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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
QT interval inn crease in milliseconds for Thioridazine
35.8
26
QT interval inn crease in milliseconds for Ziprasidone
20.6
27
QT interval inn crease in milliseconds for Haloperidol
4.7
28
Early neurological adverse effects of FGAs
Acute dystonia Akathisia Parkinsonism
29
Acute dystonia w/ FGAs
1-5 days = maximal risk Treat with: biphenhydramine IM benztropin IM
30
Akathisia w/ FGAs
5-60 days | Usual treatment for agitation is more drugs -> not in this case
31
Parkinsonism w/ FGAs
5-30 days
32
Late neurological adverse effects of FGAs
``` Neuroleptic malignant syndrome (weeks; 10% mortality; antiparkinson agents not effective) Tardive dyskinesia (after months - years of treatment) Perioral tremor (rabbit sundrome; months -> years) ```
33
Neuroleptic malignant syndrome (NMS)
more common in pts on high potency FGAs, depot FGAs, deyhydrated, or exhausted pts
34
NMS Tx
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
35
NMS follow up
Use only SGAs for rechallenge post-NMS
36
Early Second Generation Antipsychotic agents (SGAs)
``` Clozapine Risperidone Olanzapine Quetiapine Ziprasidone Arpiprazole ```
37
Later SGA agents
Paliperidone Iloperidone Asenapine Lurasidone
38
What additional therapeutic mechanisms do SGAs have
D1, D4 antagonism | NE, 5-HT (serotonin) antagonism
39
Why are SGAs atypical APs
Due to their non-D2 antagonism | Significantly less risk of extrapyramidal effects
40
Tradeoff of SGAs
Increased risk of metabolic effects like weight gain
41
Atypical APs
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
SGA SE
``` Mod-severe weight gain DM Clozapine: 1) Seizures 2) Nocturnal salivation 3) Agranulocytosis 4) Myocarditis 5) Lens opacities ```
43
Clozapine
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
Early SGAs
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
Paliperidone (late SGA)
9-OH metabolite of risperidone
46
Iloperidne (late SGA)
Increased risk of orthostatic hypotension
47
Asenapine (late SGA)
ODT SL tabs don't chew or swallow increased risk of anaphylaxis and angioedema
48
Schizophrenia tx
3 phases: 1) Acute 2) Stabilization 3) Maintenance
49
Tx of first acute psychotic episode
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
Suicide risk ______ as other sx improve
Increases!!!!!!!
51
When do we use clozapine
Lack of response with other SGAs | Intolerable SE from other APs
52
Role of FGAs
Typically not first line | May be used before a SGA if chronically ill pts have a previously satisfactory response
53
Stage 1 pharmacotherapeutic algorithm
Only for pts w/ first schizophrenic episode | SGAs = FIRST LINE
54
Stage 2 | pharmacotherapeutic algorithm
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
Stage 3 pharmacotherapeutic algorithm
Switch to clozapine (monotherapy) Increased efficacy for suicidal behavior Consider earlier use in suicidal pts Monitor CBC pts (Look for agranulocytosis)
56
Stage 4 pharmacotherapeutic algorithm
Continue clozapine | Add additional AP (combination therapy)
57
Stage 5 pharmacotherapeutic algorithm
Trial of monotherapy AP | Use FGA or SGA not previously used
58
Stage 6 pharmacotherapeutic algorithm
Consider combination therapy When switching APs -> overlap 2nd agent for 1-2 weeks Taper and DC first agent (taper clozapine SLOWLY)
59
Combination treatment of schizophrenia
Using 2 APs simultaneously
60
Augmentation treatment of schizophrenia
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
Augmentation Agents
Mood stabelizers SSRIS Beta blockers
62
Mood stabilizers as augmentation agent
Lithium Valproic acid Carbamazepine
63
Beta blockers as augmentation agents
Antiaggressive effect Propranolol Pindolol Nadolol
64
Combination of therapy (step 4-6)
Multiple MOAs Combos should be time limited (12 weeks) If no improvement -> taper one and discontinue Series of monotherapies preferred over AP combination
65
Maintenance tx of schizophrenia
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
Long acting depot injectable APs
Recommended in unreliable pts Not 1st line Look for SE as a cause for nonadherence
67
Depot APs
``` Haloperidol decanoate (FGA) Fluphenazine decanoate (FGA) Risperidone microspheres (SGA) ```
68
Haldol lactate vs haldol decanoate
immediate vs sustained release
69
Haloperidol decanoate
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
Fluphenazine decanoate
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
Risperidone micropsheres
Only SGA depot agent; needs reconstitution Optimum dose is 25-50 mg Higher doses have no more benefit, but more EPS
72
Bipolar disorder
1 disorder: mania 2 disorder: hypomania Must rule out amphetamine use and pheochromocytoma Most distinctive syndromes in psychiatry
73
What did bipolar disorder used to be called
Manic depression
74
Bipolar disorder (BP) characterizations
Elevated mood Overactivity Lack of need for sleep Increased optimism
75
Unique hallmark of bipolar disorder
Mania
76
BP mania
Different from usual behavior Single episode significant for diagnosis Types: one, alternating, every few year episodes
77
Classic bipolar disorder
Bipolar 1 | manic phase-usually requires hospitalization
78
Major depression + hypomania
bipolar 2
79
Rapid cyclers and BP disorder
>4 manic or depressive cycles per year
80
Genetics of BP disorder
50% of pts have family hx of BP disorder | Risk -> 10% in siblings of affected parients
81
Acute mania tx
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
More tx for acute mania
Lithium Valproic acid Carbamazepine
83
DX for bipolar depression
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
Mood stabilizers:Lithium
Classic | Good for: mania, bipolar disorder; bipolar deressin
85
Lithium therapeutic index
Therapuetic (acute mania) =0.6-1.2% Tremor Seizures/sudden death >2.5 mEq/L
86
Tx of bipolar depression
Depressive episodes need a response will give SSRIs then, Tricyclic antidepressants (TCAs) Monoamine oxidasing inhibitors
87
Caution with use of antidepressants with BP disorder
Induce switch from depression to mania | Don't use w/ h/o mania episodes
88
Lithium for BP disorder
Classic mood stabilizer | Good for mania, bipolar disorder, and bipolar depression (last 2 = prophylactically)
89
Narrow therapeutic index of Lithium
Acute mania: 0.6-1.2 mEq/L Tremor: 1.5-2 mEq/L Seizures/death: >2,5 mEq/L
90
Remember w/ lithium
Draw blood levels twice/week until stable | Collect trough samples just prior to next dose
91
Cabamazepine
Anticonvulsant found useful in the 80s .5 of all doses were for bipolar illness Weekly dosing
92
Valproic acid
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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