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AUBF LEC MIDTERMS > RENAL DISEASES > Flashcards

RENAL DISEASES Flashcards

1
Q

RENAL DISEASES
CLASSIFICATION (5)

A
  • GLOMERULAR DISORDERS
  • TUBULAR DISORDERS
  • INTERSTITIAL DISORDERS
  • RENAL FAILURE
  • RENAL LITHIASIS
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2
Q
  • IMMUNOLOGIC
    +Immune system components produce changes and damage to the membranes (deposition of antibodies, trapped circulating immune complexes)
A

GLOMERULAR DISORDERS

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3
Q

Glomerular injury: caused by ___

A

chemical mediators and toxic substances

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4
Q

SYNDROMES/MANIFESTATIONS THAT INDICATE GLOMERULAR INJURY
* ASYMPTOMATIC:
* SYMPTOMATIC:

A

ASY: HEMATURIA OR PROTEINURIA
SY: ACUTE NEPHRITIC SYNDROME AND NEPHROTIC SYNDROME

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5
Q

Increased permeability to plasma proteins (> 3.5 g/day)

A

NEPHROTIC SYNDROME

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6
Q

GLOMERULAR DISORDERS
*ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
+Symptoms appear 1-2 weeks following respiratory infections
and 6 weeks after skin infection caused by _____ that contain ____ in the cell wall.

A

group A Streptococcus (1)
M protein (2)

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7
Q

+Major cause of nephrotic syndrome in adults

A

MEMBRANOUS GLOMERULONEPHRITIS

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8
Q

Causes: immune complex formation in glomerulus or deposition of complement; associated with persistent hepatitis C, autoimmune diseases, and cancer

A

*MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

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9
Q

GLOMERULAR DISORDERS
*MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

+Increased cellularity in the subendothelial cells of the
mesangium, causing _____

A

thickening of the capillary walls and
extremely dense deposits in the GBM

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10
Q

+ Glomerulus looks normal in light microscopy but there is loss
of podocyte foot processes in electron microscopy

A

MINIMAL CHANGE DISEASE

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11
Q

Major cause of nephrotic syndrome in children

A

MINIMAL CHANGE DISEASE

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12
Q

+Affects only certain numbers and areas of glomeruli
(sclerosis/scar tissue)

A

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

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13
Q

+Deposition of immune complexes containing IgA in the glomerular membrane or in situ formation of immune complexes after deposition of galactose-deficient IgA

A

IMMUNOGLOBULIN A (IgA) NEPHROPATHY

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14
Q

Similar pathophysiology and renal presentation with IgA nephropathy BUT…HSP also shows signs of systemic
vasculitis, younger patients, preceding infection, and abdominal complaints

A

ENOCH-SCHONLEIN PURPURA/IgA VASCULITIS

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15
Q

+ Progression of previously discussed glomerular disorders
+ Depends on the amount and duration of the damage to the glomerulus

A

CHRONIC GLOMERULONEPHRITIS

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16
Q

+Cytotoxic autoantibody (antiglomerular basement membrane
antibody) against the glomerular basement membranes after
viral respiratory infections
+If with lung hemorrhage (Goodpasture’s syndrome)

A

ANTIGLOMERULAR BASEMENT MEMBRANE DISEASE

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17
Q

+Causes a granuloma-producing inflammation of the small
blood vessels of the kidney and respiratory system
* MICROSCOPIC POLYANGIITIS: same but w/o granuloma
formation

A
  • WEGENER GRANULOMATOSIS/GRANULOMATOSIS WITH POLYANGIITIS
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18
Q

TESTING for ANCA
+ Common in Churg-Strauss and microscopic polyangiitis

A

p-ANCA

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19
Q

TESTING for ANCA
+ Common in Wegener’s

A

+ c-ANCA: granular pattern throughout the cytoplasm (directed against
proteinase 3)

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20
Q

+Like Wegener’s but with elevated eosinophils (severe asthma)
+Most accurate test is lung biopsy showing granulomas and eosinophils

A

EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS/CHURG-STRAUSS VASCULITIS

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21
Q

+Most common hereditary nephritis
+Inherited disorder of collagen production affecting the GBM

A

ALPORT SYNDROME

22
Q

Deposition of amyloid in the glomeruli
* Primary amyloidosis (AL amyloidosis): deposition of Ig light
chains in plasma cell dyscrasias

A

AMYLOIDOSIS

23
Q

+ Common autoantibodies: ANA or antinuclear antibody (best screening test) and anti-dsDNA or anti-double stranded DNA
+ Kidney involvement is usually its most serious manifestation
* Microscopic hematuria and proteinuria

A

SYSTEMIC LUPUS ERYTHEMATOSUS/LUPUS NEPHRITIS

24
Q

An autoimmune disease in which organs and cells undergo damage initially mediated by tissue-binding autoantibodies and immune complexes followed by destruction mediated by complement activation and release of cytokines/chemokines

A

SYSTEMIC LUPUS ERYTHEMATOSUS/LUPUS NEPHRITIS (SAME PARIN IKAW JUD)

25
Q

+Thickening of GBM (due to the loss of heparan sulfate) and expansion of the mesangium due to the accumulation of extracellular matrix

A

DIABETIC NEPHROPATHY

26
Q
  • May be due to actual damage to tubules (infection or toxic
    substances) or if a metabolic or hereditary disorder
    affects the intricate functions of the tubules
A

TUBULAR DISORDERS

27
Q

May be due to decreased blood flow that causes lack of oxygen presentation to the tubules or the presence of nephrotoxic substances in the filtrate

A

ACUTE TUBULAR NECROSIS

28
Q

+ Generalized failure of tubular reabsorption in PCT
+ May be inherited, acquired through exposure to toxic agents, or as a complication of multiple myeloma and renal transplant

A

FANCONI SYNDROME

29
Q

+ Inability of tubules to secrete adequate hydrogen ions despite normal GFR
+ Patients have acidosis but unable to produce an acid urine

A

RENAL TUBULAR ACIDOSIS

30
Q

inability of the PCT to reabsorb sodium

A

+ Bartter’s syndrome

31
Q

excessive sodium reabsorption in the PCT

A

Gordon’s syndrome

32
Q

excessive sodium reabsorption in the DCT

A

+ Liddle’s syndrome

33
Q

+ Inherited disorder caused by an autosomal mutation in the gene
that produces uromodulin
+ Increased production of abnormal uromodulin

A

UROMODULIN KIDNEY DISEASE

34
Q

only protein produced by the kidney

A

Uromodulin

35
Q
  • URINARY TRACT INFECTION
    +Lower UTI: ___ and ___
    +Upper UTI: ___ and ___
A

lower: urethritis and cystitis
upper: pyelitis and pyelonephritis

36
Q

85% of UTI is caused by

A

Gram-negative rods (E. coli, Proteus,
Klebsiella, Enterobacter, Pseudomonas)

37
Q

+ Most frequently occurs because of the ascending movement of
bacteria from a lower UTI into the tubules and interstitium

A

ACUTE PYELONEPHRITIS

38
Q

+Bacteria multiply in the interstitium and cause acute inflammation
+Tubular necrosis
+Bacterial toxins and leukocyte enzymes cause the formation of abscess

A

ACUTE PYELONEPHRITIS

39
Q

+Persistent inflammation of renal tissue and causes permanent scarring

A

CHRONIC PYELONEPHRITIS

40
Q

Cell-mediated immune response that causes damage to the interstitium
and renal tubular epithelium (3-21 days after exposure to the
offending agent)

A

ACUTE INTERSTITIAL NEPHRITIS

41
Q

Occurs when the bacterial flora is disrupted by antibiotics or
pH changes

A

YEAST INFECTIONS

42
Q
  • Renal calculi or kidney stones
  • Vary in size from barely visible to large, staghorn calculi
A

NEPHROLITHIASIS

43
Q

PATHOGENESIS OF STONES
* Conditions favoring the formation of renal calculi: (4)

A

+Chemical concentration or supersaturation of chemical
salts in urine
+Optimal pH
+Urinary stasis
+Nucleation or initial crystal formation

44
Q

NEPHROLITHIASIS
75-85% of calculi are

A

calcium oxalate or calcium phosphate

45
Q

NEPHROLITHIASIS

accompanied by chronic urinary infections involving urea-splitting bacteria, usually Proteus species

A

+ Magnesium ammonium phosphate/struvite/staghorn (5%):

46
Q

NEPHROLITHIASIS

food rich in purine and with uromodulin-associated
kidney disease

A

Uric acid (5-10%)

47
Q

NEPHROLITHIASIS

in conjunction with hereditary disorders of cystine
metabolism

A

Cystine (1%)

48
Q

NEPHROLITHIASIS

medication for HIV patients; poor solubility in physiologic
pH

A

Indinavir

49
Q

+ Sudden loss of renal function caused by sudden decrease in renal blood flow (25%), acute glomerular and tubular disease (65%, 99% of cases is due to ATN), or renal calculi or obstructions (10%, high BCHP equates to low GFR)

A

Acute Renal Failure

50
Q

+ One of the most common causes of acute renal failure in children
+ Commonly occurs after ingestion of meat infected with
verocytotoxin-producing E. coli, most often serotype O157: H7

A
  • HEMOLYTIC-UREMIC SYNDROME
51
Q

+ Progressive loss of renal function caused by an irreversible and
intrinsic renal disease and progresses to end-stage renal disease

A

Chronic Renal Failure

AUBF LEC MIDTERMS (3 decks)

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