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Drug Action III > Psychoses and Bipolar (Patho) - Block 3 > Flashcards

Psychoses and Bipolar (Patho) - Block 3 Flashcards

1
Q

What is psychotic?

A

Unable to separate real from unreal experiences
* hallucinations
* Delusions

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2
Q

Psychotic diagnosis is based on ____?

A

Degree and length of symptoms

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3
Q

Types of psychotic related disorders?

A

Brief psychotic: 1 day -1 month
Schizophreniform: 1-5 months
Schizophrenia: 6 months or longer
Schizoaffective: Schizo and mood disorder
Delusional: Delusions of persecution, jealousy, being followed, erotomania, somatic delusions

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4
Q

What are the subtypes of schizo?

A
  1. Paranoid
  2. Disorganized (hebephrenic)
  3. Catatonic
  4. Undifferntiated
  5. Residual
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5
Q

Describe paranoid schizo?

A

Primarily positive sx occupied wth 1+ delusion

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6
Q

What is disorganized schiz?

A

Diorganized behavior, speech, thought
* Flatten affect or rapidly changing effect, or inappropriate emotions

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7
Q

What is catatonic schizo?

A

Striking motor behavior, hyperactivity and agitation

Or states of almost complete immobility

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8
Q

What is undiferentiated schizo?

A

Non conforming to general diagnostic criteria for schizo

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9
Q

What is residual schizo?

A

Recovery with continuing negative or mild positive sx

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10
Q

What is the characteristics of schizoid personalities?

A

Premorbid personality: introverted, withdrawn, eccentric, impulsive, paranoid, suspicious

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11
Q

What is the prodromal phase?

A

Precedes the active phase: not acting like themselves and deterioration of functioning

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12
Q

What occurs in the active psychotic phase?

A

Delusions and hhallucination

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13
Q

What is the residual phase

A

without psychotic sx, functionally impaired (sometimes), lack motivation and judgement

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14
Q

What occurs before the prodromal phase?

A

Relapses: anxiety, epression, agitation, anger, hostility, withdrawn

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15
Q

What are the phases of schizo?

A
  1. Prodrome
  2. Actve psychotic phase
  3. Residual phase
  4. Relapse
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16
Q

Chlorpromazine

Brand, ADR

A

Largactil
ADR: Parkinsonian ADR due to dopanimergic activity

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17
Q

Drug that became the benchmark of schizo treatment?

A

Chlorpromazine

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18
Q

What are the positive sx of schizo>

A
  1. Hallucinations
  2. Delusions
  3. Disordered thoughs
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19
Q

What are the negative sx of schizo?

A
  1. Lack of motivation (anhedonia, avolition)
  2. Social withdrawal (asociality)
  3. Blunted affect
  4. Impoverished speech (Alogia)
  5. Inappropriate affect
  6. Avolition (apathy)
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20
Q

What are examples of delusions?

A
  1. People spying on them
  2. Thoughts are stolen from them
  3. Thoughts are broadcasted to others
  4. Being controlled by external forces
  5. Impulses to do something
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21
Q

What is the difference between delusions and hallucinations?

A

Delusion: fa;se personal beliefs not a part of social culture
Hallucinations: Sensory experiences that don’t exist
* auditory: hearing voices
* visual: seeing things that aren’t there
* Tactile: feeling invisible fingers touching body

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22
Q

What is the most common hallucination of schizo?

A

Hearing voices

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23
Q

Differentiate disorganized speech, incoherence, and loose associations?

A

Disorganized speech: problems in organizing ideas so that others can understand them
Incoherence: hard to follow speech, inability to make connections
Loose associations: difficulty sticking to one topic

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24
Q

Differentiate blunted affect, asociality, and inappropriate effect?

A

Blunted: stimulus fails to elicit emotion
Asociality: severe impairment in social relationships, poor social skills
Inappropriate affect: rapid shift from one emotional state to other (laughing at sad stories)

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25
Q

What is avolition?

A

Lack of energy, absence of interest or care

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26
Q

What is alogia?

A

Poverty of speech and though, speech without content

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27
Q

What is anhedonia?

A

Inability to experience pleasure (not able to enjoy things)

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28
Q

What are the disadvantages of having negative sx?

A

Inability to:
1. Hold job
2. Attend school
3. Form friendships
4. Having intimacy

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29
Q

What is catatonia?

A

Motor abnormalities of schizo of repeaed gestures with peculiar movements
* Catatonic immobility: unusual postures for long periods of time
* Waxy flexibility: Place the patient’s limbs in any position, and they can maintain it fo a long period of time

30
Q

Schizo neurocgnitive impairments?

A
  1. Memory deficits
  2. Attention deficits
  3. Lack in executive functioning
  4. Lack in verbal fluency
31
Q

What is the cause of schizophrenia?

A

Neuochemical or molecular basis for schizo is unknown

32
Q

What are the causes of silent lesions or functional abs of the brain?

A

Prenatal/perinatal: Obstetrical problems and hypoxia from perinatal complications
Children: poor maternal nutrition and birth in winter or early spring months

32
Q

What is the neurodevelopmental model?

A

Implies the presence of silent lesin or functional abnormalities in the brain
* lesions occur long before the onset of psychotic symptoms and generally do not interfere with the basic brain function or development in the early years

33
Q

What are the structural problems of the schizo brain?

A
  1. Enlarged ventricles
  2. Temporal lobe atrophy (reduced volume of the amygdala and hippocampus)
  3. Abnormal migration and development of the hippocampus
  4. Prefrontal and frontal cortical atrophy
  5. Reduced volume of the basal ganglia
  6. Reduced neurons in the mediodorsal thalamus
  7. Grey matter loss in parietal lobe
34
Q

Many behaviors disrupted in schizo are governed by what?

A

Prefrontal cortex (speech, decision making, affect)

35
Q

How does cortical connection differ in schizo?

A
  1. Samller soma
  2. Decreased spine density
  3. Decreased dendritic length
  4. Decreased presynaptic terminal
36
Q

What are the neurotransmitter abnormalities associated with Schizo?

A

Dopamie, seratonin, GABA, glutamate

37
Q

What is the most prominent theory related to abnormal dopamine reg in schizo brain?

A

Dopamine hypothesis

38
Q

What is the dopamine hypothesis?

A

Increased (hyperactivity) subcortical dopamine activity: increased D2 receptors
Decreased (hypoactivity) prefrontal cortical dopamine activity: stimulationof D1 receptors

39
Q

What are your dopamininergic pathways?

A
  1. Nigrostriatal
  2. Mesolimbic (+ sx)
  3. Mesocortical (- sx)
  4. Tuberoinfundibular: regulates prolactin
40
Q

Describe the mesolimbic system?

A
  1. Dopaminergic neurons originating in the ventral tegmental area (VTA) and terminating in the nucleus accumbens (NAc), amygdala, and hippocampus.
  2. Influences limbic cognitive function and behavior
  3. Hyperactivity -> + sx
41
Q

Describe the mesocortical system?

A
  1. Dopaminergic neurons originating in the ventral tegmental area (VTA) and terminating in the prefrontal cortex influencing cognitve processing.
  2. Hypoactivity -> - sx
  3. Hyperactivity -> psychomotor agitation (with amphetamines)
42
Q

What is the purpose for mesocortical system?

A

Provides negative feedback loop to mesolimbic pathways in the nucleus accumbens

43
Q

Describe the mechanism of the tuberoinfundibular pathway?

A

Short neurons running from the arcuate nucleus of the hypothalamus to the pituitary:
1. Inhibits prolactin secretion
2. Blockade of D2 recepotrs can increas secretion
* Lactation, galactorrhea, amenorrhea in females
* Gynocomastia and impotence in males

44
Q

What is the use of antipsychotics for schizo?

A

Blocks D2 receptors to reduce positive sx

45
Q

What is the hypofrontality theory?

A

Normally the prefrontal cortex feeds back to the limbic system to inhibit the N. Accumbens
Hyperactivity of limbic, hypoactivity of cortical in schizo patients

46
Q

What is the NMDAR hypofunction hypothesis?

A

Based on the induction of psychosis and negative sx by NMDA receptor glutamatergic noncompetivie antagonists (ketamine, phencyclidine)

47
Q

ADR of noncompetitive NMDA antagonist?

A
  1. Auditory hallucinations
  2. Depersonalization
  3. Delusions

Exacerbates schizo

48
Q

What are the outcomes of NMDAR hypofunction?

A

Leads to disinhibition of fast spiking parvalbumin GABAergiv interneuorns in cortex
* Glutamate also interacts with dopaminergic and GABAergic neurotrasmission

49
Q

What is the seratonin involvement of schizo?

A

LSD and other hallucinogenic drugs target 5HT2A and 5HT2C receptors
* serotonergic receptor binding profile of atypical antipsychotics, which block 5HT2A receptors with high affinity
* Serotonin modulates dopaminergic, glutamatergic, cholinergic, noradrenergic and GABAergic neurotransmitter systems in the CNS
* Serotonin 5HT2 receptors modulateDA release in the limbic system

50
Q

What is postmortem studies in schizo?

A

Increased 5-HT transporte density in subcortical regions

51
Q

What is agoinsit challenge studies?

A

Admi of mCPP (5HT agonist): exacerbates sx in unmedicated schizos

52
Q

Describe GABA neurotransmission in schizo?

A

GABA is found in prefrontal cortex, Lower levels of GABA in schizo
* Reduced density of neurons positive for GAD (marker for GABA neurons)

53
Q

Ach and schizo?

A

Decreases in muscarinic (M1 and M4) and nicotinic receptor (α4β2 and α7 subtypes) numbers are observed in schizophrenic patients

54
Q

What is unipolar depression?

A

Serious mood disorder that consists of unremitting depression or period of (no mania)

55
Q

What is bipolar disorder?

A

Depression that alternates to mania

56
Q

What is a manic episodes?

A

Mood disturbances characterized by elation, irritability, expansiveness

57
Q

What is hypomania?

A

marked elevated and expansive mood where sx are not severe enough to cause impairment in functioning
* Less severe than mania, ≥4days, no hallucinatiosn or delusions

58
Q

What is mania?

A

Abnormally, persistently elevated, expansive mood for >1 week, may include hallucinations and/or delusions

59
Q

What is major depression?

A

low mood, sadness, decreased interest or decreased activity > 2 weeks
* altered appetite
* Altered sleep
* Suicidal ideation

60
Q

What are mixed episodes?

A

Cycling between manic and depressive stages every day for at least a week

61
Q

What is the cause of biopolar?

A

Largely unknown:
1. Dysregulation of neurotransmitters (increased NE, DOPA, 5-HT in mania, and decreased in depression)
2. Dysfunction in ion distribution (increase Ca2+ in mania, decreased in depression)
3. Dysregulation of transport / transduction systems (NAK ATPase, cAMP, G proteins)
4. Neuroendocrine dysregulation (hypothyroidism in depression, hyperthyroidism in mania)
5. Genetic mutation

62
Q

Most common sx of bipolar?

A

Depressed mood/hopelessness
Mania/hyperactivity

63
Q

Target sx of major depression?

A
  1. Sleep disturbances
  2. Decreased enerfgy
  3. Psychomotor retardation
  4. Anhedonia
  5. Poverty of speech
  6. Carb craving
  7. Weight gain
64
Q

Target sx of mania?

A
  1. Euphoria
  2. Grandiosity
  3. Flight of ideas
  4. Delusions/hallucinations
  5. Pressured speech
  6. Imparied judgement
  7. Poor social functioning
65
Q

Sx of hypomania?

A
  1. Happy
  2. Creative
  3. Funny
  4. Productive
66
Q

Sx of cyclthymia?

A
  1. Hypomania
  2. Mild depression
67
Q

What is the difference between bipolar 1 and 2

A

1: >1 Manic or mixed episodes and major depression
* Female = males
* : Changes in sleep/wake cycle; sleep deprivation
* 20-30% dont recover between episode

2: Hypomania + mjor depression
* Female > males
* 15% dont recover between episodes

68
Q

What is cyclothymic disoder?

A

Hypomania and depressive sx (not major depression) for ≥ 2 years

69
Q

Bipolar Disorder Not Otherwise Specified?

A

Bipolar that doesn’t fulfill the criteria for any other bipolar disorder

Drug Action III (23 decks)

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