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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
A patient w/ CHF or cirrhosis develops hypertension. Labs show increased renin level. Explain
Secondary hyperaldosteronism -- hypovolemia-induced increased renin
26
A chronic diabetic has hypertension. Renal biopsy shows nephrosclerosis. Labs show increased renin level. Explain
Secondary hyperaldosteronism -- decreased renal perfusion causes increased renin
27
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?
Adrenocortical adenoma - aldosterone-secreting Spironolactone bodies Conn syndrome
28
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?
Hypokalemia Weakness, paresthesias, visual disturbances, occasional tetany
29
Confirmatory test for hyperaldosteronism
Aldosterone suppression test
30
Adrenal androgen formation is regulated by what? What androgens are released from the adrenal cortex? What happens to these androgens?
ACTH DHEA and androstenedione Converted to testosterone in peripheral tissues
31
A baby girl presents with body hair, deeper voice and muscle bulk. ACTH level is high. Her adrenals are both enlarged. Most likely?
Congenital adrenal hyperplasia -- deficiency in cortisol-producing enzyme, causing steroid precursor excess that leads to increased androgens
32
Most common mutation in congenital adrenal hyperplasia What can this lead to? (bad)
21-hydroxylase deficiency -- SALT-WASTING SYNDROME Lack of aldosterone --> hyponatremia, hyperkalemia, acidosis, hypotension, shock
33
A baby is born w/ ambiguous genitalia. Over time, it develops body hair and deeper cry. It's BP and labs are normal.
21-hydroxylase deficiency -- SIMPLE VIRILIZING SYNDROME w/o salt wasting
34
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.
PARTIAL 21-hydroxylase deficiency --Nonclassic/late-onset virilism
35
Which 21-hydroxylase deficiency syndrome, of the 3, is the most common?
Nonclassic/late onset -partial deficiency
36
Bilateral adrenal enlargement, thickened nodular cortex w/ brown color, lack of lipid on biopsy
Congenital adrenal hyperplasia
37
How does a male child present w/ CAH?
Enlarged external genitalia, increased pubic and facial hair, etc.
38
How does an adult male present w/ CAH?
Oligospermia/infertility
39
How can severe salt-wasting 21-hydroxylase deficiency affect vascular tone?
Low glucocorticoids = low epinephrine production = adrenomedullary dysplasia and hypotension/circulatory collapse
40
Treatment of CAH What about salt-wasting?
Exogenous glucocorticoids --> replace glucocorticoids and suppress ACTH Exogenous mineralocorticoids
41
3 settings of acute adrenocortical insufficiency
- 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
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?
Waterhouse-Friderichsen syndrome Bilateral adrenal hemorrhage (from DIC)
43
Weakness, easily fatigued, N/V/D, weight loss, neural symptoms when standing, skin hyperpigmentation in sun-exposed areas and creases
Primary Addison disease (adrenocortical insufficiency)
44
Progressive destruction of the adrenal cortex (from whatever cause), leading to adrenocortical insufficiency
Primary Addison disease
45
Caucasian woman presents w/ weakness, fatigue, weight loss, and skin hyperpigmentation. Most likely diagnosis? What to look for on labs?
Autoimmune adrenalitis Autoantibodies against 21-hydroxylase or 17-hydroxylase
46
Caucasian woman presents w/ weakness, fatigue, weight loss, and skin hyperpigmentation. 2 potential clinical settings?
Autoimmune polyendocrine syndrome 1 or 2 (APS1, APS2)
47
APS1 - clinical findings
Chronic candidiasis in mouth, skin/teeth/nail deficits, autoimmune disorders
48
APS1 - what are the autoimmune disorders possible? (4)
Adrenalitis, Hypoparathyroidism, Hypogonadism, Pernicious anemia
49
APS1 - genetics Causes what?
AIRE gene (chromosome 21) Breakdown in T-cell self-tolerance in thymus
50
APS1 - why chronic candidiasis?
Autoantibodies against IL-17 and IL-22 are common, which are normally used to fight fungal infections
51
APS2 - findings
Adrenal insufficiency + (thyroiditis or type 1 DM)
52
Addison's disease - infectious causes
TB, fungi
53
Addison's disease - malignant cause
Metastatic carcinoma (lung, breast mostly)
54
Addison's disease, irregularly-shrunken glands, cortex has scattered residual cortical cells w/in collapsed network of connective tissue and lymphoid infiltrate
Primary autoimmune adrenalitis
55
Addison's disease, adrenal glands show inflammation w/ clusters of multinucleated giant cells and various other immune cells
TB/fungal disease
56
A patient has chronic fatigue, weakness, and hyperpigmentation. She presents to the ER w/ vomiting, abdominal pain, hypotension, hyponatremia, hyperkalemia Causes?
Adrenal crisis Infection, trauma, surgery
57
Symptoms not seen in secondary adrenocortical insufficiency compared to primary
``` No hyperpigmentation (no ACTH excess) No hyponatremia or hyperkalemia (aldosterone not affected) ```
58
Diagnosing secondary adrenocortical insufficiency
Give exogenous ACTH, see prompt rise in cortisol level
59
2 syndromes w/ increased risk of adrenocortical carcinoma
Li-Fraumeni syndrome - TP53 mutation | Beckwith-Wiedemann syndrome - IGF-2 overactivity
60
Adenoma or carcinoma: - Hyperaldosteronism - Cushing syndrome - Virilizing neoplasm
Adenoma Adenoma Carcinoma
61
Adrenocortical carcinoma - most common mets
Regional and periaortic LNs, lungs, viscera
62
Adrenocortical carcinoma - often invades what?
Adrenal vein, vena cava, lymphatics
63
Undifferentiated carcinoma in the adrenal cortex...what must be distinguished?
Primary carcinoma vs. distant metastasis of other cancer
64
Mass in adrenal gland composed of fat and hematopoietic stem cells (CD34+)
Adrenal myelolipoma
65
A patient has abdominal imaging after a car accident. The doc finds a mass in the adrenal gland. No adrenal symptoms are present.
Adrenal incidentaloma (4% of population)
66
Cells of the adrenal medulla
``` Chromaffin cells (neuroendocrine) Supporting sustentacular cells ```
67
Most important neoplasms of the adrenal medulla
Pheochromocytoma Neuroblastoma Neuroblastic tumors
68
Episodic palpitations, increases in BP, headache, sweating, tremor, sense of apprehension (impending doom)
Pheochromocytoma
69
Rule of 10s
Pheochromocytoma - 10% are extra-renal (paragangliomas) - 10% are bilateral (especially familial) - 10% are malignant (especially paraganglioma and familial) - 10% don't have hypertension
70
5 familial syndrome's w/ pheochromocytoma
MEN2A, MEN2B, NF1, VHL, Familial paraganglioma (1,3,4)
71
Pheo, medullary thyroid carcinoma, hyperparathyroidism
MEN-2A
72
Pheo, medullary thyroid carcinoma, marfanoid, mucocutaneous ganglioneuromas
MEN-2B
73
Pheo, cafe-au-lait spots, optic nerve glioma
NF1
74
Pheo, renal cell carcinoma, hemangioblastoma, pancreatic endocrine neoplasm
VHL
75
SDH mutation
Familial paraganglioma
76
Diagnosis of pheo
Urinary excretion of catecholamines, metanephrines, vanillylmandelic acid

Endocrine 2 (12 decks)

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