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Clin Med3: Endocrine > D/o of the adrenal cortex - McGowan > Flashcards

D/o of the adrenal cortex - McGowan Flashcards

1
Q

what hormones does the adrenal gland secrete

A

mineralocorticoids
glucocorticoids
androgens
catecholamines
peptides

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2
Q

what are the mineralocorticoids and where are they made

A

aldosterone and corticosterone
found within the Zona Glomerulosa in the adrenal gland

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3
Q

what are the glucocorticoids and where are they made

A

cortisol and cortisone
zona fasciculata in adrenal gland

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4
Q

what are the androgens and where are they made

A

estrogen and testosterone
zona reticularis in adrenal gland

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5
Q

what are the catecholamines and where are they made

A

epinephrine and norepinephrine
medulla of the adrenal gland

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6
Q

what are the peptides and where are they made

A

Somatostatin and Substance P
medulla of adrenal gland

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7
Q

what is the make up of the adrenal gland

A

cortex and medulla

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8
Q

what is the function/purpose of glucocorticoids and mineralocorticoids

A

physiologic stress response (long term)
blood pressure regulation and electrolyte homeostasis
aldosterone and cortisol

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9
Q

what is aldosterone responsible for

A

controls sodium/potassium/water balance
regulation of Blood volume
BP regulation (RAA system)

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10
Q

what is Cortisol responsible for

A

glucose production
BP regulation
anti-inflammatory

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11
Q

what are adrenal androgen precursors

A

DHEA (hehydroepiandrosterone)
converted to sex steroids in gonads or target tissues (estrogen and testosterone)

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12
Q

what are the actions of androgen hormones

A

male and female reproductive development
secondary sex characteristics
menstruation
muscle strenth/mass

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13
Q

what are the catecholamines responsible for

A

fight or flight response
regulates HR
regulates contractility
vasodilation/constriction
BP regulation
bronchodilation
glycogenesis

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14
Q

what are the 4 S’s of adrenal hromones

A

Aldosterone = Salt
Cortisol = sugar
Androgen = Sex
Epi, Norepi = Stress

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15
Q

what are hyperfunctioning adrenal disorders

A

Cushings syndrome
Pheochromocytoma
Multiple endocrine neoplasia
Adrenal adenoma
Adrenal Cancer

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16
Q

what are hypofunctioning adrenal disorders

A

Addisons disease
Adrenal deficiency

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17
Q

what can cause hypofunction

A

primarily due to glandular destruction: autoimmune, infection, surgery, inflammation, infarction, hemorrhage or tumor

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18
Q

what can cause hyperfunction

A

neoplasms (functional), autoimmune disorders, exogenous administration

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19
Q

What is Cushing Syndrome

A

secondary to glucocorticoid excess, F>M (4:1)
increased ACTH production (dependent vs independent)
pituitary adenomas
cortisol unchecked
excess blood glucose production
increase lipolysis
increase catabolism
decreased insulin production and increased glucagon

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20
Q

what is the presentation of Cushing syndrome

A

central obesity
rounded face (moon facies)
enlarged fat pad between shoulders (buffalo hump) abdominal striae (purple* stretch marks)

weight gain, Hirsutism, facial plethora (swelling/erythema)

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21
Q

what is the workup for Cushing syndrome

A

elevated 24 hour urine free cortisol
elevated midnight plasma cortisol
dexamethasone suppression test
Plasma ACTH
Localizing the source - ACTH dependent - MRI/CT; ACTH independent - CT of adrenals

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22
Q

what can impact 24 hour urine free cortisol tests

A

anti-epileptics, estrogen, testosterone and exogenous steroids

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23
Q

what is the overnight dexamatheasone suppression test

A

baseline plasma cortisol (high dose only)
give 1mg or 8mg dexamethasone at 11pm
check plasma cortisol at 8-9am

24
Q

what is the difference between ACTH dependent and ACTH independent

A

Dependent: problem upstream/outside of adrenals - pituitary
Independent: problem is in the adrenal gland

25
Q

What is the treatment of Cushing syndrome

A

piruitary source (dependent): trans-sphenoidal resection of mass
Ectopic ACTH-secreting tumors: local surgical resection
benign adrenal adenoma: laparoscopic resection
adrenal carcinomas: surgical resection

26
Q

what is required for longterm treatment of cushing syndrome

A

long-term glucocorticoid replacement
younger = more likely to fully recover

27
Q

what are negative prognostic indicators for Cushings

A

older age at diagnosis
higher pre-op ACTH
longer disease presence

28
Q

what is a sympathetic nervous system tumor arising from the adrenal medulla

A

pheochromocytoma
avg. age at dx is 40 yo
cause of death in 1/3 of pts prior to dx

29
Q

what is secreted from pheochromocytomas

A

catechomaines (epi and norepi)

30
Q

what are the rule of 10 for pheo

A

~10% bilateral
~10% exra-adrenal
~10% malignant

31
Q

what is the presentation for variable presentation

A

‘the great masquerader’- variable presentation
HA, Profuse sweating, palpitation and tachycardia, HTN (sustained or paroxysmal), Anxiety/panic attacks

32
Q

What is the classic triad of PHEo

A

Palpitations
Headache
Episodic sweating

diagnosis likely if all three + HTN

33
Q

what can pheo result in

A

catastrophic HTN crisis, fatal arrhythmias, pulmonary edema or HF
may see ARDS and mutisystem failure

34
Q

what is the workup for Pheo

A

plasma fractionated free metanephrines (most sensitive)
other lab tests: elevated plasma catecholamines, 24 hour urine catecholamines, serum chromogranin A (CgA), clonidine suppression test
Non-contrast abdominal CT
MRI with or without Gadolinium contrast

35
Q

what are the treatment options for pheo

A

tx of choice: surgical resection
must medically optimize HTN and tachycarrhythmias preop
caution: tx resistant hypotesion post-op => AKI, MI

36
Q

what is the treatment for malignant pheo

A

add chemo
recheck BP and plasma free metanephinres
follow up for serum chromogranin
a (CgA)

37
Q

what is multiple endocrine neoplasia (MEN)

A

inherited tumor syndromes
- autosomal dominant (genetic testing)
tumor in 2+ endocrine glands
4 distinct types

38
Q

what is the presentation of MEN1

A

90% have mutation in Menin gene
abnormalities can be deltected around 14-18 years old
clinical symptoms appear in 20s-30s
mean life expectancy: 55 years
classic triad: parathyroids, pancreatic islets, anterior pituitary

39
Q

What is the presentation of MEN2 (2A) and Men 3 (2B)

A

ret protooncogene mutation
difference is clinical presentation
Classic triad: meduallary thyroid carcinoma (MTC), pheochromocytomas, parathyroid tumors

40
Q

what gene is mutated in MEN4

A

CDKN1B

41
Q

what is the presentation of MEN2

A

classic triad: Medullary thyroid carcinoma (MTC), pheochromocytomas, parathryoid tumors

42
Q

What is the presentation of MEN3

A

characterized by mucosal neuromas
marfan like habitus
medullary thyroid carcinomas

43
Q

what is the presentaiton of MEN4

A

most rare of MEN subsets
often pituitary, parathyroid and pancreatic tumors

44
Q

how do you work up MEN

A

genetic testing
screen patients with known FH
screen for neuroendocrine tumors with targeted tests/imaging

45
Q

what is the treatment of MEN1

A

parathyroidectomy if symptomatic
prophylactic thymectomy if getting parathyroidectomy
high does PPIs and control of hyeprcalcemia if gastrinomas

46
Q

what is the treatment for MEN 2 and MEN3

A

if known FH and + genetic screening
total thyroidectomy : by age 6 for MEN2, by 6 months for Men 6
no GLP-1 inhibitors for DM
screening for pheo and thyroid cancer

47
Q

what can cause adrenal insufficiency

A

primary of secondary causes
primary - adrenal gland dysfunction (cortisol and aldosterone)
secondary - ACTH deficiency due to hypothalamus or pituitary dysfunction

48
Q

What is a primary adrenal disease

A

Addison’s Disease (Adrenal Deficiency)
primarily autoimmune in origin

49
Q

what is the classic presentation of adrenal insufficiency

A

fatigue, reduced stamina, weakness, anorexia and weight loss

50
Q

what are the later presenting facors for adrenal insufficiency

A

N/V, abdominal pain +/- diarrhea
pain: arthralgia, myalgias, CP, abdominal pain, back/leg pain, HA
Psych: irritability, depression, anxiety
hyperpigmentation

51
Q

what is acute adrenal crisis

A

more common with primary insufficiency
life threatening
N/V/Fever, dehydration, profound hypotension
progression to shock, unresponsive to fluids or vasopressors

52
Q

what is the workup for adrenal insufficiency

A

plasma cortisol
low serum DHEA levels
confirmation with cosynotropin stimulation test (synthetic ACTH)

53
Q

what is the treatment for adrenal insufficiency

A

glucocortioid replacement therapy (15-30mg hydrocortisone daily in 2-3 doses)
mineralocorticoid replacement therapy (fludrocortisone acetate)
+/- DHEA supplementation for women

54
Q

what is the treatment of adrenal crises

A

loading dose of hydrocortisone 100-300mg IV
rehydration with saline solution (generous resuscitation, plus dextrose)
then, hydrocortisone 50-100mg q6h IV, titrate down to PO as able
broad spectrum ABX if infection ruled out as cause

55
Q

how do you prevent adrenal criese

A

patient education of times of increased risk
give extra doses and plenty of refills
stress dose steroids
dose adjustment for hot weather, vigorous exercise
anti-emetics PRN to prevent N/V
consider other routes of administration if unable to take PO due to N/V

Clin Med3: Endocrine (7 decks)

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