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Pharmacology > Cardio/Respiratory Drugs > Flashcards

Cardio/Respiratory Drugs Flashcards

1
Q

Direct acting sympathoneumonic

A

directly acts on the post synaptic receptor. NE,E

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2
Q

indirect acting sympathoneumonic druc

A

increases the release of the transmit in the presynaptic terminal. amphetamine, meth, MDMA

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3
Q

Block the re-uptake of sympathetics

A

amytriptiline, coains

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4
Q

block the degeneration of NE

A

MAO inhibitors, phenylezene

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5
Q

Phenylephrine

A

A1 agonist, vasconstriction/venoconstriction.

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6
Q

Phenylpherine indications and doses

A

decongestion, eye dilator (Mydriatic), raises BP. Given topically or IV.

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7
Q

Phenyephrine

A

Less potent vasoconstrictor, not inactivated by COMT

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8
Q

Clonidine class/action

A

pharmacologic class—central α2 agonist; therapeutic class–antihypertensive, adjunct to Rx of opioid withdrawal, prophylaxis of migraine

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9
Q

Clonidine pharmacodynamics/kinetics

A

stimulates α2 adrenoceptors in brainstem, thereby leading to down-regulation of sympathetic output. : Onset 1 h, duration 8 h, F~85%, also available as cutaneous patch

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10
Q

Clonidine toxcities/interactions

A

withdraw gradually because of risk of rebound HTN; risk of bradycardia in sinus node disease; letharagy, fatigue, depression. additive effects with most other antihypertensives; additive sedation with other CNS drugs

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11
Q

Selective alpha agonists

A

clonidine and phenylephrine

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12
Q

Selective beta agonists

A

isoproterenol, dobutamine, albuterol

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13
Q

Isoproterenol class/action

A

B1, B2 agonist. Increases HR, contractility, cardiac conduction

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14
Q

Isoproterenol dosage/side effects

A

IV administration. Not used as much as causes tachyarrythmias and vasodilation

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15
Q

Dobutamine mech

A

B1 agonist. highly effective beta agonist, also causes dilation of renal and mesenteric blood vessels

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16
Q

Dobutamine administration, indiciations, side effects

A

increases contractility more than heart rate, therefore useful in cardiogenic shock, stimulates ventricles. Administered via IV. can cause tachycardia, hypertension, and ectopy

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17
Q

Albuterol

A

B2 agonist, brochodilation

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18
Q

albuterol indiciations/ doses/ side effects

A

bronchodilation for acute exacerbation of asthma, prevents premature labor. Most often given as meter dose. also given as nebulizer/IV. Can cause tachy, anxiety, tremor

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19
Q

Mirabegron mech

A

B3 agonist. stimulates the detrusor muscle, reducing tone

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20
Q

Mirabegron indications/administrations

A

for overactive bladder. Relaxes detrusor and increases bladder capacity. administered orally

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21
Q

Epinephrine class

A

direct acting adernegic agonist, cardiac stimulator, bronchodilator

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22
Q

Epinephrine pharmacodynamics

A

Acts on A1 receptors to stimulate vasoconstriction venoconstriction in peripheral vasculature, b1 receptors to increase contractility and HR, and b2 receptors to cause bronchodilation. Also inhibits mast cell release of histamine

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23
Q

Epinephrine pharmacokinetics

A

Administer IV for immediate effect, IM for variable effect, SM 5-15 minutes, Inhalation 1- 5 min. Degraded by COMT and excreted renally

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24
Q

Epinephrine indications/ dosing

A

anaphalaxis .1-.5 mcg IM or SC, for cardiac arrest 1-5mg IV, , for infusion 1-4mcg per minute

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25
Q

Epinephrine toxicity and interactions

A

excessive HTN, vasconstriction, hemorrhagic stroke, tachycardia, arrhythmias. Risk of severe htn interaction with propranolol.

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26
Q

Epinephrine monitoring

A

BP, HR, extravasation, rhythm, infusion site

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27
Q

Norepinephrine drug class

A

direct acting adernergic agonist, vasoconstrictor, cardiac stimulator

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28
Q

Norephinephrine pharmacodynamics

A

A1 stimulation- vasoconstriction and venoconstriction peripherally. Does lead to decreased BF to kidneys, skin, and muscle. B1 agonist-cardiac stimulation (HR, contractility).

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29
Q

Norepinephrine pharmacokinetics

A

F-100%. given IV only, half life 1-2 minutes, must be given on continuous drip. metabolized by COMT and MAO, excreted in the urine. Crosses placenta but not BBB

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30
Q

Norepinephrine toxicities/interactions

A

can cause excessive vasoncostriction, especially in mesenteric and renal vessels causing ischemia, infection, and gangrene. Can cause reflex bradycardia. Potential interactions with increase HTN with propranolol and MAO inhibitors.

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31
Q

Norepinephrine special considerations

A

patients must be volume stable before administering drug. Extravasation is a major concern, so site must be monitored closely, as well as HR and BP. Excersise caution when administering to adults and children.

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32
Q

Dopamine-description/actions

A

DA, A1,B1 agonist. DA agonist at low dose, B1 agonist at medium dose, A1 agonist at high dose.

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33
Q

Dopamine-usages and indications

A

shock-stimulates heart, vasoconstriction, increases mesenteric and renal perfusion. given for short periods of time

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34
Q

Ephedrine class/action

A

from ephedra plant, stimulates stored NE from neurons, some direct agonism.

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35
Q

Ephedrine indications/ usage

A

mild to moderate hypotension, nasal congestion. Used for short acting (15 minutes) effect in surgery. potent CNS stimulant, can cause HTN and insomnia

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36
Q

Pseudoephedrine class/action

A

vasoconstricor, stimulates NE neurons to release stored NE. , some direct A and B agonism.

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37
Q

Pseudoephedrine indications/usage

A

nasal decongestion, doesn’t dilate bronchioles as well. Behind the counter product

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38
Q

Amphetamine

A

indirect NE agonist (release of NE from nerve endings). Used for narcolepsy, obesity, and ADHD. No FDA approved indications, high risk of dependence, tremors, restlessness.

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39
Q

Tyramine

A

chemical present in many fermented foods (wine, cheese, cured meats), that acts as a indirect agonist. Can act similarly to amphetamine (obesity, narcolepsy, ADHD). Potential interactions with people taking MAO inhibitors, as metabolized by MAO.

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40
Q

Cocaine

A

purified extract of coca, blocks repute of NE, E, D. used in bad cases of epistaxis, CNS stimulant. Side effects include tachycardia, arrythmias, seizures, MI

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41
Q

Prazosin-drug class

A

selective alpha 1 inhibitor, vasodilator, antihypertensive, bPH

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42
Q

Prazosin-pharmk/pharmd

A

selectively blocks alpha 1 receptors, preventing vaso and venoconstriction by blocking NE binding. Administered orally/transdermally, variable bioavailability, available 2 hours after administration, in system for 12-24 hours. Extensivly metabolized by the liver.

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43
Q

Prazosin toxicity/side effects

A

hypotension, especially when standing. Addititive effect with diuretics.

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44
Q

Prazosin-considerations/doasage

A

start at bedtime, slowly build up dose. Begin with 1mg tid, up to 20mg tid. continue to monitor BP, weight, edema

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45
Q

Pheotolamine class

A

non-selective, competitive alpha adernergic receptor antagonist. Used for hypertension in individuals with pheochromocytoma

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46
Q

Phenotolamine pharmk/d

A

blocks A1 and A2 receptors at the presynaptic and post synaptic membranes. This decreases preload and afterload. Administered IV, half life 20 minutes

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47
Q

Phentolamine toxicities/interactions

A

excessive hypotension and syncope, especially orthostatic. Additive effects with most other hypertensives, especially diuretics.

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48
Q

Phentolamine special considerations/dose

A

rule out carcinoma BP before use. Used for intra-opp hypotensive crisis. hypotensive crisis in response to sympathomimetic amines. prevent dermal sloughing after extravasation. Dose 5 mg IV, titrate, repeat. Monitor BP

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49
Q

Atenolol/metoprolol class

A

b1 antagonist, anti hypertensive, anti arrythmic, MI prevention, anti anginal.

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50
Q

Atenolol/metoprolol pharmacodynamics/kinetics

A

Binds directly to B1 site, preventing binding of norepinephrine. lowers htn via various mechanisms including decreasing CO, and inhibiting RAAS system. less effective for preventing stroke. Available oral or IV, variable F. Renally excreted for longer half life (12-24 hours). renally excreted for longer half life. metoprolol is hepatically metabolized

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51
Q

Atenolol toxicities/interactions

A

can worsen CHF in severe cases, cause bronchospasm in severe asmatics, as well as bradycardia, hypotention, and heart block. Additive effect with most other anti-hypertensives. Additive AV block with CEBs

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52
Q

Atenolol dosages/considerations

A

25-100mg po qd/bid. especially good for individuals with exertional angina, MI, atria fib. May no longer be first line defense. Monitor BP, excersize tolerance, HR

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53
Q

Labetalol drug class

A

anti hypertensive, treatment of stable CHF. Mixed alpha/beta antagonist.

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54
Q

Labetalol pharmacokinetics/dynamics

A

blocks A1 and B1 receptors, lowering BP via multiple mechanisms. Different patients will have different degrees of blocks on each receptor. High first pass effect, so only 25%F. 1-2 hours for effect orally, 2-5 minutes iv. extensively metabolized by liver 2D6

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55
Q

Labetalol toxicities and interactions

A

bradycardia, hypotension. Do not use in patients in shock, asthma, CHF. Caution in patients with pheochromocytoma and cardiomyopathy. Pregnancy level b/c. Additive effect with most other anti-hypertensives

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56
Q

Labetalol dosage and considerations

A

generally used for hypertensive crisis. additive effect with most other hypertensives. Give small 20mg bolus initially than 1-2mg bolus subsequently. not generally given orally. Monitor BP and heart rate.

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57
Q

Carbachol class/actions

A

non-selective muscarinic and nicotinic receptor agonist. Ocular agent causing miosis and increased aqueous humor outflow, for use in open angle glaucoma

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58
Q

Carbachol toxicity/other factors

A

overuse could cause excessive adernergic toxicity but unlikely since topical. Not broken down efficiently by acetylcholinesterase so long lasting

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59
Q

Bethanechol class/actions

A

non-selective muscarinie receptor agonist, used to increase detrusor muscle tone and stimulate GI motility after surgery. Given orally for urinary retention, neurogenic bladder, GERD.

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60
Q

Bethanechol toxicities/considerations

A

can cause reflex tachycardia, bronchoconstriction, increased secretory activity

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61
Q

Pilocarpine class/indications

A

non selective muscarinic receptor agonist. used for open and closed angle glaucoma, decreasing IOP and dry mouth(xerostomia), Sjogren syndrome, and head and neck cancer associated.

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62
Q

Pilocarpine toxicity/administration

A

can cause execssive acetylcholine symptoms. adminstered topical and oral

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63
Q

Methacholine class/actions/use

A

non selective muscarinic agonist. used to diagnos bronchial hyperactivity in the diagnosis of asthma. Inhaled only

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64
Q

Nicotine class/action

A

nicotinic cholinergic agonist, binds to nicotinic receptors but has slower action thn that found in cigarettes

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65
Q

Nicotine indications/side effects

A

smoking cessation, nicotine withdrawal. can cause bronchospasm and nicotine dependence transferance. Administered in gum, patch, nasal

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66
Q

Varenicline class/actions

A

partial nicotinic receptor agonist. reduces cravings for and pleasure associated with smoking by reducing the ability of nicotine to stimulate the mesolimbic dopamine system

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67
Q

Vareincline indications/side effects

A

given orally for smoking cessation. Can cause nausea, headaches, insomnia, abnormal dreams

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68
Q

Metoclopramide is…?

A

largely replaced bethanachol for post surgery gastroparaesis and antiemetic. stimulates D2 receptors to trigger Ach release

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69
Q

Edrophonium (Tensilon test)

A

reversible acetylcholinesterase inhibitor adminstered to test for myasthenia gravis. Can cause excessive cholinergic reaction, though does have a very short half life (10-30 minutes. Does not cross BBB

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70
Q

Neostigmine class/actions

A

reversible cholinesterase inhibtior. Increases acetylcholine availability for post synaptic membrane receptors

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71
Q

Neostigmine Indications/ toxicity

A

Myasthenia gravis, nondepolarizing neuromuscular blockade reversal, urinary retention. Can cause excessive cholinergic rxn. Can be given IV, IM, SC. Does not enter CNS

72
Q

Physostigmine class/action

A

reversible cholinesterase inhibitor, leading to indirect increased stimulation of M and N receptors.

73
Q

Physostigmine indicatoions, toxicities

A

indicated for glaucoma, alzheimers, delayed gastric emptying, anticholinergic toxicicty (CNS effects, atropine OD, non depolarizing neuromuscular blockade reversal. Can cause cholinergic excessive excitation, does cross BBB so not used for myasthenia gravis

74
Q

Pyridostigmine class/action

A

reversible cholinesterase inhibitor, indirectly stimulates both muscarinic and cholinergic inhibitors.

75
Q

Pyridostigmine indications/toxicities

A

myasthenia gravis, shorter half like than Neostigmine. Does not cross BBB, low oral availability

76
Q

Donepezil class/actions

A

reversible cholinesterase inhibitor, indirectly stimulates both nicotinc and muscarinic receptors.

77
Q

Donepezil indications/toxicities

A

azheimers associated dementia.. can cause GI upset. Crosses the BBB, F= 100%

78
Q

Usueful drugs for dimetia

A

Rivastigmine = revesible cholinesterase patch for GI upset. Galantamine = Nn agonist and acetylcholinesterase inhibitor.

79
Q

Echothiophate class/action

A

irreversible cholinesterase inhibitor. binds irreversibly to acetylcholinesterase.

80
Q

Echothinophate indications/tox

A

given topically for glaucoma. Can cause lacrimation and stinging. Very long half life

81
Q

Atropine class/action

A

non-selective muscarinic antagonist. prevents actions of acetylcholine and down regulates cholinergic controlled processes and glands

82
Q

Atropine indications/side effects

A

Indicated for organophosphate poisonings, to slow heart rate, pupil dilation, reduce secretions. Can cause anti-cholinergic set syndrome

83
Q

Atropine dosing

A

Given IV, SC, IM. Lipid soluble, crosses the blood brain barrier for when toxins have as well.

84
Q

Pralidoxime class/action

A

reactivates cholinesterase. Binds to deactivated acetylcholinesterase and speeds reactivation.

85
Q

Pralidoxime indications/toxicities

A

cholinesterase inhibitor overdose. exposure to organophosphates. When paired with atropine, can worsen anti-cholinergic syndrome

86
Q

Pralidoxime administration

A

IV, IM only. Must be used soon after exposure. Military stockpiles large amounts of these.

87
Q

Bentropine class/action

A

M1 receptor antagonist and histamine receptor blocker. Centrally acting

88
Q

Bentropine indications/tox

A

used for parkinsonism, disorders of extrapyramidal system, dystonia. Can cause anticholinergic excess syndrome

89
Q

Bentropine administration

A

IV IM

90
Q

Scopolamine class/action

A

non-selecitve muscarinic receptor blocker. Possibly some specificity for M1 receptors, anti emetic.

91
Q

Scopolamine indication/side effects/adminstration

A

given to prevent sea sickness and dilate eyes. Can cause anti-cholinergic syndrome. transdermal, can cross BBB

92
Q

Ipratropium class/action

A

non selective muscarinic receptor antagonist. Inhaled bronchodilator. Generally slower acting, combined with albuterol.

93
Q

Ipratropium indications/side effects

A

asthma/COPD. Can cause bad taste and dry mouth. could cause anticholinergic syndrome but only with overdose

94
Q

Dicyclomene class/actions

A

non-selective muscarinic antagonist. Relaxes smooth muscle, inhibits bradykinin and histamine to reduce bowel spasm.

95
Q

Dicyclomene indications, side effects

A

used for IBS. Can cause anticholinergic syndrome with delerium at higher doses. Administered orally

96
Q

Succinylcholine class/action

A

nicotinic NMJ blocker, Nm receptor agonist. Depolarize muslce, not terminated, resulting in flaccid paralysis. Not brocken down acetylcholinesterase.

97
Q

Succinylcholine indications/toxicities

A

short term muscle relaxation and paralysis, as for intubation. Can cause Black box, rare rhabdomyalgia with hyperkalemia and subsequent Ventricular dysrhythmias causing cardia arrest and death. Occurs in children with previously undiagnosed myopathys, most commonly duchennes.

98
Q

Succenycholine special considerations

A

do not give in children with myopathies, do not give in individuals llackin acetylcholinesterase, as no way to reverse and long time to break down. IV only

99
Q

D-tubocurarine class/action

A

reversible NMJ receptor antagonist. Directly blocks receptor on end plate, causing muscle paralysis.

100
Q

D-tubocurarine indications/toxicities

A

produces complete skeletal muscle paralysis. First used in surgery, has subsequently been replaced. can cause respiratory failure, tachy, paralysis in fully consiouce patients, histamine release, ganglionis and muscarinic side effects

101
Q

D-tubocurarine administration/reversal

A

duration 30-60 minutes, neostigmine will reverse.

102
Q

Vecuronium class/action

A

NMJ receptor antagonist, reversible, non-competitive inhibitor. Directly blocks receptors on NJM endplate

103
Q

Vecuronium indications/toxicities

A

Used as paralytic in lethal injection. Can be used as a paralytic in surgery. Black box warning, can cause paralysis in conscious patients, histamine release, tachy, muscarinic and gangliosidic side effects

104
Q

Vecuronium duration/reversile

A

lasts 30-60 minutes, neostigmine will reverse Can cause hepatic damage

105
Q

Cisatracurium class/action

A

nicotinic NJM blocker, reversible competitive inhibition. Antagonizes muscular endplate

106
Q

Cisatracurium indications/toxicities

A

production of complete paralysis for intubation and surgery. Can cause respiratory failure, complete paralysis in concious patients, tachy, histamine release, gangliosidica and muscarinic side effects

107
Q

Cisatracurium duration/reversile

A

30-60 minutes. Neostigmine will reverse.

108
Q

Trimetaphan class/action

A

competive gangliosidic blocker, acts as a non-depolarizing gangliosidic antagonist. Antihypertensive. Blocks the parasympathetic and sympathetic systems.

109
Q

Trimetaphan pharamcodynamics/kinetics

A

: blocks nicotinic transmission within both sympathetic and parasympathetic ganglia (by blocking NN receptors); produces veno- and vaso-dilatation. useful only when given iv; produces fall in BP within minutes; partly metabolized, and partly excreted by kidneys

110
Q

Trimetaphan toxicities/interactions

A

sudden, severe drop in BP; also fall in HR; also, reduction in just about any sympathetic or parasympathetic response. Additive effect with most other anti-hypertensives.

111
Q

Botulinum class/action

A

bacterial exotoxin, derived from C. botulinism. Cleaves snare proteins, inhibiting release of acetylcholine.

112
Q

Botulinum indications/tox

A

reduce wrinkles, prevent hyperhydrosis, prevent migranes. Can cause botulism symtoms. Asthenia, muscle weakness, diplopia, blurred vision, ptosis dysphagia, urinary incontinence, breathing difficulties, life threatening, and death. Inject locally to prevent systemic effects.

113
Q

HCTZ- class/action

A

thiazide diuretic. diuretic, anti-hypertensive

114
Q

HCTZ pharmacodynamics/kinetics

A

blocks uptake of Cl and Na in the distal tubule leading to fluid loss resulting in reduced blood pressure. Also reduces SVR. F = 70%, excreted unchanged in urine; short half-life (hours); HCTZ not available in IV formulation; onset 2 h, peak 5 h, duration 10 h

115
Q

HCTZ side effects/toxicities

A

allergy to sulfa antibiotics (?); cause K and Mg depletion; cause Na and Cl depletion, metabolic alkalosis; volume depletion; worsen hyperuricemia. additive effects with most other antihypertensives.

116
Q

HCTZ administration, special considerations

A

: more side effects in geriatric patients; Pregnancy Class D; much less effective in patients with reduced GFR, 12.5mg or 25 mg PO QD.

117
Q

Lisinopril class/action

A

Ace inhibitor. anti-hypertensive, CHF control, MI recurrence reduction, acute MI reduction, preserve renal function

118
Q

Lisinopril pharmacodynamics/kinetics

A

inhibits conversion of AT I to AT II by ACE; diminishes both vasocontriction and stimulation of aldosterone secretion by AT II. well absorbed; onset 1 h, peak 6 h, duration 24 h; once a day is fine; excreted primarily in urine as unchanged drug

119
Q

Lisinopril toxicities/interactions

A

orthostatic hypotension; use with caution in patients with impaired renal function, or renal artery stenosis; be careful in patients on diuretics, or those with aortic stenosis; angioedema, cough; acute renal failure. additive effects with most other antihypertensives; NSAIDs may reduce ability to lower BP; hyperkalemia with KCL.

120
Q

Lisinopril special considerations/administration

A

often discontinue diuretics prior to beginning use to reduce hypotension; Category C/D in pregnancy, abnormal cartilage development. Start with 10mg PO QD and slowly titrate up to 40. Continue to monitor BP, creatinie, etc. USE ACE inhibitor in diabetics, because preserves kidney function.

121
Q

Losartan class/action

A

ARB. antihypertensive, preserve renal function, treatment of CHF

122
Q

Losartan pharmacodynamics/kinetics

A

block stimulation of AT I receptor by angiotensin II, thereby reducing vasoconstriction and production of aldosterone. : F ~30%; onset 6 h; extensive first pass effect; active metabolite is 40x more potent, much longer half-life.

123
Q

Losartan toxicities/interactions

A

dizziness; orthostatic hypotension; worsening of renal failure. : additive effects with most other antihypertensives

124
Q

Losartan special considerations/dosage

A

Pregnancy class C/D; use care in patients on diuretics, those with renal artery stenosis, those with mitral or aortic stenosis. For HTN, daily doses 25-100 mg qd. Monitor stuff plus creatinie. USE in diabetics, for preserved kidney function.

125
Q

Hydralazine class/action

A

peripheral vasodilator; therapeutic class– antihypertensive, treatment of CHF, vasodilator

126
Q

Hydralazine pharmacodynamics/kinetics

A

“direct” acting vasodilator; seems to act by inducing endothelium to produce NO, which then passes to SM cells and induces production of cGMP, minimal venodilating effect. given po, im, iv; metabolized extensively in GI mucosa and in liver, eventually excreted as metabolites in urine; F ~40%; onset 30 after po dose, 10 min after iv dose; persist for 2-6 hours

127
Q

Hydralazine side effects/toxicities

A

more dangerous in patients with renal disease, prior stroke, angina; watch for hypotension, edema, occasionally drug-induced lupus. additive with most other hypertensive drugs

128
Q

Hydralazine special considerations/dosage

A

dont give long term, reflex tachy and edema. Also some concern giving to patients with CAD. 10-50 mg PO daily. monitor the usual + symptoms of lupus and angina

129
Q

Nitroprusside class/action

A

pharmacologic class– vasodilator; therapeutic class–antihypertensive, management of severe CHF, management of pulmonary hypertension, produce controlled hypotension to reduce bleeding during surgery

130
Q

Nitroprusside pharamcodynamic/kinetics

A

acts “directly” on vascular smooth muscle to cause dilatation of both veins and arterioles; metabolized to release CN- and NO, which activates guanylate cyclase, leads to production of cGMP from GTP, which then leads to vasodilation; cGMP then hydrolyzed to GMP by PDE. : only route is iv; rapid onset (minutes) and cessation (minutes), thereby allowing minute-by-minute titration; CN- metabolite is converted to SCN in liver, then excreted in urine; must be given by continuous infusion

131
Q

Nitroprusside toxicities/interactions

A

excessive hypotension; accumulation of CN- and thiocyanate; headache; decreased blood flow to brain.
additive effects with most other antihypertensives

132
Q

Nitroprusside special considerations/administration

A

monitor patient VERYclosely—must be in ICU with arterial line; avoid high infusion rates or prolonged infusions, to prevent accumulation of CN-; use with caution in patients with increased intracranial pressure. Given IV in continuous infusion 0.3-10 mcg/kg per minute, must have arterial central line. Monitor BP, CN-, HR, metabolic acidosis

133
Q

Amlodipine class/action

A

pharmacologic class—dihydropyridine calcium entry blocker; therapeutic class– antihypertensive, antianginal (classical and variant).

134
Q

Amlodipine pharmacodyamics/kinetics

A

reduces BP by inhibiting influx of calcium through “slow channels”, thereby dilating peripheral arterioles; also, produces negative inotropic effect as well in myocardial cells; for angina, reduces afterload, thus decreasing oxygen consumption; also, inhibits spasm of coronary arteries in vasospastic angina. F 64-90%; peak effects 6-12 hours post dose; duration 24 hours; extensively metabolized in liver 90% excreted in urine as inactive metabolites

135
Q

Amlodipine toxicities/interactions

A

hypotension, AV block, worsening of CHF, bradycardia, headache, edema; watch out in patients with aortic stenosis, heart failure, severe liver disease. additive effects with most other antihypertensives; additive toxic effects on heart when given with beta-blockers (negative inotropic and dromotropic effects)

136
Q

Amlodipine special considerations/administration

A

shorter-acting nifedipine (and similar CEBs) can increase risk of MI (unclear why); Pregnancy C . 2.5-10mg daily. Pregnancy class C

137
Q

Clonidine Special considerations/ administration

A

Pregnancy class C; avoid in patients with renal insufficiency, Begin .2mg PO BID, up to 1.2 mg per day. Transdermal administration as well. BP, HR, fatigue

138
Q

Trimethaphan special considerations, administration

A

patients are quite miserable, hence only used during general anesthesia; also, helps to tilt patient to help control BP. Given only briefly to treat hypertensive crisis, or for controlled hypotension during surgery. Must monitor BP minute to minute.

139
Q

Reserpine

A

historic drug, first sympathneumetic drug used to treat hypertension. Prevents endocytosis of vesicles containing NE and serotonin, preventing firing of nerves. Takes several weeks to build up, not used clinically anymore

140
Q

Non selective beta receptor agonists

A

propranolol, nodalol

141
Q

Cholestyramine class/action

A

bile sequestering drug, cholesterol lowering drug

142
Q

Cholestyramine pharamcodynamics

A

forms a non-absorbable complex with bile acids in small bowel (releasing Cl); inhibits enterohepatic reuptake of intestinal bile salts; increases fecal loss of bile acids > increases bile acid synthesis > increases cholesterol synthesis > increases expression of LDL receptors on cell surface of hepatocytes > reduces LDL chol by 10-20% (maximum)

143
Q

Cholestyramine pharmacokinetics

A

virtually no absorption; excreted in feces; peak effect 3 weeks

144
Q

Cholestyramine toxicities/interactions

A

> 10% of patients have GI problems including gas, bloating, diarrhea, constipation; may interfere with absorption of fat-soluble vitamins, and drugs including digoxin, warfarin, thyroxine. may diminish absorption of statins, steroids, digoxin, warfarin.

145
Q

Cholestyramine special considerations/dose

A

given in oral suspension multiple times a day. not used much anymore, as was first one.

146
Q

Nicotinic Acid/Niacin classes

A

vitamin, cholesterol lowering medicine.

147
Q

Nicotinic acid/niacin pharamcodynamics

A

lowers BOTH TG and LDL-chol; decreased production of VLDL > decreased production of LDL > increase in LDL receptor in liver; modestly effective as single agent, usually used in combination; can also raise HDL; Note: recent study NEJM 2011 showed that while adding niacin to a statin can further reduce TG and raise HDL, these changes were NOT associated with improved clinical outcomes

148
Q

Nicotinic Acid pharmacokinetics

A

well absorbed, large first pass effect (to nicotinamide); Tmax 45 min; half-life 45 min; urinary excretion of unchanged drug and metabolite

149
Q

Nicotinic Acids toxicities/Interactions

A

many patients develop skin flushing, which can be lessened by taking aspirin; some patients develop hepatitis. Reduced absorption with cholesyteramine

150
Q

Gemfibrozil class/action

A

Pharm–Fibric acid derivative; Rx–Lipid-lower agent

151
Q

Gemfibrozil pharamcodynamics

A

cellular mechanism of action remains unclear (prob related to inhibition of lipolysis and decrease hepatic fatty acid uptake, inhibit hepatic secretion of VLDL); produces slight reduction in LDL-chol levels (-4%); most useful in treatment of hypertriglyceridemia in types IV and V hyperlipidemia (-31%); may increase HDL-chol (+6%)

152
Q

Gemfibrozil pharamcokinetics

A

well absorbed; oxidized in liver to two inactive metabolites; half-life 1-2 h

153
Q

Gemfibrozil toxicities/interactions

A

elevation of LFTs; myositis; GI distress; avoid in patients with renal, hepatic, or biliary tract disease. increased theraputic effect with statins, but possibly increased toxicity as well.

154
Q

Gemfibrozil considerations/administrations

A

600mg PO bid. contraindicated in individuals with liver or kidney disease.

155
Q

Atorvastatin class/action

A

HMG-CoA reductase, lipid lowering drug, primary and secondary CAD preventer.

156
Q

Atorvastatin pharmacodynamics

A

Parent drug (lactone) is transformed to an active metabolite, which inhibits HMG-CoA reductase, the early and rate-limiting step in the synthesis of cholesterol. Inhibition is not complete. Leads to up-regulation of LDL receptors on hepatocytes, so that liver cells can import more cholesterol. Leads to reduction in LDL-chol (-10-65%), increase in HDL (small)

157
Q

Atorvastatin pharmacokinetics

A

Rapidly absorbed; extensively metabolized, likley mostly by CPT 3A4; metabolites account for most of its activity; active metabolites have half-life of 20-30 h

158
Q

Atorvastatin toxicities/interactions

A

Check LFTs and CPK during first year. may cause rhabdomyolysis, myositis, myopathies, hepatitis. Additive effects with cholestyramine, nicotinic acid, ezetimibe; gemfibrozil and niacin may increase risk of myopathy; erythromycin, cyclosporine, fluconazole, and others may inhibit CYP 3A4 metabolism, thereby causing increased accumulation and increasing toxicity. Avoid in patients with pre-existing hepatitis, muscle disease, and pregnancy

159
Q

Ezitemibe class/action

A

Pharm class–2-azetidinone compound; Therapeutic class–cholesterol absorption inhibitor

160
Q

Ezitemibe pharmacodynamics

A

Selectively blocks the intestinal absorption of cholesterol and related phytosterols, by acting at the level of the small bowel brush border; causes reduction of hepatic cholesterol stores, and an increase in the blood clearance of cholesterol; when used as monotherapy, can lower LDL-chol by up to 18%; often used with a statin; recent work suggests that while it can lower LDL-chol, it may not add to overall clinical efficacy (clinical endpoints)

161
Q

Ezitemibe pharmacokinetics

A

Given orally; Tmax 4-12h; extensively metabolized to the glucoronide; F 35-60%; t 1/2 = 22 h

162
Q

Ezitemibe toxicities/interactions

A

HA in about 8%, diarrhea in about 4%. Use in combination with dietary therapy, as monotherapy, or in combination with a statin (is available as Vitorin, ezetimibe + simvastatin); bile acid sequestrates may decrease F. Use in caution in patients with renal or hepatic impairment.

163
Q

Nitroglycerin class

A

nitrate. vaso/venodilator. anti-anginal

164
Q

Nitroglycerin pharmacodynamics/kinetics

A

reacts directly with sm cells to casue reduction of organic nitrate to NO, resulting in upregulation cGMP. High bioavailability, rapid onset, can be given in mutliple formats

165
Q

Nitroglycerin toxicities/interactions

A

excessive hypotension, throbing headaches, flushing. excessive hypotension, severe hypotension with viagra

166
Q

Nitroglycerin fun facts

A

can develop tolerance quickly, remove patch before defibrulating

167
Q

Asprin class

A

salicilate. antiplatlet, antipyretic, anti-inflammatory, analgesic

168
Q

Asprin pharmacodynamics/kinetics

A

in low doses, irreversibly inhibits cox-1 in platlets preventing platlet aggregation and vasoconstriction. transiently inhibits cox-2 (vasodilation, platlet dispersal). F= 60%, Tmax variable, excreted in urine.

169
Q

Asprin toxicities/interactions

A

GI bleed, GI ulcer, tinnitus. prevents methotrexate excretion, predisopose to bleeding with if taking warfarin. avoid in patients with nasal polyps or asthma

170
Q

Clopidogrel class

A

inhibitor of ADP induced platlet aggregation. anti-platlet

171
Q

Clopidogrel pharmacodynamics/kinetics

A

blocks ADP receptor directly preventing recruitment of other platlets via llb-llla. useful in primary prevention of stroke and tia, angina blah blah. parent drug not active, must be metabolized. Well absorbed, onset 1-2 hours, hepatic metabolism, half life 8 hours

172
Q

Clopidogrel toxicities/interactions

A

hemorrhage, bruising, skin discloeration. increased risk of bleeding with aspirin but also increased effectiveness. May inhibit CYP3A

173
Q

Abciximab class

A

Fab fragment of chimeric monocolonal antibody. Adjunct to to PCI, prevents ischemia, prevents MI.

174
Q

Abciximab pharmacodynamics/kinetics

A

binds non-competitively to IIb/IIIa receptor, preventing binding of VWF anf fibrinogen, to prevent active platlet aggregations. IV bolus + IV infusion. half life 30 minutes, decrease in clot time after 12 hours.

175
Q

Abciximab toxicities/interactions

A

contraindicated in GI bleed, intracranial mass, bleeding, trauma, etc. Additive effects with aspirin, clopiderol, heparin, low dose tPA.

Pharmacology (7 decks)

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