ENDOCRINE

Question 1

endocrine problems often result in abnormalities of what?

Answer 1

serum osmolality

Question 2

what is normal osmolality of body fluids?

Answer 2

275-295 mOsm/kg
<275 = hypo-osmolar
>295 = hyperosmolar

Question 3

what variables affect serum osmo?

Answer 3

serum sodium, BUN, and glucose; an increase in any of these will INCREASE serum osmolality

Question 4

what does the hypothalamus (via pituitary gland) regulate?

Answer 4

• temperature
• intake drives
• autonomic NS (sympathetic/parasympathetic)

Question 5

what part of the kidney does ADH affect to reabsorb water?

Answer 5

distal convoluted and collecting tubule

Question 6

where is ADH formed and stored?

Answer 6

hypothalamus; posterior pituitary

Question 7

what happens in SIADH?

Answer 7

too much ADH –> H2O retention –> decreased serum Na –> decreased UO –> decreased osmolality

Question 8

what are some causes of SIADH?

Answer 8

most common: oat cell carcinoma, viral PNA, head problems

increased osmolality, anesthesia, stress, thiazide diuretics (esp. elderly)

Question 9

how is SIADH treated?

Answer 9

• treat cause
• fluid restriction
• 3%
• phenytoin (Dilantin) –> inhibits ADH secretion
• NO hypotonics or free water

Question 10

what happens in DI?

Answer 10

not enough ADH –> water loss –> increased serum Na, high UO (6-24L/day), increased serum osmolality

DILUTE urine (specific gravity 1.001-1.005)

Question 11

what causes DI?

Answer 11

• head surgery, tauma

- phenytoin

Question 12

what are some complications of DI?

Answer 12

hypovolemia, hypovolemic shock

Question 13

how is DI treated?

Answer 13

• ADH (pitressin, DDAVP), use cautiously in those with heart disease, may cause coronary artery ischemia
• fluids to replenish intravascular volume
• monitor UO/specific gravity

Question 14

what causes DKA?

Answer 14

• younger population
• type I diabetes
• new onset type I
• infection
• stress
• noncompliance

Question 15

what are some S/S of DKA?

Answer 15

• glucose >250
• develops rapidly over 1-2days
• no insulin production
• fluid loss 4-6L
• acidosis
• serum ketones
• normal/high serum osmolality
• Kussmaul respirations
• elevated K (although decreases as acidosis is corrected)

Question 16

how is DKA treated?

Answer 16

• insulin, fluids
• NS, 0.45 NS (if Na high and BP normal/high)
• decrease BS by 50-100/hr
• add dextrose to IV fluids after serum glucose reaches ~250mg/dL
• continue insulin infusion until acidosis is resolved

Question 17

what causes hyperosmolar hyperglycemic state (HHS)?

Answer 17

• older
• type II diabetes
• pancreatitis
• TPN
• steroid use

Question 18

what are some S/S of HHS?

Answer 18

• BS >600
• develops slowly 5-7 days (still making insulin, but inadequate)
• fluid loss 6-9L
• no acidosis
• small serum ketones
• serum osmolality >320 mOsm/kg
• rapid, shallow respirations
• K elevated due to insulin deficiency

Question 19

how is HHS treated?

Answer 19

• fluids, insulin
• NS
• decrease BS by 5-100mg/dL/hr
• add dextrose to IVF after serum glucose reaches ~300mg/dL

Question 20

in metabolic acidosis, where do hydrogen ions and potassium move into?

Answer 20

• H+ ions move into intracellular space

- K leaves intracellular space and moves into extracellular space

Question 21

what type of medications may mask early signs of hypoglycemia (for Type I diabetics)?

Answer 21

beta blockers; pt’s first sign’s of hypoglycemia will be later signs)

Question 22

what are some S/S of hypoglycemia?

Answer 22

• early (due to sympathetic effects of adrenaline release in an attempt to raise glucose): tachycardia, palpitations, diaphoresis, irritability, restlessness
• late (due to lack of glucose in brain): confusion, lethargy, slurred speech, sz, coma

Question 23

what is the treatment for hypoglycemia?

Answer 23

• complex carbs PO
• D50 if NPO
• D10 infusion for refractory hypoglycemia
• glucagon 1mg –> decreases GI motility, monitor for n/v