Mood Disorders II

Question 1

Depressive episode diagnostic criteria

Answer 1

Question 2

Associations w/ development of depression

Answer 2

• Depression may follow CVA (post-stroke depression)
• Depression may follow MI (post-MI depression)
• Cancer patients at >3-4x risk for depression

Question 3

Screening for depression

Answer 3

PHQ-2 and PHQ-9 are used to screen patients

Question 4

Summary of depression pharmacology

Answer 4

Question 5

Persistent Depressive Disorder (including Dysthymia)

Answer 5

Question 6

Manic episode diagnostic criteria

Answer 6

Question 7

Hyponamnic episode diagnostic criteria

Answer 7

Question 8

Differential for mania

Answer 8

Question 9

Types of bipolar

Answer 9

Question 10

Peak age of onset for bipolar disorder

Answer 10

Age of Onset: peak late teens 15-19, retrospective report of significant childhood depression is common

Second peak between age 35-45

Question 11

Before perscribing any antidepressant, you must ALWAYS . . .

Answer 11

. . . screen for a history of mania

You don’t want to make mania worse by treating depression with the wrong antidepressant

You should ask about:

1. An uncharacteristic episode of increased energy or elevated/irritable mood
2. Decreased need for sleep is most specific symptom
3. FHx bipolar disorder

Question 12

Summary of bipolar pharmacology

Answer 12

Question 13

Premenstrual Dysphoric Disorder (PMDD) Summary

Answer 13

Question 14

Substance/Medication-Induced Mood Disorder Summary

Answer 14

Question 15

Mood Disorder due to Another Medical Condition Summary

Answer 15

Question 16

Appetite disturbances in childhood may be marked by. . .

Answer 16

. . . failure to demonstrate expected weight gain, rather than weight loss

Another use for growth curves!

Question 17

Disruptive Mood Dysregulation Disorder

Answer 17

Question 18

Current state of the monoamine theory of depression

Answer 18

It is now believed that it is the downstream adaptation of the neuron to the increased levels of monoamines over time which results in the efficacy of SSRIs, SNRIs, MAOis, etc, not JUST the increase in levels of monoamines.

This argument is based on the notion that synaptic monoamine levels increase rapidly after taking these drugs, however they take weeks to months to have any effect, suggesting that the true therapeutic mechanism lies downstream of increasing monoamine levels.

Question 19

Neuroplasticity hypothesis

Answer 19

That it is a lack of neural connection in the prefrontal cortex which causes depression, likely caused by excessive neural pruning.

Question 20

Neuroendocrine hypothesis

Answer 20

Theory that depression represents a dysregulated response to psychosocial stress.

The HPA axis’s feedback is impaired, increasing cortisol levels and having downstream effects on limbic circuits.

Question 21

Inflammation hypothesis

Answer 21

Considered an adendem to the neuroendocrine hypothesis.

Some patients w/ depression have elevated CRP even in the absence of illness. Depression patients with this elevated CRP have depression that responds to anti-inflammatories.

This may represent a subset of patients.

Question 22

Role of 5HT1A receptor downregulation in the mechanism of action of SSRIs

Answer 22

When this receptor is stimulated it inhibits firing of serotonergic neurons, this means that it works as an autoreceptor that inhibits serotonergic activity.

As a response to serotonin stimulation, the serotonergic neuron downregulates 5HT1A receptors. This occurs over weeks, and has been proposed as the explanation of delayed monoamine antidepressant effects.

Thus, the neurons are disinhibited to release more serotonin in the synaptic space and to fire more frequently.

Question 23

SERT

Answer 23

The serotonin transporter (SERT) is a monoamine transporter protein. This is a membrane protein that transports serotonin from synaptic spaces into presynaptic neurons.

It is the target of inhibition of SSRIs

Question 24

BDNF

Answer 24

The neurotrophic hypothesis of depression proposes that depression is associated with reduced brain BDNF levels in the hippocampus. So, antidepressant treatments alleviate depressive symptoms and increase BDNF levels.

BDNF, in turn, upregulates neuronal mTOR, which then promotes the expression many other proteins, including glutamate receptors in the synaptic cleft.

Question 25

Adjustment disorder

Answer 25

Not a psychiatric condition necessarily! This is often on the ddx for depression.

Question 26

The DSM V got rid of the ___ with regards to MDD diagnosis, which places more emphasis on ___ when diagnosing depression.

Answer 26

The DSM V got rid of the bereavement exception with regards to MDD diagnosis, which places more emphasis on functional impairment when diagnosing depression.

Question 27

Imortant side effects of lithium

Answer 27

• Tremors (HUGELY important for certain occupations)
• Nephrogenic diabetes insipidus