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Physiology Pt. 4 > Endocrine 4 - Adrenal Roids > Flashcards

Endocrine 4 - Adrenal Roids Flashcards

1
Q

What are the four histologic zones of the adrenal gland and what do the cells in each zone make?

A 
From superficial to deep:
Zona Glomerulosa --> aldosterone
Zona Fasciculata --> cortisol
Zona Reticularis --> androgens
Medulla --> catecholamines
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2
Q

What is a mineralocorticoid?

A

Cholesterol-derived hormone that influences salt/water balance. Aldosterone is the big boy.

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3
Q

What is a glucocorticoid?

A

Cholesterol-derived hormone that influences glucose metabolism. Cortisol is the major one in the plasma.

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4
Q

In aldosterone synthesis, cholesterol is first converted to _________ by the enzyme _______. However, the rate limiting step is prior to this reaction. What is the rate limiting step?

A

cholesterol –> pregnenolone by CYP1A1

Before that, though, StAR (steroid acute regulatory protein) brings cholesterol from the plasma membrane into the mitochondria, and that is the rate-limiting step.

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5
Q

Describe the two forms in which cortisol can be found in the plasma.

A

The large majority of cortisol is bound to transcortin (a protein), and a small amount is free in the plasma. The free cortisol is what actually does stuff, and its in equilibrium with the transcortin-bound cortisol.

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6
Q

When should a clinician measure cortisol levels? Explain.

A

In the morning shortly after the patient wakes up, cuz that’s when they peak.

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7
Q

What is the cellular location of the cortisol receptor? What happens after cortisol binds the receptor?

A

In the cytoplasm. Cortisol binds, displaces Hsp90 (a thing that prevents nuclear binding), then transcription happens after that.

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8
Q

Which tissues bind cortisol? What are the effects of cortisol on each tissue?

A

Liver - cortisol stimulates gluconeogenesis.

Skeletal muscle - cortisol inhibits GLUT-4 glucose uptake.

Adipose tissue - cortisol (1) stimulates lipolysis, (2) inhibits lipogenesis, and (3) inhibits GLUT-4 glucose uptake.

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9
Q

Does gluconeogenic enzyme activity increase after administration of cortisol?

A

Yeah

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10
Q

Why do people with Cushing’s have muscle weakness? What hormone counteracts this effect?

A

Cortisol promotes proteolysis, insulin counteracts it.

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11
Q

How does cortisol effect catecholamine (epi, norepi) and glucagon signaling?

A

It enhances signaling by increasing (1) the amount of receptors, (2) adenylate cyclase, (3) cAMP, and (4) protein kinase A - which are all involved in the signaling process.

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12
Q

What are the five effects of glucocorticoids on the immune system?

A
  1. Inhibits production of inflammatory cytokines.
  2. Inhibits T cell proliferation.
  3. Promotes T cell apoptosis.
  4. Inhibits leukocyte chemotaxis.
  5. Inhibits prostaglandin production.
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13
Q

How exactly do glucocorticoids inhibit prostaglandin production?

A

Glucocorticoids promote synthesis of Annexin A1 aka Lipocortin, which inhibits phospholipase A2, the enzyme that acts on plasma membrane phospholipids to make arachidonic acid (precursor for prostaglandin).

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14
Q

Does the hypothalamus integrate a bunch of info, then release CRH if it wants to?

A

Yeah

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15
Q

Describe the hypothalamic-pituitary-adrenal axis and its feedback mechanism as it relates to cortisol.

A

Long feedback loop.

Also note that ADH acts synergistically with CRH to promote ACTH release, but cortisol doesn’t feed back to inhibit ADH.

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16
Q

What receptor binds ACTH? What second messengers are used?

A

7TM receptor. G protein –> cAMP –> protein kinase A –> decrease in glycogen synthesis, increase in cholesterol synthesis

17
Q

When does Addison’s disease cause hyperpigmentation of the skin?

A

When there is a primary defect in the adrenal glands (usually from autoimmune destruction of the gland). There is no cortisol to feedback to the pituitary –> tons of ACTH. alpha-MSH is also cleaved from POMC, the precursor of ACTH, so more ACTH = more MSH.

18
Q

When does Addison’s disease not cause skin hyperpigmentation?

A

When there is a defect in the hypothalamus or pituitary –> low ACTH levels cause hypocorticism, and low ACTH means low MSH.

19
Q

What is the difference between Cushing’s disease and Cushing’s syndrome? Which one causes hyperpigmentation and why?

A

Cushing’s disease is when there is a tumor of the hypothalamus or pituitary –> lots of ACTH, lots of MSH (pigmented).

Cushing’s syndrome (without Cushing’s disease) is hypercorticism from a defect in the adrenals, not pigmented cuz ACTH levels are low.

20
Q

Name five clinical features of Cushing’s diasease.

A
  1. Moon face
  2. Buffalo hump
  3. Abdominal striae
  4. Poor wound healing
  5. Muscle weakness
21
Q

Describe the exact action of aldosterone.

A

Acts on distal tubule and CD cells, upregulates the Na+/K+ ATPase to pump sodium into the cell and potassium into the tubule lumen (gain of sodium, loss of potassium) –> increased BP and volume.

22
Q

What are the four stimulants of the renin-angiotensin-aldosterone system?

A
  1. Decreased blood pressure
  2. Reduced blood volume
  3. Reduced osmolarity
  4. Elevated plasma K+
23
Q

Which two adrenal cortex hormones exhibit receptor cross-reacivity? Describe the mechanism that protects against inadvertent cross-stimulation.

A

Cortisol and aldosterone can activate each other’s receptors. There is a lot more cortisol in the blood than there is aldosterone, so in order for aldosterone receptors to not go nuts over cortisol, the aldosterone receptors express 11beta-hydroxysteroid dehydrogenase, which converts cortisol to cortisone, an inactive metabolite.

24
Q

Which amino acid are the catecholamines derived from? How does cortisol control their synthesis?

A

Derived from tyrosine. Cortisol regulates the expression of PNMT, a methyl transferase that converts norepinephrine to epinephrine.

25
Q

What are the two major enzymes that degrade the catecholamines? What is the end product?

A

MAO and COMT. End product is vanillylmandelic acid, ends up in the urine.

26
Q

One action that cortisol does NOT have is to:

a) stimulate gluconeogenesis in the liver
b) increase the sensitivities of tissues to epinephrine
c) stimulate skeletal muscle proteolysis between meals
d) promote wound healing
e) inhibit ACTH production

A

d) promote wound healing

- it suppresses the immune system

27
Q

ACTH acts on the adrenal cortex through what second messenger systems?

a) cGMP and PIP3/diacylglycerol
b) tyrosine kinases and Ca+2
c) Ca+2 and PIP3/diacylglycerol
d) cAMP
e) cGMP

A

d) cAMP

28
Q

Aldosterone acts in the kidney to:

a) reduce K+ reabsorption
b) stimulate Ca+2 reabsorption
c) stimulate K+ reabsorption
d) reduce Na+ reabsorption
e) stimulate Na+ reabsorption

A

e) stimulate Na+ reabsorption

Physiology Pt. 4 (14 decks)

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