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Fiser absite > 21 Adrenal > Flashcards

21 Adrenal Flashcards

1
Q

Blood supply to adrenal gland

A 
Superior adrenal (inferior phrenic artery)
Middle adrenal (aorta)
Inferior adrenal (renal artery)
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2
Q

Superior adrenal artery

A

Inferior phrenic artery

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3
Q

Middle adrenal artery

A

Aorta

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4
Q

Inferior adrenal artery

A

Renal artery

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5
Q

Left adrenal vein goes to:

A

Left renal vein

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6
Q

Right adrenal vein goes to:

A

Inferior vena cava

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7
Q

Adrenal cortex innervation?

A

Nothing

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8
Q

Medulla innervation?

A

Sympathetic nervous system

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9
Q

Adrenal lymphatics

A

Subdiaphragmatic and renal lymph nodes

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10
Q

Incidentaloma

A

Seen in 1-2% of abdominal CT

5% are mets

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11
Q

Work up for incidentaloma

A

Check for functioning tumor: urine metanephrines, VMA< catecholamines, hydroxycorticosteroids, serum K with plasma renin/aldosterone
CXR
Colonoscopy
Mamography

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12
Q

Ominous characteristics for an incidentaloma

A 
Non-homogenous
>4-6cm
Functioning 
Enlarging
--> surgery
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13
Q

Common mets to adrenals

A

Lung CA
Breast CA
Melanoma
Renal CA

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14
Q

Cancer history with asymptomatic adrenal mass?

A

Biopsy

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15
Q

Adrenal cortex

A

From mesoderm
Glomerulosa - aldosterone
Fasciuclata - glucocorticoids
Reticularis - androgens/estrogens

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16
Q

Production of adrenal cortex hormones

A

Cholesterol -> progesterone -> androgens/cortisol/aldosteronew
All zones have 21- and 11-beta hydroxylase

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17
Q

Cortisol

A 
Inotropic
Chronotorpic
Increases vascular resistance
Proteolysis and gluconeogensis
Decrease inflammation
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18
Q

Aldosterone

A

Stimulates renal sodium resoprtion and secretion of K+ and H+
Stimulated by angiotensin II an dhyperkalemia

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19
Q

Excess estrogen and androgen by adrenals?

A

Almost always cancer

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20
Q

21-hydroxylase deficiency

A

Precocious puberty in males, virilization in females
Salt wasting and hypotension
Tx: cortisol, genitoplasty

Excess 17-OH progesterone

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21
Q

11-hydroxylase deficiency

A

Precocious puberty in males, virilization in females
Salt saving - HTN
Tx: cortisol, genitoplasty

Excess deoxycortisone (acts as mineralcorticoid)

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22
Q

Hypertension without edema, hypokalemia, weakness, polydipsia, polyuria

A

Hyperaldosteronism (Conn’s syndrome)

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23
Q

Primary hyperaldosteronism

A

Low renin

Adenoma (85%), hyperplasia (15%), ovarian tumor (rare), cancer (rare)

24
Q

Secondary hyperaldosteronism

A

Renin is high - more common than primary
CHF, renal artery stenosis, liver failure, diuretics
Batter’s syndrome (renin-secreting tumor)

25
Q

Diagnosis for primary hyperaldosteronism

A

Salt-load suppression test (urine aldosterone will stay high)
Aldosterone:renin ration >20
Labs: decreased K+, increased Na, increased urine K, metabolic alkalosis
Plasma renin activity will be low

26
Q

Localizing studies for hyperaldosteronism

A

MRI
NP-59 scintigraphy (hyperfunctional adrenal tissue - differentiates adenoma from hyperplasia - 90% accurate)
Adrenal venous sampling

27
Q

What do you need to fix preoperative for hyperaldosteronism?

A

Hypertension

Hypokalemia

28
Q

Treatment for hyperaldosteronism secondary to an adenoma?

A

Adrenalectomy

29
Q

Treatment for hyperaldosteronism secondary to hyperplasia

A

Medical therapy - spironolactone, CCB, potassium supplementation
Bilateral resection only done for refractory hypokalemia (increased morbidity) - need fludrocortisone postop

30
Q

Hypocortisolism

A

Adrenal insufficiency, Addison’s disease
MCC - withdrawal of exogenous steroids
MCC primary disease - autoimmune destruction
Other - pituitary disease, infection/hemorrhage/metastasis/resection
Low cortisol, high ACTH, low adosterone
Dx: Cosyntropin test (give ACTH, measure urine cortisol - positive if it stays low)

31
Q

Acute adrenal insufficiency

A

Hypotension, fever, lethargy, abdominal pain, nausea, vomiting
Decreased glucose, increased potassium
Tx: Dexamethasone, fluids
Confirmation: cosyntropin test (dexamethasone does not interfere)

32
Q

Chronic adrenal insufficiency

A

Hyperpigmentation, weakness, weight loss, GI symptoms
Increased potassium, decreased sodium
Tx: Corticosteroids

33
Q

Hypercortisolism

A

Cushing’s syndrome
MCC - iatrogenic
- Measure 24-hr urine cortisol and ACTH
If high cortisol, with low ACTH - cortisol secreting lesion (done)
If high cortisol, with high ACTH - ACTH secreting lesion;
Then do High-dose dexamethasone suppression test:
- Urine cortisol suppressed - pituitary adenoma
- Not suppressed - ectopic producer of ACTH

34
Q

In hypercortisolism - how do you localize tumors and differentiate adrenal adenomas from hyperplasia?

A

NP-59 scintography

35
Q

Pituitary adenoma

A 
Cushing's disease
Cortisol is NON-suppressable
Microadenoma
Localization - petrosal sampling, MRI
Tx: transsphenoiodal, XRT
36
Q

Ectopic ACTH

A

MCC small cell lung CA
Cortisol is NON-suppressable
Localization - chest and abdominal CT
Tx: Resection

37
Q

Adrenal adenoma (cushing’s syndrome)

A

Decreased ACTH - unregulated steroid production

Tx: Adrenalectomy

38
Q

Adrenal hyperplasia (cushing’s syndrome)

A

Medical tx:
- Metyrapone (blocks cortisol synthesis)
- Aminoglutethimide (inhibits steroid production)
Bilateral adrenalectomy is medical treatment fails

39
Q

Adrenocortical carcinoma

A

Before 5yo, after 50yo, more common in females
50% functioning - cortisol, aldosterone, sex steroids
Viralization, androgeny
Sx: abdominal pain, weight loss, weakness
Tx: Radical adrenalectomy, debulking
- Mitatane (adrenal-lytic) - residual, recurrent, metastatic

40
Q

Catecholamine production

A

Tyrosine > dopa > dopamine > NE > Epi

41
Q

Rate limiting step for catecholamine production?

A

Tyrosine hydroxylase

42
Q

Origin of adrenal medulla?

A

Ectoderm - neural crest cells

43
Q

Why can Epi only be produced in adrenal medulla?

A

PNMT (phenylethanolamine N-methyltransferase)
Converts NE to EPi
Only found in adrenal medulla

44
Q

What breaks down catecholamines?

A

Monoamine oxidase (MAO)
NE > normetanephrine
EPI > metanephrine
Then turned into vanillylmandelic acid (VMA)

45
Q

Extra-adrenal rests of neural crest tissue locations?

A

Retroperitoneum

Organ of Zuckerkandl at the aortic bifurcation

46
Q

Pheochromocytoma - 10% rule

A

Malignant, bilateral, in children, familial, extra-adrenal

47
Q

Pheochromocytoma - associated syndromes

A 
MEN IIa
MEN IIb
ZVon Recklinghausen's disease
Tuberous sclerosis
Struge-Weber disease
48
Q

Pheochromocytoma - symptoms

A

HTN (episodic)
Headache
Diaphoresis
Palpitations

49
Q

Pheochromocytoma - Diagnosis

A

Urine metanephrines and VMA*
MIBG scan (NE analogue) (localization)
Clonidine suppression test (tumor does NOT respond)
DO NOT DO venography - can cause HTN crisis

50
Q

Pheochromocytoma - preoperative treatment

A

Volume replacement
A-blocker first (phenoxybenzamine)
then B-blocker (if needed for tachcyardia or arrhythmias)

51
Q

What happens if you don’t alpha blockade before giving a pheo b-blocker?

A

Unoppsed alpha stimulation –> HTN crisis, stroke, heart failure

52
Q

Pheochromocytoma - treatment?

A

Adrenalectomy - ligate adrenal veins first to avoid spilling catecholamines during tumor manipulation
Metyrosine - inhibits tyrosine hydroxylase\
Have ready - Nipride, Neo-=synephrine, antiarrhythmic agents (just in case)

53
Q

Post-op conditions associated with Pheochromocytoma?

A 
Persistent HTN
Hypotension
Hyperglecmia
Bronchospasm
Arrhythmias
Intracerebral hemorrhage
CHF
MI
54
Q

Other sites of pheo?

A

Organ of zuckerland (most common - inferior aorta near bifurcation)
Vertebral bodies
Opposite adrenal gland
Bladder

55
Q

What can cause falsely elevated VMA?

A 
Coffee
Tea
Fruits
Vanilla
Iodine contrast
Labetalol
A- and b-blockers
56
Q

Ganglioneuroma

A

Rare
Benign
Asymptomatic tumor of neural crest origin in adrenal medulla or sympathetic chain
Tx: Resection

Fiser absite (58 decks)

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