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Module 201/202 > Hematuria (Mod 202) > Flashcards

Hematuria (Mod 202) Flashcards

1
Q

What are 6 common causes of hematuria?

A
  1. Infections (any age) 2. Nephrolithiasis (>20yo) 3. Neoplasms (>40yo except Wilms) 4. BPH (Males>40yo) 5. Glomerulonephritis (young children) 6. Schistosomiasis (any age; most common worldwide)
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2
Q

What are some causes of pigmenturia?

A
  1. Meds (azathioprine, doxorubicin, ibuprofen) 2. Metabolites (bilirubin, melanin, methemoglobin) 3. Food Dyes (blackberries, beets, food colouring)
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3
Q

Define Macroscopic Hematuria

A
  • visible with the naked eye - Always pathologic - “tea coloured/ cola coloured” - Malignancy until proven otherwise
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4
Q

Define Microscopic Hematuria

A
  • nonvisible to the naked eye - microscopy of 2 properly collected urine specimens show >2 RBCs per high powered field - no hx of recent exercise, menses, sexual activity, or instrumentation
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5
Q

What is transient microscopic hematuria

A

UTIs, strenuous exercise - Would likely resolve on testing 48hs after tx/ 72h post exercise

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6
Q

What is spurious microscopic hematuria?

A

contamination of urine sample from menstruation or sexual intercourse for women

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7
Q

What is persistent microscopic hematuria?

A

true hematuria

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8
Q

What are Sx of lower UTIs (urethritis/ cystitis)

A

Urethritis; Acute onset, dysuria Cystitis; Acute onset, dysuria, frequency, urgency, hematuria (micro or macro), suprapubic pain, ?nocturia, hesitancy

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9
Q

What are the Sx of Upper UTI (pyelonephritis)

A
  • infection of renal parenchyma and renal pelvis/ calyces - symptoms of cystitis + fever/chills, flank pain/ CVA tenderness - systemic sx; N&V
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10
Q

What are features of asymptomatic bacteruria

A
  • no specific sx - positive urine culture - no/insignificant # of WBCs in urine - common in elderly women - tx pregnant females/preschoolers
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11
Q

What is an uncomplicated UTI

A

UTI with no structural or functional abnormality within the urinary tract or kidney parenchyma & no comorbidities that would increase likelihood of complications; not associated with instrumentation

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12
Q

What are some RF for increased risk of tx failure in uncomplicated UTIs?

A
  1. hx of polycystic renal disease 2. nephrolithiasis 3. neurogenic bladder 4. DM 5. immunosuppression 6. pregnancy 7. indwelling catheter 8. recent instrumentation
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13
Q

What is a complicated UTI?

A

infection with anatomical/functional problems of the urinary tract, or the presence of comorbidities that increase risk for complications.

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14
Q

What are the RF for complicated UTIs

A
  1. Male sex 2. Anatomic abnormality of the urinary tract or external drainage system 3. Recurrent UTI 4. Advanced age in men 5. Nursing home residency 6. Neonatal state 7. Comorbidities 8. Pregnancy 9. Immunosuppression 10. Advanced neurologic disease 11. Known or suspected atypical pathogens 12. Known or suspected resistance to typical antimicrobial agents for UTI`
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15
Q

What does the development of UTI depend on?

A
  1. Ability of the microbe to establish itself and to cause disease-virulence factors. 2. ability of the host to resist the microbe (host factors)
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16
Q

What are 5 virulence factors?

A
  1. Adherence to epithelial cells via fimbriae and pili 2. Resistance to cidal compounds in serum 3. Production of hemolysins (membrane damaging toxins that target RBCs, WBCs etc) 4. Motility 5. Activitiy of endotoxins and other toxins
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17
Q

What are the 4 modes of entry into the urinary tract?

A
  1. Periurethral bacteria ascending into the urinary tract 2. Hematogenous spread esp in immunocompromised + neonates (staph aureus, candidia, mycobacterium TB) 3. Lymphatogenous spread 4. Spread of bacteria from adjacent organs
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18
Q

What are 7 elements of host defence in UTIs?

A
  1. Periurethral flora 2. Prostate (secretions contain zinc which act as antimicrobial) 3. Flow of urine 4. Urine osmolality, low pH, organic acid content and increased urea concentration (inhibit growth/colonization) 5. Urinary proteins (inhibit bacterial adherence) 6. Serum/ urine antibodies (bacterial opsonization/phagocytosis) 7. Urinary tract epithelium (barrier)
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19
Q

What causes 80% of uncomplicated cystitis and plyelonephritis?

A

E.coli

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20
Q

What are the pathogens that cause UTIs?

Community Acquired

Nosocomial Organisms

Immunocompromised/Speical

A
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21
Q

Diagnostic Flow Chart Below

A
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22
Q

What Ix do you do to Dx UTI?

A
  1. Dipstick ( urine specific gravity, pH, protein, blood, glucose, ketones, bilirubin, nitrite and leukocyte esterase)
  2. Urinalysis (microscopy) of mid stream sample
  3. Urine culture (gold standard) & sensitivity
  4. Children with first UTI may need renal US & voiding cystourethrogram (r/o anatomic defect)
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23
Q

What are you looking for in a urine dipstick with regards to UTI?

A
  1. Nitrites (reduction of urinary nitrites by Gram - bacteria)
    - Note Gram + cocci do not convert nitrate to nitrite so negative nitrite does not r/o UTI
  2. Leukocyte esterase (breakdown of WBCs)
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24
Q

What are you looking for on Renal U/S with relation to UTIs?

A

Size and shape of kidneys

anatomic abnormalities

difference between cyst & mass

bladder obstruction

ureteral obstruction

hydronephrosis

Kidney stones (not good for stone in ureter)

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25
Q

What is the Tx of acute uncomplicated UTI?

A

Acute uncomplicated; TMP/SMX or nitrofurantoin

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26
Q

What is the tx for pyelonephritis?

A

Fluorouinolone (pyelonephritis)

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27
Q

What is the tx for pregnant women with UTI

A
  1. Cephalexin, Ampicillin, Nitrofurantoin = 1st line
    - Avoid Nitrofurantoin at 36+ weeks (hemolytic anemia of neonate)
    - DO NOT USE TMP/SMX - Teratogenic in early pregnancy + kernicterus in late pregnancy
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28
Q

What is the uti tx for Men?

A

Fluoroquinolone or TMP-SMX for 7 - 14 days

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29
Q

How do you divide renal causes of hematuria?

A
  1. Glomerular
  2. Non Glomerular
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30
Q

What are the three glomerular (renal) causes of hematuria?

A
  1. IgA nephropathy
  2. Alport disease and thin basement membrane nephropathy (TBMN)
  3. Other primary & secondary glomerulonephropathies
    - post infectious
    - SLE
    - Goodpasture Syndrome
    - Henoch Schunlein purpura or vasculitides
    - Hemolytic Uremic Syndrome
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31
Q

What are the 4 categories of non glomerular (renal) causes of hematuria?

A
  1. Neoplastic
  2. Tubulointersitial
  3. Vascular
  4. Metabolic
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32
Q

What are two neoplastic (non glomerular - renal) causes of hematuria?

A
  1. Rnal cell or transitional cell Ca
  2. Benign Renal Mass
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33
Q

What are 5 Tubulointerstitial (non glomerular renal) causes of Hematuria?

A
  1. Nephrolithiasis
  2. PCKD or medullary sponge kidney
  3. Pyelonephritis
  4. Papillary Necrosis
  5. Acute interstitial Nephritis
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34
Q

What are 5 vascular (non glomerular renal) causes of hematuria?

A
  1. aterial embolus/ thrombosis
  2. AV malformation or fistula
  3. Renal vein thrombosis
  4. Nutcracker syndrome (compression of Left renal vein)
  5. Malignant HTN
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35
Q

What two metabolic (non glomerular renal) causes of hematuria?

A
  1. Hypercalciuria
  2. Hyperuricosuria
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36
Q

What are four things that glomerular hematuria will show?

(do not see these abnormalities if origin is distal to kidney or because of structural abnormalities)

A
  1. Dysmorphic RBCs (changes because cells are squeezed through the capillary wall of the glomerulus & tubules of nephron.
  2. Red cell casts
  3. New/ worse HTN or proteinuria
  4. Increased creatinine
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37
Q

What are the classes of extra renal causes of hematuria (4)

A
  1. Ureter
  2. Bladder
  3. Urethra
  4. Prostate
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38
Q

What are three ureter causes of hematuria?

A
  1. stricture
  2. stone
  3. Mass; benign or malignant polyp
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39
Q

What are 4 bladder causes of hematuria?

A
  1. Infectious cystitis
  2. Noninfectious cystitis
  3. Transitional cell or squamous cell Ca
  4. Stone
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40
Q

What are 4 urethral causes of hematuria?

A
  1. Urethritis
  2. Urethral diverticulum
  3. Traumatic Catheterization
  4. Urethral Stricture
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41
Q

What are 4 prostate causes of hematuria?

A
  1. Prostate Cancer
  2. BPH
  3. Post procedural
  4. Prostatitis
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42
Q

What is an approach to macroscopic hematuria?

A
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43
Q

What is an approach to microscopic hematuria?

A
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44
Q

What is eGFR measuring, what is the normal range?

A

measuring renal function

normal = 100 - 120mL/min/1.73m2 of body surface area

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45
Q

What are 3 things that can interfere with secretion of creatinine?

A
  1. dietary protein intake
  2. volume of muscle mass

meds (cimetidine, trimethoprim, probenecid)

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46
Q

Will eldery, cachexic patients & spinal cord injury patients have more or less serum createnine?

A

lower serum creatinine –> less muscle mass

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47
Q

Define Proteinuria

A
  1. >150mg/day of protein excretion
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48
Q

What are the three main classes of proteinuria?

A
  1. Glomerular
  2. Tubular
  3. Overflow
49
Q

What is and what causes glomerular proteinuria?

A

Causes; diabetic nephropathy & glomerular disease

Pathophys; Increased filtration of albumin across glomerular capillary wall

50
Q

Define tubular proteinuria? What causes it?

A

Definition; defective reabsorptive capacity in the proximal tubules, instead of proteins being normally reabsorbed they are excreted in urine

Cause; underlying tubulointerstitial disease (mostly low molecular weight proteins like immunoglobulin light chains)

51
Q

Define overflow proteinuria? What causes it?

A

Define; Maximum threshold for reabsorption by tubules is exceeded

Causes; Multiple myeloma = overabundance of Ig light chains secondary to overproduction

52
Q

What are Ix for proteinuria?

A
  1. Urine dip; only detects albumin
  2. Random urine protein: creatinine ratio; similar to 24h urine protein
53
Q

What are 5 signs of Nephrotic Syndrome?

A
  1. Proteinuria >3.5g/1.73m2/24h (40 - 50mg/kg/day)
  2. Hypoalbuminemia
  3. Edema
  4. Hyperlipidemia
  5. Lipiduria

Some hematuria may occur in nephrotic syndrome - usually transient and less striking than that of nephritic syndrome

54
Q

The glomerular capillary wall normally acts as a filter; what is it composed of?

A
  1. Fenestrated endothelium
  2. Basement membrane
  3. Podocytes + foot processes
55
Q

WHat is the pathogenesis of nephrotic syndrome?

A
  1. Noninflammatory damage to glomerular capillary wall > altered/ increased permeability to plasma proteins of sizes and charge that would have typically been restricted from entering bowman’s capsule (esp albumin)
  2. Etiology of noninflammatory change is often immune complex deposition under the epithelial cells + morphology changes in podocyte foot processes
  3. Non inflammatory process is a double edged sword; may limit the damage done to the glomerulus however, it also slows down recover (months- years for resolution)
56
Q

Why do you get hyperlipidemia in nephrotic syndrome?

A

liver is constantly producing protein to replace the significant amounts lost in the urine. This increases production of lipoprotiens.

Decreased plasma oncotic pressure stimulated production of VLDL

Hyperlipidemia may be from hypercholesterolemia, hypertriglyceridemia, and increased LDL and VLDL. Treat with statin +/- bile acid sequestrant

57
Q

What is lipiduria?

A

urine microscopy may show fatty casts –> fatty casts originate from the lipiduria which results in cholesterol precipitation

Urine microscopy may show oval fat bodies –> lipid is embedded in the plasma membrane of epithelial cells (maltese crosses)

58
Q

Why are you at increased risk of blood clotting with proteinuria?

A

loss of protein C and S, antithrombin, Factors IX, XI, and XII

Synthesis of both procoagulatn and anticoagulant proteins is increased however, there is greater production of procoagulants (fibrinogen), so nephrotic syndrome results in a higher risk of clotting

59
Q

Why does loss of protein result in;

  1. increased change of infection
A

loss of IgG and defects in complement cascade

60
Q

Why does loss of protein result in;

Anemia?

A

loss of erythropoietin and transferrin

61
Q

Why does loss of protein result in;

Altered thyroid function tests

A

loss of thyroxine - binding globulin

62
Q

Why does loss of protein result in;

Deficiency of Vitamin D and secondary hyperparathyroidism

A

loss of vitamin D binding protein

63
Q

What are 4 examples of primary (idiopathic) nephrotic syndrome?

A
  1. Membranous nephropathy (idiopathic, hepB, SLE, malignancy)

thickening of basement membrane

dense deposit on epithelial side of basement membrane

hypercoaguable state

  1. Focal segmental glomerular sclerosis (often in african americans, associated with heroin, HIV, obesity)

HTN, hematuria, renal dysfunction

area of sclerosis in focal segments of glomeruli

effacement of foot processes

poor response to steroids

  1. Minimal change disease (most common nephrotic syndrome in children)

post infectious

effacement of podocyte foot processes > increased permeability of glomerular membrane

responds to steroids

4. Membranoproliferative glomerulonephritis (Immunoglobulin mediated; SLE, HepC, monoclonal gammopathy)

complement mediated

glomerular mesangial cells grow along capillary wall and split the BM

serum complement may be low

64
Q

What are secondary causes of Nephrotic syndrome?

A
  1. Stems from systemic disease of hereditary conditions (DM, SLE, amyloidosis, Leukemia)

Tx underlying cause and you can reverse

65
Q

What are the lab findings for the following in nephrotic syndrome;

Renal Function Tests;

  1. Serum creatinine
  2. Serum Albumin
  3. Cholesterol and Triglyceride Levels
  4. Total serum calcium level;
  5. Ionized calcium level
  6. Serum sodium level;
A

Nephrotic Syndrome

Renal Function Tests;

  1. Serum creatinine; N
  2. Serum Albumin; L (<3.5mg/dl)
  3. Cholesterol and Triglyceride Levels; H
  4. Total serum calcium level; L
  5. Ionized calcium level; N
  6. Serum sodium level; L (secondary to increased triglycerides
66
Q

What are the lab findings for the following in nephrotic syndrome;

Blood Studies

  1. Hematocrit;
  2. Complement C3 & C4, ANA, HepB/C;
A

NEPHROTIC SYNDROME

Blood Studies

  1. Hematocrit; N or high (secondary to hemoconcentration)
  2. Complement C3 & C4, ANA, HepB/C; (may be abnormal and help to identify cause)
67
Q

What are the Urine Lab findings in Nephrotic Syndrome?

  1. Presence of Protein (via test strip;
  2. Presence of Blood;
A

NEPHROTIC SYNDROME

  1. Presence of Protein (via test strip); 3+
  2. Presence of Blood; Absent; rarely seen
68
Q

When do you do a renal biopsy for nephrotic syndrome?

A

doubt as to the etiology of proteinuria

pt has comorbidities that “confound” the diagnosis

before cytotoxic medications started

when course of disease not expected

69
Q

What is the tx for nephrotic syndrome?

A
  1. Consider corticosteroids/cytotoxic agents/monoclonal antibodies (tx of secondary causes)
  2. Use statin +/- bile acid sequestrant to control hyperlipidemia
  3. reduce sodium intake and use loop diuretics to resolve edema; avoid hypovolemia/hypotension
  4. Thrombosis; consider anticoagulation until nephrotic syndrome resolves
  5. Give children pneumococcal vaccine to prevent bacterial peritonitis
70
Q

What are the S&S of Nephritic Syndrome?

A

S&S of Nephritic Syndrome;

  1. Hematuria
  2. RBC casts
  3. Variable proteinuria
  4. Renal Insufficiency
  5. Salt retention (htn/edema)
71
Q

Compare and Contrast Nephrotic vs Nephritic Syndrome S&S

A

Nephrotic;

  1. Proteinuria >3.5g
  2. Hypoalbuminemia
  3. Edema
  4. Hyperlipidemia
  5. Lipiduria

Nephritic;

  1. Hematuria
  2. RBC Casts
  3. Variable Proteinuria (usually <3g/day)
  4. Renal Insufficiency
  5. Salt Retention
72
Q

What is the pathogenesis of nephritic syndrome?

A

Glomerulonephritis is an inflammatory process causing renal dysfunction

Antibodies may bind to a structural componenet of the glomerulus (eg Goodpastures)

antigen- antibody complezes aren’t captured by the spleen and are deposited in glomerulus (eg SLE, DNA nucleosome complexes, cryoglobulins in HepC)

Antigen deposited in glomerulus and causes activated of complement > tissue injury or inflammation + cellular proliferation (mesangial, endothelial + epithelial cells)

73
Q

What are 3 causes of acute, rapidly progressive glomerulonephritis?

A
  1. Goodpastures
  2. Wegeners Granulomatosis
  3. Polyarteritis Nodosum
74
Q

What lab work would you order for nephritic syndrome?

A

CBC +diff

electrolytes

serum Cr+

BUN

eGFR

urinalysis

antibody specific levels

75
Q

What are you looking for in a CBC and electrolyte panel of a pt with nephritic syndrome?

A

CBC; Anemia, Thrombocytopenia or leukopenia (eg SLE)

Electrolyte abnormalities with renal dysfunction

76
Q

What imagine would you order for a patient with nephritic syndrome and why?

A

CXR; wegeners granulomatosis/ Goodpastures

Renal US; decreased eGFR

77
Q

What special test would you order in a patient with nephritic syndrome where you want a definitive dx?

A

Renal Biopsy;

-prompt dx needed in RPGN

gives info on inflammation, amount of fibrosis & prognosis

78
Q

What is the tx for nephritic syndrome?

A
  1. underlying or systemic disease
  2. immunosuppressive agents (IgA nephropathy- help presever renal function)
  3. Cytotoxic agents; Goodpasture’s, Wegener’s granulomatosis, SLE
  4. Plasmapheresis; removes pathogenic autoantibodies (goodpasture’s, pauci-immune)
  5. Treat underlying HepB, HepC and HIV
  6. Tx of post streptococcal glomerulonephritis > supportive
79
Q

WHat is the prognosis in nephritic syndrome?

A

Post streptococcal; excellent; spontaneous recoverin in 70 - 85%

Wegener’s/ Goodpasture’s can be fatal if left untreated

80
Q

What is the most common type of glomerulonephritis?

A

IgA Nephropathy

81
Q

What sex and what ages is IgA nephropathy most common?

A

Males

10 - 30 years

82
Q

What is the pathogenesis of IgA nephropathy?

A

higher amounts of IgA molecules that are galactose- deficient at the hinge region > person develops IgG and IgA autoantibodies against this deficient type

Hypothesis; may be a second hit phenomenon;

  • infection/ oxidative stress results in production of these antibodies > deposition of immune complexes in glomeruli > inflammatory reaction, glomerulosclerosis and interstitial fibrosis
83
Q

What are S&S of IgA Nephropathy?

A
  • asymptomatic microscopic hematuria +/- proteinuria
  • episodic gross hematuria after URTI or exercise
  • 20 - 50 % have HTN
  • serum complement is normal
84
Q

How do you diagnose IgA nephropathy?

A
  • IgA deposits seen in glomerulus is dominant/codominant on microscopy + mild mesangial proliferation to severe crescentic glomerulonephritis
85
Q

What is the tx for IgA nephropathy?

A
  • ACEI/ ARB to decrease intraglomerular pressure/protect kidneys, corticosteroids, consider cytotoxic agents
86
Q

What is the prognosis for IgA nephropathy?

A

variable; some show no decline in GFR over decades, and other develop nephrotic syndorme + HT + renal failure

87
Q

Mesangial proliferation and IgA deposition

A
88
Q

What does the PEAL acronym stand for with relation to Nephrotic Syndrome?

A

Proteinuria >3.5g/day

Edema

hypo Albuminema

hyper Lipidemia

89
Q

When is post infectious glomerulonephritis common?

A

Typically after pharyngitis but can occur after strep infections anywhere.

Occurs after infection with nephritogenic strains of Group A - beta hemolytic streptococci

90
Q

What age category is post- infectious glomerulonephritis diagnosed?

A

children. the answer is always children.

91
Q

what is the pathogenesis of post infectious glomerulonephritis?

A

immune complexes of strep antigen + antibodies are deposited in glomerulus –> complement activation

92
Q

What are the S&S of post infectious glomerulonephritis?

A

hematuria, proteinuria, htn 10 days - weeks post strep infection

93
Q

what is depressed in 90% of patients during post infectious glomerulonephritis?

A

depressed serum complement C3

94
Q

What antibodies are present in post infectious glomerulonephritis?

A

antistreptolysin O

antihyaluronidase

antistreptokinase

anti DNAase

95
Q

Is renal biopsy needed for post infectious glomerulonephritis?

A

may not be necessary if clinical picture + serum antibodies + depressed serum

96
Q

What is Henoch - Schonlein Purpura?

A

IgA immune complex mediated leyckocytoclastic vasculitis

97
Q

What is the classic tetrad presentation of Henoch-Schonlein Purpura?

A

Palpable purpua (+/- thrombocytopenia), abdominal pain, arthralgies, renal disease

98
Q

What is Pauci-immune acute glomerulonephritis?

A

rapidly progressive glomerulonephritis with no immune deposits seen with immunoflourescence on histo

99
Q

What are S&S of pauci immune acute glomerulonephritis?

A

Progressive renal failure, nephritic syndrome

100
Q

What is Goodpasture’s syndrome?

A

Antiglomerular basement membrane antibody Glomerulonephritis (effects lung & kidney)

101
Q

What is the triad fo goodpasture’s syndrome?

A

glomerulonephritis, pulmonary hemorrhage, antiglomerular BM antibodies ( deposit in lungs/ kidneys leads to alveolar hemorrhage & glomerulonephritis)

102
Q

What is multiple myeloma

A

plasma cells produce large amounts of a monoclonal Ig (monoclonal gammopathy). Bone marriw produces malignant plasma cells.

103
Q

What is does the CRAB acronym stand for in relation to multiple myeloma?

A

CRAB (calcium elevation, renal insufficiency, anemia, bone lesions) –> end organ damage

104
Q

What is seen on urine protein immunoelectrophoresis in multiple myeloma?

A

Proteinuria (Bence Jones protein); from overproduction/secretion of free monoclonal kappa or lambda light chains

105
Q

What is seen on serum protein electrophoresis in multiple myeloma?

A

tall homogenous monoclonal spike (M spike) usually IgG (70%), other Ig are decreased

106
Q

What is Lupus Nephritis?

A

SLE is a chronic disease with production of autoantibodies that disrupt function in multiple body systems, including the kidneys; class detemines treatment.

107
Q

What are the VI classes of lupus nephritis?

A

Minimal mesangial LN, mesangial proliferative LN, focal proliferative LN, diffuse proliferative LN, membranous LN, advanced sclerosing LN

108
Q

Explain the pathophys of kidney stone formation

A

calcium and phosphate not needed for bone mineralized are excreted in urine. Oxalate (end product of metab) also excreted in urine.

If H20 content low or increased products in urine then urine is saturated and there is crystalization iof products.

109
Q

What is a struvite stone most likely to form?

A

staghorn calculi but cystine and uric acid stones can do this too

110
Q

when are struvite stones most common

A

women, urinary stasis (indwelling catheter, neurogenic bladder)

111
Q

WHat causes a cystine stone?

A

autosomal recessive disorder (mutation= decreased tubular reabpsorption/ increased excretion of AA cystine, lysine, arginine and ornithine

112
Q

What are precipitating factors of calcium oxalate/ phosphate stones?

A

High protein diet (transient metabolic acidosis/increased GFR).

Increased calcium filtation.

Inhibition of distal Ca2+ resorption.

113
Q

What causes uric acid stones?

A

Low pH & volume . Obese, DM, gout, myeloproliferative disorders, chemo, chronic diarrhea

114
Q

What are the complications of urolithiasis?

A

infection/sepsis, ureteral sticture, renal failure, urine extravasation, perinephric abscess, xanthogranulomatous pyelonephritis

115
Q

What are 6 recommendations to prevent calcium kidney stones?

A

1. increase fluid intake 2. reduce salt 3. reduce animal protein 4. moderate ca intake 5. moderate consumption of high oxalate foods (spinach, strawberries, nuts, rhubarb, wheat germ) 6. increased intake of citrate rich foods

116
Q

What is polycystic kidney disease?

A

autosomal dominant disorder leading to development of renal cysts

117
Q

What side of renal vein thrombosis is most common?

A

Left is more common.

2/3 of cases are bilat.

118
Q

What are the RFs for Bladder Ca

A

White, Male, Smoker, age >40, hx of pelvic rads, phenacetin/chlornophazine/cyclophasphamide use, urothelial ca, chronic UTIs, Scchistosomiasis, toxin exposure. VIT A PROTECTIVE

119
Q
A

Module 201/202 (5 decks)

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