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IMCP I > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Hydralazine and minoxidil MOA?

A

Opens K+ channels –> hyperpolarization of membrane and inhibition of calcium entry into smooth muscle –> Art VD –> (-) PVR AND (-) afterload pressure.

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2
Q

What are the Adverse Effects of sodium nitroprusside?

A

profound hypotension, Profound hypotension, reflex tachycardia. **Cyanide vs thiocyanate toxicity • Liver impairment (↑CN), or renal impairment (↑thiocyanate)

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3
Q

What are the Adverse Effects of hydralazine?

A

Reflex tachycardia, edema. Systemic lupus erythematosus-like syndrome- esp. in slow-acetylators

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4
Q

What are the Adverse Effects of minoxidil?

A

Reflex tachycardia, edema, more potent vasodilator. Therefore, it has the potential to precipitate angina and congestive heart failure.
Hirsutism.

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5
Q

PK of hydralazine?

A

t1/2 ~ 2-4 hrs.

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6
Q

PK of minoxidil?

A

Pro-drug - Activated by hepatic sulfotransferase.
last over 24 hrs (2-5 days).

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7
Q

What is the MOA of sodium nitroprusside?

A

vascular metabolism/ activation to NO by RBCs (heme) , NO then diffuses into the blood vessel ↑ cGMP –> smooth muscle relaxation, Opens K+ channels –> hyperpolarization and inhibition of calcium entry. Venous and Arterial Vasodilation)à Drop in Preload and Afterload

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8
Q

PK of sodium nitroprusside?

A

BP reduction < 2 minutes. Short-acting: Duration: 1-10 minutes.

Metabolism:
Blood Nitroprusside → cyanide (CN) ions. Liver CN → thiocyanate by rhodanase mitochondrial enzyme. Rate limiting step is the availability of thiosulfate donors. Kidney Thiocyanate slowly eliminated.

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9
Q

What is special about minoxidil?

A

Hirsutism.

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10
Q

What is special about sodium nitroprusside?

A

Methemoglobinemia, Photosensitive

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11
Q

What are the DHP CCBs?

A

Nicardipine, Nifedipine, Amlodipine

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12
Q

What is the MOA of DHPs?

A

Block L-type vg-calcium channels in arterial VSM –> (+) Ca2+ influx –> Arterial vasodilation

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13
Q

PK of nicardipine?

A

IV: 10 min.

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14
Q

PK nifedipine?

A

t1/2 = 2 hrs (IR). ER has biphasic peaks first at 2 hrs and at 6-12 hrs (ER).

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15
Q

PK of amlodipine?

A

Duration of action ~ 18-24 hrs; t1/2 = 30-50 hrs.

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16
Q

Adverse effects of DHPs?

A

Reflex tachycardia, edema and Hypotension.

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17
Q

DDIs of DHPs?

A

CYP 3A4 substrates, inhibitors / inducers.

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18
Q

What is special about nicardipine?

A

Indication: acute hypertensive crisis.
Has less negative inotropic effects than nifedipine.

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19
Q

What is special about nifedipine?

A

Short-acting is associated with an increased risk for MI or mortality. Long-acting CCB’s are preferred in chronic treatment of HTN.

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20
Q

What is special about amlodipine?

A

amlodipine is administered once daily in its standard formulation

(immediate release).

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21
Q

What are the Non-DHPs?

A

Verapamil, diltiazem

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22
Q

MOA of Non-DHPs?

A

inhibit calcium influx in myocardium and VSM.

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23
Q

Verapamil PK?

A

Metabolism: CYP 3A4 (N-demethylation) –> active (~20%) metabolite (norverapamil t1/2: 6-10 hrs).CYP 2D6 (O-demethylation) to inactive metabolite.

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24
Q

Diltiazem PK?

A

Deacetylation (major route) –> active metabolite (~25-50%). CYP 3A4 (N-demethylation) and CYP 2D6 (O- demethylation).

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25
Q

AEs of Non-DHPs?

A

Edema, Hypotension, HF, Arrhythmias, AV block, bradycardia.

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26
Q

DDIs of Non-DHPs?

A

CYP 2D6 & 3A4 substrates, inducers, inhibitors. an inhibitor of P-gp and CYP 3A4. inhibits Pgp efflux → ↑[digoxin] → digoxin toxicity (verapamil?).

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27
Q

Verapamil special?

A

Indication: atrial fibrillation, angina, HTN.
(Negative chronotrope, Moderate negative inotrope.
Can precipitate heart failure esp. in patients with limited cardiac reserve.

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28
Q

Special diltiazem?

A

Mild negative inotropic effects. Intermediate affinity to cardiac cells. safer than verapamil.

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29
Q

DDI barbituates and felodipine, nifedipine, and verapamil?

A

Decreased effects of CCBs

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30
Q

DDI Beta-blockers and CCBs?

A

Additive or synergistic (more verapamil and diltiazem); inhibition of beta-blocker metabolism

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31
Q

DDI cimetidine and CCBs?

A

Increased 1,4 DHP levels

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32
Q

DDI digoxin and nifedipine, diltiazem, and verapamil?

A

Increased digoxin levels

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33
Q

DDI HMG CoA reductase inhibitors and diltiazem, verapamil?

A

Increased levels of HMG CoA reductase inhibitors

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34
Q

DDI phenytoin and CCBs?

A

Decreased effectiveness of CCBs due to induction

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35
Q

DDI rifamin and diltiazem, nifedipine, nisoldipine, verapamil?

A

Decreased levels of CCB

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36
Q

Angiotensin II on blood vasculature?

A

Direct rapid vasoconstriction

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37
Q

Angiotensin II on kidneys?

A

Increased Na+ reabsorption, increased vasocontriction

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38
Q

Angiotensin II on heart?

A

Increased HR

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39
Q

MOA of ACE inhibitors?

A

Reversible inhibition of ACE.

(block angiotensin –> VD, No aldosterone releaseàno Na and Water retention, block hydrolysis of bradykinin).

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40
Q

Lisinopril PK?

A

No activation required o t1/2 = ~ 12 hrs.

41
Q

Captopril PK?

A

Poor bioavailability with food

42
Q

Benazipril PK?

A

Metabolism by liver esterase to active benazeprilat

43
Q

Enalapril PK?

A

Metabolism via liver esterase to active drug, enalaprilat. Enalaprilat is available in IV formulation for HTNsive crisis

44
Q

Quinapril PK?

A

Metabolism via liver esterase to active drug, quinaprilat

45
Q

Fosinopril PK?

A

Metabolism via liver esterase to active drug, fosinoprilat.

46
Q

AEs of ACEIs?

A
  1. Angioedema 2. Hypotension – first dose effect 3. Chronic dry cough 4. Hyperkalemia. contraindicated in pregnancy.
47
Q

DDIs of ACEIs?

A

Digoxin: increase or decrease digoxin plasma level.
K preps.: hyperkalemia.
NSAIDs: decrease hypotensive effect.

48
Q

Indications for all ACEIs?

A
  1. Hypertension 2. Heart failure 3. Myocardial infarctions 4. Left ventricular dysfunction 5. Diabetic nephropathy.
49
Q

Captoril special?

A

AE: rashes and taste disturbance due to sulfhydryl group.

50
Q

AT1 recptor activation?

A

Gaq ——–> vasocontriction

51
Q

AT2 recptor activation?

A

Balance AT1, vasodilation

52
Q

What are the ARBs?

A

Losartan, olmesartan, candesartan, irbesartan, telmisartan, valsartan, azilsartan

53
Q

MOA of ARBs?

A

Selective AT1–R antagonist to inhibit constriction of VSM in arterial and venous.

54
Q

What is special about the MOA of azilsartan?

A

Highly selective.

55
Q

PK olmesartan?

A

(Pro-Drug). t1/2=10–15hrs.

56
Q

Special PK candesartan?

A

Ester prodrug.

57
Q

Special PK valsartan?

A

Food markedly decreases absorption. Metabolism by non-CYP mechanism. Elimination is primarily via hepatic elimination.

58
Q

DDIs of ARBs?

A

Digoxin: increase or decrease digoxin plasma level.
K preps.: hyperkalemia. NSAIDs: decrease hypotensive effect.

59
Q

Special ARBs?

A

Contraindicated in pregnancy.

60
Q

What are the NItrates?

A

NTG, isosorbide di, isodorbide mono

61
Q

MOA of Nitrates?

A

VSM relaxation. Nitroglycerin is denitrated by glutathione S- transferase which releases the free nitrite ion. A second enzymatic reaction releases free radical nitric oxide (NO). NO in turn causes direct activation of guanylyl cyclase –> Increased levels of cGMP –> activate a Myosin Light Chain Phosphatase –> VSM Relaxation.

62
Q

PK NTG?

A

t1/2: 1-3 mins.

63
Q

PK isosorbide di?

A

sublingual route. t1/2: 45 mins

Active metabolites have much longer half-life ~ 3-6 hrs

64
Q

PK Isosorbide mono?

A

No first pass effects. t1/2: 3-6 hrs. Metabolism via glucuronidation

65
Q

AE Nitrates?

A

Headache, Orthostatic hypotension, Reflex tachycardia. Serious: Syncope, Methemoglobinemia. Tolerance due to frequent dosing.

66
Q

NTG special?

67
Q

Isosorbide di special?

68
Q

Isosorbide mono

A

Slower than NTG

69
Q

Special all Nitrates?

A

have more impact on preload than afterload

70
Q

DDI nitrates?

A

Phosphodiesterase-5 inhibitors (PDE5-I).

71
Q

What are the diuretics?

A

Acetazolamide, Mannitol, Furosemide, Bumetanide, Torsemide, Ethacrynic

72
Q

Loop diurectic site of action?

73
Q

MOA Loop?

74
Q

Inhibition of Na/K/2Cl co-transporter in luminal renal epithelium of TALH.

Most potent class. (Fast action and short duration).

75
Q

PK furosemide?

A

t1/2 ~ 2 hrs.

76
Q

PK bumetanide?

A

1/2 =1 - 3 hrs.

77
Q

PK torsemide?

A

t1/2 = 2-4 hrs.

78
Q

PK ethacrynic?

A

t1/2 1-4 hr.

79
Q

AE Loop?

A

hyponatremia, hypokalemia, hypochloremia, hypocalcemia and hypomagnesemia.

Orthostatic hypotension, Hyperuricemia.

80
Q

DDI Loop?

A

Decrease lithium clearance à lithium toxicity. Digoxin toxicity.

hypokalemia and hypomagnesemia enhance Na-K-ATPase inhibition by (digoxin).

81
Q

Special Acetazolamide?

A

Indication: Acute mountain sickness.

Glaucoma.

82
Q

What are the thiazide and thiazide-like diuretics?

A

HCTZ, chlorthalidone, metolazone

83
Q

Site of Action thiazide and thiazide-like diuretics?

A

Na/Cl co-transporter at DCT.

84
Q

MOA of thiazide and thiazide-like?

A

Inhibition of Na/Cl co-transporter in DCT.

85
Q

PK HCTZ?

A

t1/2 = 6-15 hrs.

86
Q

PK chlorthalidone?

A

t1/2 = 40-60 hrs.

87
Q

PK metolazone?

A

t1/2 = 8-14 hrs. duration of action ~ 12-24 hrs.

88
Q

AE thiazide and thiazide-like?

A

Hyponatremia, hypokalemia, hypomagnesemia, hypophosphatemia, hypochloremia alkalosis. Hypercalcemia, hyperuricemia, hyperlipidemia, Hyperglycemia.

89
Q

DDI thiazide and thiazide-like?

A

Decrease lithium clearance –> lithium toxicity. Digoxin toxicity. hypokalemia and hypomagnesemia enhance Na-K-ATPase inhibition by (digoxin).

90
Q

Thiazide and thiazide-like special?

A

Sulfonamide group (Rash). Chlorthalidone most potent.

91
Q

What are the ENaC Inhibitors?

A

Triamtrene, amiloride

92
Q

SIte of action triamtrene, amiloride?

A

ENac at CD & CT

93
Q

ENaC Inhibitor MOA?

A

Inhibits (ENaC) –> (-) Na reabsorption and K secretion.

94
Q

Triamtrene PK?

A

t1/2 = 1 – 3 hrs. duration of action ~ 8-10 hrs.

95
Q

Special triamtrene?

A

Used in combination with Thiazide or loop.

96
Q

Aldosterone Receptor Antagonists (K sparing) antagonist?

A

Spironolactone

97
Q

Spironolactone Site of Action?

A

Aldosterone Receptor at CD&CT.

98
Q

Spironolactone special?

A

(pro-Drug) not potent antihypertensive/diuretic by itself. Contraindicated: acute renal insufficiency, concomitant ENaCI, hyperkalemia.

IMCP I (32 decks)

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