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AUBF - Lec > UNIT 7 - Renal Disorders > Flashcards

UNIT 7 - Renal Disorders Flashcards

1
Q

Deposition of immune complex formed in conjunction with Group A Streptococcus infection on the glomerular membranes

A

Acute Glomerulonephritis

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2
Q

Rapid onset of hematuria and edema

Permanent renal damage seldom occurs

A

Acute Glomerulonephritis

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3
Q

Urinalysis Results for Acute Glomerulonephritis

A

 Macroscopic hematuria
 Proteinuria
 Red blood cell casts
 Oliguria
 Granular casts

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4
Q

Significant Test for Acute Glomerulonephritis

A

 Anti-streptolysin O titer
 Anti-Group A Streptococcal enzyme

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5
Q

Deposition of immune complex from System immune disorders on the glomerular membrane

A

Rapidly Progressive (Crescentic) Glomerulonephritis

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6
Q

Rapid onset with glomerular damage

Possible progression to End-stage renal failure

A

Rapidly Progressive (Crescentic) Glomerulonephritis

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7
Q

Urinalysis Results for Rapidly Progressive (Crescentic) Glomerulonephritis

A

 Macroscopic hematuria
 Proteinuria
 Red blood cell casts

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8
Q

Significant Test for Rapidly Progressive (Crescentic) Glomerulonephritis

A

 Blood Urea Nitrogen
 Creatinine
 Creatinine Clearance

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9
Q

Attachment of Cytotoxic Antibody formed during viral respiratory infections to glomerular and alveolar basement membranes

A

Goodpasture Syndrome

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10
Q

Hemoptysis and Dyspnea, followed by Hematuria

Possible progression to End-stage renal failure

A

Goodpasture Syndrome

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11
Q

Urinalysis Result of Goodpasture Syndrome

A

 Macroscopic hematuria
 Proteinuria
 Red blood cell casts

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12
Q

Significant Test for Goodpasture Syndrome

A

 Anti-Glomerular Basement Membrane Antibody

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13
Q

Antineutrophilic Cytoplasmic Autoantibody binds to neutrophils in vascular walls producing damage to small vessels in the
lungs and glomerulus

A

Wegener’s Granulomatosis

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14
Q

Pulmonary symptoms including Hemoptysis, followed by Renal Involvement

Possible progression to End-stage renal
failure

A

Wegener’s Granulomatosis

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15
Q

Urinalysis Results for Wegener’s Granulomatosis

A

 Macroscopic hematuria
 Proteinuria
 Red blood cell casts

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16
Q

Significant Test for Wegener’s Granulomatosis

A

 Anti-neutrophilic Cytoplasmic Antibody

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17
Q

Occurs primarily in children following viral respiratory infections

Decrease in platelets disrupts vascular integrity

A

Henoch-Schonlein purpura

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18
Q
  • Initial appearance of Purpura
  • followed by Blood in SPUTUM and STOOL and
  • eventual Renal involvement

COMPLETE RECOVERY is COMMON but may progress to renal failure

A

Henoch-Schonlein purpura

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19
Q

Urinalysis Results for Henoch-Schonlein purpura

A

 Macroscopic hematuria
 Proteinuria
 Red blood cell casts

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20
Q

Significant Test for Henoch-Schonlein purpura

A

 Stool occult blood

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21
Q

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

A

IgA Nephropathy “Berger’s Disease”

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22
Q

Recurrent macroscopic hematuria following exercise with slow progression to chronic glomerulonephritis

A

IgA Nephropathy “Berger’s Disease”

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23
Q

Urinary Results for IgA Nephropathy “Berger’s Disease”

A

EARLY STAGES:
 Macro/microscopic hematuria

LATE STAGES:
 Chronic glomerulonephritis

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24
Q

Significant Test for IgA Nephropathy “Berger’s Disease”

A

 Serum immunoglobulin A

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25
Q

Thickening of the glomerular membrane following IgG immune complex deposition

A

Membranous Glomerulonephritis

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26
Q

Slow progression to Nephritic Syndrome or possible remission

A

Membranous Glomerulonephritis

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27
Q

Urinary Results for Membranous Glomerulonephritis

A

 Macroscopic hematuria
 Proteinuria

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28
Q

Significant Test for Membranous Glomerulonephritis

A

 Antinuclear antibody
 Hepatitis B Surface Antigen
 Fluorescent treponemal antibody absorbent test (FTA-ABS)

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29
Q

Cellular proliferation affecting the capillary walls or the glomerular basement membrane

Possibly immune mediated

A

Membranoproliferative Glomerulonephritis
“TRAM TRACKING PATTERN OF THE GLOMERULUS”

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30
Q

Noticeable progression to Chronic Glomerulonephritis to Nephritis Syndrome

A

Membranoproliferative Glomerulonephritis

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31
Q

Urinalysis Results for Membranoproliferative Glomerulonephritis

A

 Hematuria
 Proteinuria

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32
Q

Significant Test for Membranoproliferative Glomerulonephritis

A

 Serum complement levels

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33
Q

Marked decrease in renal function resulting from glomerular damage precipitated by other renal disorders

A

Chronic Glomerulonephritis

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34
Q

Noticeable decrease in Renal function
progressing to Renal Failure

A

Chronic Glomerulonephritis

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35
Q

Urinalysis Results for Chronic Glomerulonephritis

A

 Hematuria
 Proteinuria
 Glucosuria
 Cellular & Granular casts
 Waxy & Broad casts

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36
Q

Significant Test for Chronic Glomerulonephritis

A

 Blood Urea Nitrogen
 Serum
 Creatine
 Creatinine clearance
 Electrolytes

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37
Q

Disruption of the electrical charges that produce the tightly fitting podocyte barrier resulting in massive loss of protein and lipids

A

Nephrotic Syndrome

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38
Q

Acute onset following systemic shock

Gradual progression from other glomerular disorders and the to renal failure

A

Nephrotic Syndrome

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39
Q

Urinalysis Results for Nephrotic Syndrome

A

 Heavy proteinuria
 Microscopic hematuria
 Renal tubular cells
 Oval fat bodies
 Fat droplets
 Fatty and waxy casts

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40
Q

Significant Tests for Nephrotic Syndrome

A

 Serum albumin
 Cholesterol
 Triglycerides

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41
Q

Disruption of podocytes occurring primarily in children following ALLERGIC REACTIONS and IMMUNIZATION

A

Minimal Change disease “Lipid nephrosis”

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42
Q

Frequent complete remission following corticosteroid treatment

A

Minimal Change disease “Lipid nephrosis”

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43
Q

Urinary Results for Minimal Change disease “Lipid nephrosis”

A

 Heavy proteinuria
 Transient hematuria
 Fat droplets

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44
Q

Significant Test for Minimal Change disease “Lipid nephrosis”

A

 Serum albumin
 Cholesterol
 Triglycerides

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45
Q

Disruption of podocytes in certain areas of glomeruli associated with

Heroin and Analgesic abuse and acquired immunodeficiency syndrome

A

Focal Segmental Glomerulosclerosis

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46
Q

May resemble nephrotic syndrome or minimal change disease

A

Focal Segmental Glomerulosclerosis

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47
Q

Genetic disorder showing lamellated and thinning of glomerular basement membrane

A

Alport Syndrome

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48
Q

Slow progression to nephritic syndrome and end stage renal disease

A

Alport Syndrome

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49
Q

Urinalysis Results for Alport Syndrome

A

See Nephrotic syndrome

50
Q

Most common cause of ESRD

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

A

Diabetic Nephropathy “Kimmelstiel-Wilson Disease”

51
Q

Urinary Results for Diabetic Nephropathy

A

 (+) Microalbuminuria
 (+) Micral test

52
Q

NEPHROTIC SYNDROME
URINE FINDINGS

A
  1. Proteinuria
  2. Lipiduria
  3. Hematuria
  4. Cylindruria (fatty cast)
53
Q

NEPHROTIC SYNDROME
PLASMA/BLOOD FINDINGS

A
  1. Increase A2-Macroglobulin in electrophoresis
  2. Hypoproteinemia & Hypoalbuminemia
  3. Hyperlipidemia
  4. Increase PLASMA SODIUM & WATER level due to increase water and sodium reabsorption in the kidney that will eventually lead to Edema
54
Q

TUBULAR DISORDERS

A
  1. Acute Tubular Necrosis
  2. Fanconi Syndrome
  3. Diabetes Insipidus
  4. Renal Glucosuria
55
Q

INTERSTITIAL DISORDERS

A
  1. Cystitis (Lower UTI)
  2. Acute Pyelonephritis (Upper UTI)
  3. Chronic Pyelonephritis
  4. Acute Interstitial Nephritis
56
Q

Damage to renal tubular cells caused by ischemic or toxic agents

A

Acute Tubular Necrosis

57
Q

Conditions producing tubular necrosis:

A

 Exposure to heavy metals
 Drug-induced toxicity
 Hemoglobin & myoglobin toxicity
 Viral infections (hepatitis B)
 Pyelonephritis
 Allergic reactions
 Malignant infiltrations
 Salicylate poisoning
 Acute allogenic transplant rejection

58
Q

Findings for Acute Tubular Necrosis

A

 Microscopic hematuria
 Hyaline, Granular, Waxy, and Broad Cast
 RTE CELLS & CASTS
 Odorless urine
 Isosthenuria

59
Q

Generalized failure of tubular reaction in the
Proximal Convoluted tubule

A

Fanconi Syndrome

60
Q

Findings for Fanconi Syndrome

A

 Glucosuria
 Cystinuria
 Proteinuria
 Phosphaturia
 Very low urinary pH (due to failure to reabsorb bicarbonate)

61
Q

 Failure to produce ADH (hypothalamus)
 Low ADH

A

Neurogenic Diabetes Insipidus

62
Q

 Inability to respond to ADH (renal tubules)
 Normal to increased ADH

A

Nephrogenic Diabetes Insipidus

63
Q

Findings for Diabetes Insipidus

A

 Low specific gravity urine
 Polyuria

64
Q

Defective tubular reabsorption of glucose

A

Renal Glucosuria

65
Q

Findings for Renal Glucosuria

A

 Normal blood glucose
 Increase urinary glucose

66
Q

Ascending bacterial infection of the urinary bladder

A

Cystitis (Lower UTI)

67
Q

Findings for Cystitis (Lower UTI)

A

 WBC
 Bacteria
 Microscopic hematuria
 Mild proteinuria
 Increase urine pH

68
Q

Infection of the renal tubules and interstitium
related to interference of urine flow to the bladder

Untreated cystitis

A

Acute Pyelonephritis (Upper UTI)

69
Q

– Reflux of urine from the bladder

A

VESICOURETERAL REFLUX

70
Q

Findings for Acute Pyelonephritis (Upper UTI)

A

 WBC
 Bacteria
 WBC & Bacterial cast
 Microscopic hematuria
 Proteinuria

71
Q

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

A

Chronic Pyelonephritis

72
Q

Findings for Chronic Pyelonephritis

A

 WBC
 Bacteria
 WBC & Bacterial cast
 Granular, waxy, broad cast
 Hematuria & Proteinuria

73
Q

Allergic inflammation of the renal interstitium in response to certain medication

A

Acute Interstitial Nephritis

74
Q

Findings for Acute Interstitial Nephritis

A

 Hematuria & Proteinuria
 WBC (increase eosinophil)
 WBC cast
 NO BACTERIA

75
Q

PCT Dysfunction

Impaired ability to reabsorb Glucose

A

Renal Glucosuria

76
Q

PCT Dysfunction

Impaired ability to reabsorb Cystine & dibasic amino acids

A

Cystinuria

77
Q

PCT Dysfunction

Impaired ability to reabsorb Glycine or mono amino-monocarboxylic amino acids

A

Hartnup disease

78
Q

PCT Dysfunction

Impaired ability to reabsorb Sodium

A

Bartter’s Disease

79
Q

PCT Dysfunction

Impaired ability to reabsorb Bicarbonate

A

Renal Tubular Acidosis Type II

80
Q

PCT Dysfunction

Impaired ability to reabsorb Calcium

A

Idiopathic hypercalciuria

81
Q

PCT Dysfunction

Excessive reabsorption of Calcium

A

Hypocalciuric familial hypercalcemia

82
Q

PCT Dysfunction

Excessive reabsorption of Sodium

A

Gordon’s Syndrome

83
Q

PCT Dysfunction

Excessive reabsorption of Phosphate

A

Pseudohypoparathyroidism

84
Q

DCT Dysfunction

Impaired ability to reabsorb Phosphate

A

Familial hypophosphatemia (vitamin D - resistant rickets)

85
Q

DCT Dysfunction

Impaired ability to reabsorb Calcium

A

Idiopathic hypercalciuria

86
Q

DCT Dysfunction

Impaired ability to Acidify

A

Renal Tubular acidosis type I & IV

87
Q

DCT Dysfunction

Impaired ability to Retain

A

Renal salt-losing disorders

88
Q

DCT Dysfunction

Impaired ability to Concentrate Urine

A

Nephrogenic diabetes

89
Q

DCT Dysfunction

Excessive absorption of SODIUM

A

Liddle’s Syndrome

90
Q

GLOMERULAR DISORDERS (ADDENDUM)

 Some forms may demonstrate increased fibrin degradation products, cryoglobulins, and the deposition of IgA immune complexes in the glomerulus

A

Rapidly progressive (Crescentic) Glomerulonephritis

91
Q

GLOMERULAR DISORDERS (ADDENDUM)

 A cytotoxic autoantibody can appear against the glomerular and alveolar basement membranes AFTER VIRAL RESPIRATORY INFECTIONS
 Initial pulmonary complaints are hemoptysis and dyspnea, followed by the development of hematuria

A

Goodpasture’s Syndrome

92
Q

GLOMERULAR DISORDERS (ADDENDUM)

 Disease occurs primarily in children after UPPER RESPIRATORY INFECTIONS. As its name implies, initial symptoms include the appearance of raised, red patches on the skin. Respiratory and gastrointestinal symptoms, including blood in the sputum and stools, may be present

A

Henoch-schonlein purpura

93
Q

GLOMERULAR DISORDERS (ADDENDUM)

 Disorders associated with membranous
glomerulonephritis development include
systemic lupus erythematosus, Sjögren
syndrome, secondary syphilis, hepatitis B, gold
and mercury treatments, and malignancy

A

Membranous Glumerulonephritis

94
Q

GLOMERULAR DISORDERS (ADDENDUM)

 Marked by two different alterations in the
cellularity of the glomerulus and peripheral
capillaries.

A

Membranoproliferative Glomerulonephritis

95
Q

GLOMERULAR DISORDERS (ADDENDUM)

  • displays increased cellularity in the
    subendothelial cells of the mesangium
    (interstitial area of Bowman’s capsule),
    causing thickening of the capillary walls
A

Membranoproliferative Glomerulonephritis Type 1

96
Q

GLOMERULAR DISORDERS (ADDENDUM)

  • displays extremely dense deposits in the
    glomerular basement membrane. Many of
    the patients are children, and the disease
    has a poor prognosis
A

Membranoproliferative Glomerulonephritis Type 2

97
Q

GLOMERULAR DISORDERS (ADDENDUM)

 Affects only certain numbers and areas of
glomeruli, and the others remain normal.
 Symptoms may be similar to the nephrotic
syndrome and minimal change disease owing to damaged podocytes

A

Focal Segmental Glomerulosclerosis

98
Q

GLOMERULAR DISORDERS (ADDENDUM)

 Patients usually present with an episode of
macroscopic hematuria following an infection or strenuous exercise. Disorder may remain essentially asymptomatic for 20 years or more

A

IgA Nephropathy

99
Q

 Characterized clinically by a SUDDEN decrease in the GFR, azotemia, and oliguria
 Nephrons are “functionally” abnormal, no histologic abnormality is usually present
 Usually, REVERSIBLE

A

Acute Renal Failure (ARF)

100
Q

Primary causes of ARF include:

A

 a sudden decrease in blood flow to the kidney (prerenal)
 acute glomerular and tubular disease (renal)
 renal calculi or tumor obstructions (postrenal)

101
Q

the most common cause of Acute Renal Failure

A

Ischemic acute tubular necrosis

102
Q

Causes of Acute Renal Failure

PRE-RENAL

A

 Decreased blood pressure
 Decreased cardiac output
 Hemorrhage
 Burns
 Surgery
 Septicemia

103
Q

Causes of Acute Renal Failure

RENAL

A

 Acute glomerulonephritis
 Acute tubular necrosis
 Acute pyelonephritis
 Acute interstitial nephritis

104
Q

Causes of Acute Renal Failure

POST-RENAL

A

 Renal calculi
 Tumors

105
Q

 PROGRESSIVE loss of renal function caused by an irreversible and intrinsic renal disease characterizes this.

 progresses to an advanced renal disease often termed End Stage Renal Disease or End-Stage Kidneys

A

Chronic Renal Failure

106
Q

CRF is associated with:

A

 Azotemia
 Acid-base imbalance
 Water and electrolyte imbalance
 Abnormal calcium and phosphorus metabolism

106
Q

Urinalysis findings associated with end-stage renal disease include a:

A
  • FIXED SPECIFIC GRAVITY (isosthenuria, at 1.010)
  • significant proteinuria
  • minimal to moderate hematuria
  • the presence of all types of casts, particularly
    waxy and broad cast
107
Q

Progression to end-stage renal disease is characterized by:

A

 marked decrease in the glomerular filtration rate less than 25 mL/min
 steadily rising serum BUN and creatinine values (azotemia);
 electrolyte imbalance; Proteinuria; Renal glycosuria;
 Lack of renal concentrating ability producing an isothenuric urine;
 An abundance of granular, waxy, and broad casts, often referred to as a TELESCOPED URINE SEDIMENT

108
Q

 Mostly formed during summer season
 are found primarily in the renal calyces, pelvis, ureter, or bladder

A

Renal Calculi / Renal Stones/ Renal Lithiasis

109
Q

Primary Microscopic Finding for Renal Calculi

A

Hematuria

110
Q

Renal Calculi may be of various sizes, commonly described as:

A
  • Sand
  • Gravel
  • Stone
111
Q

Conditions Favoring/Enhancing Formation of Renal calculi:

A

a. Urinary pH
b. Chemical/solute concentration
c. Urinary stasis
d. Metabolic disorders (ex. Gout, and inbom error of metabolism)
e. Infections (ex. UTI)
f. Nucleation (initial crystal deposition and formation)
g. Endocrine disorders (ex. Hyperparathyroidism)

112
Q

 Major constituent of renal calculi
 Very hard, dark brown color with rough
surface

A

Calcium Oxalate

113
Q

 Associated with increase intake of foods
with high purine content, and
uromodulin-associated kidney
 Yellowish to brownish red and
moderately hand

A

Uric Acid

114
Q

 Seen in hereditary disorders of cystine
metabolism
 Yellow brown, greasy and resembles an
old soap
 Least common calculi (1-2%)

A

Cystine

115
Q

 Pale and friable constituent of Renal Calculi

A

Phosphate

116
Q

ADDITIONAL INFO for RENAL CALCULI

A
  1. Calcium oxalate or a mixture of oxalate and calcium phosphate is often found in stones 80%
    Mixed calcium phosphate, magnesium ammonium phosphate, and uric acid are the next most common constituents 3% - 10%
    each followed by cystine stones 1% to 2%
  2. Males are more often affected with calcium stones than females, and children are not often affected with calcium stones
  3. Struvite (Triple phosphate) stones may become large, forming casts of the kidney pelvis and showing staghorns
  4. Staghorn calculi resembling the shape of the renal pelvis and smooth, round bladder stones with diameters of 2 or more inches
117
Q

Simultaneous appearance of the elements of acute/chronic glomerulonephritis, ESRD and nephrotic syndrome

A

Telescoped Sediments

118
Q

A telescoped sediment might therefore include:

A

 red blood cells
 red blood cell casts
 cellular casts
 broad waxy casts
 lipid droplets
 oval fat bodies
 fatty casts

119
Q

Telescoped sediment may be found in

A

COLLAGEN VASCULAR DISEASE (notably lupus nephritis) and SUBACUTE BACTERIAL ENDOCARDITIS

120
Q

 Associated with strenuous exercise such as marathon running
 Normal /physiologic condition characterized by appearance of CELLS AND CASTS (shower of cast) in urine

A

Athletic Pseudonephritis

121
Q

Athletic Pseudonephritis is positive in

A

 RBC WBC
 Granular cast
 Hyaline cast

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