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65 Cards in this Set

  • Front
  • Back
What are the 4 other receptors that are involved with imipramine's side effects?
1. Cardiac fast channels = arrhythmias, cardiotoxicity, wide QRS complex
2. muscarinic Ach receptors = flushing, hyperthermia, dilated pupils, ileus, urinary retention, sinus tachy, confusion, hallucination
3. alpha 1 receptors = hypotension, vasodilation
4. H1 receptors = sedation
mechanism of methadone, meperidine, dextromethorphan, codeine
opioids open K+ channels, close Ca2+ channels --> hyperpolarization and inhibition, causing decrease synaptic transmission of ACh, NE, 5-HT, glutmate, substance P/
opiod rx for diarrhea
loperamide, diphenoxylate
how do you treat a person who comes in ODing on a substance that causes:
-respiratory/CNS depresion
-constipation
-PINPOINT pupils
Opioid toxicity treated with naloxone, naltrexone
In chronic opioid use, what 3 things do you build tolerance to, what 2 things can you not develop tolerance to?
Build tolerance to:
-CNS depression
-Resp depression
-cough

Do NOT develop tolerance to:
-miosis (pinpoint pupils)
-constipation
Partial agonist at opioid mu receptor, agonist at kappa receptor
Butrophanol

*used for pain- has less resp. depression than full mu agonists.
Tramadol
-mechanism
-uses
very weak opioid agonist- also inhibits serotonin and NE reuptake.

Used for chronic pain, has similar opioid side effects, also has decreased seizure threshold.
3 drugs that are 1st line for tonic clonic
phenytoin, carbamazepine, valproic acid
5 indications for carbamazepine
1. tonic clonic seizures
2. partial (simple or complex) seizures
3. trigeminal neuralgia
4. diabetic neuropathy
5. mood stabilizer
5 classes of side effects for phenytoin
1. neuro: nystagmus*, diplopia, ataxia, sedation, peripheral neuropathy*

2. cosemtic: gingival hyperplasia*, hirsutism*, acne

3. megaloblastic anemia

4. teratogen "fetal hydantoin syndrome"

5. SLE like syndrome*

*also induces CYP450
we all know agranulocytosis, aplastic anemia, liver toxicity are the 3 feared side effects of carbamazepine.

what are 5 other, less famous, side effects?
1. diplopia, ataxia
2. teratogen (like phenytoin)
3. induces CYP450 (like phenytoin)
4. SIADH
stevens-johnson syndrome
This drug blocks voltage gated Na+ channels and has the dreaded side effect of Stevens-Johnson syndrome
Lamotrigine (used 2nd line for partial and tonic clonic)
Mechanism and 3 uses of Gabapentin
mechanism: designed as GABA analog, but ironically inhibits HVA Ca2+ channels.

Uses =
-partial, tonic clonic.
-peripheral neuropathy (post herpetic neuralgia)
-bipolar disease.
Blocks Na+ and GABA

Causes mental dulling, kidney stones, weight loss
Topiramate
4 uses of barbituates (which increase duration of Cl- channel opening)
1. anxiety
2. seizures partial or generalized - phenobarbital
3. insomnia
4. induction of anestheia - thiopental
3 epilepsy drugs that induce CYP450
PCP induce (thus would make heparin subtherapeutic)

phenytoin, carbamazepine, phenobarbital (barbituates)
Use for patient with absence seizure AND has tonic clonic.

Inactivates Na+ channels, and increases GABA concentration.
Valproic acid

*also 1st line for MYOclonic seizures
1st line for absence seizures

what are 5 main side effects?
ethosuximide - blocks thalamic T-type Ca2+ channels

fatigue
GI symptoms
headache
urticaria
stevens johnson syndrome
rare side effect of valproic acid
rare but fatal hepatotoxicity
also, tremor, weight gain

*teratogen = neural tube defects in fetus
Inhibits GABA reuptake
tiagabine
irreversibly iinhibits GABA transaminase --> increased GABA
vigabatrin
4 short acting benzos
triazolam
oxazepam
midazolam
alprazolam
3 intermediate acting benzos
lorazepam
estazolam
temazepam
4 long acting benzos
diazepam
chloridazepoxide
clorazepate
flurazepam
4 clinical uses of benzos
1. anxiolytic
2. sedative - night terrors, sleepwalking, insomnia
3. anticonvulsant (used acutely and for alcoholic DTs)
4. muscle relaxant - spasticity
OD of benzo rx
flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Which are more likely for withdrwal, oxazepam or flurazepam?
oxazepam = short acting (along with triazolam, midazolam, alprazolam)

short acting are more likely to cause withdrawl

flurazepam = long acting along with diazepam, chlordiazepoxide, clorazepate
act via BZ1 receptor and treats insomnia with less addictive potential because it is rapidly metabolized and has less psychomotor depression.
zolpidem (ambien), zaleplon, eszopiclone

*side effects = ataxia, headache, confusion
what determines rapid induction and recovery times in anesthetics?
less solubility in blood = rapid induction and recovery times

*high blood solubility = high blood/gas partition coefficient = increased gas to saturate blood = slower onset of action
what determines potency in anesthestics?
drugs with more lipid solubility = increased potency = 1/MAC (minimum alveolar conc.)
inhaled anesthetic side effects = CV/resp depression, nausea/emesis, increased cerebral blood flow, rarely malignant hyperthermia

what are specific side effects for:
-halothane
-methoxyflurane
-enflurane
-halothane: fulminant hepatoxicity
-methoxyflurane: nephrotoxicity
-enflurane: proconvulsant
thiopental has one weird side effect
decreases cerebral blood flow

*high potency, rapid entry. effect terminated by redistribution in to tissue/fats.
anesthetic commonly used for endoscopy with inhaled anesthetics, can cause severe postoperative resp depression
midazolam (short acting benzo)
ketamine mechanism and side effects
block NMDA receptors- cardiovascular stimulants.

cause disorientation, hallucination, bad dreams.

increase cerebral blood flow.
order of nerve blockade with local anesthetics (esters-procaine, amides-lidocaine)
small myelinated > small unmyelinated > large myelinated > large unmyelinated
order of pain loss with local anesthestics (esters-procaine, amides-lidocaine)
pain > temperature > touch > presure
side effects of bupivicaine (amide local anesthetic) and cocaine (ester local anesthetic)
bupivicaine = severe CV tox

cocaine = arrhythmias

*all local anesthetics cause CNS excitation
reversal of succinylcholine phase 1 and phase 2

what happens when given cholinesterase inhibitors (neostigmine)
phase 1 = prolonged depolarization, no antidote, block POTENTIATED by cholinesterase inhibitors

phase 2 = repolarized but blocked, neostigmine works.

*general side effects of succinylcholine = hypercalcemia, hyperkalemia
neuromuscular blocking drugs that block ACh receptors
tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

*can reverse with neostigmine
Rx for neuroleptic malignant syndrome
dantrolene
3 parkinson's drugs that are dopamine agonists
bromocriptine
pramipexole
ropinirole
3 drugs that prevent dopamine breakdown
selegiline = selectively inhibits MAO-B, which preferentially metabolizes dopamine ofver NE/5-HT

COMT inhibitors, prevent L-dopa degradation
entacapone
tolcapone
What side effects will NOT be prevented by carbidopa
Carbidopa is administereed with L-Dopa to prevent peripheral conversion to dopamine, which can cause arrhythmias, vomiting, nausea.

However, it will NOT prevent axiety/agitation of parkinson's disease as these are CNS symptoms and carbidopa only works peripherally.
NMDA receptor antagonist for Alzheimers
memantine

remember alzheimers = low ACh, high NE, high glutamate

by blocking NMDA you can decrease the effect of the increased glutamate (which works on NMDA receptors) and help prevent excitotoxicity.

side effects can include hallucinations
acetylcholinesterase inhibitors that treat alzheimers
donepezil, galantamine, rivastigmine

side effects can include insomnia
two treatment options for huntingtons
disease = high dopamine, low ACh, low GABA

1. reserpine + tetrabenazine - prevent neurotranmitter entry to presynpatic vesicles, amine depleting

2. haloperidol - dopamine receptor antagonist
major side effect of sumatriptan
sumatriptan = 5HT IB/ID agonist which causes vasoconstruction, inhibition of trigeminal activationa and vasoactive peptide release.

used for acute migrane, cluster headaches.

tox = coronary vasospasm - contraindicated in patients with CAD or prinzmetal's angina.
ADHD treatment
methylphenidate (ritaline), dextroamphetamine

*can also be used for narcolepsy
Evolution of EPS side effects with typical antipsychotics:
4h
4d
4wk
4mo
4h: acute dystonia (muscle spasm, stiffness, oculogyric crisis)
4d: akinesia (parkinsonian symptoms)
4wk: akathasia (restlesness)
4mo: tardative dyskinesia (lock smaking, tongue chewing)

*occurs from upregulation or hypersensitivity of dopamine receptors and a decrease in cholinergic tone.
4 main symptoms of neuroleptic malignant syndrome
hyperthermia (dopamine is involved in temp regulation)
rigidity
autonomic instability/encephalopathy
myoglobinuria
Other than EPS side effects and NMS, what are 4 other side effects (things blocked) by typical antipsychotics (haloperidol + -azines)
1. endocrine side effects --> hyperprolactinemia
2. blocking muscarinic (dry mouth, constipation)
3. blocking alpha (hypotension)
4. blocking histamine (sedation)

*also remember that typical antipsychotics are highly lipid soluble and are very slow to be removed by the body.
Which are the high potency and which are the low potency typical psychotics?
High potency: haloperidol, trifluoperazine, fluphenazine *have more neurologic side effects (EPS)

Low potency: thioridazine, chloropromazine (non neuro side effects- anticholinergic, antihistamine, alpha blocker)
special side effects of chloropromazine and thirodazine (both low potency)
chloropromazine - corneal deposits

thioridazine - retinal deposits
mechanism of olanzapine
block 5-HT2, dopamine, alpha, H1 receptor

*used to treat pos + neg symptoms of schizophrenia.
-Olanzapine is also used for OCD, anxiety, depression, mania, Tourette's

*has less EPS/anticholinergic symptoms than typicals.
side effects of olanzapine and clozapine
both olanzapine and clozapine cause weight gain.

clozapine also can cause agranulocytosis.
mood stabilizer for bipolar disorder and can treat SIADH
lithium
What are the 5 side effects of lithium
Movement (tremor)
Nephrogenic diabetes inspidus- hypernatremia, polyuria, polydispia
hypOthyroidism
Pregnancy problems
Fetal cardiac defects- ebstein abomaly (fucked up tricsupid valve), malformation of the great vessels
What is the mechanism of TCAs?

what are the names of 5 common TCAs
imipramine (bed wetting), amitriptyline (very anticholinergic), nortryptiline (not so anticholinergic), desipramine, clomopramine (OCD), doxapine, amoxapine

block reuptake of NE + Serotonin
what are the 4 other things that TCA can accidentally block?
1. Cardiac fast channels = arrhythmias, cardiotoxicity, wide QRS complex

2. muscarinic ACh receptor = flushing, hyperthermia, dilated pupils, ileus, urinary retention, sinus tachy, confusion, hallucination

3. alpha 1 block = hypotension

4. H1 block = sedation
which drug TCA has the least anticholinergic effects?

what about least sedating?
amitriptyline has more anticholinergic side effects than nortriptyline

desipramine is the least sedating and has lower seizure threshold (desis keep you awake)
rescue for TCA cardiotoxicity (wide QRS from blocking Na+ fast channels)
NaHCO3
patient presents with hyperthermia, muscle rigidity, CV collapse, flushing, diarrhea, seizures. what is the treatment?
serotonin syndrome - occurs when you comine MAOi + SSRI

treat with cyproheptadine (5-HT2 receptor antagonist)

*differentiate from NMS because it has flushing, diarrhea, seizures
2 SNRIs and their main toxicity
venlafaxine (depression + GAD), duloxetine (depression + diabetic peripheral neuropathy)

main tox: high BP
name the 4 SSRIs
fluoxetine, paroxetine, sertraline, citaprolam

rx for depression, OCD, bulimia, social phobias, PTSD, panic disorder
4 common MAOi's

what is the mechanism
phenezline, tranylcypromine, isocarboxazid, selegiline (selective for dopamine)

*mechanism: inhibit breakdown of NE, serotonin, dopamine