-
Reserpine
- deplete dopamine stores within nerve endings
- may diminish striatal dopaminergic transmission to affect both direct and indirect pathways of basal ganglia --> producing parkinsonism
-
Carbidopa and I-dopa
- reduces peripheral metabolism of I-dopa
- administer together with I-dopa to treat Parkinson's disease
-
a metabolite of MPTP
- contaminant produced during improper preparation of synthetic narcotic
- causes parkinsonism by damage in nigral Mtc
-
cocaine, amphetamine, benztropine
- inhibition of dopamine reuptake
- increase dopamine level at the synaptic cleft
-
what are prophylactic (preventive) treatments for depression? (name 5)
lithium, carbamacepines, lamotrigine, valproate, anitepileptics (mood stablizers)
-
Tricyclics, Fluoxetine (prozac)
- selective seratonine reuptake inhibitors
- used for treatment of anti-depression
could also use MAO inhibitors, ECT...
-
cocaine, amphetamine, benztropine
- treatment for anti-psychotic
- blocks reuptake of Dopamine
- short-term SE: tremor, rigidity (parkinson like symptom)
- Long-term SE: tardive dyskinesia
-
what would you substitute for opiate addiction?
methadone
-
what is common treatment for alcohol withdrawal?
- Benzodiazepine
- (GABA enhancer)
-
Haldrol, haloperiodol, perphenazine
- typical antipsychotic drugs
- treatment for schizophrenics
- block D1 and D2 receptors
- side effect as parkinson like movements ie. tremor, rigidity,
also, if haloperidol were applied to ppl with addictions, it would reduce euphoric/rewarding effect
-
Clozapine, olanzapine
- atypical antipsychotic medications
- block D3 and D4 receptors
- no side effects
- treatment for schizophrenics
-
Levetiracetam
- aka KEPPRA
- treatment for epilepsy
- decrease the voltage-operated delayed rectifier K+ current without affecting Na+ and A-type K+ current --> reduced repetitive action potential generation
- reduction of N-type and P/Q type Ca currents ==> decreased NT release
- binds to synaptic vesicle protein, SV2A (= believed to impede conduction across synapses)
-
Benzodiazepines, barbiturates (Gabanergic)
- treatment of epilepsy
- potentiate inhibitory GABA A receptors and inhibit AMPA receptors
- Enhance inhibition
-
Phenytoin, carbamazepine, lamotriginum
- treatment for epilepsy
- reduce the flow of Na+ and Ca+ ions into the neurons
- increase the level of GABA
- suppress the release of NT (glutamate)
- less excitability
-
Thiazide (from physio)
blocks NCCT at distal convoluted tubule (mutation in this channel: Gittelman's syndrome)
-
Bumetanides, furosemide (from physio)
- blocks NKCC2 at TAL.
- diuretics
- mutation in NKCC2 or ROMK, or CLC-kb = Bartter's syndrome
-
Phenothiazine
- block D2 receptor in the forebrain
- used in the treatment of psychosis
- may cause parkinsonism by limiting dopamine -mediated inhibition of striatal neurons contributing to the indirect pathway
-
acetazolamide (from physio)
- inhibits carbanic anhydrase
- turns H2CO3 --> CO2 and H2O
Carbanic anhydrase is considered diuretics because it excretes out H+ in urine
-
PTU
- inhibit iodine oxidation
- inhibit organification (formation of MIT or DIT by iodine and thyroglobulin)
- inhibit coupling between MIT and DIT
-
Thyocyanate
inhibit Na/I cotransporter in thyroid gland
-
Perchlorate
inhibit Na+/I Cotransporter in thyroid gland
-
what are the drugs that induce fetal gamma globulin formation to avoid HbS formation to express AR sickle cell? name 3
- 5-azacytidine, (decitabine, demethylating agent)
- hydroxyurea, (demethylating agent?)
- butyrate compounds (histone deacetylation)
-
Bromocriptine (from physio)
- treatment for prolactinoma
- tumor on prolactin secreting anterior pituitary --> causes excessive release of prolactin
- treat with dopamine agonist
-
sodium benzoate (genetics)
- trap excess ammonia made from protein degradation when urea cycle is defect
- chemical diversion
-
sulfonamides, animaralials, chloramphenicol
-->what disease is associated?
- G6PD
- cannot produce NADPH oxidase
- oxidative drug will cause hemolytic anemia
- example of idiosyncratic drug effects
-
Warfarin --> explain pharmakokinetic and pharmakodynamic dual polymorphism
warfarin --> anticoaggulant drug by inhibiting vitamin K-expoxide reducatse (VKORC1 gene)
- warfarin is racemic -->S-warfarin is more potent since it follows single pathway with CYP2C9
- pharmakokinetic effect
- expression of CYP2C9 is polymorphic-->individual has different alleles
- Pharmakodynamic effect
- VKROC1 is also polymorphic --> requires different effective dosage of warfarin
-
Butyrylcholinesterase (BChE)-->what does it metabolize?
succinylcholine
AR ppl with BChE will experience prolonged muscle paralysis due to succinylchoine
-
N-acetyltransferase (NAT2) -->what does it metabolize?
isoniazid
slow acetylaters(AR)-->adverse effects --> more prone to drug toxicity ie. hepatotoxicity, neuropathy
fast acetylaters
-
Codeine and metoprolol --> what metabolizes them?
metabolized by CYP2D6
- codeine: convered to morphine by CYP2D6
- -ultrarapid metabolizers have extra copy of CYP2D6 --> codeine gets covereted to morphine too fast --> leads to respiratory arrest
- -opposite affect for poor metabolizers; too slow conversion, thus codeine is ineffective drugs for them
- metroprolol
- -poor metabolizers take time to detoxify--> increased adverse effects
- -ultrarapid metabolizers need higher dosage
-
6-marcaptopurine and azathiopurine --> what metabolizes them?
- anti-cancer drug
- metabolized by thiopurine-methyltransferase
- autosomal recessive ppl with TPMT will suffer from myelosuppresion due to prolonged presence of these drugs
-
amiloride (from physio)
blocks ENac at collecting duct
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