Exam 2: Ch 18 Blood Vessel Disorders & Cholesterol Flashcards

(54 cards)

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
how do statins work
higher intake of LDL causes it to decrease less cholesterol production in liver causes higher LDL receptors
26
ASCVD
atherosclerotic cardiovascular disease
27
how are statins perscribed
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
other CHD risk factors
smoking HTN low HDL DM
29
non modifiable CHD risk
family history age males > 45 females > 55 (post-menopausal)
30
diet therapy for cholesterol
lower calories, sat fat, cholesterol higher fruits, veggies, fish used for 3 months before starting meds
31
statins
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
heart attack and plaques
plaques lead to rupture clot forms at rupture site... hole in endothelium
33
some artery locations are more likely to accumulate...
plaques
34
atherosclerosis
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
CHD death rates
low since 1960 but CHD remains #1 killer in US
36
risk factors for atherosclerosis
hypercholesterolemia #1 HTN (stress injury to edothelium), smoking (chemical injury), obesity aging family history
37
C-reactive protein
marker of systemic inflammation (CHD is an inflammatory process) anti-inflammatory effect so less plaque forms
38
homocysteine
methionine metabolite in animal protein damages endothelium and stimulates clotting Vit B breaks down, but do not decrease risk
39
lipoprotein A
Altered LDL Increases cholesterol delivery to injured blood vessels increases risk of CHD
40
fatty streak
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
fibrous plaque
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
what happens in fibrous plaques
LDL infiltrates to subendothelial space monocytes bind to site of endothelial injury and enter space to oxidize LDL (which is toxic to endothelium)
43
what happens when LDL is oxidized by monocytes in fibrous plaques
rapid uptake by monocytes inhibition of NO release stimulation of cytokine release from T cells
44
cytokine release in fibrous plaques stimulated by monocytes oxidizing LDL
activate monocytes to differentiate into macrophages SMC proliferation
45
macrophages take up...
LDL to form foam cells
46
SMC in fibrous plaques
lay down collagen in plaque take up LDL to form foam cells
47
atherosclerotic occlusive disease (peripheral artery disease)
commonly affect lower extremities same risk factors as atherosclerosis...smoking really bad intermittent claudication
48
intermittent claudication
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
thromboangitis obliterans (Buerger disease)
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
Raynaud's disease
arterial vasospasm in arteries of fingers pallor and cold followed by hyperemia cause ulceration and gangrene
51
Primary Raynaud's disease--no known cause
overactive SNS most common in healthy young women triggered by cold or strong emotion
52
Secondary Raynaud's disease
Associated with previous vessel injury like frostbite Trauma from use of vibrating tools
53
diagnosis of Raynaud's disease
cold to trigger
54
treatment of Raynau's disease
eliminate triggers (cold) quit smoking calcium channel blockers alpha-blockers avoid stress