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Kaplan Physio > Adrenal Cortex and Adrenal Medulla (Endocrine) > Flashcards

Adrenal Cortex and Adrenal Medulla (Endocrine) Flashcards

1
Q

Circulating Epinephrine originates mainly from

A
  • the adrenals

- epi increases the metabolic rate. This won’t occur without thyroid hormones or the adrenal cortex.

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2
Q

Circulating NE originates mainly from

A
  • sympathetic nerve endings
  • removal of adrenal medulla reduces plasma epi to very low levels, but doesn’t alter plasma NE
  • bc many of the actions of epi are also mediated by NE, the adrenal medulla isn’t essential for life
  • episodic release (particularly of NE) can induce a hypertensive crisis
  • most reliable test is urine metanephrines
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3
Q

Epinephrine is a stress hormone secreted in response to

A

exercise, exposure to cold, emergencies, hypoglycemia

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4
Q

Epinephrine increases blood glucose via

A
  • liver glycogenolysis

- it also stimulates muscle glycogenolysis, but muscle does not release glucose

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5
Q

Epinephrine increase the release of FA from adipose by

A

increasing the activity of hormone-sensitive lipase

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6
Q

pheochromocytomas

A
  • secrete epinephrine and NE and

- are most consistently assoc w HTN

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7
Q

paragangliomas

A
  • extra-adrenal pheochromocytomas of sympathetic ganglia
  • located primarily within the abdomen
  • secrete NE
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8
Q

PMNT (phenylethanolamine-N-methyltransferase)

A

converts NE into Epi

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9
Q

Half-life of catecholamines = approx 2 min and Metabolic end-products =

A
  • metanephrines and VMA (vanillylmandelic acid)

- both can be measured in plasma and urine

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10
Q

episodic release of catecholamines (particularly of NE) can induce

A
  • a hypertensive crisis
  • can be induced by physical stimuli that displaces abdominal contents
  • most reliable test is urine metanephrines
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11
Q

The ____ action of NE is essential for the maintenance of normal BP, esp ____

A
  • VASOCONSTRICTIVE
  • esp when a person is standing
  • Plasma NE levels double when one goes from lying to standing
  • Ppl with inadequate production of NE suffer from orthostatic hypotension
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12
Q

Major effect of Epi on the liver

A
  • increases activity of liver and muscle phosphorylase
  • promotes glycogenolysis
  • this increases glucose output by the liver
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13
Q

Major effect of Epi on skeletal muscle

A
  • promotes glycogenolysis
  • but bc muscle lacks G6Phosphatase, glucose can’t be released by skeletal muscle
  • instead, it’s metabolized to lactate before being released into circulation
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14
Q

Major effect of Epi on adipose tissue

A
  • increases lipolysis in adipose tissue
  • by increasing the activity of hormone-sensitive lipase
  • Glycerol from TG breakdown is a major substrate for gluconeogenesis
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15
Q

People with inadequate production of NE suffer from

A

orthostatic hypotension

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16
Q

Pheochromocytomas

A
  • adrenal tumors that secrete Epi and NE in various ratios
  • usually unilateral benign tumors
  • highly vascular and encapsulated
  • characteristic of MEN2A and MEN2B
  • paragangliomas (pheochromocytomas on sympathetic ganglia)
  • most consistent feature = HTN
  • Sx: headache, diaphoresis, palpitations, anxiety
  • increased metabolic rate and hyperglycemia also occur
  • can cause hypertensive crisis
  • usually curable, but fatal if undiagnosed
  • tx: alpha blocker followed by surgical removal
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17
Q

Secretion of the adrenal medulla is

A
  • 20% NE and 80% epinephrine

- half-life of catecholamines is approx 2min.

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18
Q

ACTH controls the release of

A

cortisol and adrenal androgens

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19
Q

Aldosterone is stimulated

A

by a rise in ATII and/or K+

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20
Q

Zona Fasciculata of Adrenal Gland

  1. location
  2. Hormone secreted
  3. controlled by
A
  1. location: between zone glomerulosa and zone reticularis
  2. secretes: Cortisol and Androgens (along w zona reticularis)
  3. controlled by: ACTH
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21
Q

Zona reticularis of Adrenal Gland

  1. location
  2. Hormone secreted
  3. controlled by
A
  1. location: between zone fasciculate and medulla
  2. secretes: Cortisol and Androgens (along w zona fasciculata)
  3. controlled by: ACTH
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22
Q

Medulla of Adrenal Gland

  1. location
  2. Hormone secreted
  3. controlled by
A
  1. location: inner-most part
  2. secretes: epinephrine
  3. controlled by: ANS
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23
Q

Zona Glomerulosa of Adrenal Gland

  1. location
  2. Hormone secreted
  3. controlled by
A
  1. location: outer-most region
  2. secretes: Aldosterone
  3. controlled by: AT II, K+
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24
Q

Consequences of loss of function of zona glomerulosa

A
  • absence of the mineralocorticoid aldosterone causes:
  • Loss of Na+
  • decreased volume of the ECF
  • low BP
  • circulatory shock, death
  • if probs develop w Ant pituitary secretion: glucocorticoid secretion may be affected, but mineralocorticoid system remains intact.
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25
Q

Consequences of loss of function of zona fasciculate, zona reticularis

A
  • absence of the glucocorticoid, cortisol. contributes to:
  • circulatory failure, bc w/o cortisol, catecholamines don’t exert their normal vasoconstrictive action
  • an inability to readily mobile energy sources (glucose and FFA) from glycogen or fat
  • under normal conditions: not life threatening; under stressful situations, severe problems can arise
  • ie fasting can result in fatal hypoglycemia
  • if probs develop w Ant pituitary secretion: glucocorticoid secretion may be affected, but mineralocorticoid system remains intact.
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26
Q

mineralocorticoid =

A

aldosterone

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27
Q

glucocorticoid =

A

cortisol

28
Q

loss of mineralocorticoid function causes

A
  • severe HYPOtension, and can be fatal
  • Lack of glucocorticoids is not life-threatening under normal circumstances. but stressful situations can cause severe problems
29
Q

cortisol, aldosterone, and adrenal androgens can easily be measured in

A

plasma and urine

30
Q

sulfated androgen is specific to

A

synthesis in the adrenals

31
Q
  • zona glomerulosa is stimulated by

- secretes

A
  • ATII and K+, and

- secretes: ALDOSTERONE

32
Q

cortisol

A
  • stress hormone that mobilizes carbs, protein and lipid

- other stress hormones: GH, glucagon, Epi

33
Q

stress hormones are

A
  • counter regulatory, bc they raise plasma glucose
34
Q

Aldosterone’s main action

A
  • increase Na reabsorption in kidney
  • bc water follows Na, aldosterone doesn’t affect [Na]
  • aldosterone also increases K+ and H+ loss by the kidney
35
Q

RAAS

A
  • the long-term regulation of BP

- activation is a decrease in BP inside the kidney

36
Q

cushing syndrome =

A

hypercortisolism

37
Q

primary hypercortisolism MCC

A
  • adrenal adenoma secreting cortisol

- ACTH, adrenal androgens disease

38
Q

secondary hypercortisolism due to

A
  • increase in ACTH
  • if the source is the Anterior pituitary = Cushing’s disease
  • Ectopic ACTH hypersecretion is MC due to small cell carcinoma of lung
39
Q

primary hypocortisolism due to

A
  • withdrawal of glucocorticoid therapy or

- anterior pituitary mass with the loss of ACTH

40
Q

primary hyperaldosteronism

A
  • aka Conn’s
  • due to an adenoma or hyperplasia of the zona glomerulosa
  • HTN, HYPOKalemia, alkalosis, low renin
  • NO EDEMA (Na escape)
41
Q

Secondary hyperaldosteronism w HTN

A
  • usually has renal vascular origin

- HTN, HYPOkalemia, HIGH renin

42
Q

Secondary hyperaldosteronism w HYPOtension

A
  • usually due to low CO
  • Low BP, HYPONatremia
  • EDEMA (no Na escape)
43
Q

in congenital adrenal hyperplasia ____ causes ____

A
  • decreased cortisol synthesis causes increased ACTH
44
Q

in 21 beta-hydroxylase deficiency

A

= a mineralocorticoid deficiency

  • salt wasting and HYPOtension
  • androgen excess and female virilization
45
Q

in 11 beta-hydroxylase deficiency

A

= mineralocorticoid EXCESS

  • salt retention and HTN
  • androgen excess and female virilization
46
Q

in 17-alpha- hydroxylase deficiency

A

= mineralocorticoid excess

  • adrenal androgen deficiency, HTN
  • but gonadal steroid deficiency and HYPOgonadism
47
Q

Aldosterone causes Na ____

A
  • Na reabsoption

- increase total body Na

48
Q

Aldosterone causes K+

A
  • secretion

- decrease plasma [K+]

49
Q

Aldosterone causes H+ ___

A
  • secretion

- promotes metabolic alkalosis

50
Q

Aldosterone causes HCO3-

A
  • production

- promotes metabolic alkalosis

51
Q

Aldosterone causes H20

A
  • reabsorption

- causes volume expansion

52
Q

renin is secreted by

A

juxtaglomerular cells (baroreceptors)

  • stimulated by a decrease in pressure in the renal afferent arteriole
  • decreased Na+ delivery to macula dense of DCT
  • increased beta-1 noradrenergic input to the juxtaglomerular cells
53
Q

renin secretion is triggered by

A
  • a decrease in pressure in the renal afferent arteriole
  • decreased Na+ delivery to macula dense of DCT
  • increased beta-1 noradrenergic input to the juxtaglomerular cells
54
Q
  • Plasma cortisol increased
  • plasma ACTH decreased
  • NO hyperpigmentation
  • Dx?
A

Dx primary hypercortisolism

55
Q
  • Plasma cortisol increased
  • plasma ACTH normal or increased
  • NO hyperpigmentation
  • Dx?
A

Dx: secondary hypercortisolism = CUSHING disease

56
Q
  • Plasma cortisol increased
  • plasma ACTH increased
  • yes (maybe) hyperpigmentation
  • Dx?
A

Dx: Ectopic ACTH secretion causing secondary hypercortisolism

57
Q
  • Plasma cortisol decreased
  • plasma ACTH increased
  • YES hyperpigmentation
  • Dx?
A

Dx: primary HYPOcortisolism

58
Q
  • Plasma cortisol decreased
  • plasma ACTH decreased
  • NO hyperpigmentation
  • Dx?
A

Dx: secondary hypocortisolism

59
Q

primary hypercortisolism effect on

  1. plasma cortisol
  2. plasma ACTH
  3. hyperpigmentation?
A
  • Plasma cortisol increased
  • plasma ACTH decreased
  • NO hyperpigmentation
60
Q

Cushing Disease effect on

  1. plasma cortisol
  2. plasma ACTH
  3. hyperpigmentation?
A
  • type of secondary hypercortisolism
  • Plasma cortisol increase
  • plasma ACTH normal or increased
  • NO hyperpigmentation
61
Q

Primary hypocortisolism effect on

  1. plasma cortisol
  2. plasma ACTH
  3. hyperpigmentation?
A
  • Plasma cortisol decreased
  • plasma ACTH increased
  • YES hyperpigmentation
62
Q

Ectopic ACTH production effect on

  1. plasma cortisol
  2. plasma ACTH
  3. hyperpigmentation?
A
  • type of secondary hypercortisolism
  • Plasma cortisol increased
  • plasma ACTH increased
  • yes (maybe) hyperpigmentation
63
Q

secondary hypocortisolism effect on

  1. plasma cortisol
  2. plasma ACTH
  3. hyperpigmentation?
A
  • Plasma cortisol decreased
  • plasma ACTH decreased
  • NO hyperpigmentation
64
Q

Secondary Hyperaldosteronism

  1. plasma renin
  2. ATII activity
  3. total body Na
  4. ECF volume
  5. plasma volume
  6. Edema
A
  1. increased
  2. increased (increased ATII activity will drive the 2ndary hyperaldosteronism)
  3. increased
  4. increased
  5. increased
  6. YES (Na escape prevents peripheral edema in primary, but not secondary hyperaldosteronism)
    - also note that the increased ECF volume remains mainly on the venous side of the circulation, accentuating the venous congestion and preventing a return of circulating blood volume to normal
65
Q

21 beta-hydroxylase deficiency effect on:

  1. glucocorticoid
  2. ACTH
  3. BP
  4. aldosterone (mineralocorticoid)
  5. DOC (mineralocorticoid)
  6. androgen
  7. estrogen
A
  1. glucocorticoid: decreased
  2. ACTH: increased
  3. BP: decreased
  4. aldosterone (mineralocorticoid): decreased
  5. DOC (mineralocorticoid): decreased
  6. androgen: increased adrenal
  7. estrogen: no change
66
Q

11 beta-hydroxylase deficiency effect on:

  1. glucocorticoid
  2. ACTH
  3. BP
  4. aldosterone (mineralocorticoid)
  5. DOC (mineralocorticoid)
  6. androgen
  7. estrogen
A
  1. glucocorticoid: decreased
  2. ACTH: increased
  3. BP: increased
  4. aldosterone (mineralocorticoid): decreased
  5. DOC (mineralocorticoid): increased
  6. androgen: increased adrenal
  7. estrogen: no change
67
Q

17 beta-hydroxylase deficiency effect on:

  1. glucocorticoid
  2. ACTH
  3. BP
  4. aldosterone (mineralocorticoid)
  5. DOC (mineralocorticoid)
  6. androgen
  7. estrogen
A
  1. glucocorticoid: decreased
  2. ACTH: increased
  3. BP: increased
  4. aldosterone (mineralocorticoid): decreased
  5. DOC (mineralocorticoid): increased
  6. androgen: decreased adrenal and testicular
  7. estrogen: decreased

Kaplan Physio (4 decks)

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