DI/SIADH Flashcards

1
Q

Define DI

A

Fluid imbalance– inability to retain fluid and lack of sugar in urine
excessive thirst and excretion of large amounts (>3L/day) of dilute urination (<300 mOsm/kg)

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2
Q

Define C-DI

A

decreased ADH released from PP causing polyuria, polydipsia, nocturia

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3
Q

where is the defect with C-DI

A

hypothalamus or PP not making enough ADH

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4
Q

where is the defect with N-DI

A

kidney (collecting tubules or loop of henle) unresponsive to ADH

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5
Q

expected labs with C-DI vs N-DI

A

Central labs: LOW BMP, UA and ADH
Nephrogenic labs: normal-high BMP, UA, ADH
Both: high serum osmo, low urine osmo, no response to water deprivation

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6
Q

what causes thirst in DI

A

elevated serum Na (increased Osmo) stimulates thirst to replace urinary water loss

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7
Q

sx of hyper-natremia

A

lethargy
weakness
edema
irritability
NM excitability

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8
Q

exogenous ADH can help with which type of DI

A

Central DI

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9
Q

expected result of fluid deprivation test in someone w/ DI

A

no response to water deprivation

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10
Q

Define N-DI

A

kidney resistant to ADH–> decreased ability to concentrate urine
polydipsia, polyuria, nocturia

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11
Q

3 must haves for SIADH diagnosis

A

hyponatremia (<135) with low serum Osm (<275)
urine Osm >100mOsm/kg
Also: normal thyroid, renal and adrenal fx and urine sodium >30

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12
Q

ADH levels in DI vs SIADH

A

DI has inadequate ADH
SIADH has excess ADH

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13
Q

SERUM vs Urine osmolarity in DI & SIADH

A

Serum: DI high (polyuria), SIADH low (oliguria)
Urine: DI low, SIADH high

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14
Q

serum sodium in SI vs SIADH

A

DI: hypernatremia
SIADH: hyponatremia

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15
Q

main treatment differences for DI vs SIADH

A

DI: desmopressin, HCTZ, chlopropamide
SIADH: fluid restriction

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16
Q

relationship between ADH levels and urine production

A

increase in ADH= water retention/decreased urine production
no ADH= water voided and higher sodium concentration

17
Q

what is the most important physiologic stimulant of ADH

A

plasma osmolaLity

18
Q

cycle of ADH & plasma osmolali

A

increased ADH–> increased reabsorption–> decreased plasma osmolality–> decreased ADH release–> increased plasma osmolality

19
Q

clinical signs of DI

A

polyuria, polydipsia, nocturia
craving cold water
hypernatremia
dehydration

20
Q

causes of central/neurogenic vs nephrogenic DI

A

central causes: pit or hypo thalamus damage from trauma or surgery, autoimmune, tumors, drugs, vascular
nephrogenic causes: renal d/o or lithium therapy, congenital, electrolyte d/o, sickle cell

21
Q

what happens if someone can’t respond to thirst stimulation?

A

severe hypernatremia= increased mortality

22
Q

diagnostic for DI

A

water deprivation test +/- serum ADH
vasopressin test (IM)
MRI to evaluate pituitary

23
Q

what is the vasopressin test (IM)

A

give IM vasopressin to determine if central or nephrogenic DI
if urine output slows- Central Di
if it remains the same- Nephrogenic DI

24
Q

first line tx in Central vs Nephrogenic DI

A

central tx: desmopressin
nephrogenic: Diuretics- amiloride

25
Q

other treatments for C-DI

A

HCTZ diuretics–causes mild hypovolemia & proximal Na & H2O reabsorption (end result is less urine output
Chlorpropamide (2nd line)– causes partial release of ADH & can cause hypoglycemia
Carbamazepine– enhances response to ADH in partial C-DI
Clofibrate– can induce SIADH

26
Q

which medication can reverse lithium effect

A

Amiloride (diuretic)

27
Q

name the only other class of meds that can work on N-DI

A

NSAIDs– inhibits prostaglandin synthesis so it doesn’t antagonize ADH
Indomethacin > Ibuprofen

28
Q

which gramulomatous disease can cause C-DI

A

sarcoid

29
Q

what drugs can cause C-DI

A

alcohol
diphenylhydantoin (seizure med)

30
Q

Sx of SIADH

A

nausea/vomiting, cramps
depressed mood, irritable
confusion, hallucinations
seizures, coma
edema/wt gain

31
Q

conditions associated w/ SIADH

A

head trauma
malignant neoplasms (esp small cell lung CA)
pulmonary dz
CNS d/o
drugs

32
Q

lab findings w/ SIADH

A

low plasma Na, low plasma Osm, high urine Osm d/t disproportionate solute excretion w/o water

33
Q

tx for SIADH

A

fluid restriction (for chronic hyponatremia)- fluids 500ml less than output
hypertonic saline if severe CNS sx (emergencies)

also: vasopressin receptor antagonist or urea to increase solute load and increase water loss

34
Q

how does desmopressin (DDAVP) work?

A

acts on collecting duct causing non suppressible ADH activity–> inability to excrete ingested water (hyponatremia)
monitor Na+ after starting the medication!