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NE Exam 3 > 11 - CIS Hypothalamic and Pituitary Relationships and Biofeedback Pt. II > Flashcards

11 - CIS Hypothalamic and Pituitary Relationships and Biofeedback Pt. II Flashcards

1
Q

This is located immediately above the kidneys.

A

Adrenal glands (also called suprarenal)

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2
Q

What are the layers of the adrenal gland?

A

Capsule
Cortex
Medulla

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3
Q

What are the components of the adrenal cortex?

A

Zona Glomerulosa
Zona Fasciculata
Zona Reticularis

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4
Q

What do each layer of the adrenal cortex and adrenal medulla secrete?

A

Zona Glomerulosa – Mineralocorticoid (Aldosterone)

Zona Fasciculata – Glucocorticoids (Cortiso); Androgens (DHEAS)

Zona Reticularis – Androgens (DHEAS); Glucocorticoids (Cortisol)

Medulla – Chromaffin cells secrete Catecholamines (NE and E)

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5
Q

These are catecholamines that are rapid responders to stress (i.e., hypoglycemia, exercise).

A

Epinephrine

Norepinephrine

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6
Q

This is a steroid (glucocorticoid) that is a longer-acting stress-response steroid hormone. It regulates glucose utilization, immune and inflammatory homeostasis.

A

Cortisol

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7
Q

This is a steroid (mineralocorticoid) that regulates salt and volume homeostasis.

A

Aldosterone

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8
Q

This is a steroid that is an androgen precursor.

A

DHEAS

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9
Q

Briefly describe the HPA axis and its negative feedback control.

A

Hypothalamus releases CRH, stimulates Anterior Pituitary to release ACTH, stimulates Adrenal Cortex to release Cortisol.

Cortisol gives negative feedback to Hypothalamus and Anterior Pituitary to inhibit release of CRH and ACTH.

***Cortisol will also inhibit the process of infection and inflammation (via cytokines)

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10
Q

What are the main things that will stimulate CRH to start producing?

A 
Physical stress (i.e., surgery)
Emotional stress (i.e., fear) 
Metabolic stress (i.e., acute hypoglycemia) 
Infection and inflammation (via cytokines)
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11
Q

Where does cortisol go and what does it do?

A

Immune system – Suppresses it
Liver – Gluconeogenesis
Muscle – Protein catabolism
Adipose tissue – Lipolysis

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12
Q

What is the circadian rhythm like for cortisol?

A

Secretory rates are high in the early morning but low in the late evening.

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13
Q

ACTH also induces the secretion of _______ from the Zona Reticularis. Unlike Cortisol, this has no feedback mechanism on CRH or ACTH.

A

Androgens (DHEAS)

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14
Q

Briefly explain the process of increasing blood pressure by using Aldosterone.

A

Low BP signals to kidney to increase its release of Renin –

The Liver also releases Angiotensinogen –

Renin cleaves Angiotensinogen into Angiotensin I –

ACE (from lungs) will make Angiotensin I into Angiotensin II –

Angiotensin II goes to the Adrenal Cortex and induces it to secrete Aldosterone –

Aldosterone increases water and sodium reabsorption –

Increases BP

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15
Q

The following symptoms are most representative of what disease?

    • Truncal obesity (abdomen)
    • Moon face
    • “Buffalo hump”
    • Easy bruising
    • Dark red or purple stretch marks
    • Acne
A

Cushing’s Syndrome

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16
Q

In this test, it differentiates patients that have CS (Cushing’s Syndrome) from those that do not have it. If there is no ACTH suppression, then they have CS.

A

Low-Dose Dexamethasone Suppression Test

  • **This inhibits ACTH (CS is caused by too much Cortisol).
  • **This test does NOT specify the source of the ACTH over-production (that is high-dose).
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17
Q

In this test, it distinguishes patients with CS caused by pituitary ACTH-secreting tumor from CS caused by a non-pituitary ACTH-secreting tumor. It is used after the initial diagnosis of CS is made.

A

High-Dose Dexamethasone Suppression Test

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18
Q

Explain how the High-Dose Dexamethasone Suppression test works.

A

A high-dose of Dexamethasone is given to the patient. If there is a pituitary tumor, there will be decreased ACTH because of the negative feedback effect on the pituitary. If there is an ectopic tumor, there is no change in ACTH because there is no negative feedback effect on this type of tumor.

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19
Q

What are the ways of getting CS?

A

Exogenous glucocorticoid excess (latrogenic – via drugs)

Pseudo-Cushing’s Syndrome – via major depression, anxiety, acute/chronic illness, alcoholism

ACTH-dependent – Pituitary adenoma (Cushing’s Disease), Ectopic ACTH-secreting tumor, CRH-secreting tumor

ACTH-independent – Adrenal Adenoma, Adrenal Carcinoma

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20
Q

Exogenous glucocorticoids have the same negative feedback effect as Cortisol, and due to their use they could cause the atrophy of the adrenal cells in the _______ _______ that produce Cortisol.

A

Zona Fasciculata

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21
Q

What are examples of synthetic glucocorticoids?

A

Prednisone
Methylprednisone
Dexamethasone

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22
Q

The primary action of Aldosterone is renal ________ reabsorption.

A

Sodium

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23
Q

Aldosterone combines with a cytoplasmic receptor (in kidney cells). This hormone-receptor complex initiates transcriptions in the nucleus. Translation and protein synthesis makes new protein channels and pumps. Aldosterone-induced proteins modulate existing channels and pumps. These result in increased ________ reabsorption and ________ secretion.

A

Sodium

Potassium

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24
Q

This is produced in the Anterior Pituitary and is derived from post-translational processing of POMC (pro-opiomelanocortin). It is a peptide hormone.

A

ACTH

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25
Q

In non-pituitary cells, what does ACTH induce?

A

Melanin synthesis (can cause hyperpigmentation)

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26
Q

What disease presents with increased ACTH and hyperpigmentation as a result?

A

Addison’s Disease

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27
Q

This test is used to detect adrenal gland insufficiency. Helps determine primary vs. secondary or tertiary.

A

Cosyntropin (synthetic ACTH) Stimulation Test

28
Q

In _________ adrenal insufficiency, BOTH Cortisol and Aldosterone secretion is decreased. Renin-Angiotensin-Aldosterone axis does not work. Hyperpigmentation occurs here.

A

Primary

29
Q

In ________ or ________ adrenal insufficiency, ONLY Cortisol secretion is decreased. The Renin-Angiotensin-Aldosterone axis is intact (Aldosterone is secreted).

A

Secondary

Tertiary

30
Q

What are causes of Primary Adrenal Insufficiency (Addison’s Disease)?

A

Autoimmune disease
Adrenal hemorrhage
Infection (Tuberculosis or N. meningitidis)
Tumor metastases to the Adrenal Gland

31
Q

In this disease, and adrenal hemorrhage can occur secondary to N. meningitidis.

A

Waterhouse-Friedrichsen Syndrome

32
Q

What is the treatment for adrenal insufficiency?

A

Replace the hormones the Adrenal Gland isn’t making.

***People with secondary or tertiary maintain aldosterone production so they don’t need mineralocorticoid replacement.

33
Q

What are some hormone replacements that can be used adrenal insufficiency?

A

Cortisol is replaced with Corticosteroid – Hydrocortisone, Prednisone, or Dexamethasone

Aldosterone is replaced with a Mineralocorticoid – Fludrocortisone

34
Q

Look at the table on slide 34! Study her, know her.

A

Review 5 minutes.

35
Q

This is due to the excessive release of Aldosterone from the Adrenal Cortex.

A

Primary hyperaldosteronism

36
Q

This syndrome is a type of primary hyperaldosteronism caused by an ademona in the Adrenal Cortex.

A

Conn’s Syndrome

37
Q

This is due to excessive renin secretion by the juxtaglomerular cels in the kidney.

A

Secondary hyperaldosteronism

38
Q

This can result from the destruction of the Adrenal Cortex, defects in Aldosterone synthesis, or inadequate stimulation of Aldosterone secretion.

A

Hypoaldosteronism

39
Q

Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio can detect what? How?

A

Primary Hyperaldosteronism

If the PRA is low but the PAC is high, that means the ratio is off and there is an overproduction of Aldosterone (hyperaldosteronism). If there is an increased ratio for both PRA and PAC then it could be secondary hyperaldosteronism (overproduction of renin).

40
Q

What is the pathway for the synthesis of Aldosterone from Cholesterol?

A

Cholesterol converted to Pregnenolone (via Cholesterol desmolase) -

Pregnenolone converted to Progesterone (via 3B-hydroxysteroid dehydrogenase) –

Progesterone converted to 11-Deoxycorticosterone/DOC (via 21B-hydroxylase) –

11-DOC converted to Corticosterone (via 11B-hydroxylase) –

Corticosterone converted to 18-OH Corticosterone (via 18-hydroxylase) –

18-OH Corticosterone converted to Aldosterone (via 18-oxidase)

41
Q

What is the pathway for the synthesis of Cortisol from Cholesterol?

A

Cholesterol converted to Pregnenolone (via Cholesterol desmolase) -

Pregnenolone converted to Progesterone (via 3B-hydroxysteroid dehydrogenase) –

Progesterone converted to 17-OH Progesterone (via 17a-hydroxylase)–

17-OH Progesterone converted to 11-Deoxycortisol (via 21B-hydroxylase) –

11-Deoxycortisol converted to Cortisol (via 11B-hydroxylase)

42
Q

What is the pathway for the synthesis of Androgens from Cholesterol?

A

Cholesterol converted to Pregnenolone (via Cholesterol desmolase) -

Pregnenolone converted to 17-OH Pregnenolone (via 17a-hydroxylase) –

17-OH Pregnenolone converted to DHEA (via 17, 20 lyase) –

DHEA converted to Androstenedione (via 3B-hydroxysteroid dehydrogenase)

43
Q

The mineralocorticoid receptor is protected from activation by cortisol by the enzyme…

A

11B-HSD2

***Deflects and produces cortisone, which targets glucocorticoids.

44
Q

All congenital adrenal enzyme deficiencies are characterized by an __________ of both adrenal glands due to _________ ACTH stimulation (due to _________ cortisol).

A

Enlargement
Increased
Decreased

***There is low cortisol, so there is no negative feedback to ACTH production, resulting in increased ACTH. This causes the enlargement.

45
Q

Look at table on slide 42. V IMPORTANT!

A

Review 5 minutes.

46
Q

This is a tumor that arises from Chromaffin cells of the Adrenal Medulla. It is rare but extremely dangerous because of hypertension. Remember, the Adrenal Medulla has Chromaffin cells that secrete NE and E. If this increased then it can lead to hypertension, headaches, palpitations, and sweating.

A

Pheochromocytoma

47
Q

Most Pheochromocytoma are benign, unilateral adrenal tumors. Catecholamines secreted by pheochromocytoma stimulate both _______ and _______ ________ receptors.

A

Alpha/Beta Adrenergic

48
Q

The Adrenal Medulla produces ______ percent Epinephrine and ______ percent Norepinephrine.

A

80

20

49
Q

This catecholamine is a responder to stress such as hypoglycemia and exercise. It influences energy metabolism and cardiac output.

A

Epinephrine

50
Q

Synthesis of catecholamines is under the control of __________ activity and the CRH-ACTH-Cortisol axis.

A

Sympathetic

***Remember, sympathetic stimulation (ACh) stimulates Tyrosine to form Dopamine, which makes Norepinephrine. Norepinephrine is converted to Epinephrine via PNMT.

51
Q

Sympathetic stimulation (ACh) stimulates Tyrosine to form Dopamine, which makes Norepinephrine. Norepinephrine is then converted to Epinephrine via the enzyme ________. This enzyme if upregulated by Cortisol.

A

PNMT

52
Q

What is the chemical signal for secretion of Catecholamine from the Adrenal Medulla?

A

ACh

53
Q

NE and E are synthesized in different cellular compartments. NE is in the ________ _______ while E is in the ________.

A

Chromaffin Granule
Cytosol

***NE is transported out of granule and into cytosol, where it converts to E.

54
Q

The rate-limiting step of NE and E synthesis is the hydroxylation of Tyrosine by ________ ________, producing DOPA.

A

Tyrosine Hydroxylase

55
Q

DOPA is converted to DA by the cytoplasmic enzyme, _______, and is then transported into the secretory vesicle (Chromaffin Granule).

A

AADC (aromatic amino acid decarboxylase)

56
Q

Within the Chromaffin Granule, DA is converted to NE by the enzyme __________.

A

DBH (dopamine B-hydroxylase)

57
Q

In most adrenomedullary cells, essentially all of the NE diffuses out of the Chromaffin Granule by facilitated transport and is methylated by the cytoplasmic enzyme ________ to form E.

A

PNMT (Phenylethanolamine-N-methyl transferase)

58
Q

Once made, E is then transported back into the Chromaffin Granule by _________. Multiple molecules of E, and some NE, are stored in the granules complexed with ATP, Calcium, and proteins called _________.

A

VMATs (Vesicular Monoamine Transporters)

Chromogranins

59
Q

These are multi molecular complexes, thought to decrease the osmotic burden of storing individual molecules of E within Chromaffin Granules. When circulating, these can be used as a marker of sympathetic paraganglion-derived tumors (paragangliomas).

A

Chromogranins

60
Q

What is used to degrade catecholamines?

A

COMT

MAO

61
Q

NE and E can both degrade to _________ _________ with MAO.

A

Dihydroxymandelic Acid

62
Q

Epinephrine degrades to _________ with COMT, while NE degrades to _________ with COMT.

A

Metanephrine

Normetanephrine

63
Q

Metanephrine and Normetanephrine both further degrade into _________ __________ with MAO.

A

Vanillylmandelic Acid (in urine)

***This is what is produced if Dihydroxymandelic Acid (from NE and E degradation with MAO) is degraded with COMT!

64
Q

These adrenergic receptors respond better to NE than E.

A

Alpha receptors

B3 receptors

65
Q

This adrenergic receptor responds equally to NE and E.

A

B1 receptors

66
Q

This receptor has a higher affinity with E than NE.

A

B2 receptor

NE Exam 3 (16 decks)

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