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MedEd Path > Histopathology 1 - Upper and Lower GI, Pancreas, Gall Bladder and Liver > Flashcards

Histopathology 1 - Upper and Lower GI, Pancreas, Gall Bladder and Liver Flashcards

1
Q

Define metaplasia

A

Reversible change in one mature and functional cell type for another mature and functional cell type

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2
Q

Example of Metaplasia

A

Barrett’s Oesophagus

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3
Q

What can Barrett’s progress to? Via what pathway?

A

Adenocarcinoma of the Oesophagus via the Metaplasia - dysplasia pathway

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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)

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5
Q

4 defining features of a cancer

A

Gland formation
Mucin Screening
Make Keratin (even in non-keratinised tissues)
Inter-celllular bridges

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6
Q

Two types of Cancer in GI

A

Adenocarcinoma

Squamous Cell Carcinoma

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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

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8
Q

Cancer cell producing Inter-cellular bridges. What is the type of cancer?

A

Squamous Cell Carcinoma

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9
Q

Cancer cell secreting mucin. What is the type of cancer?

A

Adenocarcinoma

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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)

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11
Q

Define Apoptosis

A

Planned energy dependent exit strategy

Cell contents are not released, they go into apoptotic bodies

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12
Q

How long is the oesphagus? What structures are near it?

A

25cm

Passes from Cricoid to Cardia of stomach through the Diaphragm

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13
Q

What are the layers of the oesophagus?

A

Longitudinal muscular layer
Circular muscular layer
Submucosal layer

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14
Q

What do submucosal glands on biopsy indicate?

A

Tissue is from the oesophagus

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15
Q

How much fluid do submucosal glands produce?

A

1 litre of alkaline fluid a day

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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.

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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.

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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

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19
Q

Generally how do you get cancer of the oesophagus?

A

It becomes inflamed.

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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

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21
Q

What causes oesophagitis?

A

Reflux

Corrosives (e.g. bleach)

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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

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23
Q

Two distinct features of Barrett’s Oesophagus

A

Columnar Metaplasia

Columnar Metaplasia with Goblet Cells

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24
Q

Where are goblet cells found normally?

A

The small bowel

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25
Q

What do we call Columnar Metaplasia with Goblet Cells?

What are the implications

A

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.

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26
Q

What are the types of oesophageal malignancy?

What is their aetiology and epidimeiology?

A

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

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27
Q

What is a common oesophageal pathology other than inflammation, malignancy and Barrett’s?

A

Oesophageal Varices

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28
Q

What is Oesophageal Varices?

A

extremely dilated sub-mucosal veins in the lower third of the esophagus

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29
Q

What causes Oesophageal Varices and what are the implications?

A

Any cause of portal hypertension

  • cirrhosis
  • portal vein thrombosis
  • IVC obstruction

It can cause torrential GI bleeding

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30
Q

How to treat Oesophageal Varices?

A

Terlipressin
Resucitate with blood and crystalloids
Score them to find risk
Infuse with PPI

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31
Q

What type of cells line the stomach?

A

Columnar Epithelium

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32
Q

What are two specialised cells in the stomach? What functions?

A

Parietal Cells - produce acid

P Cells / Chief cells - produce pepsin –> pepsinogen (broken down by acid)

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33
Q

What do goblet cells in the stomach indicate?

A

Goblet Cells are NOT seen in the stomach

Indicated intestinal-type metaplasia

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34
Q

What causes Gastritis?

Give Acute and Chronic

A

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
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35
Q

What is pernicious anaemia?

A

Antibodies against intrinsic factor
Stops Vitamin B12 absorbtion
Causes Pernicious macrocytic aneamia
Most common cause of VitB12 deficiency in UK

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36
Q

BONUS: For what disease are 10% of our lymphocytes created for?
Implications?

A

CMV

thus transplant patients who are immunosupressed are at risk of CMV infection. esp. renal transplant patients.

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37
Q

4 Complications of Gastritis

A

Ulceration
Perforation
Haemorrhage
Cancer

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38
Q

What kind of bacteria is H. pylori? How does it get energy?

A

Gram Negative Curved Rod

Breaks down acid in the stomach using hydrogenase

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39
Q

What makes H. pylori outcome worse?

A

Cag pathogenicity Island

It is a toxin injected into the submucosa

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40
Q

What does H. pylori cause and what does this lead to?

A

Chronic Gastritis –> Ulcers and Scarring
Adenocarcinoma
LYMPHOMA

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41
Q

What is onr bacterial cause of Lymphoma?

A

H. pylori

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42
Q

What is the treatment of H. pylori?

A

One week of Triple Therapy
PPI (-razole)
Clartihromycin
Amoxicillin or Metronidazole

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43
Q

How does H. pylori cause Lymphoma?

A

Induces MALT –> Germinal Centre + Lymphoid Follicles –> Adenocarcinoma via columnar epithelium metaplastic change

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44
Q

What is MALT?

A

Mucosa Associated Lymphoid Tissue

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45
Q

What are the different types of Gastric cancer and what are their percentages?

A

Adenocarcinoma 95%

SCC, Lymphoma, GIST (Gastrointestinal stromal tumors( benign/malignant)) 5%

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46
Q

What are two features of adenocarcinoma?

A

Gland forming

Mucin Secretion

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47
Q

What are two features of Squamous Cell Carcinoma?

A

Keratin Producing

Intercellular Bridges

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48
Q

What are the two main types of adenocarcinoma? Describe them.

A

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

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49
Q

What is AKA a classic adenocarcinoma?

A

Intestinal Adenocarcinoma

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50
Q

What is a poorly differntiated adenocarcinoma?

A

Diffuse adenocarcinoma

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51
Q

What is a signet ring cell indicative of and how is it formed?

A 
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
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52
Q

What type of epithelium is found in the duodenum?

A

intestinal-type epithelium

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53
Q

What is the villous crypt ratio?

A

> 2:1

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54
Q

What is a villi?

A

Villi are small, finger-like projections in the small intestine

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55
Q

What is a crypt?

A

These are folds inbetween villi. They are in the lamina propria layer and are mostly absorbative. They sometimes contain goblet cells.

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56
Q

What happens when there is damage in the small intestine?

A

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

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57
Q

Where are goblet cells seen and where are they definitely not expected to be?

A

Seen in the small intestine

Not normally seen in the stomach

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58
Q

What disease is most commonly caused by H.pylori?

A

Duodenal Ulcers

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59
Q

What are anterior and posterior (duodenal) ulcers?

A

Ulcers on the anterior aspect and posterior aspect of the duodenum respectively. (simple)

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60
Q

What are you worried about with anterior and posterior (duodenal) ulcers? What do you have to prepare for?

A

Anterior Ulcers –> perforate –> peritonitis

Posterior Ulcers –> Near Gastroduodenal Artery –> Haemorrhage –> more likely to require surgery

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61
Q

What causes a major haemorrhage from the small bowel?

A

Posteriorly sided duodenal ulcer

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62
Q

How to diagnose Coeliac Disease?

A

anti-endomysial Ab +ve
Anti-TTG +ve (tissue transglutaminase)
OGD on gluten diet

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63
Q

What pathological changes occur in Coeliac malabsorbption?

A

villous atrophy
crypt hyperplasia (hence reduction in villi:crypt ratio)
increased intraepithelial lymphocytes = CD8+ T cells
(20:100 lymphocytes: enterocytes or higher)

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64
Q

What can be difficult for patients when trying to diagnose them with Coeliac Disease?

A

Diagnosis requires 6 weeks of eating gluten before an OGD which can make patients feel very unwell

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65
Q

BONUS: What does ERCP stand for?

A

Endoscopic Retrograde Cholangio-Pancreatography

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66
Q

What are complications of Coeliac Disease?

A

Malabsorption
Deficiencies
Lymphoma EATL (Enteropathy Associated T-cell Lymphoma)

Treating Coeliac reduces risk of lymphoma

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67
Q

What is a similar condition to Coeliac Disease? What is it?

A

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
Q

What are GI polyps?

A

GI Polyps are abnormal tissue growths on the lining of the large intestine or rectum. Most are asymptomatic.

69
Q

Are polyps benign?

A

Most polyps are benign, however some may be adenomas and may develop into cancer of the large intestine or rectum.

70
Q

What are different groups of polyps of the large bowel?

A

Two Groups: Non-neoplastic polyps and Neoplastic polyps

71
Q

What are the different types of polyps of the large bowel?

A

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
Q

What are inflammatory pseudo-polyps?

A

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
Q

What is a feature of hamartomatous polyps?

A

They are benign and have high Eosinophils. One example is a strawberry naevus.

74
Q

What increases risk of Cancer from polyps?

A

Larger Polyps
More Polyps (people normally have 1-4 if any)
Higher villous component
Dysplastic Features

75
Q

How does tissue in large bowel form Cancer?

How does this inform treatment?

A

Normal –> Adenoma –> Adenocarcinoma

Remove the adenoma –> Reduce the risk of cancer

76
Q

What type of cancer are colorectal cancers?

A

98% of colorectal cancers are adenocarcinomas

77
Q

What causes Colitis?

A 
Acute:
Infection
Drugs (notably Abx)
Chemotherapy
Radiation

Chronic / acute on chronic diseases:
Crohn’s
Ulcerative Coiltis
TB

78
Q

What can cause Ischaemic Colitis?

A

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
Q

What is Ischaemic Colitis?

A

Inflammation and injury of the large intestine resulting from inadequate blood supply

80
Q

What are some common symptoms of Ischaemic Bowel?

A 
Abdominal Pain
malaena
diarrhoea
abdominal tenderness
weight loss
abdominal bruit
81
Q

Where does the Liver receive its blood from?

A

Dual Blood Supply:
Portal Vein (blood from spleen, stomach, pancrease and gut)
Hepatic Artery

82
Q

Where does the Hepatic Artery originate from?

A

The Coeliac Artery, which is the first major branch of the Aorta, positioned at T12

83
Q

BONUS: What does Coeliac mean?

A

Relating to the abdomen

84
Q

What is characterisitc of pathology of the liver?

A

Ischaemic disease of the liver is very rare.

Most commonly iatrogenic.

85
Q

What are the most metabolically active cells of the liver?

A

Hepatocytes

86
Q

What cells line the bile ducts in the liver?

A

Cholangiocytes

87
Q

What are the macrophages of the liver called?

A

Kupffer cells

88
Q

What cells store Vitamin A?

A

Stellate Cells

89
Q

Which cells in the liver become very significant in disease?

A

Stellate Cells - when activated they become myofibroblasts, deposit collagen and cause most of the scarring in liver diseases
Normally they store Vitamin A

90
Q

Which cells cause scarring in liver pathology?

A

Stellate cells laying down collagen

91
Q

What are the big pink cells on liver tissue slides?

A

Hepatocytes

92
Q

How to tell if you are looking at a central vein?

A

It looks like a hole in the tissue slide (not a great Q)

93
Q

What are the big pink cells on liver tissue slides?

A

Hepatocytes

94
Q

What is a central vein in the liver?

A

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
Q

What is a portal vein?

A

It is what drains blood from the spleen, stomach, pancreas and gut

96
Q

What is the flow of a RBC in liver?

A

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
Q

What is in a portal tract/portal triad?

A

Chiefly: blood from portal vein and hepatic artery
Hepatic Artery, Portal Vein, Bile Duct
(also lymphatic vessels, branch of vagus nerve)

98
Q

What are the 3 zones in liver histopathology? Where are they situated?

A

1, 2, 3

1 is near the portal tract, 2 is inbetween 1 & 3 and 3 is near the central vein

99
Q

What are the 3 zones in liver histopathology? Where are they situated?

A

1, 2, 3

1 is near the portal tract, 2 is inbetween 1 & 3 and 3 is near the central vein

100
Q

Where are liver macrophages located?

A

Kuppfer cells are found in the sinusoids

101
Q

Where are liver macrophages located?

A

Kupffer cells are found in the sinusoids

102
Q

Where are (quiescent) stellate cells located?

A

Inbetween the endothelial cells lining the sinusoids and the hepatocytes AKA the Space of Disse.
In liver injury, they deposit scar matrices here.

103
Q

What are sinusoids?

A

Spaces inbetween adjacent rows of hepatocytes

104
Q

What happens to liver microanatomy in liver injury?

A

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
Q

How are hepatocytes arranged?

A

In lobules, that are hexagonal

106
Q

What does ‘portal’ indicate?

A

Blood is returning to the liver

107
Q

What occurs in the three zones of cells in the liver?

A

Zone 1: Hepatocytes born near portal tract
Zone 2: Hepatocytes mature
Zone 3: Hepatocytes are most metabolically active

108
Q

How is microvasculature of the liver arranged? How does blood flow

A

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
Q

What is difference between portal veins and hepatic veins?

A

Portal veins take blood to the liver, hepatc veins take blood from the liver to the heart

110
Q

How is liver sinusoid epithelium / endothelial cells unique?

A

Do not have a basemenet membrane

Discontinuous (no tight junctions) aka fenestrated

111
Q

What is the key element of liver histopathology?

A

Stellate cells become activated and deposit Collagen (/scar tissue/BM type collagens) in the Space of Disse (space between sinusoid epithelium and hepatocytes)

112
Q

What are key features of cirrhosis?

A

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
Q

What occurs to blood leaving the intestine normally compared to when there is liver shunting?

A

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
Q

How to classify Cirrhosis?

A

According to Aetiology:

1) alcohol or insulin resistance –> fatty liver
2) Viral Hepatitis B, C, D etc.

115
Q

What are complications of liver cirrhosis?

A

Portal Hypertension –> shunting (e.g. Oesophageal Varices)
Hepatic encephalopathy
Liver Cell Cancer

116
Q

Where may blood flow through if there is portal hypertension?

A

The spleen –> splenomegaly

117
Q

Is Cirrhosis always fatal?

A

No it can be reversible

118
Q

What causes acute hepatitis?

A

Viruses and Drugs

119
Q

What are the histological features of acute hepatitis?

A

Spotty Necrosis: little foci of inflammation e.g. apoptosis, many lymphocytes and macrophages

120
Q

What causes chronic hepatitis?

A

Viruses, Drugs and Auto-Immune

121
Q

What is used to describe the severity of chronic hepatitis?

A 
Grade = Severity of Inflammation
Stage = Severity of Fibrosis F0 - F4
122
Q

What is Portal Inflammation?

A

Inflammation confined within limiting plate

123
Q

What is the limiting plate in liver histology?

A

Interface between portal tract and hepatocytes

124
Q

What is Interface Hepatitis?

A

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
Q

What is lobular inflammation?

A

Inflammation across the entire lobule

126
Q

What is F4 in the liver describing?

A

Compensated Cirrhosis

127
Q

How does fibrosis look like on liver tissue slides?

A

it is blue (strands of collagen) and links the portal tract to the central vein

128
Q

What causes intrahepatic shunting?

A

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
Q

When does chronic hepatitis begin shunting?

130
Q

When does chronic hepatitis become Cirrhosis?

A

Stage F4 (compensated Cirrhosis)

131
Q

What are the grades of inflammation in Chronic Hepatitis?

A

Portal Inflammation: within limiting plate
Interface Hepatitis: across limiting plate
Lobular Inflammation: across entire lobule

132
Q

What does a Prussian Blue stain indicate?

A

Haemochromatosis (bronzed diabetes)

133
Q

What does Rhodanine indicate?

A

Wilson’s Disease

134
Q

What are major causes of Cirrhosis?

A
  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
Q

What are the stages of Alcoholic Hepatitis?

A

Fatty Liver
Alcoholic Hepatitis
Cirrhosis

136
Q

What are the microscopic characteristics of fatty liver?

A

Fatty Infiltrates:
accumulation of fat droplets in hepatocytes (steatosis)
chronic exposure –> fibrosis

(fully reversilbe if alcohol avoided)

137
Q

What are the microscopic characteristics of Cirrhosis?

A

Fibrosis
Loss of Parenchymal Tissue
Small regnerative nodules of hepatocytes

138
Q

What are the microscopic characteristics of Alcoholic Hepatitis?

A

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
Q

What are the macroscopic characterisitcs of Fatty Liver?

A

Large, pale, yellow and greasy liver

140
Q

What is NAFLD?

A

Non-Alcoholic Fatty Liver Disease

141
Q

Describe NAFLD

A

Very similar histological features as Alcoholic Liver Disease however no drinking

142
Q

What causes NAFLD?

A

T2DM
Obesity
=Metabolic Syndrome

143
Q

What does NAFLD cause?

A

Non-alcoholic Steatohepatitis AKA NASH

equivalent to alcoholic hepatitis

144
Q

What causes Liver Cancer?

A

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
Q

What is HCC?

A

Hepatocellular Carcinoma

146
Q

Which Hepatic Lobular Zone is most at risk of injury?

147
Q

What are the two components of the pancreas? What do they include? What do they produce?

A 
Endocrine component (Islets of Langerhans)
Insulin, Glucagon, Somatostatin
Exocrine component (Acini)
Protease, Lipase, Amylase
148
Q

What is acute pancreatitis?

A

Aberrant release of pancreatic enzymes

Caused by duct obstruction and reflux + Direct Acinar Injury

149
Q

What causes acute pancreatitis generally?

A

Duct obstruction and Reflux + Direct Acinar Injury

150
Q

What are all the causes of Acute Pancreatitis?

A 
Duct Obstruction: Gallstones (50%) and Tumours
Metabolic / Toxic: Alcohol (33%)
Ischaemia: Shock ('low flow states')
Infection: Mumps
Autoimmune (IGG4 Diease)
Idiopathic
151
Q

What is the most common cause of Chronic Pancreatitis?

A

Alcohol Use

152
Q

What are the patterns of injury in Acute Pancreatitis?

A

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
Q

What is the pathological process that underpins Acute Pancreatitis?

A

Reflux enzymes –> Acinar Necrosis –> Release of more enzymes
Release of lipases –> Fat Necrosis –> Soaponification with calcium (pancreas becomes mush)

154
Q

What are the complications of Acute Pancreatitis?

A 
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
Q

How to manage Acute Pancreatitis?

A

Diagnose with Serum Lipase: raised
IV Fluids (sequestration & 3rd spacing)
Antibiotics are not recommended unless necrotising pancreatitis (give Merapenem)
Electrolyte Replacement

156
Q

What is Chronic Pancreatitis?

A

Relapsing or persistent pancreatitis

Fibrosis is present, duct strictures, loss of parenchyma –> insufficiency

157
Q

What causes Chronic Pancreatitis?

A 
Alcohol (80%)
Gallstones + Tumours
Haemochromatosis
Idiopathic
Autoimmune (IgG4 Disease)
158
Q

What are the tumours of the Pancreas?

A

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
Q

What does the position of a pancreatic tumours suggest?

A

Ductal carcinomas are common in the head of the pancreas (60% found here)

Neuroendocrine tumours are common in the tail

160
Q

Give 3 features of Pancreatic Carcinoma

A

5YSR 5%

K-ras mutations 95%
Peri-neural invasion very common
above two together v specific for pancreatic tumour

161
Q

Give 3 features of Neuroendocrine Tumours

A

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
Q

What percentage of the general population have Gall Stones?

A

20% of all people

163
Q

What are the most common type of Gall Stone?

A

50% are cholestrol stones

164
Q

What are complications of Gall stones?

A

Bile Duct Obstruction
Acute (neutrophils) on chronic cholecystitis (scarring + Rokitansky-Aschoff sinuses)
Gall Bladder Cancer
Pancreatitis

165
Q

What are Rokitansky-Aschoff sinuses?

A

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

MedEd Path (5 decks)

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