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Pathology > Kidney and Bladder, TBP > Flashcards

Kidney and Bladder, TBP Flashcards

1
Q

Reason why many kidney disease do not become clinically apparent until majority of the organ is affected

A

Large physiologic reserve

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2
Q

Reason why many kidney disease do not become clinically apparent until majority of the organ is affected

A

Large physiologic reserve

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3
Q

Prerenal vs Renal: FENa less than 1%

A

Prerenal

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4
Q

Prerenal vs Renal: FENa >1%

A

Renal

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5
Q

Prerenal vs Renal: BUN/Cr ratio >20:1

A

Prerenal

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6
Q

Prerenal vs Renal: BUN/Cr ratio less than 20:1

A

Renal

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7
Q

Prerenal vs Renal: Urine sodium

A

Prerenal

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8
Q

Prerenal vs Renal: Urine sodium >20 mEq/L

A

Renal

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9
Q

Prerenal vs Renal: Urine osm >500 mOsm/kg

A

Prerenal

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10
Q

Prerenal vs Renal: Urine osm less than 400 mOsm/kg

A

Renal

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11
Q

Diagnostic test of choice in post renal azotemia

A

Ultrasound

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12
Q

Electrolyte disturbances in acute renal failure

A

1) Hyponatremia
2) Hyperkalemia
3) Hyperphosphatemia
4) Hypocalcemia

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13
Q

Acid-base disorder in acute renal failure

A

Metabolic acidosis

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14
Q

Oliguria is defined as

A

Less than 400 mL/day

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15
Q

Very sensitive test for differentiating pre renal from renal cause of ARF

A

FENa

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16
Q

Chronic renal failure: Electrolyte imbalance

A

1) Hyperkalemia
2) Hyperphosphatemua
3) Hypocalcemia

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17
Q

Chronic renal failure: Acid-base disorder

A

Metabolic acidosis

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18
Q

Chronic renal failure: Urine SG

A

Less than 1.010

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19
Q

Acute renal failure: Urine SG in renal cause

A

Less than 1.010

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20
Q

Prerenal vs Renal: FENa

A

Prerenal

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21
Q

Prerenal vs Renal: FENa >1%

A

Renal

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22
Q

Prerenal vs Renal: BUN/Cr ratio >20:1

A

Prerenal

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23
Q

Prerenal vs Renal: BUN/Cr ratio

A

Renal

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24
Q

Prerenal vs Renal: Urine sodium

A

Prerenal

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25
Q

Prerenal vs Renal: Urine sodium >20 mEq/L

A

Renal

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26
Q

Prerenal vs Renal: Urine osm >500 mOsm/kg

A

Prerenal

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27
Q

Prerenal vs Renal: Urine osm

A

Renal

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28
Q

Diagnostic test of choice in post renal azotemia

A

Ultrasound

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29
Q

Electrolyte disturbances in acute renal failure

A

1) Hyponatremia
2) Hyperkalemia
3) Hyperphosphatemia
4) Hypocalcemia

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30
Q

Acid-base disorder in acute renal failure

A

Metabolic acidosis

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31
Q

Oliguria is defined as

A

Less than 400 mL urine per day

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32
Q

Very sensitive test for differentiating pre renal from renal cause of ARF

A

FENa

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33
Q

Chronic renal failure: Electrolyte imbalance

A

1) Hyperkalemia
2) Hyperphosphatemua
3) Hypocalcemia

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34
Q

Chronic renal failure: Acid-base disorder

A

Metabolic acidosis

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35
Q

Chronic renal failure: Urine SG

A

Less than 1.010

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36
Q

Acute renal failure: Urine SG in prerenal cause

A

> 1.020

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37
Q

Acute renal failure: Urine SG in renal cause

A

Less than 1.010

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38
Q

Chronic renal failure: Hematologic complications (2)

A

1) Normocytic normochromic anemia

2) Platelet dysfunction

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39
Q

Chronic renal failure: Skeletal complications (2)

A

1) Renal osteodystrophy

2) Hyperparathyroidism

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40
Q

Earliest and most sensitive clinical indication of hypovolemia

A

Oliguria

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41
Q

Stains in LM: Basement membrane and mesangium

A

PAS

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42
Q

Stains in LM: Fibrosis

A

Trichrome

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43
Q

Stains in LM: Basement membrane

A

Silver

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44
Q

Igs used in IF

A

IgG, IgM, IgA

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45
Q

IF pattern: Reaction of Ab with pathogenic Ab directed against Ag in the GBM

A

Linear

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46
Q

IF pattern: Reaction of Ab with pathogenic Ag-Ab complexes on GBM

A

Granular

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47
Q

Allows for detection and determination of location of ICs and evaluation of basement membrane

A

EM

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48
Q

Origin of MOST glomerular diseases

A

Immunologic

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49
Q

Mechanism of destruction in IC deposition

A

Complement activation and chemotaxis via C5a

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50
Q

Type of edema caused by nephrotic syndrome

A

Generalized (anasarca)

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51
Q

Nephrotic syndrome: Mechanism for hyperlipidemia

A

Response of liver to loss of albumin by producing more apolipoprotein to compensate for low serum osmotic pressure

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52
Q

Nephrotic syndrome: Key component of the slit diaphragm found between the podocyte foot processes which may help control permeability

A

Nephrin

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53
Q

Nephrotic syndrome: Risk of thrombosis is secondary to

A

Urinary loss of antithrombin III, protein C, and protein S

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54
Q

Appearance of lipid droplets under polarised light

A

Maltese cross

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55
Q

Most common cause of nephrotic syndrome in all populations

A

Primary

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56
Q

LM: Minimal change disease

A

Normal

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57
Q

LM: FSGS

A

Segmental sclerosis of glomeruli

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58
Q

LM: Membranous glomerulopathy

A

Spike and dome on silver stain

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59
Q

LM: PSGN

A

Lumpy-bumpy on silver stain

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60
Q

LM: RPGN (all types)

A

Glomerular crescents

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61
Q

LM: MPGN (all types)

A

Tram-track appearance on silver stain

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62
Q

IF: MCD

A

Negative

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63
Q

IF: FSGS

A

IgM and C3

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64
Q

IF: Membranous GN

A

IgG, granular

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65
Q

IF: PSGN

A

IgG, IgM and C3, granular

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66
Q

IF: RPGN I

A

IgG (anti-GBM) Linear

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67
Q

IF: RPGN II

A

IgG Granular

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68
Q

IF: RPGN III

A

Negative

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69
Q

IF: MPGN I

A

IgG and C3, granular

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70
Q

IF: MPGN II

A

C3

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71
Q

EM: MCD

A

Effacement of foot processes

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72
Q

EM: FSGS

A

No immune complexes

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73
Q

EM: Membranous GN

A

Subepithelial IC deposits

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74
Q

EM: PSGN

A

Predominantly subepithelial IC deposits; also subendothelial, intramembranous, and mesangial

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75
Q

EM: RPGN Type I

A

No IC

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76
Q

EM: RPGN Type II

A

Subendothelial IC deposits

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77
Q

EM: RPGN Type III

A

No IC

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78
Q

EM: MPGN Type I

A

Subendothelial IC

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79
Q

EM: MPGN Type II

A

Long dense band in lamina densa and sub endothelial region

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80
Q

Nephrotic syndrome: 4 main conditions

A

1) Minimal change disease
2) Membranous GN
3) FSGS
4) DM nephropathy

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81
Q

MCD: Also known as

A

Lipoid nephrosis

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82
Q

MCD: Male vs female

A

Male

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83
Q

MCD: Selective vs nonselective proteinuria

A

Selective

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84
Q

MCD: Conditions associated (3)

A

1) Hodgkin’s lymphoma
2) Other lymphomas and leukemias
3) NSAIDs

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85
Q

T/F FSGS is immunologic in origin

A

F

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86
Q

Mechanism of FSGS

A

Epithelial injury

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87
Q

FSGS: Type of proteinuria

A

Nonselective

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88
Q

FSGS: Variant that has worse prognosis and similar to injury seen with HIV infection

A

Collapsing variant

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89
Q

Significant independent risk factors for the development of FSGS

A

1) IV heroin

2) HIV

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90
Q

Risk of FSGS in IV heroin users

A

30x that of the general population

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91
Q

FSGS: Treatment

A

None –> chronic GN

92
Q

50% of patients with FSGS develop ESRD within

A

10 years

93
Q

Membranous GN: Spikes represent

A

Basement membrane between IC

94
Q

Membranous GN: Domes represent

A

Thickened basement membrane that cover IC

95
Q

Pathogenesis of membranous GN

A

Fomation of MAC

96
Q

Membranous GN: Proteinuria

A

Nonselective

97
Q

T/F Most membranous GN is idiopathic in origin

A

T

98
Q

Membranous GN: Related causative drugs

A

1) Pencicillamine
2) Captopril
3) NSAIDs

99
Q

Membranous GN: Associated conditions

A

1) Infections (syphilis, HBV, HCV, malaria)
2) Cancers (lung and colon)
3) Melanoma
4) SLE

100
Q

Membranous GN: Rule

A

1/3

1) Remission
2) Proteinuria and stable renal functions
3) Progress to ESRD within 5-10 years

101
Q

Single most important cause of ESRD

A

DM

102
Q

DM nephropathy: GFR

A

1) Elevated early in the disease

2) Progressive decline later

103
Q

Predicts development of DM nephropathy

A

Microalbuminuria

104
Q

DM nephropathy: Most common finding

A

Diffuse glomerulosclerosis (diffuse thickening of the basement membrane)

105
Q

DM nephropathy: Found in 15-20% of patients with DM nephropathy

A

Kimmelsteil-Wilson nodules or nodular glomerulosclerosis

106
Q

What are Kimmelsteil-Wilson nodules

A

ACELLULAR nodules within GBM

107
Q

T/F Damage to the glomerulus is more severe in nephritic syndrome than nephrotic syndrome

A

T

108
Q

Pathogenesis of nephritic syndrome

A

IC triggers proliferation of glomerular cells and chemotaxis

109
Q

Nephritic syndrome: Hematuria described as

A

Smoky brown or cola-colored

110
Q

Nephrotic vs nephritic: Proteinuria >3.5 g/d

A

Nephrotic

111
Q

Nephrotic vs nephritic: Proteinuria less than 3.0/d

A

Nephrotic

112
Q

Nephrotic vs nephritic: Presence of oliguria

A

Nephritic

113
Q

Nephrotic vs nephritic: Presence of hematuria

A

Nephritic

114
Q

Nephrotic vs nephritic: Hypertension

A

Nephritic

115
Q

Nephrotic vs nephritic: Elevated BUN/Cr

A

Nephritic

116
Q

Nephritic syndrome: Low serum complement level found in (4)

A

1) PSGN
2) MPGN
3) SLE
4) Bacterial endocarditis

117
Q

Nephritic syndrome: Normal serum complement level (3)

A

1) IgA nephropathy
2) Idiopathic RPGN
3) Anti-GBM Ab disease

118
Q

Nephritic syndrome: 3 conditions

A

1) PSGN
2) RPGN
3) MPGN

119
Q

Nephritogenic GABHS

A

1, 4, 12

120
Q

Markers of streptococcal infection (2)

A

1) ASO

2) Anti-DNAse B

121
Q

RPGN: Most primary or secondary

A

Secondary

122
Q

Distinguishing feature: Type I RPGN

A

Linear immunofluorescence due to binding of IGG to GBM antigens

123
Q

Distinguishing feature: Type II RPGN

A

Immune complex mediated

124
Q

Distinguishing feature: Type III RPGN (2)

A

1) Pauci-immune (no ICs)

2) Majority ANCA-positive

125
Q

Manifestations of MPGN in order of frequency

A

1) Nephrotic syndrome
2) Asymptomatic hematuria
3) Nephritic syndrome

126
Q

~50% of patients with MPGN develop CRF within

A

10 years

127
Q

MPGN is aka

A

Mesangioproliferative GN

128
Q

Function of C3 nephritic factor

A

Stabilizes C3 convertase

129
Q

Most common glomerular cause of asymptomatic hematuria

A

IgA nephropathy

130
Q

4 most common conditions causing asymptomatic hematuria

A

1) IgA nephropathy
2) HSP
3) Alport syndrome
4) Thin basement membrane disease

131
Q

Most common primary cause of glomerulonephritis

A

IgA nephropathy

132
Q

IgA nephropathy: Male vs female

A

Male

133
Q

IgA nephropathy: 2 associated diseases

A

1) Celiac disease

2) HSP

134
Q

IgA nephropathy: IF

A

IgA and C3, granular

135
Q

IgA nephropathy: EM

A

IgA in mesangium

136
Q

IgA nephropathy: Pathogenesis

A

Abnormal glycosylation

137
Q

IgA-mediated vasculitid\s

A

HSP

138
Q

HSP: Commonly preceded by

A

Streptococcal or viral infection

139
Q

Alport syndrome: Characteristic cells on LM

A

Interstitial foam cells due to accumulation of neutral fats and mucopolysaccharides

140
Q

Alport syndrome: IF

A

Negative

141
Q

Alport syndrome: EM

A

Splitting, thickening, and thinning (Basket-weave pattern)

142
Q

Alport syndrome: Most common pattern of inheritance

A

X-linked

143
Q

Alport syndrome: Associated symptoms

A

1) Nerve deafness
2) Lens dislocation
3) Cataracts

144
Q

Alport syndrome: Male vs female

A

Male

145
Q

Normal thickness of GBM

A

300-400 nm

146
Q

Tubulointerstitial disease: 4 categories

A

1) Acute tubulointerstitial nephritis
2) Chronic tubulointerstitial nephritis
3) Acute interstitial nephritis
4) Acute tubular necrosis

147
Q

Tubulointerstitial disease: Edema, neutrophils, focal necrotizing infiltrates

A

Acute tubulointerstitial nephritis

148
Q

Tubulointerstitial disease: Noninfectious causes of acute tubulointerstitial nephritis

A

Acute interstitial nephritis

149
Q

Tubulointerstitial disease: Cellular infiltrate composed of lymphocytes and macrophages in combination with interstitial nephritis

A

Chronic tubulointerstitial nephritis

150
Q

Acute tubulointerstitial nephritis, causes: Drugs (4)

A

1) Methicillin
2) Rifampin
3) Sulfonamides
4) Ciprofloxacin

151
Q

Acute tubulointerstitial nephritis, causes: Systemic infections (4)

A

1) Legionnaire’s
2) Sterp
3) CMV
4) IM

152
Q

Acute tubulointerstitial nephritis, causes: Primary renal infections

A

Acute bacterial pyelonephritis

153
Q

Acute tubulointerstitial nephritis, causes: Immune d/o (2)

A

1) SLE

2) Sjogren

154
Q

Responsible for most cases of acute tubulointerstitial nephritis

A

Drugs

155
Q

Usual cause of acute interstitial nephritis

A

Drugs

156
Q

Drugs that cause acute interstitial nephritis

A

1) Methicillin
2) Rifampin
3) Thiazides
4) Sulfonamides

157
Q

Tubulointerstitial disease: Tubular injury combined with a persistent and severe decrease in blood flow

A

Interstitial nephritis

158
Q

Tubulointerstitial disease: Interstitial lymphocytes and macrophages, edema, eosinophils; sometimes giant cells and granulomas

A

Acute interstitial nephritis

159
Q

Chronic tubulointerstitial disease: More common in older women, typically with a history of arthritis or headaches and a long history of chronic heavy analgesic use (e.g., aspirin, phenacetin, acetaminophen)

A

Analgesic nephropathy

160
Q

Chronic tubulointerstitial nephritis: Most important cause

A

Urinary tract obstruction

161
Q

Chronic tubulointerstitial nephritis: Heavy metals that can cause (2)

A

1) Lead

2) Cadmium

162
Q

Chronic tubulointerstitial nephritis: Malignancy that can cause

A

MM

163
Q

2 categories of acute tubular necrosis

A

1) Ischemic

2) Toxic

164
Q

Toxic causes of ATN (7)

A

1) Aminoglycosides
2) Amphotericin B
3) IV contrast
4) Mercury
5) Oxalic acid (ethylene glycol poisoning)
6) Myoglobinuria, hemoglobinuria
7) Hyperuricemia

165
Q

Stages of acute tubular necrosis

A

1) Initiating
2) Maintenance
3) Recovery

166
Q

Stages of acute tubular necrosis: Maintenance phase is characterized by

A

Oliguria within 24 hours of initiating event

167
Q

Stages of acute tubular necrosis: Recovery phase is characterized by

A

Increased UO up to 3L

168
Q

Increases risk of death during the recovery phase of ATN

A

Electrolyte disturbance

169
Q

Protein casts are composed of

A

Tamm-Horsfall protein

170
Q

More common organism when acute pyelonephritis is acquired hematogenously

A

Staphylococcus aureus

171
Q

Gross morphology of acute pyelonephritis

A

Abscesses in the cortex

172
Q

Complication of pyelonephritis almost exclusively seen in diabetics

A

Emphysematous pyelonephritis

173
Q

Emphysematous pyelonephritis is most commonly due to what organism

A

E. coli

174
Q

Patients at risk for papillary necrosis

A

1) Diabetics with obstruction
2) Patients with sickle cell disease
3) Patients abusing analgesics

175
Q

Acute vs chronic pyelonephritis: U-shaped cortical scars

A

Chronic

176
Q

Acute vs chronic pyelonephritis: Blunting of renal papillae

A

Chronic

177
Q

Chronic pyelonephritis microscopically presents as

A

Thyroidization of tubules

178
Q

T/F Xanthogranulomatous pyelonephritis is unilateral

A

T

179
Q

T/F Kidney affected by xanthogranulomatous pyelonephritis is enlarged

A

T

180
Q

Calcium stones: Most are secondary to deranged serum calcium levels for whatever reason

A

F, idiopathic

181
Q

Pseudomonas and Providencia are associated with what kidney stones

A

Struvite

182
Q

Why are urease producing organisms commonly associated with struvite stones

A

Urea –> CO2 + Ammonia; Ammonia raises urine pH, struvite precipitates

183
Q

Complication of struvite stones

A

Xanthogranulomatous pyelonephritis

184
Q

T/F Most kidney cysts are simple and usually of little clinical signficance

A

T

185
Q

Most common site of renal cyst

A

Cortex

186
Q

T/F Patients on chronic renal dialysis may have an increased risk of developing renal cell CA

A

T

187
Q

Genes mutated in autosomal dominant polycystic disease

A

PKD1 and PKD2

188
Q

Most common cause of death in patients with autosomal dominant polycystic kidney disease

A

Renal failure

189
Q

T/F Adult polycystic kidney disease is associated with chronic urinary tract infections

A

T

190
Q

Adult polycystic kidney disease: Associated vascular anomaly

A

Berry aneurysms

191
Q

Adult polycystic kidney disease: Other associated anomalies besides berry aneurysms

A

1) Cysts of liver and pancreas

2) Myxomatous mitral valve

192
Q

T/F Autosomal recessive polycystic kidney disease has its clinical onset during adulthood

A

F, infancy or childhood

193
Q

Autosomal recessive polycystic kidney disease: Gene mutated

A

PKHD1

194
Q

PKHD1 in autosomal recessive polycystic kidney disease encodes for

A

Fibrocystin

195
Q

APCKD vs ARPCKD: Multiple cysts (up to 4 cm in size), which usually distort the normal architecture of the kidney to a point where it is no longer identifiable as a kidney

A

Adult

196
Q

APCKD vs ARPCKD: Multiple cysts in cortex and medulla; normal kidney architecture (i.e., the general shape of the kidney) is pre- served

A

Autosomal recessive

197
Q

Most common renal tumor in adults

A

RCC

198
Q

Most common renal tumor in children

A

Wilms tumor

199
Q

RCC: M:F

A

Male

200
Q

RCC: Risk factors (3)

A

1) Smoking
2) Cadmium
3) Chronic dialysis

201
Q

RCC: Most common type

A

Clear cell

202
Q

Type of RCC: Yellow (from glycogen) and hemorrhagic

A

Clear cell

203
Q

Type of RCC: Brown mass

A

Chromophobe

204
Q

Type of RCC: Fibrovascular papillae lined with neoplastic cells; foamy macrophages are within the papillae

A

Papillary

205
Q

RCC: Propensity to invade what

A

Renal vein > IVC > Heart

206
Q

Most common mode of metastasis

A

Hematogenous

207
Q

3 most common sites of RCC metastasis

A

1) Lung (most common)
2) Bone
3) Liver

208
Q

T/F Renal cell CA is known to metastasise to unusual locations such as the forehead and arm

A

T

209
Q

Classic clinical triad of RCC

A

1) Hematuria
2) Flank pain
3) Palpable mass

210
Q

Urothelial neoplasm is aka

A

Transitional cell carcinoma

211
Q

Urothelial neoplasm: T/F Many are papillary and noninvasive hence can be removed without removing the bladder itself

A

T

212
Q

Urothelial neoplasm: Poor prognostic indicator

A

Muscularis propria invasion

213
Q

Urothelial neoplasm: Usual cause of death

A

Ureteral obstruction, eventual renal failure

214
Q

Urothelial neoplasm: Clinical presentation

A

Painless hematuria

215
Q

Acid-base disorder: Lung CA

A

Chronic respi alka

216
Q

Causes of hypochloremic metabolic alkalosis (3)

A

1) Vomiting
2) NGT suction
3) Diuretics

217
Q

Causes normochloremic metabolic alkalosis

A

Exces mineralocorticoids

218
Q

T/F Met alka carries a much graver prognosis than met acid

A

T

219
Q

Anion gap wherein the patient has a probable met acid

A

> 15 mEq/L

220
Q

Anion gap wherein the patient has a definitive met acid

A

> 25 mEq/L

221
Q

Acute respi acid: Increase in HCO3 per mmHG CO2

A

1 mEq/L HCO3 per 10 mmHg CO2

222
Q

Chronic respi acid: Increase in HCO3 per mmHG CO2

A

3.5 mEq/L per 10 mmHg CO2

223
Q

Acute respi alka: Decrease in HCO3 per mmHg CO2

A

2 mEq/L HCO3 per 10 mmHg CO2

224
Q

Chronic respi alka: Decrease in HCO3 per mmHg CO2

A

5 mEq/L HCO3 per 10 mmHg CO2

225
Q

Metabolic acidosis: Change in pCO2

A

Winter’s formula: 1.5 (HCO3) + 8 +/-2

226
Q

Metabolic alkalosis: Change in pCO2

A

0.9 (HCO3) + 9

Pathology (16 decks)

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