Lecture 11 Flashcards

1
Q

What is Depression

A

“the common cold of mental illness” 3% of the population in the USA experiences a depressive episode in any 6 month period. 6% experience a major depressive episode in their life time. In western societies clinical depression has increased since 1945. Effects females twice as men. Less than 20% of individuals with symptoms seek treatment

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2
Q

Outlook for Depression as chronic illness

A

Over 80% of patients treated with drugs improve within 6 months
Less than 1/3 remain well; 2/3 will relapse.

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3
Q

What are some symptoms of Clinical Depression

A

A recurrent, persistent, deep depression with no clear trigger, Anhedonia, Weight loss
Lethargy, Insomnia, Decreased feelings of self worth, Increased feelings of guilt
Thoughts of death and suicidal ideation

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4
Q

Hormones and Depression

A

Individuals with depression have reduced Thyroid function.

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5
Q

Whats the result of exogenous THR?

A

Exogenous TRH results in a decrease in depression symptoms. Depressed patients displayed blunted TSH in response to TRH. Deficit is noticeable across system.

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6
Q

what is often present in patients with clinical depression?

A

High levels of antibodies against the thyroid gland (autoimmune??) High TRH levels in the CSF. Enhancement of antidepressant efficacy when T3 is co-administered

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7
Q

Growth Hormone and Depression

A

GH response in induced -Hypoglycemia is impaired in depressed patients (acute vs chronic stress). TRH causes an abnormal increase in GH in depressed patients.

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8
Q

Prolactin and Depression

A

Elevated plasma levels of prolactin are associated with depression.

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9
Q

Depression and inhibition of the HPA via cortisol.

A

Cortisol would normally inhibit HPA. The negative feedback actions of the HPA are impaired in depressed patients. 50% of individuals with depression have elevated levels of cortisol.

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10
Q

Dexamethasone Suppression Test

A

Dexamethasone is a synthetic steroid similar to gluccorticoids. It should activate negative feedback, resulting in decreased synthesis of cortisol, but fails. Suggesting failure of neural mechanism.

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11
Q

Depression, Cortisol and Dexamethasone.

A

Cortisol levels are usually at their peak in the early morning. In depressed patients, cortisol levels are at their highest 3-4 hours after start of sleep. Dexamethasone results in early suppression of cortisol followed by a surge in circulating levels.

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12
Q

Cortisol and Adrenal disorders

A

Addison disease: Insufficient cortisol secretion
Associated with depression
Cushings Disease: Excessive cortisol secretion
Associated with depression.

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13
Q

Depression and Estrogens

A

Depressed women have low levels of estradiol. Physiological doses of estrogen alleviates depressed mood in post-menopausal women and improves mood in healthy women
Supraphysiological doses reduces symptoms in women with severe clinical depression

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14
Q

Postpartum Depression and CRH Involvement

A

Elevated mid-gestational CRH levels are predictive of postpartum depression
Source of elevated CRH is the placenta
Relationship between CRH and postpartum depression is not known.

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15
Q

Postpartum Depression and progesterone

A

Highest difference between gestational and Post-Partum progesterone levels in post-partum depressed women
Progesterone replacement may ameliorate some symptoms.

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16
Q

Postpartum Depression and role β-endorphin

A

Levels of β-endorphins rise in third trimester of pregnancy and plummet 3-4 hours post-parturition. Highest levels of β-endorphin during gestation correlates with more depression postpartum
“Maternity blues” might results from withdrawal of β-endorphin

17
Q

Seasonal Affective Disorder

A

Also Known as Winter depression. Characterized by: Depressed affect
Lethargy, Loss of libido, Anxiety, Inability to concentrate, Hypersomnia, Hyperphagia
Carbohydrate craving, Symptoms go away as days get longer. Some may have hypomania/ mania. 1-10% of the population women more than men (3.5:1)

18
Q

Seasonal Affective Disorder and Serotonin (5HT)

A

Serotonin is synthesized from Tryptophan
A diet rich in carbohydrates increases tryptophan levels in the brain.
High levels of serotonin decrease carbohydrate consumption
It is possible that patients with SAD have cyclic disruptions of the serotonin-carbohydrate regulatory system

19
Q

Describe the increasing Serotonin Path way

A

Glucose and insulin stimulate uptake of NON-tryptophan AA into peripheral cells. the more tryptophan in brain the more serotonin in brain

20
Q

what do High levels of serotonin stimulate?

A

High levels of serotonin decrease carbohydrate consumption. It is possible that patients with SAD have cyclic disruptions of the serotonin-carbohydrate regulatory system.

21
Q

Seasonal Affective DisorderRole of Serotonin (5HT)

A

Serotonin transporter (5HTT) a transmembrane molecule that brings Serotonin back into the presynaptic neuron. Elevated 5HTT binding reflects low levels of 5HT. More 5HTT in winter produces less 5HT, which leads to sad mood.

22
Q

Melatonin is a major regulator of the circadian rhythm what are its effects in SAD

A

5HT is converted to melatonin in the pineal gland. Melatonin levels are higher during the night than during the day. Shifting sleep patterns also shifts melatonin secretion pattern.

23
Q

how does exposure to light affects Melatonin

A

Brief exposure to light inhibits night time secretion of melatonin. Light has two functions
To synchronize the daily melatonin rhythm
Acutely suppress daily melatonin secretion

24
Q

Melatonin Light Transduction and SAD

A

1500 lux (high levels of light) stimulates the suppression of melatonin. People with SAD are 5.6x more likely to have a mutation in melanopsin, which causes a deficits in light transduction.

25
Q

What is the two classification of Anorexia Nervosa?

A

Restricting: Maintain low weight by excessive dieting and exercise.
Binge eating-purging
ONLY psychiatric disorder that requires a endocrine dysfunction (menstrual abnormalities) as a diagnostic criteria.