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Medical Studies 2A > 6.3 Mental Health Disorders > Flashcards

6.3 Mental Health Disorders Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the “classic” depressive disorder?

A

Major depressive disorder (MDD). When you think depression, this is what you’re referring to.

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2
Q

What characterises Major Depressive Disorder?

A
  • Feeling low most of the time on most days
  • Not being interested in things that were once enjoyable
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3
Q

Describe the diagnostic criteria for Major Depressive Disorder

A

> 5 of the following must be present within a 2-week period, and represent a change from previous functioning:

  1. Depressed mood
  2. Markedly diminished interest or pleasure in all/almost all activities
  3. Change in weight/appetite
  4. Change in sleep
  5. Excessive/reduced movement
  6. Fatigue/loss of energy
  7. Worthlessness/excessive or inappropriate guilt
  8. Diminished concentration/decision making
  9. Recurrent suicidal ideation or suicide attempt (or thoughts of death)

These must cause clinically significant distress/impairment in important areas of life.

Cannot be attributable to medication/condition.

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4
Q

A man presents to the GP after losing his wife: loss of energy, depressed mood, high appetite, increased sleep, suicidal ideation. Should we diagnose him with Major Depressive Disorder?

A
  • Not necessarily.
  • Need to distinguish between a major depressive episode and grief.
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5
Q

Why is it incorrect to say that mental health conditions (like depression and bipolar I) are purely an additive function of genes and environment?

A

Because this neglects the influence of epigenetics.

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6
Q

Is MDD heritability thought to be monogenic or polygenic?

A

Highly polygenic.

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7
Q

First degree relatives have a _-fold increased risk of MDD. The genetic contribution is thought to be ~__%.

A
  • 3-fold risk increase
  • 35% genetic contribution
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8
Q

How does childhood adversity affect the risk, treatment and symptoms of Major Depressive Disorder?

A
  • 2-fold risk of increase
  • Increased symptom severity
  • Less responsive to treatment
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9
Q

True or false: low socioeconomic status is linked to Major Depressive Disorder

A
  • Yes
  • Money really can buy happiness
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10
Q

List three monoamine neurotransmitters

A
  • Norepinephrine
  • Serotonin
  • Dopamine
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11
Q

Outline the monoamine hypothesis of Major Depressive Disorder.

A

Low levels of monoamines (e.g. serotonin, dopamine, norepinephrine) may underlie symptoms of depression.

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12
Q

Which hypophysiotrophic hormone is often elevated in Major Depressive Disorder. More broadly, which axis is implicated in this?

A
  • Elevated Corticotropin releasing hormone
  • HPA axis
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13
Q

How is peripheral immune dysfunction linked to MDD?

A
  • Severe infection/autoimmune conditions increase risk
  • Increase levels of serum cytokines increase risk
  • Also show increased microglial activation in CNS
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14
Q

How do peripheral immune dysfunction and HPA axis dysfunction interact in the setting of Major Depressive Disorder?

A
  • They “egg each other on”
  • Both of these processes can reduce neuroplasticity by decreasing levels of brain-derived neurotrophic factor (BDNF)
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15
Q

What occurs when BDNF levels are decreased? What is the consequence of this?

A
  • Decreased dendritic branching
  • Leads to neuronal atrophy and death
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16
Q

What is the most consistent neuroanatomical finding in Major Depressive Disorder. How might cortisol play a role in this?

A
  • Decreased volume of hippocampus
  • This may be linked to increased levels of cortisol (perhaps decreasing BDNF)
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17
Q

Which area of the prefrontal cortex show decreased activity in Major Depressive Disorder?

A

Left dorsolateral prefrontal cortex (Robert Greene area). Maybe atrophy secondary to high cortisol levels.

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18
Q

What does a PET scan of the brain show?

A

Metabolic activity in different regions

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19
Q

Which brain areas are thought to show decreased/increased connectivity in the setting of Major Depressive Disorder?

A
  • Hypoconnectivity in frontoparietal network (emotional/attentional regulation)
  • Hyperconnectivity in default mode network (inward thinking/introspection; Peterson)

Super fucking interesting

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20
Q

This disorder is considered the bridge between depressive and psychotic disorders…

A

Bipolar disorder

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21
Q

Describe three classifications of Bipolar disorder

A
  • Bipolar class 1 (Manic-Major Depression)
  • Bipolar class 2 (Hypomanic-Major depression)
  • Cyclothymia (hypomanic-minor depression)
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22
Q

What is the criteria necessary for a diagnosis of Bipolar I?

A

At least one manic episode:

High energy and irritable for at least one week for most of nearly every day. At least three of the following must be present:

  1. Higher self esteem
  2. Less sleep
  3. More talkative
  4. Racing thoughts
  5. Distractability
  6. More goal-directed behaviour
  7. High risk behaviours

Like depression, needs to cause disruption to daily life, and cannot be attributed to other cause (e.g. Cheese abuse)

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23
Q

Do you need depression in order to be diagnosed with Bipolar I Disorder?

A

Nope.

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24
Q

Are men or women more likely to be depressed? How does this link to Bipolar II rates?

A
  • Women more likely to be depressed
  • Since depression dominates Bipolar II, they’re also more likely to get this
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25
Q

Describe the age peak(s) of depression

A
  • Early adulthood (coming to terms with life)
  • 60s (coming to terms with impending death)
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26
Q

At what age are people most likely to get Bipolar disorder?

A

Early 20s (that checks out)

27
Q

Does Bipolar disorder have a stronger genetic component than depression?

A
  • Yes: up to 85%, whereas depression is ~35%
  • Unlike depression, recurrent genetic trends have been found, but still polygenic
28
Q

Misuse of which drug in adolescence is thought to possibly cause bipolar disorder?

A

Cannabis

29
Q

Describe “permissive theory” of mania and depression; it’s probably oversimplistic, but even still…

A

Depression = low monamines (norepinephrine, dopamine, serotonin)

Mania = high dopamine and norepinephrine, but low serotonin

Perhaps low serotonin “permits” other molecules to define symptoms

30
Q

Describe the decreased areas of grey matter seen in bipolar disorder. What might the effects of this be?

A
  • Less in right fronto-insular cortex (important for inhibitory control)
  • Less in left anterior cingulate (important for cognition/emotions)

Less inhibition + lower cognition and lower emotional control = BAD

31
Q

Describe two changes in brain activity seen in Bipolar disorder

A
  • More activity in medial temporal lobe (e.g. hippocampus)
  • Less activity in inferior frontal gyrus (important for cognition)
32
Q

Lithium is one of the most effective drugs for treating depressive and manic episodes. How does it do this, both broadly and specifically?

A

Broadly: decreases excitability, and increases inhibition

  • Decreases glutamate
  • Increases serotonin
  • Regulates calcium efflux
33
Q

Which kinds of drugs are more useful for bipolar patients who are more manic vs more depressive

A

Manic: Antipsychotic
Depressive: antiseizure, antidepressant

34
Q

Describe the diagnostic criteria for Generalised Anxiety Disorder

A

A. Excessive anxiety and worry about many things most of the time for 6 months
B. It is difficult to control the worrying.
C. The anxiety is associated with at least 3:
1. Being restless
2. Fatigue
3. Difficulty concentrating
4. Irritability
5. Muscle tension
6. Disturbances to sleep

Need to cause significant distress in other areas of life (e.g. work, socialising etc.)

35
Q

Which gender is more likely to experience GAD? What is the most common age of onset?

A
  • Women 2x more likely
  • ~30 is common age of onset
36
Q

Does Generalised Anxiety Disorder ever completely go away?

A
  • Not usually
  • Has a relapsing course
37
Q

Outline the genetic aetiology of Generalised Anxiety Disorder

A
  • First-degree relatives 2x as likely to be diagnosed
  • ~30% heritability
  • Strong genetic link to neuroticism
38
Q

What are some environment causes of Generalised Anxiety Disorder

A
  • Childhood separation
  • Parental overprotection
  • Dysfunctional family
  • Inhibited childhood temperament
39
Q

Outline the potential role of GABA in GAD. Provide an example of an expertiment that supports this theory.

A
  • Decreased GABA may be linked with GAD (decreased inhibition)
  • Infusing GABA antagonists into amygdala can cause anxiety
40
Q

What happens to serotonin and norepinephrine in Generalised Anxiety Disorder?

A
  • Serotonin signalling interrupted
  • Norepinephrine (and NE metabolites) increased in blood and saliva in response to a stressor
41
Q

What is anxiety?

A

Shares features with:

  • Fear
  • Emotional response to a threat
  • Anticipation of a threat
42
Q

People with GAD show increased activity in the anterior cingulate cortex during decision making. This trend is most pronounced in those who reported an intolerance for…

A

Uncertainty (oops)

43
Q

Which brain regions light up in response to fearful faces, and how does this change in a patient with GAD?

A
  • Amygdala and prefrontal cortex are activated
  • Trend is more pronounced in those with GAD (even when image processing is subconscious)
44
Q

How is the waking cortisol spike (Huberman) changed in those with GAD?

A

It is more pronounced.

45
Q

Describe the feedback loop between the amygdala, the HPA axis, and the hippocampus. How is this dysregulated in GAD?

A
  • Amygdala can activate HPA axis
  • Cortisol causes atrophy of hippocampus through overactivation
  • Ordinarily, the hippocampus can inhibit the hypothalamus from releasing CRG
  • In GAD, this brake is lost
46
Q

Decreased signalling of serotonin receptors in the ____ seem to be key to anxiety symptoms. How are these receptors regulated, and how might this help explain GAD?

A
  • Forebrain receptors
  • Regulated by glucocorticods; in the setting of high cortisol release, this receptors ability to signal may be decreased
47
Q

How might benzodiazepines help to treat Generalised Anxiety Disorder?

A
  • Benzos bind to allosteric (other than GABA) site on GABA receptors
  • Increases probability that channels will stay open for longer in response to GABA
  • It is thought that increased GABAergic transmission in Amygdala may be key to efficacy
48
Q

Hallucination vs delusion

A

Hallucination: false sensory experience
Delusions: false belief

49
Q

What are the three classes of symptoms present in schizophrenia, and what do they mean?

A
  • Positive: (addition) delusions or hallucinations
  • Negative: (removal) Anhedonia, poverty of speech
  • Cognitive: (assocated) working memory and attention problems
50
Q

Which type of schizophrenia symptoms form the basis for diagnosis?

A

Positive

51
Q

Describe the diagnostic criteria for schizophrenia

A

A. Two or more present in a month, at least one is 1, 2 or 3.
1. Delusions
2. Hallucinations
3. Disorganised speech
4. Disorganised or catatonic
5. Negative symptoms

B. Level of functioning below normal

C. Symptoms present for 6 months

D. Schizoaffective disorder ruled out

E. Symptoms not due to medical condition or substance

52
Q

Schizoaffective disorder vs schizophrenia

A

Schizoaffective disorder has more prominent mood symptoms (i.e. a depressive or manic aspect).

53
Q

Are men or women more likely to have schizophrenia? What is the peak age of diagnosis?

A
  • 4x more common in men
  • Peaks in early adulthood
54
Q

Is schizophrenia heritable?

A

Yes. Highly.

55
Q

What environmental factors can lead to schizophrenia?

A
  • Higher paternal age at conception
  • Maternal vitamin D deficiency
  • Urbanicity
  • Drug abuse
56
Q

What is the apparent link between dopamine pathways and schizophrenia?

A
  • Dopamine transmission is mesolimbic pathway is overactive
  • Dopamine transmission in mesocortical pathway is underactive
57
Q

What kind of schizophrenia symptoms does dopamine dysfunction seem to cause (out of the 3 kinds)

A

Positive symptoms.

58
Q

What is an NMDA receptor?

A

Ionotropic glutamate receptor.

59
Q

How might NMDA receptor dysfunction cause schizophrenia (with reference to dopamine)?

A
  • NDMA receptor dysfunction
  • Counterintuitively, causes increased excitation of post-synaptic neuron
  • Leads to increased dopamine release, which we know is associated with the positive symptoms of schizophrenia
60
Q

Outline the disinhibition hypothesis of schizophrenia — how can decreased activation of NMDA receptors cause MORE post-synaptic firing?

A

Because the decreased receptor activation is occuring on inhibitory interneurons. Less inhibition = more firing.

This leads to greater dopamine release, and it appears that increased dopamine is associated with schizophrenia.

61
Q

What macroscopic brain changes occur during schizophrenia

A
  • Global loss of brain volume, particularly in prefrontal cortex
  • Increased ventricular volume

(I guess the brain just gets cooked a little bit)

62
Q

Maria is pregnant, and catches the flu in the first trimester of her pregnancy. What are the implications of this with regards to epilepsy?

A
  • 7-fold risk increase
  • Neuroinflammation in early brain development can drive later neurodegeneration and volume loss
63
Q

People with schizophrenia show increased midbrain activity in salience processing. Why is this notable?

A

Because misattributing salience could be the cause of hallucination.

64
Q

True or false: during auditory hallucinations, a patient with schizophrenia will only experience increased activity in their auditory cortex?

A
  • False
  • Also increased in speech processing areas

Medical Studies 2A (110 decks)

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