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pharm sci exam 2 > Cruthirds > Flashcards

Cruthirds Flashcards

0
Q

Vasopressin

A

Increase water reabs
Increase BP
Vasoconstriction

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1
Q

Aldosterone

A

Increase na+ and water reabs
Increase BP
Secretes k+

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2
Q

Spiromolactone

A 
Aldosterone antagonist 
Potassium sparing diuretic 
Decrease sodium and water reabs 
Decrease BP
Increase potassium
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3
Q

Heart failure

A

Progressive clinical syndrome

Abnormality in the structure or function that impairs the ability of the ventricle to contract or eject blood

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4
Q

In heart failure is the heart meeting the metabolic demand?

A

No bc cardiac output is low

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5
Q

Heart failure compensation occurs when?

A

Sns and raas is activated

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6
Q

SMS activation in heart failure

A

Activate beta 1 and alpha 1 causing increase co, increase hr, increase contraction, increase pressure, increase vasoconstriction, increase ne release

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7
Q

Raas activation in heart failure

A

Ang 2 vasoconstrictor that increases map

Aldosterone increases sodium and water reabs increase bv, increase preload, increase FOC

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8
Q

Digoxin is a ?

A

Cardiac glycoside

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9
Q

What’s the critical component for contraction of all muscle cells?

A

Calcium

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10
Q

Calcium role in cardiac myocytes

A

Tropinin C binds calcium which results in a conformational change exposing the actin binding site on the myosin filament allowing cross bridge formation

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11
Q

Sodium movement is tied with what?

A

Calcium movement

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12
Q

Scra pump

A

Moves calcium into scarp plasmid reticulum

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13
Q

MOA of digoxin

A

Inhibits the sodium-potassium ATPase on cardiac myocytes

Increases sodium conc
Increases calcium in the cell

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14
Q

Where does intracellular calcium get moved to?

A

Scarce plastic reticulum

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15
Q

What will happen to heart failure patients on digoxin?

A

Increase contraction because more calcium In sarcoplasmic reticulum
Increases pumping ability
Beneficial for heart failure patients

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16
Q

Digoxin acts in what type of manner?

A

Pns

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17
Q

Digoxin and what binds near the same site on the sodium potassium ATPase pump?

A

Potassium

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18
Q

Effect of potassium on digoxin activity

A

Increase potassium then decrease digoxin activity

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19
Q

At therapeutic doses what is the effect that digoxin exhibits?

A

Vagiometic effect allowing digoxin to slow av node- good for a fib pts

Norm baroreceptor reflex is getting activated frequently, digoxin lowers the sensitivity so it’s not being constantly activated

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20
Q

Clearance and secretion of digoxin

A

Cleared renally

Secreted by PGP

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21
Q

Digoxin has good absorption where?

A

Gi tract

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22
Q

Half life of digoxin

A

36 hrs

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23
Q

Digoxin have a wide or narrow therapeutic range?

A

Narrow

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24
Q

ADR of digoxin

A 
N/v
Vision disturbances(yellow and green halos) 
Av node block 
Ventricular arrhythmias
Fatigue
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25
Q

Drug interactions with Digoxin

A

Hyper or hypo kalemia
Beta blockers and non-dhp cause decrease contractility
Macrolide antibiotics- increase bioavailability
Amiodarone, propane one, verapamil, spironolactone increase conc of drug

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26
Q

MOA spironolactone

A

Potassium sparing
Decrease bv
Decrease BP
Dis in vol overload

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27
Q

Aldosterone in hf

A

If increase vol, increased aldosterone causes cardiac remodeling, nicreae collagen deposits and fibrosis occurs
Inhibit pumping
Increase stiffness and thickness of walls of heart

28
Q

Half life of spironolactone

A

7-20 hrs

29
Q

Protein binding of spironolactone

A

91-98%

30
Q

Pk of spironolactone

A

Food increases bioavailability

Hepatic metabolism to active metabolites

31
Q

ADR of spironolactone

A

N/v/d
Gynecomastia
Irregular menses
Impotence

32
Q

Drug interactions with spironolactone

A

Acei and arbs and digoxin cause hyper kalemia

33
Q

Milrinone used for?

A

De compensated heart failure

34
Q

MOA of Milrinone

A

Inhibitor of pde3

Inodilator

35
Q

Define Inodilator

A

Increase FOC, dilation

36
Q

Where are the effects of Milrinone present?

A

Cardiac and vascular smooth muscle

37
Q

If you inhibit PDE3 what happens to camp and amp

A

Blocks camp which inhibits amp

38
Q

Milrinone prevents block of camp to amp which enhances what effects?

A

Sns

Includes beta1, beta2, and alpha1

39
Q

Onset of action of Milrinone

A

5-15 minutes

40
Q

Half life of Milrinone

A

2.5 hrs

41
Q

How is Milrinone cleared?

A

Active tubular secretion

42
Q

How is Milrinone admin?

A

Iv only

43
Q

ADR of Milrinone?

A

Hypotension
Arrhythmias
Thrombocytopenia

44
Q

Nesirtide is used in what?

A

Acute de compensated hf

45
Q

Nesiritide is what? Released when?

A

Recombinant bnp

Released in response to vol overload

46
Q

Nesiritide results in what?

A

Natriuresis
Diuresis
Vasodilation

47
Q

MOA of Nesiritide

A

Binds Npr a
Increases intracellular cGMP which increases natures is and diuresis including sm relaxation in venous and arterial systems
Results in decrease in preload and decrease TPR

48
Q

Onset of action of Nesiritide

A

15 min

49
Q

Half life Nesiritide

A

18 minutes

50
Q

Elimination of Nesiritide

A

1 binds cell surface receptor NPR-C and cellular internalization and degradation
2 proteolytic cleavage by neutral endopeptidases
3 renal filtration

51
Q

ADR of Nesiritide

A

Hypotension

Gi upset

52
Q

Vasopressin treats?

A

Cardiac arrest

53
Q

Vasopressin is what?

A

Non- adrenergic peripheral vasoconstrictor which also increases blood flow to heart and brain

54
Q

MOA vasopressin

A

Binds v1 receptor activates ip3 mediated signaling which activated ip3 cascade results in vasoconstriction and water reabs

55
Q

Npr-a

A

Cell surface receptor that has intrinsic guanylyl Cyclades activity

56
Q

V1 receptor

A

Gq coupled receptor on vsm

When activated causes vasoconstriction

57
Q

Vasopressin can cause vasodilation where? How?

A

Where- cerebral and coronary vessels

How/why- MOA is calcium activates enos increases no, causes vsm relaxation

58
Q

Half life vasopressin, cleaved by?

A

17-35 min

Cleaved by proteases

59
Q

ADR vasopressin

A

N/v

Ab cramps

60
Q

ADH Antagonist treats?

A

Hf associated with hyper oil hyponatermia

61
Q

V2 receptor

A

Abso lateral side of collecting duct
Activation of Gs coupled receptor leads to activation of adenylyl Cyclades resulting in increased camp and increased activity of pka which increases water perm across apical mem

62
Q

To.vaptan

A

Selective v2 antagonist
Half life 12 hr
3a4 substrate
Pgp substrate and inhibitor

63
Q

ADR of tolvaptan

A 
Dry mouth 
Thirst 
Urinary freq
Constipation
Hyperglycemia
64
Q

Drug interactions with tolvaptan

A

CYP3a4 and pgp inhib or inducers

Digoxin may increase digoxin levels

65
Q

Conivaptan

A

V1a/v2 antagonist
Iv
Half life 5 to 8 hrs
3a4 substrate and inhibitor

66
Q

ADR conivaptan

A

Orthodtatic hypotension
Fever
Hypo kalemia
Local injection site rxns

67
Q

Drug interactions with conivaptan

A

3a4 inhib/ inducers

Increase levels of simvastatin, digoxin, amlodipine, midazolam

pharm sci exam 2 (7 decks)

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