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Drug Action I > Block 2 - CHF Med Chem > Flashcards

Block 2 - CHF Med Chem Flashcards

1
Q

Describe what MAO metabolism is?

A

Primary amine → aldehyde

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2
Q

Describe what COMT metabolism is?

A

Metabolism of meta OH of catechol adding a methyl group

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3
Q

What receptors are found in arterioles? Response?

A

a1 and 2: Constriction

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4
Q

What receptors are found in the heart? Response?

A

b1: Increased rate and force

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5
Q

What is glycosides?

A

Molecules in which a sugar molecule is bound to another functional group (eg: steroid) by a glycosidic bond

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6
Q

The sugar portion of glycosides is called ___ while the non sugar is known as ___

A

Glycone; aglycone or genin

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7
Q

If they act on the heart they are referred to as _____

A

Cardiac glycosides

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8
Q

T or F: Aglycone is considered a steroid.

A

True: it has a steroid nucleus

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9
Q

How does digoxin differ from digitoxin? And how do it affect the PK properties?

A

Digoxigenin has an extra OH → More hydrophilic → lower absorption → Shorter half-life → Lower protein binding

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10
Q

What gives aglycone its U shape?

A

A-B and C-D are cis-fused, whereas B-C are trans-fused

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11
Q

Describe the SAR of aglycone?

A
  1. 2 methyl group at C-10 and 13
  2. Hydroxyl groups are present at C-3 and C-14
    • C-14 unsubstituted hydroxyl is necessary for cardiotonic activity
  4. Lactone ring at C-17 required and varies with source (usually 5-membered if from plants, 6-membered if from animals)
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12
Q

OH increases ______ and _____ half-life for algycones

A

Hypophilicity; shorter

Lowers absorption

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13
Q

Describe the SAR of glycone?

A
  1. C-3 of steroid linked to monosaccharide or polysaccharide
  2. O-acetyl groups on sugars affect PK/lipophilicity
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14
Q

What is the dual effect of glycosides?

A

Directly (on cardiac muscle and SA node, AV node and His-Purkinje system)

Indirectly (through autonomic nervous reflexes)

Dose-dependent

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15
Q

What electrophysiologic properties does glycosides change?

A
  1. Contractility
  2. HR
  3. Excitability
  4. Conductivity
  5. Refractory period
  6. Automaticity of atrium, ventricle, Purkinje fibers, AV node, and SA node
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16
Q

What is the MOA of cardioglycosides

A

Inhibits Na/K-ATPase pump:
→ Restores membrane potential to normal
→ Inhibit Na+ exchange with K+ → Increased intracellular Na+ → increased intracellular Ca2+
→ Increased Ca2+ → increase in contraction (positive inotropic)

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17
Q

What are examples of cardioglycosides?

A

Digoxin (Lanoxin)

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18
Q

What are the DDIs with digoxin? and why?

A

Digoxin is a substrate for P-gp therefore interacts with drugs that are substrates, inhibitors, and inducers of P-gp

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19
Q

Digoxin is considered toxic due to its ____ therapeutic window

A

Narrow

20
Q

What are the toxic ADRs associated with digoxin?

A
  1. High intracellular Ca levels
  2. Hypokalemia
  3. GI effects ventricular tachycardia, AV block → ventricular fibrillation → Give K+ salts
21
Q

What are the MOA of PDE3i? Common ADR?

A

Gs protein activation → formation of intracellular cAMP → increases Ca2+ → cardiac muscle contraction → relaxation is when cAMP is hydrolyzed by PDE3 → Inhibitor of PDE3 → increased cAMP

Ventricular arrhythmias

22
Q

____ is the suffix for PDE3is while ___ is the suffix for PDE5is

A

-ones; -fils

23
Q

Example of PDE3i?

A
  1. Inamrinone
  2. Milrinone
24
Q

What are ADRS associated with Inamrinone? Dosage form?

A
  1. Thrombocytopenia
  2. GI and liver impairments
25
Q

What are warnings associated with milrinone?

A
  1. Incompatible with Lassie → precipitation with milrinone lactate salts
26
Q

How does Ivabradine differ from other PDE3i?

A

Blocks the “funny” (If) current/channel from the SA node
1. NA-K inward current
2. Reduces cardiac pacemaker activity, slows heart rate
3. Decrease rate without reducing contractility

27
Q

Compare the PK properties of the 2?

A
28
Q

How does structure affect the PK property? How does it impact its counseling points

A

Complete oral absorption due to lipophilicity → food may slow absorption and increase plasma exposure

29
Q

What is shock?

A

Inadequate tissue perfusion associated with hypotension

30
Q

What do you treat shock with?

A

Want both a and b activity

31
Q

Why do we need both alpha and beta agonistism?

A

Only β agonist → increased blood flow but risk of myocardial ischemia

Only α agonist → increased blood pressure and vascular tone but can decrease cardiac output and impair tissue blood flow

32
Q

Differentiate NE from E?

A

NE: predominantly α but modest β effects → increased BP

E: all receptors but more β1 effects → Increased heart rate

33
Q

What is dopamine MOA?

A

B1 agonist: G protein signal transduction process → increases intracellular cAMP levels → increase in intracellular calcium

34
Q

Why do you rarely use dopamine for shock?

A

Acts on too many receptors including dopamine receptors → too many ADRS including arrhythmias

35
Q

How are catecholamines metabolized and how does it affect its availability in the body?

A

COMT and MAO → short DOA with no oral activity

36
Q

How does dobutamine differ from dopamine?

A

Metabolized only by COMT → IV push to avoid rapid first-pass metabolism

Catecholamine increases air oxidation → sodium bisulfate it used for stabilization

37
Q

Describe the activity of dobutamine mixtures?

A

S-(-) enantiomer = β1 agonist, α1-agonist
R-(-) enantiomer = Non-selective β agonist, α1-antagonist

Overall just β1 agonist

38
Q

What is the structure and MOA of nediritide? ADRs?

A

Synthetic BNP

Increase cGMP in smooth muscle cells, reduces venous and arteriolar tone

Excessive hypotension

39
Q

Why does nesiritide have a short half-life despite its size?

A
  1. Peptides is easily metabolized → low oral bioavailability
  2. BNP is already in the body → body recognize it and metabolize

Short half-life and should not be PO

40
Q

Describe the structure and activity of sacubitril?

A

Prodrug activated by by carboxyl esterase 1 (CES1) in the liver to sacubritrilat

41
Q

What is the MOA of sacubitril?

A

Inhibits the enzymeneprilysin

42
Q

What degrades BNP and ANP?

A

Endopeptidase

42
Q

What degrades BNP and ANP?

A

Endopeptidase

43
Q

What is Entresto?

A

Combination of sacubitril, the first-in-class neprilysin inhibitor, and the angiotensin II receptor blocker valsartan

44
Q

What is the MOA of SGLT2 inhibitors?

A
  1. No SGLT2 in heart
  2. Inhibition of glucose reuptake in kidney tubules -> improved diuresis and preload reduction
  3. May also inhibit sodium hydrogen exchanger or later sodium influx

Drug Action I (32 decks)

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