pharm exam 2

anxiolytic/hypnotic,

which is more likely to be perscribed, BZ or barb?

BZ bc less effects

when to use BZ (indications)?

anxiety, seizures, muscle relax

MAO of BZ

GABA agonist

potentiates GABA by binding to GABAa receptor

what does BZ cause in the cell?

increased Cl influx which makes cell negatively charged

can BZ work without GABA

no, BZ needs GABA and can only potentiate it

which increases inhibition

where are more GABA receptors with BZ subunits located

located in limbic system

think emotions

what do BZ do when used?

reduce anxiety, cause sedation/hypnosis, cause amnesia (anterograde), anticonvulsant, muscle relaxant

how does BZ cause sedation/hypnosis

uses a1-GABAa receptor

sleep areas are below limbic system so easy access

what is amnesia due to BZ mediated by

a1-GABAa receptors

first line of treatment in status epilepticus

BZ

not daily treatment bc its too sedating

how does BZ conduct muscle relaxation

a2-GABAa receptors

what therapies are BZ used for

GAD, sleep disorders, certain severe muscle disorders

what is special about kinetics of BZ

lipid soluable and variations in ½ life (short, med, long)

BZ metabolism?

hepatic which forms ACTIVE metabolites

BZ excreted?

excreted renally

why is it important to taper BZ

can potentiate SZ if not tapered correctly

adverse effects of BZ

drowsiness, ataxia (stumbling), memory loss (amnesia), hepatic impairment

depressive if everything combined

BZ antagonist used when?

during overdose, depending on half life if its long acting we many need to use ALOT of the drug

other anxiolytics?

antidepressants (concurrent treatment), and buspirone (uses serotonin and dopamine receptors instead of BZ)

MAO of barbiturates

binds to GABAa (like BZ) but not only limited to limbic system

blocks LTP (excitatory glutamate)

blocks Na+ channels

barb dont stop pain by instead can

prevent formation of chronic pain

negative effects of barb

causes addiction, drowsiness, nausea, vertigo, tremors, and enzyme induction (more liver action and CYP which metabolizes OTHER drugs way more quickly)

barb kinetics?

ultra-short acting, short-acting, long-acting

similar to BZ

actions of barb

causes CNS depression based on dose

effects like sedation, hypnosis, anesthesia, coma, death

is barb/BZ an analgesic?

no they do not kill pain

what causes death for those who OD on barb?

respiratory depression- slower slower breath till death

decreased sensors to low O2 and H+(co2)so brain doesnt know to do anything

theraputic uses of barb

anesthesia (induction agent), anticonvulsant, sedation/hypnosis (prevent rem and disturbs sleep)

kinetics of barb

narrow TI (so more dangerous), induction of CYP (metabolizes other drugs faster), and distribution to other tissues, withdrawl can cause death,

effects of other hypnotics

psychomotor effects (uncontrolled movements), melatonin agonist (help blind ppl with circadian rhythm)

effect of antidepressants on mania

increase mania and make it worse`

monoamine theory

depression happens bc theres not enough norepi, serotonin, dopamine

monoamine theory related to mania

mania is bc theres an over production of monoamines

how does ssri work

SPECIFICALLY targets serotonin receptors

how much time do antidepressants need to have an effect

LONG LONG time

kinetics of ssri

good oral absorption but long ½ life

SLOWW

BZ/barb effect on cyp

increase cyp activity (faster metabolism of other drugs)

ssri effect on cyp

inhibit cyp (prolong action of other drugs)

adverse effects of ssri

sexual dysfunction, hyponatremia (low sodium), sleep disturbed

why is ssri not used in children

concern that it can make depression worse nad increase suicidal ideation

overdose of ssri

cause cadiac arrthymia, seizures, serotonin syndrome

what is disocntinuation syndrome

causes bad effects with antidepressants when there is abrupt withdrawl

causes serotonin syndrome (bruxism -grinding teeth, agitation)

second line of defense for antidepressants

snri

mechanism of snri

prevents reuptake of serotonin and epi causing more NT in synapse

other use for snri

can decrease pain perception (acts as analgesic)

atypical antidepressants

can increase serotonin and norepi activity, antihistaminic activity (heavy sedation), weight gain, messes with serotoning receptors, can decrease BP

mechanisms of TCA

side effects due to blocking muscarinic causing sympathetic response

what can TCA do

elevate mood, decrease suicidal thoughts, pain relief, increase sleep

kinetics of tca

lipid souable and variable bioavailability (1st pass metabolism)

adverse effects of TCA

muscarinic bloackage causes sympathetic response due to stress, decrase alertness, LOW TI, can cause worse arrhythmias, epilepsy

MAOI

prevent MAO from killing NT in axon terminal when in excess so they can build up and go out of the cell

food relation of maoi

tyramine in food will cause hypertensive crisis bc more monoamines

kinetics of maoi

good oral, enzymes regenerate soon

adverse effects of maoi

hypertensive episode, drowsy, hypotension, serotonin syndrome

treatment for mania/biopolar

lithium, low TI