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Pathophysiology > endocrine- adrenal > Flashcards

endocrine- adrenal Flashcards

1
Q

where are the adrenal glands located? what are the two parts to them?

A

Retroperitoneal, superior pole of each kidney

2 separate glands-cortex & medulla

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2
Q

cortex of adrenal gland - essential? what does it secrete? # of zones?

A

Outer cortex-mesoderm
Essential for life (only source of cortisol)
Secretes steroid hormones
3 zones

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3
Q

medulla of adrenal gland - essential? what does it secrete?

A

Inner medulla-ectoderm
Secretes catecholamines
not essential for life

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4
Q

what are the 3 zones of the outer adrenal cortex? which is the thickest?

A
  1. outer: zona glomerulosa
  2. middle: Zona fasciculata -thickest
  3. Zona reticularis
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5
Q

what are each of the 3 zones of the outer adrenal cortex made of?

A

“Salt, sugar, & sex…the deeper you go, the sweeter it gets”
Zona glomerulosa- Mineralocorticoids: Aldosterone
Zona fasciculata- Glucocorticoids: Cortisol
Zona reticularis - Glucocorticoids: androgens
(think “GFR” - as its right about kindey)

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6
Q

which adrenal cortex zone responds to ACTH? which doesnt?

A

zona glomerulosa - not affected

zona fasisculata- responds to ACTH

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7
Q

adrenocortical steroids are all dervied from _____.

A

cholesterol

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8
Q 
Glucocorticoids & mineralocorticoids have \_\_\_ carbons
Androgens have\_\_\_carbons (kinda weeds)
A

21

19

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9
Q

cholesterol –> glucocorticoid: changes to molecular structure? what about for glucocorticoid –> cortisol?

A

Glucocorticoids require C11 & C21 hydroxylation

Cortisol requires C17 hydroxylation as well

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10
Q

cholesterol –> aldosterone: changes to molecular structure?

A

Aldosterone requires C11 hydroxylation & has C18 double bond

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11
Q

cholesterol –> androgens: changes to molecular structure?

A

Androgens lack C20-21 side chain & have C17 double bond (ketone group)

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12
Q

adrenal cortical steroid synthesis: zone contain enzymes specific to hormones produced… ZG has _____, ZR has _____

A

ZG has aldosterone synthase

ZR has 17, 20-lyase

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13
Q

the rate limiting step in adrenal cortical steroid synthesis: ______ stimulates initial conversion of cholesterol to ______?

A

ACTH stimulates conversion cholesterol –> pregnenolone

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14
Q

what are the precursor molecules that can sub for our key adrenal hormones?

A

Corticosterone has glucocorticoid activity (can sub for cortisol)
Corticosterone & 11-deoxycorticosterone have mineralocorticoid activity (can do what aldosterone does but not as well - can sub for it)
* from pathway: deoxy –> corticosterone –> aldosterone

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15
Q

when are the highest levels of adrenal hormones ? (time of day)

A

Highest levels between 4am-8am

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16
Q

what causes the secretion of adrenal corticosteroid? what is it affected by?

A

Results from pulsatile secretion of hypothalamic CRH

Affected by sleep-wake cycles & sensory input

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17
Q

cortisol’s effect on the HPA axis?

A

inhibits it

- comes out adrenal cortex- inhibits both ant. pituitary (release of ACTH) and hypothalamus (release of CRH)

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18
Q

6 functions of cortisol

A
  1. Promotes gluconeogenesis
  2. Decreases peripheral glucose utilization (diabetogenic)
  3. Potent anti-inflammatory effects
  4. Inhibits immune response
  5. Upregulates α1 receptors on vascular smooth muscle (too much cortisol = HTN)
  6. Increases GFR
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19
Q

why is cortisol necessary for survival?

A

needed for times of metabolic stress (like a broken bone)

–> hyperglycemia –> more glucose available to brain.

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20
Q

what two things does aldosterone increase?

A
  1. Increases Na+ reabsorption
    - Water follows
    - Increases ECF volume
  2. Increases K+ (or H+) secretion
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21
Q

what do androgens do?

A

Promote masculinization

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22
Q

what is addison’s disease?

A 
chronic hypoadrenocorticism: 
 Insufficient glucocorticoid (cortisol) (& usually mineralocorticoid - androgen) production
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23
Q

most common cause of addison’s (chronic hypoadrenocorticocism)?

A

Iatrogenic:
Rapid withdrawal of glucocorticoids, post-adrenalectomy, ketoconazole/fluconazole.
(adrenal gland goes on strike when we give steroids, if you take them off fast- we didnt give it enough time for gland to recover)

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24
Q

most common cause of non-iatrogenic hypoadrenocorticocism? (kinda weeds)

A

Autoimmune adrenalitis -auto antibodies against adrenal cortex
(comes with hashimoto’s (thyroiditis that causes hypothyroid): treating without covering with steroids- known as Schmidts syndrome)

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25
Q

3 other causes of hypoadrenocorticocism? (addisons)

A
  1. Corticosteroid insufficiency of critical illness: ICU patients
  2. Infections
  3. Secondary (ACTH deficiency)
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26
Q

5 S+S and hypo adrenocorticisim (kinda weeds) (addisons)

A
  1. Weakness
  2. Weight loss
  3. low BP (hypotension)
  4. Often labeled as being “mental”
  5. Sudden unexpected death :from common cold, flu, etc.
    * none specific enough to raise suspicion
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27
Q

4 substance level changes in hypoadrenocorticism (kinda weeds)

A 
metabolic acidosis 
Hypoglycemia
Hyperkalemia
Hyperpigmentation (high ACTH)-check nipples, palmar creases, old scars
*none specific enough to raise suspicion
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28
Q

what is acute hypoadrenocorticism known as? what does it cause?

A

adrenal apoplexy/ Addisonian crisis (unexplained deaths from relatively minor infections/illness)
“Sudden onset “warm” shock, accompanies stress, often fatal.”

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29
Q

what are the two causes of acute hypoadrenocorticism (adrenal apoplexy/ addisonian crisis)

A
  1. Undiagnosed adrenal insufficiency

2. Known Addison’s without supplemental steroids

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30
Q

what is Waterhouse-Friderichsen syndrome?

A

type of hypoadrenocorticism:

  • Massive intra-adrenal hemorrhage in setting of sepsis (usual meningococcal, but not always.. still suspect acute addisons)
  • Shock, death within hours
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31
Q

txt for waterhouse-friderishsen?

A

Give the steroids without waiting for the labs to come back.

32
Q

treatment for hypoadrenocorticism: primary addisons

A
  1. glucocorticoid & mineralocorticoid: (Hydrocortisone/fludrocortisone)
    - Maintenance & stress doses
    - when you anticipate someone will be under metabolic stress- bump up to dose to cover metabolic stress
33
Q

treatment for hypoadrenocorticism: acute adrenal insufficiency (3)

A
  1. Salt, sugar, steroid replacement
  2. Support organ function
  3. Search for underlying cause
34
Q

what is cushing’s syndrome? who gets it?

A

hyperadrenocorticism - excessive glucocorticoid production

-most common in women

35
Q

2 keys to signs of hyperadrenocorticism

A
  • Excess fat deposits in the body*

- Diagnosis is partially a lack of circadian rhythm when cortisol is secreted

36
Q

S+S of hyperadrenocorticisim

A 
Weight gain
Truncal obesity/moon face
Thin skin, striae, poor healing
Hirsutism
Hypertension
Glucose intolerance
Osteoporosis
Amenorrhea
Often labeled as being “mental”
37
Q

Dx test for hyperadrenocorticism

A 
24 hour urinary free cortisol test: 
800/2000 cortisol levels = NORMAL 
(high cortisol 8am, low 8pm = normal) 
-reversal of these levels = pos. Dx 
**document hypersecretion of cortisol & loss of circadian rhythm
38
Q

how do you distinguish cushing’s disease vs syndrome?

A

low (syndrome) vs high (disease) dose dexamethasone suppression test

39
Q

txt of hyperadrenocorticism is usually based on cause, often involve surgery, but what are two drugs that can be used? (kinda weeds)

A

Metyrapone & ketoconazole inhibit steroid synthesis

40
Q

primary hyperaldosteronism: what is it and what causes it?

A

Overproduction of mineralocorticoid (causes water and sodium reabs)
Due to adrenal hyperplasia or adrenal adenoma (Conn’s syndrome)

41
Q

surgery-correctable cause of hypertension? (0.5%)

A

primary hyperaldosteronism

42
Q

S+S of hyperaldosteronism

A 
Hypertension
Hypokalemia
Metabolic alkalosis
Low renin levels
No edema
43
Q

primary hyperaldosteronism-caused HTN: with thiazide diuretics can cause what?

A

fatal hypokalemia!

44
Q

Dx of primary hyperaldosteronism

A

Diagnosis via high aldosterone-to-renin activity ratio

- if renin is low and aldosterone is high, then aldosterone level is inappropriate

45
Q

removal of adrenal adenoma (cause of hyperald.): what should you be sure to do?

A

theyre often small..

Renal vein sampling can determine laterality (which side the adenoma is on so you know which side to remove*)

46
Q

txt of adrenal hyperplasia (cause of hyperald.)

A

Spironolactone (K sparing*)

47
Q

what is congenital adrenal hyperplasia (CAH) ?

A

a group of autosomal recessive disorders

  • deficiency of an enzyme involved in the synthesis of cortisol, aldosterone, or both
  • Lack of negative feedback from cortisol on ant pituitary causes increased ACTH (to try to stimulate adrenal glands) = adrenal hyperplasia
  • Because of the blocks, most of the precursors go down the androgen pathway*
48
Q

adrenogenital syndrome: two types? which is most common ?

A

a type of CAH
- many types: two main types we care about
21- hydroxylase deficieny (MOST COMMON)
11-β-hydroxylase deficiency

49
Q

adrenogenital syndrome: 21-hydroxylase deficiency vs 11- beta hydroxylase (maybe weeds)

A 
21-hydroxylase deficiency
No cortisol, aldosterone, or DOC
Severe deficit: Salt-wasting, dehydration, death in severe forms
MORE LIFE THREATENING
11-β-hydroxylase deficiency
Huge amounts DOC produced
Don’t get much cortisol produced*
Hypertension, salt-retention
50
Q

what do you want to Consider in females with amenorrhea or moustaches?

A

adrenogenital syndrome (kind of CAH)
- 21-hydroxylase deficiency most common
Dx: Serum 17-OH-progesterone
If normal-ish, provoke with ACTH stimulation

51
Q

Dx adrenogenital syndrome

A

Stimulation test:
1. Administer ACTH
2. Measure 17-OH-progesterone in 1 hour
Even mild elevations suggest disease

52
Q

txt adrenogenital syndrome

A

Treat with glucocorticoid ± mineralocorticoid replacement (depends on the block type*)
Reconstructive surgery in severely affected female infants

53
Q

what are most adrenal masses like?

A

about 75% are adenomas

- most can be left alone

54
Q

what is the purpose of the adrenal medulla?

A

Not essential for life
produces catecholamines:
Source of adrenalin (epinephrine) & norepinephrine

55
Q

what are the two disorders of the adrenal medulla?

A 
both usually functional - secrete catecholamines 
1. Pheochromocytoma: Adults
Well-differentiated
2. Neuroblastoma: Children
Poorly-differentiated
56
Q

“paroxysms of extreme hypertension (230s/150 ex), headache, sweating, other autonomic disturbances”- what is this a classic presentation of?

A

pheochromocytoma

  • result from compression/ischemia of tumor = secrete more Epinephrine
  • more commonly produce sustained HTN
57
Q

what % of pheochromocytoma are familial? who has to be screened?

A

30%
- family members need to be screened if someone has MEN IIa or IIb (RET oncogone) or von Recklinghausen’s neurofibromatosis (NF-1 mutation)

58
Q

Dx of pheochromocytoma

A

24 hr urinary vanillylmandelic acid (VMA)

Plasma free metanephrines (can test this in urine too*)

59
Q

txt of pheochromocytoma

A
  1. Surgical resection- subtle movement of the tumor can cause sudden BP drop**
  2. Careful fluid & BP management
60
Q

Multiple endocrine neoplasia disorders (MENs) - what type hereditary nature?

A

Autosomal dominant disorders

-Predispose people to endocrine tumors

61
Q

MEN I

A

“PPP”, “Wermer’s syndrome”
Chromosome 11, gene MENI, protein menin, tumor suppressor gene
1. Parathyroid hyperplasia/adenoma(s) (95%)
2. Pituitary adenoma
3. Pancreatic endocrine tumors (usually gastrinoma)

62
Q

MEN IIa

A 
“PPM”, “Sipple’s syndrome”
Chromosome 10, gene RET, protein tyrosine kinase, proto-oncogene
1. Medullary thyroid cancer (100%) 
2. Parathyroid adenoma(s) 
3. Pheochromocytoma
63
Q

which MEN do people get prophylactic thyroidectomy for?

A

MEN IIa and MEN IIb

64
Q

MEN IIb

A

“PMM”, “Wagenmann-Froboese syndrome”
Chromosome 10, gene RET, protein tyrosine kinase, proto-oncogene
1. Mucosal neuromas (100%), also Marfanoid body habitus
2. Medullary Thyroid cancer (85%)
3. Pheochromocytoma

65
Q

consequences of Dx a adrenal disease that is NOT actually there?

A

-lifelong medication, unnecessary surgery or radiation

66
Q

consequences of failure to Dx adrenal disease?

A

death from disease that maybe had an excellent prognosis

67
Q

general guidelines for adrenal testing?

A
  • Single tests seldom establish adrenal disease
  • Often utilize “stimulation” or “suppression” tests
  • Get consultation with endocrinologist in equivocal cases or when screening is positive
68
Q

Thin, tired patient with no appetite: what should you do? (3 steps to Dx and treatment)

A

maybe addisons
1. Screening-early morning (between 4 and 8am) serum cortisol
2. if <13 mg /dL –> get rapid ACTH stimulation test
(give 250 mcg synthetic ACTH IV)
3. check Serum cortisol in 30-60 min
if > 18 mcg/dL = NORMAL
if < 18 mcg/dL =primary or secondary Addison’s
Consider giving dexamethasone pre-test to prevent crisis

69
Q

Depressed, overweight patient with hypertension & hyperglycemia

A

maybe cushings- check cortisol levels (3 possible ways)
1. serum cortisol: 8pm levels over 1/2 of 8am levels (higher at night) = Dx
2. 24 hr urine free cortisol: >108 mcg/dL (high) =Dx
3. low dose dexamethasone suppression test: give at midnight and measure cortisol in morning.
lack of suppression = Dx
4. late night salivary cortisol

70
Q

when might someone get falsely high positive cortisol tests? (giving false impression of cushings)

A

False-positives in severe depression, hard drinkers, pregnancy

71
Q

two tests to distinguish cushings Dz from others?

A
  1. high dose desamethasone suppression test: Pituitary adenomas are suppressed, adrenal tumors & ectopic sources of ACTH are not
  2. metyrapone stimulation test: Potent inhibitor of 11-β-hydroxylase (enzyme important for aldosterone + cortisol production)
    - normal response: decr. cortisol, compensatory increase ACTH and 11-deoxycortisol
    - -> Pituitary adenomas (cushings) stimulated
    - -> adrenal tumors are not:
    - -> ectopic ACTH sources maybe?
72
Q

Hypertensive patient with hypokalemia off meds

A

hyperaldosteronism: renin-independent increase in aldosterone
Dx: serum aldosterone-renin activity ratio
> 920: primary aldosteronism
< 28 : Addisons

73
Q

Nervous patient with hypertension & headaches: what do you think? 3 possible ways to Dx?

A

pheochromocytoma

  1. 24 hr urinary vanylmandelic acid (VMA) & metanephrines
  2. Plasma free metanephrines
  3. I131 metaiodobenzylguanidine isotope scan
74
Q

low vs high serum ACTH suggest what?

A

Low indicates adrenal tumor Cushing’s syndrome

High indicates ectopic ACTH Cushing’s syndrome

75
Q

Corticotrophin-releasing factor stimulation test

A

pituitary adenomas respond, others dont

76
Q

low dose vs high dose dexamethasone tests results

A

Low-dose dex suppressions rule in/out Cushingism

High-dose dex suppressions attempt to differentiate Cushing’s disease from other causes

Pathophysiology (28 decks)

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