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Endocrine Physiology > ACTH/Glucocorticoids > Flashcards

ACTH/Glucocorticoids Flashcards

1
Q

The adrenal gland is made up of the cortex and the medulla. Which one is essential for life?

A

The cortex.

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2
Q

What is the blood supply of the adrenal gland?

A

Supply: branches off the aorta, phrenic and renal arteries
Drainage: adrenal veins

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3
Q

What is the nerve supply of the adrenal gland?

A

Pre-ganglionic sympathetic fibers from the splanchnic nerves

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4
Q

What is the embryonic origin of the adrenal cortex and medulla

A

Cortex: mesenchyme in the area of the urogenital ridge
Medulla: neural crest cells

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5
Q

What are the 3 layers of the adrenal cortex?

A
  1. zona glomerulosa
  2. zona fasciculata
  3. zona reticularis
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6
Q

What does the zona glomerulosa do?

A

It secretes our good old friend aldosterone, which acts to increase Na+ retention and K+ and H+ excretion in the kidney. This system is controlled by the renin-angiotensin system

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7
Q

What’s going on in the zona fasciculata?

A

Secretes glucocorticoids (cortisol mainly) which effects lots of things (carb breakdown, immune suppression etc). This system is controlled by ACTH from the anterior pituitary, which is controlled by CRH from the hypothalamus.

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8
Q

What’s happening in the zona reticularis?

A

Secretes sex hormones and dehydroepiandrosterone (DHEAS) (a weak androgen that effects immune response differently than glucocorticoids)

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9
Q

What is special about the fetal adrenal gland and what is it’s role?

A
  1. It contains a provisional cortex between the medulla and adult cortex, which secretes mainly DHEAS, which is converted to androgens and estrogens by the placenta.
  2. Interestingly, this estrogen enters the maternal blood stream and is the major source of estrogen during gestation.
  3. The provisional cortex rapidly involutes after birth
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10
Q

What kind of cells does the adrenal medulla contain and what do they secrete

A

Chromaffin cells, which are modified sympathetic postganglionic nerves. They secrete norepinephrine and epinephrine in response to the preganglionic cholinergic neurons that innervate the medulla.

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11
Q

What is the rate limiting enzyme in cortisol biosynthesis

A

20,22 desmolase

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12
Q

Describe how ACTH works on the adrenal gland

A

ACTH binds to surface receptors and activates adenylyl cyclase, which converts ATP to cAMP which activates PK, which activates desmolase enzymes.

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13
Q

What players influence the release of ACTH (and B-END and B-LPH) from the corticotrophs of the anterior pituitary?

A

Mostly CRH from the hypothalamus. Epinephrine and ADH both act on the corticotroph to increase its sensitivity to CRH.

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14
Q

What are the 4 main secretory mechanisms of ACTH release

A
  1. negative feedback by cortisol
  2. Episodic secretion
  3. Diurnal secretion
  4. Stress
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15
Q

Describe the negative feedback regulation of cortisol secretion

A

Cortisol inhibits the release of CRH at the level of the hypothalamus and the release of ACTH at the level of the anterior pituitary

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16
Q

The hell is episodic secretion and why do you (should you) care?

A

Normally, ACTH (and cortisol) are released 7-15x/day in a pulsatile fashion. This prevents constant simulation that would down-regulate the receptors. Pulsatile release maintains receptor sensitivity

17
Q

What do we mean when we say diurnal rhythm of ACTH secretion?

A

ACTH and cortisol levels are highest in the early morning, and lowest in the evening. The pulsatile rhythm is superimposed on this 24 hour variation. This cycle may play a role in sleep cycle disruption due to jet-lag or emotional disturbances

18
Q

You’re SUPER STRESSED about the midterm. How will this influence your ACTH and cortisol levels.

A

ACTH will continue to be produced, and overcomes the negative feedback loop from cortisol. It is thought that higher centers in the brain can push CRH release despite the negative feedback loop.

19
Q

What is the name of cortisol’s travel buddy in the blood?

A

Cortisol binding globulin (CBG) or transcortin. 80% of cortisol is bound to CBG, and most of the other 20% is bound to albumin, with ~5% floating free.

20
Q

How does cortisol have both anabolic and catabolic effects?

A
  1. Anabolic: in the liver, it is increasing glucose through gluconeogeneis and ketogenesis
  2. Catabolic: breakdown of peripheral proteins and fat to support gluconeogenesis and ketogenesis in the liver
21
Q

Effect of cortisol on glucose levels?

A

Increased glucose supply via gluconeogenesis and decreased utilization by insulin dependent tissues (cortisol causes insulin resistance so that the brain keeps getting glucose since it’s insulin independent)

22
Q

What is the effect of cortisol on protein metabolism?

A
  1. Increased protein metabolism to supply amino acids for gluconeogenesis in the liver.
  2. Decreased protein synthesis everywhere except the liver
23
Q

Effect of cortisol on fat metabolism?

A

Increased fat metabolism as fat is broken down into glycerol and fatty acids for the liver

24
Q

How does cortisol effect the circulatory system? What role does it play in the kidneys specifically

A

It causes vasoconstriction and increases BP. The kidneys use cortisol to maintain proper glomerular filtration rate.

25
Q

Effects of high doses of cortisol on the immune system?

A
  1. stabilizes lysosomal membranes
  2. decrease capillary permeability
  3. depresses white cell proliferation and phagocytosis.
26
Q

Cushing’s Syndrome Due to an Adrenal Tumor

A

Adrenal tumor makes too much cortisol

27
Q

What causes Cushing’s syndrome from Ectopic ACTH

A

Some lung and GI tumors produce lots of ACTH, which in turn produces lots of cortisol

28
Q

What causes alcohol induced Cushing’s Syndrome

A

Due to excessive CRH secretion from the hypothalamus

29
Q

What causes Iatrogenic Cushing’s syndrome

A

Due to excessive consumption of glucocorticoids, which suppresses the whole hypothalamic-pituitary-adrenal axis.

30
Q

What are the three types of hypocortisolism?

A
  1. Primary Hypocortisolism: Addison’s Disease, hypocortisolism due to adrenal destruction.
  2. Secondary Hypocortisolism: from the failure of the pituitary to produce ACTH.
  3. Tertiary Hypocortisolism: failure of the hypothalamus to produce CRH.

Endocrine Physiology (9 decks)

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