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Psychiatric disorders Flashcards

1
Q

What are the major psychiatric disorders we will be focusing on

A

Bipolar disorder

Schizophrenia

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2
Q

Life time prevalence of schizophrenia in the US

A

1%

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3
Q

Lifetime prevalence of suicide among schizophrenic patients

A

10%

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4
Q

Genetic risks of schizophrenia

A

3% if 2nd degree relative has it
10% if first degree relative has it
40% if both parents have it
Mono-zygotic twin risk 48%

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5
Q

Presentation of schizophrenia

A

NOT split personality

Chronic diagnosis of thought and affect

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6
Q

Acute schizophrenic psychotic episodes

A 
Auditory hallucinations (especially voices)
Delusions (fixed false beliefs)
Ideas of influence (outside forces control their actions)
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7
Q

Positive schizophrenic symtoms

A

Most obvious/dramatic

Suspiciousness, unusual thought content, hallucinations, etc.

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8
Q

Negative schizophrenic sx

A

Functional impairments

Affect flattening, alogia, anhedonia

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9
Q

Cognitive schizophrenic sx

A

Impaired attention, working memory, executive function

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10
Q

Schizophrenia tx overview

A

Pharmacotherapy = mainstay

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11
Q

Nonpharmacological tx for schizophrenia

A

Psychosocial rehab = mainstay

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12
Q

What measurements should you be looking at when getting ready to start treatment for schizophrenia to establish a baseline?

A 
**Doing so to rule out medical or substance abuse causes**
Vitals
EKG
CBC (fasting glucose)
Electrolytes
Lipid studies
LFTs
Thyroid functions
Renal fx
Urine drug screen
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13
Q

Original rationale for pharmacotherapy of schizophrenia

A

Acute psychotic episodes increase DA neurotransmission
Results in hypersensitivity to stimuli
(this is the original dopamine hypothesis)

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14
Q

Current rationale for pharmacotherapy of schizophrenia

A

Since inhibitory neurons are modulated by DA 5-HT, Ach and NE, these become targets for new Aps
Newer dysregulation hypothesis

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15
Q

Neurochemistry associated with schizophrenia

A

AP efficacy is proportional to D2 affinity

Non-D2 receptors are associated with SEs/AEs

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16
Q

First generation antipsychotics (FGAs)

A

DA antagonism = MOA

MOA characterizes “typical” anti-psychotics

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17
Q

Neuroleptic

A

Prominent D2-dopamine receptor antagonism
Typical anti psychotic
Contrasted with atypical mechanism of action of second generation anti-psychotics
Preferred term = First Generation Antipsychotic (FGA)

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18
Q

Examples of First Generation Antipsychotics

A

Fluphenazine 2-20 mg/day

Haloperidol 2-25 mg/day

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19
Q

Traditional Equivalent dose of FGAs

A

2 for both

allows for switching to equivalent dose of another FGA

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20
Q

Efficacy of FGA

A

Immediate D2 receptor blockaged

Theraputic effect develops over 6-8 weeks

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21
Q

Percentages of decreased presynaptic release of DA

A

> 60% D2 blockade = clinical response
70% D2 blockade = hyperprolactinemia
80% D2 blockage = increased risk of EPS

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22
Q

Adverse effects FGAs

A 
Sedation
Dystonias/Parkinsonian movement disorders (EPS)
Anticholinergic effects
Orthostatic hypotension
Seizures
Hyperprolactinemia
Moderate weight gain
Prolonged QT interval (incidence of sudden death 0.015% only about twice that of the healthy population)
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23
Q

Anticholinergic effects of antipsychotic drugs

A 
constipation
Urinary retention
blurry vision
tachycardia
dry eyes, mouth, and throat
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24
Q

Antipsychotics (APs) that increase QT interval

A

Thioridazine
Ziprasidone
Haloperidol

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25
Q

QT interval inn crease in milliseconds for Thioridazine

A

35.8

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26
Q

QT interval inn crease in milliseconds for Ziprasidone

A

20.6

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27
Q

QT interval inn crease in milliseconds for Haloperidol

A

4.7

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28
Q

Early neurological adverse effects of FGAs

A

Acute dystonia
Akathisia
Parkinsonism

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29
Q

Acute dystonia w/ FGAs

A

1-5 days = maximal risk
Treat with:
biphenhydramine IM
benztropin IM

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30
Q

Akathisia w/ FGAs

A

5-60 days

Usual treatment for agitation is more drugs -> not in this case

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31
Q

Parkinsonism w/ FGAs

A

5-30 days

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32
Q

Late neurological adverse effects of FGAs

A 
Neuroleptic malignant syndrome (weeks; 10% mortality; antiparkinson agents not effective)
Tardive dyskinesia (after months - years of treatment)
Perioral tremor (rabbit sundrome; months -> years)
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33
Q

Neuroleptic malignant syndrome (NMS)

A

more common in pts on high potency FGAs, depot FGAs, deyhydrated, or exhausted pts

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34
Q

NMS Tx

A

DISCONTINUE antipsychotic
DA agonist bromocriptine reduces rigidity, fever, and CK in up to 94% of pts
Amantadine (another DA agonist) works up to 63% of the time

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35
Q

NMS follow up

A

Use only SGAs for rechallenge post-NMS

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36
Q

Early Second Generation Antipsychotic agents (SGAs)

A 
Clozapine
Risperidone
Olanzapine
Quetiapine
Ziprasidone
Arpiprazole
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37
Q

Later SGA agents

A

Paliperidone
Iloperidone
Asenapine
Lurasidone

38
Q

What additional therapeutic mechanisms do SGAs have

A

D1, D4 antagonism

NE, 5-HT (serotonin) antagonism

39
Q

Why are SGAs atypical APs

A

Due to their non-D2 antagonism

Significantly less risk of extrapyramidal effects

40
Q

Tradeoff of SGAs

A

Increased risk of metabolic effects like weight gain

41
Q

Atypical APs

A

ability to produce antipsychotic responses with few or no acutely occurring extrapyramidal effects
Enhanced efficacy
Absence of tardive dyskinesia
Ex: clozapine (only SGA to fulfill all criteria)

42
Q

SGA SE

A 
Mod-severe weight gain
DM
Clozapine:
1) Seizures
2) Nocturnal salivation
3) Agranulocytosis
4) Myocarditis
5) Lens opacities
43
Q

Clozapine

A

FDA approved despite risk of agranulocytosis (.39%)
Risk of death = 0.013%
Weekly CBCs for 6 months; then q2 weeks
Reserved for pts who fail other methods

44
Q

Early SGAs

A

Virtually no extrapyramidal sx
Greatly reduced risk of tardive dyskinesia
Good for negative sx
Significantly less relapse than with FGAs (25% w/ Risperidone vs 40% with haloperidol)

45
Q

Paliperidone (late SGA)

A

9-OH metabolite of risperidone

46
Q

Iloperidne (late SGA)

A

Increased risk of orthostatic hypotension

47
Q

Asenapine (late SGA)

A

ODT SL tabs
don’t chew or swallow
increased risk of anaphylaxis and angioedema

48
Q

Schizophrenia tx

A

3 phases:

1) Acute
2) Stabilization
3) Maintenance

49
Q

Tx of first acute psychotic episode

A

First goal: calm agitated pt
Immediate treatment improves long term outcomes
Most psychiatrists will prescribe SGA (not clozapine; decreased anger and anxiety seen in 24-48 hours)

50
Q

Suicide risk ______ as other sx improve

A

Increases!!!!!!!

51
Q

When do we use clozapine

A

Lack of response with other SGAs

Intolerable SE from other APs

52
Q

Role of FGAs

A

Typically not first line

May be used before a SGA if chronically ill pts have a previously satisfactory response

53
Q

Stage 1 pharmacotherapeutic algorithm

A

Only for pts w/ first schizophrenic episode

SGAs = FIRST LINE

54
Q

Stage 2

pharmacotherapeutic algorithm

A

Chronically ill pts recently started on APs
Or new onset pt with poor response to Stage 1
Monotherapy w/ FGA or SGA
Chose different AP than used in stage 1

55
Q

Stage 3 pharmacotherapeutic algorithm

A

Switch to clozapine (monotherapy)
Increased efficacy for suicidal behavior
Consider earlier use in suicidal pts
Monitor CBC pts (Look for agranulocytosis)

56
Q

Stage 4 pharmacotherapeutic algorithm

A

Continue clozapine

Add additional AP (combination therapy)

57
Q

Stage 5 pharmacotherapeutic algorithm

A

Trial of monotherapy AP

Use FGA or SGA not previously used

58
Q

Stage 6 pharmacotherapeutic algorithm

A

Consider combination therapy
When switching APs -> overlap 2nd agent for 1-2 weeks
Taper and DC first agent (taper clozapine SLOWLY)

59
Q

Combination treatment of schizophrenia

A

Using 2 APs simultaneously

60
Q

Augmentation treatment of schizophrenia

A

Addition of non-AP drug to an AP
Use only in inadequately responding pts
Augmentation agents are rarely effective for schizophrenia used alone
Responders will usually improve rapidly
If no sx improvement -> DC augmentation agent

61
Q

Augmentation Agents

A

Mood stabelizers
SSRIS
Beta blockers

62
Q

Mood stabilizers as augmentation agent

A

Lithium
Valproic acid
Carbamazepine

63
Q

Beta blockers as augmentation agents

A

Antiaggressive effect
Propranolol
Pindolol
Nadolol

64
Q

Combination of therapy (step 4-6)

A

Multiple MOAs
Combos should be time limited (12 weeks)
If no improvement -> taper one and discontinue
Series of monotherapies preferred over AP combination

65
Q

Maintenance tx of schizophrenia

A

1st presentation may respond sooner
Meds may reduce sx -> None are curative
All sx may not abate
Prevents relapse (18-32% on drugs vs. 60-80% on placebo)
Continue at least 12 months past remission

66
Q

Long acting depot injectable APs

A

Recommended in unreliable pts
Not 1st line
Look for SE as a cause for nonadherence

67
Q

Depot APs

A 
Haloperidol decanoate (FGA)
Fluphenazine decanoate (FGA)
Risperidone microspheres (SGA)
68
Q

Haldol lactate vs haldol decanoate

A

immediate vs sustained release

69
Q

Haloperidol decanoate

A

Use 10-15xs the oral daily dose
Round dose up to nearest 50 mg
Give dose via deep IM (not IV) injection once a month
Overlap with PO haloperidol for first month

70
Q

Fluphenazine decanoate

A

Use 1.2 times oral daily dose
Use 1.6 times PO dose for more acutely ill pts
Round up dose to nearest 12.5 mg interval
Overlap w/ PO fluphenazine for 1 week

71
Q

Risperidone micropsheres

A

Only SGA depot agent; needs reconstitution
Optimum dose is 25-50 mg
Higher doses have no more benefit, but more EPS

72
Q

Bipolar disorder

A

1 disorder: mania
2 disorder: hypomania
Must rule out amphetamine use and pheochromocytoma
Most distinctive syndromes in psychiatry

73
Q

What did bipolar disorder used to be called

A

Manic depression

74
Q

Bipolar disorder (BP) characterizations

A

Elevated mood
Overactivity
Lack of need for sleep
Increased optimism

75
Q

Unique hallmark of bipolar disorder

A

Mania

76
Q

BP mania

A

Different from usual behavior
Single episode significant for diagnosis
Types: one, alternating, every few year episodes

77
Q

Classic bipolar disorder

A

Bipolar 1

manic phase-usually requires hospitalization

78
Q

Major depression + hypomania

A

bipolar 2

79
Q

Rapid cyclers and BP disorder

A

> 4 manic or depressive cycles per year

80
Q

Genetics of BP disorder

A

50% of pts have family hx of BP disorder

Risk -> 10% in siblings of affected parients

81
Q

Acute mania tx

A

Medical emergency
Marriage, job, and life of pt at risk
AP drugs = effective in acute mania
Rapid onset may be lifesaving in violent pts
Newere atypical AP (SGAs) are they effective in complaining pts

82
Q

More tx for acute mania

A

Lithium
Valproic acid
Carbamazepine

83
Q

DX for bipolar depression

A

Depressive episodes respond to: SSRIs, TCAs, MAOIS
Note: antidepressants may induce switch from depression to mania
Dont use AD in pts w/ hx of dangerous mania episodes

84
Q

Mood stabilizers:Lithium

A

Classic

Good for: mania, bipolar disorder; bipolar deressin

85
Q

Lithium therapeutic index

A

Therapuetic (acute mania) =0.6-1.2%
Tremor
Seizures/sudden death >2.5 mEq/L

86
Q

Tx of bipolar depression

A

Depressive episodes need a response
will give SSRIs then,
Tricyclic antidepressants (TCAs)
Monoamine oxidasing inhibitors

87
Q

Caution with use of antidepressants with BP disorder

A

Induce switch from depression to mania

Don’t use w/ h/o mania episodes

88
Q

Lithium for BP disorder

A

Classic mood stabilizer

Good for mania, bipolar disorder, and bipolar depression (last 2 = prophylactically)

89
Q

Narrow therapeutic index of Lithium

A

Acute mania: 0.6-1.2 mEq/L
Tremor: 1.5-2 mEq/L
Seizures/death: >2,5 mEq/L

90
Q

Remember w/ lithium

A

Draw blood levels twice/week until stable

Collect trough samples just prior to next dose

91
Q

Cabamazepine

A

Anticonvulsant found useful in the 80s
.5 of all doses were for bipolar illness
Weekly dosing

92
Q

Valproic acid

A

Recent study found Li prophylaxis much more effective than valproate for suicide prevention (JAMA 2003; 290(11): 1467-73)

Pharm (32 decks)

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