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Block 9 Week 1 > CV System-Fung > Flashcards

CV System-Fung Flashcards

1
Q

What do arteries have more of in their media than veins?

A

smooth muscle

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2
Q

What is the weight of a female heart?
Male heart?
What is the ventricular wall thickness of the right ventricle?
Left ventricle?

A

250-300 grams
300-350 grams

right: 0.3-0.5 cm
left: 1.3-1.5 cm

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3
Q

What are the four major components of cardiac muscle?

A

tropomyosin
troponin
actin
myosin

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4
Q

Where do you find the SA node?
AV node?
Accessory pathway connection?
Bundle of his?

A

Right atrium
interatrial septum
Right side atrioventricular septum
interventricular septum

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5
Q

What are the four major components of cardiac muscle?

A

tropomyosin
troponin
actin
myosin

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6
Q

Where do you find the SA node?
AV node?
Accessory pathway connection?
Bundle of his?

A

Right atrium
interatrial septum
Right side atrioventricular septum
Ventricular septum

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7
Q

What does the left coronary artery branch into?

A

the circumflex, LAD, Large marginal artery

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8
Q

What does the right coronary artery branch into?

A

right (acute) marginal artery and posterior descending artery

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9
Q

What do endothelial cells due for the structure of the vascular system?

A
  • maintain non-thrombogenic blood-tissue interface
  • modulate vascular resistance
  • metabolize hormones
  • regulate inflammation
  • regulate cell growth
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10
Q

What do the smooth muscle cells of the vascular system do?

A
  • proliferate when stimulated
  • synthesize collagen, elastin, proteoglycans
  • Elaborate growth factors and cytokines
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11
Q

What is found within the ECM of the vascular system?

A
  • Elastin
  • Collagen
  • Glycosoaminoglycans
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12
Q

What are the layers of the vascular system?

A

intima
media
adventitia

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13
Q

What kind of arteries are the radial and femoral arteries?

A

muscular arteries

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14
Q

Where do you find elastin in muscular arteries?

A

internal and external elastic lamina

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15
Q

What are the six mechanisms of dysfunction in cardiovascular disease and what is the major mechanism of dysfunction?

A

Failure of the pump
Obstruction to flow
Regurgitant flow
Shunted flow (congenital heart disease)
Disorders of cardiac conduction (bundle branch blocks)
Rupture of the heart or a major blood vessel (dissection of aorta)

FAILURE OF PUMP

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16
Q

What happens when there is endothelial cell loss or dysfunction?

A

stimulates smooth muscle cell growth/proliferation and extracellular matrix synthesisi leading to intimal thickening

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17
Q

Sustained increased BP is associated with increased risk of (blank X 5)

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

When you have decreased blood pressure what will your peripheral resistance look like and why?

What will your cardiac output look like and why?

A

Decreased resistance i.e dilation

-increased NO,prostacyclin, kinins, ANP, and decreased neural factors

Decreased CO-> due to decreased BV, HR, Contactility

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19
Q

How do you increased BP?

A

renin released from kidney, converts angiotensinogen from liver into angiotensin in lung which makes adrenal glands secrete aldosterone which will make the kidneys resorb Na and water which will increase your BV and thus your BP. and you will vasconstrict

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20
Q

How do you lower blood volume?

A

kidney excretes sodium and water and you vasodilate

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21
Q

Whats normal systolic and diastolic?
Whats prehypertensive?
Whats abnormal?
Whats malignant?

A
  • less than 120, less than 80
  • 120-139, 80-89
  • greater than 140, greater than 89
  • greater than 200, greater than 120
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22
Q

What is essential HTN?

A

idiopathic without any real known cause

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23
Q

What are the Contributing factors of essential HTN?

A

single gene defects
polymorphisms
vascular
environmental factors

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24
Q

What are some single gene defects that cause essential HTN?
Polymorphisms?
Vascular?
Environmental Factors?

A
  • aldosterone metabolism, sodium reabsorption
  • angiotensinogen locus, angiotensin receptor locus, renin-angiotensin system
  • vasoconstriction, structural changes
  • diet, stress, obesity, smoking, physical inactivity
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25
Q

What are the causes of secondary hypertension?

A
  • renal
  • endocrine
  • CV
  • Neuroogic
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26
Q

What are the renal causes of secondary htn?

A
  • acute glomerulonephritis
  • chronic renal disease
  • polycystic disease
  • renal artery stenosis
  • renal vasculitis
  • renin-producing tumors
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27
Q

What are the endocrine causes of secondary htn?

A
  • adrenocortical dysfunction
  • exogenous hormones
  • pheochromocytoma
  • acromegaly
  • hypothyroidism
  • hyperthyroidism
  • pregnancy-induced
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28
Q

What are the CV causes of secondary HTN?

A
  • coarctation of aorta
  • polyarteritis nodosa
  • increased intravascular volume
  • increased CO
  • rigidity of aorta
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29
Q

What are the neurologic causes of secondary HTN?

A
  • psychogenic
  • increased ICP
  • sleep apnea
  • acute stress
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30
Q

What is this:
an eosinophilic deposition of material around arterioles in the kidney, looks like a rough kidney and is associated with benign essential htn

A

hyaline arteriosclerosis

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31
Q

What is this:

deposition of smooth muscle cells around the arterioles of the kidney. Associated with malignant htn.

A

Hyperplastic arteriosclerosis

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32
Q

Atheromas protrude into the vessel lumen and can…..?

A
  • obstruct blood flow
  • rupture and cause vessel thrombosis
  • lead to aneurysm formation
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33
Q

What are atheromas?

A

raised lesions with a soft yellow core of lipid covered with a fibrous cap

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34
Q

What all makes up an atheroma?

A

SM cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, calcium

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35
Q

What are the constitutional risk factors of atherosclerosis?
What are the modifiable risk factors?
What are other risk factors?

A
  • age, gender, genetics
  • hyperlipidemia, HTN, cigarette smoking, diabetes
  • inflammation, hyperhomocystinemia, metabolic syndrome, lipoprotein a, hemostatic factors, sedentary life style, type A personality, obesity
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36
Q

What is the risky age for females to have atherosclerosis?

For males?

A

above 55

above 45

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37
Q

(blank) is a chronic inflammatory and healing response to arterial wall and endothelial injury

A

Atherosclerosis

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38
Q

What are the pathologic events that lead to atherosclerosis?

A

-endothelial injury-> lipoprotein accumulation (in media) -> monocyte adhesion and formation of foam cells->platelet adhesion-> smooth muscle cell recruitment-> smooth muscle cell proliferation and ECM production-> lipid accumulation

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39
Q

Where do you get lipoprotein accumulation in the formation of atherosclerosis?

A

in media

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40
Q

How do you get monocyte adhesion and formation of foam cells?

A

Through scavenger pathway and LDL breakdown

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41
Q

What are ways you can get endothelial injury?

A
  • Mechanical denudation (wearing down)
  • immune complex deposition
  • irridiation
  • chemicals
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42
Q

What are causes of endothelial dysfunction?

A
  • hemodynamic disturbances
  • hypercholesterolemia
  • hypertension
  • smoking
  • infectious agents
  • homocysteine
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43
Q

Plaques tend to occur at areas of disturbed blood flow… such as?

A
  • ostia of exiting vessels
  • branch points
  • posterior wall of abdominal aorta
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44
Q

Why kind of flow protects against atherosclerosis?

A

non-turbulent, laminar flow

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45
Q

What are the dominant lipids in plaques?

A

cholesterol and cholesterol esters

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46
Q

Genetic (blank) is associated with accelerated atherosclerosis

A

hyperlipoproteinemia

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47
Q

What 2 diseases are associated with hypercholesterolemia?

A

DM and hypothyroidism

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48
Q

Lower serum (blank) slows the rate of atherosclerosis

A

cholesterol

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49
Q

Lipid accumulation reduces (blank) ability of vessels. Why?

A

vasodilation

-because hyperlipidemia increases oxygen free radical production which then accelerates nitric oxide decay

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50
Q

Atherosclerosis increases production of foam cells. Explain why?

A

oxygen free radicals (created by hyperlipidemia) oxidizes LDL which is then ingested by macrophages through a scavenger receptor.

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51
Q

What will oxidized LDL increase release of? what will this recruit?

A

growth factors, cytokines, and chemokines

-monocytes!!!!!

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52
Q

Atherosclerotic lesions are in a chronic (blank) state

A

inflammatory state (t-lymphocytes)

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53
Q

What promotes smooth muscle cell proliferation and ECM synthesis? How will this affect the fatty streak?

A

Chemokines and growth factors

It will convert the fatty streak into a mature atheroma

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54
Q

What are the major consequences of atherosclerosis?

A
  • MI
  • Cerebral Infarction
  • Aortic Aneurysm
  • Peripheral vascular disease
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55
Q

Critical stenosis occurs at (blank) occlusion

A

70%

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56
Q

With stenosis, you get decreased profusion which leads to …..?

A
  • Bowel Ischemia
  • Chronic IHD
  • Ischemic encephalopathy
  • Intermittent Claudication
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57
Q

What are acute plaque changes?

A
  • Rupture exposing plaque contents to blood
  • Erosion or ulceration exposing BM to blood
  • Rupture and hemmorhage into atheroma
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58
Q

What are the pre-clinical phases of atherosclerosis?

A
  • fatty streak
  • fibrofatty plaque
  • advanced vulnerable plaque
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59
Q

What are the clinical phases of atherosclerosis?

A

Aneurysm and Rupture
Occlusion by Thrombus
Critical stenosis

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60
Q

What is this:

generic designation for a group of pathologically related syndromes resulting from myocardial ischemia :)

A

Ischemic Heart Disease

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61
Q

(blank) is an imbalance between the supply and demand of the heart for oxygenated blood. What is this frequently referred to as?

A

Myocardial ischemia

-coronary artery disease

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62
Q

90% of the time ischemic heart disease results from (blank)

A

obstructive atherosclerotic lesions in the coronary arteries

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63
Q

What are minor causes of ischemic heart disease?

A
  • Tachycardia
  • Myocardial Hypertrophy
  • Hypoxemia
  • Coronary Emboli
  • Blockage of coronary arteries
  • Severe hypotension
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64
Q

What are some acute coronary syndromes that cause ischemic heart disease?

A
  • angina pectoris
  • myocardial infarction
  • chronic IHD with heart failure
  • sudden cardiac death
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65
Q

What is angina pectoris?

What is it caused by?

A

Paroxysmal and recurrent attacks of substernal and precordial chest discomfort
-Caused by transient myocardial ischemia that falls short of inducing myocyte necrosis

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66
Q

What are the three variants of angina?

A
  • stable (typical)
  • prinzmetal
  • unstable (crescendo)
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67
Q

What causes stable angina?

A

caused by an imbalance of perfusion (75% occlusion) relative to myocardial demand
-physical activity, emotional excitement or increased cardiac workload causes it.

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68
Q

What percentage of occlusion can cause stable angina?

A

75%

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69
Q

What relieves stable angina?

A

rest or vasodilators

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70
Q

What causes prinzmetal angina?

What relieves this?

A
  • coronary artery spasm unrelated to physical activity, heart rate or BP
  • vasodilators and calcium channel blockers
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71
Q

What is unstable angina?

A

pattern of increasingly frequent pain of prolonged duration that is precipitated at low levels or activity or at rest

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72
Q

What percent of artery occlusion do you have to have for unstable angina to occur?

A

90% or greater

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73
Q

What is unstable angina caused by?

Unstable angina gives you a warning for an impending (blank)

A
  • acute plaque change with superimposed thrombosis/embolism
  • vasospasm

-acute MI

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74
Q

What is this;

Death of cardiac muscle due to prolonged severe ischemia

A

Myocardial infarction

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75
Q

What is the typical sequence of an MI?

A
  • atheromatous plaque exposes thrombogenic contents
  • platelets adhere to plaque and degranulate and initiate vasospasms
  • tissue factor activates the coagulation cascade adding to the bulk of the thrombus
  • thrombus completely occludes the lumen of the vessel
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76
Q

10% of MI can occur without (blank)

A

coronary vascular pathology

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77
Q

What can cause vasospasm with/without atherosclerosis resulting in MI?

A

cocaine abuse

platelet aggregation

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78
Q

What can cause emboli resulting in MI?

A
  • atrial fibrillation of left atrium
  • vegatations from infective endocarditis
  • left sided mural thrombus
  • paradoxical right sided emboli
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79
Q

What can cause ischemia without atherosclerosis or thrombosis ?

A 
vasculitis
sickle cell disease
amyloid deposition
vascular dissection
severe hypotension (shock)
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80
Q

MI can be divided into phases of (blank) and (blank) injury

A

reversible and irreversible

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81
Q

Reversible injury is ischemia lasting no more than (blank) minutes.

A

20-30

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82
Q

Reversible injury is ischemia lasting no more than 20-30 minutes. What will happen within seconds? What will happen within 60 seconds?

A
  • cessation of aerobic metabolism within seconds

- loss of contractility within 60 seconds

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83
Q

Irreversible injury is when you have prolonged severe ischemia leading to myocyte necrosis. Necrosis is complete within (blank) hours of onset

A

6

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84
Q

The morphologic features of a myocardial infarction depends on ….?

A
  • location and severity of the atherosclerosis
  • size of the vascular bed perfused by the obstructed vessel
  • duration of the occlusion
  • oxygen demands of the affected myocardium
  • extent of collateral circulation
  • heart rate, cardiac rhythm and 02 saturation
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85
Q

Myocardial ischemia proceeds from the (blank) outward

A

endocardium

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86
Q

What is a transmural infarction?

A
  • necrosis involves the full thickness

- associated with chronic atherosclerosis, acute plaque change, superimposed thrombus

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87
Q

What causes a transmural infarction?

What will it look like on an EKG?

A
  • associated with chronic atherosclerosis, acute plaque change, superimposed thrombus
  • ST elevation infarcts
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88
Q

What is a subendocardial infarction?
What is this due to?
What does it look like on an EKG?

A
  • Necrosis limited to the inner 1/3-1/2 of the ventricular wall
  • any reduction in coronary flow (plaque disruption with lysed thrombus, global hypotension)
  • non-ST elevation infarcts
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89
Q

What does the LAD supply?

A

apex
anterior wall of LV
anterior 2/3 of ventricular septum

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90
Q

What does the Right coronary artery supply?

A

posterior 1/3 of septum (dominant)
RV free wall
Posterobasal wall of LV

91
Q

What does the Left circumflex artery supply?

A

LV myocardium

92
Q

What happens within hours of an infarction?
within days?
Within weeks?
Within months?

A
  • Coagulative necrosis
  • Neutrophils then macrophages
  • granulation tissue
  • scarring
93
Q

What are the clinical features of an MI?

A

rapid, weak pulse
diaphoresis
dyspnea
asymptomatic

94
Q

When do you get a rise in myoglobin, CK-MB, Troponin I and T

A

0-2 hours
2-4 hrs
2-4 hrs

95
Q

When do you have peak levels of myoglobin, CK-MB, Troponin I and T?

A

Myoglobin: 6-8 hrs
CK-MB: 24 hrs
Troponins: 48 hrs

96
Q

What test is sensitive but not specific?

What test is sensitive and specific?

A

CK-MB

Troponin I and T

97
Q

Whats awesome about troponins besides they are specific and sensitive?

A

their levels persist for 7-10 days post MI so you can tell if someone had a heart attack days ago

98
Q

What is the treatment of MI?

A 
aspirin (inhibits platelets)
heparin (inhibits coag)
oxygen (higher O2 sat)
nitrates (vasodilate)
beta-adrenergic inhibitors
ACE inhibitors 
Reperfusion
99
Q

What does reperfusion do and how do you do this?

A
  • thrombolysis
  • angioplasty
  • stent placement
  • coronary artery bypass graft (CABG)
100
Q

What is reperfusion limited by?

A
  • rapidity of alleviating the obstruction

- extent of the correction and the underlying causal lesion

101
Q

What are the adverse complication of reperfusion?

A
  • arrhythmias
  • myocardial hemorrhage with contraction bands
  • irreversible cell damage superimposed on the original injury (reperfusion injury)
  • microvascular injury
  • prolonged ischemic dysfunction (myocardial stunning)
102
Q

What are complications of MI?

A 
contractile dysfunction
arrhythmias
myocardial rupture
pericarditis
right ventricular infarction
Infarct extension
Infarct expansion
Mural thrombus
Ventricular aneurysm
Papillary muscle dysfunction
Progressive late heart failure
103
Q

What is chronic ischemic heart disease?

What is this commonly called?

A

progressive heart failure as a consequence of ischemic myocardial damage
-ischemic cardiomyopathy

104
Q

How can sudden cardiac death occur?

A

consequence of lethal arrhythmia normally triggered by myocardial ischemia.

105
Q

What are 2 types of lethal arrhythmias?

A

asystole

ventricular fibrillation

106
Q

arrhythmia normally occurs at a site (blank) from the conduction system

A

distant

**also found adjacent to scars of previous MI

107
Q

What are some nonatherosclerotic conditions that can cause sudden cardiac death?

A

Congenital structural or coronary arterial abnormalities
Aortic valve stenosis
Mitral valve prolapse
Myocarditis
Cardiomyopathies
Pulmonary hypertension
Drug abuse (cocaine, meth)
Hereditary or acquired cardiac arrhythmias
Systemic metabolic and hemodynamic alterations
Catecholamines

108
Q

What are hereiditary or acquired cardiac arrhythmias that can cause sudden cardiac death?

A 
Long QT
Short QT
WPW
Sick sinus syndrome
Catecholamine polymorphic VT
109
Q

When does heart failure occur?

A
  • when the heart is unable to pump blood sufficiently to meet the demands of the tissue
  • When the heart can only pump blood sufficiently at elevated filling pressures
110
Q

Why will heart failure develop?

A
  • chronic or acute valve disease
  • long standing htn
  • ischemic heart disease with MI
  • Fluid overload
111
Q

What is forward heart failure characterized by?

A

decreased cardiac output and tissue perfusion

112
Q

What is backward heart failure characterized by?

A

pooling of blood in the venous system (pulmonary and/or peripheral edema)

113
Q

What is the frank-starling mechanism?

A

dilation and increased filling pressure INCREASES contractility

114
Q

What are adaptive mechanisms for heart failure?

A
  • frank starling mechanism
  • ventricular remodeling (hypertrophy with or without dilation)
  • neurohomonal mechanisms
115
Q

What are the neurohormonal mechanisms of the heart that are adaptive in the case of heart failure?

A
  • norepinephrine release to increase heart rate
  • activation of renin-angiotensin-aldosterone system to adjust filling volumes and pressures
  • release of ANP to adjust filling volumes and pressures
116
Q

What is this:
increased mechanical work due to pressure or volume overload or due to trophic signals causes the myocytes to increase in size

A

Hypertrophy

117
Q

What will myocytes due in heart failure?

A
  • increase protein synthesis to increase sarcomeres
  • increase mitrochondria to gain more energy
  • increase nuclear size due to ploidy
118
Q

In heart failure, you will get pressure overload hypertrophy and volume overload hypertrophy, what will this result in?

A

increased cardiac weight
sarcomeres increase in parallel and in series
ventricle wall thickness changes (increases, decreases, or no change)

119
Q

In volume or pressure overload hypertrophy will you get sarcomeres increasing in parallel to long axes of cells?
What about in series?

A
  • Pressure overload hypertrophy

- Volume overload hypertrophy

120
Q

In pressure overload hypertrophy what will your heart look like?
In volume overload?

A
  • Concentric increase in wall thickness

- Ventricular dilation

121
Q

THe changes in the heart used to compensate for hypertrophied hearts can end up damaging the heart, why?

A
  • hypertrophy isnt accompanied by increase in capillaries
  • change in myocardial metabolism
  • alteration in calcium homeo
  • apoptosis of myocytes
  • reprogramming of gene expression
122
Q

What causes left sided heart failure?

A

-Ischemic heart disease
-Hypertension
-Aortic and valvular diseases
-Myocardial disease
Systolic and Diastolic failure

123
Q

How do you get systolic failure?

How do you get diastolic failure?

A

insuffiicient cadiact output (pump failure)

stiff ventricle that cannot expand and increase its output

124
Q

Why do symptoms develop from left sided heart failure?

A

BECAUSE YOU GET:

  • congestion of pulmonary circulation
  • stasis of blood in left chambers
  • hypoperfusion of tissues
125
Q

What are the symptoms of left sided heart failure?

A 
Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Renal failure
Loss of attention span, restlessness
126
Q

What causes right sided heart failure (cor pulmonale)?

A

Left sided heart failure and its causes and pulmonary hypertension.

127
Q

WHat causes pulmonary htn?

A

parenchymal disease of the lung
pulmonary vasculature disease
pulmonary thromboembolism
hypoxic conditions

128
Q

What is the general symptom of cor pulmonale (right sided heart failure)?
What are the specific symptoms?

A

Systemic and Venous congestion

  • Hepatosplenomegaly
  • Peripheral edema
  • Pleural effusions
  • Ascites
  • Abnormal mental function
  • Renal failure
129
Q

In heart failure, pnts frequently present with (blank) with symptoms of both right and left sided heart failure.
How do you treat this?

A

biventricular

  • Diuretics
  • Renin-angiotensin-aldosterone blockers (ACE inhibitors)
  • Beta-blockers (lower adrenergic tone)
130
Q

What will sustained htn cause?

How do you classify it?

A 
pressure overload and ventricular hypertrophy i.e hypertensive heart disease (HHD)
Left sided (systemic) HHD or Right sided (cor pulmonale) HHD.
131
Q

What is the diagnostic criteria for systemic HHD (left sided)?

A
  • Left ventricular hypertrophy without any other cardiovascular pathology
  • History or pathologic evidence of HTN
132
Q

What is the diagnostic criteria for pulmonary HHD (right sided)?

A
  • Characterized by right ventricular hypertrophy and dilation
  • can be acute (pulmonary embolism) or chronic
133
Q

How can you have acute pulmonary HHD?

A

pulmonary embolism

134
Q

What do you find on the AV valves?

What do you find on the semilunar valves?

A

papillary muscles/chordae tendineae

cusps

135
Q

What is this:
Failure of a valve to open completely, which impedes flow
Leads to pressure overload

A

Stenosis

136
Q

What is this:
Failure of a valve to close completely, allowing reversed flow
Leads to volume overload
Functional regurgitation

A

Insufficiency/Regurgitation

137
Q

What disease will you see mitral stenosis?

A

rheumatic heart disease

138
Q

What diseases will you see mitral regurgitation?

A 
Rheumatic fever 
Infective endocarditis
Mitral valve prolapse
Drugs
Rupture of papillary muscle
Papillary muscle dysfunction 
Rupture of chordae tendinae
LVH
Calcification
139
Q

What diseases will you see aortic stenosis?

A

Rheumatic heart disease
Senile calcifications
Calcification of a congenitally deformed valve

140
Q

What disease will you see aortic regurgitation?

A 
Rheumatic heart disease
Infective endocarditis
Marfan syndrome
Degenerative aortic dilation
Syphilitic aortitis
Ankylosing spondylitis
Rheumatoid arthritis
Marfan syndrome
141
Q

What is a valvular disease associated with calcification of the aorta?
What is it due to?
Who is it present in?
What can this result in?

A
  • Calcific aortic stenosis
  • Normal wear and tear
  • Normally presents in the 7th to 9th decades of life
  • Obstruction results in pressure overload and LVH
142
Q

What is the most frequent congenital CV malformation?
What is it due to?
When does it present?

A

Calcific stenosis of congenitally bicuspid aortic valve

  • normal wear and tear
  • 5th to 7th decades of life
143
Q

How does mitral annular calcification present? HOw does it affect valvular function?
What are some rare complications of mitral annular calcification?

A
  • with calcifications in the peripheral fibrous ring.
  • It doesn’t affect it and is thus not clinically important.
  • Regurgitation, Stenosis, Arrhythmias and sudden cardiac death
144
Q

What is this:
mitral valve leaflet are floppy and prolapse into the left atrium during systole
-myxomatous degeneration (weakening of CT)
-most patients are asymptomatic and associated with a midsystolic click

A

Mitral valve prolapse

145
Q

What are the rare complications associated with mitral valve prolapse?

A

Infective endocarditis
Mitral insufficiency
Stroke
Arrhythmias

146
Q

What is this:
Acute, immunologically mediated multisystem inflammatory disease that occurs a few weeks after group (blank) streptococcal pharyngitis

What is a frequent consequence?

A

Rheumatic fever
Group A

Acute rheumatic carditis

147
Q

What are clinical features of rheumatic heart disease?

How do you diagnose it?

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

Jones criteria

148
Q

What is the jones criteria?

A

There are five major criteria:

  • carditis
  • polyarthritis
  • chorea
  • erythema marginatum
  • subcutaneous nodules
149
Q

Acute rheumatic heart disease is characterized by (blank). What is this composed of?

A

Aschoff bodies
inflammation (plasma and lymphocytes), Antischkow cells (reactive histiocytes with slender, wavy nuclei)
Giant cells
Fibrinoid material

150
Q

What layer can aschoff bodies be found?

A

any layer (pancarditis)

151
Q

Vegetations with underling fibrinoid necrosis is found in what type of RHD?

A

Acute rheumatic heart disease

152
Q

(blank) plaques within the left atrium are found in acute rheumatic heart diseease

A

MacCallum plaques

153
Q

What is this:
a deforming fibrotic valvular disease which is the only cause of mitral stenosis.
Other valves can be involved.
Aschoff bodies not identified

A

Chronic rheumatic heart disease

154
Q

In chronic rheumatic heart disease what does the mitral valve show?

A
  • leaflet thinkening
  • commissural fusion and shortening
  • thickening and fusion of tendinous cords
155
Q

What is this:

serious condition characterized by colonization or invasion of the heart valves or mural endocardium by a microbe.

A

Infective endocarditis

156
Q

What are the vegetations made up in infective endocarditis?

A

thrombotic debris and organisms

157
Q

What are the 2 forms of infective endocarditis?

A

acute or subacute

158
Q

How do you diagnose infective endocarditis?

A

duke criteria

pathologic criteria, major clinical criteria, minor clinical criteria

159
Q

What is this:
previously normal heart valve infected by a highly virulent organism.
Necrotizing, ulcerative, destructive lesions

Is it easy to cure?

A

Acute infective endocarditis

No, it is difficult to cure with antiobiotics

160
Q

What is this:
Insidious infections of deformed valves by organisms of lower virulence
Less destructive lesion

Is it easy to cure?

A

Subacute infective endocarditis

Yes, cure produced with antibiotics

161
Q

What organism is most commonly seen in subacute infective endocarditis?

A

S. viridans

native but attacks previously damaged or abnormal valves

162
Q

What organism is most commonly seen in acute infective endocarditis and is the most virulent?

A

S. aureus

attacks healthy or deformed valves

163
Q

What organism is seen in prosthetic valves?

A

S. epidermis (coagulase (-) staph)

164
Q

What are the other organisms that can cause infective endocarditis organisms?

A
  • HACEK (Hemophilus, Actinobaccilus, Cardiobacterium, Eikenella, Kingella)
  • Enterococci
  • Gram negative bacilli
  • Fungi
165
Q

What is this:

non-infected (sterile) vegetations caused by non-bacterial thrombotic endocarditis.

A

Non-infective endocarditis (Libman-Sacks endocarditis (SLE)

166
Q

What is this:
characterized by deposition of small sterile thrombi on the leaflets of cardiac valves. Vegetations are thrombi that do not invade or elicit an inflammatory reaction. May be the source of systemic thrombi.

A

Non-bacterial thrombotic endocarditis (previously referred as marantic endocarditis)

167
Q

Who does non-bacterial thrombotic endocarditis appear in?

A

patients with cancer (mucinous adenocarcinoma), sepsis, or hypercoagulable state

168
Q

What is this:
Patients have systemic lupus erythematosus and have vegetations located on the mitral and tricuspid valves, valvular endocardium, chords, and mural endocardium of the atria

A

Libman-Sacks disease

169
Q

What are the vegetations made up of in Libman-Sacks disease?

A

composed of finely granular, fibrinous eosinophilc material with hematoxylin bodies

170
Q

In libman-sacks disease you have intense (blank) with (blank) necrosis of the valve

A

valvulitis

fibrinoid

171
Q

What are the complications associated with artificial valves (mechanical prostheses, tissue valves)?

A
  • thromboembolism
  • infective endocarditis with ring abscess
  • structural deterioration
172
Q

What is this:

Lesions are firm and plaque like endocardial fibrous thickenings found at the tricuspid and pulmonary valves

A

Carcinoid heart disease

173
Q

What is carcinoid heart disease due to?

A

carcinoid syndrome that results in carcinoids emptying into the IVC

174
Q

What are the three primary cardiomyopathies (disorders confined to the heart muscle)?

A
  • Dilated
  • Hypertrophic
  • Restrictive
175
Q

What are secondary cardiomyopathies?

A

myocardial involvement as a component of a systemic or multiorgan disorder

176
Q

What is the most common form of primary cardiomyopathy?

What is it characterized by?

A

Dilated cardiomyopathy (90%)

Progressive cardiac dilation and contractile dysfunction

177
Q

What is hypertrophic cardiomyopathy characterized by?

A
  • myocardial hypertrophy
  • poorly compliant LV myocardium
  • abnormal diastolic filling
  • intermittent ventricular outflow obstruction
178
Q

What is the leading cause of unexplained LVH?

A

hypertrophic cardiomyopathy (caused by gene mutation, seen in HS athletes)

179
Q

What is restrictive cardiomyopathy characterized by?

A

decreased ventricular compliance resulting in impaired filling during diastole

180
Q

What is the mechanism of impairment of dilated cardiomyopathy?

A

contractility (systolic dysfunction)

181
Q

What is the mechanism of impairment of hypertrophic cardiomyopathy?

A

compliance (diastolic dysfunction)

182
Q

What is the mechanism of impairment of restrictive cardiomyopathy?

A

compliance (diastolic dysfunction)

183
Q

What are the causes of dilated cardiomyopathy?

A 
Genetic
Myocarditis
Alcohol abuse
Childbirth
Chronic anemia
Medications
Hemochromatosis
184
Q

What are the causes of hypertrophic cardiomyopathy?

A

Genetics

185
Q

What are the causes of restrictive cardiomyopathy?

A

idiopathic
amyloidosis
radiation induced
fibrosis

186
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

An inherited disorder (autosomal dominant) that breaks down the myocardium increasing risk of abnormal heartbeat (arrhythmia) and sudden death.

187
Q

What will arrhythmogenic right ventricular cardiomyopathy cause?

A

right ventricular failure and various rhythm disturbances (ventricular tachycardia, ventricular fibrillation)
Thinned right ventricular wall

188
Q

Why is the right ventricle wall severely thinned in arrhythmogenic right ventricular cardiomyopathy?

A

loss of myocytes, fatty infiltration and fibrosis

189
Q

Arrhythmogenic right ventricular cardiomyopathy is related to defective (blank) in the desmosomes that link adjacent myocytes

A

cell adhesion proteins

190
Q

What is this:
Thickened interventricular wall
Enlarged myofibrils with big nuclei
Myofibral disarray

A

Cardiomyopathy

191
Q

What will you see on a histogram of restrictive cardiomyopathy?

A

amyloid deposition

192
Q

What will a histogram look like of arrhthmogenic right ventricular cardiomyopathy?

A

fatty deposits due to a genetic mutation that causes a fatty mutation of the myocardium which causes expansion

193
Q

What is myocarditis?

A

infectious or inflammatory processes that cause myocardial injury

194
Q

What are the infectious processes that cause myocardial injury?

A 
Viruses
Bacteria
Fungus
Protozoa (trypanosoma)
Helminths
195
Q

What are the viruses that cause myocardial injury?

A

Coxsackie A/B
Enterovirus
HIV
CMV

196
Q

What are the bacteria that cause myocardial injury?

A

Chlamydia
Neisseria
Borrelia
Rickettsia

197
Q

What are the causes of immune-mediated myocarditis?

A 
post-viral
poststreptococcal
SLE
Drug Hypersensitivity
-methyldopa
-sulfoamides
Transplant rejection
198
Q

What are 2 other cause of myocarditis?

A

sarcoidosis

giant cell myocarditis

199
Q

The normal pericardial space contains (blank) mL of thin, clear, straw colored fluid.

A

30-50

200
Q

Chronic pressure allows effusion of up to (blank) mL in the pericardial space.
Rapid effusion allows up to (blank) mL

A

500

200-300

201
Q

What is this:

pericardial space distended by serous fluid

A

Pericardial effusion

202
Q

What is this:

pericardial space distended by blood

A

Hemopericardium

203
Q

What is this:

Pericardial space distended by pus

A

Purulent pericarditis

204
Q

What are types of acute pericarditis?

A 
Serous pericarditis
Fibrinous/serofibrinous pericarditis
Purulent pericarditis
Hemorrhagic pericarditis
Caseous pericarditis
205
Q

What are types of chronic pericarditis?

A

adhesive pericarditis

constructive pericarditis

206
Q

What is serous pericarditis produced by? What is the infiltrate like and where is it found?

A
  • non-infectious inflammatory disease

- mild lymphocytic infiltrate in the epipericardial fat

207
Q

What is the most frequent type of acute pericarditis?

A

Fibrinous/ serofibrinous

208
Q

What is characteristic of fibrinous/serofibrinous acute pericarditis?

A

loud pericardial friction rub

209
Q

What is this:

composed of serous fluid mixed with fibrinous exudate

A

fibrinous/serofibrinous acute pericarditis

210
Q

What is fibrinous/serofibrinous acute pericarditis associated with?

A

acute MI, postinfarction syndrome, uremia, chest radiation, Rheumatoid Factor, systemic lupus erythematosus, trauma

211
Q

What causes acute purulent pericarditis?

A

invasion of microbes into the pericardial space by direct extension, seeding from the blood, lymphatic extension, introduction during cardiotomy

212
Q

Acute purulent pericarditis is an acute inflammatory reaction that can produce a (blank). What can occur after this and what type of pericarditis is that associated with?

A

mediastinopericarditis

Scarring and re-organization which results in constrictive pericarditis.

213
Q

What is the appearance of hemorrhagic acute pericarditis?

A

blood with a fibrinous or suppurative effusion

214
Q

What causes hemorrhagic acute pericarditis?

A

metastatic malignant neoplasm

also found in TB and bacterial infections and post-cardiac surgery

215
Q

What does caseous acute pericarditis lead to?

A

a disabling, fibrocalcific, chronic constrictive pericarditis

216
Q

What is caseous acute pericarditis due to and is it common?

A

due to TB by direct spread, but sometimes fungus

-rare

217
Q

What are the four types of chronic pericarditis?

A
  • no clinical consequence
  • adhesive pericarditis
  • adhesive mediastinopericarditis
  • constrictive pericarditis
218
Q

When do you get adhesive mediastinopericarditis?

What is it?

A
  • following infectious pericarditis, cardiac surgery, radiation
  • pericardial sac is obliterated and pericardium adheres to surrounding structures
219
Q

What is constrictive pericarditis?

A

heart is encased in a fibrous/ fibrocalcific scar that limits diastolic expansion and cardiac output

220
Q

What does constrictive pericarditis mimic?

What are the heart sounds like in constrictive pericarditis?

A

restrictive cardiomyopathy

muffled or distant

221
Q

What is the most common primary cardiac tumor in adults? Are they malignant or benign
What chromosomes are abnormal?
Where do these arise from?
What part of the heart are they found?
10% of these are associated with (blank) complex

A
  • myxoma
  • benign
  • 12 & 17
  • primitive multipotent mesenchymal cells
  • atria but can arise in any chamber
  • Carney complex
222
Q

What is the most common cardiac tumor in children? What is it associated with? what are they considered?

A 
Rhabdomyoma
tuberous sclerosis (disease that causes benign tumor growth in essential organs and skin)
hamartomas (normally present cells with abnormal structure but is benign and resembles a tumor)
223
Q

What is this:
A cardiac benign tumor of mature adipose tissue
most often located in the LV, RA or atrial septum

A

Lipoma

224
Q

What is this:
A cardiac benign neoplasm often discovered at autopsy
Resemble Lambl excrescences (filiform fronds that occur at sites of valve closure)

A

Papillary fibroelastoma

Block 9 Week 1 (7 decks)

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