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59 Cards in this Set
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glaucoma drugs
epinephrine |
a-agnoist
decrase aqueous humor synthesis due to vasoconstriction. ae: mydriasis, stinging; do not use in closed-angle glaucoma |
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glaucoma drugs
brimonidine |
decrease aqueous humor synthesis
no pupillary or vision changes |
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glaucoma drugs
timolol, betaxolol, carteolol |
decrease aqueous humor secretion
no pupillary or vision changes |
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glaucoma drugs
acetazolamide |
diuretic (ca inhibitor)
decrease aqueous humor secretion due to decrased bicarb. no pupillary or vision changes |
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glaucoma drugs
pilocarpine, carbachol |
direct cholinomimetics
incrase outflow of aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies; very effective at opening meshwork into cancal of Schlemm ae: miosis, cyclospasm |
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glaucoma drugs
physostigmine, echothiophate |
indirect cholinomimetics
direct cholinomimetics incrase outflow of aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies; very effective at opening meshwork into cancal of Schlemm ae: miosis, cyclospasm |
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glaucoma drugs
latanoprost |
PGF2a
increase outflow of aqueous humor ae: darkens color of iris (browning) |
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opioid analgesics
morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan |
act as agonist at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission - open K channels, close Ca channels: decreases synaptic transmission. Inhibit releaes of ACh, NE, 5-HT, glutamate, substance P.
use: pain, cough suppression (dextromethorphan), diarrhea )loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone). toxicity: addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with othe rdrugs. tolerance does not develop to miosis and constipation. toxicity treated with naloxone or naltrexone (opioid receptor antagonist). |
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butorphanol
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partial agonist at opioid mu receptors, agnoist at kappa receptors.
use: pain; causes less respiratory depression than full agnoist. toxicity: causes withdrawal if on full opioid agnoist. |
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tramadol
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very weak opioid agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters - "tram it all" in)
use: chronic pain toxicity: similar to opioids. decreases seizure threshold |
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epilepsy drug uses
phenytoin |
simple/complex partial seizures
1st line for tonic clonic generalized 1st line for status generalized. |
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epilepsy drug uses
carbamazepine |
simple/complex partial seizures
1st line for tonic clonic generalized |
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epilepsy drug use
lamotrigine |
simple/complex partial seizures
tonic clonic generalized |
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epilepsy drug use
gabapentin |
simple/complex partial seizures
tonic clonic generalized |
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epilepsy drug use
topiramate |
simple/complex partial seizures
tonic clonic generalized |
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epilepsy drug use
phenobarbital |
simple/complex partial seizures
tonic clonic generalized |
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epilepsy drug use
valproic acid |
simple/complex partial seizures
1st line for tonic clonic generalized absence genearlized |
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epilepsy drug use
ethosuximide |
1st line for absence generalized
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epilepsy drug use
benzodiazepines |
1st line for acute status generalized
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epilepsy drug use
tiagabine |
simple/complex partial seizures
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epilepsy drug use
vigabatrin |
simple/complex partial seizures
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epilepsy drug use
levetiracetam |
simple/complex partial seizures
tonic clonic generalized |
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epilepsy drug toxicities
benzodiazepines |
sedation, tolerance, dependence
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epilepsy drug toxicities
carbamazepine |
diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of p450, SIADH, Stevens-johnson syndrome.
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epilepsy drug toxicities
ethosuximide |
gi distress, fatigue, ha, urticaria, stevens-johnson syndrome
EFGH - ethosuximide, fatigue, gi, ha |
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epilepsy drug toxicities
phenobarbital |
sedation, tolerance, dependence, induction of p450
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epilepsy drug toxicities
phenytoin |
nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome), SLE like syndrome, induction of p450
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epilepsy drug toxicities
valproic acid |
gi distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defets in fetus (spina bifida), tremor, weight gain. CI in pregnancy
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epilepsy drug toxicities
lamotrigine |
stevens-johnson syndrome
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epilepsy drug toxicities
gabapentin |
sedation, ataxia
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epilepsy drug toxicities
topiramate |
sedation, mental dulling, kidney stones, weight loss
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phenytoin
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use-dependent blockade of Na channels; increased refractory period; inhibition of glutamate release from excitatory presynaptic neuron
use: tonic clonic seizures. also a class IB antiarrhythmic. toxicity: nystagmus, ataxia, diplopia, sedation, SLE like syndrome, induction of p450. chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decrase folate absorption). teratogenic (fetal hydantoin syndrome). |
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barbiturates
phenobarbital, pentobarbital, thiopental, secobarbital |
facilitate BAGAa action by icnrased duration of Cl channel opening, thus decreasing neuron firing.
use: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental). toxicity: dependence, additive CNS depression effects with alcohol, respiroatry or CV depression (can lead to death), drug interactions owing to induction of p450. treat OD with symptom management (assist respiration, increase BP). barbiDURATe (increase DURATion) CI in porphyria |
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benzodiazepines
diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam |
faciliate GABAa action by icnrasing frequency of Cl channel opening. decrease REM sleep. most have long half lives and active metabolites.
useS; anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification 9esp. alcohol withdrawaal-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia). toxicity: dependence, additive CNS depression effets with alcohol. less risk for respiratory depression and coma than with barbiturates. treat OD with flumazenil (competitive antagonist at GABA benzodiazepine receptor) Short acting = TOM thumb - Triazolam, Oxazepam, Midazolam. highest addictive potential. Benzos, barbs, and EtOH all bind BAGA(A)-R, which is a ligand gated Cl channel. |
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Anesthetics
General Principles |
CNS drugs must be lipid soluble (cross BBB) or be actively transported.
drugs with decreased solubility in blood = rapid induction and recovery times. drugs with increased solubility in lipids = increased potency = 1/MAC MAC = minimal alveolar concentration at which 50% of population is anesthetized. varies with age. |
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Anesthetics effect on lungs
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increases rate, depth of ventilation = increased gas tension
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Anesthetics effect on blood
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increases blood solublity = increased blood/gas partition coefficient = increases solubility = increases gas required to saturate blood = slower onset of action.
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Anesthetics effect on tissue (eg. brain)
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AV concentration gradient increased = increased solubility = increasd gas required to saturate tissue = slower onset of action.
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inhaled anesthetics
halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide |
unknown mechanism
effects: myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand). toxicity: hepatotoxicity (halothane) nephrotoxicity (methoxyflurane) proconvulsant (enflurane) malignant hyperthermia (rare), expansion of trapped gas (nitrous oxide) |
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IV anesthetics
barbiturates - thiopental |
high potency, high lipid solubility, rapid entry into brain. used for inductino of anesethesia and short surgical procedures. effect terminated by rapid redistribution into tissue and fat. decreased cerebral blood flow
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IV anesthetics
benzodiazepines |
midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. may cause severe postoperative respiratory depression, decrease BP (treat OD with flumazenil), and amnesia.
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IV anesthetics
Arycyclohexylamines (ketamine) |
PCP analogs that act as dissociative anesthetics. block NMDA receptors. CV stimulants. cause disorientation, hallucination and bad dreams. increase cerebral blood flow.
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IV anesthetics
opiates |
morphine, fentanyl used with other CNS depressants during general anesthesia
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IV anesthetics
propofol |
used for rapid anesthesia induction and short procedures. less postoperative nausea than thiopental. potentiates GABAa.
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local anesthetics
esters - procaine, cocaine, tetracaine amide - lidocaine, mepivacaine, bupivacaine (amides have 2 I's in name) |
block Na channels by binding to specific receptors on inner portion of channel. preferentially bind to activated Na channels, so most effective in rapid firing neurons. tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels a charged form.
use: minor surgical procedures, spinal anesthesia. if allergic to esters, give amides. toxicity: CNS excitation, severe CV toxicity (bupivacaine), HTN, hypotension, and arrhythmias (cocaine). |
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local anesthetics principles
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1. in infected (acidic) tissue, alkaline anesthetics are charged and can't penetrate membrane effectively. more anesthetic is needed in these cases.
2. order of nerve blockade - small diameter fibers > large diameter. myelinated fibers > unmyelinated fibers. overall size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers. order of loss - pain (lose first) > temperature > touch > pressure (lose last). 3. except for cocaine, given with vasoconstrictors (usually epinephrine) to enhance local action - decrease bleeding, increase anesthesia by decreasing systemic concentration. |
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neuromuscular blocking drugs
depolarlizing |
used for muscle paralysis in surgery or mechanical ventilation. selective for motor (vs. autonomic) nicotinic receptors
depolarizing - succinylcholine (complications include hypercalcemia nd hyperkalemia). reversal of blockade: phase I (prolonged depoarlization) - no antidote. block potentiated by cholinesterase inhibitors. phase II (repolarized by blocked ) - antidoe consists of cholinesterase inhibitiors (eg. neostigmine) |
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neuromuscular blocking drugs
nondepolarizing |
used for muscle paralysis in surgery or mechanical ventilation. selective for motor (vs. autonomic) nicotinic receptors
tubocurarine, atracurium, mivacurium, pancuronium, vecuoniu, rocuronium. competitive - compete with ACh for recptors. reversal of blockade - neostigmine, edrophonium, and other cholinesterase inhibitors. |
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Dantrolene
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used in treatment of malignant hyperthermia, which is caused by concomitant use of inhalation anesthetic (except N2O) and succinylcholine. also used to treat neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).
mechanism: prevents the release of Ca from the sarcoplasmic reticulum of SK.M |
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PK disease drugs
agnoize DA receptors |
bromocriptine, pergolide (ergot alkaloid and partial dopamine agonist), pramipexole, ropinirole (non-ergot); non-ergots are preferred.
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PK disease drugs
increase dopamine |
amantadine (may increase da release); also used as an antiviral against influenza A and rubella; toxicity = ataxia
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PK disease drugs
prevent da breakdown |
selegiline (selective MAO type B inhibitor);
entacapone, tolcapone (COMT inhibitors - prevent L-dopa degradation, thereby increasing da availability |
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PK disease drugs
curb excess cholinergic activity |
benztropine (antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia)
for essential or familiar tremors, use b-blockers |
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levodopa/carbidopa
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increases level of da in brain. unlike dopamine, L-dopa can cross BBB and is converted by dopa decarboxylase in teh CNS to dopamine.
use: PK toxicity: arrhythmias from peripheral converstion to da. long term use can lead to dyskinesia following administration, akinesia between doses. carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa in order to increase bioavailabity of l-dopa in the brain and to limit peripheral side effects. |
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selegiline
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selectively inhibits MAO-B, which preferentially metabolizes dopamine over Ne and 5-HT, thereby increasing the availability of da.
use: adjunctive agent to L-dopa in treatment of PK. toxicity: may enhance adverse effects of L-dopa |
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alzheimer's drugs
memantine |
NMDA recpetor antagonist; helps prevent excitotoxicity (mediated by Ca)
toxicity: dizziness, confusion, hallucinations. |
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alzheimer's drugs
donepezil, galantamine, rivastigmine |
acetylcholinesterase inhibitors.
toxicity: nausea, dizziness, insomnia. |
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huntington's drugs
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disease: increase da, decrease GABA + ACh
reserpine + tetrabenazine - amine depleting. haloperidol - da receptor antagonist. |
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sumatriptan
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5-HT 1b-1d agonist. cause vasoconstriction, inhibition o trigeminal activation and vasoactive peptide release. 1/2 life < 2 hrs.
use: acute migraine, cluster ha attacks. toxicity: coronary vasospasm (CI in patients with CAD or prinzmetal angina), mild tingling. |
