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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
How does aldosterone act on the kidney?
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
26
Where is ACTH produced?
Anterior pituitary; derived from post-translational processing of POMC
27
How does ACTH act on non-pituitary tissues?
activates alpha-MSH which promotes melanin synthesis
28
How does increased ACTH lead to hyperpigmentation in Addison's disease?
ACTH above physiological levels will bind to MC1R in melanocytes and increase melanin synthesis
29
Result of primary adrenal insufficiency
both cortisol and aldosterone secretion is reduced because adrenal cortex is damaged
30
Secondary adrenal insufficiency
cortisol is decrease since no ACTH is released from pituitary, but the renin-angiotensin axis still produces aldosterone
31
Causes of primary adrenal insufficiency (Addison's Disease)
- autoimmune - adrenal hemorrhage - Waterhouse-Freidrichsen syndrome (adrenal hemorrhage secondary to N. meningitidis) - hemorrhage caused by anticoagulant treatment - infection - tumor metastases to adrenal gland
32
Treatment for adrenal insufficiency
hormone replacement
33
Dx for primary (adrenal) excess
- increased cortisol - decreased CRH - decreased ACTH - no hyperpigmentation
34
Dx for secondary (pituitary) excess
- increased cortisol - decreased CRH - increased ACTH - hyperpigmentation
35
Dx for primary deficiency
- decreased cortisol - increased CRH - increased ACTH - hyperpigmentation
36
Dx for secondary deficiency
- decreased cortisol - increased CRH - decreased ACTH - no hyperpigmentation
37
Dx for steroid administration
- decreased cortisol (but symptoms of excess) - decreased CRH - decreased ACTH - no hyperpigmentation
38
Primary hyperaldosteronism
excessive release of aldosterone from the adrenal cortex
39
Conn's Syndrome
primary hyperaldosteronism as a result of an adenoma in the adrenal cortex
40
Secondary hyperaldosteronism
excessive renin secretion by the juxtaglomerular cells in the kidney
41
Hypoaldosteronism
- destruction of adrenal cortex - defects in aldosterone synthesis - inadequate stimulation of aldosterone secretion
42
PAC to PRA ratio to detect primary hyperaldosteronism
- increase PAC | - decreased PRA
43
Steroid synthesis pathway in zona glomerulosa
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
Steroid synthesis pathway in zona fasciculata
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
Steroid synthesis in zona reticularis
1) cholesterol- cholesterol desmolase 2) pregnenolone- 17a 3) 17OH progesterone- 17,20 lyase 4) DHEA- 3B 5) androstenedione
46
How is the mineralocorticoid receptor protected from activation by cortisol in the kidney?
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
What are all congenital adrenal enzyme deficiencies characterized by?
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
Dx 17a enzyme deficiency
- increased mineralocorticoids - decreased cortisol - decreased sex hormones - increased blood pressure - decreased K+ - decreased androstenedione - undescended testes, lack of secondary sexual development
49
Dx 21B enzyme deficiency
- 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
Dx 11B
- decreased aldosterone - increased DOC; increased BP - decreased cortisol levels - increased sex hormone - increase BP - decreased K+ - decreased renin activity - virilization
51
What occurs with a pheochromocytoma?
- tumor in adrenal cortex - increased release of catecholamines - hypertension, headaches, palpitations, sweating
52
What produces catecholamines?
``` Adrenal medulla (Epi = 80%; norepi = 20%) ```
53
How are catecholamines synthesized?
1) tyrosine 2) XDOPA 3) Dopamine 4) Norepi 5) Epi
54
Synthesis of catecholamines is under the control of what?
sympathetic activity and the CRH-ACTH-cortisol axis
55
What does cortisol do to PMNT enzyme?
Upregulates it | PMNT = enzyme that converts norepinephrine to epinephrine
56
What is the chemical signal for secretion of catecholamines from the adrenal medulla?
Acetylcholine
57
Contrast the location of norepi and epi synthesis?
Norepinephrine is synthesized in the chromaffin granule vesicle while epinephrine is synthesized in the cytosol
58
What is the rate limiting step of catecholamine synthesis?
hydroxylation of tyrosine by tyrosine hydroxylase producing DOPA
59
How does norepi get into the granule?
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
What happens after norepi is produced inside the granule?
norepi diffuses out of the granule by facilitated transport and is methylated by PMNT to form epi
61
What happens to epi after it is produced?
epi is transported back into the granule by VMATs and is stored in the granule with ATP, Ca2+, and proteins called chromogranins
62
How are catecholamines degraded?
MAO | COMT
63
How can a diagnosis of pheochromocytoma be confirmed?
elevated levels of catecholamines and their metabolic byproducts
64
alpha-1 receptor
- increases IP3 and Ca2+, DAG | - increase vascular smooth muscle contraction
65
alpha-2 receptor
- decreases cAMP - inhibit norepi release - inhibit insulin release
66
beta-1 receptor
- increase cAMP | - increases cardiac output
67
beta-2 receptor
- increases cAMP - increases hepatic glucose output - decreases contraction of blood vessels, bronchioles, and uterus - epinephrine has higher affinity for beta-2 than norepi
68
beta-3 receptor
- increases cAMP - increases hepatic glucose output - increases lipolysis
69
Which receptors respond better to norepi than epi?
- alpha receptors | - beta3 receptors
70
What occurs during a short-term stress response?
1) stress sends nerve impulses to spinal cord lateral horn 2) sympathetics released to adrenal medulla 3) adrenal medulla secretes catecholamines
71
What occurs during a long-term stress response?
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
Long term stress responses from mineralocorticoids
- kidneys retain sodium and water | - BV and BP rise
73
Long term stress responses to glucocorticoids
- proteins and fats converted to glucose or broken down for energy - blood glucose increase - immune system suppressed
74
Short term responses to strss
- 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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