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Neuroendocrine I: Exam 3 > Hypothalamic-Pituitary Relationships and Biofeedback Pt 2 > Flashcards

Hypothalamic-Pituitary Relationships and Biofeedback Pt 2 Flashcards

1
Q

Actions of cortisol

A
  • Secreted predominantly from the zona fasciculata
  • Longer-acting stress-response steroid hormone
  • Suppresses the immune system via an anti-inflammatory action
  • Stimulates gluconeogenesis in the liver to increase plasma glucose (diabetogenic effect)
  • Promotes protein catabolism w/in muscles
  • Promotes lipolysis w/in adipose tissue
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2
Q

Regulation of aldosterone secretion

A
  • Main stimulus is decreased Na+ or increased K+ in blood, decreased blood volume or decreased BP through the renin-angiotensin-aldosterone axis
  • Can also be stimulated by adrenocorticotrophic hormone
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3
Q

Actions of aldosterone

A
  • Targets distal kidney tubules to increase absorption of Na+ and, secondarily, water, as well as, increasing K+ excretion –> increases blood volume and BP
  • Steroid hormone that alters the transcription/translation of protein channels and pumps
  • Secreted from the zona glomerulosa
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4
Q

Signs/symptoms of Cushing’s syndrome/Disease

A
  • Hypercorticolism
  • Truncal/central obesity
  • Round face
  • “Buffalo hump” –> excess fat on back of neck
  • Easy bruising/poor wound healing
  • Osteoporosis
  • Purple striae
  • HTN
  • Edema
  • Weakness
  • Osteoporosis
  • Hirsutism
  • Acne
  • Virilization
  • Diabetes
  • Immunosuppression
  • Cognitive effects
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5
Q

Dexamethasone suppression test: Low dose

A
  • Provide a low-dose of synthetic glucocorticoid at night –> measure cortisol and ACTH lvls in morning b/c it should inhibit adrenocorticotropic hormone and corticotropin releasing hormone secretion by acting like cortisol in negative feedback
  • Differentiates pts w/ Cushing’s syndrome versus Cushing’s disease –> If there is no ACTH suppression it indicates Cushing’s Disease (ACTH-dependent hypercorticolism)
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6
Q

Dexamethasone suppression test: High dose

A

-When identified pt has Cushing’s Disease (ACTH-dependent hypercortisolism), we can administer high lvls of synthetic glucocorticoid to distinguish the source of the elevated ACTH lvls:

a) Anterior pituitary ACTH-secreting tumor –> high lvls will negatively feedback and cause decreased ACTH
b) Ectopic ACTH-secreting tumor –> no negative feedback effect and therefore will continue to see elevated ACTH

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7
Q

Consequences of glucocorticoid excess

A
  • Overall diabetogenic effect
  • promotes visceral obesity
  • Osteoporosis
  • Protein catabolism/collagen breakdown
  • Anti-inflammatory immunosuppression
  • Salt & water retention –> HTN b/c has cross reactivity w/ mineralocorticoid receptors at high lvls
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8
Q

Etiologies of Cushing’s syndrome (hypercortisolism)

A
  1. Exogenous glucocorticoid excess
  2. Pseudo-Cushing’s syndrome (major depression, anxiety, acute/chronic illness)
  3. ACTH-dependent (Cushing’s disease, ectopic ACTH-secreting tumors, CRH-secreting tumors)
  4. ACTH-independent (adrenal adenoma vs adrenal carcinoma)
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9
Q

How do the normal lab values (CRH, ACTH, Cortisol) compare to values seen in Cushing’s syndrome caused by: adrenal tumor

A

primary disorder:

  1. decreased CRH
  2. decreased ACTH
  3. increased cortisol lvls
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10
Q

How do the normal lab values (CRH, ACTH, Cortisol) compare to values seen in Cushing’s syndrome caused by: ectopic ACTH-secreting tumor

A
  1. decreased CRH
  2. INCREASED ACTH (very abnormally high) –> hyperpigmentation
  3. increased cortisol
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11
Q

How do the normal lab values (CRH, ACTH, Cortisol) compare to values seen in Cushing’s syndrome caused by: ACTH-secreting pituitary tumor

A

secondary disorder:

  1. decreased CRH
  2. Increased ACTH (but not as much as an ectopic tumor) –> hyperpigmentation
  3. increased cortisol
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12
Q

How do the normal lab values (CRH, ACTH, Cortisol) compare to values seen in Cushing’s syndrome caused by: excess exogenous glucocorticoid drugs

A
  1. decreased CRH
  2. decreased ACTH
  3. decreased cortisol (but drugs mimic cortisol actions and pt has symptoms of excess)
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13
Q

How do the normal lab values (CRH, ACTH, Cortisol) compare to values seen in: primary adrenal insufficiency (Addison’s disease)

A
  1. increased CRH
  2. increased ACTH –> hyperpigmentation
  3. decreased cortisol
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14
Q

How do the normal lab values (CRH, ACTH, Cortisol) compare to values seen in: secondary adrenal insufficiency

A
  1. Increased CRH
  2. decreased ACTH
  3. decreased cortisol
    - Normal levels of aldosterone b/c renin-angiotensin-aldosterone axis maintained
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15
Q

How do the normal lab values (CRH, ACTH, Cortisol) compare to values seen in: tertiary adrenal insufficiency

A
  1. decreased CRH
  2. decreased ACTH
  3. decreased cortisol
    - Normal levels of aldosterone b/c renin-angiotensin-aldosterone axis maintained
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16
Q

How does increased ACTH cause hyperpigmentation?

A

-When there is a loss of feedback on the HPA axis causing supraphysiological lvls of ACTH, it can bind to low-affinity MC1R on melanocytes in skin to increase melanin synthesis and dispersal –> skin darkening

17
Q

Explain how the cosyntropin stimulation test detects adrenal gland insufficiency

A
  • Cosyntropin is a synthetic ACTH analog
    1) Measure cortisol @ 8 am:
    a. if pt has >15 microgram/dL –> r/o adrenal insufficiency
    b. if pt has < 3 microgram/dL –> adrenal insufficiency confirmed (see step 2)
    c. if pt has 3-15 micrograms/dL –> administer cosyntropin and measure cortisol lvls in 30 min to see if able to produce it –> if lvls are WNL (>/= 18), AI r/o but if they are less than normal (<18), AI confirmed

2) AI confirmed –> measure ACTH lvls:
a. if low/normal –> secondary or tertiary AI
b. if elevated –> primary AI

18
Q

Primary vs secondary hyperaldosteronism

A
  • Primary due to excessive release of aldosterone from adrenal cortex (Conn’s syndrome = alderosterone-secreting adenoma in zona glomerulosa of adrenal cortex)
  • Secondary due to excessive renin secretion by juxtaglomerular cells in kidney
19
Q

Signs/symptoms of Addison’s Disease (primary adrenocortical insufficiency)

A

Primary deficiency of cortisol and aldosterone due to adrenal cortex atrophy

  • Hypoglycemia
  • Anorexia, weight loss, nausea, vomiting
  • Weakness
  • Hypotension
  • Hyperkalemia
  • Metabolic acidosis
  • Decreased pubic and axillary hair in females
  • Hyperpigmentation
20
Q

Explain how we can use the ratio of plasma aldosterone concentration (PAC) / plasma renin activity (PRA) to detect primary hyperaldosteronism

A
  • Hypertension and hypokalemia –> hyperaldosteronism
  • decreased PRA and increased PAC –> ratio of >/= 20 AND PAC >/= 15 ng/dL
  • Since the primary problem is elevated aldosterone lvls, it is increasing BP and therefore decreasing activity of the renin system
21
Q

21beta-hydroxylase deficiency

A
  • Blocks cortisol and mineralocorticoid production, therefore increasing production of androgens
  • Hypotension due to salt wasting, hypoglycemia, masculinization of external genitalia (penis-like clitoris and scrotum-like labia) in females, early appearance of pubic/axillary hair (precocious puberty), suppression of gonadal function, early acceleration of linear growth, virilization
  • ACTH lvls will be elevated due to low cortisol lvls –> adrenal hyperplasia
22
Q

17alpha-hydroxylase deficiency

A
  • Blocks glucocorticoid and androgen production –> impaired formation of secondary sex characteristics and overproduction of mineralocorticoids
  • Symptoms of glucocorticoid deficiency (hypoglycemia)
  • Symptoms of mineralocorticoid excess (HTN, hypokalemia, metabolic alkalosis) –> will also have decreased aldosterone lvls b/c of HTN negative feedback on renin-angiotensin-aldosterone system
  • Lack of pubic/axillary hair in females, undescended testes in males
  • ACTH lvls will be elevated due to low cortisol lvls –> adrenal hyperplasia
23
Q

11beta-hydroxylase deficiency

A
  • blocks cortisol production and mineralocorticoid products downstream of 11-deoxycorticosterone (DOC)
  • increased levels of DOC cause symptoms of mineralocorticoid excess –> HTN, hypokalemia, metabolic alkalosis
  • Also causes an increase in androgen production (masculinization)
  • ACTH lvls will be elevated due to low cortisol lvls –> adrenal hyperplasia
24
Q

Expected levels of mineralocorticoids, cortisol, androgens, BP, [K+], and other labs compared to normal in pts w/:

17alpha-hydroxylase deficiency

A
  • increased mineralocorticoids
  • decreased cortisol
  • decreased androgens
  • increased BP
  • decreased [K+]
  • decreased androstenedione
25
Q

Expected levels of mineralocorticoids, cortisol, androgens, BP, [K+], and other labs compared to normal in pts w/:

21beta-hydroxylase deficiency

A
  • decreased mineralocorticoids
  • decreased cortisol
  • increased androgens
  • decreased BP
  • increased [K+]
  • increased renin activity and increased 17-hydroxy-progesterone
26
Q

Expected levels of mineralocorticoids, cortisol, androgens, BP, [K+], and other labs compared to normal in pts w/:

11beta-hydroxylase

A
  • decreased aldosterone, increased DOC (increased BP)
  • decreased cortisol
  • increased androgens
  • increased BP
  • decreased [K+]
  • decreased renin activity (negative feedback)
27
Q

Classic symptoms of pheochromocytoma

A

Increased catecholamine release causing:

  • HTN
  • Headaches
  • palpitations
  • sweating

Neuroendocrine I: Exam 3 (18 decks)

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