atherosclerosis

Question 1

what is atherosclerosis

Answer 1

arterial plaque

Question 2

endothelial damage is a result of

Answer 2

mechanical stress

immune response

oxidative stress

Question 3

mechanical stress (hemodynamic)

Answer 3

hypertension
fluctuating pressure

Question 4

immune response

Answer 4

preeclampsia
high serum cholesterol (lipid)
cytokine release, WBC

Question 5

oxidative stress

Answer 5

free radicals
ex, aging

Question 6

mechanical stress, immune response and oxidative stress all stimulate

Answer 6

atherosclerosis and clotting (thrombogenesis)

Question 7

plaque pathogenesis steps 1-3

Answer 7

1. site of injury or trigger (ex. high cholesterol level) - endothelial cells begin to produce VCAM 1 (surface adhesion molecule)
2. circulating monocytes- stick to endothelium and migrate beneath it by squeezing through endothelial cells
3. monocytes turn into macrophages and release free radicals which is oxidative stress

Question 8

plaque pathogenesis steps 4-6

Answer 8

4. this oxidizes ciculating lipids (LDL) which become toxic to endothelial cells, this injures them and becomes platelet aggregation
5. oxidized LDL are phagocytosed by macrophage and they keep the lipid they take so theyre called foam cells
6. apoptosis of foam cells and left with a fatty streak (lipid residue)

Question 9

fatty streak (lipid deposit)

Answer 9

first sign of atherosclerosis

first occur in aorta and coronary arteries

most people by age 20

Question 10

atheroscleritic plaque includes (2)

Answer 10

foam cells (macrophages and lipids)

aggregated platelt (clot)

Question 11

as the clot matures and stabilizes (2)

Answer 11

collagen and fibrin

Question 12

plaque causes an increase and 2 risks in what?

Answer 12

increase in PVR= HTN

risk for obstruction of blood flow

risk for rupture- bleeding

Question 13

nitroglycerin (nitro)

Answer 13

organic nitrate

its exogenous nitric oxide

1st line acute coronary obstructive flow

SL tablet/spray or IV

Question 14

how much nitro

Answer 14

q5 min but if over 3 doses in 15 mins call ems

Question 15

fats (lipids)- energy source

Answer 15

9cal/g

Question 16

triglyceride

Answer 16

3 fatty acids + glycerol

Question 17

fatty acids

Answer 17

saturated, trans, unsaturated

Question 18

structural of fats (2)

Answer 18

cholesterol- hepatic and diet

phospholipids- diet

Question 19

cholesterol

Answer 19

necesarry for hormone/ vitamin D and bile synthesis

Question 20

phospholipids

Answer 20

necessary for cell membrane synthesis

Question 21

unused food stuffs converted into

Answer 21

triglycerides and stored in adipose cells

Question 22

LDL

Answer 22

primary cholesterol carrier

Question 23

VLDL

Answer 23

primary triglyceride carreier

Question 24

HDL

Answer 24

return to liver for excretion; primarily cholesterol

excreted in bile

Question 25

obesity... increased LDL, VLDL and total cholesterol levels

Answer 25

hyperlipidemia hypercholesterolemia

Question 26

lowering lipids (3)

Answer 26

statin niacin fibrate

Question 27

statin (HMG coA reductase inhibitor)

Answer 27

1st for post MI lower LDL lovastatin, atorvastain, simvastatin PO qd liver function dependent side effects: myopathy, CYP 3A4, CYP 2C9 interactions

Question 28

Niacin- vit b3

Answer 28

increases HDL good for pt with low HDL 3g/day decrease liver cholesterol synthesis and increasees clearance

Question 29

Fibrates

Answer 29

decreases VLDL increases lipolysis and metabolism eg. fenofibrate (lipidil)

Question 30

2 used for synergy mainly

Answer 30

niacin an vibrates

Question 31

risk factors for atherosclerosis

Answer 31

HTn high lipids (fats) oxidative stress ... nicotine other: family and age

Question 32

oxidative stress

Answer 32

caused by free radicals reactive molecules (unpaired electron)

Question 33

example of oxidative stress

Answer 33

ROS - reactive oxygen species unstable o2 (oh,h202) endogenous byproduct of respiration and cellular metabolism or cytotoxic substances (nicotine, drugs)

Question 34

how does oxidative stress cause direct damage to individual cells?

Answer 34

through electron reaction and that decreases normal function (insulin resistance, decresed immunity and aging) also cytokine release= inflammation balanced by antioxidants

Question 35

antioxidants reduce...

Answer 35

reactive molecules= formation of water molecules support normal cellular enzyme ex. grape (proanthocyanidins), berries

Question 36

clotting and coagulation (steps)

Answer 36

1. injury or percieved- endothelin released 2. vascular spam- vasoconstriction 3. clotting- vWfactor, platelet degranulation, signals for more aggregation (ADP, thromboxane and thrombin), exposure of glycoprotein 4. coagulation ex. plaque rupture

Question 37

thrombin (4)

Answer 37

fibrinogen to fibrin activates factor 13 platelet aggregation facilitate its own synthesis

Question 38

antiplatelet meds- block thromboxane a2 in degranulation

Answer 38

asprin, asa, dipyridamole ASA + cox 1 inhibition= decreased platelet aggregation aggrenox= combo drug of ASA + dipyridamole

Question 39

antiplatelet med- block adp in degranulation

Answer 39

clopidogrel (plavix) good for peds

Question 40

antiplatelt med- glycoprotein 2b and 2a receptor inhibition

Answer 40

abciximab (repro), integrillin, aggrastat decreased receptor binding and fibrin adhesion iv bolus= continuous influsion used pre/during interventions to remove obstruction

Question 41

baby aspririn

Answer 41

recommended dose for pain/inflammation 325-650mg q4h recommended for CV- 81mg peds NOT unless kawasaki (10-15mg/kg)

Question 41

baby aspririn

Answer 41

recommended dose for pain/inflammation 325-650mg q4h recommended for CV- 81mg peds NOT unless kawasaki (10-15mg/kg)

Question 42

anticoagulants (blood thinners) inhibit factor Xa and ||a= no thrombin

Answer 42

heparin IV low molecular weight heparins enoxaparin, SC dalteparin apixaban (eliquis)- good for LT

Question 43

anticoagulants (blood thinners) block thrombin receptors and factor ||a

Answer 43

dabigatran (pradaxa), PO ex efficacy in CVA

Question 44

anticoagulants (blood thinners) inhibit hepatic synthesis of specific clotting factors

Answer 44

warfarin (coumadin), PO long t1/2, high pub, narrow ti

Question 45

HIT: heparin induced thrombocytopenia

Answer 45

immune reaction to heparin ( and platelet factor 4) activation of thrombin -> disseminated coagulation incidence: up to 20% of patients life threatening: up to 3% of patients .. DIC

Question 46

prothrombin time (PT/INR) 1

Answer 46

warfarin

Question 47

activated partial thromboplastin time 2

Answer 47

heparin

Question 48

anti factor Xa levels 3

Answer 48

lmwh

Question 49

complete blood count (CBC) 4

Answer 49

bleeding risk

Question 50

thrombolytics

Answer 50

based on endogenous clotting control: plasmin (dissolves fibrin clot) plasminogen (inactive) in bloodstream

Question 51

med for thrombolytics

Answer 51

tissue plasminogen activator (tPA) t1/2= 13/16 min administer IV

Question 52

reverse heparin overdose

Answer 52

protamine sulfate

Question 53

anticoagulant

Answer 53

pradbind

Question 54

overdose of warfarin

Answer 54

vitamin k

Question 55

clinical manifestations - narrowing of the vessel

Answer 55

ischemia turbulent flow CAD, angina, PVD, arrythmia, heart failure

Question 56

clinical manifestations -vessel obstruction - plaque rupture

Answer 56

ischemia MI, heart failure, CVA

Question 57

clinical manifestations - thrombosis (emboli)

Answer 57

ischemia MI, CVA, DVT, PE

Question 58

clinical manifestations - weakening of vessel wall

Answer 58

aneurysms hemmorhage or rupture (cardiac tamponade, CVA)

Question 59

high risk BW results

Answer 59

hyperlipidemia, hyppercholesterolemia