Final - Psychopathology Flashcards

1
Q

Schizophrenia

Statistics

A

Afflicts ~ 0.8% of the population.

Age of onset ~ 19.2 years

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2
Q

Positive Symptoms of Schizophrenia

A
  • Hallucinations
  • Delusions
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3
Q

Hallucinations

A

Positive symptom of schizophrenia.

  • Auditory (hearing things that aren’t really there) is the most common, followed by somatosensory (e.g., bugs crawling on skin) and olfactory.
  • Visual hallucinations are rare.
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4
Q

Delusions

A
  • A fixed false belief.
  • Grandeur
  • Paranoid (“out to get me”)
  • Religiousity

Religiousity and paranoia make SZ very hard to treat because patients won’t trust advice.

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5
Q

Negative Symptoms of Schizophrenia

A

Negative symptoms are the first to appear but are hard to recognize.

  • Flat affect
  • Anhedonia (inability to experience joy)
  • Social withdrawal
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6
Q

Theories of Schizophrenia

A
  • Genetic
  • Dopamine
  • Seasonality/2nd Trimester Hypothesis
  • Brain Damage/Abnormalities
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7
Q

MZ twins are _______ times as likely to be concordant for SZ than DZ twins.

A

4

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8
Q

MZ Twin

A

“Identical.”

One egg travels down falopian tube and upon fertilization, splits into 2.

Twins from the same egg are therefore 100% genetically identical.

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9
Q

DZ Twin

A

“Fraternal.”

2 eggs travel down falopian tube and are fertilized.

Share 50% genetic similarity (same amount as a normal sibling).

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10
Q

What are the rates of SZ for a child of a SZ parent and a child of the non-SZ parent who have MZ twin grandparents who are concordant for SZ?

A
  • Offspring of parent with SZ = 16.8% have SZ
  • Offspring of non-SZ parent = 17.2% have SZ

BOTTOM LINE = You’re just as likely to be SZ if your MZ twin grandparents both have SZ regardless of whether your parent had SZ.

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11
Q

SZ Candidate Gene

A

DISC-1

(Disrupted in Schizophrenia 1)

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12
Q

DISC-1

A
  • Gene that codes for a protein that is involved in neurite outgrowth and neuronal growth.
  • The DISC-1 aberration was present in a family with a high incidence of SZ.
  • If take neuronal cells and grow them in a dish and knock-out the DISC-1 proten, the neurons won’t spread their “arms”.
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13
Q

Support for the Dopamine Hypothesis of SZ

A
  1. If you block D2 receptors, the positive symptoms of SZ will be decreased.
    * Thorzine, Haldol (anti-psychotics)
  2. If you give a DA agonist to a SZ, their symptoms will become much worse.
    * E.g., amphetamine, cocaine
  3. DA agonists can mimic the SX of SZ in normal, healthy human populations.
    * In a 1972 experiment, experimenters gave 10mg of meth round the clock for 5 days straight to normal volunteers. Had to stop study early b/c participants had full-blown SZ-like symptoms.
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14
Q

Meth Use for _______ days straight invokes SZ like positive symptoms

A

3

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15
Q

DA Pathways

A
  1. Nigrostriatal Pathway [SN–>Striatum (part of basal ganglia that has to do with movement)]
  2. Mesolimbic Pathway/Median Forebrain Bundle (MFB) [VTA–>Limbic System (NaC, Amygdala, Anterior cingulate)].

The MFB is implicated in SZ and can view positive symptoms as dysfunction of emotion/limbic system.

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16
Q

NaC

A

Pleasure/Reinforcement

Bottom of frontal lobe above lateral sulcus

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17
Q

Amygdala

A

Fear, Anger (paranoia)

Temporal lobe

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18
Q

Anterior Cingulate

A

Plays a key role in thought processes and how emotions drive behavior.

Above CC.

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19
Q

4 Characteristics of Atypical Antipsychotics

&

An Example

A
  1. Block D4 receptors instead of D2 receptors.
  2. No EPS (“extrapyramidal symptoms”) (movement problems)
  3. Capable of treating patients who are “treatment refractory” (= failed on at least 3 typical anti-psychotics).
  4. Help alleviate negative symptoms.

Ex. Clozapine

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20
Q

DA Receptors & Antipsychotics

A

DA receptors range from D1-D5.

  • Striatum = Primarily D2 receptors
    • Haldol, Thorazine
    • Parkinsonian-Like Symptoms
  • Limbic System = Primarily D4 receptors (want to block these receptors to mitigate positive symptoms). No parkinsonian-like symptoms.
    • Clozapine
      • Must get weekly blood tests to monitor WBC count (some ppl will develop agranuloytosis (no immune cells)
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21
Q

Seasonality/2nd Trimester Hypothesis of SZ

A

Based on fact that a majority of SZs are born in the Spring. Mother would be in the height of the flu season in 2nd trimester.

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22
Q

Neurodevelopment During 2nd Trimester

A

Neural stem cells are (1) proliferating, (2) migrating and (3) differentiating.

If a flu virus disrupts this process, a “disorganized pattern later results in disorganized thoughts.” If examine the brains of SZs, there won’t be neatly formed layers because as the neural stem cells climb the radial glia guide cells, they get stuck and the traffic jam will result in cells jumping off at whatever layer they can.

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23
Q

Hypofrontality & SZ

A

Hypofrontality is decreased function in the frontal lobe. SZs typically exhibit hypofrontality and have difficulty with sorting tasks and switching tasks/gears.

Ex. Wisconsin Card Sorting Test, Raven’s Progressive Matrices/Patterns Test.

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24
Q

MZ Twin Study: SZ Rates in MZ Twins That Are Monochorionic vs Dichorionic

A
  • Monochorionic = Share placental sack
    • 60% concordant for SZ
  • Dichorionic = Individual placental sacks
    • 17% concordant for SZ

Some viruses may only pass through one placental sack.

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25
Q

Brain Damage/Abnormalities in SZ

A
  1. Enlarged Ventricles
  2. Hypofrontality
  3. Don’t have too much DA.
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26
Q

Enlarged Ventricles & Schizophrenia

A
  • Enlarged ventricles can be caused by a shrinking of the structures next to the ventricles (e.g., brain tissue, caudate, cingulate gyrus, hippocampus).
  • Enlarged ventricles can also be caused by hydrocephaly (fluid on brain). If have too much CSF, the structures of the brain can start separating.
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27
Q

Do SZs have too much DA?

A

NO.

Studies show that they have too many receptors byt it’s hard to believe these studies because they’re usually done on SZs who have taken anti-psychotics already (which can cause receptors to up-regulate or down-regulate).

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28
Q

Depression Stats

A

50% of the population will experience depression at some point in their lifetime.

29
Q

Support for the Monoamine Hypothesis of Depression

A
  1. Agonists (drugs in the catecholamine and indolamine pathways) provide relief
  2. Antagonization (blocking) of monamines leads to worsened symptoms.
    1. Can block anywhere along the indolamine pathway (e.g., block l-tryptophan with a diet low in amino acids).
30
Q

5 Depression Treatments

A
  1. Psychopharmacology
  2. Light Therapy
  3. Sleep Deprivation
  4. ECT
  5. Talk Therapy
31
Q

Light Therapy

A

Resets circadian rhythms. When awake, people’s brain waves are in alpha waves (highest). Don’t want people walking around in theta waves.

Effective treatment for SAD (a disorder caused by disruption of circadian rhythms).

32
Q

Sleep Deprivation

A

If a person sleeps too much, they are releasing melatonin all the time and the brain is in a sedated state.

33
Q

ECT

A
  • Works when medication doesn’t
  • Single most effective treatment
  • Side effect = memory loss.
  • Short, effective, but results are not long-lived (usually wear off b/w 1-2 years).
  • Memory loss seems to occur b/w 3-6 treatments which is also when depression symptoms start to be alleviated (memory loss can take away ruminating thoughts).
34
Q

Bipolar: What Mood Do Ppl Normally Find Themselves In?

A

Depressed state

35
Q

Frequency of Manic Episodes

A
  • Usually occurs 1x every 2 years.
  • Can be induced by lack of sleep.
  • In height of manic episode, have SZ-like statements (psychosis).
36
Q

Bad Treatments for People with Bipolar

A
  • Sleep deprivation
  • Drugs that are agonists of NE (e.g., MAOI inhibitors)
37
Q

Potential Causes of Bipolar

A
  • Dysregulation of circadian rhythms (problem in SCN)
  • Genetics
  • Abnormality of locus ceureleus & release of NE
38
Q

3 Categories of SZ Symptoms

A
  1. Positive
  2. Negative
  3. Cognitive
39
Q

Positive Symptoms of SZ

A
  1. Thought disorders (disorganized, irrational thinking)
  2. Hallucinations (auditory, olfactory)
  3. Delusions (persecution, grandeur, control)
40
Q

Most common form of hallucination?

A

Auditory

41
Q

Negative Symptoms of SZ

A

Absence or diminution of normal behaviors.

  1. Flattened emotional response
  2. Poverty of speech
  3. Lack of initiative and persistence
  4. Anhedonia (inability to experience pleasure)
  5. Social withdrawal
42
Q

Cognitive Symptoms of SZ

A
  1. Difficulty in sustaining attention
  2. Low psychomotor speed
  3. Deficits in learning and memory
  4. Poor abstract thinking
  5. Poor problem solving
43
Q

How long does it usually take symptoms of SZ to appear?

A

Appear slowly over period of 3-5 years.

Negative symptoms are the first to appear, followed by cognitive symptoms.

44
Q

DISC-1

A

Involved in regulation of embryonic and adult neurogenesis, neuronal migration during embryonic development, function of the postsynaptic density in excitatory neurons and function of mitochondria.

45
Q

Mutation of DISC-1

A

Mutation of the DISC-1 gene have been found in some families with a high incidence of SZ.

Mutation appears to increase the likelihood of SZ by a factor of 50.

46
Q

SZ and Effect of Paternal Age

A
  • Children of older fathers more likely to develop SZ. Caused by mutations in spermatocytes.
47
Q

Epigenetic

A

“On Top of the Genes”

Mechanisms that control the expression of genes.

48
Q

Chlorpromazine

A

A first generation antipsychotic drug.

DA receptor blocker.

Eliminated/diminished positive symptoms.

Block D2 and D3 receptors.

49
Q

Which DA Pathway Is Implicated in SZ?

A

Mesolimbic (MFB)

  • Begins in VTA and ends in NaC and amygdala.
50
Q

DA Agonists That Produce Positive Symptoms of SZ

A
  • Amphetamine, cocaine, and methylphenidate (block re-uptake of DA)
  • L-DOPA (stimulates synthesis of DA).
  • Symptoms can be alleviated with anti-psychotics.
51
Q

Amphetamine Injections in normal controls vs SZ patients

A
  • Amphetamine caused the release of more DA in the striatum of SZ patients than in normal subjects.
52
Q

Tardive Dyskinesia

A

A movement disorder that can occur after prolonged treatment with antipsychotic medication, characterized by involuntary movements of the face and neck.

Explained by phenomenon of supersensitivity.

53
Q

Supersensitivity

A

The increased sensitivity of NT receptors; caused by damage to afferent axons or long-term blockage of NT release.

A compensatory mechanism in which some types of receptors become more sensitive if they are inhibited for a period of time by a drug that blocks them. When D2 receptors are chronically blocked, they become supersensitive (which in some cases overcompensates for effects of the drugs).

54
Q

Clozapine

A

An atypical antipsychotic drug; blocks D4 receptors in the NaC.

In monkeys, causes decrease in the release of DA by the mesolimbic system (reduces positive symptoms) and also causes an increase in the release of DA in the PFC (which reduces negative and cognitive symptoms).

55
Q

MZ Twins Discordant for SZ: Brain Abnormalities

A
  • SZ: Larger lateral and 3rd ventricles, smaller anterior hippocampus, total volume of gray matter in left temporal lobe reduced.
56
Q

Hypofrontality

A

Decreased activity of the PFC; believed to be responsible for the negative symptoms of SZ.

***dlPFC

57
Q

PCP & Ketamine

A

Elicit full range of SZ symptoms. The negative and cognitive symptoms produced by the drugs are caused by a decrease in the metabolic activity of the frontal lobes.

Both are indirect antagonists of NMDA receptors (which inhibits activity of dlPFC) and both decrease the level of DA utilization in the dlPFC.

58
Q

What’s unique about atypical antipsychotics?

A

They increase DA activity in the PFC and reduce it in the mesolimbic system.

59
Q

Partial Agonist

A

Ex. Aripiprazole

A drug that has a very high affinity for a particular receptor but activates that receptor less than the normal ligand does; serves as an agonist in regions of low concentration of the normal ligand and as an antagonist in regions of high concentration.

60
Q

Monoamine Oxidase (MAO) Inhibitors

A
  • MAO destroys excess monoamine transmitter substances within terminal buttons.
  • Drug increases the release of DA, norepinephrine, and 5-HT.

Monoamine agonists.

61
Q

Tricyclic Antidepressant

A

A class of drugs used to treat depression; inhibits the reuptake of NE and 5-HT but also affects other NTs; named for molecular structure.

Monoaminergic Agonist

62
Q

SNRI

A

Specifically inhibits the reuptake of NE and 5-HT w/o affecting reuptake of other NTs.

63
Q

Monoamine Hypothesis of Depression

A

Depression is caused by a low level of activity of one or more monoaminergic synapses.

Focus is on NE and 5-HT

Monoamine antagonists can produce the symptoms of depression and agonists can reduce them.

64
Q

Tryptophan Depletion Procedure

A

Used to study the role of 5-HT in depression.

A procedure involving a low-tryptophan diet and a tryptophan-free amino acide “cocktail” that lowers brain tryptophan and consequently decreases the synthesis of 5-HT (and therefore impacts mood in depressed patients).

65
Q

5-HT Transporter

A

Stressful life experiences increase the likelihood of depression in people with one or two short alleles of the 5-HT transporter promoter gene, and a better response to antidepressant treatment is seen in depressed people with 2 long alleles.

66
Q

Where can neurogenesis occur?

Neurogenesis & Depression?

A

Dentate gyrus (region of hippocampus).

Stressful experiences that produce the symptoms of depression suppress hippocampal neurogenesis and the administration of antidepressant treatments, including MAO inhibitors, tricyclic antidepressants, SSRIs, ECT and lithium, increase neurogenesis.

67
Q

Characteristic Sleep of People with Depression

A

Shallow, fragmented

Slow-Wave delta sleep (stages 3 and 4) is reduced and stage 1 is increased.

REM occurs earlier, the first half of the night contains a higher proportion of REM periods and REM sleep contains an increased number of rapid eye movements.

68
Q

Drugs that block the reuptake of NE and 5-HT

A

Tricyclic antidepressants

SSRIs

SNRIs