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

Adrenal Cortex and Adrenal Medulla (Endocrine) Flashcards

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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
Consequences of loss of function of zona fasciculate, zona reticularis
- 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.
26
mineralocorticoid =
aldosterone
27
glucocorticoid =
cortisol
28
loss of mineralocorticoid function causes
- severe HYPOtension, and can be fatal - Lack of glucocorticoids is not life-threatening under normal circumstances. but stressful situations can cause severe problems
29
cortisol, aldosterone, and adrenal androgens can easily be measured in
plasma and urine
30
sulfated androgen is specific to
synthesis in the adrenals
31
- zona glomerulosa is stimulated by | - secretes
- ATII and K+, and | - secretes: ALDOSTERONE
32
cortisol
- stress hormone that mobilizes carbs, protein and lipid | - other stress hormones: GH, glucagon, Epi
33
stress hormones are
- counter regulatory, bc they raise plasma glucose
34
Aldosterone's main action
- 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
RAAS
- the long-term regulation of BP | - activation is a decrease in BP inside the kidney
36
cushing syndrome =
hypercortisolism
37
primary hypercortisolism MCC
- adrenal adenoma secreting cortisol | - ACTH, adrenal androgens disease
38
secondary hypercortisolism due to
- 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
primary hypocortisolism due to
- withdrawal of glucocorticoid therapy or | - anterior pituitary mass with the loss of ACTH
40
primary hyperaldosteronism
- aka Conn's - due to an adenoma or hyperplasia of the zona glomerulosa - HTN, HYPOKalemia, alkalosis, low renin - NO EDEMA (Na escape)
41
Secondary hyperaldosteronism w HTN
- usually has renal vascular origin | - HTN, HYPOkalemia, HIGH renin
42
Secondary hyperaldosteronism w HYPOtension
- usually due to low CO - Low BP, HYPONatremia - EDEMA (no Na escape)
43
in congenital adrenal hyperplasia ____ causes ____
- decreased cortisol synthesis causes increased ACTH
44
in 21 beta-hydroxylase deficiency
= a mineralocorticoid deficiency - salt wasting and HYPOtension - androgen excess and female virilization
45
in 11 beta-hydroxylase deficiency
= mineralocorticoid EXCESS - salt retention and HTN - androgen excess and female virilization
46
in 17-alpha- hydroxylase deficiency
= mineralocorticoid excess - adrenal androgen deficiency, HTN - but gonadal steroid deficiency and HYPOgonadism
47
Aldosterone causes Na ____
- Na reabsoption | - increase total body Na
48
Aldosterone causes K+
- secretion | - decrease plasma [K+]
49
Aldosterone causes H+ ___
- secretion | - promotes metabolic alkalosis
50
Aldosterone causes HCO3-
- production | - promotes metabolic alkalosis
51
Aldosterone causes H20
- reabsorption | - causes volume expansion
52
renin is secreted by
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
renin secretion is triggered 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
54
- Plasma cortisol increased - plasma ACTH decreased - NO hyperpigmentation - Dx?
Dx primary hypercortisolism
55
- Plasma cortisol increased - plasma ACTH normal or increased - NO hyperpigmentation - Dx?
Dx: secondary hypercortisolism = CUSHING disease
56
- Plasma cortisol increased - plasma ACTH increased - yes (maybe) hyperpigmentation - Dx?
Dx: Ectopic ACTH secretion causing secondary hypercortisolism
57
- Plasma cortisol decreased - plasma ACTH increased - YES hyperpigmentation - Dx?
Dx: primary HYPOcortisolism
58
- Plasma cortisol decreased - plasma ACTH decreased - NO hyperpigmentation - Dx?
Dx: secondary hypocortisolism
59
primary hypercortisolism effect on 1. plasma cortisol 2. plasma ACTH 3. hyperpigmentation?
- Plasma cortisol increased - plasma ACTH decreased - NO hyperpigmentation
60
Cushing Disease effect on 1. plasma cortisol 2. plasma ACTH 3. hyperpigmentation?
- type of secondary hypercortisolism - Plasma cortisol increase - plasma ACTH normal or increased - NO hyperpigmentation
61
Primary hypocortisolism effect on 1. plasma cortisol 2. plasma ACTH 3. hyperpigmentation?
- Plasma cortisol decreased - plasma ACTH increased - YES hyperpigmentation
62
Ectopic ACTH production effect on 1. plasma cortisol 2. plasma ACTH 3. hyperpigmentation?
- type of secondary hypercortisolism - Plasma cortisol increased - plasma ACTH increased - yes (maybe) hyperpigmentation
63
secondary hypocortisolism effect on 1. plasma cortisol 2. plasma ACTH 3. hyperpigmentation?
- Plasma cortisol decreased - plasma ACTH decreased - NO hyperpigmentation
64
Secondary Hyperaldosteronism 1. plasma renin 2. ATII activity 3. total body Na 4. ECF volume 5. plasma volume 6. Edema
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
21 beta-hydroxylase deficiency effect on: 1. glucocorticoid 2. ACTH 3. BP 4. aldosterone (mineralocorticoid) 5. DOC (mineralocorticoid) 6. androgen 7. estrogen
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
11 beta-hydroxylase deficiency effect on: 1. glucocorticoid 2. ACTH 3. BP 4. aldosterone (mineralocorticoid) 5. DOC (mineralocorticoid) 6. androgen 7. estrogen
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
17 beta-hydroxylase deficiency effect on: 1. glucocorticoid 2. ACTH 3. BP 4. aldosterone (mineralocorticoid) 5. DOC (mineralocorticoid) 6. androgen 7. estrogen
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

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