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Pathology Flashcards

1
Q

What supplies blood to the small intestine

A

Superior mesenteric artery

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2
Q

What can cause Ischaemia of small bowel

A

Mesenteric artery atherosclerosis, thromboembolism from heart, shock, drugs, hyperviscosity, drugs (cocaine)

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3
Q

Hypoxia affects what part of the gut wall the greatest

A

Mucosa, most metabolically active

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4
Q

How is degree of small bowel ischaemia classified

A

By the degree of infarction caused. from mucosal (lamina propriae is preserved) to mural (penetrates lamina propriae but can be regenerated, fibrosis occurs) to transmural infarction (gangrene, needs to be resected)

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5
Q

What is Meckels diverticlum

A

A congenital diverticulum, a slight bulge in the small intestine present a birth, a vestigial remnant of the vitello-intestinal duct. Most are asymptomatic

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6
Q

Which tumours are more common in small intestine, primary or secondary

A

Secondary tumours are more common, metastases from ovary, colon and stomach

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7
Q

What type of Lymphomas of small bowel

A

Non-Hodgkin type - No Reed-Sternberg cell (crippled germinal centres mainly of B cells)

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8
Q

How can MALTomas of small bowel be treated

A

Surgery and chemotherapy

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9
Q

Identify - Small, yellow, slow growing tumour. Locally invasive and can cause intussusception and obstruction. Produce hormone like substances, cause diarrhoea and flushing if metastasize to liver.

A

Carcinoid tumour of small bowel

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10
Q

What is Intussusception

A

Folding of the intestine into the section next to it

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11
Q

What predisposes to rare tumours of small bowel

A

Crohns and coeliac disease

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12
Q

Most common cause of Appendicitis

A

Idiopathic

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13
Q

Pathology of acute appendicitis

A

Acute inflammation, mucosal ulceration, serosal congestion, exudate and pus in lumen

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14
Q

Complications of appendicitis

A

Peritonitis, rupture, abscess, fistula, sepsis, liver abscess

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15
Q

What are Coeliac diseases

A

Autoimmune disorder of the small intestine due to an abnormal immune response to Gluten. This leads to production of various antibodies and inflammation. This reduces absorptive capacity and leads to anaemia.

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16
Q

What serology is associated with coeliac disease

A

Human Leukocyte Antigen (HLA) - B8. This is part of the HLA family and codes for Major Histocompatibility Complex (MHC) which distinguishes different antigen

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17
Q

What is Dermatitis Herpetiformis associated with

A

It is an itchy, burning skin rash indicating gluten intolerance and sometimes coeliac disease

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18
Q

Suspected toxic agent causing coeliac disease

A

Gliadin, component of Gluten

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19
Q

What can coeliac disease cause

A

Loss of villi, flat duodenal mucosa, loss of surface area. Thus reduces absorption and anaemia. Steatorrhea occurs due to inabsorption of fats. Reduced intestinal hormone production leads to reduced pancreatic secretion and bile flow causing gallstones

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20
Q

There is an increase in intraepithelial lymphocytes and inflammation in lamina propria

A

True

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21
Q

Diagnosing coeliac disease

A

Endoscopy - Mucosa maybe normal or attenuated, Serology - For anti-Tissue Transglutinamase, anti-endomesial and anti-gliadin

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22
Q

Which oesophagitis is more common, acute or chronic

A

Chronic due to gastric acid reflux causing metaplastic change. Acute oesophagitis is more common in immunocompromised patients such as candiasis, herpes

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23
Q

What is reflux oesophagitis

A

Inflammation of oesophagus due to reflux gastric acid

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24
Q

Cause of reflux oesophagitis

A

Hiatus hernia (stomach moves into chest cavity), defective sphincter, increased abdominal pressure (pregnancy), abnormal oesophageal motility

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25
Q

How is increased desquamation due to reflux oesophagitis compensated for

A

By basal zone hyperplasia and elongation of connective tissue papillae

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26
Q

Complications of reflux oesophageal

A

Ulceration, bleeding, stricture, Barrett’s oesophagus

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27
Q

What is Barrette’s oesophagus

A

Metaplastic change of oesophageal stratified squamous epithelium to gastric golumnar goblet cells.

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28
Q

How does Barrette’s mucosa look macroscopically

A

Red velvety mucosa in oesophagus

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29
Q

Allergic oesophagitis is more common in what gender

A

Male > females, increased eosinophils in blood

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30
Q

What is spotty/feline/corrugated oesophagus known as

A

Allergic oesophagus

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31
Q

How is allergic oesophagitis seen microscopic

A

Increased intraepithelial eosinophils

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32
Q

Treatment of allergic oesophagitis

A

Steroids, chromoglycate, montelukast (leukotriene receptor antagonist)

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33
Q

What is a papilloma

A

Small wart like growth on the skin or mucous membrane, derived from epidermis and usually benign

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34
Q

Common causes of small cell carcinoma

A

Vitamin A or Zinc deficiency, tannic acid, smoking, alcohol, HPV, genetic, gastric reflux

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35
Q

What cancer of oesophagus is more common in caucasians

A

Adenocarcinoma of oesophagus, more common in obese males

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36
Q

Pathogenesis of adenocarcinoma of oesophagus

A

Chronic reflux oesophagitis - Barrett’s oesophagus - Low grade dysplasia - High grade dysplasia - Adenocarcinoma

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37
Q

Adenocarcinoma can cause?

A

Dysphagia and obstruction

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38
Q

General symptoms of metastases

A

Anaemia, weight loss, loss of energy

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39
Q

How can oral squamous cell carcinoma present

A

Variable, usually - red, white, speckled, ulcer lump

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40
Q

What is verrucous carcinoma

A

Uncommon variant of squamous cell carcinoma often seen in those who chew tobacco or use snuff orally.

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41
Q

What can cause gastrooesophageal reflux disease

A

Incompetent lower oesophagus sphincter, poor oesophageal clearance, barrier function/visceral sensitivity

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42
Q

What is water brash

A

Sour taste in the mouth due to stomach contents rising up the oesophagus.

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43
Q

What is odynophasia

A

Painful swallowing

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44
Q

Investigations for GORD

A

Endoscopy, barium swallow (ancient, not used anymore), oesophageal manometry & pH studies, nuclear studies

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45
Q

Common cause of dyspepsia

A

Indigestion is commonly caused by GORD

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46
Q

What is pernicious anaemia

A

Anaemia in which the body has lost stomach cells that are involved in the synthesis of intrinsic factor. This intrinsic factor helps absorb vitamin B12.

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47
Q

LIfestyle modifications for GORD

A

Stop smoking, lose weight, avoid provoking, prop up bed head

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48
Q

Are antacids useful for GORD

A

Symptomatic relief, however it does not heal oesophagitis nor prevent further complications

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49
Q

Histamine (H2) receptor antagonists that can be used for GORD

A

Cimetidine - Rapid symptomatic relief, less effective at healing than placebo
Ranitidine - Poor in preventing relapse and complications, tolerance after 4/52 week therapy

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50
Q

Proton pump inhibitors vs H2 receptor antagonist in treatment of GORD

A

Proton pump inhibitors such as Omeprazole are more effective at symptom relief and healing than H2 antagonists (ranitidine, cimetidine)

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51
Q

Treatment of GORD or hiatus hernia in young patients

A

Nissen fundoplication, heals oesophagitis with good control of symptoms

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52
Q

Is Barrett’s oesophagus reversible

A

No but recent findings point otherwise

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53
Q

Type of hiatus hernia

A

Sliding where the stomach slides into the oesophagus increasing risk of GORD. Second type is paraoesophageal hiatus hernia where the stomach pushes through beside the oesophagus

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54
Q

What is gastroparesis

A

Disease of the muscles of stomach or nerves controlling these muscles that causes it to stop working. It results in inadequate grinding and poor emptying of food from stomach.

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55
Q

Symptoms of gastroparesis

A

Feeling of fullness, nausea, vomiting, weight loss, upper abdominal pain

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56
Q

Causes of gastroparesis

A

Idiopathic, diabetes mellitus, cannabis, medication (opiates, anticholinergics), systemic disease (systemic sclerosis)

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57
Q

Management of gastroparesis

A

Remove precipitating factors (drugs), liquid diet, eat little and often, promotility agents, gastric pacemaker

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58
Q

What is achalasia

A

Disease of muscles of lower oesophagus that prevents relaxation of sphincter and absence of contractions and hence peristalsis of oesophagus.

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59
Q

Common cause of chronic gastritis

A

ABC - Autoimmune, bacterial and chemical

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60
Q

Cause of autoimmune chronic gastritis

A

Anti-parietal and auto-intrinsic factor antibodies leads to atrophy and intestinal metaplasia in body of stomach

61
Q

What can autoimmune gastritis lead to

A

Pernicious anaemia causing B12 vitamin deficiency. This can lead to subacute combined degeneration of spinal cord (SACDC)

62
Q

What is subacute combined degeneration of spinal cord (SACDC)

A

Degeneration of spinal cord at posterior and lateral columns due to vitamin B12 deficiency. Usually associated with pernicious anaemia

63
Q

Most common cause of chronic gastritis

A

Helicobacter pylori infection. Lives between epithelial cell surface and mucous barrier.

64
Q

What are peptic ulcerations

A

Breach in the gastrointestinal mucosal lining as a result of acid and pepsin attack

65
Q

Pathogenesis of peptic ulcers

A

Excess acid in duodenum produces gastric metaplasia and leads to H.pylori infection, inflammation, epithelial damage and ulceration. The GALT is also unable to cope with this increased acid and H.pylori infection

66
Q

Morphology of peptic ulcers

A

2-10 cm across, edges are clear cut and punched out

67
Q

What are gastrointestional stromal tumours (GIST)

A

Most common in stomach but can be found in small intestine. Begin in interstitial cells of Cajal (ICC)

68
Q

Other causes of gastric adenocarcinoma

A

Pernicious anaemia, partial gastrectomy, HNPCC, Menetrier’s disease

69
Q

What is hereditary nonpolyposis colorectal cancer (HNPCC)

A

Lynch syndrome is an autosomal dominant genetic condition that predisposes to high risk of colon cancer.

70
Q

What is Menetrier’s disease

A

Premalignant disease of stomach characterized by massive gastric folds, excessive mucous production with resultant protein loss and little or no acid production

71
Q

Types of gastric adenocarcinoma

A

Intestinal - Polypoid mass

Diffuse - Expands/infiltrates stomach

72
Q

Are all gastric ulcers malignant

A

No, however all gastric ulcers must be regarded as potentially malignant.

73
Q

Benign peptic ulcer vs malignant

A

Benign peptic ulcer mimics caner however is more punched out and lacks a raised rolled edge

74
Q

What is linitis plastica

A

Leather bottom stomach which is a morphological variant of diffuse stomach cancer.

75
Q

What is signet ring cell gastric adenocarcinoma

A

Rare form of malignant adenocarcinoma of stomach. Presence of signet ring cells (cells with a large vacuole)

76
Q

Some types of diffuse gastric adenocarcinoma

A

Linitis plastica, signet ring type, sclerosis

77
Q

Intestinal vs diffuse gastric adenocarcinoma, which has better prognosis

A

Intestinal as it spreads relatively less

78
Q

What is a Krukenberg tumour

A

A tumour that has metastasized into the ovary from a primary site, classically the GI tract. It’s most common site is from gastric adenocarcinomas

79
Q

Gastric lymphoma is also known as

A

MALToma

80
Q

Low grade vs high grade tumour

A

Low grade - Grow slowly and less likely to spread

High grade - Grow faster and more likely to spread

81
Q

How can dyspepsia be divided

A

According to Rome III criteria -
Epigastric pain syndrome - Epigastric pain or burning
Postprandial distress syndrome - Postpradial fullness and early satiety

82
Q

Cause of dyspepsia

A

Peptic ulcer disease, drugs (NSAID, Cox2 inhibitors), gastric cancer, idiopathic, GORD, irritable bowel syndrome

83
Q

Alarm symptoms of dyspepsia which constitutes referral to hospital

A

Dysphagia, evidence of GI blood loss, persistent vomiting, unexplained weight loss, upper abdominal mass. This is complicated dyspepsia

84
Q

Test and treat strategy of dyspepsia

A

Check H.pylori status and eradicate if infected. Continue acid inhibition if still symptomatic

85
Q

Causes of peptic ulcer disease

A

H.pylori is the main cause for gastric and duodenal. NSAIDs can also cause the same

86
Q

B cell gastric lymphoma is also called

A

MALToma

87
Q

How can H.pylori infection be identified

A

Gastric biopsy urease breath test, faecal antigen test, IgA serology (less accurate with increasing age)

88
Q

What is the urease breath test

A

Diagnostic procedure to test for H.pylori infection. Based on the ability of the bacteria to convert urea to ammonia and CO2

89
Q

What are stool antigen tests

A

Non-invasive diagnostics for H.pylori. Less expensive than urea breath test

90
Q

How can peptic ulcer disease be tested

A

Proton pump inhibitor, presence of H.pylori, withdraw NSAIDs, change lifestyle

91
Q

Treatment for non-H.pylori/non-NSAID ulcer

A

Nutrition and optimise comorbidities

92
Q

Anti-secretory therapy for peptic ulcer disease

A

PPI (Omeprazole 20-40mg/day) heals duodenal ulcers more rapidly than histamine H2 receptor (Ranitidine) antagonists for the first four weeks of therapy.

93
Q

Antacids in ulcer therapy

A

Antacids and sucralfate are superior to placebo in healing duodenal ulcers but not other types.

94
Q

Treatment of H.pylori infection

A

Triple therapy for one week -
PPI + Amoxicillin 1 g bd + Clarithromycin 500mg BD
PPI+Metronidazole 400mg bd+Clarithromycin 250mg bd

95
Q

Are 2 week regimes for H.pylori infection better?

A

Yes, higher eradication rate however low compliance

96
Q

Is dual therapy of PPI + 1 antibiotic recommended

A

No

97
Q

What is patient is still symptomatic despite H.pylori eradication therapy

A

Re-test

98
Q

Complications of peptic ulcer disease

A

Anaemia, bleeding, perforation, gastric outlet/duodenal obstruction - fibrotic scar

99
Q

Follow up for ulcers

A

Duodenal ulcers -
No follow up required unless there’s ongoing symptoms
Gastric ulcers -
Endoscopy at 6-8 weeks to ensure healing and no malignancy

100
Q

What is achlorhydria

A

Absent HCl in gastric secretions. Up risk gastric cancer

101
Q

Correa’s hypothesis of gastric cancer

A

H.pylori infection - chronic gastritis - atrophy - intestinal metaplasia - dysplasia - neoplasia

102
Q

How does H.pylori inhibit gastric secretions

A

Direct effect of bacterial product - ammonia, methyl histamine, cave’s factor
Effect of body inflammation induced by H.pylori -
IL-1B in H.pylori gastritis, powerful inhibition of gastric secretion

103
Q

How does host genetic affect H.pylori infection outcome

A

Presence of IL-1B pro-inflammatory host genotype -
Acid hyposecretion leading to body predominant gastritis, atrophic gastritis and cancer
Absence of IL-1B pro-inflammatory host genotype
Normal or high acid secretion, antral predominant gastritis and duodenal ulcer or no disease

104
Q

Is a GI bleed an medical emergency

A

Yes

105
Q

Major cause of upper GI tract bleeding

A

Duodenal ulcer, gastric erosions and gastric ulcers

106
Q

What is a Mallory-Weiss syndrome/tear

A

Tear in mucous membrane of the lining where oesophagus meets the stomach. Often haematemesis

107
Q

First step management for upper GI bleeding

A

Resuscitation (A,B,C) -
Airway protection, oxygen, IV access, fluids
After resuscitation, endoscopy

108
Q

Poor prognostic group for upper GI bleed

A 
The 100 rule
Systolic BP < 100mmHg
Pulse > 100/min
Hb < 100 g/l
Age > 60, comorbid disease, postural drop in BP
109
Q

What is OGD also known as

A

Oesophageal-gastroduodenoscopy or endoscopy

110
Q

What can be used to quantify GI bleeding risk after successful resuscitation

A

Blatchford score in NHS Tayside

111
Q

Signs of recent haemorrhage

A

Active bleeding/oozing, overlying clot/ visible vessel

112
Q

How does Haemospray work

A

Absorbs water, then acts as a cohesive and adhesive, forming a mechanical barrier over bleeding site

113
Q

Peptic ulcer found on endoscopy, bleeding or stigmata of recent haemorrhage

A

Adrenaline injection/heater probe thermo-coagulation/clips

114
Q

Treatment course for peptic ulcer on endoscopy after bleeding stops

A

Omeprazole 80mg IV + 8mg/hr for 72 hours

H.pylori eradication and course of oral PPI

115
Q

Re-bleed after initial haemostasis

A

Omperazole 80mg IV + 8mg/hr for 72 hours
Further attempt at endoscopic therapy
Surgery if bleed continues

116
Q

Risk factors for variceal bleeding

A

Portal pressure > 12 mmHg
Varices > 25% oesophageal lumen
Presence of red signs
Degree of liver failure (Child’s A<b></b>

117
Q

Aims of management of varicose veins

A

Resuscitation, haemostasis , prevent complications of bleeding, prevent deterioration of liver function, prevent early re-bleeding

118
Q

Common cause of variceal bleeding

A

Liver cirrhosis

119
Q

What are your initial considerations for variceal bleeding

A

Coagulopathy (excessive bleeding), parenteral nutrition, replace electrolytes, antibiotics, hypoglycaemia, central venous vs portal pressure monitoring

120
Q

How can haemostasis after variceal bleed be achieved

A

Terlipressin, endoscopic variceal lighting, sclerotherapy, sengstaken-blakemore balloon, TIPS

121
Q

What is Terlipressin

A

A vasopressin prodrug used in variceal bleed haemostasis. Splanchnic vasoconstrictor with beneficial effect on renal perfusion

122
Q

What is endoscopic variceal ligation

A

Banding of bleeding varices via endoscopy

123
Q

What is sclerotherapy

A

Chemical called sclerosant is injected into a vein. This causes it to shrink and then dissolve over a period of weeks.

124
Q

What’s a Sengstaken-Blakemore tube (S-B tube)

A

Tube passed down into the oesophagus with a gastric balloon in the stomach. This is inflated to apply pressure and reduce blood flow to oesophageal varices and stop bleeding. This is rarely used nowadays

125
Q

How is TIPS used in variceal bleeding

A

Transjugular intrahepatic portosystemic shunt (TIPS) is used to reduce portal hypertension and its complications such as variceal bleeding. A stent is inserted between the hepatic and portal vein

126
Q

First step management of variceal bleeding

A

Resuscitation, antibiotics, terlipressin + early OGD with/out endoscopic variceal ligation (EVL)

127
Q

Variceal bleeding stops after first step treatment

A

Propanolol + banding to follow up

128
Q

Variceal bleed continues after first step management

A

Endoscopic variceal ligation or S-B tube

If bleed continues, TIPS. If hepatic function remains poor consider transplant

129
Q

What are polyps

A

Abnormal growth of tissue projecting from mucous membrane.

130
Q

Pedunculated vs sessile polyps

A

Pedunculated polyps have a narrow elongated stalk attached to the surface whereas sessile polyps have no stalk

131
Q

Are all polyps cancerous?

A

No, they can also be due to adenoma inflammation such as in inflammatory bowel disease

132
Q

Which polyps have better prognosis, pedunculated or sessile

A

Pedunculated as it hangs by a stalk. This stalk can be cut off easily

133
Q

Molecular genetics of adenoma-carcinoma sequene

A

Normal epithelium - APC mutation - Small adenoma - k-ras mutation - Large adenoma - chromosome deletion, p53 mutation - Invasive carcinoma - nm23 deletion - Metastases

134
Q

Why must all adenomas be removed

A

As they can become malignant

135
Q

Primary treatment for adenocarcinoma

A

Surgery

136
Q

Explain duke staging A of colorectal carcinoma

A

Confined by muscularis propriae, usually day discharge

137
Q

Explain duke staging B of colorectal carcinoma

A

Through muscularis propriae, may or may not need chemotherapy depending on other features such as age, health

138
Q

Explain duke staging C of colorectal carcinoma

A

Metastatic and lymph nodes, needs adjuvant chemotherapy

139
Q

Which side is generally presented with colorectal carcinoma problems

A

Left (75%). Generally present with altered bowel habits, obstruction, blood in rectum

140
Q

Why do caecal carcinoma not usually bleed

A

Caecum has high capacity to expand. It can easily swell to accommodate the tumour and hence no bleeding is seen.

141
Q

If constipation with sudden diarrhoea and blood is seen, what might this suggest

A

Colorectal carcinoma on the left side, rectum or sigmoid

142
Q

Typical histopathological appearance of large bowel carcinoma

A

Adenocarcinoma

143
Q

Which lymph nodes does colorectal cancer affect

A

Mesenteric nodes

144
Q

Why are metastases from large bowel commonly found on the liver

A

As the blood supply from the large bowel is to the liver

145
Q

Inherited bowel cancer syndromes

A

Familial adenomatous polyposis (FAP) > 100 polyps, patient presents early on (16) and develops colorectal cancer by 27
Hereditary non polyposis colorectal cancer (HNPCC) or Lynch syndrome < 100 polyps. Patient has late presentation of colorectal cancer, around 50 - 60

146
Q

Differentiate between inherited colorectal carcinoma between their causes

A

Familial adenomatous polyposis - Defect in tumour suppression
Hereditary non-polyposis colorectal cancer - Defect in DNA mismatch repair

147
Q

Which of the inherited colorectal carcinoma affects right side more

A

Lynch syndrome with more mucinous tumours

148
Q

Most common genetic mutation in large bowel cancer

A

APC gene mutation

GI (32 decks)

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