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Cardiology > Atherosclerosis All Lectures > Flashcards

Atherosclerosis All Lectures Flashcards

1
Q

Why has CVD deaths among men gone down more than among women?

A

reduction in smoking and differential efficacy/role of drugs in men

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2
Q

How do we evaluate risk of CVD events for person without known CHD, atherosclerotic disease, or diabetes?

A

count risk factors and use framingham scoring to determine absolute 10yr event risk and use this to decide LDL goals (secondarily, non-HDL goals)

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3
Q

How does CRP and its genotype contribute to ischemic heart disease?

A

CRP is causal but genotype is not causal for ischemic heart disease; however genotype is obviously causal for CRP level –> the relationship doesn’t carry through but the CRP level is still a good marker

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4
Q

What is atherosclerosis?

A

arterial intimal disease of large-medium size arteries characterized by lipid accumulation and inflammation

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5
Q

Clinical consequences of atherosclerosis

A
  1. CHd, MI, sudden death, CAD, stroke, vascular dementia, PAD, renal artery stenosis
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6
Q

Clinical risk factors for atherosclerosis

A

M, age, lipoprotein disorders, htn, DM2, family hx, smoking

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7
Q

What happens to it during atherosclerosis? endothelia

A

inflammation, dysfunction

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8
Q

What happens to it during atherosclerosis? oxidation

A

modifies lipoproteins

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9
Q

What happens to it during atherosclerosis? monocytes

A

macrophage mediated inflammation and become foam cells, t cell changes

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10
Q

What happens to it during atherosclerosis? platelets

A

drive thrombosis

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11
Q

What happens to it during atherosclerosis? matrix proteolysis

A

ruptures plaques

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12
Q

What happens to it during atherosclerosis? smooth muscle

A

secrete ECM that leads to plaque stability

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13
Q

Why does this factor lead to endothelial injury and dysfunction? htn

A

shear stress

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14
Q

Why does this factor lead to endothelial injury and dysfunction? smoking

A

oxidant stress

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15
Q

Why does this factor lead to endothelial injury and dysfunction? diabetes

A

glycation

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16
Q

_____ and _____ induce endothelial cell dysfunction that promotes inflammation and fatty streak formation.

A

mechanosignal trandsuction and hypercholesterolemia

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17
Q

Which molecules are involved in leukocyte rolling and in leukocyte adhesion?

A

p/e selectin and vcam/icam

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18
Q

Which molecules are involved in the migration of monocytes through the arterial intima?

A

chemokines like ccr5 and cx3cr1 and ccr2

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19
Q

How do macrophages become foam cells?

A

scavenger receptors recognize ldl/chylomicrons/remants/etc as foreign pathogens and consume them in the intima

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20
Q

What is the status of native LDLRs in macrophages as they become foam cells?

A

they are normally downregulated in monocytes and don’t lead to the consumption of lipids –> it’s scavenger receptors that pick up ldl and lead to formation of foam cells

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21
Q

Which T-cells are powerful activators of monocytes and are seen in early atherosclerosis formation?

A

TH1 CD4+ (CD3+, alphabetaTCR+) cells that express high levels of IFN gamma, IL12, and TNFalpha which leads to further IL12 production by macrophages

  • also have TH17 cells
  • TH2 plays a small role
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22
Q

How do treg cells contribute to early atherosclerotic lesions?

A

they suppress the disease to an extent

23
Q

How does LDL end up in the intima?

A

It enters the intima through endothelial cells and between them and then release mediators that drive up MCP1 which mediates monocyte migration –> AKA it calls up the monocytes which come and eat them

24
Q

How does HDL inhibit early atherosclerotic lesions?

A
  1. inhibits oxidation of LDL to modified LDL which can generate mediators of inlammation
  2. soaks up cholesterol from the blood vessel wall cells like macrophages etc via ABCA1 etc
25
Q

What factors lead to the progression of atherosclerosis from an early lesion?

A
  1. smooth muscle production of ECM and scarring
  2. macrophage death leading to a necrotic core
  3. thrombosis due to endothelial sloughing
  4. rupture and cycling of the fibrous cap of the lesion that can expose blood to tissue factor leading to thrombosis
  5. calcification and remodeling
26
Q

What is Glagov’s coronary remodeling hypothesis?

A

the lumen of blood vessels expand to compensate for plaques –> only after this compensation fails do you get severe CAD

27
Q

Factors that drive rupture-ability of plaques

A
  1. thin fibrous cap
  2. low VMSC count
  3. large lipid pool
  4. high oxLDL content
  5. high macrophage content
  6. high t-cell count
  7. thin shoulder region
  8. neovascularization
28
Q

How does vessel stenosis lead to plaque rupture?

A

extent of vessel stenosis IS NOT a factor in making a plaque prone to rupture

29
Q

Can atherosclerotic lesion regress?

A

yes –> lower LDL atherogenic lipoproteins, increased HDL (lipid efflux), regulate inflammation/macrophages

30
Q

What is metabolic syndrome?

A

a constellation of risk factors (3 or moreof following) strongly associated with obesity such as triglycerides, low hdl, blood pressure, fasting glucose, abdominal obesity

31
Q

What is the rationale for the increased weight loss that results from a low carb diet vs a low fat diet?

A

simply caloric restriction. fat is not magical.

32
Q

How do the low carb and low fats diet fare on triglyceride reduction?

A

low carb > low fat w/regards to reduction

33
Q

What is the ideal diet and why do we like it?

A

Mediterranean diet –> balance between low carb/low fat and discriminates based on type of fat (e.g. olive oil)

*low carb = basically making body pretend it’s in fasting state

34
Q

What’s the story on trans fat?

A

manmade, makes liquid fat solid so better for processed foods that need to sit for a long time, also likes sitting around in your body and causing trouble because of it’s unkinked double bond

35
Q

rate of energy expenditure expressed in mets

A

absolute intensity

36
Q

% of maximal aerobic power that is maintained during exercise, expressed as % of maximal hr or VO2 max

A

relative intensity

37
Q

Relationship between fitness and risk of cvd

A

curvilinear with more fit = fewer events (bigger impact among men)

38
Q

T/F Going from unfit-fit reduces your risk of cvd events as if you were fit and stayed fit.

A

F –> but reduces risk by half vs people who are unfit and stay unfit

39
Q

What accounts for the decline in CV events in the US?

A

about half due to tech like stents and CABGs and the other half due to identification and modification of risk factors

40
Q

What’s better for STEMI? for stable angina? PCI or fibronolytic tx

A

PCI is more expensive but more efficacious (better survival and LV functionality) and cost efficient in the US in a STEMI …but no advantage in pts with stable angina

41
Q

Where do VSMCs control blood pressure?

A

arterioles not large arteries

42
Q

Characteristics of Stage 1 Atherosclerosis:

A

foam cells

43
Q

Characteristics of Stage 2 Atherosclerosis:

A

fatty streak with foam cell penetration of internal elastic lamina

44
Q

Characteristics of Stage 3 Atherosclerosis:

A

extracellular lipid pools

45
Q

Characteristics of Stage 4/5 Atherosclerosis:

A

formation of lipid core w/fibrous cap (aka: fibroatheroma), calcification

46
Q

Characteristics of Stage 6 Atherosclerosis:

A

hematoma/hemorrhage, thrombi, plaque rupture, aneurysmal dilation

47
Q

Why does restenosis occur after PCI and stenting?

A
  1. damage from the stent expose VSMCs under the internal elastic lamina to the lumen allowing further proliferation/ECM production/inflammation and constrictive remodeling
  2. pressure from the stent leads to remodeling of the artery which downsizes and increases luminal occlusion
48
Q

Which growth factors induce SMC migration from media to intima during restenosis?

A

PDGF

49
Q

Which growth factors induce SMC proliferation during restenosis?

A

basic FGF and Angiotensin II

50
Q

Which growth factors induce ECM secretion during restenosis?

A

TGF beta

51
Q

What is the effect of stenting with a drug eluting stent w/rapamycin?

A

rapamycin is a cell cycle inhibitor –> less restenosis

52
Q

MOA of rapamycin (in drug eluting stents)

A

macolide antibiotic blocks cytokine and growth factor-mediated cell proliferation by inhibiting TOR (binds to FKBP12 receptor) and arrests SMCs at end of G1

53
Q

MOA of paclitaxel (in drug eluting stents)

A

anti-neoplastic agent polymerizes tubulin resulting in nonfunctional microtubules and inhibition of cell replication at G2/M phase and inhibits cell migration

54
Q

What is the risk with drug eluting stents?

A

if you inhibit growth of cells in the area of the stent, the stent does not get a lining of endothelial cells over time –> increases thrombosis risk

Cardiology (41 decks)

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