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Cardio Exam 1 > Lec 14 Atherosclerosis > Flashcards

Lec 14 Atherosclerosis Flashcards

1
Q

What is role of endothelial cells in normal vascular homeostasis?

A
  • physical barrier to large molec
  • secrete substances that are anti-inflammatory and promote vasodilation [NO] and resist thrombosis

= maintains homeostasis

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2
Q

What is role of smooth muscle cells in normal vascular homeostasis?

A
  • effect vasoconstriction/ vasodilation in response to local/circulating molec = maintain vascular tone
  • produce extracellular matrix to maintain vascular integrity
  • contained within arterial media
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3
Q

What is role of collagen and elastin?

A

collagen maintains strength
elastin maintains flexibility

both produced by smooth muscle cells

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4
Q

What are the 3 layers of normal arterial wall?

A

intima = closest to lumen, consists of single layer endothelial cells

media = middle, bounded by elastin [internal and external elastic laminae], consists of smooth muscle cells and extracellular matrix

adventitia = outer, contains nerves, lymphatics, blood vessels

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5
Q

What makes up the extracellular matrix?

A

collagen + elastin + proteoglycans

maintain structural integrity of vessel

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6
Q

What is the earliest visible lesion of atherosclerosis?

A

fatty streak

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7
Q

What is the order:
plaque disruption
fatty streak
plaque progression

A

fatty streak –> plaque progression –> plaque disruption

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8
Q

What is mech/pathway of fatty streak?

A
  • endothelial cell dysfunction: endothelial cell no longer physical barrier
  • increased endothelial permeability allows entry LDL into intima where it stays in subendothelial space
  • LDL gets modified [by oxidation or glycation] = mLDL
  • mLDL promotes leukocyte recruitment and foam cell formation] + stimulates inflammation directly + indirectly
  • recruitment leukocytes [monocytes + T cells] to vessel wall
  • monocytes into intima –> become phagocytes –> take up mLDL to become foam cells via unregulated scavenger receptor
  • foam cell apoptosis, necrosis, persistent inflammation = make up core of plaque formation
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9
Q

What are risk factors for initial endothelial cell dysfunction that leads to fatty streak/atherosclerosis formation?

A

smoking, high cholesterol, diabetes

associated with hydrodynamic stress –> high BP, branch points in vessels

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10
Q

How does mutated apolipoprotein B lead to atherosclerosis?

A

b/c it allows easier entry of LDL into the subendothelial space

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11
Q

What is the necrotic core?

A

lipid rich center of a plaque formed by necrotic foam cells

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12
Q

When do fatty streaks appear?

A

start to appear in early life, by late teens can be found but are asymptomatic

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13
Q

What is mech/pathway of plaque progression?

A

-

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14
Q

What happens in early plaque growth?

A

have outward remodeling of arterial wall to preserve diameter of lumen and does not limit blood flow so you don’t get ischemic symptoms

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15
Q

What happens in later plaque growth?

A

over time vessel can no longer compensate with outward remodeling –> start to restrict vessel lumen and impede perfusion –> tissue ischemia –> symptoms like angina or claudication of extremities

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16
Q

What is underlying pathology of most coronary syndromes?

A

fibrous cap of an atherosclerotic plaque ruptures –> exposes prothrombic molec within lipid core and precipitates actual thrombus that occludes arterial lumen

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17
Q

What is mech/pathways of plaque progression from fatty streak to fibrous plaque?

A
  • smooth muscle cells migrate from arterial media into intima and proliferate [signaled by foam cells, platelets, endothelial cells]
  • smooth muscle cells secrete collagen/extracellular matrix to form fibrous cap on plaque
  • T-lymphocyte IFN-g inhibits smooth muscle collagen synthesis + local foam cells secrete MMP both degrade fibrous cap
  • balance betwen cap degradation in synthesis results in stable vs vulnerable plaque
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18
Q

What are characteristics of stable vs vulnerable plaque?

A

stable = small lipid pool thick fibrous cap, preserved arterial lumen

vulnerable = large lipid cores, thin fibrous cap, many inflammatory cells

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19
Q

What happens in plaque disruption?

A
  • fibrous cap ruptures due to hemodynamic stress and matrix degradation
  • subsequent development of superimposed thrombus consisting of fibrin, RBCs, platelets
  • clinical manifestion depends on vascular territory and stability of overlying thrombus = rupture may heal and just narrow lumen [=silent] or may cause complete occlusion and major event [ex. MI]
20
Q

Why higher risk of MI in the morning?

A

higher BP in the morning = more hemodynamic stress = more likely to plaque to rupture

21
Q

What is order of location where atherosclerotic plaques happen first?

step1

A

ab aorta > coronary aorta > popliteal artery > carotid artery

22
Q

What are traditional non-modifiable risk factors of atherosclerosis?

step1

A
  • age [older]
  • gender [male or post-menopausal female]
  • family history
23
Q

What are modifiable risk factors for atherosclerosis?

step1

A
  • smoking
  • hypertension
  • hyperlipidemia
  • diabetes
  • physical inactivity
24
Q

What are gender risk factors for atherosclerosis?

step1

A

higher risk in men and in post-menopausal women

25
Q

What are symptoms of atherosclerosis?

step1

A

angina
claudication = pain in legs in exercise due to insufficient blood flow
or can be asymptomatic

26
Q

How does risk of cardiovascular disease increase with age?

A

linearly

27
Q

What is difference high vs low density lipoprotein?

A

higher density = bigger ration proteins:lipids

higher density = less bad

28
Q

What is structure of lipoproteins?

A
  • lipid core of cholesteryl esters and triglycerides

- surrounded by hydophilic phospholipid/protein/cholesterol layer

29
Q

What does LDL do?

A

= bad cholesterol

- deposits cholesterol in subendothelial space leading to atherosclerosis

30
Q

What does HDL do?

A

= good cholesterol

  • reverses cholesterol transport
  • takes cholesterol from macrophages in subendothelial space and brings it back to liver to be processes
31
Q

What is synergism of HDL and LDL risk factors for atherosclerosis?

A

pts with low HDL and high LDL have triple risk of those on opposite end of spectrum

low HDL + high LDL is worse than either risk factor alone

32
Q

What is non-pharm mech for lowering LDL?

A

diet/exercise

33
Q

How do you medically lower LDL?

A

give statins = HMG-CoA reductase inhibitors

  • increase expression of LDL receptor in liver so lower serum LDL
34
Q

What is effect of statins of cardiovascular resik?

A
  • benefit proportional to degree of LDL lowering

- also has some elevation in HDL

35
Q

What are the non-LDL lowering mech of statins?

A
  • modulate vascular tone [dilate]
  • stabilize plaque
  • reduce inflammation
  • rase HDL a little
36
Q

What are the major risk factors that affect LDL level?

A
  • cigarette smoking
  • hypertension
  • low HDL
  • family history of premature coronary heart disease
  • age
37
Q

What is effect of DM on cardiovascular?

A

accelerates atherosclerosis + puts you in prothrombotic state

38
Q

Who has same risk “risk equivalent” for CHD as a diametic without prior MI?

A

a normal pt with a prior MI

39
Q

What are treatment objectives in diabetic pt?

A

preven microvascular complications [nephropathy, neuropathy, retinopathy] by glycemic control

prevent macrovascular [stroke, MI] by control of midfiable cardiac risk factors

40
Q

Why does obesity put you at risk for vascular events?

A
  • more adipose tissue –> secretes pro-inflammatory cytokines
  • higher BP –> higher CO to meat higher metabolic demands
  • endothelial dysfunction
  • insulin resistance
41
Q

What is obesity?

A

BMI > 30

42
Q

What is the physical activity recommendation?

A

Every US adult should accumulate 30 minutes or more of moderate-intensity physical activity on most, preferably all, days of the week

43
Q

What is effect of smoking on vasculature?

A

causes endothelial damages, platelets more aggregable [prothrombic]

44
Q

What is role of homocystein in atherogenesis?

A

CVD pts have high levels homocysteine but reductions don’t benefit CV risk

45
Q

What is lipoprotein A?

A

variant of LDL
may impair endogenous thrombolysis + promote inflammation

people with high lipoprotein A have higher CV risk

46
Q

What is c reactive protein role in atherogenesis?

A

marker of inflammation and associated wtih increased CV risk

unclear if marker or mediator of atherosclerosis

Cardio Exam 1 (16 decks)

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