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FHB Hormone/Repro > 76 - Adrenal gland continued > Flashcards

76 - Adrenal gland continued Flashcards

1
Q

What are mineralocorticoids and what do they do?

A

Hormones that promote Na+ retention by the kidney (secondary result is water retention)

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2
Q

What is the primary endogenous mineralocorticoid?

A

Aldosterone

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3
Q

What part of the adrenal gland does mineralocorticoid synthesis occur?

A

Zona glomerulosa (primary cells in body that have aldosterone synthase)

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4
Q

What are the 4 big sites of action for aldosterone?

What receptor would you expect to find there in high abundance?

A
  • Distal tubule in kidney; colon; salivary ducts, sweat ducts
  • MR
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5
Q

Increased extracellular K+ will (stimulate/inhibit) aldosterone?

A

Stimulate (Basolateral NKP- Na reabsorbed, K excreted)

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6
Q

RAA system:

Decreased blood pressure stimulates _______ release from kidney (juxtaglomerular apparatus).

A

Renin

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7
Q

RAA system:

Renin cleaves _________ (from what organ?) to __________.

A

Angiotensinogen (liver) to angiotensin I

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8
Q

RAA system:

______________ converts ANG I to ______________.

A
  • ACE (angiotensin converting enzyme)

- Angiotensin II

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9
Q

RAA system:

- Angiotensin II stimulates ___________. It also acts to ___________.

A
  • Aldosterone

- Vasoconstrict

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10
Q

What are the effects of aldosterone?

What is the net result?

A

Increase Na+ reabsorption and K+ secretion at cortical collecting ducts
- Net Result = increased extracellular fluid volume and BP (sodium in extracellular space retains water)

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11
Q

How would you differentiate aldosterone vs. ADH/AVP?

A

Aldosterone: The Na hormone
- primary regulator of extracellular volume

ADH/AVP: The water hormone
- primary regulator of free water balance

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12
Q

What is the primary effect of ADH?

What is the secondary effect?

A

Decreases plasma osmolality which secondarily affects sodium concentration in the blood

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13
Q

Recall: aldosterone primarily binds ____, while cortisol primarily binds ____.

A

MR, GR

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14
Q

What is the name of the hormone that converts cortisol to cortisone and vice versa?

A
  • Cortisol to cortisone: 11beta-HSD2

- Cortisone to cortisol: 11beta-HSD1

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15
Q

Why is cortisol converted to cortisone by 11beta-HSD2?

A

Inactivates it (so aldosterone can bind to the MR)

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16
Q

Which is higher concentration in the blood, glucocorticoids or mineralocorticoids?

A

Glucocorticoids (100-1000x)

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17
Q

What are the binding proteins for cortisol and for aldosterone?

A
  • Cortisol: CBG (95% bound)

- Aldosterone: doesn’t have a binding protein

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18
Q

What would be the effect of inhibiting 11beta-HSD2?

A

Increased levels of cortisol, excessive MR activation! (competes w/aldosterone and has much higher blood conc.)

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19
Q

What would be the effect of excessive licorice consumption?

A

Licorice (glycyrrhetinic acid) inhibits 11β-HSD2. - - Excessive consumption can lead to increased Na+ (due to cortisol binding MRs) and subsequent H2O retention

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20
Q

(extra) What’s a drug that was mentioned that inhibits 11beta-HSD2?
What is it used to treat?

A

Carbenoxolone

- Treats esophageal inflammation by increasing cortisol (anti-inflammatory)

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21
Q

What is DHEA/S and where is it produced?

A

Weak androgen

- Produced in zona reticularis

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22
Q

What is DHEA/S a precursor for?

A

Precursor for more potent androgen testosterone, and for estrogens (converted in reproductive tissues)

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23
Q

How does DHEA/S change w/age?

When does it peak?

A

Declines with age

- Peaks between 20 – 30.

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24
Q

How does DHEA/S affect women

A

Increases libido; primary source of androgen and estrogen in postmenopausal women

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25
Q

What is the first step in steroid hormone biosynthesis? What 2 enzymes are required?

A

Convert cholesterol to pregnenolone

  • Requires CE hydrolase- stimulated by ACTH
  • Requires StAR, which xfers chol from OMM to IMM
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26
Q

What is the primary product of steroid hormone synthesis in the zona fasciculata?

A

Cortisol

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27
Q

What genes and intermediates are clinically relevant in cortisol formation in the ZF?

A
  1. Chol -> pregnenolone (CYP11A1)
  2. Pregnenolone -> progesterone
  3. Progesterone -> 17(OH)-progesterone (CYP17)
  4. 17(OH)-progesterone -> 11-deoxycortisol (CYP21A2)
  5. 11-deoxycortisol -> cortisol (CYP11B1)
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28
Q

What are the enzyme names for CYP11A1?

chol -> prenenolone

A

Desmolase/P450scc (chol. small chain cleavage)

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29
Q

What are the enzyme names for CYP21A2?
(Progesterone -> 11-DOC in ZG)
(17-OH-progesterone -> 11-deoxycortisol in ZF)

A

21alpha-hydroxylase/p450c21

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30
Q

What are the enzyme names for CYP11B1?

11-deoxycortisol -> cortisol in ZF

A

11-hydroxylase/P450c11

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31
Q

What are the enzyme names for CYP11B2?

last 3 rxns in ZG

A

Aldosterone synthase/P450aldo

32
Q

What are the enzyme names for CYP17?
(Progesterone -> 17(OH)progesterone in ZF)
(Pregnenolone -> 17(OH)pregnenolone in ZR)

A

17alpha-hydroxylase/P450C17

33
Q

What enzyme/gene is deficient in Congenital Adrenal Hyperplasia (CAH)?
What adrenal pw’s are affected?
What steps are interrupted?
What accumulates?

A

21α hydroxylase deficiency (P450c21 or CYP21A2)

  • ZG and ZF blocked, ZR builds up
  • No mineralocorticoids cuz it interrupts progesterone -> 11-DOC in ZG
  • No cortisol cuz it interrupts 17(OH)progesterone -> 11-deoxycortisol in ZF
  • Excess DHEA/S (ACTH has no negative feedback cuz no cortisol, so everything shunts to ZR pw)
34
Q

*What are the clinical indications of CAH? (explain how the sx are caused)

A
  • Virilization (masculinization due to shunt to ZR pw of DHEA/S)
  • Ambiguous genitalia at birth (^ ZR)
  • Na+ loss (no mineralocorticoids)
  • Hypotension (no mineralocorticoids or glucocorticoids to stimulate MR’s)
  • Hyperkalemia (no aldosterone so no K+ secretion)
  • High plasma renin (response to low BP from low aldosterone)
  • High ACTH (lack of negative feedback from the absent cortisol/aldosterone production)
35
Q

What is the primary product of steroid hormone synthesis in the zona glomerulosa?

A

Aldosterone

36
Q

What genes and intermediates are clinically relevant in aldosterone formation in the ZG?

A
  1. Chol -> pregnenolone (CYP11A1)
  2. Pregnenolone -> progesterone
  3. Progesterone -> 11-DOC (CYP21A2)
  4. 11-DOC -> corticosterone (CYP11B2)
  5. Corticosterone -> 18(OH)corticosterone (CYP11B2)
  6. 18(OH)corticosterone -> aldosterone (CYP11B2)
37
Q

What would be the effects of a CYP11B1 (11-hydroxylase) deficiency?
(explain each effect)

A
  • No cortisol (interrupts 11-deoxycortisol -> cortisol in ZF)
  • High ACTH (no neg feedback from cortisol)
  • High MR activity (11-DOC is active, still can activate MR receptors)
  • Low aldosterone (due to HTN, Ang II not present to stimulate aldosterone synthase)
  • Increased androgens (ZR shunt)
38
Q

Which pw’s would be affected in CYP11B1/11-hydroxylase deficiency? (NOT CYP11B2)

What would be the clinical presentation of CYP11B1 (11-hydroxylase) deficiency? (explain why)

A

ZF blocked, would stimulate ZG and ZR.

  • Hypertension* due to excess 11-DOC (aldosterone levels low because its synthase is regulated by Ang II, not HPA axis)
  • Hypokalemia due to MR stimulation by 11-DOC
  • Masculinization (increased ZR androgens)
  • High ACTH (no negative feedback)
39
Q

What is the primary product of steroid hormone synthesis in the zona reticularis?

A

DHEA/S

40
Q

What genes and intermediates are clinically relevant in DHEA/S formation in the ZR?

A
  1. Chol -> pregnenolone (CYP11A1)
  2. Pregnenolone -> 17(OH)pregnenolone (CYP17)
  3. 17(OH)pregnenolone -> DHEA
    4a. DHEA -> DHEAS
    4b. DHEA -> Androstenedione (minor product)
41
Q

Which pw’s would be affected in CYP17 (17α-hydroxylase) deficiency?

What would be the effects of a CYP17 (17α-hydroxylase) deficiency? (explain why)

A

ZF and ZR blocked, would stimulate ZG

  • No cortisol (interrupts progesterone -> 17(OH)progesterone in ZF)
  • Low aldosterone, high MR activity (11-DOC builds up and binds MRs, aldosterone inhibited because requires Ang II, but BP is high)
  • Decreased androgens (interrupts pregnenolone -> 17(OH)pregnenolone, low DHEA/S)
42
Q

What would be the clinical presentation of CYP17 (17α-hydroxylase) deficiency? (explain why)

A
  • Hypertension (increased 11-DOC which binds MRs, but low aldosterone because it’s regulated by Ang II, which would be low)
  • Hypokalemia (low aldosterone)
  • Feminization/pseudohermaphroditism (ZR blocked, decreased weak androgens)
  • High ACTH (no cortisol negative feedback)
43
Q

Which of the steroidogenic genes are stimulated by ANG II (not ACTH)?

A

CYP11B2 (makes aldosterone)

  • AKA aldosterone synthase, p450aldo
  • Only in ZG
44
Q

What are the major targets/effects of ACTH in adrenals?

A
  • Stimulates conversion of cholesterol to pregnenolone by activating StAR activity
  • Stimulates cellular hypertrophy
  • Stimulates biosynthesis of cortisol
  • *Stimulates biosynthesis of DHEA (CYP17)
  • Stimulates 11β-hydroxylase (CYP11B1)
  • Stimulates conversion of dopamine to NE (medulla)
45
Q

Adrenal medullary cells are innervated by:

A

Sympathetic preganglionic fibers
(Originates from same neural crest area that forms sympathetic ganglia)
- Considered to be modified post-ganglionic sympathetic neurons (no dendrites or axons).

46
Q

Most cells of the adrenal medulla release ____________. (stored in granules)

A

Epinephrine

47
Q

What system controls the release of epinephrine from the adrenal medulla?

A

Sympathetic NS

48
Q

What does the cellular architecture of the adrenal medulla look like?

A

Cords of polyhedral shaped epithelial cells

49
Q

What stimulates the conversion of NE to E in the adrenal medulla?

A

Cortisol

50
Q

What generally causes the release of epinephrine?

How long does it take for release to occur?

A

Response to acute stress: (pain, cold, perceived danger)

- Rapid activation/return

51
Q

Epinephrine release is mediated by the symp NS, but what nerve in particular innervates its release from the medulla?

A

Splanchnic nerve

52
Q

What types of receptors do epi/NE bind?

A

Alpha and beta adrenergic receptors

53
Q

What is the overall goal of releasing adrenaline during the “fight or flight” sympathetic response, in terms of the brain and muscle?
What are the 3 main targets?

A
  • Increase nutrient supply to muscle, and adequate supply of O2/Glucose for brain
  • Muscle, liver, adipose tissue
54
Q

What are the physiological effects of epi (and NE) through beta2 receptors? (think it out)

A

Dilation + other effects

  • SkM: arteriolar vasodilation, ^ glycogenolysis, v Glucose uptake
  • Bronchiolar dilation
  • Decreased GI motility
  • Adipose: ^ Lipolysis, v Glucose uptake (beta3 as well)
  • Liver: ^ Glycogenolysis, ^ GNG, ^ ketogenesis
  • Pancreatic alpha cells: ^ Glucagon
55
Q

What are the physiological effects of epi (and NE) through alpha receptors? (think it out)

A

Constriction + other effect

  • Vein and lymphatic constriction
  • Splanchnic arteriolar vasoconstriction
  • Pancreatic beta cells: v Insilin
  • Iris dilation
56
Q

What are the physiological effects of epi (and NE) through beta1 receptors?

A

HEART:

  • ^ Inotropy (myocardial contraction strength)
  • ^ Chronotropy (rate of SA node)
  • ^ Lusitropic (myocardial relaxation)
57
Q

During acute stress, what catecholamine is actually released?

A

NE

58
Q

What catecholamine stimulates the release of CRH, which will eventually release cortisol?

A

NE

59
Q

What is the longer-term response to stress, and what is the shorter term response?

A
  • Short-term: directly release NE (symp NS)

- Long-term: release CRH, leads to cortisol and epi

60
Q

What is released at the site of tissue injury that can stimulate the stress response?

A

Cytokines

61
Q

In the metabolism of catecholamines, what does MAO break down epi and NE into in the adrenal medulla, liver, and kidney? (1 thing)

A

DHPG

62
Q

What can act on DHPG in the liver and kidney to make VMA (vanillylmandelic acid)?

A

COMT/AD

63
Q

In the metabolism of catecholamines, what does COMT break down epi and NE into in the adrenal medulla, liver, and kidney? (2 things)

A

Metanephrine, normetanephrine

64
Q

What can act on metanephrine and ormetanephrine in the liver and kidney to make VMA (vanillylmandelic acid)?

A

MAO

65
Q

How can VMA be used clinically?

A

VMA levels can be used to detect tumors producing excess EPI or NE (indicating their breakdown)

66
Q

What is a pheochromocytoma?

A

Tumors originating from chromaffin cells: catecholamine overproduction

67
Q

Sx of pheochromocytomas?

A

HTN (no response to medication), headaches, tachycardia

68
Q

How do you dx pheochromocytomas?

A

Measurements of urinary metanephrines

69
Q

Tx for pheochromocytomas?

A

Surgery. Pre-surgery, give alpha/beta blockers

70
Q

Why is a pheochromocytoma known as the 10% tumor?

A
  • 10% malignant
  • 10% bilateral
  • 10% in children
  • 10% familial (have family member w/same tumor)
  • 10% recur (5 - 10 years)
  • 10% associated with MEN* syndromes (rare syndromes of endocrine tumors)
  • 10% present w/CVA
  • 10% extra-adrenal (found within nervous tissue outside adrenal glands)
71
Q

What gene/enzyme converts pregnenolone to progesterone?
What zones is this in?
What other rxn does it catalyze?

A

3beta-HSD

  • All 3 zones
  • Also converts DHEA to androstenedione (minor product)
72
Q

Where are 11beta-HSD 1 and 2 found?

A

Kidney (type 2- not sure what this means)

- Not p450 family

73
Q

What adrenal cortex zones contain CYP11A1/desmolase/p450scc?

A

All 3

74
Q

What adrenal cortex zones contain CYP21A2/21alpha-hydroxylase/p450c21?

A

ZG and ZF

75
Q

What adrenal cortex zones contain CYP11B2/aldosterone synthase/p450aldo?

A

ZG only

76
Q

What adrenal cortex zones contain CYP11B1/11-hydroxylase/p450c11?

A

ZF only, I believe

77
Q

What adrenal cortex zones contain CYP17/17alpha-hydroxylase/P450c17?

A

ZF and ZR

FHB Hormone/Repro (16 decks)

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