Module 4: Renal: Renal Cell Carcinoma, Bladder Cancer, cystitis Flashcards

1
Q

Starting off will be Renal Cell Carcinoma, what is the pathogenesis for this?

A

Mutation of VHL (von-hippel lindau) tumor supressor gene (3p)

  • -more common in older men 60-70
  • -unilateral and unifocal for sporadic and bilateral and multifocal for inherited
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2
Q

What is the origin for renal cell carcinoma?

A

Proximal tubule epithelial cells that arise from the cortex

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3
Q

What are the pre-disposing factors for renal cell carcinoma sporadic?

A
HTN
Obesity 
Smoking 
Cadmium (batteries)
 Acquired polycystic kidney disease
B2 microglobulin 
--long standing dialysis
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4
Q

There is also renal cell carcinoma that is inherited (5%) that is seen in younger adults. What is it associated with?

A

Bilateral and Multifocal

–associated with pheochromocytoma, cerebellar and retinal hemangioblastomas

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5
Q

What are the three types of renal cell carcinoma?

A

Clear cells (most common): has glycogen and lipids
Papillary: has psammoma bodies
Chromophobe

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6
Q

What is the classic triad of manifestations for patients with renal cell carcinoma?

A

Painless hematuria (no casts because the problem is in the kidney not below)
Flank Pain
Flank Mass

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7
Q

What is the treatment for renal cell carcinoma?

A

Subtotal nephrectomy (excisional biopsy)
–urine cytology not good
Dont take incisional biopsy because you can spread it in the blood
–dx can be confirmed by renal ultrasound scan — bilateral shrunken kidneys

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8
Q

What is seen on histology for patients with clear cell renal carcinoma?

A

scanty stroma containing blood vessels and glycogen and lipids (Hence why its clear)

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9
Q

What other diseases have a mutation in the VHL gene?

A

Renal Cell Carcinoma
Phenochromocytoma
Retinal and Cerebellar Hemangioblastomas

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10
Q

What are complications associated with renal cell carcinoma?

A

Hematogenous spread: lungs (cannonball lesions), brain and bones (lytic lesions)
–does not spread through lymph (Exception)
FSGS from subtotal nephrectomy: due to compensatory hyperfiltration by the other kidney now.

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11
Q

What other carcinomas spread through the blood and not the lymph?

A
Renal Cell Carcinoma 
Choriocarcinoma 
Follicular Carcinoma 
Hepatocellular Carcinoma 
--liver, lung, brain, bone and kidneys
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12
Q

Renal cell carcinoma also is responsible for paraneoplastic syndromes, which ones?

A

Renin: HTN
EPO: polycythemia (high EPO does not allow for negative feedback)
ACTH: cushing’s syndrome
PTH-like peptide: Hypercalcemia
Leukamoid Reaction: neutrophilia (elevated LAP score–unlike CML with normal LAP score)
Amyloidosis: AA

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13
Q

Moving onto pathologies associated with the bladder. What is a diverticula in the bladder?

A

Pouch-like eversion/evagination of the bladder wall

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14
Q

What is the congenital versus acquired pathogenesis for Diverticula?

A

Congenital: due to defect in development of muscle wall of the bladder
Acquired: due to increased intravesical pressure secondary to obstruction to urine outflow (BPH)

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15
Q

What are complications seen with Diverticula?

A

Urine Stasis, infection, stone formation and carcinomas

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16
Q

What is a urachus in regards to bladder pathology?

A

Persistent tubular structure

  • -between bladder and umbilicus
  • -fibrosis of the cord is basically formed
  • -if not surgically excised patients can pee out of the belly button and patients have an increased risk for adenocarcinoma
17
Q

Now moving onto cystitis, what are some features?

A

Occurs secondary to infection or radiation (hemorrhagic cystitis)

  • -bacteria: E.coli, proteus, klebsiella, and enterobacter
  • -fungus: Candida
  • -parasites: S. hematobium
18
Q

What are pre-disposing factors to cystitis?

A

More common in females (short urethra)

  • -DM
  • -Instrumentation (catheter or cystoscopy)
  • -bladder calculi
  • -bladder outlet obstruction (BPH)
19
Q

What is the presentation for cystitis?

A
Urinary frequency 
Dysuria 
Suprapubic pain 
Fever 
Chilis 
Microhematuria
20
Q

There is also chronic interstitial cystitis which is common in middle aged females. What is seen on cystoscopic exam?

A

Edema, hemorrhage, ulceration of bladder mucosa

21
Q

What is seen on pathology of chronic interstitial cystitis?

A

Chronic inflammation (macrophages) and mast cells

22
Q

What is the presentation for cystitis?

A

Severe suprapubic pain, frequent/urgent urination, dysuria and hematuria

23
Q

The next big bladder pathology will focus on Bladder Cancer. What type is the most common?

A

Transitional or Urothelial Carcinoma

–also have adenocarcinoma and squamous

24
Q

What are the risk factors for transitional or urothelial carcinoma?

A
Smoking 
Analgesic abuse (phenacetin) 
Cyclophosphamide (immunosuppressant) 
Naphthylamine (Rubber factories) 
Mutations in p53, Rb and p16 
--more common in males
25
Q

What are the different types of transitional bladder cancer?

A

Papillary carcinoma or invasive papillary carcinoma (invades the actual bladder )
Flat non invasive carcinoma (carcinoma in situ) and flat invasive carcinoma (invasion into the bladder)
–most invasive flat comes from the non invasive flat carcinoma

26
Q

How do all the bladder cancers present?

A

Painless hematuria
Dysuria
Urgency and Frequency
Flank pain

27
Q

Now first lets talk about papillary urothelial carcinoma, what are some features?

A

Note 1a and 1b
Projects into lumen of the bladder and causes obstructive symptoms so patient presents early — better prognosis
–much more common
–exophytic, multifocal, low grade with a high chance of recurrence
More common, more likely to re-occur after surgery and more likely to cause hydroureter/hydronephrosis

28
Q

What is the histology seen for papillary urothelial carcinoma?

A

More than 5 layers with non-uniform layers — if there is infiltration as seen on the image then this is invasive carcinoma

29
Q

Once papillary carcinoma becomes invasive what are features?

A

greater than 10 layers with atypica and invasion of fibrovascular core

30
Q

What are complications of invasive papillary carcinoma?

A

Obstruction — back up of urine — bilateral hydroureters/hydronephrosis – chronic renal failure — recurrent kidney and bladder stones/infections and acute urinary retention

31
Q

What is seen on the urine results for invasive papillary carcinoma?

A

Two casts: WBC (Acute pyelonephritis) and waxy (chronic renal failure)
–patients also get iron deficiency anemia due to the painless hematuria
RBC without casts because its below the kidney

32
Q

The second type of urothelial cancer is flat carcinoma and again it can be invasive and non invasive. What are some features?

A

High Grade Tumor
Presents late
Poor prognosis b/c it invades bladder wall
–most invasive flat come from non invasive not de novo.

33
Q

How is a diagnosis made of flat or papillary carcinoma?

A

Cystoscopy and biopsy most accurate test

  • -atypical epithelial cells and multilayering
  • -flat is worse because it can invade the bladder wall
  • -papillary is more likely to cause bilateral hydronephrosis (also more likely to recur following resection)
34
Q

Now very briefly, when do you see patients with squamous bladder cancer?

A

Only seen in Egyptian Immigrants
–S. hematobium: causes squamous dysplasia, squamous carcinoma and keratin pearls
—has to be purely squamous
Also seen in patients with bladder stones

35
Q

Now again very briefly, when do you see patients with adenocarcinoma of the bladder?

A

Associated with bladder urachus (persistence of a cystic structure from umbilicus to the dome of the bladder)

  • -glandular dysplasia – adenocarcinoma –malignant glands invading the bladder wall
  • -has to be purely adenocarcinoma
36
Q

What is more common mets to the bladder or primary bladder cancer?

A

Mets to the bladder is more common than primary bladder cancer