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psych drugs Flashcards

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1
Q

MOA of lithium

A

works on multiple NT (5-HT, NE, Glu, GABA, Da)

-modifies 2nd messenger system

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2
Q

What conditions does lithium work for?

A
  • Bipolar Mania (FDA)
  • bipolar Prophylaxis (FDA)
  • Adjunct to antidepressants to help treat MDD
  • Acute tx of mania or agitation
  • Better at preventing mania than depression but does help prevent depression
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3
Q

What are the side effects of lithium

A

!!Dec. renal function!! (kidney drug!)

  • tremor
  • polyuria +/- polydipsia
  • cognitive slow/memory probs
  • hypothyroid
  • acne
  • N/V/D
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4
Q

Can lithium be used in pregnancy?

A
  • category D
  • avoid in 1st trimester (Ebstein’s abnormality=congenital heart defect)
  • can use after 1st trimester if benefts>risks
  • do not use while breastfeeding
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5
Q

Does lithium interact with any drugs?

A
  • THINK KIDNEY
  • diuretic–>inc. Li levels
  • urinary alkalinizers–>dec. LI level
  • iodide salts–>inc. hypothyroidism
  • NSAIDS–>inc. Li levels
  • sodium bicarb–>dec. Li levels
  • antipsychotics–>inc. Li toxicity
  • buproprion–>inc. sz risk
  • inc. or dec. levels of verpamil
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6
Q

does lithium interact with any foods?

A

inc. sodium–>dec Li level

inc. caffeine–>dec. Li level

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7
Q

What are the sx of lithium toxicity?

A
  • Coarse tremor, muscle fasciculations, confusion, stupor

- Slurred speech, ataxia (wobbly), vomiting, arrhythmia & seizures

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8
Q

What things do you need to monitor in a patient taking lithium?

A
  • narrow therapeutic window (blood level 0.8–1.2mmol/liter)
  • monitor kidney function (Li excreted through the kidneys
  • monitor TSH (worried about hypothyroid, though it is reversible if you discontinue Li)
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9
Q

what is the MOA of anticonvulsants as mood stabilizers?

A
  • Act on sodium, potassium and calcium ion channels in cell
  • This modulation changes both excitatory (GLU) and inhibitory (GABA) neurotransmission
  • Augment synthesis/release of GABA
  • Inhibit reuptake and breakdown of GABA
  • Decrease release of Glu
  • ->work to dec. excitatory NT (glu) and inc. inhibitor NT (GABA)
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10
Q

What drug class is valproic acid? What conditions can it be used to treat?

A
  • Acute mania (FDA)
  • Seizure d/o (FDA)
  • Bipolar prophylaxis (may be effective)
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11
Q

what are the side effects of valproic acid?

A

Scary side effects are:

  • pancreatitis
  • hepatitis (esp. children)
  • thrombocytopenia

Less scary but undesirable side effects are:

  • wt gain
  • sedation
  • GI upset (take w/ food)
  • Dizziness
  • hair loss
  • polycystic ovaries
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12
Q

Can you use valproic acid in pregnancy?

A

category D

inc. risk of NTD

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13
Q

What sx will you see with valproic acid overdose?

A

N/V, CNS depression, seizures

check drug levels, target is 50-100g/mL

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14
Q

Which drugs will inc. the serum level of valproic acid?

A

CAFE PI

  • cemetidine (PPI)
  • Aspirin
  • Fluoxetine (antidepressant SSRI)
  • Erythromycin
  • Phenothiazines
  • Ibuprofen
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15
Q

Which drugs will dec. the serum level of valproic acid?

A

CREPes

  • Carbamazepine
  • Rifampin
  • Ethosuximide
  • Phenobarbitol
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16
Q

Valproic acid inhibits the metabolism of which drugs?

A

I sAW LAND (I=inhibited by)

  • Amitriptyline
  • Warfarin (inc. risk bleeding)
  • lamotrigine
  • AZT
  • Nortriptyline
  • Diazepam (benzo)
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17
Q

what is the MOA of carbamazepine?

A

Acts on Na and K channels to enhance GABA availability

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18
Q

What conditions would you use carbamazepine with?

A
  • trigeminal neuralgia
  • seizures
  • can use in bipolar but there are better drugs with fewer side Effx
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19
Q

What are the side effects of carbamazepine?

A

HLA typing in asians

Scary ones are:

  • thrombocytopenia and aplastic anemia
  • hepatitis
  • exfoliative dermatitis, toxic epidermal necrolysis

Less scary but unpleasant ones:

  • sedation
  • dizziness
  • fatigue
  • N/V, constipation or diarrhea
  • ataxia (wobbly)
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20
Q

carbamazepine and pregnancy?

A

category D

-assoc. w/ congenital malformations (spina bifida)

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21
Q

What are the important clinical take-home points concerning carbamazepine?

A
  • Avoid in patients with cardiac, hematological, liver or kidney disease
  • Think of it as a drug that interacts with almost everything
  • If you ever rx must check it doesn’t interact with other meds pt is taking (it interacts with itself)
  • Must have 14 day washout period before initiate MAOI—can have serotonin syndrome
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22
Q

what is the MOA for lamotrigine?

A

dec the excitatory actions of Glu via interference with Na channels

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23
Q

what disorders can you treat with lamotrigine?

A

bipolar d/o (mania, hypomania, and depression)

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24
Q

what are the side effects of lamotrigine?

A

scary:
-toxic epidermal necrolysis (10% pt’s get rash but only small subset progress)

less scary but unpleasant:

  • sedation
  • dizziness
  • ataxia
  • dec. coordination
  • headache
  • N/V
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25
Q

lamotrigine in pregnancy?

A

Category C
Avoid in first trimester
Use after first trimester if other meds don’t work
Avoid in breast feeding – risks unknown

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26
Q

When can you use antipsychotics?

A

Psychotic illness – unable to distinguish unreality from reality
-Schizophrenia, Bipolar Mania, Depression w/psychosis, drugs (eg. Cocaine)

Augmentation of antidepressant (eg SSRI)—makes them work better
-Aripiprazole & Quetiapine

Mood Stabilizer – Acute Mania
-Quetiapine, olanzepine, aripiprazole, ziprasidone & risperidone

Mood Stabilizer – Maintenance
-Olanzapine & aripiprazole

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27
Q

What are the typical first generation antipsychotics?

A

dopamine antagonists:

  • chlorpromazine
  • thiordazine
  • prochlorperazine
  • trifluoperazine
  • haloperidol
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28
Q

What are the second generation atypical antipsychotics?

A

serotonin/dopamine antagonists:

  • Clozapine
  • Risperidone
  • Olanzapine
  • Quetiapine
  • Ziprasidone

dopamine agonist/antagonist:
-arpiprazole

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29
Q

what is the mesolimbic pathway? What does this pathway control?

A
  • Midbrain ventral tegmental area –>nucleus accmbens
  • Pathway of all things pleasurable
  • Pathways for drugs of abuse to create “high” feeling
  • Pathway of delusions and hallucinations of pscyhosis
30
Q

What is the mesocortical pathway? What does this pathway control?

A
  • Midbrain ventral tegmental area –> limbic cortex
  • May have role in mediating +/- psychotic symptoms
  • May have role in cognitive side effects of FGA’s
31
Q

what is the nigrostriatal pathway? what does this pathway control?

A
  • Substantia nigra –> basal ganglia

- Controls movement

32
Q

What ist he tubuloinfundibular pathway? What does this pathway control?

A
  • Hypothalamus –> anterior pituitary gland
  • Controls prolactin secretion
  • Dopamine & prolactin have an inversely proportionate relationship (i.e. inc of one =dec of the other)
  • Lower dopamine–>inc. prolactin–>galactorrhea/gynecomastia
33
Q

what is the dopamine hypothesis of schizophrenia?

A 
-Hyperdopaminergic activity in mesolimbic system -->positive sx
Delusions
Hallucinations
Catatonia
Thought disorder

-Hypodopaminergic activity in mesocortical system –>neg sx
Apathy
Motor retardation
Social withdrawal

34
Q

what is the MOA of FGA dopamine antagonists?

A
  • Competitively block Da receptors (D2, D3 & D4 subtypes)
  • D2 receptors located in limbic, extrapyramidal & endocrine structures
  • D3 & D4 subtypes located primarily in limbic structures
  • Receptors linked to enzyme adenyl cyclase via G protein which inhibits activation of enzyme
  • Blocking receptors decreases +sx (mesolimbic pathway)
  • Bind to D2 receptors 10-50x more avidly than D3 receptors
35
Q

Which FGAs are high potency? What profile will they have?

A

haloperidol & fluphenazine

  • Low anticholinergic & low sedating properties
  • Fewer CV abnormalities
  • Higher rate of EPS
36
Q

Which FGAs are low potency? What profile will they have?

A

chlorpromazine and thioridazine

  • high anticholinergic and high sedating properties
  • more pronounced CV abnormalities
  • low incidence of EPS
37
Q

What is the MOA of dopamine/serotonin antagonists (SGAs)?

A

clozapine, risperidole, olanzapine, quetiapine, ziprasidone

More selective for mesolimbic Da pathway (origin + symptoms)

Less active on nigrostriatal pathway (origin EPS)

Competitively block serotonin receptors (5-HT2 subtype)

Have >5x binding affinity for 5-HT2 than D2
-5-HT2 located in cortical structures where neg sx thought to originate

Higher degree of binding/blockade of D4 & D3 receptors vs D2
-D4 & D3 receptors located in limbic structures where + sx thought to originate

Blockade of 5-HT receptors therefore–>

  • Improves negative & positive sx
  • Dec EPS
38
Q

what is the MOA of dopamine agonist/antagonist?

A

*Establishes balanced dopamine availability

-Acts as antagonist when there is excess Da 
Mesolimbic pathway (positive sx-delusions)

-Acts as agonist when there is too little Da
Nigrostriatal pathway & frontal lobes (negative sx)

-Aripiprazole (abilify) only drug in this class

39
Q

What other receptors can antipsychotics act on? What are the side effects based on these receptors?

A

Anticholinergic (M1)

  • Dry mouth
  • Mydriasis
  • Urinary retention
  • Constipation

Antihistaminergic (H1)

  • Weight gain (can be VERY significant)
  • diabetes
  • sedation

Alpha Adrenergic Blockade

  • Orthostatic (postural) hypotension
  • sedation

Dopaminergic Blockade
-EPS

40
Q

what are the extrapyramidal side effects of antipsychotics?

A
  • Parkinsonian syndrome (blockage of D2 receptors in striatum–>muscle rigidity, slow movements, shuffling gait, resting tremor, mask like facies, cogwheel rigidity)
  • acute dystonia (prolonged muscle spasm tx’ed with dephenhydramine or benztropine)
  • tardive dyskinesia (more common with FGAs, abnormal writing movement of tongue, face, limbs, trunk; D2 blockade in hypothalamus and striatum, may not go away with discontinuation of meds)
  • Neuroleptic malignant syndrome: life threatening, more common in men, hyperthermia, hypertension, tachycardia, tremor, sz, dyskinesias, STOP antipsychotic
  • akithisia: subject feeling of motor restlessness, give patient dephenhydramine, propanolol, benzodiazepine
41
Q

what are the endocrine side effects of antipsychotics?

A

Blockade of D2 in hypothalamus &/or anterior pituitary

  • Inc prolactin –>gynecomastia in men and galactorrhea in women
  • Dec gonadotropin–> amenorrhea
  • Dec growth hormone, Luteinizing hormone & ACTH
42
Q

what are the cardiovacular side effects of antipsychotics?

A
  • Prolongation of QT interval on EKG (Torsades)

- Can result in potentially lethal cardiac -arrhythmia

43
Q

What is metabolic syndrome? Which has more risk FGA or SGA? What should you monitor in patients taking antipsychotics?

A

Group of findings–> inc risk of heart disease, stroke & diabetes
-Inc BP, inc insulin, xs abdominal fat or inc cholesterol

  • SGAs have inc. risk
  • Monitor: weight, waist circumference, fasting glucose, fasting lipids, BP
44
Q

What are the general clinical guidelines for antipsychotics?

A
  • Choose based on past response and side effects
  • SGA’s generally 1st line, especially if past tardive dyskinesia
  • Avoid SGA’s for behavioral disorders in patients with dementia–> inc mortality

-Pregnancy category C
FGA’s – slight inc in anomalies
SGA’s – need inc data

  • Smoking increases metabolism of antipsychotics
  • Must adjust dose for patients with liver or kidney disease
45
Q

When would you use clozapine? What are the side effects?

A

-For patients who have failed 2+ other antipsychotic agents

  • Risk of agranulocytosis & neutropenia must monitor CBC
  • Risk seizures on doses > 600mg/day
  • Myocarditis – rare
  • Low association with TD
  • For patients who have failed 2+ other antipsychotic agents
  • Sedation, orthostatic hypotension & hypersalivation
  • Decreased risk of suicide in patients with schizophrenia (FDA approval)
46
Q

which 2 antipsychotics are less likely to cause weight gain?

A

aripiprazole

ziprasidone

47
Q

all addictive drugs activate what part of the brain

A

the mesolimbic dopamine system

this originates in the VTA–>nucleus accumbens, amygdala, hippocampus, prefrotnal cortex

48
Q

SSRIs

A
  • Sertraline, paroxetine, citalopram, escitalopram, fluvoxamine
  • Good b/c decr. wt. gain, decr. sedation, decr. orthostatic hypotn
  • Biggest drawback is decrease sex drive
49
Q

SNRIs

A
  • serotonin and norepi reuptake inhibitors
  • Venlafaxine, duloxetine
  • Duloxetine can be used for DM peripheral neuropathy
50
Q

tricyclic antidepressants

A
  • Desipramine, Imipramine, Nortriptyline, Amitriptyline
  • Block reuptake of NE & Serotonin
  • Yes they’re efficacious but they come with a whole host of AE’s
  • CARDIAC – arrhythmias, prolonged QT
  • ANTI – histaminergic, - cholinergic, - adrenergic
  • Still sexual AEs
  • OD will KILL you
51
Q

MAOIs

A

-Phenelzine, Tranylcypromine
Not use as much because…
-Foods that contain TYRAMINE –>stroke
-Mixing with drugs can –> HTN crisis
-React with other medications, including anesthetics so have to go off 2 weeks before surgery
-SEROTONIN SYNDROME – do not mix w/ SSRIs**

52
Q

buproprion

A
  • Only one, along with mirtazapine, that doesn’t cause sexual side effects
  • Can also be used to help quit smoking – marketed as Zyban for that
  • NDRI (norepi and dopamine reuptake inhibitors)
53
Q

Why are SSRI’s better than Tricyclics?

A

a. Do NOT block cholinergic receptors, histamine receptors (less sedation) or a1-adrenergic receptors (less orthostatic hypotension)
b. Do NOT have quinidine-like action on the heart
c. Do NOT cause significant weight gain
d. Do NOT require monitoring of blood levels
e. Have higher safety margins in overdose

54
Q

Serotonin syndrome occurs when SSRIs are combined with which drugs?

A

a. MAOIs
b. Tricyclic antidepressants
c. Lithium
d. Carbamazepine

55
Q

What are the indications for using SSRIs

A 
o	Depression (1st line)
o	OCD, panic disorders, posttraumatic stress disorder, eating disorders, generalized anxiety disorder, premenstrual syndrome
56
Q

which SSRI has the longest half-life?

A

fluoxetine

57
Q

what are the indications for using Tricylcics?

A 
o	Depression (resistant to SSRIs)
o	Childhood enuresis, chronic pain, neuralgias, migraine, diabetic neuropathy
58
Q

What is the MOA of benzodiazepines?

A

enhance frequency of GABA mediated Cl- channel opening

59
Q

what is the MOA of barbituates?

A

enhance duration of GABA mediated Cl- channel opening

60
Q

What drug classes and drug names can you use to treat insomnia?

A
  1. antihistamines (diphenhydramine)
    2 . antidepressants w/ sedative activity (trazodone)
  2. melatonin receptor agonists (ramelteon)
  3. benzo’s (temazepam, estazolam, flurazepam, quazepam, triazolam)
  4. non-benzo hypnotics (zolpidem, zaleplon)
61
Q

What are the adverse effects when using benzodiazepines?

A

o Sedation (ALL benzodiazepines are sedating)
o Daytime drowsiness
o Dizziness and ataxia (<2%), can lead to falls and hip fractures in the elderly
o Amnesia and memory impairment
o Rebound insomnia upon discontinuation

caution in patients with COPD, sleep apnea and cognitivie deficits

teratogenic in pregnancy

other issues: abuse, withdrawal

62
Q

what are the best drugs to use to treat insomnia?

A

zolpidem
zaleplon

act on subunit of GABA receptor and inc. Cl- channel opening

63
Q

All addictive drugs activate what

A

mesolimbic dopamine system

VTA=addiction center

64
Q

Which drugs of abuse work on GPCR pathways?

A
  1. opioids
  2. cannabinoids
  3. GHB
  4. LSD
65
Q

which drugs of abuse work on ion channels?

A

nicotine
alcohol
benzo’s
phencyclidine, ketamine

66
Q

Which drugs of abuse work on dopamine transporters?

A

cocaine, amphetamine

ecstasy

67
Q

tolerance

A

escalation in dose to maintain comparable effect

  1. PK changes (eg. enzyme induction–barbituates)
  2. pharmacodynamic changes (receptor change in number–morphine)
  3. immunological changes (antibody formation–insulin)
  4. behavioral changes (compensation–alcohol)
68
Q

physical dependence

A

drug need to prevent withdrawal syndrome
alcohol,barbituates=severe
narcotic analgesics=moderate
stimulants=mild

69
Q

you suspect drug toxicity. Patient presents with respiratory depression, mental status depression, miosis. What drug?what is the treatment?

A

opioid

naloxone

70
Q

patient is drug addict going through withdrawal. He presents with lacrimation, rhinorrhea, mydriasis, N/V/D, diaphoresis, insomnia, piloerection. What drug is he withdrawing from?

A

heroind

71
Q

how do you treat benzo toxicity?

A

flumazenil

neuro.psych.optho (8 decks)

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