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BIOL 432 Final > Steroids Glucocorticoids > Flashcards

Steroids Glucocorticoids Flashcards

(67 cards)

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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
The SCN also receives non-photic input. Where is this from?
- neuropeptide Y projections from intergeniculate leaflet | - serotonergic projections from median raphe nucleus
26
What does the suprachiasmatic nucleus controls and how?
- various rhythms (body temp, activity, hormone levels) | - through nervous projections to other nuclei of the hypothalamus and other brain regions
27
Specifically how are sleep-wake cycles regulated?
- through projections from the SCN to the dorsomedial hypothalamus and posterior hypothalamic area
28
What can the central clock be adjusted by?
- light or day-night cycles of the environment
29
Where is rhythmic information relayed to?
- pineal gland, pituitary, periphery through autonomic nervous system
30
Peripheral oscillators can by entrained by which three things?
- neuronal pathways - hormones - feeding rhythms!
31
What are the external time cues tat entrain circadian rhythm?
- feeding schedule - light - activity - social cues
32
What are the central outputs of the SCN?
- sleep-wake cycles | - cognitive performance
33
What are the peripheral outputs of the SCN?
- heart - liver - muscle - kidney
34
What do the outputs of the SCN ultimately affect?
- physiology and behaviour
35
What are the adrenal disorders?
- Cushing syndrome
36
What is cushing syndrome characterized by?
- excess cortisol (hyperadrenocorticism) | - caused by adrenal tumor or excess ACTH
37
What are the 4 main symptoms of cushing syndrome?
1. Protein depletion 2. Fat redistribution 3. Mental problems 4. Inhibition of bone formation (suppression of calcium absorption)
38
In what two situations are excess levels of glucocorticoids seen?
1. excessive endogenous production of cortisol | 2. Administration of glucocorticouds for therapeutic purposes
39
What is cushing's disease?
- specific type of cushing's syndrome due to excessive ACTH from a pituitary tumor
40
What is addison's disease?
- insufficient production of cortisol - often aldosterone deficiency - hypoadrenocorticism
41
What are the common causes of addison's disease?
- infectious disease | - autoimmune destruction of adrenal cortex
42
What are the symptoms of addison's disease?
- cardiovascular disease, lethargy, disarrhea, and weakness | - hypoglemciam, Na and K imbalances, hypotension, weight loss, and weakness
43
Why is addison's disease on the rise?
- association with AIDs and cancer | - can be side effect of glucocorticoid treatment
44
Addison disease results in a hyposecretion of?
- glucocorticoids and mineralocorticoids
45
Underproduction of cortisol causes downstream effects. What are these?
- lack of effect on target tissues - lack of negative feedback on the pituitary - increase in pituitary ACTH secretion stimulates melanin synthesis
46
What could glucocorticoid therapy lead to?
- if taking glucocorticoids in excess leads to negative feedback and gland atrophy and addisons disease
47
What is the main mineralocorticoid?
- aldosterone
48
What enzyme is specifically expressed in the zona glomerulosa? What does it lack?
- p450aldo | - lacks 17alpha-hydroxylase so cannot produce cortisol or androgens
49
What are the physiological effects of mineralocorticoids?
- regulating extracellular concentrations of minerals | - major target is distal tubule of the kidney (exchange Na and K)
50
What happens if there is an imbalance or loss of minerals?
- leads to rapidly life-threatening abnormalities in electrolyte and fluid balance
51
What are the three primary physiological effects of aldosterone?
- 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
How does aldosterone specifically increase resorption of sodium?
- activation of sodium channels (aldosterone-regulated kinase) - stimulation of transcription of Na-K ATPase gene
53
What is the major effect of aldosterone?
- conserve body sodium | - conservation of water follows
54
What regulates aldosterone secretion?
- concentration of potassium ion in extracellular fluid - angiotensin II - sodium deficiency stimulates aldosterone secretion
55
How does the concentration of potassium in the extracellular fluid regulate aldosterone secretion?
- increase plasma K | - increase aldosterone secretion (pump K out and take up Na)
56
How does angiotensin II regulate the secretion of aldosterone?
- 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
What does the renin-angiotensin system do?
- regulates blood pressure
58
What is a source of renin?
- juxtaglomerular cells
59
What inhibits renin secretion?
- excess aldosterone
60
What is ACE?
- angiotensin-converting enzyme | - angiotensin I to II
61
What is the renin-angiotensin-aldosterone axis?
- angiotensinogen get converted to angiotensin I by renin - angiotensin I to II by ACE - activates angiotensin II receptors
62
What does activation of angiotensin II receptors result in?
- aldosterone secretion - vasoconstriction - sympathetic activation - all contribute to blood pressure regulation
63
What does mineralocorticoid receptor bind with equal affinity?
- aldosterone and cortisol
64
Since cortisol serum concentrations are higher is this an issue with the mineralocorticoid receptor?
- no | - aldosterone-responsive cells express enzyme 11-beta-hydroxysteroid dehydrogenase
65
What does 11-beta-hydroxysteroid dehdrogenase do?
- converts cortisol to cortisone | - allows aldosterone to bind its receptor without competition
66
Why does chronic licorice intoxication occur?
- licorice inhibits 11-beta-hydrozysteroid dehydrogenase - no inactivation of cortisol - net effect similar to aldosterone excess (pseudohyperaldosteronism - endogenous mineralcorticoid secretion is normal)
67
What is chronic licorice intoxication?
- 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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