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AUBF LEC > Renal Diseases > Flashcards

Renal Diseases Flashcards

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

A

MELANURIA

23
Q

Homogentisic Acid Oxidase

A

ALKAPTONURIA

24
Q

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

A

ALKAPTONURIA

25
Q

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)

A

MAPLE SYRUP URINE DISEASE

26
Q

UA TEST/FINDINGS: Maple syrup odor / 2,4-dinitrophenyl- hydrazine (DNPH) test – (+ Yellow turbidity or precipitate)

A

MAPLE SYRUP URINE DISEASE

27
Q

Amino acids involved are leucine, isoleucine and valine

A

MAPLE SYRUP URINE DISEASE

28
Q

Etiology: Deficiency of Isovaleryl coenzyme A in the leucine pathway

A

ISOVALERIC ACIDEMIA

29
Q

Sweaty feet odor

A

ISOVALERIC ACADEMIA

30
Q

Etiology: errors in the metabolic pathway converting isoleucine, valine, threonine, and methionine to succinyl coenzyme A

A

PROPIONIC & METHYLMALONIC ACIDEMIA

31
Q

Methylmalonic academia- detected using p- nitroaniline test= (+) EMERALD GREEN COLOR

A

PROPIONIC & METHYLMALONIC ACIDEMIA

32
Q

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

A

INDICANURIA

33
Q

UA TEST/ FINDINGS: Hartnup’s disease- blue staining of infant’s diaper / OBERMAYER TEST
FeCl3 + urine + Chloroform = (+) violet color

A

INDICANURIA

34
Q

increased amounts of tryptophan are converted to indole

A

INDICANURIA

35
Q

Etiology: due to excess amounts of serotonims

A

5-HYDROXYINDOLE- ACETIC ACID

36
Q

UA TEST: Silver Nitroprusside Test- (+) Purple-black color

A

5-HYDROXYINDOLE- ACETIC ACID

37
Q

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

A

5-HYDROXYINDOLE- ACETIC ACID

38
Q

Etiology: Inability of renal tubules to reabsorb cystine filtered by the glomerulus

A

CYSTINURIA

39
Q

UA TEST: Rotten egg URINE odor / Cyanide Nitroprusside test- (+) Red purple color

A

CYSTINURIA

40
Q

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

A

CYSTINOSIS

41
Q

UA TEST: Infantile nephropathic cystinosis / Polyuria Generalized aminoaciduria (+) Clinitest for urinary substances Lack of urinary concentration

A

CYSTINOSIS

42
Q

Etiology: Defects in the metabolism of the amino acid Methionine

A

HOMOCYSTINURIA

43
Q

UA TEST: Cyanide Nitroprusside test- (+) red purple color / Silver Nitroprusside Test- (+)red purple color

A

HOMOCYSTINURIA

44
Q

increased homocystine can result in failure to thrive, cataracts, mental retardation, thromboembolic problems, and death / included in Newborn Screening test

A

HOMOCYSTINURIA

45
Q

disorders of porphyrin metabolism

A

PORPHYRIAS

46
Q

can be inherited or acquired from erythrocytic and hepatic malfunctions or exposure to toxic agents

A

PORPHYRIAS

47
Q

Common causes of acquired porphyrias include lead poisoning, excessive alcohol intake, iron deficiency, chronic liver disease, and renal disease.

A

PORPHYRIAS

48
Q

free erythrocyte protoporphyrin (FEP) as a screening test for lead poisoning, whole blood is analyzed

A

PORPHYRIAS

49
Q

Abnormal skeletal structure

A

Hurler

50
Q

Severe mental retardation

A

Hurler

51
Q

Mental retardation

A

San Filippo

52
Q

Etiology: Failure to inherit the gene to produce the enzyme hypoxanthine phosphoriboxyl transferase

A

LESCH- NYHAN SYNDROME

53
Q

Clinical manifestation: motor defects, mental retardation, a tendency toward self-destruction, gout, and renal calculi

A

LESCH- NYHAN SYNDROME

54
Q

Lab result: Increased uric acid

A

LESCH- NYHAN SYNDROME

AUBF LEC (3 decks)

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