General Pharm Flashcards
a2 receptor protein class and function
Gi
decrease sympathetic outflow
decrease insulin release
decrease lipolysis
Increase platelet aggregation
B1 receptor protein class and function
Gs
Increase heart rate
Increase contractility
Increase renin release
Increase lipolysis
B2 receptor protein class and function
Gs
Vasodilation Bronchodilation Increase HR Increase contractility Increase lipolysis Increase insulin release decrease uterine tone Ciliary muscle relaxation Increase aqueous humor production
M1 protein class and function
Gq
Located in CNS and enteric nervous system
M2 protein class and function
Gi
Decrease HR
Decrease contractility of atria
M3 protein class and function
Gq
Increase exocrine gland secretions (lacrimal, salivary, gastric acid)
Increase gut peristalsis
Increase bladder contraction
Bronchoconstriction
Increase pupillary sphincter muscle contraction (miosis)
Ciliary muscle contraction (accommodation)
D1 receptor protein class and function
Gs
Relaxes renal vascular smooth muscle
D2 protein class and function
Gi
Modulates transmitter release, especially in brain
H1 receptor protein class and function
Gq
Increase nasal and bronchial mucus production Increase vascular permeability contraction of bronchioles pruritus pain
H2 receptor protein class and function
Gs
increases gastric acid secretion
V1 receptor protein class and function
Gq
Increase vascular smooth muscle contractiion
V2 receptor protein class and function
Gs
Increase water permeability and reabsorption in collecting tubules of the kidney
Bethanechol
MOA: cholinomimetic
Activates bowel and bladder smooth muscle
Resistant to AChE
Clinical: postoperative ileus, neurogenic ileus, and urinary retention
Normal post void residual volume
Carbachol
MOA: Choinomimetic
Clinical: glaucoma, pupillary constriction, and relief of intraocular pressure
Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Pilocarpine
MOA: Cholinomimetic
Clinical: stimulatory of sweat, tears, and saliva
Contracts ciliary muscle of eye (open-angle glaucoma)
Pupillary sphincter (closed-angle glaucoma)
Resistant to AChE
Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Methacholine
MOA: cholinomimetic
Clinical: challenge test for asthma
Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Neostigmine
MOA: AChE inhibitor
increasing endogenous ACh
Clinical: postoperative and neurogenic ileus, urinary retention, myasthenia gravis, reversal of postoperative neuromuscular junction blockade
Due to quaternary amine structure will not cross CNS
Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Pyridostigmine
MOA: AChE inhibitor
Increases endogenous ACh
Increases strength
Clinical: Myasthenia gravis (long acting)
Does not penetrate CNS
Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Physostigmine
MOA: AChE inhibitor
Increases endogenous ACh
Clinical: Atropine or other anticholinergic toxicity
Crosses BBB
Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Donepezil, rivastigmine, galantamine
MOA: AChE inhibitor
Increases endogenous ACh
Clinical: Alzheimers
Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Endrophonium
MOA: AChE inhibitor
increases endogenous ACh
Clinical: Diagnosis of myasthenia gravis (short acting)
Quaternary amine structure does not allow CNS penetration
Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
AChE inhibitor toxicity
Often due to organophosphates (parathion-insecticides)
SLUDGE: Salivation, Lacrimation, Urination, Defecation, GI distress (diarrhea), Eye Problems (miosis)
Also bronchospasm, bradycardia, Excitation of skeletal muscle, Sweating, confusion, low BP, flushing
Antidote: atropine
homatropine
MOA: Muscarinic Antagonists
Act on eye
Clinical: produce mydriasis and cyclopegia
Benztropine
MOA: muscarininc antagonist
Act on CNS
Clinical: Parkinsons
Anti-psychotic overdose treatment
Scopolamine
MOA: Muscarinic Antagonist
Act on CNS
Clinical: Motion Sickness
Over treatment of myasthenia gravis side effects (also hyoscyamine can be used)
Ipratropium, tiotropium
MOA: muscarinic antagonists
Act on Respiratory system
Clinical: COPD, asthma
Oxybutynin
MOA: muscarinic antagonists
Act on Genitourinary system
Clinical: reduce urgency in mild cystitis and reduce bladder spasms
Urge incontinence
Also can be used with tolterodine, fesoterodine, trospium
darifenacin and solifenacin
MOA: muscarinic antagonists
Act on Genitourinary system
Clinical: reduce urgency in mild cystitis and reduce bladder spasms
Urge incontinence
tolterodine and fesoterodine
MOA: muscarinic antagonists
Act on Genitourinary system
Clinical: reduce urgency in mild cystitis and reduce bladder spasms
Urge incontinence
Trospium
MOA: muscarinic antagonists
Act on Genitourinary system
Clinical: reduce urgency in mild cystitis and reduce bladder spasms
Urge incontinence
Glycopyrrolate
MOA: muscarininc antagonist
Acts on Gastrointestinal and respiratory system
Clinical: Given parenteral for peroperative use to reduce airway secretions
Given orally for drooling, peptic ulcer
Tropicamide
MOA: muscarinic antagonist
Acts on Eye
Clinical: produce mydriasis and cycloplegia
Atropine
MOA: muscarinic antagonist eye: pupil dilation, cycloplegia Airway: decrease secretion Stomach: decrease acid secretion Gut: decrease motility Bladder: decrease urgency in cystitis
Clinical: bradycardia, produce mydriasis and cycloplegia, before bronchoscopy to decrease respiratory mucous secretions and promote bronchodilation
Organophosphate poisoning (no effect on muscle paralysis due to nicotinic receptors-use pralidoxime early on) Pralidoxime restores cholinesterase from its receptors
Toxicity: increase in body temperature (decreased sweating), rapid pulse, dry mouth, dry-flushed skin, cyclopegia, constipation, disorientation,
Can cause acute angle closure glaucoma in elderly due to mydriasis
Urinary retention in men with BPH
Hyperthermia in infants
1/2 life increases in elderly enhancing the chance of toxicity
Treat toxicity with physostigmine which inhibits AChE bot peripherally and centrally due to its tertiary amine properties
Epinephrine
Acts on B>a
B1=Increase HR
B1 and a1=systolic BP
B2>a1 at low dose leading to decreased diastolic pressure (vasodilation)
a1>B2 at high dose leading to increased diastolic pressure
Clinical: anaphylaxis, open angle glaucoma, asthma, hypotension,
a effects predominate at high doses
Norepinephrine
a1>a2>B1
Clinical: hypotension but decreased renal perfusiion
NE extravasation (induration and pallor) a1 vasoconstriction can lead to tissue necrosis Prevent necrosis by sodium solution of phentolamine mesylate (a1 blocker)
Isoproterenol
B1=B2
Increase contractility via B1
Decreased vascular resistance via B2
Clinical: electrophysiologic evaluations of tachyarrhythmias
Can worsen ischemia
Dopamine
D1=D2>B>a
Clinical: unstable bradycardia, heart failure, shock,
inotropic and chronotropic a effects predominate at high doses
Low doses: stimulates D1 receptors in renal vasculature and tubules leading to increased GFR, RBF, and Na excretion and mesenteric vasodilation
Moderate doses: Stimulates B1 receptors of heart leading to increased contractility, increased pulse pressure, and increase of systolic BP
High doses: stimulates a1 receptors leading to vasoconstriction which causes decreased CO (used for hypotension while maintaining kidney perfusion)
Phenylephrine
a1>a2
Clinical: hypotension (vasoconstrictor), ocular procedures (mydriatic), rhinitis (decongestion)
Albuterol
B2>B1
Clinical: acute asthma
Salmeterol
B2>B1
Clinical: long acting asthma or COPD control
Terbutaline
B2>B1
Clinical: reduce premature uterine contractions
Amphetamine
MOA: Indirect sympathomimetic
Reuptake inhibitor and releases stored catecholamines
Clinical: narcolepsy, obesity, attention deficit disorder
Ephedrine
MOA: indirect sympathomimetic
releases stored catecholamines
Clinical: nasal decongestion, urinary incontinence, hypotension
Cocaine
MOA: indirect sympathomimetic
Reuptake inhibtor
Clinical: causes vasoconstriction and local anesthesia
Never give B blockers if cocaine Intoxication is suspected
Dobutamine
B1 effects (increase cAMP)
Passive inotropic effect increasing contractility and CO decreased ventricular filling pressures
Weakly positive chonotropic effect leading to Increased HR and increased myocardial oxygen consumption
increased conduction velocity leading to arrhythmias
Clonidine
MOA: a2 agonist
Clinical: hypertensive urgency (doesn’t decrease renal flow)
ADHD, severe pain
Off label-ethanal and opioid withdrawal
Toxicity: CNS depression, bradycardia, hypotension, respiratory depression and small pupil size
a-methyldopa
MOA: a2 agonist
Clinical: hypertension in pregnancy
toxicity: direct Coombs + hemolytic anemia, SLE-like syndrome
Phenoxybenzamine
MOA: irreversible a-blocker
Clinical: pheochromocytoma preoperatively to prevent catecholamine crisis
Toxicity: orthostatic hypotension, reflex tachycardia
Prazosin, terazosin, doxazosin, tamsulosin
MOA: a1 selective blockers
Relaxation of smooth muscle in arterial and venous walls decreasing TPR
Clinical: urinary symptoms of BPH, PTSD (prazosin)
Hypertension (not tamsulosin)
Toxicity: 1st dose othostatic hypotension, dizziness, headache, vertigo
Mirtazapine
MOA: a2 selective blocker
Clinical: depression
Toxicity: sedation, increased serum cholesterol, increased appetite
-olols and carvedilol, labetalol
MOA: Beta Blockers
Clinical:
Angina pectoris: decreased HR, contractility leading to less O2 consumption
MI: metoprolol, carvedilol and bisoprolol lead to decreased mortality
SVT: metoprolol and esmolol lead to decreased AV conduction velocity (class II antiarrythmics)
Hypertension: decreased CO, decreased renin secretion (due to B1 receptor blockade on JGA cells)
CHF: slow progression of chronic failure
Glaucoma: timolol decreased secretion of aqueous humor
Toxicity: impotence, bradycardia, AV block, CHF, Seziures, sedation, sleep alterations, dyslipidemia (metoprolol), asthmatics/COPD may exacerbate
Avoid in cocaine users
May block hypoglycemia symptoms in diabetes but no Contraindicated
Selectivity: B1=A through M
Nonselective: M through Z,
Nonselective a and B antagonists: carvedilol and labetaolol
Nebivolol can stimulate B3 receptors which activate NO synthase in vasculature
CYP inducers
Chronic Alcohol Modafinil St. John's Wort Phenytoin Phenoarbital Nevirapine Rifampin Griseolfulvin Carbamazepine
CYP substrates
Anti-epileptics Antidepressants Antipsychotics Anesthetics Theophylline Warfarin Statins OCPs
CYP inhibitors
Acute alcohol abuse Gemfibrozil Ciprofloxacin Isoniazid Grapefruit Juice Quinidine Amiordarone Ketoconazole (all azoles) Macrolides Sulfonamides Cimetidine Ritonavir
a1 receptor protein class and function
Gq
Increase vascular smooth muscle contraction
Increase pupillary dilator muscle contraction (mydriasis)
Increase intestinal and bladder sphincter muscle contraction
Hemicholinium
Blocks Choline uptake into axon
Vesamicol
Block ACH intake into vesicles
Metyrosine
Blocks tyrosine to DOPA
Reserpine
Blocks Dopamine into vesicles
Bretylium
NE release from axon
Guanethidine
blocks NE release
