GU Flashcards

1
Q

What BUN/creatinine ratio is indicative of a prerenal azotemia?

A

> 20

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2
Q

How does Proteus mirabilis change urine pH?

A

Makes it more alkaline (e.g. 8). Uses urease to split urea into ammonia and carbon dioxide. Alkaline urine increases risk for struvite stones (magnesium ammonium phosphate)

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3
Q

How are simple renal cysts managed?

A

Reassurance only if asymptomatic, even if large

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4
Q

What shape are the crystals in cystinuria?

A

Hexagonal

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5
Q

What kind of stones does a urinary cyanide-nitroprusside test detect?

A

Detects elevated cystine levels - cystinuria crystals

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6
Q

What is treatment for uric acid stones?

A

Hydration, alkalization of the urine (e.g. potassium citrate), and a low-purine diet

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7
Q

What structural changes can be seen in the kidneys in pts with hypertension?

A

Benign nephrosclersis: Bilateral shrunken kidneys with damage to aterioles (nephrosclerosis) that progresses to damage to glomerular capillary tufts.
Nephrosclerosis: hypertrophy and intimal medial fibrosis.
Glomerulosclerosis: progressive loss of the glomerular capillary surface area with glomerular and peritubular fibrosis.

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8
Q

What insults can lead to minimal change disease in adults?

A

NSAIDS and lymphoma

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9
Q

What risk factors are associated with focal segmental glomerulosclerosis?

A

African American and Hispanic ethnicity, obesity, HIV, and heroin use

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10
Q

What are risk factors for membranous nephropathy?

A

Adenocarcinoma (e.g. breast, lung), NSAIDs, hep B, and SLE

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11
Q

What are risk factors for membranoproliferative glomerulonephritis?

A

Hep B and C

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12
Q

What is the timeline of crystal-induced acute kidney injury vs acute interstitial nephritis from medications?

A

Crystal-induced: <7 days after starting drug

AIN: 7-10 days after drug exposure

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13
Q

What medications/etiologies are associated with crystal-induced acute kidney injury?

A

Acyclovir, sulfonamides, MTX, ethylene glycol, protease inhibitors, and uric acid (tumor lysis syndrome)

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14
Q

What is Bartter’s syndrome?

A

A rare inherited defect in the thick ascending limb of the loop of Henle. It is characterized by low potassium levels (hypokalemia), increased blood pH (alkalosis), and normal to low blood pressure.

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15
Q

What are ways to prevent renal injury when using contrast?

A

Pre and post procedure hydration, N-acetylcysteine, and urine alkalization

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16
Q

What is the most common cause of acute epididymitis in a patient >35 yo?

A

Most often due to bladder outlet obstruction (e.g. BPH). Ascending coliform bacteria such as E. coli are most common pathogens

17
Q

What is the most common cause of acute epididymitis in a patient <35 yo?

A

STI such as Chlamydia or gonorrhea

18
Q

What are causes of type I renal tubular acidosis?

A

Lithium/Ampho B, analgesics, SLE, Sjogrens, sickle cell, hepatitis

19
Q

How do you dx and tx type I renal tubular acidosis?

A

Urine pH > 5.4, HypoK, Kidney stones (due to problem with excreting H+ in distal tubules/collecting duct).
Tx with PO bicarb

20
Q

What are causes of type II renal tubular acidosis?

A

Fanconi’s syndrome, multiple myeloma, amyloidosis, vitD def, autoimmune dz

21
Q

How do you dx and tx type II renal tubular acidosis?

A

Due to problem reabsorbing bicarb in proximal tubule –> HypoK and osteomalacia.
Treat with potassium and mild diuretic (bicarb will not help)

22
Q

What are causes of type IV renal tubular acidosis?

A

Due to hypoaldosteronism (also have high renin levels)- >50% caused by diabetes! Other causes include Addison’s, sickle cell, or any other cause of aldosterone def

23
Q

How do you dx and tx type IV renal tubular acidosis?

A

Presents with hyperK, hyperCl, and high urinary sodium concentration even with salt restriction.
Treat with fludrocortisone

24
Q

How is FENa calulated?

A

(urinary Na x serum creatinine)/(serum Na x urine creatinine)

25
Q

What is the earliest renal abnormality in diabetic nephropathy?

A

Glomerular hyperfiltration

26
Q

What dietary recommendations should be made to patients with recurrent renal calculi?

A
  1. Increase fluid intake
  2. Decrease sodium intake (decreasing sodium leads to increased calcium reabsorption from renal tubules)
  3. Normal dietary calcium intake
27
Q

What is the mechanism behind membranoproliferative glomerulonephritis type 2 (dense deposit disease)?

A

IgG antibodies against C3 convertase of the alternative complement pathway which leads to persistent complement activation and kidney damage. Causes dense intramembranous deposits

28
Q

What should you be thinking in a patient with worsening kidney function and flank pain after starting acyclovir?

A

Crystal-induced acute kidney injury (AKI)

29
Q

What is hyposthenuria?

A

The inability of the kidneys to concentrate urine (results in very low specific gravity)