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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
•Progression to renal failure
Chronic Glomerulonephritis
26
(result of tubular dysfunction)
Glucosuria
27
•most common cause of glomerulonephritis
IgA nephropathy/Berger’s Disease
28
•IgA deposition on the glomerular membrane leading to thickening
IgA nephropathy/Berger’s Disease
29
•Disruption of the electrical charges of the basement membrane leading to massive loss of proteins and lipids
NephroticSyndrome
30
•Genetic disorder showing lamellatedand thinning of glomerular basement membrane.
AlportSyndrome
31
•Lipid nephrosis
Minimal Change Disease
32
•Little cellular changes
Minimal Change Disease
33
•Disruption of podocytesoccurring primarily in children following allergic reactions and immunizations
Minimal Change Disease
34
•Most common cause of end-stagerenal disease
Diabetic Nephropathy/Kimmelstiel-Wilson
35
•Glomerular membrane thickening
Diabetic Nephropathy/Kimmelstiel-Wilson
36
•Increased proliferation of mesangialcells
Diabetic Nephropathy/Kimmelstiel-Wilson
37
•Increased deposition of cellular and noncellularmaterials
Diabetic Nephropathy/Kimmelstiel-Wilson
38
•Deposition of glycosylated proteins on the glomerular basement membranes caused by poorly controlled blood glucose levels
Diabetic Nephropathy/Kimmelstiel-Wilson
39
•actual damage to the tubules and those in which a metabolic or hereditary disorder affects the intricate functions of the tubules.
Tubular Disorders
40
•Damage to the renal tubular epithelial cells due to ischemiaand nephrotoxic agents
Acute Tubular Necrosis
41
•Odorless urine
Acute Tubular Necrosis
42
•Failure of tubular reabsorption in the PCT (glucose, amino acids, phosphorus, sodium, potassium, bicarbonate and water)
Fanconi’sSyndrome
43
Cystinosis; Hartnupdisease
Fanconi’sSyndrome
44
a.Neurogenic DI –failure of the hypothalamus to produce ADH
Diabetes Insipidus
45
b.NephrogenicDI –renal tubules fail to respond to ADH
Diabetes Insipidus
46
•Inherited defect in the production of uromodulinby the renal tubules
Uromodulin-associated kidney disease (UKD)
47
•Increased uric acid causing gout
Uromodulin-associated kidney disease (UKD)
48
•Normal uromodulinis replaced by abnormal forms that destroy the RTE cells
Uromodulin-associated kidney disease (UKD)
49
•Inherited autosomal recessive trait
Renal Glycosuria
50
•Normal blood glucose
Renal Glycosuria
51
•Increased urine glucose due to defective tubular reabsorption
Renal Glycosuria
52
•Disorders affecting the interstitiumalso affects the tubulesdue to their close proximity
C. TUBULOINTERSTITIAL DISEASES
53
•Majority of these disorders involve infectionsand inflammatory conditions
C. TUBULOINTERSTITIAL DISEASES
54
•Lower UTI
Cystitis
55
•Bacterial infection of the urinary bladder
Cystitis
56
•Upper UTI
Acute Pyelonephritis
57
•Infection of the renal tubules and interstitiumrelated to interference of urine flow to the bladder, reflux of urine from the bladderand untreated cystitis
Acute Pyelonephritis
58
•Recurrent infection of the renal tubules and interstitium caused by structualabnormalities affecting the flow of urine.
Chronic Pyelonephritis
59
•Allergic inflammation of the renal interstitiumin response to certain medications
Acute Interstitial Nephritis
60
•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
RENAL FAILURE
61
•GENERAL CHARACTERISTICS: •Decreased GFR •OLOGURIA •Edema •Azotemia
ACUTE RENAL FAILURE
62
Decreased blood pressure/cardiac output
PRERENAL
63
Hemorrhage
PRERENAL
64
Burns
PRERENAL
65
Surgery
PRERENAL
66
Septicemia
PRERENAL
67
Acute glomerulonephritis
RENAL
68
Acute tubular necrosis
RENAL
69
Acute pyelonephritis
RENAL
70
Acute interstitial nephritis
RENAL
71
Renal calculi
POSTRENAL
72
Tumors
POSTRENAL
73
Crystallization of ingested substances
POSTRENAL
74
•Formation of stones in the renal calyces, renal pelvis, ureters and bladder
Renal Calculi/Lithiasis
75
•May be passed in the urine and obstruct the urinary tract
Renal Calculi/Lithiasis
76
-Major constituent of renal calculi
a. Calcium oxalate/phosphate (~75%)
77
-Very hard, dark in color with rough surface
a. Calcium oxalate/phosphate (~75%)
78
-May be due to metabolic disorders or diet
a. Calcium oxalate/phosphate (~75%)
79
: -Frequently accompanied by UTI involving urea-splitting bacteria
b. Magnesium ammonium phosphate
80
-Formed in the pelvis –resembling antlers of deer
b. Magnesium ammonium phosphate
81
:-associated with increased intake of foods with high purine content
c. Uric acid
82
-Yellowish to brownish red and moderately hard
c. Uric acid
83
-seen in conjunction with hereditary disorders of cysteine metabolism
d. Cystine
84
-Yellow-brown, greasy and resembles an old soap
d. Cystine
85
-Least common calculi (1-2%)
d. Cystine
86
-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.
LITHOTRIPSY
87
•Glycosuria
Fanconi’sSyndrome
88
•Possible mild proteinuria
Fanconi’sSyndrome
89
•Low specific gravity
Diabetes Insipidus
90
•Polyuria
Diabetes Insipidus
91
•Pale yellow color of urine
Diabetes Insipidus
92
–failure of the hypothalamus to produce ADH
Neurogenic DI
93
–renal tubules fail to respond to ADH
Nephrogenic DI
94
•RTE cells
Uromodulin-associated kidney disease (UKD)
95
•Hyperuricemia
Uromodulin-associated kidney disease (UKD)
96
•+ WBCs
97
•+ Bacteria
98
Ik
99
•Mild proteinuria
100
•Increased pH

ANURBF MIDTERM (10 decks)

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