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N216 A/B > Perfusion Part 3 - Atherosclerosis > Flashcards

Perfusion Part 3 - Atherosclerosis Flashcards

1
Q

Atherosclerosis is an the build up of arterial ____

A

plaque

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2
Q

What are 3 causes of damage to the endothelium lining of blood vessels?

A
  • Mechanical stress
  • Immune response
  • Oxidative stress
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3
Q

Example of:
Mechanical stress - ____
Immune response - ____ ____
Oxidative stress: ____

A

HTN
Inflammatory sequelae
ROS

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4
Q

How do you balance ROSs?

A

Antioxidants

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5
Q

All 3 causes of endothelial damage lead to blood ____

A

clotting

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6
Q

Increased cholesterol levels lead to endothelial cells producing an adhesion molecule called ___-_

A

VCAM-1

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7
Q

Circulating ____ attach to VCAM-1 on the endothelium

A

monocytes

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8
Q

What do monocytes do after attaching to VCAM-1? How does this affect permeability?

A

Squeeze between endothelium cells and move into the intima; increases permeability

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9
Q

Monocytes differentiate into ____ in the intima and release ____

A

macrophages, ROSs

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10
Q

Circulating ____ are phagocytosed by macrophages, turning the macrophage into a ____ cell

A

LDLs, foam

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11
Q

Foam cells undergo ____, the lipid residue remaining turning into a ____ ____

A

apoptosis, fatty streak

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12
Q

Fatty streaks are commonly first found in the ____ and ____ arteries

A

aorta, coronary

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13
Q

What are the 4 components of plaque?

A
  • Foam cells
  • Collagen
  • Fibrin
  • Calcium deposits
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14
Q

What are 4 examples of clin. manifestations of atherosclerosis?

A
  • Narrowing of vessel
  • Vessel obstruction
  • Thrombosis + emboli formation
  • Weakening of vessel wall
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15
Q

What is ischemia?

A

Decreased oxygen to tissues

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16
Q

What is tamponade?

A

Coronary arteries rupture + bleed into the pericardium

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17
Q

State the most common locations these are found:
Ischemia & infarction - ____ + ____ arteries
Thrombus formation - ____

A

Coronary, cerebral

Aorta

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18
Q

What are some risk factors for athersclerosis?

A
  • HTN
  • High cholesterol/lipids
  • Male
  • Age
  • Smoking
  • Family history
  • Diabetes mellitus
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19
Q

What are 2 strategies to lowering amount of lipid in the body?

A
  • Lifestyle/diet

- Pharmacotherapy

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20
Q

What are the 3 drug classes used during pharmacotherapy of lowering lipids?

A
  • Statins
  • Niacin
  • Fibrates
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21
Q

Which drug class is 1st line treatment post MI?

A

Statins

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22
Q

Which 2 drug classes are mainly for synergy?

A

Niacin + fibrates

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23
Q

Niacin ____ HDLs while fibrates ____ VLDLs

A

increase, decrease

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24
Q

Statins inhibit what?

A

HMG-CoA Reductase

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25
Q

HMG-CoA Reductase is the primary regulatory site for ____ ____ and is under a ____ feedback system

A

Cholesterol synthesis, negative

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26
Q

Statins lower LDLs by decreasing ____ ____ and increasing ____ ____

A

Cholesterol synthesis, hepatic circulation

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27
Q

What time of day are statins usually given and why?

A

Night, cholesterol synthesis peaks at night

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28
Q

What are 3 examples of statins?

A
  1. Lovastatin (mevacor)
  2. Atorvastatin (lipitor)
  3. Simvastatin (zocor)
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29
Q

All statins are dependent on ____ function

A

liver

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30
Q

Statins are considered pregnancy category ___, meaning:

A

X, meaning pregnant people should NOT take them (interfere with fetal CNS myelination).

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31
Q

What are some side effects of statins?

A
  • Myopathy (muscle weakness)

- Drug-drug interactions

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32
Q

What are 2 types of disorders of CVD?

A
  • Acute

- Chronic

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33
Q

Describe acute CVD

A
  • Unstable angina
  • Unstable plaque (–> rupture)
  • Risk of MI
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34
Q

Describe chronic CVD

A
  • Stable angina

- Thick fibrous cap over plaque

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35
Q

What are the 4 steps from plaque rupture to clotting?

A
  1. Rupture/injury
  2. Vascular spasm
  3. Platelet plug formation
  4. Coagulation
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36
Q

What are the 2 steps of platelet plug formation?

A
  1. Platelet activation

2. Signaling for aggregation

37
Q

What are released to signal aggregation?

A
  • ADP
  • Thromboxane A2
  • Thrombin
38
Q

What is glycoprotein IIB/IIIa responsible for?

A

Makes platelet sticky + stabilizes fibrin through binding

39
Q

Factor _ converts prothrombin into thrombin

40
Q

Thrombin activates ____ into fibrin

A

fibrinogen

41
Q

Thombrin activates factor _, which makes fibrin from a ____ meshwork to a ____ one.

A

XIII, loose, stable

42
Q

What are 3 drug classes to counter atherosclerosis?

A
  1. Antiplatelet
  2. Anticoagulant
  3. Thrombolytic
43
Q

Describe at which point in the clotting process the drug classes work on:
Antiplatelet: ____ ____
Anticoagulant: ____ ____
Thrombolytic: ____ –> ____

A

Platelet aggregation
Coagulation cascade
Post-clot –> lysis

44
Q

What does STEMI mean?

A

ST wave Elevation MI

45
Q

STEMI is a total ____ artery blockage, which means the heart is unable to ____ and ____ oxygenation

A

coronary, rest, no

46
Q

Ischemia goes hand in hand with cellular ____

47
Q

What are some signs and symptoms of ischemia?

A
  • Pain
  • SOB
  • Hypoxemia
  • No contractility
48
Q

Injury of myocardial cells can lead to the leakage of what 3 enzymes?

A
  • Troponin
  • Creatine Kinease
  • Myoglobin
49
Q

What is the 1st line acute intervention for stable angina?

A

Nitroglycerin (Nitro) - nitric oxide

50
Q

Nitroglycerin has ____ coronary circulation efficacy

51
Q

Nitroglycerin can be administered ____ by _ tablet(s) q _ min x _

A

sublingually, 1 tablet q5min x3

52
Q

Angioplasty (PTCA) treats ____ within arterial vessels and ____ ____ within cerebral vessels

A

obstruction (CAD), thrombic CVA

53
Q

CABG is a ____ common treatment for obstruction

54
Q

What are 3 meds that can induce cardiac arrest?

A
  • Calcium channel blockers
  • Beta 1 blockers
  • Potassium
55
Q

Which 2 substances are blocked by anti-platelets?

A
  1. Thromboxane A2.

2. ADP.

56
Q

What is the function of Thromboxane A2 normally?

A

Calls other platelets to initiate aggregation.

57
Q

What are 2 examples of antiplatelets that block Thromboxane A2?

A
  1. ASA (aspirin/acetasalycilic acid)

2. Dipryridamole

58
Q

Which 2 drug classes does ASA belong to?

A

Anti-platelet & NSAID

59
Q

ASA causes _____ __ inhibition.

60
Q

____ is a combination of ASA and Dipyridamole.

61
Q

What is the normal function of ADP in platelet aggregation?

A

Promotes platelet adhesion.

62
Q

What is an example of an anti-platelet that blocks ADP?

A

Clopidogrel (Plavix)

63
Q

Which anti-platelet is contraindicated in children? Why?

A

ASA: dose is too high & will increase intracranial pressure.

64
Q

Which anti-platelet is the drug of choice for children?

A

Clopidogrel (Plavix).

65
Q

What is the recommended dose (amount of drug q_h) of ASA for pain/inflammation?

A

325-650 mg, q4h

65
Q

What is the recommended dose (amount of drug q_h) of ASA for pain/inflammation?

A

325-650 mg, q4h

66
Q

What is the recommended dose of aspirin per kg if it was indicated to be used in children?

A

10-15mg per kg

67
Q

What is one situation where aspirin would be indicated for treatment in children?

A

Kawasaki syndrome.

68
Q

What are 3 mechanisms of action for anticoagulants?

A
  1. Inhibit thrombin by targeting Active Factor X (activates thrombin).
  2. Block thrombin receptors & Factor IIa (2a).
  3. Inhibit hepatic (liver) formation of specific clotting factors (specifically II, VII, IX and X)
    All ultimately result in fibrin not being produced so the clot does not stabilize.
69
Q

What is the primary anticoagulant that inhibits thrombin via Factor X?

70
Q

What are 2 low-molecular weight heparins (LMWHs)?

A
  1. Enoxaparin (Lovenox)

2. Dalteparin (Fragmin)

71
Q

What is the antidote to heparins?

A

Protamine sulfate

72
Q

Which anticoagulant blocks thrombin receptors & factor IIa (2a)?

A

Dabigatran (Pradaxa)

73
Q

What is special about Dabigatran (Pradaxa) when it comes to ADME?

A

It is a prodrug.

74
Q

What are anticoagulants that block thrombin receptors & Factor IIa (2a) used to prevent?

75
Q

Which anticoagulant inhibits hepatic formation of clotting factors II, VII, IX and X?

A

Warfarin (coumadin)

76
Q

What are 3 PD characteristics of Warfarin (coumadin)?

A
  1. Long half-life.
  2. Highly PPB.
  3. Narrow TI.
77
Q

What is the antidote to Warfarin (Coumadin) overdose?

A

Vitamin K to ensure that blood doesn’t get too think & can still clot if needed (ie: if you had an injury).
Vit K promotes formation of clotting factors.

78
Q

What is heparin-induced thrombocytopenia (HIT)?

A

Emergency: immune reaction to heparin & platelet Factor IV (4).

79
Q

What lab monitoring test (besides monitoring serum drug levels) should patients taking warfarin undergo?

A

Prothrombin time (PT/INR - internal normalized ratio): evaluation of blood clotting by measuring the number of seconds taken for a clot to form after clotting reagents are added.

80
Q

Which lab monitoring test (besides measuring serum drug levels) should patients taking unfractioned heparins take?

A

aPTT (activated partial thromboplastin time): evaluates clotting (same mechanism as PT/INR - number of seconds taken for a clot to form after reagents are added)

81
Q

What lab test should we use to monitor a patient taking LMWHs (low molecular weight heparins)?

A

Anti Factor Xa levels: measures plasma drug levels

82
Q

What is the mechanism of action of thrombolytics?

A

Promotes dissolution of the fibrin by converting plasminogen (inactive) to plasmin (active)

83
Q

Which drug is considered a thrombolytic?

A

tPA (tissue plasminogen activator) - Alteplase, Reteplase

84
Q

Which 2 drug classes do we use for an acute atherosclerosis-related event?

A
  1. Antiplatelets (ASA in adults, Plavix in children)

2. Thromolytics (tPA)

85
Q

Which drug class would we use for a patient who is at high risk for clotting (ex: due to dysrhythmias, complex surgeries, or a severe MI)?

A

Anticoagulants.

86
Q

Which drug class would we use for routine prevention of clotting?

A

Antiplatelets (specifically baby ASA).

87
Q

Which of the atherosclerosis drugs is also used to treat atrial fibrillation patients?

A

Warfarin (Coumadin)

N216 A/B (26 decks)

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