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nurs 216 > atherosclerosis > Flashcards

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
lipoprotein
type of apoprotein - LDL and VLDL
26
LDL
"bad" cholesterol - distributes to cells and is primary cholesterol carrier
27
VLDL
distributes to cells and is primary triglyceride carrier
28
HDL
"good" cholesterol - returns to liver for excretion and is excreted in bile - primary cholesterol
29
mono-unsaturated fat
lowers LDL and raises HDL - main source comes from olives, oils, nuts, avocados
30
poly-unsaturated fat
lowers LDL and raises HDL - main source comes from corn and fish
31
saturated fat
raises LDL - main source comes from most dairy products, red meat, chocolate, coconut
32
trans fat
raises LDL - main source comes from margarine, fast foods, commercial baked goods
33
trans fat
raises LDL - main source comes from margarine, fast foods, commercial baked goods
34
excess fats
converted to triglycerides and stored into adipose tissue or cells and contributes to obesity
35
increase in LDL and VLDL
may cause hyperlipidemia and hypercholesterolemia
36
drug subclasses for lowering lipids
statins, niacin, fibrates - niacin and fibrates used as synergy
37
statins
HMG-CoA reductase inhibitors - lower LDL through decreased synthesis and increased hepatic metabolism
38
lovastatin (mevacor), atorvastatin (lipitor), simvastatin (zocor)
statins - PO, can only use in patients with good liver function, may cause myopathy - 1st line treatment for post MI
39
Niacin
increases HDL - decreases liver cholesterol synthesis and increases clearance - ideal for patients with low HDL - 3g/day
40
fibrates
increases lipolysis and metabolism
41
fenofibrate (lipidil)
fibrate
42
atherosclerosis risk factors
hypertension, high lipid (fat), oxidative stress
43
mechanism of action for oxidative stress
direct damage to individual cells by electron reaction which causes decreased normal function and cytokine release eg. insulin resistance
44
antioxidants
reduce reactive molecules; formation of water molecules - support normal cell enzyme function
45
proanthocyanidins
type of antioxidant
46
platelet aggregation
triggered by mechanical stress (HTN, vessel injury)
47
clotting pathway
1. injury 2. vascular spasm 3. clotting initiated by vWf factor (glycoprotein)
48
clotting
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
coagulation
platelet rupture --> foam cells/lipids released --> tissue thromboplastin synthesis and secretion --> extrinsic coagulation pathway
50
extrinsic coagulation pathway
tissue trauma --> release of thromboplastin
51
thrombin
essential to blood coagulation - converts fibrinogen to fibrin - activates factor XIII - enhances platelet aggregation - facilitates own synthesis
52
antiplatelet medications
block thromboxane A2 in degranulation, block ADP in degranulation, glycoprotein IIB and IIIA receptor inhibition
53
ASA, Dipyridamole, aggrenox
antiplatelet medications, block thromboxane A2 in degranulation
54
clopidogrel (plavix)
antiplatelet medication, block ADP in degranulation
55
abciximab (reopro), integrilin, aggrastat
antiplatelet medication; glycoprotein IIb/IIIa receptor inhibition - decreased receptor binding and fibrin adhesion - used pre/during interventions to remove obstruction
56
baby aspirin
recommended dose for pain/inflammation is 325-650 recommended dose for CV is 81mg 10-15mg/kg in Kawasaki disease
57
anticoagulant medications
inhibit factor Xa and IIa--> no thrombin, block thrombin receptors and factor IIa, inhibit hepatic synthesis of specific clotting factors
58
Heparin (IV)
anticoagulant - inhibit factor Xa and IIa which leads to no thrombin - aPTT test
59
enoxaparin (lovenox), dalteparin (fragmin), apixaban (eliquis)
low molecular weight heparins - inhibit factor Xa and IIa which leads to no thrombin - anti factor Xa level test
60
dabigatran (pradaxa) PO
anticoagulant - block thrombin receptors and IIa - CVA prevention
61
warfarin (coumadin)
anticoagulant; inhibit hepatic synthesis of specific clotting factors (II, VII, IX, X) - PO, long half life, high PPB, narrow TI - PT/INR test
62
HIT (heparin induced thrombocytopenia)
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
prothrombin time test (PT/INR)
used for patients on warfarin
64
activated partial thromboplastin time (aPTT)
used for patients on heparin
65
anti factor Xa levels
used for patients on low molecular weight heparins
66
thrombolytics
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
Alteplase, Reteplase
tPA (tissues plasminogen activator); thrombolytics - half life 13-16 min; IV

nurs 216 (8 decks)

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