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Cardiology Flashcards

1
Q

First pharyngeal arch

A

CN V, maxillary artery

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2
Q

Second pharyngeal arch

A

CN VII, stapedial artery (regresses)

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3
Q

Third pharyngeal arch

A

CN IX, common carotid, prox internal carotid artery

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4
Q

Fourth pharyngeal arch

A

CN X, true aortic arch, subclavian arteries

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5
Q

5th pharyngeal arch

A

Oblitered!

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6
Q

6th pharyngeal arch

A

CN X (recurrent laryngeal), pulmonary arteries, ductus arteriosus

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7
Q

Down syndrome

A

endocardial cushion defects (ostium primum) ASD, regurgitant AV valves

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8
Q

DiGeorge

A

TOF, interrupted AA

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9
Q

Friedreich ataxia

A

Hypertrophic cardiomyopathy

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10
Q

Marfan

A

Cystic medial necrosis (dissection, aneurysm), MV prolapse. Cardiovascular dz most likely cause of death (esp aortic dissection)

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11
Q

Tuberous schlerosis

A

cardiac rhabdomyomas -> valvular obstruction

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12
Q

Turner

A

Aortic coarction, bicuspid valve

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13
Q

Vancomycin MOA, SE

A

blocks glycoprotein polymerization by binding to D-ala, D-ala; redman syndrome, nephrotoxicity

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14
Q

Daptomycin MOA, SE

A

Depolarization of bacterial (cannot penetrate GN bacteria outer cell membrane, is inactivated by lung surfactant); myopathy & CK elevation

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15
Q

Linezolid MOA, SE

A

Inhibit protein synthesis by binding to 50s subunit; thrombocytopenia, optic neuritis, serotonin syndrome

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16
Q

Post-MI: 0-4 hours

A

Minimal change

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17
Q

Post MI: 4-12 hours

A

Early coag necrosis: edema, hemorrhage, wave fibers

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18
Q

Post MI: 12-24 hours

A

Coag necrosis, marginal contraction band necrosis

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19
Q

Post MI: 1-5 days

A

Coag necrosis, PMN infiltrate

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20
Q

Post MI: 5-10 days

A

MO phagocytosis of dead cells

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21
Q

Post MI: 11-14 days

A

Granulation tissue, neovascularization

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22
Q

Post MI: 2 weeks - 2 months

A

Collagen deposition, scar formation

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23
Q

Local amyloid production: cardiac, thyroid, pancreatic islets, cerebrum/cerebral blood vessels, pituitary gland

A

atrial naturietic protein, calcitonin, islet amylin protein (TIID), beta-amyloid protein, prolactin

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24
Q

Systemic amyloid protein

A

IG light chain, esp gamma light chains; associated with MM

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25
Q

Malignancy re: exposure to arsenic, thorotrast, polyvinyl chloride; cells express CD-31 (PECAM-1)

A

Hepatic angiosarcoma from vascular endothelial cells

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26
Q

Familial chylomicronemia syndrome (Type I)

A

Lipoprotein lipase/ApoC-II (cofactor) defect; elevated chylomicrons; pw acute pancreatitis, eruptive skin xanthelomas, HSM, lepemia retinalis

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27
Q

Familial hypercholesterolemia (Type II A)

A

LDL receptor/ApoB-100 defect; elevated LDL; pw premature CAD, corneal acrus, tendon xanthomas, xanthelesmas

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28
Q

Familial dysbetalipoproteinemia

A

ApoE; chylomicrons/LDL; pw premature CAD/PVD, palmar xanthelomas

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29
Q

Familial hypertriglyceridemia

A

ApoA-V; VLDL; pancreatitis, obesity/insulin resistance

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30
Q

Atrial myxoma

A

preference for LA; mid-diastolic rumble; histo: scattered cells w/ mucopolysaccharide stroma; VEGF & IL6

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31
Q

Sx of wide pulse pressure

A

head pounding, head bobbing

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32
Q

m/c cause of AR

A

aortic root dilatation, bicuspid aortic valve

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33
Q

CABG: LAD alone, multile arteries

A

Left internal mammary; great saphenous vein

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34
Q

IVDU endocarditis

A

R-side, TR, Staph A, early systolic murmur accentuated by inspiration

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35
Q

MI healing require what kind of collagen, when?

A

Type I; 2 weeks post-MI

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36
Q

Type II collagen

A

Cartilage, vitreous humor, nucleus pulposus

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37
Q

Type III collagen

A

skin, lung, GI, blood vessels, lympatic, granulomatous tissue

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38
Q

Type IV collagen

A

Basement membrane (Alport)

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39
Q

Niacin SE, mediated by, rx

A

Flushing, prostaglandin, aspirin

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40
Q

Vanc SE, mediated by

A

Redman syndrome, histamine

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41
Q

Capsaicin MoA

A

Decrease pain by decreasing substance P

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42
Q

Digoxin toxicity induced by; rx

A

hypokalemia, hypovolemia, renal failure; anti-digoxin antibody fragments

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43
Q

Heart sound: Loud P2

A

Pulmonary HTN

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44
Q

Post-MI complication days 3-7

A

Rupture LV free wall

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45
Q

TOF/truncus arteriosus/TGV embryology

A

NC cells migrate into truncus arteriosus and bulbar ridges to induce aorticopulmonary septation

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46
Q

Nitroglycerin MoA

A

venodilator of large veins, reduces pre-load and oxygen demand to rx angina pectoris

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47
Q

Arterial baroreceptors: where? nerves?

A

Carotid, glossopharyngeal; aortic arch, vagus nerve

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48
Q

atrial myoxoma pw, histo, cytokines

A

large pedunculated mass on LA with mid diastolic rumble @ apex, SOB w/ sitting up, fever; scattered cells with mucopolysaccharide stroma, abnormal blood vessels, hemorrhage; VEGF (angiogenesis), IL-6 (weight loss, fever)

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49
Q

AR pw, etiology

A

Early diastolic murmur (if severe, holodiastolic) with palpitations, head pounding, head bobbing; aortic root dilatation, bicuspid aortic valve

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50
Q

CABG: vessel source if LAD alone, multiple arteries

A

left internal mammary; great saphenous vein (surgeons access the vein inside femoral triangle)

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51
Q

R-side tricuspid regurgitation moa, pw

A

IV drug use, staph endocarditis; early systolic, accentuated by inspiration

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52
Q

Vertebral levels at which IVC branches into renal veins, common iliac veins

A

L1/L2, L4

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53
Q

MI healing culminates in what type of collagen? how long does deposition last?

A

type I collagen, 1 week - 2 months

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54
Q

niacin-induced flushing mediated by what molecule? rx with what drug?

A

prostaglandin; aspirin

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55
Q

Digoxin toxicity induced by what situations?

A

hypokalemia, hypoveolemia, renal failure

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56
Q

Digoxin toxicity pw, rx

A

nonspecific GI (anorexia, N/V), neuro (confusion, fatigue, weakness, color vision change), arrhythmia (most dangerous); rx with anti-digoxin antibody fragments

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57
Q

constrictive pericarditis moa, pw

A

thick, fibrous tissue in percardial space that restricts ventricular filling during diastole, reduces CO, and causes RHF (kussmaul sign: JVP increases with inspiration); pw pulsus paradoxicus, pericardial knock, increased JVP

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58
Q

constrictive pericarditis etiologies

A

idiopathic, viral, cardiac surgery/radiation, tuberculosis

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59
Q

heart sounds: loud P2

A

pulmonary HTN

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60
Q

heart sounds: S3

A

dilated ventriclesdecreased ventricular wall compliance (intrinsic in restrictive cardiomyopathy, extrinsic in constrictive cardiomyopathy)

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61
Q

pulsus paradoxicus moa

A

during inspiration, increased systemic venous return; but if pericardium cannot expand (2/2 tamponade, constrictive/restrictive pericarditis, severe obstructive lung dz), then RV pushes into LV and CO/BP decreases

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62
Q

Post-MI rupture of LV free wall moa

A

days 3-7 after coagulative necrosis, PMN infiltration, and enzymatic lysis of connective tissue reduces stability

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63
Q

Asthma: beta-agonist, steroid moa

A

Stimulated beta-2 adrenergic receptor on lungs, stimulation of Gs receptor leads to increased activation of AC and increased cAMP; steroids impair eosinophilic degranulation

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64
Q

Recent respiratory illness may lead to what heart condition?

A

serous viral pericarditis, significant acute pericardial effusion, and tamponade

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65
Q

rheumatic heart dz most commonly affects what valve?

A

MV (but can affect both MV and AV in a quarter of cases)

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66
Q

tetrology of fallot pw and development

A

most common cause of cyanotic congenital heart disease (may not present in neonate if pulmonary stenosis is mild); in beginning, VSD allows L to R shut, thus infrequent cyanotic episodes; however, over time pulmonary HTN develops and R to L shunt leads to frequent cyanotic episodes

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67
Q

ToF, truncus arteriosis, TGV developmental misfortune

A

aorticopulmonary septation requires NC cells to migrate into truncal (truncus arteriosis) and bulbar ridges (bulbus cordis) in order to grow into the aorta and pulmonary artery; failure of this process

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68
Q

main myocardial energy source:

A

FA oxidation (60%), but FA oxidation requires more O2, produces more ATP, thus shift of FA to glucose oxidation can improve stable angina

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69
Q

longer QT means highe rrisk of torsades; which anti-arrhythmic, thought it increases QT interval, does not increase risk of torsades?

A

amiodarone

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70
Q

adenosine moa

A

binds to A1 receptors on cardiac cells and activates K+ channels and increases K+ clearance; results in transient conduction delay through AV and briefly treats SVT

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71
Q

nitrate limitation on use

A

around-the-clock administration results in tolerance; thus give nitrate-free interval at night

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72
Q

statins 2 moa, main se

A
  1. lower cholesterol, 2. stabilize atheromatous plaque (decrease chance of second MIA); risk of myositis (increased CK), myalgias (normal CK)
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73
Q

statin risk of myositis increases with which drugs?

A

niacin, fibrates

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74
Q

persistent lymphadema increases risk of what disease?

A

lymphangiosarcoma, rare malignancy of the endothelial lining of lymph system

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75
Q

cavernous hemangioma

A

benigh neoplasm of small blood endothelial cells

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76
Q

carvernous lympangioma

A

network of endothelium lined lymph spaces below epidermis

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77
Q

cystic hygroma

A

cavernous lympangioma + absence of luminla blood cells, common in H&N, turner’s syndrome

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78
Q

pyogenic granuloma

A

capillary form of cappilary hemangioma, exophitic red nodules attached by stalk to oral mucucosa and skin;

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79
Q

MS-related enlargement impinges on what nerve and causes what symptom?

A

L recurrent laryngeal nerve, hoarseness

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80
Q

PDA associated with what congenital dz?

A

rubella

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81
Q

ventricular septal defect associated with what pregnancy condition?

A

fetal alcohol syndrome

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82
Q

MVP increases or decreases with squatting?

A

decreases. squatting increases preload and PVR; thus it increases LV volume. this returns leaves to normal arrangement (in MVP, mitral redundancy occurs 2/2 elongation, overlap of leaflets).

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83
Q

native valve bacterial endocarditis (NVBE): most common etiology

A

MVP among 15-60 yo americans; upon which plt and fibrin deposit and is colonized by bacteria

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84
Q

nitroglycerin moa

A

converts to NO at vascular SM cell membrane; NO converts GTP to cGMP; increased cGMP decreases Ca in cytosol, which decreases activity of myosin LC kinase, myosin LC dephosphorylase; muscle relaxation

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85
Q

congenital QT prolongation: responsible mutation

A

K+ channel protein

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86
Q

After contraction, how does myocyte achieve Ca efflux?

A

Ca-ATPase (SR) and Na/Ca exchange mechanism (plasma membrane)

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87
Q

cystic medial degeneration moa, histology

A

myxomatous changes in the media of large arteries; fragmentation of elastic tissue (“basket weave”), separation of elastic/fibromuscular componenets that produce small cleft-like spots with amorphous ECM filling

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88
Q

lysyl oxidase fxn, required cofactor

A

cross-link collagen fibers, elastin; copper (Menkes)

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89
Q

organ susceptibility to infarction

A

CNS (5 min), myocardium (20-30 min), kidney (30 min), spleen, liver (less likely 2/2 dual blood supply, unless transplanted)

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90
Q

Class I anti-arrhythmic: binding strength to Na channel

A

1C>1A>1B

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91
Q

Anti-arrhythmic medication for ischemia-induced ventricular arrhythmias

A

1B (lidocaine, mexiletine, tocainide) as dissociation is rapid with minimal cumulative effective

92
Q

ANP fxn

A
  1. kidney (increase diuresis); 2. adrenal gland (increase naturesis by inhibiting aldosterone secretion); 3. blood vessels (vasodilation)
93
Q

Veramapil fxn, SE, c/i

A

rate control for A-fib with RVR; negative ionotrope (helpful for angina, HTN); bradycardia, AV block, constipation; CHF pt (2/2 negative ionotropic effect)

94
Q

Which statin is not metabolized by P-450 system?

A

pravastatin

95
Q

P-450 inducers

A

phenytoin, phenobarbitol, rifampin, griseofulvin, carbamazapine

96
Q

P-450 inhibitors

A

macrolides (erythromycin/clarithromycin) , ketoconazole, isoniazid, cipro, grapefruit

97
Q

turner’s syndrome: unusual findings

A

cystic hygroma (located in neck, cystic spaces rich in lymphoid tissue); aortic co-arction

98
Q

atherosclerotic plaques, likely locations

A

aorta > coronary arteries > popliteal > internal carotid > circle of willis

99
Q

muscular/elastic arteries

A

coronary, poplitleal/ aorta, carotid, iliac

100
Q

hypertrophic cardiomyopathy mutation

A

AD mutations of sarcomere protein leads to deficiency in force generation

101
Q

what is unique about staph a in infectious endocarditis?

A

sports a surface adhesion molecule that can invade intact valvular endothelium; thus, can affect pts without pre-existing valvular dz

102
Q

embryology: vein development (vitilline, umbilical, cardinal)

A

vitilline - portal veins; umbilitcal veins - degenerate; and cardinal - systemic veins

103
Q

furosemide moa, effect on K, Ca

A

at ascending limb, loop diuretic that blocks Na/K/2Cl symporter; decreases K, Ca

104
Q

thiazide moa, effect on K, Ca

A

at distal tubule, blocks Na/Cl symporter; decreases K, increases Ca

105
Q

amiloride moa, effect on K

A

block ENaC, at apical membrane of principal cells K sparing

106
Q

primary pulmonary HTN

A

medial hypertrophy of arteries/arterioles, concentric laminar intimal fibrosis that reduces lumina

107
Q

most common cause of cor pulmonale

A

COPD-related obliteration of segments of pulmonary vasculature

108
Q

intimal injury 2/2 athersclerosis: key cytokines in reactive intimal hyperplasia

A

PDGH: encourage SMC migration, proliferation; VCAM: adherence of monocytes/lymphocytes

109
Q

syndenham chorea moa

A

anti-strep antibodies cross-react w basal ganglia

110
Q

TGA: moa, aorta position relative to pulmonary artery

A

failure of aorticopulmonary septum to spiral normally; aorta lying anterior to (normally posterior)

111
Q

Gq pathway

A

activates phospholipase C, degrades membrane lipids into DAG (activate protein kinase C) or IP3 (release Ca from SR)

112
Q

nitroprusside SE, rx

A

cyanide poisoning (altered mental status, lactic acidosis); rx with Na thiosulfate, which adds sulfate to liver rhodonase to help with metabolism

113
Q

ebstein’s anomaly: what is it, what causes it

A

apical displacement of tricuspid valve, decreased RV volume, atrialization of RV; lithium

114
Q

nitroglycerin + sildenafil

A

hypotension

115
Q

milrinone moa

A

phosphodiesterase isoenzyme 3 inhibitor, increases conductance of Ca channels on SR at the heart; at the periphery, can lead to vasodilation so don’t use in hypotensive patient

116
Q

ACE-I and bilateral renal artery stenosis

A

do not use ACE-I - can limit efferent arteriole constriction to maintain renal artery perfusion

117
Q

aortic coarctation adults vs children

A

adults: stenosis is post-PDA; children: pre-PDA

118
Q

pritzmetal angina: dx

A

ergonavine (ergot alkaloid that acts via alpha-adrenergic receptor to induce vascular smooth muscle constriction )

119
Q

carcinoid heart dz: moa, why limited to R side?

A

fibrous intinal thickening and endocardial plaques; limited to R-heart because serotonin and bradykinin inactivated by pulmonary vascular endothelial monoamine oxidase

120
Q

hemosiderin-laden MO in alveoli: histo, how to differentiate with lipofuschin (age-related byproducts of lipid oxidation)

A

golden-yellow/brownish cytoplasmic capsule; prussian blue stain (blue=hemosiderin)

121
Q

normal aging and effect on heart macro/micro appearance

A

macro: decreased LV size 2/2 ventricular septum becoming sigmoidal; micro: increased interstitial CT with concomitant amyloid deposition (w/i myocites, progressive accumulation of lipofuscin)

122
Q

PDA more likely with

A

prematurity, rubella

123
Q

functional heart murmur

A

2/2 acute hemodynamic change

124
Q

VSD: heart sound, pulse ox finding

A

loud, holosystolic murmur over LLSB with Sp02 difference between RA and RV

125
Q

class III anti-arrhythmics

A

amiodarone, ibutilide, dofetilide, sotalol

126
Q

dopamine low, medium, high dose effect

A

low: kidney (increased GFR, Na excretion); med: cardiac (increased contractility, SBP, pulse pressure via beta-1); high: vasculature (increased SVP, decreased CO 2/2 alpha-1 )

127
Q

epi/phenylephrine difference

A

phenyl: pure alpha-1 (vasoconstriction, decreased HR); epi: added beta effect (increased SBP, decreased DBP, increased HR, increased contractility)

128
Q

likelihood of plaque rupture is associated with

A

mechanical strength of overlying fibrous cap

129
Q

cellular sign of irreversible cardiac injury

A

mitochondrial vacuolization: myofibril relaxation, polysome disaggregation, TG droplet accumulation

130
Q

niacin SE

A

vasodilation (decrease HTN meds), insulin resistance (increase DM meds), increase uric acid (careful in gout)

131
Q

digoxin deadly SE

A

AV block, ventricular tachyarrhythmias

132
Q

digoxin electrolyte SE that reflects serum toxicity

A

hyperkalemia

133
Q

class III antiarrhythmic with beta-adrenergic blocking abilityes and QT prolongation

A

sotalol

134
Q

verapamil vs diltiazam

A

more cardioselective

135
Q

TGF-beta

A

arrest of cell cycle, angiogenesis, stimulation of fibroblasts to lay down ECM

136
Q

hypertrophic cardiomyopathy histo findings

A

myocyte hypertrophy, haphazard arranged myocyte and myocyte bundles and fibrosis in interstitial spaces

137
Q

thiamine deficiency leads to what cardiac outcome

A

wet beriberi leads to DCM

138
Q

acute rheumatic fever pw

A

pericarditis: weak heart sound, increased HR, pericardial friction rub, arrhythmias; myocarditis: dilatoin, MR and acute heart failure; chronic ARF: MS

139
Q

aortic rupture occurs most often at what location?

A

isthmus, tethered by ligamentum arteriosum, relatively fixed/immobile place

140
Q

BB overdose rx

A

glucagon (increased cAMP, Ca, independent of adrenergic receptors)

141
Q

PE prefers what lobes?

A

lower lobes

142
Q

isoprotenolol

A

nonselective beta agonst (beta 1: increased contractility, beta 2: vasodilation)

143
Q

labetolol moa

A

combined alpha, beta blocker (beta 1 blocker: decreased contraction; beta2 blocker/alpha1 blocker: decreased SVR)

144
Q

fenoldopam moa, function

A

rx for HTN emergencies, esp in pt with renal insufficiency; selective DA-1 agonist: at periphery, decreases blood pressure and at kidney, increases renal blood flow)

145
Q

NE in peripheral vein causes what, and how to you reverse

A

extravation can cause vasoconstriction, induration/pallor of tissue; prevent with alpha-1 antagonist like phentolamine

146
Q

congenital QT prolongation: two kinds

A

jervell and lange-nelson (AR) with neurosensory deficiency; romano-ward (AD) no deafness

147
Q

congenital DCM moa

A

cardiac cell cytoskeleton (problem with force transfer) and mitchondrial enzymes of oxidative phosphorylation (problem of force generation)

148
Q

spontaneous intracranial hemorrhage: m/c etiology

A

AVM, ruptured aneurysm, cocaine

149
Q

What’s the basis of association between cerebral aneurysm and coarction of aorta?

A

HTN means more likely to rupture

150
Q

hallmarks of lightning strike

A

lichtenburg figures (fern-leaf pattern erythema) + second degree burns; most common reason for death is arrhythmias, respiratory failure

151
Q

acute pericarditis most common causes

A

MI, rheumatic fever, uremia, viral

152
Q

embryo: truncus arteriosus

A

ascending aorta, pulmonary trunk

153
Q

embryo: bulbus cordis

A

smooth part of L/R ventricles

154
Q

embryo: primitive atrium

A

trabeculated part of L/R atria

155
Q

embryo: primitive ventricle:

A

trabeculted part of L/R ventricles

156
Q

embryo: primitive pulmonary vein

A

smooth part of left atrium

157
Q

embryo: right horn of sinus venosus

A

smooth part of right eatrium

158
Q

embryo: left horm of sinus venosus

A

coronary sinus

159
Q

embryo: right common cardinal vein and right anterior cardinal vein

A

SVC

160
Q

Defect in L/R dynein (Kartagener’s) affects what organ and what time in development?

A

looping of the primary heart tube at week 4

161
Q

PFO moa

A

failure of septum primum and septum secundum to fuse

162
Q

VSD moa

A

membranous septum

163
Q

sequence of fetal erythropoiesis organs

A

yolk sac, liver, spleen, bone marrow

164
Q

allantois/urachus

A

median umbilical ligament

165
Q

foramen ovale

A

fossa ovalis

166
Q

notocord

A

nucleus pulposus

167
Q

umbilical arteries

A

medial umbilical ligaments

168
Q

umbilical vein

A

ligamentum teres hepatis (in falciform ligament)

169
Q

coronary blood flow peaks during

A

early diastole

170
Q

arterioles provide most of; veins provide most of

A

TPR, blood storage capacity

171
Q

organ remove has what effect on TPR and CO?

A

increase TPR and decrease CO

172
Q

speed of conduction

A

purkinje > atria > ventricles > AV node

173
Q

pacemaker pace

A

SA > AV > bundle of his/purkinje/ventricles

174
Q

ABCDE of drugs that induce long QT

A

anti Arrhythmics (IA, III), antiBiotics (macrolides), anti Cychotics (e.g. haloperidol); anti-Depressants (TCA); antiEmetics (ondansetron)

175
Q

rx for torsades

A

give magnesium sulfate

176
Q

brugada syndrome

A

AD d/o of asian males, ECG shows pseudo-RBB with ST elevation in V1-V3; increased risk of ventricular tachyarrhythmias and SCD; preven with implantable cardioverter-defibrillator

177
Q

WPW anatomic cause, pw, complication

A

abnormal fast accessory conduction pathway (bundle of Kent); delta wave, widened QRS, shortened PR; supraventricular tachycardia

178
Q

lyme dz heart problemz

A

3rd degree heart block

179
Q

BNP and ANP difference

A

BNP has longer half life

180
Q

hypoxia: pulmonary vs systemic reaction

A

vasoconstriction (to move blood to well-perfused areas), vasodilation

181
Q

ApoB-48

A

mediates chylomicron secretion (chylomicron)

182
Q

ApoB-100

A

binds LDL receptor (VLDL, IDL, LDL)

183
Q

ApoC-II

A

lipoprotein lipase cofactor (VLDL, chylomicron)

184
Q

ApoA-I

A

activates LCAT (HDL, chylomicron)

185
Q

ApoE

A

mediates remnant uptake (all but LDL)

186
Q

dystrophic calfcification

A

hallmark of cell injury and necrosis; m/c in age/damaged cardiac valve or atheromatous plaques; pw fine, gritty white clumps with dark purple, sharp-edged granules on H&E

187
Q

dofetelide moa

A

class 3 (K+ blocking in cardiac myocytes in phase 3)

188
Q

ARF: aschoff bodies

A

interstitial granulomas in cardiac cells

189
Q

ARF: anotschkov cells

A

macrophages with abundant cytoplasm and central nucleus that become aschoff giant cells

190
Q

prostacycline synthesized by, role, disease

A

synthesized in capillary endothelium by prostacyclin synthase; maintain capillary patency by promoting vasodilation and inhibiting platelet adhesion; damaged endothelial cells can’t synthesized PG so increased risk of thrombus formation

191
Q

beta-1 antagonist moa

A

receptors on cardiac and renal tissue (JG cells) that blocks catecholamine-induced renin release and inhibits RAS

192
Q

digoxin moa

A
  1. slow depolarization and increase diastolic filling time; 2. reduced Na influx slows Ca efflux, thus allowing more Ca inside
193
Q

Class 1C and Class III different effect on QT duration

A

1C prolong QRS more with high HR (“use dependence”); III prlonged more with low HR (“reverse use dependence”)

194
Q

phentolamine moa

A

reversible, competitive non-specific alpha-antagonist used in catacholamine induced HTN crisis (pheo, MAOI crisis, cocaine)

195
Q

phenoxybenzamine moa

A

irreversible non-specific alpha antagonist, used in pheo

196
Q

very important difference between epi and NE

A

epi has more beta-2 effect than NE

197
Q

hydralazine/minoxidal moa, SE

A

direct arterial vasodliators; tachycardia and edema

198
Q

ulcertaed atherosclerotic plaque with partially obstructive thrombus leads to what conditions

A

UA, subendocardial MI, and sudden death

199
Q

ruptured plaque with fully obstructed thrombus

A

transmural MI

200
Q

Post-catheterization atheroembolic dz presents with

A

renal failure, toe gangrene, livedo reticularis; light microscopy showing cholesterol emboli obstructing renal arterioles

201
Q

cilostazol 2 moa

A

decreased plt phosphodiesterase, increase cAMP, reduce plt aggregation; direct arterial vasodilator

202
Q

churg-strauss moa

A

antibodies against PMN myeloperoxidase (p-ANCA); pw adult-onset asthma, eosinophilia, atopia, neuropathy

203
Q

plt dysfunction

A

increased bleeding time, mucocutaneous bleeding

204
Q

intrinsic/extrinsic coagulation pathway measured by

A

aPTT; PT

205
Q

during exercise, what changes occur? what does not change? why?

A

increased CO, venous constriction, arterial constriction (all but muscles); MAP does not change; decreased SVR 2/2 vasodilation of muscle arterioles

206
Q

myocardial “hibernation”

A

reduced metabolism 2/2 persistant hypoperfusion or reptitive ischemia

207
Q

ventricular tachycardia: preferred treatment

A

amiodarone

208
Q

drug-inced SLE

A

hyralazine, procainimide, isoniazide; positive ANA, anti-smith; negative dsDNA

209
Q

HCM: obstruction etiology

A

abnormal systolic anterior motion of the anterior leaflet of MV toward hypertrophied interventricular septum

210
Q

CXR findings of CHF

A

cardiomegaly, pleural effusion, kerley B lines (edema of intralobular septa)

211
Q

NBTE etiology, pw

A

hypercoagulable state (2/2 pro-coagulant mucin of mucinous adenoma of pancreas/lungs); small, sterile, nondestructive fibrinous vegetations along the closure lines of cusps (bland thrombus without inflammation or valvular damage); if cancer-related, called “morantic”

212
Q

Silly reason to get secondary pulmonary HTN

A

extended consumption of appetite suppresants like fenfluramine, phentemine

213
Q

most common cause of death in MI patient pre-hospital, in-hospital

A

cardiac arrhythmia, ventricular failure

214
Q

coagulase-negative staphlococcal infection of prosthetic valve is most likely what bacteria, and what is the rx?

A

S. epidermidis (polysaccharide slime); vanc with rifamin or gent

215
Q

digeorge syndrome

A

maldevelopment of third/fourth branchial pouches 2/2 deletion on chromosome 22

216
Q

precapillary spincters sensitive to

A

epi, NE; histamine, low Ox

217
Q

AV block: origin of conduction

A

AV node

218
Q

nitroprusside effect

A

balanced venous/arterial vasodilator

219
Q

AVM effect on preload and afterload

A

increase preload, decrease afterload

220
Q

eruptive skin xanthomas

A

hypertriglyceridemia

221
Q

tendon xanthomas/xanthelasmas

A

hypercholesterolemia

222
Q

thromboangiitis obliterans (buerger’s dz)

A

vasulitis of medium/smal arteries (tibial, radial); acute/chronic inflammation of arterial walls, thrombosis of lumen with recanalization; segmental, and fibrosis extends into contiguous veins and nerves

223
Q

polyarteritis nodosa

A

transmural inflammatoin of the arterial wall

224
Q

noncyanotic congenital heart defect

A

ASD, VSD, PDA, coarctation

225
Q

within 60 seconds of the onset of total ischemia

A

loss of cardiomycocyte contractility

226
Q

NO mechanism

A

stimulate GC, increase cGMP, decrease Ca, decrease myosin LC kinase, myosin LC dephosphorylation and smooth muscle relaxation

227
Q

constrictive pericarditis: chronic or acute

A

chronic process

step 1 (17 decks)

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