Module 6 - Endocrine Emergencies Flashcards
causes of polyuria
neurogenic/nephrogenic diabetes insipidus; hyperglycemia; excessive IV fluids; hypokalemia; hypercalcemia; renal disorder; psychogenic polydipsia; diuretics/litium
what is diabetes insipidus
absences of vasopressin or inadequate response to vasopressin
plasma sodium > 145
hypotonic polyuria - urine inappropriately dilute
-SG <1.010; urine osmolality < 300
polyuria: > 300 mL/h for 2 consecutive hours or > 3 L/day
diagnosis of diabetes insipidus
if patient is dehydrated w/ elevated plasma osmolality and dilute urine no further dehydration is necessary
draw blood for plasma vasopressin level
-to determine nephrogenic vs neurogenic DI
determine response to desmopression
what is formal water deprivation test?
- withhold all fluids
- weight, serum sodium, plasma/urine osmolality (Uosm > 800 eliminates DI & >600 eliminates it in most cases)
- record volume, osmolality of each urine
- weigh patient after each liter of urine
- stop test when urine osmolality plateaus (<10% change over 2 measurements) weight decreased by 3-5% or Na >145
- serum sodium, plasma & urine osmolality & vasopressin level
- administer DDAVP 1 mcg subQ
- record urine volume and osmolality hourly x 2 hours
]central DI, partial central DI, nephrogenic DI, psych/polydipsia chart
picture #1
causes of acquired central DI
trauma, vascular (CNS hemorrhage), neoplastic, granulomatous, infectious, inflammatory/autoimmune, drug/toxin induced, hydrocephalus, hypothalamic; idiopathic
acquired nephrogenic DI?
- renal tubules fail to respond appropriately to vasopressin. caused by:
- electrolyte disorder
- drug induced - cisplatin, amphotericin B
- tubulointerstitial renal disease (sickle cell, renal amyloidosis, multiple myeloma, Sjogren’s)
treatment of DI
correct water deficits; decrease urine volume; goal decrease Na by 1 mmil Q2h
what is desmopressin (DDAVP)
- synthetic analogue of AVP/vasopressin
- 2000xmore spcific for antidiuresis than vasopressin
- decrease pressor activity and increase half life compared to vasopressin (don’t have to worry as much about pressure going up when you give this drug vs. vasopressin)
treatment of neurogenic DI
- start DDAVP on PRN basis - start on evening dose of medication so they don’t have to get up at night to urinate
- repeat DDAVP when urine output is 20—250 mL/hour for > 2 hours
- standing order for DDAVP only if persistent polyuria > 48 hours
- treat hypokalemia (can cause resistance to DDAVP)
how do you dose DDAVP?
in partial DI, 0.1 mg at night
complete DI, 0.1 mg BID or TID
treatment of nephrogenic DI
- stop offending drug
- correct electrolyte abnormalities
- thiazide diuretic + low sodium diet (blocks Na absorption in critical diluting site –>modest hypovolemia–>stimulates proximal tubular solute reabsorption –>decrease urine volume)
- use amiloride or indomethacin (this one has GI side effects long term)
how should you monitor nephrogenic DI
Q4-6 h (serum sodium, osmolality & urine sodium, osmolality & SG)
-consider withdrawal of DDAVP, monitor urine output
presentation of hyponatremia?
asymptomatic, nausea, malaise, headache, lethargy, confusion, stupor, seizures, coma
diagnosis of SIADH
euvolemia (hanging on to water, but not so much that they are edematous), decreased serum sodium, decreased plasma osmolality, increased urine osmolality, urine sodium > 20, normal BUN/Creatinine, normal adrenal and thryroid function (confirm this if you suspect SIADH)
causes of SIADH?
- malignancy
- CNS (stroke, hemorrhage, infection, psychosis
- pulmonary: PNA, viral, pneumothorax
- drug induced: SSRI, opiates,
treatment of SIADH
depends on acute vs chronic, sodium level, and symptom level
goals of emergency therapy for SIADH
- raising serum Na by 4-6 meq/L should alleviate symptoms and prevent herniation
- increase in Na should not exceed 9 meq/L in 24 hours -if you do over correct then give DDAVP in D5W to re-lower the serum Na
- rapid correction increases risk of osmotic demyelination
when is osmotic demyelination have the highest risk?
sodium < 105; hypokalemia; alcoholism; malnutrition; liver disease; women/childre post op; massive water ingestion; intracranial pathology
treatment of SIADH?
- fluid restriction to < 1 L/day
- normal saline + loop diuretic
- 3% saline
- salt tablets
- demeclocycline - long term for increasing Na
- vasopressin receptor antagonists-selective water diuresis w/o affecting sodium & potassium excretion (tolvaptan)
monitoring for SIADH?
- serum sodium measured Q2-4Hrs
- urine output
- urine osmolality, urine sodium and urine potassium
epidemiology of adrenal insufficiency
PRIMARY -increasing prevalence d/t higher incidence of autoimmune adrenalitis -peak incidence in 4th decade of life -more common in women SECONDARY -peak incidence in 6th decade of life -more common in women
what is primary adrenal insufficiency
- loss of both cortisol and aldosterone
- causes: autoimmune, tuberculosis, hemorrhage, infection, medication, metastatic replacement, surgical, congenital
what is secondary adrenal insufficiency
- loss of cortisol production (don’t have as many problems with their pressures as primary adrenal insufficiency)
- causes: exogenous glucocorticoid use, Apoplezy/Sheehan’s syndrome, infiltrative diseases, infection, head trauma, drugs (megestrol, opiates)
glucocorticoid induceded AI
- potency, dose & duration of glucocorticoid use are important but imperfect predictors of HPA suppression
- more likely w/ prednisone 20 mg x 3 weeks w/o taper
- less likely on lower doses, shorter duration, when given in morning vs evening/alternative day regimens
- suppression of axis can last for up to 12 months
- can be caused by inhaled, nasal, intra-articular or topical steroid use
- do formal testing on those where clinical indicated
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