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60 Cards in this Set

  • Front
  • Back
Cholinergic agonists (3)
Carbachol - ganglion stimulating
Bethanechol, Pilocarpine - muscarinic agonists
Actions of cholinergic agonists
Decrease HR, CO, and BP
Vasodilation
GI, bronchiolar, salivary secretions
GI motility
GU detrussor muscle contraction
Eye: Miosis
Acetylcholinesterase Inhibitors (Reversible, 4)
Neostigmine
Physostigmine
Pyridostigmine
Edrophonium
Types of muscarinic receptors on target tissue
M1: Gastric parietal cells
M2: Cardiac cells, smooth muscle
M3: Exocrine glands, smooth muscle
Hexamethonium
Nicotinic ACh receptor antagonist: ganglionic blocker. Blocks both SNS and PSNS.
AchE toxicity (Organophosphate poisoning)
DUMBBELSS:
diarrhea
urination
miosis
bronchospasm
bradycardia
excitation of CNS, skeletal muscle
lacrimation
salivation
sweating
Antidote for AchE toxicity
Atropine (muscarinic antagonist)
Pralidoxime (chemical antagonist, regeneratives active cholinesterase)
Muscarinic antagonists (and uses)
Atropine: mydriasis and cycloplegia
Benztropine: Parkinson's, decreases movement
Scopolamine: motion sickness
Ipratropium: Asthma, COPD
Atropine: Effects and side effects
Effects: blocks SLUD
salivation
lacrimation
urination
defecation

Side effects:
hot as a hare: increased body temperature
dry as a bone: decreased secretions (saliva, sweat)
mad as a hatter: SNS-type effects
blind as a bat: pupil dilation
red as a beet: flushed skin
Sympathomimetics: Catecholamines and main receptors
Epinephrine: a1, a2, b1, b2
Norepinephrine: a1, a2, b1
Isoproterenol: b1=b2
Dopamine: D1 = D2 > b > a
Dobutamine: b1 > b2
Amphetamine
Sympathomimetic, indirect general agonist, releases stored catecholamines.
Uses: narcolepsy, obesity, ADD
Ephedrine
Sympathomimetic: indirect agonist, releases stored catecholamines.
Uses: nasal decongestion, urinary incontinence, hypotension
Phenylephrine
Sympathomimetic: a1 > a2 agonist.
Uses: pupil dilator, vasoconstriction, nasal decongestion.
Albuterol, Terbutaline
Sympathomimetic: B2 > B1.
Uses: short acting beta agonist in asthma, bronchodilation
Cocaine
Sympathomimetic: Indirect general agonist, uptake inhibitor.
Uses: causes vasoconstriction and local anesthesia.
Clonidine, methyldopa
Sympathomimetic: centrally-acting a-agonist. Decreases central adrenergic outflow.
Uses: hypertension, especially with renal disease.
Ganglionic cholinergic agonists (3)
Nicotine
Trimethaphan
Mecamyline
- No therapeutic use; widespread effects
NMJ cholinergic drugs: agonists and antagonists
Depolarizing drugs are agonists (nicotine, succinylcholine).
Non-depolarizing drugs are antagonists (tubocurarine).
Non selective alpha blocker
Phenoxybenzamine (irreversible)
Phentolamine (reversible)
Used for pheochromocytoma, can cause orthostatic hypotension, reflex tachycardia.
Alpha 1 blockers
Prazosin
Terazosin
Doxazosin
Used for HTN, urinary retention in BPH. Can cause hypotension, dizziness, headache.
Alpha 2 blockers
Mirtazapine
Used in depression
Causes sedation, increased serum cholesterol, increased appetite.
Beta 1 blockers
A BEAM:
acebutolol
betaxolol
esmolol
atenolol
metaprolol
Uses: Cardioselective. Decreases CO, renin secretion in HTN. Decreases HR and contractility, O2 consumption in angina pectoris. Slows progression of CHF. Decrease mortality after MI.
Non selective beta blockers and toxicities
Propanolol, timolol, pindolol, nadolol, labetalol.
Toxicities: impotence, exacerbation of asthma, cardiovascular side effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations)
*Use with caution in diabetics - hides effects of hypoglycemia
Glaucoma drugs: approaches
a agonists (epinephrine, brimonidine)
b blockers (timolol, betaxolol, carteolol)
diuretics (acetazolamide)
cholinomimetics (pilocarpine, physostigmine, echothiophate)
prostaglandin (Latanoprost)
Goals of glaucoma treatment
Constrict pupil (more PSNS, less SNS effect)
Increase fluid outflow (a agonist)
Decrease fluid production (b blocker)
Treatment of Parkinson's
Parkinsons: destruction of dopaminergic neurons in substantia nigra.
Dopamine agonists: l-dopa/carbidopa, bromocriptine, pramipexole, ropinirole, amantadine (enchances DA release)
MAO inhibitors: selegiline (MAO-B selective)
Antimuscarinics: Benztropine
COMT inhibitors: entacapone, tolcapone
BALSA
bromocriptine
amantadine
levodopa (L-dopa/carbidopa)
selegiline
antimuscarinics
Levodopa/Carbidopa
Parkinson's treatment.
L-dopa can cross BBB, is converted to DA by dopa decarboxylase in CNS. Carbidopa inhibits peripheral decarboxylase to prevent peripheral activation of DA.
Peripheral DA effects: arrythmias.
Other SE: dyskinesia.
MAO selectivity
MAOa: breaks down 5HT, NE.
MAOb: breaks down DA.
Selegiline
MAOb-selective inhibitor. Increases CNS DA, used in treatment of Parkinson's.
Sumatriptan
Serotonin agonist, used for acute migraines, cluster headache attacks. Causes chest discomfort, mild tingling (contraindicated in pts with CAD or Prinzmetal's angina). Strong anticholinergic side effects.
Phenytoin: MOA
Blocks the voltage-gated Na channel once it is open (activity dependent INACTIVATION).
Uses: simple & complex partial seizures, tonic-clonic seizures.
Carbamazepine: MOA
Blocks the voltage-gated Na channel once it is open (activity dependent INACTIVATION).
Lamotrigine: MOA
Inhibits voltage-gated Na+ and Ca+2 channels.
Uses: Simple & complex partial seizures, tonic-clonic seizures.
Gabapentin: MOA
Increase GABA release
Used for Simple & complex partial seizures, tonic-clonic seizures.
Epilepsy drugs (9)
Phenytoin
Carbamazepine
Lamotrigine
Gabapentin
Topiramate
Phenobarbital
Valproate
Ethosuximide
Benzodiazepines (Diazepam, lorazepam)
Topiramate: MOA
Inhibits Na+ channels, potentiates GABAergic function.
Uses: partial seizures (simple & complex)
Phenobarbital: MOA
Barbiturate. Bind to GABAa receptors and potentiate them by increasing the duration of their opening. Can work even if GABA is not bound (unlike BZD).
Uses: Simple & complex partial seizures, tonic-clonic seizures.
Treatment for absence seizures
Valproate
Ethosuximide
Valproate: MOA
Increases Na channel inactivation, increases GABA concentration - subtle effects on multiple channels.
Uses: all seizures, especially absence.
Ethosuximide: MOA
Blocks thalamic T-type Ca++ channels, disrupting slow rhythmic firing of thalamic neurons.
First choice for absence seizures.
*Hepatic toxicity
Benzodiazepines: MOA
Potentiates GABAa receptor by increasing frequency with which it opens.
Uses: Status seizures.
Drugs for status epilepticus seizures
Benzodiazepines, phenytoin
Phenytoin: profile
MOA: use-dependent blockade of Na+ channels.
Clinical use: grand-mal seizures, class IB anti-arrythmic.
Toxicity: nystagmus, ataxia, diplopia, lethargy. Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decrease vitamin B12), malignant hyperthermia (rare), teratenogenic (fetal hydantoin syndrome)
Psychiatric drugs: Classes (5)
Benzodiazepines
Barbiturates
Neuroleptics (work on DA)
Atypicals (DA, 5HT)
Lithium
Barbiturates: drugs, MOA
Phenobarbital
Pentobarbital
Thiopental
Secobarbital
MOA: facilitate GABAa action by increasing duration of Cl- channel opening, thus decreasing neuron firing.
(BarbiDURATE = increased DURATion of Cl- channel opening)
Barbiturates: uses, side effects
Use: sedative for anxiety, seizures, insomnia, induction of amnesia (thiopental).
Side effects: dependence, additive CNS depression with alcohol, respiratory or CV depression (can lead to death), induction of cytochrome P450.
Benzodiazepines: drugs, MOA
Diazepam
Lorazepam
Triazolam
Temazepam
Oxazepam
Midazolam
Chlordiazepoxide
MOA: facility GABAa action by increasing frequency of Cl- channel opening
(FREnzodiazepines have increased FREquency of Cl- channel opening)
Benzodiazepines: Clinical use, side effects
Uses: anxiety, spasticity, status epilepticus (diazepam), detoxification (esp alcohol withdrawal with DT)
Side effects: dependence, additive CNS depression with alcohol. Less risk of respiratory depression & death than with barbiturates.
Treat OD with flumazenil (competetive GABA antagonist).
Overdose antidotes:
Organophosphates
Benzodiazepines
Morphine
Organophosphates: atropine
Benzodiazepines: flumazenil
Morphine: naloxone
(all antagonists)
Neuroleptics
thioridazine, haloperidol, fluphenazine, chlorpromazine
MOA: most antipsychotics block D2 receptors (excess DA effects connected with schizophrenia)
Use: schizophreniz, psychosis
Toxicity: extrapyramidal effects, sedation, endocrine side effects, anti- muscarinic, a adrenergic, and histaminic effects (orthostatic hypotension).
Conditions associated with antipsychotics
(antipsychotics block dopamine)
Neuroleptic malignant syndrome: rigidity, autonomic instability, hyperpyrexia - treat with dantrolene and DA agonists.
Tardive dyskinesia: stereotypic oral-facial movements probably due to DA receptor sensitization; results of long-term antipsychotic use.
Atypical antipsychotics
Clozapine, olanzapine, risperidone
MOA: block 5HT2 and DA receptors.
Uses: schizophrenia, positive and negative sxs.
Olanzapine is also used for OCD, anxiety disorder, and depression.
SE's: fewer extrapyramidal, anticholinergic than other antipsychotics
Lithium
Antipsychotic.
MOA not established - inhibition of IP3 cascade?
Use: mood stabilizer for bipolar disorder, blocks relapse and acute manic events.
Toxicity: tremor, hypothyroidism, polyuria (ADH antagonist --> nephrogenic DI), teratogen (cardiac). Narrow therapeutic index.
Antidepressants: Classes (4)
SSRI's
TCA's
Heterocyclics
MAOI's
SSRI's
Fluoxetine
Sertraline
Paroxetine
Citalopram
MOA: blocks reuptake of serotonin into presynaptic cell.
Use: endogenous depression.
Toxicity: fewer than TCA's. CNS stimulation - anxiety, insomnia, tremor, anorexia, nausea, and vomiting.
With MAOI's: Serotonin syndrome - hyperthermia, muscle rigidity, cardiovascular collapse.
Tricyclic antidepressants
Imipramine
Amitriptyline
Desipramine
Nortriptyline
Clomipramine
Doxepin
MOA: block reuptake of NE and serotonin
Use: endogenous depression, bedwetting (imipramine decreases stage 4 sleep), OCD
SE's: sedation, alpha-blocking, anticholinergic effects (tachycardia, urinary retention).
Toxicity: Tri-C's - Convulsion, Coma, Cardiotoxicity.
Heterocyclics
Used in major depressive disorders:
Tazodone - inhibits 5HT reuptake
Buproprion - Smoking cessation. MOA unknown.
Venlafaxine - Inhibits 5HT, DA, NE reuptake, used in GAD.
Mirtazapine - a2 antagonist (increased release of Ne, 5HT), potent 5HT2 receptor antagonist
Maprotiline - blocks NE reuptake.
MAO inhibitors
Phenelzine
Tranylcypromine
MOA: nonselective MAO inhibition (A > B, so NE and 5HT increased)
Use: atypical depression (psychotic or phobic), anxiety, hypochondriasis
Toxicity: hypertensive crisis with tyramine ingestion and meperidine; CNS stimulation. Contraindicated with SSRI's, B agonists (serotonin syndrome).
Opioid analgesics: drugs and MOA
Morphine
Fentanyl
Codeine
Heroin
Methadone
Meperidine
Dextromethorphan
MOA: act as agonists at opioid receptors to modulate synaptic transmission.
Mu = morphine
Delta = enkephalin
Kappa = dynorphin
Opioid analgesics: clinical uses, toxicities
Dextromethorphan = pain, cough supression
Loperamide, diphenoxylate = diarrhea
Methadone = maintenance programs for addicts.
Toxicity: addiction, respiratory depression, constipation, miosis, additive CNS depression with other drugs. Tolerance does NOT develop to miosis and constipation.
Treat OD with naloxone, naltrexone (opioid receptor antagonist).