CAM202 Path Pots Flashcards
1
Q
A
Squamous Cell Carcinoma of the Buccal Mucosa
2
Q
A
Pleumorphic Adenoma of the Parotid
3
Q
A
Oesophageal Varices
4
Q
A
Chronic Oseophagitis
(active, with scarring)
Reflux oesophagitis*
5
Q
A
Squamous Cell Carcinoma of the Oesophagus
6
Q
A
Chronic Gastric Ulcer
7
Q
A
Leather Bottle Stomach
Strikingly thickened stomach wall - loss of plasticity
(secondary to a plaque-like tumour involving the entire mucosal surface and infiltrating through the muscular layers and into the serosal tissues)
8
Q
A
Adenocarcinoma of the stomach
9
Q
A
Adenocarcinoma of the Stomach
10
Q
+ microscopically?
A
Perforated Pre-Pyloric Gastric Ulcer
4 zones of chronic gastric ulcer:
- Thin Layer of Necrositc Debris
- Non-specific Inflammatory Cell Infiltrate
- Granulation Tissue
- Scar Tissue beneath the granulation tissue
11
Q
A
Squamous Cell Carcinoma of the Tongue
The specimen includes: sagitally sliced tongue, epiglottis, larynx, and upper trachea & bit of upper oseophagus
Tumour extends through tongue and into the hyoid bone
Does not invulve the epiglottis
12
Q
A
Pleumorphic Adenoma of the Parotid
Encapsulated oval shaped tumour mass from the parotid salivary gland
13
Q
A
Oesophageal Varices
In the lower part of the oesophagus, there are distended, congested venous channels underlying the oesophageal mucosa
14
Q
A
Squamous Cell Carcinoma of the Oesophagus
Shows a segment of oesophagus encircled with tumour mass 5cm in length that shows ulceration
Grey-white tumour tissue has infiltrated the entire thickness of the oesophagus wall
15
Q
+ Microscopically?
A
Chronic Gastric Ulcer
Four zones of a chronic ulcer:
- Thin layer of Necrotic Cellular Debris
- Non-specific Inflammatory Cell Infultrate
- Granuluation Tissue
- Scar Tissue (lying beneath the granulation tissue)
*Surrounding mucosa exhibits some intestinal metaplasia and inflammatory vhanges - mild atropic gastritis
16
Q
+ Microscopically
A
Miltiple Perforated Gastric Ulcers
Stomach has been opened to demonstrate the two ulcers which are both adjacent to the Lesser Curvature
Four zones of chronic ulcers:
- Thin layer of Necrotic Cellular Debris
- Non-specific Inflammatory Cell Infiltrate
- Granulation Tissue
- Scar Tissue (unerdlying the granulation tissue)
17
Q
A
Leath Bottle Stomach
Specimen = part of the stomach showing grossly thickened walls. Grey white tumous tissue extends through the muscular layer and into the serosal tissue.
Loss of normal Rugal pattern of the mucosa
This has produced the rigid thickening of ‘leather bottle’
18
Q
A
Adenocarcinoma of the Stomach
This specimen = posteror wall of the stomach and the pre-pyloric region
Fungating tumour 6cm in diameter situated mostly in the lesser curvature and the upper part of the posterior wall
19
Q
+ microscopically?
A
Crohn Disease
Specimen = terminal ileum and caecum w/ appendix
Ileal mucosa has irregular polypoid appearance with elongated ulcers in the proximal portaion
Wall of the ileum is grosly thickened and the lumen is narowed
Serosal surface shows marked focal congestion in the area relating to the fistula track
Caecum and appendix are macroscopically normal
Microscopically:
- Chronic Mucosal Damage
- Transmural Inflammation
- Focal Non-Caseating Granulamata
- Fibrosis
- Knife-like clefts lined with granulation tissue (suggestive of active disease)
20
Q
+ Histologically
A
Acute Supporative Appendicitis
Enlarged, swollen appendix with a thickened, congested wall
Fibrinous Exudate covers Serosal Surface
Faecal Concretion is Impacted in the Proximal part of the Lumen
Distal Appendix = dilated with pus
Microscopically:
- All layers neutrophil infiltration
- Fibrinous inflammatory exudate coating the serosa
- Oedema
21
Q
A
Acute Gangrenous Apendicitis
Specimen = appendix with fatty mesoappendix
Serosal surface is partly covered in a grey-rellow fibro-purulent inflammatory exudate
Appendiceal tip shows congestion and dark necrotic tissue
22
Q
+ Histologically
+ common causative organism
A
Pseudomembranous Colitis
Specimen = two short lengths of opened bowel
Mucosal surface of colon is studded by multiple pale yellow plaques up to 5mm in size
Interventin mucosa appears normal
Muscle and serosal layers are normal
Microscopically:
- Multiple foci of ulceration
- Gland crypts in foci of ulceration are distended by muco-purulent exudate
- Fibrin and neutrophil admix that errupts from the glands forms the ‘pseudomembranes’
Cause
Often post-Abx therapy, and caused by clostridium difficile
23
Q
+ Microscopically
A
Ulcerative Colitis
Specimen = opened segment of colon
Mucosal surface shows numeroas coalescent areas of ulceration. Between areas of ulceration appear to by islands of regenerating mucosa (appear pale and slightly protuberant) = pseudo polyps.
Microscopically:
- Intanct mucosa shows crypt abscess formation
- Areas of ulceration show:
- loss of mucosa and lamina propria; submucosa partially replaced by acutely inflamed granulation tissue
24
Q
A
Multiple Colonic Adenomas
Specimen = section of opened bowel
Polyps are long, thin delicate projections
(unusual appearance)
Intervening Mucosa appears normal
25
Adenocarcinoma of Ascending Colon and Caecum
Specimen = terminal ileum, appendix, caecum and ascending colon
Tumour tissue has invaded the entire thickness of the bowel wall and is invading the pericolic adipse tissue
Small abscess is present within the tumour on the lateral side of the bowel\*
26
Diverticular Disease of the Colon
Numerous outpouchings alligned with the margins of the Teniae Coli
From the mucosal surface, numerous flask-shaped outpouchings, lined by mucosa, extend into the muscularis propria of the bowel
Diverticulae have thin walls - attenuated or absent muscularis propria
27
Adenocarcinoma of the Rectum
Specimen = Sigmoid Colon, Rectum, Anus and Peri-anal skin
Large, ulcerated and fungating tumour mass with villous sirface is in the rectum
Tumour has extendend through the muscle layer and into the peri-rectal fat at the back of the specimen
28
+ Histologically
Chrons Disease of the Terminal Ileum
Specimen = ~45cm of terminal ileum, the caecum and !20cm of colon
Loops of small bowel are adhered to one another
Ileo-colic fistula is present
Most of the ileal wall is markedly thickened with narrowed lumen
Normal mucosa has been replaced by flattened granular mucosa with longitudinal zones of ulceration
Creeping fat wraps around the bowel surface
Microscopically:
1. Chronic mucosal damage
2. Ulceration
3. Mucosal Atrophy
4. Heavy plasma cell infiltrate
5. Non Caseating granulomatas
6. Transmural inflammation
29
+ Histologically
Acute Obstructive Appendicitis
Appendix containing faecal concretion
Above concretion the appendix appears normal, but below, the lumen is dilated and contained pus
Serosal surface has thin inflammatory exudate, visible at the junction with the mesoappendix
Microscopically:
1. All layers have neutrophillic infiltration
2. Fibrinous exudate coats the serosa
30
Acute Gangrenous Appendicitis
Specimen = appendix attacked to mesoappendiceal fat
Serosal surface is dull & shows focal areas of vascular congestion and dark discoloration (gangrenous necrosis)
Adherant fibrino-purulent exudate is present, particularly towards the appendiceal tip
31
+ Histologically
Pseudomembranous Colitis
Specimen = two segments of large bowel
Mucosa is studded with plaques of fibrino-purulent debris and mucous
Distal segment shows greater involvement
Intervening mucosa appears normal
Microscopically:
1. Multiple foci of superficial mucosal ulceration
2. Gland crypts are distended by micro-purulent exudate with fibrin and neutrophils
3. This exudate errupts out of the glands, forming the 'pseudomembrane'
32
Adenocarcinoma of the Caecum with Metastases to Mesenteric Lymph Nodes
Specimen = Caecum and part of ascending colon
Caecum contains large, circumferential fungating tumour mass
Tumour has infiltrated transmurally, into the para-caecal tissues
Tumour has polypoid surface that is focally ulcerated
There are several enlarged mesenteric lymph nodes on the back of the specimen
\*Would be Dukes Grade C\*
33
Ulcerative Colitis
Specimen= length of ascending colon, including the caecum and terminal ileum (toawrds the top)
(sparing of the proximal caecum and terminal ileum)
Mucosa of the colon is congested and has shaggy, polypoid appearahce
These are pseudopolyps formed by islands of regenerating mucosa
Between these islands, are flat areas of mucosal ulceration (slightly paler in colour)
Bowel wall does not appear thickened
34
Diverticular Disease of Sigmoid Colon with Perforation
Specimen = length of sigmoid colon
Fibrous thickening of the wall
Large numbers of flask-shaped diverticulae extend through the bowel wall into the pericolic adipose tissue
Diverticulae are arranged in rows between the teniae coli
A number of the diverticulae appear to have ruptured, and faeces can be seen impacted in one diverticulum
Perforation of the colon with localised paracolic abscess and vesico-colic fistula
35
Villous Adenoma of the Sigmoid Colon
Specimen = section of sigmoid wall mucosa
Shows papillary tumour of the bowel mucosa, with a relatively narrow base, projecting into the lumen
Given the size and macroscopic papillary appearance, you would highly suspect that this tumour would show areas of malignancy
(Villous architecture and increasing size correlate with increased risk of malignancy)
36
Adenocarcinoma of the Rectum
Specimen= Part of the sigmoid colon, the rectum, anus and peri-anal skin
Just above the recto-anal margin as a rount, raised flattened tumour
Tumour is superficially ulcerated with raised margins
Does not appear to have infiltrated deeply into the bowel wall
37
Cirrhosis of the Liver
Specimen = Greater part of the liver
Diffuse nodularity of the liver surface
Cut surface shows variably sized patches of regenerating hepatic parenchyma, separated by bands of pale grey fibrous scar tissue
38
+ Histology
Hepatic Steatosis with Early Cirrhosis
Specimen= section of enlarged liver
Liver is yellowy/orange in colour (which would be a result of fixation of a steatoic liver)
No obvious nodularity or fibrosis
Microscopically:
1. Panlobar steatosis
2. Increased fibrous connective tissue in the portal tracts
3. Increased inflammatory infiltrate
4. Suggestive of early-stage cirrhosis
\*Steatosis is reversible, but cirrhosis is not\*
39
Metastatic Squamous Cell Carcinoma of the Cervix, in the liver
Specimen= Slice of enlarged liver
Most of the normal liver tissue has been replaced by variably shaped and sized masses of pale tumour tissue
Some of the tumour deposits show central pale foci, suggestive of necrosis
Also some facal areas of congestion and necrosis
\*Most liver cancers in the western world are metastasies\*
40
Primary Hepatocellular Carcinoma of the Liver
Specimen = Slice of a massively enlarged liver
Liver shows infiltrative, multinodular tumour mass of yellow-grey tissue, with areas of necrosis and haemorrhage
Portal vein is seen adjacent to the tumour and is completely filled with tumour
\*Hepatocellular carcinoma has a propensity to invade in this way\*
Uninvolved hepatic parenchyma shows nodular cirrhosis
41
+ Histologically
Acute on Chronic Cholecystitis with Cholelithiasis
Specimen = gallbladder containing multiple gallstones
Mucosa is focally congested
Wall is odematous and expanded by grey-white fibrous connective tissue, particularly towards the tip
Serosal surface is focally congested
Microscopically:
1. Fibrosis
2. Chronic inflammatory cell infiltrate
3. Vascular congestion
4. Acute inflammation and fibrinous exudate indicative of a super-imposed acite inflmammatory process
42
Acute on Chronic Cholecystitis with obstruction by a cholsterol gallstone
Specimen = small, thick-walled gallbladder
Mucosal surface is intensely congested - in one place, the congestion involves the full wall thickness
Congestion indicitive of acute inflammation
Obstructing the neck of he gallbladder is a single cholesterol stone ~1cm
43
+ Histologically
Cholesterolosis of the gallbladder
(Strawberry Gallbladder)
Specimen = opened gallbladder mucosa
Mucosa shows delicate lace-like pattern of yellow flecks
Flecks are 1-2mm in diameter and are slightly pedunculated
Histologically:
Yellow flecks = collections of cholesterol-laden macrophages within the lamina propria
These collections can form small polyps, recognisable on US
Aetiology: change in gallbladder wall due to excess cholesterol
44
+ its affect on the liver?
Gallstone Obstructing the Common BIle Duct (causing Ascending Cholangitis)
Specimen= Thick-walled, scarred gallbladder with several stones trapped in the fundus
The cytis, left and right hepatic ducts are grossly dilated
The common bile duct is also grossly dilated, and it is completely obstructed by a gallston ~3cm superior to the Ampulla of Vater
Affect on the liver:
1. Bile ducts completely obstructed
2. Infection ascends the biliary tract and directly invades the liver
3. Areas of hepatic necrosis
45
+ Histologically
+ Cause of white specks
Acute Haemorrhagic Pancreatitis
Specimen= Portion of the pancreas (above) and portion of the omentum (below)
Pancreas is swollen and congested
Areas of necrosis and haemorrhage
Small white chalky deposits are visible in the adipose tissue around the pancreas, and in the omentum - these are areas of fat necrosis
White Specks:
* Areas of fat necrosis
* Lipase released from the exodrine pancreas and prematurely activated breaks down the fat
* The resultant free fatty acids combine with calcium salts, forming these characteristic deposits
* People with this may have extremely low serum calcium levels due to this process\*
Histologically:
1. Acute inflammatory process
2. Oedema
3. Congestion
4. Neutrophillic Infiltrate
5. Extensive Tissue Necrosis
6. Haemorrhage
7. Characteristic Fat Necrosis
46
+ What is this pathology?
Pseudocyst of the pancreas
Specimen = Spleen and a cystic structure 3.5 x 4.5cm
Cystic structure is present within the splenic hilar connective tissue, and intimately related to the tail of the pancreas (seen on the left side)
The cyst has been opened
It would have been filled with blood-stained material and fluid
The wall of the cyst consists of pale grey fibrous connective tissue
\*\*There is no epithelial lining to the pseudocysts - hence the term 'pseudo'
What are Pancreatic Pseudocysts?
1. Walled-off collections of necrotic debris rich in pancreatic enzymes
2. Usually arise in the setting of acute pancreatitis
3. May also follow trauma to the pancreas
4. Wall consists of organizing granulation tissue
5. \*Secondary Infection can occur
47
+ Histologically
Cirrhosis of the Liver
Specimen = portion of the liver
Diffuse nodularity of the liver surface
Nodules are fairly uniform in size, and are separated out from each other by delicate bands of grey fibrous connective tissue
Cut surface shows similarly diffuse nodularity with intervening bands of fibrous connective tissue
Microscopically:
1. Regenerating nodules of hepatic parenchya
2. Between bridging fibrosis between portal tracts and between central veins and portal tracts
3. Moderate Steatosis also present
48
+ Microscopically
Hepatic Steatosis
Specimen = slice of liver
Brighter orange colour now due to fixation. But was originally pale yellow and greasy in appearance
No evidence of nodularity or fibrosis
Microscopically:
1. Intracytoplasmic accumulation of lipid droplets within hepatocytes
2. Initially in the centre of lobules, but spreads
3. \*Note steatosis is reversible\*
49
Metastatic Adenocarcinoma of the Liver
Specimen = Slice of liver
Most of the liver has been replaced by tumour tissue
Liver has numerous, large infiltrative nodules of pale tumour tissue
Areas of central necrosis - the opaque yellow tissue - can be seen
Intervening liver tissue shows congestion
50
Primary Hepatocellular Carcinoma of the Liver with Cirrhosis
Specimen = portion of the liver showing diffuse nodularity of the parenchyma (cirrhosis).
The nodules of regenerating hepatic parenchyma measure 0.2-0.5cm and are separated by thin grey fibrous connective tissue 'bridges'
Several large oval rounded nodues of slightly paler more homogenous looking tumour tissue are present
They have necrotic foci
51
+ Histologically
Chronic Cholecystitis with Cholelithiasis and granulomatous Cholecystitis
Specimen = opened thick-walled gallbladder containing 4 gallstones
Microscopically:
1. Fibrous wall
2. Chronic inflammatory cell infiltrate
3. Large numbers of foamy macrophages containing bile
52
Acute Cholecystitis with Abscess formation
Specimen = opened gallbladder and separate gallstone
The neck of the gallbladder shows a rounded space where the gallstone was situated, causing obstruction
Wall of the gallbladder is thickened and contains several small abscesses
Serosal surface is congested
53
+ Histologically
Cholesterolosis of the Gallbladder
(Strawberry gallbladder)
Specimen = small, opened gallbladder
Mucosa is studden with tiny yellow flecks 1-2mm in size
No gallstones where found in the gallbladder - is assumed these would have passed before the surgery
Microscopically:
1. Yellow flecks comprise build-up of cholesterol-laden macrophages in the lamina propria
2. These collections may form multiple small polyps which can be detected on US
54
Cholecystitis with Obstruction of the Extra-Hepatic Bile Duct, Resulting in Ascending Cholangitis
Specimen = enlarged, thick-walled gallbladder with focally ulcerated mucosa
The cystic, hepatic and common bile ducts are all markedly dilated
Common bile duct is obstructed by an orange-coloured gallstone, 1cm in diameter, wich has impacted in the ampulla of vater
The gallstone appears to be eroding its way into the duodenum
The ampulla and the gallstone are partially obstructing the duodenum
55
+ Histologically
+ Cause of chalky white flecks
Acute Haemorrhagic Pancreatitis
Specimen = Two thin slices of pancreas and a portion of adjacent mesentery with vessels and lymph nodes
Much of the pancreatic tissue is necrotis and haemorrhagic - these areas appear blackish
The included fat shows scattered chalk-white deposits of fat necrosis (best seen on the reverse of the spicimen)
Islands of spared, essentially normal, pancreatic tissue can be seen between areas of necrosis
Histologically:
1. Acute Inflammation
2. Oedema
3. Neutrophillic Infiltrate
4. Congestion
5. Widespread necrosis and haemorrhage
6. Fat Necrosis
Cause of fat necrosis:
* Release of prematurely activated lipase from pancreatic exocrine acinar
* Lipase breaks down adipose tissue (fat)
* The resultant free fatty acids bind with calcium salts
* Forms the typical fat necrosis deposits
* \*These patients will often have very low serum calcium due to this process\*
56
Horseshoe Kidney
Congenital abnormality\*
The ureters of the fised kidneys pass anteriorly to the kidney parenchyma
This anomaly is quite common - twice as common in males
Fusion of the upper poles accounts for 90% of hoseshoe kidneys
~1/3 of patients are asymptomatic and this will be an incidental finding
However, rates of various diseases are more common in horseshoe kidneys:
* Hydronephrosis
* Stone Formation
* Infection
* Certain Cancers
57
Cause of that massive thing...?
Neohrolithiasis and Pyelonephrosis
Specimen = kidney
Renal parenchyma has been destroyed and replaced by a thin rim of fibrous tissue, stretched over grossly expanded calyces which were filled with pus
Large Staghorn Calculus filling the renal pelvis and obstructing the ureter
Pus can be seen on the surface of the staghorn calculus
Cause of Staghorn Calculi:
* Almost always a consequence of infection by urea-splitting organisms - e.g. proteus and staphylococci
* The resultant alkaline urine causes the precipitation of magnesium ammonium phosphate salts
* These stones account for 15-20% of all renal stones and tend to be some of the largest
58
+ Likely Causes?
Hydronephrosis
Specimen = part of the kidney
Opened to show the distended pelvis and calyces
Small remnants of renal parenchyma are present
But most of the kidney has been reduced to thin-walled cystic structure
The hydronephrotic 'cysts' are all connected with the hydronephrotic cavity
Cuases:
* Hydronephrosis may follow an abstruction at any level of the urinary tract
* Obstruction ultimately leads to reflux and build up of pressure thatn damages the delicate kidney parenchyma
* This also predisposes to infection, inflammation and stone formation
59
+ Epidemiology of this pathology
+ Diagnosis of this pathology
Solitary Cyst of the Kidney
Specimen = A kidney
Kdney displays a large thin-walled cyst of the upper pole, which is compressing surrounding renal parenchyma
This is a solitary simple cyst of the kidney
Renal cysts are present in 50% of people over 50yo
Usually asymptomatic but can sometimes cause symptoms similar to that of a malignant renal lesion:
* Flank Pain
* Haematuria
* Palpable Mass
US and CT scan help in the differentiation of cysts from other renal masses - particularly malignancy
Bosniak system of classification of renal cysts on CT is also a useful method
60
+ Aetiology
+ Incidence and consequences
Austosomal Dominant Adult Polycystic Kidney Disease (ADPKD)
Sepcimen = Part of the Right Kidney
Sliced to show numerous cysts
In some, the sero-sanguinous contents are retained
Kidney has retained its classical 'kidney' shape, but the renal parenchyma is just about completely destroyed
Aetiology:
* AD type Polycystic Kidney Disease affects 1 in 400-1000 live births
* Accounts for 5-10% of chronic renal failure cases
* Genetic mutations alter mechanical signalling by the tubular epithelium
* This alters growth and differentiation of the epithelium
* Resulting in the progressive formation of cysts
* And destruction of functioning parenchyma
* By 60yo, 70% of these patients will be in renal failure
\*I.e. require transplants
61
+ Histologically
+ Aetiology
Clear Cell Carcinoma of the Kidney
Specimen = Right Kidney, Sliced
Sliced edge shows large, expansile tumour of the lower pole
It is infiltrating the renal parenchyma superiorly
Tumour tissue is pale yellow in colour and shows foci of haemorrhage and cystic degeneration
Hilum of the kidney appears unaffected\*
Microscopically:
1. Tumour formed by large polygonal epithelial cells with abundant clear cytoplasm
2. Show trabecular and tubular growth patterns
\*Clear Cell Carcinomas are the most common type of renal cell carcinomas
Aetiology:
* 98% of these tumours are associated with a loss of sequences on chromosome 3p at the locus of the VHL gene
62
+ Epidemiology
+ Histologically
+ Prognosis
Nephroblastoma Kidney - Wilms Tumour
At the upper pole, the small distorded kidney can be seen
Below it, is a large expansile tumour mass
Tumour is lobulated and comprised of pale tan tissue with areas of necrosis, haemhorrage, and cystic degeneration
The tumour has distorted the calyceal system and appears to be encapsulated
Microscopically:
1. Tumour made up of large sheets of neoplastic cells
2. Some areas are of embryonic type (blastema)
3. Other areas show differentiation into primitive tubular and glomerular structures (epithelial)
4. Loose stroma is also seen
5. The triphasic histology represents the tumour's attempt at nephrogenesis
6. In 5% of cases, cellular anaplasia can be seen - associated with worse prognosis
Epidemiology:
* Most common primary renal tumour in children
* Usually diagnosed in children 2-5 years old
Prognosis:
Usually good - 90% at 2 years, even where there has been spread beyond the kidney
63
Carcinoma of the Renal Pelvis
Specimen = Right kidney sliced open
Shows massive papillary carcinoma 9 x 5.5 cm
Tumor appears to be arising over most of the surface of the lower half of the renal pelvis
Upper half of the pelvis is dilated and the calyces are blunted
Ureter not involved
\*5-10% of renal tumours arise from the renal pelvic urothelium, and they tend to present quite early with haematuria or obstruction
64
+ Histologically
Horseshoe Kidney and Renal Hamartoma
Horseshoe kidney
Also present is a small subcapsular tumour-like mass at the upper pole of the left kidney
This tumour appears to have arisen from the cortex of the kidney
The tumout projectes from the capsular surface to form an irregularly shaped mass of pale yellow-grey tissue
Microscopically:
As a hamartoma of the kidney:
* Tumor composed of thick walled blood vessels
* Adipose tissue
* Interlacing bundles of smooth muscle
65
+ Aetiology
Staghorn Calculus and Pyelonephrosis
Specimen = Kidney sliced open to reveal a large, fragmented staghor calculus
The calculus filles the dilated renal pelvis and calyceal system
Pus was present in the calyces and renal pelvis
There is thinning of the renal cortex in the areas adjacent to the calculus - especially the upper pole
Aetiology:
* Staghorn calculi are almost always due to urea-splitting organisms - proteus or staphylococci
* The result is alkaline urine which causes the precipitation of magnesium ammonium phosphate salts (struvite)
* These stones are some of the largest renal calculi and account for 15-20% of renal stones
66
+ Histologically
Hydronephrosis and Chronic Pyelonephritis
Specimen = Shrunken kidney
Capsular surface shows multiple, deep, irregular scars
Cut surface shown dilated pelvis/calyceal system
Thinning of the overlying cortex and loss of medullary tissue too
Mucosal lining of the renal pelvis shown congestion - consistent with inflammation
Microscopically:
* Renal parenchyma largely replaced by fibrous tissue
* Chronic inflammatory cell infiltrate
* The pelvis/ureteric junction is narrowed and distorted by dense fibrous tissue
67
+ Epidemiology
+ Diagnosis
Solitary Cyst Kidney
Specimen = Right Kidney
Kidney has large, thin-walled solitary cyst ~8cm diameter
Cyst is in the mid-zone, overlying the front of the hilar region
Aberrant renal artery and vein also present at the lower pole\*
Simple Renal Cysts:
* Present in over 50% of individuals over 50yo
* Usually asymptomatic but may produce similar signs and symptoms to malignant lesions: flank pain, haematuria and palpable masses
Diagnosis:
* US and CT scan help in differentiating cysts from other renal masses
* Bosniak system of classification also helpful
68
+ Involvement of other organs?
+ Histologically
Polycystic Kidney Disease
Specimen = part of the right kidney
Slided to show numerous irregularly sized cysts
Some retain gelatenous material
Other caontain a watery fluid and some contain altered blood
Histologically:
1. Cysts lined with cuboidal epithelium
2. Thin rims of renal tissue around the cysts
3. Tubules filled with proteinaceous casts
4. Vessels showing hypertensive changes
~40% of patients with ADPKD have liver cysts as well
69
+ Aetiology and incidence
Clear Cell Carcinoma of the Kidney
Specimen = Right Kidney
Sliced to reveal a large expansile tumour
Largely of the lower pole of the kidney, and infiltrating the renal parenchyma superiorly
TUmour tissue is pale yellow with areas of haemorrhage, necrosis, and cystic degeneration
Hilar region appears tumour free
Aetiology
* Loss of sequences on chromosome 3p at the loci of the VHL gene
70
+ Histologically
Neohroblastoma Kidney - Wilms Tumour
Specimen = small distorted kidney, at the top of the specimen. The rest is a large expansile tumour
Tumour tissue is pale tan - white
SHows extensive areas or haemorrhage and necrosis centrally, with some areas of cystic degeneration
Tumour appears contained within a delicate fibrovascular capsule
Microscopically:
1. Small embryonic-type cells
2. And formation of primitive tubules
3. Characteristic of a nephroblastoma
4. This triphasic histology represents the tumour's attempts at nephrogenesis
5. Anaplasia only seen in ~5% of cases and is associated with worse prognosis
71
Papillary Transitional Cell Carcinoma of the Renal Pelvis
Specimen = Slice shows a papillary tumour mass finning and distorting the calyceal system of the upper pole
No evidence of haemorrhage or necrosis
\*Note that 5-10% of renal tumours arise from the pelvic urothelium. These tumours tend to present early with haematuria or obstruction
72
