Term
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Definition
Only NT in parasympathetic, first NT in sympathetic
Muscarninc and nicotinic receptors
acetyl CoA + choline via choline acetyltransferase -> acetylcholine
Hydrophilic-> poorly absorbed, poorly distributed to CNS; rapidly hydrolyzed
Effects: DUMBELSS |
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Term
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Definition
Muscarinic cholinergic receptor agonist
Effects: miosis; vasodialation, slowing of HR (at higher levels of receptor activation); bronchial constriction, increased respiratory secretion; increased GI motility and secretion, sphincter relaxation=> DUMBELSS
High resistance to hydrolysis
Use: post-op urinary retention or paralytic ileus
Oral or parenteral; does not enter CNS
Toxicity: parasympathomimetic effects, bronchospasm in asthmatics |
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Term
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Definition
Muscarinic cholinergic receptor agonist (partial agonist)
Effects: miosis; vasodialation, slowing of HR (at higher levels of receptor activation); bronchial constriction, increased respiratory secretion; increased GI motility and secretion, sphincter relaxation=> DUMBELSS
Use: test for CF by promoting sweat secretion
Oral or topical |
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Term
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Definition
Muscarinic cholinergic receptor agonist
Metabotropic receptor
Effects: miosis; vasodilation, slowing of HR (at higher levels of receptor activation); bronchial constriction, increased respiratory secretion; increased GI motility and secretion, sphincter relaxation=> DUMBELSS
Occurs through actions on effector cells |
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Term
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Definition
Nicotinic cholinergic receptor agonist
Ionotropic receptor- increased Na+ influx and depolarization
Nn receptor: PNS, SNS, ganglion cells
Nm receptor: neuromuscular junction
Activate both the sympathetic and parasympathetic nervous systems, but the net effect depends on the organ and the predominant tone
Highly lipophilic-> penetrates BBB, well absorbed across skin
Toxicity: increased GI activity; increased BP; continued agonist occupancy is associated w/ desensitization (depolarization blockade)-> flaccid paralysis/respiratory arrest
Can also be used as a pesticide |
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Term
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Definition
AchE inhibitor; carbamate ester
MOA: forms covalent bond w/ AchE that is resistant to hydrolysis; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic affects predominate=> DUMBELSS
Hydrolysis can occur but at a slow rate (30min-6hr)
Well absorbed but in general carbamates are not
Use: glaucoma; antimuscarinic drug intoxication |
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Term
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Definition
AchE inhibitor; 4° alcohol
MOA: Forms an electrostatic/H-bond with AchE that is reversible; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic affects predominate=> DUMBELSS
Short-lived inhibition (~2-10 min)
Poorly absorbed in brain due to its permanent charge
Use: diagnosis and treatment of myasthenia gravis; paralytic ileus; arrhythmias
Given parenterally |
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Term
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Definition
AchE inhibitor; Organophosphate
MOA: Prevents breakdown of acetylcholine; phosphorylates the active site of AchE and forms a bond that is extremely stable; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic effects predominate=> DUMBELSS
Hydrolyzes at an extremely slow rate (100s of hours)
Can undergo aging where there is strengthening of the AchE-phosphorus bond
Poorly absorbed
Uses: glaucoma
Toxicity: brow ache, uveitis, blurred vision |
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Term
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Definition
Antimuscarinic
Treatment: asthma or COPD
Muscarinic receptor antagonist- competitive antagonist
MOA: reversible blockade of Ach receptors
Effects: eye dilation (mydriasis); cycloplegia (loss of accommodation); tachydcardia; bronchodilation; dry mouth; reduced GI motility; reduced urination; reduced sweating
Use: cholinergic poisoning; eye examination
Given IV, topically (drops)-> well absorbed from conjunctival and gut membranes
Toxicity: dry mouth, flushed skin; agitation; delirium; hyperthermia-> dry as a bone, blind as a bat, red as a beet, mad as a hatter |
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Term
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Definition
Muscarinic receptor antagonist
Effects: eye dilation (mydriasis); tachydcardia; bronchodilation; dry mouth; reduced GI motility
Use: vertigo; nausea
Given IM or transdermal
Faster onset of action than Atropine but shorter duration of effect and crosses CNS more readily -> well absorbed from gut and conjunctival membranes; can also cross skin
Toxicity: tachycardia, blurred vision, delirium, xerostomia (dry mouth), drowsiness, amnesia, hallucinations, coma |
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Term
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Definition
Antimuscarinic
MOA: competitive, nonselective antagonist for muscarinic receptors
Treatment: asthma/COPD-> reduces bronchospasm
Given via aerosol; poorly absorbed into circulation and does not enter CNS
Toxicity: xerostomia (dry mouth), cough |
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Term
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Definition
Antimuscarinic
MOA: binds M1, M2, and M3 receptors but dissociates from M2 quickly-> prevents Ach effects and does not prevent M2 mediated release inhibition
Long acting (24hr), taken by inhalation once daily
Treatment: asthma, COPD-> reduces incidences of exacerbations |
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Term
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Definition
Ganglion blocker
MOA: block the action of Ach at sympathetic and parasympathetic nicotinic receptors; blockade by occupying sites in/on nicotinic ion channel but not the actual cholinoceptor
Use: HTN
Effects: cycloplegia/loss of accommodation; decreased BP (decreased arteriolar and venomotor tone)-> orthostatic hypotension; decreased GI motility/secretion-> constipation; urinary retention; sexual dysfunction (erection and ejaculation); reduced sweating |
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Term
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Definition
Ganglion blocker
MOA: block the action of Ach at sympathetic and parasympathetic nicotinic receptors; blocks the nicotinic receptor, not the pore
Use: hypertensive emergency, dissecting aortic aneurysm, reduce surgical bleeding, ECT
Short acting; given IV infusion (inactive orally)
Effects: cycloplegia/loss of accommodation; decreased BP (decreased arteriolar and venomotor tone)-> orthostatic hypotension; decreased GI motility/secretion-> constipation; urinary retention; sexual dysfunction (erection and ejaculation); reduced sweating |
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Term
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Definition
Ganglion blocker
MOA: competitively blocks the action of Ach at symp and parasymp nicotinic receptors
Use: adjunct for smoking cessation
Effects: readily crosses BBB-> sedation, tremor, choreiform movements, mental aberrations; cycloplegia/loss of accommodation; decreased BP (decreased arteriolar and venomotor tone)-> orthostatic hypotension; decreased GI motility/secretion-> constipation; urinary retention; sexual dysfunction (erection and ejaculation); reduced sweating |
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Term
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Definition
Indirect acting sympathomimetic
MOA: drug taken up via DAT/NET which causes increased release of dopamine and NE/serotonin from presynaptic neuron by reversal of transporters and preventing normal reuptake via NET/DAT/SERT/VMAT
Readily enters CNS; d-isomer is most potent
SE: insomnia, anorexia, tics, headaches, visual hallucinations, emotional lability, growth retardation
Contraindications: history of mania, psychosis, drug/alcohol abuse; closed angle glaucoma (increases alpha adrenergic receptor activation)
Drug Interactions: other sympathomimetics (increased BP/HR); MAO-I (hypertensive crisis); phenobarbital/phenytoin/tricyclic antidepressants (inhibits their metabolism)
Abuse: oral, smoked, or injected
Effects: alertness, euphoria, agitation, confusion, bruxism (tooth grinding), skin flushing, tachycardia, arrhythmia, HTN crisis, stroke |
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Term
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Definition
Indirect acting sympathomimetic; Local anesthetic
MOA: PNS- inhibits voltage gated Na+ channels; CNS- blocks uptake of DA, NE, serotonin
Produces an amphetamine-like effect that is shorter acting and more intense
Penetrates brain quickly
Effects: rush; tachycardia, ventricular arrhythmia, appetite loss, hyperactivity, insomnia; increased risk of stroke, intracranial hemorrhage, MI, seizure; hyperthermia, coma/death |
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Term
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Definition
Antihypertensive-> Adrenergic Neuron Blocker
Now rarely used
MOA: irreversibly blocks VMAT, depleting stores of NE, DA, and serotonin in central and peripheral neurons and adrenal medulla
Rapidly crosses BBB; half-life 24-48hrs
Toxicity: diarrhea, GI cramps, increases gastric acid secretion; sedation, lassitude, nightmares, depression, EPS/Parkinsonism
Contraindications: depression |
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Term
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Definition
Indirect acting sympathomimetic
Byproduct of tyrosine metabolism; found in fermented foods
MOA: increase synaptic levels of catecholamines by mimicking excitation of SNS; increases release
Use with caution in patients on MAO-A inhibitors-> normally degraded by MAO in liver
Low oral bioavailability b/c of first pass effect (concentration is reduced in liver); parenteral injection
Side effects: elevated BP |
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Term
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Definition
Antihypertensive
Guanethidine-like drug available in USA
Antihypertensive-> Adrenergic Neuron Blocker
Now rarely used
MOA: uptake into symp nerves by NET and replaces NE stores
Too polar to enter CNS-> no central SE
Half-life 5days (120hrs); maximal effect in 1-2wks
May require reduction of dosage in moderate renal insufficiency
Toxicity: orthostatic and exercise hypotension; delayed/retrograde ejaculation; diarrhea
DI: TCAs/sympathomimetics (cocaine, amphetamine)-> block uptake and cause hypertension
Contraindications: pheochromocytoma-> hypertensive crisis |
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Term
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Definition
Mixed-Acting Sympathomimetic
MOA: Directly stimulates alpha-adrenergic receptors of respiratory mucosa causing vasoconstriction; directly stimulates beta-adrenergic receptors causing bronchial relaxation, increased heart rate and contractility
Higher bioavailability and duration of effects than catecholamines; longer acting than Epi w/ lower potency
Excreted in urine-> a significant fraction remains unchanged
Use: decongestant |
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Term
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Definition
Mixed α/β agonist; α1=α2; β1>>β2
Increased PVR, total BP, and contractility
Compensatory baroreflex overcomes positive chronotropic effects-> decrease in HR
Use: acute hypotension |
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Term
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Definition
Mixed α/β agonist; α1=α2; β1=β2
Vasoconstriction and cardiac stimulant (increase HR); bronchodilator
Use: asthma; anaphylaxis (EpiPen)
For asthma, maximal bronchodilation in 15mins, lasts 60-90mins
Given as aerosol, nebulizer, or parenteral |
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Term
ALBUTEROL
TERBUTALINE
METAPROTERENOL |
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Definition
Beta agonist; β2>>β1
Treatment: asthma, COPD, premature labor (uterine relaxation)
Maximal bronchodilation 15-30mins, lasts 3-4hrs
All given by inhalation, albuterol and terbutaline also by tablet, terbutaline also subcutaneous
Tox: tremor, tachycardia, arrhythmia |
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Term
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Definition
MOA: selective β2 agonist
Slow onset, long acting (12hrs+)-> high lipid soluble so dissolves in sm musc cell memb
Has no anti-inflammatory component- not for monotherapy
Treatment: asthma prophylaxis
Given via inhalation
Tox: tremor, tachycardia, arrhythmia |
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Term
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Definition
Antihypertensive; Antiarrhythmic- Class 2
MOA: nonselective β-adrenergic receptor antagonist; local anesthetic action
Anti-ischemic effects-> decrease in CO (decreased HR); inhibits renin production (β1)
Half-life 3-5hrs; given orally (sustained release prep available) or parenterally; highly lipid soluble
Toxicity: bradycardia; asthma; fatigue; vivid dreams; cold hands; withdrawal from β-receptor upregulation-> nervousness, tachycardia, angina, increase BP, MI
Contraindications: bradycardia, cardiac conduction disease, asthma, peripheral vascular insufficiency, diabetes |
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Term
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Definition
Antihypertensive
MOA: β-adrenergic receptor partial agonist, but greater agonist for β2-> intrinsic sympathomimetic effect; local anesthetic action
Moderate lipid solubility; half-life 3-4hrs; given orally
May potentiate actions of antidepressants
Toxicity: fatigue, cold hands, vivid dreams |
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Term
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Definition
Antihypertensive; Antiarrhythmic- Class 2
MOA: cardioselective β-adrenergic receptor antagonist (β1>>>β2) w/ local anesthetic action
Anti-ischemic effects-> lower HR/BP; reduce renin
High 1st pass metabolism; half-life 3-7hrs; moderate lipid solubility
Sustained release version effective in HTN + heart failure
Toxicity: bradycardia, fatigue, vivid dreams, cold hands |
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Term
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Definition
Antihypertensive
Treatment: angina; HTN; arrhythmia
MOA: cardioselevtive β-adrenergic receptor antagonist (β1>>>β2)
Lowers HR/BP and renin
Half-life 6-9hr; not extensively metabolized; given once daily
Reduction in dosage required in moderate renal insufficiency
Toxicity: bradycardia, fatigue, vivid dreams, cold hands |
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Term
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Definition
Antihypertensive
MOA: selective β1 adrenergic receptor antagonist (β1>>>β2)
Rapidly metabolized via hydrolysis by RBC esterases; half-life 9-10mins
Given constant IV infusion for intra and postop HTN
Toxicity: bradycardia, hypotension |
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Term
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Definition
Antihypertensive- racemic mixture of 4 isomers
MOA: reversible adrenergic antagonist (β≥α1>α2) w/ partial agonist and local anesthetic activity
Decreases BP w/ limited HR increase
Half-life 5hrs; given oral or parenteral
Toxicity: less tachycardia than other α1 blockers |
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Term
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Definition
MOA: reversible α-adrenoceptor competitive antagonist (α1=α2); minor inhibition of 5-HT receptor and agonism of M, H1, and H2 receptors
Given IV and oral; half-life 45mins
Toxicity: severe tachycardia, arrhythmia, MI |
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Term
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Definition
MOA: irreversible α-adrenoceptor antagonist (α1>α2); inhibits reuptake of NE; blocks H1, Ach, and 5-HT receptors
Long duration (14-48hrs); given orally
Toxicity: orthostatic hypotension, tachycardia, MI; nasal stuffiness; inhibits ejaculation, fatigue, sedation, nausea |
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Term
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Definition
Antihypertensive
MOA: reversible α1 adrenergic receptor antagonist; allows NE to exert neg feedback on its own release (via α2)
α1 in arterioles and venules-> lowers BP by reducing vascular pressure
Toxicity: retention of salt and water; dizziness, palpitations, headache, lassitude, positive test for antinuclear factor (no rheumatic symptoms) |
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Term
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Definition
MOA: competitive α1 antagonist
High bioavailability; half-life 9-15hrs; hepatic metabolism
Greater potency for inhibiting prostate sm musc vs vascular sm musc
Little effect on standing BP
Use: benign prostatic hyperplasia
SE: orthostatic hypotension (uncommon) |
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Term
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Definition
L-arginine --NOS--> L-citrulline + NO
NOS requires O2 and NADPH
Enzyme bound cofactors: heme, BH4, FAD |
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Term
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Definition
NO Scavenger
MOA: NO is inactivated by superoxide; superoxide dismutase scavenges superoxide anion, protecting NO
Enhances NO potency, prolongs its duration |
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Term
| L-NMMA (Nω-monomethyl-L-arginine) |
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Definition
Nitric Oxide Synthase Inhibitor- nonselective
MOA: competitive inhibitor; binds arginine binding site in NOS
Treatment: hypotension |
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Term
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Definition
Soluble guanylyl cyclase inhibitor
MOA: NO activates soluble guanylyl cyclase to convert GTP->cGMP which activates PKG, an inhibitor of VSMC Ca2+ release and contraction; methylene blue inhibits guanylyl cyclase
Treatment: hypotension |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also antagonize NMDA receptor; may also increase K+ channel conductance and decrease nACh receptors conductance
Low solubility; rapid onset and recovery; MAC >100%
Incomplete anesthetic; no metabolism; eliminated via lungs
Toxicity: postoperative nausea and vomiting; decreased methionine synthase-> megaloblastic anemia |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
Low solubility; low volatility; poor induction agent; rapid recovery
Very little metabolism; eliminated via lungs
Effects: decrease BP; increased HR; decreased tidal V w/ increased respiratory rate; increased apneic threshold; depressed mucociliary function |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
Low solubility; rapid onset and recovery
Major elimination via lungs; metabolism-> formation of F-; also degraded by CO2 in anesthesia machine yielding compound A=> renal damage
Effects: decrease BP; decreased tidal V w/ increased respiratory rate; increased apneic threshold; depressed mucociliary function; bronchodilation
Induction agent of choice for underlying lung disease
Toxicity: decreased renal filtration |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
Moderate-high solubility; medium rate of onset and recovery
Effects: decrease BP; increased HR; decreased tidal V w/ increased respiratory rate; increased apneic threshold; depressed mucociliary function
Toxicity: tachycardia |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
Moderate-high solubility; medium rate of onset and recovery
Major elimination via lungs; renal metabolism-> formation of F-=> decreased renal concentrating ability
Effects: decrease BP; decreased tidal V w/ increased respiratory rate; increased apneic threshold; depressed mucociliary function
Toxicity: decreased renal filtration |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
High solubility; medium rate of onset and recovery
Major elimination via lungs; oxidative metabolism-> formation of trifluoroacetic acid, Br-, and Cl-; further metabolized-> chlorotrifluoroethyl free radical which interacts w/ hepatic membrane=> induced hepatitis
Effects: decrease BP; decreased HR; decreased tidal V w/ increased respiratory rate; increased apneic threshold; depressed mucociliary function; bronchodilation
Induction agent of choice for underlying lung disease
Toxicity: bradycardia; hepatotoxicity-> hepatitis (esp. obese) |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
High solubility; very slow onset and recovery
Major elimination via lungs; hepatic > renal metabolism releases fluoride ions
Effects: decrease BP; decreased tidal V w/ increased respiratory rate; increased apneic threshold; depressed mucociliary function
Toxicity: nephrotoxicity |
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Term
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Definition
Colorless, tasteless, odorless, nonirritating gas-> byproduct of combustion
MOA: combines reversibly w/ Hb at a much higher affinity than O2-> carboxyHb cannot transport O2 and prevents O2 from dissociating from oxyHb
Present in higher concentrations in smokers
CO intoxication: psychomotor impairment; headache/temporal tightness; confusion, loss of visual acuity; tachycardia/tachypnea, syncope, coma; convulsions, shock, respiratory failure
Treatment: removal from exposure, 100% O2
Elimination half-life about 320min at room air, 80min at 100% O2, 20min w/ hyperbaric O2 |
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Term
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Definition
Colorless, irritant gas-> byproduct of combustion of S containing fuels
On contact w/ moist membranes-> forms sulfurous acid=> irritant for eyes, mucous membranes, skin
Effects: bronchial constriction, bronchospasm-> asthmatics are more susceptible; delayed onset pulmonary edema |
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Term
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Definition
Brownish, irritant gas-> produced in fires and silos (silo-filler's disease)
Relatively insoluble, deep lung irritant
Effects: irritation of eyes/nose, cough, mucoid/frothy sputum, dyspnea, chest pain, pulmonary edema (w/in 1-2hrs), pulmonary lesions, death
Signs may subside but a 2nd stage of increased severity may occur about 2 wks from onset-> bronchiolitis obliterans; chronic exposure may cause emphysematous changes
Treatment: oxygenation, bronchodilators, sedatives, antibiotics |
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Term
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Definition
Bluish, irritant gas-> produced from high-voltage electrical equipment, air and water purification devices
Irritant of mucous membranes; severe exposure- pulmonary edema
Effects: rapid, shallow breathing, decrease in pulmonary compliance, upper airway irritation, changes in visual acuity, substernal pain, dyspnea, enhanced sensitivity to bronchoconstrictors, airway hyperresponsiveness/inflammation
Chronically-> bronchitis, bronchiolitis, fibrosis, emphysema |
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Term
| Halogenated aliphatic hydrocarbons |
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Definition
Industrial solvents, degreasing agents, cleaning agents
Effects:
CNS depressant- chloroform > tri- and tetrachloroethylene
Impaired memory/peripheral neuropathy- tetrachloroethylene, 1,1,1-trichloroethane
Hepatotoxicity- carbon tetrachloride
Nephrotoxicity- carbon tetrachloride, chloroform, trichloroethylene
Carcinogenic- chloroform, carbon tetrachloride, tri- and tetrachloroethylene=> renal, prostate, and testicular cancer |
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Term
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Definition
Benzene- solvents, synthesis of chemicals-> CNS depression, euphoria, nausea, locomotor problems, vertigo, coma, death, bone marrow injury (aplastic anemia, leukopenia, pancytopenia, leukemia, lymphoma, myeloma)
Toluene-> CNS depressant; skin and eye irritant, fatigue, ataxia, fetotoxic
Xylene- solvent degreasing-> CNS depressant, skin irritant |
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Term
THEOPHYLLINE
Aminophylline |
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Definition
Methylxanthines- found in tea
Aminophylline = theophylline-ethylenediamine complex
Treatment: asthma, COPD
MOA: inhibit PDE4-> increased cAMP/cGMP = sm musc relaxation; PDE4 inhibition causes reduction in inflammatory response; inhibition of adenosine receptors-> prevent contraction and histamine release; enhancement of histone deacetylation-> prevents inflammatory gene transcription (enhanced by corticosteroids-> recruit deacetylators)
Tolerance does not develop; given orally; duration 8-12hr
Hepatic metabolism (increased by smoking)-> faster in children than adults; slowest in infant
Effects: bronchodilation; increased arousal/alertness; positive chronotropic/inotropic; weak diuretic; improve contractility of diaphragm
Tox: GI; tremor; arrhythmia; seizure |
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Term
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Definition
MOA: nonselective endothelin receptor blocker-> ETA-ETB antagonist
ETB- initial transient depressor; ETA- prolonged response
Active orally
Used in pulm HTN-> causes vasodilation and decreased BP
SE: hypotension, tachycardia, facial flushing/edema, teratogenic, fatal hepatotoxicity
CI: pregnancy |
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Term
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Definition
Formed by decarboxylation of histidine via histidine decarboxylase
Self-regulated negative feedback via H2 receptors
Effects: vasodilation; chemotaxis of inflammatory cells; hypotension (vasodilation); tachycardia (stimulatory & reflex); flushing; headache; urticaria; diarrhea; bronchoconstriction
Intradermal rxn-> red spot, edema (wheal), flare response
Uses: test of bronchial hypersensitivity
Contraindications: asthma; active ulcer/GI bleeding
Physiologic antagonist-> epinephrine (acts at different receptors) |
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Term
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Definition
H1: sm musc; endothelium; brain-> increases IP3/DAG
->modulate respiratory neurons signaling inspiration/expiration; pain/itching; vasodilation (via NO); decrease cardiac contractility; bronchoconstriction; GI contraction
H2: gastic mucosa; cardiac musc; mast cells brain-> increases cAMP
->cardiac stimulation (HR and contractility); vasodilation
H3: presynaptic (brain mysenteric plexus)-> decreases cAMP (inhibitory); incr GI secretions
->reduce release of NT; inhibit GI secretions
H4: eosinophils; neutrophils; CD4 Tcells-> decreases cAMP (inhibitory) |
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Term
|
Definition
H1 antagonist- 1st Generation
Anticholinergic activity
SE: slight to moderate sedation; urinary retention and blurred vision (anticholinergic)
Hepatic metabolism |
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Term
Diphenhydramine (Benadryl)
Dimenhydrinate (Dramamine) [salt of diphenhydramine] |
|
Definition
H1 antagonist- 1st Generation
Anticholinergic activity; anti-motion sickness
Diphenhydramine-> antiparkinsonism (decrease EPS)-> given parenterally for acute dystonic rxns to antipsychotics
SE: marked sedation; urinary retention and blurred vision (anticholinergic); local anesthesia
Hepatic metabolism |
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Term
Brompheniramine
Chlorpheniramine |
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Definition
H1 antagonist- 1st Generation
Slight anticholinergic activity
SE: slight sedation
Found in OTC cold medication
Hepatic metabolism |
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Term
|
Definition
H1 antagonist- 1st Generation
SE: marked sedation
Hepatic metabolism |
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Term
|
Definition
H1 antagonist- 1st Generation
Anti-motion sickness
Meclizine = long acting (12-24hrs)
SE: slight sedation
Hepatic metabolism |
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Term
|
Definition
H1 antagonist- 1st Generation
Anticholinergic activity; antiemetic; alpha block
SE: marked sedation; orthostatic hypotension (alpha block); local anesthesia
Hepatic metabolism |
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Term
|
Definition
H1 antagonist- 1st Generation AND Serotonin antagonist
Slight anticholinergic activity; no effect on GI secretions
SE: moderate sedation
Hepatic metabolism
Treatment: sm musc manifestations of carcinoid tumor; cold-induced urticaria |
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Term
Fexofenadine (Allegra)
Loratadine (Claritin)
Cetirizine (Zyrtec) |
|
Definition
H1 antagonist- 2nd Generation
Less sedation than 1st generations-> don't cross BBB as well
Loratadine = longer acting
Cetirizine-> inhibits mast cell release of histamine via H4
Hepatic cytP450 metabolism-> inhibited by ketoconazole, itraconazole, macrolides, and grapefruit juice
Treatment: allergic rhinitis; chronic urticaria |
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Term
|
Definition
H2 antagonist
Effects: blocked acid secretion |
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Term
|
Definition
Potent vasodilators
HMW kininogen converted to bradykinin by plasma kallikrein
LMW kininogen converted to kallidin by tissue kallikrein; kallidin converted to bradykinin by aminopeptidases
MOA: binding B1 and B2 receptors (bradykinin is more specific for B2)-> arterial vasodilation but venoconstriction
Causes rapid but brief drop in BP; causes efflux of fluid into tissues
Bradykinin causes redness, heat, swelling, and pain
Metabolism via kininases; half-life 15sec
B receptor antagonists-> treatment of angioedema, pain, and bronchoconstriction |
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Term
|
Definition
Treatment: asthma; stimulation of fetal lung maturation (if delivery is expected before 34wks) by increasing surfactant
MOA: receptor (hGR) is cytoplasmic in complex w/ Hsp90-> hormone binds and Hsp90 dissociates; hormone/hGR dimerizes and binds glucocorticoid receptor elements (GRE) on DNA to initiate transcription; also bind aldosterone receptors (AR) w/ equal affinity as aldosterone
hGR alpha- steroid ligand activation; hGR beta- inhibits hGR alpha
Effects: antiinflammatory-> inhibit mast cells, lymphocytes, monocytes, basophil, and eosinophils but increase plasma neutrophils; reduce bronchial reactivity and reduce frequency of asthma exacerbations-> contraction of engorged vessels
Administer early morning after peak ACTH secretion to limit adrenal suppression; taper oral therapy slowly to prevent adrenal insufficiency
Natural = highly bound to CBG; Synthetic = highly bound to albumin; CBG increased w/ pregnancy, hyperthyroidism, and estrogen administration
SE: oral candidiasis (w/ inhaled forms); osteoporosis; cataracts; slow rate of growth in children; hyperglycemia; Cushing's syndrome |
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Term
| Hydrocortisone (cortisol) |
|
Definition
Cortisol- naturally occurring; hydrocortisone- synthetic
Short to medium acting glucocorticoid; half life 60-90mins
Oral, injectable, topical; production governed by ACTH
Increased w/ stress, hypothyroidism, and liver disease
Greatest metabolism in liver; 20% by 11-hydroxysteroid dehydrogenase in kidney |
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Term
Prednisone
Methylprednisolone |
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Definition
Short to medium acting glucocorticoids
Methylprednisone is the is the active form of prednisone
Pred- oral
Methyl- oral, injectable |
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Term
Beclomethasone
Budesonide
Flunisolide
Fluticasone |
|
Definition
Glucocorticoid
Inhalational
Fluticasone- used to wean pts from chronic prednisone therapy |
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|
Term
Betamethasone
Dexamethasone |
|
Definition
Long acting glucocorticoids
High anti-inflammatory activity
Treatment: stimulation of fetal lung maturation when given to mother-> betamethasone readily crosses placental barrier b/c of low protein binding |
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Term
|
Definition
Intermediate acting glucocorticoid
Inhalational |
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Term
|
Definition
MOA: alteration of delayed Cl- channel in cell membranes which inhibits cell activation
Effects: histamine release inhibitor-> reduce mast cell degranulation; cough inhibition; eosinophil inhibition
Treatment: asthma prophylaxis-> no effect on airway tone (ineffective in reversing symptoms); reducing symptoms of allergic rhinoconjuctivitis
Taken via aerosol
Tox: cough, all others are minimal-> chest tightness/wheezing (can be prevented w/ β2 agonist); dermatitis; myositis; gastroenteritis; eosinophilia/anaphylaxis |
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Term
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Definition
Leukotriene pathway inhibitor
Treatment: asthma-> improve control, reduce exacerbations; aspirin-induced asthma
MOA: 5-lipoxygenase inhibition
Taken orally
Tox: hepatotoxicity |
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Term
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Definition
Leukotriene pathway inhibitor
Treatment: asthma-> improve control, reduce exacerbations; aspirin-induced asthma
MOA: LTD4-receptor antagonist
LTD4 causes bronchoconstriction, bronchial reactivity, mucosal edema, mucus hypersecretion
Taken orally
Montelukast- approved for children as young as 6yo; can be taken once daily w/o regard to meals |
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Term
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Definition
MOA: anti-IgE monoclonal Ab against FC receptors on mast cells and inflammatory cells-> prevents IgE binding to mast cells and may inhibit IgE synthesis by plasma cells
Treatment: asthma-> reduces early and late bronchospastic responses; less frequent attacks; improves nasal/conjunctival symptoms
Given parenteral; duration 2-4days
Tox: injection site rxn; anaphylaxis (rare) |
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Term
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Definition
Chemo 1st line: small-cell lung cancer
MOA: displacement of Cl in cisplatin by water activates-> crosslinks DNA by binding guanines to prevent replication; cisplatin-DNA complex attracts HMG-1 (high mobility group-1) repair proteins which become irreversibly bound-> prevents effective repair and leads to apoptosis
Carboplatin activation occurs more slowly
MOR: increased nucleotide excision repair protein; loss of function of mismatch repair (HMG-1)
Tox: nephrotoxicity, ototoxicity, marked nausea/vomiting (given w/ anti-emetic); myelosuppression (Carboplatin)
Carboplatin = less toxic |
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Term
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Definition
Chemo 1st line: small-cell lung cancer
MOA: forms complex w/ topoisomerase II and DNA that cannot dissociate and blocks replication and breaks DNA
Cell cycle specific-> S or G2; used in combo w/ Cisplatin-> decreased cross-resistance
MOR: efflux pump, decreased topo II, mutation of p53
Tox: leukopenia, nausea/vomiting |
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Term
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Definition
Chemo
Topotecan = 2nd line: small-cell lung cancer
MOA: topoisomerase I inhibitor-> prevents breakage/resealing during DNA repair
Irinotecan=prodrug-> activated by carboxylesterase; no longer used for pulmonary cancers; used for colon cancers; low therapeutic index
Tox: diarrhea (irinotecan); neutropenia (topotecan) |
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Term
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Definition
Chemo
MOA: binds beta-tubulin to prevent cell division
Given IV
MOR: efflux pump
Tox: neurological (peripheral neuropathy), limited myelosuppresion, alopecia
Vinorelbine = less toxic |
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Term
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Definition
Chemo- Antimetabolite
MOA: enters cell via nucleotide transporter; binds DNA-> chain termination and apoptosis
Effective for both rapidly dividing and solid tumor cells
Synergistic w/ platinum based drugs for non-small cell cancers
Inactivated by deoxycytidine deaminase
MOR: increased deoxycytidine deaminase
Tox: myelosuppression
Contraindications: radiation use |
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Term
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Definition
Chemo
MOA: inhibit mitosis by binding to beta-tubulin-> blocks disassembly of microtubule strands
MOR: multidrug resistance pumps, beta-tubulin mutations
Tox: neutropenia, peripheral neuropathy, hypersensitivity (can use w/ dexamethasone)
Docetaxel = more predictable blood levels |
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Term
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Definition
Given IV
MOA: intercalates, inhibits topoisomerase II, ROS
SE: cardiotoxicity, bone marrow suppression, alopecia, GI, red urine |
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Term
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Definition
Chemo
MOA: EGFR-tyrosine kinase reversible inhibitor-> blocks EGFR phosphorylation and signal transduction=> decreased proliferation/angiogenesis/metastasis and increased apoptosis
Given orally
Gefitinib- low response rate
Tox: diarrhea |
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Term
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Definition
Chemo- non-small cell lung cancers
MOA: humanized monoclonal Ab against VEGF-> inhibits interaction with VEGF receptors=> inhibits angiogenesis in tumors
Tox: severe HTN, proteinurea, congestive HF, hemorrhage, stroke, MI, gastric perforation |
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Term
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Definition
Antimycobacterial
MOA: inhibits mycolic acid synthesis (cell wall component); reacts w/ NAD to inhibit a reductase of FA synthase II
Some people acetylate drug faster/slower-> determines dosage
MOR: mutation of activating enzyme (catalase peroxidase), target enzyme (INHA gene), or NADH dehydrogenase
Causes Vit B6 deficiency-> prophylactic administration of pyroxidine prevents peripheral neuritis
Tox: convulsions, optic neuritis, optic nerve atrophy, hepatotoxicity |
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Term
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Definition
Antimycobacterial
MOA: inhibits microbial RNA synthesis by inhibiting DNA-dependent RNA polymerase
MOR: target mutations
Induces cytP450s-> contraindicated for PTs on HIV drugs
Rifabutin- used for HIV PTs (no P450 effects)
Tox: possible additive hepatotoxicity in combo w/ isoniazid,
nephrotoxicity-> red-orange urine |
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Term
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Definition
Antimycobacterial
Also used for Mycobacterium avium complex (+ macrolide)
Bacteriostatic for isoniazid-resistant M. tuberculosis
MOA: inhibits mycobacterial wall synthesis by blocking arabinosyl transferases
Tox: optic neuritis-> cannot differentiate green and red; gout |
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Term
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Definition
Antimycobacterial
MOA: blocks mycobacterial FA synthase I gene involved in mycolic acid biosynthesis-> inhibits cell wall synthesis
Tox: gout (decreased urate excretion); hepatotoxicity |
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Term
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Definition
Antimycobacterial- aminoglycoside
MOA: binds 30S ribosomal subunit and interferes with protein synthesis
Contraindications: pregnancy |
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Term
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Definition
Antimycobacterial- aminoglycoside
MOA: binds 30S ribosomal subunit and interferes with protein synthesis
MOR: decreased access, increased deactivation, altered ribosome structure
Tox: ototoxicity; nephrotoxicity; neuromuscular blockade |
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Term
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Definition
Antimycobacterial- 2nd line
MOA: cyclic peptide that decreases microbe protein synthesis
Given IM for multidrug resistant TB
Tox: deafness |
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Term
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Definition
Antimycobacterial- 2nd line
MOA: inhibits D-alanine-> blocks cell wall synthesis
Tox: neurotoxicity |
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Term
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Definition
Antimycobacterial- 2nd line
MOA: activated by mycobacterial redox system; same MOA as isoniazid-> inhibits mycolic acid synthesis (cell wall component); reacts w/ NAD to inhibit a reductase of FA synthase II
Low cross resistance w/ isoniazid
Tox: nausea/vomiting; GI; neurotoxicity |
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Term
| Para-Aminosalicyclic Acid |
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Definition
Antimycobacterial- 2nd line
MOA: inhibits thymidylate synthase (TS)-> interrupts folate pathway
MOR: mutation of TS |
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Term
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Definition
Antimicrobial
MOA: inhibit cell wall synthesis
Piperacillin: activity against gram +/- aerobic/anaerobic bacteria; used together with a beta-lactamase inhibitor tazobactam
Effective against Pseudomonas aeruginosa
Tox: defect of hemostasis |
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Term
| TICARCILLIN-CLAVULINIC ACID |
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Definition
Antimicrobial
MOA: inhibit cell wall synthesis in combo w/ beta-lactamase inhibitor
Highly effective against Pseudomonas
Tox: defect of hemostasis |
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Term
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Definition
Antimicrobial
Effective against Pseudomonas
MOA: beta-lactam antibiotics, bind to penicillin-binding proteins, disrupt bacterial cell wall synthesis, and cause death of susceptible microorganisms
Very resistant to hydrolysis by most beta-lactamases |
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Term
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Definition
Antimicrobial
MOA: beta-lactam antibiotic; activity only against gram-negative bacteria; effective against P. aeruginosa |
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Term
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Definition
Beta-lactamase Inhibitor
MOA: suicide inhibitor that irreversibly binds and inhibits beta-lactamase
Effective against H. influenzae, aerobic gram - bacilli, S. aureus |
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Term
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Definition
Beta-lactamase Inhibitor
MOA: beta-lactamase inhibitor
Poor activity against the inducible chromosomal beta-lactamases; good activity against the plasmid beta-lactamases |
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Term
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Definition
Beta-lactamase Inhibitor
MOA: beta-lactamase inhibitor
Effective against gram + cocci, including S. aureus, gram - aerobes and anaerobes |
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Term
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Definition
Antimicrobial-> 2nd generation cephalosporin
MOA: interferes w/ cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking
Effective against Klebsiella, Haemophilus influenzae, Moraxella catarrhalis
Given parenterally every 8 hours or orally in the acetil form every 12 hours |
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Term
CEFTRIAXONE
CEFOTAXIME
CEFPODOXIME PROXETIL
CEFOPERAZONE |
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Definition
Antimicrobial-> 3rd generation cephalosporin
Effective against S. aureus, Streptococcus pneumoniae, Pseudomonas aeruginosa
MOA: interferes w/ cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking
MOR: beta-lactamase
Given IV every 12-24 hours; half-life = 8hrs |
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Term
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Definition
Antimicrobial-> 4th generation cephalosporin
MOA: interferes w/ cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking; even more resistant to beta-lactamases than 3rd generations
MOR: beta-lactamase |
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Term
ERYTHROMYCIN
AZITHROMYCIN
CLARITHROMYCIN |
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Definition
Antimicrobial Macrolide; Antimycobacterial- 2nd line
Especially effective against gram + cocci like S. pneunomiae
Also used for Mycobacterium avium complex (+ ethambutol)
MOA: binds 50S peptidyltransferase to block translocation
Drug interactions: decrease cytP450s (except azithromycin)
Large tissue distribution, high cellular concentration (not erythromycin)
MOR: efflux pumps; these drugs induce methylation of 50S and cannot bind-> cause resistance to self
Tox: hypersensitivity; GI problems; arrhythmia (QT prolongation); hepatitis (erythromycin) |
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Term
LEVOFLOXACIN
GATIFLOXACIN
MOXIFLOXACIN |
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Definition
Antimicrobial; Antimycobacterial- 2nd line; fluoroquinolones
Effective against S. pneumoniae and mycobacteria
MOA: inhibition of bacterial DNA gyrase (gram negative E. coli) or topoisomerase IV (gram positive streptococcus)
Tox: GI; arthropathy in children; decrease cytP450s
Contraindications: children |
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Term
| TRIMETHOPRIM-SULFAMETHOXAZOLE |
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Definition
Antimicrobial
MOA: inhibits 2 steps of the THF synthesis pathway; sulfamethoxazole inhibits incorporation of PABA into folic acid; trimethoprim inhibits DHFR
20:1 sulfamethoxazole:trimethoprim concentration
MOR: altered DHFR
Effective against S. pneumoniae and H. influenzae
Tox: myelosuppression, Stevens-Johnson syndrome |
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Term
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Definition
Antifungal- polyene
MOA: binds ergosterol in fungal cell wall which produces ion channels-> destroys osmotic integrity of cell; also induces direct membrane damage
Broad spectrum
Given IV or topical (not absorbed orally); wide tissue distribution; administration may cause fever/chills
MOR: replacement of ergosterol w/ other sterols
Toxicity: nephrotoxicity (lipid formulation = less toxic) |
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Term
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Definition
Antifungal- antimetabolite
MOA: enters cell via permease; pyrimidine analogue-> converted to pyrimidine via cytosine deaminase in fungal cells-> inhibits thymidylate synthase production of dTMP-> halt DNA synthesis
Given orally; used in combo w/ Amphotericin B and Fluconazole
MOR: decrease permease
Tox: myelosuppression |
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Term
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Definition
Antifungal- imidazole
MOA: inhibits lanosterol 14α-demethylase-> prevents conversion of lanosterol to ergosterol=> disrupts cell memb synthesis
Given oral or topical; highly lipid bound-> doesn't cross BBB
Tox: decreased hepatic cytP450s and sex steroid synthesis |
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Term
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Definition
Antifungal- triazole
MOA: inhibits lanosterol 14α-demethylase-> prevents conversion of lanosterol to ergosterol=> disrupts cell memb synthesis
Broad spectrum
Given oral or IV
Tox: decreased hepatic cytP450s; hepatotoxicity |
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Term
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Definition
Antifungal- triazole
MOA: inhibits lanosterol 14α-demethylase-> prevents conversion of lanosterol to ergosterol=> disrupts cell memb synthesis
Limited spectrum; good CNS penetration
Given oral or IV
Tox: decreased hepatic cytP450s; nausea/vomiting |
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Term
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Definition
Antiviral- Influenza A
MOA: targets M2 membrane protein on Influenza-> prevents uncoating and viral release
MOR: M2 mutation
Rimantadine-> less toxic, doesn't have to be adjusted for renal disease
Amantidine-> can improve Parkinson's disease symptoms
Tox: neurotoxicity |
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Term
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Definition
Antiviral- Influenza
MOA: targets neuraminidase glycoprotein on Influenza envelope-> prevents viral release from cells
Effective for prophylaxis and treatment in first 24-48hrs
MOR: mutation of NA or hemagglutinin
Oral
Tox: GI |
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Term
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Definition
Antiviral- Influenza
MOA: targets neuraminidase glycoprotein on Influenza envelope-> prevents viral release from cells
Effective for prophylaxis and treatment in first 24-48hrs
MOR: mutation of NA or hemagglutinin
Inhaled-> dry powder
Contraindications: chronic airway disease-> bronchospasm |
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