Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine > 172. Adrenal Cortex > Flashcards

172. Adrenal Cortex Flashcards

1
Q

Most common type of isolated hypoaldosteronism

AKA type IV renal tubular acidosis

A

Hyporeninemic hypoaldosteronism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Located in:

  • liver
  • lung
  • omental fat

Converts cortisone to cortisol

A

11B-hydroxysteroid DH Type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical manifestations:

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

Adrenal androgen excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Leads to:

  • hyponatremia
  • hyperkalemia
  • dehydration
  • hypotension

Rare for this to occur in an isolated manner

A

Aldosterone deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Measure in women:

  • DHEA-S
  • Androstenedione
  • Testosterone

Measure in men:

  • Testosterone
A

Androgen testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

Mixed hypo- and hyperfunction

A

Congenital adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

Aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Etiologies:

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

Primary selective mineralocorticoid excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

This enzyme is important in men for bone health

Converts testosterone to estradiol

Enzyme blocked in women w/ breast cancer

A

Aromatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Effects:

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

Diseases involving these are call “salt-wasting”

  • pts crave salt
A

Mineralocorticoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Carcinoma of lung

Carcinoma of pancreas

Thymoma

Benign bronchial adenoma (including carcinoid)

A

Sources of ectopic ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What kind of sweet snack blocks 11B-hydroxysteroid Type II

A

Black licorice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Mineralocorticoids are made in this zone of the adrenal cortex

  • aldosterone
A

Zona glomerulosa

27
Q

Structural similarity amongst all the separate types

  • can have activity on each others’

Used for:

  • Glucocorticoid
  • Mineralocorticoid
  • Progesterone
  • Androgen
  • Estrogen
A

Steroid receptors

28
Q

Unable to convert to cortisol

Clinical manifestations:

  • Girls: ambiguous genitalia
  • Na+ retention, hypertension (bc 11-DOC is a mineralocorticoid)
  • Short stature
  • Hirsutism
  • Hypo/amenorrhea
A

11-hydroxylase deficiency

29
Q

Enzyme responsible for transporting cholesterol into mitochondria

A

StAR

30
Q

Leads to pigmentation in Addison’s

A

Excess ACTH

31
Q

Located in kidneys Converted cortisol to cortisone

A

11B-hydroxysteroid Type II

32
Q

Leads to:

  • anorexia
  • nausea
  • weakness
  • salt craving
  • hypoglycemia
  • hyponatremia (SIADH)
  • hyperkalemia
  • dehydration
  • death
  • adrenal crisis in a pt w/ adrenal insufficiency
A

Cortisol deficiency

33
Q

Causes these hyperglycemic actions:

  • gluconeogenesis
  • glycogen deposition in liver
  • insulin antagonism in peripheral tissues
A

Cortisol

34
Q

Leads to axillary and pubic hair loss

Also leads to loss of libido (women only)

A

Adrenal androgen deficiency

35
Q

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

A

Congenital adrenal hyperplasia

36
Q

Androgens are made in this zone of the adrenal cortex

A

Zona reticularis

37
Q

There is cortisol and adrenal androgen deficiency, but largely normal aldosterone secretion

A

Secondary adrenal insufficiency (ACTH deficiency)

38
Q

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
A

Androgens

39
Q

DHEA-sulfur Androstenedione Androstenediol

A

Main androgens from adrenal cortex

40
Q

Aldosterone receptor antagonists used to treat HTN and hyperaldosteronism

A

spironolactone and eplerenone

41
Q

Low SHBG will lower But bioavailability may be normal

A

Total testosterone

42
Q

This mineralocorticoid is brought about by way of:

  • RAS
  • derives from angiotensin II
  • Hyperkalemia
  • ACTH
A

Aldosterone

43
Q

Unable to convert to cortisol or aldosterone

Clinical manifestations:

  • Girls: ambigious genitalia
  • sodium wasting, shock
  • short stature
  • hirsutism
  • hypo/amenorrhea
A

21-hydroxylase deficiency

44
Q

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

A

11-DOC (deoxycorticosterone)

45
Q

Highly protein bound to albumin and sex binding globulin (SHBG) Inactive when bound to SHBG Active when bound to albumin or free

A

Testosterone

46
Q

Corticosteroids are made in this zone of the adrenal cortex

  • cortisol
A

Zona fasciculata

47
Q

Clinical manifestations:

  • Weight loss
  • Psychosis
  • Pigmentation
  • HTN
  • Acne
  • Hypokalemic acidosis
  • Hyperglycemia
  • Weakness (hypokalemia)
  • Polyuria-polydipsia (hypokalemic nephropathy, hyperglycemia)
A

Ectopic ACTH

Acute

48
Q

MSH receptor located in hypothalamus

Its action leads to satiety

Mutations in this receptor cause Auto dominant obesity

A

MCR-4

49
Q

Widely expressed throughout the system

Action: when acted on by angiotensin II

  • cell growth and differentiation
  • incompletely understood
A

AT receptor type 2

50
Q

Breakdown product of ACTH

Melanocyte stimulating hormone to help melanocytes differentiate and proliferate

Expressed in the skin

  • keratinocytes and melanocytes
A

alpha-MSH

51
Q

Acts on AT receptor types 1 and 2

A

Angiotensin II

52
Q

Replace with hydrocortisone

  • lowest does needed
  • risk of iatrogenic

Cushing’s Replace with fludrocortisone if necessary

  • can monitor renin level
A

Endocrine therapy of congenital adrenal hyperplasia - 21-hydroxylase deficiency

53
Q

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

A

Nonclassical congenital adrenal hyperplasia

54
Q

Autoimmune primary adrenal disease

Adrenal cortex is destroyed by antibodies

Excess ACTH causes hyperpigmentation (bronze skin)

A

Addison’s Disease

55
Q

ACTH receptor expressed in the adrenal cortex

Its action leads to steroid production

Requires accessory protein for membrane display and function

A

MCR-2

56
Q

Senses lowering blood pressure leading to renin release

A

Juxtaglomerular apparatus

57
Q

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

A

P450c21 (21 hydroxylase)

58
Q

Replacement therapy with hydrocortisone = cortisol

Replacement therapy with 9-alpha-fluorocortisol (fludrocortisone, a synthetic mineralocorticoid)

Replacement of adrenal androgens not generally necessary

A

Adrenal hypofunction therapy

59
Q

Diagnostic testing shows:

  • renin and aldosterone high
  • renin and aldosterone are suppressible (Na+ loading, volume repletion)
A

Secondary hyperaldosteronism

60
Q

Performed in IR Sample ACTH and prolactin coming from both sides to see where it is coming from

Looks for Cushing’s Syndrome results

A

Inferior petrosal vein sampling

61
Q

Diagnostic testing shows:

  • renin suppressed and aldosterone high
  • renin not stimulatable (Na+ depletion, posture)
  • Aldosterone not suppressible (Na+ loading)
A

Primary hyperaldosteronism

62
Q

Glucocorticoid receptor antagonist

  • also a progesterone receptor antagonist

Can lower cortisol action

A

Mifepristone

63
Q

Androgen receptor antagonists used to treat adrenal androgen excess

A

Flutamide, finasteride, and spironolactone

64
Q

Can be part of Carney complex

  • mutation of a subunit of protein kinase A

Type of nodular adrenal hyperplasia leading to glucocorticoid excess

A

Micronodular

Endocrine (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions