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PSYCH 102 > Mental Disorders > Flashcards

Mental Disorders Flashcards

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1
Q

Etiology

A

Supernatural explanations
Demonology
Biological Perspectives
Biological Cases

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2
Q

Supernatural explanations

A

Babylonians, chinese, greeks, egyptians
Wrath of god for some transgression
1700s moved asylums away from others

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3
Q

Demonology

A

Genital mutilations
Beatings
Removal of teeth
Removal of parts of the intestine
Animal blood transfusion
Venesection and leeches

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4
Q

Biological Perspectives

A

Hippocrates tried to classify disorders as imbalances in the humours
Too much black bile = depression(melancholia)
Toay mental model psychological disorcers have a biological cause

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5
Q

Biological Cases

A

Genetics
Imbalances in neurotransmitters
Brain abnormalities
Function + size

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6
Q

Environment and genes interact Diathesis-Stress model

A

Diathesis (plus)
genes/brain structure/early learning/thinking style
(plus) Stress
abuse/illness/traumatic event/change in situation
Lead to expression of a mental disorder

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7
Q

Harmful dysfunction

A

Internal mechanisms (cognition learning perception serve purpose to keep us alive)
Fear anger sadness are adaptive
When these internal mechanisms break down = dysfunction
When that dysfycntion leads to negative consequences (harmful)

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8
Q

Definition according to APA (harmful dysfuntion)

A

There are significant disturbances in thoughts, feelings, and behaviors.
The disturbances reflect some kind of biological, psychological, or
developmental dysfunction.
The disturbances lead to significant distress or disability in one’s life.
The disturbances do not reflect expected or culturally approved
responses to certain events.

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9
Q

Categories of disorders

A

Diagnostic criteria
Prevalence information
Risk factors
Predict the course of the disorder\
Suggest Treatment
Prognosis
Comorbidity
70% of people with depressive disorder also have anxiety disorder

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10
Q

DSM 1- 106 diagnoses

A

Homosexuality was classified as one
Removed in DSM 2

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11
Q

DSM 4- 297 disorders

A

OCD = anxiety idorser
Depression didn’t equal grief(bereavment)

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12
Q

DSM 5- 237

A

OCD = its own disorder
Depression from bereavement
Autistic and aspergers both put under autism spectrum disorder

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13
Q

Generalized Anxiety Disorder

A

A general worry about nothing specific
Considerable time worrying
Difficult ot control
Associated: tension headaches, nausea, shaking, grinding teeth, insomnia, fatigue, difficulty concentrating

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14
Q

Diagnostic Criteria
(GAD)

A

Excessive worry and anxiety > 6 months

Difficult to control worry

Experience 3 or more

Restlessness or feeling on edge
Easily fatigued
Difficulty concentrating or mind going blank
Irritability
Muscle tension
Sleep disturbance

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15
Q

Life time prevalence GAD

A

5.7%
Women twice as likley as Men
32.5% of healthcare workers during COVID19

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16
Q

Causes? GAD

A

Mild genetic component (15-20%)
Early traumatic experiences (childhood abuse)
Mental strategy to avoid stronger negative emotions
Family history

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17
Q

Panic Disorder

A

Consists of Panic Attacks

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18
Q

Panic Attack

A

Accelerated heartrates
Sweating
Shaking
Shortness of breat
Feeling o fChoking
Chest pain or discomfort
Nausea or abdominal stress
Feeling dizzy/lightheaded
Derealization or depersonalization
Fear of losing c ontorl or going crazy
Fear of dyimg
Paresthesias (numbing or tingling sensation)
Chills or hot flushes

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19
Q

Panic Disorder DSM-5 Diagnositc Criteria

A

Two (or more) reocurrent unexpected panic attacks within two weeks
1 month (or more) of the following
Persistent concern about having more attacks
Worryinga bout the implications of that panic attack
Significant change in behaviour
Symptoms not due to drugs/medication
“Fear of Fear”

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20
Q

Life Time Prvelance
(panic)

A

23% of pop will experience 1 panic attack
Life time prevelance of disorder 4.7%
Women > Men

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21
Q

Causes? (panic)

A

Locus coerelus (top of midbrain) (bundle of nerves)
WHERE NOREPINEPHRINe is made
Making to omuyxh norepinephrine
Modderate genetic ocmponent 43%
Classical conditioning (associate shallow bretaing witha panic attack)

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22
Q

Specific Phobia

A

Intense fesar of particular fear of a particular object or situation
- interfered with daily functioning
May or may not be aware that their fear is irrational
Difficult to control

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23
Q

Specifc Phobia - DSM 5

A

Stimulus
Persistent fear that is unreasonable / excessive
Presence / anticipated presence of the thing
Anxiety response (ie panic attack
More than 6 months
Recognition that the fear = disproportionate
Steps are taken to avoid - interferes with normal daily living

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24
Q

Lifetime prevalence (specific phobia)

A

12.5% (phobias)
1.4% (agoraphobia)
12% (social anxiety disorder)
Safety behaviours

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25
Q

Causes? (specific phobia)

A

Classical conditioning

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26
Q

Learning theories

A

Classical conditioning
Vicarious learning
- observational learning
Prepared learning
- More likely to develop phobias towards things that are not as dangerous to us
- Fear stimuli that look a certian way

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27
Q

Mood Disorders

A

Depressive Disorders
Unipolar depression
Bipolar Disorders
Bipolar depression/manic depression

28
Q

Major Depressive Disorders DSM-5

A

At least 5 or more of these things for 2 or more weeks
Depressed mood most of the time
Dramatically reduced interest or enjoyment in most activities most of the time
CORE^
Significant challenges regulating appetite and weight
Significant challenges regulating sleep
Physical agitation or lethargy
Feeling listless with or with much lessenergy
SOMATIC^
Feeling worthless or feeling unwarranted guilt
Problems in thinking, concentrating, or decision making
Thinking repetitively of detah and suicide
COGNITIVE^

29
Q

Lifetime prevelence Depressive

A

16.9%
Highly recurrent
High rate sof morbidity
Females>Males
Underdiagnosis in minority populations
Heretability
45%

30
Q

Depression and Neurotransmitters

A

Synapses
Neurotransmitetr
Big role in mood disorders

31
Q

Neurotransmitter pathing and explanation

A

Flow of information from one axon to the dendrite, with the synapse in the middle
Inside our axons, are vesicles filled with neurotransmitters
Action potential through the axon body and stimulates the vesicles, they move to the end of teh axon, then release neurotransmitters into the synapse, neurotransmitters travel across synapse and then bind to gates, receptors pick up neurotransmitters, critical mass(sodium ions) = sets off action potential, sodium ions flow into the dendrites, continuing the action potential into the dendrites
Sodium comes from the extracellular fluid

Leftover neurotransmitters?
Some get sucked up - reuptake into the axon
Some float away and are broken down
Some stay

32
Q

Excitatory neurotransmitters

A

(more likely for a signal)
Dopamine
Norepinephrine
Glutamate
Substance P

33
Q

Inhibitory neurotransmitters

A

(less liley for brain to be active)
Serotonin
GABA
Endorphins

34
Q

Depression and serotonin

A

Not enough serotonin (in the synapse)
Too few serotonin receptors
Receptors not sensitive enough to the serotonin

35
Q

Genes and Alleles

A

Same genes that make up our eyes
Different alleles that determine eye colour
Important for ion gates
Some peoples arevery effective and get all the serotonin back into the axon
Some dont
Different alleles for transpotreter gate
5 HTTLPR transporter gene
Long / short
We all have 2, will receive short or long from father and mother
People who had short-short and maltreatmentin childhood have mor elikleyhood to develop depression
The opposite for long long

36
Q

Amygdala

A

Emotional responses
Heightened amygdala responses(depression)

37
Q

Profrontal cortex

A

Downregulate amygdala
Regulation of emtions
Lower activityin prefronatl cortex (depression)

38
Q

Cognitive explanations

A

Diathesis
Our thoughts, interpretations, self evaluations, expectations
Predispose people to developing depressive disorder
Cognitive biases
Hopelessness theory
Rumination

39
Q

Bipolar Disorder

A

Manic Vs Depressive Episodes

Minimum for diagnosis
1 manic episode

40
Q

Manic Episodes

A

Extremley positive or irritable mood AND increased energy/goal-driected behaviour
Lasting more than a week (less of hospitilization is required)
Accompanied by 3 of the following
Inflated self esteem or grindiosity
Decreased need for sleep
Extremely talkative
Racing thoughts
Distractibility
Goal directed activity (socially, at work, sexually) or psychomotor agitation
Excessive engagement in risky but pleasur seeking activities

41
Q

Bipolar 2 disorder

A

Dont experience full blown mania
Hypomania
Rapid cycling - many many episodes in a year

42
Q

Life time prevelence (bipolar)

A

1-2.4%
Often combined with anxiety (70%) / substance abuse (50%) / Physical Health issues (64%)
Men = women
Misdiagnosis of minority populations
Age of onset <25
High sucdie rates, attemp: 25-50% Complete: 8-19%

43
Q

Bipolar disorder causes

A

Strong heritability 70%
Polygenetic
Pleiotropic effects - same gene involved in multiple disorders
Norepeinephrine - too much
(dopamine and serotonin hypothesis)

44
Q

Schizophrenia

Symptoms

A

At least 2 of the following (4?) for longer than 1 moth

Delusion
Hallucinations
Disorganized speech
Disorganized behaviour or catatonia (holds an uncomfortable position for prolonged period)
- First 4^ = positive symptoms (add things)
Negative symptoms (take away things)
- Ahedonia (lose enjoyment of things you enjoy)
- Flat Effect (lack of enjoyment, ie flat tone when given good news)
- Social withdrawl (pulling away)
More than 6 month prodromal (onset to full blown) or residual symptoms (tail end)
AND Impaired function (work, school, elf-care, social) (cognitive symptoms)

45
Q

Hallucinations

A

False sensory perceptions that are experiences without an external source
Visual / Auditory / Olfactory / Tactile\
Auditory most common (⅓)
Neuroimaging studies
Same area in brain as inner speech (broca’s area)
Difficulty distinguishing which is inner voice
Culture influences what we hallucinate about

46
Q

Delusions

A

False belief based on incorrect inferences about reality
Types
Persecturoy (gov agency out to get you)
Referential (news is giving me a secret message) (mundane things having a special reference or meaning towards you)
Grandiose (I am the best!)
Identity (I am Jesus, etc. Someone that I am not)
Guilt (MISSED THIS)
Control (someone trying to take info to control you, microchip!)
Though withdrawal
Though insertion

47
Q

Disorganized speech

A

Disorganized speech/thoughts
Tangentiality/loose associations
“ got mad as I was waiting in line at grocery store, i connot stand lines, i waited a long time to get my drivers lisence, driving these days in crazy”
Clanging
“I’m not trying to make noise Im trying to make sense, im not making cents anymore, i have to make dollars”
One word sound slike another word, starting someone off in another direction
Rare: word salad, neologisms
Words taken and jumbles up
Neologisms = make up words

48
Q

Lifetime Prevalence Schizophrenia

A

1%
Life expectancy 15-20 years less than general population
High rates of physical comorbidities
Lifestyle risks, eg, 70% smoke tobacco
Substance abuse
Men = Women
Lower prevalence in developinh countries
Prognosis is also better in developing countries

49
Q

Causes? (Schizophrenia)

A

Neurobiological factors
Heratabiltity
79%

50
Q

The brain (Schizophrenia)

A

Mutationson genees that deal with brain development and neurological function
Dopamine
Limbic system - hallucinations (TOO MUCH)
Frontal lobe - negative symptoms (too little
People with schizophrenia = 6x normal dopamine receptors
Loss of control of information
Hallucinations
Smaller corpus callosum
Connects brains hemispheres
Enlaarged Ventricles
Thalamus (disregulation
Regulates sleep, consciousness and sensory information
Speech area (broca’s area)
Reduced gray matter in frontal lobes
Illness of the whole brain

51
Q

Causes? (Schizophrenia)

A

Risk factors

Forst trimester is important
Influenza
Maternal Stress
Environmental stressors
Living in urban areas
Stressful family relationships
Substance Abuse
Cannabis
Using string cannabis on daily basis, increased chance of development, 5x more likely fro psychosis than rgeular use
Self medication

52
Q

Schizophrenia Summary

A

Symptomd: episode of psychosis (.>1month) involving positive and negative symptoms, longer term (>6month) mild sumptom + functional impairment
Biological factors: genetics, disregulated dopamine
Environmenta factors: stressful environments, substance use
Psuchological factors: cognitive biases

53
Q

Treatment 1 (schizophrenia)

A

75% of people who need treatment don’t get it (50% children 40% candian)
They dont think that they need it

54
Q

Barriers for schizophrenia treatment

A

Culture
Belief
Not serious
Ineffective
Stigma
Finances
Clinical availability
Transportation
The system

55
Q

Approches to Treatment
Biomedical

A

Psychotropic drugs
Attempts to help with the “dysfunction”
Typical, medications help regulate our neurotransmitters
Treat the symptom, no the cause - they are not a cure
Became popular in 1958 - antipsychotic drugs
LECTURE - ion lightbulb comparison

56
Q

Neurotransmitters and Anxiety

A

Benzodiazepines
Increase the amount of GABA around amygdala
Less likely amygdala will fire
Calming effect
Pro - fast working, very effective
Con - works too well, very addictive, tolerance and withdrawal
Selective Serotonin Reuptake Inhibitors (SSRI’s)
Inhibit reuptake of serotonin
Increase amount of serotonin in synapse
Used for anxiety and depressiom

57
Q

Neurotransmitetr sabd depression

A

Monoamine Oxidase Inhibitor
Stop the breakdown of serotonin
(blocks enzymes from breaking serotonin, norepinephrine, dopamine)
Con - manu side effects
Tricyclics:
stops reuptake if nerepinephrine / serotonin
Cons: side effects
SSRI’s
Works specifically on serotonin
Takes 2 weeks - month to start working
Reduces sex drive, eight gain, nausea, nubess
New SNRIs
Serotonin and Norepinephrine Reuptake Inhibitors

58
Q

Neurotransmitterd and Bipolar disorder

A

Mood stabilizers
Lithium - replaces sodium slowing neuron travel speed
Only works with ⅓ of patients
Help regulate how the signals travel along neuron

59
Q

Neurotransmitters and Schizophrenia

A

Dopamine
Several pathways for it to take
Limbic system, prefrontal cortex, motor cortex
Mesolymbic pathway
Disregulayion common for hallucination
Mesocortical

60
Q

Dopamine hypothesis

A

Antipsychotics - blocks dopamine, reduces positive sumptoms
Mesolymbic system
Tardive dyskinesia (flailing arm movements - no control)
Less hallucinations more ^
Atyplica antipsyvhotics - focus on negative symptoms by regulatings erotonin and dopamine pathways
Mesocortical pathway

61
Q

Psychotherapy

A

A variety of techniques used to overcome personal problems and for personal growth
Several psychotherapeutic orientation
Psychoanalysis Vs behavioural therapy, cognitive therapy, humanistic therapy

62
Q

PSYCHOTHERAPY

A

PSYCHOANALYSIS
HUMANISTIC
BEHAVIOURAL
COGNITIVE
COGNITIVE-BEHAVIOURAL

63
Q

Psychoanalysis

A

Freudian
Psychological dysfunction result of repression of childhood trauma
Need to bring trauma to light
Techniques: free Association and dream analysis
Free association
Resistance: ego’s hesitation to talk about certain topics
Therapist listens to themes in patients free speech
Dream Analysis
Write down dreams and Freud would interpret them
Psychoanalysis takes years
4 to 5 sessions per week
3 to 6 years
Transference
Strong positive or negative feelings are attached to the therapist

64
Q

Humanism

A

Current relationships
Conscious process
Opportunity for change

Carl rogers = client centered therapy
Non directive - you know you better than yourself, mirror, empathy, acceptance
Nondirective therapy - therapist does not provide feedback or advice
Person comes to their own realizations
Active listening
Aknowlegdes, restates, paraphrases, clarifies what the client is saying
Listen wth empathy and with unconditional positive regard - client doe snot feel judged

65
Q

^Insight Therapies

A

Freud: unresolved conflicts
Rogers: feelings

66
Q

Psychotherapy is not enogh

A

½ patients benefit
½ benefit from medication

Therapy AND medication give you the highest sucess

67
Q
A

PSYCH 102 (10 decks)

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