Step 1 Flashcards

1
Q

The most common cause of pericarditis is ______

A

Coxsackie B virus, which causes inflammation of the pericardial membrane. This is a picornovirus, the smallest RNA virus. Positive, single-stranded, naked, icosohedral virus.

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2
Q

Tertiary syphilis can cause what cardiac problems?

A

Tertiary syphilic disrupts the vasa vasorum of the aorta, dilating the aortic root and the aortic valve ring. This can lead to aneurysm and aortic valve insufficiency. “Tree barking” of the aorta may also occur which is due to the wrinkling of the tunica intima.

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3
Q

Cystic fibrosis

A

Autosomal recessive causing a defect in CFTR gene, leading to dysfunctional chloride channel that secretes Cl- into lungs and GI tract and reabsorbs Cl- in sweat glands. This often leads to mucus plugging and recurrent pulmonary infections, chronic bronchitis, and bronchiectasis. Often present with meconium ileus in newborns. N-acetylcysteine can be used to loosen mucus plugs (it cleaves disulfide bonds within mucus glycoproteins).

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4
Q

CF can lead to problems associated with absorption of fat-soluble vitamins. Which condition can arise from this?

A

Fat soluble vitamins include A, D, E, and K. Deficiency in D can cause rickets in children due to decreased bone formation. Hypocalcemic tetany and muscle spasm can also occur. Vitamin A deficiency can result in night-blindness and dry skin. Deficiency in E and K can lead to RBC dysfunction and defective coagulation, respectively.

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5
Q

Which antitumor antibiotic can cause pulmonary fibrosis?

A

Bleomycin - it induces free radical formation resulting in breaks in DNA strands. It is used to treat testicular cancer and Hodgkin’s lymphoma. Skin changes may also occur on this drug such as darkening.

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6
Q

What is osteomalacia?

A

It is a disorder of bone mineralization/calcification of osteoid in adults. It is often due to vitamin D deficiency (rickets in children), which leads to low to normal levels of calcium, low vitamin D, and low phosphate. Bone matrix can be laid down but it cannot be mineralized. These patients have reduced bone densities and prone to pathologic fractures. Lab profiles might show elevated alkaline phosphatase or increased PTH secretions (this decreased phosphate levels in serum and tries to increase calcium levels). There is a hyperactivity of osteoblasts which require an alkaline environment hence why alkaline phosphatase is increased.

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7
Q

What is osteoporosis?

A

This is a decreased synthesis of new bone matrix, which is contrasted from osteomalacia, where bone matrix is laid down but not mineralized.

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8
Q

What time of chronic gastritis (nonerosive) affects the first part of the stomach?

A

Type A - it affects the fundus/body of stomach and spares the antrum. It is an autoimmune condition where antibodies attack parietal cells in the stomach.

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9
Q

What is Gerstmann’s syndrome?

A

(1) an inability to distinguish right from left; (2) an inability to identify fingers; (3) a writing disability known as agraphia or dysgraphia; and (4) a lack of understanding the rules for calculation or arithmetic known as acalculia or dyscalculia. Reading ability remains intact. The syndrome results from damage to the visual association cortex (angular gyrus).

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10
Q

Name one enzyme responsible for renal gluconeogenesis.

A

Fructose-1,6-bisphosphatase

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11
Q

Stable angine usually presents at what percentage of artery stenosis?

A

75% and greater.

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12
Q

What is most likely cause of death a few hours post-MI?

A

Fatal arrythmia, specifically polymorphic ventricular tachycardia. Cardiac arrythmia is an important cause of death before reaching hospital. Cardiogenic shock may also arise when heart completely fails and cannot supply vital organs.

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13
Q

What causes arrythmia post-MI?

A

It is due to a disruption of the vascular supply to the conduction system, combined with myocardial irritability after injury.

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14
Q

What are some etiologies of dilated cardiomyopathy?

A

ABCCCD: Alcohol abuse, Beriberi (lack of thiamine pyrophosphate - active form of thiamine or B1), Coxsackie B myocarditis (direct toxicity via receptor-mediated entry of virus into cardiac myocytes), chronic Cocaine use, Chagas’ disease, and Doxorubicin toxicity.

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15
Q

What is the S3 heart sound?

A

S3, or ventricular gallop, occurs in early diastole, following opening of the AV valves during rapid ventricular filling phase. In adults, it is a sign of volume overload owing to congestive heart failure, or increased transvalvular flow that accompanies advanced mitral or tricuspic regurgitation.

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16
Q

What is the S4 heart sound?

A

S4, or atrial gallop, occurs in late diastole and coincides with contraction of atria. It is generated by the left or right atrium contracting vigorously against stiffened ventricle. It is a sign of decreased compliance due to ventricular hypertrophy or MI.

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17
Q

A cocaine user is exeriencing an MI. Physicians decide not to give a beta-blocker. Why?

A

Beta blockers are not given with cocaine use due to unopposed alpha effects. By blocking presynaptic uptake of norepinephrine and increased release of catecholamines from the adrenal gland, cocaine results in a high degree of adrenergic activity. Beta blockers will isolate these effects to a-receptors amplifying the a-1-agonists activity leading to vascular smooth muscle contraction.

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18
Q

Which beta blockers are nonselective antagonists?

A

Think “N to Z” for “n”onselective: nadolol, pindolol, propranolol, timolol

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19
Q

What is a classic histologic finding of rheumatic fever?

A

It can lead to damage of the heart valves (mitral > aortic&raquo_space; tricuspid). Aschoff bodies (granulomas with giant cells), Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus) are commonly seen. The murmur is usually a late diastolic murmur with delayed rumbling.

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20
Q

Which heart valve is most likely damaged in IV drug users?

A

The tricuspid valve, usually tricuspid regurgitation due to tricuspid endocarditis. This results in a holosystolic, high-pitched blowing murmur. It is enhanced by maneuvers that increase RA return (like inspiration).

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21
Q

What are characteristics of septic shock?

A

Patients generally have high cardiac output and low SVR. The low SVR is due to inflammatory mediators released causing vasodilation, often presenting as flushing of the skin. Cardiac output is generally 4-8 L/min.

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22
Q

Which lipid-lowering agent results in most significant decrease in triglycerides?

A

Fibrates (like gemfibrozil). The are ligands for the peroxisome proliferator-activated receptor-alpha (PPAR-alpha) protein, a receptor that regulates the transcription of genes involved in lipid metabolism. Increase PPAR results in increased expression of LPL on endothelial cells and thus increased clearance of TG-rich lipoproteins. Also has the effect of increasing HDL synthesis.

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23
Q

What is the mechanism of calcium-channel blockers?

A

Amlodipine, nimodipine, nifedipine (dihydropyridine); diltiazem, verapamil (non-DHP) - block voltage-gated Ca++ channels (L-type) of cardiac and smooth muscle, thereby reducing muscle contractility. They close the channels during Phase 2 of the AP. Drugs like verapamil slows conduction through AV node via calcium channel blocking.

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24
Q

What is Kawasaki’s disease?

A

It is an acute necrotizing vasculitis of medium to small muscular arteries, usually affecting children <5 years old. This is the only condition in which you should given children aspirin with a high fever. IV immunoglobins should also be considered. The condition can present with fever, cervical lymphadenitis, conjuctival infection, strawberry tongue, and hand-foot erythema.

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25
Q

What is first line therapy for severe hypertriglyceridemia (increased blood levels of VLDL, TG)?

A

Fibrates and nicotinic acid.

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26
Q

What is secreted by carcinoid tumors?

A

Serotonin. This leads to flushing, watery diarrhea, and right-side valvular lesions. 5-HIAA is a metabolite of serotonin that can be detected in urine. Carcinoid tumors and IV drug use are likely pathology with pathology involving right-sided valves.

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27
Q

What is quinidine?

A

This is a sodium-channel blocker, Class I antiarrythmic. It slows or blocks conduction especially in depolarized cells. It decreased slope of Phase O and increases threshold of firing in abnormal pacemaker cells. Toxicity can cause torsades de pointes.

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28
Q

What is torsades de pointe?

A

It is a polymorpic ventricular tachycardia, characterized by shifting sinusoidal waveforms. Often caused by prolonged QT interval due to drugs, decreased K+, decreased Mg++, and other abnormalities. Treat with magnesium sulfate.

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29
Q

What is the most effective treatment for low HDL cholesterol levels?

A

Niacin is excellent for patients with low HDL (normal is >40 mg/dL for men). Niacin inhibits lipolysis in adipose tissue, reduces hepatix VLDL synthesis. It can cause hyperglycemia (FFA have undergone “rebound” from suppression and TG increase in skeletal muscle –> some lipase breaks this down into diacylglycerol, which activated PKC –> insulin receptors become flooded with serine phosphorylation, which impairs tyrosine phosphorylation, thus limiting the uptake of glucose) and hyperuricemia.

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30
Q

How does amiodarone work and what are potential complications?

A

It is a class III antiarrythmis - K+ channel blocker. It serves to increase AP duration and increase effective refractory period. It can increase QT interval, lead to pulmonary fibrosis, hepatotoxicity, hyper or hypothyroidism, corneal deposits, skin deposits resulting in photodermatitis, neurological effects, constipation, cardivascular effects (bradycardia, heart block, CHF)

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31
Q

What can cause a hypertensive crisis in a patient being treated with depression?

A

Taking an MAOI like tranylcypromine, phenelzine, iscocarboxazid, or selegiline with a food containing tyramine (eg. wine, cheese, chocolate, soy sauce, aged meats). Hypertensive crisis has the following symptoms: headache, disorientation, dilated pupils, tachycardia, and systolic blood pressure >170.

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32
Q

What is polyarteritis nodosa (PAN)?

A

It is characterized by necrotizing immune complex inflammation of medium-sized, muscular arteries. PAN typically is associated with fever, malaise, weight loss, abdominal pain, headache, myalgias, and hypertension. Inflammation of the arterial wall and surrounding connective tissue, resulting from immune complex formation and deposition, is associated with fibrinoid necrosis and leads to loss of elasticity. This fibrinoid necrosis can also lead to transmural inflammation of the arterial wall.

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33
Q

What is the most common cause of subacute bacterial endocarditis?

A

Viridans streptococci. It can be treated with penicillin. It leads to endocarditis commonly affecting the mitral valve. The tricuspid valve is associated with IV drug abuse.

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34
Q

What is the sympathetic effect on dromotropy of the heart?

A

There is a positive dromotropic effect due to increased inward Ca++ current. This is an increase in conduction velocity through the AV node.

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35
Q

What is Kussmaul’s sign?

A

It is a paradoxical rise in JVP on inspiration. It is usually a sign of limited right ventricular filling due to RHF or pericardial effusion (blood cannot enter the RA upon inspiration because of all the fluid surrounding the heart)

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36
Q

What is fibrinoid necrosis?

A

It is amorphous and pink on H&E. Examples are vasculitides (Henoch-Schonlein purpura, Churg-Strauss syndrome), malignant hypertension. It is usually a result of leakage of fibrin from epithelial cells.

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37
Q

An MI presents with ____.

A

ST-segment elevations on ECG. Also substernal chest pain with diaphoresis and dyspnea.

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38
Q

What are the features of type IIa-familial hypercholesterolemia?

A

There is increased blood levels of LDL and cholesterol due to absent or defective LDL receptors. Homozygotes have cholesterol levels over 700. Patients can present with xanthomas (plaques or nodules composed of lipid-laden histiocytes in the skin, especially eyelids). or on the Achiles tendon (tendinous xanthomas). Corneal arcus is also common - opaque ring around iris - it is a lipid deposit in the cornea.

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39
Q

What are the derivatives of each aortic arch?

A

1st - part of maxillary artery (branch of external carotid); 1st arch is maximal
2nd - stapedial artery and hyoid artery, Second = Stapedial
3rd - Common carotid artery and proximal part of the internal carotid artery, “C is the 3rd letter of the alphabet”
4th - on the left, aortic arch; proximal part of right subclavian artery, “4th arch (4 limbs) = systemic”
6th - proximal part of pulmonary arteries and (on left) ductus arteriosus

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40
Q

Where does intermittent claudication normally occur?

A

It usually occurs in arteries particularly where there is high turbulent flow like the iliac, femoral, popliteal, tibial, and peroneal arteries. Calf pain while walking is usually narrowing of popliteal artery. Medical therapy such as antiplatelet drugs may help and revascularization may be left for more severe cases.

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41
Q

What does massaging the carotid sinus do?

A

This stimulates the firing of baroreceptors in the carotid sinus (respond to stretching of the arterial wall - if arterial pressure rises, the walls of these vessels passively expand and the receptors fire). The baroreceptors synapse in the medulla, leading to autonomic changes that leads to decrease in heart rate due to slowed conduction through SA and AV nodes as a result of increased parasympathetic activity.

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42
Q

What drug can cause peaked T waves and prolonged PR intervals?

A

Spironolactone (aldosterone receptor antagonist - aldo normally aids in secretion of K+ and reabsorption of water and Na+). This is a potassium-sparing diuretic that inhibits potassium secretion at the cortical collecting duct leading to hyperkalemia.

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43
Q

What beta blocker used to treat arrythmias prolongs the repolarization phase of the cardiac action potential?

A

Sotelol - an antiarrhythmic with classes II and III properties. As a class III, it prolongs repolarization by blocking outward K+ conductance. This can lead to long QT. Amiodarone is another class III.

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44
Q

What is MPA?

A

It is microscopic polyangiitis. This is a small vessel vasculitis (like Wegener’s). It commonly involves the kidneys, skin, and lungs with pauci-immune glomerulonephritis and palpable purpura. MPO-ANCA/p-ANCA are detectable.

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45
Q

What is a common cause of aortic dissection?

A

HTN, cystic medial necrosis associated with Marfan’s syndrome, which typically causes ascending aortic aneurysms.

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46
Q

What is an aortic dissection?

A

It is a longitudinal intraluminal tear forming a false lumen. It can present with tearing chest pain of sudden onset, radiating to back with markedly unequal BP in arms. CXR shows mediastinal widening.

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47
Q

What heart medication should be (theoretically) avoided in diabetic patients?

A

Beta-blockers like metoprolol because they can mask the effects of hypoglycemia like tachycardia.

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48
Q

What is Beck’s triad and what is it a sign of?

A

It is jugular venous distention, hypotension, and muffled heart sounds which is a sign of tamponade. Patients will often also have pulsus paradoxus.

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49
Q

What is cardiac tamponade and what is the treatment?

A

It is compression of heart by fluid in pericardium, leading to decreased CO. There is an equilibration of diastolic pressure in all 4 chambers. It is treated with a pericardiocentesis.

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50
Q

What is a complication of nitroglycerine withdrawal?

A

It is a vasodilator, so withdrawal can lead to vasoconstriction, which can be unopposed in critical areas such as the coronary vessels, leading to nonatherosclerotic-related ischemia. Toxicity can lead to reflex tachycardia, hypotension, flushing, and headache.

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51
Q

What is cinchonism?

A

It is a pathologic condition caused by an overdose of quinidine of its natural source. Symptoms include flushed or sweaty skin, ringing of ears, blurring of vision.

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52
Q

What is a complication of quninidine and digoxin?

A

Quinidine decreased digoxin clearance and displaces digoxin from tissue-binding sites. This causes dangerous levels of digoxin which can lead to atrial tachycardia with AV block.

53
Q

What is temporal arteritis?

A

It is a large-vessel vasculitis that commonly affects elderly females. It usually presents with unilateral headache and jaw claudication. May lead to irreversible blindness if not treated quickly with corticosteroids. It is also called giant cell (temporal ateritis) and is characterized by granulomatous inflammation.

54
Q

What are the effects of a beta blocker?

A

β-Blockers decrease contractility and heart rate (resulting in decreased oxygen consumption) by inhibiting β-1 receptors in the heart. A decrease in heart rate will then allow more time for diastolic filling (increasing EDV) and systolic ejection (increasing ejection time). In addition, β-blockers will decrease the secretion of renin, thus diminishing the renin-angiotensin cascade.

55
Q

What are the effects of digoxin on ejection fraction and vascular resistance?

A

It increased ejection fraction due to sequestration of calcium due to Na/K pump inhibition. Since cardiac output is increased, there is a decrease in sympathetic activity, which will consequently reduce vascular resistance, resulting in a reduced heart rate.

56
Q

Superficial arch is a continuation of the _____ artery. The deep arch is a continuation of the ____ artery.

A

Ulnar; radial - both ensure collateral flow to hand when the other is occluded

57
Q

What cardiac defect is associated with a continuous, machine-like murmur?

A

Patent ductus arteriosus

58
Q

What type of diuretic results in loss of calcium?

A

Furosemide. The triple transporter is blocked meaning there is not enough K+ back-leak into lumen, which does not create the positive charge gradient to push calcium and magnesium paracellularly to the interstitial/blood space.

59
Q

What is malignant hypertension?

A

This is a hypertensive emergency that happens suddenly and leads to target organ damage. The characteristic vascular lesion is fibrinoid necrosis of arterioles and small arterties, manifesting as end-organ damage. Great than or equal to BP of 180/120.

60
Q

What does malignant hypertension predispose a person to?

A

Thoracic aortic dissection, a sudden tear along the aorta that often presents as pain radiating to the back. They present with not typical MI ECG findings.

61
Q

What is mitral valve prolapse?

A

It presents as a late systolic crescendo murmur with midsystolic click (MC due to sudden tensing of the chordae tendineae). It is when the mitral valve fails to close properly because the leaflets of the mitral valve bulge (prolapse upward) or back into the left atrium as the heart contracts.

62
Q

What is a treatment for dilated cardiomyopathy?

A

Furosemide or another loop diuretic because systolic dysfunction ensues as the heart becomes unable to pump blood, leading to heart failure. Fluid overload can ensue so a loop diuretic can be good for controlling fluid balance.

63
Q

What is a treatment for hypertrophic obstructive cardiomyopathy?

A

It is the hypertrophied septum can become too close to anterior mitral leaflet leading to outflow obstruction and failure of filling. The patient relies heavily on atrial kick for filling. One form of treatment is a beta blocker to reduce the heart rate to increase filling time and reduce myocardial oxygen demand. Calcium channel blockers (non-DHP), like verapamil, are also a good option because they decrease conduction velocity, increase ERP and increase PR interval to allow for filling and increase preload.

64
Q

What is a characteristic of von Hippel-Landau disease?

A

It is an autosomal dominant disorder characterized by abnormal blood vessel growth. The overgrowth of blood vessels leads to angiomas and hemangioblastomas in the retina, brain, and spinal cord. The disease is due to loss of VHL tumor suppressor gene on the short arm of chromosome 3 (3p).

65
Q

What is Kawasaki’s disease?

A

It is a acute necrotizing vasculitis of small and medium sized vessels. It can lead to vasculitic changes in the coronary arteries with subsequent aneurysms and possible MI. It can be treated with aspirin and IV immunoglobulin. It usually presents with fever, conjuctivitis, erythema of oral mucosa, cervical lymphadenopathy, hand-foot erythema, and desquamating rash,

66
Q

What is prolonged with aortic stenosis?

A

Isovolumetric contraction. The aortic valve opens when the ventricular pressure builds up and exceeds that of the aorta, but with aortic stenosis a higher pressure is required which takes longer to generate. It can lead to syncope. Can be due to bicuspic aorta or age-related calcific aortic stenosis.

67
Q

What are the cardiac effects of norepinephrine?

A

It has both alpha and beta receptor agonists activity. It will boost heart rate and contractility while clamping down on peripheral vessels with beta-agonisms to increase PVR. It has alpha-1 (increase vasc. smooth muscle contraction) > alpha-2 (decrease sympathetic outflow) > beta-1 effects (increase HR, contractility, and renin release).

68
Q

What is metoprolol?

A

It is a beta-blocker. It decreases SA and AV nodal activity by decreasing cAMP and Ca++ currents. Suppress abnormal pacemaker cells by decreasing slope of phase 4. AV node is particularly sensitive so it increases PR interval.

69
Q

What are the 3 D’s of B3?

A

Diarrhea, dementia, and dermatitis

70
Q

What does the carotid sinus do?

A

It transmits information via glossopharyngeal nerve to solitary nucleus of medulla (responds to decrease or in crease in stretch due to change in BP via altering efferent sympathetic activity)

71
Q

What does the aortic arch respond to?

A

Only to increase in BP (responds by decreasing sympathetic activity).

72
Q

What is Buerger’s disease?

A

Also known as thromboangiitis obliterans - it is a small to medium vessel vasculitis. The pathophysiology is essentially small-vessel ischemia. Its clinical presentation mimics that of peripheral artery disease (i.e. weak distal pulses). Raynaud’s common due to peripheral nerve ischemia. Smoking cessation is the first-line treatment.

73
Q

What toxicity can occur from digoxin?

A

Digoxin competes with K+ at its binding site on the Na+/K+-ATPase; thus hypokalemia can occur. Antidote for digoxin toxicity is the normalization of K+ and anti-digoxigenin Fab fragments.

74
Q

What is digoxin’s effect on the heart?

A

It increases contractility by making more calcium available for the next contraction. It also increases vagus nerve output, which is parasympathetic (ACh) to decrease heart rate.

75
Q

How does niacin work?

A

It works by reducing hepatic triglyceride synthesis and VLDL secretion and significantly increases HDL cholesterol levels.

76
Q

What does the calcium-calmodulin complex due in smooth muscle?

A

It activates myosin light chain kinase, which serves to phosphorylate myosin light chains. This facilitates cross-bridge formation and smooth muscle contraction.

77
Q

What are cardiac symptoms of Turner’s syndrome?

A

Preductal coarctation of the aorta (discrete narrowing of aorta just distal to left subclavian artery) - presents with difference in systolic pressure between upper and lower extremities, biscuspid aortic valve

78
Q

What virus can cause dilated cardiomyopathy?

A

Coxsackie B virus –> myocarditis

79
Q

What are some signs of CHF?

A

Edema, JVD, elevated B-type natriuretic peptide (highly sensitive for CHF - cardiac neurohormone secreted from ventricles when they are volume overloaded), S3 heart sound. Serum ANP is also increased in LHF because of left atrial dilatation.

80
Q

What is presence of hemosiderin in lungs a sign of?

A

This implies that pulmonary capillaries have ruptured under pressure, and RBCs entered the alveoli and were phagocytosed by alveolar macrophages.

81
Q

Describe a mitral stenosis murmur.

A

It often causes a sharp, high-pitched opening snap during diastole (due to opening of stiffened mitral valve leaflets) followed by a harsh rumbling murmur. The murmur is low pitched and is best hear at the apex. The number one cause of this is a untreated Group A streptococcal pharyngitis –> Rheumatic fever. Mitral stenosis can lead to LA dilation. It is enhanced by maneuvers that increase LA return, like expiration.

82
Q

What are the classic signs of an abdominal aortic aneurysm rupture?

A

Abdominal or back pain, hypotension (from blood spilling into retroperitoneum), lightheadedness, and a pulsatile mass. AAAs affect all layers of the aorta and do not create a false lumen. This needs to be surgically repaired immediately. Atherosclerosis usually weakens the wall and wall stress increases the vessel diameter.

83
Q

What are the clinical presentations of cardiac tamponade?

A

Hypotension, elevated JVP, pulsus paradoxus (drop in systolic blood pressure > 10 mmHg on inspiration) and Kussmaul’s sign (failure of JVP to decrease on inspiration). Typical ECG findings include sinus tachycardia with low QRS voltage; electical alternans is pathognomonic of tamponade.

84
Q

What is Kussmaul’s sign?

A

Failure of JVP to decrease on inspiration. Ordinarilly JVP falls due to decreased intrathoracic pressure due to expansion of thoracic cavity and the increased volume available for right ventricle expansion. This is a sign of RV filling problem due to tamponade or restrictive cardiomyopathy.

85
Q

What is pulsus paradoxus?

A

Drop of more than 10 mmHg of systolic BP during inspiration. During inspiration, since LV filling is lesser relative to that during expiration (pulmonary vessels dilate and fill more with blood so less blood brought to LV), the diastolic dysfunction is also proportionally greater, so the systolic pressure drops >10 mm Hg. This mechanism is also likely with pericarditis, where diastolic function is chastened. Inspiration causes further increase in pressure of blood in RV, displacing the interventricular septum to the left, lowering LV volume, thereby dropping the systolic BP.

86
Q

What diuretic is contraindicated for CHF?

A

Mannitol because it can cause pulmonary edema due to hypernatremia and exacerbate volume expansion.

87
Q

What disease is caused by a deficiency of lysosomal alpha-1,4-glucosidase (Acid maltase)?

A

Pompe disease (Type II) glycogen storage disease. Glycogen is deposited in the myocardium leading to cardiomyopathy, shortened PR interval and large QRS complexes, evidencing biventricular hypertrophy.

88
Q

What is a cardiac complication of SLE?

A

Libman-Sacks endocarditis (LSE). It is a late feature of SLE and is characterized by small, wart-like vegetations comprised of fibrin and inflammatory cells that line either or both surfaces of the valve leaflets. Rarely causes valve dysfunction or embolus.

89
Q

What can a post ductal coarctation of the aorta do to the brain?

A

Increased cerebral blood flow can increase risk of berry aneurysm, which is a saccular dilatation typically found around the circle of Willis and base of the brain.

90
Q

Marfan’s can lead to aortic ____.

A

Regurgitation and dissection.

91
Q

In diastolic heart failure, use caution when prescribing ______ because these may produce volume depletion and decrease CO.

A

Diuretics

92
Q

What is a cause of high-output heart failure?

A

Hyperthyroidism, decrease in blood viscosity (decreased PVR which increases venous return to heart –> anemia), vasodilation of PVR arterioles –> increases venous return to heart, caused by thiamine deficiency which decreases ATP synthesis, and early phase of endotoxic shock (NO release), ateriovenous fistula

93
Q

What is Prinzmetal variant angina?

A

Intermittent coronary artery vasospasm at rest with or without superimposed coronary artery athersclerotic disease. Vasoconstriction may be due to increase in platelet thromboxane A2 origination from thrombus material overlying an atherosclerotic plaque.

94
Q

What does thromboxane A2 do?

A

It is a vasoconstrictor and increases platelet aggregation by increasing expression of the GP IIb/IIIa in membranes of platelets.

95
Q

What is chronic ischemic heart disease?

A

Progressive CHF resulting from long-term ischemic damage to myocardial tissue due to replacement of myocardial tissue with non-contractile scar tissue.

96
Q

What is the sequence for developing an acute MI?

A

1) atheromatous plaque is suddenly disrupted 2) subendothelial collagen and thrombogenic necrotic material are exposed 3) platelets adhere to the exposed material and eventually form an occlusive platelet thrombus

97
Q

What is associated with ST-elevation?

A

Prinzmetal variant angine and acute MI (new Q-waves in ECG).

98
Q

What is the difference between STEMI and non-STEMI?

A

STEMI has ST elevation and Q waves - full thickness of myocardium is involved (transmural). Non-STEMI has no Q waves and involves inner third of myocardium (subendocardium).

99
Q

What is a sign of previously injured cells experiencing reperfusion following MI?

A

Reperfusion of irreversibly damaged cells results in their death and the formation of contraction bands due to entry of Ca++ into the cytosol causing hypercontraction of the myocytes.

100
Q

What is the mechanism of irreversible myocardial injury?

A

Superoxide radicals are locally produced by xanthine oxidase.
Acute inflammation ensures from neutrophils –> occlude capillaries, decrease blood flow, they also increase production of ROS

101
Q

What is a hallmark 3 to 7 days after AMI?

A

Red granulation tissue surrounds the area of infarction. Macrophages begin to remove debris. This is dangerous time for rupture.

102
Q

Why does MI pain radiate to arms and jaw?

A

Heart innervted by T1-T5 (inner arm is T1; epigastrium is T4-T5)

103
Q

What are complications of STEMI AMI?

A

Cardiogenic shock, arrythmias (v fib, VPC most common, heart block), CHF, rupture, mural thrombus

104
Q

What is a mural thrombus?

A

A blood clot in contact with the endocardial lining of cardiac chamber.

105
Q

What is the name of the autoimmune pericarditis that occurs following a STEMI infarction? Autoantibodies are directed against damaged pericardial antigens.

A

Dressler syndrome (relieved by leaning forward). Presents with fever and precordial friction rub,

106
Q

What is the timing of cardiac enzymes post-MI?

A

CK-MB (within 4-8 hours) and troponin (normally regulate calcium-mediated muscle contraction, arrive within 3-12 hours after MI) peak after 24 hours, but CK-MB falls after 3 days, and troponin falls after 7 days. cTnI and cTnT are measured (I and T).

107
Q

Which type of group A strep causes rheumatic fever and valve damage?

A

Step pyogenes but specifically only if in the pharynx because the nephrogenic strain that causes PSGN does not have the M virulence factor that leads to valvular damage.

108
Q

On auscultation, a patient has a three-component, scratchy sound. What is this? How do I differentiate it from something similar?

A

This is pericardial friction rub. It can be differentiated from a pleural friction rub because it does not go away when the patient holds his or her breath.

109
Q

What is the pathophysiology of constrictive pericarditis?

A

There is incomplete filling of the cardiac chambers due to thickening of the parietal pericardium.

110
Q

How does excess Na+ lead to an increased blood pressure?

A

1) it is increases plasma volume which increases stroke volume and leads to increased systolic BP.
2) An increase of sodium in smooth muscle increases calcium-mediated contraction of the muscle, leading to vasoconstriciton of PVR arterioles, which increases diastolic BP.

111
Q

When is a Kussmaul’s sign seen?

A

In conditions where the negative intrathoracic pressure during inspiration is not transmitted to the heart (i.e. the heart is “isolated” from the thorax). This includes constrictive pericarditis, restrictive cardiomyopathy, right atrial or ventricular tumors.

112
Q

What cardiac problem has an irregularly, irregular rhythm with no p waves?

A

Atrial fibrillation - chaotic rhythm from atria from foci in sleeves of atrial muscle extending into pulmonary vein (increased size of atria increases risk - so diseases that increase atrial pressure increase risk of a. fib.)

113
Q

What is Trousseau’s sign?

A

It is a superficial migratory thrombophlebitis due to pancreatic cancer, which causes a hypercoaguable state.

114
Q

What is chronic myeloid leukemia caused by?

A

It it caused by a t(9;22) chromosomal translocation (Philadelphia chromosome). It reuslts in the overproduction of myeloid cells (left-shifted toward more mature forms). BCR-ABL gene results in production of constitutively active tyrosine kinase, which activated pro-growth, pro-survival in granulocytic and megakaryocytic precursor cells.

115
Q

What is MGUS?

A

It is the monoclonal expansion of plasma cells with serum monoclonal protein <10% monoclonal plasma cells. Asymptomatic precursor to multiple myeloma.

116
Q

What is renal osteodystrophy?

A

This is a complication of chronic renal insufficiency. The impaired synthesis of active 1,25-dihydroxycholecalciferol leads to decreased calcium absorption leading to increased PTH, which will increase bone reabsorption and increase phosphate exretion (reduce renal reabsorption).

117
Q

What is PTH function?

A

1) increase bone resorption to increase Ca++ and PO43- (Increases RANK-L, which binds RANK on osteoblasts –> osteoclast stimulation and increased calcium)
2) increase kidney reabsorption of calcium in distal tubule
3) decrease reabsorption of phosphate in the proximal convoluted tubule
4) increase 1,25-(OH)2D3 (calcitriol) production by stimulating kidney 1-alpha-hydroxylase.

118
Q

vWF is a carrier protein for what?

A

VIII - Factor VIII participates in blood coagulation; it is a cofactor for factor IXa which, in the presence of Ca2+ and phospholipids forms a complex that converts factor X to the activated form Xa.

119
Q

What kind of virus is influeza?

A

Single stranded, enveloped, segmental linear virus. IT is an orthomyxovirus.

120
Q

Is prednisone a prodrug?

A

YEs - it is a prodrug of prednisolone. It must be reduced to its active form for its anti-inflammatory effects to occur. 11-Beta-hydroxysteroid dehydrogenase does this.

121
Q

What is DIC?

A

This is acute disseminated intravascular coagulation (DIC) resulting from overwhelming sepsis. It results from activation of the coagulation cascade, which leads to deposition of microthrombi and consumption of platelets, fibrin, and coagulation factors, with subsequent bleeding. The deposition of fibrin in the microcirculation leads to hemolytic anemia as RBCs are fragmented. This condition is known as microangipathic hemolytic anemia, which ic characterized by schistocytes on the peripheral blood smear.

122
Q

What is imatinib mesylate (Gleevec)?

A

It is a tyrosine kinase inhibitor that acts on BCR-ABL.

123
Q

Why is warfarin contraindicated in pregnancy?

A

It can cross the placenta and is teratogenic.

6-9 weeks: associated with nasal and midface hypoplasia and stippled vertebral and femoral epiphyses.

2nd and 3rd trimester: hemorrhage, disharmonic growth and scarring of organs; can lead to optic atrophy, blindness, Dandy-Walker malformation (hypoplasia of the cerebellum), developmental delay

124
Q

What is used to treat vWF?

A

Desmopressin (DDAVP) - it releases vWF stored in endothelium.

125
Q

How does N-acetylcysteine help with cystic fibrosis?

A

It loosens mucus plugs by cleaving disulfide bonds within mucus glycoproteins

126
Q

What is a Factor V Leiden mutation?

A

Production of mutant factor V that is resistant to degradation by activated protein C. Most common cause of inherited hypercoagulability in whites.

127
Q

What disorder is assocaited with a decreased amount of ADAMTS13?

A

Thrombotic thrombocytopenic purpura (TTP) - ADAMTS13 cleaves vWF

128
Q

What is a key differentiation test to decide between B12 and folate deficiency?

A

Methylmalonic acid levels. Although B12 hands a methyl group to homocysteine forming methylmalonic acid, homocystein levels are elevated in both conditions. B12 is a cofactor for conversion of methylmalonic acid to succinyl CoA so a B12 deficiency will lead to increased levels of methylmalonic acid.