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Winter P2 > Exam 2 - Medchem 753, Stevens Inotropics > Flashcards

Exam 2 - Medchem 753, Stevens Inotropics Flashcards

1
Q

What effects are seen during cardiac failure?

A 
Inability of heart to pump blood effectively
- Force of contraction of Cardiac Muscle
 - dec CO; dec BP; Dec Renal Q
Edema in legs/Lungs
Renal failure
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2
Q

What is the action of all positive Inotropes?

A

They affect the availability of intracellular Ca or inc sensitivity of contractile proteins

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3
Q

What is the basic action of cardiac steroids?

A

inhibit the Na/K ATPase

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4
Q

What is the basic action of Phospodiesterase inhibitors?

A

Block cAMP degradation

  • inc [cAMP]; activating cAMP dependent protein kinases
  • stimulate Ca influx through VG channels,
  • inc release and reaccumulation of CA in SR
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5
Q

What is the basic action of Ca2+ sensitivity stimulants

A

Inc the effect of existing Ca2+ levels

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6
Q

What is the basic action of B-adrenergic agonists?

A

Leads to inc cAMP production, more forceful contractions due to inc calcium presence

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7
Q

How are cardiac steroids different from other average steroids?

A

They are characterized by their 5B, 14B stereochemistry, which results in a curved, or convexely shaped molecule

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8
Q

What are the 2 different groups of cardiac steroids?

A
  1. Cardenolides

2. Bufadienolides

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9
Q

Cardenolides

  1. Origin
  2. Chemical structure
A
  1. Plant Origin

2. C-17R group is an alpha-B-unsaturated butyrolactone

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10
Q

Bufadienolides

  1. Origin
  2. Chemical structure
A
  1. Found in Toad Skin

2. C-17R group is a Pyrrone Ring

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11
Q

Most cardiac sterols naturally occur as ______ and have approximately ______ sugars attached where?

A

Glycosides
1-4 sugars
3B-OH of steroid

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12
Q

Digitalis Purpurea

A

Flox Glove (purple), it is the commercial source of digitoxin

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13
Q

Digitalis lanata

A

Woolly foxglove (white) commercial source of digoxin

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14
Q

in 1785, Digitalis leaves were used to treat several things including swelling. What were some remarkable side effects of the drug?

A

Yellow Vision

Nausea

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15
Q

What kept most physicians from using digitalis preparations until the 1900s?

A

Narrow therapeutic index

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16
Q

What site difference between digitoxigenin, Digoxigenin and Gitoxigenin makes the large pharmacological difference in their chemistry?

A

12-OH (Digoxin)
12-H (Digitoxin)
16-OH (gitoxigenin); pharmaceutically irrevelevant

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17
Q

What is the main cardiac glycoside found in Digitalis Lanata leaves?

A

Lanatoside C

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18
Q

How is Digoxin extracted from Digitalis leaves?

A

Lantoside C is treated w/ Bglucosidase, to form acetyldigoxin, which is then treated with NaOH and neutrialized with Ch3COOH to become digoxin

19
Q

Inhibition of Na/K-ATPase has what effect on calcium levels?

A

Increased intracellular Na levels –> increased release of Ca from intracellular stores

20
Q

Why is simultaneous treatment of Lasix and Digoxin dangerous?

A

Lasix lowers extracellular K levels, which increases phosphorylation and eventually the binding affinity of Digoxin

21
Q

What is the result of coadministration of Digoxin and Erythromycin?

A

Erythromycin kills microbes that would otherwise help metabolize orally available digoxin, increasing the amount of Digoxin available.

22
Q

What neuro-hormonal effect does Digoxin have in CHF patients?

A 
Inc Parasympathetic (vagal activation)
and decreased sympathetic activity
23
Q

What is the preferred cardiac glycoside for CHF?

A

Digoxin

24
Q

What is the metabolism for Digoxin?

A

minimal (80% unchanged) Hepatic Metabolism by:

  • Hydrolysis
  • Sulfation
  • Glucuronidation
25
Q

What result would be seen from Quinidine coadminstration with Digoxin?

A

Increased plasma levels of Digoxin

26
Q

What result would be seen with coadminstration of Verapamil and Digoxin

A

Increased absorption of Digoxin

Verapamil inhibits intestinal pgp efflux of digoxin

27
Q

What result would be seen with coadministration of Rifampin and Digoxin

A

Decreased absorption of Digoxin

Rifampin induces intestinal pgp efflux expression

28
Q

What would the results of coadministration of Bile Acid binding resins such as Cholestryamine and Digoxin be?

A

Decreased Digoxin Absorption

29
Q

What is the plasma protein binding, onset, and 1/2 life for Digoxin?

A

PPB - 30%
Onset - 15-30min
T1/2 - 1-2 days

30
Q

What is the plasma protein binding, onset and 1/2 life for digitoxin?

A

PPB - ~95%
onset - 05-2hrs
T1/2 - 4-7 days

31
Q

What are the primary problems and side effects of Cardiac Glycosides?

A

Narrow Therapeutic WIndow

SE: Loss of appetite, blurred vision, GI distress, potentially proarrhythmmic (Afib, Vtach, MI)

32
Q

How would you treat acute toxicity of Digoxin?

A

Digibind (digoxin immune Fab)

33
Q

What are the disappointing results of most PDE inhibitors?

A

Inc Mortality rates
Inc Incidence of arrhythmias
Causes tachycardia
Loss of positive inotropic effect w/ chronic use

34
Q

When are PDE3 inhibitors used for CHF?

A

Acute CHF

35
Q

Why was amrinone renamed in the year 2000?

A

Was confused with Amiodarone, which led to some fatal medication errors

36
Q

What is the difference in naming between PDE3 inhibitors and PDE5 inhibitors?

A

PDE3 - ends in ‘one’

PDE5 - ends in ‘fil’

37
Q

Inamrinone

  1. Class, indication
  2. Metabolism/T1/2
  3. SE
  4. Formulations
A
  1. PDE3 inhibitor, Acute CHF
  2. 3-4hrs, mainly excreted unchanged in urine
  3. Thrombocytopenia (10%)
  4. Short term IV
38
Q

Milrinone

  1. Class, Indication
  2. Metabolism/T1/2
  3. SE
  4. Formulation
A
  1. PDE3 inhibitor, Acute CHF
  2. 30-60min, Mainly excreted unchanged in urine
  3. Fewer side effects than Inamrinone
  4. Lactate for IV
39
Q

MoA for Ca sensitizing agents

A

Increase contractility by binding the N-terminus of troponin C and stabilizing the Ca-bound conformation.
Activation of ATP-regulated K channels and cause vasodilation in vascular smooth muscle.

40
Q

Levosimendan

  1. Class/Indication
  2. Formulations
A
  1. Calcium sensitizing agent, CHF

2. IV formulation for Acute CHF

41
Q

B-adrenergic agent for treatment of CHF

A

Dobutamine

42
Q

Dobutamine Racemate actions results in what overall effect?

A

In vasculature, A1 agonist negated by A1-antagonist (no vasodilation)
Overall: B1 effect: increased stroke volume and little increase in HR.

43
Q

Dobutamine Administration and Availbility

A

T1/2 ~2min
Only active
Rapid first pass COMT
(Wrap IV bags in aluminum to prevent oxidation to ortho-quinone)

Winter P2 (6 decks)

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