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Endo/Repro Exam 1 > 10. Adrenal Gland > Flashcards

10. Adrenal Gland Flashcards

1
Q

What does the adrenal CTX and adrenal medulla secrete?

A

Adrenal CTX will secrete corticoids and androgens.

Adrenal medulla will secrete catecholamines.

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2
Q

What do the layers of the adrenal CTX secrete?

A
  1. Zona glomerulosa-> mineralcorticoids (aldoesterone)
  2. Zona fasciculata -> glucocorticoids (cortisol) and androgens (DHEA and DHEAs)
  3. Zona reticularis -> glucorticoids (cortisol) and adrogens (DHEA and DHEAs)
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3
Q

The HPA axis is under negative feedback control by what?

A

Cortisol.

It will inhibit cortisol ACTH release from adrenal medulla and inhibit CRH release from the hypothalamus.

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4
Q

Steroidogenesis starts with what?

A

Cholesterol in the adrenal cortex

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5
Q

If we have a deficiency in 21-hydroxylase (gene: _______), what occurs?

Mineralcorticoids: ______

Cortisol: ______

Androgens: ______

A

21-hydoxylase (CYP21A2) is the most common. We will see

  1. decreased mineracorticoid (aldosterone)
  2. decreased cortisol,
  3. increased sex hormones (d/t increase in 17-OH-pregnenolone)
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6
Q

What are the signs and symptoms for 21-hydroxylase deficiency?

BP

Na+

K

Labs

Other presentations

A
  1. Hypotension d/t decreased aldosterone causing Na+ and H20 loss.
  2. Hyperkalemia (High K)
  3. Elevated renin
  4. Precocious puberty and Virulization of fetus
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7
Q

11B-hydroxylase (gene: _____) deficiency, we see what in steroids?

Mineralcorticoids: _____

Cortisol: ______

Androgens: _____

A

CYP11B1

  • Mineralcorticoids: decrease aldosterone and increase deoxycorticosterone and lead to sx similar to hyperaldosteronism (increase BP)
  • Decreased cortisol
  • Increased androgens
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8
Q

What are the signs and symptoms for 11-B-hydroxylase deficiency?

BP

K

Labs

Other presentations

A
  1. Increase BP (HTN)
  2. Decrease K+ (hypokalemia)
  3. Decrease renin
  4. Virulization and F have ambigious genitals
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9
Q

In 17-alpha hydroxylase/17,20 lyase defiviency, what would we see?

Mineralcorticoids: _____

Cortisol: _____

Androgens: _____

A

EXTREMEY RARE- prevents formation of any andrenocortical hormone other than aldosterone.

Mineralcorticoids: excess

Cortisol: decrease

Androgens: decreas

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10
Q

What are the signs and symptoms for 17-a-hydroxylase/17-20 lyase deficiency?

BP

K

Labs

Other presentations

A
  • BP: High BP (HTN) d/t Na+ and water reabsorption.
  • K: low (hypokalemia)
  • Because of loss of cortisol, ACTH builds up.
  • Labs: decrease androstenedione causing hypogonadism
  • Other presentations: patients are dx at puberty
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11
Q

Cortisol:

Target tissue

Actions:

Too much glucorticoid (cortisol): _______

Too little glucocorticoid (cortisol): ________

A
  • Target: NTS the cell and binds to receptors in the nucleus or cytosol of all tissue t/o the body.
  • Actions: numerous: it binds to GRE (glucocorticoid response elements) and alters gene transcription
  • Too much: Cushings dz or cushings syndrome
  • Too little: Addisons disease
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12
Q

What are the effects of cortisol on the

Immune system:

Liver:

Muscle:

Adipose tissue:

A
  • Immune system: immune supression, increasing chances of infection
  • Liver: increase gluconeogenesis and glycogenolysis
  • Muscle: break down protein
  • Adipose tissue: lipolysis.

Goal is to increase glucose levels. there are differences in acute and chronic states.

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13
Q

Describe the stimulus, release and regulation of cortisol release:

A
  1. Stimulus: Circadian rhythm (secrete most in the early morning and lease in the late evening) and stress
  2. CRF (CRH) is released from the paraventricular nucleus of the hypothalamaus
  3. Binds to CRF1 receptor (GCPR) on the AP.
  4. Stimulates the release of ACTH (derived from POMC) from the anterior pituitary -> adrenal CTX.
  5. Adrenal CTX (zona fasiculata and reticularis) releases cortisol onto any target tissue.

Feedback: Cortisol can neg backback to AP and hypothalamus to inhibit ACTH and CRH release.

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14
Q

What is the principle hormone that stimulates the adrenal glucocorticoids?

A

ACTH

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15
Q

Why does an increase in ACTH cause hyperpigmentation?

A

When ACTH is cleaved in non-pituitary tissues, it contains alpha-melanocyte stimulating hormone (a-MSH), leading to hyperpigmentation.

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16
Q

What are the HPA axis feedback loops?

A
  1. Long feedback loop: Cortisol (glucocorticoids) inhibits
  • POMC transcription/mRNA synthesis of ACTH from AP
  • mRNA synthesis of CRH from hypothalamus.
  1. Short feedback loop: ACTH inhibits CRH from the hypothalamus.
  2. Ultrashort loop: CRH inhibits itself.
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17
Q

What is the dexamethasone supression test (DST)?

A

Dexamethsone is synthetic glucocorticoid. There are 2 types of DST tests done to test to see if someone has hypercortisolism: Low-dose and high-dose.

  • Low dose DST: run to help us differentiate patients with Cushings from patients who do not have Cushings (hyperglucorticoids). A normal response is supression of ACTH and cortisol. If there is no ACTH supression -> Cushings.
  • High dose DST: Helps to distinguish the SOURCE of the problem: Cushings syndrome (d/t non-pituitary ACTH secreting tumor) or Cushings disease (d/t a pituitary ACTH secreting tumor).
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18
Q

What is the cosyntropin (synthetic ____) stimulation test?

A

CST (synthetic ACTH) is used to detect primary or secondary adrenal gland insufficiency.

  1. Administer ACTH
  2. See what happens:
  • In a normal healthy person: cortisol should increase from baseline
  • If the adenal is unresponsive and cortisol remains the smae or rises only a small amount -> adrenal insufficiency.
  • If the adrenal responds dramatically and you see a cortisol increse GREATLY -> secondary adrenal insufficiency
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19
Q

What is the difference between cushings syndrome and cushings disease?

A

Cushing’s disease is caused by a pituitary tumor.

Cushing’s syndrome is caused by an adrenal CTX tumor.

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20
Q

What is Cushings disease?

A

Hypersecretion of cortisol d/t hypersecretion of ACTH due to a pituitary tumor -> excess cortisol is secreted.

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21
Q

What is Cushings syndrome?

A
  • Cushing syndrome is a high secretion of cortisol. The amount of ACTH will depend on the etiology.
  • Can be d/t: adrenal tumor, administration of steriod hormones or e_ctopic (non-pituitary) ACTH-secreting tumor._
  • If an adrenal tumor, low ACTH.
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22
Q

In a DMT test, how would we determing if Cushings syndrome is d/t adrenal tumor or a ectopic ACTH secreting tumor?

A
  1. Low dose DMT test will determine if positive for hypercorticoidism (Cushings). Cortisol will not be supressed; it will be normal or high.
  2. High DMT test:
  • Adrenal tumor: Decrease ACTH d/t negative feedback on pituiary, but cortisol will be high.
  • Ectopic ACTH secreting tumor: ACTH stay same, cortisol stays the same.
23
Q

In a DMT test, how would we determing if Cushings disease (pituitary tumor)?

A
  1. Low dose- will only tell if pt has hypercortisolism
  2. High Dose DMT:
    * Pituitary tumor: decrease ACTH will supress cortisol, and will result in in normal to high levels of cortisol.
24
Q

If a patient with Cushings syndrome was injected with exogenous glucocorticoids (dexmethasone), what do you predict would happen to their ACTH levels and cortisol supression?

A

ACTH would be undetectable and dexamethsomne FAILS to supress cortisol because the negative feedback loop is functional, but hypercortisolism continues.

25
Q

If a patient with Cushings disease was injected with exogenous glucocorticoids (dexmethasone), what do you predict would happen to their ACTH levels and cortisol supression?

A

ACTH would be normal or slighly. high and dexamethsone would successfully. supress cortisol secretion because of abnormal negative feedback at the level of the pituiary.

26
Q

What is Addison’s disease (aka _________)?

  • ____ ACTH
  • ____ cortisol
  • ____ aldosterone.
A
  • Primary adrenal insuffiency where ALL the adrenal CTX is destructed- hyposecretion of ALL adrerenal steroids.
    • High ACTH
    • Low cortisol
    • Low aldosterone.
  • Thus, adrenal gland cannot respond to ACTH.
27
Q

What is secondary adrenal insufficiency?

____ ACTH

____ cortisol

____ aldosterone.

A

Cause: exogenous glucocortioid administration, damaging the pituitary, reducing ACTH secretion.

  • Low ACTH
  • Low cortisol
  • Normal aldosterone
28
Q

If a pt with Addisons dz is injected with synthetic ACTH (cosyntropin), what would happen to cortisol levels?

A

No change

29
Q

If a pt with secondary adrenal insuffiency is injected with synthetic ACTH (cosyntropin), what would happen to cortisol levels?

A

Increase because the adrenals are functional.

30
Q

What is Addisons Dz and what are key signs?

A

Addison’s disease is an inability of the adrenal gland produce ANY adrenal hormones due to autoantibodies, but this results in increased ACTH in an attempt to compensate.

Key signs:

  1. This leads to more α-melanocyte stimulating hormone, and more pigmentation.
  2. Hypoglycemia
  3. Hypotension
  4. Hyponatremia and hyperkalemia (d/t loss of aldosterone)
31
Q

What can cause Addisons disease?

A
    1. Autoimmune disease of adrenal gland
    1. Adrenal hemorrhage secondary to infection or anticoagulants
    1. Infections (TB or N. meningitidis)
    1. Tumor.
32
Q

What is the main mineralcorticoid that controls Na+ and K+ exchange in the distal nephron?

A

Aldosterone

33
Q

What is the main result of Aldosterone and how does it do so?

A

Main result: Increases Na+ reabsorption, increases K+ secretion and increase H+ secretion.

It does do by:

    1. Increasing synthesis and activity of Na+ channels on the apical membrane
    1. Increases synthesis and activity of Na+/K+ ATPase in the BL membrane.
34
Q

While there is an effect from ACTH on aldosterone secretion, the most important regulator is the _________.

A

RAAS system.

35
Q

What causes activation of RAAS system?

A

1. Decrease Na+ or increased K+ in blood.

2. Decreased BV or BP.

36
Q

Primary hyperaldosteronism (________)

____ plasma aldosterone

_____ plasma renin

A

Primary aldosteronism is called Conn syndrome.

  • High aldosterone, and thus high H20, Na+ and BP, low K+
  • Low renin
37
Q

Secondary hyperaldosteronism

____ plasma aldosterone

_____ plasma renin

A

kidney problem

Cause: excess renin from juxtaglomerular cells, feedback to the adrenal gland and causes high aldosterone.

  • high plasma aldosterone
  • high plasma renin
38
Q

What is primary hypoaldosteronism?

A

Hyposecretion of aldosterone d/t destruction of the adrenal CTX or problems with aldosterone synthesis.

39
Q

What is secondary hypoaldosteronism?

_____ aldosterone

_____ renin

A

kidney problem

Cause: hyposecretion of renin -> decrease in aldosterone

  • decrease aldosterone
  • decrease renin
40
Q

The effect of ACTH on aldosterone is what?

A

modest at best

41
Q

Primary adrenal failure

____ cortisol

____ aldosterone

A

low

low

42
Q

ACTH deficiency

______ cortisol

______ aldosterone

A

low cortisol

no change in aldosterone, because RAAS is still functional

43
Q

Adrenal androgens: _____ and _____, which are precurors to ________.

A

DHEA and DHEAS (DHEA sulfate) are precursors to human sex steroids.

44
Q

Catecholamines are made in the __________ and derived from ______.

A

adrenal medulla

L-tyrosine

45
Q

Chromaffin cells in the adrenal medulla make ____% EPI and ____% NE

A

80% EPI

20% NE.

46
Q

Synthesis of catecholamines is under control of what axis?

A

CRH- ACTH- Cortisol

47
Q

How do we make our catecholamines?

A
    1. Tyrosine
    1. Sympathetic stimulation (ACh) releases ACh onto nicotenic receptors, increasing synthesis of tyrosine hydroxlase (rate limiting step) to make L-DOPA.
    1. L-DOPA -> Dopamine, which gets stored in secretory vesicles called chromaffin granules.
    1. In the granules. sympathetic stimulation (ACh) releases ACh onto nicotenic receptors to increase synthesis of dopamine-B-hydroxylase (DBH) to go from Dopamine -> NE
    1. NE diffuses out of granules
    1. To make EPI: cortisol increases the PNMT enzyme and EPI is made in the cytosol.
    1. VMATS move EPI from cytosol -> back into the granule
    1. Sympathetic stimulation triggers release.
48
Q

Are NE and EPI made in the same cellular compartments?

A
  • No. NE is made in the chromaffin granule.
  • EPI is made in the cytosol.
49
Q

Action of catecholamines is short: only about 10 seconds.

What two things help us degrade catecholamines?

A
  1. MAO (monoamine oxidase) oxidizes things
  2. COMT (catechol-O-methyl-transferase) methylates things: its the main enzyme that inactivates catecholamines that are released by the adrenal hland.
50
Q

How can we determine total catecholamine production?

A

Measure the breakdown products; such as VMA.

51
Q

What is a pheochromacytoma?

Symtoms?

A

Tumor in the chromaffin tissue that produces excess catecholamines that bind to both alpha and B adrenergic R.

Symtoms wax and wane:

  1. HTN,
  2. HA,
  3. palpitations and
  4. sweating.
52
Q

Are pheochromacytomas malignant?

A

No. Most are benign, unilateral adrenal medulla tumors.

53
Q

REVIEW NOTECARDS ON ADRENERGIC RECEPTORS

A

Endo/Repro Exam 1 (14 decks)

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