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ENRP Exam II > Adrenal Pathology (Hillard) > Flashcards

Adrenal Pathology (Hillard) Flashcards

1
Q

the 3 layers of the adrenal cortex

A

Zona glomerulosa = mineralcorticoids (aldosterone)
Zona fasciculata = glucocorticoids (cortisol)
Zona reticulata = androgens

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2
Q

the 3 components of the adrenal gland

A

capsule, adrenal cortex, adrenal medulla

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3
Q

Clinical features of Cushing’s syndrome

A

hypertension, truncal obesity, fat on neck and upper back “buffalo hump”, round fcae ‘moon facies”, thin fragile skin, stretch marks (striae) and secondary diabetes

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4
Q

Pathophysiology of secondary diabetes in Cushing’s syndrome

A

increased cortisol production cortisol is potent driver of gluconeogenesis; increased glucose from energy stores creating secondary hyperglycemia leading to secondary diabetes.

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5
Q

What is the most common cause of Cushing’s syndrome?

A

exogenous or iatrogenic; too much cortisol or cortisol-like substances being absorbed, ingested or injected

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6
Q

What is the most common cause of ectopic Cushing’s?

A

Paraneoplastic production by small cell carcinoma of the lung

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7
Q

What are the three forms of endogenous Cushing

A
  1. Cushing Disease (ACTH dependent pituitary adenoma)
  2. Ectopic Cushing (paraneoplastic dependent ACTH)
  3. Adrenal Gland Cushing (independent ACTH adrenal tumor)
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8
Q

What is the most common cause of ACTH independent endogenous hypercortisolism?

A

Adrenal cortical adenoma; well demarcated yellow cut surface

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9
Q

Carney complex

A

genetic disease resulting in adrenal hyperplasia; mut PRKAR1A; will have pigmented skin lesions and myxomatous tumors

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10
Q

Reason why chronic corticosteroid use needs to be tapered slowly

A

adrenals become shrunken and atrophic when there is chronic corticosteroid use (due to decreased demand of body to make corticosteroids), when stopped body is not able to produce sufficient cortisol to keep up with body’s demand

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11
Q

Screening test for Cushing’s syndrome

A

low dose dexamethasone suppression test
24 hour urinary free cortisol
late night salivary cortisol

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12
Q

a high dose dexamethasone suppression test distinguishes between what?

A
  1. Pituitary Cushing syndrome - cortisol production will be suppressed
  2. Ectopic Cushing syndrome - cortisol production will NOT be suppressed (out of HP axis)
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13
Q

What are the two types of hyperaldosteronism

A

Primary - adrenal produces too much aldosterone; renin is low
Secondary - extra-adrenal cause (renal stenosis/CHF); renin is high

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14
Q

Primary hyperaldosteronism is caused by abnormalities in what?

A

the zona glomerulosa

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15
Q

What is the most common cause of primary hyperaldosteronism?

A

idiopathic hyperaldosteronism - bilateral nodular hyperplasia of the zona glomerulosa

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16
Q

Clinical presentation of Primary hyperaldosteronism?

A

hypertension (excessive reabsorption of water and sodium) and HYPOkalemia

17
Q

What screening test should you do if you suspect Primary hyperaldosteronism?

A

increased aldosterone to renin ratio

18
Q

What is a histological hallmark of an adrenal adenoma causing Conn syndrome?

A

Spironolactone bodies

19
Q

What are some causes of secondary hyperaldosteronism?

A

localized decreased renal artery perfusion (renal artery stenosis) or global vascular hypovolemia (heart failure)

20
Q

Clinical manifestation of congenital adrenal hyperplasia of 21 hydroxylase deficiency?

A

adrenal hyperplasia
decreased cortisol
decreased aldosterone
virilization

21
Q

Virilization in XX infants with congenital adrenal hyperplasia of 21 hydroxylase deficiency?

A

clitorial enlargement and labial fusion

22
Q

Virilization in XY infants with congenital adrenal hyperplasia of 21 hydroxylase deficiency?

A

marked enlargement of penis; not appropriate for age

23
Q

What is the confirmatory test for congenital adrenal hyperplasia of 21 hydroxylase deficiency?

A

elevated serum 17-hydroxyprogesterone

24
Q

What are the three forms of congenital adrenal hyperplasia of 21 hydroxylase deficiency?

A
  1. Classic form - neonatal form w/ salt wasting
  2. Simple virilizing - neonatal w/o salt wasting
  3. Non-classic form - late onset
25
Q

What is the classic form of congenital adrenal hyperplasia of 21 hydroxylase deficiency?

A

neonatal form with salt wasting;
-virilization
-hyponatremia, HYPERkalemia
-HYPOtension with cardiovascular collapse

26
Q

What are the 3 main causes of acute primary adrenocortical insufficiency

A
  1. chronic steroid use (atrophy with rapid withdrawal) = adrenal withdrawal syndrome
  2. massive adrenal hemorrhage
  3. Waterhouse-Friderichsen syndrome (Neisseria meningitidis infection)
27
Q

Waterhouse-Friderichsen syndrome

A

fulminant meningococcemia caused by an Neisseria meningitidis infection; bilateral adrenal hemorrhaging resulting in blood vessels rupture

28
Q

Clinical features of Addison’s Disease

A

chronic fatigue, HYPOtension, hyperpigmentation of the skin (decreased cortisol, increased ACTH, POMC, MSH, melanocytes)

29
Q

What are the 4 common causes of Addison’s disease?

A
  1. autoimmune adrenalitis (90%)
  2. infections (tuberculosis)
  3. Metastatic neoplasms
  4. Congenital (CAH and adrenoleukodystrophy)
30
Q

Autoimmune adrenalitis

A

most common cause of Addison’s disease; APS-1 mutation - predisposes to fungal infections; APS-2 mutations causes adrenal insufficiency and autoimmune thyroiditis

31
Q

Adrenoleukodystrophy

A

congenital adrenal insufficiency caused by an accumulation of very long fatty acts that accumulate in the brain, nervous system and adrenal glands; rare x-linked; learning disability, seizures and deafness

32
Q

Adrenocortical carcinoma

A

LARGE >20cm; necrosis and hemorrhaging on histo; metastases or local invasion confirms malignancy; very poor prognosis (2 yrs)

33
Q

Incidentalomas

A

incidental adrenal mass of >1 cm; typical nonfunctioning and asymptomatic; often followed by repeat imaging

34
Q

Adrenal myelolipoma

A

benign lesion of mature fat; will show trilineage of hematopoietic elements (RBCs, WBCs and platelets) similar to bone marrow

35
Q

Pheochromocytoma

A

tumor of adrenal medulla; secretes catecholamines; increased sympathetics; test urinary or plasma metanephrines (breakdown of catecholamines)

36
Q

Confirmatory test for pheochromocytoma?

A

test urinary or plasma metanephrines (breakdown of catecholamines)

37
Q

Cells with a nesting (Zellballen) appearance

A

Pheochromocytoma; tumor of adrenal medulla; secretes catecholamines

38
Q

Rule of 10’s for pheochromocytoma?

A

10% are extra-adrenal
10% of sporadic tumors are bilateral
10% are malignant
10% do NOT show hypertension

25% show familial mutations

ENRP Exam II (10 decks)

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