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Cardiovascular pathology

Q: What are the stages of stenosis?

Grade 1 (<25%) Grade 2 (25-50%) Grade 3 (50-75%) Grade 4 (>75%)

43 important questions on Cardiovascular pathology

What are the 3 layers of the normal artery?

Initima
Media: smooth muscle cells and elastin
Adventia: fat/blood vessels

What happens with atherosclerosis (layers)

Initima increases
Media decreases
Fibrosis adventitia

What can cause a aorta dissection?

Perforation of an atherosclerotic plaque
Bleeding within the vessel wall --> hematoma

What happens with mucoid media degeneration?

loss of elastic fibers (black): less elastic aorta
mucoid depositions (glycosaminoglycans): weakening of the media

What is the genetic cause of aneurysm and dissection?

disease of fibrilin (stabilizes elastin) or collagen

Consequence Marfan disease

thin and fragmented elastin

Definition degeneration heart valves

Thickening of the valve with fibrosis and inflammation

What is more increased in atherosclerotic valves?

CRP/sPLA2-IIA and complement

What is the consequence of a left coronary artery occlusion?

Massive antero-lateral MI

What is the consequence of left anterior descendens?

Antero-septal MI

What are the stages of stenosis?

Grade 1 (<25%)
Grade 2 (25-50%)
Grade 3 (50-75%)
Grade 4 (>75%)

Definition unstable atherosclerotic plaque

Thin fibrous cap or thick fibrous cap with inflammation

What are the cause of acute MI?

Thrombus
(plaque) bleeding
Dissection
Intramyocardial coronary artery
Small vessel disease

Definition small vessel disease

thickness basal membrane >1000 nm:
causus decrease in oxygen diffusion
Normal: thickness basal membrane <70-80 nm

What cause calcium related depositions in the mitochondria?

AMI

What cause loss of NBT?

AMI

Function actue phase proteins

sPLA2-IIA hydrolysis phospholipids. This forms binding sites for CRP. CRP activates complement. This is important for chemotaxis and cell damage plasma membrane.

Definition myocardial bridging cor art

Compression lumen in systole and dilation in diastole in inhibited related to fibrosis surrounding the vessel

In which forms of myocarditis are granuloma's and/or giant cells?

Tuberculosis
Sarcoidosis (no necrosis of cardiomyocytes)
Giant cell myocarditis (limited granuloma’s; extensive necrosis of cardiomyocytes) : poor prognosis

Consequences alcoholic cardiomyopathy

Dilated left ventricle
Fatty changes LV
Cardiomyocytes have a decreased densitiy of myofibrils
Fat inclusion

What are the most heart tumors?

Myxoma (benign) and angiosarcoma (malignant)

What is the major basis of vascular disorders?

Injury to the vessel wal

What is the response to vascular injury?

Recruitment of smooth muscle cells or smooth muscle precursor cells to intima
smooth muscle cell mitosis
elaboration of ECM

What characterizes atherosclerosis?

Intimal lesions called atheromas (atheromatous/plaques)

Describe the fibrous cap

Smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteiglycans and neovascularization

Describe the necrotic center

Cell debris, cholesterol crystals, foam cells and calcium

Steps of response to injury in atherogenesis

Chronic injury (vessel is still normal)
Endothelial injury with monocyte and platelet adhesion
Monocyte and smooth muscle cell migration into the intima, with macrophage activation.
Macrophage and smooth muscle cell uptake of modified lipids and further activation.
Intimal smooth muscle cell proliferation and extracellular matrix elaboration, forming a well-developed plaque.

What are the three components of a plaque?

Cells, including SMCs, macrophages, and T cells
ECM, including collagen, elastic fibers, and proteoglycans
Intracellular and extracellular lipid

What are the major consequences of atherosclerosis?

Myocardial infarction
Cerebral infarction
Aortic aneurysm
Peripheral vascular disease

How thrombosis is triggerd?

Due to plaque erosion or rupture. This leads to complete vascular obstruction and tissue infarction

Consequence stable plaques

It produces symptoms related to chronic ischemia by narrowing vessels

Consequences unstable plaques

It causes dramatic and fatal ischemic complications related to rupture, thrombosis or embolization

What is the consequence of transient/partial obstruction?

Subendocardial infarct

What is the consequence of global hypotension?

Circumferential subendocardial infarct

What is the consequence of small intramural vessel occlusion?

Microinfarcts

What is the most consistent sign of endocarditis?

Fever

Where leads valvular heart disease to?

Occlusion, regurgitation (insufficiency), abnormal ECM synthesis, neovascularization and scaring.

Non bacterial thrombotic endocarditis occurs ...

on previously normal valves as a result of hypercoagulable states; embolization is an important complication

What is the major cause of hypertrophic cardiomyopathy?

Missense mutation of the contractile apparatus

What characterizes restrictive cardiomyopathy?

Primary decrease in ventricular compliance, resulting in impaired ventricular filling during diastole

What are the three categories of cardiomyopathy?

Dilated, hypertrophic and restrictive

Where results dilated cardiomyopathy in?

Systolic (contractile) dysfunction. Causes include myocarditis, toxic exposures (e.g., alcohol), and pregnancy. In 20% to 50% of cases, mutations affecting cytoskeletal proteins are responsible

Where result HCM in?

HCM results in diastolic (relaxation) dysfunction. Virtually all cases are due to autosomal dominant mutations in the proteins that make up the contractile apparatus, in particular β-myosin heavy chain.

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Pathology

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