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Endocrine Week 1 > ICL 2.2: Adrenal Disorders > Flashcards

ICL 2.2: Adrenal Disorders Flashcards

1
Q

which disorders are corticosteroids used to treat?

A
  1. inflammatory
  2. allergic

3 .immunlogic disorders

  1. immunosuppressive agents for transplant and chemo
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2
Q

what are the long term effects of glucocorticoid use?

A

they suppress the function of the HPA axis which can lead to iatrogenic Cushing syndrome

however, the sudden cessation fo corticosteroid therapy can result in adrenal failure (iatrogenic adrenal insufficiency) so you have to wean people off

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3
Q

A 25-yo male comes to the ER with fever, hypotension and vomiting.
Prior to this event, he experienced sore throat, runny nose and body aches for 2-3 days. He has experienced increased pigmentation, gradual weakness, weight loss (6 kg) and salt craving for several months.
P/E: Pale skin, appears dehydrated, BP: 110/60 mmHg, HR: 110/min, Temp 37.5 °C

  1. excess or deficiency?
  2. which hormone(s)?
  3. location?
  4. mass?
A

hypotension: suggests deficiency since it has to do with BP maintenance

weight loss: indication of glucocorticoid deficiency

salt craving: mineralocorticoid deficiency

increased pigmentation: increased ACTH production

primary adrenal insufficiency

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4
Q

what are the clinical features of primary adrenal insufficiency?

A
  1. increased pigmentation of skin and buccal mucous due to increased acth
  2. autoimmune conditions
  3. clubbing
  4. weight loss, anorexia, nausea, vomting
  5. hypotension
  6. abdominal pain
  7. salt craving
  8. diarrhea
  9. constipation
  10. syncope/vitiligo

with secondary adrenal insufficiency there’s lack of ACTH so you won’t have hyperpigmentation

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5
Q

what are the lab findings in primary adrenal insufficiency?

A
  1. electrolyte disturbance
  2. hyponatremia
  3. hyperkalemia
  4. azotemia
  5. anemia
  6. eosinophilia
  7. hypercalcemia

hyperkalemia and eosinophilia are only in primary adrenal insufficiency, not secondary

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6
Q

why is there hyponatremia in primary adrenal insufficiency?

A

hyponatremia happens in primary because of salt loss due to mineralocorticoid deficiency

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7
Q

why is there hyperkalemia in primary adrenal insufficiency?

A

this is only in primary adrenal insufficiency not secondary

it’s due to lack of mineralocorticoids

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8
Q

what are the causes of primary adrenal insufficiency?

A
  1. anatomic destruction of adrenal gland
    ex. metastatic, hemorrhage, infection, surgical removal, Addison’s
  2. metabolic failure in hormone production
  3. ACTH blocking antibodies
  4. mutation in ACTH receptor gene
  5. adrenal hypoplasia congenita
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9
Q

what are the causes of secondary adrenal insufficiency?

A
  1. hypopituitarism due to hypothalamic-pituitary disease
    ex. sellar/suprasellar tumor/surgery, pituitary apoplexy, hemorrhage/infarct
  2. suppression of hypothalamic-pituitary axis
    ex. steroids, endogenous steroid from tumor
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10
Q

what are the 3 zones of the adrenal gland? what hormones do they produce and what are they regulated by?

A
  1. zona glomerulosa

makes mineralocorticoids like aldosterone, DOC and is regulated by the RAAS system and K+

  1. zona fasciculata

makes glucocorticoids like cortisol and corticosterone and is regulated by ACTH

  1. zona reticularis

makes androgens like DHEA and androstenedione and is regulated by ACTH

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11
Q

how can you differentiate between primary and secondary adrenal insufficiency based on which hormones are deficiency?

A

with primary adrenal insufficiency, mineralocorticoids, glucocorticoids and androgens are all deficienct because the adrenal gland itself is damaged/not working

with secondary adrenal insufficiency, mineralocorticoids and androgens are deficient but mineralocorticoids are fine because it’s a problem with impaired ACTH secretion from the anterior pituitary; the adrenal gland itself is function –> dont’require mineralocorticoid replacement!

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12
Q

what are the lab differences in primary vs. secondary adrenal insufficiency?

A

PRIMARY
1. cortisol low

  1. ACTH high
  2. renin/aldosterone high/low
  3. ECF volume low
  4. Na+ low (total body sodium depletion)
  5. K+ high
  6. cosyntropin response absent

SECONDARY
1. cortisol low

  1. ACTH low or inappropriately normal
  2. renin/aldosterone normal
  3. ECF volume normal
  4. Na+ low (dilutional)
  5. K+ normal
  6. cosyntropin response normal or blunted
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13
Q

how is the hyponatremia different in primary vs. secondary adrenal insufficiency?

A

mineralocorticoids aren’t around in primary to reabsorb sodium

in secondary they are there but cortisol decreases H2O excretion so it’s a dilutional hyponatremia

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14
Q

why are ACTH and renin levels high in primary adrenal insufficiency?

A

there’s no cortisol to act as negative feedback to ACTH and renin secretion

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15
Q

why is ECF volume low in primary and normal in secondary adrenal insufficiency?

A

in primary there’s no mineralocorticoids to regulate Na absorption so ECF is low but in secondary, mineralocorticoids aren’t effected by ACTH so they’re around and can regulate ECF volume

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16
Q

what is cosyntropin?

A

synthetic ACTH

if you give it in primary insufficiency, there won’t be an elevated cortisol levels

but if you give it in secondary, it will show a normal response and increase cortisol levels – however, this depends on how long they’ve had the insufficiency and how damaged the adrenal gland has become

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17
Q

how do you evaluate pituitary-adrenal function?

A
  1. check baseline cortisol +/- ACTH and maybe DHEA
  2. dynamic studies: insulin tolerance test, cosyntropin stimulation test, glucagon test, metyrapone test, CRH stimulation test
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18
Q

how does cortisol secretion change throughout the day?

A

circadian rhythmia

8 AM peak

12 AM peak

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19
Q

what does a lack of cortisol circadian peak suggest?

A

adrenal insufficiency

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20
Q

how do you assess adrenal insufficiency?

A

assess cortisol level and ACTH at 8 AM

if it’s under 140 mol/L then it’s most likely AI; especially if there’s elevated acth

if cortisol is over 285 then it’s controversial and unlikely that it’s AI

make sure you draw blood for diagnostic purposes before any steroid treatment is given so you have a baseline cortisol and ACTH levels

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21
Q

what is a dynamic test for adrenal function?

A

tests that asses whether the patient can provide a stress-induced rise in cortisol similar to a normal person

  1. insulin tolerance test
  2. cosyntropin stimulation test
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22
Q

what is an insulin tolerance test?

A

put the patient on insulin until the blood glucose drops to under 50 and simultaneously measure the cortisol to test the integrity of the entire HPA axis

normal response is a peak cortisol around 500-520 and you can also test growth hormone too

do NOT give to patients with cerebral disease and cardiac arrhythmias

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23
Q

what is the cosyntropin stimulation test?

A

cosyntropin is synthetic ACTH

check baseline cortisol then give ACTH and check cortisol again, and cortisol levels should rise and it doesn’t have as many side effects as the insulin tolerance test so it’s better and used more in practice

24
Q

what hormone replacement do you give if someone has acute adrenal insufficiency crisis?

A

IV hydrocortison 50-100 mg immediately and every 6-8 hrs

or

continuous infusion of 150-200 mg/d

also make sure to rehydrate with normal saline because they’ll have a lot of salt loss

25
Q

what hormone replacement do you give if someone has chronic adrenal insufficiency?

A

oral hydrocortisone 15-25 mg a day

if they have primary AI then you also have to give fludrocortisone which is a mineralocorticoid; this isn’t needed in secondary AI though

26
Q

19 year old female with hypotension and dehydration at birth. ambiguous genitalia that was surgically corrected. menarche at 9 years old and irregular menstrual cycles. used to be taller than her friends as a child but not her height as an adult is below average. hair growth over her upper lip and chin at about the time of menarche and it has progressed to involve the chest and abdomen

  1. excess of deficiency
  2. which hormones
  3. location
  4. mass
A

hypotension and dehydration is indicative of mineralocorticoid deficiency

ambiguous genitalia and early genitalia and hair growth indicates androgen access

she has congenital adrenal hyperplasia

27
Q

what is congenital adrenal hyperplasia?

A

genetic defect in steroidogenic enzymes that’s AR inheritance

presentation depends on which pathways are blocked

can have increased or decreased virilization and salt loss or retention depending on the blocked pathway

most common is 21-hydroxylase deficiency

28
Q

what is 21-hydroxylase deficiency?

A

without 21-hydroxylase you can’t make mineralocorticoids or glucocorticoids so there’s no aldosterone or cortisol made and it all gets shunted towards androgen production

so this results in increased ACTH and excess androgen

29
Q

what is there’s 11-B-hydroxylase defieicny?

A

lack of cortisol and mineralocorticoid production again which results in increased ACTH and increased androgens

30
Q

what is a 17-alpha-dehydroylase deficiency?

A

glucocortiocoid and androgen production is decreased

without cortisol there’s no negative feedback on ACTH so it’ll be elevated and increased mineralocorticoids resulting in HTN – this suppresses the RAAS system and aldosterone will be suppressed

without androgen, patients will have delayed secondary sex characteristics

31
Q

what is the clinical presentation of 21-alpha-hydroxylase deficiency?

A

you can only make androgens; mineralocorticoid and corticosteroid production is inhibited

if severe infants present with acute adrenal insufiency

females may be virilized with ambiguous genitali and have early “puberty”with accelerated early growth but short stature as adults due to early closure of growth plates

adrenal enlargement

32
Q

what are the two therapeutic goals in congenital adrenal hyperplasia due to 21-alpha-hydroxylase deficiency?

A
  1. replace deficiency hormones

2. reduce excessive androgen levels

33
Q

38 year old with gradual weight gain. a lump on the back of her neck. easy brusibility. hair growth on the upper lips and chin. difficulty climbing stairs

BP 155/90 with round and ruddy face, bilateral supraclavicular fullness

A

excess glucocorticoid

cushing’s syndrome!

34
Q

what is Cushing’s syndrome?

A

excess exposure to cortisol whether exogenous or endogenous

can cause avascular necrosis of humeral head

35
Q

what are the signs and symptoms of Cushing syndrome?

A
  1. typical habits; centripetal obesity
  2. increased body weight
  3. fatiguability and weakness
  4. HTN
  5. hirsutism
  6. amenorrhea
  7. broad violaceous cutaneous striae
  8. personality changes

10 ecchymoses

  1. proximal myopathy
  2. edema
  3. polyuria, polydipsia
  4. hypertrophy of clitoris
36
Q

what are the categories of causes of Cushing syndrome?

A
  1. ACTH-dependent
    ex. pituitary-dependent CS, ectopic ACTH syndrome, ectopic CRH syndrome
  2. ACTH-independent
    ex. adrenal adenoma, adrenal carcinoma, macro nodular adrenal hyperplasia, micro nodular adrenal hyperplasia
  3. exogenous, iatrogenic causes
    ex. prolonged glucocorticoid use
  4. pseudo-Cushing syndrome
    ex. alcoholism, depression, obesity
37
Q

what are the steps to diagnosing Cushing’s syndrome?

A
  1. screening tests
  2. diagnostic tests
  3. establish ACTH dependency
  4. differential diagnostic tests
38
Q

what are the screening tests for Cushing?

A
  1. 24 hr UFC
  2. overnight 1 mg DST
  3. late night salivary cortisol
39
Q

what are the diagnostic tests for Cushing?

A

perform 1 or 2 other studies from the screening tests and if they’re abnormal again they confirm CS

40
Q

how do you differentiate whether Cushing’s is ACTH dependent or independent?

A

after you confirm CS, give ACTH

measure ACTH; if it’s suppressed then it points to adrenal problem

if you measure ACTH and it’s normal then it’s ACTH-dependent disease

41
Q

how do you treat Cushing’s?

A

to reduce pituitary ACTH production do a transphenoidal resection of the adenoma or radiation therapy

if that failure you can do bilateral adrenalectomy or medical therapy – medical therapy isn’t curative but effective as long as chronically administered in selected patients

42
Q

34 year old male with chronic uncontrolled HTN for 6 years despite 3 medications. chronic hypokalemia. renal US shows normal kidneys with no renal artery stenosis. no HTN in family. 2 cm left adrenal mass on CT

A

high BP indicates salt retention so probably mineralocorticoid excess

43
Q

what is primary hyperaldosteronism?

A

adrenal tumor or hyperplasia is leading to increased aldosterone which results in increased Na absorption and K+ excretion

this results in increased EVF volume and increased BP ultimately resulting in renin suppression

renin suppression

44
Q

what are the causes of primary aldosteronism?

A
  1. idiopathic adrenal hyperplasia (60%)
  2. aldosterone producing adenoma (30%)
  3. primary adrenal hyperplasia (2%)
45
Q

what is secondary aldosteronism? how do you differentiate from primary aldosteronism?

A

elevated aldosterone due to volume depletion like from blood loss or diarrhea

increased concentration of aldosterone leads to increased Na but since the volume is decreased renin levels will be increased

so this is how you differentiate between primary and secondary aldosteronism because in secondary, aldosterone is high inherently resulting in increased blood volume and decreased renin

46
Q

how do you screen for primary aldosteronism?

A

morning blood sample for plasma aldosterone concentration and plasma renin activity

47
Q

what are the confirmatory tests for primary aldosteronism?

A
  1. oral sodium loading test
  2. salien infusion test
  3. fludrocortisone suppression test
  4. captopril challenge test
48
Q

what are the subtypes of primary aldosteronism?

A

aka is it unilateral or bilateral aldosterone production

  1. adrenal CT will show large masses like adrenal cortical carcinoma
  2. adrenal venous sampling

if it’s unilateral, you need surgery but if it’s bilateral medical treatment is better so you don’t take out both adrenal glands

HOWEVER, if they are under 35 year old with unilateral adrenal cortical adenoma on CT then dont do adrenal venous sampling and you just go straight to unilateral laparoscopic adrenalectomy

49
Q

what is adrenal venous sampling?

A

check venous blood and give cosyntropin to stimulate aldosterone production

if there is extremely elevated aldosterone production then you do a the adrenalectomy

50
Q

26 year old male with palpitations, s sweating, remotely severe anxiety 4-5 times a week. no triggers. BP during episodes is 160-180/75-110

A

probably due to increased catecholamines

pheochromocytoma!

51
Q

what is pheochromocytoma?

A

tumors of chromatin cells that take up, produce, store, release and metabolize catecholamines

these cells arise from the adrenal medulla or sympathetic ganglia

results in sweating attacks, palpitations, HTN, anxiety, nausea, abdominal pain, weakness, headaches

52
Q

what is the peri-operative management for pheochromocytoma?

A

alpha blocker is st line to control bP

phenoxybenzamine is non-selective and non-competitive so it’s not as good

calcium channel blockers are 2nd line

you can also add a b-blocker to control expected reflex tachycardia from the alpha blocker

increase their salt intake because even though they’re HTN it’s because of the vasoconstriction

53
Q

what is adrenal incidentalomas?

A

tumor in the adrenal gland found on accident

need to assess imaging characteristics and growth to exclude malignancy;

54
Q

A 45 year-old man has blood pressure of 150/100 mmHg on two separate visits. He was diagnosed with hypertension at age 18 years and antihypertensive medications have been gradually added. Currently he is on four antihypertensive medications. His serum sodium is 141 mEq/L [normal 135-145] and potassium is 3.1 mEq/L [normal 3.5-5.3]. His kidney panel is normal. He was recently found to have a 2.2 cm left homogenous adrenal mass on a CT-scan. Which of the following is correct for his condition?

A. Increased urinary free cortisol

B. Increased plasma free metanephrine/normetanephrine

C. Suppressed ACTH

D. Urinary salt wasting

E. Decreased plasma renin activity

A

E. Decreased plasma renin activity

primary aldosteronism

55
Q

A 29-year-old woman comes to the clinic complaining of fatigue. She denies fever, vomiting, or diarrhea, but physical examination shows dry mucous membranes. Her blood pressure is 90/60 mm Hg. Laboratory studies show a plasma sodium level of 129 mEq/L [normal 135-145] and a potassium level of 5.5 mEq/L [normal 3.5-5.3]. Which of the following is the most likely cause of her hyponatremia?

A. Addison disease

B. Diabetes insipidus

C. Hyperaldosteronism

D. Psychogenic polydipsia

E. Syndrome of inappropriate ADH secretion

A

A. Addison disease

56
Q

A 22 year-old woman was noted to have hypertension at age 10 years, for which she was given antihypertensive therapy. Despite three antihypertensive medications, her hypertensionhasn’t beenwell controlled.She never had a menstrual flow. She is 173 cm tall and weighs 73 kg (BMI 24.2 kg/m2), BP 145/90 mmHg, with breastdevelopmenttanner stage 1, no pubic or axillary hair.
Which enzyme is most likely defective in her condition?

A. 21 α-hydroxylase

B. 11 β-hydroxylase

C. 17 α-hydroxylase

D. 3 β-hydroxysteroid dehydrogenase

E. 11 β-hydroxysteroid dehydrogenase

A

C. 17 α-hydroxylase

mineralocorticoid excess and lack of sexual characteristics so sex hormone production is blocked

Endocrine Week 1 (11 decks)

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