Fcm Atherosclerosis And Ischemic Heart Disease I& Ii

Front 1

List the biological functions of endothelial cells

Back 1

1. permeability barrier
2. non-thrombogenic properties
3. prothrombotic/procoagulant factors
4. vasoactive substances
5.Growth-promoting and immunoactive factors
6. Connective tissue

Front 2

What is the role of the endothilium?

Back 2

metabolic and endocrine functions of its cells play a critical role in health and disease by synthesizing a number of biologically active factors

Front 3

describe the non-thrombotic properties of the endothilium.

Back 3

a. Cell surface: heparan sulfate proteoglycans
b. Production of antithrombotic agents: prostacyclin (PGI2) which relaxes SMC & inhibits platelet aggregation

Front 4

list the prothrombotic, procoagulant factors of the endothelium

Back 4

Factor VIIIa (vWF), tissue factor, plasminogen activator/inhibitor, factor V

Front 5

list the vasoactive substances prod. by the endothilium

Back 5

a. Nitric oxide: inhibits platelet adhesion &aggregation & reduces vascular tone

b. Endothelin & angiotensin II, two potent vasoconstrictor peptides

Front 6

list the growth promoting and imunnoactiev factors produced by the endothilium

Back 6

PDGF, IGF, FGF, VEGF, Class II histocompatibility antigens

Front 7

what connective tissue components are produced by the endothilium

Back 7

Basement membrane constituents

Front 8

list the biological functions of smooth muscle cells

Back 8

1. Mechanical functions
2. Metabolism of blood-borne substances including lipids, and secretion of cytokines
3. Synthesis of extracellular matrix constituents
4. Ability to proliferate in response to injury

Front 9

describe the mechanical function of endothilial smooth muscle

Back 9

a. Maintain the integrity of vessel wall by providing support for the endothelium

b. Control of artery wall tone, primarily via cytoskeletal proteins, actin and myosin

c. Control of blood flow by contracting or dilating in response to specific stimuli

Front 10

which extracellular matrix components does ESM synthesize

Back 10

elastin, collagen and proteoglycans

Front 11

what is atherosclerosis?

Back 11

progressive disease characterized by the accumulation within the intima of smooth muscle cells, lipids and connective tissue

Front 12

how common is atherosclerosis?

Back 12

It is the primary cause of heart disease and stroke in westernized societies

Front 13

how many death is atherosclerosis responsible for ?

Back 13

It’s the underlying cause of ~50% of all deaths

Front 14

describe the etiology of athersclerosis

Back 14

complex; polygenic, multifactorial, and evolving over a long period of time

Front 15

describe the pathogenesis of athersclerosis.

Back 15

a chronic condition that can be converted into an acute clinical event by plaque rupture and thrombosis

Front 16

is there agreement regarding the atherogenic process?

Back 16

no. several hypotheses exist.

Front 17

what is the source of controversy between hypotheses?

Back 17

initiation” of the lesion and their “progression/complication” into a clinically relevant disease

Front 18

which hypotheses are based upon changes in blood constituents or flow?

Back 18

1.Encrustation
2.Insudation
3.Response to retention
4.Hemodynamic

Front 19

which hypotheses are based on alterations of cellular components?

Back 19

1.Intimal cell mass
2.Monoclonal theory
3.Response to injury

Front 20

according to the encrustation hypothesis, what is the initial event in atherogensis?

Back 20

small mural thrombi

Front 21

has the encrustation hypothesis held up in studies?

Back 21

no. studies have shown the formation of mural thrombi is NOT the initial step in atherogenesis.

Front 22

what is the insudation hypothesis?

Back 22

accumulation of intimal lipids derived from plasma proteins.

Front 23

what is the response to retention hypothesis?

Back 23

recent theory, lipid retention (a single, key event) is sufficient for atherogenesis.

Front 24

what is the hemodynamic hypothesis?

Back 24

atherosclerotic lesions tend to occur at regions of rapidly fluctuating shear stress.

Front 25

what is the effect of shear stress on endothelial cells?

Back 25

damaging, cause expression of atherogenic factors - FGF2, tissue factor, plasminogen

*also induces expression of ANTI-atherogenic factors like NO synthase, PAI-1

Front 26

what is the initimal cell mass hypothesis?

Back 26

accumulation of smooth muscle cells in the intima at the same site as the plaque.

Front 27

what are the other factors required for this to occur?

Back 27

hyperlipidemia, hypertension chronic injury

Front 28

what is the monoclonal hypothesis?

Back 28

plagues are composed of progeny of a single SMOOTH MUSCLE CELL

the first theory to focus on cellular events

Front 29

what is the monoclonal nature equivalent to? what are the various mutagens?

Back 29

benign monoclonal neoplasms like leiomyomas

mutagens: hydrocarbons, cholesterol or its oxidants, viruses (herpes)

Front 30

(T/F) endothelial cells can completely re-endothelialize damaged (denuded) vessels

Back 30

False their regenerstive ability is limited

Front 31

what does the limited ability of endothelial cells to regenerate result in?

Back 31

recruitment of platelets, adhesion of platelets to the denuded vessel (exposed basement membrane) release of PDGF into the subjacent intima.

Front 32

what is PDGF?

Back 32

chemo attractant for, and powerful mytogen of, smooth muscle cells.

Front 33

what is the reaction to injury hypothesis?

Back 33

atherogenesis in response to endothelial injury

Front 34

endothelial injury also results in what physical changes?

Back 34

proliferation and migration of smooth muscles into the intima, chronic inflammation and fibroproliferative response to injury.

Front 35

what other effects does endothelial damage have?

Back 35

endothelial cell dysfunction, activation of leukocyte adhesion molecules and platelet/macrophage deposition, release of growth factors into the wall and accumulation of lipids

Front 36

what are some of the cellular phenomena that occur in atherogenesis?

Back 36

altered endothelial integrity
intimal smooth muscle proliferation

sysnthesis and deposition of connective tissue matrix proteins (collegen, elastic fibers and proteoglycans) by smooth muscle

accumulation of lipids within the proliferating smooth muscle cells and macrophages as well as the newly formed CT

Front 37

define ischemic heart disease

Back 37

imbalance between oxygen needs of myocardium and the oxygen supply (can be acute or chronic)

Front 38

what are the three types of ischemic disease?

Back 38

1. MI
2. angina pectoris
3. ischemic cardiomyopathy

Front 39

what causes MI?

Back 39

sudden arrest or reduction of coronary blood flow. commonly due to severe coronary artery disease (w/ or w/o thrombotic occlusion)

Front 40

what is angina pectoris?

Back 40

TRANSIENT ischemia including severe paroxysmal chest pain.

precipitated by exertion and relieved by rest and or nitroglycerine.

assoc with coronary atherosclerosis.

Front 41

what is ischemic cardiomyopathy?

Back 41

diffuse FIBROTIC changes in the myocardium.

later in life following multiple ischmic episodes

angina and high risk of MI

Front 42

what is the cause for MI in the majority of cases?

Back 42

acute coronary thrombosis

Front 43

what is the frequency of coronary involvement?

Back 43

LAD-40-50%
RCA-30-40%
L circumflex artery-15-20%

Front 44

what are the two types of infarcts?

Back 44

subendocardial and transmural

Front 45

what is hemorrhagic infarct? how is it caused?

Back 45

a reperfusion injury following protracted ischemia.

cause: anoxia injures capillary endothelium hemorrhage with reperfusion

Front 46

what are the most common complications of MI?

Back 46

arrythmias (account for ~ 50% of deaths from ischemia)

Front 47

what are other complications?

Back 47

L ventricular failure and cardiogenic shock

rupture of myocardial wall (7 to 10 days post MI)

extension of the infarct

ventricular aneurysm

pericarditis

mural thrombosis