adrenal hormones and testing Flashcards

(57 cards)

1
Q

where is the adrenal gland located

A

on top of the kidney (one for each kidney)

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2
Q

adrenal cortex

A

produces and secretes steroid hormones, including cortisol aldosterone, and androgens

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3
Q

adrenal medulla

A

produces and secretes catecholamines

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4
Q

areas of the adrenal cortex (outside to inside)

A

zone glomerulosa, zona fasciculata, zone reticularis

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5
Q

what hormones are released from the zona glomerulosa

A

mineral corticoids - aldosterone
- regulate blood pressure by increasing Na2+ retention in blood excreting K+ and H+ in return

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6
Q

what hormones are released from the zona fascicularta

A

glucocorticoids - cortisol, corticosterone, cortisone

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7
Q

what hormones are released from the zona reticularis

A

androgens - dehydroepiandrosterone

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8
Q

what hormones are released from the adrenal medulla

A

epinephrine, norepinephrine

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9
Q

RAAS system

A

renin
angiotensin
aldosterone
system

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10
Q

true or false: there is no involvement of the hypothalamus or pituitary in the regulation of aldosterone

A

TRUE: however, aldosterone does stimulate the third reflex through the hypothalamus and secretion of ADH

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11
Q

primary aldosterone excess disorders

A

adrenal disorder
autonomous aldosterone production by the adrenal tumor (Conn’s disease)
too much aldosterone in the gland

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12
Q

secondary aldosterone excess disorders

A

too much aldosterone in other organs/ conditions
renin producing tumour
renal artery stenosis - impaired blood flow to the kidney
drugs - laxatives, some diuretics

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13
Q

increased aldosterone causes

A

Na+ retention: increased blood volume and hypertension hypernatremia
K+ loss: muscle weakness and cardiac arrhythmia
H+ loss: increased blood pH

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14
Q

investigation of aldosterone excess (high blood pressure) / deficiency

A

aldosterone levels
renin levels
aldosterone:renin ratio
serum or urine samples can be measured
reported in pmol/L

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15
Q

aldosterone excess lab testing workflow

A
  1. if the patient has excess aldosterone, measure aldosterone
  2. primary or secondary? measure renin and aldosterone/renin ratio
    prim: decreased renin increased ratio
    secondary: increased renin ratio not drastically increased
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16
Q

primary aldosterone deficiency

A

addison’s disease - destruction of adrenal cortex
enzyme deficiency in the aldosterone synthesis pathway

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17
Q

secondary aldosterone deficiency

A

renin deficiency

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18
Q

aldosterone deficiency causes

A

Na2+ loss: water loss, dehydration, decreases blood pressure, weakness
K+ retention: muscle weakness and cardiac arrhythmia
H+ retention: decreased blood pH (blood is more acidic)

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19
Q

aldosterone deficiency lab workflow

A
  1. does the patient have decreased aldosterone? measure aldosterone
  2. is the case primary or secondary? measure renin and aldosterone/renin ratio
    primary: increased renin decreased ratio
    secondary: decreased renin not drastically decreased ratio
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20
Q

renin activity testing

A
  • not well standardized
  • fairly manual and time-consuming
  • can incubate for prolonged period of time to generate a signal in low renin samples
  • technical process dependant on many variables
  • have been used longer
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21
Q

renin mass

A
  • calibrated against an international reference standard
  • can be automated
    -may not be able to measure renin concentrations as low as renin activity assays
    -better intra and inter-assay reproducibility
  • in use for a shorter period
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22
Q

true or false: cortisol increases during times of stress

A

true

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23
Q

the effect of cortisol on carbohydrate, protein, and lipid metabolism

A

increases blood glucose through gluconeogenesis
increases protein breakdown
increased lipolysis
cortisol is an insulin antagonist

24
Q

… facilitates catecholamine effects by increases blood pressure

25
this hormone suppresses the immune system
cortisol
26
levels of cortisol in humans undergoes diurnal variation
highest in the morning and lowest at midnight
27
regulation of cortisol
1. During period of high stress catecholamines are released and then cortisol 2. cortisol monitored by the hypothalamus 3. the release of cortisol signals the hypothalamus to stop further release 4, hypothalamus released CRH stimulating th anterior pituitary 5. the anterior pituitary released ACTH which acts in the adrenal cortex to produce and release cortisol
28
primary adrenal disorder due to increased cortisol
autonomous cortisol production by an adrenal tumor s- cushing's syndrome
29
secondary adrenal disorder due to increased cortisol
autonomous ACTH production by pituitary tumor (cushing's disease)
30
other adrenal disorder due to an increased cortisol
ectopic acth - producing tumor
31
limitations of cortisol assay
does not measure active form diurnal variation difficult for patients testing not widely available
32
lab evaluation of cortisol
serum total cortisol 24 urinary cortisol salivary cortisol
33
why can't cortisol be measured freely
cortisol is closely bound to protein in the serum - cortisol binding globulin and albumin - free cortisol is active
34
diagnosing cushing's syndrome
- diabetes - skin thinning, easy bruising, poor wound healing, muscle weakness - abnormal fat distribution - moon face, buffalo hump, central obesity - hypertension - immune system suppresion - osteoporosis
35
how are cortisol levels measured
24 hr free urinary cortisol
36
how can cortisol be suppressed
dexamethasone suppression test - measure cortisol, serum before, and after given DXM - if cortisol not supressed suggests autonomous production tumor - if cortisol not supressed ACTH measurements can help determine whether it is primary or secondary
37
decreased acth
adrenal
38
increased acth
pituitary or ectopic
39
addison's disease
cortisol deficiency
40
presentations of addison's disease
hypoglycemia low blood pressure sever weakness and fatigue weight loss and decreased appetite nausea and vomiting mayne hyperpigmentation
41
if addisons disease coexists with an aldosterone deficiency we will see...
Na+ loss and K+ retention
42
how is cortisol in patient tested
am serum levels
43
how is cortisol production stimulated
measrue serum cortsiol before and after given synthetic acth
44
healthy individuals
large increase in cortisol
45
primary cortisol deficiency
no increase in cortisol
46
secondary cortisol deficiency
small increase in cortisol
47
what is the structure variant in catecholamines
monoamine structure
48
what hormones do catecholamines create
dopamine, epinephrine, norepinephrine
49
what are catecholamines synthesized from
amino acid tyrosine and produced by the nervous system
50
what is epinephrine and norepinephrine
fight or flight response from the sympathetic nervous system
51
cause of catecholamine excess
pheochromocytoma: tumor in medulla - can be hereditary - occurs commonly in people ages 30-50
52
what are the 4 P's of catecholamine excess
perspiration palpitation pain increased blood pressure
53
what is the best to test excess catecholamine
metanephrine and normetanephrine - methylated metabolites or norepinephrine and epinephrine
54
affected pheochromocytoma patients should avoid
food with tyramine medication with monoamine oxidase inhibitors
55
treatment for pheochromocytoma
surgery, chemotherapy, and radiation therapyc
56
catecholamine deficiecy
rare but congenital due to defects in the development of the adrenal medulla impaired mechanism of release
57
functional deficiencies can stem from and cause
impaired mechanism of release impaired reuptake impaired receptor sensitivity - can cause mood and attention dysregulation