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Neuro Endo 3 > Hypothalamic-Pituitary Relationship and Biofeedback Pt. 2 > Flashcards

Hypothalamic-Pituitary Relationship and Biofeedback Pt. 2 Flashcards

1
Q

What hormone is released by the zona glomerulosa?

A

Mineralcorticoids (ADH)- regulates salt and volume homeostasis

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2
Q

What hormone is released by zona fasciculata?

A

Glucocorticoids (cortisol)- regulates glucose utilization, immune and inflammatory homeostasis
Androgens (DHEAS)- androgen precursor

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3
Q

What hormone is released by zona reticularis?

A

Glucocorticoids (cortisol)- regulates glucose utilization, immune and inflammatory homeostasis
Androgens (DHEAS)- androgen precursor

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4
Q

What hormone is released by medulla’s chromaffin cells?

A

Catecholamines (epi and norepi)- rapid responders to stress

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5
Q

What things activate CRH in the hypothalamus?

A
  • physical stress
  • emotional stress
  • metabolic stress
  • infection/inflammation
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6
Q

How is cortisol regulated?

A

Cortisol inhibits ACTH and CRH production

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7
Q

When are cortisol levels the highest? Lowest?

A

Highest in early morning
Lowest late at night
ACTH levels remain constant

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8
Q

How does ACTH release act on the zona reticularis?

A
  • binds to MC2R
  • promotes secretion of androgens
  • no feedback
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9
Q

How does ACTH release act on zona fasciculata?

A
  • binds to MC2R
  • promotes cortisol release
  • negative feedback
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10
Q

What is the mechanism of aldosterone secretion?

A

1) low BP stimulates acts on kidney via renin-angiotensin cascade
2) stimulates zona glomerulosa of adrenal cortex to release aldosterone
3) aldosterone targets kidney tubule
4) leads to increased absorption of Na+ followed by water; increased K+ excretion
5) increased BP and BV

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11
Q

Symptoms and signs of Cushing’s syndrome

A
  • truncal obesity
  • moon face
  • buffalo hump
  • easy bruising
  • purple striae
  • hypertension
  • edema
  • weakness
  • osteoporosis
  • hirsutism
  • virilization
  • diabetes
  • immunosuppression
  • cognitive effects
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12
Q

What is dexamethasone?

A

exogenous gluccocorticoid

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13
Q

What will happen if dexamethasone if given to a normal patient?

A

suppression of ACTH levels

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14
Q

What does a low-dose dexamethasone test differentiate?

A

Patients with CS will not have ACTH suppression while those that do not have CS will have ACTH suppression
(does not specify source of ACTH over production)

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15
Q

What does a high-dose dexamethasone test differentiate?

A

Distinguishes people with Cushing’s disease

Used after diagnosis of Cushing syndrome is made

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16
Q

What kind of CS results in decreased ACTH levels after high dose dexamethasone?

A

Pituitary tumor (lowered ACTH mediated by negative feedback on pituitary)

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17
Q

What kind of CS results in not change in ACTH levels?

A

Ectopic tumor (no negative feedback effect on ectopic source of ACTH)

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18
Q

Exogenous glucocorticoid excess

A

Iatrogenic (caused by drug/medication)

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19
Q

Pseudo Cushing’s Syndrome

A
  • major anxiety/depression
  • acute/chronic illness
  • alcoholism
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20
Q

ACTH dependent

A
  • Cushing’s disease
  • ectopic ACTH secreting tumor
  • CRH-secreting tumor
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21
Q

ACTH independent

A
  • adrenal adenoma

- adrenal carcinoma

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22
Q

Plasma ACTH concentrations in patients with Cushing’s syndrome

A

Cushing disease= higher ACTH levels than normal (pituitary tumor, so excess secretion of ACTH)
Adrenal tumor = lower than normal ACTH (excess cortisol produced feedback inhibits ACTH release)
Ectopic = extremely high ACTH

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23
Q

What is the effect of exogenous administration of glucocorticoids?

A

Atrophied zona fasciculata cells which produce cortisol

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24
Q

What is the primary action of aldosterone?

A

renal sodium reabsorption

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25
Q

How does aldosterone act on the kidney?

A

1) aldosterone combines with a cytoplasmic receptor in the nephron of the kidney
2) hormone receptor complex initiates transcription in the nucleus
3) translation and protein synthesis makes new protein channels and pumps
4) aldosterone-induced proteins modulate existing channels
5) results in increased Na+ reabsorption and K+ secretion
6) Na+ reabsorption leads to water retention which increased BP

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26
Q

Where is ACTH produced?

A

Anterior pituitary; derived from post-translational processing of POMC

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27
Q

How does ACTH act on non-pituitary tissues?

A

activates alpha-MSH which promotes melanin synthesis

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28
Q

How does increased ACTH lead to hyperpigmentation in Addison’s disease?

A

ACTH above physiological levels will bind to MC1R in melanocytes and increase melanin synthesis

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29
Q

Result of primary adrenal insufficiency

A

both cortisol and aldosterone secretion is reduced because adrenal cortex is damaged

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30
Q

Secondary adrenal insufficiency

A

cortisol is decrease since no ACTH is released from pituitary, but the renin-angiotensin axis still produces aldosterone

31
Q

Causes of primary adrenal insufficiency (Addison’s Disease)

A
  • autoimmune
  • adrenal hemorrhage
  • Waterhouse-Freidrichsen syndrome (adrenal hemorrhage secondary to N. meningitidis)
  • hemorrhage caused by anticoagulant treatment
  • infection
  • tumor metastases to adrenal gland
32
Q

Treatment for adrenal insufficiency

A

hormone replacement

33
Q

Dx for primary (adrenal) excess

A
  • increased cortisol
  • decreased CRH
  • decreased ACTH
  • no hyperpigmentation
34
Q

Dx for secondary (pituitary) excess

A
  • increased cortisol
  • decreased CRH
  • increased ACTH
  • hyperpigmentation
35
Q

Dx for primary deficiency

A
  • decreased cortisol
  • increased CRH
  • increased ACTH
  • hyperpigmentation
36
Q

Dx for secondary deficiency

A
  • decreased cortisol
  • increased CRH
  • decreased ACTH
  • no hyperpigmentation
37
Q

Dx for steroid administration

A
  • decreased cortisol (but symptoms of excess)
  • decreased CRH
  • decreased ACTH
  • no hyperpigmentation
38
Q

Primary hyperaldosteronism

A

excessive release of aldosterone from the adrenal cortex

39
Q

Conn’s Syndrome

A

primary hyperaldosteronism as a result of an adenoma in the adrenal cortex

40
Q

Secondary hyperaldosteronism

A

excessive renin secretion by the juxtaglomerular cells in the kidney

41
Q

Hypoaldosteronism

A
  • destruction of adrenal cortex
  • defects in aldosterone synthesis
  • inadequate stimulation of aldosterone secretion
42
Q

PAC to PRA ratio to detect primary hyperaldosteronism

A
  • increase PAC

- decreased PRA

43
Q

Steroid synthesis pathway in zona glomerulosa

A

1) cholesterol- cholesterol desmolase
2) pregnenolone- 3B
3) progesterone- 21B
4) DOC- 11B
5) corticosterone- 18 hydroxylase
6) 18OH corticosterone- 18 oxidase
7) Aldosterone

(If you block at the step after DOC, still can have an increase in BP since DOC can act as a weak mineral corticoid)

44
Q

Steroid synthesis pathway in zona fasciculata

A

1) cholesterol- cholesterol desmolase
2) pregnenolone- 3B
3) progesterone- 17a
4) 17 OH progesterone- 21B
5) 11-Deoxycortisol- 11B
6) Cortisol

(blockage at any step will lead to decreased cortisol levels)

45
Q

Steroid synthesis in zona reticularis

A

1) cholesterol- cholesterol desmolase
2) pregnenolone- 17a
3) 17OH progesterone- 17,20 lyase
4) DHEA- 3B
5) androstenedione

46
Q

How is the mineralocorticoid receptor protected from activation by cortisol in the kidney?

A

11B-HSD2 enzyme converts cortisol to cortisone which is then transferred back to the bloodstream so just aldosterone can act on the mineralocorticoid receptor

47
Q

What are all congenital adrenal enzyme deficiencies characterized by?

A

enlargement of both adrenal glands due to increased ACTH stimulation due to decreased cortisol

(enzyme deficiency > decreased cortisol > decreased negative feedback > increased ACTH > adrenal hyperplasia

48
Q

Dx 17a enzyme deficiency

A
  • increased mineralocorticoids
  • decreased cortisol
  • decreased sex hormones
  • increased blood pressure
  • decreased K+
  • decreased androstenedione
  • undescended testes, lack of secondary sexual development
49
Q

Dx 21B enzyme deficiency

A
  • decreased mineralocorticoids
  • decreased cortisol
  • increased sex hormones
  • decreased blood pressure
  • increased K+
  • increased renin activity
  • increased 17 hydroxyprogesterone
  • most common
  • salt wasting
  • precocious puberty
  • virilization
50
Q

Dx 11B

A
  • decreased aldosterone
  • increased DOC; increased BP
  • decreased cortisol levels
  • increased sex hormone
  • increase BP
  • decreased K+
  • decreased renin activity
  • virilization
51
Q

What occurs with a pheochromocytoma?

A
  • tumor in adrenal cortex
  • increased release of catecholamines
  • hypertension, headaches, palpitations, sweating
52
Q

What produces catecholamines?

A 
Adrenal medulla 
(Epi = 80%; norepi = 20%)
53
Q

How are catecholamines synthesized?

A

1) tyrosine
2) XDOPA
3) Dopamine
4) Norepi
5) Epi

54
Q

Synthesis of catecholamines is under the control of what?

A

sympathetic activity and the CRH-ACTH-cortisol axis

55
Q

What does cortisol do to PMNT enzyme?

A

Upregulates it

PMNT = enzyme that converts norepinephrine to epinephrine

56
Q

What is the chemical signal for secretion of catecholamines from the adrenal medulla?

A

Acetylcholine

57
Q

Contrast the location of norepi and epi synthesis?

A

Norepinephrine is synthesized in the chromaffin granule vesicle while epinephrine is synthesized in the cytosol

58
Q

What is the rate limiting step of catecholamine synthesis?

A

hydroxylation of tyrosine by tyrosine hydroxylase producing DOPA

59
Q

How does norepi get into the granule?

A

DOPA is converted to dopamin by AADC in the cytoplasm and is then transported into the chromaffin granule where it is converted to norepi by DBH

60
Q

What happens after norepi is produced inside the granule?

A

norepi diffuses out of the granule by facilitated transport and is methylated by PMNT to form epi

61
Q

What happens to epi after it is produced?

A

epi is transported back into the granule by VMATs and is stored in the granule with ATP, Ca2+, and proteins called chromogranins

62
Q

How are catecholamines degraded?

A

MAO

COMT

63
Q

How can a diagnosis of pheochromocytoma be confirmed?

A

elevated levels of catecholamines and their metabolic byproducts

64
Q

alpha-1 receptor

A
  • increases IP3 and Ca2+, DAG

- increase vascular smooth muscle contraction

65
Q

alpha-2 receptor

A
  • decreases cAMP
  • inhibit norepi release
  • inhibit insulin release
66
Q

beta-1 receptor

A
  • increase cAMP

- increases cardiac output

67
Q

beta-2 receptor

A
  • increases cAMP
  • increases hepatic glucose output
  • decreases contraction of blood vessels, bronchioles, and uterus
  • epinephrine has higher affinity for beta-2 than norepi
68
Q

beta-3 receptor

A
  • increases cAMP
  • increases hepatic glucose output
  • increases lipolysis
69
Q

Which receptors respond better to norepi than epi?

A
  • alpha receptors

- beta3 receptors

70
Q

What occurs during a short-term stress response?

A

1) stress sends nerve impulses to spinal cord lateral horn
2) sympathetics released to adrenal medulla
3) adrenal medulla secretes catecholamines

71
Q

What occurs during a long-term stress response?

A

1) stress signal hypothalamus to release CRH
2) CRH signals pituitary to release ACTH
3) ACTH signal adrenal cortex to secrete steroid hormone (glucocorticoids and mineralcorticoids)

72
Q

Long term stress responses from mineralocorticoids

A
  • kidneys retain sodium and water

- BV and BP rise

73
Q

Long term stress responses to glucocorticoids

A
  • proteins and fats converted to glucose or broken down for energy
  • blood glucose increase
  • immune system suppressed
74
Q

Short term responses to strss

A
  • HR increases
  • BP increases
  • liver converts glycogen to glucose and releases glucose to blood
  • blood flow changes, reducing digestive system activity and urine output
  • metabolic rate increases

Neuro Endo 3 (13 decks)

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