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CPR2 Exam 1 > Drugs For Stable Angina And Vasospastic Angina - Dr. Konorev > Flashcards

Drugs For Stable Angina And Vasospastic Angina - Dr. Konorev Flashcards

1
Q

4 drugs used for stable and vasospastic angina

A
  1. Nitrates
  2. CCB
  3. B-Blockers
  4. Ranolazine
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2
Q

stable angina

A

occlusion of coronary artery not complete, from atherosclerotic plaque
SX during stress+exertion

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3
Q

Vasospastic angina

A

vasosconstiction episodes in coronary arteries
= genetic
= SX at rest

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4
Q

if a drug lowers O2 demand in the body what does it do

A

lowers CO

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5
Q

how to increase or restore coronary BF in stable angina

A
  1. coronary artery bypass grafting
  2. Percutaneous coronary intervention (PCI)
  3. Stent : expandable tube used as scaffolding to keep vessel open
    = drugs dont help**
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6
Q

when do coronary arteries have the most BF

A

during diastole

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7
Q

drugs for decrease O2 demand do what during stable angina

A

prevent high HR (when systole increase and diastole shortens = lower BF)

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7
Q

drugs for decrease O2 demand do what during stable angina

A

prevent high HR (when systole increase and diastole shortens = lower BF)

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8
Q

phenotolamine does what

A

vasodilates BV causing tachycardia = decrease BF in coronary arteries not good for stable angina

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9
Q

3 Nitrates drugs for stable angina

A
  1. Nitroglycerine
  2. Isosorbide dinitrate
  3. Isosorbide mononitrate
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10
Q

nitrates delivered how

A

metabolized by liver fast

= so skin, subQ, spray, cream, patch

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11
Q

Nitrates Drugs do what MOA

A

vasodilation = making NO in endothelial cells

  1. Guanylyl cyclase activated
  2. PKG activated
  3. Myosin-LC Dephosphorylation —-> SM relaxation
  4. K+ channels open = hyperrepolarization, reducing Ca+ entry = relaxes SM
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12
Q

Nitrate Drugs actions

A
  1. venous dilatin
  2. reduce preload
  3. lower O2 demand
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13
Q

Nitrates drugs tolorance happens how

A
  1. depletion thiol needed
  2. superoxide radicals bind to it and use it up
  3. salt and water retention due to the lower BP
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14
Q

short acting vs long acting nitrate drugs in preventing attack

A

All are long acting and short acting except Isosorbide mononitrate is only long-acing
= LONG usually oral instead of spray , sublingual,

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15
Q

adverse effects of nitrate drugs

A
  1. headache
  2. orthostatic hypotension
  3. tachy, increases contractility and sympathetic side effect
  4. Na + and H2O reabsorption
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16
Q

nitrates are also used to tx, drug interaction

A

erectile dysfunction

= should not be given with already drugs for this, can cause deadly hypotension , acute MI

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17
Q

2 types of CCB

A
  1. Non-cardioactive (dihydropyridines)

2. Cardioactive (non-dihydropyridines)

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18
Q

Non-cardioactive (dihydropyridines) 3

A
  1. amlodipine
  2. Nifedipine
  3. Nicardipine
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19
Q

Cardioactive (non-dihydropyridines) 2

A
  1. Diltiazem

2. Verapamil

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20
Q

CCB MOA

A
  1. lower Ca+2 entering the cell
  2. lower activation of MLCK (myosin light chain kinase)
  3. lowering contraction of SM
    ==== decrease O2 demand
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21
Q

dihydropyridines act where

A

non-cardiogenic

= vascular SM

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22
Q

(non-dihydropyridines) Cardioacitve act where

A
  1. vascular SM
  2. cardiac SM
  3. Cardiac Pacemaker
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23
Q

CCB adverse effects major

A
  1. brady
  2. cardiac depression
  3. severe hypo
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24
Q

CCB adverse effects minor

A

flushing, headache, anorexia, dizzy, edema peripheral, C

25
Q

what can diltiazem do and not nifedipine

26
Q

B-blockers for stable angina 4

A
  1. Propranolol
  2. Nadolol
  3. Metoprolol
  4. Atenolol
27
Q

B- Blockes MOA

A
  1. inhibit B1 R
  2. decrease HR + decrease BP and contractility
    ==== decrease O2 demand
28
Q

B- Blockers adverse effects

A

MAJOR : low CO, bronchoconstriction, low glucose mobilization in liver, high VLDL, low HDL

29
Q

B blockers contraindicated for

A

asthma
T1D
arrhythmia in brady
AV conducition problem

30
Q

Ranolazine MOA

A

inhibits LATE Na+ into the cardiomyocytes (during rapid repolarization)
1. cell relies on Na+/Ca to get Na into cell releasing Ca+ into ICM**

31
Q

Ranolazine effects

A

vasodilates and reduce diastolic tensino and lower contractility
= NO effect on HR
= used when other meds didnt work

32
Q

steps in drugs given for stable angina

A
  1. asprin
  2. if several attacks
    give nitrates
  3. then give other drugs like BB, CCB, long acting nitrate and combination of this
  4. surgery (CABG)
33
Q

undesirable effects of nitrates 2

A

reflex :

increase HR, increase contractility

34
Q

undesirable effects of BB or CCB 2

A

reflex :
increase End Diastolic Volume (EDV)
increase Ejection time

35
Q

Vasospastic angina drugs used

A

vasodilate to increase BF
= CCB** (diltiazem, amlodipine)
= if pt has hypo, brady, AV block : use nitrates

36
Q

2 drug classes for acute coronary syndrome

A
  1. Antiplatelet drug

2. Thrombolytic (fibrinolytic) drugs

37
Q

antiplatelet drugs 3 types

A
  1. Inhibit of thromboxane A2 synthesis
  2. ADP Receptor Blockers (P2Y12 R B)
  3. Platelet glycoprotein receptor blocker
38
Q

Thrombolytic (fibrinolytic) drugs 3 classes

A
  1. Tissue - type Plasminogen Activator drugs

2. Streptokinase preparation

39
Q

red thrombus vs white thrombus

A

RED: fibrin rich + RBCs, low pressure V,

WHITE : plt rich, high P A, acute coronary syndrome

40
Q

drug to prevent clots in A

A

anti-plt drugs (white thrombus)

41
Q

drug to prevent clot in veins

A

Anti-coags (Red thrombi)

42
Q

drug to re-establish BF through BV once clots have formed

A

thrombolytics = destroy blood clots after formed

= INHIBIT FIBRIN

43
Q

Inhibitor of thromboxane A2 synthesis drug

A

Aspirin (anti-plt)

44
Q

P2Y12 (ADP) R Blocker 3 of them

A

Anti- Plt

  1. Clopidogrel
  2. Prasugrel
  3. Ticagrelor
45
Q

Plt glycogen R Blocker 3

A

Anti-plt

  1. Abciximab
  2. Eptifibatide
  3. Tirofiban
46
Q

Aspirin MOA

A

irreverible acytylation inhibition of COX 1 and 2 (cyclooxygenase) = no TxA2 (thromboxane) production —-> no plt aggregation

47
Q

aspirin used for

A
  1. acute coronary events immediate drug, + P212 Blocker with it
  2. prevention of coronary event (low dose)
48
Q

P2Y12 R Blocker MOA

A
  1. cAMP prevents plt aggregation
  2. ADP CANT activate P2Y12 R
    = usually this R inhibits adenylyl cyclase and lower cAMP
49
Q

Clopidogrel resistance

A

a type of P2Y12 B
= from CYP2C19**
= common to be non-functional in chinese (50%) and high in AA

50
Q

P2Y12 R B use

A
  1. acute coronary event with aspirin
  2. pts with aspirin hypersensitivity
  3. prevention of coronary event
51
Q

Glycoprotein IIB/IIIA Inhibitors MOA

A
  1. BLOCKS an integrin that binds to fibrinogen, vWF

2. so prevents this trigger of plt aggregation

52
Q

Glycoprotein IIB/IIIA Inhibitors clinical use

A

high risk pts during PCI

53
Q

Glycoprotein IIB/IIIA Inhibitors adverse effects

A

bleeding esp CKD

thrombocytopenia (most in abciximab)

54
Q

Tissue - type plasminogen activator drugs 3

A
  1. Alteplase
  2. Reteplase
  3. Tenecteplase
55
Q

Tissue - type plasminogen activator MOA

A
  1. induce fibrinolysis
  2. converts plasminogen to plasmin
  3. streptokinase binding to plasminogen
56
Q

streptokinase

A

streptokinase from bacteria binds to plasminogen activating it

57
Q

Tissue - type plasminogen activator

A

alteplase and reteplase and tenecteplase are human t-PA serine proteases cleaving plasminogen to plasmin

58
Q

Tissue - type plasminogen activator and streptokinase clinical use

A
  1. when PCI cant be performed in timely manner

2. STEMI within 12hr (Sometimes NSTEMI)

59
Q

PCI means what

A

percutaneous coronary intervention

CPR2 Exam 1 (19 decks)

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