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Step 1 > Cardio Pharmacology > Flashcards

Cardio Pharmacology Flashcards

memories those meds

1
Q

What are the classes of Calcium channel blockers

A

Dihydropyridines (All the divines) and non-Dihydropyridines (Diltiazem and Verapimil)

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2
Q

Whats the mechanism of action of Ca channel blockers

A

Block voltage dependent L-type calcium channels of Cardiac (non-dihydropyridines) and Smooth muscles(Dihydropyridines).

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3
Q

Uses of Calcium Channel blockers by class

A

Dihydropyridines (except nimodipine): HTN, Angina, and Raynauds
Nicardipine and Clevidipine: HTN urgency and emergency
Non-Dihydro: HTN, Angina, A.fib/flutter. Verap in Migraine prophylaxis

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4
Q

Which Ca channel blocker is used in Pregnancy and postpartum

A

Nifidipine

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5
Q

Side effects of Ca channel blockers by class

A

Non-Dihydropyridines: Cardiac depression, AV block, Bradycardia, Hyperprolactinemia, constipation, gingival hyperplasia
Dihydropyridines: Oedema, flushing dizziness, reflex tachycardia

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6
Q

Which Ca channel blockers exacerbates MI

A

Nifidipine due to reflex tachycardia, avoid in Angina its

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7
Q

Uses of Nimodipine

A

used in Subarachnoid hemorrhage (prevents cerebral vasospasm)

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8
Q

Mechanism of action of Hydralazine

A

Increases cGMP which leads to smooth muscle relaxation, vasodilates arterioles more than veins
Causes afterload reduction

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9
Q

Uses of Hydralazine

A

Severe HTN (Acute), HF, safe in pregnancy

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10
Q

Side effects of Hydralazine

A

Excacerbates MI due to compensatory tachycardia, fluid retention, headache, SLE like syndrome

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11
Q

Fenoldepam Mechanism of action

A

Its a Dopamine D1 receptor agonist. causes coronary, peripheral, renal and splanchnic vasodilation.
Reduces BP and causes increased natriuresis

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12
Q

Uses of Fenoldepam

A

Post-op as an anti-HTN

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13
Q

Side effects of Fenoldepam

A

Hypotension and tachycardia

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14
Q

Nitroprusside mechanism of action

A

Increases cGMP via direct release of NO, can cause Cyanide toxicity

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15
Q

Uses of Nitroprusside

A

Hypertensive emergency

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16
Q

Nitrates Mechanism of action

A

Vasodilate by increasing NO in vascular smooth muscles, which leads to increase in cGMP and smooth muscle relaxation
Dilates Veins more than arteries
Reduce end-diastolic volume (PRELOAD), ejection time, MVO2
increases HR (reflex response)

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17
Q

Uses of Nitrates

A

ACS, Angina, and pulmonary oedema

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18
Q

Side effects of Nitrates

A 
REFLEX TACHYCARDIA (treat with B-blockers)
HYPOTENSION
FLUSHING
HEADACHE
MONDATY DISEASE
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19
Q

Contraindications of Nitrates

A

Right ventricular infarction & Hypertrophic CM

Absolute contraindication with Sildenafil

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20
Q

Why does oral Isosorbide Dinitrate requires higher doses than sublingual nitrate

A

absorbed via GI tract and undergoes extensive first pass metabolism in the liver prior to release in circulation, leading to low bioavailability

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21
Q

What are the determinants of MVO2 (Myocardial Oxygen consumption)?

A

End-diastolic volume
BP
HR
Contractility

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22
Q

Ranolazine mechanism of action

A

Reduces diastolic wall tension and oxygen consumption by inhibiting late phase of sodium current

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23
Q

Ranolazine Uses

A

Refractory Angina

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24
Q

Milrinone Mechanism of action

A

Selective PDE-3 inhibitor
In cardiomyocytes: Increas cAMP accumulation –> high Ca–> +ve Inotropy and chronotrop
In vascular smooth muscles: increase cAMP –> inhibition of MLCK activity–>general vasodilation

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25
Q

Uses of milrinone

A

Acute decompensated HF (short-term)

26
Q

Side effects of Milrinone

A

Hypotension, arrhythmias

27
Q

Digoxin Mechanism of action

A

Cardiac glycoside, inhibits NA/K ATPase exchanger, and also indirect inhibitor of Na /Ca exchanger Leading to higher Ca–> Positive Inotropy
Stimulates vagus nerve (parasympathetic ganglionic transmission) –> lower HR

28
Q

Uses of Digoxin

A

A.fib/flutter (reduces conduction at AV node and depression of SA node) HF (increases contractility)

29
Q

Side effects of Digoxin

A
  • Cholinergic–Nausea, vomiting, diarrhea, blurry yellow vision, arrhythmias, AV block
  • Hyperkalaemia
30
Q

Factors that predispose to Digoxin Toxicity

A
  • Renal failure (low excretion)
  • Hyokalemia
  • Drugs: Verapimil, Amiodarone, Quinidine)
31
Q

Antidote for Digoxin Toxicity

A

Digi-Fab fragments, Cardiac pacer, MG, slowly normalize K levels

32
Q

Negative Chronotropic Medications

A
  1. B-blockers
  2. Non-Dihydropyridine Ca-channel blockers
  3. Digoxin
  4. Amiodarone & Sotalol
  5. Cholinergic Agonists (Pilocarpine, Rivastigmine)
33
Q

Class I Anti-Arrhythmic Mechanism of action

A

Na- channel blockers:

  • Slow/block conduction (depolarized cells)
  • Lower slope of Phase 0 in myo. AP
  • State dependent (selectively depress tissue that is frequently depolarized, eg. tachycardia)
34
Q

Class IA Anti-arrhythmic names

A

Quinidine, Procainamide, Dysopyramide

35
Q

Class IA Anti-arrhythmic Mechanism of action

A 
Prolongs AP duration
Prolongs ERP
Prolongs QT interval
(similar to class III actions)
36
Q

Class IA Anti-arrhythmic Uses

A

Atrial and Ventricular arrhythmias specially SVT & VT

37
Q

Class IA Anti-arrhythmic Side effects

A 
Torsades de pointes due to prolonged QT
Cinchonism with Quinidine
Reversible SLE-like syndrome with Procainaide
HF with Disopyramide
Thrombocytopenia
38
Q

Class IB Anti-arrhythmic names

A

Lidocaine, Mexiletine (+Phenytoin)

39
Q

Class IB Anti-arrhythmic Mechanism of action

A

Decreases AP duration (sp in ischemic or depolarized purkinje and ventricular tissue)

40
Q

Class IB Uses

A

Arrhythmias (post-MI), Digoxin induced arrhythmia

41
Q

Class IB side effects

A

CNS stimulation/depression, cvs depression

42
Q

Class IC Anti-arrhythmic names

A

Flecainide, propafenone

43
Q

Class IC Anti-arrhythmic mechanism of action

A

Prolongs ERP in AV node and accessory bypass tracts
Minimal effect on AP duration
Prolongs QRS in a rate dependent manner (tachycardia)

44
Q

Class IC anti-arrhythmic Uses

A

SVTS, VT (last resort)

45
Q

Class IC anti-arrhythmics side effects

A

Proarrhythmic specially post MI (CI)

CI with structural heart disease

46
Q

Class II Anti-arrhthmics names

A

Beta-blockers:

Metoprolol, Carvidelol, Labetolol, Esmolol, Atenolol, Timolol, Propranolol

47
Q

Class II Anti-Arrhythmics mechanism of action

A

Decrease SA and AV nodal activity by decreasing cAMP –> decreasing Ca currents.
Suppress abnormal pacemakers by decreasing slope of PHASE 4
AV node is more sensitive–> increased PR interval

48
Q

Class II Anti-arrhthmics Uses

A

SVT, rate control in fib/flutter

49
Q

Class II Anti-Arrhythmias Side effects

A

Impotence, exacerbation of COPD and asthma, CVS effects are bradycardia and AV block and HF
CNS effects: sedation and sleep alteration. may mask signs of hypoglycemia
Metoprolol- dyslipidemia
Propranolol-exacerbates vasospasm in Prinzmetal angina

50
Q

Class III Anti-arrhythmics names

A 
K-channel blockers: AIDS
Amiodarone
Ibutilide
Dofetilide
Sotalol
51
Q

Class III Anti-arrhythmics Mechanism of action

A 
Prolongs AP duration
Prolongs ERP
Prolongs QT interval 
(similar to class IA actions)
works on phase 3 in myo AP
52
Q

Class III Anti-arrhythmics Uses

A

Afib/flutter, VT (A & S)

53
Q

Class III Anti-arrhythmics Side effects

A

Sotalol & Ibutilide: Torsades de pointes
Amiodarone: Pulmonary fibrosis, hypo or hyperthyroidism, hepatotoxicity, corneal deposits, blue/grey skin and photo dermatitis, neurologic effects, constipation, cvs (bradycardia, heart block, HF)

54
Q

Class IV Anti-arrhythmics names

A

non-dihydropyridines- Diltiazem & Verapimil

55
Q

Class IV Anti-arrhythmics Mechanism of action

A

Decreases conduction velocity
Prolongs ERP
Prolongs PR interval
PHASES 4 & 0 in PM

56
Q

Class IV Anti-arrhythmics uses

A

prevention of SVT, rate control in afib

57
Q

Class IV Anti-arrhythmics side effects

A

cardiac (HF, AV block, SA depression)

constipation, flushing , oedema

58
Q

Adenosine mech of action

A

Increases K leaving the cell–>hyperolarizing the cell and reducing Ca influx–> AV node conduction

59
Q

Adenosine Uses

A

SVT (diagnosis and treatment)

60
Q

Adenosine Side effects

A

Chest pain, feeling of impending doom, flushing, hypotension, bronchospasm (contraindicated in asthma)

61
Q

Ivabradine mech of action

A

Selective inhibition of funny Sodium channels (If) prolonging depolarization phase (PHASE 4)

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