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BIOL 432 Final > Steroids Glucocorticoids > Flashcards

Steroids Glucocorticoids Flashcards

1
Q

In what three ways is cortisol regulated?

A
  • circadian rhythm
  • stress
  • feedback (cortisol and ACTH)
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2
Q

What causes the pulsatile secretion of cortisol?

A
  • combination of positive and negative control on CRH secretion
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3
Q

What is the short feedback in the regulation of cortisol?

A
  • ACTH inhib own secretion
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4
Q

What is the long feedback in the regulation of cortisol?

A
  • cortisol paths
  • fast (non-nuclear): cortisol acts on pituitary or hypothalamus depending on the rate of change of cortisol levels
  • slow (nuclear): depends on the absolute levels of cortisol to decrease ACTH synthesis
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5
Q

What are the three mechanisms for neuroendocrine control?

A
  • episodic/circadian rhythm of ACTH release
  • stress responsiveness of HPA axis
  • feedback inhibition by cortisol of ACTH release
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6
Q

What time of day do we see a rise in ACTH and glucocorticoid?

A
  • in the morning

- CRH and ACTH peak before awakening and decline during the day

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7
Q

ACTH and cortisol follow a ____ _____ but so does body temperature.

A
  • circadian rhythm
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8
Q

For what three reasons is body temperature used as a marker for circadian rhythm?

A
  • studying hypothalamus is invasive
  • heart rate and work level are noninvasive but dominated by external influence
  • core body temperature is easily measured and suitable marker
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9
Q

What are the five cues for circadian rhythm?

A
  • sleep pattern
  • light/dark
  • feeding time
  • physical work
  • stress
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10
Q

What are are five ways that the circadian rhythm becomes dysregulated?

A
  • CNS/pituitary
  • Cushing’s syndrome
  • liver disease
  • renal failure
  • drug addication
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11
Q

What plays important roles in maintaining alertness and modulating sleep?

A
  • hypothalamic-pituitary-adrenal axis
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12
Q

What does CRH play a role in?

A
  • stress response

- circadian dependent alerting and cueing

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13
Q

Where is CRH found?

A
  • in the hypothalamic paraventricular nucleus
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14
Q

The circadian rhythm of cortisol secretion derives from connections between?

A
  • PVN and the primary endogenous pacemaker, the suprachiasmatic nucleus (SCN)
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15
Q

Where is the CRH released from and in what way?

A
  • released from the parvocellular cells of PVN

- in a circadian-dependent pulsatile fashion

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16
Q

What are circadian rhythms generated by?

A
  • endogenous clocks which can function independently from external cues
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17
Q

Where is the main circadian clock located in mammals?

A
  • suprachiasmatic nuclei of the anterior hypothalamus

- situated just above optic chiasm on each side of third ventricle

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18
Q

Around how many neurons are in each nuclei (SCN)?

A

~10, 000 for mouse

~16, 000 for humans

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19
Q

What does lesions of the SCN result in? What does grafting SCN tissue onto lesions result in?

A
  • abolish locomotor activity rhythms and more

- restores its circadian rhythmicity with characteristics of the donor

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20
Q

The SCN is the ___ ___ in the organism.

A

master clock

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21
Q

What is the circadian clock in the SCN reset by and why is this important?

A
  • it can function autonomously but can be reset by light-dark cycles
  • this ensures that it is entrained to 24 hour cycles
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22
Q

What kind of input does the “core” of the SCN receive?

A
  • photic input from the retina through the retino-hypothalamic tract
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23
Q

What kind of response does the photic input result in?

A
  • induction of various genes

- chromatin remodeling

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24
Q

Photoreceptive cells that are involved in entrainment of the SCN clock are ____ from those involved in vision, and constitute a subset of ____ _____ cells.

A
  • distinct

- retinal ganglion

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25
Q

The SCN also receives non-photic input. Where is this from?

A
  • neuropeptide Y projections from intergeniculate leaflet

- serotonergic projections from median raphe nucleus

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26
Q

What does the suprachiasmatic nucleus controls and how?

A
  • various rhythms (body temp, activity, hormone levels)

- through nervous projections to other nuclei of the hypothalamus and other brain regions

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27
Q

Specifically how are sleep-wake cycles regulated?

A
  • through projections from the SCN to the dorsomedial hypothalamus and posterior hypothalamic area
28
Q

What can the central clock be adjusted by?

A
  • light or day-night cycles of the environment
29
Q

Where is rhythmic information relayed to?

A
  • pineal gland, pituitary, periphery through autonomic nervous system
30
Q

Peripheral oscillators can by entrained by which three things?

A
  • neuronal pathways
  • hormones
  • feeding rhythms!
31
Q

What are the external time cues tat entrain circadian rhythm?

A
  • feeding schedule
  • light
  • activity
  • social cues
32
Q

What are the central outputs of the SCN?

A
  • sleep-wake cycles

- cognitive performance

33
Q

What are the peripheral outputs of the SCN?

A
  • heart
  • liver
  • muscle
  • kidney
34
Q

What do the outputs of the SCN ultimately affect?

A
  • physiology and behaviour
35
Q

What are the adrenal disorders?

A
  • Cushing syndrome
36
Q

What is cushing syndrome characterized by?

A
  • excess cortisol (hyperadrenocorticism)

- caused by adrenal tumor or excess ACTH

37
Q

What are the 4 main symptoms of cushing syndrome?

A
  1. Protein depletion
  2. Fat redistribution
  3. Mental problems
  4. Inhibition of bone formation (suppression of calcium absorption)
38
Q

In what two situations are excess levels of glucocorticoids seen?

A
  1. excessive endogenous production of cortisol

2. Administration of glucocorticouds for therapeutic purposes

39
Q

What is cushing’s disease?

A
  • specific type of cushing’s syndrome due to excessive ACTH from a pituitary tumor
40
Q

What is addison’s disease?

A
  • insufficient production of cortisol
  • often aldosterone deficiency
  • hypoadrenocorticism
41
Q

What are the common causes of addison’s disease?

A
  • infectious disease

- autoimmune destruction of adrenal cortex

42
Q

What are the symptoms of addison’s disease?

A
  • cardiovascular disease, lethargy, disarrhea, and weakness

- hypoglemciam, Na and K imbalances, hypotension, weight loss, and weakness

43
Q

Why is addison’s disease on the rise?

A
  • association with AIDs and cancer

- can be side effect of glucocorticoid treatment

44
Q

Addison disease results in a hyposecretion of?

A
  • glucocorticoids and mineralocorticoids
45
Q

Underproduction of cortisol causes downstream effects. What are these?

A
  • lack of effect on target tissues
  • lack of negative feedback on the pituitary
  • increase in pituitary ACTH secretion stimulates melanin synthesis
46
Q

What could glucocorticoid therapy lead to?

A
  • if taking glucocorticoids in excess leads to negative feedback and gland atrophy and addisons disease
47
Q

What is the main mineralocorticoid?

A
  • aldosterone
48
Q

What enzyme is specifically expressed in the zona glomerulosa? What does it lack?

A
  • p450aldo

- lacks 17alpha-hydroxylase so cannot produce cortisol or androgens

49
Q

What are the physiological effects of mineralocorticoids?

A
  • regulating extracellular concentrations of minerals

- major target is distal tubule of the kidney (exchange Na and K)

50
Q

What happens if there is an imbalance or loss of minerals?

A
  • leads to rapidly life-threatening abnormalities in electrolyte and fluid balance
51
Q

What are the three primary physiological effects of aldosterone?

A
  • increased active resorption of sodium
  • increased passive resorption of water
  • increased renal excretion of potassium
  • all result in increase in blood pressure and volume
52
Q

How does aldosterone specifically increase resorption of sodium?

A
  • activation of sodium channels (aldosterone-regulated kinase)
  • stimulation of transcription of Na-K ATPase gene
53
Q

What is the major effect of aldosterone?

A
  • conserve body sodium

- conservation of water follows

54
Q

What regulates aldosterone secretion?

A
  • concentration of potassium ion in extracellular fluid
  • angiotensin II
  • sodium deficiency stimulates aldosterone secretion
55
Q

How does the concentration of potassium in the extracellular fluid regulate aldosterone secretion?

A
  • increase plasma K

- increase aldosterone secretion (pump K out and take up Na)

56
Q

How does angiotensin II regulate the secretion of aldosterone?

A
  • decreased renal blood stimulates increase in angiotensin II which increases aldosterone secretion
  • if blood pressure high, release atrial natriuretic peptide, decrease blood pressure, decrease water and sodium, decrease aldosterone secretion
57
Q

What does the renin-angiotensin system do?

A
  • regulates blood pressure
58
Q

What is a source of renin?

A
  • juxtaglomerular cells
59
Q

What inhibits renin secretion?

A
  • excess aldosterone
60
Q

What is ACE?

A
  • angiotensin-converting enzyme

- angiotensin I to II

61
Q

What is the renin-angiotensin-aldosterone axis?

A
  • angiotensinogen get converted to angiotensin I by renin
  • angiotensin I to II by ACE
  • activates angiotensin II receptors
62
Q

What does activation of angiotensin II receptors result in?

A
  • aldosterone secretion
  • vasoconstriction
  • sympathetic activation
  • all contribute to blood pressure regulation
63
Q

What does mineralocorticoid receptor bind with equal affinity?

A
  • aldosterone and cortisol
64
Q

Since cortisol serum concentrations are higher is this an issue with the mineralocorticoid receptor?

A
  • no

- aldosterone-responsive cells express enzyme 11-beta-hydroxysteroid dehydrogenase

65
Q

What does 11-beta-hydroxysteroid dehdrogenase do?

A
  • converts cortisol to cortisone

- allows aldosterone to bind its receptor without competition

66
Q

Why does chronic licorice intoxication occur?

A
  • licorice inhibits 11-beta-hydrozysteroid dehydrogenase
  • no inactivation of cortisol
  • net effect similar to aldosterone excess (pseudohyperaldosteronism - endogenous mineralcorticoid secretion is normal)
67
Q

What is chronic licorice intoxication?

A
  • syndrome of water and sodium retention coupled wit low plasma K hypertension and low renin activity

BIOL 432 Final (14 decks)

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