CVS Pathology II Flashcards
1
Q
Ischemic heart disease (IHD) results from an imbalance of the _______ and ______ of the heart
A
Blood supply and oxygen demand
2
Q
Name modifiable risk factors of IHD
A
Diet, hyperlipidemia, hypertension, DM, cigarette smoking
3
Q
Name non-modifiable risk factors of IHD
A
Age, gender (male), familial dispostion
4
Q
Factors associated with a decreased risk in IHD
A
Alcohol (red wine), regular exercise, high HDL, estrogen, folate
5
Q
Causes of IHD
A
Fixed stenosing atherosclerosis, Fissure/rupture/ulceration/hemorrhage, Coronary artery thrombosis, Coronary artery vasoconstriction/vasospasm (no plaque), Critical stenosis
6
Q
At what percentage is stenosis considered critical? Why?
A
> 70%; at this fixed level of obstruction compensatory mechanisms areinsufficient to meet moderate increases in myocardial O2 demand
7
Q
Acute plaque changes are associated with
A
Acute coronary syndromes (unstable angina, AMI, Sudden cardiac death)
8
Q
Name some acute plaque changes
A
rupture/fissuring, erosion/ulceration, hemorrhage into atheroma
9
Q
What is the underlying cause of a typical angina pectoris
A
Fixed coronary obstruction, causing transient myocardial ischemia that falls short of infarction
10
Q
Occlusive thrombus is associated with…
A
acute transmural myocardial infarction
11
Q
Name some atheromatous Coronary arterial occlusions
A
embolism, dissecting aneurysm, vasospasm, congenital anomaly, trauma
12
Q
Inflammation plays a role in later stages of IHD by…
A
secretion of metalloproteinases by macrophages
13
Q
Inflammation plays a role in the initial stages of IHD by…
A
interaction of endothelial cells and circulating leukocytes
14
Q
IHD syndromes are _____ manifestations of coronary atherosclerosis
A
late
15
Q
What are the syndromes of IHD
A
1) Angina Pectoris
2) Acute MI
3) Chronic Ischemic heart disease (Ischemic cardiomyopathy)
4) Sudden Cardiac death
16
Q
Angina pectoris is cause by increased myocardial demand with decreased perfusion d/t:
A
Chronic stenosing coronary atherosclerosis, disrupted atherosclerotic plaques, vasospasm, thrombosis, coronary artery embolization
17
Q
3 types of Angina Pectoris
A
Stable, Prinzmetal, Unstable
18
Q
In stable angina, chest pain is precipitated by _______ and relieved by _______
A
exertion and emotion, rest and vasodilators
19
Q
Prinzmetal Angina Pectoris is d/t and ECG changes are suggestive of _____
A
Vasospasm; transmural ischemia (ST segment elevation)
20
Q
In Prinzmetal angina pectoris, there is episodic pain at _____ that responds to _____
A
Rest; nitroglycerin, Ca-channel blockers, vasodilators
21
Q
% vessel blocked in Unstable Angina Pectoris
A
90%
22
Q
In unstable angina, pain __________ in frequency and duration and occurs _______
A
progressively increases; at rest
23
Q
Unstable angina pectoris is associated with
A
Acute plaque change with superimposed partial thrombosis or vasospasm
24
Q
In MI, coronary obstruction produces what kind of cardiac muscle necrosis?
A
coagulative
25
Major risk factors of AMI
HTN, cigarette smoking, DM, hyperlipidemia
26
Minor risk factors of AMI
Obesity, sex, age, stress, physical inactivity
27
What is the hallmark myocardial change in AMI? In what region and what type of progression?
Ischemic coagulative necrosis; Subendocardial region; wavefront progression
28
Biochemical changes in AMI
Anaerobic glycolysis, ATP and creatinine phosphate reduction, lactic acidosis (increase muscle death)
29
Ultrastructural changes in AMI
mitochondrial swelling, myofibrillar relaxation, glycogen depletion, sarcolemmal membrane damage
30
In AMI, irreversible myocardial damage is seen in sever ischemia lasting from _____ or longer
20-40 minutes (another part says 10 minutes is the window period)
31
The patient may present with arrhythmia if the obstruction occurs in the _____
Anterior descending coronary artery
32
A rapid rate of occlusion development is mosre severe than a slow one b/c...
there is no time for collateral vessels to form
33
Types of infarction; Describe the difference in terms of wall thickness affected
Transmural (full thickness), Subendocardial (limited to inner 1/3 or 1/2 of ventricle)
34
Transmural Infarctions are associated with
CHRONIC atherosclerotic obstruction, acute plaque change, superimposed complete occlusive thrombosis
35
Subendocardial infarctions are associated with
Diffuse stenosing coronary atherosclerosis WITHOUT thrombosis and acute plaque change
36
What infarcts are referred to as ST elevation infarcts? Non-ST elevation infarcts
Transmural; Subendocardial
37
In the gross morphology of AMI, using triphenyl tetrazollium chloride stain, the infarct will show as _______
unstained area
38
Gross & microscopic findings 0-18 hours post MI
no gross change; wavy myocyte fibers
39
Dark mottling is seen _____ hours after AMI; What are the microscopic changes related this?
12-24 hours; coagulation necrosis, pyknosis of nuclei, myocytehypereosinophilia, marginal contraction band with beginning neutrophilic infiltrate
40
Gross & microscopic findings 7-28 days post MI
Central pallor with a red border; granulation tissue
41
Gross & microscopic findings 1-7 days post MI
Yellow pallor; Coagulative necrosis (4-24 hours), neutrophilic infiltrate (1-4 days), macrophages (4-7 days)
42
Gross & microscopic findings months post MI
White firm scar; fibrotic scar
43
Mottling with yellow-tan infarct center is seen _____ days post MI
1-3 days
44
Hyperemic border with a central yellow-tan softening is seen ____ days post MI
3-7 days
45
Maximally yellow-tan and soft with depressed red-tan margin margins seen _____ days post MI
7-10 days
46
10-14 days post MI, what are the gross features and microscopic features
red-gray depressed infarct borders; well-established granulation tissue WITH new blood vessels and collagen deposition
47
2-4 weeks post MI, what are the gross features and microscopic features
Gray-white scar progressive from border toward core of infarct; Increased collagen deposition with DECREASED cellularity
48
> 2 months post MI, what are the gross features and microscopic features
Scarring complete; Dense collagenous scar
49
What is the most effective way to rescue ischemic myocardium?
Reperfusion
50
Give complications of reperfusion
arrhythmias, myocardial hemorrhage with contraction bands, irreversible cell damage superimposed on the original ischemic injury, mircovascular injury, prolonged ischemic dysfunction
51
Reperfusion beyond _____ does not appreciable reduce myocardial infarct size
6 hours
52
Symptoms of AMI
Rapid weak pulse , diaphoresis
53
In AMI, cardiac troponins I and T are ______
elevated
54
_______ in levels of CK, CKMB troponin I in the 1st 2 days following chest pain essentially EXCLUDES a diagnosis of MI
Absence of change
55
CK-MB is sensitive and specific for MI (T/F)
False; it is sensitive but NOT specific b/c it is found in other muscles
56
Lab increase of ______ is found EARLIEST post MI
troponin
57
Time frame for use of SGOT and LDH as markers of AMI
1-3 days
58
Treatment for AMI
Aspirin and heparin, oxygen, nitrates, beta adrenergic blockers, ACE Inhibitors
59
Complications of AMI
Contractile dysfunction, Arrhythmias, Myocardial rupture, Pericarditis, R-ventricular infarct, Infarct extension, Infarct expansion, Mural thrombus, Ventricular aneurysm, Papillary muscle dysfunction, Progressive late heart failure
60
In AMI, prognosis and complications are dependent on
Infarct size, site, fractional thickness of myocardial wall damaged
61
Types of infarct modifications
Thrombolysis, Angioplasty, Stent, CABG,
62
It is the development of progressive heart failure as a result of chronic ischemic myocardial damage
Chronic Ischemic Heart Disease (Ischemic cardiomyopathy)
63
In Ischemic cardiomyopathy, postinfarct decompensation is d/t
exhaustion of compensatory hypertrophy of non-infarcted viable myocardium
64
Describe the gross morphology of the heart in ischemic cardiomyopathy
Large and heavy d/t L-ventricular dilation and hypertrophy, Moderate to severe stenosing atherosclerosis, Mural endocardium may have patchy fibrous thickenings and mural thrombi
65
Describe the microscopic morphology of the heart in ischemic cardiomyopathy
gray-white scars of healed infarcts, myocardial hypertrophy, diffuse subenedocardial vacuolization
66
In sudden cardiac death, there is unexpected death in _______ patients or those with symptoms less than _______
Asymptomatic; 1 hour
67
Major cause of sudden cardiac death
Atherosclerosis
68
Non-atherosclerotic causes of sudden cardiac death
Congenital structural or coronary arterial abnormalities, AV stenosis, MV prolapse, dilated or hypertrophic cardiomyopathy, myocarditis, Pulmonary HTN, Hereditary or acquired abnormality of cardiac conduction system, isolated hypertrophy
69
(T/F) In sudden cardiac death, there will be no apparent changes in morphology of the heart
true
70
A consistent finding in patients with sudden cardiac death is _____
Marked coronary atherosclerosis involving 1 or more major vessels and severe chronic ischemia is commonly seen
71
2 types of hypertensive heart disease
Systemic (left-side) and Pulmonary (right-sided)
72
What is the adaptive response of the heart in systemic hypertensive heart disease
CONCENTRIC left ventricular hypertrophy
73
What is the adaptive response of the heart in pulmonary hypertensive heart disease
Right ventricular dilation
74
What are the diagnostic criteria for What is the adaptive response of the heart in systemic hypertensive heart disease
Left ventricular hypertrophy, Hitory or pathologic evidence of HTN, Absence of other CVS lesions that may induce hypertrophy (ex valvular disease)
75
In systemic hypertensive heart disease, papillary muscles and the intraventricular septum are ________ and there is stiffness and impairment of ________
thick, diastolic filling
76
In systemic hypertensive heart disease, there is an increase in the ________ diameter of the myocytes with ______ nuclei
transverse, enlarged
77
Pulmonary hypertensive heart disease is characterized by
RV hypertrophy, dilation and potentially failure d/t increased pulmonary resistance
78
Different types of pulmonary hypertensive heart disease
Acute cor pulmonale; Chronic cor pulmonale
79
How do you differentiate between acute and chronic cor pulmonale?
Acute = RV dilation WITHOUT hypertrophy; Chronic = RV dilation WITH hypertrophy
80
Why is there no hypertrophy in acute cor pulmonale?
Because there is no time for adaptation (hypertrophic change)
81
What kinds of disorders predispose you to chronic cor pulmonale?
Diseases of pulmonary parenchyma, pulmonary vessels, affecting chest movements, inducing pulmonary arterial constriction
82
Name diseases of pulmonary parenchyma
COPD, diffuse pulmonary interstitial fibrosis, Pneumoconiosis, Cystic fibrosis, Bronchiectasis
83
Name diseases of Pulmonary vessels
Recurrent pulmonary thromboembolism, primary pulmonary hypertension, extensive pulmonary arteritis, drugs, extensive pulmonary tumor microembolism
84
Name diseases affecting chest movement
kyphoscoliosis, marked obesity, neuromuscular disease,
85
Name diseases inducing pulmonary arterial constriction
hypoxemia, metabolic acidosis, chronic altitude sickness, obstruction to major airways, idiopathic alveolar hypoventilation
86
Gross morphology of the heart in cor pulmonale
Compression of LV or tricuspid thickening and regurgitation
87
Microscopic changes of the heart in cor pulmonale
Loss of fat in wall with myocytes aligned circumferentially (normally haphazard)
88
Different kinds of myocardial disease
Inflammatory disorders, Immunologic and systemic metabolic disorders, genetic abnormalities
89
4 types of cardiac myopathies (CMP)
Dilated, Hypertrophic, Restrictive, Arrhythmogenic Right Ventricular Dysplasia
90
What is the most common type of cardiomyopathy
Dilated
91
Ejection fraction in dilated cardiomyopathy
Low
92
In dilated cardiomyopathy, death is usually attributable to
progressive heart failure or arrhythmia
93
(T/F) The heart is hypocontracting in dilated cardiomyopathy
True
94
S/S of dilated cardiomyopathy
(Manifestations of progressive CHF) SOB, easy fatigability, poor exertional capacity
95
(T/F) Cardiac transplantation is recommended in dilated cardiomyopathy
True
96
Causes of Dilated cardiomyopathy
Idiopathic, Previous viral or complicated myocarditis, alcohol abuse, Pregnancy, Genetic, Malnutrition (B12, B1), Cobalt (added to beer), Adriamycin therapy
97
4 Criteria for diagnosis of dilated cardiomyopathy
NEGATIVE CRITERIA:
1) NO major CAD
2) NO valvular disease
3) NO systemic HTN
4) NO shunts within or outside the heart
98
Gross morphology in dilated cardiomyopathy
Generalized chamber dilation (flabby), mural thrombi common, regurgitation d/t annular ring dilation, abnormal release of blood flow, increased weight, global enlargement
99
What is the most important finding in Hypertrophic cardiomyopathy
Myocardial hypertrophy
100
Differentiate Dilated and Hypertrophic cardiomyopathy in terms of chamber and contraction
DCM --> flabby and HYPOcontracting
| HCM --> muscular and HYPERcontracting
101
Differentiate Dilated and Hypertrophic cardiomyopathy in terms of abnormalities
DCM --> cytoskeleton; HCM --> mutations of proteins in sarcomere
102
(T/F) HCM causes both diastolic and systolic dysfunction
False. Only diastolic dysfunction, systolic dysfunction is preserved
103
What 2 diseases must be distinguished clinically from HCM
Amyloidosis, Hypertensive heart disease
104
Clinical features of HCM
Decreased diastolic filling, reduced chamber size, reduced SV and CO, increased pulmonary venous pressure, exertional dyspnea; Harsh systolic ejection murmur
105
In HCM, what is the cause of the harsh systolic ejection murmur
Ventricular outflow obstruction as the anterior mitral leaflet moves toward the ventricular septum during systole
106
What are the major clinical problems in HCM
A.fib with mural thrombosis, infective endocarditis of MV, Intractable cardiac failure, Ventricular arrhythmias, Sudden death
107
Describe the gross morphology of the heart in HCM
Massive myocardial hypertrophy WITHOUT ventricular dilation, Asymmetric septal hypertrophy, Banana-like ventricular cavity, endocaridal thickening, anterior mitral valve thickening
108
Describe the microscopic morphology of the heart in HCM
Extensive myocardial hypertrophy, Haphazard myocardial fiber disarray (Most important), Interstitial fibrosis
109
In restrictive cariomyopathy there is a ______ in cardiac compliance, ventricular filling during diastole and ejection fraction
Decrease
110
What are the causes of Restrictive cardiomyopathy
Idiopathic, Amyloidosis, radiation fibrosis, sarcoidosis, immune, metabolic, metastatic tumors, deposition of metabolites d/t inborn errors of metabolism
111
Gross morphology in Restrictive cardiomyopathy
Normal or slightly enlarged heart with non-dilated stiff ventricles; BI-ATRIAL DILATION
112
What are the other types of RCM
Endomyocardial fibrosis, Leoffler endomyocarditis, Endocardial fibroelastosis
113
Autosomal dominant Inherited cardiomyopathy that causes right ventricular failure and various rhythym disturbances (v.tach)
Arrhythmogenic Right ventricular cardiomyopathy
114
Heart morphology in Arrhythmogenic Right ventricular cardiomyopathy
Severely thinned R-ventricular wall d/t loss of myocyte with extensive fatty infiltration and fibrosis
115
Arrhythmogenic Right ventricular cardiomyopathy with hyperkeratosis of plantar palmar skin surfaces
Naxos syndrome
116
Defect in Arrhythmogenic Right ventricular cardiomyopathy
Cell adhesion proteins in desmosomes that link adjacent cardiac myocytes
117
Major causes of myocarditis are related to
Infections, Immune-mediated reactions, can be unknown, drugs
118
Type of myocarditis with an aggressive clinical course
Giant cell myocarditis
119
Myocarditis associated with ADR, with little or no necrosis, granulomas
Hypersensitivity myocarditis
120
ADR of what drug is most of the time related to hypersensitivity myocarditis
Methyldopa
121
In myocarditis, the heart is _______ d/t vascular congestion and the ventricular myocardium is _____
Beefy red; flabby and mottled by focal hemorrhagic lesions
122
In myocarditis, the heart is _______ d/t vascular congestion and the ventricular myocardium is _____
Beefy red; flabby and mottled by focal hemorrhagic lesions
