FA Cardiology

8/12/2019 FA Cardiology

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1. Truncus

arteriosus gives

rise to what?

ascending aorta and pulmonary trunk

2. bulbus cordis gives

rise to what?

smooth parts (outflow tract) of left and

right ventricles

3. primitive ventriclegives rise to what?

trabeculated left and right ventricles

4. primitive atria

give rise to what?

trabeculated left and right atria

5. left horn of sinus

venosus gives rise

to what?

coronary sinus

6. right horn of SV

gives rise to what?

smooth part of right atrium

7. right common

cardinal vein and

right anteriorcardinal vein give

rise to what?

SVC

8. what happens in

the normal

development of the

truncus

arteriosus?

neural crest migration truncal and

bulbar ridges that spiral and fuse to

form the aorticopulmonary (AP)

septumascending aorta and

pulmonary trunk

9. what are the

truncus arteriosus

pathologies?

1. TGA

2. ToF

3. TA

10.

what is the defectin transposition of

the great vessels?

failure to spiral

11.what is the TA

defect in tetralogy

of Fallot?

skewed AP septum development

12.what is the defect

in persistent TA?

partial AP septum development

13. 3 steps in

embryologic

formation of

interventricular

septum?

1. muscular ventricular septum forms-

opening= interventricular foramen

2. AP septum rotates and fuses with

muscular ventricular septum to form

membranous interventricular septum,

closing interventricular foramen

3. Growth of endocardial cushions

separates atria from ventricles and

contributes to both atrial separation

and membranous portion of the

interventricular septum

14. improper neural

crest migration

into the TA can

result in what?

transposition of the great arteries or a

persistent TA

15. in interventricular

septum development,

membranous septal

defect causes what?

an initial left to right shunt, which

later reverses to a right to left shunt

due to onset of pulmonary

hypertension (Eissenmenger's

syndrome)

16. 8 steps in interatrial

septum

development?

1. foramen primum narrows as

septum primum grows toward

endocardial cushions

2. perforations in septum primum

form foramen secundum (foramen

primum disappears

3. foramen scundum maintains

right to left shunt as septum

secundum begins to grow

4. septum secundum contains a

permanent opening (foramen ovale)

5. foramen secundum enlarges and

upper part of septum primum

degenerates6. remaining portion of septum

primum forms the valve of the

foramen ovale

7. septum secundum and septum

primum fuse to form the atrial

septum

8. foramen ovale usually closes soon

after birth because ofLA pressure

17.what happens in

pathology of

interatrial septal

development?

patent foramen ovale, caused by

failure of the septum primum and

septum secundum to fuse after birth

18.when is there fetal

erythropoiesis in the

yolk sac?

3-10wk



liver?

6wk-birth



spleen?

15-30wk


erythropoiesis in thebone marrow?

22wk-adult

22. mnemonic for fetal

erythropoiesis?

young liver synthesizes blood

23. structure of HbF? 22

24. structure of HbA? 22

25. O2 content of fetal

blood in the umbilical

vein?

PO2~30

80% saturated with O2

26. O2 sat of umbilican

arteries?

low

FA CardiologyStudy online at quizlet.com/_ohup5


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27. sites of 3

important

shunts of fetal

circulation?

1. ductus venosus

2. foramen ovale

3. ductus arteriosus

28. action of shunt at

ductus venosus

in fetal

circulation?

blood entering the fetus through the

umbilical vein is coducted via the ductus

venosus into the IVC to bypass the

hepatic circulation

29. action of the

shunt at the

foramen ovale in

fetal circulation?

most oxygenated blood reaching the

heart via the IVC is diverted through the

foramen ovale and pumped out the aorta

to the head and body

30. action of the

shunt at the

ductus

arteriosus in

fetal circulation?

deoxygenated blood entering the RA from

the SVC enters the RV, is expelled into

the pulmonary artery, then passes

through the ductus arteriosus into the

descending aorta

31.what happens to

fetal circulation

at birth when the

infant takes a

breath?

resistance in pulmonary vasculature

causesLA pressure vs RA pressure

foramen ovale closes (now called fossa

ovalis)

in O2 leads to in prostaglandins,

causing closure of ductus arteriosus

32.what helps close

PDA?

indomethacin

33.what keeps PDA

open?

PGE1, PGE2

34. post natal

derivative of the

umbilical vein?

liga mentum teres hepatis, contained in

falciform ligament

35. postnatal

derivatives of

umbilical

arteries?

medial umbilical ligaments

36. postnatal

derivatives of

ductus

arteriosus?

liga mentum arteriosum

37. postnatal

derivative of

ductus venosus?

liga mentum venosum

38. postnatal

derivative of

foramen ovale?

fossa ovalis

39. postnatal

derivative of

allantois?

urachus-median umbilical ligament

40.what is the

urachus part of?

the allantoic duct between the bladder

and the umbilicus

41.what finding is a

remnant of the

urachus?

urachal cyst, or sinus

42. postnatal derivative

of the notochord?

nucleus pulplosus of intervertebral

disc

43. LCX supplies what? lateral and posterior walls of left

ventricle

44. LAD supplies what? anterior 2/3 of interventricular

septum, a nterior papillary muscle,

and anterior surface of left ventricle

45. PD supplies what? posterior 1/3 of interventricular

septum and posterior walls of

ventricles

46. acute marignal

artery supplies

what?

right ventricle

47. SA and AV nodes are

usually supplied by

what?

RCA

48. frequency and

features of right

dominant coronarycirculation?

85%

PD arises from RCA

49. frequency and

features of left-

dominant coronary

circulation?

8%

PD arises from LCX

50. frequency and

features of

codominant

circulation?

7%

PD arises from both LCX and RCA

51. coronary artery

occlusion mostcommonly occurs

where?

in LAD

52.when do coronary

arteries fill?

during diastole

53. most posterior part

of the heart is what?

LA

54. enlargement of LA

can cause what?

dysphagia (due to compression of the

esophagus) or hoarseness (due to

compression of the left recurrent

laryngeal nerve)

55. transesophagealechocardiography is

useful for

diagnosing what?

LA enlargementaortic dissection

thoracic aortic aneurysm

56. equations for

cardiac output?

CO= SV x HR

Fick's:

CO= (rate of O2

consumption)/((arterial O2 content)-

(venous O2 content))


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57. equation for MAP? MAP= CO x TPR

MAP= 2/3 diastolic pressure + 1/3

systolic

58. pulse pressure=? systolic pressure - diastolic pressure

59. pulse pressure is

proportional to

what?

stroke volume

60. equations for stroke

volume?

SV = CO/HR = EDV - ESV

61. during the early

stages of exercise CO

is maintained by

what?

HR and SV

62. during the late stages

of exercise, CO is

maintained by what?

HR only (SV plateaus)

63.what happens during

exercise if HR is toohigh?

diastolic filling is incomplete and

CO

64. cardiac variables that

affect stroke volume?

SV CAP

Stroke Volume affected by

Contractility, Afterload, and Preload

65. SV when what? preload, afterload,

contractility

66. contractility (and SV)

with what?

1. catecholamines

2. intracellular Ca++

3. extracellular Na+

4. Digitalis

67. how do

catecholamines

contractility?

activity of Ca++ pump in

sarcoplasmic reticulum

68. how does a in

extracellular Na+

contractility?

activity of Na+/Ca++ exchanger

69. how does digitalis

contractility?

blocks Na+/K+ pump

intracellular Na+Na+/Ca++

exchanger activityintracellular

Ca++

70. contractility and SV

with what?

1. blockade

2. heart failure (systolicdysfunction)

3. acidosis

4. hypoxia/hypercapnia

(PO2/PCO2)

5. Non-dihydropyridine Ca++

channel blockers

71. effect of anxiety,

exercise, and

pregnancy on SV?

72. myocardial O2 demand is by

what?

a fterload (proportional

to arterial pressure)

contractility

heart rate

heart size (wall

tension)

73. preload = ? ventricular EDV

74. afterload=? MAP (proportional toperipheral resistance)

75. agents thatpreload? vEnodilators

(nitroglycerin)

76. agents thatafterload? vAsodilators

(hydrAlazine)

77. preload with what? 1. exercise (slightly)

2. blood volume

(overtransfusion)

3. excitement (

sympathetic activity)

78. on Starling curve, force ofcontraction is proportional to

what?

end-diastolic length ofcardiac muscle fiber

(preload)

79. on Starling curve, what are the

factors that increase

contractility?

sympathetic stimulation

catecholamines

digoxin

80. on starling curve, which

factors contractility?

loss of myocardium (MI)

blockers

Ca++ channel blockers

81. equation for EF? EF= SV/EDV = (EDV-

ESV)/EDV

82. EF is an index of what? ventricular contractility

83. normal EF? >=55%

84. EFin what? systolic heart failure

85. P =? Q x R

86. equation for resistance? resistance = (driving

pressure P)/(Flow Q)=

(8l)/r^4

87. equation for total resistance of

vessels in series?

= R1 + R2 + R3

88. 1/Toral Resistance of vesselsin parallel?

= 1/R1 + 1/R2 + 1/R3...

89.viscosity in what? 1. polycythemia

2. hyperproteinemic

states (multiple myeloma)

3. hereditary

spherocytosis

90.viscosity in what? anemia

91. pressure gradient drives

blood flow where?

from high pressure to low

pressure


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92. resistance is proportional to what? viscosity and

vessel length

93. viscosity is inversely proportional to

what?

the radius to

the 4th power

94. what accounts for most of total

peripheral resistance?

arterioles

95. what vessels regulate capillary flow? arterioles

96. where is the operating point of the

heart on the cardiac and vascular

function curve?

intersection

where cardiac

output and

venous return

are equal

97. what causes the operating point of the

heart on the cardiac and vascular

function curve to shift straight down?

TPR,

hemorrhage

before

compensation

can occur


heart on the cardiac an vascularfunction curve to shift straight up?

TPR,

exercise, AVshunt


heart to shift downward and rightward

along the venous return curve on the

cardiac and vascular function curve?

heart failure

narcotic

overdose

100. what causes an upward shift in the CO

curve?

+ inotropy

101. what causes a downward shift in the CO

curve?

- inotropy

102. what causes a rightward shift in the

venous return curve?

blood

volume

103. what causes a leftward shift in the

venous return curve?

blood

volume

104. what is the X intercept of the venous

return curve?

mean

systemic

filling

pressure

105. what are the 5 phases of the left

ventricle in the cardiac cycle?

1.

isovolumetric

contraction

2. systolic

ejection3.

isovolumetric

relaxation

4. rapid filling

5. reduced

filling

106. what is isovolumetric contraction? period between

mitral valve

closure and aortic

valve opening

107. what is the period of highest O2

consumption during the cardiac

cycle?

isovolumetric

contraction

108. what is systolic ejection? period betweenaortic valve

opening and

closing

109. what is isovolumetric relaxation? period between

aortic valve

closing and

mitral valve

opening

110. what is rapid filling? period just after

mitral valve

opening

111. what is reduced filling? period just before

mitral valve

closure

112. what causes a rightward EDV

expansion without an upward

pressure expansion in the LV

cardiac cycle P/V curve?

preload SV

113. what causes a leftward ESV

expansion with an upward pressure

expansion on a LV cardiac cycle P/V

curve?

contractility

SV

EF

ESV

114. what causes a leftward ESV

contraction with an upward

pressure expansion on a LV cardiac

cycle P/V curve?

afterload

aortic pressure

SV

ESV

115. what causes S1 sound? mitral and

tricuspid valve

closure

116. S1 is loudest where? at mitral area

117. what causes S2 sound? aortic and

pulmonary valve

closure

118. where is S2 loudest? at left sternal

border

119. when is S3 heard? in early diastole

during rapid

ventricular filling

phase

120. S3 is associated with what? filling

pressures (MR,

CHF)


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121. S3 is more common in

which types of ventricles?

dilated ventricles, but normal

in children and pregnant

women

122. when do you hear S4? "atrial kick" in late diastole

123. what causes S4? high atrial pressure

LA must push against stiff LV

wall

124. S4 associated with what? ventricular hypertrophy

125. what does JVP a wave

correspond to?

atrial contraction

126. what does the JVP c wave

correspond to?

RV contraction (closed

tricuspid valve bulging into

atrium)

127. what does the JVP x

descent correspond to?

atrial relaxation and

downward displacement of

closed tricuspid valve during

ventricular contraction

128. what does the JVP v wavecorrespond to?

right atrial pressure due to

filling against closed tricuspid

valve

129. what does the JVP y

descent correspond to?

blood flow from RA to RV

130. what happens in normal

splitting?

inspiration

drop in intrathoracic pressure

venous return to the RV

RV stroke volume

RV ejection time

delayed closure of the

pulmonic valve

131. what else contributes to

the delayed closure of the

pulmonic valve in normal

splitting?

pulmonary impedance (

capacity of the pulmonary

circulation)

132. what does normal

splitting sound like?

A2 and P2 are close during

expiration,

A2 and P2 are only slightly

more separated during

inspiration

133. wide splitting is seen in

which conditions?

those that delay RV emptying

(pulmonic stenosis, RBBblock)

134. what happens in wide

splitting?

delay in RV emptying causes

delayed pulmonic sound

(regardless of breath)

135. what does wide splitting

sound like?

an exaggeration of normal

splitting

Ex: A2 and P2 are split as

wide as normal inspiration

Ins: A2 and P2 are split much

wider than normal

136. fixed splitting is

seen in what?

ASD

137. what happens in

fixed splitting?

ASD left to right shunt RA and

RV volumesflow through pulmonic

valve such that, regardless of breath,

pulmonic closure is greatly delayed

138. paradoxical

splitting is seenin what?

conditions that delay LV emptying

(aortic stenosis, LBB block)


paradoxical

splitting?

normal order of valve closure is reversed

so that P2 sound occurs before A2.

140. what does

paradoxical

splitting sound

like?

on inspiration, P2 closes later and moves

closer to A2, thereby 'paradoxically'

eliminating the split

141. what can cause a

systolic murmur

in the aorticarea?

aortic stenosis

flow murmur

aortic valve sclerosis

142. where is the

aortic

auscultation

area?

2nd intercostal space RSB

143. what causes a

systolic ejection

murmur in the

pulmonic area?

pulmonic stenosis

flow murmur (ASD, PDA)

144. where is the

pulmonic area

for ausculation?

2nd interspace LSB

145. what causes a

pansystolic

murmur at the

tricuspid area?

tricuspid regurgitation

ventricular septal defect

146. what causes

diastolic

murmur at the

tricuspid area?

tricuspid stenosis

ASD

147. where is the

tricuspid area

for

auscultation?

5th interspace LSB

148. what causes a

systolic murmur

in the mitral

area?

mitral regurgitation

149. what causes a

diastolic

murmur in the

mitral area?

mitral stenosis


6/25

150. where is the mitral area for

auscultation?

5th interspace mid

clavicular line

151. what causes diastolic

murmur at the left sternal

border?

aortic regurgitation

pulmonic regurgitation

152. what causes systolic murmur

at left sternal border?

hypertrophic

cardiomyopathy

153. what are the auscultation

findings in ASD?

pulmonary flow murmur

diastolic rumble

(tricuspid)

blood flow across the ASD

doesn't cause a murmur

because there is no

pressure gradient

murmurlouder

diastolic murmur of

pulmonic regurgitation

from dilation of

pulmonary artery

154. the continuous, machine-like

murmur of PDA is best

appreciated where?

left infraclavicular region

155. what is the effect of

inspiration on ausculation?

intensity of right heart

sounds

156. what is the effect of

expiration on auscultation?

intensity of left heart

sounds

157. what is the effect of hand grip

maneuver on auscultation (

systemic vascular

resistance)?

intensity of MR, AR,

VSD, MVP murmurs

intensity of AS,

hypertrophic

cardiomyopathy murmurs

158. what is the effect of the

vasalva maneuver (venous

return) on auscultation?

intensity of most

murmurs

intensity of MVP,

hypertrophic


159. what is the effect of rapid

squatting (venous return,

preload,afterload with

prolonged squatting)?

intensity of MVP,

hypertrophic


160. conditions associated with

systolic heart sounds includewhat?

aortic/pulmonic stenosis

mitral/tricuspidregurgitation

VSD

161. conditons associated with

diastolic heart sounds

include what?

aortic/pulmonic

regurgitation

mitral/tricuspid stenosis

162. what does mitral/tricuspid

regurgitation sound like?

holosystolic, high-pitched

"blowing murmur"

163. mitral regurgitation is

loudest where?

at apex and radiates to

toward axilla

164. mitral regurgitation sound

is enhanced by what?

maneuvers that TPR

(squatting, hand grip) or

LA return (expiration)

165. MR is often due to what? ischemic heart disease,

mitral valve prolapse, LV

dilation

166. where is tricuspid

regurgitation loudest?

loudest at tricuspid area

and radiates to rightsternal border

167. tricuspid regurgitation

sound enhanced by what?

maneuvers that RA

return (inspiration)

168. TR can be caused by what? RV dilation

169. rheumatic fever and

infective endocarditis can

cause which heart sounds?

MR or TR

170. what does Aortic stenosis

sound like?

crescendo-decrescendo

systolic ejection murmur

following ejection click

radiates to carotids/heartbase

171. what causes ejection click in

aortic stenosis?

EC due to abrupt halting of

valve leaflets

172. pressure gradient in aortic

stenosis?

LV>> aortic pressure

during systole

173. pulse findings in aortic

stenosis?

'pulsus parvus et tardus'

pulses are weak with a

delayed peak

174. aortic stenosis can lead to

what?

Syncope, Angina, Dyspnea

on exertion (SAD)

175. aortic stenosis is due to

what?

age related calcific aortic

stenosis or bicuspid aortic

valve

176. what does VSD sound like? holosystolic, harsh

sounding murmur

177. where is VSD loudest? tricuspid area

178. VSD sound can be

accentuated how?

hand grip maneuver due to

increased afterload

179. what does MVP sound like? late systolic crescendo

murmur with midsystolic

click

180. what causes MC? sudden tensing of the

chordae tendineae

181. what is the most frequent

valvular lesion?

MVP

182. MVP is best heard where? over apex

183. when is MVP loudest? S2

184. severity of MVP? usually benign

185. MVP can predispose to

what?

infective endocarditis


7/25

186. MVP can be caused

by what?

myxomatous degeneration

rheumatic fever

chordae rupture

187. MVP enhanced by

what?

maneuvers thatVenous return

(standing or vasalva)

188. what does aortic

regurgitation

sound like?

immediate high pitched "blowing"

diastolic decrescendo murmur

189. pulses in AR? wide pulse pressure when chronic;

can present with bounding pulses

and head bobbing

190. AR is often due to

what?

aortic root dilation, bicuspid aortic

valve, endocarditis, rheumatic fever

191. whatmurmur in

AR?

hand grip

192. effect of

vasodilators on AR?

intensity of murmur

193. what does MS

sound like?

follows opening snap

delayed rumbling late diastolic

murmur

194. what causes OS in

MS?

abrupt halt in leaflet motion in

diastole, after rapid opening due to

fusion at leaflet tips

195. pressure gradient

in MS?

LA>>LV during diastole

196. MS often occurs

secondary to what?

rheumatic fever

197. chronic MS can

result in what?

LA dilation

198. MS sound is

enhanced by what?

maneuvers thatLA return

(expiration)

199. what does PDA

sound like?

continuous machine like murmur

200. when is PDA

loudest?

S2

201. PDA is often due to

what?

congenital rubella or prematurity

202. where is PDA best

heard?

left infraclavicular area

203. ventricular action

potential also

occurs where?

in bundle of His and Purkinje fibers


Phase 0 of

ventricular action

potential?

rapid upstroke- voltage gated Na+

channels open


Phase 1 of

ventricular action

potential?

initial repolarization- inactivation of

voltage gated Na+ channels. Voltage

gated K+ channels begin to open


Phase 2 of

ventricular action

potential?

plateau-Ca++ influx through voltage

gated Ca++ channels balances K+

efflux

Ca++ influx triggers Ca++ release from

sarcoplasmic reticulum and myocyte

contraction


phase 3 of

ventricular action

potential?

rapid repolarization= massive K+

efflux due to opening of voltage-gated

slow K+ channels and closure of

voltage gated Ca++ channels


phase 4 of the

ventricular action

potential?

resting potential- high K+ permeability

through K+ channels

209. difference between

cardiac muscle AP

and skeletal

muscle?

1. cardiac muscle AP has a plateau,

which is due to Ca++ influx and K+

efflux, myocyte contraction occurs due

to Ca++ induced Ca++ release from the

sarcoplasmic reticulum

2. cardiac nodal cells spontaneouslydepolarize during diastole resulting in

automaticity due to If channels

3. Cardiac myocytes are electrically

coupled to eachother by gap junctions

210. what do If chanels

do?

funny current channels responsible for

a slow, mixed Na+/K+ inward current

211. what is the

direction of the

leak currents in

cardiac

ventricular

myocytes?

K+ out

Na+, Ca++ in

212. pacemaker action

potential occurs

where?

in the SA and AV nodes


phase 0 of the

pacemaker action

potential?

upstroke- opening of VG Ca++

channels

fast VG Na channels are permanently

inactivated because of the less negative

resting voltage of these cells

214. permanent fast VG

Na channel

inactivation in thepacemaker cells

results in what?

slow conduction velocity that is used

by the AV node to prolong

transmission from the atria to theventricles


Phase 2 or

pacemaker

potential?

plateau is absent


phase 3 of the

pacemaker

potential?

inactivation of the Ca++ channels and

activation of K+ channelsK+

efflux


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217. what happens

in phase 4 of

the pacemaker

potential?

slow diastolic depolarization- membrane

potential spontaneously depolarizes as

Na+ conductance (If different from Ina

in phase 0 of ventricular action potential)

218. phase 4 of the

pacemaker

potential

accounts for

what?

automaticity of SA and AV nodes

219. slope of phase

4 in the SA

node

determines

what?

HR

220. effect of

ACh/adenosine

on SA node?

the rate of diastolic depolarization and

HR

221. effect of

catecholamines

on SA node?

depolarization and heart rate

222. effect of

sympathetic

stimulation on

SA/AV node?

the chance that If channels are open

and thusHR

223. P wave

corresponds to

what?

atrial depolarization

224. atrial

repolarization

in ECG?

masked by QRS complex

225. PR interval

corresponds to

what?

conduction delay through AV node

226. normal PR

interval?

ventricles >

AV nodes

235. relative speed of

conduction in the

pacemaker cells?

SA node> AV> Bundle of

his/purkinje/ventricles

236. what is the conduction

pathway in the heart?

SA node atriaAV node

common bundlebundle

branchespurkinje fibers

ventricles

237. dominant pacemaker in

heart?

SA node pacemaker inherent

dominance with slow phase of

the upstroke

238. what is the delay in the

AV node?

100ms delay- a trioventricular

delay; allows time forventricular filling


torsades de pointes?

ventricular tachycardia,

characterized by shifting

sinusoidal waveforms on ECG,

can progress to ventricular

fibrillation

240. what predisposes to

torsades de pointes?

anything that prolongs the QT

interval

241. treatment for torsades

de pointes?

magnesium sulfate

242. congenital long QT

syndromes are most

often due to what?

defects in cardiac sodium or

potassium channels

243. what condition has long

QT syndrome that

presents with severe

sensorineural

deafness?

Jervell and Lange-Nielsen

syndrome

244. how does atrial

fibrillation look?

chaotic and erratic baseline

(irregularly irregular) with no

discrete P waves in between

irregularly spaced QRScomplexes

245. atrial fibrillation can

result in what?

atrial stasis and lead to stroke

246. tx for atrial fibrillation? rate control

anticoagulation

possible cardioversion

247. what does atrial flutter

look like?

a rapid succession of identical,

back-to-back atrial

depolarization waves

'saw tooth' appearance


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248. pharmacologic

conversion to sinus

rhythm in atrial

flutter?

Class IA, IC, or III antiarrhythmics

249. rate control in atrial

flutter?

-blocker or calcium channel

blocker

250. what does ventricular

fibrillation look like?

a completely erratic rhythm with no

identifiable waves

251. severity of

ventricular

fibrillation?

fatal arrhythmia without

immediate CPR and defibrillation

252. features of 1st degree

AV block?

prolonged PR interval >200ms

asymptomatic

253. features of 2nd

degree AV block

Mobitz type I

(Wenckebach)?

progressive lenghtening of the PR

interval until a beat is dropped

usually asymptomatic

254. features of Mobitz

type II?

dropped beats that are not preceded

by a change in the length of the PRinterval

255. severity of Mobitz

type II?

these abrupt, nonconducted p

waves result in a pathologic

condition

256. mobitz type II is often

found as what?

2:1 block, where there are >=2 p

waves to 1 QRS

257. mobitz type II often

treated with what?

pacemaker

258. mobitz type II may

progress to what?

3rd degree block

259. what happens in 3rd

degree (complete)

heart block?

the atria and ventricles beat

independently of each other

both p waves and QRS complexes

are present, though P waves bear

no relation to the QRS complexes

260. which rate is faster in

3rd degree heart

block?

atrial rate is faster than ventricular

rate

261. 3rd degree heart

block is usually

treated with what?

a pacemaker

262. which disease can

result in 3rd degree

heart block?

Lyme disease

263. ANP is released from

where?

atrial myocytes

264. ANP is released in

response to what?

blood volume and pressure

265. ANP causes what? generalized vascular relaxation

and Na+ reabsorption at the

medullary collecting tubule

266. effect of ANP on

renal blood flow?

constricts efferent renal arterioles and

dilates afferent arterioles (cGMP

mediated), promoting diuresis and

contributing to the escape from

aldosterone mechanism

267. aortic arch

baroreceptors

transmit info

where?

via vagus nerve to solitary nucleus of

medulla (responds only to BP)

268. carotid sinus

baroreceptor

transmits info

where?

via glossopharyngeal nerve to solitary

nucleus of medulla (responds to and

in BP)

269. what happens at

baroreceptors in

response to

hypotension?

arterial pressure

stretch

afferent baroreceptor firing

efferent sympathetic firing and

efferent parasympathetic stimulation

vasoconstriction, HR, contractility,

BP

270. baroreceptors

are important in

the response to

what?

severe hemorrhage

271. effect of carotid

massage on

baroreceptors?

pressure on carotid arterystretch

afferent baroreceptor firingHR

272. baroreceptors

contribute to

which reaction?

Cushing reaction

273. what happens inCushing

reaction?

triad of hypertension, bradycardia, andrespiratory depression

274. mechanism of

Cushing

reaction?

ICP constricts arteriolescerebral

ischemia and reflex sympathetic

increase in perfusion pressure

(hypertension)stretchreflex

baroreceptor induced-bradycardia


stimulation of

peripheral

chemoreceptors?

carotid and aortic bodies are stimulated

byPO2 (


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279. what is the organ with

the largest share of

systemic cardiac output?

liver

280. which organ has the

highest blood flow per

gram of tissue?

kidney

281. which organ has the

largest arteriovenous O2difference?

heart

282. why does heart have the

largest arteriovenous O2

difference?

becuase O2 extraction is 80%

283. how is O2 demand met in

heart?

O2 demand is met by

coronary blood flow, not by

extraction of O2

284. what is the normal

pressure in the RA?


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312. which congenital heart

diseases make up the

right to left shunts

(early cyanosis)-blue

babies?

5T's

Tetralogy of Fallot

Transposition of the great vessels

persistent Truncus arteriosus

Tricuspid atresia

Total anomalous pulmonary

venous return

313. features of Persistent

Truncus Arteriosus?

failure of truncus arteriosus to

divide into pulmonary trunk and

aorta

314. most patients with

persistent truncus

arteriosus have what?

accompanying VSD

315. tricuspid atresia is

characterized by what?

absence of tricuspid valve and

hypoplastic RV

316. tricuspid atresia

requires what for

viability?

both ASD and VSD

317. what happens inTAPVR?

pulmonary veins drain into rightheart circulation (SVC, coronary

sinus, etc)

318. TAPVR is associated

with what?

ASD and sometimes PDA to

allow for right to left shunting to

maintain CO

319. which congenital heart

abnormalities make up

the left to right shunts

(late cyanosis)-blue

kids?

VSD

ASD

PDA

320. what is the most

common congenital

cardiac anomaly?

VSD

321. findings in ASD? loud S1, wide, fixed split S2

322. what do you use to

close PDA?

indomethacin

323. what is the frequency

of the congenital left to

right shunts?

VSD > ASD > PDA


Eisenmenger's

syndrome?

uncorrected VSD, ASD, or PDA

causes compensatory pulmonary

vascular hypertrophy, whichresults in progressive pulmonary

hypertension


Eisenmenger's

syndrome as

pulmonary resistance

increases?

the shunt reverses from left to

right to right to left, which causes

late cyanosis, clubbing, and

polycythemia

326. tetralogy of fallot is

caused by what?

anterosuperior displacement of

the infundibular septum

327. what is the

mnemonic for the

components of ToF?

PROVe

1. Pulmonary infundibular stenosis

2. RVH

3. Overriding aorta (overrides the

VSD)

4. VSD


important

determinant for

prognosis in ToF?

pulmonary infundibular s tenosis

329. in ToF early cyanosis

(tet spells) caused by

what?

a right to left shunt across the VSD

330. difference between

isolated VSD and

VSD in ToF?

isolated VSDs usually flow left to

right (acyanotic)

in tetralogy, pulmonary stenosis

forces right to left (cyanotic) flow

and causes RVH

331. how does RVH in

ToF look?

boot shaped heart on CXR

332. patients with ToF

learn what

compensatory

mechanism?

squat to relieve cyanotic symptoms

333. why do patients with

ToF squat?

reduces blood flow to the legs,

PVR, and thus the cyanotic right

to left shunt across the VSD

334. what is the preferred

treatment for ToF?

early, primary surgical correction


transposition of

great vessels?

aorta leaves RV (anterior) and

pulmonary trunk leaves LV

(posterior)separation of systemic

and pulmonary circulations

336. transposition of the

great vessels not

compatible with life

unless what?

a shunt is present to allow adequate

mixing of blood (VSD, PDA, or

patent foramen ovale)

337. transposition of

great vessels is due

to what?

failure of aorticopulmonary septum

to spiral

338. prognosis of

transposition of

great vessels?

without surgical correction, most

infants die within the first few

months of life

339. coarctation of the

aorta can result in

what?

AR

340. what is infantile type

of coarctation of the

aorta?

aortic stenosis proximal to insertion

of ductus arteriosus (preductal)


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341. preductal coarctation

of the aorta is

associated with what?

Turner syndrome

342. what needs to be

checked in infantile

coarctation of the

aorta?

check femoral pulses on physical

exam

343. what is adult typecoarctation of the

aorta?

stenosis is distal to ligamentumarteriosum (postductal)

344. postductal coarctation

of the aorta is


notching of the ribs (due to

collateral circulation),

hypertension in upper extremities,

weak pulses in lower extremities

345. postductal coarctation

of the aorta is most

commonly associated

with what?

bicuspid aortic valve

346. what is going on inpatent ductus

arteriosus in the fetal

period?

shunt is right to left (normal)

347. what happens to

patent ductus

arteriosus in the

neonatal period?

lung resistance and shunt

becomes left to right with

subsequent RVH and/or LVH and

failure (abnormal)

348. patent ductus

arteriosus is

associated with what

finding?

continuous machine like murmur

349. in PDA, patency is

maintained with

what?

PGE synthesis and low O2 tension

350. uncorrected PDA can

eventually result in

what?

late cyanosis in the lower

extremities (differential cyanosis)

351. when is PDA normal? PDA is normal in utero and only

closes after birth

352. which congenital

cardiac defect is

associated with 22q11

syndromes?

truncus arteriosus

ToF


cardiac defects are

associated with Down

syndrome?

ASD

VSD

AV septal defect (endocardial

cushion defect)


cardiac defects are

associated with

congential rubella?

septal defects

PDA

PA stenosis

355. which congenital cardiac

defects are associated with

turner syndrome?

coarctation of the aorta

(preductal)


defects are assciated with

Mafan's syndrome?

aortic insufficiency and

dissection (late

complication)


defects are associated withinfants of diabetic

mothers?

transposition of great

vessels

358. hypertension is defined as

what?

BP >= 140/90

359. what are the risk factors

for hypertension?

age

obesity

smoking

genetics

black>white>asian

360. 90% of hypertension is

what?

1 (essential) and related to

CO and

TPR

361. 10 % of hypertension is

what?

mostly 2 to renal disease

362. features of malignant

hypertension?

severe

>180/120

rapidly progressing

363. hypertension predisposes

to what?

athersclerosis

LVH

stroke

CHF

renal failure

retinopathy

aortic dissection

364. what are the signs of

hyperlipidemia?

atheromas

xanthomas

tendinous xanthoma

corneal arcus

365. what are atheromas? plaques in blood vessel wall

366. what are xanthomas? plaques or nodules

composed of lipid-laden

histiocytes in the skin,

especially the eyelids

367. what do you call axanthoma of the eyelid?

xanthelasma

368. what is a tendinous

xanthoma?

lipid depost in the tendon,

especially the achilles

369. what is corneal arcus? lipid deposit in cornea,

nonspecific (arcus senilis)

370. what are the 3 classes of

arteriosclerosis?

Monckberg

arteriosclerosis

atherosclerosis


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371. what is

Monckberg

arteriosclerosis?

calcification in the media of the arteries,

especially radial or ulnar

372. severity of

monckberg

arteriosclerosis?

usually benign

does not obstruct blood flow

intima not involved

373. typical

presentation ofmonckberg

arteriosclerosis?

pipestem arteries

374. what are the two

subtypes of

arteriosclerosis?

hyaline

hyperplastic

375. what is hyaline

arteriosclerosis?

thickening of small arteries in essential

hypertension or DM

376. what is

hyperplastic

arteriosclerosis?

onion skinning in malignant

hypertension

377. what isatherosclerosis?

fibrous plaques and atheromas form inintima of arteries

378. what type of

disease is

atherosclerosis?

disease of elastic arteries and large and

medium sized muscular arteries

379. what are the

modifiable risk

factors for

atherosclerosis?

smoking

hypertension

hyperlipidemia

diabetes

380. what are the

non-modifiable

risk factors foratherosclerosis?

age, gender (in men and

postmenopausal women), and positive

family history

381. what is

important in the

pathogenesis of

atherosclerosis?

inflammation

382. what is the

progression of

atherosclerosis?

endothelial cell dysfunction

macrophage and LDL accumulation

foam cell formation fatty streaks

smooth muscle cell migration (involves

PDGF and FGF), proliferation and ECM

depositionfibrous plaquecomplex

atheromas

383. important

histological

finding in

atherosclerosis?

cholesterol crystals

384. what are the

complications of

atherosclerosis?

aneurysms

ischemia

infarcts

peripheral vascular disease

thrombus

emboli

385. what is the relative

frequency of

location of

atherosclerosis?

abdominal aorta > coronary artery >

popliteal artery > carotid artery

386. what are the

symptoms of

atherosclerosis?

angina

claudication

but can be asymptomatic

387. what is an aorticaneurysm?

localized pathologic dilation of theaorta

388. what are the 2 types

of aortic

aneurysm?

AAA

TAA

389. AAA is associated

with what?

atherosclerosis

390. AAA occurs more

frequently in who?

hypertensive male smokers> 50yo

391. TAA is associated

with what?

hypertension, cystic medial necrosis

(Marfan's) and historically 3

syphilis


aortic dissection?

longitudinal intraluminal tear

forming a false lumen

393. aortic dissection

associated with

what?

hypertension

bicuspid aortic valve

cystic medial necrosis

inherited connective tissue disorders

(Marfans)


presents how?

tearing chest pain radiating to the

back

395. in aortic

dissection, CXR

shows what?

mediastinal widening

396. possibilities for the

false lumen in

aortic dissection?

can be limited to the ascending aorta,

propagate from the ascending aorta,

or propagate from the descending

aorta


can result in what?

pericardial tamponade

aortic rupture

death

398. what are the

ischemic heart

diseasemanifestations?

angina

coronary steal syndrome

myocardial infarctionsudden cardiac death

chronic ischemic heart disease

399. pathology involved

in angina?

CAD narrowing >75%

no myocyte necrosis

400. stable angina is

mostly 2 to what?

atherosclerosis

401. presentation of

stable angina?

ST depression on ECG

retrosternal chest pain with exertion

402. Prinzmental angina

occurs when?

at rest 2 to coronary artery spasm


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403. ECG finding in

prinzmental

angina?

ST elevation

404. pathology involved

in unstable angina?

thrombosis with incomplete coronary

artery occlusion

405. presentation of

unstable/crescendo

angina?

ST depression on ECG

worsening chest pain at rest or with

minimal exertion


coronary steal

syndrome?

vasodilator may aggravate ischemia

by shunting blood from area of

critical stenosis to an area of h igher

perfusion

407. myocardial is most

often due to what?

acute thrombosis due to coronary

artery atherosclerosis with complete

occlusion of coronary artery with

myocyte necrosis

408. ECG findings in

MI?

ECG initially shows ST depression

progressing to ST elevation with

continued ischemia and transmuralnecrosis

409. what is sudden

cardiac death?

death from cardiac causes within 1

hour of onset of symptoms, most

commonly due to a lethal arrhythmia

(V-fib)

410. sudden cardiac

death is associated

with what?

CAD up to 70% of cases

411. what is chronic

ischemic heart

disease?

progressive onset of CHF over many

years due to chronic ischemic

myocardial damage

412. relative frequency

of coronary artery

occlusion in MI?

LAD >RCA > circumflex

413. what are the

symptoms of MI?

diaphoresis

nausea

vomiting

severe retrosternal pain

pain in left arm and or jaw

shortness of breath

fatigue

414. what are the gross

findings within 0-

4h of MI?

none

415. what are the LM

findings within 0-

4h of MI?

none

416. what are the risks

within 0-4h of MI?

arrhythmia

CHF

exacerbation

cardiogenic shock

417. what are

the gross

findings

within 4-

24h of MI?

infarct and dark mottling; pale with

tetrazolium stain distal to occluded artery

418. what are

the LM

findings

within 4-

12h of MI?

early coagulative necrosis

edema

hemorrhage

wavy fibers

419. what is the

risk within

4-12h of

MI?

arrhythmia

420. what are

the LM

findings

within 12-

24h of MI?

contraction bands from reperfusion injury

release of necrotic cell content into blood

beginning of neutrophil migration

421. what is the

risk within

12-24h of

MI?

arrhythmia

422. what are

the gross

findings

within 1-3

days of MI?

hyperemia

423. what are

the LM

findingswithin 1-

3days of

MI?

extensive coagulative necrosis

tissue surrounding infarct shows acute

inflammationneutrophil migration

424. what is the

risk within

1-3 days of

MI?

fibrinous pericarditis

425. what are

the gross

findings

within 3-

14days ofMI?

hyperemic border;

central yellow-brown softening

maximally yellow and soft by 10 days

426. LM

findings

within 3-

14days of

MI?

macrophage infiltration followed by

granulation tissue at the margins

427. what is the

risk within

3-14 days of

MI?

free wall rupture leading to tamponade,

papillary muscle rupture, ventricular

aneurysm, interventricular septal rupture due

to macrophages that have degraded important

structural components


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428. what are the gross

findings 2weeks-

months post MI?

recanalized artery

gray white

429. LM findings 2 weeks-

months post MI?

contracted scar complete

430. risk 2weeks-months

post MI?

dressler's syndrome

431. what is the gold

standard for dx of MI

in first 6h?

ECG

432. use of cardiac troponin

I in diagnosis of MI?

rises after 4 hours and is elevated

for 7-10 days; more specific than

other protein markers

433. use of CK-MB in

diagnosis of MI?

useful in diagnosing reinfarction

following acute MI because levels

return to normal after 48 hours

434. CK-MB predominantly

found where?

in myocardium but can also be

released from skeletal muscle

435. ECG changes in MI? ST elevation (transmural infarct)

ST depression (subendocardial

infarct)

Q waves (transmural infarct)

436. necrosis in transmural

infarct?

necrosis

437. subendocardial

infarcts due to what?

ischemic necrosis of < 50% of

ventricle wall

438. transmural infarct

affects how much of

cardiac structure?

affects entire wall

439. subendocardial infarct

affect what structure?

subendocardium especially

vulnerable to ischemia

440. ECG in transmural

infarcts?

ST elevation

Q waves

441. ECG in subendocardial

infarct?

ST depression

442. Q waves in V1-V4,

where is the infarct?

Anterior wall (LAD)

443. Q waves in V1-V2,


Ateroseptal (LAD)

444. Q waves in V4-V6,where is the infarct?

anterolateral (LCX)

445. Q waves in I, aVL,


lateral wall (LCX)

446. Q waves in II, III, aVF,


inferior wall (RCA)

447. in MI, what is an

important cause of

death before reaching

hospital?

cardiac arrhythmia

448. cardiac arrhythmia in

MI is common when?

in first few days

449. what are the

complications of MI?

cardiac arrhythmia

LV failure and pulmonary

edema

Cardiogenic shock

Ventricular free wall rupture

papillary muscle rupture

IVS rupture

ventricular aneurysm

formation

postinfarction fibrinous

pericarditis

450. what is Dressler's

syndrome?

autoimmune phenomenon

resulting in fibrinous

pericarditis (several weeks post

MI)

451. factors associated with

cardiogenic shock in MI?

large infarct- high risk of

mortality

452. in MI ventricular free

wall rupture?

cardiac tamponade

453. in MI, papillary muscle

rupture?

severe mitral regurgitation

454. in MI, IVS rupture? VSD

455. factors associated with

ventricular aneurysm

formation in MI?

CO

risk of arrhythmia

embolus from mural thrombus

456. when is the greatest risk

for ventricular aneurysm

formation in MI?

1 week post MI

457. what is the most common

cardiomyopathy?

dilated (congestive)

cardiomyopathy 90%

458. dilated cardiomyopathy

is usually what origin?

often idiopathic, up to 50%

familial

459. specific etologies of

dilated cardiomyopathy

include what?

ABCCCD

Alcohol abuse

wet Beriberi

Coxsackie b virus myocarditis

chronic Cocaine use

Chaga's disease

Doxorubicin toxicity

hemochromatosis

peripartum cardiomyopathy

460. what are the findings in

dilated cardiomyopathy?

S3

dilated heart on U/S

balloon appearance on chest X

ray

461. what is the treatment for

dilated cardiomyopathy?

Na+ restriction

ACE inhibitors

diuretics

digoxin

heart transplant


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hypertrophic

cardiomyopathy?

hypertrophied interventricular

septum is too close to mitral valve

leaflet, leading to outflow tract

obstruction

463. 60-70% of

hypertrophic

cardiomyopathy are of

what origin?

familial

AD

myosin heavy chain mutation

464. hypertrophic

cardiomyopathy is


Friedreich's ataxia

465. morphologic findings

in hypertrophic

cardiomyopathy?

disoriented, tangled,

hypertrophied myocardial fibers

466. what is a cause of

sudden death in young

athletes?

hypertrophic cardiomyopathy

467. what are the findings

in hypertrophiccardiomyopathy?

normal sized heart

S4apical impulses

systolic murmur

468. what is the treatment

for hypertrophic

cardiomyopathy?

blocker or non-dihydropyridine

calcium channel blocker

(verapamil)

469. what ensues in

hypertrophic

cardiomyopathy?

diastolic dysfunction

470. gross appearance in

hypertrophic

cardiomyopathy?

asymmetric concentric

hypertrophy (sarcomeres added in

parallel)

471. pathogenesis of

hypertrophic

cardiomyopathy?

proximity of hypertrophied

interventricular septum to mitral

leaflet obstructs outflow tract,

resulting in systolic murmur and

syncopal episodes

472. major causes of

restrictive/obliterative

cardiomyopathy

include what?

sarcoidosis

amyloidosis

postradiation fibrosis

endocardial fibroelastosis

Lofflers syndrome

hemochromatosis

473. what is endocardial

fibroelastosis?

thick fibroelastic tissue in

endocardium of young children

474. what is Loffler's

syndrome?

endomyocardial fibrosis with a

prominent eosinophilic infiltrate

475. what ensues in

restrictive/obliterative

cardiomyopathy?

diastolic dysfunction

476. what is CHF? a clinical syndrome that occurs in patients

with an inherited or acquired abnormality

of cardiac structure or function, which is

characterized by a constellation of clinical

symptoms (dyspnea, fatigue) and signs

(edema, rales)

477. in CHF RHF

most often

results from

what?

LHF

478. isolated RHF

is usually due

to what?

cor pulmonale

479. which drugs

reduce

mortality in

CHF?

ACE inhibitors

blockers

ARBs

spironolactone

480. when do you

not give

blockers in

CHF?

acute decompensated HF

481. which drugs

are used for

symptomatic

relief in CHF?

thiazides

loop diuretics

482. which drugs

improve

symptoms and

mortality in

select patients

with CHF?

hydralazine with nitrate therapy

483. what are the

abnormalities

seen in CHF?

cardiac dilation

dyspnea on exertion

LHF

RHF

484. what is the

cause of

cardiac

dilation in

CHF?

greater ventricular EDV

485. what is the

cause of DOE

in CHF?

failure of cardiac output toduring

exercise

486. what are the

manifestations

of LHF in

CHF?

pulmonary edema/PND

orthopnea

487. what is the

cause of

pulmonary

edema/PND in

CHF?

pulmonary venous pressurepulmonary

venous distentions and transudation of

fluid


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488. histological finding in

LHF in CHF?

presence of hemosiderin laden

macrophages (heart failure

cells) in the lungs

489. what is the cause of

orthopnea in CHF?

venous return in supine

position exacerbates

pulmonary vascular

congestion

490. what are themanifestations of RHF in

CHF?

hepatomegaly (nutmeg l iver)peripheral edema

jugular venous distention


hepatomegaly (nutmeg

liver) in CHF?

central venous pressure

resistance to portal flow

492. rarely, hepatomegaly in

RHF leads to what?

cardiac cirrhosis


peripheral edema in

CHF?

venous pressurefluid

transudation

494. what is the cause ofjugular venous distention

in CHF?

venous pressure

495. what are the symptoms of

bacterial endocarditis?

Bacteria FROM JANE:

Fever

Roth spots

Osler nodes

Murmur

Janeway lesions

Anemia

Nail-bed hemorrhage

Emboli

496. what is the most common

symptom of bacterial

endocarditis?

fever

497. what are roth spots? round white spots on retina

surrounded by hemorrhage

498. what are osler's nodes? tender raised lesions on finger

or toe pads

499. what are janeway

lesions?

small, painless, erythematous

lesions on palm or sole

500. what is necessary for

diagnosis of bacterialendocarditis?

multiple blood cultures

501. organism that causes

acute bacterial

endocarditis?

S aureus

502. virulence of organism

that causes acute


S aureus (high virulence)

503. presentation in acute

bacterial endocarditis

caused by S aureus?

large vegetations on previously

normal valves

504. what is the onset of acute

bacterial endocarditis caused

by S aureus?

rapid onset

505. organism that causes

subacute bacterial

endocarditis?

viridans streptococcus

506. virulence of the organism

that causes subacutebacterial endocarditis?

low virulence

507. presentation in subacute


smaller vegetations on

congenitally abnormal or

diseased valves

508. subacute bacterial

endocarditis can be sequelae

of what?

dental procedures

509. what is the onset of subacute


more insidious onset

510. endocarditis may be

nonbacterial secondary towhat?

malignancy

hypercoagulable statelupus (marantic/

thrombotic endocarditis)

511. S bovis is present in which

cause of endocarditis?

colon cancer

512. S epidermidis is present in

which cause of endocarditis?

prosthetic valves

513. which valve is most

frequently involved in


mitral

514. tricuspid valve endocarditis

is associated with what?

IV drug use (dont TRI

DRUGS)

515. tricuspid endocarditis is

associated with which

organisms?

S aureus

Pseudomonas

Candida

516. what are the complications of


chordae rupture

glomerulonephritis

suppurative pericarditis

emboli

517. rheumatic fever is a

consequence of what?

pharyngeal infection with

group A hemolytic

streptococci

518. early deaths in rheumatic

fever due to what?

myocarditis

519. late sequelae of rheumatic

fever include what?

rheumatic heart disease

520. relative frequency of valves

affected by rheumatic heart

disease?

mitral > aortic >>

tricuspid (high pressure

vavles affected most)

521. early lesion in rheumatic

fever is what?

MR


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522. what is the late lesion in

rheumatic fever?

MS

523. Rheumatic fever is


Aschoff bodies

Anitschkow's cells

elevated ASO titers

524. what are Aschoff bodies? granuloma with giant cells

525. what are anitschkow's

cells?

activated histiocytes

526. immunology of rheumatic

fever?

Type II HSR; not a direct

effect of bacteria

Ab to M protein

527. symptoms of Rheumatic

fever?

FEVERSS:

Fever

Erythema marginatum

Valvular damage

ESR

Red hot joints (migratory

polyarthritis)

Subcutaneous nodulesSt. Vitus' dance (Sydenham's

chorea)

528. acute pericarditis

commonly presents with

what?

sharp pain, aggravated by

inspiration, and relieved by

sitting up and leaning

forward

friction rub

529. ECG findings in acute

pericarditis?

widespread ST-segment

elevation and/or PR

depression

530. acute fibrinous

pericarditis is caused by

what?

Dressler's syndrome,

uremia

radiation

531. fibrinous pericarditis

presents with what?

loud friction rub

532. what are the causes of

serous pericarditis?

viral

noninfectious inflammatory

diseases

533. course of viral serous

pericarditis?

often resolves spontaneously

534. non infectious

inflammatory diseasesthat cause acute serous

pericarditis?

RA

SLE

535. what causes

suppurative/purulent

pericarditis?

bacterial infections with

pneumococcus or

streptococcus

536. frequency of purulent

pericarditis?

rare with antibiotics

537. what happens in cardiac

tamponade?

compression of heart by fluid

(blood effusions) in

pericardium leading toCO

538. what happens to

pressures in cardiac

tamponade?

equilibration of pressures in all 4

chambers

539. what are the findings

in cardiac

tamponade?

hypotension

venous pressure (JVD)

distant heart sounds

HR

pulsus paradoxus

540. what is pulsus

paradoxus?

in amplitude of systolic blood

pressure by >=10mHg during

inspiration

541. pulsus paradoxus

seen in what?

severe cardiac tamponade

asthma

OSA

pericarditis

croup


syphilitic heart

disease?

3 syphilis disrupts the vasa

vasorum of the aorta with

consequent atrophy of the vessel

wall and valve ring

543. in syphilitic heart

disease you may see

what?

calcification of the aortic root and

ascending aortic arch

544. syphilitic heart

disease leads to what

appearance?

tree bark appearance of the aorta

545. syphilitic heart

disease can result in

what?

aneurysm of the ascending aorta or

aortic arch and aortic insufficiency

546. what are the most

common primary

cardiac tumors in

adults?

myxomas

547. 90% of cardiac

myxomas occur

where?

in the atria (mostly left atrium)

548. myxomas are usually

described as what?

ball valve obstruction in LA

associated with multiple syncopal

episodes


frequent primary

cardiac tumor in

children?

rhabdomyomas

550. cardiac

rhabdomyomas are

associated with

what?

tuberous sclerosis

551. most common heart

tumor is what?

mets from melanoma or lymphoma

552. what is Kussmaul's

sign?

in JVP on inspiration instead of

normal


19/25

553. what happens

in Kussmaul's

sign?

inspiration negative intrathoracic

pressure not transmitted to the heart

impaired filling of RV blood backs up

into the venae cavaeJVD

554. Kussmaul's sign

may be seen in

what?

constrictive pericarditis

restrictive cardiomyopathies

RA or RV tumors

cardiac tamponade

555. Raynaud's

phenomenon

affects what

type of vessels?

small vessels

556. what happens

in Raynaud's

phenomenon?

blood flow to the skin due to arteriolar

vasospasm in response to cold

temperature or emotional stress

557. Raynauds

phenomenon is

most often seen

where?

fingers

toes

558. when is it called

Raynaud's

disease?

when primary (idiopathic)

559. when is it called

Raynaud's

syndrome?

when secondary to a disease process such

as mixed connective tissue disease, SLE,

or CREST

560. temporal

arteritis

generally affects

who?

elderly females

561. symptoms in

temporal

arteritis?

unilateral headache (temporal artery)

jaw claudication

562. temporal

arteritis may

lead to what?

irreversible blindness die to ophthalmic

artery occlusion

563. temporal

arteritis is

associated with

what?

polymyalgia rheumatica

564. temporal

arteritis most

commonly

affects which

vessels?

branches of carotid artery

565. pathology/labs

seen in

temporal

arteritis?

focal granulomatous inflammation

ESR

566. what is the

treatment for

temporal

arteritis?

high dose corticosteroids

567. Takayasu arteritis

typically affects who?

asian females


20/25

581. symptoms associated

with kawasaki

disease?

fever cervical lymphadenitis

conjunctival injection

changes in lips/oral mucosa

(strawberry tongue)

hand-foot erythema

desquamating rash

582. children with

kawasaki disease

may develop which

complications?

coronary aneurysmsMI, rupture

583. treatment for

kawasaki disease?

IV immunoglobulin and aspirin

584. Buerger's disease

affects who?

heavy smokers, males


21/25

609. incidence of cherry

hemangioma?

frequencywith age

610. what is a pyogenic

granuloma?

polypoid capillary hemangioma

that can ulcerate and bleed

611. pyogenic granuloma

is associated with

what?

trauma and pregnancy

612. what is a cystic

hygroma?

cavernous lymphangioma of the

neck

613. cystic hygroma is

associated with

what?

Turner syndrome

614. what is a glomus

tumor?

benign painful red-blue tumor

under fingernails

615. glomus tumor arises

from what?

modified smooth muscle cells of the

glomus body

616. what is bacillary

angiomatosis?

benign capillary skin papules found

in AIDS patients

617. bacillary

angiomatosis is

caused by what?

Bartonella henselae infections

618. bacillary

angiomatosis is

frequently mistaken

for what?

kaposi sarcoma

619. what is

angiosarcoma?

rare blood vessel malignancy

typically occuring in the head,

neck, and breast areas

620. angiosarcoma is

associated with

what?

patients receiving radiation

therapy, especially for BRCA and

hodgkins lymphoma

621. course of

angiosarcoma?

very aggressive and difficult to

resect due to delay in diagnosis

622. what

lymphangiosarcoma?

lymphatic malignancy associated

with persistent lymphedema (post

radical mastectomy)

623. what is kaposi

sarcoma?

endothelial malignancy most

commonly of the skin but also

mouth, GIT, and respiratory tract

624. kaposi sarcoma isassociated with

what?

HHV-8 and HIV

625. kasposi sarcoma is

frequently mistaken

for what?

bacillary angiomatosis

626. what is sturge-weber

disease?

congenital vascular disorder that

affects capillary sized blood vessels.

627. Sturge-weber

disease

manifests how?

with port wine stain (nevus flammeus) on

face

ispilateral leptomeningeal angiomatosis

(intracerebral AVM)

seizures

early onset glaucoma

628. what are the

antihypertensive

therapies for

essential

hypertension?

diuretics

ACEI

ARBs

Ca channel blockers

629. what are the

antihypertensive

therapies used

in CHF?

diuretics

ACEI/ARBs (compensated CHF)

K+ sparing diuretics

630. blockers must

be used

cautiously in

what?

decompensated CHF

631. blockers are

contraindicated

in what?

cardiogenic shock

632. what are the

antihypertensive

therapies used

in DM?

ACEI/ARBs

Ca channel blockers

diuretics

blockers

blockers

633. ACEIs are

protctive against

what in DM?

diabetic nephropathy

634. which drugs areCa channel

blockers?

nifedipineverapamil

diltiazem

amlodipine

635. MOA of Ca

channel

blockers?

block voltage dependent L type calcium

channels of cardiac and smooth muscle an

thereby reduce muscle contractility

636. relative effect on

smooth muscle

of Ca channel

blockers?

Vascular smooth muscle-

amlodipine=nifedipine>diltiazem>verapa

637. relative effect onheart of Ca

channel

blockers?

heart-verapamil>diltiazem>amlodipine=nifedip

Verapamil-ventricle

638. clinical use of Ca

channel

blockers?

hypertension

angina

arrhythmias (not nifedipine)

prinzmental's angina

Raynauds


22/25

639. toxicity of Ca

channel

blockers?

cardiac depression

AV block

peripheral edema

flushing

dizziness

constipation

640. MOA of

hydralazine?

cGMPsmooth muscle relaxation

vasodilates arterioles > veins

afterload

641. clinical use of

hydralazine?

severe hypertension

CHF

first line tx for htn in pregnancy, with

methyldopa

frequently coadministered with blocker to

prevent reflex tachycardia

642. toxicity of

hydralazine?

compensatory tachycardia (CI in

angina/CAD), fluid retention, nausea, HA,

angina

Lupus like syndrome

643. commonly

used drugs for

malignant

hypertension

treatment?

nitroprusside

nicardipine

clevidipine

labetalol

fenoldopam

644. features of

nitroprusside

for malignant

hypertension?

short acting

cGMP via direct release of NO

645. toxicity of

nitroprusside?

can cause cyanide toxicity

646. MOA offenoldopam?

dopamine D1 receptor agonistcoronary,peripheral, renal, splanchnic

vasodilationBP and natriuresis

647. MOA of

nitroglycerine,

isosorbide

dinitrate?

vasodilate by releasing NO in smooth

muscle, causing cGMP in and smooth

muscle relaxation

dilates veins>>arteries

preload

648. clinical use of

GTN, ISDN?

angina

pulmonary edema

649. toxicity of

GTN, ISDN?

reflex tachycardia, hypotension, flushing,

HA, "monday disease" in industrialexposure

650. what is

monday

disease in

industrial

GTN, ISDN

exposure?

development of tolerance for the

vasodilating action during the work week

and loss of tolerance over the weekend

results in tachycardia, dizziness, and HA

upon reexposure

651. what is the goal

of antianginal

therapy?

reduction of myocardial O2 consumption

(MVO2) by decreasing >=1 of the

determinants of MVO2: EDV, BP, HR,

contractility, ejection time

652. effect of nitrates on EDV?

653. effect of blockers on EDV?

654. effect of nitrates+ blockers on

EDV?

no effect or

655. effect of nitrates on BP?

656. effect of blockers on BP?

657. effects of nitrates + blockers

on BP?

658. effect of nitrates on

contractility?

(reflex response)

659. effects of blockers on

contractility?

660. effect of nitrates + blockers on

contractility?

little/no effect

661. effect of nitrates on HR? (reflex)

662. effect of blockers on HR?


HR?

664. effect of nitrates on ejection

time?

665. effect of blockers on ejection

time?


ejection time?

little/no effect

667. effect of nitrates on MVO2?

668. effect of blockers on MVO2?


MVO2?

670. how do Ca channel blockers

compare to the effects of

nitrates and beta blockers on

MVO2?

nifedipine is similar to

nitrates

verapamil is similar to

beta blockers

671. which are the partial agonists

contraindicated in angina?

pindolol and acebutalol

672. effect of HMG-CoARI's on LDL?

673. effect of HMG-CoARIs on HDL?

674. effect of HMGCoARI's on TG?

675. MOA of HMGCoARIs? inhibit conversion of

HMG-CoA to

mevalona te, a

cholesterol precursor

676. AE of HMGCoARIs? hepatotoxicity (LFT)

rhabdomyolysis

677. effect of niacin on LDL?

678. effect of niacin on HDL?


23/25

679. effect of niacin

on TG ?

680. MOA of niacin? inhibits lipolysis in adipose tissue;

reduces hepatic VLDL secretion into

circulation

681. AE of niacin? red, flushed, face which is by aspirin or

long term use

hyperglycemia (acanthosis nigricans)hyperuricemia (exacerbates gout)

682. effect of bile

acid resins on

LDL?

683. effect of bile

acid resins on

HDL?

slightly

684. effect of bile

acid resins on

TG?

slightly

685. MOA of bile acidresins?

prevent intestinal reabsorption of bileacids; l iver must use cholesterol to make

more

686. AE of bile acid

resins?

patients hate it-

tastes bad and causes GI discomfort

absorption of fat soluble vitamins

cholesterol gallstones

687. effect of

ezetimibe on

LDL?

688. effect of

ezetimibe onHDL ?

no effect

689. effect of

ezetimibe on

TG?

no effect

690. MOA of

ezetimibe?

prevent cholesterol reabsorption at small

intestinal brush border

691. AE of ezetimibe? rare in LFTs

diarrhea

692. effects of

fibrates on

LDL?

693. effects of

fibrates on

HDL?

694. effects of

fibrates on TG?

695. MOA of

fibrates?

upregulate LPLTG clearance

696. AE of fibrates? myositis

hepatotoxicity

cholesterol gallstones

697. PK of digoxin? 75% bioavailability

20-40% protein bound

t1/2=40h

urinary excretion

698. MOA of digoxin? direct inhibition of Na+/K+

ATPase leads to indirect

inhibition of Na+/Ca++

exchanger/antiport

[Ca++]ipositive inotropy

stimulates vagusHR

699. clinical use of digoxin? CHF

atrial fibrillation

700. why use digoxin in

CHF?

contractility

701. why use digoxin in

atrial fibrillation?

conduction at AV node and

depression of SA node

702. what are the major

types of side effects seen

in digoxin toxicity?

cholinergic

ECG

hyperkalemia- poor prognosticindicator

703. what are the cholinergic

side effects associated

with digoxin toxicity?

nausea

vomiting

diarrhea

blurry yellow vision (VanGogh)

704. ECG side effects seen in

digoxin toxicity?

PR

QT

ST scooping

T wave inversion

arrhythmia

AV block

705. factors predisposing to

digoxin toxicity?

renal failure

hypokalemia

quinidine

706. how does renal failure

predispose digoxin

toxicity?

excretion

707. how does hypokalemia

predispose digoxin

toxicity?

permissive for digoxin binding

at K+ binding site on Na/K

ATPase

708. how does quinidine

predispose digoxin

toxicity?

digoxin clearance; displaces

digoxin from tissue binding

sites

709. what is the antidote for

digoxin toxicity?

slowly normalize K+

lidocaine

cardiac pacer

anti-digoxin Fab fragments

Mg++

710. what type of drug are all

the type I Na channel

blocker

antiarrhythmics?

local anesthetics


24/25

711. MOA of class I

antiarrhythmics?

conduction (especially in

depolarized cells)

slope of phase 0 depolarization

and threshold for firing in

abnormal pacemaker cells

712. what does it mean

that class I

antiarrhythmics are

state dependent?

selectively depress tissue that is

frequently depolarized

(tachycardia)

713. what causes

toxicity for all class I

antiarrhythmic

drugs?

hyperkalemia

714. which drugs are the

Class IA

antiarrhythmics?

Quinidine

Procainamide

Disopyramide

The Queen Proclaims Diso's

Pyramid

715. MOA of Class IA

antiarrhythmics?

AP duration

ERP

QT interval

716. Class IA

antiarrhythmias

affect what kind of

arrhythmias?

atrial and ventricular arrhythmias,

especially reentrant and ectopic

supraventricular a nd ventricular

tachycardia

717. quinidine toxicity? cinchonism- headache, tinnitus

718. procainamide

toxicity?

reversible SLE-like syndrome

719. disopyramide

toxicity?

heart failure

720. toxicities common to

all Class IA

antiarrhythmics?

thrombocytopenia,

torsades de pointes due to QT

interval

721. which drugs are the

class IB

antiarrhythmics?

Lidocaine

Mexilitine

Tocainide

I'd Buy Lidy's Mexican Tacos

(phenytoin)

722. which type of

antiarrhythmic is

best post MI?

IB

723. MOA of class IB

antiarrhythmics?

AP duration

Preferentially affect ischemic or

depolarized Purkinje and

ventricular tissue

724. Class IB

antiarrhythmics are

useful in what?

acute ventricular arrhythmias

(especially post MI) and in digitalis

induced arrhythmias

725. toxicity of Class IB

antiarrhythmics?

local anesthetic

CNS stimulation/depression

cardiovascular depression

726. which drugs are class IC

antiarrhythmics?

flecainide

propafenone

727. mnemonic for IC

antiarrhythmics?

IC is CI in structural heart

disease and post MI

728. MOA of class IC

antiarrhythmics?

no effect on AP duration

729. clinical use of class IC

antiarrhytmics?

useful in ventricular

tachycardias that progress to

VF and in intractable SVT

usually used only as last resort

in refractory tachyarrhythmias

for patients without structural

abnormalities

730. toxicity of class IC

antiarrhythmics?

proarrhythmic, especially post

MI

significantly prolongs

refractory period in AV node

731. effects of class I

antiarrhythmics onventricular AP graph?

all class I- clockwise decrease

in slope of phase 0IA- prolong AP- rightward

stretch of phase 3

IB- shorten AP- leftward

shrink of phase 3

IC- no effect- barely to the left

of normal AP

732. the class II

antiarrhythmics are

what type of drugs?

blockers

733. which drugs are used as

class II

antiarrhythmics?

metoprolol

propanolol

esmololatenolol

timolol

734. MOA of class II

antiarrhythmics drugs?

SA and AV nodal activity by

cAMP, Ca++ currents

suppress a bnormal pacemakers

byslope of phase 4

735. which class II

antiarrhythmic is very

short acting?

esmolol

736. what part of the heart is

particularly sensitive toclass II

antiarrhythmics?

AV node

737. ECG changes seen with

class II

antiarrhythmics?

PR interval

738. clinical use of class II

antiarrhythmics?

ventricular tachycardia, SVT,

slowing ventricular rate during

atrial fibrillation and atrial

flutter


25/25

739. toxicity of class II

antiarrhythmics?

impotence

exacerbation of asthma

CV effects

CNS effects

may mask the signs of

hypoglycemia

740. CV AE of class II

antiarrhythmics?

bradycardia

AV block

CHF

741. CNS effects of class II

antiarrhythmics?

sedation

sleep alterations

742. AE specific to

metoprolol?

dyslipidemia

743. treat overdose of

metoprolol with what?

glucagon

744. cardiac AE specific to

propanolol?

can exacerbate vasospasm in

Prinzmental's angina

745. which are the class III

antiarrhythmics?

Amiodarone

IbutilideDofetilide

Sotalol

AIDS

746. all class III

antiarrhythmics are

what type of drug?

K+ channel blockers

747. MOA of class III

antiarrhythmics?

AP duration, ERP

748. when are class III

antiarrhythmics used?

when others fail

749. ECG changes caused by

class III

antiarrhythmics?

QT interval

750. AE of sotalol? torsades de pointes

excessive block

751. AE of ibutilide? torsades de pointes

752. AE of amiodarone? pulmonary fibrosis

hepatotoxicity

thyroid dysfunction (40% I by

weight)

corneal deposits

skin deposits (blue/grey)resulting in photodermatitis

neurologic effects

constipation

CV effects (bradycardia, heart

block, CHF)

753. what are the

antiarrhythmic effects

of amiodarone?

has class I , II, III, and IV

effects because it a lters the lipid

membrane

754. what do you need to check

when using amiodarone?

PFTs

LFTs

TFTs

755. effect of all class III

antiarrhythmics on

ventricular AP curve?

wide rightward stretch in

phase 3 prolongs AP and

ERP

756. which drugs are class IV

antiarrhythmics?

verapamil

diltiazem

757. all class IV antiarrhythmics

are what type of drug?

Ca channel blockers

758. MOA of class IV

antiarrhythmics?

conduction velocity,

ERP, PR interval

759. clinical use of class IV

antiarrhythmics?

prevention of nodal

arrhythmias (SVT)

760. toxicity of class IV

antiarrhythmics?

constipation

flushing

edema

CV effects (CHF, heart

block, sinus nodedepression)

761. MOA of adenosine as

antiarrhythmic?

K+ out of cells

hyperpolarizing the cell

+Ica

762. adenosine is the drug of

choice for what?

diagnosing/abolishing

supraventricular

tachycardia

763. duration of action of

adenosine?

~15s

764. toxicity of adenosine? flushing

hypotension

chest pain

765. effects of adenosine blocked

by what?

theophylline and caffeine

766. clinical use of Mg++ as

antiarrhythmic?

effective in torsades de

pointes and digoxin

toxicity

FA Cardiology

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