tricyclic antibiotics 2 Flashcards
how long for therapeutic effect tricyclics? ssri?
2-3 weeks
mech action tca
unknown, inhibits norepi neuronal uptake mild 5-h serotonin receptor
metabolism tca
liver, 1/2 life is 8-84hr, large vol distribution
s/e TCA
orthostatic hypotension, tachycardia, tachy, blurred vision, dry mouth, sedation, delirium, tremors, weight gain, neurolepitc malignant
cns toxicity tca s/s
cognitive, motion, psych changes
overdose tCA-
fatal arrhythmias
SSRIs mech action
modulate serotonin neurons in the brain
s/e ssris
no anticholinergic/cardiac s/e, nausea, vomiting, anxiety, insomnia, weight loss
1/2 life ssri
2-3 days
MAOIs
ihibit MAO-A and MAO-B but action at MAO-a, which inhibits metabolism of norepi
s/e maois
hepatotoxic,cardiac toxic with tyrosine, tremors, orthostatic htn, hyperpyrexia with certain meds
trazodone
mech unknown
s/e trazodone
no muscarinic effects, CNS stim with insomnia, tremors
contraindications trazodone
seizures and head trauma
lithium
replaces sodium at certain synapses mood stabilizer, narrow therapeutic window
s/s lithium toxicity
n,v,diarrhea, abd pain, polyuria, sedation
what may occur with chronic lithum use?
hypothyroidism
antipsych meds do what
block dopamine in the brain which is therapeutic at the mesolimbic-mesocortical system but the nigostraital system causes extrapyrimidial side effects
s/e antipsychotics
sedation secondary to histamine release, extrapyradamidal side effects (acute dystonia, akathisa, parkinsonism, tardive dyskinesia
what is a late, occuring s/e of antipsychotics
tardive dyskinesia- usually irreversible
how do you treat acute dystonia
treat with congentin
how do you treat akathisia
benzo/beta block
s/s neuroleptic malignant syndrome
fever, diffuse muscle pain, severe eps, autonomic dysfunction
tx neuroleptic malignant syndrome
tx with parlodel, cooling, hydration, dantrium
s/e antipsychotics
postural hypotension, hyperprolactinemia, jaundice, corneal opacities, photosensitivity, agranulocytosis
contraindications antipsych
parkinsons, hepatic failure, bone marrow dep
whoch meds do pt on antipsychotics respond to better?
norepi vs. epi with hypotension
levodopa/carbidopa is for
tx parkinsons, considered replacement therpy, precuror of dopamine
levodopa is
an amino acid, transported across bbb and converted to dopamine by the enzyme L-aromatic amino acid decorboxylase
why is carbidoba given with levodopa?
carbidopa blocks conversion of levodopa to dopamine in the periphery b/c carbidopa is there, but cannot cross bbb. if not pt would have hypertensive crisis secondary to carbidopa which increases blood pressure
prob with pt with parkinsons
not enough dopamine, which is necessary for movement. insufficient amount makes them not able to move
where is carbiopa activated and what is it
decarboxylase inhibitor, ative liver, kidney, gi
which symptoms improve first with levo/carbo
rigidit and bradykinesia before tremor
s/e levo/carbo
nausea, vomiting, anorexia, secondary to ctz activation in the area postrema in the medulla by dopamine, orthostatic hypotension adn cardiac arrhythmias by beta dopamine stim
2nd set side effects levo/dop after long term therapy
abn movement of limbs, hands, trunk, tongue, serious mental disturbances (drug holiday x 1 week)
contraindications levo/carbi
MAO inhibitors, narrow angle glaucoma, heart arrhythmias, recent MI
what that is given with levo/carbi can cause EPS
phenothiazines, reserpine, butyrophenones
selegine
first choice drug parkinsons, enhances endogenous dopamine it is an MAO-B inhibitor
precautions slegiline
same as MAOs
seleginline and tcas
fever, agitation, delirium, coma
belladonna alkaloids
mild parkinsons, helps in drug induced dysonia
dopamine agonists
parlodel, permax
s/e dopamine agonists
anorexia, nausea
parkinsons and anesthesia
have pt take meds pre op, avoid phenothiazines, butyrophenones and reglan, increased risk aspiration, intravascularly vol depleted, increased risk laryngospasm
pt on deprenyl what drug cant give
ephedrine
ketamine can cause what with parkinsons
exagg symp response
succ and parkinsons
potential hyperkalemic response
anticonvulsants goal
to raise seizure threshold
% pt who become seizure free on anticonvulsants
40%
anticonvulsants mech of action
sodium channel blockers, block the sustained high frequency repetitive firing of action potentials
type I anticonvuls
enhance sodium channel inactivation
type I anticonvulsant meds
phenytoin, carbamezepine, oxcarbazepine, lamotrigine, felamate
type II anticonvulsants
enhance gaba inhibition, reduce t calcium currents, block ssustained high freq repetitive firins
type II anticonvulsant drugs
valproic acid, benzos, phenobarb, primidone,
type III anticonvulsants
block T calcium channels only
type of type II anticonvulsants
ethosuximide, trimethadione
type IV anticonvulsants
only enhances GABA inhibtition
type of type IV anticonfulsants
vigabatrin
noncategorized anticonvulsents
no effect on any known causes
drugs asso with noncat.
gabapentin
dilantin treats
tonic-clonic seizures and partial
dilantin is metabolized by
zero order kinetics which leads to induction of hepatic micorsomal enzymes
dilantin and protein binding
highly
s/e dilantin
gingival hyperplasia, enlargement lips and nose, fetal hydantoin syndrome, folate def
acute overdose diantin signs
nystagmus, ataxia, vertigo, diplopia, cognitive changes
drug interactions dilantin
cimetidine, chloramphenicol, disulfram, isoniazid
tegretol type of seizures treated
tonic-clonic and abcesnse
common side effect tegretol
drowsiness
what will tegretol do with metaboism
increase rate of metabolism of other anticoags
barbiturates mech action
facilitation of GABA inhibition
main side effect barbs
sedation
all anticonvulsants bascially cause
hepatic microsomal enzyme
depakene mech action
blockage sodium channels that are voltage dependent, cause increase brain GABA
s/e Depakene
hepatotoxicity, fetal neural tube defects, alopecia
benzos mech action
interaction with GABA- not first line therapy
administer phenytoin rate
25-50mg/min to avoid hypotension
phenytoin causes
resistance to NBMR
what can phenytoin cause
stevens johnson syndrome
people on anticonvulsants show
a toleratnce to opiods secondary to enzyme activation caused by anticonvulsant
