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
2
Q
Reason why many kidney disease do not become clinically apparent until majority of the organ is affected
A
Large physiologic reserve
3
Q
Prerenal vs Renal: FENa less than 1%
A
Prerenal
4
Q
Prerenal vs Renal: FENa >1%
A
Renal
5
Q
Prerenal vs Renal: BUN/Cr ratio >20:1
A
Prerenal
6
Q
Prerenal vs Renal: BUN/Cr ratio less than 20:1
A
Renal
7
Q
Prerenal vs Renal: Urine sodium
A
Prerenal
8
Q
Prerenal vs Renal: Urine sodium >20 mEq/L
A
Renal
9
Q
Prerenal vs Renal: Urine osm >500 mOsm/kg
A
Prerenal
10
Q
Prerenal vs Renal: Urine osm less than 400 mOsm/kg
A
Renal
11
Q
Diagnostic test of choice in post renal azotemia
A
Ultrasound
12
Q
Electrolyte disturbances in acute renal failure
A
1) Hyponatremia
2) Hyperkalemia
3) Hyperphosphatemia
4) Hypocalcemia
13
Q
Acid-base disorder in acute renal failure
A
Metabolic acidosis
14
Q
Oliguria is defined as
A
Less than 400 mL/day
15
Q
Very sensitive test for differentiating pre renal from renal cause of ARF
A
FENa
16
Q
Chronic renal failure: Electrolyte imbalance
A
1) Hyperkalemia
2) Hyperphosphatemua
3) Hypocalcemia
17
Q
Chronic renal failure: Acid-base disorder
A
Metabolic acidosis
18
Q
Chronic renal failure: Urine SG
A
Less than 1.010
19
Q
Acute renal failure: Urine SG in renal cause
A
Less than 1.010
20
Q
Prerenal vs Renal: FENa
A
Prerenal
21
Q
Prerenal vs Renal: FENa >1%
A
Renal
22
Q
Prerenal vs Renal: BUN/Cr ratio >20:1
A
Prerenal
23
Q
Prerenal vs Renal: BUN/Cr ratio
A
Renal
24
Q
Prerenal vs Renal: Urine sodium
A
Prerenal
25
Prerenal vs Renal: Urine sodium >20 mEq/L
Renal
26
Prerenal vs Renal: Urine osm >500 mOsm/kg
Prerenal
27
Prerenal vs Renal: Urine osm
Renal
28
Diagnostic test of choice in post renal azotemia
Ultrasound
29
Electrolyte disturbances in acute renal failure
1) Hyponatremia
2) Hyperkalemia
3) Hyperphosphatemia
4) Hypocalcemia
30
Acid-base disorder in acute renal failure
Metabolic acidosis
31
Oliguria is defined as
Less than 400 mL urine per day
32
Very sensitive test for differentiating pre renal from renal cause of ARF
FENa
33
Chronic renal failure: Electrolyte imbalance
1) Hyperkalemia
2) Hyperphosphatemua
3) Hypocalcemia
34
Chronic renal failure: Acid-base disorder
Metabolic acidosis
35
Chronic renal failure: Urine SG
Less than 1.010
36
Acute renal failure: Urine SG in prerenal cause
> 1.020
37
Acute renal failure: Urine SG in renal cause
Less than 1.010
38
Chronic renal failure: Hematologic complications (2)
1) Normocytic normochromic anemia
| 2) Platelet dysfunction
39
Chronic renal failure: Skeletal complications (2)
1) Renal osteodystrophy
| 2) Hyperparathyroidism
40
Earliest and most sensitive clinical indication of hypovolemia
Oliguria
41
Stains in LM: Basement membrane and mesangium
PAS
42
Stains in LM: Fibrosis
Trichrome
43
Stains in LM: Basement membrane
Silver
44
Igs used in IF
IgG, IgM, IgA
45
IF pattern: Reaction of Ab with pathogenic Ab directed against Ag in the GBM
Linear
46
IF pattern: Reaction of Ab with pathogenic Ag-Ab complexes on GBM
Granular
47
Allows for detection and determination of location of ICs and evaluation of basement membrane
EM
48
Origin of MOST glomerular diseases
Immunologic
49
Mechanism of destruction in IC deposition
Complement activation and chemotaxis via C5a
50
Type of edema caused by nephrotic syndrome
Generalized (anasarca)
51
Nephrotic syndrome: Mechanism for hyperlipidemia
Response of liver to loss of albumin by producing more apolipoprotein to compensate for low serum osmotic pressure
52
Nephrotic syndrome: Key component of the slit diaphragm found between the podocyte foot processes which may help control permeability
Nephrin
53
Nephrotic syndrome: Risk of thrombosis is secondary to
Urinary loss of antithrombin III, protein C, and protein S
54
Appearance of lipid droplets under polarised light
Maltese cross
55
Most common cause of nephrotic syndrome in all populations
Primary
56
LM: Minimal change disease
Normal
57
LM: FSGS
Segmental sclerosis of glomeruli
58
LM: Membranous glomerulopathy
Spike and dome on silver stain
59
LM: PSGN
Lumpy-bumpy on silver stain
60
LM: RPGN (all types)
Glomerular crescents
61
LM: MPGN (all types)
Tram-track appearance on silver stain
62
IF: MCD
Negative
63
IF: FSGS
IgM and C3
64
IF: Membranous GN
IgG, granular
65
IF: PSGN
IgG, IgM and C3, granular
66
IF: RPGN I
IgG (anti-GBM) Linear
67
IF: RPGN II
IgG Granular
68
IF: RPGN III
Negative
69
IF: MPGN I
IgG and C3, granular
70
IF: MPGN II
C3
71
EM: MCD
Effacement of foot processes
72
EM: FSGS
No immune complexes
73
EM: Membranous GN
Subepithelial IC deposits
74
EM: PSGN
Predominantly subepithelial IC deposits; also subendothelial, intramembranous, and mesangial
75
EM: RPGN Type I
No IC
76
EM: RPGN Type II
Subendothelial IC deposits
77
EM: RPGN Type III
No IC
78
EM: MPGN Type I
Subendothelial IC
79
EM: MPGN Type II
Long dense band in lamina densa and sub endothelial region
80
Nephrotic syndrome: 4 main conditions
1) Minimal change disease
2) Membranous GN
3) FSGS
4) DM nephropathy
81
MCD: Also known as
Lipoid nephrosis
82
MCD: Male vs female
Male
83
MCD: Selective vs nonselective proteinuria
Selective
84
MCD: Conditions associated (3)
1) Hodgkin's lymphoma
2) Other lymphomas and leukemias
3) NSAIDs
85
T/F FSGS is immunologic in origin
F
86
Mechanism of FSGS
Epithelial injury
87
FSGS: Type of proteinuria
Nonselective
88
FSGS: Variant that has worse prognosis and similar to injury seen with HIV infection
Collapsing variant
89
Significant independent risk factors for the development of FSGS
1) IV heroin
| 2) HIV
90
Risk of FSGS in IV heroin users
30x that of the general population
91
FSGS: Treatment
None --> chronic GN
92
50% of patients with FSGS develop ESRD within
10 years
93
Membranous GN: Spikes represent
Basement membrane between IC
94
Membranous GN: Domes represent
Thickened basement membrane that cover IC
95
Pathogenesis of membranous GN
Fomation of MAC
96
Membranous GN: Proteinuria
Nonselective
97
T/F Most membranous GN is idiopathic in origin
T
98
Membranous GN: Related causative drugs
1) Pencicillamine
2) Captopril
3) NSAIDs
99
Membranous GN: Associated conditions
1) Infections (syphilis, HBV, HCV, malaria)
2) Cancers (lung and colon)
3) Melanoma
4) SLE
100
Membranous GN: Rule
1/3
1) Remission
2) Proteinuria and stable renal functions
3) Progress to ESRD within 5-10 years
101
Single most important cause of ESRD
DM
102
DM nephropathy: GFR
1) Elevated early in the disease
| 2) Progressive decline later
103
Predicts development of DM nephropathy
Microalbuminuria
104
DM nephropathy: Most common finding
Diffuse glomerulosclerosis (diffuse thickening of the basement membrane)
105
DM nephropathy: Found in 15-20% of patients with DM nephropathy
Kimmelsteil-Wilson nodules or nodular glomerulosclerosis
106
What are Kimmelsteil-Wilson nodules
ACELLULAR nodules within GBM
107
T/F Damage to the glomerulus is more severe in nephritic syndrome than nephrotic syndrome
T
108
Pathogenesis of nephritic syndrome
IC triggers proliferation of glomerular cells and chemotaxis
109
Nephritic syndrome: Hematuria described as
Smoky brown or cola-colored
110
Nephrotic vs nephritic: Proteinuria >3.5 g/d
Nephrotic
111
Nephrotic vs nephritic: Proteinuria less than 3.0/d
Nephrotic
112
Nephrotic vs nephritic: Presence of oliguria
Nephritic
113
Nephrotic vs nephritic: Presence of hematuria
Nephritic
114
Nephrotic vs nephritic: Hypertension
Nephritic
115
Nephrotic vs nephritic: Elevated BUN/Cr
Nephritic
116
Nephritic syndrome: Low serum complement level found in (4)
1) PSGN
2) MPGN
3) SLE
4) Bacterial endocarditis
117
Nephritic syndrome: Normal serum complement level (3)
1) IgA nephropathy
2) Idiopathic RPGN
3) Anti-GBM Ab disease
118
Nephritic syndrome: 3 conditions
1) PSGN
2) RPGN
3) MPGN
119
Nephritogenic GABHS
1, 4, 12
120
Markers of streptococcal infection (2)
1) ASO
| 2) Anti-DNAse B
121
RPGN: Most primary or secondary
Secondary
122
Distinguishing feature: Type I RPGN
Linear immunofluorescence due to binding of IGG to GBM antigens
123
Distinguishing feature: Type II RPGN
Immune complex mediated
124
Distinguishing feature: Type III RPGN (2)
1) Pauci-immune (no ICs)
| 2) Majority ANCA-positive
125
Manifestations of MPGN in order of frequency
1) Nephrotic syndrome
2) Asymptomatic hematuria
3) Nephritic syndrome
126
~50% of patients with MPGN develop CRF within
10 years
127
MPGN is aka
Mesangioproliferative GN
128
Function of C3 nephritic factor
Stabilizes C3 convertase
129
Most common glomerular cause of asymptomatic hematuria
IgA nephropathy
130
4 most common conditions causing asymptomatic hematuria
1) IgA nephropathy
2) HSP
3) Alport syndrome
4) Thin basement membrane disease
131
Most common primary cause of glomerulonephritis
IgA nephropathy
132
IgA nephropathy: Male vs female
Male
133
IgA nephropathy: 2 associated diseases
1) Celiac disease
| 2) HSP
134
IgA nephropathy: IF
IgA and C3, granular
135
IgA nephropathy: EM
IgA in mesangium
136
IgA nephropathy: Pathogenesis
Abnormal glycosylation
137
IgA-mediated vasculitid\s
HSP
138
HSP: Commonly preceded by
Streptococcal or viral infection
139
Alport syndrome: Characteristic cells on LM
Interstitial foam cells due to accumulation of neutral fats and mucopolysaccharides
140
Alport syndrome: IF
Negative
141
Alport syndrome: EM
Splitting, thickening, and thinning (Basket-weave pattern)
142
Alport syndrome: Most common pattern of inheritance
X-linked
143
Alport syndrome: Associated symptoms
1) Nerve deafness
2) Lens dislocation
3) Cataracts
144
Alport syndrome: Male vs female
Male
145
Normal thickness of GBM
300-400 nm
146
Tubulointerstitial disease: 4 categories
1) Acute tubulointerstitial nephritis
2) Chronic tubulointerstitial nephritis
3) Acute interstitial nephritis
4) Acute tubular necrosis
147
Tubulointerstitial disease: Edema, neutrophils, focal necrotizing infiltrates
Acute tubulointerstitial nephritis
148
Tubulointerstitial disease: Noninfectious causes of acute tubulointerstitial nephritis
Acute interstitial nephritis
149
Tubulointerstitial disease: Cellular infiltrate composed of lymphocytes and macrophages in combination with interstitial nephritis
Chronic tubulointerstitial nephritis
150
Acute tubulointerstitial nephritis, causes: Drugs (4)
1) Methicillin
2) Rifampin
3) Sulfonamides
4) Ciprofloxacin
151
Acute tubulointerstitial nephritis, causes: Systemic infections (4)
1) Legionnaire's
2) Sterp
3) CMV
4) IM
152
Acute tubulointerstitial nephritis, causes: Primary renal infections
Acute bacterial pyelonephritis
153
Acute tubulointerstitial nephritis, causes: Immune d/o (2)
1) SLE
| 2) Sjogren
154
Responsible for most cases of acute tubulointerstitial nephritis
Drugs
155
Usual cause of acute interstitial nephritis
Drugs
156
Drugs that cause acute interstitial nephritis
1) Methicillin
2) Rifampin
3) Thiazides
4) Sulfonamides
157
Tubulointerstitial disease: Tubular injury combined with a persistent and severe decrease in blood flow
Interstitial nephritis
158
Tubulointerstitial disease: Interstitial lymphocytes and macrophages, edema, eosinophils; sometimes giant cells and granulomas
Acute interstitial nephritis
159
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)
Analgesic nephropathy
160
Chronic tubulointerstitial nephritis: Most important cause
Urinary tract obstruction
161
Chronic tubulointerstitial nephritis: Heavy metals that can cause (2)
1) Lead
| 2) Cadmium
162
Chronic tubulointerstitial nephritis: Malignancy that can cause
MM
163
2 categories of acute tubular necrosis
1) Ischemic
| 2) Toxic
164
Toxic causes of ATN (7)
1) Aminoglycosides
2) Amphotericin B
3) IV contrast
4) Mercury
5) Oxalic acid (ethylene glycol poisoning)
6) Myoglobinuria, hemoglobinuria
7) Hyperuricemia
165
Stages of acute tubular necrosis
1) Initiating
2) Maintenance
3) Recovery
166
Stages of acute tubular necrosis: Maintenance phase is characterized by
Oliguria within 24 hours of initiating event
167
Stages of acute tubular necrosis: Recovery phase is characterized by
Increased UO up to 3L
168
Increases risk of death during the recovery phase of ATN
Electrolyte disturbance
169
Protein casts are composed of
Tamm-Horsfall protein
170
More common organism when acute pyelonephritis is acquired hematogenously
Staphylococcus aureus
171
Gross morphology of acute pyelonephritis
Abscesses in the cortex
172
Complication of pyelonephritis almost exclusively seen in diabetics
Emphysematous pyelonephritis
173
Emphysematous pyelonephritis is most commonly due to what organism
E. coli
174
Patients at risk for papillary necrosis
1) Diabetics with obstruction
2) Patients with sickle cell disease
3) Patients abusing analgesics
175
Acute vs chronic pyelonephritis: U-shaped cortical scars
Chronic
176
Acute vs chronic pyelonephritis: Blunting of renal papillae
Chronic
177
Chronic pyelonephritis microscopically presents as
Thyroidization of tubules
178
T/F Xanthogranulomatous pyelonephritis is unilateral
T
179
T/F Kidney affected by xanthogranulomatous pyelonephritis is enlarged
T
180
Calcium stones: Most are secondary to deranged serum calcium levels for whatever reason
F, idiopathic
181
Pseudomonas and Providencia are associated with what kidney stones
Struvite
182
Why are urease producing organisms commonly associated with struvite stones
Urea --> CO2 + Ammonia; Ammonia raises urine pH, struvite precipitates
183
Complication of struvite stones
Xanthogranulomatous pyelonephritis
184
T/F Most kidney cysts are simple and usually of little clinical signficance
T
185
Most common site of renal cyst
Cortex
186
T/F Patients on chronic renal dialysis may have an increased risk of developing renal cell CA
T
187
Genes mutated in autosomal dominant polycystic disease
PKD1 and PKD2
188
Most common cause of death in patients with autosomal dominant polycystic kidney disease
Renal failure
189
T/F Adult polycystic kidney disease is associated with chronic urinary tract infections
T
190
Adult polycystic kidney disease: Associated vascular anomaly
Berry aneurysms
191
Adult polycystic kidney disease: Other associated anomalies besides berry aneurysms
1) Cysts of liver and pancreas
| 2) Myxomatous mitral valve
192
T/F Autosomal recessive polycystic kidney disease has its clinical onset during adulthood
F, infancy or childhood
193
Autosomal recessive polycystic kidney disease: Gene mutated
PKHD1
194
PKHD1 in autosomal recessive polycystic kidney disease encodes for
Fibrocystin
195
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
Adult
196
APCKD vs ARPCKD: Multiple cysts in cortex and medulla; normal kidney architecture (i.e., the general shape of the kidney) is pre- served
Autosomal recessive
197
Most common renal tumor in adults
RCC
198
Most common renal tumor in children
Wilms tumor
199
RCC: M:F
Male
200
RCC: Risk factors (3)
1) Smoking
2) Cadmium
3) Chronic dialysis
201
RCC: Most common type
Clear cell
202
Type of RCC: Yellow (from glycogen) and hemorrhagic
Clear cell
203
Type of RCC: Brown mass
Chromophobe
204
Type of RCC: Fibrovascular papillae lined with neoplastic cells; foamy macrophages are within the papillae
Papillary
205
RCC: Propensity to invade what
Renal vein > IVC > Heart
206
Most common mode of metastasis
Hematogenous
207
3 most common sites of RCC metastasis
1) Lung (most common)
2) Bone
3) Liver
208
T/F Renal cell CA is known to metastasise to unusual locations such as the forehead and arm
T
209
Classic clinical triad of RCC
1) Hematuria
2) Flank pain
3) Palpable mass
210
Urothelial neoplasm is aka
Transitional cell carcinoma
211
Urothelial neoplasm: T/F Many are papillary and noninvasive hence can be removed without removing the bladder itself
T
212
Urothelial neoplasm: Poor prognostic indicator
Muscularis propria invasion
213
Urothelial neoplasm: Usual cause of death
Ureteral obstruction, eventual renal failure
214
Urothelial neoplasm: Clinical presentation
Painless hematuria
215
Acid-base disorder: Lung CA
Chronic respi alka
216
Causes of hypochloremic metabolic alkalosis (3)
1) Vomiting
2) NGT suction
3) Diuretics
217
Causes normochloremic metabolic alkalosis
Exces mineralocorticoids
218
T/F Met alka carries a much graver prognosis than met acid
T
219
Anion gap wherein the patient has a probable met acid
> 15 mEq/L
220
Anion gap wherein the patient has a definitive met acid
> 25 mEq/L
221
Acute respi acid: Increase in HCO3 per mmHG CO2
1 mEq/L HCO3 per 10 mmHg CO2
222
Chronic respi acid: Increase in HCO3 per mmHG CO2
3.5 mEq/L per 10 mmHg CO2
223
Acute respi alka: Decrease in HCO3 per mmHg CO2
2 mEq/L HCO3 per 10 mmHg CO2
224
Chronic respi alka: Decrease in HCO3 per mmHg CO2
5 mEq/L HCO3 per 10 mmHg CO2
225
Metabolic acidosis: Change in pCO2
Winter's formula: 1.5 (HCO3) + 8 +/-2
226
Metabolic alkalosis: Change in pCO2
0.9 (HCO3) + 9
