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138 Cards in this Set
- Front
- Back
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antidote for cyanide poisoning and biochem
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hydroxocobalamin bind to cyanide to form cyanocobalamin for renal excretion
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antidotes for acetaminphen, opiates, CCB, hydrofluroci acid, acetaminophen, bzd, ehtylene gycol, methanol, crotalidae envenomation, bblocker, CCB, antigoagulatns, iron
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NAC, naloxone, calcium, calcium, flumazenil, fomepizole, fomepizole, antivenom fab, glucagon, phytonadione, deferozamine
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bradycardia overdose drugs
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PACED propanolol, AchE-I, chlonidine, CCB, ethanol,. digoxin
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Tachycardia od drugs
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FAST free based cocain, antichol, antihis, amphetamine, sym-mimetics, solvent, theophyline (theo drives fast car)
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hypotension od drugs
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CRASH clonidine, CCB, reserpine, antidepressant, antiHTN, sedative hyptonitcs, heroin
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hypertension od drugs
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CT SCAN cocaine, thyroid supplements, sym-mimics, caffeine, antichol, amthetamine, nicotine
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sympathomimetics OD effects
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SHHiTy MD diaphoresis, mydriasis, tachycardia, hypertension, hyperthermia, seizures
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narcotic OD effects
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B/C Much Heroine
miosis, hypoventilation, hypotension, coma bradycardia |
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cholinergic OD effects
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DUMBBELS
diarrhea, diaphoresis, urination, miosis, bradycardia, bronchorhea, emesis, lacrimation, salivation |
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antichol OD effects
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hot, dry, red, delirium, dilated pupils, tachy, urinary retention
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Not used in activated charchols
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PHAILS
pesticides, hydrocarbons, acids, alkali, iron lithium, solvents |
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use hemodialysis
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ISTUMBLE isopropanol, salicylates, theophyline, uremia, metahnol, barbs, lithium, ethylene glycol
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acetaminophen
1. metabolism 2. tox biochem 3. 4 stages of clinical manifestation 4. toxic dose |
1. hepatic flucoronide, sulfate, excreted in urine.
2. 2E1 turn into NAPQI 3. stage 1, N/V, 2, elevated AST, PT, bili, hypoglycemia, met acidosis, 3, fulminant hepatic failure, elevated ast, pt bili, hypoglycemia, el lactat, acidemia, 4, recovery 4. 7g/4 hours adults |
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toxic alcohol
1. toxic metabolites 2. tx |
1. methanol -> formic acid, met acidosis
ethylene glycol -> oxalic acid 2. fomepizole. ethanol, hemodialysis |
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aspirin tox
1. mechs 2. dose 3. acute tox si/sx 4. chronic tox si/sx 5. tx |
1. central stim respiratory center, uncouple ox phos, interrupt glucose/FA metabolism
2. acute 200mg/kg, chronic, 100mg/kg for >2 days 3. acute mild, vomit, hyperpnea, tinnitus, lethargy, acute severe: coma seizures, hypoglycemia, hyperthermia pulm edema, chronic: elderly confusion, dehydration, cerebral pulm edema; higher mortality than acute 4. sodium bicarbonate, urine alk, hemodialysis |
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Drugs of abuse
1. prototypes (3) 2. ADHD (4) 3. anorexients (5) 4. CNS stim 5. CNS depressants 6. dissociative 7. hallucinogens (3) 8. designer drugs (4) 9. anabolic steroids (2) |
1. amphetamine (dexedrine), methamphetamine, cocain
2. methylphenidate, pemoline, adderall, atomoxetine 3. phenteramine, benzphetamine, phendimetrazine, fenfluramine, phenyulpropanolamine 4. caffeine, nicotine 5. ehtanol choral hyrate, methanol, disulfiram 6. phencyclidine PCP, MJ 7. LSD, mesaline, psilocybin 8. MDMA, GHB, antichol (shrooms), volatile inhalants 8. DHEA, androstenedione |
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gateway drugs (3)
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nicotine, alcohol , MJ, higher incidence of use of other drugs of abuse in future
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recreation use vs. situational use
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recreational leads to more dependence b/c diff. mind set, higher dose schedule
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addiction vs. dependence definition
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addiction: ADL are altered by constant desire to consume drug.
dependence: chronic pain pt who needs drugs to cope with illness |
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what is seeking personality
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genetic predisposition to consume drugs b/c lower threshold for activation of DA in n. accumbens
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what determines abuse liability
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drugs stim increased DA in n accumbens, induce reverse tolerance, incentive salience
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psychochostim
1. effects (5) 2. MOA |
1. euphoria, reduce sleep, improve concentration when fatigued, alter judgment, SANS
2. inhibit reuptake at DA=NE >>5HT |
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amphetamine, methylphenidate MOA
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substrates for reuptake pumps, induce calcium independent releast, inhibti reuptake DA, NE, 5HT, inhibit MAO
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cocaine MOA
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inhibit transporter, not substrate for it, caine property in free base form, crack, NO CEILING EFFECT (kills!)
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anorexients
1. routes 2. MOA |
1. iv, po, insufflation, bagging, pyrolysis
2. NE=>5HT>>>DA NO ABUSE POTENTIAL (b/c low DA stim) |
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caffeine
1. MOA 2. od effects |
1. adenosine antag, inhibit release of ACh from PPN in thalamus -> facilitate sensoery entry into cortical processing; phosphodiesterase inhibitor
2. tremors |
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nicotine MOA
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1. MOAI -->improve concentration by increasing DA; nicotinic direct agonist.
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ethanol
1.MOA 2. metab induced, not induced 3. disulfiram MOA and effect |
1. bind GABA A, potentiate inhibition, disinhibition release
2. alcohol DH, aldehyde DH not inducible; p450 induceable 3. blocks DA beta hydroxylase -> orthostasis, blocks acetaldehyde dehydrogenase --> acetaldehyde build up. |
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methanol tox
1. metabolite, effect 2. tx |
1. formaldehyde, blindness
2. alcohol dehydrogenase inhibitor (fomepizole, EtOH) |
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what is mickey finn
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alcohol + chloral hydrate -> synergistic sedation due to shared metabolic pathway. EtOh drives conversion of chloral hydrate to trichloroethanol (Active) and reduce nicotine amide- needed for EtOH metab (so more EtOH).
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PCP
1. MOA 2. pathognomic tox effect 3. effects |
1. indirect antag Glu receptor at sigma site, DA release, DA reuptake inhibitor
2. cyclic coma 3. belligerence, hiccoughing, impaired thinking |
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MJ
1. MOA 2. phases 3. effects 4. t1/2 |
cannabinoid receptor, indirect cholinergic antag;
phase 1: DA decrease, 5TH increase phase 2: DA increase, 5TH decrease phase 3: Ach decrease 3. vasodilate, bronchodilate, analgesic, reduce IOP, stim appetite, REM inhibit. 4. 30 days in feces |
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LSD
1. short term effects 2. MOA 3. long term effects |
1. hallucination with intact cognition, perceptual si (synesthesia)
2. stim 5HT1D -> inhib raphe firing 3. hallucinogen persisting perceptual disorder, flashbacks (decreased critical flicker fusion, images fusion together -> hallucinations) |
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MDMA
1. effects 2. tox |
1. psychic effects w/o hallucinations
2. sertonin syndrome |
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GHB
MOA |
gamma hydroxybutyrate alcohol effects stim GH
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mushrooms
effects |
antichol syndrome, SLUDEGM
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anabolic steroid
Use, effects |
pyramiding (increase, decrease) in a month and one month of drug free, belligerence/violent effects
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AD
1. cholinergic hypothesis 2. nootropic definition, agents 3. other agents 4. nootropic tox |
1. decreased cholinergic cells in basal forebrain, basalis of meynert
2. AchE-I, enhance memory, tacrine, donepezil, rivastigmine, galantamine 3. a-tocopherol(vit E), piracetam, gingko biloba, hydergine, memantine, tramiprosate, NSAIDS 4. SLUDGE (salivation, lacrimation, urination, defecation, GI, Emesis |
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tacrine
MOA, USE, TOX |
MOA: reversible AchE inhibitor
USE: short action duration, lots first pass met TOX: liver tox require monitoring |
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donepezil
MOA, USE, TOX |
MOA: non-comp reverisble AchE-I selective at CNS
USE: t1/2 60 hours, qd doing TOX: tox if renal impaired |
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rivastigmine
MOA |
MOA: pseudo-irreversible comp AchE I
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galantamine
MOA, USE |
USE: reversible AchE-I, noncompetitive nicotinic agonist -> activate post synaptic receptor good for AD.
USE: t1/2 6 hours |
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a-tocopherol MOA
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MOA: free radical scavenger
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piracetam
MOA |
MOA: GABAA, muscarinic, AMPA Glu receptors
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memantine
MOA |
noncomp inhibitor of NMDA
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tramiprosate
MOA |
amyloid beta antag
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migraine Headache tx
1. prototypes 2. 7 other classes 3. tx of choice 4. tension headache tx |
1. aspirin, erogotamine, sumatriptan
2. NSAIDS ergot alkaloids (ergotamine) CGRP (sumatriptan, no x BBB) CC antag (verapamil) prophylactics (methysergide, propranolol, amitriptyline) prokinetics/antiemetics (metoclopramide, ondansteron) prochlroperazine) 3. sumatriptan, propranolol for prophalax 4. cyclobenzapine |
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tension headache tx and MOA
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bzd (cyclobenzapine), muscle relaxant and axiolytic
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migraine headache hypotheses and asso. tx
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1. vascular hypothesis of Wolff:
MOA: platelets release 5HT-> vasoconstriction n the opthal limb ot trgeminal nn -> 5HT depletion -> atony -> pulse pressure increase -> pain methysergide: 5HT antag ergots: vasodilate 2. sterile inflam -> central deficient 5HT --> leaky vessels, edema -> calcitonin gene realted peptide -> pain triptan: 5HT agonist 3. biobehavioral/spreading depression -> inability of astrocytes to perform potassium spatial buffering, by not absorb extracellular K propranolol: helps astrocyte K buffer |
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1. NSAIDS tx of headaches MOA, USE
2. role of caffeine |
MOA: block PG production, no phosphorylation of nerve ending
USE: early b/c once nn ending are phos'ed they're more sensitive to pain. 2. facilaite GI motility, increased potency of NSAIDS. |
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rebound headaches
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headaches from rapid withdrawal after chronic use, need to taper.
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ergotism
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n/v/parethesis, cramps, seizures, gagrene from vasoconstriction (GI si before CNS si)
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tox:
1. triptans 2. methysergide |
1. chest tightness, contraindicated in CAD
2. retroperitoneal fibrosis, need drug holiday. |
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migraine headaches
causes, sx |
peripheral, pulse pressure increase (throbbing), prodome, aura, pain, constipation.
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Opioid analgesics
1. prototype 2. full agonist 3. partial agonist/antagonists 4. antagonists 5. others contraindication |
1. morphine
2. codeine (high oral bio, converted to morphine, antitussive, constipation), heroin (biotrans to morphine), hydromorphone (dilaudid)/hydrocodone/oxymorphone (used w/ acetaminophen, ibuprofen, more analgesic and antitusssive potency, less histamine release), meperidine (CNS excitation), fentanyl (CNS excitation), methadone (oral, long t1/2), oxycodone (sustained release formulation). 3. pentazocine, buprenorphine 4. naloxone, naltrexone 5. dextromethorphan (antitussive), diphenoxylate w/atropine (antidiarrheal), loperamide (antidiarrheal) contraindication: pregnancy and respiratory problems, head injury |
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slow/fast pain and role of opioids
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opioids blocks slow pain and suffering
fast pain is localizing |
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neuropathic pain tx
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neuronal in nature as in shingles, use anticonvulsants not opioids
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1. morphine MOA
2. what is morphine flush. |
1. MOA: mimic effects of enkephalins, binds to enkephaline sites in periaqueductal gray to diminish the appreciation of pain, and substantail gelatinosa to inhibit release of sub P.
2. release of histamine |
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4 enk receptors and functions
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1. mu: pain and resp depression
2. kappa: segmental analgesia (krappy and krazy) 3. delta: limbic strucures 4. epsion: unknonw |
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opiods class
1. side effects 2. pathgnomic triad |
1. respiratory depression (O2 used is contraindicated), constiptation, miosis, euphoria, dependence, sedation. Meperizine is mydriasis instead of miosis, cyanosis
2. pinpoint pupils, coma, resp depression. |
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USE of naloxone, methadone
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naloxone: full antagonists in opioid OD
metahdone: substitute metahdone for morphine. |
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antileptic drugs
1. prototype 2. primary tx 3. adjunctive tx 4. status epilepticus tx |
1. phenytoic
2. phenobarbital, carbamazepine, valpoate (broad for generalized and absence), clonazepan, ethosuzimide 3. lamotrigine, gabapentin, topiramate, zonisamide, tiagabine, levetiracetam 4. diazepam, lorazepam, pentobarbital, phenytoin. |
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AED common side effects
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1. withdrawl seizures
2. cerebellar signs (intention tremor, nystagmus, ataxia, diplopia, hyperreflexia) 3. seizures (high dose induction, absence seizures by phenytoin. |
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Seizures tx
1. general strategies 2. types and tx of choice |
1. reduce activity in seizure focus for partial seizures (inhibit Na Channels), and inhibit spread in generalized seizures (inhibit CNS)
2. partial (simple, complex, 2ndary tonic clonic): carbamazepine generalized - tonic clonic, tonic atonic: valproic avid, lamotrigine (in preg F) - myoclonus: clonazpine - absence: ethosuiximide Status: lomazepam |
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phenytoin
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MOA: block Na channels
USE: generalized and partial TOX: induce p450, gingival hyperplasia, hirsutism, bleeding, reduce steroid/birth control efficacy, peripheral neuropathy, osteomalacia, cardiac arrthymia if protein binding is displaces by ASA |
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phenobarbital
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MOA: enhance GABA A
USE: generalized, partial TOX: autoinducer fo p450 |
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ethosuximide MOA, USE, TOX
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MOA: decrease Ca2+ current (T type) in thalamus
USE: absence TOX: GI, dizzy, headahce, photosensitivity, parkinsonism, restlessness, anxiety |
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carbamazepine
MOA, USE, TOX |
MOA: block voltage gated Na channels, decreased glutamate release
USE: generalized and partial #1 for partial and secondarily generalized TOX: aplastic anemia, autoinduce p450, diplopia, resp. depression. |
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clonazepam
valproic |
MOA: enhance GABA a receptor
USE: absence, myoclonic, infantile spasms, #1 in myoclonic TOX: sedation USE: broad based, generalized, partial, myoclonic, absence TOX: wt gain, alopecia, blackbox for hepatic failure, pancreatitis, spina bifida (teratogenic) |
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gabapentin, pregablin
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MOA: block Ca channels
USE: gabapentin: generalized, partial; pregablin: partial |
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vigabatrin
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MOA: inhibti GABA transaminase (breakdown)
USE: partial TOX: psychosis, ocular effects |
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excipient definition
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stuff other than drug present in drug and can cause side effects
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mech of CNS drug absorption
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1. mostly simple diffusion
2. few transported (levodopa) |
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ion trapping definition, and drugs
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1. drug get to a location by diffusion or faciliated transport then a change in pH in that compartment, the drug gets ionized and tapped. Basic drug trapped in acidic environment, acidic drugs trapped in basic environment
2. PCP, local anesthetics, NT |
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role of fat solubility of CNS drugs
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Can cross BBB, faster onset, shorter duration b/c faster redistribution
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definition of thrapeutic window
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TD50/ED50
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LADME
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= bioavailability
liberation absorption distribution metabolism excretion |
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central emesis
1. location 2. NT's 3. emetic drugs 4. anti-emetic drugs |
1. chemoreceptor trigger zone (no BBB)
2. DA 5HT 3. apomorphine, syrup of ipecac 4. prochloperazine, ondasteron, metoclopramide |
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why don't drugs distribute widely in brain?
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1. least etracellular space, 2. reuptake and uptake sites, 3. barriers to diffusions 4. enzymes break drugs down.
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definitions:
1. hepatic induction 2. hepatic polymorphisms 3. pharmacokineitc tolerance 4. CYP3A4 inducer, inhibitor |
1. more enzymes are produced to biotransform drugs more quickly
2. p450 variants have diff rates of biotransformation 3. a reduction in biovailability of a drug due to chronic exposure to a drug resulting from hepatic induction. 4. SJW induce, grapefruit juice inhibit. |
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affinity/efficacy for
1. direct agonist 2. indirect agonist 3. direct antagonist 4. indirect antagonists |
1. affinity and efficacy
2. no affinity but efficacy 3. affinity but no efficacy 4. no affinity, no efficacy |
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definition of
1. target specificity 2. receptor specificity 3. ionotropic receptors 4. metabotropic receptors |
1. location of brain, low target specificity mean drugs goes lots of different parts of brain
2. non receptor specificity means binding to lots of different types of receptors 3. open up ion channels only 4. activate second messenger to open up channels (can have lon g term effects) |
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long term effects of drugs on physical brain strucutre
efficacy delay |
1. product traphic factor in their targets
2. autotrophic factors in bed nuclei of origin efficacy delay in antidepressants |
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definitions:
1. pharmacological dennervation hypersensitvity 2. pharmacodynamic tolerance 3. physiologic tolerance 4. cross tolerance 5. reverse tolerance |
1. chonic exposure to agonists down regulates receptors, antagonists up regualtes receptor number.
2. reduction in potency due to chagne at site of drug action 3. reduction in potency due to normal physiology system outside of site of drug action (insulin/glucagon) 4. one drug produce tolerance to another member of same drug class (EtOh induce tolerance to another sedative hypnotic drug) 5. continued exposured to a drug increases potency |
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1. what determines side effects
2. counteradaptations 3. disinhibition release |
1. lack of target and receptor specificity
2. opposite effect of drug manifests once drug is withdrawn 3. paradoxical excitement from drugs taht depress CNS |
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PD drugs
1. prototype 2. indirect acting DA agnoists 3. antimusc 4. direct acting DA agonists 5. others |
1. carbidopa/levodopa
2. amantadine, benztrophine, slegiline, rasagiline, tolcapone, entacapone, stalevo 3. trihezyphenidyl, benztropine 4. pramipexole, ropinirole, cabergoline 5. calozapine, olanzapine, orphenadrine, benedryl |
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HD Tourette drugs
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tetrabenzpine + haloperidol, risperidone, ziprasidone, fluphenazine, clonidine, guanfacine
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anti tremor drugs
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propranolol, ethanol
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dystonia drugs
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antimusc, BZD's, botox
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ADHD drugs
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methylphenidate- indirect DA agonists
pemoline adderall: longer t1/2 atomoxetine: more NE reuptake effect |
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DA's CNS pathways and MOA
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1. nigrostriatal (movement), mesolimbic (emotion/addition), mesocortical (cognition), tuberoinfundibular (prolactin inhibition)
2. regulate rate that information information flow throuh glutamate-neurons from striatum to cortex (more DA, more activity) |
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1. balance hypothesis of striatal function
2. end of dose wearing off effect 3. on-off phenomenone |
1. balance of DA-Ach control movementm, lower DA = hypokinesia (PD, dystonia), higher DA hyperkinesia (chorea, ADD, tourettes, dyskinesia)
2. as PD progress, fewer DA terminals and less recycling of DA, so levodopa is less effective, increase dose will produce more side effect b/d DA neuron not degenerated in other parts of brain. 3. sudden onset of full PD symptoms during dosage due to Glu sensitization in striatum from saw toothing DA/intermittent dosing (so use longer action DA) |
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levodopa/carbidopa
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levodopa MOA: absorbed by LNAA pump in gut (protein will compete), turned into DA by AAAD (precurosor load strategy).
Carbidopa MOA: inhibit AAAD in periphery to reduce first pass effect and peripheral side effect of levodopa but increase CNS effect/tox of levodopa. |
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side effects of levodopa and otehr DA agonsit
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levodopa more prone for dyskinesia, direct agonists more prone to psychosis.
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benztropine, trihezyphenidyl MOA
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amantadine MOA, USE, TOX
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MOA: antiviral and DA reuptake inhibitor food for late stage PD
USE: good for late stage PD TOX: livido reticualris |
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selegiline/rasagiline
MOA, USE differences |
MOA: MAOB-inhibitor
USE: symptom benefits and prevent MTPT conversion to MTT+ Difference: selegiline is converted to amphetamine while rasagiline is not. |
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1. entacapone tolcapone
MOA and differences 2. Stalevo |
1. MOA: COMT inhibitor
Tolcapone: central and peripheral, liver tox 2. entacapone with carbidopa levodopa |
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bromocriptine, pergolide
MOA USE Apomorphine,USE, MOA |
MOA: direct DA agonists
USE: not for monotherpy and not used anytmore Apomorphine: short acting agonists, rescue infuse/injection |
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pramipexole ropinirole
MOA, USE, TOX |
MOA: direct DA agonists
USE: monothperay, neuroprotection TOX: more hallucinations/compulsive behaviors, sleep attacks. |
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1. Huntington tx
2. MOA 3. USE |
1. haloperidol, tetrabenazine
2. DA antag 3. tx chorea and later psychosis. |
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dystonia
1. generalized tx 2. focal tx 3. MOA |
1. antimusc
2. botox 3. antichol |
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tourette's tx
1. MOA 2. side effect |
1. DA antag
2. unmask ADHD |
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benztropine trihexyphenidyl, orphenadrine, benedryl as PD tx
1. MOA 2. TOX |
1. antimus for Ach-DA balance theory, benztrophine (antimus, DA Reuptaker Inhibitor), trihexy (anti musc), orphenadrine, benedryl ( antimus, antihis)
2. TOX: constipation, impair cognitive function in elderly. |
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role of clozapine and olanzapine
1. MOA 2. USE 3. TOX |
1. DA 2 antagonists that have least affinity for striatal DA receptors
2. tx psychosis ss of DA agonists 3. clozapine can cause agranulocytosis, must monitor CBC |
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tx comorb tourettes and ADHD
MOA |
clonidine and guanfacine
alpha adrenergic agonists b/c no DA increase |
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antipsychotic drugs
1. prototype MOA 2. typical, atypical MOA 3. tx EPSE MOA 4. tx TD |
1. chlorpromazine (DA antag
2. typical (DA antag): thioridazine, flyphenaine, haloperidol; atypical (DA + 5HT antag): clozapine, risperidone, olanzapine, quetiapine, aripiprazole, ziprasidone 3. antimus: benztropine, trihezyphenidyl 4. reserpine, tetraneazine |
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1. dopamine theory of schizophrnia
2. hypofrontality hypothesis of psychosis |
1. pharmacoecentric hypothesis that DA antag are effective in psychosis, and DA agonists (ampethamine, cocaine) induce psychotic behavior in normal pt.
2. failure of development of parahippocampal gyrus --> weak projection to prefrontal cortex --> reduced function in prefrontal cortex = negative sx; prefrontal's reduced inhibition of n. accumbens = positive sx. |
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typical psychotic
TOX |
EPSE
extrapyramidal side effects due to DA blockage 1. parkinsonian: occurs last 2. akathisia (happen 2nd, most common): inability to be still (rabbit syndrome iwt perioral tremor) 3. dystonia (with in days): abnormal maintained postuer |
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Why are they atypical?
receptors 1. thioridazine 2. risperidone 3. olanzapine, clozapine |
EPSE occurs less.
1. DA antag, antimus (tx EPSE) 2. DA and 5HT antag 3. DA4 antag, antimus (tx EPSE) USE to treat bipolar too! |
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antipsychotic tox
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1. EPSE
2. orthostasis 3. lower seizure threshold (reduced DA) 4. cardio (antimus, quidinine) 5. prolactin, glatorrhea/gynecomasti (reduced DA) 6. NMS (rigidity, hyperthermia, tx wtih dantrolene bromocriptine) |
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clozapine tox
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agranulocytosis, paradoxical wet pillow
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Tardive dyskinesia
sx, cause, tx, types |
sx: lingual facial buccal movement, dyskinesia of limbs, trunks
withdral TD: more common, antipsychot dosage reduced or stopped breakthrough TD: while drug is still given cause: DA receptor upregulation from chronic use (pharmacological denervation hypersensitivity). tx: DA depleting agents: reserpine, tetrabenazine. |
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1. depot form of antipsychotic
2. drug with highest TI 3. which drugs produce NMS |
1. haloperidol, flyphnazine.
2. haloperidol 3. all |
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amine theory of depression
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deficiecney in brain biogenic amiane (NE) and serotoinei (indoleamine)
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antidepressant drugs
antimanic |
1. TCA: imipramine, amitriptyline, clomipramine, despramine
2. heterocyclics: amaxapine, trazodone 3. fluxetine, paroxetine, sertraline, gluvoxamien 4. MAOI: isocarboxazid, phenlzine, tranylcypromine 5. new heterocyclics: bupropion, velafaxine, mertazapine antimanic: lithium, carbamazepine, valproate, aripiprazole (antipsychotic) |
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Cause of SAD
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inadequte light -> excess melotonin produce deplete substrate for 5HT production.
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TCA tox
bupropion |
bupropion - enhance sexual functioning, but decreases seizure theshold,
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SSRI
TOX, Indications |
TOX:
1. serotonin syndrome (hyperthermia, rigidity, MYOCLONUS, rapid fluc in vital sign) with use wtih MAO I or merperidine (SSRI), SJW, sumatryptans for migranines! 2. wt gain 3. impotence Indications - suicide ideation, reduced 5HIAA, negative dexamethasone suppression test |
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MAOI MOA, TOX, USE
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MOA: suicide inhibition of MAO to increase NE and 5HT; block breakdown of 5HT > NE b/c COMT also breaks down NE.
TOX: 1. pickled herring, chianti wine and cheese effect from accumulation of tyramine -> HTN crisis. 2. chronic use -> orthostasis b/c tyramine convert in to octopamine as a false NE -> can't mount SANS effect at alpha receptor. USE: last resort, #1 for atypical depression (increase eating and sleeping, developing phobias) |
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lithium MOA, TOX
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MOA: blocks myoinositol1 phosphatase reduce production if IP3 and DAG
TOX: tremor, lithium decrease ADH -> diuresis -> dehydration. seizures, coma, CV collapse. |
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Receptors MOA
1. SSRI 2. SNRI (drug) 3. TCA 4. trazadone 5. bupropion 6. mirtazapine 8. MAOI |
1. bind to SERT, inhibit bindign of 5HT to SERT
2. venlafaxine: inhibit SERT >NET 3. inhibit SER, NET and others (dirty) 4. 5HT2 antag -> increase glu 5. NET DAT inhibitor, release NE 6. 5HT2 antag, release NE, 5HT 8. MAOA 5HT>>NE>>DA, MAOB DA >>5HT>> NE |
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sedative hypnotics/anxiolytics
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BZD: diazepam (mm relaxant decrease spinal cord reflex), chlodiazepoxide, trazolam, alprazolam, temazepam, oxazepam, lorazepam, flurazepam, midazolam, estazolam
BZD antag: flumazenil Barbs: amobarbital, secobarbital, pentobarbital, phenobarbital Others: aolpidem, meprobromate chloral hydrate, paraldehyde, eszopiclone, Remelteon, zeleplon Selective anxiolytics: buspirone, propranolol. |
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effects of CNS depressants
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disinhibitiosn release, sedation, anxiolysis, repiratory depression (except benzo), mm relaxant, motor coordination, alteration in judgement, anterograde amnesia, rebound, drug hangover
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Benzo MOA
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1. GABAA receptor increased frequency of CL gate opening in presence of GABA.
2. inhibit adenosine reuptake to facilitate sleep (caffeine inhitbi adenosine receptors in thalamsu -> no sleep!) 3. inhibit Na Ca cahnnels at high concentration tx status epilepticus 4. have ceiling effect on respiratory depression due to state dependent action. |
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Barb MOA
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1. bind GABA A recepotrs increae duraiton of CL gate opening in presence of GABA
2. open gate independent of HABA. 3. p450 autoinducers -> high tolerance |
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Benzo no metabolized by liver
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oxazepam, temazapam, lorazepam; congujated only.
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1. continuum of consciousness
2. factors of benzo's long half life |
1. alert, sedated, hypnosis, obtunded, stuporous comatose, dead.
2. more lipid, shorter action duration despite long t1/2, enteroherpatic recirculation. |
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USES
1. eszopiclone 2. remelteon 3. zeleplon 4. baclofen 5. propanolol 6. buspirone 7. chloroal hydrate 8. zopidem |
1. safe for chronic sleep aid use
2. melaonin agonists as sleep aid 3. short duration for pt with problem falling alseep 4. GABA B receptors in spinal cord tx. spasticity 5. propranolol: situation anxiety 6. anxioselective, no sedation, 5HT1A partial agonsits. 7. hyptontic min effect on REM 8. hypnotic min effect on REM |
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anethetics
1. gases 2. IV 3. IV opiods 4. combo's 5. local anesthetics |
1. halothane, enflurane, isoflurane, desflurane, sevoflurane, nitrous oxide, ether, chloroform
2. thipental, etomidate, propofol, ketamine 3. fentanyl 4. fentanyl/droperidol (enurolept-analgesia), droperidol-nitrous oxide (neurolefpt-anesthesia) 5. ester: procaine, cocaine, benzocaine, tetracaine amides: lidocaine, mepivacaine, etidacine, bupivacaine, ropivacaine, articaine |
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GAS
1. Safety 2. MAC 3. diffusion hypoxia 4. metabolism |
1. lowest TI
2. partial pressure volume needed to produce anethetic plan ein 50% of pt's. 3.nitrous race back to lung from blood take up too much partial pressure that O2 tensions is low. 4. not metabolized except halothane |
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anethetics
MOA, effects |
1. receptors interface between GABA A receptors and membrane lipid
2. not good analgesics (except nitrous), OK mm reaxers, produce vasodilation (problem in long procedues) |
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anesthetics TOX
1. general 2. halothane |
1. + succiylcholine -> malignant hyperthermia (it's genetic, and dantrolene is tx)
2. catecholamien sensitization burst fo epi can indcue reentry arrhtyhmias, hepatitis |
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adjuvants in anesthesia
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neurolept-anesthesia
neurolpt-analgesia mm relax: reduce motor excition during recovery from anestehsia BZD: increase drowsiness, anterograde amnesia antiemetics: post-op emesis atropine: reduce bronchial secretion and counteract cardiac depression, reduce GI discharge opioids: reduce pain |
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USE:
IV anesthetics, ketamine |
1. outpt
2. outpt and low blood volume circumstances. |
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local anesthetics
1. MOA 2. effects of inflamation 3. how to keep it local 4. tox |
1. block NA channel from inside nn, x membrane as non-ionized free base, then ionized to bind receptor (ion trapping)
2. inflammation are more acidic, so free base form is lower and less drugs are crossing membrane, less potent) 3. epinephrine, to vasoconstrict but need acidificaiton vehicle to keep epi in solution 4. ester drugs convert into PABA -> delayed type hypersensitivity. |
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Do not use appreviations
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1. MS, MSO4, mgSO4 magSO4 - write out morphine or magnesium sulfate
2. U or u - write out unit 3. IU - write out international unit, or unit 4. qd, qod - write out dailu or q24h or q48h 5. No trailing 0 (don't use 2.0), do use leading 0 (0.2) 6. ug - write mcg 7. > < - write out greater than and less than 8. x3d: write days or doses |
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SALADS
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1. DOBUTamine DOPamine
2. traMADol traZODone 3. caPTOPRil, cefaDROXil, cephaLEXin 4. gliPIZide glyBURide 5. metoCLOPRamide, metoPROlol, metRONIDazole, metoLAZone 6. proMETHazine, proPANTHeline, proPRANpol 7. amiLORide, amiODARone, admiTRIPTYline, amLODIPine |
