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Renal > Renal First Aid Pathology II > Flashcards

Renal First Aid Pathology II Flashcards

1
Q

Oxalate crystals

A

ethylene glycol (antifreeze) or vitamin C abuse.

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2
Q

Conditions that cause hypercalcemia (cancer,

t PTH) can -+ hypercalciuria and

A

radioopaque stones (calcium oxalate, calcium phosphate, or both).

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3
Q

Most common kidney stone presentation:

A

calcium oxalate stone in a patient with hypercalciuria and normocalcemia.

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4
Q

Can lead to severe complications, such as hydronephrosis and pyelonephritis. Treat and prevent by encouraging fluid intake.

A

kidney stones

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5
Q

Treatments for recurrent calcium oxalate/phosphate stones

A

thiazides and citrate

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6
Q

Caused by infection with urease-positive bugs
(Proteus mirabilis, Staphylococcus, Klebsiella)
that hydrolyze urea to ammonia -+ urine alkalinization. Can form staghorn calculi that can be a nidus for UTis.

A

Ammonium magnesium phosphate (“struvite”)

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7
Q

three urease positive bugs that can cause struvite stones

A

(Proteus mirabilis, Staphylococcus, Klebsiella)

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8
Q

Visible on CT and ultrasound but not x-ray.
Strong association with hyperuricemia
(e.g., gout). Often seen in diseases with
t cell turnover, such as leukemia. Treat with alkalinization of urine.

A

uric acid stone

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9
Q

Most often 2ndary to cystinuria. Hexagonal crystals. Treat with alkalinization of urine.

A

Cystine stones

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10
Q

kidney stones on xray

A

calcium + struvite + cystine = radioopaque

Uric acid = radiolUcent

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11
Q

Back-up of urine into the kidney. Can be caused by urinary tract obstruction or vesicoureteral reAux. Causes dilation of renal pelvis and calyces proximal to obstruction. May result in parenchymal thinning in chronic, severe cases.

A

hydronephrosis

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12
Q

RCC originates from

A

proximal tubule cells

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13
Q

Most common renal malignancy.

A

Renal cell carcinoma

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14
Q

RCC originates from proximal tubule cells

-+ polygonal clear cells filled with accumulated

A

lipids and carbohydrates.

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15
Q

RCC risk factors

A

Most common in men 50-70 years of age. t incidence with smoking and obesity.

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16
Q

Manifests clinically with hematuria, palpable mass, 2° polycythemia, flank pain, fever, and weight loss.

A

RCC

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17
Q

hematagenous spread of rcc

A

Invades renal vein then IVC and spreads hematogenously; metastasizes to lung and bone.

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18
Q

Associated with gene deletion on chromosome

WHAT (deletion may be sporadic or inherited as von Hippel-Lindau syndrome).

A

3

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19
Q

3 paraneoplastic syndromes w. wh/ Rcc is associated

A

ectopic EPO,
ACTH,
PTHrP

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20
Q

Why is RCC “silent?”

A

in retroperitoneum, commonly presents as a metastatic neoplasm.

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21
Q

Treatment of RCC:

A

resection if localized disease.

Resistant to conventional chemotherapy and radiation therapy.

22
Q

Most common renal malignancy of early childhood (ages 2-4). Contains embryonic glomerular structures. Presents with huge, palpable flank mass and/or hematuria.

A

WIlms’ tumor (nephroblastoma)

23
Q

With what gene deletion is Wilms’ tumor associated?

A

tumor suppressor gene WTl on chromosome ll.

24
Q

Syndromes with which Wilm’s tumor is associated

A

Beckwith­ Wiedemann syndrome or WAGR complex : Wilms’ tumor, Aniridia, Genitourinary malformation, and mental Retardation.

25
Q

WAGR complex is: : Wilms’ tumor, Aniridia, Genitourinary malformation, and mental Retardation.

A

: Wilms’ tumor, Aniridia, Genitourinary malformation, and mental Retardation.

26
Q

Most common tumor of urinary tract system (can occur in renal calyces, renal pelvis, ureters, and bladder)

A

Transitional cell carcinoma

27
Q

Presentation of transitional cell carcionma

A

painless hematuria with no casts

28
Q

Transitional cell carcinoma is associated with problems in your Pee SAC:

A

Phenacetin,
Smoking,
Aniline dyes, and
Cyclophosphamide.

29
Q

White blood cell casts in urine

A

acute pyelonephritis

30
Q

presentation of acute pyelonephritis

A

fever, CVA tenderness, nausea, vomiting

31
Q

what part of kidney is most affected with acute pyelonephritis?

A

affects cortex with relative sparing of glomeruli/vessels

32
Q

Coarse, asymmetric corticomedullary scarring, blunted calyx

A

chronic pyelonephritis

33
Q

Presentation of drug-induced interstitial nephritis

A

pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as HAPTENS, inducing hypersensitivity

34
Q

drugs that may cause interstitial nephritis

A

1-2 wks later: diuretics, PCN derivatives, sulfonamides, rifampin;
months later: NSAIDs

35
Q

Acute generalized cortical infarction of both kidneys. Likely due to a combination of vasospasm and DIC.

A

Diffuse cortical necrosis

36
Q

Associated with obstetric catastrophes (e.g., abruptio placentae) and septic shock.

A

Diffuse cortical necrosis

37
Q

Most common cause of intrinsic renal failure.
Self-reversible in some cases, but can be fatal if left untreated. Death most often occurs during initial oliguric phase.

A

Acute tubular necrosis

38
Q

describe three stages of ATN

A
  1. Inciting event
  2. Maintenance phase-oliguric; lasts 1-3 weeks; risk of hyperkalemia
  3. Recovery phase-polyuric; BUN and serum creatinine fall; risk of hypokalemia
39
Q

risk in maintenance phase of ATN

A

hyperkalemia

40
Q

risk in recovery phase of ATN

A

hypokalemia

41
Q

Sloughing of renal papillae –> gross hematuria and proteinuria. May be triggered by a recent infection or immune stimulus.

A

Renal papillary necrosis

42
Q

Renal papillary necrosis is associated with four things:

A
  • Diabetes mellitus
  • Acute pyelonephritis
  • Chronic phenacetin use (acetaminophen is phenacetin derivative)
  • Sickle cell anemia and trait
43
Q

In normal nephron, BUN is reabsorbed (WHY?!), but creatinine is not.

A

for countercurrent multiplication

44
Q

As a result of decrease RBF (e.g., hypotension) –> decreased GFR, Na+fH20 and urea retained by kidney in an attempt to conserve volume, so BUN/creatinine ratio t.

A

prerenal azotemia

45
Q

Generally due to ATN or ischemia/toxins and less commonly to acute glomerulonephritis (e.g., RPGN). Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule –> dec GFR. Urine has epithelial/granular casts. BUN reabsorption is impaired –> BUN/creatinine ratio.

A

Intrinsic renal failure

46
Q

Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction.

A

Post renal azotemia

47
Q

Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia –> 2° hyperparathyroidism. Hyperphosphatemia also independently decreases serum Ca2+ by causing tissue calcifications, whereas decreased 1,25-(0H)z vitamin D –> decreased intestinal Ca2+ absorption. Causes subperiosteal thinning of bones.

A

Renal osteodystophy

48
Q 
Na+, H2O retention
Hyperkalemia
Metabolic acidosis
Uremia
Anemia
Renal osteodystrophy,
Dyslipidemia
Growth retardation and developmental delay
A

consequences of renal failure

49
Q

Multiple, large, bilateral cysts that ultimately destroy the kidney parenchyma. Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure.

A

ADPKD

50
Q

Autosomal-Dominant mutation in PKDl or PKD2 . Death from complications of chronic kidney disease or hypertension (caused by
inc renin production). Associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts.

A

ADPKD

51
Q

Infantile presentation in parenchyma. AR. Associated with congenital hepatic fibrosis. Significant renal failure in utero can lead to Potter’s syndrome. Concerns beyond neonatal period include hypertension, portal hypertension, and progressive renal insufficiency.

A

ARPKD

52
Q

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. Medullary cysts usually not visualized; shrunken kidneys on ultrasound. Poor prognosis.

A

Medullary cystic kidney disease

Renal (22 decks)

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