Pathology VI Flashcards Preview

Endocrinology > Pathology VI > Flashcards

Flashcards in Pathology VI Deck (26):
1

What lab test result points to a diagnosis of acromeagly?

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

2

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

Pituitary mass seen on brain MRI (p.301)

3

How is acromeagly treated?

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

4

What is diabetes insipidus?

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

5

What are the most common causes of central diabetes insipidus?

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

6

What is nephrogenic diabetes insipidus?

Lack of renal response to ADH (p.301)

7

What causes nephrogenic diabetes insipidus?

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

8

What two drugs are associated with nephrogenic diabetes insipidus?

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

9

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

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

10

What test is used to diagnose diabetes insipidus?

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

11

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

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

12

What is the treatment for central Diabetes Insipidus?

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

13

What is the treatment for nephrogenic Diabetes Insipidus?

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

14

What is desmopressin?

An ADH analogue (p.301)

15

What are the clinical features of SIADH?

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

16

How does the body respond to states of SIADH?

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

17

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

Seizures (p.301)

18

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

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

19

What are four common causes of SIADH?

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

20

How is SIADH treated?

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

21

What are the most common causes of hypopituitarism?

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

22

What is hypopituitarism?

Undersecretion of pituitary hormones (p.301)

23

What is Sheehan's syndrome?

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

24

How does Sheehan's syndrome usually present?

With failure to lactate (p.301)

25

What is empty sella syndrome?

Atrophy or compression of pituitary (p.301)

26

What causes empty sella syndrome?

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