Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CVPR > CVPR Cardiovascular pharmacology 3 > Flashcards

CVPR Cardiovascular pharmacology 3 Flashcards

(67 cards)

Start Studying
1
Q

Adverse effects of Niacin

A

Red flushed face which is ↓ by NSAIDs or long-term use Hyperglycemia Hyperuricemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Hyperuricemia?

A

Excess uric acid in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PCSK9 inhibitors effect on LDL

A

↓↓↓

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PCSK9 inhibitors effect on HDL

A

↑

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

PCSK9 inhibitors effect on triglycerides

A

↓

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

PCSK9 inhibitors MOA

A
  • Inactivation of LDL-receptor degradation
  • Increasing amount of LDL removed from bloodstream
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Adverse effects of PCSK9 inhibitors

A
  • Myalgias
  • Delirium
  • Dementia
  • Other neurocognitive effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Examples of PCSK9 inhibitors

A
  • Alirocumab
  • Evolocumab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cardiac glycosides

A

Digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Digoxin MOA

A

Direct inhibition of Na/K ATPase → indirect inhibition of Na/Ca exchanger ↑[Ca] → (+) ionotropy

Stimulates vagus nerve → ↓ HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical use of Digoxin

A
  • HF (↑ contractility)
  • Atrial fibrillation (↓ conduction at AV node and depression of SA node)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Adverse effects of digoxin

A

Cholinergic: NVD Blurry yellow vision (think Van Gogh) Arrhythmias AV block Can lead to hyperkalemia which is a poor prognostic indicator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Factors predisposing to Digoxin toxicity

A
  • Renal failure (↓ excretion)
  • Hypokalemia (permissive for Digoxin binding at K-binding site on Na/K/ATPase)
  • Drugs that displace digoxin from tissue-binding sites ↓ clearance (eg verapamil, amiodarone and quinidine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Antidote to Digoxin

A

Slowly normal K Cardiac pacer Anti-digoxin Fab fragments Mg2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Digoxin diagram

A

314

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Class I sodium channel blockers

A

Slow or block (↓) conduction (especially in depolarized cells) ↓ slope of phase 0 depolarization Are state dependent (selectively depress tissue that is frequently depolarized [tachycardia]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Antiarrhythmics Class IA

A

Quinidine Procainamide Disopyramide “The Queen Proclaims Diso’s pyramid”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Class IA Antiarrhythmics MOA

A

Sodium channel blockers ↑ AP duration ↑ effective refractory period (ERP) in ventricular action potential ↑ QT interval Some potassium channel blocking effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical uses of Class IA Antiarrhythmics

A

Both atrial and ventricular arrhythmias Especially re-entrant and ectopic SVT and VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Adverse effects of Class IA Antiarrhythmics

5 listed

A
  • Cinchonism (headache, tinnitus with quinidine)
  • Reversible SLE-like syndrome (procainamide)
  • HF (disopyramide)
  • Thrombocytopenia
  • Torsades du Pointes due to ↑ QT interval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Class IA Antiarrhythmics AP effects

A

Pg 315

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Class IB Antiarrhythmics mnemonic

A

Lidocaine MexileTine I’d buy Liddy’s Mexican Tacos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Class IB Antiarrhythmics MOA

A
  • ↓AP duration
  • Preferentially affect ischemic or depolarized Purkinje and ventricular tissue
  • Phenytoin can also fall into the IB category
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Phenytoin Class of Antiarrhythmics

A

Can also fall into the IB category

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Clinical uses of Class IB Antiarrhythmics
* Acute ventricular arrhythmias (especially post-MI) * Digitalis-induced arrhythmias * IB- is Best post-MI
26
Adverse effects of Class IB Antiarrhythmics
* CNS * stimulation/depression * Cardiovascular depression
27
Class IB Antiarrhythmics AP
315
28
Class IC Antiarrhythmics Mnemonic
Class IC Flecainide Propafenone Can I have Fries, Please
29
Class IC Antiarrhythmics MOA
* Significantly prolongs ERP in AV node and accessory bypass tracts * No effect on ERP in Purkinje and ventricular tissue * Minimal effect on AP duration
30
Clinical use of Class IC Antiarrhythmics
* SVTs (including atrial fibrillation) * Only as a **last resort in refractory VT**
31
Adverse effects of Class IC Antiarrhythmics
* Proarrhythmic, especially Post-MI (contraindicated) * Class IC is Contraindicated in structural and ischemic heart disease
32
Class IC Antiarrhythmics contraindicated in?
* Proarrhythmic, especially post-MI (contraindicated) * IC is Contraindicated in structural and ischemic heart disease
33
Class IC Antiarrhythmics AP
315
34
Class II Antiarrhythmics and examples
**_β-blockers_** Metoprolol Propranolol Esmolol Atenolol Timolol Carvedilol
35
Class II Antiarrhythmics MOA
* Decrease SA and AV nodal activity by ↓ cAMP which ↓Ca currents * Suppress abnormal pacemakers by ↓ slope of phase 4 AV node is particularly sensitive - ↑PR interval
36
Esmolol duration of action
Very short acting
37
Very short acting β-blockers
Esmolol
38
Class II Antiarrhythmics affinity
AV node is particularly sensitive - ↑PR interval
39
Class II Antiarrhythmics AP
316
40
Class II Antiarrhythmics Clinical uses
* SVT * Ventricular rate control for atrial fibrillation and atrial flutter
41
Adverse effects of Class II Antiarrhythmics
* Impotence * Exacerbation of COPD and asthma * Cardiovascular effects (Bradycardia, AV block, HF) * CNS effects (sedation, sleep alterations) * May mask the signs of hypoglycemia (caution in diabetes) * Metoprolol can cause dyslipidemia * Propranolol can exacerbate vasospasm in Prinzmetal angina * β-blockers (except non-selective α- and β-antagonists carvedilol and labetalol) cause unopposed α1 agonism if given alone for pheochromocytoma or cocaine toxicity
42
Treatment of β-blocker OD
* Saline * Atropine * Glucagon
43
Class III Antiarrhythmics Mnemonic and main action
Potassium channel blockers **AIDS** * Amiodarone * Ibutilide * Dofetilide * Sotalol
44
Class III Antiarrhythmics MOA
* ↑AP duration * ↑ERP * ↑QT interval
45
Class III Antiarrhythmics AP
316
46
Clinical use of Class III Antiarrhythmics
* Atrial fibrillation * Atrial flutter * Ventricular tachycardia (amiodarone, sotalol)
47
Adverse effects of Class III Antiarrhythmics
Sotalol - torsades de pointes, excessive β-blockade Ibutilide - torsades de pointes Amiodarone - pulmonary fibrosis, hepatotoxicity, hypothyroidism or hyperthyroidism (amiodarone is 40% iodine by weight) acts as a hapten (corneal deposits, blue/gray skin deposits resulting in photodermatitis), neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, HF)
48
Considerations when using amiodarone?
Remember to check PFTs, LFTs and TFTs when using amiodarone Amiodarone is lipophilic and has class I, II, III and IV effects
49
Class IV Antiarrhythmics main action and examples
Ca channel blockers Verapamil Diltiazem
50
Class IV Antiarrhythmics MOA
↓ conduction velocity ↑ ERP ↑ PR interval
51
Clinical uses of Class IV Antiarrhythmics
* Prevention of nodal arrhythmias (eg SVT) * Rate control in atrial fibrillation
52
Adverse effects of Class IV Antiarrhythmics
Constipation Flushing Edema Cardiovascular effects (HF, AV block, sinus node depression)
53
Class IV Antiarrhythmics AP
317
54
Other antiarrhythmics
* Adenosine * Mg2+
55
Adenosine as an antiarrhythmic
↑K efflux out of cells → hyperpolarizing the cell and ↓ Ica, ↓AV node conduction
56
Adenosine clinical uses for antiarrhythmia
Drug of choice in diagnosin/terminating certain forms of SVT
57
Adenosine duration of action
Very short acting (≈ 15 seconds)
58
Adenosine effects are blunted by?
Caffeine and theophylline (both are adenosine receptor antagonists)
59
Adverse effects of adenosine
* Flushing * Hypotension * Chest pain * Sense of impending doom * Bronchospasm
60
Mg2+ as an antiarrhythmic
Effective in torsades de pointes and digoxin toxicity
61
Ivabradine MOA
Selective inhibition of funny Na channels (If) prolonging slow depolarization phase 4 ↓ SA node firing: Negative chronotropic effect without ionotropy Reduces cardiac O2 requirement
62
Clinical uses of Ivabradine
* Chronic stable angina in patients who cannot take β-blockers * Chronic HF with reduced Ejection fraction
63
Adverse effects of Ivabradine
Luminous phenomena/visual brightness HTN bradycardia
64
Adverse effects of quinidine
Cinchonism (headache, tinnitus with quinidine)
65
Adverse effects of procainamide
Reversible SLE-like syndrome (procainamide)
66
Adverse effects of disopyramide
HF (disopyramide)
67
Digoxin drug interactions
* verapamil * amiodarone * quinidine

CVPR (93 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions