Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRAAB 3 > Nordgren: DRUGS- K and Ca channel blockers > Flashcards

Nordgren: DRUGS- K and Ca channel blockers Flashcards

1
Q

CE: Amiodarone

A

Prolong AP

*Also a NA channel blocker and weak blocker of Beta receptors and Ca channels > slows HR and AV node conduction (partial class 4 drug)

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

ECE: Amiodarone

A

Peripheral vasodilation

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

Toxicity: Amiodarone

A
  1. Bradycardia and heart block in pts w/ preexisting SA/AV node disease–> slow HR
  2. Drug accumulates in tissues
  3. Blocks peripheral conversion of T4 to T3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PK: Amiodarone

A

Stays in body and has effects for up to 3 months.

Substrate for CYP3A4–> level of drug influenced by other drugs that might inhibit cyp3A4.

Amiodarone also inhibits other p450s –> can lead to increased levels of statins, digoxin and warfarin

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

TU: Amiodarone

A
  1. Ventricular tachycardia (v. fib)

2. A. fibrillation and flutter

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

What is the most important adverse effect of amiodarone?

A

dose related PULMONARY TOXICITY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are other adverse effects of amiodarone?

A

Related to tissue accumulation:

  1. Abnormal liver function–> hypersensitivity hepatitis
  2. Skin deposits > photodermatitis, gray-blue skin discoloration in sun-exposed areas
  3. Corneal microdeposits (in nearly ALL patients), halos develop in peripheral visual fields, rarely optic neuritis leading to blindness
  4. Hypo- and Hyperthyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CE: Dofetilide

A
  1. Selective K channel blocker
  2. Prolongs AP
  3. Increase in QT interval (prolonged ERP in His-Purkinje system and ventricles)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Toxicity: Dofetilide

A

Life-threatening ventricular arrhythmias

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

PK: Dofetilide

A

100% bioavailable!

Hepatic metabolism via CYP3A4

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

TU: Dofetilide

A

Maintain/restore normal sinus rhythm in a. fib.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dofetilide is contraindicated in?

A

long QT, bradycardia, hypokalemia

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

CE: Ibutilide

A
  1. Prolongs AP

2. Slow inward Na activator> delays repolarization > inhibits Na channel inactivation > increases ERP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Toxicity: Ibutilide

A
  1. Excessive QT interval prolongation and torsades de pointes
  2. Can cause life-threatening ventricular arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PK: Ibutilide

A

Hepatic metabolism

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

TU: Ibutilide

A
  1. ACUTE conversion of a. flutter and a. fib to normal sinus rhythm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Is ibutilide more effective at treating flutter or fib?

A

Flutter.

The mean time to termination is 20 mins so it’s not good for chronic treatment.

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

CE: Verapamil

A

Blocks both activated and inactivated L type Ca channels

19
Q

Where does verapamil have it’s greatest effects?

A

In tissues that fire frequently, those less polarized, or nodal tissue.

20
Q

ECE: Verapamil

A

Peripheral vasodilation.

21
Q

Toxicity: Verapamil

A

AV block at large doses in pts w/ AV nodal disesase

22
Q

PK: Verapamil

A

Hepatic metabolism

23
Q

TU: Verapamil

A
  1. Supraventricular tachycardia

2. A. fib/flutter (reduces ventricular rate, not convert back to sinus rhythm)

24
Q

Verapamil is contraindicated for what disease?

A

Wolff parkinson white

25
Q

CE: Diltiazem

A

Similar to verapamil but w/ more smooth muscle-relaxing effect and produces less bradycardia.

26
Q

ECE: Diltiazem

A

k

27
Q

Toxicity: Diltiazem

A

k

28
Q

PK: Diltiazem

A

k

29
Q

TU: Diltiazem

A

k

30
Q

MOA: Adenosine

A

Activation of inward rectifier K channels and inhibition of L type Ca channels > hyperpolarization and suppression of Ca dependent AP (nodal tissue)

31
Q

What does Adenosine do to AV conduction and AV refractory period?

A

Suppresses AV conduction and INCREASES AV refractory period

32
Q

What is the drug of choice for conversion of paroxysmal supraventricular tachycardia but NOT a. flutter and fibrillation?

A

Adenosine

33
Q

What are the SE of adenosine?

A

Related to vasodilatory properties of the drug.

  1. flushing and HA
  2. Hypotension that can develop rapidly (reversed quickly if you stop drug)
  3. AV block
34
Q

How do methylxanthines relate to adenosine?

A

Methylxanthines (like caffeine), competitivley antagonize the binding of adenosine at its purinergic receptor

35
Q

Adenosine is contraindicated in patients with what condition?

A

2 and 3 AV block

36
Q

What is digitalis primarily used for?

A
  1. Heart failure (primarily)

2. Reducing ventricular rate when it is being driven by a high atrial rate (a. fib or flutter)

37
Q

What is the MOA of digitalis?

A
  1. Activation of vagal efferent nerves in the heart > reduces conduction in the AV node
  2. Inhibits Na/K/ATPase pump
38
Q

What effect does the inhibition of Na/K/ATPase pump have on cardiac cells?

A

Increaes the intracellular Na concentration > reverses action on Na/Ca exchanger > more Ca in the cell > improves cardiac contractility (Ca binds troponin)

39
Q

What is the net effect of increased contractility (d/t inhibition of Na/K/ATPase) have on HR?

A

Increased SV > increased Co> Decreased HR

40
Q

What does activation of vagal efferent nerves to the heart by digitalis do?

A

Reduces the conduction in the AV node > partial block > fewer impulses reach ventricles > ventricular rate falls

41
Q

How does a decrease in intracelluar K and an increase in intracellular Na contribute to afterpolarizations?

A

Contribute to the depolarization of RMP which contributes to afterdepolarizations at high doses.

42
Q

What are the SE of digitalis?

A
  1. Exterme AV block (contraindicated in pts who have it already)
  2. shouldn’t be used by pts w/ impaired renal function b/c it’s eliminated by hte kidenys
43
Q

Digitalis toxicity looks like what on an EKG?

A

Salvador Dali’s checkmark moustache

44
Q

What should you ask before you initiate antiarrhythmic therapy?

A
  1. Eliminate the cause if possible
  2. Make a firm diagnosis
  3. Determine the baseline condition
  4. Questions the need for therapy

CRAAB 3 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions