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AUBF LEC > Renal Diseases > Flashcards

Renal Diseases Flashcards

(54 cards)

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1
Q

Examples of Glomerular Diseases

A

Acute Post- Streptococcal glomerulonephritis, Rapidly progressive glomerulonephritis, Goodpasture Syndrome, Wegener granulomatosis, Henoch-Schonlein purpura, Membranous Glomerulonephritis, Membranoproliferative glomerulonephritis, Chronic Glomerulonephritis, Ig A nephropathy (Berger’s Disease), Minimal Change disease, Focal Segmental Glomerulosclerosis, Diabetic Nephropathy (Kimmelstiel-Wilson Disease), Alport Syndrome

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2
Q

Etiology: Formed in conjunction w/ Grp A Streptococcus infection in the glomerular membranes

A

Acute Post- Streptococcal glomerulonephritis

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3
Q

Etiology: Immune complex decomposition from systemic immune disorders

A

Rapidly progressive glomerulonephritis

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4
Q

Attachments of a cytotoxic antibody formed during viral respiratory infections to glomerular & alveolar basement membranes

A

Goodpasture Syndrome

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5
Q

Etiology: Antineutrophilic cytoplasmic autoantibody (ANCA) binds to neutrophils in vascular walls producing damage to small vessels in the lungs and glomerulus

A

Wegener granulomatosis

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6
Q

Etiology: Occurs primarily in children following viral respiratory infections

A

Henoch-Schonlein Purpura

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7
Q

Etiology: Thickening of glomerular membrane

A

Membranous Glomerulonephritis

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8
Q

Etiology: Cellular proliferation
affecting the capillary walls or the glomerular basement membrane, possibly immune- mediated

A

Membranoproliferative glomerulonephritis

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9
Q

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

A

Chronic Glomerulonephritis

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10
Q

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

A

Ig A nephropathy (Berger’s Disease)

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11
Q

Etiology: Disruption of the shield of negativity and damage to the right podocyte barrier resulting in massive loss of protein and lipids

A

NephroticSyndrome

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12
Q

Etiology: Disruption of the podocytes occurring primarily in children following allergic reactions and immunizations

A

Minimal change disease

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13
Q

Etiology: Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and AIDS

A

Focal Segmental Glomerulosclerosis

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14
Q

Etiology: Deposition of glycosylated
proteins on the glomerular basement membranes caused by poorly controlled glucose levels

A

Diabetic Nephropathy (Kimmelstiel-Wilson Disease)

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15
Q

Etiology: Genetic disorder showing lamelled of thinning glomerular basement membrane (Prob: Collagen Type IV)

A

Alport Syndrome

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16
Q

UA TEST/FINDINGS: Mousy odor/ Ferricchloride
Tube test- used to detect presence of urine phenyl pyruvic acid (+) permanent (Blue green color)

A

PHENYLKETONURIA

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17
Q

Most well-known of the aminoaciduria

A

PHENYLKETONURIA

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18
Q

ENZYME DEF: Fumarylacetoacetate hydrolase (TYPE 1) / Tyrosine Aminotransferase (TYPE 2) / p-hydroxyphenylpyruvic acid dioxygenase (type 3)

A

TYROSYLURIA

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19
Q

UA TEST/FINDINGS: Rancidodor / Nitroso-Naphthol test- orange-red color (tyrosine metabolites)

A

TYROSYLURIA

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20
Q

accumulation of excess tyrosine in the plasma (tyrosinemia) producing urinary overflow

A

TYROSYLURIA

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21
Q

UA TEST/FINDINGS: Dark urine

A

MELANURIA

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22
Q

Darkening appears after the urine is exposed to air / Elevatedurinary melanin is a serious finding that indicates proliferation of the normal melanin- producing cells (melanocytes), producing a malignant melanoma

23
Q

Homogentisic Acid Oxidase

24
Q

UA TEST/FINDING: Blackurine / Homogentisic
Acid test- (+) black color

25
Etiology: Failure to inherit the gene for the enzyme necessary to produce oxidative decarboxylation of these keto acids (a- ketoisovaleric, a-ketoisocaproic, and a-keto-b-methylvaleric)
MAPLE SYRUP URINE DISEASE
26
UA TEST/FINDINGS: Maple syrup odor / 2,4-dinitrophenyl- hydrazine (DNPH) test – (+ Yellow turbidity or precipitate)
MAPLE SYRUP URINE DISEASE
27
Amino acids involved are leucine, isoleucine and valine
MAPLE SYRUP URINE DISEASE
28
Etiology: Deficiency of Isovaleryl coenzyme A in the leucine pathway
ISOVALERIC ACIDEMIA
29
Sweaty feet odor
ISOVALERIC ACADEMIA
30
Etiology: errors in the metabolic pathway converting isoleucine, valine, threonine, and methionine to succinyl coenzyme A
PROPIONIC & METHYLMALONIC ACIDEMIA
31
Methylmalonic academia- detected using p- nitroaniline test= (+) EMERALD GREEN COLOR
PROPIONIC & METHYLMALONIC ACIDEMIA
32
Etiology: excess indole is then reabsorbed from the intestine into the blood-stream and circulated to the liver, where it is converted to indican and then excreted in the urine
INDICANURIA
33
UA TEST/ FINDINGS: Hartnup’s disease- blue staining of infant’s diaper / OBERMAYER TEST FeCl3 + urine + Chloroform = (+) violet color
INDICANURIA
34
increased amounts of tryptophan are converted to indole
INDICANURIA
35
Etiology: due to excess amounts of serotonims
5-HYDROXYINDOLE- ACETIC ACID
36
UA TEST: Silver Nitroprusside Test- (+) Purple-black color
5-HYDROXYINDOLE- ACETIC ACID
37
5-HIAA is a degradation product of serotonin / excretion of greater than 25 mg/24 h can be an indication of argentaffin cell tumors / Patient should avoid eating bananas, pineapple & tomatoes prior to testing 5-HIAA
5-HYDROXYINDOLE- ACETIC ACID
38
Etiology: Inability of renal tubules to reabsorb cystine filtered by the glomerulus
CYSTINURIA
39
UA TEST: Rotten egg URINE odor / Cyanide Nitroprusside test- (+) Red purple color
CYSTINURIA
40
Etiology: defect in the lysosomal membranes prevents the release of cystine into the cellular cytoplasm for metabolism / The incomplete metabolism of cystine results in crystalline deposits of cystine in many areas of the body
CYSTINOSIS
41
UA TEST: Infantile nephropathic cystinosis / Polyuria Generalized aminoaciduria (+) Clinitest for urinary substances Lack of urinary concentration
CYSTINOSIS
42
Etiology: Defects in the metabolism of the amino acid Methionine
HOMOCYSTINURIA
43
UA TEST: Cyanide Nitroprusside test- (+) red purple color / Silver Nitroprusside Test- (+)red purple color
HOMOCYSTINURIA
44
increased homocystine can result in failure to thrive, cataracts, mental retardation, thromboembolic problems, and death / included in Newborn Screening test
HOMOCYSTINURIA
45
disorders of porphyrin metabolism
PORPHYRIAS
46
can be inherited or acquired from erythrocytic and hepatic malfunctions or exposure to toxic agents
PORPHYRIAS
47
Common causes of acquired porphyrias include lead poisoning, excessive alcohol intake, iron deficiency, chronic liver disease, and renal disease.
PORPHYRIAS
48
free erythrocyte protoporphyrin (FEP) as a screening test for lead poisoning, whole blood is analyzed
PORPHYRIAS
49
Abnormal skeletal structure
Hurler
50
Severe mental retardation
Hurler
51
Mental retardation
San Filippo
52
Etiology: Failure to inherit the gene to produce the enzyme hypoxanthine phosphoriboxyl transferase
LESCH- NYHAN SYNDROME
53
Clinical manifestation: motor defects, mental retardation, a tendency toward self-destruction, gout, and renal calculi
LESCH- NYHAN SYNDROME
54
Lab result: Increased uric acid
LESCH- NYHAN SYNDROME

AUBF LEC (3 decks)

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