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AY Gastrointestinal > Pathology > Flashcards

Pathology Flashcards

1
Q

Causes of reflux oesophagitis

A

Hiatus hernia
Abnormal oesophageal motility
Increased intra-abdominal pressure (pregnancy)

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2
Q

What is the main pathological feature of reflux oesophagitis?

A

Basal zone expansion

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3
Q

Complications of GORD

A

Ulceration (bleeding)
Stricture
Barrett’s oesophagus

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4
Q

What is Barrett’s oesophagus?

A

Metaplasia of squamous epithelium to columnar epithelium

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5
Q

What are the complication of Barrett’s oesophagus?

A

Increased risk of d ve loping dysplasia and carcinoma of the oesophagus

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6
Q

How do you diagnose allergic oesophagitis?

A

Increased eosinophils in blood
PH probe negative for reflux
Young male with asthma

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7
Q

Treatment for allergic oesophagitis

A

Steroids
Cromoglycate
Montelukast

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8
Q

Most common benign oesophageal tumour

A

Squamous papilloma

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9
Q

2 most common malignant oesophageal tumours

A

Squamous cell carcinoma

Adenocarcinoma

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10
Q

Is squamous cell carcinoma of the oesophagus more common in makes or females?

A

Males

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11
Q

Causes of squamous cell carcinoma of the oesophagus

A 
Vitamin A, zinc deficiency 
Smoking 
Alcohol 
HPV 
Oesophagitis 
Genetic
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12
Q

Which type of cancer does Barrett’s oesophagus predispose to?

A

Adenocarcinoma

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13
Q

3 mechanisms of metastasis of carcinomas of the oesophagus

A

Direct invasion
Lymphatic permeation
Vascular invasion

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14
Q

Clinical presentation of oesophageal carcinoma

A

Dysphasia
Anaemia
Weight loss
Fatigue

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15
Q

Where are rare sites for oral squamous cell carcinoma?

A

Hard palate

Dorsum of tongue

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16
Q

Causes of oral squamous carcinoma

A

Smoking
Alcohol
Nutritional deficiencies
Post transplant

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17
Q

How are oral squamous cell carcinomas graded?

A

How differentiated they are

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18
Q

What staging system is used to grade tumours?

A

TNM system

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19
Q

Treatment of oral squamous cell carcinoma

A

Surgery

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20
Q

Causes of acute gastritis

A 
Chemical injury 
Severe burns 
Shock 
Severe trauma 
Head injury
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21
Q

Causes of chronic gastritis

A

Autoimmune
Bacterial
Chemical

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22
Q

What is the main Bacteria that causes chronic gastritis?

A

H. pylori

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23
Q

What antibodies cause autoimmune chronic gastritis?

A

Anti-parietal

Anti-intrinsic factor

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24
Q

Does autoimmune chronic gastritis carry an increased risk of malignancy?

A

Yes

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25
Q

Which interleukin is critical in h. pylori associated chronic gastritis?

A

IL8

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26
Q

Is H. pylori gram negative or gram positive?

A

Gram negative

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27
Q

Where does H. pylori bacteria inhabit within the stomach?

A

Between the epithelial cell surface and mucous barrier

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28
Q

What does H. pylori gastritis cause increased risk for?

A

Duodenal ulcer
Peptic ulcer
Gastric carcinoma
Gastric lymphoma

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29
Q

What chemicals can cause gastritis!

A

NSAID’s
Bile reflux
Alcohol

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30
Q

What is peptic ulceration?

A

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

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31
Q

Microscopic structure of peptic ulcers?

A

Layer appearance
Base of inflamed granulation tissue
Deepest layer is fibrotic scar tissue

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32
Q

Complications of peptic ulcers

A 
Perforation 
Penetration 
Haemorrhage 
Stenosis 
Intractable pain
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33
Q

Examples of benign gastric tumours

A

Hyperplastic polyps

Cystic funding gland polyps

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34
Q

Examples of malignant gastric tumours

A

Carcinoma
Lymphoma
Gastrointestinal stromal tumours (GISTs)

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35
Q

Pathogenesis of gastric adenocarcinoma

A 
H. Pylori infection 
Chronic gastritis 
Intestinal metaplasia 
Dysplasia 
Carcinoma
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36
Q

Premalignant conditions for gastric adenocarcinoma

A

Pernicious anaemia
Partial gastrectomy
Lynch syndrome
Menetrier’s disease

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37
Q

Which type of gastric adenocarcinoma has a better prognosis?

A

Intestinal type

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38
Q

Which is more common acute or chronic oesophagitis?

A

Chronic

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39
Q

How is small bowel infarction classified?

A

Mucosal infarction
Mural infarction
Transmural infarction

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40
Q

Complications of small bowel infarction

A 
Fibrosis 
Chronic ischaemia obstruction 
Gangrene 
Perforation 
Peritonitis 
Sepsis 
Death
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41
Q

What is Meckel’s diverticulum?

A

Congenital diverticulum disease

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42
Q

Complications of Meckel’s diverticulum?

A

Bleeding
Perforation
Diverticulitis

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43
Q

Which is more common in the small bowel primary or secondary tumours?

A

Secondary

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44
Q

Where do secondary tumours of the small intestine metastasise from?

A

Ovary
Colon
Sto,ACh

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45
Q

What disease are T cel, lymphomas of the small intestine associated with?

A

Coeliac disease

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46
Q

All lymphomas of the small bowel are non-hodkins in thoe. True/False

A

True

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47
Q

How are lymphomas of the small bowel treated?

A

Surgery and chemotherapy

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48
Q

Where is the most common site of carcinoid tumours?

A

The appendix

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49
Q

What is intussusception?

A

One part of the bowel slides into another

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50
Q

Clinical presentation of appendicitis

A

Vomiting
Abdominal pain
RIF pain
Increased WCC

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51
Q

Complications of appendicitis

A 
Peritonitis 
Rupture 
Abscess 
Fistula 
Sepsis and liver abscess
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52
Q

What is coeliac disease?

A

Abnormal reaction to a constituent of wheat flour, gluten which damages enterocytes and reduces absorptive capacity

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53
Q

What antibody is looked for in diagnosis of coeliac disease?

A

Anti-TTG

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54
Q

What is steatorrhea?

A

Fat in faeces

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55
Q

How can coeliac disease cause gallstones?

A

Reduced intestinal hormone production leads to reduced pancreatic secretion and bile flow (CCK) leading to gallstones

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56
Q

Clinical presentation of coeliac disease

A 
Weight loss 
Anaemia 
Abdominal bloating 
Failure to thrive
Vitamin deficiencies
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57
Q

What can cause ischaemia of the small bowel?

A 
Mesenteric artery atherosclerosis 
Thromboembolism from heart (e.g. AF) 
Shock 
Strangulation obstructing venous return
Drugs 
Hyperviscosity
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58
Q

Which part of the bowel wall is most sensitive to hypoxia?

A

Mucosa

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59
Q

What is Crohn’s disease?

A

Chronic inflammatory and ulcerative conditions of the GI tract that can affect anywhere from mouth to anus (most common in terminal ileum and colon)

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60
Q

Crohn’s disease is more common in females. True/False.

A

False.

It is more common in males

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61
Q

What is the clinical presentation of Crohn’s disease?

A 
Abdominal pain 
Small bowel obstruction 
Diarrhoea 
PR bleeding 
Anaemia 
Weight loss
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62
Q

Endoscopic pattern of Crohn’s disease?

A

Patchy, segmental with skip lesions anywhere in the GI tract

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63
Q

Which IBD involves granulomatous inflammation?

A

Crohn’s

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64
Q

Histological appearance of Crohn’s disease

A

Increased chronic inflammatory cells in the lamina progeria and crypt branching with granulomas

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65
Q

What type of inflammation is found in Crohn’s disease?

A

Transmural granulomatous inflammation

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66
Q

Complications of Crohn’s disease?

A 
Malabsorption 
Iatrogenic short bowel syndrome (due to surgery) 
Anaemia 
Hypoproteinemia 
Vitamin deficiency 
Gallstones
FISTULAS 
Anal disease 
Bowel obstruction 
Perforation 
Malignancy 
Amyloidosis
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67
Q

How can Crohn’s disease give you gallstones?

A

Can interupt enterohepatic circulation

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68
Q

Why are fistulas a more common complication in Crohn’s disease then ulcerative colitis?

A

As Crohn’s has transmural inflammation whereas ulcerative colitis is superficial

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69
Q

What is ulcerative colitis?

A

Chronic inflammatory disorder confined to colon and rectum

Mucosal and submucosal inflammation

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70
Q

Clinical presentation of UC

A

Diarrhoea
Mucus
PR bleeding

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71
Q

Investigations for UC

A

Endoscopy and mucosal biopsy

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72
Q

What is the endoscopic pattern of UC?

A

Diffuse continuous disease almost always involving the rectum

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73
Q

When is UC inflammation not confined to the mucosa and submucosa?

A

Toxic megacolon

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74
Q

Complications of UC

A 
Toxic megacolon 
Colorectal carcinoma 
Blood loss 
Hypokalemia
Extra GI manifestations
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75
Q

Extra GI manifestations of UC

A 
Uveitis 
Primary sclerosing cholangitis 
Arthritis 
Ank spondylitis 
Pyoderma gangrenous
Erythema nodosum
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76
Q

Does smoking have a protective effect in UC or Crohn’s?

A

UC

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77
Q

Is the cancer risk higher in UC or Crohn’s?

A

UC

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78
Q

Are extra GI manifestations more common in UC or Crohn’s?

A

UC

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79
Q

Which has skip lesions UC or Crohn’s?

A

Crohn’s

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80
Q

What is the normal composition of bile?

A

Cholesterol, phospholipid, bile salts and bilirubin

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81
Q

What signals for the release of bile into the second part of the duodenum?

A

CCK

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82
Q

What is the pathogenesis of cholesterol gallstones?

A

Gallstones form when their is an imbalance between the ratio of bile salts to cholesterol disrupting micelles formation

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83
Q

Five F’s for gallstones

A 
Fair 
Fat 
Female 
Fertile 
Forty
84
Q

What is the pathogenesis of pigment stones?

A

Excess bilirubin cannot be solubilised in bile salts

85
Q

Is the gallbladder wall thickened or distended in chronic cholecystitis?

A

Thickened but not distended

86
Q

What is carcinoma of the bile ducts associated with?

A

UC

PSC

87
Q

What effect does acute pancreatitis have on serum amylase?

A

Elevated

88
Q

Complications of acute pancreatitis

A 
Death 
Shock 
Pseudocysts formation 
Abscess formation 
Hypocalcemia 
Hypoglycaemia
89
Q

Where does adecarcinoma of the pancreas spread?

A

Direct spread to other organs (duodenum, stomach, spleen)
Spread to local lymph nodes
Haematogenous spread to liver

90
Q

What is a polyp?

A

Protrusion above an epithelial surface

91
Q

Differential diagnosis of a colonic polyp

A

Adenomas
Serrated polyp
Polyploid carcinoma
Other

92
Q

How do you confirm a diagnosis of a polyp?

A

Histopathology

93
Q

What are adenomas of the colon?

A

Benign tumours that do not metastasise

94
Q

What are adenomas precursors of?

A

Adenocarcinoma

95
Q

Why must all adenomas be removed?

A

They are ALL premalignant

96
Q

What are the 2 procedures for removing adenomas?

A

Endoscopic ally or surgically

97
Q

How are adenocarcinomas diagnosed?

A

Biopsy

98
Q

What are the patterns of spread of colorectal carcinoma?

A

Local invasion (peritoneum, other organs)
Mesenteric lymph nodes
Haematogenous spread to liver

99
Q

What are the 2 types of genetically related colorectal cancers?

A

HNPCC

FAP

100
Q

Common pathologies of the large bowel

A 
Diverticular disease 
Ischaemia 
Colitis 
IBD 
Colon cancer
101
Q

What causes Diverticular disease?

A

Increased intralumenal pressure related to low fibre diet

102
Q

Complications of Diverticular disease

A 
Inflammation 
Rupture 
Abscess 
Fistula 
Massive bleeding
103
Q

What can cause ischaemia of the bowel?

A 
CVS disease 
AF 
A bolus 
Shock 
Vascular is 
Atherosclerosis of Mesenteric vessels
104
Q

Histological appearance of ischaemic colitis

A

Withering of crypts
Pink smudgy lamina propria
Fewer chronic inflammatory cells

105
Q

Clinical context of ischaemic colitis

A

Elderly people
Left sided
SegmentL on endoscopy

106
Q

Complications of ischaemic colitis

A

Massive bleeding
Rupture
Stricture

107
Q

What organism causes damage in antibiotic induced ‘pseudomembranous’ colitis?

A

C. diffn

108
Q

Treatment of antibiotic induced pseudomembranous colitis?

A

Vancomycin
May need collecting
May be fatal

109
Q

What is the histological appearance of collagenous colitis?

A

Thickened basement membrane
Disease is patchy
Associated with intraepthelial inflammatory cells

110
Q

What is raised in lymphocytic colitis?

A

Intraepthelial lymphocytes

111
Q

What can be a possible cause of lymphocytic colitis?

A

Coeliac disease

112
Q

What is the basic pathogenesis of liver disease

A

Insult to hepatocytes
Inflammation
Fibrosis
Cirrhosis

113
Q

Causes of acute onset of jaundice?

A

Viruses
Alcohol
Drugs
Bile duct obstruction

114
Q

How is jaundice classified?

A 
Pre-hepatic 
Intra-hepatic 
Post-hepatic 
OR 
Conjugated 
Unconjugated
115
Q

What is pre-hepatic jaundice?

A

Jaundice caused by too much haem to break down

116
Q

What can cause pre-hepatic jaundice?

A

Haemolysis of all causes
Haemolytic anaemias
Unconjugated bilirubin

117
Q

What is intra-hepatic jaundice?

A

Liver cells injured or dead

118
Q

Causes of infra-hepatic jaundice

A 
Acute liver failure 
Alcoholic hepatitis 
Cirrhosis 
Bile duct loss (PBC, PSC)
Pregnancy
119
Q

What is post-hepatic jaundice?

A

Bile cannot escape into the bowel

120
Q

Causes of post-hepatic jaundice

A

Congenital biliary atresia
Gallstones block CBD
Strictures of CBD
Tumours (head of pancreas)

121
Q

How is cirrhosis defined?

A

Bands of fibrosis separating regenerative nodules of hepatocytes

122
Q

Complications of cirrhosis?

A

Portal hypertension

  • oesophageal varices
  • caput medusa
  • haemorrhoids

Ascites

Liver failure

123
Q

Liver damage caused by a heavy weekend binge?

A

Fatty liver

124
Q

Liver damage caused by excessive drinking for 4-6 weeks

A

Hepatitis

125
Q

Liver damage caused by months-years of heavy drinking?

A

Fibrosis

126
Q

Histological features of alcoholic hepatitis?

A

Hepatocytes necrosis
Neutrophils
Mallory bodies
Pericellular fibrosis

127
Q

Outcomes of alcoholic liver disease?

A

Cirrhosis
Portal hypertension (varices & ascites)
Malnutrition
Hepatocellular carcinoma

128
Q

What does NASH stand for?

A

Non Alcoholic SteatoHepatitis

129
Q

What patients does NASH tend to occur in?

A

Diabetes
Hyperlipidaemia
Obesity

130
Q

What viruses causes Hep A?

A

Epstein-Barr virus

131
Q

What viruses causes Hep B?

A

Yellow fever virus

132
Q

What virus causes Hep C?

A

Heroes Simplex virus

133
Q

What virus causes Hep E?

A

Cytomegalovirus

134
Q

How is Hep A spread?

A

Faecal-oral route

135
Q

What is the outcome of hep A?

A

Short incubation period
Mild illness
Usually full recovery

136
Q

How are Hep B & C spread?

A

Blood, blood products, sexually

137
Q

What causes the liver damage in hep B?

A

Antiviral immune response

138
Q

Outcomes of Hep B

A

Fulminant acute infection (death)
Chronic hepatitis
Cirrhosis
Hepatocellular carcinoma

139
Q

Outcomes of Hep C

A

Chronic hepatitis

140
Q

Causes of chronic hepatitis

A 
Hep B 
Hep C 
PBC
Autoimmune hepatitis 
Drug  induced hepatitis 
PSC
141
Q

What is PBC?

A

Rare autoimmune disease, unknown aetiology associated with autoantibodies to mitochondria

142
Q

Who is PBC most common in?

A

Women

143
Q

Histological signs of PBC

A

Granulomas
Bile ducts inflamed
Chronic portal inflammation

144
Q

Who is autoimmune more common in?

A

Female

145
Q

What is PSC?

A

Chronic inflammatory process affecting intra and extra hepatic bile ducts
Leads to periodical fibrosis, duct destruction, jaundice and fibrosis

146
Q

What is PSC associated with?

A

UC

147
Q

Who is PSC more common in?

A

Males

148
Q

What can PSC predispose patients to?

A

Malignancy in bile ducts & colon

149
Q

Buzzword for histological appearance of PSC

A

Periductal onion-skinning fibrosis

150
Q

Examples of storage diseases in the liver

A

Haemochromatosis
Wilson’s disease
Alpha-1-antitripsin deficiency

151
Q

What is haemochromatosis?

A

Excess iron within the liver

152
Q

What are primary causes of haemochromatosis?

A

Genetic condition

Increased absorption of iron

153
Q

What are secondary causes of haemochromatosis?

A

Iron overload from diet
Transfusions
Iron therapy

154
Q

How is primary haemochromatosis passed genetically?

A

Autosomal recessive

155
Q

What can primary haemochromatosis also cause?

A 
Diabetes
Cardiac failure 
Impotence 
Cirrhosis 
Hepatocellular carcinoma
156
Q

Examples of primary tumours of the liver?

A

Hepatocellular adenomas

Hepatocellular carcinoma

157
Q

Who is Hepatocellular adenomas more common in?

A

Women

158
Q

What is Hepatocellular carcinoma associated with?

A

Hep B
Hep C
Cirrhosis

159
Q

What are the normal ordered LFT’s?

A

ALT/AST
ALP
GGT

160
Q

What are the true liver function tests?

A

Bilirubin
Albumin
Prothrombin time m

161
Q

Clinical features of acute liver disease

A 
Jaundice 
Lethargy 
Nausea 
Anorexia 
Pain 
Itch 
Arthralgia
162
Q

Common causes of acute liver disease

A 
Viral 
Drugs (paracetamol) 
Shock liver
Cholangitis 
Alcohol 
Malignancy 
Chronic liver disease
163
Q

Rare causes of acute liver disease

A

Budd Chirac
AFLP
Cholestatsis of pregnancy

164
Q

Investigations for acute liver disease

A

LFT’s
Prothrombin time
Ultrasound
Virology

165
Q

Treatment of acute liver disease

A 
No alcohol 
Increase caloriesn
Avoid high fat foods 
For itch - sodium bicarc bath, cholestryamine or uresodeoxycholic acid
Observation for FHF
166
Q

Drugs that can cause liver disease

A 
ANY 
Co-amoxiclav 
Flucloxacillin 
NSAID 
Paracetamol
167
Q

Common causes of fulminant hepatic failure

A

Paracetamol
Fulminant viral
Drugs
Hep B

168
Q

Rare causes of FHF

A 
AFLP
Mushrooms 
Malignancy 
Wilsons 
Budd Chiari
Hep A
169
Q

Clinical problems caused by FHF

A 
Encephalopathy 
Hypoglycaemia 
Coagulation 
Circulatory failure 
Renal failure 
Infection
170
Q

FHF treatment

A

Inotropes & fluids
Renal replacement
Transplantation

171
Q

What is the basic pathogenesis of liver disease

A

Insult to hepatocytes
Inflammation
Fibrosis
Cirrhosis

172
Q

Causes of acute onset of jaundice?

A

Viruses
Alcohol
Drugs
Bile duct obstruction

173
Q

How is jaundice classified?

A 
Pre-hepatic 
Intra-hepatic 
Post-hepatic 
OR 
Conjugated 
Unconjugated
174
Q

What is pre-hepatic jaundice?

A

Jaundice caused by too much haem to break down

175
Q

What can cause pre-hepatic jaundice?

A

Haemolysis of all causes
Haemolytic anaemias
Unconjugated bilirubin

176
Q

What is intra-hepatic jaundice?

A

Liver cells injured or dead

177
Q

Causes of infra-hepatic jaundice

A 
Acute liver failure 
Alcoholic hepatitis 
Cirrhosis 
Bile duct loss (PBC, PSC)
Pregnancy
178
Q

What is post-hepatic jaundice?

A

Bile cannot escape into the bowel

179
Q

Causes of post-hepatic jaundice

A

Congenital biliary atresia
Gallstones block CBD
Strictures of CBD
Tumours (head of pancreas)

180
Q

How is cirrhosis defined?

A

Bands of fibrosis separating regenerative nodules of hepatocytes

181
Q

Complications of cirrhosis?

A

Portal hypertension

  • oesophageal varices
  • caput medusa
  • haemorrhoids

Ascites

Liver failure

182
Q

Liver damage caused by a heavy weekend binge?

A

Fatty liver

183
Q

Liver damage caused by excessive drinking for 4-6 weeks

A

Hepatitis

184
Q

Liver damage caused by months-years of heavy drinking?

A

Fibrosis

185
Q

Histological features of alcoholic hepatitis?

A

Hepatocytes necrosis
Neutrophils
Mallory bodies
Pericellular fibrosis

186
Q

Outcomes of alcoholic liver disease?

A

Cirrhosis
Portal hypertension (varices & ascites)
Malnutrition
Hepatocellular carcinoma

187
Q

What does NASH stand for?

A

Non Alcoholic SteatoHepatitis

188
Q

What patients does NASH tend to occur in?

A

Diabetes
Hyperlipidaemia
Obesity

189
Q

What is the outcome of hep A?

A

Short incubation period
Mild illness
Usually full recovery

190
Q

What is reflux oesophagitis?

A

Linflammation of oesophagus due to reflexes low pH gastric content

191
Q

How are Hep B & C spread?

A

Blood, blood products, sexually

192
Q

What causes the liver damage in hep B?

A

Antiviral immune response

193
Q

Outcomes of Hep B

A

Fulminant acute infection (death)
Chronic hepatitis
Cirrhosis
Hepatocellular carcinoma

194
Q

Outcomes of Hep C

A

Chronic hepatitis

195
Q

Causes of chronic hepatitis

A 
Hep B 
Hep C 
PBC
Autoimmune hepatitis 
Drug  induced hepatitis 
PSC
196
Q

What is PBC?

A

Rare autoimmune disease, unknown aetiology associated with autoantibodies to mitochondria

197
Q

Who is PBC most common in?

A

Women

198
Q

Histological signs of PBC

A

Granulomas
Bile ducts inflamed
Chronic portal inflammation

199
Q

Who is autoimmune more common in?

A

Female

200
Q

What is PSC?

A

Chronic inflammatory process affecting intra and extra hepatic bile ducts
Leads to periodical fibrosis, duct destruction, jaundice and fibrosis

201
Q

What is PSC associated with?

A

UC

202
Q

Who is PSC more common in?

A

Males

203
Q

What can PSC predispose patients to?

A

Malignancy in bile ducts & colon

204
Q

Buzzword for histological appearance of PSC

A

Periductal onion-skinning fibrosis

205
Q

Examples of storage diseases in the liver

A

Haemochromatosis
Wilson’s disease
Alpha-1-antitripsin deficiency

206
Q

What is haemochromatosis?

A

Excess iron within the liver

207
Q

How is Hep A spread?

A

Faecal-oral route

AY Gastrointestinal (21 decks)

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