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NURA 671 Advanced Pharmacology > Psychopharmacology > Flashcards

Psychopharmacology Flashcards

1
Q

What is monoamine oxidase?

A

enzyme found in presynaptic nerve endings, the liver, and the intestinal wall that metabolizes biogenic amines

dopamine
serotonin
epi
norepi

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2
Q

MAO A metabolizes which neurotransmitters?

A

serotonin
norepi
epi

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3
Q

MAO B metabolizes which neurotransmitters?

A

phenylethylamine
dopamine

may see these used in parkinson’s because they enhance dopamine levels

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4
Q

MAOI (Monoamine oxidase inhibitors): MOA

A

MAOIs form a stable irreversible complex with MAO –> increasing availability of these neurotransmitters in the CNS and peripheral autonomic nervous system

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5
Q

MAOIs: Agents

A

Phenelzine (nardil)
Tranylcypromine (parnate)
Isocarboxazid (marplan)
Selegine (eldepryl) - selective for MAO B, but at higher doses become non selective

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6
Q

MAOIs: Side Effects

A 
Most common: orthostatic hypotension
--ESPECIALLY PROMINENT IN ELDERLY
anticholinergic like effects
impotence/anorgasmy
weight gain
sedation or mild stimulant effects

MAO A enzyme present in liver, GI, tract, kidneys, lungs
–metabolizes dietary tyramine

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7
Q

Dietary to amino acid to avoid with MAOIs and why?

A

MAO A enzyme present in liver, GI tract, kidneys, lungs
—metabolizes dietary tyramine

dietary tyramine + certain medications
---massive release of endogenous catecholamines/serotonin --> 
hypertensive crisis 
hyperpyrexia
CVA
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8
Q

S/S of MAOIs + certain medication interactions

A 
serious headache
vomiting
chest pain
tachycardia
HTN
hyperthermia
CNS excitation
delirium
seizure
death
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9
Q

Foods to avoid with MAOIs (containing tyramine)

A 
cheese
fava beans
wine
avocado
liver
cured meats
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10
Q

MAOIs: adverse drug interactions

A 
antidepressants (TCAs, SSRI, etc)
opioids (NO meperidine)
cold - allergy drugs
sympathomimetics
nasal decongestants (often alpha 1 agonists)
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11
Q

MAOI + meperidine (demerol)

A

SEROTONIN SYNDROME

Excitatory response (type I) enhanced serotonin activity in the brain

  • -agitation
  • -skeletal muscle rigidity
  • -hyperpyrexia

Depressive response (type II) slowed breakdown of meperidine

  • -hypotension
  • -resp depression
  • -coma
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12
Q

MAOIs: Anesthesia Considerations

A

may need a higher MAC with volatile agents

MINIMIZE POSSIBILITY OF SYMPATHETIC NERVOUS STIMULATION OR DRUG INDUCED HYPOTENSION (just don’t have many drugs that we can give)

Sympathomimetics

  • -may get an exaggerated response from indirect acting drugs, NO EPHEDRINE!!!!!!!!
  • -USE DIRECT ACTING ONLY IF NEEDED AT ALL
  • -decrease dose by 1/3 and titrate to effect
  • -Art line

vigilant about using drugs that are short acting, easily titratable, can easily reverse

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13
Q

Antidepressant discontinuation syndromes

A

All should be tapered!

  • can get dizziness
  • myalgias
  • parasthesia
  • irritability
  • insomnia
  • visual disturbances
  • tremors
  • lethargy
  • N/V/D
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14
Q

Ketamine IV: MOA

A

Unclear

  • -NMDA antagonist
  • -promote synaptic plasticity
  • —activation of brain derived neurotrophic factor (BDNF)
  • —modulate rapamycin (mTOR) signaling pathways
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15
Q

Ketamine IV: use and dose

A

sub anesthetic doses used OFF LABEL for treatment-resistant depression with potential suicidal ideation

0.5mg/kg and 1.0mg/kg most effective

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16
Q

Benzodiazepines: MOA and use

A

Facilitates the action of GABA (major inhibitory neurotransmitter in the CNS)

allosteric agonist - binds between alpha and gamma whereas GABA is between alpha and beta

widely prescribed for anxiety and insomnia
panic disorder
some muscle relaxation (not surgical level obvi)

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17
Q

alprazolam: class, use

A

benzo, anxiolytic

high potency; short acting

can depress cortisol secretion

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18
Q

clonazepam

A

longer acting benzo

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19
Q

Buspirone: Class, use, MOA, E 1/2

A

anxiolytic, non benzo

partial agonist at serotonin receptor
no direct effect on GABA so no cross reactivity with benzo, barbs, ETOH

used for treatment of generalized anxiety disorder but not panic disorder

E1/2t: 2 - 11 hours

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20
Q

Antipsychotics: “typical agents*

A

FIRST GENERATION - phenothiazines, thioxanthenes (DOPAMINE ANTAGONISTS)

chlorpromazine (low potency)
thioridazine
perphenazine
trifluoperazine
thiothixene

SECOND GENERATION - butyrophenone (DOPAMINE ANTAGONISTS)

haloperidol (high potency)
droperidol

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21
Q

1st gen/2nd gen antipsychotics: MOA

A

dopamine antagonists at D2 receptors (high potency) in the basal ganglia and limbic portions of the forebrain (expect to see parkinson like effects because antagonizing dopamine receptors)

also muscarinic cholinergic, antihistamine, and alpha blocking properties

  • -sedation (H1 receptor blockade)
  • -anticholinergic effects (dry mouth, constipation, urinary hesitancy)
  • -anti adrenergic effects: alpha blocking effect usually seen as orthostatic hypotension
  • -interference with dopamine –> extrapyramidal side effects
  • -blockade of dopamine receptors in chemoreceptor trigger zone of medulla –> antiemetic effects
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22
Q

1st gen/2nd gen antipsychotics: extrapyramidal symptoms

A

parkinsoniasm, dyskinesia

ANESTHESIA PERSPECTIVE

  • -acute dystonia: acute skeletal muscle rigidity & cramping of muscles of eyes, tongue, face, larynx, neck, and back
  • —resp distress from laryngeal dyskinesia (LARYNGOSPASM)
  • —responds well to diphenhydramine 25-50 mg IV
  • -tardive dyskinesia: involuntary jaw or oral musc movements expanding over time to include muscles in the extrem and trunk
  • —results of long term therapy
  • —concern for ASPIRATION RISK
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23
Q

Mesolimbic tract in brain

A

behavior, mood

excessive dopamine signaling –> schizophrenia, psychoses

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24
Q

Antipsychotics: “Atypical agents”

A

clozapine (clozaril)

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25
Q

1st gen/2nd gen antipsychotics SE: neuroleptic malignant syndrome – ONSET + S/S

A

develops over 24-72 hours after administration usually in young men

  • hyperthermia
  • hypertoniciy of skeletal muscles
  • –myoglobinuria
  • instability of ANS
  • fluctuating LOC

4% fatality with early intervention
30% mortality with delayed intervention

related to respiratory failure, CV collapse, dysrhythmias

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26
Q

neuroleptic malignant syndrome: treatment

A

treatment is supportive and includes:

  • dantrolene (will produce flaccid paralysis)
  • dopamine agonists
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27
Q

1st gen/2nd gen antipsychotics: other adverse effects

A

-severe dysrhythmias: QT PROLONGATIONS (rare) leading to torsades & v fib (potentially fatal)

  • decreases in BP
  • –due to depression of vasomotor reflexes/peripheral alpha adrenergic blockade
  • –relaxants on vascular smooth muscle
  • –direct cardiac depression
  • agranulocytosis: (rare) check WBC
  • Pregnancy: 3rd trimester babies may develop w/d symptoms and EPS
  • sedation
  • –due to antagonism of alpha 1, muscarinic, & histamine receptors
  • –tolerance to sedation develops with chronic therapy

-seizure threshold decreased (in people w/ seizure hx) - similar EEG pattern as seen with seizure disorders, and sensory evoked potentials often decreased in amplitude

  • skeletal muscle relaxation
  • –by CNS action not neuromuscular junction
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28
Q

1st gen/2nd gen antipsychotics: drug interactions - intensification of effect

A

anticholinergics

CNS depressants

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29
Q

1st gen/2nd gen antipsychotics: drug interactions - reduction of effect

A

levodopa

dopamine agonists

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30
Q

1st gen/2nd gen antipsychotics: drugs to avoid (QT prolongation)

A

Many of these antipsychotics are metabolized by CYP450 enzymes, others are inhibitors of CYP450

avoid drugs that prolong the QT interval:

  • amiodarone
  • erythromycin
  • quinidine
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31
Q

Neuroleptanalgesia: INNOVAR

A

Fentanyl + droperidol

  • prolonged action of fentanyl, intense analgesia
  • potentiation of opioid side effects (sedative, ventilatory, analgesic)
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32
Q

Droperidol (2nd gen antipsychotic): CNS effects

A
  • extrapyramidal reactions
  • cerebral vasoconstrictor (decreased CBF, but not CMRO2)
  • dysphoria
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33
Q

Droperidol (2nd gen antipsychotic): Metabolism and clearance

A
  • clearance is PERFUSION DEPENDENT - hepatic metabolism opposed to hepatic enzyme activity
  • accumulation of drug with decreased hepatic blood flow
  • maximal excretion of metabolites in 1st 24 hrs
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34
Q

Droperidol (2nd gen antipsychotic): CV effects

A
  • dec in systemic BP from alpha blockade - usually minimal
  • antidysrhythmic, protects against epi induced dysrhythmia
  • large doses dec conduction along accessory pathways responsible for tachy-dysrhythmias helpful in WPW syndrome
  • prolonged QT interval
  • torsades
  • –have occurred at low doses
  • –pts with no risk factors
  • –no precise cause
  • –some have been fatal
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35
Q

Droperidol (2nd gen antipsychotic): BLACK BOX WARNING

A
  • ALL pts get 12 lead prior to administration of droperidol
  • must be monitored prior to and continued for 2-3 hrs
  • Caution with patients at risk of developing QT syndrome -CHF
  • bradycardia
  • use of a diuretic
  • cardiac hypertrophy
  • hypokalemia
  • hypomagnesemia
  • admin of other drugs known to increase the QT interval
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36
Q

Atypical antipsychotics: MOA

A

multi receptor antagonists,

  • less potent dopamine blocker than typical agents
  • potent serotonin receptor antagonist

also blocks receptors for alpha 1, histamine, ach

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37
Q

atypical antipsychotics: CV risk factors

A

decreased risk of EPS and tardive dyskinesia
increased risk of metabolic disease - ages CV system

weight gain
t2dm
dyslipidemia
myocarditis/pericarditis

ANESTHESIA CONSIDERATIONS:
recent cardiologist report, heavy CV work if they have been on this drug for a while

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38
Q

Clozapine: Class + use

A

atypical antipsychotic

indicated for schizophrenia - especially high suicide risk and bipolar disorder

39
Q

clozapine: serious side effects

A

-agranulocytosis: dec WBCs (clozapine only)
CONTRAINDICATED IN WBC < 3500

  • All agents (atypical agents): NMS
  • tonic clonic seizures
  • myocarditis
40
Q

clozapine: common side effects

A

-weight gain - leading to metabolic syndrome, sedation, orthostatic hypotension, anticholinergic side effects

41
Q

Lithium: Class + MOA

A

Mood stabilizer

MOA: unknown despite considerable research

  • inhibition of glycogen synthase kinase 3 beta?
  • promotion of neuronal survival factors and reversal of atrophy?
42
Q

Lithium: pharmacokinetics

A

positively charged
distributed throughout total body H20 and excreted by the kidneys

E1/2t: 24 hours

proximal reabsorption of lithium and NA is competitive
—Na depletion can inc plasma concentration of drug by 50%

43
Q

Lithium: pharmacokinetics

A

positively charged
distributed throughout total body H20 and excreted by the kidneys

E1/2t: 24 hours

proximal reabsorption of lithium and NA is competitive
—Na depletion can inc plasma concentration of drug by 50%

BE MINDFUL OF HYDRATION STATUS

44
Q

Lithium: side effects (kidneys)

A
  • evaluate renal function every 6 months
  • -polydipsia and polyuria; >3 L/day
  • -impaired renal concentrating ability
  • —amiloride (potassium sparing diuretic) can dec urine volume
45
Q

Lithium: side effects (CV)

A
  • EKG - T wave changes, flattening or inversion
  • —no related clinical effects and reversible
  • heart block (rare)
  • —CI in pts with SA node dysfunction
46
Q

Lithium: side effects (neuro)

A
  • fine tremor
  • sedation
  • memory disturbances/cognitive slowing
47
Q

Lithium: side effects (other)

A

-new onset psoriasis/acne

  • hypothyroidism can develop - more common in females
  • —-assess for goiter! - THINK AIRWAY - awake intubation
48
Q

Lithium toxicity: mild

A 
sedation
nausea
skeletal muscle weakness
wide QRS complex
AV heart block
hypotension
dysrhythmia
seizure
49
Q

lithium: significant toxicity

A

> 2.5 mEq/L

  • medical emergency
  • aggressive RX
  • hemodialysis
  • osmotic diuresis and IV Na+ bicarbonate
50
Q

lithium: anesthesia considerations

A
  • pre op labs and ECG (BMP, creatinine)
  • anesthetic requirements may be decreased
  • —esp CNS depressants
  • action of neuromuscular blocking agents may be PROLONGED - use PNS for sure

AIRWAY ASSESS FOR GOITER

51
Q

lithium: drug interactions

A

diuretics - inc lithium levels/risk of tox by dec NA levels

NSAIDs - in lithium levels ~60%

ACE - inhibitors - inc lithium levels

anticholinergics: urinary retention with polyuria can be uncomfortable

52
Q

Epilepsy pharmacotherapy: mechanisms

A
  • inhibiting voltage activated ion channels (Na, Ca2+)
  • promote the efflux of K = hyper-polarization
  • antagonize glutamate (primary excitatory neurotransmitter of CNS)
  • enhance function of GABA - inhibitory neurotransmitter
53
Q

Many anti-epileptics are associated with which life threatening side effects

A

BONE MARROW SUPPRESSION
HEPATOTOXICITY

Consider:

  • liver function tests
  • hematologic studies
54
Q

Phenytoin (dilantin): Class + MOA

A

anti-epileptic

MOA: regulates neuronal excitability and thereby the spread of seizure activity from a seizure focus by regulating Na and Ca ion transport across neuronal membranes

55
Q

Phenytoin (dilantin): atypical pharmacokinetics

A

non linear pharmacokinetics; metabolism is saturable

“zero order kinetics” above low doses

narrow therapeutic window; therapeutic drug monitoring

highly protein bound - 90% to plasma protein

56
Q

Phenytoin: Administration and dosing

A
  • IV formulation: very basic (pH 12), precipitates in solutions with pH < 7.8 - PHLEBITIS (extravasations are concern)
  • Not recommended IM - precipitates, poorly absorbed
  • Infusion no faster than 50 mg/min in adults to prevent hypotension and cardiac dysrhythmias

Peds: 1 - 3 mg/kg/min or 50 mg/min - whichever is slowe

57
Q

Phenytoin: side effects

A

-dose related CNS toxicity

  • non dose related
  • -allergic reaction –> steven johnson syndrome/toxic epidermal necrolysis
  • -gingival hyperplasia
  • -hirsutism
  • -acne
  • -measles like rash
  • -hepatotoxicity
  • -purple glove syndrome
  • -severe congenital malformations (POTENTIAL FOR PREGNANCY)
  • GI irritation
  • hepatotoxicity
58
Q

phenytoin: metabolism

A

induces CYP450 (POTENT, POTENT, POTENT)

increases metabolism of other antiepileptics, BCP (birth control pills), warfarin, corticosteroids

59
Q

fosphenytoin: MOA, PK, Use, dose

A

FOS = PRO DRUG

antiepileptic

  • acts on on Na ion channel blockade
  • highly protein bound
  • water soluble phenytoin pro drug
  • used in hospitals for status epilepticus and in neurosurgery to prevent/treat seizures
  • –10-20 mg/kg IV LOADING DOSE
60
Q

Carbamezapine (tegretol): Class + MOA

A

anti epileptic

sodium channel blocker

61
Q

Carbamezapine (tegretol): drug interactions

A

enzyme inducer, auto induction

  • accelerated metabolism of warfarin and oral contraceptives are of particular concern
  • grapefruit juice can inc levels (inhibitor?)
  • phenytoin and phenobarb can decrease levels (inc dose)
62
Q

Carbamezapine (tegretol): Adverse effects

A
  • minimal cognitive impairment: mild CNS
  • rash mild –> steven johnson syndrome
  • hematological effects: aplastic anemia, thrombocytopenia, anemia, leuokopenia (CBC)
  • inappropriate ADH secretion (FLUID/ELECTROLYTE)
  • congenial defects (neural tube defects)
63
Q

lamotrigine (lamictal): Class + MOA

A

anti epileptic, can also be used as a mood stabilizer

MOA: blocks sodium channels, also:
–decreases glutamate via calcium channel block

64
Q

lamotrigine (lamictal): side effects

A

CNS effects
-sedation, visual disturbances, HA, N/V, depression, suicide risk

Rash is a major concern (steven johnson’s sydrome); MUST TITRATE DOSE SLOWLY

65
Q

lamictal: metabolism

A

metabolism can be induced by other anti - epileptics that are inducers (phenytoin, phenobarbital, carbamezapine)

Inhibited by valproate!

66
Q

Inhibited by valproate

A

lamictal

67
Q

Phenobarbital: Class + MOA

A

anti epileptic; long acting barbiturate

MOA: modulation of post synaptic actions of GABA and glutamate; prolong duration of chloride channel opening; limiting spread of SZ

68
Q

phenobarbital: metabolism

A

enhances cyp450 system in liver

69
Q

phenobarbital: side effects

A

cognitive and behavioral SE limit usefulness - 2nd line drug

sedation in adults; hyperactivity in children

depression

confusion in elderly

70
Q

Valproate/valproic acid (depakote) Class, MOA, use

A

anti epileptic; bipolar disorder, migraine prevention

MOA:

  • blocks Na channel
  • blocks t type calcium currents
  • promotes synthesis of GABA
71
Q

Valproate/valproic acid (depakote): drug interactions

A

-not metabolized by CYP450

ENZYME INHIBITOR - when administered with topiramate - high levels of ammonia can accumulate and cause CNS toxicity

72
Q

valproate/valproic acid (depakote): side effects

A
  • MAJOR congenital malformations - category D
  • fatal pancreatitis
  • fatal hepatotoxicity (esp in peds <2 yo)
  • n/v, weight gain, alopecia, thrombocytopenia (CBC)
73
Q

Topiramate (topamax): MOA + Class

A

anti epileptic

MOA: multiple modes of action

  • blocks sodium channels, enhances GABA
  • blocks calcium channels
  • glutamate antagonist
74
Q

Topiramate: drug interactions

A
  • phenytoin and carbamazepine can decrease levels of drug

- topiramate can increase phenytoin levels

75
Q

Topiramate: adverse effects

A

drowsiness, impaired cognition, ataxia, weight loss

SERIOUS: psychomotor slowing, renal stones, metabolic acidosis (ABG), glaucoma, congenital malformations

76
Q

Keppra (levetiracetam):

A

MOA: unknown

adverse effects much less significant

very few drug interactions, not metabolized by CYP450

pregnancy safety uncear = category C

77
Q

Pharmacotherapy of Parkinson’s: goals of therapy

A

Tx is palliative

RESTORE DOPAMINE

  • inc dopamine synthesis
  • inc dopamine release
  • dopamine receptor agonism
  • dec dopamine re uptake
  • dec dopamine metabolism
78
Q

Levodopa/carbidopa (sinemet): MOA

A

dopamine does not cross BBB

immediate precursor levadopa, does via active transport

carbidopa does not cross BBB, but does inhibit peripheral conversion of levodopa to dopamine by blocking peripheral dopamine decarboxylase; therefore, levadopa is available to cross the BBB

79
Q

Levodopa: side effects

A
  • N/V - dop induced stimulation of the chemoreceptor trigger zone
  • CV - alpha and beta responses evoked by higher plasma levels of dop resul in transient flushing of skin, sinus tach, PACs, PVCs, and orthostatic hypotension
  • abnormal involuntary movements - tics, grimacing, develops after 1-4 months of therapy in 50% of pts
  • psychiatric disturbances
80
Q

Levodopa: lab measurements

A
  • urinary metabolites can cause false positive tests for ketoacidosis
  • transient increase in BUN
  • increase in liver enzymes

usually not reflective of any long term effects

81
Q

Levodopa: drug interactions

A

butyrophenones and phenothiazines

  • ANTAGONIZE EFFECTS OF DOPAMINE - avoid them!
  • metoclopramide - worsens effects of disease
  • droperidol - skeletal muscle rigidity and pulmonary edema d/t sudeen antagonism of dopamine

MAO inhibitors
-interferes with inactivation of catecholamines including dopamine

Anticholinergics

  • act synergistically with levodopa to improve tremor
  • levodopa (bringing dopamine level up), anticholinergic (bringing ach level down) –> restoring balance
82
Q

Catechol - O - Methyl Transferase (COMT) Inhibitors: MOA + Agent

A

MOA: prevent breakdown of dop - more levodopa to cross BBB; in amount of dop available to CNS (prolongs half life 50-75%)

Agent: Entacapone (prototype) - used with levodopa

83
Q

Catechol - O - Methyl Transferase (COMT) Inhibitors: adverse effects

A
  • similar to levodopa as it intensifies those effects
  • urine discoloration (orange)
  • hallucinations
84
Q

Direct dopamine agonists: MOA, use + agents

A

MOA: selectively binds to D2 and D3 receptor subtypes: delayed onset of effect 2-3 weeks

used as 1st line monotherapy and then combined with levodopa as disease progresses

Agents:
Prototype: pramipexole (mirapex)
bromocriptine
pergolide
ropinirole (requip
85
Q

Direct dopamine agonists: adverse effects

A
  • n/v
  • postural hypotension
  • hallucinations
  • vivid dreams
  • sleepiness
  • dyskinesias (less than with levodopa)
  • impulsive
  • high risk behaviors
86
Q

Parkinson’s drug therapy, Anticholinergics: MOA + agents

A

MOA: blunt effects of excitatory neurotransmitter ach correcting balance between dopamine and Ach

Agents:

  • trihexyphenidyl (artane)
  • benztropine (cogentin)
87
Q

Parkinson’s drug therapy, Anticholinergics: side effects

A
  • confusion
  • hallucination
  • urinary retention

think CAS

88
Q

Parkinson’s drug therapy, Amantadine (symmetrel): MOA, use

A
  • anti viral
  • MOA: anti parkinsons action unclear: weak, non competitive antagonist of the NMDA receptor, enhances dop release into the synapse and delays reuptake into the nerve endings
  • symptomatic improvement of parkinsonian symptoms
89
Q

Parkinson’s drug therapy, Selegine (eldepryl): MOA, use

A

MOA: highly selective irreversible inhibitor of MAO B (selective for MAO B so not quite as worried about serotonin syndrome, but should still treat conservatively)

used as an adjunct to carbidopa - levodopa

90
Q

Non pharmacologic Rx: Parkinson’s

A
  • deep brain stimulation

- stem cell transplantation and other therapeutic mechanisms are under investigation

91
Q

Cholinesterase Inhibitors: use, moa, agents

A

Use: alzheimers

MOA: inhibit acetylcholinesterase; thereby inc Ach concentrations in the synapse

  • donepezil (aricept)
  • rivastigmine (exelon)
  • galantamine (razadyne)
92
Q

cholinesterase inhibitors: side effects

A
  • nausea
  • diarrhea
  • dizziness
  • HA
  • bronchoconstriction
93
Q

Memantine: Class, Use, MOA

A

Class: NMDA receptor antagonist

Use: indicated for moderate to severe AD, very modest benefits

MOA: 2 proposed mechanisms

  1. blocking “leaky” channels to help reduce calcium induced excitotoxicity
  2. blocking “leaky” channels helps reduce background noise, making signals relatively stronger
94
Q

Memantine: side effects and considerations

A

(NMDA receptor antagonist)

  • dizziness
  • HA
  • fatigue
  • sedation
  • HTN
  • rash
  • diarrhea
  • wt gain
  • urinary frequency
  • anemia

CBC, HTN, FLUID/ELEC BALANCE

NURA 671 Advanced Pharmacology (9 decks)

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