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Analysis of Urine and Other Body Fluids > Chapter 8 - Renal Disease > Flashcards

Chapter 8 - Renal Disease Flashcards

1
Q

3 Classifications of renal dse

A

Glomerular disorders, tubular disorders, interstitial disorders

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2
Q

Majority are of immune origin (immune complexes, IgG, IgA)

A. Glomerular disorders
B. Tubular disorders
C. Interstitial disorders

A

A. Glomerular disorders

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3
Q

UTI belongs to which of the ff:

A. Glomerular disorders
B. Tubular disorders
C. Interstitial disorders

A

C. Interstitial disorders

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4
Q

How would you diff acute post-strep GN from other GN?

A

Positive ASO titer

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5
Q

Thickening of glomerular membrane ff IgG immune complex deposition assoc w/ systemic disorders

A

Membranous GN

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6
Q

Deposition of antiglomerular basement membrane antibody to glomerular and alveolar basement membranes

A

Goodpasture syndrome

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7
Q

Occurs in children ff viral respiratory infections; decrease in platelets disrupts vascular integrity

A

Henoch Schönlein purpura

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8
Q

Antineutrophilic cytoplasmic auto-antibody binds to neutrophils in vascular walls producing damage to small vessels in the lungs & glomerulus

A

Wegener’s granulomatosis

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9
Q

Deposition of immune complexes from systemic immune disorders on the glomerular membrane

A

Rapidly progressive GN

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10
Q

Cellular proliferation of epithelial cells inside the Bowman’s capsule form “crescents”

A

Rapidly progressive (crescentic) GN

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11
Q

Tram-track; cellular proliferation affecting the capillary walls or the glomerular basement membrane, possibly immune-mediated

A

Membranoproliferative GN

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12
Q

Deposition of IgA on the glomerular membrane resulting from increased levels of IgA

A

IgA nephropathy / Berger’s disease

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13
Q

Genetic disorder showing lamellated and thinning of the glomerular basement membrane

A

Alport syndrome

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14
Q

Narked decrease in renal fxn resulting from glomerular damage precipitated by other renal disorders; progression to renal failure; less painful but irreversible

A

Chronic GN

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15
Q

Little cellular changes in glomerulus, disruption of podocytes primarily in children ff allergic rxns & immunization

A

Minimal change dse / Nil dse / Lipoid nephrosis

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16
Q

Disruption of podocytes in certain numbers & areas of glomeruli, others remain normal

A

Focal segmented glomerulosclerosis

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17
Q

Most common cause of ESRD; deposition of glycosylated proteins on the glomerular basement membranes caused by poorly controlled blood glucose levels

A

Diabetic nephropathy / Kimmelstiel-Wilson dse

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18
Q

Disruption of the electrical charges that produce the tightly fitting podocyte barrier resulting in massive loss of proteins & lipids; progression from other dses.

A

Nephrotic syndrome

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19
Q

Enunerate findings for each of the ff dses:

  1. Acute post-strep GN
  2. Rapidly progressive GN
  3. Goodpasture syndrome
  4. Wegener’s granulomatosis
  5. Henoch-Schonlein purpura
  6. Membranous GN
  7. Membranoproliferative GN
  8. Chronic GN
  9. IgA nephropathy
  10. Minimal change dse
  11. Focal segmental glomerulosclerosis
  12. Diabetic nephropathy
  13. Alport syndrome
  14. Nephrotic syndrome
A
  1. Macroscopic hematuria, proteinuria, dysmorphic RBCs, RBC casts, granular casts, positive ASO titer
    2, 3, 4 & 5. Macroscopic hematuria, proteinuria, RBC casts
  2. Microscopic hematuria, proteinuria
  3. Henaturia, proteinuria
  4. Hematuria, proteinuria, glucosuria, cellular & granular casts, waxy & broad casts
  5. Early stages: hematuria ; late stages: same w/ chronic GN
  6. Heavy proteinuria, transient hematuria, fat droplets
  7. Proteinuria, hematuria
  8. Microalbuminuria, positive micral test
    13, 14. Lipiduria, albuminuria, proteinuria
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20
Q

How would you diff chronic from acute GN based on findings?

A

Waxy & broad casts

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21
Q

Determine whether the ff would increase or decrease for px with nephrotic syndrome:

  1. Serum albumin
  2. Serum gammaglobulins
  3. Urine albumin
  4. Urine alpha-1 globulins
  5. Serum alpha-1 globulins
  6. Serum Beta globulin (LDL)
  7. serum Alpha-2 macroglobulin
  8. Urine alpha-2 macroglobulin
  9. Oval fat bodies in urine
  10. Fatty casts in urine
  11. Waxy casts in urine
A
  1. Dec
  2. Dec
  3. Inc
  4. Inc
  5. Dec
  6. Inc
  7. Inc
  8. Neg
  9. Inc
  10. Inc
  11. Inc
22
Q

Generalized failure of tubular reabsorption in the PCT

A

Fanconi syndrome

23
Q

Normal blood glucose, increased urine glucose; defective tubular reabsorption of glucose

A

Renal glucosuria

24
Q

Damage to renal tubular cells caused by ischemia or toxic agents

A

Acute tubular necrosis

25
Q

Failure of hypothalamus to produce ADH

A

Neurogenic DI

26
Q

Renal tubules fail to respond to ADH

A

Nephrogenic DI

27
Q

Inherited defect in the production of normal uromodulin by the renal tubules & increased uric acid causing gout; normal uromodulin is replaced by abnormal forms that destroy the RTE cells

A

Uromodulin-assoc kidney dse (UKD)

28
Q

Enumertae the findings for each of the ff tubular disorders:

  1. Acute tubular necrosis
  2. UKD
  3. Fanconi syndrome
  4. DI
  5. Renal glucosuria
A
  1. Microscopic hematuria, proteinuria, RTE cells, RTE casts, hyaline, granular, waxy, broad casts
  2. RTE cells, hyperuricemia
  3. Glucosuria, POSSIBLE CYSTINE CRYSTALS
  4. Low SG, polyuria (>15 L/day)
  5. Glucosuria
29
Q

Lower UTI, bladder infection

A

Cystitis

30
Q

Upper UTI, kidney infection

A

Acute pyelonephritis

31
Q

Recurrent infection of the renal tubules & interstitium caused by structural abnormalities affecting the flow of urine

A

Chronic pyelonephritis

32
Q

Allergic inflammation of the renal interstitium in response to certain medications

A

Acute interstitial nephritis

33
Q

Ascending bacterial infection of the urinary bladder; acute onset of urinary frequency & burning

A

Cystitis

34
Q

Infection of urine flow to the bladder, reflux of urine from the bladder (vesicoureteral reflux) & untreated cystitis

A

Acute pyelonephritis

35
Q

Enumerate the findings expected from the ff interstitial disorders:

  1. Cystitis
  2. Acute pyelonephritis
  3. Chronic pyelonephritis
  4. Acute interstitial nephritis
A
  1. WBCs, bacteria, NO CAST, microscopic hematuria, mild proteinuria, increased pH
  2. WBCs, bacteria, WBC casts, bacterial casts, microscopic hematuria, proteinuria
  3. WBCs, bacteria, WBC casts, bacterial casts, granular casts, waxy & broad casts, hematuria, proteinuria
  4. Hematuria, proteinuria, WBCs (increased eos), WBC casts, NO BACTERIA
36
Q

Normal value for GFR

A

120 mL/min

37
Q

Decreased GFR, increased blood BUN & crea, electryte imbalance, negative renal concentating ability (isosthenuria), proteinuria & renal glycosuria

A

Renal failure

38
Q

Increased BUN & crea in blood

A

Azotemia

39
Q

Simultaneous appearance of the elements of acute / chronic GN & nephrotic syndrome ; increased cells & casts (RBC, granular, waxy, broad, fatty), lipid droplets, oval fat bodiest

A

Telescoped sediment

40
Q

Conditions favoring the formation of renal calculi

A

pH, chemical concentration, urinary stasis

41
Q

Primary UA finding for renal calculi

A

Microscopic hematuria

42
Q

Identify the rebal calculi described:

  1. Yellowish to brownish red & moderately hard
  2. Yellow-brown, greasy & resembles an old soap
  3. Pale & friable
  4. Branching/staghorn calculi resembling antlers of a deer
  5. Major constituent of renal calculi
  6. Accompanied by urinary infections involving urea-splitting bacteria (like Proteus vulgaris)
  7. Very hard, dark in color w/ rough surface
  8. Least common calculi (1-2%)
A
  1. Uric acid & urate calculi
  2. Cystine calculi
  3. Phosphate calculi
  4. Triple phosphate calculi
  5. Calcium oxalate
  6. Triple phosphate calculi
  7. Calcium oxalate
  8. Cystine calculi
43
Q

Identify the ff rare calculi:

  1. Assoc. w/ inherited enzyme def & hyperuricemia
  2. Insoluble diuretic; mustard colored stones
  3. Ingestion of silica over a long period of time
  4. Assoc. w/ a genetic disorder w/ an absence of xanthine oxidase
A. Sulfonamide calculi
B. Silica calculi
C. Adenine calculi
D. Triamterene calculi
E. Xanthine calculi
A
  1. C
  2. D
  3. B
  4. E
44
Q

Methods for calculi analysis

A

Optical crystallography, radiograph diffusion, infrared spectroscopy, electron beam analysis, mass spectroscopy

45
Q

If neutrophils are fixed in ____, the ANCA form a perinuclear pattern called p-ANCA

A

Ethanol

46
Q

If neutrophils are fixed with ____, the pattern is granular throughout cytoplasm called c-ANCA

A

Formalin

47
Q

The rate of proteinuria in nephrotic syndrome is ____

A

> 3.5 g/day

48
Q

HLA-B12 antigen has been assoc w/ ______

A

Minimal change dse

49
Q

True or false: renal calculi can be formed in nephrons

A

False. It is formed in calyces & pelvis of kidney, ureters & bladder

50
Q

____ uses high energy shockwaves to break kidney stones into pieces

A

Lithotripsy

51
Q

_____ is often found in stones (~80%)

A

CaOx / mixture of oxalate & calcium phosphate

52
Q

The next common renal calculi constituents after caox

A

Miced calcium phosphate, triple phosphate & uric acid

Analysis of Urine and Other Body Fluids (18 decks)

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