Adrenal

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Clinical Chemistry
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1

adrenal glands

multifunctional organs that produce steroid hormones and neuropeptides; paired organs that sit on top of the kidneys

2

blood pressure, electrolyte balance, and androgen excess

three functions of the adrenal glands

3

hormone replacement therapy

hypofunction treatment

4

pharmacologic suppression and/or surgery

hyperfunction treatment

5

hyperaldosteronism

causes hypertension, hypokalemia, and metabolic alkalosis

6

pheochromocytoma

causes hypertension, anxiety, palpitations, dizziness, diaphoresis

7

Cushing's syndrome

causes hypertension, unexplained weight gain, red/purple stretch marks, proximal muscle weakness

8

congenital adrenal hyperplasia

causes inappropriate hirsutism/virilization and inability to conceive

9

primary adrenal insufficiency

causes loss of appetite, unintentional weight loss, pigmented skin

10

adrenal cortex and adrenal medulla

adrenal gland regions

11

zona reticularis, zona fasciculata, and zona glomerulosa

adrenal cortex zones

12

mineralcorticoids

hormones released from zona glomerulosa

13

glucocorticoids

hormones released from zona fasciculata

14

androgens

hormones released from zona reticularis

15

stress hormones

hormones released from adrenal medulla

16

mineralcorticoids

regulate mineral balance

17

glucocorticoids

regulate glucose metabolism

18

androgens

stimulate masculinization

19

stress hormones

stimulate sympathetic ANS

20

aldosterone

1 type of mineralcorticoids

21

cortisol, corticosterone, and cortisone

3 types of glucocorticoids

22

dehydroepiandrosterone

1 type of androgen hormone

23

epinephrine and norepinephrine

two types of stress hormones

24

adrenocorticotropic hormone

a cortex steroidogenesis stored in pituitary gland

25

cortex steroidogenesis

controls substrate availability, enzyme activity, inhibitory feedback specific to zone

26

pregnenolone

rate limiting step of steroidogenesis

27

cholesterol

common substrate of adrenal gland for cortex steroidogenesis; stored in parenchymal cells; additional synthesis possible via Acetyl-CoA; free enters pathway; ACTH stimulates free availability while LDL inhibits free availability

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Hypothalamus releases corticotropin releasing hormone -> anterior pituitary releases ACTH -> adrenal cortex releases cortisol

cortex steroidgenesis

29

figures 21.1 and 21.3

...

30

pregnenolone by cytochrome P450

rate limiting step cholesterol

31

returned to cortex for zonal reactions

...

32

increased glucocorticoids

what suppresses CRH and ACTH

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cortisol

primary regulator of ACTH

34

increased ACTH and CRH to stimulate cortisol

results of decreased enzymatic activity

35

leads to adrenal hyperplasia and possible overproduction of androgens

...

36

congenital adrenal hyperplasia

group of conditions due to absent or diminished enzymes involved in steroidgenesis

37

mineralcorticoid, glucocorticoid, androgen production

pathways affected by congenital adrenal hyperplasia due to substrate build-up

38

21-hydroxylase

commonly affected enzyme of congenital adrenal hyperplasia

39

figure 21.4

...

40

decreased glucocorticoid and increased 17-hydroxyprogesterone

hormonal result of congenial adrenal hyperplasia

41

failure to thrive and low blood pressure

classic form of congenital adrenal hyperplasia in infants

42

hirsutism, menstrual irregularities, and infertility

nonclassic form of congenial adrenal hyperplasia in women

43

aldosterone

60% transported bound to albumin or corticosteroid-binding globulin; 40% transported free

44

morning

diurnal variation of aldosterone where concentration is highest

45

upright position

postural changes that increase aldosterone levels

46

regulates extracellular fluid volume and potassium metabolism

aldosterone functions

47

renin-angiotensin system, potassium, and ACTH

three things that control aldosterone release

48

hyperkalemia, decreased blood pressure, and decreased Na+ concentration

three factors that stimulate aldosterone

49

primary aldosteronism

excessive secretion of aldosterone that cannot be suppressed by salt or volume replacement; symptoms include hypertension, metabolic alkalosis, vascular disease risk

50

aldosterone-producing adrenal adenoma and unilateral or bilateral hyperplasia

two of the most common primary aldosteronism

51

increased plasma aldosterone and increased plasma renin

lab tests seen in primary aldosteronism

52

isolate hypoaldosteronism

insufficient aldosterone secretion due to adrenal gland destruction; caused by chronic heparin therapy, adrenalectomy, G-zone enzyme deficiency, and mild renal insufficiency

53

adrenal insufficiency

inadequate hormone secretion from adrenal cortex

54

primary adrenal insufficiency

adequate stimulation but not release of hormones of adrenal cortex; inadequate release of glucocorticoids, mineralcorticoids, or adrenal androgens

55

secondary adrenal insufficiency

insufficient stimulus for adrenal gland hormone release such as pituitary gland insufficient release of ACTH

56

autoimmune destruction of the adrenal gland (Addison's disease)

most common cause of adrenal insufficiency

57

decreased blood pressure, glucose, and sodium, and increased potassium

nonspecific adrenal insufficiency diagnostics along with fatigue, weight loss, decreased appetite, and nausea

58

decreased cortisol and increased ACTH

adrenal insufficiency diagnostic labs

59

ACTH stimulation test

used to diagnose primary adrenal insufficiency; measures baseline ACTH and cortisol in the morning, give synthetic ACTH IV or IM, and remeasure cortisol at 30 and 60 minutes

60

rise in cortisol

normal ACTH stimulation test result

61

secondary adrenal insufficiency

ACTH stimulation test may be normal or abnormal depending on the issue; other stimulation tests optional

62

replacement of glucocorticoids or mineralcorticoids

treatment for adrenal insufficiency

63

maintains normal blood pressure, hematological effects, increased during stress, and regulation of metabolism

four functions of cortisol

64

stimulates GFR and decreases water reabsorption by kidneys

two ways cortisol maintains normal blood pressure

65

stimulates erythropoiesis, causes leukocytosis and lymphocytopenia, and suppresses inflammatory and immune reponse

three ways cortisol effects hematologically

66

carbohydrates, proteins and lipids, and anabolic effect on liver metabolism

three ways cortisol regulates metabolism

67

increase plasma glucose levels and antagonistic to effects on insulin

two ways cortisol regulates carbohydrate metabolism

68

catabolic effect

the way cortisol regulates protein and lipid metabolism

69

high levels of free cortisol in urine

indicates adrenal hyperfunction

70

cortisol

96% bound to Cortisol binding globulin, 6% to albumin; 4% free in plasma

71

high in morning, low in late afternoon to evening

normal diurnal variation of cortisol

72

CRH

synthesized and released by hypothalamus and acts on pituitary to release ACTH

73

ACTH

acts on adrenal cortex

74

stimulates CRH and cortisol

hypoglycemia effects on cortisol

75

CRH, ACTH, stress, and hypoglycemia

four ways cortisol is controlled and regulated

76

Cushing's Syndrome

excess cortisol production; manifestations are not unique to the condition but include hypertension, glucose intolerance, depression, obesity, skin changes; characteristic moon face and buffalo hump

77

adrenal tumors which produce excess cortisol causing ACTH to be low

primary cause of hypercortisolism

78

pituitary/non-pituitary tumor produces excess cortisol due to increased ACTH

secondary cause of hypercortisolism

79

ACTH dependent Cushing's disease

elevation of ACTH due to pituitary gland

80

ACTH independent Cushing's syndrome

increased cortisol no due to elevated ACTH

81

dexamethasone suppression test

synthetic cortisol (30x more potent) given in evening and blood cortisol drawn in AM; normal <140 mmol/L, Cushing's response >280 mmol/L

82

immunoradiometric test IRMA

used to determine the reason for hypercorticolism, the degree of ACTH elevation, and identify if it is ACTH dependent or independent

83

resection of pituitary tumor

Cushing's disease treatment

84

tumor resection or medical therapy to suppress ACTH

Cushing's syndrome treatment

85

DHEA and DHEA-S

precursors of adrenal androgens

86

androstenedione, testosterone, 5-dihydrotestosterone, and estrogen, some testosterone

5 active androgens

87

androgen edxcess

ambiguous genitalia in female infants and precocious puberty in children; simulates organ development and linear growth; physical affects in both girls and boys; short stature; infertility in men and women; additional physical effects in men and women

88

measure DHEA, DHEA-S, urinary 17-ketosteroid, and testosterone

4 diagnostic markers for adrenal androgens

89

adrenal medulla

responsible for synthesis of catecholamines from tyrosine; first responders to regulate body's response to stress

90

fight or flight response by adrenal medulla

increases cardiac output and blood pressure moving blood to muscle and brain tissue

91

epinephrine, norepinephrine, dopamine, and serotonin

four naturally occurring catecholamines

92

epinephrine

catecholamine produced in adrenal medulla

93

norepinephrine

catecholamine neurotransmitter produced in central nervous system and postganglionic sympathetic nerves

94

dopamine

highest concentration in brain and some peripheral organs

95

serotonin

signal transmitter in CNS and peripheral organs

96

phenylalanine

sequentially converted to epinephrines

97

increase cortisol and increase epinephrine production

product of norepinephrine to epinephrine by phenylethanolamine-N-methyltransferase (PNMT)

98

neurosecretory vesicles

location of NE and EPI storage

99

epinephrine

the main catecholamine

100

dopamine

sympathetic neuron vesicles in norepinephrine; hypothalamus synthesis

101

catecholamines (dopamine and epinephrine)

important transmitters of nerve signals that influence the vascular system

102

vanillylmandelic acid

principle end product of epinephrine and norepinephrine

103

fall in blood pressure or blood volume, thyroid hormone deficiency, congestive heart failure, arrhythmias, and stress

5 causes of excess levels of catecholamines

104

idiopathic postural hypotension

cause of decreased levels of catecholamines

105

pheochromocytoma

hypersecretion of catecholamines producing tumors; symptoms include weight loss, sustained or paroxysmal hypertension, headache, palpitations, and anxiety

106

urine metanephrine and VMA and plasma catecholamines

used to diagnose adrenal medulla disorders

107

neuroblastoma

one of the most common malignant tumors in children; 80% in children less than 5 years old; increased dopamine excretion is diagnostic; also increased norepinephrine, VMA, and HVA

108

fluorometric, spectrophotometric, chromatographic (HPLC), and imaging studies

analytic methods for measurement