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Pathophysiology > Exam 2: Ch 18 Blood Vessel Disorders & Cholesterol > Flashcards

Exam 2: Ch 18 Blood Vessel Disorders & Cholesterol Flashcards

1
Q

3 layers of a blood vessel

A

tunica externa

tunica media (smooth muscle activity)

tunica intima (only layer capillaries have)

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2
Q

endothelial cells

A

simple squamous epithelium that lines cardiovascular system

maintains selectively permeable barrier in brain

regulates clotting, inflammation, vessel reactivity

influences growth of smooth muscle

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3
Q

how do endothelial cells regulate clotting

A

produces thrombogenic factors and prevents platelet adhesion

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4
Q

how do endothelial cells regulate vessel reactivity

A

produce dilators (NO)

produce constrictors (ACE)

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5
Q

endothelial dysfunction (plaques)

A

reversible changes in response to environmental stimuli

modulate blood flow (NO, ACE)

regulate SMC proliferation (growth factors)

regulate inflammation (produce IL)

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6
Q

vascular SMCs

A

can constrict and relax

synthesize collagen

migrate and proliferate

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7
Q

lipids are transported in the blood as…

A

lipoproteins

chylomicrons: carry triglycerides and cholesterol from intestine to tissues and liver

VLDL: main carrier of triglycerides

LDL: main carrier of cholesterol

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8
Q

hypercholesterolemia means

A

high blood lipids

risk factor for MI and stroke

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9
Q

VLDL

A

made in liver from cholesterol

deliver triglycerides to tissues…becomes cholesterol rich IDL

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10
Q

lipoprotein and apoprotein structures

A

micelles

hydrophilic outside, hydrophobic core

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11
Q

apolipoproteins

A

Proteins that bind lipids

control fate of lipids b/c receptors

activate enzymes for lipoprotein metabolism (remove lipids from lipoproteins)

recognized by tissue cell receptors – endocytosis takes in lipoproteins

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12
Q

chylomicrons

A

synthesized in cells of sm. intestinal wall

Carry dietary triglycerides and cholesterol from intestines to tissues and liver

Exogenous pathway

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13
Q

exogenous lipid transport

A

chylomicrons transfer triglycerides to cells for storage and energy use

remnant (cholesterol rich) chylomicrons taken up by liver

cholesterol used to make VLDL or is excreted in bile acid

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14
Q

the liver makes and releases ____ & _____

A

VLDL, HDL

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15
Q

endogenous lipid transport

A

VLDL delivers triglycerides to tissues, turns into cholesterol rich IDL

IDL recycled to VLDL by liver or to LDL in circulation

LDL in blood taken up by LDLr if low

LDL scavenged by macrophages and monocytes in tissues and into blood vessel walls if high –> plaque

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16
Q

low LDLr leads to

A

high circulatory LDL –> plaque

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17
Q

HDL

A

returns cholesterol from peripheral tissues to the liver…requires ABCA1

exercise increases HDL

smoking decreases HDL

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18
Q

ABCA1

A

ATP binding cassette transporter A, class 1

transports cholesterol out of vessel wall cells

genetic defect = Tangier disease (low HDL)

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19
Q

a low HDL is indicative of

A

early atherosclerosis

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20
Q

type 1 familial hyperchylomicronemia is high in..

A

french-americans

high chylomicrons means deficiency in LPL (lipoprotein lipase) or apo cells

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21
Q

hypercholesterolemia diagnoses and causes

A

Dx: LDL based on fasting blood sample every 5 yrs (20+ older)

causes: deit, co-morbidities like diabetes mellitus, meds, genetics

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22
Q

calculate total cholesterol

A

LDL + HDL + tF/S

23
Q

genetic basis of hypercholesterolemia

A

LDLr gene abnormality

heterozygoes have LDLs of 250-500 mg/dl (1st heart attack in 30s)

homozygotes have LDLs of ~1000 mg/dl (see fat in blood)

xanthomas and atherosclerosis common

heart attack in 20s

24
Q

treatment of hypercholesterolemia

A

not based on LDL goals

risk reduction

statins

25
Q

how do statins work

A

higher intake of LDL causes it to decrease

less cholesterol production in liver causes higher LDL receptors

26
Q

ASCVD

A

atherosclerotic cardiovascular disease

27
Q

how are statins perscribed

A

moderate to high for people with clinical ASCVD

no ASCVD but LDL > 190 mg/dl

DM w/o ASCVD regardless of LDL or 10-yr risk

10-yr risk > 7.5% regardless of LDL, DM

28
Q

other CHD risk factors

A

smoking

HTN

low HDL

DM

29
Q

non modifiable CHD risk

A

family history

age

males > 45

females > 55 (post-menopausal)

30
Q

diet therapy for cholesterol

A

lower calories, sat fat, cholesterol

higher fruits, veggies, fish

used for 3 months before starting meds

31
Q

statins

A

HMG CoA inhibitors, block cholesterol syn. in liver –> upregulate LDLr

bile acid resins bind bile acids in intestine

nicotinic acid and fibrates block VLDL syn.

32
Q

heart attack and plaques

A

plaques lead to rupture

clot forms at rupture site… hole in endothelium

33
Q

some artery locations are more likely to accumulate…

A

plaques

34
Q

atherosclerosis

A

Thickened artery wall due to plaque

Preference for medium to large arteries –> CHD is one type

fibrous plaques at ~20 take decades for disease to develop

35
Q

CHD death rates

A

low since 1960 but CHD remains #1 killer in US

36
Q

risk factors for atherosclerosis

A

hypercholesterolemia #1

HTN (stress injury to edothelium), smoking (chemical injury), obesity

aging

family history

37
Q

C-reactive protein

A

marker of systemic inflammation (CHD is an inflammatory process)

anti-inflammatory effect so less plaque forms

38
Q

homocysteine

A

methionine metabolite in animal protein

damages endothelium and stimulates clotting

Vit B breaks down, but do not decrease risk

39
Q

lipoprotein A

A

Altered LDL

Increases cholesterol delivery to injured blood vessels

increases risk of CHD

40
Q

fatty streak

A

yellow lines in tunica intima of major arteries

composed of SMC filled with cholesterol and macrophages –> foam cells (fatty macrophages

present from ~20yr old

41
Q

fibrous plaque

A

fibrous cap over lipids and necrotic core

reduce flow in vessel

rupture and suddenly occlude vessel

inhibition of NO by oxidized LDL lowers vasodilation

42
Q

what happens in fibrous plaques

A

LDL infiltrates to subendothelial space

monocytes bind to site of endothelial injury and enter space to oxidize LDL (which is toxic to endothelium)

43
Q

what happens when LDL is oxidized by monocytes in fibrous plaques

A

rapid uptake by monocytes

inhibition of NO release

stimulation of cytokine release from T cells

44
Q

cytokine release in fibrous plaques stimulated by monocytes oxidizing LDL

A

activate monocytes to differentiate into macrophages

SMC proliferation

45
Q

macrophages take up…

A

LDL to form foam cells

46
Q

SMC in fibrous plaques

A

lay down collagen in plaque

take up LDL to form foam cells

47
Q

atherosclerotic occlusive disease (peripheral artery disease)

A

commonly affect lower extremities

same risk factors as atherosclerosis…smoking really bad

intermittent claudication

48
Q

intermittent claudication

A

pain when walking, atrophy of skin, blanching when leg elevated

occurs when vessels > 50% occluded

Dx. tibial:brachial systolic BP ratio less than .9, ultrasound, CT, MRI

Rx. ASA, surgery, reduce CHD risk

49
Q

thromboangitis obliterans (Buerger disease)

A

vasculitis that causes thrombus formation

effects medium sized arteries of foot and hand

smoking and genetics

Dx: similar to intermittent claudication

Rx: stop smoking, sympathectomy

50
Q

Raynaud’s disease

A

arterial vasospasm in arteries of fingers

pallor and cold followed by hyperemia

cause ulceration and gangrene

51
Q

Primary Raynaud’s disease–no known cause

A

overactive SNS

most common in healthy young women

triggered by cold or strong emotion

52
Q

Secondary Raynaud’s disease

A

Associated with previous vessel injury like frostbite

Trauma from use of vibrating tools

53
Q

diagnosis of Raynaud’s disease

A

cold to trigger

54
Q

treatment of Raynau’s disease

A

eliminate triggers (cold)

quit smoking

calcium channel blockers

alpha-blockers

avoid stress

Pathophysiology (24 decks)

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