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Liz's Clinical Chemistry Module 4 > Endocrine Function III: Adrenal Cortex and Adrenal Medulla Hormones > Flashcards

Endocrine Function III: Adrenal Cortex and Adrenal Medulla Hormones Flashcards

1
Q

Basic anatomy of the adrenal cortex

A
  • Capsule (outer)
  • Adrenal cortex
  • Adrenal medulla (inner)
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2
Q

Three layers of the adrenal cortex

A
  • Zona glomerulosa (outermost)
  • Zona fasciculata (middle)
  • Zona reticularis (innermost)
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3
Q

Three major hormone classes of the adrenal cortex

A
  • Estrane
  • Andosane
  • Pregnane
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4
Q

Major hormone(s) produced by the zona glomerulosa layer

A

Mineralocorticoids

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5
Q

Major hormone(s) produced by the zona fasciculata layer

A

Glucocorticoids

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6
Q

Major hormone(s) produced by the zona reticularis layer

A

Sex hormones

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7
Q

Number of carbons on estrogens, androgens, and adrenal steroids

A
  • Estrogens: 18
  • Androgens: 19
  • Adrenal steroids: 21
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8
Q

First biosynthetic pathway for adrenocorticosteroid formation

A

Acetate → Cholesterol → Pregnenolone → Adrenocorticoids

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9
Q

Second biosynthetic pathway for adrenocorticosteroid formation (not preferred)

A

Pregnenolone → DHEA → Androstenedione → Testosterone → (Estradiol)

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10
Q

Causes of adrenocorticosteroids utilizing alternate pathway instead of the preferred pathway

A

Enzyme deficiencies

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11
Q

Importance of enzymes in steroid biogenesis

A

Takes enzymes to make conversions to final product

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12
Q

Major site of steroid metabolism

A

Liver

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13
Q

Form of adrenocorticosteroids excreted in the urine

A
  • Liver is the site of catabolism

- Water-insoluble hormones must be conjugated w/ sulfates or glucuronic acid to be excreted in urine

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14
Q

Which steroid has a negative feedback effect on adrenocorticotrophic hormone (ACTH)

A

Cortisol

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15
Q

Name of the principle cortisol-binding protein

A

CBG

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16
Q

Mineralocorticoids

- Metabolic effects

A
  • Maintain sodium and potassium balance

- Aldosterone

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17
Q

Four regulatory factors for aldosterone secretion (order of importance)

A
  1. Potassium concentration
  2. RAAS
  3. Total body sodium concentration
  4. ACTH (has minor effect unless ACTH is pathologically in excess or is deficient)
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18
Q

Glucorticoids

- Metabolic effects

A
  • Promotion of gluconeogenesis and lipolysis
  • Promotion of liver glycogenesis
  • Promotion of liver glycogenolysis
  • Inhibition of protein synthesis and promotion of protein catabolism
  • ↑ anti-inflammatory and immunosuppressive action
  • ↓ intestinal absorption of Ca2+; ↑ loss of Ca2+ from bone matrix
  • Miscellaneous: enzyme production, appetite promotion, regulation of blood pressure
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19
Q

Most potent glucocorticoid

A

Cortisol

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20
Q

Most potent mineralocorticoid

A

Aldosterone

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21
Q

Most potent adrenocortical androgen

A

Testosterone

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22
Q

What is the role of RAAS on the regulation of aldosterone?

A

Releases aldosterone and reabsorbs Na+ and releases K+

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23
Q

Three regulatory factors for the release of glucocorticoids

A
  • ACTH stimulation of hormone
  • Normal diurnal variation
  • Stress
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24
Q

Feedback mechanism utilized in glucocorticoid hormonal regulation

A

Cortisol causes negative feedback on hypothalamus and anterior pituitary

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25
Q

Normal diurnal variation in cortisol

A
  • While sleeping, cortisol is very low so negative feedback is removed
  • ACTH is released and there is a sharp ↑ while waking up (BP and sugar ↑ so you don’t pass out)
    The cortisol levels ↓ over the day
  • By 4pm it should be 1/3 the level it was at 8am
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26
Q

What androgen is produced in the greatest quantity by the adrenal cortex?

A

Testosterone

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27
Q

Six conditions associated w/ a hypofunctioning adrenal cortex

A
  • Primary hypoaldosteronism
  • Secondary hypoaldosteronism
  • Addison’s disease
  • Acute adrenal insufficiency
  • Secondary and tertiary adrenal insufficiency
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28
Q

Differentiate causes of primary hypoaldosteronism

A

Inability to adjust to stress, low Na+, high K+, high renin, low aldosterone

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29
Q

Differentiate causes of secondary hypoaldosteronism

A

Occurs in patient w/ renal disease,

- Kidney is unable to produce and release renin and therefore cause low aldosterone

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30
Q

List the typical sodium, potassium, and renin levels observed in hypoaldosteronism

A
  • Low Na+
  • High K+
  • High renin
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31
Q

Addison’s disease

- Clinical symptoms due to glucocorticoids deficiency

A
  • Fatigue
  • Weakness
  • Weight loss
  • GI disturbances
  • Post-parandial hypoglycemia
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32
Q

Addison’s disease

- Clinical symptoms due to mineralacorticoid deficiency

A
  • Dehydration
  • Hypotension
  • Hyperkalemia
  • Metabolic acidosis (↓H+ secretion)
  • Hyponatremia (↓Na+ reabsorption into blood)
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33
Q

Addison’s disease

- Reason for hyperpigmentation and infertility

A

No negative feedback on anterior pituitary (e.g., hyperpigmentation present b/c excess ACTH stimulates MSH production)

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34
Q

Addison’s disease

  • Na
  • K
  • Blood sugar
  • Cortisol
  • ACTH
A
  • ↓ Na+
  • ↑ K+
  • ↓ Blood sugar
  • ↓ Cortisol
  • ↑ ACTH
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35
Q

What is the cause of the Addisonian crisis?

A

During infection or acute stress, Addison’s patient cannot respond with ↑ aldosterone and cortisol and can go into shock with hypotension, fever, hypovolemia, and hyperkalemia (life threatening)

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36
Q

What is the cause of Waterhouse-Friderichsen?

A

Caused by meningococcal meningitis and septicemia; this causes acute adrenal insufficiency

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37
Q

What is the most common cause of tertiary adrenal insufficiency?

A

Chronic pharmacological administration of glucocorticoids

38
Q

Four conditions associated w/ a hyperfunctioning adrenal cortex

A
  • Primary aldosteronism (Conn’s syndrome)
  • Secondary aldosteronism
  • Cushing’s syndrome
  • Congenital adrenal hyperplasia
39
Q 
Primary aldosteronism (Conn's syndrome)
- Cause
A

Adenoma in outermost layer (tumors)

40
Q 
Primary aldosteronism (Conn's syndrome)
- Outstanding clinical symptom
A

Hypertension

41
Q

Primary aldosteronism (Conn’s syndrome)

  • Na+ (blood)
  • K+ (blood and urine)
  • Aldosterone
  • Renin
A
  • ↑ Aldosterone
  • Hypernatremia (b/c of ↑ aldosterone)
  • Hypokalemia
  • Hypokaluria
  • ↓ Renin
  • Metabolic alkalosis (↑H+ secretion in urine caused by ↑ Na+ reabsorption)
42
Q

Secondary aldosteronism

- Two causes

A

Characterized by elevated aldosterone in the absence of an adrenal tumor

  • ↓ blood flow to kidney causing ↓ GFR
  • Hyperactivity of RAAS causing ↑ renin production
43
Q

Secondary aldosteronism

  • Na+
  • K+
  • Aldosterone
  • Renin
A
  • Hypernatremia
  • Hypokalemia
  • Hypokaluria
  • ↑ Aldosterone (b/c of ↑ Na+)
  • ↑ Renin
  • Metabolic alkalosis (↑H+ secretion in urine caused by ↑ Na+ reabsorption)
44
Q

Why is renin increased in secondary aldosteronism?

A

RAAS is continuously being activated

45
Q

Secondary aldosteronism

- Clinical symptoms

A

↓ blood flow to kidney:

  • Nephrosis
  • CHF
  • Obstructive renal disease
  • Cirrhosis w/ Na+ depletion
  • Pregnancy
  • Diuretic use
46
Q

Cushing’s Syndrome

- Five clinical symptoms

A
  • Moon face
  • Buffalo hump
  • Truncal obesity
  • Purple striae
  • Hypertenion
47
Q

Cushing’s Syndrome

- Three general causes

A
  • Exogenous glucocorticoid therapy (prednisone)
  • ACTH-dependent syndrome
  • ACTH-independent
48
Q

Cushing’s Syndrome

- Two specific causes of ACTH-dependent Cushing’s

A
  • Cushing’s disease (ACTH-producing tumors)

- Ectopic ACTH-secreting tumors

49
Q

Cushing’s Syndrome

- Two specific causes of ACTH-independent Cushing’s

A
  • Adrenal adenoma (all 3 layers)

- Nodular adrenal hyperplasia (out of control)

50
Q

Cushing’s Syndrome

- Two recommended screening tests and typical results if patient has syndrome

A
  • 24 hour free cortisol (>120 = Cushing’s)
  • Overnight dexamethasone suppression test
  • AM/PM cortisol levels
51
Q

Cushing’s Syndrome

- Expected morning and afternoon cortisol levels

A

↑ in AM, ↓ over the day normally

- In Cushing’s, it’s increased all the time)

52
Q

Cushing’s Syndrome

  • Na+
  • K+
  • Blood sugar
  • Cortisol
  • ACTH
A
  • ↑ Na+
  • ↓ K+
  • ↑ Blood sugar
  • ↑ Cortisol
  • ↑ ACTH (due to adrenal cortex being continuously stimulated in Cushing’s Disease, ectopic ACTH-secreting tumor, and Cushing’s Syndrome)
53
Q

CAH

- Full name (as well as the name of the adult condition)

A
  • Congenital adrenal hyperplasia

- Aka adrenogenital syndrome

54
Q

CAH/adrenogenital syndrome

- Pathogenesis

A
  • Caused by enzyme deficiencies in the pathways to produce the glucocorticoids and mineralocorticoids
  • No negative feedback since cortisol is not produced and aldosterone is ↓
55
Q

CAH/adrenogenital syndrome

- Two common enzyme deficiencies

A
  • 21-hydroxylase

- 11-beta-hydroxylase

56
Q

CAH/adrenogenital syndrome

  • Cortisol
  • ACTH
  • Progesterone
  • DHEA
  • Sodium
  • Potassium
A
  • ↓ Cortisol
  • ↑ ACTH
  • ↑ Progesterone
  • ↑ DHEA
  • ↓ Sodium
  • ↑Potassium
57
Q

CAH/adrenogenital syndrome

- Typical symptoms in boys and girls

A 
Females
- Abnormalities of external genitalia at birth (cannot tell if male or female)
- Hirsutism
- Infertility
- Breast atrophy
Males
- Appear normal at birth but have sexual precocity (too much testosterone)
Both
- Acne
- Coarsening of voice
- Scalp recession early in life
58
Q

CAH/adrenal hyperplasia

- Lab test included in newborn screen to check for this condition

A

17-hydroxyprogesterone

59
Q

This is an enzyme kinetic assay used to measure angiotensin I produced from angiotensinogen by renin

A

Plasma renin activity test (PRA)

60
Q

Stimulation tests are used to assess ____ hormonal states (hypofunctioning vs. hyperfunctioning)

A

Hypofunctioning

61
Q

Suppression tests are used to assess ____ hormonal states (hypofunctioning vs. hyperfunctioning)

A

Hyperfunctioning

62
Q

ACTH stimulation test

- Diagnostic use

A

Differentiate primary adrenal insufficiency (Addison’s) from secondary (hypopituitarism)

63
Q

ACTH stimulation test

- Analyte measured

64
Q

ACTH stimulation test

- Expected normal response

A

Serum cortisol should double in 30 minutes

65
Q

ACTH stimulation test

- Results in Addison’s disease

A

Little or no change in cortisol levels

66
Q

ACTH stimulation test

- Results in hypopituitarism

A

Increased levels of cortisol on successive days (2-3) of ACTH stimulation (delayed or “staircase” response)

67
Q

Metyrapone test

- Principle

A

Selectively inhibits 11-beta-hydroxylase, so the conversion of 11-deoxycortisol to cortisol is inhibited, allowing unrestricted release of ACTH

68
Q

Metyrapone test

- Diagnostic use

A

Differentiation of normal patients from secondary adrenal insufficiency (hypopituitarism);
- Assesses pituitary ACTH reserve basically to see how much ACTH the patient can produce

69
Q

Metyrapone test

- Expected normal response

A
  • ↓ cortisol
  • ↑ 11-deoxycortisol
  • ↑ ACTH
70
Q

Metyrapone test

- Results in hypopituitarism

A

Unchanged cortisol, 11-deoxycortisol, and ACTH levels

71
Q

Clinical use of the corticotropin releasing hormone (CRH) test

A

Differentiates secondary (pituitary) and tertiary (hypothalamic) adrenal sufficiency

72
Q

Overnight Dexamethasone Suppression Test (screening test)

- Principle

A

Feedback mechanism of hypersecretion can be tested by administering a potent glucocorticoid and judging suppression of ACTH secretion

73
Q

Overnight Dexamethasone Suppression Test (screening test)

- Analytes measured

A

Serum or urine cortisol levels

74
Q

Overnight Dexamethasone Suppression Test (screening test)

- Diagnostic use

A

Differentiate normal patient from Cushing’s syndrome (either due to Cushing’s disease, adrenal tumor, or ectopic ACTH syndrome)

75
Q

Overnight Dexamethasone Suppression Test (screening test)

- Expected normal response

A

↓ cortisol (<3 ug/dL)

76
Q

Overnight Dexamethasone Suppression Test (screening test)

- Cause of abnormal results

A

↑ cortisol (>10 ug/dL) = Cushing’s Syndrome

77
Q

Which causes of Cushing’s syndrome may be differentiated using the high-dose test?

A
  • Adrenal tumors
  • Nonendocrine ACTH-secreting tumors
  • Pituitary Cushing’s disease
78
Q

What do normal results look like in high dose dexamethasone suppression test look like?

A

50% suppression of cortisol production

79
Q

How do abnormal results differ in Cushing’s and adrenal/ectopic tumors during the high dose test?

A
  • Cushing’s = mostly suppressed cortisol production

- Adrenal/ectopic tumors = no change in cortisol levels

80
Q

Three principle hormones classified as catecholamines and their sites of synthesis.

A
  • Epinephrine (80-90% medulla production)
  • Norepinephrine (10-20% medulla production)
  • Dopamine (small amt produced in adrenal medulla)
81
Q

These catecholamines have a marked influence on the vascular system

A

Dopamine and norepinephrine

82
Q

This catacholamine influences metabolic processes, especially carbohydrate metabolism

A

Epinephrine

83
Q

This catecholamine inhibits phenylethanolamine-N-methyltransferase

A

Epinephrine

84
Q

This catecholamine inhibits tyrosine hydroxylase

A

Norepinephrine

85
Q

Pheochromocytomas

- Cause

A
  • Tumor in adrenal medulla

- Too much catecholamines

86
Q

Pheochromocytomas

- Principle clinical symptom

A

Hypertension

87
Q

Pheochromocytomas

- Best specific urine screening test

A

Urinary metanephrines

88
Q

Pheochromocytomas

- Best diagnostic test

A

Urinary VMA

89
Q

Neuroblastomas

- Commonly affected age group

90
Q

Neuroblastomas

- Clinical symptoms

A

Tumor in or near adrenal gland producing a lot of dopamine, causing transient hypertension and tachycardia

91
Q

Neuroblastomas

- Best specific urine screening test

A

Urinary HVA (diagnostic0

Liz's Clinical Chemistry Module 4 (5 decks)

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