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Cardiovascular > Atherosclerosis, Thrombosis, Vascular Biology > Flashcards

Atherosclerosis, Thrombosis, Vascular Biology Flashcards

1
Q

When you analyze blood lipids, what are the 3 things u can test for in the plasma?

A

total cholesterol, HDL, TG’s

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2
Q

Gib me the Friedewald eqn to predict LDL values

A

LDL = (Total Chol) - HDL - (TG’s/5)

only if TG’s are < 400mg/dL

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3
Q

This molecule is a varient of LDL with an ApoA protein covalently attached to it.

A

Lipoprotein A (LpA)

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4
Q

ApoA is structurally similiar to what plasma factor, thereby inhibiting normal clot lysis and leads to thrombus formation?

A

plasminogen

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5
Q

So if a pt has elevated LpA, what conditions are they at risk for?

A

coronary heart disease, cerbrovascular disease, atherosclerosis, thrombosis, and stroke.

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6
Q

Which vitamin can lower LpA levels by up to 20%?

A

Niacin

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7
Q

This is the marker that functions in immune reactions to bind to foreign materials or damaged cells to ID them as targets for phagocytosis.

A

CRP

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8
Q

Where is CRP made?

A

Liver

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9
Q

CRP is a good marker for the prediction for the risk of what events?

A

Cardiovascular events

holy balls i dont know how to write questions anymore.

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10
Q

After injury, what is the time span where CRP raises to very high levels in acute inflammation?

A

4-6 hrs

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11
Q

So if a pt has SLIGHTLY elevated CRP (3-10mg/L), what might be going on?

A

chronic, low grade inflammation

LIKE A PLAQUE BITCH

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12
Q

Which mediator is released by endothelial and SM cells to stimulated CRP release?

A

IL-6

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13
Q

This protein modifies lipid transport during inflammation and increases with atherosclerosis.

A

Serum amyloid A protein (SAA)

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14
Q

These are thin walled outpouchings of the arteries at the circle of willis.

A

Berry aneurysms

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15
Q

These are abnormal, small, direct connections between aa and vv.

A

Arteriovenous fistulas

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16
Q

What is the most common cause of arteriovenous fistulas?

A

developmental defects

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17
Q

This is focal, irregular thickening of the walls of the medium and large muscular aa.

A

Fibromuscular dysplasia

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18
Q

What 2 layers of the areteries undergo hyperplasia and fibrosis to cause fibromuscular dysplasia?

A

intima and and media

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19
Q

What are the pathological manifestations of fibromuscular dysplasia?

A

luminal stenosis, renovascular HTN, development of aneurysms

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20
Q

These are the cells that form a barrier and maintain homeostasis of the vessel.

A

Endothelial cells

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21
Q

How does endothelial cells maintain homeostasis throughout the bodayyy?

A

permeability barrier, elaboration of prothrombic molecules, ECM production, modulation of blood flow, regulation of inflammation and immunity, regulation for cell growth, oxidation of LDL

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22
Q

Endothelial cells are activated when exposed to what stimuli?

A

cytokines, bacterial products, hemodynamic stresses, lipid products that cause atherosclerosis, advanced glycosylation end products, viruses, complement components, and hypoxia

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23
Q

This is the condition when endothelial cells have an altered phenotype that impairs vasoractivity or induces a surface that is thrombogenic or abnormally adhesive to inflammatory cells.

A

Endothelial dysfunction

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24
Q

So if endothelial cells become sticky under dysfunction, what does that predispose the body to creating?

A

Thrombi

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25
Q

Vascular injury causes matrix synthesis which thickens which layer of the vessel?

A

Intima

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26
Q

This subtype of arteriolosclerosis is characterized by thickening with eosinophilic deposition, and usually results in coagulative necrosis.

A

Hyaline subtype

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27
Q

What 3 things is the hyaline substype of arteriolosclerosis associated with?

A

diabetic microagiopathy, aging, and HTN

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28
Q

This subtype of arteriolosclerosis occurs with severe HTN, which shows onion-skinning of the vessel, and usually accompanied by fibrinoid necrosis.

A

Hyperplastic subtype

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29
Q

These are dark purple cacific deposits in the tunica media of muscular arteries in people >50, and can undergo metplastic change into bone.

A

Moenckeberg medial sclerosis

30
Q

What layer in the vessel does atherosclerotic plaques form?

A

Intima

31
Q

Where in the world is atherosclerosis mostly found?

A

Western world and developed nations

32
Q

Which ages are at risk for atherosclerosis?

A

40-60. but as u age u increase risk.,

33
Q

Which gender is at risk for atherosclerosis?

A

perimenopausal woman < men < postmenopausal women

estogen is a protective factor.

34
Q

Is there genetic component to atherosclerosis?

A

YESH

35
Q

Which lipoprotein puts u at a higher risk for atherosclerosis?

A

LDL

36
Q

Hypertrophy of which chamber of the heart puts u at a higher risk for atherosclerosis?

A

LV

37
Q

How much is the death rate doubled by smoking 1 pack/day by ischemic heart disease (IHD)?

A

doubled

38
Q

There is a 100x increased risk of atherosclerosis-induced gangrene in what condition?

A

Diabeetus

39
Q

Just give me the atherosclerosis process from injury to the atheroma.

A

endothelial injury (irritants) –> endothelial dysfxn and monocyte adhesion –> smooth muscle recruitment and macrophage activation –> macrophage engulf lipids (foam cells) –> fatty streaks –> ECM deposition –> fatty adenoma

40
Q

Which big ass artery is the most common location of atherosclerotic plaques?

A

abdominal aorta

41
Q

What is the main targets of atherosclerosis? what size of vessels?

A

large and medium-sized muscular arteries

42
Q

HOWEVER, which arteries is the most common location of atherosclerotic stenosis?

A

small aa.

43
Q

What 3 things can happen in acute plaque change?

A
  1. rupture
  2. erosion/ulceration
  3. hemorrhage into the atheroma
44
Q

A pipe-like rigidity and subsequent fragility is from what manifestation of atherosclerosis?

A

calcification

45
Q

How can atherosclerosis cause a stroke?

A

embolization

46
Q

A slowly growing atherosclerotic plaque with a thick cap in a coronary artery can cause what type of condition?

A

Angina pectoris

47
Q

This blood lipoprotein is produced in the intestinal epithelial cells and carries TG’s in the blood.

A

Chylomicrons bitch

48
Q

This blood lipoprotein is produced in the bloood, contains high concentration of cholesteol, and endocytosed by the liver and periphereal tissues.

A

LDL

49
Q

This blood lipoprotein is produced in the liver and carries TG’s in the blood.

A

VLDL

50
Q

This blood lipoprotein is produced in the blood from VLDL remnants and endocytosed by the liver or converted to LDL

A

IDL

51
Q

This blood lipoprotein is produced in the liver and intestine, exchanges protein and lipids with other lipoproteins, and returns cholesterol from the tissues to the liver

A

HDL

52
Q

By what reaction does HDL obtain cholesterol from other lipoproteins?

A

LCAT

53
Q

By what protein does HDL deliver cholesterol to the liver?

A

CETP

54
Q

What is the substance that smooth muscle cells secrete to thin the fibrous cap of atherosclerotic plaques?

A

metalloproteinases

55
Q

After the cap has been thinned and rupture, internal plaque contents come in direct contact with procoagulant elements, leading to the formation of what?

A

thrombus

56
Q

What chemical modifications to LDL can lead to atherogenesis?

A

oxidative dmg

57
Q

High concentrations of which lipoprotein correlated with an increased risk of coronary artery disease, even in pts witch the lipid profile is otherwise normal.

A

LpA

58
Q

This type of hyperlipidemia is caused from apoCII or LPL deficiency and causes increased chylomicrons and TG’s.

A

I (familial hypercholomicronemia)

59
Q

This type of hyperlipidemia is caused from defect in LDLR, so there are increased LDL’s in the blood.

A

IIa (familial hypercholesterolemia)

60
Q

This type of hyperlipidekmia is caused by inadequate LDLR internalization, leading to increased LDL, VLDL, and TG’s in teh blood.

A

IIb (familial mixed hyperlipidemia)

61
Q

This type of hyperlipidemia is caused from many factors, leading to increased levels of VLDL and TG’s.

A

IV (familial hypertiglyceridemia)

62
Q

This type of hyperlipidemia is caused from a defect in Apo E, leading to increased VLDL (IDL) and Tg’s in the blood.

A

III (familial dysbetalipoproteinemia)

63
Q

This type of hyperlipidemia is caused from LPL deficiency + increased production of VLDLs, leading to VLDL, chylomicrons, and TG accumulations in the blood.

A

V (familial mixed hypertriglyceridemia)

64
Q

This compound is the stabilizing component of cell membranes, and is the precursor to bile salts and steroids.

A

Choelsterol

65
Q

What is the rate limiting step of cholesterol synthesis?

A

HMG-CoA reductase

66
Q

What is the substrate and product for HMG-CoA R?

A

HMG-CoA –> mevalonate

67
Q

Which drugs act of HMG-CoAR to stop cholesterol synth?

A

Statins

68
Q

Which 2 foods offer delicious, nutritious essentials which lower the effect of starutated fats?

A

Veggies and fish

69
Q

Which organ uses FA’s for surfactant protection?

A

lungs

70
Q

Which tissues use Fa’s for beta oxidation?

A

muscles

71
Q

What do free radicals from free iron and copper do to polyunsaturated FA’s?

A

peroxidate them

72
Q

What are the peroxidated FA’s a risk for?

A

Athrogenic changes

Cardiovascular (4 decks)

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