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Behavioral Med: Test 4 > Schizophrenia > Flashcards

Schizophrenia Flashcards

1
Q

What is Schizophrenia?

A
  1. “Split mind-” irrational divergence between behavior and thought content
  2. Chronic, debilitating illness associated with deterioration in mental function and behavior
    A. Clearly involves a gene by environment interaction
    B. Not caused by any known social or environmental factor
    C. Exacerbated by social stress
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2
Q

Schizophrenia Characterisitics

A
  1. One of most debilitating psychiatric illnesses and utilizes many resources
    a. Welfare
    b. Social Security Income
    c. Social Security Disability
    d. Inpatient and group home stays
    e. Incarceration facilities
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3
Q

What is the Downward Drift? (Means you never return to baseline after diagnosis)

A
  • Prior to schizophrenia, patients are psychosocially fully functional (10% may lead normal lives…)
  • As years progress, the average patient loses social stature, income, relationships, support network… You become more and more disabled with each episode
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4
Q

The hallmark symptom of schizophrenia

A
  1. Psychosis is a hallmark symptom
    a. Impairment in reality testing that may present as:
    - Alteration in sensory perceptions(hallucinations)
    - Abnormalities in thought content (delusions)
    - Abnormalities in thought process/organization
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5
Q

Symptoms of Psychosis

A
  • Illusion
  • Hallucinations
  • Ideas of reference
  • Delusions
  • Loss of ego boundaries
  • Alogia
  • Echolalia
  • Thought Blocking
  • Neologisms
  • Circumstantiality
  • Tangentiality
  • Loose associations
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6
Q

What is an Illusion?

A

Misperception of real external stimuli

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7
Q

What is an hallucination?

A

Sensory perceptions not generated by external stimuli

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8
Q

What are ideas of reference?

A

False conviction that one is subject of attention by other people (Crowds, TV, Radio, Internet). Feeling as though people are referring to you in their conversations

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9
Q

What are Delusions?

A

False beliefs not correctable by logic or reason, not based on simple ignorance, and not shared by culture; delusions of persecution most common

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10
Q

What is loss of ego boundaries?

A

Not knowing where one’s mind and body end and those of others begin

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11
Q

What is alogia?

A

Lack of informative content in speech, lacking/poverty of speech
ex. “Patient is mute or speaks few words.”

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12
Q

What is Echolalia?

A

Repeating Statements of Others/Associating words by their sounds, not by their meaning
ex. “I’m very sure I’ve got the cure and I’m not pure.”

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13
Q

What is thought blocking?

A

Abrupt halt in the train of thinking, often because of hallucinations
Ex. I have to take my……

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14
Q

What is neologisms?

A

Inventing new words

Ex. Patient states he is ‘fatigloo’ which means he is tired

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15
Q

What is circumstantiality?

A

In responding to questions, one presents unnecessary and voluminous details ultimately arriving at an answer to the question posed

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16
Q

What is tangentiality?

A

Beginning a response in a logical fashion but then getting further and further away from the point and fail to answer the question initially posed (can understand topic transition)

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17
Q

What is loose associations?

A

Loss of logical meaning between words or thoughts; when asked a question, illogically jumps from one subject to another

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18
Q

What is loose associations?

A

Loss of logical meaning between words or thoughts; when asked a question, illogically jumps from one subject to another

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19
Q

Schizophrenia vs delirium

A
  1. At least one episode of psychosis with persistent disturbances of thought, behavior, appearance, speech and affect (emotion) as well as impairment in occupational and social functioning
  2. In contrast to delirium or substance abuse, patients with schizophrenia do not have clouding of consciousness
    a. Attention and memory capacity typically intact, when not psychotic
    b. Alert and oriented, do not fluctuate in/out of consciousness/stupor
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20
Q

DSM 5 Diagnostic Criteria

A

A. Characteristic symptoms: 2 or more of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated):

  • Delusions
  • Hallucinations
  • Grossly disorganized or catatonic behavior
  • Negative symptoms (flat affect, alogia, or avolition)
  • Disorganized speech (frequent derailment or incoherence)
  • the DSMIV only req’d 1 symptom

B. Social/occupational dysfunction: One or more major areas of functioning (ie. work, interpersonal relations, or self care) are markedly below level achieved prior to onset

C. Duration: Continuous signs of the disturbance persist for at least 6 months. This 6-month period must include at least 1 month of symptoms (or less if successfully treated) that meet Criterion A (i.e., active phase symptoms) and may include periods of prodromal (symptomatic of the onset) or residual symptoms.

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21
Q

Positive Symptoms

A 
The patient develops these! ADDED
Positive symptoms: are additional to expected behavior (i.e. symptoms that are added to a patient’s normal functioning) 
-Delusions 
-Hallucinations 
-Agitation 
-Talkativeness 
-Thought Disorder

Respond well to traditional & atypical antipsychotics

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22
Q

Negative Symptoms

A 
Negative symptoms: are missing from expected behavior (i.e. decreased or loss of usual function)
-Lack of motivation
-Social withdrawal
-Flattened affect/emotion
-Cognitive disturbances
-Poor grooming
-Poor/impoverished speech 
Sometimes a better response with atypical antipsychotics.
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23
Q

How do atypicals or second generation antipsychotics work?

A

They block D2 dopamine receptors and 5HT2a serotonin receptors where their predecessors only accomplished the former

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24
Q

Subtypes of Schizophrenia (Not in the DSM5 anymore) Be aware but don’t memorize

A
  1. Undifferentiated: Most common
    Characteristics of more than one subtype
  2. Paranoid: Delusions of persecution
    Older age of onset, better functioning than other types
  3. Residual (all - sxs)
    At least one psychotic episode with subsequent negative symptoms, mild positive symptoms if any
  4. Disorganized: Onset often before age 25
    Incoherent speech, bizarre behavior (mirror gazing, facial grimacing, stereotypic movts), poor grooming, inappropriate emotional responses
  5. Catatonic: Rare since introduction of antipsychotic agents
    Stupor or extreme agitation, incoherent speech, blank facial expression, bizarre posturing, waxy flexibility
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25
Q

DSM 5 Revisions

A
  1. DSM-5 raises the symptom threshold, requiring that an individual exhibit at least two of the specified symptoms.
    -In DSM-IV, that threshold was one.
  2. Subtypes of schizophrenia are eliminated due to their limited diagnostic stability, low reliability, and poor validity.
    -Have not been shown to exhibit distinctive
    patterns of treatment response or longitudinal
    course.
    -Instead, a dimensional approach to rating
    severity for the core symptoms
26
Q

Three phases of schizophrenia (more - sxs the longer you have it)

A
  1. Three phases:
    A. Prodromal: prior to first psychotic break
    Avoidance of social activities
    Quiet and passive or irritable
    Sudden interest in religion or philosophy
    May have physical complaints
    Anxiety and depression common
    B. Psychotic/Active: loss of touch with reality
    -Associated with positive symptoms
    C. Residual: period between psychotic episodes, in touch with reality, but doesn’t behave normally
    -Negative symptoms, peculiar thinking, eccentric behavior and withdrawal from social interactions
27
Q

Etiology

A
  1. Genetics
  2. Advanced paternal age?
    - De novo mutations in paternal germ cells
  3. Gender differences
    - Occurs equally in men and women
    - Age of onset: 15-25 years in men, 25-35 years in women
    - Women respond better to antipsychotic medication
    - Greater risk of tardive dyskinesia (TD) though
    - Cumulative days of D2 receptor (dopamine) drug blockade can lead to this permanent movement disorder
    - Choreic movts
    - Athetotic movts
    - Most often oro-facially
28
Q

Environmental Factors

A
  1. Viral infection and exposure to drugs during development have been implicated in the etiology of schizophrenia
  2. Increased incidence when born in cold-weather months
    - Due to viral infections that occur seasonally?
  3. Third-trimester maternal use of diuretics
    - Severe maternal HTN requiring use of diuretics

Anti- NMDA receptor antibodies??? In adults

29
Q

Neurological Abnormalities (frontal lobe is under active)

A
  1. Abnormalities of the frontal lobes**
    - Decreased use of glucose in prefrontal cortex (hypofrontality)
  2. Lateral and third ventricle enlargement**(similar to dementia)
  3. Abnormal cerebral symmetry (loss of asymmetry) (brain doesn’t rotate)***
  4. Changes in brain density
    a. Decreased volume of hippocampus, amygdala and parahippocampal gyrus
  5. Decreased alpha waves, increased theta and delta waves and epileptiform activity on EEG (abnormal EEGs)
  6. Abnormalities in eye movements (ex. poor saccadic smooth visual pursuit)
30
Q

What part of the brain is hyperactive while hallucinations occur?

A

The Auditory Cortex

31
Q

Neurotransmitter abnormalities: Dopamine Hypothesis

A
  1. Excessive dopaminergic (DA) activity in mesolimbic tract
    - Stimulant drugs, amphetamines and cocaine, can cause psychotic symptoms by amplifying this tract/pathway
    - Negative symptoms; may involve different abnormality of dopaminergic mechanism: hypoactivity of mesocortical dopamine tract/pathway
    - Elevated levels of homovanillic acid, a metabolite of DA in bodily fluids of patients with schizophrenia suggests more DA activity and use in the central nervous system (CNS)
32
Q

Neurotransmitter abnormalities

A
  1. Serotonin (5HT) hyperactivity
    a. Hallucinogens such as LSD,
    which increase serotonin,
    cause hallucinations and
    delusions
    b. Newer atypical antipsychotics
    (ex. clozapine) have anti-5HT2A receptor activity
  2. Norepinephrine hyperactivity?
    a. Paranoid subtype may have increased metabolites
  3. Glutamate Hypothesis
    a. Glutamate (GLU) is the major excitatory neurotransmitter in the central nervous system
    b. Antagonists of NMDA subtype of GLU receptors aggravate and create psychosis (ie. Ketamine, PCP) while agonists of NMDA receptors may experimentally relieve symptoms
    c. In fact a leading hypothesis is the NMDA receptor (NMDAR) hypoactivity hypothesis
    -NMDAR proteins, if mutated become ineffective or underactive
    -If they sit on GABA interneurons positioned between a cortical GLU pyramidal neuron and its secondary neuron, a loss of inhibition occurs in the secondary GLU allowing excessive firing and ultimately an increase in firing in the VTA which sends extra DA into the limbic system thus causing psychosis
    Perhaps the DA hypothesis, is created buy the GLU hypothesis
33
Q

Differential Diagnosis

A
  1. Psychotic disorder caused by a general medical condition
    a. B12/Folate deficiency, temporal lobe epilepsy, cortico-steroid induced, etc…
  2. Manic phase of bipolar disorder
  3. Substance-induced psychotic disorder
    a. Cocaine, crystal meth, ritalin/adderall(stimulants), ketamine, PCP, LSD, bath salts
  4. Other psychotic disorders
    a. Brief psychotic disorder (1-29 days of schizophrenia symptoms)
    b. Schizophreniform disorder (1 month-6 months of symptoms)
    c. Schizoaffective disorder (schizophrenia + mania and/or depression)
    d. Delusional disorder (delusions, but no other schizophrenia symptoms)
    e. Shared psychotic disorder (one person is delusional and a second person develops same delusion)
34
Q

What is Schizoaffective Disorder?

A

Meets criteria for recurrent depression or recurrent mania much of the time BUT must have periods of >2 weeks without affective symptoms and only schizophrenia symptoms

35
Q

What is Delusional Disorder?

A

Delusions only, no other schizophrenia symptoms

36
Q

What is brief psychotic disorder?

A

Schizophrenia symptoms up to 1 month, after this the diagnosis changes to ‘schizophreniform disorder

37
Q

What is Schizophreniform disorder?

A

Schizophrenia symptoms 2 -6 months. After this the diagnosis changes to ‘schizophrenia’

38
Q

What is Schizophreniform disorder?

A

Schizophrenia symptoms 2 -6 months. After this the diagnosis changes to ‘schizophrenia’

39
Q

Medication Management

A
  1. All effective antipsychotics block D2 receptors in the hyperactive mesolimbic DA path
  2. Often a life long treatment
    a. This does not lower DA availability, but blocks neurons from excessively firing even in the face of high DA concentrations
40
Q

Dopamine Diminishing Drugs

A
  1. Synapse Depleters (a. & b. not used much anymore)
    a. Reserpine
    - Is used for hypertension, it blocks VMAT so that vesicles with monoamines cannot be released into synapses. (opposite of stimulants perhaps)
    - Less Norepi –> less depression (and less blood pressure)
    - Less Dopamine  more depression and perhaps less psychosis
    b. Tetrabenazine
    - Is used to for Huntington’s Chorea
    - By lowering DA availability (VMATi) in the synapse, choreic movements lessen
    c. D2 Receptor Antagonists (Schizophrenia meds)
    - First generation (typical) antipsychotics = FGAs
    - 2nd generation (atypical) antipsychotics = SGAs
41
Q

First generation antipsychotics (good but movement disorder SE)

A
  1. D2 receptor antagonism
  2. Non selective, occurs in all DA 4 pathways
    - Tuberoinfundibular where antagonism causes prolactinemia
    - Nigrostriatal where it causes extrapyramidal syndomes (later)
    - Mesocortical where it causes executive dysfunction, negative sx
    - Mesolimbic where it causes DA firing to lower and psychosis to lessen
  3. High Potency Agents (high affinity, clean agents)
    a. Have high affinity for D2 receptor antagonism and require only a few mg of drug to occupy 60% of D2 receptors to alleviate psychosis
    b. Very selective and have few side effects outside of those from lowering D2 activity
    c. Blocking D2 in the mesolimbic pathway alleviates psychosis by returning this pathway from high DA activity back to normal
    d. Blocking D2 activity in the nigrostriatal pathway causes abnormally low DA activity and extrapyramidal side effects (EPS to occur)
42
Q

First Gen Antipsychotics High Potency SE

A
  1. Extrapyramidal Syndromes (EPS) occur when DA activity is forced too low
    a. Akathisia = restlessness
    b. Dystonia = muscle spasm
    c. Parkinsonism= identical to Parkinson’s Disease but is reversible (tremor, rigidity, instability, bradykinesia, etc)
    d. Neuroleptic Malignant Syndrome (NMS) also called lead pipe rigidity - can kill people
    - Hyperthermia
    - Muscle rigidity
    - Vital sign instability
    - Rhabdomyolysis
43
Q

What is the treatment for neuroleptic malignant syndrome?

A
  1. Dantrolene

2. Or a D2 agonist like Pramipexole

44
Q

Blocking the Anticholinergics can cause?

A

Dopamine to come back into the nigra stratal

45
Q

What is Tardive Dyskinesia?

A

SLOW UNCOORDINATED MOVEMENTS (can develop a movement disorder, can happen with 1st and 2nd gen antipsychotics - less w 2nd)
1. Chronic D2 receptor antagonism may cause permanent movement disorder called TD
2. Choreic Movements are fast, quirky in nature
3. Athetotic Movements are slow, writhing in nature
-Pushing DA too low creates dyskinesia
-Pushing DA too high with levodopa can too
NO TREATMENT, JUST STOP DRUG

46
Q

Low Potency Antipsychotic Agents

A
  1. Have low affinity for D2 antagonism and require more mg of drug to provide antipsychotic effects
  2. They antagonize D2, but are ‘messy’ or ‘multifactorial’ as they also manipulate other receptors associated with side effects
47
Q

First Gen Antipsychotics low potency SE (

A
  1. D2 receptor antagonism –> EPS (less than high potency FGA)
  2. Histamine 1 (H1) receptor antagonism
    a. Fatigue and increased appetite/weight
  3. Anticholinergic muscarinic antagonism
    a. Dry mouth, blurred vision, constipation…
  4. Noradrenergic Alpha 1 receptor antagonism
    a. Orthostasis (faint/dizzy)
48
Q

FGA Drugs High Potency

A

Haloperidol
Fluphenazine
Thiothixine

49
Q

FGA Drugs Low Potency

A

Chlorpromazine

Thioridazine

50
Q

Second Generation Antipsychotics MOA

A
  1. D2 receptor antagonism–> improves psychosis, mania, aggression
  2. Serotonin 2a (5HT2a) antagonism–> lessens EPS risks (MUCH BETTER, less EPS, opens up nigra stratal system)
  3. In fact, this allows greater blocking of DA in the mesolimbic system, while allowing better transmission in all other DA pathways (improving selectivity compared to FGA)
    - These could be called selective antipsychotics as they block the key pathway and tend to leave other pathways as is
51
Q

SGA Drugs: The ‘Dones

A 
Risperidone
Paliperidone
Ziprasidone
Iloperidone
Lurasidone
52
Q

SGA Drugs: The ‘Pines

A 
Olanzapine
Quetiapine (XR)
Asenapine
Clozapine*** BEST*****
Antagonizes D4 and D1 receptors too
53
Q

SGA Drugs: The ‘Rips

A

Aripiprazole

-Actually is a partial agonist at D2 and D3 receptors

54
Q

DONES SE

A

Possibly more EPS (Extra pyramidal sxs)

Though all SGA have much less EPS than any FGA

55
Q

PINES SE

A
  1. More sedating due to more antihistamine activity
  2. More metabolic syndrome inducing as well
    - Weight gain
    - Abdominal girth increase
    - Hyperlipidemia
    - Hypertension
    - Hyperglucosemia
56
Q

Second Generation Antipsychotics FDA Precautions/Boxed Warnings

A

-Suicide risk in ages

57
Q

Clozapine Details

A 
Is the original ‘atypical’ antipsychotic and used for refractory schizophrenia
-Antagonizes D2 and 5HT2a
-Also antagonizes D1 and D4
Risk of agranulocytosis
Requires WBC and ANC monitoring
Most metabolic risk of any agent
Little to zero EPS/TD
GREATEST METABOLIC RISK OF DEVELOPING DM ETC
58
Q

Management: Psychotherapy

A
  1. Provide long-term support for patient and family
  2. Foster compliance with drug regimen
  3. Types of psychotherapy:
    a. Cognitive Behavioral Therapy (CBT)
    -Improve executive dysfunction
    (Memory, concentration, planning, prioritizing)
  4. Family Therapy
  5. Peer and Mentor support or social skills Group
59
Q

Drug that causes niagara falls type drooling?

A

Clozapine

60
Q

Good prognostic indicators:

A 
Female gender
Older age at onset
Married 
Have social relationships
Good employment history
Presence of mood symptoms
Presence of positive symptoms
Few relapses

Behavioral Med: Test 4 (5 decks)

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