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Cardiac Pharmacology > EXAM 3 > Flashcards

EXAM 3 Flashcards

1
Q

fibromuscular dyplasia will appear how?

A

can occur anywhere, but tends to look like beads on a string - tends to occur in the kidney

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2
Q

wht is conn syndrome

A

when you have a tumor in the zona glomerulosa that releases excess aldosterone –> Na+ retention and SVR increase

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3
Q

explain DOC hypersecretion

A

increased ACTH from the anterior pituitary for any reason leads to hypersecretion of deoxycortisone, an aldoserone precurosor –> retention of Na+

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4
Q

explain GRA: Glucocortocoid remediable aldosteronism

A

genes encoding aldosterone synthase and 11b hydroxylase are linked during embryogenesis

  • get hypersecretion of glucocortocoids and aldsterone
  • have very severe HTN that starts early in life
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5
Q

how to treat GRA

A

glucocortocois

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6
Q

three adrenal gland disorders

A

Con syndrome, DOC hypersecretion, glucocortocoid remediable aldosteronism

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7
Q

cushing’s syndrome

A

incidence of HTN is greater in cushing’s - excess glucocortocoid. this increases angiotensinogen

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8
Q

most common risk of cushings

A

oral corticosteroids

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9
Q

symptoms of cushings

A

buffalo hump, broomstick arm+ legs,

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10
Q

pheochromacytoma

A

increased NE from the adrenal medulla leading to an increase in systolic and diastolic pressure

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11
Q

symptoms of pheo

A

palpittions, hypertension, glycosuria and extree systolic HTN

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12
Q

how do natriuretic hormones work

A

they dump Na+ into the urine, but cause Ca to accumulate –> vascular smooth muscle contraction

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13
Q

2x more likely to develop ____ than ____ in smoking

A

PAD

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14
Q

explain the ankle-brachial index

A

on the arms and ankles the BP should be the same, but in peripheral artery disease, sometimes it is not

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15
Q

in PAD, a drop of ____ as you go down the leg is significant

A

20mmHg

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16
Q

how do you treat PAD

A
  • smoking cessation, HTN control, statin,
  • antiplatelet therapy: ASA
  • exercise
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17
Q

the timing of surgical repair of an aortic aneurysm is related to

A

the diameter and the rate of increase

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18
Q

pulsatile abdominal mass is a

A

abdominal aortic aneurysm

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19
Q

what will you find in a thoracic abdominal aneurysm

A

cystic medial necrosis - a mucoid material accumulation in the media of the aorta

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20
Q

risk factors of AAA

A

smoking, male, atherosclerosis

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21
Q

descending thoracic AA due to

A

atherosclerosis

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22
Q

ascending thoracic AA due to

A

bicuspid aortic valve, connective tissue disease, syphillis

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23
Q

genetic factors leading to an ascending thoracic AA

A

Marfan, ehlers danlos and loeys deitz

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24
Q

defect in marfan

A

FBN1

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25
Q

defect in ehlers danlos

A

type III collagen

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26
Q

defect in loeys deitz

A

TGFBR

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27
Q

ideal size to operate on an aortic aneurysm

A

5cm

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28
Q

what is the genetic inheritance pattern of marfan

A

autosomal dominant

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29
Q

what tears in an aortic dissection

A

intimina

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30
Q

where is the blood located in an aortic dissection

A

in the media

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31
Q

what structures can a debakey typeI/ ascending Aortic dissection damage

A

the aortic annulus and RCA

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32
Q

abrupt onset of severe chest pain radiating to the back

A

aortic dissection

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33
Q

what does a negative D-dimer test tell you about aortic dissection

A

rules out dissection

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34
Q

how does one treat an aortic dissetion

A

1) lower BP + HR with IV labetolol and nitroprusside, BB if the BP is already low to decrease HR

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35
Q

what do we want to AVOID in aotic dissections

A

pure venous dillators such a nitroglycerin

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36
Q

treating type A dissection

A

surgical emergency

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37
Q

mutation leading to vascular ehlers danlos

A

COL3A

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38
Q

best way to diagnose aortic dissecction

A

Computer thomography angiography

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39
Q

how to diagnose PAD

A

non-invasive flow studies

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40
Q

type of arteriolar disease seen in diabetes

A

hyaline arteriosclerosis

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41
Q

what cases the hyerplastic appearance of arteriosclerosis

A

smooth muscle proliferation

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42
Q

acute renal failure from which type of arteriosclerosis

A

hyperplastic

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43
Q

lipo proteins that are pro-atherogenic

A

cylomicrons/ VLDL

LDL - apo B (90% of apo B is LDL)

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44
Q

anti atherogenic lipoproteins

A

HDL

Apo A

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45
Q

what parameter of HDL so i care about

A

how many of the particles you have, not how much cholesterol is in the body

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46
Q

higher LDL leads to an increased risk of

A

coronary artery disease

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47
Q

what does HDL take from the VLDL and LDL

A

cholesterol

and takes it from the periphery and back to the liver.

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48
Q

most genetic causes of dyslipidemia are due to a

A

LDL receptor defect

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49
Q

if LDL> ______ you are likely to have a heterozygrous LDL R problem

A

LDL>190

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50
Q

when Triglycerides are mre than 1000 you suspect ____ and worry about what condition

A

genetic defect and pancreatitis

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51
Q

drugs that can make your cholesterol very high

A

protease inhibitors for HIV

corticosteroids and immunosupressant like rapamycin

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52
Q

major statins

A

atrovastatin and rosuvastatin

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53
Q

what do statins do

A

they block the production of cholesterol by the liver

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54
Q

statin side effects

A

transaminitis - increase in ASL and ALT,

Rhabdomyalasis

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55
Q

rhabdomyalasis high risk population

A

advaced age, women, frailty, alcohol abuse

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56
Q

statin drug interaction that can put at risk for rhabdomyalysis

A

fibrates

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57
Q

what does ezetamide fo

A

blocks uptake fo bile acids back into the circulation

58
Q

PCSK9 acts how

A

is a cofactor for the LDL receptor, which marks it for degredation. so the more PCSK9 you have the less LDL receptor and higher cholesterol

59
Q

how do PCSK9 inhibitors work

A

if not PCSK9, LDL receptors stay on the liver all the time and are never broken down, so very low cholesterol in the circulation

60
Q

golden standard for cholesterol treatments?

A

statins - most effective for reducing cardiovascular risk - and ezetamide

61
Q

dyslipidemia is driven by _____ containing proteins

A

apo b on LDL and VLDL

62
Q

what do fibrates decrease the most?

A

TAGs

63
Q

what causes hyaline arteriolosclerosis

A

diabetes and HTN

64
Q

most predicitive inflammatory marker of MI risk

A

CRP + Total cholesterol:HDL - markers of the acute phase repsonse

65
Q

prostacyclin is a

A

vasodillator

66
Q

Platelet aggrivating factor is a

A

vasoconstrictor

67
Q

what do statins do to eNOS and what does eNOS do

A

statins inrease

68
Q

where are nicotinic Ach receptors found

A

preganglionic synapse of PNS, SNS and at skeletal muscle post ganlgionic

69
Q

post mi, cardiac arrhthmias occur

A

within 1st few days after Mi

70
Q

post MI, fibrinous pericarditis occurs

A

1-3 days after MI

71
Q

post Mi, papillary muscle rupture occurs

A

2-7 days

72
Q

IC setpum rupture after an MI will occur

A

3-5 post Mi

73
Q

aneurysm formation after an Mi will occur

A

5-14 days post MI

74
Q

dressler syndrome occurs how long after an Mi

A

weeks-months

75
Q

probability of death from CVD

A

47%

76
Q

normal response of a vessel to acetycholine is to

A

dillate

77
Q

what drugs promote eNOS function

A

statins

78
Q

EXCESS NO CAN predispose to

A

shock

79
Q

too little NO leads to

A

atherosclerosis

80
Q

what molecue to chemokines use to attract an activate monocytes

A

monocyte chemoattractant protein-1 MCP-1

81
Q

smooth muscle cels in atheroscelerosis secrete

A

collagen and elastin

82
Q

what moleculae to platelets make that results in vasconstriction and anginal pain

A

TXA2

83
Q

what is the singel most important determinany of stenosis for any given level of flow

A

the minimum cross sectional area within the stenosis

84
Q

low ATP, due to MI, and inability to relax the LV leads to

A

diastolic dysfuntion

85
Q

transient sarcomeric dyskinesis due to low O2 leads to

A

systolic sydfunction

86
Q

what releases TPA

A

endothelial cells

87
Q

what activates tpa

A

thrombin

88
Q

what does tpa do

A

it converts plasmin to plasminogen, which breaks down fibrin

89
Q

what is an inhibitor of thombolysis

A

plaminogen activator inhibitor, PAI-1

90
Q

elevation in cardiac biomarkers in untable angina?

A

no

91
Q

describe prinzmetal agina

A

episodic chest pain that occurs at rest, that is secondary to vasospasm

92
Q

does prinzmetal angina respond to vasodillators?

A

yes, responds promtly to nitroglycerin

93
Q

ST segment requirements for dianogsis of a STEMi

A
  • St elevation in 2 contiguous leads or new LBBB

- St elevation = 1mm limb, and 2mm in precordial

94
Q

which leads indicate an ateroseptal infarct

A

V1-V4

95
Q

what artery would be occluded in an ateroseptal infarct

A

LAD

96
Q

what leads indicate a lateral infarct

A

I, AVL, V5 and V6

97
Q

what arteries supply the lateral heart

A

L circumflex and the LAD diagonal

98
Q

what leads indicate an inferior infarct

A

II, III and Avf

99
Q

what arteries supply the inferior part of the heart

A

RCA if right dominant
Lcx if left cominant
and mid LAd

100
Q

see yellowing alone, how old is the Mi?

A

1-3 days

101
Q

see yellow with rd borders, how old si the Mi

A

2-4 day range

102
Q

no red or yellow, jsut mushy or necrotic, how old is the infarct

A

7-10 days old

103
Q

red-grey infarct with red rim is how old?

A

more than 10 days

104
Q

previous myocarditis pointsyou towards a diagnosis of

A

dilated cardiomyopathy

105
Q

an s3 sound makes you think that the heart is

A

dilated

106
Q

s4 heart sound makes you think the heart is

A

hypertrophic

107
Q

hypertrophic cardioyopathy due to what mutation

A

b-myosin heavy chain

108
Q

what disease is caused by defects in adhesion proteins such a desmosomes

A

arrhythmogenic right ventricular cardiomyopathy

109
Q

describe arrhythmogenic right ventricular cardiomyopathy

A

the RV wall is thinned with fatty ifnilatrates and fobrosis

110
Q

most common reason for a restrictive cardiomyopathy

A

amyloidosis

111
Q

what is seen on histo in restricitive cardiomyopathies

A

eosinophilic protein deposited btw cardiac myositis

112
Q

key sign in sarcoid cardiomyopathy

A

non caseating granulomas leading to a thick and stiffened paricardium

113
Q

how to diagnose sarcoid cardiomyopathy

A

MRI

114
Q

viral infections leading to myocarditis

A

group b coxackie and chagas disease

115
Q

fibrinous/serofibrinous pricarditis is usally associated with what findings or conditions

A

pericardial rub and dresslers syndrome

116
Q

myofilbrillar disarray seen in

A

hypertrophic idiopathic subaortic stenosis

117
Q

organiss that infect vascular endothelial cells

A

Rickettsia, Orientsia

118
Q

organisms that infect circulating granuocytes

A

Ehrlichia, Anaplasma

119
Q

intrcellular pathogen that ifnects erythrocytes

A

Bartonella bacilliformis

120
Q

most bacterial spread is via

A

lymphatic capillaries through the lymph nodes into the thoracic duct.

121
Q

Prototype parasitic bloodstream pathology

A

malaria `

122
Q

homes of a malria virus

A

in the misuito, in the RBC and in the liver hepatocyte

123
Q

requirement to be on the blod borne pathoge list

A

characterized by a phase in which the microbes causing the disease may circulate in the blood for a prolonged period. They are therefore capable of being transmitted through blood or other potentially infectious materials.

124
Q

histo findings in rheumatic fever

A

ashoff bodies and antischow cells

125
Q

syptoms of aortic stenosis

A

Syndope
Angina
Dyspnea
pulsus parvus et tardus

126
Q

pulsus parvus et tardus means

A

weak pulses w a delayed

127
Q

murmur of aortic stenosis

A

crescendo-decrescndo murur radiating to the corotids

128
Q

a late aortic stenosis murmur means

A

more severe

129
Q

drugs to avoid in aortic stenosis

A

preload reducers such a diuretics and nitroglycerin

130
Q

most coomon cause of aortic regurg

A

aortic root dilation

131
Q

a wide pulse pressure points you towards which valve deformity

A

aortic insufficiency

132
Q

in aortic regurg you want to to treat by

A

lowering the afterload

133
Q

describe sound of aortic insufficiency

A

high pitched diasotlic

134
Q

widely split S2 think

A

pulmonic stenosis

135
Q

notched alongated sick looking p wave think

A

mitral stenosis

136
Q

opening snap wiht loud first heart sound heard in

A

mitral stenosis

137
Q

does a short or longer time between S2 and the opening snap worse?

A

shorter time btw OS and S2 is worse

138
Q

main reason for mitral insufficiency

A

myxamatous degenertion

139
Q

for mitral stenosis, what mediation should you NOT use

A

b blockers or negative inotropes

140
Q

kleinfelters assocaited with

A

mitral valve prolapse

141
Q

opening click heard btw S1 and S1 think

A

mitral valve prolapse

Cardiac Pharmacology (3 decks)

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