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Acute Care I - Spring 2017 > Module 6 - Endocrine Emergencies > Flashcards

Module 6 - Endocrine Emergencies Flashcards

1
Q

causes of polyuria

A

neurogenic/nephrogenic diabetes insipidus; hyperglycemia; excessive IV fluids; hypokalemia; hypercalcemia; renal disorder; psychogenic polydipsia; diuretics/litium

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2
Q

what is diabetes insipidus

A

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

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3
Q

diagnosis of diabetes insipidus

A

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

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4
Q

what is formal water deprivation test?

A
  • 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
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5
Q

]central DI, partial central DI, nephrogenic DI, psych/polydipsia chart

A

picture #1

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6
Q

causes of acquired central DI

A

trauma, vascular (CNS hemorrhage), neoplastic, granulomatous, infectious, inflammatory/autoimmune, drug/toxin induced, hydrocephalus, hypothalamic; idiopathic

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7
Q

acquired nephrogenic DI?

A
  • 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)
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8
Q

treatment of DI

A

correct water deficits; decrease urine volume; goal decrease Na by 1 mmil Q2h

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9
Q

what is desmopressin (DDAVP)

A
  • 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)
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10
Q

treatment of neurogenic DI

A
  • 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)
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11
Q

how do you dose DDAVP?

A

in partial DI, 0.1 mg at night

complete DI, 0.1 mg BID or TID

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12
Q

treatment of nephrogenic DI

A
  • 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)
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13
Q

how should you monitor nephrogenic DI

A

Q4-6 h (serum sodium, osmolality & urine sodium, osmolality & SG)
-consider withdrawal of DDAVP, monitor urine output

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14
Q

presentation of hyponatremia?

A

asymptomatic, nausea, malaise, headache, lethargy, confusion, stupor, seizures, coma

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15
Q

diagnosis of SIADH

A

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)

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16
Q

causes of SIADH?

A
  • malignancy
  • CNS (stroke, hemorrhage, infection, psychosis
  • pulmonary: PNA, viral, pneumothorax
  • drug induced: SSRI, opiates,
17
Q

treatment of SIADH

A

depends on acute vs chronic, sodium level, and symptom level

18
Q

goals of emergency therapy for SIADH

A
  • 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
19
Q

when is osmotic demyelination have the highest risk?

A

sodium < 105; hypokalemia; alcoholism; malnutrition; liver disease; women/childre post op; massive water ingestion; intracranial pathology

20
Q

treatment of SIADH?

A
  • 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)
21
Q

monitoring for SIADH?

A
  • serum sodium measured Q2-4Hrs
  • urine output
  • urine osmolality, urine sodium and urine potassium
22
Q

epidemiology of adrenal insufficiency

A 
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
23
Q

what is primary adrenal insufficiency

A
  • loss of both cortisol and aldosterone

- causes: autoimmune, tuberculosis, hemorrhage, infection, medication, metastatic replacement, surgical, congenital

24
Q

what is secondary adrenal insufficiency

A
  • 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)
25
Q

glucocorticoid induceded AI

A
  • 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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Acute Care I - Spring 2017 (10 decks)

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