Pathology Flashcards
1
Q
Significance of casts in urine
A
Indicates hematuria/pyuria is of glomerular or renal tubular in origin
2
Q
Type of casts seen in glomerulonephritis and malignant HTN
A
RBC casts
3
Q
Type of casts seen in tubulointerstitial inflammation
A
WBC casts
4
Q
Type of casts seen in acute pyelonephritis
A
WBC casts
5
Q
Type of casts seen in transplant rejection
A
WBC casts
6
Q
Type of casts seen in nephrotic syndrome
A
Fatty casts (oval fat bodies)
7
Q
Type of casts seen in acute tubular necrosis
A
Granular, muddy brown casts
8
Q
Type of casts seen in end-stage renal disease or chronic renal failure
A
Waxy casts
9
Q
Significance of hyaline casts
A
Non-specific normal finding seen in concentrated urine
10
Q
Mechanism of nephrotic syndrome
A
Podocyte disruption leads to charge barrier impairment
11
Q
Findings in nephrotic syndrome
A
Proteinuria > 3.5 g/day Hypoalbuminemia Hyperlipidemia Edema Fatty casts in urine (oval fat bodies)
12
Q
Mechanism of nephritic syndrome
A
GBM disruption
13
Q
Findings in nephritic syndrome
A
HTN Proteinuria < 3.5 g/day BUN and Creatine increased Oliguria Hematuria RBC casts in urine
14
Q
LM findings in PSGN
A
Enlarged hypercellular glomeruli
15
Q
IF findings in PSGN
A
“Starry sky”, granular appearance and “lumpy-bumpy”
16
Q
Type of deposits seen in PSGN
A
IgG, IgM and C3 deposits along GBM and mesangium
17
Q
EM findings in PSGN
A
Subepithelial immune complex humps (look like camel humps)
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)
19
Q
Which plasma protein is deficient in PSGN
A
C3
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)
21
Q
Treatment for PSGN
A
Supportive
22
Q
Type II hypersensitivity reaction affecting glomerulus presenting with hematuria and pulmonary symptoms with doubling of creatinine in < 3 months
A
Goodpasture syndrome
23
Q
IF findings in Goodpasture RPGN
A
Linear pattern of antibodies to GBM
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)
25
Type II hypersensitivity reaction affecting glomerulus presenting with hematuria and MPO-ANCA/p-ANCA positive with doubling of creatinine in < 3 months
Microscopic polyangiitis
26
Presents with malar rash and has nephrotic and nephritic symptoms
Diffuse proliferative glomerulonephritis
27
LM findings in diffuse proliferative glomerulonephritis
Wire looping of capillaries
28
EM findings in diffuse proliferative glomerulonephritis
Subendothelial and/or intramembranous IgG-C3 immune complex deposits
29
IF findings in diffuse proliferative glomerulonephritis
Granular pattern
30
Glomerular disease presenting with episodic gross hematuria with RBC casts after respiratory or GI tract infection
IgA nephropathy
31
LM findings in IgA nephropathy
Mesangial proliferation
32
EM findings in IgA nephropathy
Mesangial immune complex deposits
33
IF findings in IgA nephropathy
IgA-based immune complex deposits in mesangium
34
Glomerular disease presents with sensory hearing loss, ocular disturbances and hematuria with basket-weave appearance on EM
Alport syndrome
35
Inheritance pattern of Alport syndrome
X-linked dominant
36
Mutation in Alport syndrome
Type IV collagen causing thinning and splitting of GBM
37
Hepatitis B patient presents with hematuria and has subendothelial immune complex deposits with granular IF - diagnosis
Membranoproliferative glomerulonephritis type I
38
Description of PAS stain and H and E stain findings
Tram-track appearance due to GBM splitting from mesangial ingrowth
39
Glomerular disease presents with decreased C3 levels and granular IF from immune complex deposition
Membranoproliferative glomerulonephritis type II
40
Mechanism of decreased C3 levels in membranoproliferative glomerulonephritis
IgG antibody stabilizes C3 convertase leading to persistent compliment activation
41
LM findings in minimal change disease
Normal glomeruli
42
IF findings in minimal change disease
No findings
43
EM findings in minimal change disease
Effacement of foot processes
44
Most common nephrotic syndrome in children
Minimal change disease
45
Malignancy associated with minimal change disease
Hodgkin lymphoma
46
Mechanism of glomerular damage in Hodgkin lymphoma
Increases cytokines damaging epithelial cells
47
Treatment for minimal change disease
NSAIDs
48
LM findings in focal segmental glomerulonephritis
Segmental necrosis and hyalinosis
49
IF findings in focal segmental glomerulonephritis
Often negative but may have IgM, C3, C1 deposits
50
EM findings in focal segmental glomerulonephritis
Effacement of foot processes
51
Most common cause of nephrotic syndrome in African Americans and Hispanics
FSGS
52
Consequence of FSGS
Chronic renal failure if fails to respond to steroids
53
Common secondary causes of FSGS
HIV infection, sickle cell disease, heroin abuse
54
LM findings in membranous nephropathy
Diffuse capillary and GBM thickening
55
Nephrotic presentation of SLE
Membranous nephropathy
56
IF findings in membranous nephropathy
Granular as a result of immune complex deposition
57
EM findings in membranous nephropathy
Spike and dome appearance with subepithelial deposits
58
Most common cause of primary nephrotic syndrome in Caucasian adults that may progress to chronic renal failure
Membranous nephropathy
59
Common secondary causes of membranous nephropathy
NSAIDs, gold, penicillamine, HBV, HCV, SLE or solid tumors
60
Kidney is most commonly affected kidney and presents with Congo red stain showing apple-green birefringement under polarized light
Amyloidosis
61
Type of deposits seen in amyloidosis
Amyloid deposits in the mesangium
62
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.
Diabetic glomerulonephritis
63
Mechanism of GBM thickening in diabetic glomerulonephritis
Non-enzymatic glycosylation of GBM causes increased permeability and thickening
64
Mechanism of hyaline arteriosclerosis in diabetic glomerulonephritis
Non-enzymatic glycosylation of efferent arterioles increases GFR causing mesangial expansion
65
How do ACE inhibitors affect diabetic glomerulonephritis
Slow progression of disease
66
Most common kidney stone with hypercalciuria and normocalcemia
Calcium oxalate stone
67
Treatment for calcium oxalate stones
Thiazides, citrate and low-sodium diet
68
Best option for treating and preventing kidney stones
Encourage fluid intake
69
Type of stone with increased pH and radiopaque on X-ray and CT that is wedge-shaped prism
Calcium phosphate stone
70
Treatment for Calcium phosphate stone
Low sodium diet and thiazides
71
Organisms implicated in ammonium magnesium phosphate (AMP) stones
Proteus, Staph saprophyticus, Klebsiella
72
Findings in AMP stones
Increased pH, radiopaque on X-ray and CT with coffin lid-shaped stones
73
Treatment for AMP stones
Treat underlying infection and surgical removal of stones
74
Radiolucent stone on X-ray with decreased pH with hyperuricemia
Uric acid stone
75
Treatment for uric acid stones
alkalinization of urine, allopurinol and hydration
76
Hexagonal-shaped radiolucent stone on X-ray
Cystine stone
77
Mechanism of cystine stone formation
Cystine-reabsorbing PCT transporter loses function causing cystinuria
78
Most common seen in children with poor reabsorption of cystine, ornithine, lysine, arginine and autosomal recessive
Cystinuria which causes cystine stones
79
Treatment for cystinuria
Low sodium diet, alkalinization of urine, chelating agents and hydration
80
Distention or dilation of renal pelvis and calyces caused by urinary obstruction, retroperitoneal fibrosis, or vesicoureteral reflux
Hydronephrosis
81
Area of dilation in hydronephrosis
Proximal to site of obstruction
82
Conditions in hydronephrosis that elevate creatinine levels
Bilateral obstruction or having only one kidney
83
Complications of hydronephrosis
Compression and possible atrophy of renal cortex and medulla
84
Conditions like renal stones, severe BPH, cervical cancer and injury to ureters can lead to what disease
Hydronephrosis
85
Malignancy presenting with polygonal clear cells filled with lipids and carbohydrates with golden-yellow due to increased lipid content
Renal cell carcinoma (RCC)
86
Population RCC most commonly affects
50 - 70 year old men
87
Risk factors that increase RCC
Obesity and smoking
88
Route RCC takes when metastasizes
Renal vein to IVC and spreads hematogenously
89
Consequence of RCC invading left renal vein
Left sided varicocele and metastases
90
Most common primary renal malignancy
RCC
91
Sites metastatic RCC most commonly invades
Lungs and bone
92
Gene defect most commonly associated with RCC
VHL gene deletion on chromosome 3 (von Hippel-Lindau syndrome)
93
Types of von Hippel-Lindau
Sporadic and Hereditary
94
Presentation of sporadic type von Hippel-Lindau syndrome
Single tumor in upper pole seen in older smoker
95
Presentation of hereditary type von Hippel-Lindau syndrome
Multiple bilateral tumors in younger patients
96
Benign epithelial cell tumor arising from collecting ducts
Renal oncocytoma
97
Presents with hematuria, palpable mass, 2ndary polycythemia, flank pain, fever, and weight loss
RCC
98
Presents with painless hematuria, flank pain, abdominal mass with large eosinophilic cells with abundant mitochondria without perinuclear clearing
Renal oncocytoma
99
Type of cells seen in RCC histology
Polyclonal clear cells
100
Type of cells seen in renal oncocytoma histology
Large eosinophilic cells without perinuclear clearing
101
Treatment for localized RCC
Surgery/ablation
102
Treatment for metastatic RCC
Immunotherapy or targeted therapy
103
What needs to be done in renal oncocytoma to exclude malignancy
Resection
104
Most common renal malignancy of early childhood presenting with large palpable, unilateral flank mass, and hematuria
Nephroblastoma (Wilms tumor)
105
What is the mutation in Wilms tumor
Loss of function in WT1 or WT2 gene on chromosome 11
106
Syndromes associated with Wilms tumor
WAGR complex, Denys-Drash, and Beckwith-Wiedemann
107
Syndrome presents with Wilms tumor, aniridia, genitourinary malformations, mental retardation
WAGR complex
108
Gene mutation associated with WAGR complex
WT1
109
Syndrome presents with Wilms tumor, early-onset nephrotic syndrome and male pseudohermaphroditism
Denys-Drash
110
Syndrome presents with Wilms tumor, macroglossia, organomegaly, hemihyperplasia and neonatal hypoglycemia
Beckwith-Wiedemann
111
Gene mutation associated with Denys-Drash
WT1
112
Gene mutation associated with Beckwith-Wiedemann
WT2
113
What does Wilms tumor contain
Embryonic glomerular structures
114
Cells RCC originates from
PCT cells
115
Most common tumor of the urinary tract system mostly affecting men in developed countries
Transitional cell carcinoma
116
Type of mutation associated with flat type transitional cell carcinoma
Early p53 mutation
117
Low-grade transitional cell carcinoma
Papillary
118
High-grade transitional cell carcinoma
Flat
119
Presents with painless hematuria with no casts in older smoker
Transitional cell carcinoma
120
Risk factors associated with transitional cell carcinoma
Phenacetin, Smoking, Aniline dyes and Cyclophosphamide (P SAC)
121
Disease in Middle Eastern men presenting with painless hematuria
Squamous cell carcinoma (SCC) of the bladder
122
Consequence of chronic irritation of urinary bladder
Squamous metaplasia to dysplasia to squamous cell carcinoma
123
Risk factors associated with SCC of the bladder
Chronic cystitis, smoking, chronic nephrolithiasis
124
Helminth infection associated with SCC of the bladder
Schistosoma haematobium
125
Population most commonly affected by SCC of the bladder
Middle Eastern men
126
Nerve that innervates the external urethral sphincter
Pudendal nerve
127
Urethral sphincter under involuntary control
Internal urethral sphincter
128
Type of urinary incontinence presenting with leak when sneezing, lifting, coughing or Valsalva maneuver from urethra with no leakage while sleeping
Stress incontinence
129
Cause of stress incontinence
Outlet incompetence from urethral hypermobility or intrinsic sphincter deficiency
130
Type of urinary incontinence presenting with involuntary loss of urine both day and night and not able to suppress urge to void
Urgency incontinence
131
Treatment for stress incontinence
Pelvic floor muscle exercise, weight loss, pessaries
132
Cause of urgency incontinence
Overactive bladder from detrusor instability
133
Treatment for urgency incontinence
Kegel exercises, bladder training or antimuscarinics like oxybutynin
134
Type of urinary incontinence with both stress and urgency incontinence
Mixed incontinence
135
Type of urinary incontinence presenting with leak, overfilling and increased post-void residual on catheterization or ultrasound
Overflow incontinence
136
Cause of overflow incontinence
Detrusor underactivity or outlet obstruction leading to incomplete emptying
137
Condition presenting with suprapubic pain, dysuria, urinary frequency, and urgency typically with no systemic signs
Urinary tract infection
138
Population most commonly affected by UTIs
Sexually active women due to shorter urethra
139
Most common cause of UTIs
E coli
140
Can cause UTIs in sexually active young women
Staph saprophyticus
141
Causes of UTIs from most to least common
E coli, Staph saprophyticus, Klebsiella, Proteus
142
Causes UTI and has strong ammonia scent
Proteus
143
Risk factors associated with UTIs
Female gender, sexual intercourse, indwelling catheter
144
Lab findings in UTIs
Positive leukocyte esterase and nitrites
145
Significance of positive urinary nitrites in UTIs
Infection with gram negative organisms
146
Significance of sterile pyuria and negative urine culture
Infection with N gonorrhoeae or Chlamydia trachomatis infection
147
Condition presenting with fevers, flank pain, nausea, vomiting, chills, WBCs in urine and WBC casts with striated parenchymal enhancement on CT
Acute pyelonephritis
148
Area of kidney affected in acute pyelonephritis
Cortex with relative sparing of glomeruli and vessels
149
Common organisms causing acute pyelonephritis
E coli, Klebsiella and Enterococcus faecalis
150
Risk factors associated with acute pyelonephritis
Indwelling catheter, urinary tract obstruction, vesicoureteral reflux, DM, pregnancy
151
Complications of acute pyelonephritis
Chronic pyelonephritis, renal papillary necrosis, perinephric abscess, urosepsis
152
Condition caused by recurrent acute pyelonephritis and vesicoureteral reflux or chronically obstructed kidney stones
Chronic pyelonephritis
153
Type of infiltrate seen in acute pyelonephritis
Neutrophilic infiltrate of renal interstitium
154
Microscopic pathology seen in chronic pyelonephritis
Eosinophilic casts resembling thyroid tissue
155
Presents with coarse asymmetric corticomedullary scarring, blunted calyx and tubules with eosinophilic casts resembling thyroid tissue
Chronic pyelonephritis
156
Condition that presents with grossly orange nodules that can mimic tumor nodules with widespread kidney damage due to granulomatous tissue containing foamy macrophages
Xanthogranulomatous pyelonephritis
157
Cause of chronic pyelonephritis in children
Vesicoureteral reflux
158
Acute cortical infarction of both kidneys
Diffuse cortical necrosis
159
Cause of diffuse cortical necrosis
Vasospasms and DIC from abruptio placentae or septic shock
160
Hypocalcemia, hyperphosphatemia and failure of vitamin D hydroxylation associated with chronic renal disease leading to 2ndary hyperparathyroidism
Renal osteodystrophy
161
Consequence of hyperphosphatemia
Decreases serum calcium by causing tissue calcifications
162
Consequence of decreased 1,25-(OH)2 D3
Decreased intestinal calcium absorption
163
Common cause of pre-renal azotemia
Decreased renal blood flow from hypotension
164
How is GFR affected in pre-renal azotemia
GFR is decreased
165
What is retained by kidney in pre-renal azotemia to conserve volume
Na/H2O and BUN
166
What happens to BUN/creatinine ration in pre-renal azotemia
BUN/creatinine ratio increases due to retained BUN
167
What happens to FeNa in pre-renal azotemia
FeNa decreases
168
Causes of intrinsic renal failure
ATN, ischemia/toxins > common
| Acute glomerulonephritis or interstitial nephritis < common
169
BUN/creatinine ratio in intrinsic renal failure
BUN/creatinine ratio decreased since BUN reabsorption impaired
170
How is GFR affected in intrinsic renal failure
Decreased GFR from debris obstructing tubule in ATN
171
Type of casts seen in intrinsic renal failure
Epithelial/granular casts
172
Cause of post-renal azotemia
Bilateral outflow obstruction from either stones, BPH, neoplasia or congenital abnormalities
173
Urine osmolality in pre-renal azotemia
> 500
174
Urine Na in pre-renal azotemia
< 20
175
FeNa in pre-renal azotemia
< 1%
176
Serum BUN/Cr in pre-renal azotemia
> 20
177
Urine osmolality in intrinsic renal failure
< 350
178
Urine Na in intrinsic renal failure
> 40
179
FeNa in intrinsic renal failure
> 2%
180
Serum BUN/Cr in intrinsic renal failure
< 15
181
Urine osmolality in post-renal azotemia
< 350
182
Urine Na in post-renal azotemia
> 40
183
FeNa in post-renal azotemia
< 1% - mild
| > 2% - severe
184
Serum BUN/Cr in post-renal azotemia
Varies
185
Disease defined as inability to make urine and excrete nitrogenous waste
Renal failure
186
Causes of acute renal failure
ATN
187
Causes of chronic renal failure
HTN, DM, congenital anomalies, glomerular disease
188
Consequence of renal failure acute or chronic
```
MAD HUNGER:
Metabolic Acidosis
Dyslipidemia
Hyperkalemia
Uremia
Na/H2O retention
Growth retardation and developmental delay
Erythropoietin failure
Renal osteodystrophy
```
189
Cause of acute interstitial nephritis
Drugs acting as haptens inducing hypersensitivity reaction type III
190
Presentation of acute interstitial nephritis
Pyuria and azotemia occurring days to weeks after administration of drugs
191
Drugs associated with acute interstitial nephritis
```
Diuretics
NSAIDs
Penicillin derivatives
PPIs
Rifampin
```
192
Secondary causes of acute interstitial nephritis
Systemic infections and autoimmune diseases
193
Most common cause of acute kidney injury in hospitalized patients
ATN
194
Stages of ATN
1. Inciting event
2. Maintenance phase
3. Recovery phase
195
ATN stage characterized by oliguria and risk of hyperkalemia, metabolic acidosis and uremia lasting 1-3 weeks
Maintenance phase
196
ATN stage characterized by polyuria, drop in BUN and creatinine and risk of hypokalemia
Recovery phase
197
Sections of kidney more susceptible to ATN injury due to ischemia
PCT and thick ascending limb of loop of Henle
198
Ischemic causes of ATN
HoTN, shock, sepsis, hemorrhage, HF
199
Nephrotoxic causes of ATN
Toxic substances, crush injury, hemoglobinuria
200
Mechanism of ATN in crush injury
Myoglobin released from cells is toxic to kidney
201
Toxic substances in ATN
Radiocontrast, aminoglycosides, lead, cisplatin, ethylene glycol
202
Section kidney more susceptible to ATN injury due to nephrotoxicity
PCT
203
Onset of ATN with radiocontrast
24-48 hours
204
Onset of ATN with aminoglycosides
10-14 days
205
Mechanism of injury in ATN from ethylene glycol
Oxalate crystal formation
206
Mechanism of injury in ATN from chemotherapy
Increased urate from tumor lysis syndrome
207
Disease characterized by sloughing of necrotic renal papillae leading to gross hematuria and proteinuria
Renal papillary necrosis
208
Conditions associated with renal papillary necrosis
Sickle cell disease, acute pyelonephritis, analgesics, DM
209
Most common mutation leading to ADPKD
PKD1 on chromosome 16
210
Disease in adult with berry aneurysms, MVP, hepatic cysts, diverticulosis and kidney cysts presenting with flank pain, hematuria, HTN and urinary infection
ADPKD
211
Mutations that cause ADPKD
PKD1 chromosome 16 > common
| PKD2 chromosome 4 < common
212
Treatment for ADPKD
ACE inhibitors or ARBs
213
Inheritance patter for ADPKD
Autosomal dominant
214
Inherited condition presenting with cystic dilatation of collecting ducts and enlarged bilateral kidneys with cysts seen in infancy
Autosomal Recessive Polycystic Kidney Disease (ARPKD)
215
Consequence of ARPKD renal failure in utero
Potter sequence
216
Complications of ARPKD beyond neonatal period
HTN, progressive renal insufficiency, portal HTN from congenital hepatic fibrosis
217
Autosomal dominant disorder with shrunken kidneys on ultrasound causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine
Medullary cystic disease
218
Very common asymptomatic finding that accounts for majority of all renal masses and filled with ultrafiltrate that is anechoic on ultrasound
Simple cysts
219
Presents with septated, enhanced or solid component on imaging requiring removal due to risk of RCC
Complex cysts
