Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSYC 304 > CH 18: Biopsychology of Psychiatric Disorders > Flashcards

CH 18: Biopsychology of Psychiatric Disorders Flashcards

1
Q

Describe the POSITIVE symptoms of Schizophrenia & provide specific examples of each (5).

A

Positive Symptoms = symptoms that seem to represent an excess of typical function, i.e)

  1. Delusions - of being controlled, persecution
  2. Hallucinations - imaginary, critical voices
  3. Inappropriate Affect - failure to react appropriately to emotion or +/- events
  4. Disorganized Speech/thought - illogical thinking, belief in supernatural
  5. Odd Behaviour - difficulty performing everyday tasks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the NEGATIVE symptoms of Schizophrenia & provide specific examples of each (3).

A

Negative Symptoms = symptoms that seem to represent a reduction/loss of typical function, i.e.)

  1. Affective Flattening - diminished emotional expression
  2. Avolition - reduced motivation
  3. Catatonia - motionless, awkward positioning for long periods of time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the causal factors implicated in the development of Schizophrenia.

A
  • ^Genetic factor
  • Many genes linked to schizo, but no single gene causes it
  • But concordance rate of schizophrenia in monozygotic twins is «100%
  • -> Suggests a diff in experience have significant effect in development schizophrenia
  • ie) maternal stress, socioeconomic factors, childhood adversity
  • -> Alters typical course of neurodevelopment
  • -> Leads to schizo in those w/ genetic susceptibility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define ANTIPSYCHOTIC DRUG.

A
  • Meant to treat certain symptoms of schizophrenia & bipolar disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List the 2 widely prescribed antipsychotic drugs.

A
  1. Chlorpromazine

2. Reserpine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the discovery of CHLORPROMAZINE.

A
  1. Chlorpromazine:
    - 1st used as antihistamine - counteracts swelling & had calming effect on some patients
  • Antagonizes transmission at synapses by binding to dopamine receptors
  • -> Chlorpromazine = receptor blocker = binds to dopamine w/o activating it
  • Doesn’t cure schizo, but reduces severity of its symptoms
  • -> Agitated patients were calmed, & emotionally blunted patients were activated by it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the discovery of RESERPINE.

A
  1. Resperine:
    - Antagonizes transmission at synapses by depleting brain of dopamine
  • No longer used to treat schizo bc produce dangerous decline in bp & the doses needed for successful treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the similarities b/w Chlorpromazine & Reserpine (3).

A
  1. Their antipsychotic effect manifested after 2-3 weeks of meds
  2. Antipsychotic effect ass. w/ motor effects similar to PD (ie. muscular rigidity)
    - -> Suggests that both drugs act through the same mechanisms, one related to PD
  3. Both antagonize transmission at dopamine synapses - but in different ways!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the DOPAMINE THEORY OF SCHIZOPHRENIA.

A

Dopamine Theory of Schizophrenia:
= Schizophrenia is caused by too much dopamine & that antipsychotic drugs exert their effects by decreasing dopamine levels

see pg 478-479 for details

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List evidence of support for the Dopamine Theory of Schizophrenia (2).

A

Support:
1. Reserpine (antipsychotic drug) depletes dopamine in brain by breaking down the synaptic vesicles in which the NTs are stored

  1. Drugs like cocaine (which trigger schizo-like episodes) ^extracellular levels of dopamine in brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe ATYPICAL ANTIPSYCHOTICS.

A

Atypical Antipsychotics:
= Drugs effective against schizophrenia but DON’T bind strongly to D2 receptors
- Discredits dopamine theory

  • see pg 479 for details
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List 3 important notes RE: Atypical Antipsychotics

A
  1. Some D2 receptor antagonists have no antipsychotic actions
  2. Drugs that ^effects of glycerine or block effects of glutamate are proving to be effective treatments of schizophrenia
  3. There’s growing appreciation for the role of glutamatergic dysregulation in development of schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe PSYCHEDELIC DRUGS.

A

Psychedelic Drugs:
= Drugs whose primary action is to alter perception, emotion & cognition
- ie) LSD, hallucinogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the conclusions made from research on its use in human brain (2).

A
  • Study effects of psychedelic drugs in human brain
  • -> Conclusions:
    1. Effects of classic hallucinogens (ie. LSD) mimic the (+) symptoms of schizophrenia (ie. hallucinations) by acting as agonists of certain SEROTONIN receptors
  1. Dissociative hallucinogens mimic the (-) symptoms of schizophrenia by acting as antagonists of GLUTAMATE receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe research on SCHIZOPHRENIA-RELATED GENES.

A
  • Learned the important roles certain genes play in developing schizophrenia
    > ie) Various schizo-relate genes shown to:
  • Disrupt neural proliferation & migration
  • Synaptic prying during neurodevelopment
  • Myelination
  • Transmission at glutamatergic & GABAergic synapses

** Some genes that ^ susceptibility to schizophrenia are also linked to other psychiatric & neurological disorders**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe research on BRAIN STRUCTURE CHANGES ass. w/ SCHIZOPHRENIA.

A
  • Neuro-imaging techniques (ie. MRIs)
  • Hippocamps, amygdla, thalamus & nucleus accumbens = significantly smaller in schizo
  • Schizo-related V reductions develop in both grey & white matter
  • -> Consistently observed in temporal lobes
  • -> May be due to reduced neuron size & reduced dendritic & axonal arborization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

List 4 important conclusions from research on schizophrenia.

A
  1. Individuals not diagnosed w/ schizophrenia but at risk of schizophrenia (ie. bc close relative) display V reductions in some parts of brain
  2. Extensive brain changes already exist when patients 1st seek medical treatment & receive 1st brain scans
  3. Subsequent brain scans reveal that the brain changes continue to develop after initial diagnosis
  4. Alterations to different areas of brain develop at different rates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define CLINICAL DEPRESSION.

A
  • Depression that’s so severe that it’s difficult for patient to meet essential requirements of daily life
  • aka Major Depressive Disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Distinguish the difference b/w REACTIVE Depression & ENDOGENOUS Depression.

A
  • Reactive Depression = triggered via obvious (-) experience

- Endogenous Depression = triggered via no apparent cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the causal factors implicated in the development of Major Depressive Disorder (3).

A
  1. Genetic factors, experience (ie. stress, trauma)
  2. SAD = Seasonal Affective Disorder
    - Depression timed during winter months
    - -> Suggest depression triggered by reduced sunlight
  3. Peripartum Depression
    = intense sustained depression experienced by some women during pregnancy, after giving birth, or both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

List 3 major classes of antidepressant drugs.

A
  1. Monoamine Oxidase Inhibitors
  2. Tricyclic Antidepressants
  3. Selective-Monoamine-Reuptake Inhibitors
  4. Atypical Antidepressants
  5. NMDA-Receptor Antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe MONOAMINE OXIDASE INHIBITORS - include an example.

A
  1. Monoamine Oxidase Inhibitors:
    - ^levels of monoamines (ie. norepinephrine, serotonin) by inhibiting activity of monoamine oxidase (MAO)
  • Has dangerous side effect = cheese effect
  • -> ^risk of stroke bc ^bp when eat cheese
  • ie) Iproniazid = 1st antidepressant drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe TRICYCLIC ANTIDEPRESSANTS - include an example.

A
  1. Tricyclic Antidepressants:
    - Blocks re-uptake of both serotonin & norepinephrine
    - -> ^levels in brain
  • Safer alternative than MAO inhibitors
  • ie) Imipramine = 1st tricyclic antidepressant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe SELECTIVE MONOAMINE-REUPTAKE INHIBITORS.

A
  1. Selective-Monoamine-Reuptake Inhibitors:
    = Serotonin agonists
    - Exerts agonistic effects by blocking the re-uptake of serotonin from synapses
  • Fewer side effects than Tricyclics &; MAO inhibitors
  • Acts against wide range of psych disorders in add. to depression
  • ie) Fluoxetine (aka Prozact) = 1st SSRI developed
  • Similar class of drugs = SNRIs = Selective Norepinephrine Re-uptake Inhibitors
  • -> as effective as SSRIs in treating depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe ATYPICAL ANTIDEPRESSANTS - include an example.

A
  1. Atypical Antidepressants:
    - A catch-all class for antidepressant drugs that didn’t fit into the above categories
    - Each of the drugs in this class has its own unique mechanism of action
  • see pg 483 for details
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe NMDA-RECEPTOR ANTAGONISTS - include an example.

A
  1. NMDA-Receptor Antagonists:
    - Positive effects of antagonizing the glutamate NMDA receptor on depressive disorders
  • ie) Ketamine = a dissociative hallucinogen
  • -> Single dose rapidly reduces depression
  • -> Has undesirable side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the various brain differences ass. w/ Major Depressive Disorder (3).

A
  1. Consistent reductions in grey matter V in:
    - Prefrontal cortex
    - Hippocampus
    - Amygdala
    - Cingulate cortex
  2. White matter reductions in several brain regions (most in frontal cortex)
  3. Atypical activity in frontal, cingulate & insular cortices, amygdala, thalamus & striatum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

List the 2 theories of the biology of Major Depressive Disorder.

A
  1. Monoamine Theory of Depression

2. Neuroplasticity Theory of Depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the MONOAMINE Theory of Depression.

List the evidence of support (2).

A

Monamine Theory of Depression:
= Depression ass. w/ under-activity as serotonergic & noradrenergic synapses

SUPPORT:
1. Fact that MAO inhibitors, tricyclic antidepressants, SSRIs & SNRIs are all agonists of serotonin, norepinephrine, or both

  1. ^Norepinephrine & serotonin receptors in brains of dead, depressed ppl w/o pharm. treatment
    - -> Implies deficit in monoamine release
    - -> When insufficient amount of a NT is released at a synapse, there’s a compensatory ^ in the #receptors for that NT
    - -> process = ‘Up-Regulation’
30
Q

Describe the NEUROPLASTICITY Theory of Depression.

List the evidence of support (2).

A

Neuropsychology Theory of Depression:
= Depression results from decrease of neuroplastic processes in various brain structures (ie. hippocampus)
–> Leads to neuron loss & other neural pathology

SUPPORT:

  1. Research showing stress & depression ass. w/ disruption of various neuroplastic processes
    - -> ie) decrease in adult hippocampal neurogenesis
  2. Research showing antidepressant treatments ass. w/ enhancement of neuroplastic processes
    - -> ie) synthesis of neurotrophins
31
Q

List 2 forms of treatment for depression that utilize brain stimulation.

A
  1. rTMS = Repetitive Transcranial Magnetic Stimulation

2. Deep Brain Stimulation

32
Q

Describe rTMS.

A
  1. Repetitive Transcranial Magnetic Stimulation (rTMS):
    = Form of TMS that involves noninvasive delivery of repetitive magnetic pulses at either high frequency or low frequency to specific cortical areas (usually prefrontal cortex)
  • HIGH frequency rTMS = stimulate activity w/in those brain regions in which it’s applied
  • LOW frequency rTMS n= inhabit activity
33
Q

Describe Deep Brain Stimulation.

A
  1. Deep Brain Stimulation:
    = Chronic brain stimulation via implanted electrode
    - Tip implanted into area of white matter of anterior cingulate gyrus in medial prefrontal cortex
    - Effective for those who don’t respond to other treatments
34
Q

Describe HYPOMANIA.

A
  • Reduced need for sleep
  • High E
  • Positive affect
  • Talkative
  • Energetic
  • Impulsive
  • Positive
  • v confident
35
Q

Describe MANIA.

A
  • Same features as hypomania but taken to extremes

Additional symptoms:

  • Delusions of grandeur
  • Overconfidence
  • Impulsivity
  • Distractibility
36
Q

Bipolar Disorder type II = bouts of _____ & _____.

A
  • Depression & hypomania
37
Q

Bipolar Disorder type I = bouts of _____ .

A
  • Mania
38
Q

Describe the various causal factors that have been identified for bipolar disorders (1).

A
  • ^^^heritable
  • Many diff genes in bipolar disorders
  • ie) genes that code for particular Ca2+ channels & for particular proteins found at nodes of Ranvier
39
Q

Describe MOOD STABILIZERS.

A

Mood Stabilizers:
= Drugs that effectively treat depression or mania w/o ^risk of mania or depression, respectively
- Acts against bouts of mania, some act against depression, & some act against both
–> But they do NOT eliminate all symptoms
- Some have adverse side effects (ie. weight gain, tremor, blurred vision)

40
Q

Describe LITHIUM.

A

Lithium
= Simple metallic ion
= 1st drug found to act as mood stabilizer
- Found that lithium rate protected guinea pigs from toxicity of urea
- **Hypo that manic patients have lower levels of lithium than non-manic patients

41
Q

Describe the brain differences ass. w/ bipolar disorder (3).

A
  1. Reductions in grey matter V
  2. Several specific brain structures smaller in bipolar disorder patients
    - ie) medial prefrontal cortex, left anterior cingulate, L superior temporal gyrus, certain prefrontal regions, & hippocampus
  3. Atypical activation in frontal cortex, medial temporal lobe structures & basal ganglia
42
Q

Describe some of the theories of the etiology of bipolar disorders (4).

A
  1. Evidence of hypothalamic-pituitary-adrenal (HPA) axis dysregulation
  2. Marked disruptions in circadian rhythms in both patients w/ bipolar disorders & their non bipolar disorders
  3. Atlerations to GABA, glutamate & monamine neurotransmission
  4. Evidence that BDNF levels lower in bipolar patients when they’re either depressed or manic
43
Q

Define ANXIETY.

A
  • Chronic fear that persists in absence of any direct threat
44
Q

Define ANXIETY DISORDER.

A
  • Anxiety that’s so extreme & pervasive that it disrupts normal functioning.
45
Q

List 4 anxiety disorders.

A
  1. Generalized Anxiety Disorder (GAD)
  2. Specific Phobias
  3. Agoraphobia
  4. Panic Disorder
46
Q

Describe GAD.

A
  1. Generalized Anxiety Disorder:

- Stress responses & extreme feelings of anxiety & worry about a large # of different activities/events

47
Q

Describe Specific Phobias.

A
  1. Specific Phobias:

- Strong fear/anxiety about particular objects/situations

48
Q

Describe Agoraphobia.

A
  1. Agoraphobia:
    - Pathological fear of public places & open spaces
    - ^incapacitating than more specific phobia
49
Q

Describe Panic Disorder.

A
  1. Panic Disorder:
    - Recurrent rapid onset attacks of extreme fear & severe symptoms of stress (ie. choking, heart palpations, shortness of breath)
  • Panic attacks occur in some cases of GAD, specific phobia, & agoraphobia
50
Q

Describe the etiological factors that have been implicated in anxiety disorders (3).

A
  1. Anxiety disorders triggered by identifiable stressful events
  2. Anxiety focused on particular objects/situations
    - Role of experience in shaping the disorder is apparent
  3. ^^GENETIC component
    - Heritable
    - ^Concordance rates for monozygotic twins than dizygotic twins
    - -> But no specific genes yet linked
51
Q

List 3 drugs used in the treatment of anxiety disorders.

A
  1. Benzodiazepines
  2. Serotonin Agonists
  3. Antidepressant Drugs
52
Q

Describe BENZODIAZEPINES..

A
  1. Benzodiazepines:
    = Class of GABAA agonists w/ anxiolytic (anti-anxiety), sedative & anticonvulsant properties
  • Adverse side effects = sedation, tremor, nausea, withdrawal reaction that includes rebound anxiety
  • ^^Addictive
  • -> Should be prescribed for short-term use
53
Q

Describe SEROTONIN AGONISTS.

A
  1. Serotonin Agonists:
    - Selective agonist effects type of serotonin receptor
    - ^specific than benzodiazepines
    - -> Produce anxiolytic effects w/o muscle relaxation &sedation
  • Side effects = dizziness, nausea, headache, insomnia
54
Q

Describe ANTIDEPRESSANT DRUGS.

A
  1. Antidepressant Drugs:
    = Atypical antipsychotics ; anticonvulsants (some of which are effective mood stabilizers) are also effective treatments for certain anxiety disorders
  • ie) SSRIs, SNRIs, & anxiolytic drugs
55
Q

List 3 animal models of anxiety disorders.

A
  1. Elevated-Plus-Maze Test
  2. Defensive-Burying Test
  3. Risk-Assessment Test
56
Q

Describe the Elevated-Plus Maze Test.

A
  1. Elevated-Plus-Maze Test:
    - Rats placed in plus-sign-shaped maze above floor
    - -> 2 arms have sides & 2 arms don’t

–> Measure anxiety as proportion of time rats spend in enclosed arms rather than venturing into exposed arms

57
Q

Describe the Defensive-Burying Test.

A
  1. Defensive-Burying Test:
    - Rats shocked by wire-wrapped wooden dowel mounted on wall of familiar test chamber

–> Measure anxiety as amount of time rats spend spraying bedding material from floor of chamber at source of shock w/ forward thrusting movements of their head & forepaws

58
Q

Describe the Risk-Assessment Test.

A
  1. Risk-Assessment Test:
    - Rats experience single brief exposure to cat then flee to their burrows & freeze
    - -> Rats engage in variety of risk-assessment behaviours (ie. scanning surface from mouth of burrow)

–> Measure anxiety as amount of time rats spend in freezing & risk assessment

59
Q

How were the above tests validated?

A
  • Validated by demonstrating that benzodiazepines reduce the various indices of anxiety used in tests
  • -> Whereas non-anxiolytic drugs do not
60
Q

Describe research findings related to the neural bases of anxiety disorders.

A
  • Overlap in brain structures involved in Major Depressive Disorder & anxiety disorders
  • ie) prefrontal cortex, hippocampus & amygdala
  • -> But difference in patterns:
  • -> Major Depression: shrinkage of these structures
  • -> Anxiety Disorders: No significant atrophy
61
Q

Define TICS.

A
  • repetitive, stereotyped movements or vocalizations
62
Q

Describe TOURETTE’s DISORDER.

A

Tourette’s Disorder:

= Disorder of tics

63
Q

Describe the symptoms of Tourette’s Disorder.

List some common motor tics & verbal tics.

A
  • Begins in early life w/ simple motor tics (ie. eye blinking or head moving)
  • ^complex & severe symptoms as patients grows older
  • Common complex MOTOR tics = hitting, touching objects, squatting, hopping, twirling
  • Common VERBAL tics = inarticulate sounds (ie. barking), repetition of words
  • Symptoms reach peak in few years then gradually subside as patient matures
  • -> Tics are involuntary but can be temporarily suppressed w/ [ ] & effort by patient
64
Q

Describe research findings related to the neural bases of Tourette’s Disorder.

A

Tourette’s patients often have:

  • Smaller stratal volumes
  • When suppress tics, fMRI activity recorded in both prefrontal cortex ; caudate nuclei
  • -> aka decision to suppress tics comes from prefrontal cortex, which initiates the suppression by acting on the caudate nuclei
65
Q

Describe how Tourette’s Disorder is treated (3).

A
  1. Educate patient & fam about nature of syndrome
  2. Focus treatment on ancillary emotional problems (ie. anxiety & depression)
  3. Treat tics via ANTIPSYCHOTICS
    - Often refused bc adverse side effects (ie. weight gain, fatigue)
    - **Blocks tics
    - -> Hypo that disorder is related to changes in the cortical-striatal-thalamic cortical circuit bc that circuit relies heavily on dopaminergic signaling
66
Q

Describe the 3 phases of clinical trials.

A

PHASE 1: Screening for safety

  • Finds maximum safe dose
  • Used on healthy, paid volunteers

PHASE 2: Establishing the testing protocol
- Establishing most effective doses & schedules of treatment

PHASE 3: Final testing
- Clear demonstration that drug is therapeutic

67
Q

Describe the 1st controversial aspect of clinical trials.

A
  1. Requirement for double-blind design & placebo controls.
    - Sick patients wanting experimental treatment may be given placebo instead
    - -> Ineffective for some patients
68
Q

Describe the 2nd controversial aspect of clinical trials.

A
  1. The need for active placebos
    - Experimental drugs may produce side effects
    - -> Obvious to patient that they’re not in placebo group
    - -> ^Contribute to positive effects of the drug
  • Active Placebos = control drugs that have no therapeutic effect but produce side effects similar to those produced by the drug under evaluation
69
Q

Describe the 3rd controversial aspect of clinical trials.

A
  1. Length of time required
    - Patients desperately seeking new treatments are frustrated by amount of time needed for clinical trials
    - -> ie) takes long time to be approved, etc.
70
Q

Describe the 4th controversial aspect of clinical trials.

A
  1. Financial issues
    - Drug companies pay scientists, physicians, technicians, etc. $$$ in drug trials
    - -> Will suppress any (-) findings bc anxious to gain money back
    - -> Rarely profitable
71
Q

Describe the 5th controversial aspect of clinical trials.

A
  1. Targets of psychopharmacology
    - Current characteristics of psychiatric disorders are the best they can be given the existing evidence
    - -> But it’s clear that most disorders are likely clusters for disorders w/ diff patterns of ass. brain changes
    - -> Thus, effective new drugs are likely to benefit only a proportion of those patients who have been given a particular diagnosis
    - -> Thus their effectiveness might go unrecognized
72
Q

Discuss the relative effectiveness of clinical trials.

A
  • Clinical trials = most objective method devised to assess efficacy of a treatment
  • Are expensive & slow
  • -> But results are trustworthy bc trials carefully monitored/conducted

PSYC 304 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions