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atherosclerosis Flashcards

1
Q

what is atherosclerosis

A

endothelial cell damage cause by mechanical stress, immune response and oxidative stress which causes plaque formation in arteries

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2
Q

plaque pathogenesis steps

A
  1. endothelial cell damage so LDL’s enter tunica intima
  2. LDL’s become oxidized which activates the endothelial cells to create adhesion receptors for WBC’s
  3. monocytes enter tunica intima and turn into macrophages
  4. macrophages eat LDL’s and make foam cells
  5. foam cells burst but lipid contents remain
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3
Q

what does plaque include

A

foam cells (macrophages, LDL), collagen, fibrin, calcium deposits

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4
Q

what is the first sign of atherosclerosis

A

a fatty streak

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5
Q

where do fatty streaks occur first

A

aorta & coronary arteries

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6
Q

what lipids are used for energy

A

triglycerides

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7
Q

what lipids are used for structure

A

cholesterol

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8
Q

what happens to unused foods

A

turns into triglycerides and stored in adipose cells

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9
Q

what are lipoproteins

A

lipid + protein carriers for transport to target tissues

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10
Q

what are LDLs what do they transport and where

A

low density lipoproteins, transport cholesterol to cells

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11
Q

what are VLDLs what do they transport

A

very low density lipoproteins, transport triglycerides to cells

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12
Q

what are HDLs what to they transport and where

A

high density lipoproteins, transport cholesterol to liver

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13
Q

ideal cholesterol in body

A

low LDL, low total cholesterol

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14
Q

what kind of foods raise cholesterol

A

hydrogenated, fast food, deep fried

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15
Q

what diet causes health issues

A

high saturated fat, high LDL and LVDL

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16
Q

risk factors of atherosclerosis

A

hypertension, hypercholesterolemia, hyperlipidemia, smoking, family history, age

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17
Q

what is dyslipidemia

A

high LDL & VLDL, hypercholesterolemia & hyperlipidemia

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18
Q

drugs for dyslipidemia

A

statins, niacin, fibrates

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19
Q

statins moa

A

HMG-coa reductase inhibitor

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20
Q

statins function

A

decreases cholesterol synthesis and increase cholesterol metabolism

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21
Q

statins examples

A

-statin suffix

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22
Q

statins s/e

A

myopathy

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23
Q

who cant use statins and why

A

pregnant women, category X- affects fetal CNS myelination

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24
Q

what is oxidative stress

A

when more free radicals are released than can be detoxified

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25
Q

what can oxidative stress do to cells

A

can cause direct damage to cells due to electron reaction which can lead to decreased function

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26
Q

what can cause oxidative stress

A

ROS, cytotoxic substances

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27
Q

how does oxidative stress cause inflammation

A

oxidative stress causes endothelial cells to attract WBCs

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28
Q

how to balance oxidative stress

A

antioxidants

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29
Q

what do antioxidants do

A

support normal enzyme function and reduce reactive molecules ( =water byproduct)

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30
Q

antioxidants example

A

grapes

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31
Q

what does atherosclerosis cause

A

narrow blood vessels, vessel obstruction due to plaque, thrombus->emboli, weakening of vessel wall

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32
Q

what does narrow blood vessels cause

A

ischemia and turbulent flow

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33
Q

examples of narrow blood vessels

A

CAD, angina, PVD, heart failure

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34
Q

what does vessel obstruction due to plaque cause

A

causes ischemia to target tissue

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35
Q

examples of vessel obstruction due to plaque

A

MI, heart failure

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36
Q

what can thrombosis lead to

A

embolus

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37
Q

what does thrombosis cause

A

ischemia to target tissue

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38
Q

examples of thrombosis

A

DVT, pulmonary embolus, MI

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39
Q

what can weakening of vessel wall cause

A

aneurysm formation, hemorrhage or rupture, tompanade

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40
Q

CAD

A

coronary artery disease can be chronic or acute

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41
Q

chronic CAD

A

stable angina, stable plaque

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42
Q

acute CAD

A

unstable angina, unstable plaque can rupture and cause MI

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43
Q

plaque rupture steps

A
  1. injury
  2. vascular spasm
  3. platelets activated
  4. coagulation cascade
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44
Q

how are platelets activated

A

thromboxane A2, ADP, thrombin are released and signal platelets to activate

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45
Q

what happens when platelets are activated

A

platelet aggregation

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46
Q

what is the coagulation cascade

A

has 2 pathways that lead to making fibrin which leads to clots

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47
Q

how is the extrinsic pathway activated

A

when external damage causes endothelial cells to release tissue factors

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48
Q

how is the intrinsic pathway induced

A

when endothelial cells are exposed to collagen

49
Q

how is thrombin made

A

active factor X + prothrombin (CF II)

50
Q

what does thrombin do

A

converts fibrinogen to fibrin, activates CF XIII which creates stable fibrin, released by platelets to increase aggregation, can synthesize itself

51
Q

what causes a STEMI

A

total blockage of coronary artery so large area of heart muscles don’t receive blood

52
Q

what happens during a STEMI

A

high ST segment so ventricles don’t contact fully before relaxing

53
Q

what is ischemia

A

reduction of blood getting to tissue = reduction of oxygen

54
Q

what happens to cells during ischemia

A

become anaerobic

55
Q

what do anaerobic cells produce and what does it do

A

lactic acid which decreases PH

56
Q

signs and symptoms of ischemia

A

pain, SOB, hypoxemia, no contractility

57
Q

onset of ischemia

A

fast onset, 1 minute

58
Q

what happens to injured myocardial cells

A

leaks intrinsic enzymes and cause inflammation

59
Q

what do myocardial cells leak

A

intrinsic enzymes like troponin and creatine kinase

60
Q

what is found in blood during MI or ischemia

A

high troponin and creatine kinase

61
Q

how to check for biomarkers

A

check levels of troponin and CK in plasma

62
Q

what happens after 20-40 mins of ischemia

A

necrosis occurs which leads to scar tissue = heart failure

63
Q

immediate ischemia treatments

A

vasodilate, oxygenate, remove obstruction, treat clotting

64
Q

drug class used to vasodilate during ischemia

A

organic nitrates

65
Q

examples of organic nitrates

A

nitroglycerin, isosorbide

66
Q

what is nitroglycerin

A

exogenous nitric oxide

67
Q

what does nitroglycerin do

A

causes vasodilation which decreases hearts oxygen demand

68
Q

nitroglycerin doses

A

3 doses in 5 min intervals, if doesn’t respond call 911

69
Q

nitroglycerin routes of administration

A

SL, IV, spray

70
Q

what kind of angina can nitroglycerin treat

A

stable angina

71
Q

obstruction treatments

A

coronary angioplasty & CABG

72
Q

what is a coronary angioplasty

A

when a narrowed coronary artery is opened using a balloon catheter

73
Q

what is a CABG

A

when a vein graft from saphenous vein in leg is used and attached to the aorta and coronary artery to bypass the obstruction

74
Q

what do antiplatelets do

A

prevent platelet aggregation and adhesion

75
Q

how do antiplatelets work

A

work to prevent thromboxane A2, ADH, and glycoprotein IIb/IIIa receptor

76
Q

meds that block thromboxane A2 release

A

ASA and aggrenox

77
Q

asa as antiplatelet

A

cox1 inhibitor which prevent thrombin production which decreases aggregation

78
Q

asa risks

A

NSAID so can cause ulcers

79
Q

aggrenox fx

A

asa+dipyridamole decrease platelet aggregation

80
Q

asa used for antiplatelet drug

A

baby asprin, low dose 81 mg

81
Q

baby asa on children is used when

A

when they have kawasaki syndrome

82
Q

meds that block ADH receptor

A

clopidogrel (plavix)

83
Q

how does clopidogrel work

A

prevent ADH from binding to platelets which prevent aggregation

84
Q

meds that block glycoprotein IIb/IIIa

A

abciximab, intrigrillin, aggrestat

85
Q

how does abciximab work

A

inhibits the glycoprotein IIb/IIIa receptor which decrease fibrin = decreased platelet adhesion

86
Q

glycoprotein IIb/IIIa receptor inhibitor ROA and uses

A

IV only, used only in hospital for pre/during obstruction treatment

87
Q

function of anticoagulants

A

lengthen clotting time

88
Q

anticoagulant target

A

coagulation cascade (clotting factors), thrombin formation, thrombin receptors, and CF formation

89
Q

meds that inhibit thrombin synthesis

A

heparin, LMWH (enoxaprin, daltaprin)

90
Q

how does heparin work

A

targets Xa and CF II which inhibits thrombin synthesis = no fibrin

91
Q

how do LMWH work

A

targets Xa which inhibits thrombin synthesis

92
Q

why are LMWH used

A

given when going home from hospital, short term use

93
Q

meds that block thrombin receptors

A

dabigatran (pradaxa)

94
Q

when is dabigatran used

A

for stroke prevention

95
Q

meds that inhibit CF 2,7,9&10

A

warfarin (coumadin)

96
Q

how does warfarin work

A

it inhibits activation of CF 2,7,9 and 10, inhibits vitamin k action

97
Q

warfarin risks

A

high PPB and narrow TI

98
Q

antidote for low dose warfarin

A

vitamin k since it activates CF

99
Q

antidote for high dose warfarin

A

protamine sulfate

100
Q

what to avoid when on warfarin

A

leafy greens, high vit K foods, other drug treatments

101
Q

what is HIT

A

herparin induced thrombocytopenia

102
Q

what causes HIT

A

immune system makes antibodies against heparin + CF 4, when the antibodies bind to the heparin complexes activating platelets

103
Q

what can HIT lead to

A

clotting = DIC

104
Q

how many ppl get HIT

A

50% of heparin users

105
Q

how much HIT is life threatening

A

3% of ppl with HIT

106
Q

how do you monitor heparin

A

monitor PT values

107
Q

how do you monitor warfarin

A

monitor PTT values

108
Q

how do you monitor LMWH

A

anti factor Xa

109
Q

what is monitored for a bleeding risk

A

complete blood count

110
Q

what are thrombolytics

A

break down clots

111
Q

how do thrombolytics work

A

they activate plasminogen in blood into plasmin, which breaks down fibrin

112
Q

thrombolytic meds

A

tissue plasminogen activators; alteplase, retelplase

113
Q

tpa half life

A

13-16 mins

114
Q

tpa roa

A

IV

115
Q

what is used during an acute event

A

antiplatelets, thrombolytics

116
Q

ppl with high clotting risk

A

ppl w dysryhthmia, complex surgery, severe MI

117
Q

meds to give patients at risk for clotting

A

anticoagulants

118
Q

routine prevention meds

A

antiplatlets

119
Q

what is used to treat hypertension in patients with MI

A

beta blockers

Nurs 216 (6 decks)

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