ASN QBank Pearls - Fluid Compartments and Electrolyte Disorders Flashcards Preview

Nephrology Board Review Pearls > ASN QBank Pearls - Fluid Compartments and Electrolyte Disorders > Flashcards

Flashcards in ASN QBank Pearls - Fluid Compartments and Electrolyte Disorders Deck (27)
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1

how much volume of 0.9% saline contributes to increasing the volume of the intravascular space?

25%

2

illicit drug that can cause AKI 2/2 nontraumatic rhabdomyolysis

MDMA (ecstasy)

3

most efficient and effective means of removing lithium

HD

4

normal kidneys echogenicity

less than that of pancreas and equal or less than that of liver and spleen

5

hypercholesterolemia with lipoprotein X associated with cholestatic or obstructive jaundice is a cause of

pseudohyponatremia

6

risk factors for osmotic demyelination syndrome (ODS)

- alcoholism
- serum Na+ ≤ 105 mEq/L
- liver disease
- malnutrition

7

complication of hypomagnesemia or hypermagnesemia

hypocalcemia

8

differential diagnosis for hypercalcemia with low PTH, normal 25(OH)D, and low 1,25(OH)2D

- hyperthyroidism
- malignancy
- immobilization
- Paget’s disease
- milk-alkali syndrome

9

initial therapy of moderate to severe hypercalcemia includes

simultaneous administration of;
- isotonic saline
- calcitonin
- bisphosphonate

10

classic triphasic response following injury or transection of the pituitary stalk

1. DI occurs because vasopressin cannot be released from nerve terminals d/t interruption of nerve impulses
2. SIADH results from unregulated release of stored vasopressin from degenerating neurons
3. permanent DI once vasopressin stores are depleted

11

can cause central pontine and extrapontine myelinolysis, similar to what occurs after rapid correction of chronic hyponatremia

acute hypernatremia; should be rapidly corrected

12

ODS prognosis even if initially ventilator dependent

complete neurological recovery in up to 1/3 of cases

13

mechanism by which hypermagnesemia causes hypocalcemia

binds to calcium-sensing Rs and reduces PTH

14

complications of acute hypermagnesemia

- hypotension
- hyperkalemia
- hypocalcemia
- at higher levels, heart block and cardiac arrest

15

familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) gene mutations

claudin-16 gene

16

medication class that inhibits claudin-16 gene

calcineurin inhibitors (cyclosporine, tacrolimus, and pimecrolimus)

17

medications that cause hypomagnesemia d/t renal magnesium wasting in distal tubule

cetuximab, panitumumab, and matuzumab

18

calcineurin inhibitors primarily reduce expression of claudin 16 where?

ascending limb in LOH

19

what test BEST demonstrates pseudohyponatremia?

plasma osmolality

20

MOST appropriate therapy for hyperuricemia prior to tumor-specific chemotherapy if G6PD deficiency?

allopurinol

21

no longer recommended for tumor lysis syndrome (TLS)

urinary alkalinization d/t r/o calcium-phosphate crystal deposition (acute phosphate nephropathy) and hypoxanthine/xanthine crystal deposition

22

renal complications of cisplatin

- hyponatremia 2/2 cisplatin-induced renal salt wasting
- ATN
- tubulopathies:
- proximal tubulopathy/Fanconi syndrome
- Mg2+ wasting
- nephrogenic DI
- CKD

23

MOST common electrolyte disturbance associated with cetuximab

hypomagnesemia

24

complications of ecstasy toxicity

- hyponatremia 2/2 SIADH and excessive hypotonic fluid ingestion
- seizures (from hyponatremia)
- lactic acidosis
- AKI 2/2 rhabdomyolysis

25

mechanisms of hyponatremia 2/2 IVIG

- pseudohyponatremia from the immunoglobulin
- true hyponatremia from the associated carrier (sucrose, maltose)

26

women who donate a kidney before becoming pregnant

increased risk for adverse outcomes DURING pregnancy

27

use of ACE inhibitors during pregnancy?

contraindicated, but can be used during breastfeeding postpartum