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atherosclerosis Flashcards

1
Q

atherosclerosis

A

arterial plaque
- mechanical stress, immune response/inflammation, oxidative stress

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2
Q

mechanical stress

A

endothelial cell damage leading to hypertension

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3
Q

immune response/inflammation

A

endothelial cell damage due to cytokines and WBC leading to preeclampsia and high serum cholesterol

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4
Q

oxidative stress

A

endothelial cell damage due to circulation of reactive oxygen species (happens in aging)
- due to cytotoxic substances and reactive oxygen species
- balanced out by antioxidants

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5
Q

plaque pathogenesis step 1

A

injury or trigger causes endothelial damage and produces surface adhesion molecules (VCAM-1)

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6
Q

plaque pathogenesis step 2

A

circulating monocytes adhere to endothelium and then migrate beneath it, increasing permeability

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7
Q

plaque pathogenesis step 3

A

monocytes turn into macrophages and release free radicals leading to oxidative stress

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8
Q

plaque pathogenesis step 4

A

oxidation of LDL which becomes toxic for endothelial cells which causes injury and then platelet aggregation

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9
Q

plaque pathogenesis step 5

A

LDL phagocytosed by macrophages and retain the lipid which turn to foam cells

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10
Q

foam cells

A

macrophages with lipid in them

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11
Q

plaque formation

A

foam cell disintegrates on cell wall and leaves the liquid

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12
Q

fatty streak (lipid deposit)

A

indication of atherosclerosis, occur initially in aorta or coronary arteries

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13
Q

coronary arteries

A

right coronary, left and descending coronary, circumflex

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14
Q

atherosclerotic plaque

A

foam cell and aggregated platelet (clot)
- as it MATURES collagen and fibrin deposit onto it
- as it AGES calcium deposits in it

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15
Q

plaque causes…

A

increase in PVR=HTN, blood flow obstruction, risk of rupture (bleeding)

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16
Q

organic nitrate

A

nitroglycerin (nitro)

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17
Q

Nitroglycerin (Nitro)

A

organic nitrate;1st line in acute coronary flow obstruction
- exogenous nitric oxide,
-SL tablet/spray/IV
- only give 3 times before calling EMS

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18
Q

fats

A

9cal/g

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19
Q

triglycerides

A

fat; only found in diet; unused food converted and deposited into adipose tissue
- 3 fatty acids and glycerol
- breakdown via glycolysis into glucose

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20
Q

fatty acids

A

saturated, trans, unsaturated

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21
Q

structural resource of fat

A

cholesterol, phospholipids

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22
Q

cholesterol

A

come from hepatic and diet; necessary for vitamin D, hormone, and bile synthesis

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23
Q

phospholipids

A

come from diet; necessary for cell membrane synthesis

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24
Q

lipid movement

A

combine with protein carriers to move to target tissues

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25
Q

lipoprotein

A

type of apoprotein
- LDL and VLDL

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26
Q

LDL

A

“bad” cholesterol
- distributes to cells and is primary cholesterol carrier

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27
Q

VLDL

A

distributes to cells and is primary triglyceride carrier

28
Q

HDL

A

“good” cholesterol
- returns to liver for excretion and is excreted in bile
- primary cholesterol

29
Q

mono-unsaturated fat

A

lowers LDL and raises HDL
- main source comes from olives, oils, nuts, avocados

30
Q

poly-unsaturated fat

A

lowers LDL and raises HDL
- main source comes from corn and fish

31
Q

saturated fat

A

raises LDL
- main source comes from most dairy products, red meat, chocolate, coconut

32
Q

trans fat

A

raises LDL
- main source comes from margarine, fast foods, commercial baked goods

33
Q

trans fat

A

raises LDL
- main source comes from margarine, fast foods, commercial baked goods

34
Q

excess fats

A

converted to triglycerides and stored into adipose tissue or cells and contributes to obesity

35
Q

increase in LDL and VLDL

A

may cause hyperlipidemia and hypercholesterolemia

36
Q

drug subclasses for lowering lipids

A

statins, niacin, fibrates
- niacin and fibrates used as synergy

37
Q

statins

A

HMG-CoA reductase inhibitors
- lower LDL through decreased synthesis and increased hepatic metabolism

38
Q

lovastatin (mevacor), atorvastatin (lipitor), simvastatin (zocor)

A

statins
- PO, can only use in patients with good liver function, may cause myopathy
- 1st line treatment for post MI

39
Q

Niacin

A

increases HDL
- decreases liver cholesterol synthesis and increases clearance
- ideal for patients with low HDL
- 3g/day

40
Q

fibrates

A

increases lipolysis and metabolism

41
Q

fenofibrate (lipidil)

A

fibrate

42
Q

atherosclerosis risk factors

A

hypertension, high lipid (fat), oxidative stress

43
Q

mechanism of action for oxidative stress

A

direct damage to individual cells by electron reaction which causes decreased normal function and cytokine release
eg. insulin resistance

44
Q

antioxidants

A

reduce reactive molecules; formation of water molecules
- support normal cell enzyme function

45
Q

proanthocyanidins

A

type of antioxidant

46
Q

platelet aggregation

A

triggered by mechanical stress (HTN, vessel injury)

47
Q

clotting pathway

A
  1. injury
  2. vascular spasm
  3. clotting initiated by vWf factor (glycoprotein)
48
Q

clotting

A

after initiation of vWf factor…
- platelet degranulation
- signal for more aggregation from ADP, thromboxane and thrombin
- exposure of glycoprotein IIB/IIIA receptor site which increases platelet adhesion

49
Q

coagulation

A

platelet rupture –> foam cells/lipids released –> tissue thromboplastin synthesis and secretion –> extrinsic coagulation pathway

50
Q

extrinsic coagulation pathway

A

tissue trauma –> release of thromboplastin

51
Q

thrombin

A

essential to blood coagulation
- converts fibrinogen to fibrin
- activates factor XIII
- enhances platelet aggregation
- facilitates own synthesis

52
Q

antiplatelet medications

A

block thromboxane A2 in degranulation, block ADP in degranulation, glycoprotein IIB and IIIA receptor inhibition

53
Q

ASA, Dipyridamole, aggrenox

A

antiplatelet medications, block thromboxane A2 in degranulation

54
Q

clopidogrel (plavix)

A

antiplatelet medication, block ADP in degranulation

55
Q

abciximab (reopro), integrilin, aggrastat

A

antiplatelet medication; glycoprotein IIb/IIIa receptor inhibition
- decreased receptor binding and fibrin adhesion
- used pre/during interventions to remove obstruction

56
Q

baby aspirin

A

recommended dose for pain/inflammation is 325-650
recommended dose for CV is 81mg
10-15mg/kg in Kawasaki disease

57
Q

anticoagulant medications

A

inhibit factor Xa and IIa–> no thrombin, block thrombin receptors and factor IIa, inhibit hepatic synthesis of specific clotting factors

58
Q

Heparin (IV)

A

anticoagulant
- inhibit factor Xa and IIa which leads to no thrombin
- aPTT test

59
Q

enoxaparin (lovenox), dalteparin (fragmin), apixaban (eliquis)

A

low molecular weight heparins
- inhibit factor Xa and IIa which leads to no thrombin
- anti factor Xa level test

60
Q

dabigatran (pradaxa) PO

A

anticoagulant
- block thrombin receptors and IIa
- CVA prevention

61
Q

warfarin (coumadin)

A

anticoagulant; inhibit hepatic synthesis of specific clotting factors (II, VII, IX, X)
- PO, long half life, high PPB, narrow TI
- PT/INR test

62
Q

HIT (heparin induced thrombocytopenia)

A

immune reaction to heparin and platelet factor 4
- activation of thrombin –>disseminated coagulation
- incidence in up to 50% of patients
- life threatening in up to 3% of patients

63
Q

prothrombin time test (PT/INR)

A

used for patients on warfarin

64
Q

activated partial thromboplastin time (aPTT)

A

used for patients on heparin

65
Q

anti factor Xa levels

A

used for patients on low molecular weight heparins

66
Q

thrombolytics

A

clotting control; plasmin dissolves fibrin clot
- plasminogen in blood stream gets activated by tPA to plasmin which causes clot lysis
- med would be tPA

67
Q

Alteplase, Reteplase

A

tPA (tissues plasminogen activator); thrombolytics
- half life 13-16 min; IV

nurs 216 (8 decks)

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