Endocrine > 172. Adrenal Cortex > Flashcards

172. Adrenal Cortex Flashcards

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1
Q

Most common type of isolated hypoaldosteronism

AKA type IV renal tubular acidosis

A

Hyporeninemic hypoaldosteronism

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2
Q

Located in:

  • liver
  • lung
  • omental fat

Converts cortisone to cortisol

A

11B-hydroxysteroid DH Type I

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3
Q

Clinical manifestations:

  • hirsutism, acne, temporal/central balding
  • ruddy complexion, purple striae
  • increased red cell mass
  • irregular periods
A

Adrenal androgen excess

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4
Q

Leads to:

  • hyponatremia
  • hyperkalemia
  • dehydration
  • hypotension

Rare for this to occur in an isolated manner

A

Aldosterone deficiency

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5
Q

Measure in women:

  • DHEA-S
  • Androstenedione
  • Testosterone

Measure in men:

  • Testosterone
A

Androgen testing

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6
Q

Expressed in:

  • vasculature
  • heart
  • kidney
  • adrenal
  • pituitary

Action: when acted on by angiotensin II

  • vasoconstriction
  • aldosterone synthesis
  • vasopressin secretion
A

AT receptor type 1

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7
Q

Can be due to aberrant receptor expression:

  • GIP
  • Vasopressin
  • LH
  • IL-1

Type of nodular adrenal hyperplasia leading to glucocorticoid excess

A

Macronodular

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8
Q

Clinical manifestations:

  • weight gain, redistribution of fat
  • Na+ retention, fluid retention, HTN
  • K+ depletion, hypokalemia
  • Hyperglycemia, CHO intolerance, diabetes
  • Ruddy complexion, purple striae
  • Hyperphagia
  • Depression, euphoria, inability to concentrate
  • Osteoporosis
  • Myopathy, muscle loss, weakness
A

Cushing’s Syndrome (glucocorticoid excess) Chronic

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9
Q

Used to differentiate b/w Cushing’s Disease and Ectopic ACTH syndrome

Cushing’s: ACTH and cortisol decrease

Ectopic: ACTH will stay elevated

A

Dexamethasone testing

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10
Q

Genetic enzyme deficiencies lead to defect of cortisol and excess of precursors

Mixed hypo- and hyperfunction

A

Congenital adrenal hyperplasia

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11
Q

Basal plasma cortisol and ACTH Cosyntropin (synthetic ACTH) stimulation test

Direct pituitary stimulation tests for ACTH

  • insulin tolerance
  • CRH Plasma aldosterone and renin
A

Endocrine testing in adrenal insuffiency

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12
Q

Important middle product of cholesterol conversion into adrenal cortex products

Used as a marker for enzyme blockage down the road

A

17-OH-progesterone

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13
Q

Leads to a decrease in K+ absorption (increase in excretion) and an increase in Na+ absorption (decrease in excretion)

A

Aldosterone

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14
Q

Decreases protein synthesis and AA uptake in extrahepatic tissues

AA diverted to gluconeogenesis in the liver

Decrease growth hormone secretion and action

A

Catabolic effects of cortisol

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15
Q

Etiologies:

  • aldosterone-producing adenoma
  • bilateral nodular hyperplasia HTN, hypokalemia (50%), alkalosis
A

Primary selective mineralocorticoid excess

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16
Q

Senses decreased osmotic pressure leading to renin release

Located b/w afferent and efferent arteriole in the kidney just in front of the glomerulus

A

Macula densa

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17
Q

Products of the adrenal cortex all derive from what being made into what

  • except DHEA which comes from pregnenolone (middle product of this reaction)
A

Cholesterol –> progesterone

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18
Q

Most common cause is prolonged steroid use

  • longterm prednisone

Could be 2/2 pituitary disease:

  • tumor
  • granuloma
  • autoimmune
  • hemorrhage
A

ACTH deficiency (secondary adrenal disease)

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19
Q

Electrolytes: in kidney, guts, and sweat glands

  • Na+ retention
  • K+ excretion

Adipose:

  • redistribution of fat (fat pads)

Red cell mass decreases

Depresses all aspects of the immune response

Anti-inflammatory

CNS effects:

  • stimulates appetite
  • mood modulation (euphoria and depression)
A

Cortisol

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20
Q

Etiologies:

  • Autoimmune
  • Addison’s
  • Infectious/granuloma
  • tuberculosis (most common worldwide)
  • Hemorrhage
  • seen in shock
  • Metastases
  • Genetic ACTH receptor or MRAP deficiency
A

Primary adrenal disease

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21
Q

This enzyme is important in men for bone health

Converts testosterone to estradiol

Enzyme blocked in women w/ breast cancer

A

Aromatase

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22
Q

Effects:

  • Na+ retention
  • K+ excretion
  • H+ excretion

Diseases involving these are call “salt-wasting”

  • pts crave salt
A

Mineralocorticoid

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23
Q

Carcinoma of lung

Carcinoma of pancreas

Thymoma

Benign bronchial adenoma (including carcinoid)

A

Sources of ectopic ACTH

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24
Q

Enzyme responsible for conversion of 11-deoxycortisol –> cortisol Second most commonly mutated in pathway - can’t make cortisol, but aldosterone is fine - 11-DOC builds up –> hypertension and salt retention —> congenital adrenal hyperplasia

A

p450c11Beta (11-hydroxylase)

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25
What kind of sweet snack blocks 11B-hydroxysteroid Type II
Black licorice
26
Mineralocorticoids are made in this zone of the adrenal cortex - aldosterone
Zona glomerulosa
27
Structural similarity amongst all the separate types - can have activity on each others' Used for: - Glucocorticoid - Mineralocorticoid - Progesterone - Androgen - Estrogen
Steroid receptors
28
Unable to convert to cortisol Clinical manifestations: - Girls: ambiguous genitalia - Na+ retention, hypertension (bc 11-DOC is a mineralocorticoid) - Short stature - Hirsutism - Hypo/amenorrhea
11-hydroxylase deficiency
29
Enzyme responsible for transporting cholesterol into mitochondria
StAR
30
Leads to pigmentation in Addison's
Excess ACTH
31
Located in kidneys Converted cortisol to cortisone
11B-hydroxysteroid Type II
32
Leads to: - anorexia - nausea - weakness - salt craving - hypoglycemia - hyponatremia (SIADH) - hyperkalemia - dehydration - death - adrenal crisis in a pt w/ adrenal insufficiency
Cortisol deficiency
33
Causes these hyperglycemic actions: - gluconeogenesis - glycogen deposition in liver - insulin antagonism in peripheral tissues
Cortisol
34
Leads to axillary and pubic hair loss Also leads to loss of libido (women only)
Adrenal androgen deficiency
35
Genetic deficiency in steroidogenic enzymes - most common: 21-hydroxylase deficiency - second most common: 11-hydroxylase deficiency Unable to make cortisol or aldosterone in 21-hydroxlyase Unable to make cortisol in 11-hydroxylase Cortisol deficiency causes ACTH overproduction, which leads to adrenal hyperplasia, excess production of precursor steroids, and shunting of precursors into the non-blocked androgen pathway
Congenital adrenal hyperplasia
36
Androgens are made in this zone of the adrenal cortex
Zona reticularis
37
There is cortisol and adrenal androgen deficiency, but largely normal aldosterone secretion
Secondary adrenal insufficiency (ACTH deficiency)
38
Effects: - hair growth (beard, pubic, axillary, body) - central and temporal balding - sebum production --\> acne - penile and clitoral growth - Erythropoietic --\> Increase O2 carrying capacity by increasing Hb - Anabolic (muscle mass) - Anti-estrogen - Voice changes
Androgens
39
DHEA-sulfur Androstenedione Androstenediol
Main androgens from adrenal cortex
40
Aldosterone receptor antagonists used to treat HTN and hyperaldosteronism
spironolactone and eplerenone
41
Low SHBG will lower But bioavailability may be normal
Total testosterone
42
This mineralocorticoid is brought about by way of: - RAS - derives from angiotensin II - Hyperkalemia - ACTH
Aldosterone
43
Unable to convert to cortisol or aldosterone Clinical manifestations: - Girls: ambigious genitalia - sodium wasting, shock - short stature - hirsutism - hypo/amenorrhea
21-hydroxylase deficiency
44
In 11-hydroxylase deficiency, one of the immediate precursors preceding the block is \_\_ - accumulates in large quantities Strong mineralocorticoid Its accumulation causes Na+ retention and hypertension
11-DOC (deoxycorticosterone)
45
Highly protein bound to albumin and sex binding globulin (SHBG) Inactive when bound to SHBG Active when bound to albumin or free
Testosterone
46
Corticosteroids are made in this zone of the adrenal cortex - cortisol
Zona fasciculata
47
Clinical manifestations: - Weight loss - Psychosis - Pigmentation - HTN - Acne - Hypokalemic acidosis - Hyperglycemia - Weakness (hypokalemia) - Polyuria-polydipsia (hypokalemic nephropathy, hyperglycemia)
Ectopic ACTH Acute
48
MSH receptor located in hypothalamus Its action leads to satiety Mutations in this receptor cause Auto dominant obesity
MCR-4
49
Widely expressed throughout the system Action: when acted on by angiotensin II - cell growth and differentiation - incompletely understood
AT receptor type 2
50
Breakdown product of ACTH Melanocyte stimulating hormone to help melanocytes differentiate and proliferate Expressed in the skin - keratinocytes and melanocytes
alpha-MSH
51
Acts on AT receptor types 1 and 2
Angiotensin II
52
Replace with hydrocortisone - lowest does needed - risk of iatrogenic Cushing's Replace with fludrocortisone if necessary - can monitor renin level
Endocrine therapy of congenital adrenal hyperplasia - 21-hydroxylase deficiency
53
Most common in Ashkenazi Jews and Hispanic populations 20-50% of 21-hydroxylase activity preserved so no salt wasting or adrenal insufficiency Main symptoms are d/t androgen excess Phenotypically similar to polycystic ovarian syndrome
Nonclassical congenital adrenal hyperplasia
54
Autoimmune primary adrenal disease Adrenal cortex is destroyed by antibodies Excess ACTH causes hyperpigmentation (bronze skin)
Addison's Disease
55
ACTH receptor expressed in the adrenal cortex Its action leads to steroid production Requires accessory protein for membrane display and function
MCR-2
56
Senses lowering blood pressure leading to renin release
Juxtaglomerular apparatus
57
Enzyme responsible for 21-hydroxylation of 17-OH-progesterone --\> 11-deoxycortisol Most commonly mutated enzyme in the pathway - can't make cortisol or aldosterone --\> congenital adrenal hyperplasia
P450c21 (21 hydroxylase)
58
Replacement therapy with hydrocortisone = cortisol Replacement therapy with 9-alpha-fluorocortisol (fludrocortisone, a synthetic mineralocorticoid) Replacement of adrenal androgens not generally necessary
Adrenal hypofunction therapy
59
Diagnostic testing shows: - renin and aldosterone high - renin and aldosterone are suppressible (Na+ loading, volume repletion)
Secondary hyperaldosteronism
60
Performed in IR Sample ACTH and prolactin coming from both sides to see where it is coming from Looks for Cushing's Syndrome results
Inferior petrosal vein sampling
61
Diagnostic testing shows: - renin suppressed and aldosterone high - renin not stimulatable (Na+ depletion, posture) - Aldosterone not suppressible (Na+ loading)
Primary hyperaldosteronism
62
Glucocorticoid receptor antagonist - also a progesterone receptor antagonist Can lower cortisol action
Mifepristone
63
Androgen receptor antagonists used to treat adrenal androgen excess
Flutamide, finasteride, and spironolactone
64
Can be part of Carney complex - mutation of a subunit of protein kinase A Type of nodular adrenal hyperplasia leading to glucocorticoid excess
Micronodular
Endocrine
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