1. Which of the following about atherosclerosis is true?
A. Intake of unsaturated fatty acid associated with decreased risk
B. Thoracic aorta involvement is more severe than abdominal aorta involvement
C. Extent of lesion in veins is same as that in arteries
D. Hypercholesterolemia does not always increase the risk of atherosclerosis perse
Ans. A. Intake of unsaturated fatty acid associated with decreased risk
Ref- Harrison 17th edition page no.2429
· Atherosclerosis is a condition in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol.
· It is a syndrome affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries, caused largely by the accumulation of macrophage white blood cells and promoted by low-density lipoproteins without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL),
· It is commonly referred to as a hardening or furring of the arteries.
· It is caused by the formation of multiple plaques within the arteries.
The athermanous plaque is divided into three distinct components:
1. The atheroma which is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery
2. Underlying areas of cholesterol crystals
3. Calcification at the outer base of older/more advanced lesions.
Role of PUFA
· "N-3 polyunsaturated fatty acids (n-3 PUFAs) are present in high concentration in fish and in flax seeds.
· The most widely used n-3 PUFAs for the treatment of hyperlipidernias are the two active molecules in fish oil: eicosapentanoic acid (EPA) and decohexanoic acid (DHA).
· N-3 PUFAs have been concentrated into tablets and decrease fasting triglycerides in doses of 3–4 g/d.
· Fish oils can result in an increase in plasma LDL-C levels in some patients.
· Fish oil supplements can be used in combination with fibrates, niacin, or statins to treat hypertriglyceridemia. In general, fish oils are well tolerated and appear to be safe, at least at doses up to 3–4 g.
· Although fish oil administration is associated with a prolongation in the bleeding time, no increase in bleeding has been seen in clinical trials.
· A lower dose of omega 3 (about 1 g) has been associated with reduction in cardiovascular events in CHD patients and is used by some clinicians for this purpose."
2. A girl presented with severe hyperkalemia and peaked T waves on ECG. Most rapid way to decreased serum potassium level?
A. Calcium gluconate IV B. Oral resins
C. Insulin + glucose D. Sodium bicarbonate
Ans C. Insulin + glucose
Ref-.Harrison 17th e/p.284.
Hyperkalemia is treated by following ways.
1. Injection calcium gluconate – It stabilizes cardiac membrane and thus prevent arrhythmia. It does not reduce serum potassium level. It is usually given when serum potassium level are very high.
2. Injection dextrose insulin drip – It is the most widely used method to reduce serum potassium level. It is the fastest method to reduce potassium level.
3. Beta 2 agonist – Like salbutamol & Albuterol can also reduce serum potassium level.
4. Potassium chelating resin – They are used orally, usually for long term use, they prevent serum potassium level to rise. Resins are slow acting used in chronic hyper kalemia
6. Injection NahCO3 – It is used to treat severe acidosis when PH is below 7.1. Acidosis is usually associated with hyperkalemia so when we treat by NahCO3, potassium level also falls. But please note NahCO3 is not used to treat hyperkalemia as such!!!
Treatment for urgent control of hyperkalemia.
Modality Onset Duration
Calcium Gluconate 0-5 minutes 1 hour
Sodium Bicarbonate 15-30 minutes 1-2 hour
Insulin 15-60 minutes 4-6 hours
Albuterol 15-30 minutes 2-4 hours
3. A 9 yr old girl has difficulty in combing hairs and climbing upstairs since 6 / months. She has Gower’s sign positive and maculopapular rash over metacarphalangeal joints. What should be the next appropriate investigation to be done?
a. ESR b. RA factor
c. Creatine kinase d. Electromyography
Ans. C. Creatine kinase
Ref. Harrison ed.17th pg no.2700
In the question, as the patient is not able to comb her hair and is unable to climb up stairs it means she is suffering most likely with proximal myopathy. She also has skin lesion over the metacarphalangeal joints, she probably has dermatomyositis & the skin lesion seem to be Gottron’s sign.
The clinically suspected diagnosis of PM, DM, or IBM is confirmed by examining the serum muscle enzymes, EMG findings, and muscle biopsy (Table 383-2).
Table 383-2 (Harrison ed.17th ) Criteria for Diagnosis of Inflammatory Myopathies
Criterion Definite Probable Dermatomyositis Inclusion Body Myositis
Myopathic muscle weaknessa Yes Yes Yesb Yes; slow onset, early involvement of distal muscles, frequent falls
Electromyographic findings Myopathic Myopathic Myopathic Myopathic with mixed potentials
Muscle enzymes Elevated (up to 50-fold) Elevated (up to 50-fold) Elevated (up to 50-fold) or normal Elevated (up to 10-fold) or normal
Muscle biopsy findings "Primary" inflammation with the CD8/MHC-I complex and no vacuoles Ubiquitous MCH-I expression but minimal inflammation and no vacuoles Perifascicular, perimysial, or perivascular infiltrates, perifascicular atrophy Primary inflammation with CD8/MHC-I complex; vacuolated fibers with -amyloid deposits; cytochrome oxygenase–negative fibers; signs of chronic myopathy
Rash or calcinosis Absent Absent Present Absent
· ESR & RA factor would not directly help in establishing the diagnosis of inflammatory myopathy Needle
· EMG shows myopathic potentials characterized by short-duration, low-amplitude polyphasic units on voluntary activation and increased spontaneous activity with fibrillations, complex repetitive discharges, and positive sharp waves.
· These EMG findings are not diagnostic of an inflammatory myopathy but are useful to identify the presence of active or chronic myopathy and to exclude neurogenic disorders.
· Muscle biopsy is the definitive test for establishing the diagnosis of inflammatory myopathy and for excluding other neuromuscular diseases.
Muscular dystrophy refers to a group of hereditary progressive diseases each within unique phenotypic and genetic features. (Table 382-5, 382-6, 382-7)
Table 382-5 (Harrison ed.17th) Progressive Muscular Dystrophies
Type Inheritance Onset Age Clinical Features Other Organ Systems Involved
Duchenne XR Before 5 years Progressive weakness of girdle musclesUnable to walk after age 12Progressive kyphoscoliosisRespiratory failure in 2d or 3d decade CardiomyopathyMental impairment
Becker XR Early childhood to adult Progressive weakness of girdle musclesAble to walk after age 15Respiratory failure may develop by 4th decade Cardiomyopathy
Limb-girdle AD/AR Early childhood to early adult Slow progressive weakness of shoulder and hip girdle muscles ± Cardiomyopathy
Emery-Dreifuss XR/AD Childhood to adult Elbow contractures, humeral and peroneal weakness Cardiomyopathy
Congenital AR At birth or within first few months Hypotonia, contractures, delayed milestonesProgression to respiratory failure in some; static course in others CNS abnormalities (hypomyelination, malformation)Eye abnormalities
Myotonica (DM1, DM2) AD Usually 2d decadeMay be infancy if mother affected (DM1 only) Slowly progressive weakness of face, shoulder girdle, and foot dorsiflexionPreferential proximal weakness in DM2 Cardiac conduction defectsMental impairmentCataractsFrontal baldnessGonadal atrophy
Facioscapulohumeral AD Before age 20 Slowly progressive weakness of face, shoulder girdle, and foot dorsiflexion DeafnessCoats’ (eye) disease
Oculopharyngeal AD 5th to 6th decade Slowly progressive weakness of extraocular, pharyngeal, and limb muscles —
aTwo forms of myotonic dystrophy, DM1 and DM2, have been identified. Many features overlap (see text).Abbreviations: XR, X-linked recessive; AD, autosomal dominant; AR, autosomal recessive; CNS, central nervous system.
The most sensitive enzyme is CK, which in active disease can be elevated as much as 50-fold. Although the CK level usually parallels disease activity, it can be normal in some patients with active IBM or DM, especially when associated with a connective tissue disease. The CK is always elevated in patients with active PM. Along with the CK, the serum glutamic-oxaloacetic and glutamate pyruvate transaminases, lactate dehydrogenase, and aldolase may be elevated.
EMG findings are not diagnostic of an inflammatory myopathy but are useful to identify the presence of active or chronic myopathy and to exclude neurogenic disorders .
4. 14 yrs old girl on exposure to cold has pallor of extremities followed by pain and cyanosis. In later ages of life she is prone to develop?
C Rheumatoid arthritis
Ans. B. Scleroderma
Ref-Harrison ed.17th pg no.2101
· "Raynaud’s phenomenon, defined as episodic vasoconstriction in the fingers and toes, develops in virtually every patient with Systemic sclerosis. In some, episodes may also affect the tip of the nose and earlobes.
5· Attacks are triggered by
a. Exposure to cold
b. Decrease in temperature
c. Emotional stress
d. Using vibration tools
· In colder climates, patients commonly experience an increase in the frequency and severity of episodes during the winter months.
Table 243-1 Classification of Raynaud’s Phenomenon
Primary or idiopathic Raynaud’s phenomenon: Raynaud’s disease
Secondary Raynaud’s phenomenon
1. Collagen vascular diseases: scleroderma, systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis, polymyositis
2. Arterial occlusive diseases: atherosclerosis of the extremities, thromboangiitis obliterans, acute arterial occlusion, thoracic outlet syndrome
3. Pulmonary hypertension
4. Neurologic disorders: intervertebral disk disease, syringomyelia, spinal cord tumors, stroke, poliomyelitis, carpal tunnel syndrome
5. Blood dyscrasias: cold agglutinins, cryoglobulinemia, cryofibrinogenemia, myeloproliferative disorders, Waldenström’s macroglobulinemia
6. Trauma: vibration injury, hammer hand syndrome, electric shock, cold injury, typing, piano playing
7. Drugs: ergot derivatives, methysergide, Beta-adrenergic receptor blockers, bleomycin, vinblastine, cisplatin
· Typical attacks start with pallor, followed by cyanosis of variable duration. Eventually erythema develops spontaneously or with rewarming of the digit.
· The progression of the three color phases reflects the underlying pathogenic mechanisms of vasoconstriction, ischemia, and reperfusion.
· Some patients with Raynaud’s phenomenon may experience only pallor or cyanosis."
· In a patient of Raynaud’s phenomena all arteries (like radial, brachial, popliteal, dorsalis pedis) are normally palpable.
· Recently a new drug, Bosentan, which is a endothelin receptor blocking drug has been approve for the treatment of Raynaud’s phenomenon.
· Extra Edge: Bosentan has also approved for the treatment of primary pulmonary arterial hypertension
5. Berry aneurysm – Defect lies in
A. Degeneration of internal elastic lamina
B. Deposition of mucoid material in media
C. Defect in muscular layer
D. Disturbance in vessel wall
Ans. C. Defect in muscular layer
Ref- Harrison 17th, Page 1727
· Saccular (Berry) aneurysms occur at the bifurcations of the large to medium-sized intracranial arteries; rupture is into the subarachnoid space in the basal cisterns and often into the parenchyma of the adjacent brain.
· Approximately 85% of aneurysms occur in the anterior circulation, mostly on the circle of Willis. About 20% of patients have multiple aneurysms, many at mirror sites bilaterally.
· As an aneurysm develops, it typically forms a neck with a dome. The length of the neck and the size of the dome vary greatly and are factors that are important in planning neurosurgical obliteration or endovascular embolization.
· The arterial internal elastic lamina disappears at the base of the neck.
· The media thins, and connective tissue replaces smooth-muscle cells. At the site of rupture (most often the dome) the wall thins, and the tear that allows bleeding is often £0.5 mm long.
· Aneurysm size and site are important in predicting risk of rupture.
· Those >7 mm in diameter and those at the top of the basilar artery and at the origin of the posterior communicating artery are at greater risk of rupture.
6. In which cotrimoxazole not use in treatment?
Ans. C. Chancroid
Uses of cotrimoxazole
· Pneumocystis pneumonia
· Toxoplasmosis and nocardiosis
· Acute exacerbations of chronic bronchitis and infections of the urinary tract where there is good rationale for use
· Acute otitis media in children where there is good rationale
Specific indications for its use include:
Being an antibiotic, co-trimoxazole does not have any activity against HIV itself, but it is often prescribed to immunocompromised patients as Pneumocystis jirovecii pneumonia prophylaxis.
· Infections caused by Listeria monocytogenes, Nocardia spp., Stenotrophomonas maltophilia (Zanthomonas maltophilia)
· Staphylococcus saprophyticus infections presenting as urinary tract infection or cystitis
· Whipple’s Disease
· Traveler’s Diarrhea
· Prophylaxis of cerebral toxoplasmosis in HIV patients
· Cyclospora cayetanensis
Chronic bacterial prostatitis treatment
· Chronic bacterial prostatitis treatment is with long-term antibiotics, up to eight weeks, with ciprofloxacin, sulfa drugs [for example, sulfamethoxazole and trimethoprim or erythromycin
· Chancroid – Treatment regimens may include the following: azithromycin, ceftriaxone, ciprofloxacin and erythromycin base
· Typhoid fever –
a. Ciprofloxacin is the most frequently used drug.
b. Ceftriaxone, an intramuscular injection medication, is an alternative
c. Ampicillin and trimethoprim-sulfamethoxazole are frequently prescribed antibiotics.
7. Thrombotic event is seen in all of following except
D. Heparin induced thrombocytopenia
Ref- .Harrison 17th edition Page 367
Table 59-3 Risk Factors for Thrombosis
Venous Venous and Arterial
Factor V Leiden Homocystinuria
Prothrombin G20210A Dysfibrinogenemia
Protein C deficiency Mixed (Inherited and acquired)
Protein S deficiency Hyperhomocysteinemia
Age Antiphospholipid antibody syndrome
Previous thrombosis Hormonal therapy
Immobilization Polycythemia vera
Major surgery Essential thrombocythemia
Pregnancy & puerperium Paroxysmal nocturnal hemoglobinuria
Hospitalization Thrombotic thrombocytopenic purpura
Obesity Heparin-induced thrombocytopenia
Infection Disseminated intravascular coagulation
APC resistance, non genetic
Elevated factor II, IX, XI
Elevated TAFI levels
Low levels of TFPI
a Unknown whether risk is inherited or acquired.
Note: APC, activated protein C; TAFI, thrombin-activatable fibrinolysis inhibitor; TFPI, tissue factor pathway inhibitor
8. A patient develops sudden palpitation with HR 150 / min, regular. What could be the cause?
b. Sinus tachycardia
c. Ventricular tachycardia
d. Atrial flutter with block
Ans. A. PSVT
Paroxysmal supraventricular tachycardia (PSVT) is an occasional rapid heart rate.
i. PSVT can be initiated in the SA node, In the atria, in the atrial conduction pathways, or other areas.
ii. PSVT can occur with digitalis toxicity and conditions such as Wolff-Parkinson-White syndrome.
iii. The condition occurs most often in young people and infants.
The following increase risk for PSVT:
i. Alcohol use
ii. Caffeine use
iii. Illicit drug use
ii. Chest tightness
iii. Palpitations (a sensation of feeling the heart beat)
iv. Rapid pulse
v. Shortness of breath
Note: Symptoms may start and stop suddenly, and can last for a few minutes or several hours. A PSVT lasting more than half of the day is considered an incessant PSVT.
Signs and tests
· A physical examination during a PSVT episode will show a rapid heart rate.
· The heart rate may be 150 to 250 beats per minute (bpm). In children, the heart rate tends to be very high. There may be signs of poor blood circulation such as lightheadedness. Between episodes of PSVT, the heart rate is normal (60 to 100 bpm).
· An ECG during symptoms shows PSVT.
· An electrophysiology study (EPS) is often necessary for an accurate diagnosis and to recommend the best treatment.
The Valsalva maneuver can be used to interrupt the fast heartbeat.
Emergency treatment of PSVT may include:
1. Medicines through a vein, including adenosine and verapamil.
2. Other medications may be used, such as procainamide, beta-blockers, and propafenone.
3. Electrical cardioversion, the use of electric shock to restore a rapid heartbeat back to normal.
Long-term treatment of PSVT may include:
1. Daily medications such as propafenone, flecainide, moricizine, sotalol, and amiodarone.
2. Pacemakers to override the fast heartbeat; very occasionally used in children with PSVT who have not responded to any other treatment.
3. Radiofrequency catheter ablation; currently the treatment of choice for most PSVTs.
The main complication is an increased risk of heart failure.
9. Where pulsatile liver and ascites is found
b. Critical pulmonary stenosis
Ans. A. TR
Ref: Harrison, 17th edition page 1479
· The clinical features of TR result primarily from systemic venous congestion and reduction of CO.
· With the onset of TR in patients with pulmonary hypertension, symptoms of pulmonary congestion diminish, but the clinical manifestations of right-sided heart failure become intensified.
· The neck veins are distended with prominent v waves and rapid y descents, marked hepatomegaly, ascites, pleural effusions, edema, systolic pulsations of the liver, and a positive hepatojugular reflux.
· A prominent RV pulsation along the left parasternal region and a blowing holosystolic murmur along the lower left sternal margin, which may be intensified during inspiration and reduced during expiration or the strain of the Valsalva maneuver (Carvallo’s sign), are characteristic findings;
· AF is usually present.
10. ln renal cell carcinoma which is not associated
c. Cushing syndrome
d. Malignant hypertension
Ans. C. Cushing syndrome
Ref-Harrison 17th/e p.2254,592.
· The presenting signs and symptoms include hematuria, abdominal pain, and a flank or abdominal mass.
· This classic triad occurs in 10–20% of patients. Other symptoms are fever, weight loss, anemia, and a varicocele (Table 90-4).
· The tumor can also be found incidentally on a radiograph. Widespread use of radiologic cross-sectional imaging procedures (CT, ultrasound, MRI) contributes to earlier detection, including incidental renal masses detected during evaluation for other medical conditions.
· The increasing number of incidentally discovered low-stage tumors has contributed to an improved 5-year survival for patients with renal cell carcinoma and increased use of nephron-sparing surgery (partial nephrectomy).
· A spectrum of paraneoplastic syndromes has been associated with these malignancies, including erythrocytosis, hypercalcemia, nonmetastatic hepatic dysfunction (Stauffer syndrome), and acquired dysfibrinogenemia.
· Erythrocytosis is noted at presentation in only about 3% of patients. Anemia, a sign of advanced disease, is more common.
Table 90-4 Signs and Symptoms in Patients with Renal Cell Cancer
Presenting Sign or Symptom Incidence, %
Classic triad: hematuria, flank pain, flank mass 10-20
Flank pain 40
Palpable mass 25
Weight loss 33
Abnormal liver function 15
Increased erythrocyte sedimentation rate 55
12. Reperfusion is useful for
a. Stunt myocardium
b. Hibernating myocardium
c. Non ischemic viable myocardium
d. Mixed ischemic myocardium
Ans. B. Hibernating myocardium
· "LV dysfunction can be due to non contractile or hypo contractile segments that are viable but are chronically ischemic (hibernating myocardium).
· As a consequence of chronic reduction in myocardial blood flow these segments down regulate their contractile function.
· These can be detected by using consequence of chronic reduction in myocardial blood flow these segments down regulate their contractile function.
· These can be detected by using radionuclide scans of myocardial perfusion and metabolism, PET, CMR imaging, or delayed scanning with thallium-20 I; or by improvement of regional functional impairment, provoked by low-dose dobutamine.
· " In such patients, revascularization improves myocardial blood flow, can return function, and can improve survival."
· Stunned myocardium can be differentiated from hibernating myocardium by three clinical parameters, namely, LV wall motion, myocardial perfusion, and myocardial metabolism.
· Stunned myocardium has abnormal wall motion that tends to normalize in response to inotrope and postextrasystolic potentiation.
· Perfusion is adequate and metabolism is also adequate. Hibernating myocardium also has abnormal wall motion, which normalizes after nitrates, inotrope, post extrasystolic potentiation (PESP), PTCA, or CABG.
· Myocardial perfusion is reduced but can be reversed with PTCA or CABG and metabolism is adequate.
Extra Edge: Recent Advances:
Following are the methods to reperfuse the myocardium
a. Thrombolytic therapy
b. Mechanical method :
c. Coronary artery bypass graft (CABG)
13. Positive hepatojugular reflux is found in all of the following conditions except?
a. Tricuspid regurgitation
b. Right heart failure
c. Decreased after load
d. Increased pulmonary capillary bed pressure
Ans. C. Decreased after load
Ref: Harrison, 17th edition, page 1384
· In patients suspected of having right ventricular failure who have a normal CVP at rest, the abdominojugular reflux test may be helpful.
· The palm of the examiner’s hand is placed over the abdomen, and firm pressure is applied for 10 s or more. In normal persons, this maneuver does not alter the jugular venous pressure significantly, but when right heart function is impaired, the upper level of venous pulsation usually increases.
· A positive abdominojugular test is best defined as an increase in JVP during 10 s of firm midabdominal compression followed by a rapid drop in pressure of 4 cm blood on release of the compression.
a. The most common cause of a positive test is right-sided heart failure secondary to elevated left heart filling pressures.
b. Increase after load is associated with LVF. That is why ACEI are used in the treatment of LVF (To reduce after load)
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