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Flashcards in MTB Endo Deck (36):
1

Panhypopituitarism is caused by

any condition that compresses or damages the pituitary gland

Tumors

Conditions such as hemochromatosis, sarcoidosis, and histiocytosis X or infec- tion with fungi, TB, and parasites infiltrate the pituitary, destroying its func- tion.

2

Panhypopituitarism presentation

prolactin: failure to lactate, galactorrhea, amenorrhea, gynacomastia, erectile dysfunction

FSH/LH: ammenorrhoea/erectile dysfunction, reduced libido,

GH: short stature and dwarfism, • Centralobesity
• IncreasedLDLandcholesterollevels • Reduced lean muscle mass

3

Kallman Syndrome

• Decreased FSH and LH f r o m decreased GnRH • Anosmia
• Renal agenesis in 50%

4

Panhypopituitarism Diagnostic Tests

TSH, LH/FSH, ACTH, (Prolactin and GH [pulsatile])
• Hyponatremia is common secondary to hypothyroidism. Potassium levels remain normal because aldosterone is not affected and aldosterone excretes potassium.

5

panhypopituitarism Treatment

Replace deficient hormones with:
• Cortisone
• Thyroxine
• Testosterone and estrogen
• Recombinant human growth hormone

Replace cortisone before starting thyroxine.

6

Diabetes insipidus (DI) is a decrease in either

the amount of ADH from the pituitary (central DI) or its effect on the kidney (nephrogenic DI).

7

xxx is a classic cause of NDI.

Lithium

8

The difference between central and nephrogenic DI is determined by the response to

vasopressin. In central DI, urine volume will decrease and urine osmolality will increase. With nephrogenic DI, there is no effect ofvasopressin use on urine volume or osmolality.

9

Acromegaly is almost always caused by a pituitary .

adenoma

10

Acromegaly. The best initial test is a level of

insulinlike growth factor (IGF-1).

11

Acromegaly responds to

transphenoidal resection ofthe pituitary in 70% of cases.

12

Acromegaly Medications:

• Cabergoline: Dopamine will inhibit GH release.
• Octreotide or lanreotide: Somatostatin inhibits GH release.
• Pegvisomant: A GH receptor antagonist, it inhibits IGF release from
the liver.

13

Hypothyroidism leads to hyperprolac- tinemia because

extremely high TRH levels will stimulate prolactin secretion.

14

Occasionally patients have hypothyroidism from:

• Dietary deficiency of iodine • Amiodarone

15

Hypothyroidism

Bradycardia
Constipation
Weight gain
Fatigue, lethargy, coma
Decreased reflexes
Cold intolerance
Hypothermia
(hair loss, edema)

16

Hyperthyroidism

Tachycardia, palpitations, arrhythmia (atrial fibrillation)
Diarrhea (hyperdefecation) Weight loss
Anxiety, nervousness, restlessness Hyperreflexia
Heat intolerance Fever

17

Thyroid Nodules

These are incredibly common, and are palpable in as much as 5% of women and 1% of men. Ninety-five percent are benign (adenoma, colloid nodule, cyst). Thyroid nodules are rarely associated with clinically apparent hyperfunction- ing or hypofunctioning.

18

When a patient has a nodule:

1. Perform thyroid function tests (TSH and T4).
2. If tests are normal, biopsy the gland.

19

The most common cause of hypercalcemia is

primary hyperparathyroidism (PTH).

20

Primary hyperparathyroidism and cancer account for xxx% of hypercalcemia patients.

90

21

Hypercalcemia presentation

Acute, symptomatic hypercalcemia presents with confusion, stupor, lethargy, and constipation.
Cardiovascular
• Short QT syndrome and hypertension
Bone lesions
• Osteoporosis
Renal
• Nephrolithiasis
• Diabetes insipidus • Renal insufficiency

22

Treatment
Acute hypercalcemia is treated with:

1. Saline hydration at high volume
2. Bisphosphonates:pamidronate,zoledronicacid

23

Calcitonin

inhibits osteoclasts. The onset of action of calcitonin is very rapid, and it wears off rapidly. Bisphosphonates take several days to work.

24

Hypocalcemia causes

surgery hypoparathyroidism
hypomagnesemia
renal failure The kidney converts 25 hydroxy-D to the more active 1,25 hydroxy-D.

25

Low calcium =
High calcium =

twitchy and hyperexcitable
lethargic and slow

26

Signs of neural hyperexcitability in hypocalcemia:

• Chvostek sign (facial nerve hyperexcitability)
• Carpopedal spasm
• Perioral numbness
• Mentalirritability
• Seizu res
• Tetany(Trousseausign)

27

Primary hyperaldosteronism is

the autonomous overproduction of aldoste- rone despite a high pressure with a low renin activity. Eighty percent are from solitary adenoma. Most of the rest is from bilateral hyperplasia. It is rarely malignant.

28

primary hyperaldosteronism =

High BP + hypokalemia

29

Pheochromocytoma is

a nonmalignant lesion of the adrenal medulla autonomously overproducing catecholamines despite a high blood pressure.

30

Pheochromocytoma is the answer when there is:

o Hypertension that is episodic in nature
o Headache
o Sweating
o Palpitations and tremor

31

Pheochromocytoma treatment

Treatment
Phenoxybenzamine is an alpha blocker that is the best initial therapy of pheochromocytoma. Calcium channel blocker and beta blockers are used afterwards.
Pheochromocytoma is removed surgically or by laparoscopy.

32

Dopamine agonists:

Cabergoline is better tolerated than bromocriptine.

33

Cushingsyndromecanbeusedinterchangeablywiththe term

hypercortisolism. Cushing disease is a term used for the pituitary overproduction of ACTH.

34

The 1 mg overnight dexamethasone suppression test should normally suppress the morning cortisol level. If this suppression occurs,

hypercortisolism can be excluded.

35

High ACTH? High dexamethasone

• suppresses: pituitary
• does not suppress: ectopic + cancer

36

Metformln is contrainidicated in those with

renal dysfunction because it can accumulate and cause metabolic acidosis.
Metformin works by blocking gluconeogenesis.