Adrenal Hormones and Alterations in Adrenal Function Flashcards

1
Q

What are corticosteroids?

A

Steroid hormones produced by the adrenal cortex including glucocorticoids (cortisol) and mineralcorticoids (aldoseteron).

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2
Q

Name the parts of the adrenal cortex and their role.

A

Outer zona glomerulosa = mineralcorticoids.

Middle zona fasciculata = glucocorticoids

Inner zona reticularis = adrenal androgens

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3
Q

Glucocorticoids are synthesized from?

A

Cholesterol.

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4
Q

What are three glucocorticoids?

A
  1. Cortisol (95% of glucocorticoids).
  2. Corticosterone = a weak glucocorticoid. Most is converted to aldosterone.
  3. Cortisone = an inactive metabolite of cortisol. Needs to be converted back to cortisol to have an effect (occurs mainly in liver).
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5
Q

Is cortisol stored in the adrenal cortex?

A

No. Lipid-soluble hormones are produced when needed.

ACTH (adrenocorticotropic hormone stimulates the cells of the adrenal cortex to immediately synthesize and secrete cortisol.

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6
Q

What is the daily rhythm of cortisol?

A

Peaks early morning (after waking).

Lowest in the evening and early hours after midnight.

Also responds (increases) with physiological or psychosocial stress.

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7
Q

How is cortisol transported?

A

80-90% binds with transcortin (a plasma glycoprotein) or albumin.

Small amount is free in blood.

Cortisol then detaches from carrier protein to act on target cell.

Diffuses across membrane and binds with an intracellular receptor to alter gene expression and protein synthesis.

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8
Q

Why is cortisol called “the stress hormone”?

A

Because it mobilizes energy stores required in times of stress.

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9
Q

How does cortisol moblise energy stores (increase blood glucose and fatty acids)?

A

Increased lipolysis = free fatty acids + glycerol = gluconeogenesis

Increased protein breakdown = release of amino acids = gluconeogenesis.

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10
Q

In addition to mobilizing energy via lipolysis and protein breakdown - what are other effects of glucocorticoids?

A
  • immune suppression
  • anti-inflammatory effects
  • increase coaguability
  • mineralcorticoid effects
  • increased bone resorption and inhibit bone formation
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11
Q

How is cortisol regulated?

A

Hypothalamus releases corticotropin releasing hormone (CRH).

CRH stimulates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland.

ACTH stimulates the synthesis and release of cortisol by the adrenal cortex.

Rising cortisol inhibits both ACTH and CRH.

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12
Q

What lab tests are preformed for cortisol?

A

Blood cortisol is not useful as it measures both bound and free cortisol - free cortisol has biological activity.

Free cortisol can be measured in urine or saliva.

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13
Q

Where is cortisol metabolized and what are it’s metabolites.

A

Cortisol and cortisone are metabolized by liver and kidneys. Metabolites = tetrahydrocortisol and tetrahydrocortisone.

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14
Q

What are factors that accelerate the degradation of cortisol and cortisone into metabolites?

A

Inflammation, obesity, insulin resistance.

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15
Q

What is Cushing disease or cushing syndrome?

A

Alteration of the adrenal cortex = hyperfunction that causes increased secretion of cortisol (hypercortisolism).

Cushings syndrome is defined as the clinical syndrome composed of signs and symptoms resulting form chronic exposure to excessive circulating levels of glucocorticoids.

Cushings disease specifically refers to a glucocorticoid excess caused by an ACTH-producing pituitary adenoma.

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16
Q

What is adrenal insufficiency?

A

Alteration of the adrenal cortex = hypofunction that causes decreased secretion of cortisol (hypocortisolism).

Typically results from:
- inadequate stimulation of the adrenal glands by ACTH
- a primary inability of the adrenal glands to produce and secrete adrenocortical hormones (e.g. Addison disease)

17
Q

What is addison’s disease?

A

A primary adrenal insufficiency that is most commonly caused by an autoimmune destruction of cells of the adrenal cortex. It can cause both hypocortisolism and hypoaldoseteronism.

18
Q

What is stress dosing in addison’s disease?

A

Adjusting levels of exogenous glucorticoids for periods of stress and increased dependence on cortisol (infection, trauma etc.)