Adrenal Dysfunction/ Adrenal Medulla Flashcards

1
Q

Primary Adrenocortical Insufficiency (Addison Disease) is characterized by what

A

defect within adrenal gland

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2
Q

Primary Adrenocortical Insufficiency (Addison Disease) is cased by what

A

destruction of gland by tuberculosis, metastatic tumor
an autoimmune disorder
inborn errors of steroid hormone synthesis

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3
Q

Clinical Features of Primary Adrenocortical Insufficiency (Addison Disease) are

A

aldosterone deficiency
cortisol deficiency
androgen deficiency

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4
Q

consequences of aldosterone deficiency are

A

decreased renal absorption of Na+ (hyponatremia and polyuria)
extracellular fluid depletion (reduced plasma volume, hypotension, dehydration)
hyperkalemia

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5
Q

consequences of cortisol deficiency

A
inability to handle stress
hypoglycemia when stressed or fasting
weakness and fatigue
hypotension
decreased appetite and weight loss
anemia
hyperpigmentation
GI discomfort, nausea and occasional vomiting
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6
Q

consequences of androgen deficiency

A

loss of pub and axillary hair in females

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7
Q

Secondary Adrenocortical Insufficiency is associated with what

A

insufficient production of ACTH

insufficient production of renin

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8
Q

clinical supraphysiological doses of synthetic glucocorticoids cause what (and how)

A

Secondary Adrenocortical Insufficiency associated with ACTH

surpasses the hypothalamic-pituitary axis and depression of ACTH leads to adrenal atrophy

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9
Q

pseudohypoaldosteronism is cased by what

A

loss of function mutant in the mineralocorticoid receptor

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10
Q

pseudohypoaldosteronism is characterized by what

A

severe salt wasting in neonate
hyperkalemia
metabolic acidosis
failure to respond to treatment with mineralocorticoids

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11
Q

cushing syndrome is characterized by what

A

excessive cortisol secretion

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12
Q

major causes of cushing syndrome are?

A

injection of pharmacological doses of glucocorticoids
excessive secretion of ACTH by pituitary (Cushing’s Disease)
ectopic, non-endocrine, ACTH secreting tumors
tumors of adrenal cortex

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13
Q

patients with cushing syndrome have what clinical facial feature

A

moon face with acne

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14
Q

clinical features of cushing syndrome are?

A
obesity
hypertension
glucose intolerance
hirsutism
amenorrhea
purple cutaneous striae
bruise easy
osteoporosis
acne
poor wound healing
mental effects
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15
Q

what are the mental effects related to cushings

A

personality changes
insomnia
depression

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16
Q

poor wound healing seen in bushings is due to the inhibitor effects of cortisol on what

A
production of mediators of inflammation
production of chemotaxic and mitogenic mediators
fibroblast proliferation
collagen biosynthesis
circulating levels of WBCs
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17
Q

Primary aldosteronism (Conn Syndrome) is caused by what?

A

autonomous secretion of aldosterone, usually by ademona arising from zona glomerulosa

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18
Q

Primary aldosteronism (Conn Syndrome) symtoms are

A

mild hypertension
hypokalemia
metabolic alkalosis
low plasma renin

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19
Q

in patients with conn syndrome plasma renin levels are what?

A

depressed (as a result of expanded extracellular volume)

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20
Q

secondary aldosteronism is cased by what

A

inappropriate activation of renin-angiotensin system

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21
Q

Congenital Adrenal Hyperplasia (CAH) refers to what

A

group of genetically transmitted enzymatic deficiencies in the biosynthesis pathway for adrenal steroids

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22
Q

hyperplasia results when?

A

deficiency in biosynthetic pathway for cortisol

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23
Q

deficiency in biosynthetic pathway for cortisol result in what

A

decrease in negative feedback inhibition resulting in rise in ACTH secretion

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24
Q

what actually induces the hyperplasia of the adrenal gland

A

tropic effect of ACTH

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25
Q

in hyperplasia there is a build up of what

A

steroid intermediates directly behind the enzymatic block

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26
Q

most frequent block in congenital adrenal hyperplasia is in what

A

21-hydroxylase enzyme

27
Q

21-hydroxylase enzyme block is characterized by what

A

virilizing syndrome due to excess androgen production in the adrenal and non-adrenal tissues from pre block intermediates

28
Q

in females 21-hydroxylase enzyme block leads to what

A

fusion of labia and clitoral hypertrophy if exposure to androgens occurs before 12 weeks
exposure after 12 weeks leads to clitoral hypertrophy alone

29
Q

in males 21-hydroxylase enzyme block leads to what

A

increase in somatic growth
premature closure of epiphyseal plate
early maturation of genitalia
development of secondary sexual characteristics

30
Q

adrenal medulla contains what type of cells

A

modified postganglionic cells (chromaffin cells)

31
Q

chromaffin cells secrete what and into what

A

catecholamines directly into the blood stream

32
Q

chromaffin cells are innervated by what fibers

A

cholinergic preganglionic fibers

33
Q

what are the principle catecholamates released from the adrenal medulla

A

epinephrine and norepinephrine

34
Q

aprox 80% of chromaffin cells secrete what

A

epinephrine

35
Q

the only source of circulating epinephrine is where

A

adrenal gland

36
Q

most norepinephrine in the blood is released from where

A

nerve terminals

37
Q

chatecholamine release by adrenal medulla is an important part in acute response to what?

A

stress

38
Q

catecholamine biosynthesis involves the stepwise modification of what to what

A

tyrosine to dopamine

39
Q

the first step of converting tyrosine to dopamine is what

A

tyrosine to dihydroxyphenylalanine (DOPA) by tyrosine hydroxylase

40
Q

what is the rate limiting step in the conversion of tyrosine to dopamine

A

tyrosine to dihydroxyphenylalanine (DOPA) by tyrosine hydroxylase

41
Q

what is the transporter that brings dopamine into the chromaffin granule

A

VMAT

42
Q

in the chromaffin granule what happens to dopamine

A

converted to norepinephrine

43
Q

what happens to norepinephrine in cromaffin granule

A

exits granule via facilitated diffusion converted to epinephrine in cytoplams

44
Q

norepi becomes epi how

A

phenylthanolamine-N-methyltransferase (PNMT)

45
Q

what happens to epinephrine created in cytoplasm of chromaffin cells

A

transported back into chromaffin granule via VMAT where it is stored until release

46
Q

catecholamines are stored in chromaffin granules in a complex with what

A

ATP, Ca2+, and chromogranin

47
Q

about 50% of circulating catecholamine pool is loosely bound to what?

A

albumin

48
Q

the adrenal medulla is usually activated in concert with what

A

rest of sympathetic nervous system

49
Q

what is released from preganglionic fibers to promote the release of catecholamines that are stored in chromaffin granules

A

acetylcholine

50
Q

acetyl choline promotes transcription of what enzyme

A

tyrosine hydroxylase

51
Q

what connects adrenal medulla and cortex

A

portal system

52
Q

cortisol promotes what (in terms of catecholamines)

A

promotes conversion of norepinephrine to epinephrine

induces phenylethanolamine-N-methyltransferase (PNMT)

53
Q

cortisol prevents chromaffin cells from what?

A

developing into postganglionic neurons

54
Q

catecholamine-degrading enzymes (name them

A
monoamine oxidase (MAO)
catecholamine-o-methyltransferase (COMT)
55
Q

what happens to NE released by nerve terminals

A

either repackaged into secretory granules or degraded by MAO and COMT

56
Q

tissues degrade catecholamines predominantly how?

A

COMT-mediated methylation

57
Q

major classes of metabolites resulting from the inactivation of catecholamines (name them)

A

metanephrines

vanillylmandelic acid

58
Q

useful measure of total catecholamine production

A

urinary levels of metanephrines and vanillylmandelic acid

59
Q

adrenal medulla releases catecholamines into the blood in response to what

A

sympathetic activation caused by fright, danger, trauma, hemorrhage, hypoglycemia, vigorous exercise

60
Q

alpha 1 adrenergic receptors work via what pathway

A

Gd: IP3, Ca2+, DAG

61
Q

alpha 2 adrenergic receptors work via what pathway

A

Gi: decreasing cAMP

62
Q

then beta adrenergic receptors work via what pathway

A

Gs: cAMP

63
Q

Pheochromocytomas (what are they)

A

catecholamine-producing tumors of chromaffin cells of the adrenal medulla or extra-adrenal ganglia

64
Q

Pheochromocytomas (clinical features)

A

hypertension, tachycardia, tremors, sweating, anxiety, headache