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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
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)
ischemic heart disease (IHD)
26
What is the primary cause of IHD
(>90%) due to coronary artery atherosclerosis
27
What are two other prominent causes of IHD
coronary artery atherosclerosis (>75% narrowing) | coronary artery thrombosis
28
What are four other causes of IHD
increased myocardial oxygen demand (hypertension) decreased blood volume (hypotension/shock) decreased oxygenation (pneumonia) decreased oxygen carrying capacity (anemia)
29
What are the four clinical types of IHD
angina pectoris myocardial infarction chronic IHD with CHF sudden cardiac death
30
This is intermittent chest pain caused by transient, reversible myocardial ischemia
angina pectoris
31
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
stable angina
32
This is the increasing frequency of chest pain with minimal/no exertion; often preceding something more serious
unstable angina
33
This results from necrosis of the cardiac muscle due to ischemia
myocardial infarction
34
What is the prevalence of MI
1.5 million annually, 1/3 die
35
Severe ischemia lasting longer than 20-40 minutes will cause what
irreversible myocyte injury
36
Myocardial ischemia contributes to this due to ischemic regions causing electrical instability
arrhythmias and may lead to ventricular fibrillation
37
What are the clinical manifestations of ischemic heart disease
``` chest pain SOB nausea/vomiting diaphoresis (sweating) low grade fever ```
38
What are two tests that can be used to test for IHD; MI
ECG | elevated serum proteins and troponin
39
What occurs during IHD:MI after a few hours
coagulation necrosis
40
What occurs during IHD:MI after 1 week
granulation tissue
41
What occurring during IHD:MI after weeks-months
scar formation
42
MIs less than this are usually not grossly apparent at autopsy
12 hours
43
At 12-24 hours after a MI the infarcted area appears what
reddish-blue
44
What are the three treatments for IHD:MI
placement of stents to open coronary vessels affected by atherosclerosis coronary artery bypass grafts (CABG) "clot-busting" drugs like streptokinase or TPA
45
Treatment of IHD; MI may result in what
reperfusion injury
46
What are eight complications of MI
``` arrhythmia CHF/shock mural thrombosis mitral valve regurgitation myocardial rupture infarct expansion to involve right ventricle ventricular aneurysm chromic ischemic heart disease ```
47
What is a mural thrombosis (MI complication)
thrombus developing on the lining of the heart chamber, which can lead to left sided embolism
48
Why is there a possibility of mitral valve regurgitation (MI complication)
due to papillary muscle dysfunction
49
This is progressive heart failure due to ischemic myocardial damage usually with a history of MI
chromic ischemic heart disease
50
What is the most common cause of sudden cardiac death; ischemia induced cardiac arrhythmia with or without myocardial necrosis
IHD (80-90%)
51
True or False | sudden cardiac death can occur in individuals with our without a previous history of IHD
True
52
This class of cardiomyopathy is when the disease is solely confined to the heart muscle
primary
53
This class of cardiomyopathy is when the myocardium is involved as part of a systemic disorder
secondary
54
What are the three functional patterns of cardiomyopathies
dilated hypertrophic restrictive
55
This type of cardiomyopathy may be primary, secondary, or genetic
dilated
56
Dilated cardiomyopathy seen in genetics cases (20-30%) is also related to what
alcoholism myocarditis pregnancy
57
Where is the dilation found in dilated cardiomyopathy
all four chambers
58
what are the clinical manifestations of dilated cardiomyopathy
poor ventricular contractility | non-specific histology with fibrosis and myocyte hypertrophy
59
This type of cardiomyopathy is either primary or genetic with AD inheritance; a missence point mutation in one of several sarcomeric gene loci
hypertrophic cardiomyopathy
60
What are the clinical manifestations of hypertrophic cardiomyopathy
stiff ventricles prevent adequate filling (diastolic dysfunction) myocyte disarray with fibrosis
61
Inappropriate (spontaneous) myocardial hypertrophy (asymmetric) is greater where in the heart
in the inter ventricular septum than the left ventricular free wall and often obstructs the left ventricular outflow tract
62
This type of cardiomyopathy is when there is a decrease in ventricular compliance (wall is stiffer) resulting in impaired ventricular filling during diastole
restrictive cardiomyopathy
63
Restrictive cardiomyopathy can be idiopathic or what
secondary to systemic conditions that happen to affect the myocardium, such as radiation fibrosis, amyloidosis, hemochromatosis and sarcoidosis
64
What is the etiology of myocarditis
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
What are some non-infectious causes of myocarditis
toxins hypersensitivity reactions auto-immune disorders but some cases are unknown
66
Viral myocarditis produces what
lymphocytic (interstitial mononuclear inflammatory cells) infiltrate with foci of necrosis
67
Pyogenic bacteria causing myocarditis produces what
abscesses
68
Parasitic myocarditis produces what
infect individual myocytes or are in interstitial areas with surrounding inflammatory cells example; trypanosomes in Chagas disease
69
Hypersensitivity reactions (usually to drugs) causing myocarditis causes what
perivascular inflammatory infiltrate with eosinophils

SP15 Pathology (17 decks)

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