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lecture 7 > atherosclerosis > Flashcards

atherosclerosis Flashcards

1
Q

what is atherosclerosis

A

arterial plaque

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2
Q

endothelial damage is a result of

A

mechanical stress

immune response

oxidative stress

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3
Q

mechanical stress (hemodynamic)

A

hypertension
fluctuating pressure

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4
Q

immune response

A

preeclampsia
high serum cholesterol (lipid)
cytokine release, WBC

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5
Q

oxidative stress

A

free radicals
ex, aging

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6
Q

mechanical stress, immune response and oxidative stress all stimulate

A

atherosclerosis and clotting (thrombogenesis)

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7
Q

plaque pathogenesis steps 1-3

A
  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
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8
Q

plaque pathogenesis steps 4-6

A
  1. this oxidizes ciculating lipids (LDL) which become toxic to endothelial cells, this injures them and becomes platelet aggregation
  2. oxidized LDL are phagocytosed by macrophage and they keep the lipid they take so theyre called foam cells
  3. apoptosis of foam cells and left with a fatty streak (lipid residue)
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9
Q

fatty streak (lipid deposit)

A

first sign of atherosclerosis

first occur in aorta and coronary arteries

most people by age 20

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10
Q

atheroscleritic plaque includes (2)

A

foam cells (macrophages and lipids)

aggregated platelt (clot)

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11
Q

as the clot matures and stabilizes (2)

A

collagen and fibrin

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12
Q

plaque causes an increase and 2 risks in what?

A

increase in PVR= HTN

risk for obstruction of blood flow

risk for rupture- bleeding

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13
Q

nitroglycerin (nitro)

A

organic nitrate

its exogenous nitric oxide

1st line acute coronary obstructive flow

SL tablet/spray or IV

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14
Q

how much nitro

A

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

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15
Q

fats (lipids)- energy source

A

9cal/g

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16
Q

triglyceride

A

3 fatty acids + glycerol

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17
Q

fatty acids

A

saturated, trans, unsaturated

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18
Q

structural of fats (2)

A

cholesterol- hepatic and diet

phospholipids- diet

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19
Q

cholesterol

A

necesarry for hormone/ vitamin D and bile synthesis

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20
Q

phospholipids

A

necessary for cell membrane synthesis

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21
Q

unused food stuffs converted into

A

triglycerides and stored in adipose cells

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22
Q

LDL

A

primary cholesterol carrier

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23
Q

VLDL

A

primary triglyceride carreier

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24
Q

HDL

A

return to liver for excretion; primarily cholesterol

excreted in bile

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25
Q

obesity… increased LDL, VLDL and total cholesterol levels

A

hyperlipidemia
hypercholesterolemia

26
Q

lowering lipids (3)

A

statin
niacin
fibrate

27
Q

statin (HMG coA reductase inhibitor)

A

1st for post MI

lower LDL

lovastatin, atorvastain, simvastatin

PO qd

liver function dependent

side effects: myopathy, CYP 3A4, CYP 2C9 interactions

28
Q

Niacin- vit b3

A

increases HDL

good for pt with low HDL

3g/day

decrease liver cholesterol synthesis and increasees clearance

29
Q

Fibrates

A

decreases VLDL

increases lipolysis and metabolism
eg. fenofibrate (lipidil)

30
Q

2 used for synergy mainly

A

niacin an vibrates

31
Q

risk factors for atherosclerosis

A

HTn
high lipids (fats)
oxidative stress … nicotine

other: family and age

32
Q

oxidative stress

A

caused by free radicals
reactive molecules (unpaired electron)

33
Q

example of oxidative stress

A

ROS - reactive oxygen species

   unstable o2 (oh,h202)
   endogenous byproduct of respiration and cellular metabolism

or cytotoxic substances (nicotine, drugs)

34
Q

how does oxidative stress cause direct damage to individual cells?

A

through electron reaction and that decreases normal function (insulin resistance, decresed immunity and aging)

also cytokine release= inflammation

balanced by antioxidants

35
Q

antioxidants reduce…

A

reactive molecules= formation of water molecules

support normal cellular enzyme

ex. grape (proanthocyanidins), berries

36
Q

clotting and coagulation (steps)

A
  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
37
Q

thrombin (4)

A

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

38
Q

antiplatelet meds- block thromboxane a2 in degranulation

A

asprin, asa, dipyridamole

ASA + cox 1 inhibition= decreased platelet aggregation

aggrenox= combo drug of ASA + dipyridamole

39
Q

antiplatelet med- block adp in degranulation

A

clopidogrel (plavix)

good for peds

40
Q

antiplatelt med- glycoprotein 2b and 2a receptor inhibition

A

abciximab (repro), integrillin, aggrastat

decreased receptor binding and fibrin adhesion

iv bolus= continuous influsion

used pre/during interventions to remove obstruction

41
Q

baby aspririn

A

recommended dose for pain/inflammation 325-650mg q4h

recommended for CV- 81mg

peds NOT unless kawasaki (10-15mg/kg)

41
Q

baby aspririn

A

recommended dose for pain/inflammation 325-650mg q4h

recommended for CV- 81mg

peds NOT unless kawasaki (10-15mg/kg)

42
Q

anticoagulants (blood thinners)

inhibit factor Xa and ||a= no thrombin

A

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

43
Q

anticoagulants (blood thinners)

block thrombin receptors and factor ||a

A

dabigatran (pradaxa), PO
ex efficacy in CVA

44
Q

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

A

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

45
Q

HIT: heparin induced thrombocytopenia

A

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

46
Q

prothrombin time (PT/INR) 1

A

warfarin

47
Q

activated partial thromboplastin time 2

A

heparin

48
Q

anti factor Xa levels 3

A

lmwh

49
Q

complete blood count (CBC) 4

A

bleeding risk

50
Q

thrombolytics

A

based on endogenous clotting control: plasmin (dissolves fibrin clot)

plasminogen (inactive) in bloodstream

51
Q

med for thrombolytics

A

tissue plasminogen activator (tPA)

t1/2= 13/16 min
administer IV

52
Q

reverse heparin overdose

A

protamine sulfate

53
Q

anticoagulant

A

pradbind

54
Q

overdose of warfarin

A

vitamin k

55
Q

clinical manifestations
- narrowing of the vessel

A

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

56
Q

clinical manifestations
-vessel obstruction - plaque rupture

A

ischemia
MI, heart failure, CVA

57
Q

clinical manifestations
- thrombosis (emboli)

A

ischemia
MI, CVA, DVT, PE

58
Q

clinical manifestations
- weakening of vessel wall

A

aneurysms
hemmorhage or rupture (cardiac tamponade, CVA)

59
Q

high risk BW results

A

hyperlipidemia, hyppercholesterolemia

lecture 7 (1 decks)

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