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ANURBF MIDTERM > LESSON 7: RENAL DISEASES > Flashcards

LESSON 7: RENAL DISEASES Flashcards

1
Q

RENAL DISEASES

A

•Glomerular •Tubular •Interstitial

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2
Q

•Majority are of immune origin

A

Glomerular Disorders

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3
Q

•Exposure to chemicals and toxins

A

Glomerular Disorders

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4
Q

•Disruption of the electrical membrane charges

A

Glomerular Disorders

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5
Q

•Deposition of amyloid material from systemic disorders

A

Glomerular Disorders

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6
Q

•Basement membrane thickening

A

Glomerular Disorders

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7
Q

refers to a sterile, inflammatory process that affects the glomerulus and is associated with the finding of blood, protein, and casts in the urine

A

glomerulonephritis

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8
Q

•Immune-mediated

A

NEPHRITIC SYNDROME

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9
Q

•Acute onset of usually grossly visible hematuria

A

NEPHRITIC SYNDROME

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10
Q

•RBC casts

A

NEPHRITIC SYNDROME

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11
Q

•Mild to moderate proteinuria

A

NEPHRITIC SYNDROME

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12
Q

•Hypertension

A

NEPHRITIC SYNDROME

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13
Q

•Oliguria

A

NEPHRITIC SYNDROME

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14
Q

Deposition of immune complexes, formed in conjunction of Group A Streptococcus infection on the glomerular membranes

A

Acute PoststreptococcalGlomerulonephritis

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15
Q

•Deposition of immune complexes from systemic immune disorders (ex: SLE) on the glomerular membrane

A

Rapidly Progressive (Crescentic) Glomerulonephritis

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16
Q

•Deposition of antiglomerularbasement membrane antibody to glomerular and alveolar basement membranes.

A

GoodpastureSyndrome

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17
Q

•causes a granuloma-producing inflammation of the small blood vessels of primarily the kidney and respiratory system

A

Wegener’s Granulomatosis

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18
Q

•Dx: (+)Antineutrophiliccytoplasmic antibody (ANCA)

A

Wegener’s Granulomatosis

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19
Q

•Occurs in children following viral respiratory infections

A

Henoch-SchonleinPurpura

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20
Q

•Allergic purpurathat causes decrease in the number of platelets and affects vascular integrity

A

Henoch-Schonlein Purpura

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21
Q

•Apronounced thickening of the glomerular basement membrane resulting from the deposition of IgGimmune complexes

A

Membranous Glomerulonephritis

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22
Q

•Seen in SLE, Sjogren’ssyndrome, secondary syphilis and hepatitis B infection

A

Membranous Glomerulonephritis

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23
Q

•Cellular proliferation affecting capillary walls or the glomerular basement membrane

A

Membranoproliferative Glomerulonephritis(MPGN)

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24
Q

•Gradual worsening of symptoms leading to loss of kidney function

A

Chronic Glomerulonephritis

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25
Q

•Progression to renal failure

A

Chronic Glomerulonephritis

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26
Q

(result of tubular dysfunction)

A

Glucosuria

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27
Q

•most common cause of glomerulonephritis

A

IgA nephropathy/Berger’s Disease

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28
Q

•IgA deposition on the glomerular membrane leading to thickening

A

IgA nephropathy/Berger’s Disease

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29
Q

•Disruption of the electrical charges of the basement membrane leading to massive loss of proteins and lipids

A

NephroticSyndrome

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30
Q

•Genetic disorder showing lamellatedand thinning of glomerular basement membrane.

A

AlportSyndrome

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31
Q

•Lipid nephrosis

A

Minimal Change Disease

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32
Q

•Little cellular changes

A

Minimal Change Disease

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33
Q

•Disruption of podocytesoccurring primarily in children following allergic reactions and immunizations

A

Minimal Change Disease

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34
Q

•Most common cause of end-stagerenal disease

A

Diabetic Nephropathy/Kimmelstiel-Wilson

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35
Q

•Glomerular membrane thickening

A

Diabetic Nephropathy/Kimmelstiel-Wilson

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36
Q

•Increased proliferation of mesangialcells

A

Diabetic Nephropathy/Kimmelstiel-Wilson

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37
Q

•Increased deposition of cellular and noncellularmaterials

A

Diabetic Nephropathy/Kimmelstiel-Wilson

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38
Q

•Deposition of glycosylated proteins on the glomerular basement membranes caused by poorly controlled blood glucose levels

A

Diabetic Nephropathy/Kimmelstiel-Wilson

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39
Q

•actual damage to the tubules and those in which a metabolic or hereditary disorder affects the intricate functions of the tubules.

A

Tubular Disorders

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40
Q

•Damage to the renal tubular epithelial cells due to ischemiaand nephrotoxic agents

A

Acute Tubular Necrosis

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41
Q

•Odorless urine

A

Acute Tubular Necrosis

42
Q

•Failure of tubular reabsorption in the PCT (glucose, amino acids, phosphorus, sodium, potassium, bicarbonate and water)

A

Fanconi’sSyndrome

43
Q

Cystinosis; Hartnupdisease

A

Fanconi’sSyndrome

44
Q

a.Neurogenic DI –failure of the hypothalamus to produce ADH

A

Diabetes Insipidus

45
Q

b.NephrogenicDI –renal tubules fail to respond to ADH

A

Diabetes Insipidus

46
Q

•Inherited defect in the production of uromodulinby the renal tubules

A

Uromodulin-associated kidney disease (UKD)

47
Q

•Increased uric acid causing gout

A

Uromodulin-associated kidney disease (UKD)

48
Q

•Normal uromodulinis replaced by abnormal forms that destroy the RTE cells

A

Uromodulin-associated kidney disease (UKD)

49
Q

•Inherited autosomal recessive trait

A

Renal Glycosuria

50
Q

•Normal blood glucose

A

Renal Glycosuria

51
Q

•Increased urine glucose due to defective tubular reabsorption

A

Renal Glycosuria

52
Q

•Disorders affecting the interstitiumalso affects the tubulesdue to their close proximity

A

C. TUBULOINTERSTITIAL DISEASES

53
Q

•Majority of these disorders involve infectionsand inflammatory conditions

A

C. TUBULOINTERSTITIAL DISEASES

54
Q

•Lower UTI

A

Cystitis

55
Q

•Bacterial infection of the urinary bladder

A

Cystitis

56
Q

•Upper UTI

A

Acute Pyelonephritis

57
Q

•Infection of the renal tubules and interstitiumrelated to interference of urine flow to the bladder, reflux of urine from the bladderand untreated cystitis

A

Acute Pyelonephritis

58
Q

•Recurrent infection of the renal tubules and interstitium caused by structualabnormalities affecting the flow of urine.

A

Chronic Pyelonephritis

59
Q

•Allergic inflammation of the renal interstitiumin response to certain medications

A

Acute Interstitial Nephritis

60
Q

•PROGRESSION TO END-STAGE RENAL DISEASE:
•Marked decreased in GFR(<25mL/min)
•Steady rise in BUN AND CREATININE(azotemia)
•Electrolyte imbalance
•Lack of renal concentrating ability producing an isosthenuricurine •Proteinuria, Renal glycosuria
•TELESCOPED URINE SEDIMENTS

A

RENAL FAILURE

61
Q

•GENERAL CHARACTERISTICS:
•Decreased GFR
•OLOGURIA
•Edema
•Azotemia

A

ACUTE RENAL FAILURE

62
Q

Decreased blood pressure/cardiac output

A

PRERENAL

63
Q

Hemorrhage

A

PRERENAL

64
Q

Burns

A

PRERENAL

65
Q

Surgery

A

PRERENAL

66
Q

Septicemia

A

PRERENAL

67
Q

Acute glomerulonephritis

A

RENAL

68
Q

Acute tubular necrosis

A

RENAL

69
Q

Acute pyelonephritis

A

RENAL

70
Q

Acute interstitial nephritis

A

RENAL

71
Q

Renal calculi

A

POSTRENAL

72
Q

Tumors

A

POSTRENAL

73
Q

Crystallization of ingested substances

A

POSTRENAL

74
Q

•Formation of stones in the renal calyces, renal pelvis, ureters and bladder

A

Renal Calculi/Lithiasis

75
Q

•May be passed in the urine and obstruct the urinary tract

A

Renal Calculi/Lithiasis

76
Q

-Major constituent of renal calculi

A

a. Calcium oxalate/phosphate (~75%)

77
Q

-Very hard, dark in color with rough surface

A

a. Calcium oxalate/phosphate (~75%)

78
Q

-May be due to metabolic disorders or diet

A

a. Calcium oxalate/phosphate (~75%)

79
Q

: -Frequently accompanied by UTI involving urea-splitting bacteria

A

b. Magnesium ammonium phosphate

80
Q

-Formed in the pelvis –resembling antlers of deer

A

b. Magnesium ammonium phosphate

81
Q

:-associated with increased intake of foods with high purine content

A

c. Uric acid

82
Q

-Yellowish to brownish red and moderately hard

A

c. Uric acid

83
Q

-seen in conjunction with hereditary disorders of cysteine metabolism

A

d. Cystine

84
Q

-Yellow-brown, greasy and resembles an old soap

A

d. Cystine

85
Q

-Least common calculi (1-2%)

A

d. Cystine

86
Q

-a procedure using high-energy shock waves, can be used to break stones located in the upper urinary tract into pieces that can then be passed in the urine. Surgical removal also can be employed.

A

LITHOTRIPSY

87
Q

•Glycosuria

A

Fanconi’sSyndrome

88
Q

•Possible mild proteinuria

A

Fanconi’sSyndrome

89
Q

•Low specific gravity

A

Diabetes Insipidus

90
Q

•Polyuria

A

Diabetes Insipidus

91
Q

•Pale yellow color of urine

A

Diabetes Insipidus

92
Q

–failure of the hypothalamus to produce ADH

A

Neurogenic DI

93
Q

–renal tubules fail to respond to ADH

A

Nephrogenic DI

94
Q

•RTE cells

A

Uromodulin-associated kidney disease (UKD)

95
Q

•Hyperuricemia

A

Uromodulin-associated kidney disease (UKD)

96
Q

•+ WBCs

A
97
Q

•+ Bacteria

A
98
Q
A

Ik

99
Q

•Mild proteinuria

A
100
Q

•Increased pH

A

ANURBF MIDTERM (10 decks)

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