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SP15 Pathology > Exam 2; Cardiovascular II > Flashcards

Exam 2; Cardiovascular II Flashcards

1
Q

This is the failure to pump an adequate amount of blood to supply the metabolic requirements of the organs

A

congestive heart failure

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2
Q

How many people a year does CHF affect

A

nearly 5 million people in the US annually; contributing to 300k deaths

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3
Q

What may cause CHF

A

pathologic conditions directly related to the hear or due to peripheral problems

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4
Q

What are two neurohormonal systems used as a compensatory mechanism for CHF

A

release of NE with increased HR and contractility

activation of renin-angiotension system with water/salt retention (increase circulatory volume)

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5
Q

What is the Frank-Starling compensatory mechanism

A

increased end-diastolic filling volume stretches the cardiac muscle fibers
the fibers at first contract for forcefully, increase CO but eventually they cannot keep up

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6
Q

This is an increase in muscle fiber size resulting in increased thickness of the ventricular wall but without increase in the size of the lumen

A

myocardial hypertrophy

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7
Q

Compensatory mechanisms usually fail due to what

A

increased oxygen requirements of myocardium but without increase capillary supply, resulting in susceptibility to ischemia

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8
Q

What are some physiologic compensatory mechanisms

A 
increased heart rate
increased intravascular volume
re-distribution of blood flow
increased catecholamines
ventricular dilation
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9
Q

What are five causes of left-sided heart failure due to CHF

A 
ischemic heart disease
hypertension
myocarditis
cardiomyopathy
valvular disease
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10
Q

What are four causes of right-sided heart failure due to CHF

A

left-sided heart failure
pulmonary hypertension
valve disease
septal defects with left-to-right shunts

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11
Q

How does left-sided heart failure cause the right side to fail as well

A

subsequent pulmonary congestion leads to increased pulmonary arterial pressure

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12
Q

What are the three clinical manifestations of left ventricular failure of CHF

A

pulmonary edema and congestion resulting in dyspnea
chronic cough
orthopnea

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13
Q

What is the clinical manifestation of right and/or left ventricular failure

A

cerebral hypoxia

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14
Q

What are the clinical manifestations of right ventricular failure

A

congestion of liver (nutmeg liver) and spleen

edema (pitting) of subcutaneous tissues, particularly lower extremities (feet and ankles)

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15
Q

What is the prevalence of CHD in live births in the US

A

6-8/1,000

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16
Q

What are three causes of CHD

A

environmental factors
chromosomal abnormalities
90% are unknown and likely multifactorial

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17
Q

What are the two forms of CHD

A

cyanotic and non-cyanotic

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18
Q

This is the 2nd most common congenital malformation of non-cyanotic CHD

A

atrial septal defect (ASD)

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19
Q

This the most common (4/1,000) of cardiac malformations of non-cyanotic CHD

A

ventricular septal defect

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20
Q

This connects aorta and pulmonary artery; should close within a few days after birth

A

patent ductus arteriosus (PDA)

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21
Q

This type of CHD generally has shunting of poorly-oxygenated systemic venous return to the systemic arterial circulation; bypassing the lungs

A

cyanotic

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22
Q

CHD include what forms

A

shunts
abnormal connections between chambers and blood vessels
absence of normal connections

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23
Q

What are the four disorders associated with teratology of fallout associated with cyanotic CHD

A

ventricular septal defect
narrowed right ventricular outflow
overriding of the aorta over the VSD
right ventricular hypertrophy

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24
Q

What is the transposition of the great arteries associated with cyanotic CHD

A

right ventricle empties into the aorta

left ventricle empties into the pulmonary artery

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25
Q

This refers to a group of related disorders that are all characterized by imbalance between myocardial blood supply and myocardial oxygen demand; it is the leading cause of death in the US (500k annually)

A

ischemic heart disease (IHD)

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26
Q

What is the primary cause of IHD

A

(>90%) due to coronary artery atherosclerosis

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27
Q

What are two other prominent causes of IHD

A

coronary artery atherosclerosis (>75% narrowing)

coronary artery thrombosis

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28
Q

What are four other causes of IHD

A

increased myocardial oxygen demand (hypertension)
decreased blood volume (hypotension/shock)
decreased oxygenation (pneumonia)
decreased oxygen carrying capacity (anemia)

29
Q

What are the four clinical types of IHD

A

angina pectoris
myocardial infarction
chronic IHD with CHF
sudden cardiac death

30
Q

This is intermittent chest pain caused by transient, reversible myocardial ischemia

A

angina pectoris

31
Q

This occurs predictably at certain levels of exertion, crushing or squeezing substantial pain that may radiate down the left arm or jaw (referred pain); received by rest or nitroglycerin

A

stable angina

32
Q

This is the increasing frequency of chest pain with minimal/no exertion; often preceding something more serious

A

unstable angina

33
Q

This results from necrosis of the cardiac muscle due to ischemia

A

myocardial infarction

34
Q

What is the prevalence of MI

A

1.5 million annually, 1/3 die

35
Q

Severe ischemia lasting longer than 20-40 minutes will cause what

A

irreversible myocyte injury

36
Q

Myocardial ischemia contributes to this due to ischemic regions causing electrical instability

A

arrhythmias and may lead to ventricular fibrillation

37
Q

What are the clinical manifestations of ischemic heart disease

A 
chest pain
SOB
nausea/vomiting
diaphoresis (sweating)
low grade fever
38
Q

What are two tests that can be used to test for IHD; MI

A

ECG

elevated serum proteins and troponin

39
Q

What occurs during IHD:MI after a few hours

A

coagulation necrosis

40
Q

What occurs during IHD:MI after 1 week

A

granulation tissue

41
Q

What occurring during IHD:MI after weeks-months

A

scar formation

42
Q

MIs less than this are usually not grossly apparent at autopsy

A

12 hours

43
Q

At 12-24 hours after a MI the infarcted area appears what

A

reddish-blue

44
Q

What are the three treatments for IHD:MI

A

placement of stents to open coronary vessels affected by atherosclerosis
coronary artery bypass grafts (CABG)
“clot-busting” drugs like streptokinase or TPA

45
Q

Treatment of IHD; MI may result in what

A

reperfusion injury

46
Q

What are eight complications of MI

A 
arrhythmia
CHF/shock
mural thrombosis
mitral valve regurgitation
myocardial rupture
infarct expansion to involve right ventricle
ventricular aneurysm
chromic ischemic heart disease
47
Q

What is a mural thrombosis (MI complication)

A

thrombus developing on the lining of the heart chamber, which can lead to left sided embolism

48
Q

Why is there a possibility of mitral valve regurgitation (MI complication)

A

due to papillary muscle dysfunction

49
Q

This is progressive heart failure due to ischemic myocardial damage usually with a history of MI

A

chromic ischemic heart disease

50
Q

What is the most common cause of sudden cardiac death; ischemia induced cardiac arrhythmia with or without myocardial necrosis

A

IHD (80-90%)

51
Q

True or False

sudden cardiac death can occur in individuals with our without a previous history of IHD

A

True

52
Q

This class of cardiomyopathy is when the disease is solely confined to the heart muscle

A

primary

53
Q

This class of cardiomyopathy is when the myocardium is involved as part of a systemic disorder

A

secondary

54
Q

What are the three functional patterns of cardiomyopathies

A

dilated
hypertrophic
restrictive

55
Q

This type of cardiomyopathy may be primary, secondary, or genetic

A

dilated

56
Q

Dilated cardiomyopathy seen in genetics cases (20-30%) is also related to what

A

alcoholism
myocarditis
pregnancy

57
Q

Where is the dilation found in dilated cardiomyopathy

A

all four chambers

58
Q

what are the clinical manifestations of dilated cardiomyopathy

A

poor ventricular contractility

non-specific histology with fibrosis and myocyte hypertrophy

59
Q

This type of cardiomyopathy is either primary or genetic with AD inheritance; a missence point mutation in one of several sarcomeric gene loci

A

hypertrophic cardiomyopathy

60
Q

What are the clinical manifestations of hypertrophic cardiomyopathy

A

stiff ventricles prevent adequate filling (diastolic dysfunction)
myocyte disarray with fibrosis

61
Q

Inappropriate (spontaneous) myocardial hypertrophy (asymmetric) is greater where in the heart

A

in the inter ventricular septum than the left ventricular free wall and often obstructs the left ventricular outflow tract

62
Q

This type of cardiomyopathy is when there is a decrease in ventricular compliance (wall is stiffer) resulting in impaired ventricular filling during diastole

A

restrictive cardiomyopathy

63
Q

Restrictive cardiomyopathy can be idiopathic or what

A

secondary to systemic conditions that happen to affect the myocardium, such as radiation fibrosis, amyloidosis, hemochromatosis and sarcoidosis

64
Q

What is the etiology of myocarditis

A

most common cause in the US is viral infection (coxsackie A and B, other Enteroviruses) but can also be caused by bacterial, fungal, and parasitic organisms

65
Q

What are some non-infectious causes of myocarditis

A

toxins
hypersensitivity reactions
auto-immune disorders
but some cases are unknown

66
Q

Viral myocarditis produces what

A

lymphocytic (interstitial mononuclear inflammatory cells) infiltrate with foci of necrosis

67
Q

Pyogenic bacteria causing myocarditis produces what

A

abscesses

68
Q

Parasitic myocarditis produces what

A

infect individual myocytes or are in interstitial areas with surrounding inflammatory cells
example; trypanosomes in Chagas disease

69
Q

Hypersensitivity reactions (usually to drugs) causing myocarditis causes what

A

perivascular inflammatory infiltrate with eosinophils

SP15 Pathology (17 decks)

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