Pathology Flashcards

1
Q

What are the two main causes of small bowel ischaemia?

A
  1. Mesenteric artery occulsion
  2. Non-occlusive perfusion insufficiency
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2
Q

Why may the mesenteric artery become occluded?

A
  • Atherosclerosis
  • Thromboembolism (from AF for example)
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3
Q

What are some causes for non-occlusive perfusion insufficiency of the small bowel?

A
  • Shock
  • Strangulation - obstructs venous return
  • Drugs - cocaine
  • Hyperviscosity
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4
Q

Which area of the small bowel is most affected by ischaemia?

A

Mucosa

(it is the most metabolically active tissue)

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5
Q

As time of ischaemia increases in the small bowel, what are the consequences?

A

Ischaemia worsens and deepens

Gangrene may eventually develop

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6
Q

What is the difference between the outcomes of:

a) Mucosal infarct
b) Mural infarct
c) Transmural infarct

A

a) Regeneration - mucosal integrity is restored
b) Repair and regeneration - a fibrous stricture forms
c) Gangrene - death occurs unless this part of the small bowel is resected

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7
Q

What is the danger of gangrene in the small bowel?

A

The small bowel will perforate, cause peritonitis, sepsis and even death

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8
Q

Which type of tumour, primary or secondary, are more common in the small bowel?

A

Secondary

(primary are very rare)

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9
Q

Which types of secondary tumours are common in the small bowel?

A

Metastases from:

  • Ovaries
  • Colon
  • Stomach
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10
Q

Which types of primary tumours are likely to affect the small bowel?

A
  • Lymphomas
  • Carcinoid tumours
  • Carcinomas
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11
Q

Which conditions are associated with carcinoma of the small bowel?

A
  • Crohn’s disease
  • Coeliac disease
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12
Q

Where will a carcinoma of the small bowel usually metastasise to?

A
  • Lymph nodes
  • Liver
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13
Q

What may be the clinical signs of appendicitis?

A
  • Vomiting
  • Abdominal pain
  • RIF tenderness
  • Increased WCC
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14
Q

What is the aetiology of appendicitis?

A
  • Idiopathic
  • Faecoliths
  • Lymphoid hyperplasia
  • Parasites
  • Tumours
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15
Q

What are faecoliths?

A

Small hard lumps of faeces which can commonly enter and inflame the appendix leading to acute appendicitis

They are often the result of dehydration

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16
Q

What are the features of an appendix during acute appendicitis?

A
  • Acute inflammation - involving the muscle coat
  • Mucosal ulceration
  • Serosal congestion
  • Pus in the lumen
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17
Q

What happens to the muscular wall in appendicitis?

A

It thickens

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18
Q

What are the complications of appendicitis?

A
  • Peritonitis
  • Rupture
  • Abscess
  • Fistula
  • Sepsis and liver abscess
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19
Q

Coeliac disease is due to an abnormal reaction to what?

A

Gliadin - a component of gluten

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20
Q

Coeliac disease is mediated by which cell type?

A

T-cells

(intraepithelial lymphocytes)

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21
Q

How is the mucosa in the small bowel affected during Coeliac disease?

A

The mucosal surface flattens and complete villus atrophy occurs

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22
Q

Which antibodies will be found in a sufferer of Coeliac disease?

A
  1. Anti-TTG
  2. Anti-endomesial
  3. Anti-gliadin
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23
Q

Why may coeliac disease often lead to anaemia?

A

There is poor absorption of iron, vitamin B12 and folate from the terminal ileum

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24
Q

Why are gallstones a potential complication of Coeliac disease?

A

There is reduced intestinal hormone production which reduces pancreatic secretion which in turn affects bile flow

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25
Q

Which inflammatory oesophageal conditions may be acute?

A
  • Chemical ingestion
  • Infection in immunocompromised patients e.g. candida, herpes, cytomegalovirus, HIV, chemotherapy
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26
Q

Which inflammatory cells are often present during reflux disease in the oesophagus?

A

Eosinophils

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27
Q

Why may reflux oesophagitis even arise?

A
  • Defective sphincter mechanism
  • Hiatus hernia
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28
Q

What are the potential complications of oesophagitis?

A
  • Ulcers - when a physical prtective barrier cannot be made quickly enough
  • Strictures and fibrosis - due to the healing process from continued injury
  • Barrett’s oesophagus - replacement of stratified squamous epithelium by columnar epithelium which include more mucous cells for protection
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29
Q

What is Barrett’s oesophagus?

A

The change of epithelium in the oesophagus from stratified squamous epithelium to columnar epithelium

This means more mucous cells are present for protection

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30
Q

What is allergic oesophagitis?

A

Eosinophilic inflammation in the oesophagus due to allergy

The oesophagus becomes corrugated and feline-like

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31
Q

Which age and gender are most likely to suffer from allergic oesophagitis?

A

Young males

(often have asthma)

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32
Q

Which rare oesophageal tumour is associated with HPV?

A

Squamous papilloma

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33
Q

Which tumours are malignant in the oesophagus?

A

Squamous cell carcinomas

Adenocarcinomas

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34
Q

Squamous cell carcinomas are related to what?

A
  • Vitamin A or zinc deficiency
  • Tannic acid or strong tea
  • Smoking and alcohol
  • HPV
  • Oesophagitis
  • Genetic
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35
Q

Which tumour type is associated with dysphagia?

A

Squamous cell carcinoma

or

Adenocarcinoma

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36
Q

Which tumour eventually arises from Barrett’s oesophagus assuming dysplasia eventually does occur and progress?

A

Adenocarcinoma

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37
Q

Where in the oesophagus does an adenocarcinoma affect?

A

Bottom 1/3rd of oesophagus

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38
Q

Carcinomas of the oesophagus can spread via metastses to which other locations in the body?

A
  • Direct invasion
  • Lymphatic permeation
  • Vascular invasion
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39
Q

What is a Mallory-Weiss tear?

A

A tear in the oesophagus 2cm above the Z-line

It is cause by severe and prolonged vomiting

It will result in bleedign and haematemesis

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40
Q

What is the term given to dilated veins in the distal oesophagus?

A

Oesophageal varices

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41
Q

What is the main cause of oesophageal varices?

A

Increased portal venous pressure due to chronic liver disease

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42
Q

Describe the TNM staging system for tumours

A

T - Greatest diameter of tumour an invasion

N - Lymph node status (how many are affected)

M - Metastases

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43
Q

Inflammatory bowel disease emcompasses which two conditions?

A
  1. Crohn’s disease
  2. Ulcerative colitis
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44
Q

What is Crohn’s disease?

A

Chronic inflammation and ulcering of the GI tract anywhere from the mouth to the anus yet most commonly in the terminal ileum and colon

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45
Q

How will Crohn’s disease present clinically?

A
  • Abdominal pain
  • Small bowel obstruction
  • Diarrhoea
  • Bleeding PR
  • Anaemia
  • Weight loss
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46
Q

Which investigations should e taken for a patient with suspected Crohn’s disease?

A
  • Endoscopy
  • Mucosal biopsy
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47
Q

In relation to the distribution of Crohn’s disease, how would it be described?

Continuous, or patchy?

A

Patchy and segmental

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48
Q

How does the body often respond to the damage caused by Crohn’s disease in the terminal ileum for example?

A
  1. Stricturing of the terminal ileum
  2. Thickening of the bowel wall
  3. Fat wrapping (from greater omentum)
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49
Q

Which inflammatory bowel disease produced cobblestoning of the mucosa?

A

Crohn’s disease

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50
Q

Deep fissures into the mucosa are associated with which IBD?

A

Crohn’s

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51
Q

Transmural inflammation occurs with which IBD?

A

Crohn’s

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52
Q

What are the main complications of Crohn’s disease?

A
  • Malabsorption - latrogenic (short bowel syndrome) due to repeated resections and removal
  • Hypoproteinemia, vitami deficiency, anaemia
  • Gallstones
  • Fistulas (colic, vaginal, blind loop syndrome)
  • Anal disease - fissures, abscesses, sinuses
  • Toxic megacolon - very rare
  • Malignancy
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53
Q

Crohn’s disease is most common in which group of people?

A

Caucasians

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54
Q

What is thought to cause Crohn’s disease?

A
  • Genetic defects - frameshift mutation in the NOD2 gene
  • Environmental factors
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55
Q

Whih environmental triggers affect Crohn’s disease?

A
  • Smoking
  • Infectious agents
  • Vasculitis
  • Sterile environment theory
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56
Q

Why is Crohn’s not an autoimmune condition?

A

It involves an unregulated and out of control immune response to a pathogen

There is persistant activation of T cells which leads to damage

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57
Q

What is ulcerative colitis?

A

Chronic inflammation confined to the colon and rectum

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58
Q

Which layers of the small intestine wall are affected in ulcerative colitis?

A

Mucosal and submucosa

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59
Q

What is the most common inflammatory bowel disease?

A

Ulcerative colitis

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60
Q

Are patients diagnosed with UC generally old or young?

A

Young

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61
Q

Is UC a patchy or continous condition along the colon and rectum?

A

Continuous

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62
Q

What is the clinical presentation of UC?

A

Diarrhoea, mucus and blood PR

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63
Q

Which inflammatory bowel disease is associated with periods of exacerbation and periods of remission?

A

UC

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64
Q

Which investigations ae required for a patient with suspected UC?

A
  • Endoscopy
  • Mucosal biopsy
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65
Q

How are the crypts in the small intestine affected in UC?

A

They become irregularly shaped and branching

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66
Q

If a patient with UC fails to respond to corticosteroids, what is the other option for treatment?

A

Subtotal colectomy

(removal of colon leaving rectum behind)

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67
Q

How do the ulcers in UC differ from those seem in Crohn’s?

A

They are broader based

They do not permeate as deep into the small bowel wall

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68
Q

In which IBD are granulomas formed?

A

Crohn’s

69
Q

Why is colorectal cancer a complication of UC?

A

Chronic inflammation leads to dysplasia and then to carcinoma

70
Q

How can UC affect electrolyte balance?

A

It can cause hypokalaemia

71
Q

How may UC present as a sign on the skin?

A

Pyoderma gangrenosum

Erythema nodosum

72
Q

How may UC affect the eye?

A

Uveitis

73
Q

Which environmental factor that causes exacerbation of Crohn’s does not affect UC?

A

Smoking

74
Q

Which IBD involves transmural inflammation?

A

Crohn’s disease

75
Q

In which IBD is cancer risk higher?

A

UC

76
Q

In which IBD are fistulas more common?

A

Crohn’s

77
Q

What are the three causes of chronic gastritis?

A
  1. Autoimmune
  2. Bacterial
  3. Chemical
78
Q

Which bacterial species is respoinsible for causing gastritis?

A

Helicobacter pylori

79
Q

What is the cause of gastritis in autoimmune gastritis?

A

Anti-parietal and anti-intrinsic factor antibodies

80
Q

What occurs in the stomach in response to autoimmune gastritis?

A

Atrophy

Intestinal metaplasia

81
Q

Why does pernicious anaemia often occur with autoimmune gastritis?

A

Anti-intrinsic factor antibodies bind to instrinsic factor preventing vitamin B12 from being absorbed

This happens because intrinsic factor must bing to vitamin B12 in order to be absorbed

82
Q

How do red blood cells present in autoimmune gastritis?

A

Macrocytic

(lack of vitamin B12)

83
Q

What is the most common cause of chronic gastritis?

A

H. pylori associated gastritis

84
Q

Where in the stomach wall does H. pylori inhabit?

A

The area between the epithelial cell surface and the mucous barrier

85
Q

H. pylori infection increases the risk of which 4 main things?

A
  1. Gastric ulcer
  2. Duodenal ulcer
  3. Gastric carcinoma
  4. Gastric lymphoma
86
Q

What is the cause of chemical gastritis? (3)

A
  1. NSAIDS
  2. Alcohol
  3. Bile reflux
87
Q

What is peptic ulceration?

A

A breach of the gastrointestinal mucosa as a result of acid and pepsin attack

88
Q

Where are chronic peptic ulcers likely to develop?

A
  • Duodenum (1st part)
  • Stomach
  • Gastro-oesophageal junction
  • Stomal area (when a patient has a stoma bag)
89
Q

Why can excess acid in the duodenum eventually allow for H. pylori infection there?

A

The acid causes metaplasia of the duodenal mucosa causing it to become more like gastric mucosa and therefore be habitable for H. pylori

90
Q

What allows for chronic peptic ulcers to occur? (2)

A
  1. Increased acid
  2. Poor mucosal defence
91
Q

What are the complications of a peptic ulcer?

A
  • Perforation
  • Penetration
  • Haemorrhage
  • Stenosis
  • Intractable pain
92
Q

What is crucial for the chronic inflammation seen with H. pylori infection?

A

IL-8

93
Q

What is the term given to benign gastric tumours?

A

Polyps

94
Q

What are the two malignant gastric tumours?

A
  • Carcinoma (adenocarcinoma)
  • Lymphoma
95
Q

Why does H. pylori increase risk for gastric adenocarcinoma?

A

It causes chronic gastritis

This leads to intestinal metaplasia, dysplasia and eventually carcinoma

96
Q

What is Lynch syndrome?

A

Lynch syndrome, often called hereditary nonpolyposis colorectal cancer(HNPCC), is an inherited disorder that increases the risk of many types of cancer - mainly colorectal cancer

97
Q

What is Menetrier’s disease?

A

A rare, acquired, premalignant disease of the stomach

It is characterised by massive gastric folds, excessive mucous production (with resultant protein loss), and little or no acid production.

The condition is associated with excessive secretion of TGF-α

98
Q

What are the two types of gastric adenocarcinoma and what is the differnece between the two?

A
  1. Intestinal type - exophytic - grows outwards
  2. Diffuse type - expands and infiltrates the stomach wall
99
Q

Of the two types of gastric adenocarcinoma, which has better prognosis?

A

Intestinal type

100
Q

Where can gastric adenocarcinomas spread?

A
  • Local - other organs, peritoneal cavity, ovaries
  • Lymph nodes
  • Haematogenous - to the liver
101
Q

What is another name gastric lymphoma?

A

Maltoma

102
Q

Gastric lyphoma is associated with what?

A

H. pylori infection

103
Q

Which type of tissue is associated with gastric lymphoma?

A

Mucosa associated lymphoid tissue (MALT)

104
Q

Acute liver failure may manifest as jaundice. What are some causes for this?

A

Viruses

Alcohol

Drugs

Bile duct obstruction

105
Q

If a patient has acute liver failure which three main ways can they progress?

A
  1. Complete recovery
  2. Chronic liver disease
  3. Death
106
Q

What are the two different forms of bilrubin in the body?

A
  1. Conjugated
  2. Unconjugated
107
Q

What is conjugated bilirubin?

A

This is synthesised by the liver

Bilirubin is conjugated with glucuronic acis by enzyme action

This type of bilirubin is then metabolised further and the products are passed out of the body in faeces and urine

108
Q

What is unconjugated bilirubin?

A

This is bilirubin that is yet to be conjugated by the liver

109
Q

What are the three types of jaundice?

A
  1. Pre-hepatic
  2. Hepatic
  3. Post-hepatic
110
Q

What is pre-hepatic jaundice?

A

Caused by haemolysis of all causes such as haemolytic anaemias resulting in large amounts of unconjugated bilirubin being produced

111
Q

What causes hepatic jaundice?

A

Any injury to the liver cells affecting their ability to process biirubin

112
Q

What are some causes for hepatic jaundice?

A
  • Acute liver failure (viruses, drugs, alcohol)
  • Alcoholic hepatitis
  • Cirrhosis
  • Bile duct loss (atresia, PBC, PSC)
  • Pregancy
113
Q

What is post hepatic jaundice?

A

The liver processes bilirubin fine, but bile cannot escape into the bowel due to ostruction

114
Q

Give some causes for post-hepatic jaundice

A
  • Congenital biliary atresia
  • Gallstones block the common bile duct
  • Strictures of the common bile duct
  • Tumours
115
Q

What is the final common end point for liver disease?

A

Cirrhosis

116
Q

What are some complications of cirrhosis?

A
  • Portal hypertension - oesophageal varices, caput medusa, haemorrhoids
  • Ascities
  • Liver failure
117
Q

A cirrhosed liver is more susceptible to what?

A

Hepatocellular carcinoma

(or other malignancies)

118
Q

What is NASH?

A

Non-alcoholic steatohepatitis

A pathologically identical disease to alcoholic liver disease, yet patients do not drink

119
Q

Which type of patients will NASH occur in?

A

Diabetes

Obesity

Hyperlipidaemia

120
Q

How is hepatitis A spread?

A

Faecal/oral

121
Q

How is hepatitis B spread?

A

Blood

Sexually

Vertically (mother to child)

122
Q

What causes the liver damage in hepatitis B?

A

Antiviral immune response

123
Q

How is hepatitits C spread?

A

Blood

Potentially sexually

124
Q

Which type of hepatitis virus is most likely to become chronic?

A

Hepatitis C

125
Q

Which type of necrosis is associated with hepatitis, most specifically viral?

A

Piecemeal (interface) necrosis

Necrosis occurs in fragments

Refers specifically to a loss and degeneration of hepatocytes at the lobular-portal-interface, producing a moth-eaten irregular appearance.

It is associated with a lymphocytic infiltrate into the adjacent parenchyma.

126
Q

What is primary biliary cholangitis?

A

Autoimmune disease associated with autoantibodies to mitochondria

It results in slow destruction of small bile ducts in the liver over time causing bile and other toxins to build up

127
Q

Which gender is most likely to develop PBC?

A

Females

128
Q

What are the outcomes if PBC is left untreated?

A
  • Cholestasis
  • Inflammation
  • Fibrosis
  • Cirrhosis
129
Q

Autoimmune hepatitis is more common in which gender?

A

Females

130
Q

What is primary sclerosing cholangitis?

A

A chronic inflammatory process affecting intra and extra hepatic bile ducts

This impedes bile flow and can lead to fibrosis

131
Q

Primary sclerosing cholangitis is more common in which gender?

A

Males

132
Q

Primary sclerosing cholangitis is associated with which other GI condition?

A

Ulcerative colitis

133
Q

What is the term given to too much iron within the liver?

A

Haemochromatosis

134
Q

What are the two types of haemochromatosis?

A

Primary - inherited

Secondary - to other factors

135
Q

Why is primary haemochromatosis bad?

A

There is excess iron absorption from the intestine

Iron is depositied in the liver

Portal connective tissue is eventually affected by these depositis

Cirrhosis wil develop and predisposed to carcinoma

136
Q

As well as cirrhosis, what else can primary haemochromatosis cause?

A

Diabetes

Cardiac failure

Impotence

137
Q

Which stain confirms the presence of iron in the liver?

A

Perls stain

138
Q

What is Wilson’s disease?

A

Inherited autosomal recessive condition affecting copper metabolism

Copper accumulates in the liver and brain

Chronic hepatitis and neurological deterioration can be caused

139
Q

What is a clinical sign of Wilson’s disease in relation to the eyes?

A

Kayser-Fleischer rings at the corneal limbus

140
Q

What is alpha-1-antitrypsin deficiency and what does it cause?

A

Inherited autsomal recessive disorder of the production of an enzyme inhibitor

Cytoplasmic globules of unsecreted protein build up

This can cause cirrhosis and emphysema

141
Q

What are the two different types of tumours which can arise in the liver?

A
  1. Primary
  2. Secondary
142
Q

What are the two most common primary tumours of the liver?

A
  1. Hepatocellular adenoma
  2. Hepatocellular carcinoma
143
Q

Where can secondary tumours of the liver originally arise?

A

Colon, pancreas, stomach, breast, lung etc.

144
Q

Hepatocellular adenoma is a ________ tumour most common in __________

A

Benign

Females

145
Q

Hepatocellular carcinoma is associated with what?

A

HBV

HCV

Cirrhosis

146
Q

What is cholelithiasis?

A

The development of gallstones

147
Q

What are the three main bile components?

A
  1. Bilirubin
  2. Cholesterol
  3. Bile salts
148
Q

When will gallstones form?

A

When there is an imbalance between the ratio of cholesterol to bile salts disrupting micelle formation

(too much cholesterol causes free crystallisation on micelle surface)

149
Q

Pigment stones in the gallbladder are caused by what?

A

Excess bilirubin

(from haemolytic anaemia for example)

150
Q

What is a complication of a fistula forming between the gallbladder and the small bowel?

A

Gallstone ileus

(gallstones can pass into the small intestines and become trapped in the ileocaecal valve)

151
Q

What is cholecystitis?

A

Inflammation of the gallbladder

152
Q

Rupture, peritonitis, septicaemia and death are complcications mainly associated with acute or chonic cholecystitis?

A

Acute

153
Q

Gallstones are formed with which type of cholecystitis, acute or chronic?

A

Chronic

154
Q

Which type of cancer is associated with the gallbladder?

A

Adenocarcinoma

(this is rare)

155
Q

Cancer of the bile ducts is called what?

A

Cholangiocarcinoma

156
Q

Cholangiocarcinoma is associated with which other GI conditions?

A

Ulcerative colitis

Primary sclerosing colitis

157
Q

Which condition will all sufferers get if they have their pancreas removed?

A

Diabetes

158
Q

When the pancreas is necrosed which enzyme is secreted?

A

Amylase

159
Q

What is the biggest cause of chronic pancreatitis?

A

Alcohol

160
Q

The inflammation and fibrosis found in chonic pancreatitis can mimic which other condition?

A

Cancer

161
Q

Why can small cancers of the pancreas be as high as stage 4 very quickly?

A

The pancreas is a very intimate organ so will spread very easily

162
Q

The oesophagus is lined with which type of epithelium?

A

Stratified squamous epithelium

163
Q

What are some complications of chronic oesophagitis?

A

Ulceration leading to stricture and fibrosis

(Barrett’s oesophagus may also occur)

164
Q

What is Barrett’s oesophagus?

A

Stratified squamous epithelium is replaced by columnar epithelium

165
Q

Allergic oesophagitis is mediated by which cell type?

A

Eosinophils

166
Q

Which benign tumour will be found in the oesophagus?

A

Squamous papilloma

167
Q

Which tumour(s) associated with the oesophagus is HPV related?

A

Squamous papilloma

Squamous cell carcinoma

168
Q

Oesophageal varices are usually formed as a result of what?

A

Portal hypertension

(often due to liver disease)