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Surgery > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

What are pheochromocytomas, by definition?

A

Chromaffin cell tumors that can arise anywhere along the sympathetic chain, most commonly in the medullary adrenal gland.

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2
Q

What are extra-adrenal pheochromocytomas associated with?

A

Malignant, versus benign disease.

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3
Q

What are bilateral pheochromocytomas associated with?

A

Familial inheritance

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4
Q

What familial diseases are associated with pheochromocytoma?

A

MEN IIA, MEN IIB, Von Hippel-Lindau disease, Neurofibromatosis I.

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5
Q

What are the most common tumors associated with VHL disease?

A

CNS and retinal hemangioblastomas, clear cell renal carcinoma, pheochromocytoma, pancreatic neuroendocrine tumors, pancreatic cysts, endolymphatic sac tumors, epididymal papillary cystadenomas

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6
Q

What are the common presenting symptoms of pheochromocytoma?

A

HTN (sustained, paroxysmal, or systained with acute elevations), anxiety, palpitations, pallor, diaphoresis

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7
Q

What is the rule of 10s for pheochromocytoma?

A

10% malignant
10% familial
10% extra-adrenal
10% bilateral

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8
Q

What are the diagnostic tests of choice for pheochromocytoma?

A
  1. 24 hour urinary collection for catecholamines, VMA, metanephrine
  2. Clonidine test: will suppress plasma catecholamines in normal patients but not in pheo
  3. CT, MRI, or nuclear scan
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9
Q

What is the preoperative treatment for pheochromocytomas, and in what specific order?

A

Alpha-adrenergic blockade, plus beta-blockers for persistent tachycardia. Alpha blockade must precede bela blockade because beta blockers have negative inotropic and chronotropic effects and would lead to unopposed vasoconstriction if given alone.

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10
Q

What perioperative monitoring is required when excising a pheochromocytoma?

A

Arterial blood pressure monitoring, as manipulation of the tumor can cause extreme changes in BP

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11
Q

What is the treatment for malignant pheochromocytosis?

A
  1. Resect recurrences and metastases when they occur
  2. Treat with catecholamine blockage
  3. Use XRT for bony mets
  4. Chemotherapy has 60% response rate
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12
Q

What is the prognosis for malignant pheochromocytoma?

A

5-year survival is 36-60%

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13
Q

What spinal cord segment is at the level of the adrenal glands?

A

T11

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14
Q

What is the size of the normal adrenal?

A

3-6 g each. 5-2.5 cm

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15
Q

What supplies the arterial vascular supply to the adrenals?

A

Branches of the aorta, inferior phrenic, and renal arteries

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16
Q

What supplies the venous drainage to the kidneys?

A

Central vein or inferior vena cava, or left adrenal vein.

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17
Q

What is the percentage breakdown of renal cell carcinoma analtomicaaly?

A
  1. 75% are fasciculata tumors growing steroids and cortisl.

Glomerulosa (15% aldoserone synthesis), 10% chance of cholesterol stones as a find result of the excise.

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18
Q

Describe the anatomy of the adrenal glands.

A

Bilateral retroperitoneal organs that rest anterior and medial to the superior pole of each kidney. Typically lie at the level of T11. They are 3-6 grams each and typically measure 5x2.5 cm in a normal, nonpregnant adult. They are supplied by branches of the aorta, inferior phrenic, and renal arteries. The right adrenal drains to the central vein or IVC. The left adrenal drains to the left renal vein.

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19
Q

Describe the hisology and function of the various parts of the adrenal gland.

A

The cortex is divided into three layers: the glomerulosa comprises 15% of the cortical mass and is responsible for the production of aldosterone. The fasciculata comprises 75% of the cortical mass; it’s cells rest in a linear configuration perpendicular to the gland surface, and they are responsible for production of steroids and cortisol. The reticularis comprises 10% of the cortical mass, and is responsible for cholesterol storage and cortisol, androgen, and estrogen secretion. The medulla is comprised of polyhedral cells organized in cords that are responsible for catecholamine synthesis.

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20
Q

Describe hyperplasia of the adrenal gland.

A

Widening of the zona reticularis with an increased number of cells that hyperfunction. Typically weighs between 6-12 g, but if caused by ectopic ACTH production can weigh between 12-30 grams.

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21
Q

What are the typical types of adrenal adenomas?

A

Typically consist of cortical cells that cause either hypercortisolism and/or hyperaldosteronism. Rarely cause androgen related symptoms. They are not typically >5cm, and weigh <100 grams. Histologically that comprise of homogenous cell populations, tumor necrosis, and low mitotic activity.

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22
Q

Describe the epidemiology of adrenal cortical carcinomas.

A

Affect women more than men, peak incidence is bimodal at either <5 years-old or 30-40 years-old.

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23
Q

What are the signs and symptoms of adrenal cortical carcinomas?

A

Vague abdominal complains secondary to mass effect, and symptoms of hormonal excess as most tumors are functional.

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24
Q

Describe the pathology of adrenal cortical carcinomas.

A

> 6cm, weigh 100-5,000 grams, necrotic and hemorrhagic, desmoplasia and mitoses seen with vascular invasion, large hyperchromatic nuclei with enlarged nucleoli.

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25
Q

What percent of adrenal cortical carcinomas secrete cortosol?

A

50%

26
Q

What are the diagnostic modalities for adrenal cortical carcinoma?

A
  1. 24 hour urine collection for cortisol, aldosterone, catecholamines, metanephrine, vanillymandelic acid, 17-OH corticosteroids, and 17-ketosteroids
  2. CT or MRI
  3. CXR to rule out pulmonary metastasis
27
Q

What is the treatment for adrenal cortical carcinoma?

A
  1. Radial en bloc resection, or debulking if total resection is not possible.
  2. XRT for palliation of bone metastasis
  3. No role for chemotherapy
  4. Post-operative monitoring of steroid levels
  5. Resection of recurrent disease
28
Q

What are the typically areas of recurrence of adrenal cortical adenomas?

A

Lungs, lymph nodes, liver, peritoneum, and bone

29
Q

What is the prognosis of adrenal cortical carcinoma?

A

70% present as stage III or IV disease. 5-year survival is 40% if patient undergoes complete resection. If local invasion medial survival is 2.3 years.

30
Q

What are prognostic features of adrenal cortical carcinomas that predict recurrence or metastatic disease?

A

High mitotic activity, high DNA ploidy, excessive prodcution of androgens or 11-deoxysteroids.

31
Q

Define Cushing syndrome.

A

Excessive cortisol production

32
Q

What are the common causes of Cushing syndrome?

A
  1. Iatrogenic administration of corticosteroids
  2. Pituitary tumors that secrete ACTH
  3. Adrenal tumors that secrete cortisol
  4. Ectopic ACTH secretion by tumor elsewhere
33
Q

What are the typical signs and symptoms of Cushing Syndrome?

A

Appearance - weight gain, truncal obesity, extremity wasting, buffalo hump, moon facies, striae, hirsutism
Physiology - mild glucose intolerance, amenorrhea, decreased libido, depression, impaired memory, muscle weakness.

34
Q

What is the most common cause of ectopic ACTH production?

A

Small cell lung cancer.

35
Q

What are the diagnostic modalities for assessment of Cushing syndrome?

A
  1. Confirm the presence of hypercortisolism first with a low dose dexamethasone suppression test.
  2. Check 24-hour urinary cortisol level.
  3. If low dose test fails to suppress, perform high dose suppression test.
  4. Image adrenals with CT (95% sensitive, but not specific); image pituitary with MRI
  5. Petrosal sinus sampling if pituitary pathology suspected.
36
Q

What laboratory and imaging patterns are typical of adrenal causes of Cushing syndrome?

A

Tumor or hyperplasia seen on CT or MRI, low plasma ACTH, no suppresion with high-dose dexamethasone.

37
Q

What are the laboratory and image findings of pituitary causes of Cushing syndrome?

A

CT abdomen showing bilateral adrenal hyperplasia, mild elevation of ACTH, suppression of cortisol with high-dose dexamethasone, +petrosal sinus sampling.

38
Q

What are the laboratory and image findings typical of ectopic ACTH production causing Cushing syndrome?

A

CT abdomen showing bilateral adrenal hyperplasia, increased plasma ACTH, no suppression of cortisol with high-dose dexamethasone, negative petrosal sinus sampling.

39
Q

Describe the low-dose dexamethasone suppression test.

A

Single dose of steroid (2mg) at 11 PM, followed by measurement of serum and urinary cortisol levels at 8 AM. Normal is <5 ug/dL serum cortisol, and decreased urinary 17-ketosteroids.

40
Q

Describe the high dose dexamethasone suppression test.

A

8 mg of steroid given at 11 PM with serum and urinary cortisol sampling in the morning. Decreases urinary cortisol to <50% if pituitary dependent, but no decrease if cause is either primary adrenal or ectopic ACTH production.

41
Q

What is the difference between Cushing syndrome and Cushing disease?

A

Cushing syndrome is descriptive of all causes of hypercortisolism. Cushing Disease is more specific for pituitary causes of Cushing Syndrome (i.e. ACTH producing pituitary adenoma)

42
Q

What is the treatment for Cushing Disease?

A

Transsphenoidal resection of pituitary adenoma

43
Q

What is the treatment for Cushing syndrome caused by an adrenal adenoma?

A

Laparoscopic adrenalectomy

44
Q

What is the treatment for Cushing syndrome caused by adrenal carcinoma?

A

Open adrenalectomy.

45
Q

What is the treatment for Cushing syndrome caused by ectopic ACTH production?

A

Resection of the primary lesion.

46
Q

What is the treatment for Cushing syndrome caused by unresectable tumors?

A

Lesions and recurrence should be debulked for palliation.

47
Q

What is the medical treatment for Cushing Syndrome?

A

Suppression of cortisol production with metyrapone, aminoglutethimide, and mitotane

48
Q

What is the mechanism of action of metyrapone?

A

blocks cortisol synthesis by inhibiting 11-beta-hydroxylase.

49
Q

What is the mechanism of action of aminoglutethimide?

A

Two MOA:

  1. Blocks aromatase
  2. Blocks conversion of cholesterol to pregnenolone by inhibiting the enzyme P450scc thus decreasing the levels of all hormonal steroids.
50
Q

What is the mechanism of action of mitotane?

A
  1. Alters peripheral steroid metabolism
  2. suppresses adrenal cortex
  3. Alters cortisone metabolism
51
Q

What are the various findings when checking urinary 17-ketosteroids?

A

60 mg/day is indicative of adrenal cortical hyperplasia.

52
Q

What is a positive petrosal sinus sampling test?

A

Sinus/plasma ACTH ratio >3 after CRH administration.

53
Q

What is the difference between primary and secondary Addison’s Disease?

A

Primary: due to destruction of the adrenal cortex with sparing of the medulla
Secondary: Failure due to hypothalamic or pituitary abnormalities.

54
Q

What is the most common cause of secondary adrenal insufficiency?

A

Iatrogenic, caused by long-term glucocorticoid therapy

55
Q

What are the most common etiologies of primary Addison’s disease?

A
  1. Autoimmune adrenalitis
  2. Tuberculosis
  3. Fungal infection
  4. AIDS
  5. Metastatic cancer
  6. Familial glucocorticoid deficiency
  7. Post-adrenalectomy
  8. Bilateral adrenal hemorrhage
56
Q

What are the most common etiologies of secondary Addison’s disease?

A
  1. Craniopharyngioma
  2. Pituitary surgery or irradiation
  3. Empty sella syndrome
  4. Exogenous steroids
57
Q

What are the sign’s and symptoms of adrenal insufficiency (Addison’s)?

A

Nausea, vomiting, weight loss, weakness, fatigue, lethargy, hyperpigmentation

58
Q

What diagnostic findings are typical in patients with Addison’s disease?

A

Hyponatremia, hyperkalemia, failed ACTH stimulation test (cortisol rise 30 minutes after administration of ACTH), Baseline ACTH

59
Q

What is the treatment for Addison’s disease?

A
  1. Glucocorticoid therapy for primary and secondary cases.

Additional mineralocorticoid therapy for primary case

60
Q

What is the treatment for Addisonian Crisis?

A
  1. Volume resuscitation

2. Glucocorticoids IV

Surgery (9 decks)

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