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Neuroendocrine Test Three > Hypothalamic Pituitary Relationships and Feedback Part 2 Dr.LH > Flashcards

Hypothalamic Pituitary Relationships and Feedback Part 2 Dr.LH Flashcards

1
Q

What does the adrenal cortex secrete? (Specifically each layer)

A
  • Zona Reticularis and Zona Fasciculata secrete Glucocorticoids and Androgens
  • Zona Glomerulosa secretes Aldosterone (Mineralocorticoids)
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2
Q

Epinephrine and Norepinephrine fall into what class of hormones?

A

Catecholamines

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3
Q

Cortisol falls under what hormone class, and what is the action?

A
  • Steroids (Glucocorticoid)
  • Longer acting stress response
  • Regulates glucose use, immune and inflammatory homeostasis
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4
Q

What class does Aldosterone fall under? Fxn?

A
  • Mineralocorticoids a steroid hormone
  • Regulates salt and ECF homeostasis
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5
Q

What is DHEAS? Fxn?

A
  • Steroid hormone
  • Androgen precursor
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6
Q

Where does CRH and ACTH come from, what regulates them, what do they target?

A
  • CRH hypothalamus
    • stimulated by stress physically, emotionally, or metabolic
  • ACTH anterior pituitary
    • stimulated by CRH
  • Cortisol has negative feedback on both CRH and ACTH
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7
Q

Actions of cortisol?

A
  • Immune suppression
  • Gluconeogenesis
  • Protein catabolism
  • Lipolysis
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8
Q

Circadian rhythm of cortisol?

A
  • Highest in the morning but low in late evening
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9
Q

Describe step by step what causes aldosterone secretion and how it fixes the issue starting with decreased BP and ending with raising the BP

A
  • BP is decreased
  • Kidney produces renin
  • Liver makes Angiotensinogen
  • Renin works on Angiotensinogen converting it to Angiotensin I
  • ACE converts Angiotensin I to Angiotensin II
  • Angiotensin II travels to Adrenal cortex and gets taken in wherer it stimulates release of Aldosterone from the cortex
  • Aldosterone causes an increase in Water and Na reabsorption
  • BP is increasaed
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10
Q

What are sx of Cushings syndrome?

A
  • Truncal obesity
  • Moon face
  • Easy bruising
  • Htn
  • Edema
  • Purple Striae
  • Weakness
  • Osteoporosis
  • Buffalo Hump
  • Acne
  • Diabetes
  • Immunosuppressioin
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11
Q

What does the Dexamethasone Suppression test do at low and high doses?

A

Low

  • Differentiates patiess with CS of any cause from patients who don’t have CS
    • No ACTH suppression indicates CS, but doesn’t tell you where this overproduction comes from

High

  • Distinguishes patients with CS caused by pituitary adenoma from a non pituitary AT+CTH secreting tumor
    • used after CS diagnosis
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12
Q

Describe the negative feedback seen in the high dose dexamethasone test.

A
  • If ACTH decreases there is a pituitary tumor, seen by -FB on pituitary
  • If ACTH doesn’t change there is an ectopic tumor as there was no -FB to decrease ACTH
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13
Q

How do exogenous glucocorticoids effect adrenal cells?

A

They c an atrophy them, they have the same negative FB effect as cortisol does

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14
Q

Etiology of Cushings?

A
  • Exogenous glucocortiocoids excess
  • Psuedo cushings- major depression, anxiety, acutre or chronic infections, alcoholism (rare)
  • ACTH depdndent- ectopic ACTH secreting tumors, CRH secreting tumors
  • ACTH independent- Adrenal adenoma/carcinoma
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15
Q

A patient with CS has hihgh cortisol levels, but low ACTH. Where is the tumor causing this located?

A

Adrenal tumor because the cortisol is exerting a -FB on the pituitary keeping ACTH low, but adrenal gland is secreting cortisol despite no signal

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16
Q

Cushing syndrome patient has high low CRH but high levels of ACTH and Cortisol, where is the tumor?

A

Pituitary tumor as it is secreting ACTH despite no signal from CRH

17
Q

CS patient has high cortisol, but low ACTH release from pituitary, (High levels of ACTH in lab) and low CRH. What is happening?

A

Ectopic ACTH secreting tumor

18
Q

Low CRH, low ACTH and low Cortisol, what caused this?

A

Decreased cortisol but the exogenous glucocorticoids can mimin cortisol actions so it caused -FB to occur decreasing everything.

Exogenous glucocorticoids can cause symptoms of excess cortisol

19
Q

How does aldosertone work at a cellular level?

A
  • Combines with cytoplasmic receptor and then ccomplex travels to nucleus
  • Initiates transcription in the nucleus, translation & protein synthesis occur making new protein channels and pumps
  • Aldosterone induced proteins mudulate existing channnels and pumps
  • Results in increased Na reabsorption and K secretion
20
Q

Where is ACTH derived from?

A

POMC, its a peptide hm also

21
Q

How does increased ACTH cause hyperpigmentation?

A
  • Formed from Pro-opiomelanocortin (POMC) in anterior pituitary
  • the POMC has many peptides and some are alpha-MSH which stimulates Melanocytes
  • High levels of ACTH competes with a-MSH it can be a source of producing melanin as well resulting in an increase in pigmentation
  • Normally UV exposure results in a-MSH producing melanin, elevated ACTH increases this
22
Q

How does the Cosyntropin stimulation test work what is it for?

A
  • Determining primary Adrenal gland insufficiency
  • Measure cortisol at 8 am where it should be high >15
  • If it is less than 3 you measure ACTH
  • if its btw 3-15 use Cosyntropin stimulation test
    • test cortisol levels 30 min later and if levels are >18 rule out AI
    • If levels are <18 after 30 min meausre ACTH comfirm AI
  • ACTH low or normal you have tertiary or secondary AI
  • If ACTH elevated you have primary AI
23
Q

Cortisol and aldosterone secretion is decreased. What disorder primary secondary tertiary is it?

A

Primary adrenal deficiency it is at adrenal cortex

24
Q

Cortisol decreased but renin angiotensin aldosterone axis exists. What kind of deficiency is this? 1 2 or 3

A
  • 2 or 3 adrenal insufficiency anterior pituitary is not secreting ACTH and cortisol is not made
25
Q

Causes of 1 adrenal insufficiency? (Addisons)

A
  • Autoimmune
  • Adrenal hemorrhage
  • Infections
    • TB
    • N. Meningitidis
  • Tumor metastases to adrenal gland
26
Q

How do you treat Adrenal Insufficiency?

A
  • Replacing hormones that adrenal glad isn’t making
  • cortisol replaced with corticosteroid
  • Aldosertone replaced with fludrocortisone a mineralocorticoid hormone
  • Usually maintain aldosterone production with 2 adrenal insufficiency
27
Q

Hyperaldosteronism

A
  • Primary Hyperaldosteronism: excesssive release of aldosterone from aderenal cortex
  • Secondary Hyperaldostetronism: excessive renin secretion by juxtaglomerular cells in kidney
28
Q

Hypoaldosteronism

A
  • Destruction of adrenal cortex
  • Defects in aldosterone synthesis
  • Inadwquate stimuation of aldosterone stimulation
29
Q

What does 11B-hydroxylase do?

A
30
Q

Pheochromocytoma presentation?

A

Htn

Headaches

Palpitations

Sweating

31
Q

What is a pheochromocytoma?

A
  • Benign unilateral adrenal tumor
  • Catecholamines secreted by this tumor stimulate alpha and beta adrenergic receptors
32
Q

Pathway to make epinephrine?

A
  • Tyrosine to DOPA via tyrosine hydroxylase
  • DOPA to Domapine via AADC and transport into vesicle called chromaffin granule
  • Inside chromaffin granule dopamine converted to NE by DBH
  • NEpi diffuses out and is methylated by PMNT to make Epi
  • EPi transported back into Chromaffin cell via VMAT
33
Q

How are catecholamines degraded?

A
  • COMT takes Epi to Metanephrine and NEpi to Normetanephrine
  • Dihydryxymandelic acid COMT to Vanillylmandelic acid
  • MAO converts Normetanephrine and Metanephrine to Vanillylmandelic acid in urine
34
Q

How can you confirm pheochromocytoma in a lab?

A
  • Measure catecholamines and their byproducts such as metanephrines and VMA to see if they are elevated
35
Q

Describe how B1 B2 B3 & alpha receptors respond to NE and Epi

A
  • alpha and B3 receptors respond better to NE than Epi
  • B1 responds equally
  • Epi is more potent than NE for B2 receptor

Neuroendocrine Test Three (19 decks)

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