Renal & Electrolytes Flashcards

1
Q

Treatment of patients with severe hypovolemic hypernatremia

A

1st correct the hypovolemia with 0.9% saline.

Then switch to 0.45% saline + 5% dextrose to correct the hypernatremia no faster than 1mEq/L/hour

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2
Q

Earliest renal abnormality in patients with diabetes? Earliest observable abnormality in these patients?

A

Earliest abnormality = glomerular hyperfiltration

Earliest observable abnormality = GBM thickening

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3
Q

Imaging modalities of choice for patients with suspected kidney stones

A

Non contrast helical CT and ultrasound (preferred if alternate dx is unlikely or pregnant)

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4
Q

Treatment of choice for uric acid stones

A

Alkalinization of the urine to a pH of 6 to 6.5 with potassium citrate.

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5
Q

Stones not observable on imaging

A

Calcium stones

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6
Q

Most common type of nephrotic syndrome where you see renal vein thrombosis?

A

Membranous glomerulopathy

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7
Q

Differentiating benign renal cysts from malignant renal cysts

A

Simple: smooth, homogenous, do not enhance with contrast, asymptomatic and unilocular.

Malignant: thick, irregular walls, loculated, heterogenous, enhance with contrast, cause pain/hematuria/HTN

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8
Q

Most common causes of anion gap metabolic acidosis

A
Methanol
Uremia
DKA
Propylene glycol
INH
Lactic acid
Ethylene glycol
Salicylates
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9
Q

Appropriate rate of correction of serum sodium for patients with hyponatremia

A

No more than 0.5mEq/dL/hr and not exceeding 12mEq in 24 hours.

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10
Q

How to calculate serum osmolarity

A

2Na + BUN/2.8 + Glc/18

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11
Q

Calculate serum osmolar gap

A

Measured Sosm - Calculated Sosm. This is typically done when you suspect ethanol, methanol or ethylene glycol toxicity.

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12
Q

Diagnostic criteria for SIADH

A

Sosm Sosm

Una > 20

Absence of hypovolemia

Normal renal, adrenal and thyroid function

No obvious stimulus to activate the neuroendocrine hormonal response that increases ADH secretion

Absence of other known causes of hyponatremia

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13
Q

Why is metabolic acidosis due to renal disease rarely seen in patients with an eGFR > 20?

A

The remaining nephrons compensate greatly for decreased H+ secretion by increasing NH3 production that gets secreted in the urine as NH4 to get rid of the H+.

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14
Q

Dietary recommendations for patients with renal calculi?

A

Increased fluid to >2L urine/day, decreased Na+ to

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15
Q

Definitive measures used to reduce serum K+

A

Cation exchange resins like sodium polystyrene sulfonate

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16
Q

How to confirm the diagnosis of cystinuria in a patient with stones?

A

Hexagonal crystals and urinary cyanide nitroprusside test showing elevated cystine levels.

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17
Q

Post-void residual volume that is significant for bladder outlet obstruction

A

> 50 mL

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18
Q

Complete vs. partial DI

A

Complete: urine osmolarity is > 600

Partial: urine osmolarity is 300-600

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19
Q

Common causes of nephrogenic DI

A

Hypercalcemia, hypokalemia, tubulointerstitial renal disease, Li, demeclocycline, foscarnet, cidofovir and amphotericin

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20
Q

Why do saline-resistant causes of metabolic alkalosis have a high urine Cl- concentration?

A

Excess mineralocorticoid stimulation results in excess serum Na+ and volume retention. The kidneys respond by secreting more Na+ and Cl-, resulting in increased Cl- concentration.

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21
Q

Treatment of UTIs and pyelonephritis in non-pregnant women?

A

Acute uncomplicated cystitis: nitrofurantoin x 5 days (avoid if GFR 20%). Fosfomycin x1. Culture urine only if treatment fails.

Complicated cystitis: fluoroquinolones 5-14 days. Amp-gent for more severe cases. Culture urine to confirm correct antibiotic choice.

Pyelo: fluoroquinolones as outpatient therapy. IV fluoroquinolones or aminoglycoside +/- ampicillin for inpatient therapy. Culture urine to confirm correct antibiotic choice.

22
Q

What constitutes a case of complicated cystitis?

A

DM, CKD, pregnancy, immunocompromised, urinary tract obstruction, hospital-acquired infection, procedure-associated infection or catheter-associated infection.

23
Q

Management of hypercalcemia?

A

Severe (sx or Ca > 14): NS at 200mL/hr with goal urine output of 100-150mL/hr + calcitonin immediately. Give bisphosphonates for long-term treatment.

Moderate (Ca 12-14): no treatment

Mild (Ca

24
Q

Tests to get in patients with BPH

A

Urinalysis and PSA if life expectancy is > 10 years

25
Q

Most common type of kidney stone

A

Ca-oxalate

26
Q

Acid-base abnormality seen with chronic vomiting

A

Hypochloremic, hypokalemic metabolic alkalosis. This is because for each H+ lost in vomit, one HCO3- is formed. Additionally, hypovolemia leads to RAAS activation, H+/K+ wasting and HCO3- retention.

27
Q

Common extrapulmonary manifestations of Tb

A

Liver disease, splenic infiltration, renal disease, Pott’s disease and adrenal insufficiency (very common in endemic regions).

28
Q

NSAID effects on kidneys

A

Prostaglandin inhibition prevents afferent arteriole dilation and can cause renal failure.

Also, it potentiates the action of ADH and can cause SIADH.

29
Q

ECG characteristics in hyperkalemia

A

Peaked T-waves, short QT, long PR and wide QRS that can progress to sine wave morphology.

30
Q

Kidney stones that will likely pass spontaneously

A
31
Q

Most common histology seen in patients with diabetic nephropathy?

A

Diffuse glomerulosclerosis

32
Q

Most common causes of nephrotic syndrome in adults with no evidence of systemic disease?

A

Membranous nephropathy and FSGS

33
Q

How do you know a patient has FHH vs. primary hyperparathyroidism?

A

They have very low urine Ca ( 0.02 due to high urinary Ca levels.

34
Q

Factors that may precipitate hepatorenal syndrome

A

Those that reduce renal perfusion or GFR

35
Q

How to diagnose hepatorenal syndrome

A

Confirm renal hypoperfusion with FeNa

36
Q

Nephrotic range proteinuria, hematuria and dense intramembranous deposits that stain positive for C3

A

Membranoproliferative GN. This is due to IgG antibodies against C3 convertase that constitutively activate C3 and the alternative complement pathway.

37
Q
Muddy brown granular casts
RBC casts
WBC casts
Fatty casts
Broad and waxy casts
A
Muddy brown granular casts - ATN
RBC casts - GN
WBC casts - AIN, pyelo
Fatty casts - nephrotic syndrome 
Broad and waxy casts - chronic renal failure
38
Q

Cardinal features of nephrotic syndrome

A

Proteinuria (glomerular injury), hypoproteinemia, hyperlipidemia (increased liver synthesis of albumin and lipids), edema (decreased oncotic pressure), hypercoaguability (loss of AT III and increased protein C/S) and hypovolemia

39
Q

Drugs that commonly cause interstitial nephritis?

A

Cephalosporins, PCN, sulfonamides, sulfa diuretics, NSAIDs, rifampin, phenytoin and allopurinol.

40
Q

Antibiotic that can cause hyperkalemia by blocking the eNaC and decreases creatinine secretion?

A

Trimethoprim

41
Q

Characteristics of interstitial cystitis? Treatment?

A

Bladder pain with filling that is relieved by voiding with no other attributable cause for > 6 weeks. Treat by avoiding triggers + amitriptylene and analgesics during flares.

42
Q

Why are loop diuretics associated with metabolic alkalosis?

A

They increase Na delivery to the DCT. This leads to increased Na resorption and K/H secretion -> metabolic alkalosis.

43
Q

How to prevent at-risk patients from getting contrast-induced nephropathy if they really need imaging done.

A

Adequate IV hydration with isotonic NaHCO3 or 0.9% NS + acetylcysteine.

44
Q

Extra-renal manifestations of ADPKD

A

Berry aneurysms
MVP/AR
Colonic diverticula
Abdominal wall/inguinal hernia

45
Q

Aspects of patients on dialysis that increase their risk of dying from heart disease?

A

Elevated homocysteine levels

Hyperphosphatemia w/elevated PTH levels

Anemia

ESRD

Accelerated atherogenesis from enhanced oxidant stress

Enhanced Ca intake

NO inhibition

46
Q

Patient has gross hematuria, low serum C3 and subepithelial humps consisting of C3 complement on renal biopsy

A

Post-strep GN

47
Q

AA amyloidosis vs. AL amyloidosis

A

AA = chronic inflammatory conditions, beta-2 microglobulin, apolipoprotein or transthyretin gets abnormally folded and deposited.

AL = MM, Waldenstroms. Lambda light chains get deposited.

48
Q

Nephritic syndromes with associated low C3 levels

A

Post-strep GN, lupus, MPGN, mixed cryoglobulinemia

49
Q

Immune complexes that form in mixed cryoglobulinemia

A

IgM complexes with anti-HCV IgG, HCV RNA and complement.

50
Q

Drugs that can cause crystal-induced nephropathy

A

Acyclovir, sulfonamides, MTX, ethylene glycol and protease inhibitors

51
Q

What do +LE and nitrites on UA mean?

A

+LE = pyuria. Nitrites = enterobacter is present.