Neuroendocrinology Flashcards

1
Q

What are the short term consequences of stress?

A

Effect on brain function ->
adaptation to environment

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2
Q

What are the consequences of long term stress?

A

Adaptation ->
Psychiatric disorders

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3
Q

How do the nervous system and endocrine system interact?

A

Neurotransmitters
Hormones

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4
Q

How do the immune system and endocrine system interact?

A

Cytokines
Hormones

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5
Q

How do the nervous system and immune system interact?

A

Neurotransmitters
Cytokines

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6
Q

What parts of the CNS are in the endocrine system?

A

Pineal gland
Hypothalamus
Pituitary gland

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7
Q

What are the pituitary hormones? What are their target organs?

A

TSH (thyroid)
ACTH (adrenal cortex)
FSH and LH (testes/ovaries)
Growth hormone (entire body)
Prolactin (mammary glands)
Endorphins (brain- pain receptors)

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8
Q

How do the endocrine and nervous system influence each other?

A

All hormones affect brain activity
Almost all endocrine secretions are controlled by the brain

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9
Q

What are the psychiatric symptoms of Cushing’s syndrome?

A

Depression
Irritability
Loss of recent memory

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10
Q

How does mineralocorticoid receptor respond to corticosterone and cortisol?

A

Binds with high affinity to regulate circadian fluctuation of these hormones

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11
Q

How does glucocorticoid receptor respond to corticosterone and cortisol?

A

Binds with low affinity
Takes a higher level of hormones to initiate response
Regulates response in times of stress, when levels are high

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12
Q

What gets is used when cortisol overproduction is suspected?

A

Dexamethasone to suporeee cortisol levels

Low dose will differentiate healthy from people producing too much

High dose will differentiate Cushing’s disease

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13
Q

How does the HPA axis regulate stress response?

A

Stress stimulates hypothalamus to release CRF
CRF stimulates the anterior pituitary to produce ACTH
ACTH stimulates the adrenal glands to produce cortisol
Cortisol stimulates physiological changes (fight or flight) and sends inhibitory signals to hypothalamus and pituitary

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14
Q

What happens when cortisol activates the glucocorticoid receptor?

A

Receptor released HSP complex and translocated into the nucleus

There the GR regulates gene transcription to initiate physiological changes

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15
Q

How is the HPA axis disrupted in patients with depression?

A

Glucocorticoid receptors are resistant to

Translocation and downstream effects cannot happen

Negative feedback is disrupted and glucocorticoid levels remain high

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16
Q

How does stress affect neuroplasticity?

A

Shortens dendrites
Effect is reversible over weeks

Effect seems to be mediated by the HPA axis (cortisol)

17
Q

What evidence points to elevated disrupted HPA axis in depression and psychosis?

A

Enlarged pituitary gland
Cortisol hypersecretion
Dexamethasone non suppression

18
Q

How does high glucocorticoid induce psychosis?

A

Glucocorticoids increase dopaminergic activity in the mesolimbic pathway

19
Q

How does cortisol correlate with hippocampal volume in psychosis?

A

Negative correlation
Higher cortisol = smaller hippocampal volume

20
Q

How do patients with psychosis differ from patients with depression I. Response to stress?

A

Patients with psychosis do not mount a stress response to social stress tests, patients with depression do

21
Q

What biomarker might be useful for predicting non-response to psychosis treatment?

A

Awakening cortisol response

22
Q

What biomarkers support the theory of higher inflammation in depression and psychosis?

A

Higher cytokine levels (TNF, IL6) preceding the onset of depression

23
Q

How does childhood trauma affect inflammation levels?

A

Higher levels of inflammatory markers even with disorder group

24
Q

Has anti inflammatory treatment proved useful in all patients with depression?

A

No, only in higher levels inflammation
Low level inflammation might be neuro protective

25
Q

How is the HPA axis involved in inflammation?

A

CRF activated the locus coeruleus to activate the sympathetic nervous system

This stimulates release of cytokines

Cytokines alter monoamine metabolism, increase excitotoxicity, decrease trophic factor (BDNF) production