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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

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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
CCB adverse effects minor
flushing, headache, anorexia, dizzy, edema peripheral, C
25
what can diltiazem do and not nifedipine
slow HR
26
B-blockers for stable angina 4
1. Propranolol 2. Nadolol 3. Metoprolol 4. Atenolol
27
B- Blockes MOA
1. inhibit B1 R 2. decrease HR + decrease BP and contractility ==== decrease O2 demand
28
B- Blockers adverse effects
MAJOR : low CO, bronchoconstriction, low glucose mobilization in liver, high VLDL, low HDL
29
B blockers contraindicated for
asthma T1D arrhythmia in brady AV conducition problem
30
Ranolazine MOA
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
Ranolazine effects
vasodilates and reduce diastolic tensino and lower contractility = NO effect on HR = used when other meds didnt work
32
steps in drugs given for stable angina
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
undesirable effects of nitrates 2
reflex : | increase HR, increase contractility
34
undesirable effects of BB or CCB 2
reflex : increase End Diastolic Volume (EDV) increase Ejection time
35
Vasospastic angina drugs used
vasodilate to increase BF = CCB**** (diltiazem, amlodipine) = if pt has hypo, brady, AV block : use nitrates
36
2 drug classes for acute coronary syndrome
1. Antiplatelet drug | 2. Thrombolytic (fibrinolytic) drugs
37
antiplatelet drugs 3 types
1. Inhibit of thromboxane A2 synthesis 2. ADP Receptor Blockers (P2Y12 R B) 3. Platelet glycoprotein receptor blocker
38
Thrombolytic (fibrinolytic) drugs 3 classes
1. Tissue - type Plasminogen Activator drugs | 2. Streptokinase preparation
39
red thrombus vs white thrombus
RED: fibrin rich + RBCs, low pressure V, | WHITE : plt rich, high P A, acute coronary syndrome
40
drug to prevent clots in A
anti-plt drugs (white thrombus)
41
drug to prevent clot in veins
Anti-coags (Red thrombi)
42
drug to re-establish BF through BV once clots have formed
thrombolytics = destroy blood clots after formed | = INHIBIT FIBRIN
43
Inhibitor of thromboxane A2 synthesis drug
Aspirin (anti-plt)
44
P2Y12 (ADP) R Blocker 3 of them
Anti- Plt 1. Clopidogrel 2. Prasugrel 3. Ticagrelor
45
Plt glycogen R Blocker 3
Anti-plt 1. Abciximab 2. Eptifibatide 3. Tirofiban
46
Aspirin MOA
irreverible acytylation inhibition of COX 1 and 2 (cyclooxygenase) = no TxA2 (thromboxane) production ----> no plt aggregation
47
aspirin used for
1. acute coronary events immediate drug, + P212 Blocker with it 2. prevention of coronary event (low dose)
48
P2Y12 R Blocker MOA
1. cAMP prevents plt aggregation 2. ADP CANT activate P2Y12 R = usually this R inhibits adenylyl cyclase and lower cAMP
49
Clopidogrel resistance
a type of P2Y12 B = from CYP2C19**** = common to be non-functional in chinese (50%) and high in AA
50
P2Y12 R B use
1. acute coronary event with aspirin 2. pts with aspirin hypersensitivity 3. prevention of coronary event
51
Glycoprotein IIB/IIIA Inhibitors MOA
1. BLOCKS an integrin that binds to fibrinogen, vWF | 2. so prevents this trigger of plt aggregation
52
Glycoprotein IIB/IIIA Inhibitors clinical use
high risk pts during PCI
53
Glycoprotein IIB/IIIA Inhibitors adverse effects
bleeding esp CKD | thrombocytopenia (most in abciximab)
54
Tissue - type plasminogen activator drugs 3
1. Alteplase 2. Reteplase 3. Tenecteplase
55
Tissue - type plasminogen activator MOA
1. induce fibrinolysis 2. converts plasminogen to plasmin 3. streptokinase binding to plasminogen
56
streptokinase
streptokinase from bacteria binds to plasminogen activating it
57
Tissue - type plasminogen activator
alteplase and reteplase and tenecteplase are human t-PA serine proteases cleaving plasminogen to plasmin
58
Tissue - type plasminogen activator and streptokinase clinical use
1. when PCI cant be performed in timely manner | 2. STEMI within 12hr (Sometimes NSTEMI)
59
PCI means what
percutaneous coronary intervention

CPR2 Exam 1 (19 decks)

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