Pathology VI

Question 1

What lab test result points to a diagnosis of acromeagly?

Answer 1

Failure to suppress GH following an oral glucose tolerance test (p.301)

Question 2

What imaging finding is often present in a patient with acromeagly?

Answer 2

Pituitary mass seen on brain MRI (p.301)

Question 3

How is acromeagly treated?

Answer 3

Pituitary adenoma resection followed by somatostain analog if surgery is non curative (p.301)

Question 4

What is diabetes insipidus?

Answer 4

Lack of ADH which causes an inability to concentrate urine and resulting in intense thirst and polyuria (p.301)

Question 5

What are the most common causes of central diabetes insipidus?

Answer 5

Pituitary tumor, trauma, surgery, histocytosis X (p.301)

Question 6

What is nephrogenic diabetes insipidus?

Answer 6

Lack of renal response to ADH (p.301)

Question 7

What causes nephrogenic diabetes insipidus?

Answer 7

Heriditary or secondary to hypercalcemia, lithium, demeclocycline (ADH antagonist) (p.301)

Question 8

What two drugs are associated with nephrogenic diabetes insipidus?

Answer 8

Lithium, demeclocycline (ADH antagonist) (p.301)

Question 9

What lab findings are consistent with a diagnosis of diabetes insipidus?

Answer 9

Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L (p.301)

Question 10

What test is used to diagnose diabetes insipidus?

Answer 10

Water deprivation test- urine osmolality doesn’t increase (p.301)

Question 11

What test response is used to distinguish central diabetes insipidus from nephrogenic diabetes insipidus?

Answer 11

Response to desmopressin (no response in nephrogenic DI) (p.301)

Question 12

What is the treatment for central Diabetes Insipidus?

Answer 12

Adequate fluid intake; intranasal desmopressin (ADH analogue) (p.301)

Question 13

What is the treatment for nephrogenic Diabetes Insipidus?

Answer 13

Adequate fluid intake; hydrochlorothiazide, indomethacin, or amiloride (p.301)

Question 14

What is desmopressin?

Answer 14

An ADH analogue (p.301)

Question 15

What are the clinical features of SIADH?

Answer 15

Excessive water retention, hyponatremia with continued urinary Na+ excretion, urine osmolarity > serum osmolarity (p.301)

Question 16

How does the body respond to states of SIADH?

Answer 16

By decreasing aldosterone (causing hyponatremia) to maintain near normal volume status (p.301)

Question 17

What is one severe clinical consequence of low serum sodium levels?

Answer 17

Seizures (p.301)

Question 18

Why must very low levels of sodium be corrected very slowly?

Answer 18

To decrease risk of central pontine myelinosis (p.301)

Question 19

What are four common causes of SIADH?

Answer 19

Ectopic ADH production (e.g. small cell lung cancer), CNS disorders/ head trauma, pulmonary disease, drugs (e.g. cyclophosphamide) (p.301)

Question 20

How is SIADH treated?

Answer 20

Fluid restriction, IV saline, conivaptan, tolvaptan, demeclocycline (p.301)

Question 21

What are the most common causes of hypopituitarism?

Answer 21

Nonsecreting pituitary adenoma, craniopharyngioma, Sheehan’s syndrome, Empty sella syndrome, brain injury/ hemorrhage, radiation (p.301)

Question 22

What is hypopituitarism?

Answer 22

Undersecretion of pituitary hormones (p.301)

Question 23

What is Sheehan’s syndrome?

Answer 23

Ischemic infarct of pituitary following postpartum bleeding (p.301)

Question 24

How does Sheehan’s syndrome usually present?

Answer 24

With failure to lactate (p.301)

Question 25

What is empty sella syndrome?

Answer 25

Atrophy or compression of pituitary (p.301)

Question 26

What causes empty sella syndrome?

Answer 26

Often idiopathic; common in obese women (p.301)