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FA > Cardio > Flashcards

Cardio Flashcards

1
Q

what does the truncus arteriosus give rise to

A

ascending aorta and pulmonary trunk

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2
Q

what does the bulbus cordis give rise to

A

smooth parts (outflow tract) of LV and RV

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3
Q

what does the primitive ventricle give rise to

A

trabeculated LV and RV

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4
Q

what does the primitive atria give rise to

A

trabeculated LA and RA

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5
Q

what does the left horn of sinus venosus (SV) give rise to

A

coronary sinus

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6
Q

what does the right horn of SV give rise to

A

smooth part of right atrium

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7
Q

what does the right common cardinal v.and right anterior cardinal v. give rise to

A

SVC

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8
Q

fetal erythropoiesis in yolk sac

A

3-10 weeks

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9
Q

fetal erythropoiesis in liver

A

6 weeks - birth

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10
Q

fetal erythropoiesis in spleen

A

15-30 weeks

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11
Q

fetal erythropoiesis in bone marrow

A

22 weeks - adult

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12
Q

fetal hemoglobin

A

alpha 2 gamma 2

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13
Q

adult hemoglobin

A

alpha 2 beta 2

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14
Q

umbilical vein

A

ligamentum teres heptatitis - falciform ligament

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15
Q

umbilical arteries

A

medial umbilical ligaments

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16
Q

ductus arteriosus

A

ligamentum arteriosum

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17
Q

ductus venosus

A

ligamentum venosum

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18
Q

foramen ovale

A

fossa ovalis

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19
Q

allantois

A

urachus - median umbilical ligament

urachus - allantoic duct (bladder-umbilicus)

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20
Q

allantois remnant

A

urachal sinus/cyst

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21
Q

notochord

A

nucleus pulposus of IV disc

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22
Q

most common site of coronary a. occlusion

A

LAD

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23
Q

what supplied SA and AV node

A

RCA

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24
Q

what determines heart domination

A

posterior descending/interventricular a.

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25
Q

when do coronary a. fill

A

diastole

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26
Q

most posteiror part of heart?

A

LA

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27
Q

LA enlargements

A

compress esophagus –> dysphagia

compress L. recurrent laryngeal n. (vagus) –> hoarseness

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28
Q

what to listen to at aortic area

A

systolic murmur - aortic stenosis, flow murmur, aortic valve stenosis

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29
Q

what to listen to at left sternal border

A

diastolic murmur - aortic and pulmonic regurg

systolic murmur - hypertrophic cardiomyopathy

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30
Q

what to listen to at pulmonic area

A

systolic ejection murmur - pulmonic stenosis, flow murmur (ASD, PDA)

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31
Q

what to listen to at tricuspid area

A

pansystolic murmur - tricuspid regurgitation, VSD

diastolic murmur - tricuspid stenosis, ASD

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32
Q

what to listen to at mitral area

A

systolic murmur - mitral regurg

diastolic murmur - mitral stenosis

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33
Q

where to listen to a PDA and what it sounds like

A

left infraclavicular region - machine-like murmur

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34
Q

inspiration effect –>

A

RILE

increase intensity right heard sounds

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35
Q

expiration effect –>

A

RILE

increase intensity left heart sounds

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36
Q

what does handgrip cause

A

increase systemic vascular resistance

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37
Q

hand grip effect –>

A

increase intensity MR, AR< VSD murmurs
decrease intensity AS, hypertrophic cardiomyopathy mumurs
MVP - increase murmur intesnity - later onset of click/murmur

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38
Q

what does valsava cause

A

decrease venous return

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39
Q

valsava effect –>

A

decrease intensity of most murmurs
increase intensity of hypertrophic cardiomyopathy mumurs
MVP - decrease murmur intensity - earlier onset click/murmur

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40
Q

what does rapid squatting cause

A

increase venous return, increase preload, increase afterload with PROLONGED squatting

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41
Q

rapid squatting effect –>

A

decrease intensity of hypertrophic cardiomyopathy mumurs

MVP - increase murmur intensity, later onset click/murmur

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42
Q

what are the systolic heart sounds

A

aortic/pulm stenosis, mitral/tricuspid regurg, VSD

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43
Q

what are the diastolic heart sounds

A

aortic/pulm regurg, mitral/tricuspid stenosis

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44
Q

holosystolic high pitched blowing murmur

A

MR/TR

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45
Q

crescendo-decrescendo systolic ejection murmur following ejection click

A

AS

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46
Q

holosystolic, harsh-sounding murmur

A

VSD

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47
Q

late systolic crescendo murmur with midsystolic click

A

MVP

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48
Q

immediate high-pitched blowing diastolic decrescendo murmur

A

AR

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49
Q

follows opening snap –> delayed rumbling late diastolic murmur

A

MS

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50
Q

continuous machine-like murmur

A

PDA

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51
Q

what enhances MR

A

increase TPR (squat/hand grip) or LA return (expiration)

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52
Q

what enhances TR

A

increase RA return (inspiration)

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53
Q

where is MR the loudest and where does it radiate

A

apex –> radiates to axilla

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54
Q

what causes MR

A

ischemic heart disease, MVP, or LV dilation

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55
Q

where is TR the loudest and where does it radiate

A

tricuspid area –> radiates to right sternal border

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56
Q

what causes TR

A

RV dilation

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57
Q

what can can either MR or TR

A

rheumatic fever and infective endocarditis

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58
Q

what causes ejection click in AS

A

abrupt halting of valve leaflets

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59
Q

AS

A

LV > aortic P in systole

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60
Q

where does AS radiate

A

carotids

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61
Q

pulsus parvus et tardus

A

AS - pulses are weak with a delayed peak

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62
Q

what can AS lead to

A

SAD - syncope, angina, and dyspnea on exertion

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63
Q

AS cause

A

age-related calcific aortic stenosis or bicuspid aortic valve - WEAR AND TEAR

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64
Q

where is VSD the loudest

A

tricuspid area

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65
Q

what accentuates VSD

A

hand grip manuever –> increased afterload

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66
Q

what causes midsystolic click in MVP

A

sudden tensing of chordae tendinae (parachute)

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67
Q

what is the most freq valvular lesion

A

MVP

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68
Q

where is MVP best heard

A

apex

loudest just before S2

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69
Q

MVP

A

benign and can predispose to infective endocarditis

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70
Q

what can cause MVP

A

myxomatous degeneration, RF, or chordae rupture

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71
Q

what does MVP occur earlier with

A

manuevers that decrease venous return - standing or valsava

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72
Q

AR

A

chronic - wide pulse pressure (hyperdynamic circulation)

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73
Q

can present with bounding pulses and head bobbing

A

AR

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74
Q

what causes AR

A

aortic root dilation, bicuspid aortic valve, endocarditis, or RF

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75
Q

what increases AR murmur

A

hand grip

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76
Q

what decreases intensity of AR murmur

A

vasodilators

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77
Q

what causes opening snap in MS

A

abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips

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78
Q

MS

A

LA > LV pressure during diastole

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79
Q

what does MS often occur secondary to

A

rheumatic fever

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80
Q

chronic MS presentation

A

LA dilation

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81
Q

what enhances MS

A

manuevers that increase LA return (expiration)

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82
Q

where is PDA the loudest

A

S2

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83
Q

what causes PDA

A

congenital rubella or prematurity

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84
Q

what is best heard at left infraclavicular area

A

PDA

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85
Q

continuous machine-like murmur

A

PDA

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86
Q

what causes R –> L shunts

A

**early cyanosis - blue babies

Tetralogy of Fallot, Transposition, Truncus arteriosus, Tricuspid atresia, TAPVR (total anomalous pulm venous return)

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87
Q

what causes L –> R shunts

A

**late cyanosis - blue kids

VSD > ASD > PDA

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88
Q

what is the most common cause of early cyanosis

A

tetralogy of fallot

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89
Q

what do most patients with persistent truncus arteriosus have

A

VSD

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90
Q

hypoplastic RV

A

tricuspid atresia

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91
Q

what is the most common congenital cardiac anomaly

A

VSD

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92
Q

flixed splitting S2

A

ASD

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93
Q

how do you close PDA

A

indomethacin - decrease prostaglandins (PGE - keeeeps PDA open)

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94
Q

fetal alcohol syndrome

A

VSD

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95
Q

what does eisenmergers syndrome cause

A

late cyanosis, clubbing + polycythemia

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96
Q

what does tetralogy of fallot consist of

A

PROVe - pulmonary infundibular stenosis, RVH, overriding aorta, VSD

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97
Q

what is the most important determinant for tetralogy of fallot prognosis

A

pulmonary infundibular stenosis

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98
Q

boot shaped heart on xray

A

tetralogy of fallot

99
Q

maternal diabetes

A

D-transpition of great vessels

100
Q

infantile coarctation of aorta

A

proximal to insertion of PDA

101
Q

adult coarctation of aorta

A

distal to ligamentum arteriosum

102
Q

turners syndrome

A

infantile coarctation of aorta

103
Q

adult coarctation of aorta sx

A

collateral circulation –> notching of ribs

UE - hypertension, LE - weak pulses

104
Q

22q11 syndromes

A

truncus arteriosus, tetralogy of fallot

105
Q

Down syndrome

A

ASD, VSD, AV septal defect (endocardial cushion defect)

106
Q

congenital rubella

A

septal defects, PDA, pulmonary artery stenosis

107
Q

turner syndrome

A

coarctation of aorta (preductal)

108
Q

marfans syndrome

A

aortic insufficiency + dissection (late complication)

109
Q

infant of diabetic mother

A

transposition of great-vessels

110
Q

definition of HTN

A

> 140/90

111
Q

definition of malignant HT

A

> 180/120

112
Q

calcification in media of a.

A

monckeberg arteriosclerosis

113
Q

fibrous plaques/atheromas in intima of a.

A

atherosclerosis

114
Q

where do you see hyaline arteriolosclerosis

A

essential HTN and diabetes mellitus

***HYALINE = PINK

115
Q

onion skinning in malignant HTN

A

hyperplastic arteriolosclerosis

116
Q

incidental finding on mammogram

A

monckeberg arteriosclerosis

117
Q

foam cells + fatty streaks

A

atherosclerosis

118
Q

coronary a. occlusion order

A

LAD > RCA > circumflex

119
Q

gold standard during first 6 hours of MI

A

ECG

120
Q

MI dx

A

troponin I

121
Q

MI reinfarction dx

A

CK-MB

122
Q

transmural infarct

A

increase necrosis

affects entire wall

123
Q

subendocardial infarcts

A

ischemic necrosis < 50% of ventricle wall

subendocardium espec. vulnerable to ischemia

124
Q

transmural infarct ECG

A

ST elevation, Q waves

125
Q

subendocardial infarct ECG

A

ST depression

126
Q

LAD infarct - anterior wall

A

V1-V4

127
Q

LAD infarct - anteroseptal

A

V1-V2

128
Q

LCX infarct - anterolateral

A

V4-V6

129
Q

LCX infarct - lateral wall

A

I, avL

130
Q

RCA infarct - inferior wall

A

II, III, aVF

131
Q

cardiomyopathy associated with systolic dysfunction

A

dilated

132
Q

cardiomyopathy associated with diastolic dysfunction

A

hypertrophic and restrictive/obliterative

133
Q

cause of sudden death in young athletes

A

hypertrophic cardiomyopathy

134
Q

most common primary cardiac tumor in adults

A

myxoma

135
Q

most common location of myxoma

A

left atrium - ball valve obstruction

136
Q

most common primary cardiac tumor in kids

A

rhabdomyoma

137
Q

what is rhabdomyoma associated with

A

tuberous sclerosis

138
Q

asian children < 4 y/o

A

kawasaki disease

139
Q

heavy male smokers < 40 y/o

A

buerfers disease

140
Q

positive HBsAg

A

polyarteritis nodosa

141
Q

wegeners granulomatosis triad

A

focal necrotizing vasculitis, necrotizing granulomas in lung + upper airway, necrotizing glomerulonephritis

142
Q

positive p-ANCA

A

microscopic polyangiitis and churg strauss syndrome

143
Q

positive c-ANCA

A

wegeners granulomatosis

144
Q

henoch-schonlein purpura

A

URI –> IgA complex deposition –> childhood systemic vasculitis

145
Q

henoch-schonlein purpura triad

A

skin - palpable purpura of butt/legs
arthralgia
GI - abdominal pain, melena, multiple lesions of same age

146
Q

elevated IgE

A

churg-strauss syndrome

147
Q

IgA nephropathy association

A

henoch-schonlein purpura

148
Q

essential HTN tx

A

diuretics, ACE inhibitors, ARBs, CCB

149
Q

CHF tx

A

diuretics, ACE inhibitors/ARBs, B-blockers (compensated CHF), K+ sparing diuretics

150
Q

DM tx

A

ACE inhibitors/ARBs, CCB, diuretics, B-blockers, alpha-blockers

151
Q

protective vs. diabetic nephropathy

A

ACE inhibitors

152
Q

Ca+ channel blockers

A

nifedipine, verapamil, diltiazem, amlodipine

153
Q

CCB MOA

A

block voltage gated L-type Ca channels of cardiac and smooth muscle –> reduce muscle contractility

154
Q

CCB for vasc smooth muscle

A

amlopdipine = nifedipine > diltiazem > verapamil

155
Q

CCB for heart

A

verapamil > diltiazem > amlodipine = nifedipine

VERAPAMIL = VENTRICLE

156
Q

CCB clinical use

A

htn, angina, arrhythmias (not nifedipine), prinzmetal’s angina, raynaud’s

157
Q

CCB toxicity

A

cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation

158
Q

hydralazine MOA

A

increase cGMP –> smooth muscle relaxation
vasodilate arterioles > veins
reduce afterload

159
Q

hydralazine clinical use

A

severe htn, CHF
first line - htn in preggers with methyldopa
freq coadminister w/ beta-blocker to prevent reflex tachycardia

160
Q

hydralazine toxicity

A

compensatory tachycardia, fluid retention, nauseua, headache, angina, lupus-like syndrome
CI - angina/CAD

161
Q

malignant htn tx drugs

A

nitroprusside, nicardipine, clevidipine, labetalol and fenoldopam

162
Q

nitroprusside

A

short acting
increase cGMP via direct release NO
releases cyanide –> can cause cyanide toxicity

163
Q

fenoldopam

A

dopamine D1 receptor agonist - coronary, peripheral, renal and splanchnic vasodilationg
decrease BP and increase natriuresis

164
Q

nitroglycerin and isosorbide dinitrate MOA

A

release NO into smooth muscle –> increase cGMP –> smooth muscle relaxation = vasodilation veins > arteries
decrease preload

165
Q

nitroglycerin and isosorbide dinitrate clinical use

A

angina, pulmonary edema

166
Q

nitroglycerin and isosorbide dinitrate toxicity

A

reflex tachycardia, hypotension, flushing, headache

167
Q

monday disease

A

nitroglycerin and isosorbide dinitrate toxicity
in industrial exposure - develop tolerance for vasodilating action during work week + lose tolerance over weekend –> tachycardia, dizziness and headache upon reexposure

168
Q

goal of antianginal tx

A

decrease EDV, BP, HR, contractility, or ejection time –> reduce myocardial O2 consumption

169
Q

nitrates vs. angina

A

PRELOAD
decrease - EDV, BP, Ejection time, MVO2
increase HR and contractility via reflex response

170
Q

b-blockers vs. angina

A

AFTERLOAD
decrease - BP, contractility, HR, MVO2
increase - EDV and ejection time

171
Q

nitrates and beta-blockers vs. angina

A

really decrease MVO2
decrease HR and BP
little/no effect on ejection time/contractility
no effect or decrease EDV

172
Q

pindolol and acebutolol

A

partial beta-agonists CI in angina

173
Q

CCB similar to nitrates/Bblockers

A

nifedipine - similar to nitrates in effect

verapamil - similar to b-blockers in effect

174
Q

HMG-CoA reductase inhibitors

A

lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

175
Q

HMG-CoA reductase inhibitors effect on LDL

A

DECREASE DECREASE DECREASE

176
Q

HMG-CoA reductase inhibitors effect on HDL

A

increase

177
Q

HMG-CoA reductase inhibitors effect on TG

A

decrease

178
Q

HMG-CoA reductase inhibitors MOA

A

inhibit conversion of HMG-CoA –> mevalonate (cholesterol precursor)

179
Q

HMG-CoA reductase inhibitors SE

A

hepatotoxicity - increase LFTs

rhabdomyolysis

180
Q

Niacin

A

Vitamin B3

181
Q

Niacin effect on LDL

A

DECREASE DECREASE

182
Q

Niacin effect on HDL

A

INCREASE INCREASE

183
Q

Niacin effect on TG

A

decrease

184
Q

Niacin MOA

A

inhibits lipolysisin adipose tissue

reduce hepatic VLDL secretion into circulation

185
Q

NIacin SE

A

red flushed fash - decrease by aspirin / long-term use
hyperglycemia - acanthosis nigricans
hyperuricemia - exacerbates gout

186
Q

bile acid resins

A

cholestyramine, colestipol, colesevelam

187
Q

bile acid resins effect on LDL

A

DECREASE DECREASE

188
Q

bile acid resins effect on HDL

A

slightly increase

189
Q

bile acid resins effect on TG

A

slightly increase

190
Q

bile acid resins MOA

A

prevent intestinal reabsorption of bile acids

liver must use cholesterol to make more

191
Q

bile acid resins SE

A

patients HATE it - tastes bad and causes GI discomfort, decrease absorption of fat-soluble vitamins
cholesterol gallstones

192
Q

cholesterol absorption blockers

A

ezetimibe

193
Q

ezetimibe effect on LDL

A

DECREASE DECREASE

194
Q

ezetimibe MOA

A

prevent cholesterol reabsorption at SI brush border

195
Q

ezetimibe SE

A

rare - increase LFT’s, diarrhea

196
Q

fibrates

A

gemfibrozil, clofibrate, bezafibrate, fenofibrate

197
Q

fibrates effect on LDL

A

decrease

198
Q

fibrates effect on HDL

A

increase

199
Q

fibrates effect on TG

A

DECREASE DECREASE DECREASE

200
Q

fibrates MOA

A

upregulate LDL –> increase TG clearance

201
Q

fibrates SE

A

myositis, hepatotoxicity (increase LFTs), cholesterol gallstones

202
Q

cardiac glycoside

A

digoxin

203
Q

digoxin MOA

A

direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchange –> increase intracellular calcium –> positive isotropy
stimualtes vagus nerve –> decrease HR

204
Q

digoxin clinical use

A

CHF - increase contractility

atrial fibrillation - decrease conduction at AV node and depress SA node

205
Q

digoxin toxicity

A

cholinergic - N&V, diarrhea, blurry yellow vision (van goh)
ECG - increase PR, decrease QT, ST scooping, T-wave inversion, arrhythmia, AV block
poor prognostic indicator = hyperkalemia

206
Q

factors predisposing to digoxin toxicity

A

renal failure - decrease excretion
hypokalemia -digoxin bdining K+ binding site on Na/K ATPASE
quinidine - decrease clearance - displace digoxin

207
Q

digoxin antidote

A

slowly normalize K+, lidocaine, cardiac pacera, anti-digoxin Fab fragments, Mg2+

208
Q

antiarrhythmics class I

A

Na+ channel blockers
local anesthetics
slow/block conduction in depolarized cells
decrease slow phase 0 depol
increase threshold for firing in abnormal pacemaker cells
state depemdent - selectively depress tissue that is freq depolarized (tachycardia)

209
Q

what causes increase toxicity for all class I drugs

A

hyperkalemia

210
Q

Class IA antiarrhythmics

A

quinidine, procainamide, disopyramide

211
Q

Class IA MOA

A

increase AP duration, effective refractory period, and QT interval
atrial and ventricular arrhythmias - reentrant and ectopic supraventricular and ventricular tachycardia

212
Q

quinidine toxicity

A

cinchonism - headache, tinnitus

213
Q

class IB antiarrhythmics

A

lidocaine, mexiletine, tocainide

214
Q

class IB MOA

A

decrease AP duration
pref affect ischemic or depolarized purkinje and ventricular tissue
used in acute ventricular arrhythmias (post-MI) and digitalis-induced arrhythmias

215
Q

class IB toxicity

A

local anesthetic, CNS stimulation/depression, CV depression

216
Q

class IC antiarrhythmics

A

flecainide, propafenone

217
Q

class IC MOA

A

no effect on AP duration
useful in ventricular tachycardia that progress to VF and in intractable SVT
last resort in refractory tachyarrythmias - pts w/o structural abnormalities

218
Q

class IC toxicity

A

proarrhythmic, especially post-MI (CI)

significantly prolongs refractory period in AV node

219
Q

procainamide toxicity

A

reversible SLE-like syndrome

220
Q

disopyramide toxicity

A

heart failure

221
Q

class IA toxicity

A

thrombocytopenia, torsades de pointes due to increase QT interval

222
Q

IB is best…

A

post-MI

223
Q

IC is contraindicated…

A

structural heart disease and post-MI

224
Q

class II antiarrhythmics

A

beta-blockers –> metoprolol, propanolol, esmolol, atenolol, timolol

225
Q

class II MOA

A

decrease cAMP and decrease CA current –> decrease SA and AV nodal activity
decrease slope of phase 4 - suppress abnormal pacemakers
AV node particularly sensitive - increase PR interval

226
Q

very short acting class II

A

esmolol

227
Q

class II toxicity

A

impotence, exacerabtion of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). may mask signs of hypoglycemia

228
Q

metoprolol toxicity

A

dyslipidemia

229
Q

metoprolol overdose tx

A

glucagon

230
Q

propanolol toxicity

A

can exacerbate vasospasm in prinzmetal’s angina

231
Q

class III antiarrhythmics

A

K+ channel blockers - amiodarone, ibutilide, dofetilide, sotalol

232
Q

class III MOA

A

increase AP duration, ERP
used when other antiarrhythmics fails
increase QT interval

233
Q

sotalol toxicity

A

torsades de pointes, excessive beta block

234
Q

ibutilide toxicity

A

torsades

235
Q

amiodarone toxicity

A

pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (40% iodine by weight), corneal deposits, skin deposits (blue/gray) –> photodermatitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF)

236
Q

alters lipid membrane - has class I-IV effects

A

amiodarone

237
Q

what do you check when using amiodarone

A

PFTs, LFTs, TFTs

238
Q

class IV antiarrhythmics

A

Ca+ channel blockers - verapamil and diltiazem

239
Q

class IV antiarrhythmics MOA

A

decrease conduction velocity, increase ERP and PR interval

used in prevention of nodal arrhythmias (SVT)

240
Q

class IV toxicity

A

constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

241
Q

adenosine MOA

A

increase K+ out of cells –> hyperpolarize the cell + decrease intracellular calclium
very short acting (15 seconds)

242
Q

drug of choice in dx/abolishing supraventricular tachycardia

A

adenosine

243
Q

adenosine toxicity

A

flushing, hypotension, chest pain

effects blocked by theophylline and caffeine

244
Q

effective in torsades de pointes and digoxin toxicity

A

Mg2+

FA (13 decks)

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