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anesthesia pharm > antipsychotics > Flashcards

antipsychotics Flashcards

1
Q

tricyclic antidepressant pharm action

A

mood elevating agents do not act as stimulants of CNS.
Only after a period of 2-3 weeks of chronic dosing will a therapeutic benefit emerge.
the precise mechanism responsible for the antidepressant action of the TCA is unknown

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2
Q

TCA theory of action

A

inhibition of norepi neuronal uptake
time dependent changes in beta adrenergic function parallel the delayed onset of clinical efficacy
mild effect on 5-HT central serotonin receptor sensitivity

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3
Q

TCA pharmacokinetics

A 
well absorbed by GI tract
large volume of distribution
half lives range from 8-89 hours
most require once a day dosing
inactivation through oxidative metabolism by hepatic microsomal enzymes
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4
Q

TCA adverse effects

A 
antimuscarinic efects (tachy, burry vision, constipated, dry mouth)
sedation
toxic delirium
seizures
weight gain
involuntary movements
neuroleptic malignant syndrome
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5
Q

TCA

A

weak alpha adrenergic antagonists, most common CV effects are ortostatic hypotension and tachy, sedation is thought to be mediated through antagonist properties at the apha 1 adrenoreceptor and H1 histaminergic receptor sites in the brain
lowers seizure threshold
CNS toxicity presents as a delirium with affective, cognitive, motor, and psych symptoms
overdose is frequently fatal with unresolvable arrhythmia’s

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6
Q

Selective Serotonin Re-uptake Inhibitors

A

produce therapeutic action through an ability to modulat serotonin neurotransmission in the brain
long cascade of events causes poentiation of serotonin neurotransmission at central synaptic sites.

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7
Q

SSRI pharm and kinetics

A

onset is the same as TCA
anticholinergic and cV side effects were not present in SSRI
side effects tolerated better:
GI effects- nausea and diarrhea
CNS stimulation- insomnia and anxiety
sexual dysfunction- aorgasmia and delayed ejaculation
weightloss

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8
Q

SSRI warnings

A

caution in combo with other antidepressants, benzos, neuroleptics, carbamepazine, and blood levels increase

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9
Q

elimination half life of fluoxetine

A

2-3 days

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10
Q

SSRI absorption dependent on food?

A

NO

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11
Q

Monoamine Oxidase Inhibitors (MAOI)

A

developed from iproniazid, a drug used to combat TB, patients noted to be happier while on med.
Reserved for atypical depression unresponsive to TCAs or SSRIs and depression resistant to ECT

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12
Q

MAOI mechanism of action

A

monoamine oxidase exists on the body as A and B
transmiter amines, such as norepi, are preferrably metabolized by MAO-A in brain tissue
MAO-B is involved in the catabolism of dopamine
drugs inhibit both A and B, but A is where therapeutic effect occurs

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13
Q

MAOI changes and side effects

A

adaptive effects occur in 2-3 weeks
side effects:
occasion with long term therapy, particulary for those who are slow acetylators
non hydrazine derivatives have low hepatotoxicity risk
CV effects- occur with ingestion of certain foods, low tyrosine diet, cheese beer and wine
tremors
ejaculatory delay
orthostaic hypotension
hyperpyrexia with meperidine dextromethorphan and TCA

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14
Q

trazadone

A

desyrel
less toxic and faster acting
anxiolytic properties acts at both seratonin and norepi sites in brain
common side effects are sedation dizziness hypotension and nausea

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15
Q

bupropion

A

wellbutrin and zyban
MOA unknown
free of muscarinic side effects
CNS stimulation with insomnia and nervousness
contraindicated in seizures or head trauma

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16
Q

lithium

A

effective 60-80% of BOD patients
mood stabilizing agent
replaces sodium at certain active sites
selective to CNS non selective excitatory tissues (CV)

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17
Q

Manic Depressive on lithium

A

adverse reactions are associated directly with therapeutic levels
narrow window (0.5-1.5mEq/L) necessitates frequent monitoring
toxicity presents as nausea, diarrhea, vomiting, abd pain, polyuria, sedation and mild tremor
many become hypothyroid after long term use

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18
Q

antipsychotic MOA

A

block synaptic actions of dopamine in the brain
the antagonism of dopamine in the medolimbic-mesocortical system is thought to be the basis of the therapeutic actions of the antipsychotic drugs, while antagonism of the nigrostriatal system in the major factor in the extrapyramidal side effects seen with antipsychotics

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19
Q

antipsychotic side effects

A

sedation- common with all antipsychotics, activate histamine receptors, given at bedtime
extrapyramidal effects- acute dystonia, akathisia, parkinsonism

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20
Q

antipsychotics extrapyramidal effects

A

actute dystonia in 5% of cases- treated centrally acting muscarinic agent (cogentin)
akathisia- unresponsive to cogentin- treated with benzos or beta blockers
tardive dyskenesia is a late occuring and usually an irreversabe phenomenon
neuroleptic malignant syndrome- fever, diffuse muscle rigidity, severe EPS, autonomic dysfunction (elev BP &HR)

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21
Q

Neuroleptic Malignant Syndrome

A

more common in men than women
80% of cases occur under age 40
can be misdiagnosed as MH
treated with cooling, hydration, dantrium has been useful
bromocriptine (parlodel) can ease the rigidity as well
discontinue the antipsychotic drug ASAP
can occur with phenothiazine admin preop

22
Q

more antipsychotic side effects

A 
autonomic- alpha adrenergic antagonists
cholinergic antagonism
postural hypotension
hyperprolactinemia- removing dopamine inhibition on prolactin secretion- amenorrhea, galactorrhea, infertility in women and impotence in men
cholestatic jaundice
cutaneous allergic reactions
photosensitive
opacities of the cornea
agranulocytosis
23
Q

antipsychotics contraindications

A

parkinsons, hepatic failure, bone marrow depression, use o other sedatives
overdose rarely fatal
hypotension responds better to norepi then to epi

24
Q

antiparkinson drugs

A

most prominent pathological finding in parkinsons disease is the degeneration of neurons that originate in the sunstantia nigra of the midbrain and terminate in the basal ganglia (caudate nucleus, putamen, palladium)

25
Q

levodopa/carbidopa

A

most reliable and effective
considered a form of replacement therapy
precursor to dopamine
levodopa, an amino acid, is transported across the BBB and converted to dopamine y the enzyme L-aromatic amoni acid decarboxylase

26
Q

levodopa/ carbidopa activity

A

carbidopa is a decarboxylase inhibitor, which is active i the lover, kidney, and GI tract
these sites are where the levodopa is metabolized prior to getting across the BBB
carbidopa does not cross the barrier, so it has peripheral effects only

27
Q

levodopa/carbidopa ….

A

pharmacologic effects are caused by newly formed dopamine in the brain
levodopa can improve the quality of life of most patients
improvements in rigidit and bradykinesia are generally more complete and appear sooner than do improvements in tremor

28
Q

Levodopa/ carbidopa sie effects

A

intial treatment side effects are nausea, anorexia, and vomiting
most patients develop a tolerance
CTZ activation in the area postrema in the medulla oblongata by newly formed dopamine
orthostatic hypotension
cardiac dysrhythmias- beta adrenergic dopamine stimulation

29
Q

levodopa/ carbidopa long term side effects

A

abnormal choreiform movements of limbs, hands, trunk, and tongue
movements improve with lower dose but parkinsons increase
serious mental disturbances
psychotic episodes
drug holiday x 1 week

30
Q

levodopa/ carbidopa contraindications

A 
MAOI
narrow angle glaucoma
cardiac arrythmias
recent MI
phenothiazines, butyrophenones and reserpine can produce EPS
31
Q

Selegiline

A

MAO-B inhibitor
first line drug for parkinsons before levodopa
enhances action of endogenous dopamine
same precautions with MAOI
interacts with TCA causing fever, agitation, delirium, and coma

32
Q

belladonna alkaloids

A

used only in mild cases
combat tremor
help in drug induced dystonias
antihistamines like diphenhydramine can be used to control monir tremors in elderly patients

33
Q

dopamine agonists

A

only 20-30% of patients respond favorably
bromocriptine (parlodel) pergolide (permax)
loss of response typically occurs over time
anorexia and nausea due to stimulation of the CTZ

34
Q

anesthetic implications of parkinsons

A

have patients take medications preop (lasts 6-12 hrs)
avoid phenothiazines, butyrphenones, and metoclopramide
muscle rigidity can impede mask ventilation
increased risk of aspiration
intravascularly volume depleted
normal responses to muscle relaxants
increased risk of laryngospasm
voilent tremors on emergence
no ephedrine if patient taking deprenyl
ketamine causes exagerated response
potential hyperkalemia for succs

35
Q

more anesthetic implications of parkinsons

A

skeletal muscle tremor may mimic VFIB on ECG
may have diminished reserve due to chronically poor exercise tolerance
muscle relaxants will relax even the most rigid of patients

36
Q

anticonvulsants

A

goal is to raise seizure threshold
therapuetic goal is to control seizures without excessive side effects
only 40% of epileptics become seizure free with medications
20% of epileptic patients get NO benefit from currently available meds

37
Q

anticonvulsants MOA

A

appears to be inhibition of neuronal sodium channels in hyperexcitable cells
disinhibition may increase seizures
reduction in GABA increases seizures
anticonvulsants are classified as the 1-4 for MOA

38
Q

type 1

A

block sustaines high frequency repetatice firing by enhancing sodium channel activation
phenytoin carbamazepine, oxycarbazepine, lamotagrine, and felbamate

39
Q

type 2

A

multiple actions: enhance GABAergic inhibition, reduce T calcium currents, and possibly block SRF
valproic acid, benzo, phenobarbitolprimidone

40
Q

type 3

A

block T calcium currents only

ethosuximide, trimethadione

41
Q

type 4

A

only enhances GABAergic inhibition. Has no known effect on SRF, GABAergic inhibition, or T calcium currents
Vigabatrin and gabqpentin

42
Q

anticonvulsants sodium channel blockers MOA

A

capacity to block the sustained high frequency repetitive firing of action potentials
anticonvulsants of this class bind preferenctially to the inactive or non inactive site
block in time dependent, because it takes a while to dissociate the drug from the site to make it active again

43
Q

phenytion

A 
generalized tonic clonic seizures
partial seizures
antiarrhythmic propertoes
slow and complete GI absorption
highly plasma potein bound (90%)
zero order kinetics
leads to hepatic induction of microsomal enzymes
44
Q

phenytoin adverse effects

A

acute overdose- nystagmus, ataxia, vertigo, diplopia, cognitive changes
idiosyncratic- skin rashes, dermatitis, heptic necrosis
common- gingival hyperplasia, enlargement of lips and nose
fetal hydantoin syndrome
folate deficiency

45
Q

phanytoin drug interatcions

A

cimetidine, chloramphenicol, disulfram, isoniazid

dilantin reduces the half life of quinidine by 50%

46
Q

carbamazepine (tegretol)

A

for tonic clonic and absence seizures
most common side effect is drowsiness
allergic response usually rash, fever SLE
can exacerbate seizures in some patients
causes significant enzyme induction
will increase rate of metabolism of other anticonvulsants

47
Q

barbituates

A

primary mechanism of action is facilitation of GABA inhibition- prolonged opening of chloride channels
main side effect is sedation- disturbance is cognitive functioning
will also cause hepatic microsomal enzyme induction

48
Q

valproic acid

A

MOA is blockage of sodium channels that are voltage dependent
causes increased brain GABA
side effects- hepatotoxicity and failure, fetal neural tube defects, alopecia

49
Q

benzodiazepines

A

interaction with GABA
cause sedation
not first line therapy
rapid development of tolerance

50
Q

anesthetic implications of phenytoin

A

resistance to nondepolarizing muscle relaxants
shorter duration of action of muscle relaxants
administer at 25-50mg/min to avoid hypotension
Stevens-Johnson syndrome

51
Q

anesthetic implications of anticonvulsants

A

induction with thiopental or propofol
N2O/ narc techniques
avoid enflurane, methohexital
show a tolerance to opiods secondary to enzyme activation caused by their anticonvulsant

anesthesia pharm (10 decks)

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