Lec 38 CVS Pharma HPN and HF Flashcards

1
Q

Alpha blockers that are more sensitive to alpha1 than alpha 2

A

Prazosin, Terazosin, Doxazosin (BASICALLY MGA SIN)

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2
Q

Facilitates urinary outflow

A

Alpha1 blockers (mga sin)

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3
Q

Toxicities of Alpha blockers

A

Orthostatic hypotension (alpha-1 is responsible in maintaining BP in postural changes)

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4
Q

Manifests with the first dose phenomenon

A

Alpha1 blockers (mga sin)

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5
Q

NERVE TERMINAL BLOCKERS

A

Reserpine and Guanethedine

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6
Q

Inhibits the Ca2+-dependent release of norepinephrine

A

Guanethedine

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7
Q

Toxicities of Guanethedine

A

Severe orthostatic hypotension and sexual dysfunction

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8
Q

Blocks vesicular amine transporter

A

Reserpine

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9
Q

Toxicities of Reserpine

A

Psychiatric depression and GI disturbances (Lowering the levels of NE, DA, 5-HTwill impair brain and gut functions)

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10
Q

Competitively block nicotinic cholinoceptors in both sympathetic and parasympathetic ganglia

A

Hexamethonium

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11
Q

Centrally acting sympathoplegic drugsthat reduce sympathetic flow and inhibit NE

A

Alpha2 agonists

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12
Q

Best for refractory hypertension as a last resort

A

Alpha2 agonists

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13
Q

Examples of Alpha 2 agonists

A

Clonidine, Methyldopa

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14
Q

Withdrawal of Methyldopa causes____.

A

Rebound hypertension

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15
Q

Examples of Beta 1 blockers

A

Acebutolol (partial agonist), Betaxolol, Esmolol,Atenolol, Metoprolol (A BEAM of beta1 blockers)

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16
Q

Examples of nonselective Alpha and Beta antagonists

A

Labetalol, Carvedilol (Curb Love)

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17
Q

Drugs with intrinsic sympathomimetic properties

A

Partial agonists (Pindolol, Acetabulol)

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18
Q

Toxicity of beta blockers

A

Increased triglycerides, hyperglycemia (can cause new onset DM)

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19
Q

Nonselective ? blocker

A

propanolol

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20
Q

Oral vasodilator that cause NO release and can be used by women since it does not cross placenta

A

Hydralazine

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21
Q

Vasodilator that dilates Arterioles NOT veins

A

Hydralazine and Minoxidil

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22
Q

Toxicities of Hydralazine

A

Angina, tachycardia, Lupus-like syndrome

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23
Q

Oral vasodilator that cause opens K channels in vascular smooth muscle

A

Minoxidil

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24
Q

Toxicities of Minoxidil

A

Angina, tachycardia, headache, sweating, hirsutism (now used as topical for baldness)

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25
Q

Examples of parenteral vasodilators

A

NITROPRUSSIDE, FENOLDOPAM, DIAZOXIDE

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26
Q

Parenteral vasodilators that release NO

A

Nitroprusside

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27
Q

Parenteral vasodilators that activates D1 receptors

A

Fenoldopam

28
Q

Parenteral vasodilators that open K channels

A

Diazoxide

29
Q

Toxicities of nitroprusside

A

excessive BP lowering and accumulation of cyanide

30
Q

What type of calcium channels do CCBs inhibit?

A

L-type

31
Q

CCBs with more affinity to heart particularly the SA node

A

non-DHPs VERAPAMIL, DILTIAZEM

32
Q

greatest depressant effect on the heart; may cause supraventricular arrhythmia

A

Verapamil

33
Q

CCBs that reduce vascular resistance and have more affinity to smooth muscles

A

DHPs (NIFEDIPINE, AMLODIPINE)

34
Q

Examples of ACE inhibitors

A

Captopril, Enalapril, Lysinopril (mga pril)

35
Q

Mode of action of ACE inhibitors

A

blocks bradykinin breakdown

36
Q

ACE inhibitor that is a prodrug and thus NOT the active drug

A

Enalapril

37
Q

Toxicities of ACE inhibitors

A

ARF with bilateral renal artery stenosis, Contraindicated during second and third trimester of pregnancy

38
Q

Example of ARBs

A

LOSARTAN, VALSARTAN

39
Q

No effect in bradykinin metabolism and hence don’t cause cough

A

ARBs

40
Q

inhibits renin action

A

Aliskiren (“Alis ka renin”)

41
Q

Contraindications of Aliskiren

A

Pregnancy (because of the toxicity of ACE inhibitors and ARBs)

42
Q

First line drug in chronic heart falure

A

HYDROCHLOROTHIAZIDES

43
Q

What is the mode of action of Thiazides?

A

Inhibit NaCl transport predominantly in the distal convoluted tubule

44
Q

Toxicities of Thiazides

A

hyperGLUC (Glycemia, Lipidemia, Uricemia, Calcemia)

45
Q

Most potent diuretics available

A

Loop diuretics

46
Q

Inhibit NaCl reabsorption in thick ascending loop of Henle (Na+/K+/2Cl- transporter)

A

Loop diuretics

47
Q

Example of loop diuretics

A

IV Furosemide

48
Q

Toxicities of loop diuretics

A

Hypokalemic metabolic alkalosis, Allergy, Nephritis, Dehydration, Ototoxicity, Gout (HANDOG)

49
Q

Example of potassium sparing diuretics

A

Spironolactone

50
Q

Mode of action of Spironolactone

A

Competitive antagonist of aldosterone

51
Q

Treatment goals of HF drugs

A

Enhance oxygen delivery, Temper compensatory mechanisms, Prevent progressive cell death and structural deterioration to decrease morbidity and mortality

52
Q

What is the mechanism of action of digoxin

A

Direct inhibition of Na+/K+ ATPase; Stimulates vagus nerve

53
Q

What are the clinical applications of digoxin?

A

CHF (inc contractility), Atrial fibrillation

54
Q

What is the mode of excretion of digoxin?

A

Urinary excretion

55
Q

Toxicities of digoxin

A

Bigeminal rhythm, hypokalemia, tachycardia, fibrillation

56
Q

Mechanism of action of digoxin

A

vasodilator, inotropic, chronotropic

57
Q

Major excretion products of dobutamine in the urine

A

conjugates of dobutamine and 3-O-methyl dobutamine

58
Q

most widely used selective beta1-agonist in heart failure

A

dobutamine

59
Q

Where is dopamine metabolized?

A

liver, kidney, and plasma by MAO and catechol-O-methyltransferase

60
Q

The drug choice for patients with congestive heart failure, hypotension and oliguria.

A

Dopamine

61
Q

Mode of action of Milrinone

A

Inhiibt phosphodiesterase (PDE3) which inactivates camP and thus leads to increased cAMP

62
Q

T or F Milrinone has a greater cardiac than vascular effect

A

F. Milrinone has a greater vascular than cardiac effect so that arterial pressure is lowered in the presence of augmented cardiac output.

63
Q

Most common side effect of Milrinone

A

Ventricular arrhythmias

64
Q

Example of a Vasopressin antagonist

A

Conivaptan

65
Q

What is the mode of action of Nesiritide?

A

Increases cGMP in smooth muscles

66
Q

Adverse effects of Nesiritide

A

excessive hypotension; reports of significant renal damage and deaths