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Block 9 Week 1 > Cardiovascular System - Fung > Flashcards

Cardiovascular System - Fung Flashcards

1
Q

what is the normal weight of a female heart?

A

250 - 300 g

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2
Q

What is the normal weight of a male heart?

A

300-350 g

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3
Q

What is the normal wall thickness of the right wall?

A

0.3-0.5 cm

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4
Q

what is the normal thickness of the left ventricle?

A

1.3-1.5 cm

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5
Q

what cell type metabolizes hormones?

A

endothelial

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6
Q

what cell type proliferates when stimulated?

A

smooth muscle

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7
Q

what cell type regulates inflamm?

A

endothelial cells

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8
Q

what cell type regulates cell growth?

A

endo

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9
Q

what part of the vascular structure contains elastin, collagen, and glycosaminoglycans?

A

extracellular matrix

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10
Q

what cell type modulates vascular resistance?

A

endotheilial cells

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11
Q

what cell type mantains non-thrombogenic blood-tissue interface?

A

endothelial cells

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12
Q

from lumen outward, what are the layers of a muscular artery?

A

internal elastic lamina
tunica media
external elastic lamina
tunica adventitia

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13
Q

do arteries or veins contain valves?

A

veins

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14
Q

what are the six mechanisms of cardiac dysfunction?

A 
Pump failure
Obstruction
regurgitation
shunt
conduction
rupture of a major vessel
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15
Q

endothelial loss or dysfunction stimulates (blank) cell growth and ECM matrix thickening

A

smooth muscle cell

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16
Q

ECM thickening leads to thickening of which layer of the vessel?

A

intima

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17
Q

what are the complications of long term HTN?

A 
atherosclerosis
HTN heart disease
multi-infarct dementia
aortic dissection
renal failure
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18
Q

increased nitric oxide, prostacyclin, kinins, and ANP will lead to….

A

decreased peripheral resistance aka dilation aka decreased blood pressure

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19
Q

decreased levels of neural factors (b-adrenergic) will lead to….

A

decreased peripheral resistance aka dilation aka decreased blood pressure

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20
Q

Decreases in blood volume, heart rate, or contractility will have what affect on BP?

A

decreased

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21
Q

increased levels of what five compounds will lead to increased peripheral resistance and therefore blood pressure?

A 
ANG II
catecholemines
thromboxane
endothelin
a-adrenergic neural factors
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22
Q

What affect does ANP have on the kidney?

A

excretes Na and Water leading to decreased blood volume and a drop in BP

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23
Q

Low volume or low resistance measured by the kidney causes it to release what to increase blood pressure?

A

Renin

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24
Q

Renin converts what enzyme from the liver?

A

angiotensin to angiotensin 1

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25
Q

what organ produce ACE?

A

lungs

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26
Q

what organ does ANG II affect?

A

adrenal glands to produce aldosterone

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27
Q

what organ does aldosterone affect and what does it do?

A

kidney; reabsorb Na and water

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28
Q

what are the two mechanisms by which ANGII causes an increase in blood pressure?

A

increase in blood volume and via vasoconstriction

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29
Q

what is normal BP?

A

120/80

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30
Q

What is prehypertensive?

A

120-139/80-89

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31
Q

What is abnormal BP?

A

> 140/>89

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32
Q

What is malignant BP?

A

> 200/>120

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33
Q

Single gene defects in what two areas can lead to essential hypertension?

A

aldosterone metabolism and sodium reabsorption

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34
Q

(blanks) in the angiotensin locus, ANG receptor, and renin-angiotensin system can lead to essential hypertension

A

polymorphisms

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35
Q

What are the vascular causes of essential hypertension?

A

vasoconstriction and structural changes

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36
Q

What are the environmental factors leading to essential hypertension?

A 
diet
stress
obesity
smoking
being a lazy ass
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37
Q

what kinds of tumors can cause secondary HTN? where do you find them?

A

renin-producing tumors in the kidney

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38
Q

what are the renal causes of secondary HTN?

A
  1. acute glomerulonephritis
  2. chronic renal disease
  3. polycystic kidney disease
  4. renal artery stenosis
  5. renal vasculitis
  6. renin-producing tumors
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39
Q

What are the endocrine causes of secondary HTN?

A
  1. adrenal dysfunction
  2. exogenous hormones
  3. pheochromocytoma
  4. acromegaly
  5. hypothyroidism
  6. hyperthyroidism
  7. pregnancy induced
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40
Q

what are the cardiac causes of secondary HTN? (think anatomy)

A
  1. coarctation of the aorta
  2. polyarteritis nodosa
  3. increased intravascular volume
  4. increaed cardiac output
  5. rigidity of aorta
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41
Q

What are the neurologic causes of secondary HTN?

A
  1. psychogenic
  2. increased ICP
  3. sleep apnea
  4. acute stress
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42
Q

what are the two types of arteriosclerosis?

A

hyaline

hyperplastic

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43
Q

what are the three things that can happen when an atheroma forms?

A

obstruction of blood flow
rupture and vessels thrombosis
aneurysm formation

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44
Q

Describe the make up of an atheroma fibrous cap?

A

fibrous cap of smooth muscle cells, macrophages, collagen, elastin proteoglycans, and NEOVASCULIZATION

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45
Q

describe the make up of the necrotic center of an athermoa?

A

cell debris, cholesterol crystals, foam cells, and calcium depositis

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46
Q

what are the constitutional risk factors in atherosclerosis?

A

age
gender
genetics

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47
Q

what are the modifiable risk factors for atherosclerosis?

A

hyperlipidemia
hypertension
cigarette smoking
diabetes

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48
Q

what are the miscellaneous risk factors for atherosclerosis?

A
  1. inflamm
  2. hyperhomocystenemia
  3. metabolic syndrome
  4. lipoprotein a
  5. hemostatic factors
  6. sedentary life style
  7. type A personality
  8. obesity
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49
Q

Describe the process of atheroma formation?

A
  1. endothelial injury
  2. lipoprotein accumulation
  3. monocyte adhesion and formation of foam cells
  4. PLT adhesion
  5. smooth muscle recruitment
  6. smooth muscle proliferation and ECM production
  7. lipid accumulation
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50
Q

what are the causes of endothelial INJURY?

A

mechanical denudation
immune complex deposition
irradiation
chemicals

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51
Q

what are the causes of endothelial DYSFUNCTION?

A
  1. hemodynamic disturbances
  2. hypercholesterolemia
  3. hypertension
  4. smoking
  5. infectious agents
  6. homocysteine
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52
Q

where do plaques tend to occur?

A

at the ostia of exiting vessels
branch points
POSTERIOR wall of the aorta

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53
Q

what type of flow protects against atherosclerosis?

A

laminar flow

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54
Q

What are the dominant lipids in plaques?

A

cholesterol and cholesterol esters

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55
Q

Genetic (blank) is associated with accelerated atherosclerosis

A

hyperlipoprotenemia

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56
Q

DM and HYPOthyroidism are associated with….

A

hypercholesterolemia

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57
Q

Lowering serum cholesterol lowers the rate of….

A

atherosclerosis

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58
Q

Lipid accumulatoin reduces the ability of vessels to…

A

vasodilate

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59
Q

Hyperlipidemia increases the production of (blank) which then accelerates nitric oxide decay

A

free radical production

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60
Q

Atherosclerosis increases the production of what cell type?

A

foam cells

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61
Q

Oxygen free radicals oxidize what type of cholestero[l?

A

LDL

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62
Q

How is oxidized LDL taken up by mac’s?

A

via a scavenger receptor

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63
Q

Oxidized LDL increases the release of (blank) factors which leads to increased monocyte recruitment

A

growth factors, cytokines, and chemokines

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64
Q

oxidized LDL is cytotoxic to what two cell types?

A

endothelial cells and SMC causing endothelial cell dysfunction

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65
Q

Atherosclerotic lesions in smooth muscle cells are in a chronic (blank) state

A

inflammatory (t cell infiltrate)

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66
Q

Chemokines and growth factors produced promote (blank) cell proliferation and ECM synth

A

smooth muscle cell

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67
Q

The ECM and smooth muscle proliferation converts the fatty streak into a mature (blank)

A

atheroma

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68
Q

critical stenosis occurs at what percent occlusion?

A

70%

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69
Q

chronically decreased perfusion leads to what four major complications?

A

bowel ishemia
chronic IHD
ischemia encephalopathy
intermittent claudication

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70
Q

What are the three types of acute plaque change?

A
  1. rupture/fissure
  2. eorsion/ulceration
  3. hemorrhage into the atheroma
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71
Q

mural thormbosis, embolization, and wall weakening will do what to an unstable plaque?

A

cause aneurysm and rupture

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72
Q

Plaque rupture, erosion, hemorrhage, mural thrombosis, or embolization will do what to an unstable plaque?

A

occlusion by thrombosis

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73
Q

Progressive plaque growth will cause a (blank) stenosis

A

critical

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74
Q

90% of ischemic heart disease arises from (blank) lesions in the coronary arteries

A

obstructive atherosclerotic lesions

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75
Q

what are the three complications of IHD?

A

tachycardia
myocardial hypertrophy
hypoxemia

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76
Q

besides atherosclerotic lesiosn, what three other things can cause IHD?

A

coronary emboli
blockage of coronary arteries
severe hypotension

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77
Q

Late manifestation of coronary atherosclerosis may have started when in life?

A

childhood or adolescence

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78
Q

According to Fung, what are the the four things included in ACS?

A

Angina pectoris
MIS
Chronic IHD with heart failure
sudden cardiac death

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79
Q

what is the causes of angina pectoris?

A

transient myocardial ischemia that falls short of inducing myocyte necrosis

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80
Q

Unstable angina is also known as….

A

crescendo angina

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81
Q

stable angina is also known as….

A

typical angina

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82
Q

what percent occlusion is needed to cause stable angina?

A

75%

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83
Q

what things relieve stable angina?

A

rest or vasodilators

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84
Q

what two meds can relieve prinzmetal angina?

A

vasodilators and calcium channel blockers

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85
Q

at what percent occlusion do you see unstable angina?

A

90% or greater`

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86
Q

what are the two things that can precipitate unstable angina?

A

acute plaque change with superimposed thrombus/embolism

vasospasm

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87
Q

unstable angina is a warning of an impending….

A

acute MI

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88
Q

Describe the sequence of events in an acute MI

A
  1. acute change of atheromatous plaque exposes thrombogenic contents
  2. PLTs adhere to exposed plaque
  3. PLTs degranulate
  4. degranulation initiates vasopasm
  5. tissue factor activates coag cascade
  6. thrombus occludes lumen of the vessel
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89
Q

what are the vaspasm causes of MI without coronary vascular path?

A

cocaine abuse

PLT aggregation

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90
Q

What are the emboli causes of MI w/o vascular path?

A

A-fib of left atrium
Vegetations from infective endocarditis
L sided mural thrombus
Paradoxical R sided emboli

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91
Q

What are the causes of ischemia without atherosclerosis or thrombosis?

A 
Vasculitis
sickle cell disease
amyloid deposition
vascular dissection
shock (severe hypotension)
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92
Q

reversible ischemia cannot last longer than…

A

20-30 minutes

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93
Q

how soon after ischemia onset does aerobic metabolism stop?

A

within seconds

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94
Q

how soon after ischemia onset does contractility stop?

A

within 60 seconds

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95
Q

Necrosis is complete within (blank) hours of onset

A

6

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96
Q

T/F: heart rate, cardiac rhythm, and O2 sat determine the morphologic features of an MI

A

true

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97
Q

myocardial ischemia begins in what layer of the heart and travels in which direction?

A

in the endocardium and travels outward

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98
Q

A transmural necrosis involves how much of the wall?

A

full thickness

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99
Q

a (blank) infarction is associated with chronic atherosclerosis, acute plaque change, and superimposed thrombus

A

transmural

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100
Q

What type of infarct is ST elevated?

A

transmural

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101
Q

How much of the wall thickness is involved in a subendocardia infarct?

A

one third to one half

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102
Q

what type of infarct is due to ANY reduction in coronary flow, aka plaque disruption with lysed thrombus, global hypotension

A

subendocardial infarct

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103
Q

what type of infarct is non-ST elevated?

A

subendocardial

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104
Q

why is the endocardium the first layer to experience ischemia?

A

its the farthest way from the coronary vessels! (which lie on the outside of the heart :) )

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105
Q

what areas of the heart does that LAD supply?

A

Apex
anterior wall of the LV
anterior 2/3 of the ventricular septum

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106
Q

What areas of the heart does that right coronary artery supply?

A

posterior 1/3 of septum (dominant/ common form)
RV free wall
posterobasal wall of LV

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107
Q

What areas of the heart does that LCx feed?

A

LV myocardium

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108
Q

List the three cardiac markers in order of first to last to appear

A

Myoglobin 0-2 hours
CK-MB 2-4 hours
Troponin I and T 2-4 hours

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109
Q

Which cardiac biomarker takes the longest to peak

A

Troponins, 48 hours

110
Q

Which cardiac biomarker is the most sensitive and specific?

A

troponins

111
Q

CK-MB is sensitive or specific?

A

sensitive but not specific

112
Q

In what other tissues do we find myoglobin?

A

skeletal muscle

113
Q

CK-MM is found in what two tissues?

A

cardiac and skeletal muscle

114
Q

CK-BB is found in what two tissues?

A

brain and lung

115
Q

CK-MB is found in what two tissues?

A

mostly cardiac, some skeletal

116
Q

when does myoglobin peak?

A

6-8 hours

117
Q

when does CK-MB peak?

A

24 hours

118
Q

how long do the troponins stay elevated after an MI?

A

7-10 days

119
Q

What are the treatments for ischemic heart disease MI?

A 
Aspirin
Heparin
Oxygen
Nitrates
Beta-adrenergic inhibitors
ACE inhibitors
Reperfusion
120
Q

what is the benefit of reperfusion?

A

rescues myocardium and limits infarct size

121
Q

what are the four ways of reperfusing?

A

thrombolysis
angioplasty
stent placement
CABG

122
Q

what are the things that limit reperfusion?

A

size of the lesion

how fast you can actually clear the obstruction

123
Q

(reperfusion/beta blockers) can cause arrhythmias

A

reperfusion

124
Q

What treatment can result in myocardia hemorrhage with contraction bands?

A

reperfusion

125
Q

What is a reperfusion injury?

A

irreversible cell damage superimposed on the original infarct

126
Q

Reperfusion can cause (micro/macro)vascular injury

A

microvascular

127
Q

What is myocardial stunning?

A

prolonged ischemic dysfunction post reperfusion

128
Q

T/F: pericarditis is a potential complication of an MI

A

true

129
Q

T/F: a ventricular aneurysm can arise from an MI

A

true

130
Q

explain the mechanism of chronic IHD? (aka ischemic cardiomyopathy)

A

function decompensation of hypertrophied noninfarcted myocardium

131
Q

Sudden cardiac death is the consequence of a lethal (MI/arrhythmia)

A

arrhythmia TRIGGERED BY mycardial ISCHEMIA

132
Q

Describe the very generally the electrical rhythm in sudden cardiac death

A

asystole followed by V-fib

133
Q

T/F: the arrhythmia in sudden cardiac death usually occurs within the main conduction system

A

false; at a site DISTANT from the conduction system;

134
Q

the arrhythmia in sudden cardiac death usually pops up near what type of tissue?

A

scars of a previous MI

135
Q

what two valve conditions can cause sudden cardiac death?

A

aortic valve stenosis

mitral valve prolapse

136
Q

What type of HTN causes sudden cardiac death?

A

pulmonary HTN

137
Q

what two street drugs can cause sudden cardiac death?

A

cocaine and meth

138
Q

(myo/peri)carditis can cause sudden cardiac death

A

myocarditis

139
Q

T/F: Congenital structural or coronary arterial abnormalities
and cardiomyopathies can cause sudden cardiac death

A

true

140
Q

what are the hereditary or acquired cardiac arrhythmias?

A 
Long QT
Short QT
WPW
Sick sinus syndrome
Catecholamine polymorphic VT
141
Q

what Rx drug can induce an arrhythmia?

A

catecholemines

142
Q

what are the causes of heart failure?

A

chronic or acute valve dz
chronic HTN
IHD with MI
fluid overload

143
Q

What is forward failure heart failure?

A

decreased cardiac output and tissue perfusion

144
Q

what is backward failure heart failure?

A

pooling of blood in the venous system seen as pulmonary and/or peripheral edema

145
Q

Apply the Frank-Starling mehanism as a compensatory system to heart failure

A

dilation and increased filling pressure increases contractility to keep yo ass alive

146
Q

What is ventricular remodeling?

A

hypertrophy with or without dilation to adapt to heart failure

147
Q

What neurohormone is released to increase HR in heart failure?

A

NorEpi

148
Q

What hormone axis is activated to adjust filling volumes and pressures in fluid overload heart failure?

A

renin-angiotensin-aldosterone

149
Q

Release of (ANP/BNP) adjusts filling volumes and pressures

A

ANP

150
Q

What part of the myocyte increases in number during hypertrophy?

A

sarcomeres
mitochondria
nuclear size due to ploidy

151
Q

What are the two types of “overload” heart failure

A

pressure

volume

152
Q

T/F: cardiac weight is increased in both volume and pressure overload hypertrophy

A

true

153
Q

In (pressure/volume) overload hypertrophy, sarcomeres increase in parallell to long axes of the cell

A

pressure

154
Q

In (pressure/volume) overload hypertrophy, sarcomeres increase in series with existing cells

A

volume

155
Q

T/F: ventricle wall thickness always increases in volume overlad hypertrophy

A

false; may be up, normal, or low

156
Q

how does hypertrophy lead to muscle failure?

A 
no increase in capillaries along with muscle mass
increased metabolism
alteration in handling of calcium
reprogramming of gene expression
apoptosis of myocytes
157
Q

Systolic left sided heart failure is pumping or filling issue

A

pumping issue

158
Q

The clinical symtpoms of left sided heart failure are caused by what complications?

A

Congestion of pulmonary circulation
Stasis of blood in left chambers
Hypoperfusion of tissues

159
Q

what are the Sx of left sided heart failure?

A 
Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Renal failure
Loss of attention span, restlessness
160
Q

What is the latin term for right sided heart failure?

A

Cor pulmonale

161
Q

what is the most common cause of right sided heart failure?

A

left sided heart failure

162
Q

What are the causes of pulmonary HTN in R sided heart failure?

A

Parenchymal disease of the lung
Pulmonary vasculature disorders
Pulmonary thromboembolism
Hypoxic conditions

163
Q

What are the Sx of the venous congestion assc’d with R sided heart failure?

A 
Hepatosplenomegaly
Peripheral edema
Pleural effusions
Ascites 
Abnormal mental function
Renal failure
164
Q

What are the three firstline treatments for heart failure?

A

Diuretics
ACEI
B-blockers (to lower adrenergic tone)

165
Q

What are the diagonstic criteria for systemic HHD?

A

Left ventricular hypertrophy without any other cardiovascular pathology
History or pathologic evidence of hypertension

166
Q

What is the acute cause of pulmonary HHD?

A

pulmonary embolus

167
Q

valve stenosis leads to (pressure/volume) overload

A

pressure overload

168
Q

valve insufficiency/regurg leads to (pressure/volume) overload

A

volume

169
Q

What is the most common path causing mitral stenosis?

A

rheumatic heart disease

170
Q

What are some things on your DDx for mitral regurg?

A 
Rheumatic heart disease
Infective endocarditis
Mitral valve prolapse
Drugs
Rupture of papillary muscle
Papillary muscle dysfunction
Rupture of chordae tendinae
LVH
Calcification
171
Q

what are some things on your DDx for Aortic stenosis?

A

Rheumatic heart disease
Senile calcifications
Calcification of a congenitally deformed valve

172
Q

what are some things on your DDx for aortic regurg?

A 
Rheumatic heart disease
Infective endocarditis
Marfan syndrome
Degenerative aortic dilation
Syphilitic aortitis
Ankylosing spondylitis
Rheumatoid arthritis
Marfan syndrome
173
Q

T/F: calcific aortic stenosis is due to normal wear and tear

A

true

174
Q

aortic stenosis leads to what complication?

A

pressure overload and LVH

175
Q

What is the most frequent congential cardiac malformation?

A

calcific stenosis of a congenitally bicuspid aortic valve

176
Q

What type of valve calcification does not affect valvular function?

A

mitral annular calcification

177
Q

What are the rare complications of mitral annular calcification?

A

Regurgitation
Stenosis
Arrhythmias and sudden cardiac death

178
Q

mitral valves can prolapse into the left…

A

atrium

179
Q

a “myxomatous degeneration” by an unknown mechanism is characteristic of what valvular prolapse?

A

mitral valve prolapse

180
Q

T/F: most pts are asymptomatic that have mitral prolapse

A

true

181
Q

what heart sound will you hear with a mitral prolapse?

A

midsystolic click

182
Q

What are the rare complications of mitral prolapse?

A

Infective endocarditis
Mitral insufficiency
Stroke
Arrhythmias

183
Q

rheumatic fever happens after infx with which bug?>

A

group A strep

184
Q

What the clinical findings in rheumatic fever?

A 
Migratory polyarthritis of large joints
Pancarditis
Subcutaneous nodules
Erythema marginatum of the skin
Sydenham chorea
185
Q

The (blank) criteria is used to diagnose rheumatic fever

A

Jones criteria

186
Q

acute rheumatic heart disease is characterized by (blank) bodies

A

Aschoff bodies

187
Q

What three cell types are found in Aschoff bodies?

A

Lymphs
plasma cells
Anitschkow cells

188
Q

Aschoff bodies can be found in (blank) layers of the heart

A

any (therefore it is a pancarditis)

189
Q

in acute rheumatic heart dz, MacCallum plaques form in what chamber?

A

left atrium

190
Q

the vegetations in acute rheumatic heart dz have underlying fibrinoid (blank)

A

necrosis

191
Q

Chronic rheumatic heart dz is a deforming (blank) valvular dz

A

fibrotic

192
Q

T/F: CRHD is the only cause of mitral stenosis

A

true!

193
Q

T/F: CRHD can involve other valves besides the mitral

A

true

194
Q

Can you see Aschoff bodies in CRHD?

A

nope

195
Q

Describe the changes to the mitral valve in CRHD?

A

leaflet thickening
commissural fusion and shortening
Thickening and fusion of the tendinous cords

196
Q

In infective endocarditis, what are the vegetations made of?

A

thrombotic debris and organisms

197
Q

what are the two forms of IE?

A

acute and subacute

198
Q

What are the three Duke Criteria for IE?

A

pathologic
major clinical
minor clinical

199
Q

what type of IE affects normal valves by highly virulent bugs?

A

acute

200
Q

what type of IE is this?

necrotizing, ulcerative, destructive lesions

A

acute

201
Q

Do you cure acute or subacute with abx?

A

subacute

202
Q

what type of IE infects already damaged valves with a lower virulence bug?

A

subacute

203
Q

What but infects healthy OR deformed valves?

A

S. aureus

204
Q

what bug infects prosthetic valves?

A

S. epidermidis (coag neg. staph)

205
Q

WHat bug infects damaged or abnl valves?

A

S. viridans

206
Q

What are the non-strep bugs that may also cause IE?

A

HACEK
Enterococci
gram neg. baccili
fungi

207
Q

what are the HACEK bugs?

A

Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

208
Q

non-infective aka sterile endocarditis is caused by what two things?

A

non-bacterial thrmbotic

Libman-Sacks endocarditis (SLE)

209
Q

da fuck is marantic endocarditis?

A

old term for non-bacterial thrombotic endocarditis

210
Q

what type of valve issue is characterized by deposition of small sterile thrombi on the leaflets of cardiac valves

A

Non-bacterial thrombotic endocarditis

211
Q

T/F: Non-bacterial thrombotic endocarditis does not elicit an inflamm response

A

true; no bacteria!

212
Q

Non-bacterial thrombotic endocarditis may be the source of systemic….

A

thrombi

213
Q

In what type of cancer do you get Non-bacterial thrombotic endocarditis?

A

mucinous adenocarcinoma

214
Q

In what other severely compromised states do you get Non-bacterial thrombotic endocarditis?

A

sepsis or hypercoagulable states

215
Q

Where are the vegetations in Libman-Sacks dz?

A

mitral and tricuspid valves
Valvular endocardium
Chords
Mural endocardium of the atria

216
Q

what type of vegetations are composed of finely granular, fibrinous eosinophilic material with hematoxylin bodies?

A

Libman-Sacks

217
Q

Libman-Sacks also causes intense valvulitis with fibrinoid (blank) of the valve

A

necrosis

218
Q

prosthetic valves can get IE with a (blank) abscess

A

ring abscess

219
Q

What valvular dz has lesions that firm plaque-like endocardial fibrous thickenings of the tricuspid and pulmonary valves

A

carcinoid heart dz

220
Q

The carcinoids that cause dz occur outside the portal system and empty directly into the..

A

IVC

221
Q

what are the three classes of primary cardiomyopathies?

A

dilated
hypertrophic
restrictive

222
Q

dilated cardiomyopathy shows (blank) dysfucntion

A

ERECTILE
jk!
contractile

223
Q

what is the leading cause of unexplained LVH?

A

hypertrophic cardiomyopathy

224
Q

the poor (blank) of the LV in hypertrophic cardiomyopathy leads to abnl diastolic filling and ventricular outflow obstruction

A

compliance

225
Q

Restrictive cardiomyopathy has a decreased compliance that leads to impaired filling during….

A

diastole

226
Q

which is the only systolic dysfunction cardiomyopathy?

A

dilated cardiomyopathy

227
Q

what are the two types of diastolic dysfunction cardiomyopathy?

A

hypertrophic and restrictive

228
Q

What are the causes of dilated cardiomyopathy?

A 
Genetic
Myocarditis
Alcohol abuse
Childbirth
Chronic anemia
Medications
Hemochromatosis
229
Q

What is the only cause of hypertrophic cardiomyopathy?

A

genetics

230
Q

what are the causes of restrictive cardiomyopathy?

A

Idiopathic
Amyloidosis
Radiation induced
Fibrosis

231
Q

what AD, variably penetrant disorder causes R ventricular failure and rhythm distrubances?

A

Arrhythmogenic right ventricular cardiomyopathy

232
Q

which ventricular wall is thinned in Arrhythmogenic right ventricular cardiomyopathy?

A

right ventricle

233
Q 
The myocytes of the R ventricle in Arrhythmogenic right ventricular cardiomyopathy
have a (blank) infiltration and fibrosis
A

fatty

234
Q

Arrhythmogenic right ventricular cardiomyopathy is caused by a defective cell (blank) proteins in the desmosomes that link adjacent myocytes

A

cell adhesion proteins

235
Q

what viruses can cause myocarditis?

A

Coxsackie A and B
Enterovirus
HIV
CMV

236
Q

what bacteria can cause myocarditis?

A

chlamydia
neisseria
Borrelia
Rickettsia

237
Q

Besides bacteria and fungi, what other infectious agents can cause myocarditis?

A 
fungus
trypanosoma (protozoa)
helminths
238
Q

hypersensitivity to what drugs can cause immune-mediated myocarditis?

A

methyldopa

sulfonomides

239
Q

WHat are the immune-mediated causes of myocarditis

A 
Post-viral
Poststreptococcal
SLE
Drug hypersensitivity
Methyldopa
Sulfonamides
Transplant rejection
240
Q

what two zebra processes can cause myocarditis?

A

sarcoidosis

giant cell myocarditis

241
Q

what is normal pericardial fluid like?

A

30-50 mL of thin, clear, straw colored fluid

242
Q

how much pericardial fluid can collect in a chronic pressure effusion?

A

500mL

243
Q

a rapid pericardial effusion can allow what volume of fluid to collect?

A

200-300mL

244
Q

Describe the three types of pericardial effusions

A

Pericardial effusion: pericardial space distended by serous fluid
Hemopericardium: pericardial space distended by blood
Purulent pericarditis: pericardial space distended by pus

245
Q

What are the types of acute pericarditis?

A 
Serous pericarditis
Fibrinous/serofibrinous pericarditis
Purulent pericarditis
Hemorrhagic pericarditis
Caseous pericarditis
246
Q

what are the types of chronic pericarditis?

A

Adhesive pericarditis

Constrictive pericarditis

247
Q

(blank) pericarditis is a non-infectious inflammatory process with a mild lymphocytic infiltrate in the epicardial fat

A

serous pericarditis

248
Q

What is the most frequent type of pericarditis that also tends to present with a loud pericardial friction rub?

A

fibrinous/serofribrinous

249
Q

What type of pericarditis is associated with MI, postinfarction syndrome, uremia, chest radiation, RF, SLE, trauma

A

fibrinous/serofribrinous

250
Q

what are the methods of microbes accessing the pericardial space?

A

Direct extension
Seeding from the blood
Lymphatic extension
Introduction during cardiotomy

251
Q

acute purulent pericarditis can cause an inflamm reaction that can produce a….

A

mediastinopericarditis

252
Q

what type of pericarditis arises as a result of the healing process post purulent pericarditis?

A

constrictive

253
Q

Hemorrhagic pericarditis has blood with what kind of effusion?

A

suppurative or fibrinous effusion

254
Q

what is the most common cause of a hemorrhagic pericarditis?

A

metastatic malignant neoplasm

255
Q

besides cancer, when else do you see a hemorrhagic pericarditis?

A

in TB and bacterial infections and post cardiac-surgery

256
Q

What causes caseous pericarditis?

A

TB; Leads to a disabling, fibrocalcific, chronic constrictive pericarditis

257
Q

T/F: chronic pericarditis is fatal

A

false; no clinical consequence

258
Q

Adhesive mediastinopericarditis follows what things?

A

Follow infectious pericarditis, cardiac surgery, radiation

Pericardial sac is obliterated and pericardium adheres to surrounding structures

259
Q

constrictive pericarditis mimmics…

A

restrictive cardiomyopathy; heart sounds are muffled or distant

260
Q

what is the most common primary cardiac tumor in adults?

A

myxoma

261
Q

which two chromosome are abnormal in myxoma?

A

12 and 17

262
Q

what cell line does a myxoma arise from?

A

mesenchymal cells

263
Q

Where in the heart do you see a myxoma?

A

atria; but can be in any chamber

264
Q

10% of cases of myxoma are assoicated with what complex?

A

Carney complex

265
Q

what is the most common primary cardiac tumor in kids?

A

rhabdomyoma

266
Q

rhabdomyoma is associated with what dz?

A

tuberous sclerosis

267
Q

a rhabdomyoma is a type of….

A

hamartoma

268
Q

T/F: lipomas are malignant

A

false

269
Q

where in the heart do you find lipomas?

A

LV, RA, or atrial septum

270
Q

T/F: papillary fibroelastomas are benign

A

true; resemble Lambl excrescences

Block 9 Week 1 (4 decks)

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