endocrine problems often result in abnormalities of what?
serum osmolality
what is normal osmolality of body fluids?
275-295 mOsm/kg
<275 = hypo-osmolar
>295 = hyperosmolar
what variables affect serum osmo?
serum sodium, BUN, and glucose; an increase in any of these will INCREASE serum osmolality
what does the hypothalamus (via pituitary gland) regulate?
- temperature
- intake drives
- autonomic NS (sympathetic/parasympathetic)
what part of the kidney does ADH affect to reabsorb water?
distal convoluted and collecting tubule
where is ADH formed and stored?
hypothalamus; posterior pituitary
what happens in SIADH?
too much ADH –> H2O retention –> decreased serum Na –> decreased UO –> decreased osmolality
what are some causes of SIADH?
most common: oat cell carcinoma, viral PNA, head problems
increased osmolality, anesthesia, stress, thiazide diuretics (esp. elderly)
how is SIADH treated?
- treat cause
- fluid restriction
- 3%
- phenytoin (Dilantin) –> inhibits ADH secretion
- NO hypotonics or free water
what happens in DI?
not enough ADH –> water loss –> increased serum Na, high UO (6-24L/day), increased serum osmolality
DILUTE urine (specific gravity 1.001-1.005)
what causes DI?
- head surgery, tauma
- phenytoin
what are some complications of DI?
hypovolemia, hypovolemic shock
how is DI treated?
- ADH (pitressin, DDAVP), use cautiously in those with heart disease, may cause coronary artery ischemia
- fluids to replenish intravascular volume
- monitor UO/specific gravity
what causes DKA?
- younger population
- type I diabetes
- new onset type I
- infection
- stress
- noncompliance
what are some S/S of DKA?
- 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)
how is DKA treated?
- 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
what causes hyperosmolar hyperglycemic state (HHS)?
- older
- type II diabetes
- pancreatitis
- TPN
- steroid use
what are some S/S of HHS?
- 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
how is HHS treated?
- fluids, insulin
- NS
- decrease BS by 5-100mg/dL/hr
- add dextrose to IVF after serum glucose reaches ~300mg/dL
in metabolic acidosis, where do hydrogen ions and potassium move into?
- H+ ions move into intracellular space
- K leaves intracellular space and moves into extracellular space
what type of medications may mask early signs of hypoglycemia (for Type I diabetics)?
beta blockers; pt’s first sign’s of hypoglycemia will be later signs)
what are some S/S of hypoglycemia?
- 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
what is the treatment for hypoglycemia?
- complex carbs PO
- D50 if NPO
- D10 infusion for refractory hypoglycemia
- glucagon 1mg –> decreases GI motility, monitor for n/v
