Cardio/Respiratory Drugs Flashcards
1
Q
Direct acting sympathoneumonic
A
directly acts on the post synaptic receptor. NE,E
2
Q
indirect acting sympathoneumonic druc
A
increases the release of the transmit in the presynaptic terminal. amphetamine, meth, MDMA
3
Q
Block the re-uptake of sympathetics
A
amytriptiline, coains
4
Q
block the degeneration of NE
A
MAO inhibitors, phenylezene
5
Q
Phenylephrine
A
A1 agonist, vasconstriction/venoconstriction.
6
Q
Phenylpherine indications and doses
A
decongestion, eye dilator (Mydriatic), raises BP. Given topically or IV.
7
Q
Phenyephrine
A
Less potent vasoconstrictor, not inactivated by COMT
8
Q
Clonidine class/action
A
pharmacologic class—central α2 agonist; therapeutic class–antihypertensive, adjunct to Rx of opioid withdrawal, prophylaxis of migraine
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
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
11
Q
Selective alpha agonists
A
clonidine and phenylephrine
12
Q
Selective beta agonists
A
isoproterenol, dobutamine, albuterol
13
Q
Isoproterenol class/action
A
B1, B2 agonist. Increases HR, contractility, cardiac conduction
14
Q
Isoproterenol dosage/side effects
A
IV administration. Not used as much as causes tachyarrythmias and vasodilation
15
Q
Dobutamine mech
A
B1 agonist. highly effective beta agonist, also causes dilation of renal and mesenteric blood vessels
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
17
Q
Albuterol
A
B2 agonist, brochodilation
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
19
Q
Mirabegron mech
A
B3 agonist. stimulates the detrusor muscle, reducing tone
20
Q
Mirabegron indications/administrations
A
for overactive bladder. Relaxes detrusor and increases bladder capacity. administered orally
21
Q
Epinephrine class
A
direct acting adernegic agonist, cardiac stimulator, bronchodilator
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
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
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
25
Epinephrine toxicity and interactions
excessive HTN, vasconstriction, hemorrhagic stroke, tachycardia, arrhythmias. Risk of severe htn interaction with propranolol.
26
Epinephrine monitoring
BP, HR, extravasation, rhythm, infusion site
27
Norepinephrine drug class
direct acting adernergic agonist, vasoconstrictor, cardiac stimulator
28
Norephinephrine pharmacodynamics
A1 stimulation- vasoconstriction and venoconstriction peripherally. Does lead to decreased BF to kidneys, skin, and muscle. B1 agonist-cardiac stimulation (HR, contractility).
29
Norepinephrine pharmacokinetics
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
30
Norepinephrine toxicities/interactions
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.
31
Norepinephrine special considerations
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.
32
Dopamine-description/actions
DA, A1,B1 agonist. DA agonist at low dose, B1 agonist at medium dose, A1 agonist at high dose.
33
Dopamine-usages and indications
shock-stimulates heart, vasoconstriction, increases mesenteric and renal perfusion. given for short periods of time
34
Ephedrine class/action
from ephedra plant, stimulates stored NE from neurons, some direct agonism.
35
Ephedrine indications/ usage
mild to moderate hypotension, nasal congestion. Used for short acting (15 minutes) effect in surgery. potent CNS stimulant, can cause HTN and insomnia
36
Pseudoephedrine class/action
vasoconstricor, stimulates NE neurons to release stored NE. , some direct A and B agonism.
37
Pseudoephedrine indications/usage
nasal decongestion, doesn't dilate bronchioles as well. Behind the counter product
38
Amphetamine
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.
39
Tyramine
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.
40
Cocaine
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
41
Prazosin-drug class
selective alpha 1 inhibitor, vasodilator, antihypertensive, bPH
42
Prazosin-pharmk/pharmd
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.
43
Prazosin toxicity/side effects
hypotension, especially when standing. Addititive effect with diuretics.
44
Prazosin-considerations/doasage
start at bedtime, slowly build up dose. Begin with 1mg tid, up to 20mg tid. continue to monitor BP, weight, edema
45
Pheotolamine class
non-selective, competitive alpha adernergic receptor antagonist. Used for hypertension in individuals with pheochromocytoma
46
Phenotolamine pharmk/d
blocks A1 and A2 receptors at the presynaptic and post synaptic membranes. This decreases preload and afterload. Administered IV, half life 20 minutes
47
Phentolamine toxicities/interactions
excessive hypotension and syncope, especially orthostatic. Additive effects with most other hypertensives, especially diuretics.
48
Phentolamine special considerations/dose
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
49
Atenolol/metoprolol class
b1 antagonist, anti hypertensive, anti arrythmic, MI prevention, anti anginal.
50
Atenolol/metoprolol pharmacodynamics/kinetics
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
51
Atenolol toxicities/interactions
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
52
Atenolol dosages/considerations
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
53
Labetalol drug class
anti hypertensive, treatment of stable CHF. Mixed alpha/beta antagonist.
54
Labetalol pharmacokinetics/dynamics
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
55
Labetalol toxicities and interactions
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
56
Labetalol dosage and considerations
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.
57
Carbachol class/actions
non-selective muscarinic and nicotinic receptor agonist. Ocular agent causing miosis and increased aqueous humor outflow, for use in open angle glaucoma
58
Carbachol toxicity/other factors
overuse could cause excessive adernergic toxicity but unlikely since topical. Not broken down efficiently by acetylcholinesterase so long lasting
59
Bethanechol class/actions
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.
60
Bethanechol toxicities/considerations
can cause reflex tachycardia, bronchoconstriction, increased secretory activity
61
Pilocarpine class/indications
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.
62
Pilocarpine toxicity/administration
can cause execssive acetylcholine symptoms. adminstered topical and oral
63
Methacholine class/actions/use
non selective muscarinic agonist. used to diagnos bronchial hyperactivity in the diagnosis of asthma. Inhaled only
64
Nicotine class/action
nicotinic cholinergic agonist, binds to nicotinic receptors but has slower action thn that found in cigarettes
65
Nicotine indications/side effects
smoking cessation, nicotine withdrawal. can cause bronchospasm and nicotine dependence transferance. Administered in gum, patch, nasal
66
Varenicline class/actions
partial nicotinic receptor agonist. reduces cravings for and pleasure associated with smoking by reducing the ability of nicotine to stimulate the mesolimbic dopamine system
67
Vareincline indications/side effects
given orally for smoking cessation. Can cause nausea, headaches, insomnia, abnormal dreams
68
Metoclopramide is...?
largely replaced bethanachol for post surgery gastroparaesis and antiemetic. stimulates D2 receptors to trigger Ach release
69
Edrophonium (Tensilon test)
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
70
Neostigmine class/actions
reversible cholinesterase inhibtior. Increases acetylcholine availability for post synaptic membrane receptors
71
Neostigmine Indications/ toxicity
Myasthenia gravis, nondepolarizing neuromuscular blockade reversal, urinary retention. Can cause excessive cholinergic rxn. Can be given IV, IM, SC. Does not enter CNS
72
Physostigmine class/action
reversible cholinesterase inhibitor, leading to indirect increased stimulation of M and N receptors.
73
Physostigmine indicatoions, toxicities
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
Pyridostigmine class/action
reversible cholinesterase inhibitor, indirectly stimulates both muscarinic and cholinergic inhibitors.
75
Pyridostigmine indications/toxicities
myasthenia gravis, shorter half like than Neostigmine. Does not cross BBB, low oral availability
76
Donepezil class/actions
reversible cholinesterase inhibitor, indirectly stimulates both nicotinc and muscarinic receptors.
77
Donepezil indications/toxicities
azheimers associated dementia.. can cause GI upset. Crosses the BBB, F= 100%
78
Usueful drugs for dimetia
Rivastigmine = revesible cholinesterase patch for GI upset. Galantamine = Nn agonist and acetylcholinesterase inhibitor.
79
Echothiophate class/action
irreversible cholinesterase inhibitor. binds irreversibly to acetylcholinesterase.
80
Echothinophate indications/tox
given topically for glaucoma. Can cause lacrimation and stinging. Very long half life
81
Atropine class/action
non-selective muscarinic antagonist. prevents actions of acetylcholine and down regulates cholinergic controlled processes and glands
82
Atropine indications/side effects
Indicated for organophosphate poisonings, to slow heart rate, pupil dilation, reduce secretions. Can cause anti-cholinergic set syndrome
83
Atropine dosing
Given IV, SC, IM. Lipid soluble, crosses the blood brain barrier for when toxins have as well.
84
Pralidoxime class/action
reactivates cholinesterase. Binds to deactivated acetylcholinesterase and speeds reactivation.
85
Pralidoxime indications/toxicities
cholinesterase inhibitor overdose. exposure to organophosphates. When paired with atropine, can worsen anti-cholinergic syndrome
86
Pralidoxime administration
IV, IM only. Must be used soon after exposure. Military stockpiles large amounts of these.
87
Bentropine class/action
M1 receptor antagonist and histamine receptor blocker. Centrally acting
88
Bentropine indications/tox
used for parkinsonism, disorders of extrapyramidal system, dystonia. Can cause anticholinergic excess syndrome
89
Bentropine administration
IV IM
90
Scopolamine class/action
non-selecitve muscarinic receptor blocker. Possibly some specificity for M1 receptors, anti emetic.
91
Scopolamine indication/side effects/adminstration
given to prevent sea sickness and dilate eyes. Can cause anti-cholinergic syndrome. transdermal, can cross BBB
92
Ipratropium class/action
non selective muscarinic receptor antagonist. Inhaled bronchodilator. Generally slower acting, combined with albuterol.
93
Ipratropium indications/side effects
asthma/COPD. Can cause bad taste and dry mouth. could cause anticholinergic syndrome but only with overdose
94
Dicyclomene class/actions
non-selective muscarinic antagonist. Relaxes smooth muscle, inhibits bradykinin and histamine to reduce bowel spasm.
95
Dicyclomene indications, side effects
used for IBS. Can cause anticholinergic syndrome with delerium at higher doses. Administered orally
96
Succinylcholine class/action
nicotinic NMJ blocker, Nm receptor agonist. Depolarize muslce, not terminated, resulting in flaccid paralysis. Not brocken down acetylcholinesterase.
97
Succinylcholine indications/toxicities
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
Succenycholine special considerations
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
D-tubocurarine class/action
reversible NMJ receptor antagonist. Directly blocks receptor on end plate, causing muscle paralysis.
100
D-tubocurarine indications/toxicities
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
D-tubocurarine administration/reversal
duration 30-60 minutes, neostigmine will reverse.
102
Vecuronium class/action
NMJ receptor antagonist, reversible, non-competitive inhibitor. Directly blocks receptors on NJM endplate
103
Vecuronium indications/toxicities
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
Vecuronium duration/reversile
lasts 30-60 minutes, neostigmine will reverse Can cause hepatic damage
105
Cisatracurium class/action
nicotinic NJM blocker, reversible competitive inhibition. Antagonizes muscular endplate
106
Cisatracurium indications/toxicities
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
Cisatracurium duration/reversile
30-60 minutes. Neostigmine will reverse.
108
Trimetaphan class/action
competive gangliosidic blocker, acts as a non-depolarizing gangliosidic antagonist. Antihypertensive. Blocks the parasympathetic and sympathetic systems.
109
Trimetaphan pharamcodynamics/kinetics
: 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
Trimetaphan toxicities/interactions
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
Botulinum class/action
bacterial exotoxin, derived from C. botulinism. Cleaves snare proteins, inhibiting release of acetylcholine.
112
Botulinum indications/tox
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
HCTZ- class/action
thiazide diuretic. diuretic, anti-hypertensive
114
HCTZ pharmacodynamics/kinetics
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
HCTZ side effects/toxicities
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
HCTZ administration, special considerations
: 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
Lisinopril class/action
Ace inhibitor. anti-hypertensive, CHF control, MI recurrence reduction, acute MI reduction, preserve renal function
118
Lisinopril pharmacodynamics/kinetics
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
Lisinopril toxicities/interactions
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
Lisinopril special considerations/administration
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
Losartan class/action
ARB. antihypertensive, preserve renal function, treatment of CHF
122
Losartan pharmacodynamics/kinetics
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
Losartan toxicities/interactions
dizziness; orthostatic hypotension; worsening of renal failure. : additive effects with most other antihypertensives
124
Losartan special considerations/dosage
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
Hydralazine class/action
peripheral vasodilator; therapeutic class-- antihypertensive, treatment of CHF, vasodilator
126
Hydralazine pharmacodynamics/kinetics
“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
Hydralazine side effects/toxicities
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
Hydralazine special considerations/dosage
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
Nitroprusside class/action
pharmacologic class-- vasodilator; therapeutic class--antihypertensive, management of severe CHF, management of pulmonary hypertension, produce controlled hypotension to reduce bleeding during surgery
130
Nitroprusside pharamcodynamic/kinetics
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
Nitroprusside toxicities/interactions
excessive hypotension; accumulation of CN- and thiocyanate; headache; decreased blood flow to brain.
additive effects with most other antihypertensives
132
Nitroprusside special considerations/administration
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
Amlodipine class/action
pharmacologic class—dihydropyridine calcium entry blocker; therapeutic class-- antihypertensive, antianginal (classical and variant).
134
Amlodipine pharmacodyamics/kinetics
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
Amlodipine toxicities/interactions
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
Amlodipine special considerations/administration
shorter-acting nifedipine (and similar CEBs) can increase risk of MI (unclear why); Pregnancy C . 2.5-10mg daily. Pregnancy class C
137
Clonidine Special considerations/ administration
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
Trimethaphan special considerations, administration
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
Reserpine
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
Non selective beta receptor agonists
propranolol, nodalol
141
Cholestyramine class/action
bile sequestering drug, cholesterol lowering drug
142
Cholestyramine pharamcodynamics
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
Cholestyramine pharmacokinetics
virtually no absorption; excreted in feces; peak effect 3 weeks
144
Cholestyramine toxicities/interactions
>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
Cholestyramine special considerations/dose
given in oral suspension multiple times a day. not used much anymore, as was first one.
146
Nicotinic Acid/Niacin classes
vitamin, cholesterol lowering medicine.
147
Nicotinic acid/niacin pharamcodynamics
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
Nicotinic Acid pharmacokinetics
well absorbed, large first pass effect (to nicotinamide); Tmax 45 min; half-life 45 min; urinary excretion of unchanged drug and metabolite
149
Nicotinic Acids toxicities/Interactions
many patients develop skin flushing, which can be lessened by taking aspirin; some patients develop hepatitis. Reduced absorption with cholesyteramine
150
Gemfibrozil class/action
Pharm--Fibric acid derivative; Rx--Lipid-lower agent
151
Gemfibrozil pharamcodynamics
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
Gemfibrozil pharamcokinetics
well absorbed; oxidized in liver to two inactive metabolites; half-life 1-2 h
153
Gemfibrozil toxicities/interactions
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
Gemfibrozil considerations/administrations
600mg PO bid. contraindicated in individuals with liver or kidney disease.
155
Atorvastatin class/action
HMG-CoA reductase, lipid lowering drug, primary and secondary CAD preventer.
156
Atorvastatin pharmacodynamics
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
Atorvastatin pharmacokinetics
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
Atorvastatin toxicities/interactions
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
Ezitemibe class/action
Pharm class--2-azetidinone compound; Therapeutic class--cholesterol absorption inhibitor
160
Ezitemibe pharmacodynamics
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
Ezitemibe pharmacokinetics
Given orally; Tmax 4-12h; extensively metabolized to the glucoronide; F 35-60%; t 1/2 = 22 h
162
Ezitemibe toxicities/interactions
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
Nitroglycerin class
nitrate. vaso/venodilator. anti-anginal
164
Nitroglycerin pharmacodynamics/kinetics
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
Nitroglycerin toxicities/interactions
excessive hypotension, throbing headaches, flushing. excessive hypotension, severe hypotension with viagra
166
Nitroglycerin fun facts
can develop tolerance quickly, remove patch before defibrulating
167
Asprin class
salicilate. antiplatlet, antipyretic, anti-inflammatory, analgesic
168
Asprin pharmacodynamics/kinetics
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
Asprin toxicities/interactions
GI bleed, GI ulcer, tinnitus. prevents methotrexate excretion, predisopose to bleeding with if taking warfarin. avoid in patients with nasal polyps or asthma
170
Clopidogrel class
inhibitor of ADP induced platlet aggregation. anti-platlet
171
Clopidogrel pharmacodynamics/kinetics
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
Clopidogrel toxicities/interactions
hemorrhage, bruising, skin discloeration. increased risk of bleeding with aspirin but also increased effectiveness. May inhibit CYP3A
173
Abciximab class
Fab fragment of chimeric monocolonal antibody. Adjunct to to PCI, prevents ischemia, prevents MI.
174
Abciximab pharmacodynamics/kinetics
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
Abciximab toxicities/interactions
contraindicated in GI bleed, intracranial mass, bleeding, trauma, etc. Additive effects with aspirin, clopiderol, heparin, low dose tPA.
