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Shit-list > Cardio - Path > Flashcards

Cardio - Path Flashcards

1
Q

polyarteritis nodosa (autoimmune) causes what kind of vasculitis

A

fibrinoid necrosis, segmental, transmural

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2
Q

3 causes of amyloidosis vasculitis

A

1) plasma cell dyscrasia
2) chronic systemic inflammation – RA
3) genetic - Transthyretin

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3
Q

what do injured endothelial cells secrete during the first step of atherosclerosis?

A

IL-1, TNFalpha (the pro-inflammatory cytokines)

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4
Q

What do injured endothelial cells have less of? (protein things)

A

decreased superoxide dismutase, less vasodilator and antithrombotic NO and prostacyclin

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5
Q

what drug protects against inflammation? specifically anti-interleukin-1beta?

A

canakinumab

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6
Q

what two things have been found to activate the inflammasome?

A

cholesterol crystals and free fatty acids

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7
Q

triggering the inflammasome results in activaiton of what enzyme

A

caspase-1

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8
Q

inflammasome –> caspase-1 –> (? inflammatory cytokine)

A

IL-1

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9
Q

why is neovascularization of atherosclerotic plaques important?

A

abnormal, irregular, small blood vessels - prone to rupture

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10
Q

what drug can be given to help reduce CV events in pts with atherosclerosis? (think anti-gout drug, b/c of similar mechanisms of urate crystals and cholesterol crystals)

A

colchicine –> improves CRP

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11
Q

effects of statins on atherosclerosis

A

1) decrease lipid content of plaques
2) decrease macrophage activity (inflammation) in plaques
3) increase stabilizing fibrous content of plaques

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12
Q

what percentage of ACD events in the LAD?

A

one-half

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13
Q

what percentage of ACD events are in the RCA?

A

one-third

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14
Q

what percentage of ACD events are in the LCX

A

one-sixth

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15
Q

a thrombus overlying an atherosclerotic plaque is result of superficial erosion - who is more common in?

A

women

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16
Q

what is thought to cause superficial erosion? what causes this?

A

apoptosis of endothelial cells –> due to oxidative stress and hypochlorous acid

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17
Q

why is methotrexate helpful in preventing atherosclerotic CV events?

A

cell proliferation of fibroblasts, SM cells, endothelial cells, and lymphocytes plays a role in atherosclerosis

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18
Q

what are common causes of coronary vasospasm?

A

stimulant abuse –> amphetamines, nose candy

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19
Q

atheroembolism is associated with what? (a histo feature)

A

eosinophilia

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20
Q

what is etiology of superficial erosion leading to thrombus formation?

A

erosion unamasks pro-coagulant stuff –> tissue factor released from apoptosed endothelial cells, or collagen

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21
Q

combination of abundant basophilic debris (nuclear dust) + geographic pattern necrosis

A

“pathergic necrosis”

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22
Q

pathergic necrosis - what disease?

A

granulomatosis with polyangiitis (Wegener’s)

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23
Q

contraction band necrosis

A

1) when the MI is caused by coronary vasospasm (cocaine, meth, epi - pheochromocytoma)
2) reperfusion

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24
Q

Trousseau syndrome

A

venous thrombi may result from elaboration of procoagulant factors from malignant tumors –> hypercoagulable state –> thromboses in different vascular beds at different times (migratory thrombophlebitis)

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25
Q

Sturge Weber Syndrome

A

(encephalotrigeminal angiomatosis) - congenital disorder, facial port wine nevi, ipsilateral venous angiomas in (something), mental retardation, seizures, hemiplegia, radiopacities of the skull

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26
Q

SVC syndrome

A

neoplasms that compress or invade the SVC (bronchogenic carcinoma or mediastinal lymphoma) - the resulting obstruction –> marked dilation of veins of the nead, neck, and arms associated w/ cyanosis

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27
Q

Osler-Weber-Rendu disease

A

hereditary hemorrhagic telangiectasia –> autosomal dominant –> mutations in genes that encode components of TGF-beta signaling pathway in endothelial cells - telangiectasias present at birth - widely distributed - shit can spontaneously rupture, causing epistaxis (nosebleed), GI bleeding, or hematuria

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28
Q

IVC syndrome

A

neoplasms that compress or invade the IVC or by thrombus –> neoplasms -

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29
Q

what neoplasma (associated w/ IVC syndrome) - tend to grow within veins

A

hepatocellular carcinoma and renal cell carcinoma

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30
Q

what happens when you occlude the IVC

A

marked lower extremity edema, distention of superficial collaterla veins of lower abdomen

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31
Q

causes of portal vein HTN

A

liver cirrhosis –> less frequently, portal vein obstruction or hepatic vein thrombosis

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32
Q

results of portal vein HTN

A

opening of porto-systemic shunts - increased blood flow into veins at gastro-esophageal junction = esophageal varices, rectum = hemorrhoids, and periumbilical veins of abdominal wall = caput medusae

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33
Q

what is the most impt result of portal vein HTN

A

esophageal varices - prone to rupture, can lead to massive upper GI hemorrhage

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34
Q

Kaposi Sarcoma caused by HHV-8–> what induces VEGF

A

virally encoded G protein induces VEGF

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35
Q

HHV-8 - what drives proliferation

A

viral homologue of cyclin D,

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36
Q

what is something else that KSHV / HHV-8 has that helps mess w/ normal proliferation

A

virally encoded proteins that inhibit p53

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37
Q

AIDS patient w/ KS, what is good tx

A

HIV antiretroviral therapy

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38
Q

KS associated w/ immunosuppression - good tx?

A

withdraw the immunosuppression

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39
Q

8 risk factors of venous stasis dermatitis

A

1) age
2) female sex
3) obesity
4) DVT
5) standing occupation
6) fam hx of venous disease
7) heart failure
8) HTN

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40
Q

how to differentiate arterial vs venous in lower extremity ulcer (factors pointing towards venous)

A

1) medial ankle location
2) surrounding area of hemosiderin deposition
3) fibrosis around ulcer
4) granulation tissue in base

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41
Q

DVT - calf measurements

A

asymmetry over 2 cm = positive screening test

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42
Q

what is negative predictive value of negative D-dimer

A

99%

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43
Q

what about the Sn and Sp of D-dimer

A

good Sn, poor Sp

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44
Q

in addition to prolonged immobilization, what is risk for DVT (5)

A

1) postoperative state
2) CHF
3) pregnancy
4) oral contraceptive use
5) obesity

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45
Q

EKG w/ no p waves - most likely scenario

A

ventricular tachycardia (but could be a fib as well technically)

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46
Q

syncope likely to be caused by what abnormality in heart rate

A

sinus bradycardia

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47
Q

normal vector of the heart

A

R –> L
top –> bottom
anterior –> posterior

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48
Q

inferior leads

A

II, III, AvF

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49
Q

anterior leads

A

v leads

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50
Q

what is the number 1 cause of stroke

A

atrial fibrillation

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51
Q

primary cause of sudden cardiac death (SCD)

A

ventricular tach

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52
Q

tx for ventricular tach

A

AED or ICD

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53
Q

where do you put ICD

A

tip of RV

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54
Q

key word/phrase for complete heart block

A

atrio-ventricular dissociation

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55
Q

tx for heart block

A

pacemaker

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56
Q

the 2 determinants of myocardial O2 demand

A

1) HR

2) systolic BP

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57
Q

what is the pathophysiology of MI and the findings on EKG

A

1) abrupt occlusion of coronary artery leading to muscle DYING
2) ST elevation (STEMI)

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58
Q

tx for bradycardia (after you have taken away Beta blockers and thyroid looks nml, but still bradycardic)

A

pacemaker

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59
Q

how long should QT interval be

A

less than 1/2 the RR interval

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60
Q

most common cause of long QT

A

certain drugs

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61
Q

complications of long QT

A

fatal arrhythmias

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62
Q

what is another example of dissociation (besides heart block - which is the most common form of dissociation)

A

ventricular tachycardia

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63
Q

what features present w/ hypertrophic cardiomyopathy cause it to be hypertrophic obstructive cardiomyopathy

A

subaortic stenosis and obstruction

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64
Q

histologic finding of hypertrophic cardiomyopathy

A

myocyte disarray

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65
Q

key clinical finding of hypertrophic cardiomyopathy

A

syncope after exercise

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66
Q

dx of hypertrophic cardiomyopathy (pt comes in w/ hx of syncope after exertion, what do you do)

A

get an echo

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67
Q

what is inheritance of HCM

A

autosomal dominant - test first degree relatives

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68
Q

what is the defect in HCM?

A

beta-myosin heavy chain - this is why it is auto dominant - you can’t have only one good copy of the gene and be aight

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69
Q

how do you qunatify LVH? where do you measure

A

measure posterior wall, cut off is 1.5 cm

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70
Q

classic clinical triad for aortic stenosis

A

dyspnea, angina, SCD

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71
Q

gross anatomical features of rheumatic valvulitis

A

fibrous adhesions extending from commisures, closing valve partially, no calcifications

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72
Q

aortic stenosis due to rheumatic disease - what else common along with it

A

mitral stenosis 95% of the time

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73
Q

HTN causes what in the arteries

A

thickening of wall –> increased SM cells and fibrous tissue

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74
Q

finding of small arteries (can be pulmonary) associated w/ HTN

A

onion skinning

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75
Q

most common cause of cor pulmonale (50% in the state of TN)

A

COPD

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76
Q

second most common cause of cor pulmonale

A

old organized pulmonary thromboembolus - chronic PE w/ numerous small (individually asymptomatic) PE

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77
Q

micro pathology (morphology) or a subacute organizing PE

A

residual condensed fibrin, fibroblasts, myxoid ground substance and hemosiderin

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78
Q

a third, common cause of pulmonary HTN leading to cor pulmonale

A

IV drug abuse - leads to accumulation of foreign bodies - elicits a foreign body giant cell reaction

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79
Q

how do you measure preload?

A

pulmonary artery catheter –> somehow getting catheter into LV to measure pressure there

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80
Q

what are 2 major determinants of afterload?

A

1) SBP

2) dimensions of LV

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81
Q

define heart failure

A

a syndrome of dysfunction of myocardial contractility, where heart cannot generate enough flow to meet the metabolic needs of the body

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82
Q

Dx of heart failure –> we talked about 4 things

A

1) PMI - displaced down and to the left
2) PMI - larger than the size of a dime
3) S3 gallop, auscultate w/ bell, goes away if you pres down
4) JVD - jugular distended above level of clavicle w/ pt supine

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83
Q

EF

A

SV/EDV

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84
Q

what does EF not tell us (4 things)

A

1) CO
2) renal blood flow
3) RAAS
4) salt and H2O retention

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85
Q

how much of CO goes to nephron

A

20%

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86
Q

when does kidney turn on RAAS?

A

if it gets less than 20% of CO

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87
Q

what other factors turn on the RAAS?

A
  • standing up

- heat

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88
Q

RAAS upregulates renin, which upregulates Ang II –> what are the 2 effects of Ang II?

A

1) vasoconstrictor –> inc afterload

2) promote secretion of aldosterone

89
Q

what does aldosterone do

A

promotes retention of salt and water

90
Q

ascites/anasarca - how much fluid has accumulated

A

30 L

91
Q

put on diuresis, how much do you diurse per day

A

1 L

92
Q

4 hypertrophic heart diseases

A

1) hypertensive
2) hypertrophic cardiomyopathy
3) aortic stenosis
4) cor pulmonale

93
Q

hypertrophic cardiomyocytes - nuclei appearance

A

boxcars

94
Q

hypertrophic heart disease - progressively develop what driven by what

A

myocardial fibrosis, driven by TGF-beta

95
Q

what group of pts are very prone to getting hypertensive heart disease

A

chronic renal failure pts

96
Q

the histologic organization of myocardial fibrosis in hypertensive heart disease is what

A

interstitial

97
Q

HCM w/ IVS hypertrophy is accompanied by systolic anterior motion of the mitral valve - what is the significance

A

can cause LVOT obstruction and mitral regurgitation

98
Q

what is the result of this systolic anterior motion of the mitral valve and hitting against the IVS

A

fibrous thickening of the mitral valve and mirror image patch of fibrosis on the subaortic upper septum

99
Q

what is a tx (other than open heart surgery) for getting rid of the obstructing upper IVS

A

inject a poison into a septal coronary artery and infarct the inner part of the hypertrophied upper septum - use alcohol (EtOH)

100
Q

what is a consequence of the fibrosis associated with hypertrophic cardiomyopathy?

A

provide a anatomic substrate for the development of reentrant ventricular tachycardia

101
Q

aortic stenosis due to rheumatic valvultits, what happens to the valve leaflets?

A

inflammation, fibrosis, and fusion start at the commissue, and moves inward

102
Q

what is a commissure?

A

heart valve commissure is where the valve opening meets the valve annulus

103
Q

calcific bicuspid aortic valve - what is the epidemiology

A

male, probably in 40s, probably presented w/ sudden death

104
Q

besides surgery to replace a stenotic aortic valve, what else can you do

A

stent

105
Q

what is the numerical relationship of the thickness of the right ventricular wall compared to the left ventricular wall -

A

thickness of RV wall is less than 1/3 of the LV wall –> constant for normal sized heart or hypertrophied heart

106
Q

what determines SV (2)

A

1) preload,

2) contractility

107
Q

what determines HR (2)

A

1) ANS,

2) conduction system

108
Q

2 things determine TPR

A

1) neurohumoral factors –> RAAS, etc

2) local autoregulation - pH, hypoxia, kinins, PGs,

109
Q

according to JNC8, what is the cutoff line for pts 60 or older for htn tx

A

150/90

110
Q

for everyone less than 60, what is the cutoff to start treating for htn

A

140/90

111
Q

what is the cardiac output like for pts w/ uncomplicated HTN

A

nml CO

112
Q

causes of essential HTN

A

1) gain of function of pathways that promote vasoconstriction and renal sodium retention
2) loss of function of pathways that promote vasodilation and renal sodium excretion

113
Q

what percentage of HTN is due to secondary causes (any HTN other than essential)

A

5%

114
Q

what is the clinical significance of HTN (nace)

A

it is the most common preventable cause of death in developed countries

115
Q

what is the upper limit of normal for pulmonary capillary pressure

A

10 mm Hg

116
Q

at what level of pulmonary cap pressure will you have interstitial pulmonary edema

A

20 mm Hg

117
Q

pulmonary capillary pressure - alveolar pulmonary edema

A

25 mm Hg

118
Q

other causes of pulmonary edema - septic shock, what will the pulmonary capillary pressure be?

A

normal

119
Q

hemorrhagic shock - pulmonary edema - pulmonary cap pressure?

A

low

120
Q

does heart failure ever lead to a pro-inflammatory cytokine profile?

A

yes - TNF, IL-1, IL-6

121
Q

what is a surgical emergency regarding the aortic valve

A

severe acute uncompensated aortic regurgitation

122
Q

what is the synthetic, recombinant BNP

A

Nesiritide

123
Q

BNP is an excellent blood test for heart failure

A

just know it

124
Q

what is impt about diastolic heart murmurs

A

there are no innocent diastolic murmurs

125
Q

arrhythmia defined by a RyR defect

A

familial catecholaminergic polymorphic ventricular tach

126
Q

what is the epidemiology of familial cathecholaminergic polymorphic ventricular tach

A

mostly children

vent tach/fib during emotional stress

127
Q

epidemiology of Brugada

A

young asian males

128
Q

what is Brugada

A

group of channelopathies causing shortened cardiac myocyte APs and risk of vent tach and SCD

129
Q

what leads do you look for the “coved type” ST elevations of Brugada

A

V1-V3

130
Q

classical clinical presentation of congenital long QT syndrome

A

young person, exercise related SCD

131
Q

pathophys of Long QT

A

phase 2 early after depolarization - LV

132
Q

pathophys of Brugada

A

phase 2 reentry - RV

133
Q

pathophys of catecholaminergic polymorphic VT

A

phase 4 delayed after depolarization - LV

134
Q

what buzzword association for Long QT

A

Torsades

135
Q

what is RV cardiomyopathy

A

disease due to genes encoding desmosomal proteins

136
Q

what does RV cardiomyopathy cause

A

reentrant ventricular tach originating from RV - related to abnormalities in myocyte adhesion - desmosomal proteins

137
Q

what is treatment of channelopathies

A

ICD

138
Q

which channelopathy can you use Beta blockers for?

A

familial catecholaminergic polymorphic ventricular tach

139
Q

type of cardiomyopathy that presents with arrhythmias

A

arrhythmogenic RV cardiomyopathy

140
Q

histologic features of arrhythmogenic RV cardiomyopathy

A

extensive replacement of myocytes by adipocytes and fibrous tissue

141
Q

asteroid body

A

sarcoidosis

142
Q

prototype restrictive cardiomyopathy

A

amyloidosis

143
Q

what is most common cause of myocarditis

A

viral infections - coxsackievirus

144
Q

what else can cause myocarditis

A

lyme disease

145
Q

drugs cause what type of myocarditis and what is a histologic feature

A

hypersensitivity myocarditis - eosinophils

146
Q

Hx - reticulonodular interstitial lung disease, bilateral hilar lymphadenopathy

A

sarcoidosis

147
Q

pathology of sarcoidosis

A

noncaseating granulomas in lungs, liver, lymph nodes, spleen, bone marrow, skin, eyes, heart

148
Q

what does sarcoidosis favor in the heart

A

favors base of heart, commonly involves conducting system

149
Q

spider cell

A

rhabdomyoma

150
Q

pre-req for giant cell arteritis

A

calcification of internal elastic lamina and tunica media

151
Q

what cells initiate immune response of giant cell art

A

dendritic cells

152
Q

what mediates the activation of dendritic cells in giant cell art

A

ligation of their TLRs

mostly TLR-4

153
Q

what do the dendritic cells produce (giant cell art)

A

IL-18, IL-12

154
Q

what do dendritic cells upregulate (giant cell art)

A

IFN-gamma

155
Q

the progression of the immune response in giant cell art depends on what

A

TH1 and TH17 CD4 T cells

156
Q

what is the dominant cell type in the intramural lesions of giant cell arteritis

A

TH1

157
Q

giant cell art - what is implicated in the response that leads to lumen stenosis

A

VEGF and PDGF

158
Q

what cell type is elevated in untreated pts of giant cell arteritis in peripheral blood

A

Th17 cells

159
Q

what is the tx for giant cell arteritis and what effect does it have on one of the cell types implicated

A

prednisone - almost complete reduction of Th17 cells - suppression of IL-1, IL-6, IL-17 axis

160
Q

what plays a primary role in the internal elastic lamina degradation characteristic of giant cell art

A

MMP-2, MMP-9 - released by macrophages

161
Q

what is the word for vacuolated cytoplasm of myocytes

A

myocytolysis

162
Q

histologic appearance of MI 4 hours old

A

wavy myocytes

163
Q

MI - when is coagulation necrosis visible

A

4-12 hrs

164
Q

MI - neutrophilic infiltration

A

12-24 hrs

165
Q

reperfusion effects of MI - contraction band necrosis

A

more contraction band necrosis

166
Q

reperfusion effects MI - effect on neutrophils

A

fewer neutrophils

167
Q

reperfusion effects MI - macrophages

A

more macrophages

168
Q

nichols question that mentions irregular rhythm - what type of arrhythmia first

A

a fib

169
Q

what is a common cause of a fib

A

heart failure

170
Q

see a high level of BNP - first thought

A

heart failure

171
Q

if you see a stroke from an MI - what time frame

A

7 days - embolus from mural thrombus

172
Q

what other cell type can be present in an infarct around 6 days

A

fibroblasts

173
Q

what is time frame for rupture of a MI

A

5 days

174
Q

color of acute MI

A

light brown to tan

175
Q

color of subacute MI

A

yellow

176
Q

when do you expect to see granulation tissue with an MI

A

3-14 days

177
Q

what is essential for making diagnosis of infective endocarditis

A

blood cultures

178
Q

what is the most common cause overall of infective endocarditis

A

staph aureus

179
Q

what causes mitral regurg from valve prolapse to go into remission

A

pregnancy - increase in blood volume causes LV to dilate

180
Q

presentation of long QT

A

childhood - syncope or SCD -

181
Q

“trigger” for long QT

A

exercise

182
Q

epsilon wave

A

ARVC

183
Q

disease of north Italy

A

ARVC

184
Q

“trigger” for ARVC

A

exercise

185
Q

channel involved in Brugada

A

sodium

186
Q

“trigger” for catecholaminergic polymorphic vent tach

A

exercise or emotional stress - increased levels of catecholamines

187
Q

Virchow’s Triad

A

1) endothelial injury
2) abnormal blood flow
3) hypercoagulability - can be congenital

188
Q

most likely underlying cause of mitral regurg

A

mitral valve prolapse

189
Q

what do we call emboli from infective endocarditis

A

septic emboli

190
Q

sites of septic embolization - common one we talked about

A

spleen

191
Q

what do septic emboli cause when they get to their final destination

A

infection, abscess - needs drainage

192
Q

what is clinical sign of septic emboli that caused abscess

A

recurrent fever

193
Q

causes and manifestations of carcinoid heart disease

A

1) bioactive compounds such as serotonin released by carcinoid tumors
2) flushing, diarrhea, dermatitis, bronchoconstriction

194
Q

what is normally affected in carcinoid heart disease?

A

endocardium and valves of Rt heart

195
Q

gross pathology of carcinoid heart disease

A

distinctive glistening white intimal plaquelike thickenings

196
Q

histologic features of carcinoid heart disease

A

SM cells and sparse collagen fibers - embedded in acid mucopolysaccharide-rich matrix

197
Q

see many tiny little vegetations on a heart valve

A

Rheumatic Heart Disease - in the acute phase does have vegetations

198
Q

what is the pattern of fibrosis in chronic rheumatic valve disease

A

starts at commissures, comes into the middle

199
Q

Anytime there is a hole in the heart/ valve - not due to a projectile, or congenital - what is the cause

A

infective endocarditis

200
Q

A pt w/ hypercoagulable state throws a DVT to their lungs and turns blue. How do you explain this?

A

If they had a probe patent foramen ovale –> cause Eisenmenger syndrome and push blood the other way and cause cyanosis

201
Q

4 things, quick, to remember about MVP

A

1) Common
2) benign
3) midsystolic click
4) +/- regurgitation

202
Q

3 things, quick, to remember Marantic Endocarditis

A

1) Common
2) Thrombi on valves
3) Precursor to infective endocarditis

203
Q

3 things about Libman-Sacks Endocarditis

A

1) part of SLE
2) most common in young black females
3) rarely embolizes

204
Q

4 things about infective endocarditis

A

1) uncommon
2) fatal if missed
3) heart murmurs
4) blood cultures

205
Q

4 things for calcific aortic stenosis

A

1) common
2) male
3) systolic ejection murmur
4) onset of symptoms = time for valve replacement

206
Q

What kind of septal defect can occur w/ transposition of great vessels?

A

VSD

207
Q

what kind of septal defect will not ocur w/ TGV

A

ASD

208
Q

What “defects” would help keep a pt alive in the case of TGV

A

VSD or PDA

209
Q

What, besides eating a hole in the valve, is a complication of infective endocarditis that can lead to problems - 3rd degree heart block and cardiac arrest

A

rupture a hole in the IVS

210
Q

when and how does the acute phase of rehumatic mitral valve disease present

A

acutely - age 10

211
Q

chronic mitral valve disease

A

20 yrs after the acute rheumatic fever (so 30 yo) –> mitral stenosis, females, diastolic murmur

212
Q

signs of heart failure –> dyspnea, ankle edema, S3, bibasilar pulmonary crackles –> what is potential pathophys of this?

A

Large acute MI –> heart failure –> inc LVEDV, inc LV dilation –> mitral regurgitation

213
Q

pericardial effusions –>

1) appearance of serous pericarditis fluid
2) common causes

A

1) tan, looks like serum

2) CHF, lymphatic obstruction, hypoalbuminemia

214
Q

for serous pericarditis as a result of lymphatic obstruction by tumor - mets - most likely site of primary tumor

A

lung, breast, skin (melanoma)

215
Q

shaggy pericarditis –> fibrinous –> most common causes

A

viral myopericarditis, uremia, acute MI, metastatic malignancy, autoimmune (SLE)

216
Q

when is the maximal neutro infiltration seen in acute MI

A

2 days

217
Q

subacute MI –>

1) what will you see
2) time frame

A

1) gray/tan w/ red rim of granulation tissue

2) 2 weeks –> sometime during the 2nd week

218
Q

what is the color progression of an MI

A

nml red/brown –> lighter brown –> tan –> yellow –> rim of red granulation tissue –> red moves in on yellow –> pink –> white

219
Q

most common fatal sequence of complications of atherosclerosis

A

hemorrhage into a thin capped (vulneralbe) plaque –> rupture –> thrombus

Shit-list (2 decks)

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