CVS Pathology II Flashcards
Ischemic heart disease (IHD) results from an imbalance of the _______ and ______ of the heart
Blood supply and oxygen demand
Name modifiable risk factors of IHD
Diet, hyperlipidemia, hypertension, DM, cigarette smoking
Name non-modifiable risk factors of IHD
Age, gender (male), familial dispostion
Factors associated with a decreased risk in IHD
Alcohol (red wine), regular exercise, high HDL, estrogen, folate
Causes of IHD
Fixed stenosing atherosclerosis, Fissure/rupture/ulceration/hemorrhage, Coronary artery thrombosis, Coronary artery vasoconstriction/vasospasm (no plaque), Critical stenosis
At what percentage is stenosis considered critical? Why?
> 70%; at this fixed level of obstruction compensatory mechanisms areinsufficient to meet moderate increases in myocardial O2 demand
Acute plaque changes are associated with
Acute coronary syndromes (unstable angina, AMI, Sudden cardiac death)
Name some acute plaque changes
rupture/fissuring, erosion/ulceration, hemorrhage into atheroma
What is the underlying cause of a typical angina pectoris
Fixed coronary obstruction, causing transient myocardial ischemia that falls short of infarction
Occlusive thrombus is associated with…
acute transmural myocardial infarction
Name some atheromatous Coronary arterial occlusions
embolism, dissecting aneurysm, vasospasm, congenital anomaly, trauma
Inflammation plays a role in later stages of IHD by…
secretion of metalloproteinases by macrophages
Inflammation plays a role in the initial stages of IHD by…
interaction of endothelial cells and circulating leukocytes
IHD syndromes are _____ manifestations of coronary atherosclerosis
late
What are the syndromes of IHD
1) Angina Pectoris
2) Acute MI
3) Chronic Ischemic heart disease (Ischemic cardiomyopathy)
4) Sudden Cardiac death
Angina pectoris is cause by increased myocardial demand with decreased perfusion d/t:
Chronic stenosing coronary atherosclerosis, disrupted atherosclerotic plaques, vasospasm, thrombosis, coronary artery embolization
3 types of Angina Pectoris
Stable, Prinzmetal, Unstable
In stable angina, chest pain is precipitated by _______ and relieved by _______
exertion and emotion, rest and vasodilators
Prinzmetal Angina Pectoris is d/t and ECG changes are suggestive of _____
Vasospasm; transmural ischemia (ST segment elevation)
In Prinzmetal angina pectoris, there is episodic pain at _____ that responds to _____
Rest; nitroglycerin, Ca-channel blockers, vasodilators
% vessel blocked in Unstable Angina Pectoris
90%
In unstable angina, pain __________ in frequency and duration and occurs _______
progressively increases; at rest
Unstable angina pectoris is associated with
Acute plaque change with superimposed partial thrombosis or vasospasm
In MI, coronary obstruction produces what kind of cardiac muscle necrosis?
coagulative
Major risk factors of AMI
HTN, cigarette smoking, DM, hyperlipidemia
Minor risk factors of AMI
Obesity, sex, age, stress, physical inactivity
What is the hallmark myocardial change in AMI? In what region and what type of progression?
Ischemic coagulative necrosis; Subendocardial region; wavefront progression
Biochemical changes in AMI
Anaerobic glycolysis, ATP and creatinine phosphate reduction, lactic acidosis (increase muscle death)
Ultrastructural changes in AMI
mitochondrial swelling, myofibrillar relaxation, glycogen depletion, sarcolemmal membrane damage
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)
The patient may present with arrhythmia if the obstruction occurs in the _____
Anterior descending coronary artery
A rapid rate of occlusion development is mosre severe than a slow one b/c…
there is no time for collateral vessels to form
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)
Transmural Infarctions are associated with
CHRONIC atherosclerotic obstruction, acute plaque change, superimposed complete occlusive thrombosis
Subendocardial infarctions are associated with
Diffuse stenosing coronary atherosclerosis WITHOUT thrombosis and acute plaque change
What infarcts are referred to as ST elevation infarcts? Non-ST elevation infarcts
Transmural; Subendocardial
In the gross morphology of AMI, using triphenyl tetrazollium chloride stain, the infarct will show as _______
unstained area
Gross & microscopic findings 0-18 hours post MI
no gross change; wavy myocyte fibers
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
Gross & microscopic findings 7-28 days post MI
Central pallor with a red border; granulation tissue
Gross & microscopic findings 1-7 days post MI
Yellow pallor; Coagulative necrosis (4-24 hours), neutrophilic infiltrate (1-4 days), macrophages (4-7 days)
Gross & microscopic findings months post MI
White firm scar; fibrotic scar
Mottling with yellow-tan infarct center is seen _____ days post MI
1-3 days
Hyperemic border with a central yellow-tan softening is seen ____ days post MI
3-7 days
Maximally yellow-tan and soft with depressed red-tan margin margins seen _____ days post MI
7-10 days
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
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
> 2 months post MI, what are the gross features and microscopic features
Scarring complete; Dense collagenous scar
What is the most effective way to rescue ischemic myocardium?
Reperfusion
Give complications of reperfusion
arrhythmias, myocardial hemorrhage with contraction bands, irreversible cell damage superimposed on the original ischemic injury, mircovascular injury, prolonged ischemic dysfunction
Reperfusion beyond _____ does not appreciable reduce myocardial infarct size
6 hours
Symptoms of AMI
Rapid weak pulse , diaphoresis
In AMI, cardiac troponins I and T are ______
elevated
_______ in levels of CK, CKMB troponin I in the 1st 2 days following chest pain essentially EXCLUDES a diagnosis of MI
Absence of change
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
Lab increase of ______ is found EARLIEST post MI
troponin
Time frame for use of SGOT and LDH as markers of AMI
1-3 days
Treatment for AMI
Aspirin and heparin, oxygen, nitrates, beta adrenergic blockers, ACE Inhibitors
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
In AMI, prognosis and complications are dependent on
Infarct size, site, fractional thickness of myocardial wall damaged
Types of infarct modifications
Thrombolysis, Angioplasty, Stent, CABG,
It is the development of progressive heart failure as a result of chronic ischemic myocardial damage
Chronic Ischemic Heart Disease (Ischemic cardiomyopathy)
In Ischemic cardiomyopathy, postinfarct decompensation is d/t
exhaustion of compensatory hypertrophy of non-infarcted viable myocardium
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
Describe the microscopic morphology of the heart in ischemic cardiomyopathy
gray-white scars of healed infarcts, myocardial hypertrophy, diffuse subenedocardial vacuolization
In sudden cardiac death, there is unexpected death in _______ patients or those with symptoms less than _______
Asymptomatic; 1 hour
Major cause of sudden cardiac death
Atherosclerosis
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
(T/F) In sudden cardiac death, there will be no apparent changes in morphology of the heart
true
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
2 types of hypertensive heart disease
Systemic (left-side) and Pulmonary (right-sided)
What is the adaptive response of the heart in systemic hypertensive heart disease
CONCENTRIC left ventricular hypertrophy
What is the adaptive response of the heart in pulmonary hypertensive heart disease
Right ventricular dilation
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)
In systemic hypertensive heart disease, papillary muscles and the intraventricular septum are ________ and there is stiffness and impairment of ________
thick, diastolic filling
In systemic hypertensive heart disease, there is an increase in the ________ diameter of the myocytes with ______ nuclei
transverse, enlarged
Pulmonary hypertensive heart disease is characterized by
RV hypertrophy, dilation and potentially failure d/t increased pulmonary resistance
Different types of pulmonary hypertensive heart disease
Acute cor pulmonale; Chronic cor pulmonale
How do you differentiate between acute and chronic cor pulmonale?
Acute = RV dilation WITHOUT hypertrophy; Chronic = RV dilation WITH hypertrophy
Why is there no hypertrophy in acute cor pulmonale?
Because there is no time for adaptation (hypertrophic change)
What kinds of disorders predispose you to chronic cor pulmonale?
Diseases of pulmonary parenchyma, pulmonary vessels, affecting chest movements, inducing pulmonary arterial constriction
Name diseases of pulmonary parenchyma
COPD, diffuse pulmonary interstitial fibrosis, Pneumoconiosis, Cystic fibrosis, Bronchiectasis
Name diseases of Pulmonary vessels
Recurrent pulmonary thromboembolism, primary pulmonary hypertension, extensive pulmonary arteritis, drugs, extensive pulmonary tumor microembolism
Name diseases affecting chest movement
kyphoscoliosis, marked obesity, neuromuscular disease,
Name diseases inducing pulmonary arterial constriction
hypoxemia, metabolic acidosis, chronic altitude sickness, obstruction to major airways, idiopathic alveolar hypoventilation
Gross morphology of the heart in cor pulmonale
Compression of LV or tricuspid thickening and regurgitation
Microscopic changes of the heart in cor pulmonale
Loss of fat in wall with myocytes aligned circumferentially (normally haphazard)
Different kinds of myocardial disease
Inflammatory disorders, Immunologic and systemic metabolic disorders, genetic abnormalities
4 types of cardiac myopathies (CMP)
Dilated, Hypertrophic, Restrictive, Arrhythmogenic Right Ventricular Dysplasia
What is the most common type of cardiomyopathy
Dilated
Ejection fraction in dilated cardiomyopathy
Low
In dilated cardiomyopathy, death is usually attributable to
progressive heart failure or arrhythmia
(T/F) The heart is hypocontracting in dilated cardiomyopathy
True
S/S of dilated cardiomyopathy
(Manifestations of progressive CHF) SOB, easy fatigability, poor exertional capacity
(T/F) Cardiac transplantation is recommended in dilated cardiomyopathy
True
Causes of Dilated cardiomyopathy
Idiopathic, Previous viral or complicated myocarditis, alcohol abuse, Pregnancy, Genetic, Malnutrition (B12, B1), Cobalt (added to beer), Adriamycin therapy
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
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
What is the most important finding in Hypertrophic cardiomyopathy
Myocardial hypertrophy
Differentiate Dilated and Hypertrophic cardiomyopathy in terms of chamber and contraction
DCM –> flabby and HYPOcontracting
HCM –> muscular and HYPERcontracting
Differentiate Dilated and Hypertrophic cardiomyopathy in terms of abnormalities
DCM –> cytoskeleton; HCM –> mutations of proteins in sarcomere
(T/F) HCM causes both diastolic and systolic dysfunction
False. Only diastolic dysfunction, systolic dysfunction is preserved
What 2 diseases must be distinguished clinically from HCM
Amyloidosis, Hypertensive heart disease
Clinical features of HCM
Decreased diastolic filling, reduced chamber size, reduced SV and CO, increased pulmonary venous pressure, exertional dyspnea; Harsh systolic ejection murmur
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
What are the major clinical problems in HCM
A.fib with mural thrombosis, infective endocarditis of MV, Intractable cardiac failure, Ventricular arrhythmias, Sudden death
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
Describe the microscopic morphology of the heart in HCM
Extensive myocardial hypertrophy, Haphazard myocardial fiber disarray (Most important), Interstitial fibrosis
In restrictive cariomyopathy there is a ______ in cardiac compliance, ventricular filling during diastole and ejection fraction
Decrease
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
Gross morphology in Restrictive cardiomyopathy
Normal or slightly enlarged heart with non-dilated stiff ventricles; BI-ATRIAL DILATION
What are the other types of RCM
Endomyocardial fibrosis, Leoffler endomyocarditis, Endocardial fibroelastosis
Autosomal dominant Inherited cardiomyopathy that causes right ventricular failure and various rhythym disturbances (v.tach)
Arrhythmogenic Right ventricular cardiomyopathy
Heart morphology in Arrhythmogenic Right ventricular cardiomyopathy
Severely thinned R-ventricular wall d/t loss of myocyte with extensive fatty infiltration and fibrosis
Arrhythmogenic Right ventricular cardiomyopathy with hyperkeratosis of plantar palmar skin surfaces
Naxos syndrome
Defect in Arrhythmogenic Right ventricular cardiomyopathy
Cell adhesion proteins in desmosomes that link adjacent cardiac myocytes
Major causes of myocarditis are related to
Infections, Immune-mediated reactions, can be unknown, drugs
Type of myocarditis with an aggressive clinical course
Giant cell myocarditis
Myocarditis associated with ADR, with little or no necrosis, granulomas
Hypersensitivity myocarditis
ADR of what drug is most of the time related to hypersensitivity myocarditis
Methyldopa
In myocarditis, the heart is _______ d/t vascular congestion and the ventricular myocardium is _____
Beefy red; flabby and mottled by focal hemorrhagic lesions
In myocarditis, the heart is _______ d/t vascular congestion and the ventricular myocardium is _____
Beefy red; flabby and mottled by focal hemorrhagic lesions
