa T Human hookworm infection is a common soil-transmitted helminth infection that is caused by the nematode parasites, Necator americanus and Ancylostoma duodenale. Worldwide, hookworm infects an estimated 740 million people, most of whom are asymptomatic. Despite this lack of symptoms, hookworm substantially contributes to the incidence of anemia and malnutrition in developing nations. The greatest number of cases occurs in the rural tropical and subtropical areas of China and sub-Saharan Africa, followed in number by India, South Asia, and Latin America. The life cycle of hookworms begins with the passing of hookworm eggs in human feces and their deposition into the soil. Larval growth is most proliferative in favorable soil that is sandy and moist, with an optimal temperature of 20-30°C. Under these conditions, the larvae hatch in 1 or 2 days to become rhabditiform larvae, also known as L1. The rhabditiform larvae feed on the feces and undergo 2 successive molts, such that, after 5-10 days, they become infective filariform larvae, or L3. These L3 go through developmental arrest and can survive in damp soil for as long as 2 years. However, they quickly become desiccated if exposed to direct sunlight, drying, or salt water. L3 live in the top 2.5 cm of soil and move vertically toward moisture and oxygen. Infection of the human host is established when filariform larvae penetrate the skin, typically on the hands or feet. This penetration may cause a local pruritic dermatitis, also known as ground itch. The larvae migrate through the dermis, entering the bloodstream and moving to the lungs within 10 days. Once in the lungs, the hookworms penetrate the alveoli and are carried to the glottis by means of the ciliary action of the respiratory tract. During pulmonary migration, the host may develop a mild reactive cough, sore throat, and fever that resolve after the worm migrates into the intestines. At the glottis, the larvae are swallowed and carried to their final destination, the small intestine. During this part of the migration, the larvae undergo 2 further molts, developing a buccal capsule and attaining their adult form. Using this buccal capsule, the worms attach themselves to the mucosal layer of the proximal small intestine, including the lower part of the duodenum, jejunum, and proximal ileum. In 3-5 weeks, the adults become sexually mature, and the female worms begin to produce eggs that appear in the person's feces. Intestinal blood loss secondary to infection is the major clinical manifestation of hookworm infection. In fact, hookworm disease historically refers to the clinically significant hypochromic, microcytic anemia and the depletion of iron stores resulting from chronic intestinal blood loss secondary to hookworm infection. Attaching to the mucosal layer and using their mouth parts, hookworms rupture the arterioles and venules along the luminal surface of the intestine. The worms ingested and digested some of the blood from the injured mucosa by means of a multienzyme cascade of metallohemoglobinases. Inhibited host coagulation due to a series of anticoagulants directed against factor Xa and the factor VIIa–tissue factor complex, as well as again platelet aggregation, further exacerbate blood loss. Diagnosis is made by finding eggs in the feces. Treatment is with anti-helminths (Albendazole, mebendazole) 50. The following are frequently seen in systemic sclerosis (scleroderma) a. Raynaud’s phenomenon T b. Ulcers on fingers T c. Dysphagia T d. Peripheral neuritis F e. Hemiplegia F Ulcers may be seen on the fingers due to digital ischemia. Systemic sclerosis is also known as scleroderma, and is classified into systemic or localized types: SYSTEMIC: - systemic sclerosis with diffuse cutaneous disease - systemic sclerosis with limited cutaneous disease (CREST) - systemic sclerosis without scleroderma (no cutaneous involvement) LOCALIZED: morphea (plaques of fibrotic skin) - linear (fibrotic bands) - “en coup de saber” = linear scleroderma of one side of scalp and forehead. Pulmonary fibrosis and pulmonary HTN, Amenorrhea and infertility Thyroid fibrosis + hypothyroidism Myocardial fibrosis, pericarditis, restrictive cardiomyopathy GERD, Biliary cirrhosis, classic facies (purse-string mouth and mouse-like facies) Renal crisis (RPGN, MAHA) CREST= Calcinosis+Raynauds+Esophageal dysmotility+Sclerodactyly+Telangiectasias 51. Abdominal pain relieved by defecation and associated with loose bowel motions is a feature of: a. Irritable bowel syndrome T b. Anorexia nervosa T c. Peptic ulcer of stomach F d. Gall stones F e. Crohn’s disease of colon F IBS is a primarily functional bowel disorder characterized by abdominal pain that is relieved by defecation, alternating loose stool and hard stool, mucus in the stool, and a frequent sensation of incomplete evacuation. Serotonin is implicated in the pathophysiology of IBS, as it modulates visceral sensation within the central nervous system. A serotonin4-receptor agonist, tegaserod, has demonstrated efficacy in the treatment of constipation-dominant IBS. As stated previously, extra-GI conditions associated with IBS are numerous. In a review of the published literature on IBS since 1966, Whitehead, Palsson, and Jones (2002) noted that non-GI, nonpsychiatric disorders with the best-documented association with IBS included fibromyalgia (49% have IBS), chronic fatigue syndrome (51%), temporomandibular joint disorder (64%), and chronic pelvic pain (50%). Similar to IBS, the female predominance in these conditions is well documented. It is certin, however, that “abdominal pain relieved by defecation” is a classic expression of functional bowel syndrome, and thus underlying pathology (gall stones, ulcer, IBD) must be excluded. The Rome criteria, rather than the Manning criteria, were applied to identify IBS subjects. IBS was defined as abdominal pain that kept recurring over a period of more than three months in the prior year, in combination with: (1) one or more of the following symptoms: (i) abdominal pain relieved by defecation, often (more than 25% of the time); (ii) more frequent and/or less frequent bowel movements with pain, often; or (iii) looser and/or harder stools with pain, often; and (2) two or more of the following: (i) more than three bowel movements a day, often and/or less than three bowel movements a week, often; (ii) stools very lumpy or hard, often and/or stools very loose or watery, often; (iii) incomplete rectal evacuation, often and/or urgency, often and/or straining, often; (iv) abdominal bloating or distension, often; or (v) mucus in stools. Eating disorders and a history of eating disorders are significantly (5-15x) more common in functional bowel diseases than in either the population at large, or nonfunctional bowel diseases. Thus, I would say this is true. 52. The following have hematuria a. Steroid sensitive but recurrent minimal change GN b. IgA nephropathy c. Nephropathy associated with diabetes d. Infective endocarditis e. Acute papillary necrosis F T T T T See question 46 53. A 50 year old woman is thought likely to have osteoporosis a. A history of alcoholism would suppose the diagnosis b. A history of thyrotoxicosis would support the diagnosis c. A-P and lateral xrays of spine are sensitive indicator of disease progression d. Bone loss is mainly cortical, not trabecular T T F F e. Vitamin D replacement is mandatory F Trabecular bone is the thin bars of bone tissue in spongy bone Cortical bone is the outer part of the bone. Osteoporosis is quantitative decrease in bone matrix components of bone. Osteoporosis may be primary or secondary. Osteoporosis is common in elderly women, especially with late menarche, early menopause, long history of oligomenorrhea. Other risk factors include alcohol, smoking, sedentary lifestyle, family history and lean body type. Secondary osteoporosis occurs in: Endocrine: Cushing’s, thyrotoxicosis, hyperparathyroidism, hypogonadism Rheumatological disease: any inflammatory arthropathy. Gastrointestinal: malabsorption, cirrhosis Drugs: Corticosteroids, heparin, warfarrin, phenytoin Neoplasia Osteoporosis causes low impact fractures and thoracic vertebral fractures loss of height, exaggerated dorsal kyphosis and pain. While plain radiographs can be used to establish fractures, it is DEXA (dual emission X-ray absorptiometry) used to measure bone density, to quantify disease progression from normal to osteopenia (mild moderate bone loss) to osteoporosis (severe bone loss). 54. Characteristic features of sarcoidosis include: a. fatigue T b. hypocalcemia F c. erythema marginatum F d. positive mantoux test F e. Uric acid stones F Sarcoidosis is a multi-system disease characterized by non-caseating granulomas. Association with HLA-B8 has been demonstrated, especially with erythema nodosum and arthalgia. Two classic presentations exist: ACUTE: erythema nodosum, arthralgia, BHL CHRONIC: Slowly progressive dyspnea as a result of progressive pulmonary fibrosis There is no relationship with TB and sarcoidosis. Mantoux test is for TB, not for sarcoidosis. Erythema marginatum is described as the presence of pink rings on the trunk and inner surfaces of the arms and legs which come and go for as long as several months. The rings are barely raised and are pruritic. The face is generally spared. It occurs in less than 5% of patients with rheumatic fever (5% from emedicine.com, 50% if you take it from Medicine at a Glance), but is considered a major Jones criterion when it does occur. It is an early feature of rheumatic fever and may be associated with mild carditis (inflammation of heart muscle). 10% get hypercalcemia. 55. With regards to acute stroke, the following statements are true a. cerebral ischemia is readily differentiated from F cerebral hemorrhage from clinical signs b. early CT scanning always demonstrates the lesion F c. Infarction of the cerebral cortex is T commonly associated with dysphagia d. cerebellar hemorrhage often requires surgical intervention T e. patients with A.fib should be anticoagulated immediately F The mechanism of stroke (infarct or bleed) must be demonstrated by CT or MRI. If infarct, the origin or the thrombus should be worked out by carotid ultrasound or transesophageal echo (aortic arch). If hemorrhage, angiography to exclude an aneurysm and sugery/intervention may be needed. INFARCTS: 1. keep BP low (don’t decrease acutely- this can cause watershed infarcts). 2. give aspirin and other antiplatelet agents. 3. thrombolysis may be indicated if given within 3 hours of symptom onset. HEMORRAGE: 1. Lower BP (rapidly if needed.) 2. If in posterior fossa, neurosurgical intervention is required to prevent coning. If intracerebral with mass effect, evacuation may be needed. The assessment and management in stroke: Imagine a Scottish lady from Glasgow with large DDDD breasts. With regards to Glasgow scale, remember how lovely Glasgow is, so lovely we Must Vacate Edinburgh! Glasgow coma scale: Assess best motor response, best verbal response, best eye response Must Motor (6) 6 Obeys commands 5 localizes to pain 4 withdraws 3 Flexes from pain 2 extends from pain 1 No limb movement Vacate Verbal (5): Edinburgh Eyes (4) D Dysphagia: D DVT 5 4 3 2 1 Oriented Disoriented speech Incoherent words Non-sensicle vocalizations No speech 4 Spontaneous eye opening 3 Eyes open on command 2 Eyes open to pain 1 No eye opening assess swallowing. If aspiration risk high, NG tube short term and PEG tube long term prevent DVT using low-dose heparin (unless BLEED in which case avoid) D D Disability Depression Assess rehabilitation needs on basis of disability 50-75% of patients get depression and antidepressants may help Clinical signs do not readily distinguish between bleeds and ischemia. Moreover, a CT scan may not always show a bleed immediately, and early ischemia may be difficult to see. Moreover, a patient with A.Fib may still get a bleed, in which case anticoagulation may be contraindicated. 56. With regards to hemochromatosis, the following statements are true a. It is an autosomal recessive condition b. Patients may present with glycosuria c. The condition may be complicated by hepatoma development d. Therapy usually involves desferrioxamine e. A genetic screen is available to aid diagnosis T T T F T Hemochromatosis is the abnormal accumulation of iron in parenchymal organs, leading to organ toxicity. It is the most common inherited liver disease in whites and the most common autosomal recessive genetic disorder. Hereditary hemochromatosis is an adult-onset disorder characterized by inappropriately high iron absorption resulting in progressive iron overload. The organs involved are the liver, heart, pancreas, pituitary, joints, and skin. In hereditary hemochromatosis, dysregulation of intestinal iron absorption occurs, wherein iron continues to be efficiently absorbed even in the face of substantial elevation of body iron stores. The gene responsible for the disease is called HFE and is located on chromosome 6. It is mutated in the vast majority of individuals with hereditary hemochromatosis. HFE interacts with the transferrin receptor and causes a clear decrease in the affinity with which the receptor binds transferrin. This interaction also may modulate cellular iron uptake and decrease ferritin levels. When a mutant or nonfunctional variant of the HFE gene is present, ferritin levels are not under influence of a normal and functional HFE gene, which leads to enhanced accumulation of iron in peripheral tissues. Firstdegree relatives can be screened for hemachromatosis using genetic mutation analysis (HFE mutation analysis). Findings suggestive of increased iron transport at the basolateral membrane of enterocytes in hemochromatosis have emerged from numerous studies of HFE-related hemochromatosis in humans and in mice. Hepcidin, a human antimicrobial peptide synthesized in the liver, plays a key role in the down-regulation of iron release by enterocytes and macrophages. The absence of this new peptide is associated with severe early-onset iron-loading phenotype. It is also inappropriately low in adult-onset HFE-related disease. Excess iron is hazardous because it produces free radical formation. The presence of free iron in biological systems can lead to the rapid formation of damaging reactive oxygen metabolites such as the hydroxyl radical and the superoxide radical. These can produce DNA cleavage, impaired protein synthesis, and impairment of cell integrity and cell proliferation, leading to cell injury and fibrosis. Symptoms usually begin between age 30 years and age 50 years, but they may occur much earlier. Clinical manifestations include the following: Liver disease (cirrhosis and later, hepatoma/hepatocellular carcinoma) Skin pigmentation Diabetes mellitus (can of course cause glycosuria…) Arthropathy Impotence in males and amenorrhea in females Cardiac enlargement, with or without heart failure or conduction defects Dilated cardiomyopathy Hypothyroidism Cirrhosis: This is one of the most common disease manifestations of the tissue damage caused by hemochromatosis, and it may progress to liver cancer years later (risk >200-fold). It also is the most common cause of death in patients with hereditary hemochromatosis. Reversibility with iron removal has been reported even with development of varices, but this is more likely early in the course of liver disease. Iron removal is typically performed with blood letting (venesection 500 g whole blood weekly until excess iron stores removed, then every 3 months after). If this is insufficient (rarely), iron-chelators such as desferrioxamine may be used. All patients with cirrhosis should undergo diagnostic endoscopy to document the presence of varices and to determine their risk of variceal hemorrhage. Patients at risk for variceal hemorrhage should be considered for primary prophylaxis with propranolol or nadolol. Most patients are asymptomatic (75%) and are diagnosed when elevated serum iron levels are noted on a routine a chemistry screening panel or when screening is performed because a relative is diagnosed with hemochromatosis. 57. The following are causes of secondary hyperlipidemia a. Loop diuretics F b. Chronic renal failure T c. Hypothyroidism T d. High alcohol intake T e. Obstructive jaundice T Secondary causes contribute to most cases of dyslipidemia in adults. The most important secondary cause in developed countries is a sedentary lifestyle with excessive dietary intake of saturated fat, cholesterol, and trans fatty acids (TFAs). TFAs are polyunsaturated fatty acids to which hydrogen atoms have been added; they are commonly used in many processed foods and are as atherogenic as saturated fat. Other common secondary causes include diabetes mellitus, alcohol overuse, chronic renal insufficiency and/or failure, hypothyroidism, primary biliary cirrhosis and other cholestatic liver diseases, and drugs, such as thiazides, β-blockers, retinoids, highly active antiretroviral agents, estrogen and progestins, and glucocorticoids. While thiazide diuretics classically cause hyperlipidemia, loop diuretics can cause a temporary increase in plasma cholesterol and triglyceride concentrations. Since this is temporary only, I’d say false for a. 58. With regards to Atrial fibrillation a. Commonly occurs in patients with a structurally normal heart b. May be precipitated by alcohol excess c. tends to be asymptomatic in patients with hypertrophic cardiomyopathy d. On careful auscultation, a fourth heart sound can be heard e. a-waves are often visible in JVP T T F F F The typical JVP appears like: Since the a wave refers to the atrial systole, there is no a wave in A.Fib. Risk factors for atrial fibrillation include age, male sex, long-standing hypertension, valvular heart disease, left ventricular hypertrophy, coronary artery disease (with or without depressed left ventricular function), diabetes mellitus, smoking, and any form of carditis. Heart sounds S1 and S2 are still present but irregularly irregular. Causes of atrial fibrillation can be divided into cardiovascular versus noncardiovascular causes. cardiovascular causes: HTN, IHD, CHF, carditis, cardiomyopathy Infiltrative heart disease of any type Sick sinus syndrome Noncardiovascular causes: Hyperthyroidism Low levels of potassium, magnesium, or calcium Pheochromocytoma Sympathomimetic drugs, alcohol, electrocution Noncardiovascular respiratory causes: Pulmonary embolism Pneumonia Lung cancer Hypothermia 59. In primary hyperparathyroidism a. Most patients present with urinary tract calculi b. Serum calcium is always higher than normal c. PTH is usually within normal limits d. Chloride:phosphate ratio is elevated F F F T The chloride/phosphate (Cl:PO[4]) ratio is known to help distinguish between the hypercalcemia of primary hyperparathyroidism (HPT) and hypercalcemia from other causes. In the absence of renal failure, the chloride phosphate ratio is elevated in primary hyperparathyroidism but not other causes of hypercalcemia. Primary hyperparathyroidism is usually (90%) caused by a parathyroid adenoma. This may or may not be in conjunction with MEN-1 syndrome (parathyroid hyperplasia+ pituitary adenoma+ pancreatic polypeptide tumors) Incidentally: MEN2a Thyroid medullary Ca, parathyroid hyperplasia, phaeochromocytoma (70% bilateral) MEN2b MEN2A+ Mucosal neuromas+ Marfanoid body habitus. KNOWN defect=Chr.10 oncogene Ret Primary hyperparathyroidism has a female to male preponderance of 2:1. It is the most common cause of hypercalcemia, although 50% are asymptomatic and only discovered because of incidental investigations. Mild or normal calcium levels may be present. Definitive treatment is surgical resection. Postoperative hypocalcemia is usually transient and treatable with calcium supplements and vitamin D. 60. Which of the following suggests that a thyroid swelling is malignant a. Thyrotoxicosis F b. Hoarseness T c. Palpable lymph glands T d. Increased uptake of iodine F Thyrotoxicosis can be caused by Hashimotos thyroiditis (transient hyperthyroidism before becoming hypothyroid), Graves disease (most common cause), toxic multinodular goiter, or toxic adenoma. Thus thyrotoxicosis does not imply malignancy. Hoarseness and thyroid swelling implies the swelling has invaded either the recurrent laryngeal nerve, or the larynx/vocal cords. This implies malignancy. Palpable lymph nodes may be present in infection, chronic inflammatory conditions (RA, etc) or neoplasms, but in the setting of a thyroid swelling, palpable lymphadenopathy would be suggestive of malignancy. Thyroid uptake scan, when increased, may suggest Graves, toxic adenoma or multinodular goiter, thus no suggestion is established. 61. The following are recognized complications of Crohns disease a. Iritis T b. Ascending cholangitis F c. Sclerosing cholangitis T d. Erythema nodosum T PBC (primary biliary cirrhosis) is associated with celiac, rheumatoid disease and autoimmune thyroid disease. This is easy to remember cause PBC has a female:male ratio of 9:1, and is similar to thyroiditis and rheumatoid disease in its female preponderance. PSC (primary sclerosing cholangitis) is associated with IBD. This is easy to remember cause IBD includes two pathologies (UC and CD), as does PSC, which includes intrahepatic and extrahepatic duct disease. The extraintestinal manifestations of Crohn’s disease include: Uveitis and iritis Ankylosing spondylitis Sacroiliitis Anemia (iron and B12 deficiency, and chronic) Hepatitis Mouth ulcers Gallstones Fistulas (enterocolic/enterovesical, etc.) PBC Monoarthritis Pyoderma gangrenosum Erythema nodosum 62. Pancreatic pseudocysts a. Are developmental in origin b. Usually arise in the lesser peritoneal sac c. May be effectively treated by internal drainage d. Occur following pancreatic abscess F F F Single or multiple fluid collections that look like cysts on pancreatic imaging are often observed during acute pancreatitis. Because of increasing sensitivity of imaging modalities and improvements in technology providing enhanced therapeutic abilities, the questions of when and whether drainage should be performed and what modality should be used to drain the cysts are often asked. Strictly defining the type of fluid collection is very important when reviewing pancreatic fluid collections. The therapeutic approach is different depending on the type of collection. Pseudocysts are best defined as a localized fluid collection that is rich in amylase and other pancreatic enzymes, that has a nonepithelialized wall consisting of fibrous and granulation tissue, and that usually appears several weeks after the onset of pancreatitis. These characteristics contrast with those of acute fluid collections, which are more evanescent and are serosanguinous inflammatory reactions to acute pancreatitis. These collections are noted in moderate-to-severe pancreatitis. Acute fluid collections usually have an irregular shape and lack a well-defined wall. In general, they resolve in about 65% of cases. Pathophysiology: Pancreatic pseudocysts can be single or multiple. Multiple cysts are more frequently observed in patients with alcoholism, and they can be multiple in about 15% of cases. Size varies from 2-30 cm. About one third of pseudocysts manifest in the head of the gland, and two thirds appear in the tail. The fluid in pseudocysts has been well characterized as clear or watery, or it can be xanthochromic. The fluid in pseudocysts usually contains very high amounts of amylase, lipase, and trypsin, though the amylase level may decrease over time. The pathogenesis of pseudocysts seems to stem from disruptions of the pancreatic duct due to pancreatitis and extravasation of enzymatic material. Two thirds of patients with pseudocysts have demonstrable connections to the pancreatic duct. In the other third, an inflammatory reaction is supposed to have sealed the connection so that it is not demonstrable. The cause of pseudocysts parallels the cause of acute pancreatitis; 75-85% of cases are caused by alcohol or gallstone disease–related pancreatitis. In children, pseudocysts and trauma are frequently associated. Sex: The male predominance in the incidence of pseudocysts mirrors the male predominance in the incidence of pancreatitis. Age: Pseudocysts may occur after pancreatitis in any age group. In children, pseudocysts are most likely observed after abdominal trauma. In elderly persons, take care not to confuse cystic neoplasms with pseudocysts. Treatment: Most pseudocysts resolve without interference and only require supportive care. Several studies have indicated that the size of the cyst and the length of time the cyst has been present are poor predictors of complications. In general, larger cysts are more likely to become symptomatic or cause complications. However, some patients with larger collections do well; therefore, size of the pseudocyst alone is not an indication for drainage. Prognosis: Most pseudocysts resolve without interference, and patients do well without intervention. Outcome is much worse for patients who develop complications or who have the cyst drained. The presence of pancreatic necrosis is a poor prognostic sign. The failure rate for drainage procedures is about 10%, the recurrence rate is about 15%, and the complication rate is 15-20%. Indications for drainage include the following: Complications Symptoms Concern about possible malignancy Drainage can be carried out by catheter drainage, ERCP, or surgical drainage. Lab Studies: CEA CEA-125 Fluid viscosity Amylase Pseudocyst fluid Low Low Low High Neoplasm sample Elevated Elevated Elevated Low Imaging Studies: CT scan is the imaging criterion standard for pancreatic pseudocysts. It has a sensitivity of 90-100% and is not operator dependent. The usual finding on CT scan is a large cyst cavity in and around the pancreas. Multiple cysts may be present. 63. Acute protrusion of L4/L5 or L5/S1 intervertebral disc a. Is usually associated with lumbar scoliosis b. Causes reduction in straight leg raising c. Commonly causes loss of knee tendon reflex d. May be associated with sensory change at the lateral border of the foot F T T T A spinal disc herniation is a pathological condition in which a tear in the outer, fibrous ring (annulus fibrosus) of an intervertebral disc allows the soft, central portion (nucleus pulposus) to be extruded (herniated) to the outside of the disc. It is normally a further development of a previously existing disc protrusion, a condition in which the outermost layers of the annulus fibrosus are still intact, but can bulge when the disc is under pressure. Disc herniation can occur in any disc in the spine, but the two most common forms are the cervical disc herniation and the lumbar disc herniation. The latter is the most common, causing lower back pain (lumbago) and often leg pain as well, in which case it is commonly referred to as sciatica. Lumbar disc herniation occurs 15 times more often than cervical (neck) disc herniation, and it is one of the most common causes of lower back pain. The cervical discs are affected 8% of the time and the upper-to-mid-back (thoracic) discs only 1 2% of the time. The upper two cervical intervertebral spaces, the sacrum, and the coccyx have no intervertebral discs and are thus exempt from herniated discs. The classic presentation of a HNP (herniated nuclear palposus) includes the complaint of sciatica (an intractable radiating pain), with associated objective neurological findings of weakness, reflex change, or dermatomal numbness. Causes of a disc herniation can include general wear and tear on the disc over time, repetitive movements, stress on the disc that occurs while twisting and lifting, or other injuries. The discs cushion the spine from compressive forces, but are weak to pressure applied during rotational movements. That is why a person who bends to one side, at a bad angle, to pick up a piece of paper may more likely herniate a spinal disc than a person falling from a ladder and landing on his or her back. Pain that radiates from your lower (lumbar) spine to your buttock and down the back of your leg is the hallmark of sciatica. You may feel the discomfort almost anywhere along the nerve pathway, but it's especially likely to follow a path from your low back to your buttock and the back of your thigh and calf. The pain can vary widely, from a mild ache to a sharp, burning sensation or excruciating discomfort. Sometimes it may feel like a jolt or electric shock. Sciatic pain often starts gradually and intensifies over time. It may be worse when you cough or sneeze, and prolonged sitting or walking can also aggravate symptoms. Usually only one lower extremity is affected. In addition to pain, you may also experience: Numbness or muscle weakness along the nerve pathway in your leg or foot. In some cases, you may have pain in one part of your leg and numbness in another. Tingling or a pins-and-needles feeling, most commonly in your toes or part of your foot. A loss of bladder or bowel control. This is a sign of cauda equina syndrome, a rare but serious condition that requires emergency care. 64. The following are features of Horner’s syndrome a. Unilateral enophthalmos b. Atrophy of the hand muscles c. Miosis d. Loss of sweating on one side of face T F T T Horner’s syndrome is a disruption in the cervical sympathetic chain, and can be caused by: Thyroid carcinoma Syringomyelia Apical lung Ca Cervical rib Aortic aneurysm MS/glioma in posterolateral brain stem Trauma Carotid dissection Signs found in all patients, regardless of the level of interruption include mild-tomoderate ptosis owing to denervation of the sympathetically controlled Müller muscle, slight elevation of the lower lid (upside-down ptosis) due to denervation of the lower lid muscle analogous to Müller muscle in the upper lid, and miosis and dilation lag, where pupillary dilation after psychosensory stimuli is slower in the affected pupil than the unaffected pupil. Depending on the level of the lesion, impaired flushing and sweating may be found ipsilaterally. 65. Diagnosis of insulinoma is suggested by the following a. Fasting hypoglycemia b. Hypoglycemia relieved by meals c. Hypoglycemia coming 1-2 hours after meals d. Hepatic disease in an alcoholic T T T F e. Hypoglycemia with very low plasma insulin F Insulinomas are the most common cause of hypoglycemia resulting from endogenous hyperinsulinism. Pathophysiology: An insulinoma is a neuroendocrine tumor deriving mainly from pancreatic islet cells that produce excessive amounts of insulin. About 90% of insulinomas are benign. In healthy individuals, insulin and C-peptide are secreted in equimolar quantities because they derive from the same inactive precursor, proinsulin. Normally, less than 20% of proinsulin is released directly into the circulation. Some insulinomas secrete additional hormones, such as gastrin, 5-hydroxyindolic acid, adrenocorticotropic hormone (ACTH), glucagon, human chorionic gonadotropin, and somatostatin. The tumor may secrete insulin in short bursts, causing wide fluctuations in blood levels. Approximately 10% of insulinomas are malignant (metastases are present), and 10% are multiple, particularly in patients with multiple endocrine neoplasia type 1 (MEN 1). Of patients with multiple insulinomas, 50% have MEN 1. Insulinomas are associated with MEN 1 in 5% of patients. On the other hand, 21% of patients with MEN 1 develop insulinomas. About 85% of patients present with symptoms of hypoglycemia with diplopia, blurred vision, palpitations, or weakness.Other symptoms include confusion, abnormal behavior, unconsciousness, or amnesia. About 12% of patients have grand mal seizures. Adrenergic symptoms (hypoglycemia causes adrenalin release) include weakness, sweating, tachycardia, palpitations, and hunger. Symptoms may be present from 1 week to as long as several decades prior to the diagnosis (1 mo to 30 y, median 24 mo, as found in a large series of 59 patients). Hypoglycemia usually occurs several hours after a meal. In severe cases, symptoms may develop in the postprandial period. Symptoms can be aggravated by exercise, alcohol, hypocaloric diet, and treatment with sulfonylureas. Weight gain occurs in 20-40% of patients. 66. The following are true of ankylosing spondylitis a. It is commonest in females over 40 F b. Can be associated with arthritis of the hip joint F c. It may present with sciatica T Ankylosing spondylitis is a chronic inflammation of the spine that may gradually result in a fusion of vertebrae. Symptoms include a slow development of back discomfort, with pain lasting for more than three months. The back is usually stiff in the morning; pain improves with exercise. In severe cases, the patient must continually stoop over. It can be quite mild, however, and it rarely affects a person's ability to work. It occurs mostly in young Caucasians in their mid-twenties. The disease is more common in men, but about 30% of the cases are in women. Researchers believe that in most cases it is hereditary. About 20% of people with inflammatory bowel disease and about 20% of people with psoriasis develop a form of ankylosing spondylitis. There are few effective treatments for this potentially disabling disease, although etanercept (Enbrel) and infliximab (Remicade), antiinflammatory agents known as TNF-blockers, are proving to be beneficial. 67. A 70 year old lady presented with a cough. She is also anorexic of late. The following should be performed immediately? a. ESR T b. CXR T c. Psychiatric evaluation F d. Sedate her, send her home and review in a week F e. Examine sputum for AFB T ESR: This presentation may be consistent with an infection or inflammatory process, both of which would raise ESR. This would gage recovery as well. CXR: May have TB or other chest infection. Psychiatric evaluation: anorexia may be psychiatric, but cough suggest organic cause. Sedation, send home and review later: Obviously this woman needs to be investigated. Examine sputum for AFB: Acid-fast bacilli may be found in TB, so do it. 68. Subdural hematoma is suggested by the following: a. Change of personality T b. Brain spinal tap F c. History of trauma T d. Central scotoma F Subdural hematoma is usually a venous bleed in brain shrinkage (old age, dementia, chronic alcoholism). Blood oozes into subdural space. Space-occupying lesions result. There may be a history of trauma. Focal neurological deficit, decreased mobility, decreased mental agility (if in frontal area, personality change may occur). CT scan is diagnostic. Brain spinal tap (I assume they mean lumbar puncture) is diagnostic in subarachnoid hemorrhage, not subdural. Evacuation should be considered. Central scotoma is an area of depressed vision that corresponds with the point of fixation and interferes with central vision. It suggests a lesion between the optic nerve head and the chiasm. Possible causes include: multiple sclerosis - which may cause unilateral or asymmetrical bilateral scotoma methyl alcohol - which may cause symmetrical bilateral scotoma nutritional causes - which may be due to, e.g. alcohol or tobacco amblyopia, B12 deficiency vascular lesions – hemorrhage (into macula) may cause unilateral scotoma; this is not subdural however gliomas of the optic nerve - this may cause unilateral scotoma simple glaucoma - which may initially cause an off-centre scotoma 69. The following investigations are indicated in a patient with bilateral hilar lymphadenopathy. a. Mantoux test T b. Kveim test T c. Serum calcium T d. CT scan T e. Lung biopsy T Bilateral hilar lymphadenopathy is classically associated with sarcoidosis, which can cause hypercalcemia and a positive Kveim test (splenic extract from sarcoid patient A injected into patient B suspected of having sarcoidosis. The reaction is biopsied and histologically examined for presence of non-caseating granuloma). This test is no longer done, however, because of concerns over infection. Instead, a lung biopsy can be 90% sensitive or a liver biopsy 70% sensitive for the pathognomonic lesion of sarcoidosis. Alternative causes of bilateral hilar lymphadenopathy include TB, for which a Mantoux test can be performed, and neoplasm, for which a CT would be indicated. 70. Complications of Diabetes mellitus include a. LOAD ? b. Liver cysts F c. Proteinuria T d. Raynaud’s phenomenon F e. Neovascularization of the retina T Diabetic complications can be categorized into microvascular or macrovascular: Microvascular typically affects nerves, eyes, kidneys (neuropathy, retinopathy, nephropathy). Macrovascular affects the large arteries (atherosclerosis increasing MI/stroke). Neuropathy includes autonomic, sensory or motor neuropathy. Retinopathy is divided into background (dot-blot hemorrages, exudates ), preproliferative (cotton wool spots + venous beading + IRMAs), and proliferative (neovascularization) diabetic retinopathy. Maculopathy risk is also increased in diabetes. Nephropathy includes basement membrane thickening to KimmelsteinWilson lesion (glomerulosclerosis). Nephrotic and nephritic syndrome may result. Raynaud’s phenomenon is episodic, painful, digital ischemia in response to cold or emotional stimuli, causing a classical color change from white to blue to red (“With Boys Rarely” as it affects mostly women!). Causes include: Idiopathic Affects young women mostly Secondary Cervical rib Vibrating tools Vasculitis CT disease (SLE, RA, dermatmyositis) Cryoglobinemia Cold agglutinins Hyperviscosity Drugs (beta-blockers, cytotoxics) 71. An alcoholic presents with hepatosplenomegaly and hematemesis a. The bleeding can be assume to be esophageal varices F b. Vitamin K will reverse all clotting defects F c. The presence of blood in the GIT may be harmful T d. Lactulose, magnesium sulphate and F neomycin may all be useful e. The features of encephalopathy include T altered consciousness The combination of lactulose (osmotic diuretic), magnesium sulphate (osmotic diuretic), neomycin (counteracts constipation)-this is seen and used in IBS (irritable bowel syndrome). Encephalopathy literally means disease of the brain. It refers to the central nervous system, or parts of it. Pathologists are more likely to use this term. Descriptions of the living usually refer to dementia. Medical Imaging has made physiopathology more practical on the living, however. Encephalopathy alters brain function and/or structure. It may be caused by an infectious agent (bacteria, virus, or prion), metabolic or mitochondrial dysfunction, brain tumor or increased intracranial pressure, prolonged exposure to toxic elements (including solvents, drugs, radiation, paints, industrial chemicals, and certain metals), chronic progressive trauma, poor nutrition, or lack of oxygen or blood flow to the brain. It is also known that concomitant use of lithium with other neuroleptics may, in rare cases, cause encephalopathy. The hallmark of encephalopathy is an altered mental state. Depending on the type and severity of encephalopathy, common neurological symptoms are progressive loss of memory and cognitive ability, subtle personality changes, inability to concentrate, lethargy, and progressive loss of consciousness. Other neurological symptoms may include myoclonus (involuntary twitching of a muscle or group of muscles), nystagmus (rapid, involuntary eye movement), tremor, muscle atrophy and weakness, dementia, seizures, and loss of ability to swallow or speak. Hematemesis is the vomiting of fresh red blood. The source is generally the upper gastrointestinal tract. Patients can easily confuse it with hemoptysis (coughing up blood), although the former is more common. CAUSES: Vomiting of ingested blood after hemorrhage in the oral cavity, nose or throat Mallory-Weiss syndrome (esophageal tear) Esophageal varices Peptic ulcer Gastritis Gastric varices Dieulafoy's lesion: Dieulafoy's lesion is an uncommon cause of gastric bleeding thought to cause less then 5% of all gastro-intestinal bleeds in adults. It was named after French surgeon Paul Georges Dieulafoy who described this condition in his paper "Exulceratio simplex: Leçons 1-3" in 1898. Dieulafoy's Lesions bleed into the gastro-intestinal tract from an arteriole protruding through a minute defect in the mucosa. 95% of Dieulafoy's lesions occur in the upper part of the stomach, within 6cm of the gastro-oesophageal junction, however they can occur anywhere in the GI tract. Interestingly and in contrast to peptic ulcer disease, a history of alcohol abuse or NSAID use is usually absent in Dieulafoy's. In a "hemodynamically significant" case of hematemesis, that is hypovolemic shock, resuscitation is an immediate priority to prevent cardiac arrest. Fluids and/or blood is administered, preferably by central venous catheter, and the patient is prepared for emergency endoscopy, which is typically done in theatres. Surgical opinion is usually sought in case the source of bleeding cannot be identified endoscopically, and laparotomy is necessary. 72. Polycystic kidney a. Is transmitted autosomal dominant b. Often presents in childhood c. Causes hypertension d. Is associated with cystic liver disease F F T T PKD is transmitted autosomal dominant OR autosomal recessive, thus a is false. PKD can present in childhood if autosomal recessive. This is rare compared to autosomal dominant variant. Polycystic kidney disease (PKD) is a progressive, genetic disorder of the kidneys. It occurs in humans and other organisms. PKD is characterised by the presence of multiple cysts (polycystic) in both kidneys. The disease can also damage the liver, pancreas and rarely the heart and brain. The two major forms of polycystic kidney disease are distinguished by their patterns of inheritance. Autosomal dominant polycystic kidney disease (ADPKD) is generally a late onset disorder characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts. Kidney manifestations in this disorder include renal function abnormalities, hypertension, renal pain, and renal insufficiency. Approximately 50% of patients with ADPKD have end-stage renal disease (ESRD) by age 60 years. ADPKD is, however, a systemic disease with cysts in other organs such as the liver (which may lead to cirrhosis), seminal vesicles, pancreas, and arachnoid mater and non-cystic abnormalities such as intracranial aneurysms and dolichoectasias, dilatation of the aortic root and dissection of the thoracic aorta, mitral valve prolapse, and abdominal wall hernias. Initial symptoms are hypertension, fatigue and mild to severe back or flank pain and urinary tract infections. The disease often leads to chronic renal failure and may result in total loss of kidney function, known as end stage renal disease (ESRD) which requires some form of renal replacement therapy (e.g. dialysis). Autosomal recessive polycystic kidney disease (ARPKD) is much rarer than ADPKD and is often lethal. The signs and symptoms of the condition are usually apparent at birth or in early infancy. 85% of Polycystic kidney disease is autosomal dominant and thus “adult-onset” while 15% is autosomal recessive and presents at birth or early infancy. 73. Extraintestinal manifestations of IBD: a. Sacroiliitis T b. Erythema nodosum T c. Syndenhams’s Chorea F d. Pyoderma gangrenosum T e. Entrapment neuropathy. F IBD extraintestinal manifestations include: Clubbing Anemia (B12 deficiency/iron deficiency/chronic disease) Arthralgia (seronegative, includes sacroiliitis) PSC (esp. UC) CRC likelihood increased Erythema nodosum and pyoderma gangrenosum 74. An 80 year old female presented in an acute confusional state with very aggressive behavior. Immediate steps in her management include: a. Acute psychiatric admission F b. Review for drug therapy if any T c. Physical examination to exclude T focus of infection d. Start broad spectrum antibiotic F e. Isolate and review in a week F IMMEDIATE steps include: History and exam, including collateral history. Vitals. Review drugs. Medications should not be started until the aetiology is established. Confusion (encephalopathy) is defined as the inability to maintain a coherent stream of thought or action. The hallmark of acute confusional states is impairment in attention and/or arousal or acute changes in perception or other higher order behaviors. Delirium is a more specific syndrome, defined as an impairment of attention or arousal. The usage of the two terms overlaps considerably. Causes: Potential causes of acute confusional states are numerous. A good clinician is thorough and systematic in the evaluation. Intoxication Intoxicants can include prescription and over-the-counter medications, as well as alcohol and illegal drugs. Although these causes often are suspected in the emergency department (ED), they may be unsuspected in other settings (eg, postoperative delirium tremens in closet alcoholics). Prescription medicines may be used inappropriately. Prednisone, dexamethasone, and other steroids can cause paradoxical confusion, as can a host of other medications. Focal brain lesions Focal brain lesions occasionally can cause acute confusion. Subdural hematomas, strokes, and mass lesions may be found on CT scan and MRI. Contrast scans are more sensitive for the above. If the confusion is due to increased intracranial pressure, as in a subdural hematoma, arousal may be most affected and the patient may be sleepy. If due to a stroke, the "confusion" is likely to be misdiagnosed aphasia, or vice-versa, unless a huge lesion is present, in which case associated hemiparesis makes the diagnosis obvious. Uncommonly, strokes can present as confusional states with highly select lesion loci. Brain tumors often develop slowly, allowing the brain to compensate; therefore, they are somewhat less likely to present as acute confusional states. Occasionally, focal lesions can result in confusion. Patients develop an agitated confusion with head lesions affecting the caudate, thalamus, or basal forebrain. Patients may appear agitated with lesions of the Wernicke area or of the mirror-image homologous area of the right hemisphere. Infections Urinary tract infections and pneumonias are common infections that cause confusion in debilitated, nursing home, and other elderly patients. If these common infections are not present, patients should be checked for other common metabolic abnormalities, including abnormalities of glucose, sodium, BUN, calcium, magnesium, and phosphorus. The blood oxygen should be checked and the anion gap measured. Once these are sent for investigation, other common conditions should be sought, including cobalamin deficiency, thyroid disease, vasculitis, and latent syphilis. Ammonia should be checked, especially if asterixis is present. Neurologic diseases Specific neurologic diseases besides stroke, tumor, and subdural hematoma need to be considered. Paramount among these are neurologic infections, especially those that are treatable. Young patients presenting with high fever and confusion should be evaluated for herpes virus and treated presumptively until the condition is ruled out. West Nile virus can present with fever. Epilepsy Epilepsy can present as confusion. Patients may have nonconvulsive status epilepticus, a condition that can be easily diagnosed and treated. Two types may occur—absence status may occur in patients who may or may not have had prior absence seizures, and complex partial status epilepticus may occur in patients with or without a history of complex partial seizures. The 2 types are differentiated by EEG. In absence epilepsy, spike-and-wave discharges are seen at a rate of 3 per second. In complex partial status (the more common type), a focal discharging pattern may be seen. Vascular dememtia, given it’s stepwise progression, may also appear like acute confusional state in some settings. 75. Multiple blood transfusions increase the risk of a. Malaria T b. Hepatitis A F c. Non-A Non-B Hepatitis T d. Chicken pox pneumonia ?? e. AIDS T I would think multiple blood transfusions would DECREASE the risk of chicken pox pneumonia, since there would be antibodies versus varicella zoster virus in the transfusion…I don’t know this one though Blood donation centers in different countries may have different guidelines about who can serve as a blood donor. Common contraindications to being a blood donor include: previous malaria or hepatitis a history of intravenous drug abuse donors who have received human-derived pituitary hormones donors with high-risk sexual behaviour (variably defined) donors who have previously been transfused (12-month min. deferral) As of mid-2005, all donated blood in the United States is screened for the following infectious agents: HIV-1 and HIV-2 Human T-lymphotropic virus (HTLV-1 and HTLV-2) Hepatitis B or C virus West Nile virus Treponema pallidum (the causative agent of syphilis) 76. The following attack both skin and mucosal surfaces a. Erythema multiforme T b. Lichen planus T c. Granuloma annulare F d. Discoid lupus F e. Herpes simplex T Erythema multiforme is a hypersensitivity rash of acute onset caused by infection or drugs. T-cell lymphocyte mediated response is seen on skin. Causes include: Idiopathic (50%) HSV, HIV, EBV, CMV, orf infection CT disease (SLE, polyarteritis nodosa) Wegener’s granulomatosis Drugs (anticonvulsants, sulphonamides) Target lesions occur symmetrically on limbs, palms and soles, and mucosal involvement occurs in “EM major” aka Stevens-Johnson syndrome. Lichen planus is a pruritic inflammatory dermatosis commonly associated with mucosal involvement, nail dystrophy and less commonly, scarring alopecia. White lacy pattern on the lesion surface may be present, and is known as “Wickham’s striae.” A T-cell mediated mechanism is postulated. Small purple, flat-topped, intensely pruritic papules seen on wrist flexors, lower legs especially. Mucosal involvement is common, with mouth, esophagus and anogenital region commonly affected. Granuloma annulare is a dermatosis of young adults and children, characterized by clusters of small dermal papules forming rings, commonly found on dorsum of hands and feet. Diffuse forms may be associated with diabetes mellitus. Mucosal involvement generally does not occur. Discoid lupus erythematosus (DLE) is a chronic, scarring, atrophy producing, photosensitive dermatosis. DLE may occur in patients with systemic lupus erythematosus (SLE), and some patients (<5%) with DLE progress to SLE. Some patients also have the lesions of subacute cutaneous lupus erythematosus (SCLE), and some may have a malar rash. DLE lesions frequently are characteristic. The primary lesion is an erythematous papule or plaque with slight-to-moderate scaling. As the lesion progresses, the scale may thicken and become adherent, and pigmentary changes may develop, with hypopigmentation in the central or inactive area and hyperpigmentation at the active border. Several unusual variants of chronic Cutaneous Lupus Erythematous, other than DLE, have been reported; in one of which mucosal surfaces may be affected by lesions that appear identical to DLE of the skin or by lesions that may simulate lichen planus. However, DLE does not involve mucosal surfaces on its own. Herpes simplex can affect the genitals (HSV-2 usually) or gingivostomatis with mouth ulcers (HSV-1 usually). Mucosal surfaces commonly involved in oral area. 77. Causes of gynecomastia include a. Puberty b. Klinefelters syndrome c. Spironolactone therapy d. Untreated essential hypertension e. decreased thyroid function T T T F F Gynecomastia occurs when excessive estrogens, prolactin or HCG are produced, as can occur in: Liver disease Tumors of: adrenal gland, testicle, lung Breast carcinoma, prolactinoma Neonatal, Puberty and old age Hyperthyroidism Drugs: spironolactone, phenytoin, digoxin, cannabis, opiates, gonadotrophins Genetic Klinefelters 78. The following are features of LVF a. Basal creps T b. Gallop rhythm T c. Pulsus alternans T d. Peripheral edema F e. Elevated pulsatile JVP F The features of right heart failure include: Increased JVP Hepatomegaly Ascites Ankle edema Features of left heart failure include Pulsus alternans (alternating large and small amplitude beats noted in pulse) Bibasal crepitations Cyanosis Pink frothy sputum Orthopnea Third heart sound (“gallop rhythm”) 79. A 23 year old man with 6/12 history of treatment of frequent bowel motions with release of blood and mucus PR. a. A perianal fistula would suggest Crohns T b. A barium enema may aid diagnosis T c. You would expect anemia and low serum iron T d. A barium follow through may be needed T e. An infective cause would be likely F 80. A 60 year old man presents with bilateral ptosis. Diplopia is worse in the evenings. Pupils are equal and reactive to light and accommodation. Bedrest improved ocular movements. The most likely diagnosis is: a. Myasthenia gravis b. Ocular myopathy c. Myotonic dystrophy d. Endocrine exopthalmic exopthalmoplegia e. Midbrain vascular lesion 81. The following murmurs are correctly associated: a. Mitral stenosis: mid diastolic murmur b. Pulmonary stenosis: pansystolic murmur c. Mitral regurgitation: pansystolic murmur d. Aortic stenosis: ejection murmur e. Aortic regurgitation: pan-diastolic murmur 82. The following are suggestive of carcinoma in a patient with hoarseness: a. Unilateral recurrent laryngeal nerve palsy b. Myxedematous thickening of the vocal cord c. Cervical lymphadenopathy d. Single nodule in the thyroid gland e. Sudden enlargement of??? 83. In Cor pulmonale a. Digoxin in the best treatment b. Diuretics are indicated c. The 5 year survival rate exceeds 75% d. Hypoxia causes reduced pulmonary vascular resistance e. Home oxygen has little or no place in the treatment 84. Heberdens nodes: a. Occur at the base of the terminal phalanges b. Occur in subacute bacterial endocarditis c. Are commoner in fat people than in thin people 85. A teacher, asthmatic, with a 2month history of epigastric pain. Barium meal is negative. She is currently taking theophylline and a B12 stimulant. No other medications. Three days later she is complaining of nausea. What is the single most appropriate action to take? a. Repeat barium meal b. Measure theophylline levels c. Gastric acid stimulation test d. Gastroscopy e. FOB 86. Cerebellar ataxia may be caused by: a. Folate deficiency b. Thiamine c. Phenytoin d. Alcohol e. Carbamazepine 87. A young man presents with rigors, dysuria and pyrexia. What do you do? a. MSU, differential wcc, blood culture b. IVP before starting treatment c. Do not treat with antibiotics before getting cultures d. Oral penicillin is the first line treatment 88. Mitral valve prolapse: a. Is found in 5-10% of the population b. Presents with a mid-late systolic cluck and late systolic murmur c. Presents with chest pain and palpitations d. Patients should receive antibiotic prophylaxis e. Patients have a higer incidence of endocarditis 89. The following statements are correct: a. Amiodarone causes corneal microdeposits and pulmonary fibrosis b. Amiodarone causes a peripheral neuropathy c. Adenosine is contraindicated in complete heart block d. Aortic incompetence is best heard with the patients sitting forward and on inspiration e. A collapsing pulse is a feature of aortic incompetence Common drugs used in arrythmias include: Arrythmia Drug Contraindications and Side effects Supraventricular Slow AV node tachycardia IV adenosine ConInd: 2nd/3rd degree heart block sick sinus syndrome Caution: SidEff: Asthma (bronchospasm) “ABCDEF” Adenosine Bronchospasm Chest pain Dyspnea ECGtransient rhythm Disturbance Flacial flushing Nausea B-blockers Esmolol ConInd: SidEff: Asthma Marked bradycardia 2nd/3rd degree heart block Metabolic acidosis Uncontrolled heart failure Phaeochromocytoma (without alphablockade) Bradycardia Heart failure Bronchospasm Peripheral vasoconstriction Verapamil ConInd GI/sleep disturbance Sexual dysfunction Exacerbation of psoriasis Renal failure Hypotension 2nd/3rd degree heart block Cardiogenic shock Hx heart failure or LV Dysfunction A.Fib/A Flutter with WPW SidEff: Syndrome Constipation N+V/headache Allergic reactions (urticaria/StevensJohnson ) Increased PRL secretion Fleicainide Atrial Fibrillation Rate Control Digoxin Beta-blockers Ca channel blockers Rhythm control Amiodarone Flecainide Sotalol Anticoagulation INR 2.5-3 Warfarrin Ventricular tachycardia Hemodynamically stable VT IV lidocaine Amiodarone Pulseless VT or Polymorphic VT DC cardioversion 90. During cardio-pulmonary resuscitation a. External cardiac massage must be discontinued during inflation of the lungs b. Intubation should be attempted immediately c. PEA should be treated with IV adrenaline d. 50 mL of 8.4% sodium bicarbonate should be given as soon as central access is established e. Ventricular fibrillation associated with hypotension is best treated with IV Lignocaine 132. Clubbing is associated with which of the following a. severe asthma F b. chronic bronchitis F c. bronchiectasis T d. cirrhosis T e. pulmonary fibrosis T The causes of clubbing can be divided into the following categories: Cardiac: Infective Endocarditis Cyanotic Congenital Heart Disease Atrial Myxoma Respiratory: Bronchial Carcinoma Chronic Suppurative Lung Diseases (e.g. Bronchiectasis, Lung Abscess, Empyema) Pulmonary Fibrosis Cystic Fibrosis Pleural Mesothelioma Asbestosis Gastrointestinal: Liver Cirrhosis Inflammatory Bowel Disease Coeliac Disease Miscellaneuous: Thyrotoxicosis Familial Pregnancy Neurogenic Diaphragmatic Tumours 133. Radioiodine treatment for hyperthyroidism a. can be given in an outpatient clinic T b. is the treatment of first choice in the elderly F c. The results of this treatment can be seen in 2-3 Weeks F d. Is absolutely contraindicated in women who are Lactating T e. Is absolutely contraindicated in women planning a future pregnancy F (T if conception planned for up to 4 months post-treatment) Radioiodine therapy for hyperthyroid patients is almost always done on an outpatient basis, because the dose required is relatively small compared with the doses typically used for treatment of thyroid cancer. If a patient has received a higher radioiodine dose for treatment of thyroid cancer, he/she may need to be admitted to hospital for several days depending on the amount of radioiodine administered, their living environment, state of residence, or local practice patterns. Radioiodine treatment is the treatment of choice in elderly people in the United States. However in the UK and Ireland, antithyroid drugs such as carbimazole or propylthiouracil in combination therapy with a beta-blocker e.g. propanolol is still the first treatment of choice. However radioiodine being used more widely in Ireland and the UK than previously, particularly in hyperthyroid patients who are not pregnant or lactating. Thus this treatment is considered more in the elderly population, particularly in those who also have thyroid-related heart disease e.g. atrial fibrillation, high-output cardiac failure. The results of radioiodine therapy for hyperthyroidism usually take 2-3 months to develop i.e. to revert back to euthyroidism. Radioiodine treatment is absolutely contraindicated in women who are lactating because there is a risk of the radioiodine being absorbed by the infant’s thyroid gland too, causing it to be irradiated and the child to become hypothyroid. Radioactive iodine is absolutely contraindicated during pregnancy, or if the patient is planning to get pregnant within 4 months after treatment, because from the third month of pregnancy the thyroid gland of the foetus absorbs iodine and therefore the baby’s thyroid would become irradiated too. As a result, the baby would not have a functioning thyroid gland. It is also important not to come into close contact with babies, children or women of childbearing years for approximately 2-3 weeks for the same reasons. The above guidelines apply to both male and female patients. However the radioiodine is completely excreted from the body 4 months post-treatment, so conception after 4 months is not harmful to the foetus. Finally radioiodine therapy has not been found to alter patient’s fertility or the viability of future pregnancies in any way. 134. Collapsing pulse is associated with: a. aortic stenosis F b patent ductus arteriosus T c. fever T d. anaemia T e. aortic regurgitation T A collapsing pulse is defined as a pulse with a fast upstroke and fast down stroke. Causes of a collapsing pulse include aortic regurgitation, patent ductus arteriosus, and hyperdynamic circulations e.g. thyrotoxicosis, pyrexia/fever, anaemia and AV fistulae. 135. Features of an innocent murmur are a. diastolic rhythm F b. loud S1 F c. Normal S2 in expiration T d. Radiation throughout precordium F e. PR interval 0.12-0.2 seconds T Characteristics of innocent murmurs include the following: 1. Systolic murmur, which is neither diastolic or pan systolic, except for the continuous murmur of a venous hum, which is reduced on lying down. 2. No other abnormality detected (no cardiac enlargement) 3. No thrills or added sound 4. Intensity of murmur often varies with a change in posture 5. No radiation of murmur heard on auscultation 136. Features of a pleural effusion a. bronchial breaths T b. increased vocal fremitus F c. Increased vocal resonance F d. Dullness on percussion T e. Crackles F A pleural effusion is fluid in the pleural space. Features of pleural effusion on clinical examination include the following: 1. Decreased chest expansion on affected side 2. Stony dull percussion note 3. Diminished breath sounds occur on the affected side. 4. Tactile vocal fremitus and vocal resonance are decreased (inconstant and unreliable) 5. Above the effusion where the lung is compressed, there may be bronchial breathing and megaphone (bleating vocal resonance). 6. With large pleural effusions, there may be tracheal deviation away from the effusion. 137. Thrombocytosis is a feature of a. Post operatively T b. Post-splenectomy T c. Malignancy T d. SLE T e. After blood transfusion F Thrombocytosis occurs when the platelet count exceeds 450,000 per cubic mm although numbers may exceed 1,000,000 per cubic mm without symptoms. Thrombosis and paradoxically, haemorrhage are the main symptoms but their occurrence is as much dependent on qualitative defects in the platelets as much as their number. Two types of thrombocytosis are recognised: reactive thrombocytosisfor which the term thrombocytosis is reserved and essential thrombocythaemia- an essential or autonomous thrombocytosis. Reactive thrombocytosis (RT) refers to thrombocytosis in the absence of a chronic myeloproliferative or myelodysplastic disorder, in patients who have a medical or surgical condition likely to be associated with an increased platelet count, and in whom the platelet count normalizes, or is expected to normalize, after resolution of this condition. Reactive thrombocytosis is commonly associated with: inflammation bacterial infection trauma bleeding malignancy iron deficiency following splenectomy following recent surgery Counts may exceed 1,000,000 per cm^3. The platelets are functionally normal. Very severe iron deficiency may cause thrombocytopenia rather than thrombocytosis. 138. Crackles can be a sign of: a. Cryptogenic fibrosing alveolitis T b. Extrinsic allergic alveolitis T c. Sarcoidosis T d. Pulmonary fibrosis T e. TB T Crackles are caused by the re-opening , during inspiration, of the small airways, which have become occluded during expiration. They may be fine and high pitched if coming from distal air spaces (e.g. pulmonary oedema, fibrosing alveolitis) or coarse and low pitched if they originate more proximally (e.g. bronchiectasis).Extrinsic allergic alveolitis and pulmonary fibrosis are also known to cause crackles to be heard on auscultation. Although 80% of patients with acidosis have lung involvement, they usually have no respiratory signs. In severe disease however, there may be signs of pulmonary fibrosis, and so crackles heard. In the case of TB, usually no abnormal chest signs are found, and clues to the diagnosis lie in the classical history of cough, haemoptysis, weight loss, night sweats and malaise. However TB, particularly primary TB, results in consolidation, and crackles can be appreciated on auscultation of some patients. 139. The following are true about hypertension a. Thiazide diuretics are treatment of choice in Elderly T b. There is more of a chance of finding a cause for the more severe malignant form than from the more common benign form T c. Headache and dizziness are signs/symptoms of mild or moderate hypertension F d. Systolic hypertension alone requires no treatment F Essential/benign hypertension (primary, cause unknown) represents 95% of cases and is usually asymptomatic. Secondary hypertension represents the remaining 5% of hypertensive patients. Malignant/secondary hypertension refers to severe hypertension (e.g. >200/>130 mm Hg )in conjunction with bilateral retinal haemorrhages and exudates, and papilloedema may or may not be present. Symptoms such as headache +/- visual disturbance are common, and malignant hypertension alone requires urgent treatment and thorough investigation of underlying cause such as renal disease, endocrine disease, forestation of aorta, pregnancy etc. Evidence from three major studies indicates, beyond doubt, that benefits of treating elderly patients with systolic hypertension are even greater than treating moderate hypertension in middle-aged patients. Systolic blood pressure is the most important determinant of cardiovascular risk in the over 50s.Thiazide diuretics are considered the first-line treatment of choice for hypertension in the elderly, being both therapeutically and cost-effective. 140. A woman presents with a facial rash of four weeks a. History is compatible with a diagnosis of acne Rosacea T b. Psoriasis could be a cause F c. Oral steroids trial is advised F d. H2 blockers could be a cause of the rash T e. Photosensitive rash is a possible diagnosis T Acne rosacea refers to a chronic relapsing and remitting facial disorder of unknown aetiology, where chronic flushing triggered by alcohol, spicy foods etc. often precedes the development of fixed erythematic (chin, nose, cheeks, forehead), telangiectasia, papules and pustules. Psoriasis is usually characterised by symmetrical well-defined red plaques with silvery scale, on the extensor surface of the elbows, knees, scalp and sacrum. The flexures are frequently also involved, but lesions are not scaly here. The face is not affected in psoriasis. Oral steroid treatment is not without its complications, and is not indicated here. Topical steroids can be used for treatment of inflammatory skin conditions (other than those arising from infection), in particular eczema, contact dermatitis and insect stings. However they are of no value in the treatment of urticaria and are contraindicated in the case of rosacea. They are also not recommended for acne vulgaris. H2-blockers can cause erythema multiforme and toxic epidermal necrolysis, the latter causing widespread erythema. Photosensitive rash or rash that is triggered by exposure to light, such as the characteristic malar rash of SLE, is a possible diagnosis. 141. A 45 year old man, non smoker, presents to casualty with chest pain of 3 hours, no history of hypertension a. IV analgesics are indicated T b. PO aspirin advised T c. IV thrombolytic therapy is not contraindicated T d. Monitoring of BP and ECG is necessary T e. Patient is allowed home to return in 24 hours for ECG F Have to manage this man’s complaint of chest pain for 3 hours as an myocardial infarct until proven otherwise. Contraindications to Thrombolytics: Absolute Contraindications to Fibrinolytic Therapy Active internal bleeding CNS neoplasm, AV malformation, or aneurysm. CNS procedure or CVA within two months. Severe uncontrolled hypertension (over 200/130 or complicated by retinovascular disease or encephalopathy) Known bleeding diathesis MI due to aortic dissection Allergy to either streptokinase or anistreplase, if streptokinase or anistreplase will be used Relative Contraindications to thrombolytic therapy Age over 75 Cerebrovascular disease Pregnancy or early postpartum Recent major surgery (less than 10 days), noncompressable vessel puncture, or organ biopsy Recent trauma, including CPR of over 2 minutes duration Recent GI bleeding or active ulcer disease (less than 10 days) Acute pericarditis or subacute bacterial endocarditis Septic thrombophlebitis High likelihood of left heart thrombus (eg. mitral stenosis with atrial fibrillation) Known coagulation defects, including anticoagulant therapy Significant liver dysfunction Conditions associated with bleeding risks, such as diabetic retinopathy. Menstruation Terminal cancer or other end-stage disease Recent streptococcal infection, if streptokinase or anistreplase will be used 142. Anemia of chronic disorders is associated with a. Low ESR F b Reduced serum iron T c. Reduced utilization of iron T d. No response to oral iron T e. Reduced serum transferring F Anaemia of chronic disorders is associated with many diseases e.g. infection, collagen vascular disease, rheumatoid arthritis, malignancy, renal failure. Investigations reveal the following: Mild normocytic anaemia (e.g. Hb <8 g/dl) Decreased Total Iron Binding Capacity Decreased serum iron Normal or increased serum ferritin Serum soluble transferrin receptor level is normal ESR is often raised as a result of an often underlying inflammatory process. Management is largely treatment of the underlying cause. The anaemia of renal failure is partly due to erythropoietin deficiency and recombinant erythropoietin is effective in raising the haemoglobin level. It is also effective in raising Hb and improving quality of life in those with malignant disease. IV iron can be given with erythropoietin safely in patients with anaemia of chronic disease with some benefit. However oral iron causes many disagreeable side-effects such as nausea and constipation which reduce patient compliance, is associated with drug-drug interactions and has limited efficacy in anaemia of chronic disorders. Randomised controlled trials of treatment of anaemia chronic disease, have shown no added efficacy in using oral iron with recombinant erythropoietin in patients, compared with recombinant erythropoietin alone. 143. Low serum potassium could be from: a. Diuretic therapy T b. Digoxin therapy F c. Addison’s disease F d. Phaeochromocytoma F e. Acute renal failure T (in recovery phase of acute tubular necrosis, where low serum potassium can occur). Causes of Hypokalaemia: Diuretics (common cause) Vomiting and diarrhoea Pyloric stenosis Villous adenoma rectum Intestinal fistulae Cushings Syndrome/glucocorticoids/ACTH Conn’s Syndrome Alkalosis Purgative and liquorice abuse Renal tubular failure Digoxin toxicity does not cause hypokalemia, but hypokalemia can worsen digoxin toxicity.Hyperkalemia is the usual electrolyte abnormality precipitated by digoxin toxicity, primarily in the acute setting. Hyperkalemia may be associated with acute renal failure that subsequently precipitates digoxin toxicity. Chronic digoxin toxicity does not usually cause hyperkalemia. 144. A 64 year old smoker presents with left pleuritic chest pain, cough and hemoptysis. On examination, clubbing was noticed. A reasonable differential diagnosis would include a. Pulmonary TB T b. Mycoplasma pneumonia F c. Cancer of bronchus T d. CFA ? e. Left Upper Lobe Strep pneumonia F Pleuritic chest pain (pain exacerbated by inspiration) implies inflammation of the pleura secondary to pulmonary infection, inflammation or infarction. Cough and haemoptysis broaden the differential diagnosis to include Tuberculosis, Pulmonary Infarction secondary to Embolism, Bronchial Carcinoma and Left-sided CommunityAcquired Pneumonia. The addition of finger clubbing however makes Bronchial Carcinoma, Chronic Suppurative Lung Diseases such as lung abscess, empyema and bronchiectasis more likely, and helps to largely rule out acute mycoplasma pneumonia and left upper lobe strep pneumonia. As pulmonary TB may sometimes cause finger clubbing and the history is certainly suggestive of possible pulmonary TB,it is still a reasonable differential here. 145. Tests on the above man should include a. Sputum for regular cytology and serology T b. Sputum for PCP and H+E F c. MRI thorax F d. Mantoux test T e. Videooptic bronchoscopy T 146. A 45 year old man presents with a 10 year history of tremor which is worse on picking up a glass. The patient says his father and sister also had the tremor a. Tremor decreases during sleep T b. Propranolol is drug of choice T c. Diagnosis is likely to be familial parkinsonism F d. Amantadine is next drug of choice F e. Tremor is thought to be a disorder of the red Nucleus F Familial tremor is a neurologic disorder that tends to run in families, which results in shaking/tremor that gets worse during movement or activity. Tremors can affect people at any age, but they are most common in older people. Familial tremors affect more than one person in a family and is usually a dominant trait, which means about 50% of a patient‘s children will also have the tremor. Over time, the tremors may affect the hands, arms, head, voice box, eyelids, or other muscles. The tremors rarely involve the legs or feet. In children, these tremors are usually limited to the hands and rarely require treatment. Tremors may not affect both sides of the body equally. The exact pathophysiology is unknown. Familial tremor worsens with voluntary movement and emotional stress, disappears during sleep and may improve with alcohol consumption. Treatment may not be necessary unless the familial tremor interferes with your ability to perform daily activities. How well medicine works depends on the individual patient. Medications that may reduce tremors include propranolol, mysoline and other anticonvulsants, and mild tranquilizers. If the above are ineffective diamox,neptazane (methazolamide), clonidine, amantadine, clonazepam, neurontin and clozapine have been suggested as other options. If tremors are severe and do not go away with medicine, surgery to implant a deep brain stimulator (DBS) in the brain may be an option. Caffeine and other stimulants should be avoided because they can make tremors worse. Alcoholic beverages in small quantities may decrease the tremor, but drinking should be carefully monitored to avoid alcohol abuse and alcohol dependence, especially if there is a family history of alcohol problems. How alcohol decreases an essential tremor is unknown. 147. A 40 year old man presents to casualty in a confused state a. Alcohol may be a cause T b. Confabulation is a feature of Korsakoff’s Syndrome T c. Ophthalmaplegia and ataxia are indications for Pyridoxine F d. Foeter and liver flap indicate hepatic Encephalopathy T e. Chlordiazepoxide is used for treatment of DTs T Pyridoxine is Vitamin B6, and is not used to prevent and treat Wernicke’s Encephalopathy triad of symptoms: ophthalmoplegia, ataxia and confusion, rather Vitamin B1/thiamine. The severe deficiency states Wernicke's encephalopathy and Korsakoff's psychosis, especially as seen in chronic alcoholism, are best treated initially by the parenteral administration of B vitamins (Pabrinex®), followed by oral administration of thiamine in the longer term. Anaphylaxis has been reported with parenteral B vitamins (see CSM advice, below). 148. In a patient who has pulsus alternans a. The pulse is irregular F b. Digitalis intoxication is the most likely cause F c. The pulse waves are unequal in size T d. It is most easily observed when taking BP F e. Pulse rate varies with respiration F Pulsus alternant refers to regular rhythm with alternating strong and weak beats. It suggests left ventricular failure for the most part, but also can be caused by cardiomyopathy and aortic stenosis. It is most easily detected on examination of peripheral pulses. 149. Pericardial rub is a recognized feature of: a. Hypertensive cardiac failure F b. Extrarenal uraemia T c. Terminal uraemia T d. Minority of cases of MI T e. Atrial flutter F Pericardial friction rub occurs in inflammation of the pericardium which may be primary or secondary to systemic disease. Causes include: Viruses (Coxsackie’s, influenza, Epstein-Barr, mumps, vermicelli, HIV) Bacteria (pneumonia, rheumatic fever, TB) Fungi Myocardial infarct Dressler’s Syndrome Uraemia Rheumatoid Arthritis SLE Myxoedema Trauma Surgery Malignancy Radiotherapy Drugs e.g. procainamide, hydralazine. 150. In active pulmonary TB: a. Physical signs are always present on careful examination of the chest F b. Clubbing is common F c. In most cases ESR is raised T d. Radiological changes are commonest in the apex of the lung T e. Pneumothorax occurs in about 10% of cases F Active pulmonary TB may be silent or present with cough, sputum, malaise, weight loss, night-sweats, pleurisy, haemoptysis, pleural effusion, or superimposed pulmonary infection. Clubbing may occur in TB, but is uncommon. As TB is a chronic infective process, the ESR in most cases should be raised. Pneumothorax occurs in about 2-3% of cases pf active pulmonary TB. 151. Mitral stenosis a. Is more likely to develop SBE than incompetence F b. Always give antibiotic prophylaxis T c. Systolic murmur F d. Give anticoagulation T e. Presents with sudden death F Mitral stenosis nearly always due to rheumatic heart disease, but rarely may be congenital. History: Many patients are asymptomatic. Some patients may develop symptoms during physiologic stress such as infection, exercise, fever, or pregnancy. Exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea (symptoms of left heart failure) are most common. Dyspnea may be accompanied by cough and wheezing. Acute pulmonary oedema may occur precipitated by exertion, pregnancy or onset of AF. Chest pain due to right ventricular ischemia, concomitant coronary atherosclerosis, or a coronary embolism may be present. Hemoptysis from pulmonary venous hypertension results in rupture of anastomosis between bronchial veins. Recurrent bronchitis In later stages, symptoms of RV failure. Patients may present with complications of mitral stenosis. New-onset atrial fibrillation Systemic embolism Infective endocarditis (more common with incompetence) Physical: Look for findings not only intrinsic to valvular deformity but also hemodynamic disturbance from the stenotic valve and its complications. Cardiac examination of stenotic mitral valve (best at the apex with the patient in the left lateral recumbent position) Palpable diastolic thrill An accentuated S1, followed by S2, and an opening snap (OS) Characteristic diastolic low-pitched, rumbling murmur The duration, and not intensity, of the murmur is a guide to the severity of mitral valve narrowing. However, murmur may diminish in intensity as the stenosis increases. Pulmonary crackles Signs of right heart strain/failure in later stages. Other findings A pansystolic murmur of mitral regurgitation may accompany the valvular deformity of mitral stenosis. “Mitral facies” characterized by pinkish purple patches on the cheeks may be present. Managemant: If in AF -digoxin +/- beta-blocker + warfarin. Diuretics decrease preload and pulmonary venous congestion. Balloon valvuloplasty, open mitral valvotomy or valve replacement if this fails to control symptoms. SBE/IE prophylaxis for dental or surgical procedures. Oral penicillin as prophylaxis against recurrent fever if < 30 years old. 152. A 35 year old Indian vegetarian presents with difficulty getting out of a chair and parasthesia; useful tests include a. Calcium b. Alkaline phosphatase c. ACTH d. bilirubin e T4 a. T. Hypocalcaemia could account for the paraesthesia and proximal myopathy b. T. alk phos will be increased in osteomalacia, which is a cause of hypocalcaemia c. T. Cushings is a cause of proximal myopathy d. F e. T. thyrotoxicosis is a cause of proximal myopathy a. and b. Difficulty getting out of a chair=proximal myopathy. In osteomalacia there is low calcium which could account for the proximal myopathy and paraesthesia. In osteomalacia there is a normal amount of bone but its mineral content is low. It occurs due to lack of vitamin D: 1. Vitamin D deficiency due to malabsorption, poor diet, lack of sunlight 2.Renal Failure-failure of hydroxylation of vitamin D 3.Liver Disease: reduced production of 25-OH Vitamin D 4. Drugs e.g. anticonvulsants as they induce liver enzymes leading to increased Vitamin D breakdown. 5. Vitamin D resistance: a number of rare inherited defects in vitamin D receptors Vitamin D increases calcium and phosphate levels. In osteomalacia therefore you get: Decreased PO4, decreased Ca and increased alk phosphate b. Cushings can cause proximal myopathy. I would say true for this although ACTH levels would certainly not be the first line investigation in Cushings. However, 90% of cushings is ACTH dependent. The majority of these are from a pituitary adenoma. Dexamethasone suppression tests would be used to confirm the diagnosis of cushings and ACTH levels can then be used to help localize the cause of the cushings. 153. A student tested Mantoux positive after contact with TB; CXR normal and there were no signs but sputum was not available for testing a. Discharge her saying she will never get TB b. Discharge her saying come back only if pregnant c. Tell her to miss college for 3 months d. Three month prophylaxis with rifampicin and streptomycin e. Six month prophylaxis with rifampicin and streptomycin a. F b. F c. F d. F e. F According to Kumar and Clark, in adults who have contact with TB even if they are mantoux test positive they do not require any treatment if CXR is negative. In children however, positive tuberculin test is taken as evidence of infection and treatment is started. 154. A 40 year old male who worked in Saudi, presented with dyspnea, slight wheeze. He had a history of smoking and alpha-1 anti-trypsin deficiency. The likely findings are: a. Enlarged lung fields on CXR b. Diagnosis of asthma c. Diagnosis of emphysema d. Reduced FEV1/FVC e. Improvement with bronchodilators a. T. the lung fields are hyperinflated in emphysema b. F. c. T. d. T. This is characteristic of an obstructive pattern e. F. I would say F here. Some patients with COPD have a bronchodilator response but this relates to reversible airways obstruction. This is unlikely if emphysema is predominating the picture as the obstruction here is due to enlargement of airsapces with destruction of the alveolar walls. This man most likely has emphysema as alpha 1 antitrypsin deficiency and smoking are the big risk factors. The symptoms of cough and wheeze also fit with this diagnosis. There would be an obstructive pattern with decreased FEV1/FVC ratio. 155. Gout: a. Commoner in females than males b. Treat an acute attack with allopurinol c. Initial attacks are commonly a polyarthritis d. May occur with a normal serum uric acid e. Tophi are an early feature of disease a. F = M:F ratio is 5:1.In fact, gout is rare in prememopausal women. b. F = allopurinol is a xanthine oxidase inhibitor which is used as a preventative agent for people who suffer recurrent attacks of gout or who have risk factors e.g. those on chemotherapy. However, allopurinl MUST NEVER be used in the acute attack as it can worsen symptoms c. F= the most common initial presentation is a monarthritis, classically of the first metartarsal d. T = serum uric acid levels are not that useful in the diagnosis of gout as the condition can occur with normal serum uric acid levels. e. F = tophi deposits are found in the peripheries, e.g. pinna, ear, only after repeated attacks of gout Gout occurs due to the deposition of monosodium urate crystals in joints which leads to synovitis and results in an acutely swollen, red, tender joint which is exquisitely painful. Attacks may be precipitated by trauma, surgery, infection, starvation or diuretics. Secondary causes include polycythaemia, leukemia, chemotherapy, renal failure and long-term alcohol excess. Treatment for the acute attack includes NSAIDS or colchicine if NSAID intolerant. Allopurionol is used as a prophylactic agent 156. These conditions cause a polymorphonuclear leucocytosis a. Acute blood loss b. Malignant infiltration of the bone marrow c. Acute brucellosis d. Chronic pyelonephritis e. Acute pyelonephritis a. T. can be caused by any trauma, sugery, burns or haemorrhage. b. F. this is a cause of pancytopenia. c. F. pancytopenia occurs in brucellosis. d. T. can be caused by any inflammation. e. T. can be caused by any bacterial infection. 157. The following statements are correct a. Hip joint disease may present as pain in the knee b. A normal joint contains as little synovial fluid that the clinical demonstration of fluid in a joint always implies an abnormality c. Joint disease alone is seldom a cause of gross muscle wasting d. A positive “patellar tap” test is a sign of patello-femoral arthritis e. Carpal tunnel syndrome typically remits during pregnancy a. T b. ? c. F. Disuse atrophy can cause extensive muscle wasting. d. T. The patellar tap: The suprapatella pouch is compressed with one hand whilst the other hand pushes the patella sharply backwards; with a positive test the patella can be felt striking the femur and bouncing off again. If positive it is a sign of an effusion. An effusion can occur in patello femoral arthritis. Other causes of an effusion would include trauma and haemarthrosis. e. F. Carpal tunnel often occurs for the first time in pregnancy 158. Characteristics of typhoid fever include: a. Incubation period of 4 weeks b. Polymorph leucocytosis in the early stages of the illness c. Macular rash on the trunk d. Profuse watery diarrhea in the first week of fever e. Resolution of the fever within 3-4 days of starting chloramphenicol in appropriate dosage a. F. The incubation period is 10 to 20 days b. F. Leucopenia occurs c. T. A maculopapular rash, so called “rose spots” occurs in 40% of cases. However this is usually scanty and difficult to see. d. F. Presentation is usually with malaise, headache, high fever and abdominal pain. Diarrhoea is more common after the first week. e. F. the temperature may stay elevated for several days after starting antibiotics, and this is not a sign of treatment failure. 159. The following drugs may aggravate or cause GI ulceration a. Paracetamol b. Codeine phosphate c. Ibuprofen d. Indomethacin e. Enteric-coated potassium chloride a. F. Side effects are rare but include rashes and blood disorders. Liver failure can occur following overdose b. F. This is a opioid analgesic, of which the common side effects are nausea and vomiting, constipation and drowsiness. Larger doses can cause respiratory depression and hypotension. No mention of GI ulceration c. T. This is an NSAID, thus GI ulceration is a possible side effect. are d. T. This is also an NSAID e. T. KCL can cause cause oesophageal and small bowel ulceration. The other main side-effect is nausea and vomiting. KCL is oral potassium which is used to treat potassium depletion, most often in patients taking digoxin or other antiarrythmics, in patients with secondary hyperakldosteronsim, and patients with excessive loss of K in the stool i.e. severe diarrhoea with intestinal malabsorption 160. Impaired elimination of the following drugs occurs in advanced renal failure and will necessitate dosage reduction when they are used in this situation a. Chlorpropamide b. Warfarrin c. Streptomycin d. Morphine e. Benzylpenicillin a. T. This is a long-acting sulphonylurea. Sulphonylureas should be avoided where possible in severe renal and hepatic failure, as reduced elimination of the drug will increase the risk of hypoglycaemia, especially in elderly patients. b. T. Caution is advised when prescribing warfarin to anyone with renal or hepataic failure c. T. This is an aminoglycoside. Excretion is principally via the kidney thus accumulation occurs in renal impairment. Aminoglycosides are also ototoxic d. T. Dose should be reduced or avoided in renal impairment. e. T. Caution in renal impaiment. 161. Harmful results are not infrequent when working with a. Asbestos b. Emulsion paint c. Beryllium d. Coarse sand e. Cotton dust a. T. Can cause asbestosis (lung fibrosis) or malignant mesothelioma (90% of malignant mesotheliomas are associated with asbestos exposure, which may have been up to 45yrs previously i.e. long latent period. It is a highly aggressive tumour with prognosis less than 2 years at diagnosis.) b. F. c. T. Berylliosis can cause an cute pneumonitis or chronic pulmonary fibrosis. However, stirct control of leverls in th workplace have made the disease a rarity. d. T. This can cause extrinsic allergic alveolitis. e. T. This can cause extrinsic allergic alveolitis 162. Low fibre diet is at present commonly believed to be a major factor in the causation of a. Diverticular disease of the colon b. Crohn’s disease c. Varicose veins d. Colon cancer e. Esophageal cancer a. T b. F c. F d. T e. F 163. Hypernatremia is an expected finding in the following disorders a. Acute renal failure caused by abruption placentae b. Dehydration complicating renal tubular acidosis c. Dehydration in an elderly confused man being treated with chlorpromazine d. Non-ketotic hyperglycemic coma e. Dehydration complicating diuretic therapy a. T. if Sheehans syndrome (pituitary infarction) occurs this can cause pituitary diabetes insipidus, which is cause of hypernatramia b. T. Renal tubular acidosis is a cause of nephrogenic diabetes insipidus c. F. d. T. Osmotic diuresis can cause hypernatraemia, for example due to HONK. e. F. Diuretic therapy causes hyponatraemia The causes of hypernatraemia are: impaired thirst or conscious state. pituitary diabetes insipidus i.e. failure of ADH secretion nephrogenic diabetes insipidus i.e. failure of response to ADH osmotic diurese excessive loss of water through the skin or lungs excessive administration of Na may contribute 164. The following are characteristic hematological findings in the named systemic disorders a. Leucopenia in active SLE b. Leucopenia in active PAN c. Lymphocytosis in acute leptospirosis d. Lymphopenia in acute sarcoidosis e. Lymphpenia in HIV infection a. T. Leucopenia, lymphopenia and thrombocytopenia may occur. b. F. PAN is a necrotizing vasculitis that causes aneurysms of medium-sized arteries. It is a multisystem condition that can affect many organs. Hamatological abnormalities include: increased WCC, eosinophilia in 30%, anaemia, increased ESR and increased CRP. c. F. Leucocytosis characteristically occurs. d. T. Sarcoidosis is a multisystem granulomatous disorder of unknown aetiology. Haematological investigations may show: lymphopenia, increased ESR, increased serum ACE and increased Igs. e. T. Laboratory abnormalities include lymphopenia with atypical reactive lymphocytes, thrombocytopenia and raised liver enzymes. 165. Hypophosphatemia is associated with a. Osteomalacia due to celiac disease b. Parathyroid adenoma-associated hypercalcemia c. Rickets due to progressive chronic renal failure d. Osteoporosis associated with exogenous steroid therapy e. Sarcoidosis associated hypercalcemia a. T. Osteomalacia can occur as a result of malabsorption of Vitamin due to Coeliac diaease. Lack of Vitamin D results in hypophosphataemia and hypocalcaeimia with an increased alk phos. b. T. parathyroid adenoma accounts for 80% of cases of hyperparathyroidism. PTH increases Ca and decreases PO4 reabsorption in the kidney; increases osteoclastic activity and increases Vitamin D production. The overall net effect is to increase serum Ca. Findings include increased Ca and decreased Po4 c. F. Although the lack of vitamin will result in decrased PO4 absorption in the gut the CRF will result in PO4 retention, therefore hypophosphataemia is unlikely. d. F. Serum Po4, Ca and alk phos are all normal in osteoporosis. e. F. Sarcoidosis associated hypercalcaemia is due to increased vitamin D action. Vitamin D acts to increase the reabsorption of both Ca and Po4 therefore hypophosphataemia will not occur in this instance. 166. The following are frequently found in association a. Chronic ulcerative colitis and membranous glomerulonephritis b. Acute-on-chronic renal failure and prolonged bleeding time c. Pericarditis and sarcoidosis d. Spironolactone treatment and gynecomastia e. Thrombocytopenia with renal failure caused by the HUS a. T?. Associations include SLE, bowel malignancy, bronchus malignancy, penicillamine therapy and hepatitis B. Since chronic UC predisposes to bowel ca this could be an association, but maybe this is a long shot. Make up your own minds b. F c. F. Cardiac involvement is rare and includes ventricular dysrhythmias, conduction defects and cardiomyopathy. No mention of pericarditis d. T. Spironolactone is a cause of gynaecomastia. Other drug causes include oestrogens, anti-androgens and digoxin. e. T. HUS is characterized by: ARF, thrombocytopenia and micrangiopathic hemolytic anaemia. 167. The following may be of value in the treatment of hirsutism a. Regular waxing b. Cyproterone acetate c. Minoxidil d. Spirolactone e. Low dose dexamethasone at night a. T b. T. This is an anti-androgen and progestogen. c. F. This is for the treatment of alopecia d. F e. F. Hirsutism can occur as a side effect of corticosteroids 166. Regarding hypoglycemia a. When insulinoma is suspected this is best diagnosed by a glucose tolerance test b. It is not a clinical problem in diabetic patients if they have diminished awareness of their symptoms c. May be precipitated in insulin-dependent patients by unaccustomed exercise d. Does not occur in diabetic patients treated with oral hypoglycemics e. Is rarely a cause of death in insulin-dependent diabetics F. A suppressive test must be administered to diagnose insulinoma. IV insulin is given and C-peptide levels are measured. Normally exogenous insulin suppresses C-peptide but this does not occur in insulinoma. F. Hypoglycamia is much more dangerous in patients who have hypoglycaemic unawareness. Normally patients will experience “warning symptoms”, such as sweating, tremor, hunger, which will allow them to ingest some glucose before symptoms progress. If a patient has hypoglycaemic unawareness they will not have any symptoms and may progress to coma very quickly. T. The following can precipitate hypoglycaemia in an insulin dependent diabetic: exercise, alcohol, excess insulin. F. Oral hypoglycamics can cause hypoglyaemia, in particular sulphonylureas. ?F. Id say false here as hypoglycaemia is the commenest endocrine emergency, however I don’t know if many people actually die from it. 167. In the jaundiced patient a. A palpable gallbladder suggests gallstones b. Pruritus suggests obstructive jaundice c. With hemolytic anemia, the urine is of normal color but contains urobilinogen d. Carcinoma of the head of the pancreas typically causes “boring” back pain e. Xanthelasmata are usually found in jaundiced patients with chronic active hepatitis a. F. Courvoisier’s law states that a palpable gallbladder in the presence of jaundice is unlikely to be due to gallstones as gallstones cause fibrosis of the gallbladder, which results in a small gallbladder. Carcinoma of head of pancreas is a more likely cause. b. T. Pruritus is due to the deposition of bile salts in the soft tissues. c. T d.?T. I would say T for this. Carcinoma of the head of the pancreas typically causes painless jaundice but carcinoma of the body and tail of the pancreas typically causes epigastric pain that radiates to the back and may be relieved by sitting forward. e. ? 168. In a patient with a pleural effusion a. Bronchial breathing may be heard above the effusion b. Protein content of 40g/L suggests heart failure may be the cause c. Pleural effusion may occur in the patient with an ovarian tumor d. Atypical pneumonia is a classical cause of a pleural effusion e. Acute pancreatitis may cause a left-sided pleural effusion and ascites a. T. This is a common finding, due to compression of the lung above the effusion. b. F. A protein content greater than 40g/L suugest an exudate, while CCF is a common cause of a transudate. The causes of an exudate include: malignancy, pneumonia, TB, pulmonary infarction, RA, SLE. The causes of a transudate are: CCF, constrictive pericarditis, cirrhosis, nephrotic syndrome, malabsorption, hypothyroidism and Meigs syndrome. c. T. Meigs syndrome is the association of a right pleural effusion (transudate) and an ovarian fibroma d. ?. Any pneumonia can cause a pleural effusion but I don’t know if is classical for atypical. Atypical pneumonias tend to have more vague symptoms and signs in general so maybe its false. I don’t know e. ? Acute pancreatitis may cause a pleural effucion but I don’t know of its left sided 169. In the patient with mitral stenosis a. History of rheumatic fever almost always obtained b. Loud first heart sound and opening snap suggests the valve is calcified c. A “p” mitrale may be seen on ECG d. Bacterial endocarditis is an uncommon complication of mitral stenosis f. Mitral stenosis may cause hoarseness T. Rheumatic fever is commonest cause. Other causes include congenital, mucopolysaccharidoses, endocardial fibroelastosis, malignant carcinoid. F. These findings are found in mitral stenosis but opening snap suggests a pliable valve, not calcified. T. P-mitrale may be seen on ECG if in sinus rhythm T. Infective endocarditis can occur but it is a rare complication T. This can occur as a complication of mitral stenosis due to pressure on recurrant laryngeal nerve from an enlarged left atrium. 170. A 65 year old man is found to have hypercalcemia a. Diarrhoea and itching would be expected symptoms b. Serum electrophoresis would be a relevant investigation c. Fluid restriction is the first line of treatment d. Thiazide diuretics may be a cause e. If he has a lung tumour, it is likely to be a squamous cell carcinoma F T F T T a) F For the symptoms of hypercalcaemia remember ‘bones, stones, groans and psychic moans’. General Features:- tiredness, weakness, dehydration, depression, weight loss, abdominal pain, vomiting Renal Features:- Renal colic from renal stones, polyuria, haematuria, and hypertension Bones:- bone pain ( bone cysts and ‘bone tumours’) Corneal calcification Cardiac arrest ( prolonged Q-T interval) b) T Serum electrophoresis to exclude multiple myeloma, a neoplastic proliferation of plasma cell which produces a monoclonal immunoglobulin band on serum or urine electrophoresis. Causes of Hypercalaemia are as follows The commonest causes are Primary Hyperparathyroidism and Malignancies Excessive Parathormone (PTH) secretion Primary Hyperparathyroidism Adenoma Hyperplasia or Carcinoma Tertiary Hyperparathyroidism Ectopic PTH secretion Malignant Disease Myeloma Secondary deposits in bone Production of osteoclastic factors by tumours PTH- related protein secretion Excess action of Vitamin D Iatrogenic or self administered Granulomatous disease e.g. Sarcoidosis, TB Lymphoma Excessive calcium intake ‘milk alkali’ syndrome Drugs Thiazide diuretics Vitamin D analogous Lithium c) F Patients with hypercalcaemia are dehydrated so fluid restriction would be a crime against humanity. Normal calcium is 2.12 – 2.65 mmol/l . While investigation of the cause is under way , immediate treatment is mandatory if the patient is seriously ill or if the serum Ca2+ is above 3.5 mmol/l 1.Rehydrate with IV 0.9% saline e.g. 4-6 L I 24 hours as needed. Correct Hypokalaemia and hypomagnesaemia. Monitor Urea and electrolytes. 2. Intravenous bisphospanate, Pamidronate. It inhibits osteoclast activity and so bone resorbption. 3. Prednisolone is effective in some instances e.g. myeloma, sarcoidosis and vitamin D excess) but in most cases is ineffective d) T, thiazides lead to increased resorption of Ca2+ in the Kidneys e) T, True ‘ectopic PTH secretion’ by the squamous cell tumour of the lung is very rare and is mostly associated with raised levels of PTH related peptide. ---------------------------------------------------------------------------------------------------------------171. In Irritable Bowel Syndrome a. Nocturnal diarrhoea is typical b. Daily stool weight is normal c. Symptoms typically develop in late middle life d. Rectal biopsy is diagnostic e. Carcinoma of the colon is a late complication F T F F F 171. In Irritable Bowel Syndrome a). Nocturnal diarrhoea is typical F More associated with diabetic autonomic neuropathy. Irritable bowel syndrome is a heterogeneous group of disorders for which no cause can be found and may be due to disorders of intestinal motility. Diagnostic Criteria (Rome II) In the preceding 12 months there should be at least 12 consecutive weeks of abdominal discomfort or pain that has two or three of the following features 1. relieved with defecation 2. onset associated with a change in frequency of stool 3. onset associated with a change in form of stool The following symptoms cumulatively support the diagnosis of IBS 1. Abnormal stool frequency (more than 3 a day or less than 3 a week) 2. Abnormal stool form (hard or loose) 3. Abnormal stool passage (straining , urgency or tenesmus) 4. Passage of mucus 5. Bloating or feeling of abdominal distension These symptoms are used to classify patients into diarrhoea or constipation predominant forms of IBS. A third group in which diarrhoea and constipation alternate also exists. Are ye bored stiff now? b). Daily stool weight is normal T 1ST step is to exclude organic disease so Look for markers of organic disease, age greater than forty, weight loss, rectal bleeding, waking at night with pain and diarrhoea. Based on clinical judgment ( what isn’t?) If young , with classic history, FBC, ESR,LFT, Coeliac serology and urinalysis, maybe sigmoidoscopy with rectal biopsy If patient greater than 45 years or has markers of organic disease do colonoscopy. If diarrhoea prominent do LFT, stool culture, B12/ Folate, Coeliac serology, TSH, referral for barium follow through , rectal biopsy c). Symptoms typically develop in late middle life F Patients are usually 20-40 yrs old and females more than males d). Rectal biopsy is diagnostic F rectal biopsy may be done to rule out a possible cause but there is no pathology ( discovered as yet) e). Carcinoma of the colon is a late complication F Has no late complications Treatment Refer to dietician, Ispaghula husk for constipation, Loperamide for diarrhoea, Mebeverine and dicloverine (antispasmodics for colic and bloating), sometimes cognitive behavioural therapy, antidepressants. --------------------------------------------------------------------------------------------------------------------------172. A 25 year old female is found to have microscopic hematuria on routine insurance exam. The following statements are correct: a. The finding is compatible with IgA nephropathy T b. The finding is consistent with Alport’s nephropathy T c. The finding is compatible with a residuum from an episode of minimal change nephrosis eight months previously F d. The finding is compatible with a residuum from an episode of post-streptococcal nephritis eight months previously F e. If the patients has insulin-dependent diabetes mellitus of 12 years standing, the finding is likely to indicate the early phase of diabetic nephropathy F 172. A 25 year old female is found to have microscopic hematuria on routine insurance exam. The following statements are correct: a). The finding is compatible with IgA nephropathy T However IgA would be more likely in children and young females. It is the commonest glomerulonephritis in the west – causing episodic haematuria that may coincide wit viral infections. IgA is deposited in glomeruli. Heavy proteinuria and hypertension indicate a poor prognosis. Tx Steroids, ACE inhibitors, dietary fish oil, tonsillectomy and renal transplantation b). The finding is consistent with Alport’s nephropathy T Alport’s syndrome is a rare condition characterised by a hereditary nephritis with haematuria, proteinuria, progressive renal failure and sensorineural deafness. Also associated lenticonus ( bulging of eye lens) seen in some. Inheritance can be Xlinked dominant, autosomal dominant or rarely autosomal recessive. Tx control Blood Pressure, supportive management of renal failure, dialysis, transplantation. c). The finding is compatible with a residuum from an episode of minimal change nephrosis eight months previously F Get proteinuria in minimal change disease, not haematuria, it can relapse however. d). The finding is compatible with a residuum from an episode of post-streptococcal nephritis eight months previously F A small number of adults develop hypertension and / or renal impairment later in life after post – streptococcal nephritis. Therefore an annual blood pressure check and estimate of serum creatinine, is a reasonable precaution, even after apparent complete recovery. e). If the patients has insulin-dependent diabetes mellitus of 12 years standing, the finding is likely to indicate the early phase of diabetic nephropathy F Type 1 DM nephropathy occurs 10-15yrs post diagnosis and is characterized by proteinuria, NOT Haematuria, (albumin excretion >300 mg/d), fall in GFR, and raise BP. Renal failure occurs 15-30 years post diagnosis. --------------------------------------------------------------------------------------------------------------------------173. Erythema nodosum may be associated with: a. OCP b. Streptococcal sore throat c. Sarcoidosis d. Pemphigus e. Diabetes Mellitus T T T F F 173. Erythema nodosum may be associated with: a). OCP T b). Streptococcal sore throat T c). Sarcoidosis T d). Pemphigus F e). Diabetes Mellitus F Erythema Nodosum is a cutaenous sign of systemic disease. It presents as painful dusky blue-red nodules, commonly over the shins which fade over 2-3 weeks. Common in young adults esp. females. The inflammation involves the dermis and the subcutaneous layer. Causes of erythema nodosum Streptococcal infection Drugs (sulphonamides, oral contraceptive) Sarcoidosis Idiopathic Yersinia infection Fungal Infection (histoplasmosis, blastomycosis) Tuberculosis Leprosy Inflammatory Bowel Disease Chlamydia Infection Treated with NSAID’s light compression bandages and bed rest. Treat underlying cause. In persistent cases try dapsone, colchicines and perdnisolone. ------------------------------------------------------------------------------------------------------174. The following are true in rheumatoid disease: a. Rheumatoid nodules are tender F b. Proximal interphalangeal joints are commonly affected T c. Presence of swan-neck deformities is a good guide to current disease activity F d. Rheumatoid nodules are usually located on the dorsum of the hand F e.Charcot’s joints are a complication F 174. The following are true in rheumatoid disease: a). Rheumatoid nodules are tender F Rheumatoid nodules are non-tender. They indicate disease activity. They are granulomata with a central zone of fibrinoid necrosis, with surrounding macrophages and fibroblasts. Poor Prognostic factors 1. Systemic features- weight loss, extra-articular manifestations 2. Slow onset 3. Rheumatoid nodules 4. Presence of Rheumatoid Factor 5. Early bone erosions 6. Persistent activity of the Disease for over 12 months b). Proximal interphalangeal joints are commonly affected T The diagnosis of Rheumatoid arthritis is typically made when 4 of 7 qualifying criteria established by the American Rheumatism Association are met. These qualifying criteria are as follows: Morning stiffness lasting longer than 1 hour before improvement Arthritis involving 3 or more joints Arthritis of the hand, particularly involvement of the proximal interphalangeal (PIP) joints, metacarpophalangeal (MCP) joints, or wrist joints Bilateral involvement of joint areas (i.e., both wrists, symmetric PIP and MCP joints) Positive serum rheumatoid factor (RF) Rheumatoid nodules Radiographic evidence of RA c). Presence of swan-neck deformities is a good guide to current disease activity F Swan neck deformities are a good guide to the chronicity i.e. how long a person has had rheumatoid arthritis. d). Rheumatoid nodules are usually located on the dorsum of the hand F Rheumatoid nodules are generally found around the elbow. However they can also be found on the flexor and extensor tendons of the hand, sacrum, Achilles tendon, sclera, lungs and myocardium. e). Charcots joints are a complication F Charcots joints are joints damaged by trauma as a result of the loss of protective pain perception. Seen in Syphilis (knees and ankles), diabetes mellitus (joints of tarsus), Syringomyelia (shoulder) and Leprosy ------------------------------------------------------------------------------------------------------175. Mark the following True or False a. In Iron deficiency anaemia, mean corpuscular volume is frequently 65-75 Fl b. Poor dietary B12 is the main cause of pernicious anaemia c. Celiac disease frequently causes folic acid deficiency d. Normal isotope bone scan is typical of multiple myeloma e. Haemolytic anaemia causes increased conjugated bilirubinemia T F T T F 175. Mark the following True or False a). In Iron deficiency anaemia, mean corpuscular volume is frequently 65-75 Fl T Normal mean cell volume (MCV) is 76-96 FL, iron deficiency anaemia causes microcytosis i.e. low MCV b). Poor dietary B12 is the main cause of pernicious anaemia F Pernicious anaemia is due to malabsorption of B12 resulting from atrophic gastritis and lack of gastric intrinsic factor. c). Celiac disease frequently causes folic acid deficiency T Due to malabsorption d). Normal isotope bone scan is typical of multiple myeloma T Isotope scans have a low sensitivity for Multiple Myeloma, so most scans would look normal as the osteoblastic response to bone destruction is diminished. Remember that all patients that have Multiple Myeloma need skeletal survey with X-rays. 99m Technetium methoxyisobutylisonitrile (99mTc-MIBI) has been shown to be superior to plain film radiography and skeletal scintigraphy in detecting bone and bone marrow involvement. e). Haemolytic anaemia causes increased conjugated bilirubinemia F Haemolytic anaemia causes an unconjugated Bilirubinemia as the red blood cells are haemolysed outside the liver, where bilirubin is conjugated ------------------------------------------------------------------------------------------------------176. The following are recognized associations a. Hypothyroidism: pretibial myxoedema b. thyrotoxicosis: Proximal myopathy c. Cushing’s disease: hypoglycaemia d. Addison’s disease: hypertension e. Acromegaly: Homonymous hemianopia F T F F F 176. The following are recognized associations a). Hypothyroidism: pretibial myxoedema F Pretibial ‘myxodema’ (oedematous swellings above the lateral malleollus) is seen in HYPERTHYROIDISM b). thyrotoxicosis: Proximal myopathy T Causes of Myopathy Hereditary Muscular Dystrophy Congenital Myopathies Acquired Myopathies (PACE PODS) Polymyositis or dermatomyosistis Alcohol, AIDS Carcinoma Endocrine e.g. hyperthyroidism, hypothyroidism, Cushing’s syndrome, acromegaly, hypopituitarism Periodic paralysis (hyperkalaemic, hypokalaemic or Normokalaemic) Osteomalacia Drugs – e.g. clofibrate, chloroquine, steroids, Zidovudine Sarcoidosis c). Cushing’s disease: hypoglycaemia F Glucocorticoids which are over secreted in Cushing’ disease, are diabetogenic. Hence they cause a hyper glycaemia d). Addison’s disease: hypertension F Addison’s Disease (adrenal insufficiency) causes postural hypotension e). Acromegaly: Homonymous hemianopia F Associated with bitemporal hemianopia due to a growth hormone secreting tumour compressing the optic chiasma ------------------------------------------------------------------------------------------------------177. The following disorders and findings on examination is correctly paired: a. Pulmonary fibrosis: fine end inspiratory crepitations b. Emphysema: increased intensity of breath sounds c. Pleural effusion: reduced tactile and vocal fremitus d. Right upper lobe collapse: trachea deviated to right e. Left apical lung tumour: Left Horner’s syndrome T F T T T 177. The following disorders and findings on examinations are correctly paired: a). Pulmonary fibrosis: fine end inspiratory crepitations T Fine (Velcro- like) late inspiratory or pan-inspiratory crackles heard over the affected lobes b). Emphysema: increased intensity of breath sounds F Breath sounds are decreased c). Pleural effusion: reduced tactile and vocal fremitus T Tactile and vocal fremitus are reduced. They are increased over consolidated lung. d). Right upper lobe collapse: trachea deviated to right T In collapse the trachea is deviated to the same side. Trachea is displaced to the opposite side in massive pleural effusion and pneumothorax e). Left apical lung tumour: Left Horner’s syndrome T ------------------------------------------------------------------------------------------------------178. True or false: a. In pulmonary TB, the presence of acid fast bacilli on a sputum smear indicated infectivity b. Treatment of TB is with combination chemotherapy for a 2 month period c. Mycoplasma pneumoniae is a common cause of community acquired pneumonia d. In meningococcal meningitis, gram+ diplococcic are seen in CSF e. IN Meningococcal meningitis, CSF neutrophilia is seen T F T F T 178. True or false: a). In pulmonary TB, the presence of acid fast bacilli on a sputum smear indicated infectivity T Patients whose bronchial washings (Bronchoalevolar lavage) are smear positive should be managed as if non-infectious unless (1) the sputum is also smear positive or becomes so after bronchoscopy, (2) they are on a ward with immunocompromised patients, or (3) they are known or suspected of having MDR-TB (Multi-drug resistant T.B.) b). Treatment of TB is with combination chemotherapy for a 2 month period F Initial chemotherapy for 2 months Rifampicin, Isoniazid, Pyrazinamide and ethambutol or streptomycin. Continue for another 4 months with Rifampicin and Isoniazid. Remember to give pyridoxine throughout treatment as Isoniazid causes pyridoxine deficit. c). Mycoplasma pneumoniae is a common cause of community acquired pneumonia True Streptococcus pneumoniae is the commonest cause of community acquired pneumoniae, followed by Haemophilus influenzae and Mycoplasma pnuemoniae. d). In meningococcal meningitis, gram+ diplococcic are seen in CSF F Nesseria Meningitis, Alias meningococcus, is a gram negative diplococcic (kisses and hugs from Prof Prentice) e). IN Meningococcal meningitis, CSF neutrophilia is seen T Meningococcus is a bacterium, Neutrophils eat bacteria. Also CSF is turbid/ purulent in appearance, with high protein and low glucose (bacteria have a sweet tooth too!) ------------------------------------------------------------------------------------------------------179. The following skin manifestations and systemic diseases are correctly paired a. Neurofibromatosis: Café-au-lait patches b. Diabetes Mellitus: Livedo Reticularis c. Chronic liver disease: Spider naevi d. Erythema nodosum: IBD e. Polyarteritis nodosa: telangiectasia T F T T F 179. The following skin manifestations and systemic diseases are correctly paired a). Neurofibromatosis: Café-au-lait patches T Café –au- lait patches are brown macules seen in Neurofibromatosis type 1 and 2 . Also seen in tuberous sclerosis, ataxia telangiectasia, Faconi’s Anaemia, Multiple endocrine neoplasia type 1, McCune-Albright syndrome. b). Diabetes Mellitus: Livedo Reticularis F Stasis in skin venules e.g. induced by cold, causes immune complex deposition and pink-blue mottling. If this becomes irreversible , it is called Livedo reticularis. Generally seen in Vasculitis like Polyarteritis nodosa. Skin Signs in Diabetes are Cutaneous infections Neuropathic ulcers Necrobiosis lipoidica diabeticorium Diabetic Dermopathy (small brown scar like lesions seen on the skin) Diabetic Bullae ~( uncommon blistering disorder of hands and feet) Xanthomas Acanthosis Nigrican’s Lipoatropy Cheiroarthropathy (scleroderma- like thickening of the skin) c). Chronic liver disease: Spider naevi T d). Erythema nodosum: IBD T e). Polyarteritis nodosa: telangiectasia F Poly arteritis Nodosa is a necrotising vasculitis that causes aneurysms of mediumsized vessels. Skin signs are utricaria, purpura, infarcts, livedo reticularis, nodules. --------------------------------------------------------------------------------------------------------------180. The following conditions are correctly paired with an accurate description of typical symptoms: a. MI: central anterior chest tightness T b. Unstable angina: central anterior chest tightness T c. Pericarditis: pain exacerbated by sitting forward F d. Psoriasis: itch T e. Subarachnoid haemorrhage: frontal headache F 180. The following conditions are correctly paired with an accurate description of typical symptoms: a). MI: central anterior chest tightness T b). Unstable angina: central anterior chest tightness T c). Pericarditis: pain exacerbated by sitting forward F Inflammation of the Pericardium. Central Chest pain worse on inspiration or lying flat +- relief by sitting forward. A pericardial friction rub may be heard. ECG classically shows concave (saddle shaped) ST segment elevation. Causes Viruses ( Epstein Barr, mumps, coxsackie), MI, Uraemia, Rheumatoid Arthritis, SLE, Hypothyroidism, Radiotherapy .Treat cause and give analgesia e.g. ibuprofen. d). Psoriasis: itch T Classically it is said that psoriasis is not itchy, a significant number of patients complain of severe itching, while most complain of itch some of the time. e). Subarachnoid haemorrhage: frontal headache F Sudden devastating headache which tends to be occipital; --------------------------------------------------------------------------------------------------------------------------181. The following occupations are correctly paired with a recognized occupational hazard a. Asbestos insulation: pleural mesothelioma T b. Pottery worker: silicosis T c. Animal laboratory worker: asthma T d. Pneumatic drill operator: Raynaud’s phenomenon T e. Deep sea diver: bony infarction T 181. The following occupations are correctly paired with a recognized occupational hazard a). Asbestos insulation: pleural mesothelioma T Can be caused by light exposure to asbestos (interval of 20-40 years from exposure to disease) Presents with pleuritic pain, increasing dyspnoea and pleural effusions. Median survival is 2 years. b). Pottery worker: silicosis T Silicosis is uncommon though it can still be encountered in stone masons, sand blasters, pottery and ceramic workers . It is caused by inhalation of silica (silicon dioxide), which is highly fibrogenic. c). Animal laboratory worker: asthma T Can be triggered by animal fur Non – IgE related Isocyanates - varnishes, spray painting Colophony fumes – soldering/ welders, electronics industry IgE related Allergens from animals, insects and antibiotics- Laboratories Allergens from flour and grain- Farmers, millers, grain workers Latex- Health care workers Complex salts of platinum- Metal refining d). Pneumatic drill operator: Raynaud’s phenomenon T Consists of episodic digital ischemia, precipitated by cold or emotion. Fingers ache and change colour pale to blue to red. It may be idiopathic and called Raynaud’s disease. It may have an underlying cause Raynaud’s phenomenon. Reflex- Raynaud’s disease, Vibrating machinery injury, cervical spondylosis Connective tissue disease – Scleroderma, SLE, Polyarteritis nodosa, Rheumatoid arthritis, polymyositis Arterial Disease- Embolism or thrombosis, trauma, Buerger’s disease Haematological – Polycthaemia, leukaemia, Dysproteinaemia, cold agglutinin disease Poison’s- drugs like beta – blockers, ergotamine, Vinyl chloride e). Deep sea diver: bony infarction T Decompression sickness ‘the bends’ occurs in divers on too rapid ascent to the surface and is caused by release of bubbles of inert gases ( nitrogen and helium).Bends can be mild with skin irritation, mottling or joint pain only. Bends can be more serious with cortical blindness, hemi paresis or cord lesions. Treatment is with oxygen in a pressure chamber. A long term problem is aseptic necrosis ( e.g. of the hip) due to nitrogen bubbles causing infarction of nutrient arteries of bone. ---------------------------------------------------------------------------------------------------------------182. The following nail findings are correctly paired with underlying disease states: a. Spoon shaped nails: B12 deficiency F b. Leuconychia: chronic liver disease T c. Splinter haemorrhages: infective endocarditis T d. Nail pitting: Steven-Johnson syndrome F e. Finger clubbing: chronic liver disease T 182. The following nail findings are correctly paired with underlying disease states: a). Spoon shaped nails: B12 deficiency F Koilonychia is associated with iron deficiency anaemia, fungal infection and Raynaud’s phenomenon b). Leuconychia: chronic liver disease T Leuconychia is caused by hypoalbunaemia which can be due to chronic liver disease c). Splinter haemorrhages: infective endocarditis T Splinter Haemorrhages are caused by nail bed infarcts due to immune complex deposition d). Nail pitting: Steven-Johnson syndrome F Steven Johnson syndrome is a severe form of Erythema Multiforme, with mucosal involvement, blisters , high fever, Anterior uveitis, pneumonia, renal failure and polyarthritis. Triggers are Herpes Simplex (the commonest), other viruses – orf, hepatitis, mumps, radiotherapy, cancers, connective tissue diseases, drugs like sulphonamides. Close attention to fluid balance and nutrition. Role of steroids controversial as morbidity from steroids may outweigh that of the disease. e). Finger clubbing: chronic liver disease T ---------------------------------------------------------------------------------------------------------------183. The following are recognized complications of diabetes mellitus: a. Impotence T b. Postural hypotension T c. Charcot’s joint T d. 3rd nerve palsy T e. Pneumothorax F 183. The following are recognized complications of diabetes mellitus: a). Impotence T Impotence is common. Part of the autonomic neuropathy of diabetes. Impotence has many causes including anxiety, depression, alcohol excess, drugs, hypothyroidism. After appropriate history and examination blood is taken for LH, FSH, testosterone, prolactin and thyroid function. Sympathetic counselling of both partners, try Phosphodiesterase type -5 inhibitors ( sildenafil, tadafil, vardenafil) b). Postural hypotension T Due to autonomic neuropathy, loss of sympathetic tone to peripheral arterioles . c). Charcot’s joint T Develops in the ankle d). 3rd nerve palsy T Isolated palsies of nerves to the external eye muscles, especially the third and sixth nerves, are more common in diabetics. In diabetic third nerve palsies the pupil reflexes are intact as the pupillomotor fibres are spared. e). Pneumothorax F Spontaneous Pnuemothorax in young men. Other causes asthma, COPD, TB, pneumonia, lung abscess, carcinoma, cystic fibrosis, lung fibrosis, sarcoidosis, connective tissue disorders, trauma, iatrogenic. -----------------------------------------------------------------------------------------------------184. Subacute bacterial endocarditis can manifest itself as: a. Cerebrovascular accident b. Anaemia c. Hematuria d. Hypertension e. Vasculitis T T T F T 84. Subacute bacterial endocarditis can manifest itself as: a). Cerebrovascular accident T Emboli from infected valves can cause infarction in the brain. Can lead to formation of cerebral abscess. b). Anaemia T Anaemia of chronic disease. There is decreased release of iron from the bone marrow to developing erythroblasts, an inadequate erythropoietin response to anaemia and decreased red cell survival. The serum iron and The Total Iron Binding Capacity are low, while the serum ferritin is normal or raised because of the inflammatory process. Patients do not respond to iron therapy and treatment in general is of the infective endocarditis. c). Hematuria T Caused by immune complex deposition due a vasculitis. Glomerulonephritis and renal failure may occur. d). Hypertension F e). Vasculitis T see above ------------------------------------------------------------------------------------------------------185. In TB meningitis a. There is usually a high polymorph cell count in CSF b. Blood glucose is usually low c. CSF protein is usually low d. Presentation can be with inappropriate ADH secretion (SiADH) e. Cranial nerve palsies may occur 185. In TB meningitis a). There is usually a high polymorph cell count in CSF F Generally tends to be mononuclear b). Blood glucose is usually low T F T F T T c). CSF protein is usually low F tends to be high d). Presentation can be with inappropriate ADH secretion (SiADH) T Meningitis (which can be due to T.B. ) and pulmonary T.B. can cause SiADH. Cause of hyponatremia. Diagnosis of SiADH requires 1. Concentrated urine (sodium > 20 mmol/l & osmolality >500 mosmol/kg) 2. Hyponatraemia (< 125 mmol/l) 3. Low plasma osmolality (< 260 mmol/kg) 4. Normal fluid volume 5. No adrenal, thyroid, pituitary, renal insufficiency or diuretic use Other Causes of SiADH are Central Nervous system – stroke, subarachnoid haemorrhage, head trauma, brain tumour Pulmonary – neoplasms, tuberculosis, pneumonia Malignancies – small cell lung cancer, pancreas, lymphoma Drugs – Antidepressants, Neuroleptics, carbamazepine e). Cranial nerve palsies may occur T Can lead to cranial nerve palsies ------------------------------------------------------------------------------------------------------186. Vasculitis lesions can be found in: a. Polyarteritis nodosa b. Drug reactions c. Hypertension d. Rheumatoid arthritis e. Hepatitis A 186. Vasculitis lesions can be found in: a). Polyarteritis nodosa T b). Drug reactions T Sulphonamides, penicillins, Thiazides c). Hypertension F Many of the conditions associated with a vasculitis can lead to hypertension. d). Rheumatoid arthritis T e). Hepatitis A F T T F T F Hepatitis B and C infection is common in Cutaneous Leucocytoclastic vasculitis and may be an aetiological agent Vasculitis is a term applied to an inflammatory disorder of blood vessels which causes endothelial damage. The clinical manifestations are due to ischaemic necrosis. The Vasculides are systemic diseases which affect the skin, musculoskeletal, renal and gastro intestinal systems. Classification of Systemic Vasculitis is usually based on the type of artery affected Types of Systemic Vasculitis Large (aorta and major tributaries) Giant cell arteritis Takayasu’s arteritis Medium ( medium and small sized arteries and arterioles) Classical polyarteritis nodosum Kawasaki’s Disease Small (small arteries, arterioles, venules and capillaries) Microscopic polyangitis (ANCA antinuetrophilic cytoplasmic antibody) Wegner’s granulomatosis (ANCA) Churg-Strauss syndrome (ANCA) Henoch-Schonlein purpura Cutaneous leucocytoclastic vasculitis Essential cryoglobulinaemia Other conditions associated with vasculities Infective- syphilis, Hepatitis B and C, T.B., group A streptococci Non Infective- Rheumatoid arthritis, SLE, Scleroderma, Polymyositis, Dermatomyositis, Bechet’s, Paraneoplastic syndromes, Inflammatory bowel disease , drugs mentioned above -----------------------------------------------------------------------------------------------------------187. Mycoplasma pneumoniae a. Occurs in young adults b. Can have CNS manifestations c. Can be accompanied by skin rash d. Responds to treatment with penicillin e. Can show a significant titre of cold agglutinins T T T F T 187. Mycoplasma pneumoniae a). Occurs in young adults T Mycoplasma Pneumonia is a relatively common cause of pneumonia and occurs in epidemics in cycles of 3-4 years. It most often occurs in patients in teenagers and twenty. (from Prof Prentice with love, Mycoplasmas are similar to bacteria but lack certain structure like cell walls. They bind to the surface of epithelial cells and cause atypical pneumonia). Presents with headache, malaise, myalgia, arthralgia which is then followed by chest symptoms like cough. There may not be any physical signs. Chest X-ray only one lobe is usually involved with patchy consolidation. There may be no correlation between x-ray appearance and the clinical status of the patient i.e. the x-ray may look horrible but the patient is well b). Can have CNS manifestations T Check out the complications below c). Can be accompanied by skin rash T Complications include skin rash (Erythema Muliforme and Steven-Johnson syndrome), meningioencephalitis or myelits, Gullian- Barre syndrome, myocarditis and pericarditis, gastro intestinal symptoms like vomiting and diarrhoea. d). Responds to treatment with penicillin F Treated with erythromycin/ clarithromycin (macrolides) or Tetracycline e). Can show a significant titre of cold agglutinins T Cold agglutins are present in 50% which can cause an autoimmune haemolytic anaemia. White cell count is not raised. Diagnosed with antibodies to mycoplasma. -------------------------------------------------------------------------------------------------188. In a patient with harsh ejection systolic murmur at the precordial base, the following might indicate aortic stenosis a. History of syncope T b. Large volume pulse F c. ECG showing left ventricular hypertrophy and strain T d. Doppler echocardiography showing a large pressure gradient across the aortic valve T e. A mid-systolic click at left sternal edge T 188. In a patient with harsh ejection systolic murmur at the precordial base, the following might indicate aortic stenosis a). History of syncope T May also have angina, dyspnoea, systemic emboli from infective endocarditis, congestive cardiac failure and sudden death b). Large volume pulse F Small volume pulse as the blood finds it difficult to get out of the heart, with narrow pulse pressure c). ECG showing left ventricular hypertrophy and strain T Can also show P- mitrale (bifid p-wave indicates left atrial hypertrophy), left anterior hemiblock, poor R wave progression, left bundle branch block or complete block d). Doppler echocardiography showing a large pressure gradient across the aortic valve T Valve gradient greater than > 50 mmhg indicates severe stenosis e. A mid-systolic click at left sternal edge T Ejection mid-systolic murmur heard at left sternal area, aortic area and radiates to the carotids. In congenital aortic stenosis where the valve cusps remain mobile and come to an abrupt halt, an ejection click may precede (come before the murmur). This click is absent if the valve is calcified. ------------------------------------------------------------------------------------------------------189. Regarding hypercholesterolemia a. Fasting sample is necessary for screening b. May be due to a decrease in LDL receptors c. Total cholesterol and LDL cholesterol are usually closely associated d. Increased HDL cholesterol is associated with an increased risk of cardiovascular disease. e. Reduction of total cholesterol has been shown to significantly reduce cardiovascular risk. F T T F T 189. Regarding hypercholesterolemia a). Fasting sample is necessary for screening F Serum cholesterol concentration does not change significantly after a meal and as a screening test a random blood sample is sufficient. It total cholesterol concentration is raised, HDL cholesterol, triglyceride, and LDL cholesterol concentrations should be quantified on a fasting sample. If a test for hypertriglyceridaemia is needed, a fasting blood sample is mandatory. b). May be due to a decrease in LDL receptors T On all the cells of the body and mainly in the liver there is a low density lipoprotein receptor that collects LDL (low-density lipoprotein) cholesterol from the bloodstream. People with Familial Hypercholesterolemia have a defect in the gene of this LDLcholesterol receptor which causes an accumulation of LDL-cholesterol in the blood and ultimately in the arterial vessel wall. There are more than 300 different gene defects that lead to FH. c). Total cholesterol and LDL cholesterol are usually closely associated T Population studies have repeatedly shown a strong association between both total and LDL Cholesterol concentration and coronary heart risk. d). Increased HDL cholesterol is associated with an increased risk of cardiovascular disease. F High Density Lipoprotein protects against cardiovascular disease e). Reduction of total cholesterol has been shown to significantly reduce cardiovascular risk. T National Cholesterol Education Program guidelines suggest that drug therapy should be used if there is inadequate response to diet therapy and the individual has a low density lipoprotein concentration above 4.1 mmol/l (corresponding roughly to a total cholesterol concentration over 6.2 mmol/l) together with existing coronary heart disease or two other coronary heart disease risk factors. -----------------------------------------------------------------------------------------------------------------------