Pathology Flashcards

1
Q

Significance of casts in urine

A

Indicates hematuria/pyuria is of glomerular or renal tubular in origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Type of casts seen in glomerulonephritis and malignant HTN

A

RBC casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Type of casts seen in tubulointerstitial inflammation

A

WBC casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type of casts seen in acute pyelonephritis

A

WBC casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type of casts seen in transplant rejection

A

WBC casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type of casts seen in nephrotic syndrome

A

Fatty casts (oval fat bodies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Type of casts seen in acute tubular necrosis

A

Granular, muddy brown casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Type of casts seen in end-stage renal disease or chronic renal failure

A

Waxy casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Significance of hyaline casts

A

Non-specific normal finding seen in concentrated urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mechanism of nephrotic syndrome

A

Podocyte disruption leads to charge barrier impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Findings in nephrotic syndrome

A
Proteinuria > 3.5 g/day
Hypoalbuminemia
Hyperlipidemia
Edema
Fatty casts in urine (oval fat bodies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mechanism of nephritic syndrome

A

GBM disruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Findings in nephritic syndrome

A
HTN
Proteinuria < 3.5 g/day
BUN and Creatine increased
Oliguria
Hematuria
RBC casts in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

LM findings in PSGN

A

Enlarged hypercellular glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IF findings in PSGN

A

“Starry sky”, granular appearance and “lumpy-bumpy”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Type of deposits seen in PSGN

A

IgG, IgM and C3 deposits along GBM and mesangium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

EM findings in PSGN

A

Subepithelial immune complex humps (look like camel humps)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Type III hypersensitivity reaction seen in children after group A strep infection affecting glomerulus presenting with peripheral and periorbital edema, coca-colored urine and hypertension

A

Post-Streptococcal Glomerulonephritis (PSGN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which plasma protein is deficient in PSGN

A

C3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

LM and IF show crescent moon shape consisting of fibrin and C3b proteins with glomerular parietal cells, monocytes and macrophages with doubling of creatinine in < 3 months

A

Rapidly progressive glomerulonephritis (RPGN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Treatment for PSGN

A

Supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Type II hypersensitivity reaction affecting glomerulus presenting with hematuria and pulmonary symptoms with doubling of creatinine in < 3 months

A

Goodpasture syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

IF findings in Goodpasture RPGN

A

Linear pattern of antibodies to GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Type II hypersensitivity reaction affecting glomerulus presenting with hematuria, sinus symptoms, PR3-ANCA/c-ANCA positive with doubling of creatinine in < 3 months

A

Granulomatosis with polyangiitis (Wegener)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Type II hypersensitivity reaction affecting glomerulus presenting with hematuria and MPO-ANCA/p-ANCA positive with doubling of creatinine in < 3 months

A

Microscopic polyangiitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Presents with malar rash and has nephrotic and nephritic symptoms

A

Diffuse proliferative glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

LM findings in diffuse proliferative glomerulonephritis

A

Wire looping of capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

EM findings in diffuse proliferative glomerulonephritis

A

Subendothelial and/or intramembranous IgG-C3 immune complex deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

IF findings in diffuse proliferative glomerulonephritis

A

Granular pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Glomerular disease presenting with episodic gross hematuria with RBC casts after respiratory or GI tract infection

A

IgA nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

LM findings in IgA nephropathy

A

Mesangial proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

EM findings in IgA nephropathy

A

Mesangial immune complex deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

IF findings in IgA nephropathy

A

IgA-based immune complex deposits in mesangium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Glomerular disease presents with sensory hearing loss, ocular disturbances and hematuria with basket-weave appearance on EM

A

Alport syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Inheritance pattern of Alport syndrome

A

X-linked dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Mutation in Alport syndrome

A

Type IV collagen causing thinning and splitting of GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Hepatitis B patient presents with hematuria and has subendothelial immune complex deposits with granular IF - diagnosis

A

Membranoproliferative glomerulonephritis type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Description of PAS stain and H and E stain findings

A

Tram-track appearance due to GBM splitting from mesangial ingrowth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Glomerular disease presents with decreased C3 levels and granular IF from immune complex deposition

A

Membranoproliferative glomerulonephritis type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Mechanism of decreased C3 levels in membranoproliferative glomerulonephritis

A

IgG antibody stabilizes C3 convertase leading to persistent compliment activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

LM findings in minimal change disease

A

Normal glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

IF findings in minimal change disease

A

No findings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

EM findings in minimal change disease

A

Effacement of foot processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Most common nephrotic syndrome in children

A

Minimal change disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Malignancy associated with minimal change disease

A

Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Mechanism of glomerular damage in Hodgkin lymphoma

A

Increases cytokines damaging epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Treatment for minimal change disease

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

LM findings in focal segmental glomerulonephritis

A

Segmental necrosis and hyalinosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

IF findings in focal segmental glomerulonephritis

A

Often negative but may have IgM, C3, C1 deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

EM findings in focal segmental glomerulonephritis

A

Effacement of foot processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Most common cause of nephrotic syndrome in African Americans and Hispanics

A

FSGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Consequence of FSGS

A

Chronic renal failure if fails to respond to steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Common secondary causes of FSGS

A

HIV infection, sickle cell disease, heroin abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

LM findings in membranous nephropathy

A

Diffuse capillary and GBM thickening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Nephrotic presentation of SLE

A

Membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

IF findings in membranous nephropathy

A

Granular as a result of immune complex deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

EM findings in membranous nephropathy

A

Spike and dome appearance with subepithelial deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Most common cause of primary nephrotic syndrome in Caucasian adults that may progress to chronic renal failure

A

Membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Common secondary causes of membranous nephropathy

A

NSAIDs, gold, penicillamine, HBV, HCV, SLE or solid tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Kidney is most commonly affected kidney and presents with Congo red stain showing apple-green birefringement under polarized light

A

Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Type of deposits seen in amyloidosis

A

Amyloid deposits in the mesangium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Disease presents with mesangial expansion, GBM thickening and eosinophilic nodular glomerulosclerosis and is the most common cause of end-stage renal disease in the U.S.

A

Diabetic glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Mechanism of GBM thickening in diabetic glomerulonephritis

A

Non-enzymatic glycosylation of GBM causes increased permeability and thickening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Mechanism of hyaline arteriosclerosis in diabetic glomerulonephritis

A

Non-enzymatic glycosylation of efferent arterioles increases GFR causing mesangial expansion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How do ACE inhibitors affect diabetic glomerulonephritis

A

Slow progression of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Most common kidney stone with hypercalciuria and normocalcemia

A

Calcium oxalate stone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Treatment for calcium oxalate stones

A

Thiazides, citrate and low-sodium diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Best option for treating and preventing kidney stones

A

Encourage fluid intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Type of stone with increased pH and radiopaque on X-ray and CT that is wedge-shaped prism

A

Calcium phosphate stone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Treatment for Calcium phosphate stone

A

Low sodium diet and thiazides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Organisms implicated in ammonium magnesium phosphate (AMP) stones

A

Proteus, Staph saprophyticus, Klebsiella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Findings in AMP stones

A

Increased pH, radiopaque on X-ray and CT with coffin lid-shaped stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Treatment for AMP stones

A

Treat underlying infection and surgical removal of stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Radiolucent stone on X-ray with decreased pH with hyperuricemia

A

Uric acid stone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Treatment for uric acid stones

A

alkalinization of urine, allopurinol and hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Hexagonal-shaped radiolucent stone on X-ray

A

Cystine stone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Mechanism of cystine stone formation

A

Cystine-reabsorbing PCT transporter loses function causing cystinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Most common seen in children with poor reabsorption of cystine, ornithine, lysine, arginine and autosomal recessive

A

Cystinuria which causes cystine stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Treatment for cystinuria

A

Low sodium diet, alkalinization of urine, chelating agents and hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Distention or dilation of renal pelvis and calyces caused by urinary obstruction, retroperitoneal fibrosis, or vesicoureteral reflux

A

Hydronephrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Area of dilation in hydronephrosis

A

Proximal to site of obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Conditions in hydronephrosis that elevate creatinine levels

A

Bilateral obstruction or having only one kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Complications of hydronephrosis

A

Compression and possible atrophy of renal cortex and medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Conditions like renal stones, severe BPH, cervical cancer and injury to ureters can lead to what disease

A

Hydronephrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Malignancy presenting with polygonal clear cells filled with lipids and carbohydrates with golden-yellow due to increased lipid content

A

Renal cell carcinoma (RCC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Population RCC most commonly affects

A

50 - 70 year old men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Risk factors that increase RCC

A

Obesity and smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Route RCC takes when metastasizes

A

Renal vein to IVC and spreads hematogenously

89
Q

Consequence of RCC invading left renal vein

A

Left sided varicocele and metastases

90
Q

Most common primary renal malignancy

A

RCC

91
Q

Sites metastatic RCC most commonly invades

A

Lungs and bone

92
Q

Gene defect most commonly associated with RCC

A

VHL gene deletion on chromosome 3 (von Hippel-Lindau syndrome)

93
Q

Types of von Hippel-Lindau

A

Sporadic and Hereditary

94
Q

Presentation of sporadic type von Hippel-Lindau syndrome

A

Single tumor in upper pole seen in older smoker

95
Q

Presentation of hereditary type von Hippel-Lindau syndrome

A

Multiple bilateral tumors in younger patients

96
Q

Benign epithelial cell tumor arising from collecting ducts

A

Renal oncocytoma

97
Q

Presents with hematuria, palpable mass, 2ndary polycythemia, flank pain, fever, and weight loss

A

RCC

98
Q

Presents with painless hematuria, flank pain, abdominal mass with large eosinophilic cells with abundant mitochondria without perinuclear clearing

A

Renal oncocytoma

99
Q

Type of cells seen in RCC histology

A

Polyclonal clear cells

100
Q

Type of cells seen in renal oncocytoma histology

A

Large eosinophilic cells without perinuclear clearing

101
Q

Treatment for localized RCC

A

Surgery/ablation

102
Q

Treatment for metastatic RCC

A

Immunotherapy or targeted therapy

103
Q

What needs to be done in renal oncocytoma to exclude malignancy

A

Resection

104
Q

Most common renal malignancy of early childhood presenting with large palpable, unilateral flank mass, and hematuria

A

Nephroblastoma (Wilms tumor)

105
Q

What is the mutation in Wilms tumor

A

Loss of function in WT1 or WT2 gene on chromosome 11

106
Q

Syndromes associated with Wilms tumor

A

WAGR complex, Denys-Drash, and Beckwith-Wiedemann

107
Q

Syndrome presents with Wilms tumor, aniridia, genitourinary malformations, mental retardation

A

WAGR complex

108
Q

Gene mutation associated with WAGR complex

A

WT1

109
Q

Syndrome presents with Wilms tumor, early-onset nephrotic syndrome and male pseudohermaphroditism

A

Denys-Drash

110
Q

Syndrome presents with Wilms tumor, macroglossia, organomegaly, hemihyperplasia and neonatal hypoglycemia

A

Beckwith-Wiedemann

111
Q

Gene mutation associated with Denys-Drash

A

WT1

112
Q

Gene mutation associated with Beckwith-Wiedemann

A

WT2

113
Q

What does Wilms tumor contain

A

Embryonic glomerular structures

114
Q

Cells RCC originates from

A

PCT cells

115
Q

Most common tumor of the urinary tract system mostly affecting men in developed countries

A

Transitional cell carcinoma

116
Q

Type of mutation associated with flat type transitional cell carcinoma

A

Early p53 mutation

117
Q

Low-grade transitional cell carcinoma

A

Papillary

118
Q

High-grade transitional cell carcinoma

A

Flat

119
Q

Presents with painless hematuria with no casts in older smoker

A

Transitional cell carcinoma

120
Q

Risk factors associated with transitional cell carcinoma

A

Phenacetin, Smoking, Aniline dyes and Cyclophosphamide (P SAC)

121
Q

Disease in Middle Eastern men presenting with painless hematuria

A

Squamous cell carcinoma (SCC) of the bladder

122
Q

Consequence of chronic irritation of urinary bladder

A

Squamous metaplasia to dysplasia to squamous cell carcinoma

123
Q

Risk factors associated with SCC of the bladder

A

Chronic cystitis, smoking, chronic nephrolithiasis

124
Q

Helminth infection associated with SCC of the bladder

A

Schistosoma haematobium

125
Q

Population most commonly affected by SCC of the bladder

A

Middle Eastern men

126
Q

Nerve that innervates the external urethral sphincter

A

Pudendal nerve

127
Q

Urethral sphincter under involuntary control

A

Internal urethral sphincter

128
Q

Type of urinary incontinence presenting with leak when sneezing, lifting, coughing or Valsalva maneuver from urethra with no leakage while sleeping

A

Stress incontinence

129
Q

Cause of stress incontinence

A

Outlet incompetence from urethral hypermobility or intrinsic sphincter deficiency

130
Q

Type of urinary incontinence presenting with involuntary loss of urine both day and night and not able to suppress urge to void

A

Urgency incontinence

131
Q

Treatment for stress incontinence

A

Pelvic floor muscle exercise, weight loss, pessaries

132
Q

Cause of urgency incontinence

A

Overactive bladder from detrusor instability

133
Q

Treatment for urgency incontinence

A

Kegel exercises, bladder training or antimuscarinics like oxybutynin

134
Q

Type of urinary incontinence with both stress and urgency incontinence

A

Mixed incontinence

135
Q

Type of urinary incontinence presenting with leak, overfilling and increased post-void residual on catheterization or ultrasound

A

Overflow incontinence

136
Q

Cause of overflow incontinence

A

Detrusor underactivity or outlet obstruction leading to incomplete emptying

137
Q

Condition presenting with suprapubic pain, dysuria, urinary frequency, and urgency typically with no systemic signs

A

Urinary tract infection

138
Q

Population most commonly affected by UTIs

A

Sexually active women due to shorter urethra

139
Q

Most common cause of UTIs

A

E coli

140
Q

Can cause UTIs in sexually active young women

A

Staph saprophyticus

141
Q

Causes of UTIs from most to least common

A

E coli, Staph saprophyticus, Klebsiella, Proteus

142
Q

Causes UTI and has strong ammonia scent

A

Proteus

143
Q

Risk factors associated with UTIs

A

Female gender, sexual intercourse, indwelling catheter

144
Q

Lab findings in UTIs

A

Positive leukocyte esterase and nitrites

145
Q

Significance of positive urinary nitrites in UTIs

A

Infection with gram negative organisms

146
Q

Significance of sterile pyuria and negative urine culture

A

Infection with N gonorrhoeae or Chlamydia trachomatis infection

147
Q

Condition presenting with fevers, flank pain, nausea, vomiting, chills, WBCs in urine and WBC casts with striated parenchymal enhancement on CT

A

Acute pyelonephritis

148
Q

Area of kidney affected in acute pyelonephritis

A

Cortex with relative sparing of glomeruli and vessels

149
Q

Common organisms causing acute pyelonephritis

A

E coli, Klebsiella and Enterococcus faecalis

150
Q

Risk factors associated with acute pyelonephritis

A

Indwelling catheter, urinary tract obstruction, vesicoureteral reflux, DM, pregnancy

151
Q

Complications of acute pyelonephritis

A

Chronic pyelonephritis, renal papillary necrosis, perinephric abscess, urosepsis

152
Q

Condition caused by recurrent acute pyelonephritis and vesicoureteral reflux or chronically obstructed kidney stones

A

Chronic pyelonephritis

153
Q

Type of infiltrate seen in acute pyelonephritis

A

Neutrophilic infiltrate of renal interstitium

154
Q

Microscopic pathology seen in chronic pyelonephritis

A

Eosinophilic casts resembling thyroid tissue

155
Q

Presents with coarse asymmetric corticomedullary scarring, blunted calyx and tubules with eosinophilic casts resembling thyroid tissue

A

Chronic pyelonephritis

156
Q

Condition that presents with grossly orange nodules that can mimic tumor nodules with widespread kidney damage due to granulomatous tissue containing foamy macrophages

A

Xanthogranulomatous pyelonephritis

157
Q

Cause of chronic pyelonephritis in children

A

Vesicoureteral reflux

158
Q

Acute cortical infarction of both kidneys

A

Diffuse cortical necrosis

159
Q

Cause of diffuse cortical necrosis

A

Vasospasms and DIC from abruptio placentae or septic shock

160
Q

Hypocalcemia, hyperphosphatemia and failure of vitamin D hydroxylation associated with chronic renal disease leading to 2ndary hyperparathyroidism

A

Renal osteodystrophy

161
Q

Consequence of hyperphosphatemia

A

Decreases serum calcium by causing tissue calcifications

162
Q

Consequence of decreased 1,25-(OH)2 D3

A

Decreased intestinal calcium absorption

163
Q

Common cause of pre-renal azotemia

A

Decreased renal blood flow from hypotension

164
Q

How is GFR affected in pre-renal azotemia

A

GFR is decreased

165
Q

What is retained by kidney in pre-renal azotemia to conserve volume

A

Na/H2O and BUN

166
Q

What happens to BUN/creatinine ration in pre-renal azotemia

A

BUN/creatinine ratio increases due to retained BUN

167
Q

What happens to FeNa in pre-renal azotemia

A

FeNa decreases

168
Q

Causes of intrinsic renal failure

A

ATN, ischemia/toxins > common

Acute glomerulonephritis or interstitial nephritis < common

169
Q

BUN/creatinine ratio in intrinsic renal failure

A

BUN/creatinine ratio decreased since BUN reabsorption impaired

170
Q

How is GFR affected in intrinsic renal failure

A

Decreased GFR from debris obstructing tubule in ATN

171
Q

Type of casts seen in intrinsic renal failure

A

Epithelial/granular casts

172
Q

Cause of post-renal azotemia

A

Bilateral outflow obstruction from either stones, BPH, neoplasia or congenital abnormalities

173
Q

Urine osmolality in pre-renal azotemia

A

> 500

174
Q

Urine Na in pre-renal azotemia

A

< 20

175
Q

FeNa in pre-renal azotemia

A

< 1%

176
Q

Serum BUN/Cr in pre-renal azotemia

A

> 20

177
Q

Urine osmolality in intrinsic renal failure

A

< 350

178
Q

Urine Na in intrinsic renal failure

A

> 40

179
Q

FeNa in intrinsic renal failure

A

> 2%

180
Q

Serum BUN/Cr in intrinsic renal failure

A

< 15

181
Q

Urine osmolality in post-renal azotemia

A

< 350

182
Q

Urine Na in post-renal azotemia

A

> 40

183
Q

FeNa in post-renal azotemia

A

< 1% - mild

> 2% - severe

184
Q

Serum BUN/Cr in post-renal azotemia

A

Varies

185
Q

Disease defined as inability to make urine and excrete nitrogenous waste

A

Renal failure

186
Q

Causes of acute renal failure

A

ATN

187
Q

Causes of chronic renal failure

A

HTN, DM, congenital anomalies, glomerular disease

188
Q

Consequence of renal failure acute or chronic

A
MAD HUNGER:
Metabolic Acidosis
Dyslipidemia
Hyperkalemia
Uremia
Na/H2O retention
Growth retardation and developmental delay
Erythropoietin failure
Renal osteodystrophy
189
Q

Cause of acute interstitial nephritis

A

Drugs acting as haptens inducing hypersensitivity reaction type III

190
Q

Presentation of acute interstitial nephritis

A

Pyuria and azotemia occurring days to weeks after administration of drugs

191
Q

Drugs associated with acute interstitial nephritis

A
Diuretics
NSAIDs
Penicillin derivatives
PPIs
Rifampin
192
Q

Secondary causes of acute interstitial nephritis

A

Systemic infections and autoimmune diseases

193
Q

Most common cause of acute kidney injury in hospitalized patients

A

ATN

194
Q

Stages of ATN

A
  1. Inciting event
  2. Maintenance phase
  3. Recovery phase
195
Q

ATN stage characterized by oliguria and risk of hyperkalemia, metabolic acidosis and uremia lasting 1-3 weeks

A

Maintenance phase

196
Q

ATN stage characterized by polyuria, drop in BUN and creatinine and risk of hypokalemia

A

Recovery phase

197
Q

Sections of kidney more susceptible to ATN injury due to ischemia

A

PCT and thick ascending limb of loop of Henle

198
Q

Ischemic causes of ATN

A

HoTN, shock, sepsis, hemorrhage, HF

199
Q

Nephrotoxic causes of ATN

A

Toxic substances, crush injury, hemoglobinuria

200
Q

Mechanism of ATN in crush injury

A

Myoglobin released from cells is toxic to kidney

201
Q

Toxic substances in ATN

A

Radiocontrast, aminoglycosides, lead, cisplatin, ethylene glycol

202
Q

Section kidney more susceptible to ATN injury due to nephrotoxicity

A

PCT

203
Q

Onset of ATN with radiocontrast

A

24-48 hours

204
Q

Onset of ATN with aminoglycosides

A

10-14 days

205
Q

Mechanism of injury in ATN from ethylene glycol

A

Oxalate crystal formation

206
Q

Mechanism of injury in ATN from chemotherapy

A

Increased urate from tumor lysis syndrome

207
Q

Disease characterized by sloughing of necrotic renal papillae leading to gross hematuria and proteinuria

A

Renal papillary necrosis

208
Q

Conditions associated with renal papillary necrosis

A

Sickle cell disease, acute pyelonephritis, analgesics, DM

209
Q

Most common mutation leading to ADPKD

A

PKD1 on chromosome 16

210
Q

Disease in adult with berry aneurysms, MVP, hepatic cysts, diverticulosis and kidney cysts presenting with flank pain, hematuria, HTN and urinary infection

A

ADPKD

211
Q

Mutations that cause ADPKD

A

PKD1 chromosome 16 > common

PKD2 chromosome 4 < common

212
Q

Treatment for ADPKD

A

ACE inhibitors or ARBs

213
Q

Inheritance patter for ADPKD

A

Autosomal dominant

214
Q

Inherited condition presenting with cystic dilatation of collecting ducts and enlarged bilateral kidneys with cysts seen in infancy

A

Autosomal Recessive Polycystic Kidney Disease (ARPKD)

215
Q

Consequence of ARPKD renal failure in utero

A

Potter sequence

216
Q

Complications of ARPKD beyond neonatal period

A

HTN, progressive renal insufficiency, portal HTN from congenital hepatic fibrosis

217
Q

Autosomal dominant disorder with shrunken kidneys on ultrasound causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine

A

Medullary cystic disease

218
Q

Very common asymptomatic finding that accounts for majority of all renal masses and filled with ultrafiltrate that is anechoic on ultrasound

A

Simple cysts

219
Q

Presents with septated, enhanced or solid component on imaging requiring removal due to risk of RCC

A

Complex cysts