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Mercy CLS 3: Urinalysis > 6. Renal Disease > Flashcards

6. Renal Disease Flashcards

1
Q

definition of GN

A

dysmorphic RBCs or RBC casts
protein > 3-3.5 g/day

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2
Q

definition of nephrotic syndrome (4)

A

protein > 3.5 g/day
hypoalbuminemia < 3.5 g/dL
edema
hyperlipidemia, lipiduria

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3
Q

4 categories of GN based on glomerular involvement

A

diffuse (all glomeruli)
focal (< 50% of glomeruli)

global (whole glomerular tuft)
segmental (part of glomerular tuft)

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4
Q

acute glomerulonephritis

etiology, onset, mechanism

A

post-streptococcal (S. pyogenes) infection
1-2 weeks post-strep
antibody complexes against M protein (Spyo) deposit in glomerular membrane

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5
Q

acute glomerulonephritis

s/s, lab findings

A

fever; edema; periorbital edema; fatigue

hematuria; RBC casts/dysphormics; mild proteinuria

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6
Q

acute glomerulonephritis

treatment, prognosis

A

supportive
self-limiting

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7
Q

goodpasture’s

etiology, onset, mechanism

A

viral respiratory infection → cytotoxic antibody attached to glomerular and alveolar basement membranes

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8
Q

goodpasture’s

s/s, lab findings

A

hemoptysis; dyspnea
hematuria (macroscopic); RBC casts; proteinuria

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9
Q

goodpasture’s

prognosis

A

leads to chronic GN and end-stage renal failure

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10
Q

Henoch-Schonlein purpura

etiology, onset, mechanism

A

viral URT infection in children
↓ platelets
renal involvement is an eventual serious complication

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11
Q

Henoch-Schonlein purpura

s/s, lab findings

A

purpura; blood in sputum and stools
macroscopic hematuria; proteinuria; RBC casts

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12
Q

Henoch-Schonlein purpura

treatment, prognosis

A

50% make complete recovery
50% → renal failure

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13
Q

Rapidly progressive crescentic glomerulonephritis

etiology, onset, mechanism

A

associated with SLE
complication of other forms of GN
macrophages damage capillary walls in glomerulus
cells, plasma released into Bowman’s space
crescentic forms: macrophages, fibroblasts, polymerized fibrin

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14
Q

Rapidly progressive crescentic glomerulonephritis

s/s, lab findings

A

↑ fibrin degradation products, cryoglobulins, IgA deposits

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15
Q

Rapidly progressive crescentic glomerulonephritis

treatment, prognosis

A

poor prognosis; often terminates in renal failure
most serious acute GN

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16
Q

Membranous glomerulonephritis

etiology, onset, mechanism

A

associated with autoimmune disorders (SLE, Sjogren’s syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, malignancy)
thickening of glomerular membrane
IgG immune complex deposition

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17
Q

Membranous glomerulonephritis

s/s, lab findings

A

microscopic hematuria; very high proteinuria

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18
Q

Membranous glomerulonephritis

prognosis

A

slow progression to nephrotic syndrome (50%)

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19
Q

Wegener’s Granulomatosis

etiology, onset, mechanism

A

antineutrophilic cytoplasmic antibody (ANCA)
antibody to neutrophils damages small vessels in lungs & glomerulus

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20
Q

Wegener’s Granulomatosis

s/s, lab findings

A

hemoptysis
macroscopic hematuria; proteinuria; RBC casts; azotemia
immunofixation test (p-ANCA/c-ANCA)

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21
Q

Wegener’s Granulomatosis

treatment, prognosis

A

possible progression to end-stage renal failure

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22
Q

Membranoproliferative Glomerulonephritis (MPGN)

etiology, onset, mechanism

A

Type 1—thickening of subendothelial & peripheral capillaries
Type 2—dense deposits in glomerular basement membrane

often in children

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23
Q

Membranoproliferative Glomerulonephritis (MPGN)

s/s, lab findings

A

variable lab results—hematuria; proteinuria; ↓ serum complement

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24
Q

Membranoproliferative Glomerulonephritis (MPGN)

treatment, prognosis

A

poor prognosis
Type 1—progress to nephrotic syndrome
Type 2—progress to chronic GN

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25
Q

IgA Nephropathy (Berger’s Disease)

etiology, onset, mechanism

A

IgA complexes deposited on glomerular membrane
maybe from mucosal infection
children and young adults
#1 cause of primary GN

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26
Q

IgA Nephropathy (Berger’s Disease)

s/s, lab findings

A

recurrent macroscopic hematuria following exercise

rust-colored urine; proteinuria; glycosuria; casts (cellular, waxy, broad)

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27
Q

IgA Nephropathy (Berger’s Disease)

treatment, prognosis

A

anti-HTN drugs; low salt, low protein diet
slow progression to chronic GN (50%)

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28
Q

Nephrotic Syndrome

etiology, onset, mechanism

A

damage to shield of negativity and podocytes; increased permeability
systemic shock ↓ blood flow to kidneys

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29
Q

Nephrotic Syndrome

s/s, lab findings

A

proteinuria > 3.5g/day; hematuria; hypoalbuminemia (stimulates lipid production in liver); edema
RTEs; OFBs; casts (fatty, waxy, RTE); cholesterol crystals; fat droplets

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30
Q

Nephrotic Syndrome

treatment, prognosis

A

medication, diet

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31
Q

Minimal Change Disease

etiology, onset, mechanism

A

1st cause of nephrotic syndrom in children

disruption of podocytes associated with allergic rxn, immunizations, HLA-B12

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32
Q

Minimal Change Disease

s/s, lab findings

A

heavy edema
other nephrotic syndrome findings

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33
Q

Minimal Change Disease

treatment, prognosis

A

corticosteroids (may lead to steroid dependence)

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34
Q

Focal Segmental Glomerulonephritis

etiology, onset, mechanism

A

disruption of podocytes
associated with heroin, analgesics, HIV
partial glomeruli involvement

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35
Q

Focal Segmental Glomerulonephritis

s/s, lab findings

A

resembles nephrotic syndrome & minimal change disease

hematuria; proteinuria

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36
Q

Alport’s Syndrome

etiology, onset, mechanism

A

sex-linked or autosomal genetic disorder
collagen IV mutation
lamellated appearance of basement membrane (thinning)
males < 6 yo associated with respiratory infections

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37
Q

Alport’s Syndrome

s/s, lab findings

A

macroscopic & microscopic hematuria
hearing/vision abnormalities

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38
Q

Alport’s Syndrome

treatment, prognosis

A

supportive
can progress to renal insufficiency, failure, nephrotic syndrome

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39
Q

Chronic Glomerulonephritis

etiology, onset, mechanism

A

“slow and silent”
progression of other GN disorders

40
Q

Chronic Glomerulonephritis

s/s, lab findings

A

hematuria; proteinuria; glycosuria; casts (cellular, waxy, broad)
↓ GFR; ↑ BUN/creatinine; ↑ phosphate; ↓ calcium

41
Q

Chronic Glomerulonephritis

treatment, prognosis

A

dialysis
renal transplant

42
Q

Diabetic Nephropathy

etiology, onset, mechanism

A

glycosylated proteins damage glomerular membrane
sclerosis of vascular structure

43
Q

Diabetic Nephropathy

s/s, lab findings

A

microalbuminemia (earliest biomarker)

44
Q

Diabetic Nephropathy

treatment, prognosis

A

1st cause of end-stage renal disease
strict control of BG, HTN

45
Q

Acute Tubular Necrosis

etiology, onset, mechanism

A

ischemic damage to RTEs or presence of toxic substances
shock, trauma, surgery, myoglobin (strenuous exercise), nephrotoxic antibiotics

46
Q

Acute Tubular Necrosis

s/s, lab findings

A

oliguria, nocturia, edema, nausea, vomiting, seizures, decreased consciousness, easy bruising, joint pain, flank pain

RTEs, RTE casts; blood strip +; ↓ specific gravity

47
Q

Acute Tubular Necrosis

treatment, prognosis

A

correct underlying cause

48
Q

Fanconi Syndrome

etiology, onset, mechanism

A

inherited
associated with cystinosis and Hartnum disease or acquired through toxic agents (ex. outdated tetracycline)

general failure of reabsorption in PCT

49
Q

Fanconi Syndrome

s/s, lab findings

A

glycosuria; proteinuria; low pH; cystine crystals

50
Q

Fanconi Syndrome

treatment, prognosis

A

supportive

51
Q

Uromodulin Associated Kidney Diseases (UMKD)

etiology, onset, mechanism

A

autosomal mutation in gene for uromodulin
↑ abnormal uromodulin builds up and damages tubular cells
teenage years

52
Q

Uromodulin Associated Kidney Diseases (UMKD)

s/s, lab findings

A

gout (teenage years)
↑ serum uric acid

53
Q

Uromodulin Associated Kidney Diseases (UMKD)

treatment, prognosis

A

eventual renal transplant

54
Q

Diabetes Insipidus

etiology, onset, mechanism

A

nephrogenic (failure to respond to ADH)—inherited sex-linked recessive or acquired (lithium, amphotericin B, PCKD, sickle cell)

neurogenic (failure to produce ADH)

55
Q

Diabetes Insipidus

s/s, lab findings

A

severe dehydration, polyuria

↓ SG; glucose =

nephrogenic—1:1 osmo after ADH injection
neurogenic— 3:1 osmo after ADH injection

56
Q

Renal Glycosuria

etiology, onset, mechanism

A

inherited autosomal recessive
failure of glucose active transport

57
Q

Renal Glycosuria

s/s, lab findings

A

glycosuria with normal BG

58
Q

Renal Glycosuria

treatment, prognosis

A

benign

59
Q

Renal Tubular Acidosis

etiology, onset, mechanism

A

distal—defects in distal H+ excretion
proximal—defect that reduces the capacity to reclaim filtered bicarbonate in PCT
voltage-dependent—defects in distal Na+ reabsorption

60
Q

Renal Tubular Acidosis

s/s, lab findings

A

metabolic acidosis

61
Q

Acute Pyelonephritis

etiology, onset, mechanism

A

ascending infection from lower UTI
rapid onset

62
Q

Acute Pyelonephritis

s/s, lab findings

A

urinary frequency, nocturia, burning, lower back pain, malaise, chills

LE +; nitrite +; mild proteinuria; hematuria; WBCs; WBC casts; bacteria; bacterial casts

63
Q

Acute Pyelonephritis

treatment, prognosis

A

antibiotics
no permanent damage

64
Q

Chronic Pyelonephritis

etiology, onset, mechanism

A

structural abnormalities affecting flow of urine → recurrent infections

65
Q

Chronic Pyelonephritis

s/s, lab findings

A

polyuria, nocturia, HTN

LE +; nitrite +; moderate proteinuria; hematuria; WBCs; WBC casts; bacteria +/=; bacterial casts; waxy and broad casts

66
Q

Chronic Pyelonephritis

treatment, prognosis

A

permanent scarring of renal tissue
correction of underlying defect

67
Q

Acute Interstitial Nephritis

etiology, onset, mechanism

A

allergic reaction to certain medications
onset 1-2 weeks of initial dose

68
Q

Acute Interstitial Nephritis

s/s, lab findings

A

skin rash, oliguria, edema
hematuria; proteinuria; urine eosinophils (Hansel stain); no bacteria; WBCs; WBC casts

69
Q

Acute Interstitial Nephritis

treatment, prognosis

A

d/c medication
corticosteroids

70
Q

Cystitis

etiology, onset, mechanism

A

frequent in women & children
#1: E. coli

71
Q

Cystitis

s/s, lab findings

A

urinary frequency, burning
LE +; nitrite +; ↑ pH; WBCs; bacteria

72
Q

Cystitis

treatment, prognosis

A

antibiotics

73
Q

Urethritis

etiology, onset, mechanism

A

bacterial or viral infection
often STI

74
Q

Urethritis

s/s, lab findings

A

dysuria, polyuria, urethral discharge
hematuria; WBCs; bacteria

75
Q

Urethritis

treatment, prognosis

A

antibiotics

76
Q

Acute Renal Failure

etiology, onset, mechanism

A

sudden loss of renal function
prerenal, renal, or postrenal

77
Q

Acute Renal Failure

s/s, lab findings

A

↓ GFR; oliguria, edema, anuria, flank pain, ↓ sensation, ↓ appetite, metallic taste, hiccups, change in mental status, seizure, tremors, nausea, vomiting, bruising, fatigue

urine sediment not distinctive

78
Q

Acute Renal Failure

treatment, prognosis

A

often reversible

79
Q

Chronic Renal Failure

etiology, onset, mechanism

A

progressive loss of renal function
usually due to DM or HTN

80
Q

Chronic Renal Failure

s/s, lab findings
GFR

A

↑↑ BUN and creatinine levels, ↑ K, electrolyte imbalance, ↓ Ca, secondary hyperparathyroidism, ↓ creatinine clearance, metabolic acidosis, anemia
GFR < 25 mL/min; isosthenuria; proteinuria; glycosuria

81
Q

Chronic Renal Failure

treatment, prognosis

A

irreversible
control sx

82
Q

Renal Lithiasis

etiology, onset, mechanism

A

pH, concentration, urine stasis contribute
increased in the summer, dehydration
increased dietary oxalates and ascorbic acid, cytotoxic drugs, endocrine disorders, foreign body seed, chemical salts in urine ultrafiltrate

83
Q

Renal Lithiasis

s/s, lab findings

A

intense pain beginning in flank and radiating forward and downward, vomiting, sweating, frequent urge to urinate

hematuria; ↑ SG; crystals (75% calcium)

84
Q

Renal Lithiasis

treatment, prognosis

A

lithotripsy
surgical removal

85
Q

Polycystic kidney disease

etiology, onset, mechanism

A

hereditary
fluid-filled cysts form on kidneys

86
Q

Polycystic kidney disease

s/s, lab findings

A

HTN, hematuria, back pain, frequent bladder or kidney infections, ↑ BUN & creatinine, anemia

87
Q

Polycystic kidney disease

treatment, prognosis

A

4th cause of chronic kidney failure
supportive care
renal transplant

88
Q

Wilm’s Tumor

etiology, onset, mechanism

A

develops in fetus
genetic component

89
Q

Wilm’s Tumor

s/s, lab findings

A

abdominal pain, swelling of abdomen, hematuria, fever, loss of appetite, n/v, malaise, ↑ BP, constipation, increased growth only on one side of body

90
Q

Wilm’s Tumor

treatment, prognosis

A

90% cure rate if localized

91
Q

bladder cancer prevalence

A

4th most common cancer in men, 9th in women

92
Q

pt hx for bladder cancer

A

older
smoking

93
Q

most common type of kidney cancer

A

renal cell carcinoma clear cell type

94
Q

hemoptysis

A

Goodpasture’s
Wegener’s granulamatosis

95
Q

kidney diseases triggered by/associated with infections (5)

A

acute GN (strep)
Goodpastures (viral resp.)
Henoch-Schonlein purpura (viral URT in children)
IgA nephropathy (maybe mucosal infection)
Alport’s syndrome (males < 6 viral respiratory)

Mercy CLS 3: Urinalysis (10 decks)

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