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Endo > SM_183b: Adrenal Cortex Physiology and Pathophysiology > Flashcards

SM_183b: Adrenal Cortex Physiology and Pathophysiology Flashcards

1
Q

Three types of steroid hormones are ____, ____, and ____

A

Three types of steroid hormones are mineralocorticoids (C21), glucocorticoids (C21), and androgens (C19)

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2
Q

Mineralocorticoids are produced in the ____

A

Mineralocorticoids are produced in the zona glomerulosa

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3
Q

Glucocorticoids are produced in the ____

A

Glucocorticoids are produced in the zona fasciculata

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4
Q

Androgens are produced in the ___

A

Androgens are produced in the zona reticularis

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5
Q

____ is the main mineralocorticoid

A

Aldosterone is the main mineralocorticoid

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6
Q

____ is the main glucocorticoid

A

Cortisol is the main glucocorticoid

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7
Q

____ and ____ are the main androgens

A

Dehydroepiandrosterone and androstenedione are the main androgens

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8
Q

StAR is responsible for ____

A

StAR is responsible for substrate delivery to enzymes

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9
Q

P450scc converts ____ to ____

A

P450scc converts cholesterol to pregnenolone

(cholesterol side chain cleavage)

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10
Q

3-beta-HSD converts to ____ to ____

A

3-beta-HSD converts to prenenolone to progesterone

(3-beta oxidation)

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11
Q

P450c17 converts ____ to ____

A

P450c17 converts prenenolone to 17-OH-prenenolone

(17-alpha hydroxylation)

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12
Q

P450c17 also converts ____ to ____

A

P450c17 also converts prenenolone to dehydroepiandosterone

(17,20-lyase)

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13
Q

P450c21 converts ____ to ____

A

P450c21 converts 17-OH-progesterone to 11-deoxycortisol

(21-hydroxylation)

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14
Q

P450c11-beta converts ____ to ____

A

P450c11-beta converts 11-deoxycortisol to cortisol

(11-beta-hydroxylation)

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15
Q

P450c11AS converts ____ to ____

A

P450c11AS converts corticosterone to aldosterone

(18-hydrol/aldo synthesis)

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16
Q

11-beta-hydroxysteroid dehydrogenase type I and II are responsible for ____

A

11-beta-hydroxysteroid dehydrogenase type I and II are responsible for cortisol-cortisone interconversion

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17
Q

17-beta-hydroxysteroid dehydrogenase III converts ____ to ____

A

17-beta-hydroxysteroid dehydrogenase III converts androstenedione to testosterone

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18
Q

5-alpha-reductase converts ____ to ____

A

5-alpha-reductase converts testosterone to 5-alpha-dihydrotestosterone

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19
Q

Aromatase converts ____ to ____

A

Aromatase converts testosterone to estradiol

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20
Q

___ regulates adrenal hormones

A

HPA axis regulates adrenal hormones

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21
Q

Describe the proopiomelanocortin cascade

A

Proopiomelanocortin cascade

  1. alpha-MSH
  2. ACTH
  3. POMC processing in the pituitary (alpha-MSH)
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22
Q

a-MSH is expressed in ___

A

a-MSH is expressed in skin (keratinocytes, melanocytes)

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23
Q

ACTH is expressed in the ____

A

ACTH is expressed in the anterior pituitary

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24
Q

MCR-2 is the ____

A

MCR-2 is the ACTH receptor

(located in adrenal cortex, responsible for steroid production)

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25
Q

MCR-2 requires ____ for membrane display and function

A

MCR-2 requires MRAP (melanocortin 2 receptor accessory protein) for membrane display and function

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26
Q

Renin is released by the ____, ____, and ____

A

Renin is released by the

  • Juxtaglomerular apparatus sensing lower BP
  • Macula densa sensing decreased osmotic pressure
  • Direct renal adrenergic input
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27
Q

Describe the RAAS

A

RAAS

  1. Angiotensinogen -> angiotensin I by renin
  2. Angiotensin I -> angiotensin II by ACE
  3. Angiotensin II promotes excretion of aldosterone
  4. Na, K decrease
  5. Na retentiona and volume expansion

(ACTH and serum K regulate aldosterone)

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28
Q

Aldosterone release is stimulated by ___, ___, and ___

A

Aldosterone release is stimulated by renin-angiotensin system, hyperkalemia, and ACTH

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29
Q

___ is the ligand for AT receptor type I and II

A

Angiotensin II is the ligand for AT receptor type I and II

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30
Q

AT receptor type I is expressed in the ____, ____, ____, and ____

A

AT receptor type I is expressed in the vasculature, heart, kidney, and adrenal pituitary

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31
Q

AT receptor type I is responsible for ____, ____, and ____

A

AT receptor type I is responsible for vasoconstriction, aldosterone synthesis, and vasopressin secretion

32
Q

AT receptor type is ____ expressed and responsible for ____

A

AT receptor type is widely expressed and responsible for cell growth / differentiation

(incompletely understood)

33
Q

Describe the action of nuclear receptors

A

Nuclear receptors

  1. Nuclear receptors bind steroid hormone (cortisol)
  2. COnformational change activates receptor protein
  3. Activated receptor-cortisol complex moves into nucleus
  4. Activated receptor-cortisol complex binds to regulatory region of target gene and activates transcription
34
Q

Describe effects of cortisol

A

Cortisol effects

  • Catabolic: decreased protein synthesis and amino acid uptake in extrahepatic tissues, amino acids diverted to gluconeogenesis in the liver, decreased growth hormone secretion and action
  • Hyperglycemic: gluconeogenesis, glycogen deposition in liver, insulin antagonism in peripheral tissues
  • Electrolytes: Na retention, K exceetion in kidney, gut and sweat glands
  • Adipose tissue: redistribution of fat
  • Erythropoietic: red cell mass
  • Lympholytic: depresses all aspects of the immune response
  • Anti-inflammatory
  • CNS effects: stimulates appetite, mood modulation
35
Q

Cortisol has ____ actions

A

Cortisol has catabolic actions

36
Q

Cortisol decreases activation of ___ and ___

A

Cortisol decreases activation of T lymphocytes and macrophages (anti-inflammatory)

37
Q

Describe effects of androgen

A

Androgen

  • Hair growth: beard, pubic, axillary, body
  • Central and temporal balding
  • Sebum production -> acne
  • Penile and clitoral growth
  • Erythropoietic
  • Anabolic (muscle mass)
  • Anti-estrogen
  • Voice changes
38
Q

Cortisol increases at start of ___ while DHEAS increases in the ___

A

Cortisol increases at start of puberty while DHEAS increases in 20s

(earlier for females than maels)

39
Q

Describe androgen testing

A

Androgen testing

  • DHEAS, androstenedione, testosterone
  • Immunometric assays for testosterone are not sufficiently accurate or sensitive to use in prepubertal boys and women
  • Testosterone is highly protein bound to albumin and sex hormone binding globulin
  • Low SHBG will lower total testosterone, bioavailable testosterone may be normal
40
Q

____, ____, and ____ are effects of mineralocorticoids

A

Na+ retention, K+ excretion, and H+ excretion are effects of mineralocorticoids

41
Q

11-beta-hydroxysteroid dehydrogenase type I is presents in the ____, ____, and ____ and converts ____ to ____

A

11-beta-hydroxysteroid dehydrogenase type I is presents in the liver, lung, and omental fat, and converts cortisone to cortisol

(can also convert cortisone back to cortisol)

(cortisone is inactive)

42
Q

11-beta-hydroxysteroid dehydrogenase type II is presents in the ____ and converts ____ to ____

A

11-beta-hydroxysteroid dehydrogenase type II is presents in the kidney and converts cortisol to cortisone

(cortisone is inactive)

43
Q
A
44
Q

____ is an enzyme that inactivates cortisol, limiting renal mineralocorticoid receptor activation in normal conditions

A

11-beta-hydroxysteroid dehydrogenase type II is an enzyme that inactivates cortisol, limiting renal mineralocorticoid receptor activation in normal conditions

45
Q

Describe causes of primary adrenal hypofunction

A

Primary adrenal hypofunction

  • Autoimmune
  • Infectious / granuloma (TB)
  • Hemorrhage (bleeding diathesis)
  • Metastases
  • Genetic ACTH receptor or MRAP deficiency
46
Q

Secondary adrenal hypofunction involves ____

A

Secondary adrenal hypofunction involves ACTH deficiency

(pituitary disease: tumor, granuloma, autoimmune, hemorrhage)

47
Q

Congenital adrenal hyperplasia (mixed hypo and hyperfunction) occurs when ___

A

Congenital adrenal hyperplasia (mixed hypo and hyperfunction) occurs when genetic enzyme deficiencies lead to a defect of cortisol and excess of precursors

48
Q

Describe clinical features of adrenal hypofunction

A

Adrenal hypofunction clinical features

  • Cortisol hypofunction: anorexia, nausea, weakness, salt craving, hypoglycemia, hyponatremia, hyperkalemia, dehydration, and death (adrenal crisis is often precipitated by a medical stress)
  • Aldosterone deficiency: hyponatremia, hyperkalemia, dehydration, hypotension
  • Adrenal androgen deficiency: axillary and pubic hair loss, loss of libido (women)
  • Excess ACTH (primary adrenal insufficiency, Addison’s disease) causes pigmentation
  • Secondary adrenal insufficiency: cortisol and adrenal androgen deficiency but largely normal aldosterone secretion
49
Q

____ adrenal insufficiency causes mucosal pigmentation

A

Primary adrenal insufficiency causes mucosal pigmentation

(excess ACTH)

50
Q

Describe endocrine testing in adrenal insufficiency

A

Endocrine testing in adrenal insufficiency

  • Basal plasma cortisol and ACTH
  • Cosyntropin (synthetic ACTH) stimulation test
  • Direct pituitary simulation tests for ACTH (insulin tolerance, CRH)
  • Plasma aldosterone and renin
51
Q

Describe cortisol testing for adrenal insufficiency

A

Cortisol testing for adrenal insufficiency

  • Measure ACTH and morning cortisol to start
  • Cortisol is highly protein bound to cortisol binding globulin: routine assays measure total (free + bound cortisol) so when CBG is abnormal there is not a normal reference range
  • Moening cortisol should be > 10 ug/dL, less than 4 likely adrenal insufficiency
52
Q

Insulin tolerance test involves measurement of ____

A

Insulin tolerance test involves measurement of blood glucose

(used to assess pituitary function, adrenal function, and insulin sensitivity)

53
Q

____ is the most common cause of isolated hypoaldosteronism

A

Hyporeninemic hypoaldosteronism is the most common cause of isolated hypoaldosteronism

(type IV renal tubular acidosis)

(common complication of diabetes)

54
Q

Describe therapy for adrenal hypofunction

A

Adrenal hypofunction therapy

  • Replacement therapy with hydrocortisone = cortisol
  • Replacement therapy with 9-alpha-fluorocortisol (fludrocortisone, a synthetic mineralocorticoid)
  • Replacement of adrenal androgens not generally necessary
55
Q

Describe clinical manifestations of Cushing’s syndrome

A

Cushing’s syndrome clinical syndrome

  • Weight gain, redistribution of fat (trunk, face)
  • Na retention, fluid retention, HTN
  • K depletion, hypokalemia
  • Ruddy complexion, purple striae
  • Hyperphagia
  • Depression, euphoria, inability to concentrate
  • Osteoporosis
  • Myopathy, muscle loss, weakness
56
Q

Describe clinical manifestations of chronic hypercorticism (Cushing’s disease)

A

Chronic hypercorticism (Cushing’s disease)

  • Centripetal obesity
  • Buffalo hump
  • Striae
  • HTN
  • Acne, hirsutism
  • Echymoses
  • Decreased CHO tolerance
  • Myopathy
  • Osteoporosis
57
Q

Describe clinical manifestations of acute hypercorticism (ectopic ACH)

A

Acute hypercorticism (ectopic ACH)

  • Weight loss
  • Psychosis
  • Pigmentation
  • HTN
  • Acne
  • Hypokalemia alkalosis
  • Hyperglycemia
  • Weakness (hypokalemia)
  • Polyuria - polydypsia (hypokalemic nephrophathy, hyperglycemia)
58
Q

Describe etiologies of glucocorticoid excess (Cushing’s syndrome)

A

Glucocorticoid excess (Cushing’s syndrome) etiologies

  • Pituitary ACTH secreting adenoma (Cushing’s disease)
  • Adrenal tumor (adenoma, carcinoma)
  • Nodular adrenal hyperplosia (macronodular can be due to aberrant receptor expression, micronodular can be part of Carney complex)
  • Ectopic ACTH syndrome
  • Exogenous steroid administration
  • Ectopic CRH-producing tu]mor
59
Q

Micronodular adrenal hyperplasia can be part of ____, which results from ____

A

Micronodular adrenal hyperplasia can be part of Carney complex, which results from mutation of a subunit of protein kinase A (autosomal dominant)

60
Q

____ is most common cause of ectopic ACTH

A

Lung carcinoma is most common cause of ectopic ACTH

(also carcinoma of pancreas, thymoma, benign bronchial adenoma)

61
Q

Hallmark of Cushing’s syndrome is ___

A

Hallmark of Cushing’s syndrome is non-suppressibility of excess hormone production

(glucocorticoid excess)

62
Q

Describe diagnosis of Cushing’s syndrome (glucocorticoid excess)

A

Cushing’s syndrome (glucocorticoid excess)

  • Biochemical confirmation: loss of diurnal rhythm of plasma cortisol, loss of suppressibility of steroid secretion, excessive production of steroids
  • Specific diagnosis: AM cortisol and ACTH, 24 h urine free cortisol excretion, midnight salivary free cortisol, dexamethasone suppression test
  • Localization procedures: pituitary, adrenal, ectopic (often obvious cancer source)
63
Q

Primary selective mineralocorticoid excess is caused by ____ or ____

A

Primary selective mineralocorticoid excess is caused by aldosterone-producing adenoma and bilateral hyperplasia

HTN, hypokalemia, alkalosis

64
Q

Secondary selective mineralocorticoid excess involves ___, ___, and ___

A

Secondary selective mineralocorticoid excess involves high renin (due to hypovolemia), hypokalemia, and alkalosis

65
Q

Hypokalemia is ___ required to consider the diagnosis of hyperaldosteronism

A

Hypokalemia is NOT required to consider the diagnosis of hyperaldosteronism

66
Q

Selective mineralocorticoid excess diagnostic tests are ____ and ____

A

Selective mineralocorticoid excess diagnostic tests are plasma renin and aldosterone

(urinary aldosterone)

67
Q

Describe diagnostic testing for primary hyperaldosteronism

A

Primary hyperaldosteronism

  • Renin suppressed and aldosterone high
  • Renin not stimulatable (Na depletion, posture)
  • Aldosterone not suppressible (Na loading)
68
Q

Describe diagnostic testing for secondary hyperaldosteronism

A

Diagnostic testing for secondary hyperaldosteronism

  • Renin and aldosterone high
  • Renin and aldosterone suppressible (Na loading, volume repletion)
69
Q

Describe clinical manifestations of androgen excess

A

Androgen excess clinical manifestations

  • Hirsutism, acne, temporal / central balding
  • Ruddy complexion, purple striae (together with glucocorticoid excess)
  • Increased red cell mass
  • Irregular periods
70
Q

____ is the main therapy of adrenal hyperfunction

A

Stopping or minimizing exogenous steroids is the main therapy of adrenal hyperfunction

71
Q

Congenital adrenal hyperplasia is caused by a ____, most often ____ but sometimes ____

A

Congenital adrenal hyperplasia is caused by a genetic deficiency in steroidogenic enzymes, most often 21-hydroxylase deficiency but sometimes 11-hydroxylase deficiency

(deficiency of cortisol and excess of precursors)

72
Q

Describe pathophysiology of congenital adrenal hyperplasia

A

Congenital adrenal hyperplasia pathophysiology

  1. Cortisol deficiency
  2. ACTH overproduction
  3. Adrenal hyperplasia, excess production of precursor steroids, and shunting of precursors into non-blocked androgen pathway
73
Q

Describe clinical manifestations of 21-hydroxylase deficiency congenital adrenal hyperplasia

A

21-hydroxylase deficiency congenital adrenal hyperplasia

  • Girls: ambiguous genitalia
  • Sodium wasting, shock
  • Short stature, hirsutism, hypo/amenorrhea
74
Q

Describe clinical manifestations of 11-hydroxylase deficiency congenital adrenal hyperplasia

A

11-hydroxylase deficiency congenital adrenal hyperplasia

  • Girls: ambiguous genitalia
  • Na retention, hypertension (11-deoxycorticosterone is a mineralocorticoid)
  • Short stature
  • Hirsutism
  • Hypo/amenorrhea
75
Q

Nonclassical congenital adrenal hyperplasia main symptoms are due to ____, is phenotypically similar to ____, and is most common in ____

A

Nonclassical congenital adrenal hyperplasia main symptoms are due to androgen excess, is phenotypically similar to polycystic ovarian syndrome, and is most common in Ashkenazi Jews / Hispanics

76
Q

Endocrine therapy of congenital adrenal hyperplasia due to 21-hydroxylase deficiency is ____ and ____

A

Endocrine therapy of congenital adrenal hyperplasia due to 21-hydroxylase deficiency is replacing with cortisone (lowest dose) and replacing with fludrocortisone if necessary

77
Q

A woman with historically regular cycles unexpectedly misses her menstrual period. Home pregnancy test is positive. She wishes to end the pregnancy, so her doctor prescribes mifepristone (RU-485). In addition to its desired progesterone receptor antagonist activity in the uterus, the hormone action producted in ___ of the adrenal gland will be most affected.

A

A woman with historically regular cycles unexpectedly misses her menstrual period. Home pregnancy test is positive. She wishes to end the pregnancy, so her doctor prescribes mifepristone (RU-485). In addition to its desired progesterone receptor antagonist activity in the uterus, the hormone action producted in zona fasciculata of the adrenal gland will be most affected.

(glucocorticoids)

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