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Antiepileptic, Antiparkinsons, Psychopharm Drugs
Terms in this set (345)
2nd most common neurodegenerative disease is...
(alzheimers is 1st)
parkinsons disease results from loss of _________________ neurons in the basal ______________
presence of __________ bodies is also a common feature of parkinsons dz
within the extrapyramidal system, _______________ is inhibitory and ________________ is excitatory
______% of dopamine in the brain is found in the basal ganglia
patients with parkinsons dz may have as little as ____% of dopamine in the basal ganglia
earliest manifestations of parkinsons dz
loss of arm swing when walking
absence of head rotation when turning body
hallmark signs of parkinsons dz
tremors (rhythmic, pill-rolling-->more obvious at rest)
paucity of emotional expression
objective of parkinsons treatment
treat debilitating symptoms by increasing amount of dopamine in basal ganglia or by reducing neuronal effects of acetylcholine
currently all approved meds for Parkinsons treatment are only ________________
(don't stop progression of the disease)
parkinsons treatment is determined by ________ of patient and ______________ of symptoms
pharmacologic treatment for Parkinsons is indicated when.....
motor symptoms become bothersome
medications for Parksinons are divided into what two categories?
those used to treat motor symptoms
those used to treat side effects of meds
most effective treatment for Parkinsons is....
can levodopa cross the BBB?
can dopamine cross the BBB?
how does Ldopa get turned into dopamine once it crosses the BBB?
aromatic-L-amino-acid decarboxylase (aka dopa decarboxylase enzyme) converts Levodopa into dopamine
two reasons to administer a peripheral decarboxylase inhibitor with levodopa
first, to prevent the conversion of Ldopa into dopamine before it even has a change to cross the BBB
second, to prevent the side effects of excess dopamine in periphery
levodopa elimination 1/2 time? why do we care?
1-3hrs....requires frequent dosing
(may have to dose in the OR)
when taken orally, _____% of levodopa is rapidly decarboxylated into dopamine after liver first pass
(this is why we MUST give a decarboxylase inhibitor)
excess dopamine in the periphery is metabolized by _____________
levodopa excreted mostly by.....
abrupt discontinuation of levodopa??
can result in Parkinsons s/s to reappear and also a neuroleptic malignant-like syndrome can occur
most common early side effects of Levodopa are...
nausea and hypotension
why dose levodopa cause nausea?
dopamine stimulates the chemoreceptor trigger zone
(minimize this side effect by taking with a meal)
orthostatic hypotension occurs in ______% of patients in early levodopa therapy
initial treatment of orthostatic hypotension from Ldopa therapy....
increase Na/fluid intake, elevate HOB, compression stockings
(usually gets better with chronic use)
most common adverse effects of levodopa with long term therapy
dyskinesias (abnormal involuntary movements)
fluctuations in mobility
psychosis (visual hallucinations, paranoia)
why do patients taking Levodopa avoid high protein meals?
large influx of dietary amino acids can interfere with transport of levodopa into the brain
is seroquel an acceptable drug to give to a patient experiencing psychosis side effects from levodopa?
you aren't supposed to give neuroleptic drugs but seroquel is okay
why can levodopa cause cardiac disrhythmias?
from metabolism of dopamine to epi and norepi->beta and adrenergic responses
which beta blocker is an effective treatment for cardiac dysrhythmias that occurs from levodopa use?
true or false,
there is some evidence showing that levodopa may speed progression of Parkinsons dz
this is why some providers may try other drugs before using levodopa
large doses of levodopa can cause ______kalemia. why?
increases plasma levels of aldosterone
pyroxidine (vitamin B6) can abolish the therapeutic effect of Ldopa by enhancing the activity of.....
dopa decarboxylase enzyme
peripheral decarboxylase inhibitors are _______________ inhibitors of decarboxylase enzymes
which side effects of Ldopa are improved by the coadministration of peripheral decarboxylase inhibitors?
nasuea, vomiting, dysrhythmias
which side effects of Ldopa are not affected by the coadmin. of peripheral decarboxylase inhibitors
abnormal involuntary movements
how do MAOIs help treat parkinsons dz?
prevent the breakdown of dopamine by MAO
how do COMT inhibitors help treat parkinsons dz?
slows the elimination of carbidopa-levodopa
selegiline and rasagiline are....
MAO inhibitors used to treat parkinsons
entacapone and tolcapone are....
COMT inhibitors used to treat parkinsons
how do dopamine agonists treat parkinsons?
they are synthetic dopamine that don't require transformation or facilitated transport across BBB, but have side effects like confusion, hallucinations, daytime sleep attacks
ropinirole, pramipexole, rotigotine, and apomorphine are....
antimuscarinic agents used to treat parkinsons help which symptoms of parkinsons?
tremor and excess salivation
don't help with muscle rigidity or bradykinesia
Benztropine, trihexyphenidyl, procyclidine, and biperiden are....
antimuscarinic drugs used to treat symptoms of parkinsons
_____________ is a glutamate receptor antagonists used to parkinsons symtpoms
can amantidine help improve skeletal muscle rigidity and bradykinesia associted with parkinsons?
what happens if you withold a patients Parkinsons meds?
they can have skeletal muscle rigidty so you may have difficulty ventilating
also, abrupt discontinuation can result in return of parkinsons s/s and possibly a neuroleptic malignant-like syndrome
ketamine with parkinsons patients...
controversial but typically avoided
(it causes SNS activity)
phenothiazines, reglan, and droperidol in parkinsons patients....
these are dopamine antagonists
volatile agents in parkinsons patients....
zofran and parkinsons patients....
alfentanil and fentayl use in parkinsons patients....
may cause acute dystonic reactions
(opioid induced decrease in central dopaminergic transmission)
non-depolarizing NMB use and parkinsons patients....
more than _____% of the population will experience a seizure in their lifetime
clinical manifestations of seizures depends on ____________ and _____________ of neurons involved
seizures that result from congenital or acquired factors
seizures that have no apparent cause or trigger
seizures that are triggered by a disorder or another condition that irritates the brain
major excitatory NT in the CNS is
major inhibitory NT in the CNS is
when there is loss of GABA activity, there is enhanced release of _____________ neurotransmitters
excessive discharge of large numbers of neurons results in depolarization in an abnormal, _____________ fashion
in epileptic patients, seizure activity has a _____________ origin
what can cause focal seizure to turn into generalized?
low PaCO2 (hyperventilation)
stress and fatigue
if you move the seizure threshold further away from the resting membrane potential, are you increasing or decreasing the seizure threshold?
is it more or less likely the person will have a seizure now?
convulsant activity and seizure threshold are _____________ related
alkalosis ______________ the seizure threshold
(more likely to have a seizure)
acidosis ___________ the seizure threshold
(more difficult to intitiate a seizure)
generalized seizures exhibit abnormal electrical discharge through....
both hemispheres of the brain
_______________ seizures usually have an immediate loss of consciousness
a seizure that occurs in one part of the brain and results in the person remaining aware during the seizure
simple partial seizure
a seizure that occurs in one part of the brain and during which the person experiences altered consciousness (they may seem dazed or confused)
complex partial seizure
seizure that results in a blank stare usually lasting less than 10 seconds; starts and ends abruptly and awareness is impaired during the seizure
absence seizure (type of generalized seizure)
seizure that has two phases; first phase involves a crying out or groan, loss of awareness, and a fall as consciousness is lost and muscles stiffen; second phase involves convulsion
tonic clonic seizure (type of generalized)
seizure that results in a sudden jerk of part of the body such as the arm or leg; the person may fall over
myoclonic seizure (type of generalized)
seizure that involves a sudden loss of muscle tone that can result in the person falling down, dropping objects, or nodding the head involuntarily
atonic seizure (type of generalized)
valproic acid aka
goal of antiepileptic drugs is to control _______________ activity with minimal __________________
are the therapeutic plasma levels of each antiepileptic drug absolute?
no, they vary from person to person
(routine plasma mointoring isn't helpful)
are the toxic plasma level of each antiepileptic drug absolute?
no, varies from person to person
(routine plasma monitoring isn't helpful)
________% of patients will achieve seizure control with monotherapy
monitoring serum levels of antiepileptic drugs is not necessary if patients have _____________ seizure control and no signs of _____________
what is the "effective dose" of antileptic drugs?
the dose at which seizure activity ceases AND side effects do not occur
phenytoin is the only antiepileptic that routine plasma monitoring is recommended for because.....
it has nonlinear saturation dose kinetics
doses of antiepileptic drugs are given at intervals of ______ half life/lives of the drug to maintain therapeutic plasma conc levels and to ensure a signle missed dosed will not drop the plasma conc level below therapeutic
1 half life
two general ways that antiepileptic drugs work
acting on voltage gated ion channels
decreasing neuronal excitability(glycine)/enhancing neuronal inhibition (GABA)
most frequently used antiepileptics work by blocking _________
voltage gated Na channels
which drugs works by blocking voltage gated Na channels?
which drug works by reducing T type calcium current (low voltage activated channels that can respond to low depolarizations or even a low RMP)
how do barbiturates treat seizures
increase duration of GABA mediated ion channel opening (hyperpolarizing cell r/t chloride ion channels)
how do benzos treat seizures?
increase the frequency of GABA mediated ion channel opening (hyperpolarize cell r/t chloride ions)
even though gabapentin isn't really used for seizures, what is it's MOA
enhances acitivty/conc of GABA
all anticonvulsants are metabolized primarily by the liver and associated with drug interactions EXCEPT for which three antiepileptics?
most anticonvulsants are hepatic enzyme ____________
carbamazepine, lamictal, oxcarbazepine, phenobarb, phenytoin, topiramate, and primidone accelerate the metabolism of estrogen and progesterone rendering _____________________________ ineffective
valproic acid is a hepatic enzyme _________________
(slows metabolism of certain drugs)
______________________ slows the metabolism of coumadin, cimetidine, and erythromycin
anticonvulsants tend to be _____________ protein bound
primary plasma protein that anticonvulsants bind to is
hypoalbuminemia and anticonvulsants?
more free drug available since theres less proteins for it to bind to=higher plasma conc of these drugs
phenytoin/dilantin binds to Na channels in the _____________ state
what kind of seizures is dilantin/phenytoin used for?
general or partial
what route is phenytoin given?
IV or PO......NOT IM
when phenytoin/dilantin is given IV, therapeutic levels are reached in ______________
IV admin of dilantin should be slow and diluted to no more than _______mg/min
phenytoin/dilantin is a weak _______ with a pkA of ________.
it will precipitate in solutions with a pH less than ___________.
pka is 8.3
dilantin is _______% protein bound
therapeutic plasma level of dilantin is ____________mcg/ml
side effects from phenytoin are likely when plasma conc exceeds __________mcg/ml
CNs disturbances caused by phenytoin/dilantin?
vertigo, nystagmus, ataxis, diplopia
phenytoin causes ___________ hyperplasia in 20% of patients
(most common side effect in children/adolescents)
how does phenytoin cause hyperglycemia?
decreased insulin secretion
phenytoin can cause GI _____________
phenytoin in pregnancy
can cause fetal hydantoin syndrome-->wideset eyes, broad mandible, finger deformities
patients chonically taking phenytoin/dilantin need ___________ doses of non depolarizing neuromuscular blockers
phenobarbital is _______ acting
peak conc of phenobarb happens in ________hrs after single dose
why is phenobarb a second line drug for seizures?
undesirbale cognitive and behavioral side effects
potentiates GABA and inhibits post-synaptic action of glutamate
(prolongs opening of chloride channels and inhibits spread of seizure)
true or false,
phenobarbital increases the seizure threshold
phenobarbital causes sedation in _____________ and irritibility/hyperactivity in _______________
sedation in adults
hyperactivity in children
chronic use of phenobarb can lead to....(3)...
tolerance to sedative effects
megaloblastic anemia from chronic use of phenobarb is responsive to
osteomalacia from chronic use of phenobarb is responsive to
nystagmus and ataxis are likely if plasma conc of phenobarb exceeds _______mcg/ml
pehnobarbital can cause abnormal collagen deposition which leads to
if phenobarb is admiinstered chronically throughout pregnancy, what can occur?
also coagulation defects and hemorrhage can occur in neonate
phenobarb is a ________ protein bound hepatic microsomal enzyme ____________
(accelerates metabolism of many drugs)
gabapentin is an amino acid related to _________
not fully known if it acts on GABA receptors, enhances GABA, or is converted to GABA
*some sources say it inhibits voltage gated Ca channels preventing the release of glutamate
gabapentin is mostly used for
gabapentin has ________ side effects
gabapentin is ________ absorbed from GI tract
gabapentin plasma protein binding
does not cauase drug interactions
gabapentin is excreted.....
unchanged in urine
alter dose for renal patients
clonazepam/klonipin works by
potentiating GABA mediated neuronal inhibition
clonazepam is effective in control and prevention of seizures, esp ___________ seizures and ___________ spasms
clonazepam is highly __________ soluble
__________ CNS effects when administered IV
clonazepam PO absorption is _________
peak plasma conc after oral admin of Klonipin/clonazepam?
elim half life of clonazepam
30-40hrs (super long)
true or false,
clonazepam is very habit forming
clonazepam is _____% protein bound
what happens if you abruptly discontinue clonazepam therapy
generalized seizure activity
Keppra is used to manage _______________ seizures in adults
Levetiracetam (Keppra) MOA
not fully known, may bind to presynaptic Ca channels to reduce excitatory neurotransmitter release
side effects of levetiracetem/keppra
what are the favorable Pkinetics of levetriacetem?
not extensively metabolized in humans (it's major metabolite is inactive)
minimal protein binding (less than 10%)
no significant drug interactions wiht coadmin of other antiepileptic drugs
>60% unchanged in urine
levetiravetem/keppra 1/2 life
increased in elderly and renal impairment
1000mg given twice daily over 10min infusions
(500mg infusion over 10 min, BID)
valproic acid/depakote is a branched-chain ______________ acid
per Stoelting, what is the MOA of valproic acid?
blocks voltage gated Na channels
valproic acid is ______ spectrum anticonvulsant
valproic acid/depakote has __________ absorption after PO admin
how is depokote taken po?
syrup or enteric coated capsule (prevents GI side effects)
peak plasma conc of depakote/valproic acid is
valproic acid is >_____% protein bound
valproic acid is partially eliminated as a ____________ containing metabolite
(may have falase positive ketones in urine)
valproic acid can displace which other two anticonvulsants from protien binding sites?
dilantin and diazepam
valproic acid is a hepatic enzyme ____________-
Valproic Acid (Depakote) _________ the metabolism of dilantin
(so you'll have increased levels of dilatin)
valproic acid increases plasma conc level of phenobarb by _____%
does valproic acid interfere with oral contraceptives?
most important side effect of valproic acid
high doses can cause thrombocytopenia from decreased platelet count, aggregation, and function
**all patients should have bleeding time monitored
valproic acid can cause weight ___________ with chronic treatment
GI side effects of valproic acid
(minimized by enteric coated capsule)
high doses of valproic acid can cause what 2 side effects
1/10,000 patients taking valproic acid will suffer from what?
what age is most likely to get it?
an unknown liver failure/hepatic necrosis
most common in pts less than 2 yrs old
incidence is GREATLY reduced after age 2
sedation from anticonvulsants may have an ______________ effect with opioids and anesthetics
it's important for us to maintain drug thearpy for anticonvulsants thoughout the ______________ periods
ketamine effects with anticonvulsants
propofol effects with anticonvulsants
it's typically used as an anticonvulsant but RARE reports of it causing seizures exist
Diazepam is the mainstay treatment for
status epilepticus and local anesthetic induced seizures
dosing for diazepam during a seizure
0.1mg/kg IV every 10-15min until suppression of seizure activity
diazepam long elim half life of....
Does diazepam have active metabolites?
lorazpeam/ativan is used for...(2)
status epilepticus and intermittant thearpy of seizure clusters
lorazepam has a _________ half life than diazepam but a __________ duration of action
(longer DOA bc it isn't rapidly redistributed from tissues)
does ativan have active metabolites?
inhaled anesthetics produce a dose depedent depression of ________ activity
N2O has no proven ___________ properties
metabolite of atracurium
laudanosine-can lead to seizure activity
demerol can cause seizures how?
rapidly metabolized to the CNS stimulant normeperidine
do barbs, opiates, or benzos lower the seizure threshold?
anticonvulsants cause a dramatic and distinct increase in NDNMB ___________________
two non depolarizing NMBs most affected by anticonvulsants?
pan and vec
two non depolarizing NMBs least affected by anticonvulsants?
atracurium and cisatracurium
does tegretol/carbamazepine have active metabolites?
topiramate/topamax has ____________ protein binding and does not affect _______________ enzymes
in addtion to seizures, topamax/topiramate can also be used in the treatment of....
topamax is a weak inhibitor of carbonic _______________
carbamazepine/tegretol ______________ the metabolism of oral contraceptives, depakote, ethosuximide, corticosteroids, antioagulants, antipsychotic drugs
(may have to increase doses of those drugs)
valproic acid ________ the metabolism of lamictal
(extendes the half time to ~60hrs)
true or false,
Stevens Johnson syndrome has been reported in cases with lamictal
the substantia ___________ is part of the extrapyramidal system and is the source of dopaminergic neurons
levodopa works by enhancing the synthesis of dopamine in the surviving neurons of the _____________________
why does levodopa eventually stop working in patients with parkinsons?
the amount of dopaminergic neurons decreases so much that fewer cells are capable of converting esogenous administered levodopa to dopamine
without coadmin of carpidopa with levodopa, what side effects are seen due to an excess of dopamine in the periphery?
should patienst take levodopa with or without food?
ingestion of meals, particularly if high in protein, can interfere with transport of levodopa into the CNS
Why does Selegiline not cause hypertensive crisis?
it only inhibits MAO-B, which is responsible for dopamine
it doesn't breakdown MAO-A, which breaks down norepi/serotonin), so you don't get a buildup of norepi
selegiline can produce insomnia because....
it is broken down into amphetamine and methamphetamine
amantidine is _____ efficacious than levodopa, and tolerance develops more readily, but has _______ side effects than levodopa
______ effects severely limit the utility of the dopamine agonists (bromocriptine, ropinirole, pramipexole, rotigotine, apomorphien)
(nausea, hallucinations, insomnia, dizziness, constipation, orthostatic hypotension)
antimuscarinic agents used to treat parkinsons dz are much _____ efficacious than levodopa
(they only plan an adjuvant role in therapy)
_______________ is a type of chornic psychosis characterized by delusions, hallucinations (often int he form of voices), and thinking or speech disturbances.
Anesthesia can be safely administered to patients taking psychopharmacologic drugs, however ___________ patients remain at esp high risk for toxicity
Antidepressants work by altering _______________ neurotransmission and/or _________________ neurotransmission
Fluoxetine, paroxtein, sertaline, fluvocamine, citalopram, and escitalopram are
amitriptyline, nortriptyline, imipramine, amoxapine, doxepin, and desipramine are..
Phenelzine, Tranylcypromine, Isocarboxazid, and selegine are...
All antidepressants work by either inhibiting the ___________ of neurotransmitter back into the presynaptic synapse OR by preventing the ____________ of the NT in the synapse
Current drugs of choice for mild to moderate depression are...
___________ are 1st line pharmacotherapy for panic disorder and obsessive compulsive syndrome
Are SSRIs effective in treating social phobia and PTSD?
Each SSRI has a different ________________ profile
(So if pt can't tolerate side effects of one, just switch to another b/c side effects are different)
Do SSRIs have anticholinergic properties?
(One reason they are beneficial compared to TCAs)
Do SSRIs cause postural hypotension or delayed cardiac conduction?
(One reason they are beneficial compared to TCAs)
Do SSRIs have a major impact on the seizure threshold?
(Another benefit over TCAs)
Are SSRIs safe even when overdosed?
MOA of SSRIs
block reuptake of serotonin which increases amount of serotonin available in the synapse
It typically takes ______ weeks for SSRIs to produce a change in mood
The max benefit may take up to _______ weeks
SSRI black box warning
Released in 2004-increased suicidal ideation in children and adolescents
(1 out of 50 children reported SI with initiation of treatment or dose change)
SSRIs are ______ absorbed with PO admin
Most SSRIs have half lives between _____________hrs
What about fluoxetine?
Most are 16-36hrs
Fluoxetine is 1-3 days (even longer in chronic therapy)
SSRIs undergo extensive metabolism by ____________
Dose should be reduced in patients with ____________ impairment
SSRIS are potent _________ of CYP450 so they can _________ plasma conc level of TCAs, neuroleptics, antidysrhythmics, and beta blockers
Do SSRIs have more or less side effects than tricyclics and MAOIs?
Less side effects
What can happen if SSRIs are combined with MAOIs?
Hyperthermia, muscle rigidity, sweating, muscle twitching, changes in mental status and vitals
Side effects of SSRIs
Headache, sweating, anxiety, agitation, GI (nausea, vomiting, diarrhea), weakness, fatigue, sexual dysfunction, changes in weight, sleep disturbances (insomnia or somnolence)
Can also have antiplatelet activity
Overdose of SSRIs is relatively safe with the exception of _____________. why?
It prolongs the QTc interval
Which SSRIs are more likely to have discontinuation syndrome?
SSRIs with shorter 1/2 lives and no active metabolites
(Prozac should'nt bc it has super long 1/2 life and metabolites)
Which antidepressants were most commonly used to treat depression before SSRIs were discovered?
tricyclic antidepressants are more commonly used to manage _____________ currently
Tricyclic antidepressants are structurally similar to ________________
MOA of tricyclic antidepressants
Block reuptake of norepinephrine and serotonin into presynaptic nerve terminals
Increase availability of both neurotransmitters
**they also block serotonin gif, alpha adrenergic, histaminergic, and muscarinic receptors which causes lots of their side effects
TCAs usually take _____ weeks to achieve therapeutic effects
TCAs that are tertiary amines inhibit the reuptake of.....
Serotonin and norepi
Examples of tertiary amine TCAs
Secondary amine TCAs primarily inhibit the re-uptake of....
Examples of secondary amine TCAs
Desipramine and nortriptyline
TCAs are _____ absorbed with PO admin
TCAs are highly lipo________ and strongly bound to plasma and tissue ___________
TCAs volume of distribution?
Up to 50l/kg
True or false,
tricyclic antidepressants readily cross the BBB
True, they are very lipophilic
TCAs have a ________ elimination half life
Allows for once daily dosing
TCAs are _________ metabolized
Drugs that induce CYP450 will __________ the plasma conc of tricyclic antidepressants
Drugs that inhibit CYP450 will __________ the plasma conc of antidepressants
TCAs are an unpopular option because of their unfavorable _____________
TCAs have a ________ therapeutic index
Plasma conc of _____________ng/ml is therapeutic for TCAs
Plasma conc of TCAs >________ng/ml are likely to cause toxicity
The three main categories of side effects from TCAs are....
Central nervous system
Which TCA causes the most intense anticholinergic effects?
Anticholinergic side effects of TCAs
Aggravation of angle closure glaucoma
Anticholinergic side effects of TCAs are exaggerated at ___________ doses and with the ____________ population
TCAs block alpha adrenergic receptors cause what side effects?
Life threatening arrhythmias (particularly with overdose)
TCAs can depress conduction of cardiac impulses through the atria and ventricles leading to
Flattened or inverted T waves
(Usually these changes are benign and will eventually go away)
TCAs may enhance the cardiac depressant effect of ____________
Sedation from TCA occurs because of binding to the ______ receptors.
TCAs _________ the seizure threshold
CNS side effects of TCAs
Lower seizure threshold
Sedation from TCAs is most prominent when?
First 2 weeks of therapy
If TCAs are taken with MAOIs, what can happen?
CNS toxicity manifesting as hyperthermia, seizures, coma
Patients recently started in TCA therapy may have __________ pressor responses.
Most pronounced with which pressor?
Patients that have been chronically taking TCAs for a while may have _____________ adrenergic receptors or depleted ____________ stores
(Pressor s may not produce a great response-levophed is usually best option in these cases)
OD of tricyclic antidepressants
Presents as agitation and seizures that lead to coma, ventilators depression, hypotension and hypothermia, striking anticholinergic effects, widened WRS.
Coma lasts 24-72 hrs
Risk of life threatening dysrhythmias persist up to 10 days
Monoamine oxidase is an enzyme found int he nerves, gut and ___________
It inactivated excess _______________
tyramine is metabolized by
Platelets exclusively contain MAO-____
Placenta contains exclusively MAO_____
MAO inihibitors ___________ bind to MAO enzyme and block it from breaking down serotonin, norepi, and _________ in the CNS and peripheral nervous system
MAO enzyme activity is inhibited after several _______ of dosing, however therapeutic effects of MAOIs are not seen for several ____________
True or false,
After termination of MAOI therapy, MAO enzymes will begin functioning again within a few days
MAOIs irreversibly bind to the MAO enzymes, so they have to be completely regenerated which takes several weeks
(If you have a patient who has recently stopped taking MAOIs, they still might not have MAO enzyme back in their body yet)
MAOIs are _____ absorbed after oral administration
They have ________ metabolism and are excreted in ___________
Is the dosing of MAOIs in elderly patients decreased or the same as in younger patients? Why?
Elderly have higher levels of MAO and the metabolism of MAOIs does not seem to be affected by age
Side effects of MAOIs are similar to those of ___________
MAOIs + other antidepressants can cause
(Esp w/ SSRIs-fluoxetine the worst)
Common side effects of MAOIs
MAOIs in the US are MAO-A and MAO-B _____________ inhibitors
Why can't people taking MAOIs eat food containing tyramine?
MAOIs inhibit the breakdown of tyramine
Buildup of tyramine causes increased released of endogenous catecholamines
Can lead to systemic HTN, tachycardia, hyperpyrexia, stiff neck, nausea, CVA
What can be used to control tyramine induced hypertension?
Nitroprusside, phentolamine, prazosin
What are some foods that contain tyramine? (Per chart in Stoelting)
MAOIs given with Demerol can cause
Excitatory or depressive response
Excitatory thought to be from excess serotonin activity
Depressive thought to be from slow breakdown of meperidine
MAOIs with sufentanil, fentanyl, and alfentanil?
Have also shown adverse affects (they are meperidine derivatives)
MAOIs given with ephedrine?
Exaggerated release of norepi from nerve endings
Prohibited drugs to be given with MAOIs (per chart in Stoelting)
Sympathomimetics (esp indirect acting)
Opioids (esp Demerol)
__________ is effective in treating 60-80% fo patients exhibiting mania and hypomania
___________ is the drug of choice for bipolar disorders
Not fully understood
Possibly inhibits a 2nd messenger system which decreases release of calcium ions
Full therapeutic effect of lithium takes ____________ weeks
Goal of lithium therapy is to maintain plasma level between _______mEq/L
Adverse effects of lithium are due to high plasma levels,
What are the adverse effects?
Polydipsia and polyuria
T wave flattening or inversion
Dermatological toxicities (acne and psoriasis)
Caution should be used with lithium in patients with __________ impairment
Lithium is really eliminated
Lithium is filtered by the glomerulus and reabsorbed by the __________ tubules
(Low sodium, thiazides, and sometimes loop diuretics can cause increased plasma levels of lithium)
Therapeutic index for lithium is very ______ and lithium salts can be __________
(Plasma conc should be monitored)
Antipsychotic drugs are also called
neuroleptics and tranquilizers
Antipsychotic drugs are primarily used to treat ____________, but also successful in other manic and psych disorders
Antipsychotic drugs reduce the intensity of __________ and __________, permitting schizophrenic patients to function in a supportive environment
Hallucinations and delusions
Three drug classes of antipsychotics
Some texts divide antipsychotics into 1st and 2nd generation
1. First gen block _________ receptors
2. Most 2nd generation block what?
1. Dopamine (haldol, prochlorperazine, trifluoperazine, Thorazine)
2. Dopamine (D2) receptors and block serotonin 5HT receptors (risperidone, quetiapine, Geodon)
Antipsychotics may also block which receptors, which are responsible for the undesired side effects?
How do antipsychotics cause an antiemetic effect?
Block D2 receptors in the chemoreceptors trigger zone
Phenothiazines and thioxanthenes have ___________ absorption after PO admin
Phenothiazines and thioxanthenes are ________ lipid soluble and can cross _______________
BBB and placenta
Phenothiazines and thioxanthenes are _________ protein bound which limits the effectiveness of ______________ to remove drugs from systemic circulation
Phenothiazines and thioxanthenes are hepatically metabolized into ______________ metabolites that are excreted in ___________
Phenothiazines and thioxanthenes have a _______ elim 1/2 time
Permits once daily dosing
Side effects of phenothiazines and thioxanthenes are related to the drug induced blockade of _____________ receptors
Phenothiazines and thioxanthenes can cause ___________ dyskinesia, which can be irreversible
(Involuntary movements, including bilateral and facial jaw movements and "fly catching" motions of the tongue
Side effects of phenothiazines and thioxanthenes
Neuroleptic malignant syndrome
Endocrine effects (galactorrhea, gynecomastia)
Reduction in seizure threshold
s/s of neuroleptic malignant syndrome
Altered mental status
Why do thioxanthenes and phenothiazines cause galactorrhea and gynecomastia?
Dopamine blockade in the ant pituitary causes increased prolactin levels
Sedation from phenothiazines and thioxanthenes is from antagonism of....
Alpha adrenergic, muscarinic and histamine 1 receptors
Obstructive jaundice from phenothiazines or thioxanthenes is considered an ___________ reaction
Ventilatory depressive and sedative side effects of __________ are likely to be exaggerated by antipsychotic drugs
Droperidol and haloperidol are ________________
Droperidol and haloperidol have the same chemical structure and MOA as other _________________
Droperidol uses (3)
Antiemetic MOA of droperidol
Not known but thought to be through postsynaptic inhibition of GABA receptors in the CRTZ
Droperidol can be administered with fentanyl to achieve "_______________" through the inhibition of GABA and ______________ ACh receptors
profound state of sedation and analgesia induced by simultaneous administration of an opioid and a tranquilizer
Haloperidol main use
Agitation and delirium in ICUs
(Not typically used in the periop period)
Butyrophenones bind to and block ________ receptors and help alleviate the ___________ symptoms of schizophrenia
Butyrophenones cause _____________ cerebral blood flow secondary to cerebral vaso_______________
Droperidol is commonly used in the preop period as an _______________
What CNS side effects do butyrophenones have?
Reduced cerebral blood flow
Akathisia->restlessness of legs
Laryngospasms (a rare extrapyramidal reaction)
Butyrophenones cause hypotension secondary to _________________ blockade
True or false,
Butyrophenones are cardiac anti-dysrhythmics
(They can protect against epinephrine induced dysrhythmias)
Butyrophenones black box warning
Prolong the QTc interval
Butyrophenones augment the ventilatory response to arterial __________________.
Why is this good for COPD patients?
COPD patients depend on the carotid body drive that responds to low O2 levels
How do butyrophenones augment the ventilatory response to hypoxemia?
Blocking the dopamine receptors in the carotid bodies
True or false,
Butyrophenones alter the ventilatory response to CO2
They augment the response to hypoxemia only (not hypercarbia)
Regular cannabis use leads to an _______________ in anesthetic requirements for surgery
Increased anesthetic requirements from chronic cannabis use is secondary to an up regulation of the
CYP450 enzyme system
There is correlation between regular cannabis use and increased post op ___________
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