Histopathology 1 - Upper and Lower GI, Pancreas, Gall Bladder and Liver Flashcards
(165 cards)
1
Q
Define metaplasia
A
Reversible change in one mature and functional cell type for another mature and functional cell type
2
Q
Example of Metaplasia
A
Barrett’s Oesophagus
3
Q
What can Barrett’s progress to? Via what pathway?
A
Adenocarcinoma of the Oesophagus via the Metaplasia - dysplasia pathway
4
Q
What are the two main pathways of GI Cancer?
Example of each
A
Metaplasia-dysplasia pathway
(Barrett’s –> Adenocarcinoma of the Oesophagus)
Adeno-carcinoma pathway
(Colorectal Cancer: benign polyps –> adenocarcinoma)
5
Q
4 defining features of a cancer
A
Gland formation
Mucin Screening
Make Keratin (even in non-keratinised tissues)
Inter-celllular bridges
6
Q
Two types of Cancer in GI
A
Adenocarcinoma
Squamous Cell Carcinoma
7
Q
How to distinguish adenocarcinoma and squamous cell carcinoma?
A
Adenocarcinoma is gland forming and/or mucin secreting
Squamous Cell Carcinoma
Make Keratin (even in non-keratinised tissues)
have Inter-celllular bridges
8
Q
Cancer cell producing Inter-cellular bridges. What is the type of cancer?
A
Squamous Cell Carcinoma
9
Q
Cancer cell secreting mucin. What is the type of cancer?
A
Adenocarcinoma
10
Q
What does necrosis represent? What is the most common cause? What are three more features?
A
Energy Failure.
Most often caused by ischaemia
Cell lysis due to loss of electro-ionic potential
It is pathological
It is energy independent - it occurs regardless of energy level (as opposed to apoptosis)
11
Q
Define Apoptosis
A
Planned energy dependent exit strategy
Cell contents are not released, they go into apoptotic bodies
12
Q
How long is the oesphagus? What structures are near it?
A
25cm
Passes from Cricoid to Cardia of stomach through the Diaphragm
13
Q
What are the layers of the oesophagus?
A
Longitudinal muscular layer
Circular muscular layer
Submucosal layer
14
Q
What do submucosal glands on biopsy indicate?
A
Tissue is from the oesophagus
15
Q
How much fluid do submucosal glands produce?
A
1 litre of alkaline fluid a day
16
Q
How does the oesophagus change in structure going down?
A
The top third is striated muscle.
The bottom third is smooth muscle.
The middle third is a mixture of both.
17
Q
What lines the oesophagus?
What are the implications of this?
A
Stratified Squamous Epithelium
No infections - lots of layers of cells i.e. not every cell is in contact with the basement membrane.
You get oesophagitis though - it is a wear and tear organ, layers are shed and new layers of cells replace it.
18
Q
Where does the stomach meet the oesophagus? Give a specific name.
A
Z-line i.e. Squamo-Columnar Junction
After this point you get columnar epithelium
19
Q
Generally how do you get cancer of the oesophagus?
A
It becomes inflamed.
20
Q
What are the two pathological mechanisms in oesophagitis?
A
Ulceration and Metaplasia
Both start with inflammation
In Ulceration, inflamation –> ulceration –> Loss of surface epithelium –> Repair –> Replacement of useful cells with myofibroblasts –> Scarring/Strictures
In Metaplasia, inflammation –> metaplasia –> metaplasia to columnar cells (±Goblet Cells) –> Dysplasia –> Cancer
21
Q
What causes oesophagitis?
A
Reflux
Corrosives (e.g. bleach)
22
Q
What are complications of oesophagitis?
A
Barrett’s Oesophagus: metaplastic columnar lined oesophagus ± goblet cells
Barrett’s –> Malignancy
Strictures due to fibrosis and scarring due to previous ulceration
Haemorrhage due to ulceration
23
Q
Two distinct features of Barrett’s Oesophagus
A
Columnar Metaplasia
Columnar Metaplasia with Goblet Cells
24
Q
Where are goblet cells found normally?
A
The small bowel
25
What do we call Columnar Metaplasia with Goblet Cells?
| What are the implications
intestinal-type metaplasia
higher risk for future cancer than simple columnar type metaplasia
thus not all Barrett's carries an equal risk. Do an OGD on patients with goblet cells more frequently.
26
What are the types of oesophageal malignancy?
| What is their aetiology and epidimeiology?
Mid-Distal Oesophagus: SCC
Commonest Type Worldwide
Caused by Smoking and Boozing
Distal Oesophagus: Adenocarcinoma
Commonest Type UK
Caused by Columnar Epithelial Transformation
Caused by GORD/Oesophagitis/H.pylori
27
What is a common oesophageal pathology other than inflammation, malignancy and Barrett's?
Oesophageal Varices
28
What is Oesophageal Varices?
extremely dilated sub-mucosal veins in the lower third of the esophagus
29
What causes Oesophageal Varices and what are the implications?
Any cause of portal hypertension
- cirrhosis
- portal vein thrombosis
- IVC obstruction
It can cause torrential GI bleeding
30
How to treat Oesophageal Varices?
Terlipressin
Resucitate with blood and crystalloids
Score them to find risk
Infuse with PPI
31
What type of cells line the stomach?
Columnar Epithelium
32
What are two specialised cells in the stomach? What functions?
Parietal Cells - produce acid
| P Cells / Chief cells - produce pepsin --> pepsinogen (broken down by acid)
33
What do goblet cells in the stomach indicate?
Goblet Cells are NOT seen in the stomach
| Indicated intestinal-type metaplasia
34
What causes Gastritis?
| Give Acute and Chronic
Acute: Alcohol, NSAIDs, H. pylori, physiological stress e..g hypovolaemia (stomach is the most sensitive organ in GIT to ischaemia)
```
Chronic: ABCCC
A: Autoimmune (pernicious anaemia)
B: bacteria (H. pylori)
C: Corrosives (bile reflux, NSAIDs)
CMV ((Renal) Transplant Patients)
Crohn's
```
35
What is pernicious anaemia?
Antibodies against intrinsic factor
Stops Vitamin B12 absorbtion
Causes Pernicious macrocytic aneamia
Most common cause of VitB12 deficiency in UK
36
BONUS: For what disease are 10% of our lymphocytes created for?
Implications?
CMV
| thus transplant patients who are immunosupressed are at risk of CMV infection. esp. renal transplant patients.
37
4 Complications of Gastritis
Ulceration
Perforation
Haemorrhage
Cancer
38
What kind of bacteria is H. pylori? How does it get energy?
Gram Negative Curved Rod
| Breaks down acid in the stomach using hydrogenase
39
What makes H. pylori outcome worse?
Cag pathogenicity Island
| It is a toxin injected into the submucosa
40
What does H. pylori cause and what does this lead to?
Chronic Gastritis --> Ulcers and Scarring
Adenocarcinoma
LYMPHOMA
41
What is onr bacterial cause of Lymphoma?
H. pylori
42
What is the treatment of H. pylori?
One week of Triple Therapy
PPI (-razole)
Clartihromycin
Amoxicillin or Metronidazole
43
How does H. pylori cause Lymphoma?
Induces MALT --> Germinal Centre + Lymphoid Follicles --> Adenocarcinoma via columnar epithelium metaplastic change
44
What is MALT?
Mucosa Associated Lymphoid Tissue
45
What are the different types of Gastric cancer and what are their percentages?
Adenocarcinoma 95%
| SCC, Lymphoma, GIST (Gastrointestinal stromal tumors( benign/malignant)) 5%
46
What are two features of adenocarcinoma?
Gland forming
| Mucin Secretion
47
What are two features of Squamous Cell Carcinoma?
Keratin Producing
| Intercellular Bridges
48
What are the two main types of adenocarcinoma? Describe them.
Intestinal (classic) and Diffuse
Intestinal: well-differentiated, mucin producing, gland forming = a classic adenocarcinoma
Diffuse: single-cell architecture, no gland formation, contains signet ring cell, spread extremely quickly
49
What is AKA a classic adenocarcinoma?
Intestinal Adenocarcinoma
50
What is a poorly differntiated adenocarcinoma?
Diffuse adenocarcinoma
51
What is a signet ring cell indicative of and how is it formed?
```
Diffuse Adenocarcinoma (pathagnomonic)
Formed as these cells contain a lot of mucin which pushes the contents of the cell to the periphery, with the nucleus flush on one end
```
52
What type of epithelium is found in the duodenum?
intestinal-type epithelium
53
What is the villous crypt ratio?
>2:1
54
What is a villi?
Villi are small, finger-like projections in the small intestine
55
What is a crypt?
These are folds inbetween villi. They are in the lamina propria layer and are mostly absorbative. They sometimes contain goblet cells.
56
What happens when there is damage in the small intestine?
Change in the villi:crypt ratio.
Shortening or blunting of villi
Crypts compensate by undergoing hyperplasia --> enlarged crypts
Ratio tends to --> 1:1 during inflammatory disease
57
Where are goblet cells seen and where are they definitely not expected to be?
Seen in the small intestine
| Not normally seen in the stomach
58
What disease is most commonly caused by H.pylori?
Duodenal Ulcers
59
What are anterior and posterior (duodenal) ulcers?
Ulcers on the anterior aspect and posterior aspect of the duodenum respectively. (simple)
60
What are you worried about with anterior and posterior (duodenal) ulcers? What do you have to prepare for?
Anterior Ulcers --> perforate --> peritonitis
Posterior Ulcers --> Near Gastroduodenal Artery --> Haemorrhage --> more likely to require surgery
61
What causes a major haemorrhage from the small bowel?
Posteriorly sided duodenal ulcer
62
How to diagnose Coeliac Disease?
anti-endomysial Ab +ve
Anti-TTG +ve (tissue transglutaminase)
OGD on gluten diet
63
What pathological changes occur in Coeliac malabsorbption?
villous atrophy
crypt hyperplasia (hence reduction in villi:crypt ratio)
increased intraepithelial lymphocytes = CD8+ T cells
(20:100 lymphocytes: enterocytes or higher)
64
What can be difficult for patients when trying to diagnose them with Coeliac Disease?
Diagnosis requires 6 weeks of eating gluten before an OGD which can make patients feel very unwell
65
BONUS: What does ERCP stand for?
Endoscopic Retrograde Cholangio-Pancreatography
66
What are complications of Coeliac Disease?
Malabsorption
Deficiencies
Lymphoma EATL (Enteropathy Associated T-cell Lymphoma)
Treating Coeliac reduces risk of lymphoma
67
What is a similar condition to Coeliac Disease? What is it?
Lymphocytic Duodenitis
Intraepithelial Lymphocytes = CD8+ve T Cells
However, architecture villous structure is normal = normal villi, normal crypts
Many have mild Coeliac Disease - likely a precursor to Coeliac. Exists on the same spectrum of pathology.
68
What are GI polyps?
GI Polyps are abnormal tissue growths on the lining of the large intestine or rectum. Most are asymptomatic.
69
Are polyps benign?
Most polyps are benign, however some may be adenomas and may develop into cancer of the large intestine or rectum.
70
What are different groups of polyps of the large bowel?
Two Groups: Non-neoplastic polyps and Neoplastic polyps
71
What are the different types of polyps of the large bowel?
Non-Neoplastic Polyps
- hyperplastic polyps = folds of mucosa that have grown a bit much
- inflammatory pseudo-polyps
- hamartomatous polyps
Neoplastic Polyps
- Tubular Adenoma
- Tubulovillous Adenoma
- Villous Adenoma (worst type, often found in rectum)
72
What are inflammatory pseudo-polyps?
These polyps are found in IBD such as UC and CD
Ulceration of the inner lining of the large bowel causes scar tissue to form during the healing process. This scar tissue resembles polyps, although it is not a true polyp.
It does not increase cancer risk.
73
What is a feature of hamartomatous polyps?
They are benign and have high Eosinophils. One example is a strawberry naevus.
74
What increases risk of Cancer from polyps?
Larger Polyps
More Polyps (people normally have 1-4 if any)
Higher villous component
Dysplastic Features
75
How does tissue in large bowel form Cancer?
| How does this inform treatment?
Normal --> Adenoma --> Adenocarcinoma
| Remove the adenoma --> Reduce the risk of cancer
76
What type of cancer are colorectal cancers?
98% of colorectal cancers are adenocarcinomas
77
What causes Colitis?
```
Acute:
Infection
Drugs (notably Abx)
Chemotherapy
Radiation
```
Chronic / acute on chronic diseases:
Crohn's
Ulcerative Coiltis
TB
78
What can cause Ischaemic Colitis?
Arterial Occlusion: Atheroma (degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue), Thromboembolism
Venous Occlusion: Thrombus, Hypercoaguable States
Small Vessel Disease: DM, Vasculitis
Low Flow States: CCF, Shock
Obstruction: Hernia, Volvulus, Intussusception
79
What is Ischaemic Colitis?
Inflammation and injury of the large intestine resulting from inadequate blood supply
80
What are some common symptoms of Ischaemic Bowel?
```
Abdominal Pain
malaena
diarrhoea
abdominal tenderness
weight loss
abdominal bruit
```
81
Where does the Liver receive its blood from?
Dual Blood Supply:
Portal Vein (blood from spleen, stomach, pancrease and gut)
Hepatic Artery
82
Where does the Hepatic Artery originate from?
The Coeliac Artery, which is the first major branch of the Aorta, positioned at T12
83
BONUS: What does Coeliac mean?
Relating to the abdomen
84
What is characterisitc of pathology of the liver?
Ischaemic disease of the liver is very rare.
| Most commonly iatrogenic.
85
What are the most metabolically active cells of the liver?
Hepatocytes
86
What cells line the bile ducts in the liver?
Cholangiocytes
87
What are the macrophages of the liver called?
Kupffer cells
88
What cells store Vitamin A?
Stellate Cells
89
Which cells in the liver become very significant in disease?
Stellate Cells - when activated they become myofibroblasts, deposit collagen and cause most of the scarring in liver diseases
Normally they store Vitamin A
90
Which cells cause scarring in liver pathology?
Stellate cells laying down collagen
91
What are the big pink cells on liver tissue slides?
Hepatocytes
92
How to tell if you are looking at a central vein?
It looks like a hole in the tissue slide (not a great Q)
93
What are the big pink cells on liver tissue slides?
Hepatocytes
94
What is a central vein in the liver?
It is what a hexagonal lobule is arranged around. After blood mixes in the sinusoids, it drains into the central veins, then into the hepatic vein which drains into the Inferior Vena Cava
95
What is a portal vein?
It is what drains blood from the spleen, stomach, pancreas and gut
96
What is the flow of a RBC in liver?
blood from portal vein/portal tract/&hepatic artery --> through sinusoids between hepatocytes (two sources of blood mix) (through zone 1, 2, 3) --> central vein --> hepatic vein --> Inferior Vena Cava
97
What is in a portal tract/portal triad?
Chiefly: blood from portal vein and hepatic artery
Hepatic Artery, Portal Vein, Bile Duct
(also lymphatic vessels, branch of vagus nerve)
98
What are the 3 zones in liver histopathology? Where are they situated?
1, 2, 3
| 1 is near the portal tract, 2 is inbetween 1 & 3 and 3 is near the central vein
99
What are the 3 zones in liver histopathology? Where are they situated?
1, 2, 3
| 1 is near the portal tract, 2 is inbetween 1 & 3 and 3 is near the central vein
100
Where are liver macrophages located?
Kuppfer cells are found in the sinusoids
101
Where are liver macrophages located?
Kupffer cells are found in the sinusoids
102
Where are (quiescent) stellate cells located?
Inbetween the endothelial cells lining the sinusoids and the hepatocytes AKA the Space of Disse.
In liver injury, they deposit scar matrices here.
103
What are sinusoids?
Spaces inbetween adjacent rows of hepatocytes
104
What happens to liver microanatomy in liver injury?
Loss of hepatocyte microvilli
Stellate cells activated (blood can't pass through)
Scar Matrix/Collagen deposited in Space of Disse (inbetween hepatocytes and epithelium lining of sinusoids)
Loss of fenestrae (gaps between) endothelial cells in endothelium lining sinusoids
Kupffer Cells Activated
105
How are hepatocytes arranged?
In lobules, that are hexagonal
106
What does 'portal' indicate?
Blood is returning to the liver
107
What occurs in the three zones of cells in the liver?
Zone 1: Hepatocytes born near portal tract
Zone 2: Hepatocytes mature
Zone 3: Hepatocytes are most metabolically active
108
How is microvasculature of the liver arranged? How does blood flow
Portal tracts around a central vein (6:1)
Blood enters portal tracts --> sinusoids --> central vein
so starts on the corners of the hexagon and all drains (and matures) into the centre
109
What is difference between portal veins and hepatic veins?
Portal veins take blood to the liver, hepatc veins take blood from the liver to the heart
110
How is liver sinusoid epithelium / endothelial cells unique?
Do not have a basemenet membrane
| Discontinuous (no tight junctions) aka fenestrated
111
What is the key element of liver histopathology?
Stellate cells become activated and deposit Collagen (/scar tissue/BM type collagens) in the Space of Disse (space between sinusoid epithelium and hepatocytes)
112
What are key features of cirrhosis?
Whole Liver Involved
Fibrosis (deposition of Collagen)
Regenerating Hepatocytes forming regenerating nodules all over the liver (visible both on tissue slide and excision)
Distortion of Liver Vascular architecture: Intra and Extra Hepatic shunting of blood (e.g. Oesophageal Varices, within the liver)
113
What occurs to blood leaving the intestine normally compared to when there is liver shunting?
Normally: toxic blood --> becomes filtered blood in liver --> heart
Intrahepatic Shunt: toxic blood --> passes through liver --> toxic unfiltered blood --> heart
Extrahepatic Shunt: toxic blood --> avoids liver --> toxic unfiltered blood --> heart
114
How to classify Cirrhosis?
According to Aetiology:
1) alcohol or insulin resistance --> fatty liver
2) Viral Hepatitis B, C, D etc.
115
What are complications of liver cirrhosis?
Portal Hypertension --> shunting (e.g. Oesophageal Varices)
Hepatic encephalopathy
Liver Cell Cancer
116
Where may blood flow through if there is portal hypertension?
The spleen --> splenomegaly
117
Is Cirrhosis always fatal?
No it can be reversible
118
What causes acute hepatitis?
Viruses and Drugs
119
What are the histological features of acute hepatitis?
Spotty Necrosis: little foci of inflammation e.g. apoptosis, many lymphocytes and macrophages
120
What causes chronic hepatitis?
Viruses, Drugs and Auto-Immune
121
What is used to describe the severity of chronic hepatitis?
```
Grade = Severity of Inflammation
Stage = Severity of Fibrosis F0 - F4
```
122
What is Portal Inflammation?
Inflammation confined within limiting plate
123
What is the limiting plate in liver histology?
Interface between portal tract and hepatocytes
124
What is Interface Hepatitis?
Inflammation across the limiting plate
Very difficult to tell difference between the portal tract and the hepatocytes as their is inflammation across the limiting plate.
T-cell mediated apoptotic inflammation
125
What is lobular inflammation?
Inflammation across the entire lobule
126
What is F4 in the liver describing?
Compensated Cirrhosis
127
How does fibrosis look like on liver tissue slides?
it is blue (strands of collagen) and links the portal tract to the central vein
128
What causes intrahepatic shunting?
Fibrosis going from the portal tract to the central vein. Creates an easier path for the blood that avoids the hepatocytes.
A bridging fibrosis
129
When does chronic hepatitis begin shunting?
Stage F2
130
When does chronic hepatitis become Cirrhosis?
Stage F4 (compensated Cirrhosis)
131
What are the grades of inflammation in Chronic Hepatitis?
Portal Inflammation: within limiting plate
Interface Hepatitis: across limiting plate
Lobular Inflammation: across entire lobule
132
What does a Prussian Blue stain indicate?
Haemochromatosis (bronzed diabetes)
133
What does Rhodanine indicate?
Wilson's Disease
134
What are major causes of Cirrhosis?
1. Alcoholic liver disease
2. Non-alcoholic fatty liver disease
3. Chronic viral hepatitis (hep B+/-D and C)
4. Autoimmune hepatitis
5. Biliary causes: Primary biliary cirrhosis & Primary sclerosing cholangitis
6. Genetic causes:
a) Haemochromatosis- HFE gene Chr 6
b) Wilson’s disease- ATP7B gene Chr 13
c) Alpha 1 antitrypsin deficiency (A1AT)
d) Galactosaemia
e) Glycogen storage disease
7. Drugs e.g. methotrexate
135
What are the stages of Alcoholic Hepatitis?
Fatty Liver
Alcoholic Hepatitis
Cirrhosis
136
What are the microscopic characteristics of fatty liver?
Fatty Infiltrates:
accumulation of fat droplets in hepatocytes (steatosis)
chronic exposure --> fibrosis
(fully reversilbe if alcohol avoided)
137
What are the microscopic characteristics of Cirrhosis?
Fibrosis
Loss of Parenchymal Tissue
Small regnerative nodules of hepatocytes
138
What are the microscopic characteristics of Alcoholic Hepatitis?
2 key features:
Ballooning of Cells
Mallory Denk Bodies (pink material within cells)
Apoptosis
Pericellular fibrosis
Zone 3 - acetaldehyde highest (most metabolically active) and relatively hypoxic (furthest from oxygenated blood)
Relatively irreversible
139
What are the macroscopic characterisitcs of Fatty Liver?
Large, pale, yellow and greasy liver
140
What is NAFLD?
Non-Alcoholic Fatty Liver Disease
141
Describe NAFLD
Very similar histological features as Alcoholic Liver Disease however no drinking
142
What causes NAFLD?
T2DM
Obesity
=Metabolic Syndrome
143
What does NAFLD cause?
Non-alcoholic Steatohepatitis AKA NASH
| equivalent to alcoholic hepatitis
144
What causes Liver Cancer?
1) Secondary Metastatic Disease (commonest)
Liver has a high blood supply so is a common site of metastases
Multiple metastases and Discrete
2) Primary Tumours
HCC (high RF: alcoholic cirrhosis/hepatitis)
Hepatoblastoma (tumours of primitive hepatocytes) (children)
Cholangiocarcinoma
Haemangiosarcoma
145
What is HCC?
Hepatocellular Carcinoma
146
Which Hepatic Lobular Zone is most at risk of injury?
Zone 3
147
What are the two components of the pancreas? What do they include? What do they produce?
```
Endocrine component (Islets of Langerhans)
Insulin, Glucagon, Somatostatin
```
```
Exocrine component (Acini)
Protease, Lipase, Amylase
```
148
What is acute pancreatitis?
Aberrant release of pancreatic enzymes
| Caused by duct obstruction and reflux + Direct Acinar Injury
149
What causes acute pancreatitis generally?
Duct obstruction and Reflux + Direct Acinar Injury
150
What are all the causes of Acute Pancreatitis?
```
Duct Obstruction: Gallstones (50%) and Tumours
Metabolic / Toxic: Alcohol (33%)
Ischaemia: Shock ('low flow states')
Infection: Mumps
Autoimmune (IGG4 Diease)
Idiopathic
```
151
What is the most common cause of Chronic Pancreatitis?
Alcohol Use
152
What are the patterns of injury in Acute Pancreatitis?
Peri-ductal = Obstructive cause (most common initiator)
- Acinar cells adjacent to the ducts undergo necrosis and pancreatic enzymes/juices are released and cycle propogates
Peri-lobular = Vascular cause
- Necrosis at the edges of the lobules
Pan-lobular: either peri-ductal or peri-lobular injury that has progressed (most likely)
153
What is the pathological process that underpins Acute Pancreatitis?
Reflux enzymes --> Acinar Necrosis --> Release of more enzymes
Release of lipases --> Fat Necrosis --> Soaponification with calcium (pancreas becomes mush)
154
What are the complications of Acute Pancreatitis?
```
Haemorrhagic Pancreatitis (50% mortality)
Metabolic Disturbances: hypoglycaemia, hypocalcaemia
Pseudocyst (collection of fluid without lining) (6 weeks after initial insult)
Abscess (any static fluid collection will become an abscess eventually and will need drainage)
```
155
How to manage Acute Pancreatitis?
Diagnose with Serum Lipase: raised
IV Fluids (sequestration & 3rd spacing)
Antibiotics are not recommended unless necrotising pancreatitis (give Merapenem)
Electrolyte Replacement
156
What is Chronic Pancreatitis?
Relapsing or persistent pancreatitis
| Fibrosis is present, duct strictures, loss of parenchyma --> insufficiency
157
What causes Chronic Pancreatitis?
```
Alcohol (80%)
Gallstones + Tumours
Haemochromatosis
Idiopathic
Autoimmune (IgG4 Disease)
```
158
What are the tumours of the Pancreas?
Carcinomas
- Ductal 85%
- Acinar
Acinar-Ductal metaplasia (most originate from acinar --> ductal carcinoma. This is a metaplastic change)
Cystic Neoplasms (predispose to adenocarcinomas) (cysts that contain mitotic changes)
- serous cystadenoma
- mucinous cystic neoplasm
Neuroendocrine Tumours (rare)
159
What does the position of a pancreatic tumours suggest?
Ductal carcinomas are common in the head of the pancreas (60% found here)
Neuroendocrine tumours are common in the tail
160
Give 3 features of Pancreatic Carcinoma
5YSR 5%
| K-ras mutations 95%
Peri-neural invasion very common
above two together v specific for pancreatic tumour
161
Give 3 features of Neuroendocrine Tumours
Associated with MEN1 (pituiutary, pancrease, thyroid)
Most are non-secretory
Commonest type of secretory tumour: insulinoma (beta cells) (v. rare)
- Glucose, C-peptide, Insulin, (proinsulin)
162
What percentage of the general population have Gall Stones?
20% of all people
163
What are the most common type of Gall Stone?
50% are cholestrol stones
164
What are complications of Gall stones?
Bile Duct Obstruction
Acute (neutrophils) on chronic cholecystitis (scarring + Rokitansky-Aschoff sinuses)
Gall Bladder Cancer
Pancreatitis
165
What are Rokitansky-Aschoff sinuses?
These are holes that are seen when you cut through a gall bladder that are diverticula of the gall bladder when there are gall stones
