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Endocrine 2 > Robbins - Adrenals > Flashcards

Robbins - Adrenals Flashcards

1
Q

Most cases of elevated cortisol are ______
Most cases of endogenous elevated cortisol are _____ and are of the _______ size
If not an adenoma, then other (rare) cause?

A

Exogenous OD
ACTH-producing pituitary adenomas; Microadenoma
Corticotroph hyperplasia (1º or 2º via hypothalamic CRH tumor)

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2
Q

Most cases of ectopic ACTH production are from _____

Neuroendocrine neoplasms can produce excess _____ instead

A

Small cell lung carcinoma

CRH

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3
Q

Increased cortisol, decreased ACTH – options?

A

Adrenal adenoma or adrenal carcinoma

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4
Q

Hypercortisolism - see what in the pituitary?

A

Crooke hyaline change (corticotroph cells become homogenous and pale)

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5
Q

Hypercortisolism + adrenal cortical atrophy

A

Exogenous glucocorticoid production

–> ACTH suppression –> ZF and ZR suppression

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6
Q

How to tell if a primary adrenocortical neoplasm is functional?

A

Functional = atrophy of rest of gland and other gland

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7
Q

Yellow, vacuolated lipid-rich cells in the adrenal cortex

A

Zona fasciculata cells – cortisol

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8
Q

Small, eosinophilic, lipid-poor cells in the adrenal cortex

A

Zona reticularis cells – androgens

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9
Q

Small, yellow mass in adrenal gland surrounded by capsule, full of vacuolated lipid-rich cells

A

Adrenal adenoma

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10
Q

Large (5-10x larger) mass in adrenal gland, no capsule

A

Adrenal carcinoma

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11
Q

Early symptoms of hypercortisolism (Cushings)

A

HTN, weight gain

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12
Q

Later, classic symptoms of hypercortisolism (Cushings)

A

Truncal obesity, moon facies, buffalo hump

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13
Q

Hypercortisolism – glucose

Results?

A

Induces gluconeogenesis, inhibits glucose uptake into cells (secondary diabetes)

Hyperglycemia, glycosuria, polydipsia

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14
Q

Hypercortisolism – catabolic effects?

Symptoms? (6)

A

Myofiber atrophy, loss of collagen, resorption of bone

Weakness, thin skin, easy bruising, cutaneous striae, osteoporosis

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15
Q

Hypercortisolism – immunity

A

Immune suppression –> increased infections, poor wound healing

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16
Q

Diagnosing Cushings (2)

A

Increased 24hr free cortisol

Loss of diurnal cortisol secretion pattern

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17
Q

Determining the cause of Cushings

A

Serum ACTH

Dexamethasone suppression test

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18
Q

Dexamethasone suppression test - results (3)

Results of dexamethasone suppression test are measured via what?

A

High ACTH/cortisol, no suppression w/ high = ECTOPIC
High ACTH, suppression w/ high dose = PITUITARY
Low ACTH, no suppression w low or high dose = ADRENAL

Measured via urinary 17-hydroxysteroid excretion (metabolic inactivation product of corticosteroids)

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19
Q

Hypercortisolism, hirsutism, mental disturbances, menstrual abnormalities

A

Other symptoms of hypercortisolism

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20
Q

Hypertension, low plasma renin, adrenal mass

A

Primary hyperaldosteronism

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21
Q

3 causes of primary hyperaldosteronism

A
  • Bilateral idiopathic hyperaldosteronism (most common)
  • Glucocorticoid-remediable hyperaldosteronism
  • Adrenocortical neoplasm
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22
Q

Older patient, minor hypertension, bilateral nodules in adrenal glands, normal ZG cells

Potential genetics?

A

Bilateral idiopathic hyperaldosteronism

KCNJ5

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23
Q

Chromosome 8 rearrangement, positive dexamethasone suppression of hyperaldosteronism

Explain

A

Glucocorticoid-remediable hyperaldosteronism

Genetic rearrangement, so aldosterone synthase is controlled by ACTH

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24
Q

A pregnant woman starts having hypertension. Labs show increased renin level. Explain

A

Secondary hyperaldosteronism – estrogen-induced increased renin

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25
Q

A patient w/ CHF or cirrhosis develops hypertension. Labs show increased renin level. Explain

A

Secondary hyperaldosteronism – hypovolemia-induced increased renin

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26
Q

A chronic diabetic has hypertension. Renal biopsy shows nephrosclerosis. Labs show increased renin level. Explain

A

Secondary hyperaldosteronism – decreased renal perfusion causes increased renin

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27
Q

Patient presents with hypertension. Small, solitary, bright yellow, well-circumscribed mass in the adrenal gland. The doc prescribes an aldosterone antagonist. After not working, biopsy shows cells w/ eosinophilic laminated cytoplasmic inclusions.

What are these in the cells (morphology)?

What is this disease called?

A

Adrenocortical adenoma - aldosterone-secreting

Spironolactone bodies

Conn syndrome

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28
Q

A patient has chronic hypertension from an adrenocortical adenoma that produces aldosterone. What will be seen on basic labs of this patient, if not controlled?

Symptoms associated w/ this?

A

Hypokalemia

Weakness, paresthesias, visual disturbances, occasional tetany

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29
Q

Confirmatory test for hyperaldosteronism

A

Aldosterone suppression test

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30
Q

Adrenal androgen formation is regulated by what?
What androgens are released from the adrenal cortex?
What happens to these androgens?

A

ACTH
DHEA and androstenedione
Converted to testosterone in peripheral tissues

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31
Q

A baby girl presents with body hair, deeper voice and muscle bulk. ACTH level is high. Her adrenals are both enlarged. Most likely?

A

Congenital adrenal hyperplasia – deficiency in cortisol-producing enzyme, causing steroid precursor excess that leads to increased androgens

32
Q

Most common mutation in congenital adrenal hyperplasia

What can this lead to? (bad)

A

21-hydroxylase deficiency – SALT-WASTING SYNDROME

Lack of aldosterone –> hyponatremia, hyperkalemia, acidosis, hypotension, shock

33
Q

A baby is born w/ ambiguous genitalia. Over time, it develops body hair and deeper cry. It’s BP and labs are normal.

A

21-hydroxylase deficiency – SIMPLE VIRILIZING SYNDROME w/o salt wasting

34
Q

An 18 y/o girl presents with increased facial hair, bad acne, and irregularities with her menstrual cycle. Labs show a decreased aldosterone level. She is otherwise normal.

A

PARTIAL 21-hydroxylase deficiency –Nonclassic/late-onset virilism

35
Q

Which 21-hydroxylase deficiency syndrome, of the 3, is the most common?

A

Nonclassic/late onset -partial deficiency

36
Q

Bilateral adrenal enlargement, thickened nodular cortex w/ brown color, lack of lipid on biopsy

A

Congenital adrenal hyperplasia

37
Q

How does a male child present w/ CAH?

A

Enlarged external genitalia, increased pubic and facial hair, etc.

38
Q

How does an adult male present w/ CAH?

A

Oligospermia/infertility

39
Q

How can severe salt-wasting 21-hydroxylase deficiency affect vascular tone?

A

Low glucocorticoids = low epinephrine production = adrenomedullary dysplasia and hypotension/circulatory collapse

40
Q

Treatment of CAH

What about salt-wasting?

A

Exogenous glucocorticoids –> replace glucocorticoids and suppress ACTH

Exogenous mineralocorticoids

41
Q

3 settings of acute adrenocortical insufficiency

A
  • Stress crisis of someone w/ chronic insufficiency
  • Withdrawal or stress of someone on exogenous steroids
  • Adrenal hemorrhage (DIC, W-F syndrome, labor complication, etc.)
42
Q

A child presents with a high fever, headache, and stiff neck. She rapidly progresses to hypotension and shock. Her skin starts turning purple. Dx?

What to be aware of?

A

Waterhouse-Friderichsen syndrome

Bilateral adrenal hemorrhage (from DIC)

43
Q

Weakness, easily fatigued, N/V/D, weight loss, neural symptoms when standing, skin hyperpigmentation in sun-exposed areas and creases

A

Primary Addison disease (adrenocortical insufficiency)

44
Q

Progressive destruction of the adrenal cortex (from whatever cause), leading to adrenocortical insufficiency

A

Primary Addison disease

45
Q

Caucasian woman presents w/ weakness, fatigue, weight loss, and skin hyperpigmentation. Most likely diagnosis?

What to look for on labs?

A

Autoimmune adrenalitis

Autoantibodies against 21-hydroxylase or 17-hydroxylase

46
Q

Caucasian woman presents w/ weakness, fatigue, weight loss, and skin hyperpigmentation. 2 potential clinical settings?

A

Autoimmune polyendocrine syndrome 1 or 2 (APS1, APS2)

47
Q

APS1 - clinical findings

A

Chronic candidiasis in mouth, skin/teeth/nail deficits, autoimmune disorders

48
Q

APS1 - what are the autoimmune disorders possible? (4)

A

Adrenalitis, Hypoparathyroidism, Hypogonadism, Pernicious anemia

49
Q

APS1 - genetics

Causes what?

A

AIRE gene (chromosome 21)

Breakdown in T-cell self-tolerance in thymus

50
Q

APS1 - why chronic candidiasis?

A

Autoantibodies against IL-17 and IL-22 are common, which are normally used to fight fungal infections

51
Q

APS2 - findings

A

Adrenal insufficiency + (thyroiditis or type 1 DM)

52
Q

Addison’s disease - infectious causes

A

TB, fungi

53
Q

Addison’s disease - malignant cause

A

Metastatic carcinoma (lung, breast mostly)

54
Q

Addison’s disease, irregularly-shrunken glands, cortex has scattered residual cortical cells w/in collapsed network of connective tissue and lymphoid infiltrate

A

Primary autoimmune adrenalitis

55
Q

Addison’s disease, adrenal glands show inflammation w/ clusters of multinucleated giant cells and various other immune cells

A

TB/fungal disease

56
Q

A patient has chronic fatigue, weakness, and hyperpigmentation. She presents to the ER w/ vomiting, abdominal pain, hypotension, hyponatremia, hyperkalemia

Causes?

A

Adrenal crisis

Infection, trauma, surgery

57
Q

Symptoms not seen in secondary adrenocortical insufficiency compared to primary

A 
No hyperpigmentation (no ACTH excess)
No hyponatremia or hyperkalemia (aldosterone not affected)
58
Q

Diagnosing secondary adrenocortical insufficiency

A

Give exogenous ACTH, see prompt rise in cortisol level

59
Q

2 syndromes w/ increased risk of adrenocortical carcinoma

A

Li-Fraumeni syndrome - TP53 mutation

Beckwith-Wiedemann syndrome - IGF-2 overactivity

60
Q

Adenoma or carcinoma:

  • Hyperaldosteronism
  • Cushing syndrome
  • Virilizing neoplasm
A

Adenoma
Adenoma
Carcinoma

61
Q

Adrenocortical carcinoma - most common mets

A

Regional and periaortic LNs, lungs, viscera

62
Q

Adrenocortical carcinoma - often invades what?

A

Adrenal vein, vena cava, lymphatics

63
Q

Undifferentiated carcinoma in the adrenal cortex…what must be distinguished?

A

Primary carcinoma vs. distant metastasis of other cancer

64
Q

Mass in adrenal gland composed of fat and hematopoietic stem cells (CD34+)

A

Adrenal myelolipoma

65
Q

A patient has abdominal imaging after a car accident. The doc finds a mass in the adrenal gland. No adrenal symptoms are present.

A

Adrenal incidentaloma (4% of population)

66
Q

Cells of the adrenal medulla

A 
Chromaffin cells (neuroendocrine)
Supporting sustentacular cells
67
Q

Most important neoplasms of the adrenal medulla

A

Pheochromocytoma
Neuroblastoma
Neuroblastic tumors

68
Q

Episodic palpitations, increases in BP, headache, sweating, tremor, sense of apprehension (impending doom)

A

Pheochromocytoma

69
Q

Rule of 10s

A

Pheochromocytoma

  • 10% are extra-renal (paragangliomas)
  • 10% are bilateral (especially familial)
  • 10% are malignant (especially paraganglioma and familial)
  • 10% don’t have hypertension
70
Q

5 familial syndrome’s w/ pheochromocytoma

A

MEN2A, MEN2B, NF1, VHL, Familial paraganglioma (1,3,4)

71
Q

Pheo, medullary thyroid carcinoma, hyperparathyroidism

A

MEN-2A

72
Q

Pheo, medullary thyroid carcinoma, marfanoid, mucocutaneous ganglioneuromas

A

MEN-2B

73
Q

Pheo, cafe-au-lait spots, optic nerve glioma

A

NF1

74
Q

Pheo, renal cell carcinoma, hemangioblastoma, pancreatic endocrine neoplasm

A

VHL

75
Q

SDH mutation

A

Familial paraganglioma

76
Q

Diagnosis of pheo

A

Urinary excretion of catecholamines, metanephrines, vanillylmandelic acid

Endocrine 2 (12 decks)

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