Depression and Bipolar Flashcards
1
Q
Mood Disorders
A
- Known as affective disorders
- Primarly disorders of mood rather than thought
- Two key emotions on the continuum: depression and mania
- Unipolar depression: only depression
- Bipolar disorder: mania that alternate with periods of depression
2
Q
Depression Prevalence
A
- 17% of adults experience depression (women more than men)
- Approx 50% of ppl will recover in 6 weeks and 90% within a year
3
Q
Suicide
A
- Between 6 and 15% of those with severe depression commit suicide
- Over 1 million people commit suicide each year
- Senior citizens have the highest rate of suicide of all age groups
4
Q
Depression: 5 main areas of functioning
A
- Emotional symptoms: feeling miserable, empty, lack of pleasure
- Motivational symptoms: lacking drive, initiative, spontaneity
- Behavioural symptoms: less active, productive, loss/gain appetite, sleep disturbances
- Cognitive symptoms: hold negative view of themselves, pessimism
- Physical symptoms: headaches, general ache and pain
5
Q
Diagnosing Unipolar Depression
A
- DSM-IV Criteria for Major Depressive Disorder
Criteria 1: Major depressive episode - Marked by 5 or more symptoms eg depresison mood or irritable, change in sleep/activity
- Present nearly everyday lasting two or more weeks
Criteria 2: NO history of mania
6
Q
Cause of Depression: Biopsychosocial Model
A
- Psychological
- Biological
- Social
7
Q
Causes of Depression: genetic factors
A
- Studies suggest some people have inherit a biological predisposition
- AS many as 20% of relatives of those with depression also have depression themselves, compared to less than 10% of the general population
- Twin studies demostrate a strong genetic component (concordance rates for identical twins = 46%)
- May be tied to specific genes eg. 5-HT transporter gene
8
Q
Causes of Depression: brain anatomy
A
Brain anatomy and circuits
- Researchers have determined that emotional reactions of various kinds are tied to brain circuits
- circuit responsible for unipolar depression has begun to emerge
- likely areas involved include: perfrontal cortex, hippocampus, amydala, subgenual cingulate, brain steam
9
Q
Causes of Depression: Biochemical factors
A
- clinical depression is associated with neurochemical alterations in the brain
- main biological theory of depression is the monoamine hypothesis first proposed in 1965
- Endocrine system/hormone release: people with depression have been found to have abnormal levels of cortisol
- People with depression have been found to have abnormal melatonin secretion (difficult sleeping)
10
Q
Monoamine Hypothesis
A
- Monoamines: include 5-HT, dopamine, NA and A
- Depression is associated with a deficiency in the neurotransmitters NA and 5HT
- Seratonin is more assoicated with mood
- NA is more associated with motor activity
11
Q
Evidence for Monoamine Hypothesis
A
- many drugs that enhance the activity of NA and seratonin will elevated mood (and conversely, drugs that decrease the activity of NA or 5HT will depress mood)
- Genetic studies linking 5HT transporter gene
12
Q
Evidence against Monoamine Hypothesis
A
- Studies aiming to show changes in monoamine pathway activity are largely negative
- Amphetamines and cocaine do not have an antidepressant effect
- Antidepressant medications boost monoamine levels immediately but therapeutic effect is delayed by weeks
13
Q
Antidepressant Drugs
A
- Main types:
- MAO Inhibitors: increases cytosolic stores of NA or 5HT
- Monoamine (NA and 5HT) reuptake inhibitors: tricyclic antidepressants (first generation) and SSRIs (second generation)
14
Q
Monoamine Oxidase (MAO) Inhibitors
A
- Slows down the body’s production of MAO
- MAO breaks down monoamines
- MAO inhibi stop this breakdown from occuring
- This leads to a rise in NA activity
- About half of patients who take these drugs are helped by them
- SE: blood pressure may rise to a potentially fatal level is one eats food with tyramine (cheese, banana and wine) while take MAOIs
15
Q
Tricyclics
A
- Tricyclics block the reuptake process, thus increasing NT activity in the synapse
Strong evidence: - 60-65% of patients find symptom improvement
16
Q
Second-generation Antidepressants
A
- SSRIs: structurally diff from MAOI and tricyclics
- Only act on 5HT
- as effective as tricyclics but clinicians prefer because it is harder to overdose and there are no dietary restrictions and fewer side effects
17
Q
Schizophrenia
A
- ‘Split mind’ - actually refers to a split from reality
- Schizophrenia spectrum disorders
- Characterised by disorganised thinking, emotions and behaviours that are disparate with their situations
- Disturbed perceptions, including delusions and hallucinations
18
Q
Pschyosis
A
- A state defined by a loss of contact with reality
- the ability to perceive and respond to the environment is significantly disturbed; functioning is impaired
- Symptoms may include hallucinations and/or delusions
- Psychosis may be substance-induced or caused by brain injury, but most appear in the form of schizophrenia
19
Q
Schizophrenia: Symptoms
A
Three categories:
- Positive symptoms
- pathological additions to a person’s behaviour e.g. delusions, hallucinations, disordered thinking - Negative symptoms
- pathological deficits to a person’s behaviour e.g. blunted/flat affect, loss of volition, social withdrawal - Psychomotor/disorganised symptoms:
- awkward movements, repeated grimaces, add gestures ( can be extreme = catatonia)
- Disorganised speech
20
Q
Course of Schizophrenia
A
Three phases:
- Prodromal: beginning of deterioration, mild symptoms
- Active: symptoms become increasingly apparent
- Residual: a return to prodromal levels, 1/4 recover, 3/4 continue to have residual symptoms
21
Q
Diagnosis: Schizophrenia
A
- DSM-IV
- Symptoms persist for 6+ months
- Type I: dominated by positive symptoms (may be more closely linked to biochemical abnormalities in the brain)
- Type II: dominated by negative symptoms (may be tied to structural abnormalities in the brain)
22
Q
What causes Schizophrenia
A
Biological View:
- Diathesis-Stress Model:
- Combination of biological and genetic vulnerabilities (diathesis) and environmental stress (stress) that both contribute to the onset of Schizophrenia - Biological Vulnerabilities
- Genetic factors
- Brain abnormailities
- Biochemical abnormalities
23
Q
Schizophrenia: genetic factors
A
- Family pedigree studies: Schizophrenia is more common among relatives of people with the disorder
- first degree relatives = 10%
24
Q
Schizophrenia: Brain structure
A
Abnormal brain structure
- radiological evidence- enlarged ventricles
- Smaller temporal lobes and abnormal BF to certain areas of brain
- Overactivity of thalamus and amygdala
25
Q
Schizophrenia: Biochemical abnormalities
A
Dopamine Hypothesis
- theory attricutes symptoms of Schizophrenia to disturbed and hyperactive dopaminergic signal transduction
- certain dopamine neurons fire too often
- particularly common in type I
26
Q
Dopamine Hypothesis evidence
A
FOR:
- antipsychotic medications which acts as antagonists of DA D2 receptors
- Extra DA receptors have been noted in the brains of Schizophrenia patients
- PD patients can develop Schizophrenia symptoms if they take too much L-Dopa
AGAINST:
- atypical antipsychotics also bind to D1 and 5HT receptors
- only seems to explain type I Schizophrenia
27
Q
Schizophrenia: Treatments
A
- Primarily antagonists of DA D2 receptor
- reduces symptoms in 65% of patients
- produce the maximal level of improvement in the first 6 months of treatment
28
Q
Antipsychotic Drugs: SEs
A
- disturbing movement problems: most common is similar to PD eg. tremour and muscle rigidity
- Tardive dyskinesia
29
Q
Bipolar: Diagnosis
A
- Criteria 1: manic episode (3 or more symptoms of mania lasting one week or more)
- criteria 2: history of mania - if currently experiencing hypomania or depression
Types:
1. Bipolar I disorder: full manic and major depressive episodes
2. Bipolar II disorder: hypomanic episodes and major depressive episodes
30
Q
Causes of Bipolar
A
- genetic factors
- brain structure abnormalities
- ion transport abnormalities
- biochemical abnormalities
31
Q
Bipolar: genetic
A
- children of a bipolar parents face 8-25% chance
- a number of SNPs and genes have been associated with increased risk of bipolar eg. CACNA1C
32
Q
Bipolar: brain structure
A
- Basal ganglia and cerebellum
33
Q
Bipolar: ion transport
A
- may cause neurons to fire too easily (mania) or too stubbornly (depression)
34
Q
Bipolar: NTs
A
Permissive theory:
- Low 5HT may ‘open the door’ to a mood disorder and permit NA to define the particular form the disorder will take
- low 5HT + low NA = depression
- low 5HT + high NA = mania
35
Q
Bipolar: treatments
A
- lithium and other mood stabilisers
