post-midterm neuro drugs

  1. Reserpine
    • deplete dopamine stores within nerve endings 
    • may diminish striatal dopaminergic transmission to affect both direct and indirect pathways of basal ganglia --> producing parkinsonism
  2. Carbidopa and I-dopa
    • reduces peripheral metabolism of I-dopa
    • administer together with I-dopa to treat Parkinson's disease
  3. a metabolite of MPTP
    • contaminant produced during improper preparation of synthetic narcotic 
    • causes parkinsonism by damage in nigral Mtc
  4. cocaine, amphetamine, benztropine
    • inhibition of dopamine reuptake 
    • increase dopamine level at the synaptic cleft
  5. what are prophylactic (preventive) treatments for depression? (name 5)
    lithium, carbamacepines, lamotrigine, valproate, anitepileptics (mood stablizers)
  6. Tricyclics, Fluoxetine (prozac)
    • selective seratonine reuptake inhibitors 
    • used for treatment of anti-depression 

    could also use MAO inhibitors, ECT...
  7. cocaine, amphetamine, benztropine
    • treatment for anti-psychotic 
    • blocks reuptake of Dopamine 

    • short-term SE: tremor, rigidity (parkinson like symptom) 
    • Long-term SE: tardive dyskinesia
  8. what would you substitute for opiate addiction?
  9. what is common treatment for alcohol withdrawal?
    • Benzodiazepine 
    • (GABA enhancer)
  10. 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
  11. Clozapine, olanzapine
    • atypical antipsychotic medications 
    • block D3 and D4 receptors 
    • no side effects 
    • treatment for schizophrenics
  12. 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)
  13. Benzodiazepines, barbiturates (Gabanergic)
    • treatment of epilepsy 
    • potentiate inhibitory GABA A receptors and inhibit AMPA receptors 
    • Enhance inhibition
  14. 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
  15. Thiazide (from physio)
    blocks NCCT at distal convoluted tubule (mutation in this channel: Gittelman's syndrome)
  16. Bumetanides, furosemide (from physio)
    • blocks NKCC2 at TAL. 
    • diuretics
    • mutation in NKCC2 or ROMK, or CLC-kb = Bartter's syndrome
  17. 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
  18. acetazolamide (from physio)
    • inhibits carbanic anhydrase 
    • turns H2CO3 --> CO2 and H2O 

    Carbanic anhydrase is considered diuretics because it excretes out H+ in urine
  19. PTU
    • inhibit iodine oxidation  
    • inhibit organification (formation of MIT or DIT by iodine and thyroglobulin)
    • inhibit coupling between MIT and DIT
  20. Thyocyanate
    inhibit Na/I cotransporter in thyroid gland
  21. Perchlorate
    inhibit Na+/I Cotransporter in thyroid gland
  22. 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)
  23. Bromocriptine (from physio)
    • treatment for prolactinoma 
    • tumor on prolactin secreting anterior pituitary --> causes excessive release of prolactin 
    • treat with dopamine agonist
  24. sodium benzoate (genetics)
    • trap excess ammonia made from protein degradation when urea cycle is defect 
    • chemical diversion
  25. sulfonamides, animaralials, chloramphenicol 
    -->what disease is associated?
    • G6PD 
    • cannot produce NADPH oxidase
    • oxidative drug will cause hemolytic anemia 
    • example of idiosyncratic drug effects
  26. 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
  27. Butyrylcholinesterase (BChE)-->what does it metabolize?

    AR ppl with BChE will experience prolonged muscle paralysis due to succinylchoine
  28. N-acetyltransferase (NAT2) -->what does it metabolize?

    slow acetylaters(AR)-->adverse effects --> more prone to drug toxicity ie. hepatotoxicity, neuropathy 

    fast acetylaters
  29. 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
  30. 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
  31. amiloride (from physio)
    blocks ENac at collecting duct
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post-midterm neuro drugs