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
2
Q
Rapid onset of hematuria and edema
Permanent renal damage seldom occurs
A
Acute Glomerulonephritis
3
Q
Urinalysis Results for Acute Glomerulonephritis
A
Macroscopic hematuria
Proteinuria
Red blood cell casts
Oliguria
Granular casts
4
Q
Significant Test for Acute Glomerulonephritis
A
Anti-streptolysin O titer
Anti-Group A Streptococcal enzyme
5
Q
Deposition of immune complex from System immune disorders on the glomerular membrane
A
Rapidly Progressive (Crescentic) Glomerulonephritis
6
Q
Rapid onset with glomerular damage
Possible progression to End-stage renal failure
A
Rapidly Progressive (Crescentic) Glomerulonephritis
7
Q
Urinalysis Results for Rapidly Progressive (Crescentic) Glomerulonephritis
A
Macroscopic hematuria
Proteinuria
Red blood cell casts
8
Q
Significant Test for Rapidly Progressive (Crescentic) Glomerulonephritis
A
Blood Urea Nitrogen
Creatinine
Creatinine Clearance
9
Q
Attachment of Cytotoxic Antibody formed during viral respiratory infections to glomerular and alveolar basement membranes
A
Goodpasture Syndrome
10
Q
Hemoptysis and Dyspnea, followed by Hematuria
Possible progression to End-stage renal failure
A
Goodpasture Syndrome
11
Q
Urinalysis Result of Goodpasture Syndrome
A
Macroscopic hematuria
Proteinuria
Red blood cell casts
12
Q
Significant Test for Goodpasture Syndrome
A
Anti-Glomerular Basement Membrane Antibody
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
14
Q
Pulmonary symptoms including Hemoptysis, followed by Renal Involvement
Possible progression to End-stage renal
failure
A
Wegener’s Granulomatosis
15
Q
Urinalysis Results for Wegener’s Granulomatosis
A
Macroscopic hematuria
Proteinuria
Red blood cell casts
16
Q
Significant Test for Wegener’s Granulomatosis
A
Anti-neutrophilic Cytoplasmic Antibody
17
Q
Occurs primarily in children following viral respiratory infections
Decrease in platelets disrupts vascular integrity
A
Henoch-Schonlein purpura
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
19
Q
Urinalysis Results for Henoch-Schonlein purpura
A
Macroscopic hematuria
Proteinuria
Red blood cell casts
20
Q
Significant Test for Henoch-Schonlein purpura
A
Stool occult blood
21
Q
Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA
A
IgA Nephropathy “Berger’s Disease”
22
Q
Recurrent macroscopic hematuria following exercise with slow progression to chronic glomerulonephritis
A
IgA Nephropathy “Berger’s Disease”
23
Q
Urinary Results for IgA Nephropathy “Berger’s Disease”
A
EARLY STAGES:
Macro/microscopic hematuria
LATE STAGES:
Chronic glomerulonephritis
24
Q
Significant Test for IgA Nephropathy “Berger’s Disease”
A
Serum immunoglobulin A
25
Thickening of the glomerular membrane following IgG immune complex deposition
Membranous Glomerulonephritis
26
Slow progression to Nephritic Syndrome or possible remission
Membranous Glomerulonephritis
27
Urinary Results for Membranous Glomerulonephritis
Macroscopic hematuria
Proteinuria
28
Significant Test for Membranous Glomerulonephritis
Antinuclear antibody
Hepatitis B Surface Antigen
Fluorescent treponemal antibody absorbent test (FTA-ABS)
29
Cellular proliferation affecting the capillary walls or the glomerular basement membrane
Possibly immune mediated
Membranoproliferative Glomerulonephritis
“TRAM TRACKING PATTERN OF THE GLOMERULUS”
30
Noticeable progression to Chronic Glomerulonephritis to Nephritis Syndrome
Membranoproliferative Glomerulonephritis
31
Urinalysis Results for Membranoproliferative Glomerulonephritis
Hematuria
Proteinuria
32
Significant Test for Membranoproliferative Glomerulonephritis
Serum complement levels
33
Marked decrease in renal function resulting from glomerular damage precipitated by other renal disorders
Chronic Glomerulonephritis
34
Noticeable decrease in Renal function
progressing to Renal Failure
Chronic Glomerulonephritis
35
Urinalysis Results for Chronic Glomerulonephritis
Hematuria
Proteinuria
Glucosuria
Cellular & Granular casts
Waxy & Broad casts
36
Significant Test for Chronic Glomerulonephritis
Blood Urea Nitrogen
Serum
Creatine
Creatinine clearance
Electrolytes
37
Disruption of the electrical charges that produce the tightly fitting podocyte barrier resulting in massive loss of protein and lipids
Nephrotic Syndrome
38
Acute onset following systemic shock
Gradual progression from other glomerular disorders and the to renal failure
Nephrotic Syndrome
39
Urinalysis Results for Nephrotic Syndrome
Heavy proteinuria
Microscopic hematuria
Renal tubular cells
Oval fat bodies
Fat droplets
Fatty and waxy casts
40
Significant Tests for Nephrotic Syndrome
Serum albumin
Cholesterol
Triglycerides
41
Disruption of podocytes occurring primarily in children following ALLERGIC REACTIONS and IMMUNIZATION
Minimal Change disease “Lipid nephrosis”
42
Frequent complete remission following corticosteroid treatment
Minimal Change disease “Lipid nephrosis”
43
Urinary Results for Minimal Change disease “Lipid nephrosis”
Heavy proteinuria
Transient hematuria
Fat droplets
44
Significant Test for Minimal Change disease “Lipid nephrosis”
Serum albumin
Cholesterol
Triglycerides
45
Disruption of podocytes in certain areas of glomeruli associated with
Heroin and Analgesic abuse and acquired immunodeficiency syndrome
Focal Segmental Glomerulosclerosis
46
May resemble nephrotic syndrome or minimal change disease
Focal Segmental Glomerulosclerosis
47
Genetic disorder showing lamellated and thinning of glomerular basement membrane
Alport Syndrome
48
Slow progression to nephritic syndrome and end stage renal disease
Alport Syndrome
49
Urinalysis Results for Alport Syndrome
See Nephrotic syndrome
50
Most common cause of ESRD
Deposition of glycosylated proteins on glomerular basement membranes caused by poorly controlled blood glucose levels
Diabetic Nephropathy “Kimmelstiel-Wilson Disease”
51
Urinary Results for Diabetic Nephropathy
(+) Microalbuminuria
(+) Micral test
52
NEPHROTIC SYNDROME
URINE FINDINGS
1. Proteinuria
2. Lipiduria
3. Hematuria
4. Cylindruria (fatty cast)
53
NEPHROTIC SYNDROME
PLASMA/BLOOD FINDINGS
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
TUBULAR DISORDERS
1. Acute Tubular Necrosis
2. Fanconi Syndrome
3. Diabetes Insipidus
4. Renal Glucosuria
55
INTERSTITIAL DISORDERS
1. Cystitis (Lower UTI)
2. Acute Pyelonephritis (Upper UTI)
3. Chronic Pyelonephritis
4. Acute Interstitial Nephritis
56
Damage to renal tubular cells caused by ischemic or toxic agents
Acute Tubular Necrosis
57
Conditions producing tubular necrosis:
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
Findings for Acute Tubular Necrosis
Microscopic hematuria
Hyaline, Granular, Waxy, and Broad Cast
RTE CELLS & CASTS
Odorless urine
Isosthenuria
59
Generalized failure of tubular reaction in the
Proximal Convoluted tubule
Fanconi Syndrome
60
Findings for Fanconi Syndrome
Glucosuria
Cystinuria
Proteinuria
Phosphaturia
Very low urinary pH (due to failure to reabsorb bicarbonate)
61
Failure to produce ADH (hypothalamus)
Low ADH
Neurogenic Diabetes Insipidus
62
Inability to respond to ADH (renal tubules)
Normal to increased ADH
Nephrogenic Diabetes Insipidus
63
Findings for Diabetes Insipidus
Low specific gravity urine
Polyuria
64
Defective tubular reabsorption of glucose
Renal Glucosuria
65
Findings for Renal Glucosuria
Normal blood glucose
Increase urinary glucose
66
Ascending bacterial infection of the urinary bladder
Cystitis (Lower UTI)
67
Findings for Cystitis (Lower UTI)
WBC
Bacteria
Microscopic hematuria
Mild proteinuria
Increase urine pH
68
Infection of the renal tubules and interstitium
related to interference of urine flow to the bladder
Untreated cystitis
Acute Pyelonephritis (Upper UTI)
69
– Reflux of urine from the bladder
VESICOURETERAL REFLUX
70
Findings for Acute Pyelonephritis (Upper UTI)
WBC
Bacteria
WBC & Bacterial cast
Microscopic hematuria
Proteinuria
71
Recurrent infection of the renal tubules and
interstitium caused by structural abnormalities
affecting the flow of urine
Chronic Pyelonephritis
72
Findings for Chronic Pyelonephritis
WBC
Bacteria
WBC & Bacterial cast
Granular, waxy, broad cast
Hematuria & Proteinuria
73
Allergic inflammation of the renal interstitium in response to certain medication
Acute Interstitial Nephritis
74
Findings for Acute Interstitial Nephritis
Hematuria & Proteinuria
WBC (increase eosinophil)
WBC cast
NO BACTERIA
75
PCT Dysfunction
Impaired ability to reabsorb Glucose
Renal Glucosuria
76
PCT Dysfunction
Impaired ability to reabsorb Cystine & dibasic amino acids
Cystinuria
77
PCT Dysfunction
Impaired ability to reabsorb Glycine or mono amino-monocarboxylic amino acids
Hartnup disease
78
PCT Dysfunction
Impaired ability to reabsorb Sodium
Bartter's Disease
79
PCT Dysfunction
Impaired ability to reabsorb Bicarbonate
Renal Tubular Acidosis Type II
80
PCT Dysfunction
Impaired ability to reabsorb Calcium
Idiopathic hypercalciuria
81
PCT Dysfunction
Excessive reabsorption of Calcium
Hypocalciuric familial hypercalcemia
82
PCT Dysfunction
Excessive reabsorption of Sodium
Gordon's Syndrome
83
PCT Dysfunction
Excessive reabsorption of Phosphate
Pseudohypoparathyroidism
84
DCT Dysfunction
Impaired ability to reabsorb Phosphate
Familial hypophosphatemia (vitamin D - resistant rickets)
85
DCT Dysfunction
Impaired ability to reabsorb Calcium
Idiopathic hypercalciuria
86
DCT Dysfunction
Impaired ability to Acidify
Renal Tubular acidosis type I & IV
87
DCT Dysfunction
Impaired ability to Retain
Renal salt-losing disorders
88
DCT Dysfunction
Impaired ability to Concentrate Urine
Nephrogenic diabetes
89
DCT Dysfunction
Excessive absorption of SODIUM
Liddle's Syndrome
90
GLOMERULAR DISORDERS (ADDENDUM)
Some forms may demonstrate increased fibrin degradation products, cryoglobulins, and the deposition of IgA immune complexes in the glomerulus
Rapidly progressive (Crescentic) Glomerulonephritis
91
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
Goodpasture's Syndrome
92
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
Henoch-schonlein purpura
93
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
Membranous Glumerulonephritis
94
GLOMERULAR DISORDERS (ADDENDUM)
Marked by two different alterations in the
cellularity of the glomerulus and peripheral
capillaries.
Membranoproliferative Glomerulonephritis
95
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
Membranoproliferative Glomerulonephritis Type 1
96
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
Membranoproliferative Glomerulonephritis Type 2
97
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
Focal Segmental Glomerulosclerosis
98
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
IgA Nephropathy
99
Characterized clinically by a SUDDEN decrease in the GFR, azotemia, and oliguria
Nephrons are "functionally” abnormal, no histologic abnormality is usually present
Usually, REVERSIBLE
Acute Renal Failure (ARF)
100
Primary causes of ARF include:
a sudden decrease in blood flow to the kidney (prerenal)
acute glomerular and tubular disease (renal)
renal calculi or tumor obstructions (postrenal)
101
the most common cause of Acute Renal Failure
Ischemic acute tubular necrosis
102
Causes of Acute Renal Failure
PRE-RENAL
Decreased blood pressure
Decreased cardiac output
Hemorrhage
Burns
Surgery
Septicemia
103
Causes of Acute Renal Failure
RENAL
Acute glomerulonephritis
Acute tubular necrosis
Acute pyelonephritis
Acute interstitial nephritis
104
Causes of Acute Renal Failure
POST-RENAL
Renal calculi
Tumors
105
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
Chronic Renal Failure
106
CRF is associated with:
Azotemia
Acid-base imbalance
Water and electrolyte imbalance
Abnormal calcium and phosphorus metabolism
106
Urinalysis findings associated with end-stage renal disease include 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
Progression to end-stage renal disease is characterized by:
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
Mostly formed during summer season
are found primarily in the renal calyces, pelvis, ureter, or bladder
Renal Calculi / Renal Stones/ Renal Lithiasis
109
Primary Microscopic Finding for Renal Calculi
Hematuria
110
Renal Calculi may be of various sizes, commonly described as:
- Sand
- Gravel
- Stone
111
Conditions Favoring/Enhancing Formation of Renal calculi:
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
Major constituent of renal calculi
Very hard, dark brown color with rough
surface
Calcium Oxalate
113
Associated with increase intake of foods
with high purine content, and
uromodulin-associated kidney
Yellowish to brownish red and
moderately hand
Uric Acid
114
Seen in hereditary disorders of cystine
metabolism
Yellow brown, greasy and resembles an
old soap
Least common calculi (1-2%)
Cystine
115
Pale and friable constituent of Renal Calculi
Phosphate
116
ADDITIONAL INFO for RENAL CALCULI
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
Simultaneous appearance of the elements of acute/chronic glomerulonephritis, ESRD and nephrotic syndrome
Telescoped Sediments
118
A telescoped sediment might therefore include:
red blood cells
red blood cell casts
cellular casts
broad waxy casts
lipid droplets
oval fat bodies
fatty casts
119
Telescoped sediment may be found in
COLLAGEN VASCULAR DISEASE (notably lupus nephritis) and SUBACUTE BACTERIAL ENDOCARDITIS
120
Associated with strenuous exercise such as marathon running
Normal /physiologic condition characterized by appearance of CELLS AND CASTS (shower of cast) in urine
Athletic Pseudonephritis
121
Athletic Pseudonephritis is positive in
RBC WBC
Granular cast
Hyaline cast
