Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

UVic BIOL 432 - Spring 2019 > Steroids and Glucocorticoids > Flashcards

Steroids and Glucocorticoids Flashcards

1
Q

During development, which tissue becomes the adrenal cortex?

A

The mesoderm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 sections of the adrenal cortex (from superficial to deep)?

A
  1. Zona glomerulosa
  2. Zona fasciculata
  3. Zona reticularis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What structural feature differentiates the zona glomerulosa and zona fasciculata from the zona reticularis? What is the purpose of this?

A

The 2 superficial layers are rich in lipids, mitochondria, and smooth endoplasmic reticulum. Allows rapid release of glucocorticoid for fight/flight response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is secretion from the zona glomerulosa regulated?

A

By the renin-angiotensin system and ACTH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is secretion from the zona fasciculata and zona reticularis regulated? How do they differ?

A

Regulated by ACTH. Fasciculata = acute reaction

Reticularis = basal level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What two endocrine organs make up the adrenal gland?

A

The adrenal cortex and the adrenal medulla.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What molecule is produced in the zona glomerulosa that is not produced in the zona fasciculata? What necessary molecule cannot be produced by the zona glomerulosa?

A

P450aldosterone only produced by the glomerulosa, though it is unable to produce 17alpha-hydroxylase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the function of the adrenal medulla?

A

Release epinephrine/norepinephrine when stimulated by the sympathetic ganglion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the function of the zona glomerulosa?

A

Release mineralocorticoids to control electrolyte balance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the function of the zona reticularis?

A

Release sex steroids (androgens, androstenedione, estrogen).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What function do the zona fasciculata and zona reticularis share?

A

They release glucocorticoids (esp. cortisol) which stimulates catabolism of fat and protein to produce glucose as well as repair tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What receptor does cortisol bind to? Where in the body are these receptors found?

A

Binds to glucocorticoid receptors found all over the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What other receptor are glucocorticoids able to bind to?

A

Glucocorticoids can also bind to mineralocorticoid receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is corticosteroid-binding globulin associated with cortisol? Is it biologically active?

A

It ferries cortisol around the body and acts as a reservoir, but is not biologically active.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How much of the cortisol which circulates in the body is not bound to a BBP? How can cortisol levels be most easily measured?

A

~10% of circulating cortisol is free. Because there are no binding protein in saliva it serves as an excellent measure of overall cortisol level.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the main function of glucocorticoids?

A

Downregulate the immune system following some stimulating event.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What 4 main factors give glucocorticoids their immunosupressive function?

A
  1. Reduces migration of inflammatory cells to injury
  2. Reduces enzymes which are involved in inflammatory response
  3. Impairs antigen and antibody production
  4. Induces apoptosis in lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What effect do glucocorticoids have on fetal development?

A

Act through other growth factors to promote development of many systems. Especially important for lung maturation and surfactant production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What effect do chronically high glucocorticoid levels have on growth?

A

Inhibits growth and may lead to Cushing’s disease (obesity, fat production).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which is the most important glucocorticoid in humans?

A

Cortisol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What lipid molecule is necessary for the biosynthesis of steroids (also Vitamin D)?

A

Cholesterol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the function of ApolipoproteinB100?

A

To deliver cholesterol to the adrenal cortex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What 5 steps describe the processing of cholesterol by receptor-mediated endocytosis?

A
  1. ApolipoproteinB100 (ApoB) absorbed into the cell by endocytosis
  2. Vesicles lose clathrin and fuse with other vesicles (make endosome)
  3. Endosome becomes acidic and dissociates receptor from lipoprotein
  4. Lysosome merges: enzymes breakdown ApoB and free cholesterol
  5. Cholesterol used, excess products recycled
24
Q

What is StAR? What is its purpose?

A

Steroidogenic acute regulatory protein. Used to transport cholesterol (and all steroids) through the cytoplasm.

25
Q

What can result from a lack of Steroidogenic acute regulatory protein? Why?

A

Lack of StAr causes deficiency of estrogen, androgen, cortisol (steroids) because there is no transport of cholesterol to the mitochondria.

26
Q

How does adrenocorticotropic hormone cause the release of cholesterol?

A

ACTH > 7TM receptors > activates Galpha-s > AC > cAMP > PKA > causes release of cholesterol from storage in the lipid droplets.

27
Q

Once cholesterol is released from the lipid droplets, how does this lead to cortisol production?

A

After delivery to the mitochondria, cholesterol is converted to pregnenolone (Preg), then undergoes 2 other modifications (in the SER) before being released from the mitochondria as cortisol.

28
Q

What zone of the adrenal cortex produces aldosterone?

A

The zona glomerulosa.

29
Q

Differentiate between the short and long feedback mechanisms to regulate cortisol.

A 
Short = ACTH inhibits own secretion
Long = Cortisol acts on the pituitary or hypothalamus in nuclear (slow) or nonnuclear (fast) manner
30
Q

What are the 3 ways cortisol is regulated?

A

Circadian rhythms, stress (all types), feedback mechanisms

31
Q

What are the external cues to affect our circadian rhythms?

A

Sleeping patterns, light/dark cycles, feeding times, physical work and stress

32
Q

Where is Corticotropin Releasing hormone (CRH) found in the hypothalamus? How does this relate to the circadian rhythm release of cortisol?

A
  • Paraventricular Nucleus (of the hypothalamus) (PVN)

- the release derives from the connections between the PVN and the superchiasmatic nucleus.

33
Q

What is the primary endogenous pacemaker :) ? Where is it located?

A
  • Superchiasmatic nucleus (SCN)

- In the anterior hypothalamus, above the optic chiasm and on each side of the third ventricle

34
Q

If you were to lesion the superchiasmatic nucleus, what happens? By replacing the SCN with a donor after lesioning, what weird phenomenon occurs?

A
  • circadian and other rhythms are off, and locomotor activity is affected
  • The rhythms are restored BUT have characteristics of the donor still, not of the acceptor
35
Q

Where does the core of the superchiasmatic nucleus’s input come from? What type of response is given after this input?

A
  • Comes from photic input from the retina, via the retino-hypothalamic tract (NOT the same photoreceptive cells as ones involved in vision)
  • induction of various genes and chromatin remodelling within SCN neurons
36
Q

What are the 2 likely candidates of the photopigments that are involved in generating input for the superchiasmatic nucleus?

A

novel opsin melanopsin and 2 cryptochromes

37
Q

Where is the non-photic information coming from for the superchiasmatic nucleus?

A

from Neuropeptide Y projections for the intergeniculate leaflet and serotinergic projections (from median Raphe nucleus)

38
Q

How are the sleep-wake cycles regulated by the superchiasmatic nucleus? (i.e. where is the output going)

A

through projections from the SCN to the dorsomedial and posterior hypothalamic areas

39
Q

How is rhythmic information regulated by the superchiasmatic nucleus? (i.e. where is the output going)

A

The pineal gland, pituitary and the periphery organs (autonomic system)

40
Q

What are the 4 main symptoms of Cushing syndrome?

A
  1. Protein depletion (muscle wasting and wound healing)
  2. Fat redistribution (abdominal fat)
  3. Mental problems
  4. Inhibition of bone formation (suppressed Ca2+ absorption and impaired Vit.D metabolism)
41
Q

What does Cushing syndrome cause?

A

hyperglycaemia, hypertension, weakness and edema

42
Q

The excessive cortisol levels seen in Cushing syndrome originate from 2 types of situations:

A
  1. Excessive endogenous production of cortisol (adrenal defect-ACTH independent, or excessive ACTH secretion)
  2. Administration of glucocorticoids for therapeutic reasons
43
Q

How is Cushings DISEASE caused?

A

(specific type of Cushing syndrome) where there is excessive ACTH secretion due to a pituitary tumor

44
Q

Describe Addison’s disease (HYPOadrenocorticism) (symptoms, causes)

A
  • Insufficient production of cortisol, accompanied by aldosterone deficiency
  • experience cardiovascular disease, lethargy, weakness, diarrhea
  • causes: infectious disease or autoimmune destruction of adrenal cortex.
45
Q

Why was Addison’s disease once rare, but is now on the rise?

A

association with AIDS and cancer, because can be a side effect of glucocorticoid treatment

46
Q

How does Addison’s disease lead to hyperpigmentation?

A

Due to the underproduction of cortisol, and therefore lack of effect on target tissues and negative feedback on the pituitary, there is an increase in ACTH pituitary secretion. This stimulates melanin synthesis and further bronzing of the skin.

47
Q

How does Cushing’s disease then lead to Addison’s disease?

A

With an excess of glucocorticoids, the leads to excessive negative feedback and eventually gland atrophy (adrenal cortex), which then leads to Addison’s disease.

48
Q

What is the main target in the body for mineralocorticoids?

A

the distal tubule in the kidney

49
Q

Describe the affects that aldosterone has on the kidney’s tubule.

A
  • activates an Na+ channel to cause reabsorption (which also means reabsorption of water)
  • stimulates transcription of a Na+/K+ ATPase gene (more Na+ reabsorption and K+ excretion)
50
Q

The conservation of water follows the conservation of _______________

A

Sodium!

51
Q

What other targets does aldosterone have where it implements the same effects as on the kidney?

A

sweat glands, salivary glands and the colon

52
Q

Describe the 3 ways in which aldosterone is regulated.

A
  1. extracellular [K+] - if increase [K+], increase aldosterone
  2. Angiotensin 2
    - (+) regulation: decreased renal blood flow –> increase angiotensin 2 –> increase aldosterone
    - (-) regulation: BP high –> atrial natriuretic peptide –> decrease water and Na+ –> decrease aldosterone
  3. Na+ deficiency - increase aldosterone
53
Q

What enzymes converts Angiotensin 1 to Angiotensin 2 :)?

A

Angiotensin-converting enzyme (ACE)

54
Q

What causes angiotensinogen to convert to Angiotensin 1? If there is an excess of __________ then that will inhibit that secretion.

A
  • Renin

- Aldosterone

55
Q

What is seen in hyperaldosteronism? What are the causes of this?

A
  • hypertension and edema

- causes: adrenal adenoma, hyperplasia, increase in mineralcorticoid-like activity, increase of renal Na+ reabsorption

56
Q

Explain how Aldosterone succeeds in competing with the high levels of cortisol in the body.

A

The enzyme 11-beta-hydroxysteroid dehydrogenase converts cortisol to the biologically inactive compound cortisone, which has a lower affinity for the mineralcorticoid receptor. This allows aldosterone to bind to the receptor without competition

57
Q

Why is eating a ridiculous amount of licorice risky for you?

A

because at toxic levels it inhibits the 11-beta-hydroxysteroid dehydrogenase, therefore not converting cortisol, and causing an excess of aldosterone floating around (pseudohyperaldosteronism)
-causes water and Na+ retention with low plasma K+ –> hypertension and low renin activity

UVic BIOL 432 - Spring 2019 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions