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Cellular pathology > GI > Flashcards

GI Flashcards

1
Q

List all the layers of the GIT

A 
Mucosa
Submucosa
Muscularis Propria
Subserosa
Serosa
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2
Q

Which layer of the GIT is the only one to change through different organs?

A

Mucosa

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3
Q

What is the function of the oesophagus?

A

Transit tube

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4
Q

What is the function of the stomach?

A

Storage and digestion

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5
Q

What is the function of the small intestine?

A

Nutrient absorption (+ digestion)

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6
Q

What is the function of the colon?

A

Water absorption

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7
Q

What is the mucosa of the oesophagus?

A

Stratified squamous

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8
Q

What is the mucosa of the stomach?

A

Thick glandular (columnar)

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9
Q

What is the mucosa of the small intestine?

A

Glandular with villi

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10
Q

What is the mucosa of the large intestine?

A

Glandular with crypts

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11
Q

What is GORD

A

Regurgitation of acidic gastric contents into the lower oesophagus

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12
Q

How does GORD damage the oesophagus

A

Regurgitation of acid into the lower oesophagus results in injury to the squamous epithelium lining the oesophagus and results in inflammation (reflux oesophagitis)

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13
Q

What are the risk factors for GORD

A

Increased intra-abdominal pressure- obesity, pregnancy
Decreased oesophageal sphincter tone- smoking, alcohol, coffee consumption
Hiatus hernia

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14
Q

What is a hiatus hernia

A

The protrusion of the upper part of the stomach into the thoracic cavity.

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15
Q

What is the cause of a hiatus hernia

A

A combination of diaphragmatic weakening and increased intraabdominal pressure

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16
Q

How does a hiatus hernia result in GORD

A

Weakens the LOS

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17
Q

List ways in which GORD may present

A
  • Regurgitation (water brash)
  • Heartburn (due to oesophagitis)
  • Progressive dysphagia (due to strictures as the oesophagus heals by fibrosis)
  • Haematemesis / malaena (large bleed)
  • Anaemia (chronic small bleeds)
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18
Q

What complication of GORD occurs in 10% patients

A

Barrett’s oesophagus

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19
Q

What is Barrett’s oesophagus

A

A metaplastic process in the lower oesophageal mucosa, occurring as an adaptive response to prolonged injury caused by GORD

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20
Q

How does Barrett’s oesophagus present

A

Asymptomatic

Often identified when patients undergo OGD due to other symptoms

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21
Q

What is the metaplastic change that occurs in Barrett’s oesophagus?

A

Squamous mucosa –[reflux of gastric acid]–> glandular mucosa

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22
Q

What percentage of patients with Barrett’s oesophagus progress to dysplasia and then to invasive adenocarcinoma?

A

2%

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23
Q

What is the most common demographic diagnosed with oesophageal cancer?

A

50-70yr old men

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24
Q

How does oesophageal cancer present

A

Progressive dysphagia - from solids to liquids as the tumour causes obstruction of the lumen
Non-specific symptoms such as weight loss

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25
Q

What are the investigations for oesophageal cancer

A

Endoscopy and biopsy.

The biopsy will tell you the type of cancer and the grade

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26
Q

What is the most common type of oesophageal cancer in the UK?

A

Adenocarcinoma

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27
Q

How does oesophageal cancer typically arise

A

Due to Barrett’s oesophagus most often

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28
Q

What is the 2nd most common type of oesophageal carcinoma in the UK?

A

Squamous cell carcinoma (most common type in Japan/China)

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29
Q

How is oesophageal cancer staged

A

TNM

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30
Q

What is the curative management option for oesophageal cancer

A

Surgery

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31
Q

What are the palliative management options for oesophageal cancer

A

Dilation
Stenting
Radiotherapy

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32
Q

What is the prognosis of oesophageal cancer

A

5 year survival is 5-10%

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33
Q

What are the 2 most important causes of gastritis?

A

NSAIDs

H Pylori infection

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34
Q

Is H. Pylori a gram positive or gram negative organism?

A

Gram negative

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35
Q

How does H. Pylori spread

A

Faecal-oral or oral-oral transmission

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36
Q

How does H Pylori survive in the stomach

A

Colonise the stomach, living in the thick mucus layer on the surface of the mucosa.
H. Pylori are able to survive in the stomach’s acidic environment by producing urease. This converts urea to ammonia and the ammonia neutralises the gastric acid and therefore improves the survival of the bacteria.

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37
Q

List the consequences of H Pylori infection

A

(1) Minority develop symptomatic gastritis (<20%)
(2) Minority develop peptic ulcer
(3) Small minority develop gastric carcinoma
(4) Very small minority develop gastric lymphoma

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38
Q

What is a peptic ulcer

A

A breach in the mucosa of the LOS, stomach or duodenum which fails to heal over a reasonable period of time

The ulcer extends through the full thickness of the mucosa - and may even extend into the submucosa / deeper layers of the wall.

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39
Q

What are the most common sites for a peptic ulcer

A

Gastric antrum / proximal duodenum.

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40
Q

What are the most common causes of peptic ulcers

A

H. Pylori (duodenum)
NSAIDs (stomach)

Mucosal ischaemia due to stress = CURLING (stress) ulcers caused by
o Massive trauma
o Extensive burns
o Sepsis
o Raised intracranial pressure
o Shock
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41
Q

What are the most common causes of oesophageal ulcers?

A

GORD

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42
Q

How do peptic ulcers illustrate chronic inflammation

A

Persistent tissue injury and destruction at the surface
On-going inflammatory response to limit the damage (macrophages, lymphocytes and plasma cells = main inflammatory cells)
Attempts to organise and heal by fibrosis

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43
Q

How does H Pylori cause peptic ulcers

A

H. Pylori burrow through and disrupt the surface mucus coving the mucosa and expose the mucosal surfaces to gastric acid and pepsin.

It overcomes the defence mechanisms: mucus layer + the epithelial cell defences

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44
Q

How do NSAIDs cause peptic ulcers

A

It overcomes the defence mechanisms: epithelial cell defences

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45
Q

How do curling ulcers occur

A

Acute ulcers (ie. CURLING) occur in clinical states of shock and affect the mucosal blood flow

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46
Q

What is Zollinger-Ellison syndrome and how does it cause peptic ulceration

A

A pancreatic/gastric gastrin secreting tumour (gastrinoma) cause excess gastric acid secretion

Peptic ulcers occur when there is a weakening of the defences or an increased acid attack.

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47
Q

What are the complications of peptic ulcers

A

Bleeding
o Acute = melaena / haematemesis
o Chronic = anaemia

Perforation - presents as peritonitis with AIR UNDER THE DIAPHRAGM (seen on erect CXR)
Stricture formation - presents as obstruction
Malignant change - ulcerated gastric carcinomas have a ROLLED EDGE

If a PU is found in oesophagus/stomach during OGD a biopsy should be taken to rule out cancer. Duodenal cancer is very rare and hence biopsy of these ulcers is rare.

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48
Q

If a gastric ulcer is found on endoscopy what should be done?

A

Biopsy should be taken to exclude cancer

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49
Q

If a duodenal ulcer is found on biopsy what should be done?

A

Nothing - duodenal cancer is very rare and hence biopsy of these ulcers is rare.

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50
Q

What demographic is most often diagnosed with gastric cancer?

A

50yr old males

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51
Q

What are risk factors for gastric cancer

A 
H. Pylori infection
Cigarette smoking
Alcohol
Diet - food with nitrates/nitrite components or salt-based preservatives 
Autoimmune gastritis
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52
Q

How does gastric cancer present

A 
new-onset dyspepsia (>55 especially)
unintentional weight loss
progressive dysphagia
vomiting
trousers sign = enlarged virchow's node
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53
Q

How do you investigate suspected gastric cancer

A

Endoscopy and biopsy

Biopsy tells you type of cancer and grade.

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54
Q

How is gastric cancer staged

A

TNM

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55
Q

How do gallstones form

A

Cholesterol is normally soluble in bile but if there is an imbalance of either, the excess will precipitate and form a gallstone

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56
Q

What are the types of gallstones

A 
Cholesterol stones (20%) = large, yellow coloured stones
Bilirubinate stones (5%) = small, pigmented stones
Mixed (75%) = Ca salts, bile pigment and cholesterol
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57
Q

List risk factors for gallstones

A

5Fs: Female, fat, forty, fertile, family history
Crohn’s
Haemolytic anaemia

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58
Q

How does Crohn’s disease cause gallstones

A

Malabsorption of bile salts from the terminal ileum = can’t maintain the cholesterol dissolved in bile

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59
Q

How does haemolytic anaemia cause gallstones

A

RBCs being broken down = increase in bilirubin = too much bile salt compared to cholesterol

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60
Q

How would you investigate a suspected gallstone

A

USS of gallbladder

LFTs - to assess liver function

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61
Q

What is Charcot’s triad

A

RUQ pain
Fever
Jaundice

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62
Q

How does biliary colic present

A

RUQ pain which can radiate to shoulder

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63
Q

Where will the gallstone be to cause biliary colic

A

Cystic duct

Gallstone impacts in and obstructs the cystic duct / neck of gallbladder. The gallbladder will contract against the acutely obstructed duct

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64
Q

How does acute cholecystitis present

A

RUQ pain which can radiate to shoulder

Fever

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65
Q

How do gallstones cause acute cholecystitis

A

If the stone occludes the duct for a prolonged period of time it will rub on and damage the mucosal lining and result in acute inflammation in the gallbladder wall.

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66
Q

What is acute acalculous cholecystitis

A

Cholecystitis without gallstones

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67
Q

What causes acute acalculous cholecystitis

A

Ischaemia - this can occur as the cystic artery is an end artery

eg. if patient has Infection / hypotension / major trauma

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68
Q

How does ascending cholangitis present

A

RUQ pain which can radiate to shoulder
Fever
Jaundice

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69
Q

Where is the stone in ascending cholangitis

A

CBD

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70
Q

What is the pathogenesis behind ascending cholangitis

A

Biliary obstruction causes stasis which predisposes to infection and gut bacteria and get into the biliary tree through the ampulla of Vater. These bacteria include E. Coli and Klebsiella

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71
Q

How will ascending cholangitis present if not treated

A

Can progress up to the liver and result in abcesses / sepsis

72
Q

What is the most common cause of acute pancreatitis

A

Gallstones

73
Q

Where is the obstruction when gallstones cause acute pancreatitis

A

Ampulla of vater

74
Q

How do gallstones cause pancreatitis

A

Blocked ampulla of vater which causes a reflux of pancreatic secretions and consequent autodigestion of the pancreas –> pancreatitis

75
Q

What is the second biggest cause of pancreatitis

A

Alcohol

76
Q

What is gallstone ileus

A

A gallstone causing mechanical SBO

77
Q

How does gallstone ileus present

A

Colicky abdominal pain; vomiting; abdominal distension; absolute constipation

78
Q

How can gallstones cause bowel obstruction

A

A fistula forms between the inflamed wall of the gall bladder and SI

79
Q

What is Courvoisier’s law

A

The presence of a palpable gallbladder means jaundice is unlikely to be caused by gallstones impacted in the biliary system

80
Q

In a jaundiced patient, what is a palpable gallbladder most likely to indicate?

A

Pancreatic cancer (head of pancreas)

81
Q

What are the functions of the pancreas

A

Endocrine - secreting hormones eg. Insulin / glucagon directly into the blood
Exocrine - secreting digestive enzymes into the pancreatic duct system

82
Q

What is the most common type of pancreatic cancer

A

Adenocarcinoma

83
Q

What cells are most likely to be affected in pancreatic cancer

A

Glandular duct cells

84
Q

What part of the pancreas is most commonly affected in pancreatic cancer

A

Head

85
Q

What is the most common demographic to be affected in pancreatic cancer

A

Elderly males who smoke

86
Q

What are the risk factors for pancreatic cancer

A

Smoking

87
Q

How does pancreatic cancer present

A

Obstructive jaundice
Weight loss
Mid-epigastric pain (radiates to the back)

88
Q

What is the prognosis of pancreatic cancer

A

Overall 5yr survival is 5%

89
Q

What is the palliative management of pancreatic cancer

A

Chemo
Stenting CBD
Symptom control

90
Q

What is the curvative management of pancreatic cancer

A

Whipple’s procedure

91
Q

When can Whipple’s procedure be done

A

If the tumour is confined to the pancreas WITHOUT lymph node involvement

92
Q

What does Whipple’s procedure remove

A

Consists of removal of the distal stomach, gallbladder, CBD, head of pancreas, duodenum, proximal jejunum, regional lymph nodes

93
Q

What is the prognosis of pancreatic cancer after Whipple’s procedure

A

5 year survival is 20-40%

94
Q

What is coeliac disease

A

Intolerance to gluten - in particular GLIADIN (the alcohol-free fraction of gluten)

95
Q

What food is gluten found in

A

Wheat, barley, rye

96
Q

What are the genetically susceptible haplotypes in coeliac disease

A

HLA-DQ2 and HLA-DQ8

97
Q

Explain the pathogenesis of coeliac disease

A
  1. Gluten is digested by luminal and brush-border enzymes in the small intestine into amino acids and peptides - including GLIADIN.
  2. The gliadin is deamidated in the mucosa by tTG (tissue transglutaminases).
  3. In individuals with HLA-DQ2 / HLA-DQ8 the deaminated form fits into MHCII and gets presented to Th cells
  4. Hence initiating a Th2 pre-dominant immune response - generating cytotoxic T cells against GLIADIN.
  5. Cytotoxic T cells migrate into the intestinal epithelium - visible on biopsy as intraepithelial lymphocytes
  6. The T cells damage and destroy epithelial cells + result in progressive villous atrophy
  7. Crypts become hyperplastic to compensate for the cell loss.
98
Q

In coeliac disease, what features can be seen on duodenal biopsy

A

Crypt hyperplasia
Intraepithelial lymphocytes
Villous atrophy

99
Q

What antibodies are generated by the humeral immune response in coeliac disease

A

Antigliadin, antiendomysial and antiTTG antibodies.

100
Q

What is the presentation of coeliac disease

A

Present at any age - but most commonly childhood or middle age.
“ Malabsorption
o Diarrhoea
o Steatorrhoea
o Weight loss
o Lethargy
o Bloating
o Abdominal pain
“ Non-specific symptoms
o Anaemia = iron deficiency (ie. As iron is absorbed in the duodenum)
o IBS-like symptoms
o Altered bowel habit
o Abdominal pain
“ In children it can cause failure to thrive and delayed puberty
“ Dermatitis herpetiformis - an intensely itchy and blistering rash over the elbows and buttocks

101
Q

What condition does dermatitis herpetiformis indicate?

A

Coeliac disease

102
Q

What must be true for the investigations for coeliac disease to be accurate?

A

Patient is consuming a gluten diet during the testing period

103
Q

What are the investigations for coeliac disease

A

Serology
o First line - total IgA and IgA tTG
o If weakly positive - IgA anti-endomysial (EMA)

Endoscopy and duodenal biopsy = gold standard; done in all patients to confirm the diagnosis
o Villous atrophy
o Crypt hyperplasia

104
Q

How is coeliac disease managed

A

Life long gluten free diet

105
Q

What are the complications of coeliac disease

A

Malabsorption - anaemia and other micronutrient deficiencies = vitamin B, folic acid, vitamin D, calcium.
Osteopenia/osteoporosis - reduced bone density (osteopenic) = likely as they fail to reach peak bone density during young adult life due to malabsorption of calcium.
Dermatitis herpetiformis - symmetrically on extensor surfaces
Lymphoma - small bowel lymphoma risk increased, but only small amount.

106
Q

What is peritonism

A

The inflammation of the peritoneum

107
Q

What is the peritoneum

A

A thin layer of cells that cover the external surfaces of the abdominal organs and pelvic organs

108
Q

What are the clinical features of peritonitis

A 
Increasing tachycardia and pyrexia
Constant abdominal pain
Abdominal tenderness and guarding
Rebound tenderness
Localised pain during distant palpation
Absence of bowel sounds
Clinical features relating to the underlying cause of peritonitis
109
Q

What are the causes of peritonitis

A

The most common cause is bacterial infection. This can be caused by:
External source - penetrating wound; peritoneal dialysis
Abdominal viscera - perforation of an inflamed appendix/diverticulum; post-operative leak; bowel infarction
From blood stream - sepsis
From the female genital tract - PID

110
Q

How will peritonitis progress without treatment

A

LEFT UNTREATED IT WILL PROGRESS TO SEPSIS, SEPTIC SHOCK AND DEATH.

111
Q

What are the investigations for peritonitis

A

It is a clinical diagnosis

FBC - marked leucocytosis
Serum amylase - to identify acute pancreatitis as the cause (prevent surgery)
Erect CXR - to see free air under the diaphragm if a perforated abdominal viscus is the cause
AXR - may show a cause
CT - best investigation to pinpoint the cause of peritonitis

112
Q

What is the management of peritonitis

A

Will depend on the cause

IV fluid and electrolyte replacement
ABx
Pain relief
Gastric aspiration to prevent further aspiration
SURGERY - indicated if the source can be removed/closed or the underlying cause of the peritonitis is not clear

113
Q

What is intestinal obstruction

A

A restriction to the normal passage of intestinal contents along the intestines.

114
Q

What are the clinical features of intestinal obstruction

A

Absolute constipation - neither faeces or flatus are passed
Colicky abdominal pain - the bowel proximal to the obstruction exhibits increased peristalsis in an attempt to overcome the blockage
Abdominal distension - the bowel proximal to the obstruction gradually becomes dilated. This is due to accumulation of gas and intestinal secretions
Vomiting - Ejection of the accumulated intestinal secretions and contents
Bowel sounds - initially hyperactive, as the bowel distends they become high-pitched and resonant. Absent in strangulation.
Dehydration
Hypotension + tachycardia
o If febrile + tachycardic think STRANGULATION
Empty rectum (PR)

115
Q

How will a SBO present differently to a LBO

A

The location of the obstruction will affect the presentation: talking about the gut in terms of a tube, a more proximal obstruction will present with vomiting (+ pain) whereas a more distal obstruction will present with absolute constipation (+ distension - extremely marked in the RIF if the ileocaecal valve is competent = closed loop obstruction here).

Also note that SBO is more rapid in onset, whereas LBO can be gradual/intermittent

116
Q

What are the 2 types of intestinal obstruction

A

Mechanical / paralytic ileum

117
Q

How can you classify mechanical obstruction

A

Speed of onset - acute
Anatomical site - SBO
Compromise of blood supply - strangulating
Loop - closed-loop

118
Q

What is ischaemia

A

Tissue dysfunction due to interference with blood flow

It is reversible

119
Q

What is infarction

A 
Tissue death (necrosis) due to interference of blood flow
It is irreversible
120
Q

What is necrosis

A

Cell death due to a pathological process

121
Q

What is gangrene

A

Infarction with a superimposed bacterial invasion and putrefaction of the tissue

122
Q

What is the mechanism behind strangulating bowel obstruction

A

As the bowel distends the pressure within the wall increases and consequently the vessels within the bowel wall collapse - compromising the blood supply to the intestine.

There are multiple causes of interference with blood flow including: occlusion to arterial supply/venous drainage and globally reduced perfusion (ie. Shock).

123
Q

How will strangulation progress if not treated

A

If not treated strangulation will progress to ischaemia, bowel infarction, perforation, peritonitis and then death.

124
Q

List the signs of strangulation

A

Toxic appearance - tachycardia and fever
Colicky pain - becomes continuous as peritonitis develops
Tenderness, guarding and rebound tenderness
Absent bowel sounds

125
Q

Describe the difference between an open and closed loop bowel obstruction

A

In open loop obstruction proximal decompression is possible (vomiting)
In closed loop obstruction (eg. voluvulus/LBO with competent ileocaecal valve) both inflow and outflow is blocked, which can’t be decompressed by vomiting. The bowel fills with air and secretions which results in dilation and increased pressure on the walls (can result in strangulation).

126
Q

What is paralytic ileus

A

Cessation of normal gut peristalsis (a functional obstruction rather than a mechanical one)
The lack of normal peristalsis means the bowel contents cannot be pushed out. Gas, fluid and electrolytes accumulate in the bowel lumen resulting in bowel distension - which can consequently affect the blood supply, resulting in ischaemia and without treatment progressing to infarction/perforation.

127
Q

List the main causes of mechanical SBO

A 
Adhesions
Hernias
Intussusception
Volvulus
Crohn's Disease - stricture
128
Q

List the main causes of mechanical LBO

A

Colorectal cancer
Diverticular disease - strictures
Sigmoid volvulus

129
Q

What is the most common cause of intestinal obstruction in the UK

A

Adhesions

130
Q

What is the most common cause of intestinal obstruction worldwide

A

Abdominal hernias

131
Q

What is an adhesion

A

A band of fibrous (scar) tissue binds together two anatomical structures which are usually separate.

132
Q

How do adhesions cause SBO

A

They cause SBO by pushing in from the outside - they can kink, twist and pull the intestine out of place.

133
Q

Do adhesions cause LBO and why

A

They rarely cause LBO because the colon is mostly retroperitoneal.

134
Q

What is a hernia

A

Abnormal protrusions of peritoneal-lined sacs through defects in the abdominal wall

135
Q

What type of bowel obstruction can hernias often lead to

A

If a segment of bowel protrudes into the sac and becomes trapped it may lead to a closed loop strangulating bowel obstruction and consequent infarction

136
Q

What are the common sites for hernias

A

Epigastric- upper abdomen at midline
Incisional- at site of previous surgical incision
Umbilical- at the navel
Direct inguinal- near the opening of the inguinal canal
Indirect inguinal- at the opening of the inguinal canal
Femoral- occur in the femoral canal

137
Q

What is intussusception

A

A segment of small bowel invaginates within the immediately adjoining bowel

138
Q

What is the most common site for intussusception

A

Ileocaecal valve

139
Q

What age group does intussusception most commonly occur in

A

Infants and young children

140
Q

What type of obstruction does intussusception result in

A

Due to the direct pressure of the outer layer, the interssusceptum (inside part) has its blood supply cut off resulting in a strangulating obstruction.

141
Q

What is volvulus

A

An abnormal twisting of a segment of bowel around its mesentery

142
Q

What type of obstruction does volvulus result in

A

Closed loop obstruction - and can result in strangulation if the vessels are occluded in the twisting.

143
Q

What are the common sites of volvulus

A

Sigmoid colon, caecum, small intestine

144
Q

What are some of the precipitating factors for volvulus

A

Long sigmoid loop
Short mesenteric attachment
Attachment - via adhesions to the apex
Constipation

145
Q

How do you manage sigmoid volvulus

A

Insert a flatus tube

146
Q

How does Crohn’s disease result in bowel obstruction

A

One of the main features of Crohn’s is transmural inflammation. Healing as a result of this results in fibrosis which may cause strictures - and hence bowel obstruction

147
Q

What type of bowel obstruction does Crohn’s disease cause

A

Crohn’s disease most commonly affects the terminal ileum and so results in SBO rather than LBO

148
Q

What percentage of CRC presents with bowel obstruction

A

20%

149
Q

In order for CRC to cause obstruction, what side is it usually on

A

A left-sided tumour is more likely to cause a LBO as the faeces are more solid at this point due to having travelled through the rest of the colon (harder to pass through).

150
Q

Is gallstone ileus a mechanical / paralytic form of bowel obstruction?

A

Mechanical

151
Q

Describe the general principles of management for bowel obstruction

A

Drip + Suck
o IV fluid / electrolyte replacement
o NG suction is used to decompress the gut
Close monitoring
NBM
IV ABx if strangulation is suspected
Need to identify the cause - eg contrast CT
Need for surgery depends on the clinical scenario - eg. SBO due to adhesions will often settle with drip and suck management. However if signs of PERITONITIS / STRANGULATION = pt needs to go to theatre

152
Q

List the causes of paralytic ileus

A

Post-operative state - handing of the bowel during surgery
o Pts kept NBM after abdominal surgery until the bowel regains function
o Usually resolves spontaneously 2-3 days later
Generalised peritonitis
Drugs - eg. Opiates / anticholinergicsc
Electrolyte imbalance - eg. Hypokalaemia / uraemia

153
Q

What is bowel infarction

A

Tissue necrosis due to interference with the blood supply

154
Q

What are the main causes of bowel infarction

A

Essentially they come under 3 categories:
- occlusion of arterial supply
- occlusion of venous drainage
- global hypo perfusion (shock)
———-
Strangulating bowel obstruction
Occlusion of a mesenteric artery by an embolus
Typically thrombi which originate from:
o Left atrium in patients with AF
o Mural thrombus secondary to myocardial infarction
o Vegetation on a heart valve in infective endocarditis
o Atheromatous plaque in the aorta which ruptures
Occlusion of a mesenteric artery by a thrombus
Often as a complication of a ruptured atherosclerotic plaque
Occlusion of a mesenteric artery by an aortic dissection extending into the mesenteric artery = reduced perfusion
Compression of veins in the bowel wall - most often due to bowel obstruction
Occlusion of a mesenteric vein by a thrombus
Vasculitis
Non-occlusive infarction - global hypoperfusion (shock)

155
Q

How does acute bowel infarction present compared to gradual

A

ACUTE interference of blood supply results in infarction - leads to bowel perforation and peritonitis.
GRADUAL may result in “intestinal angina” - severe abdominal pain following meals. May be associated steatorrhoea.

156
Q

What is the textbook clinical presentation of bowel infarction

A

Acute colicky pain
Rectal bleeding
Shock
Often in a patient with AF.

May cause abdominal pain which is out of proportion with the physical signs OR peritonism.

157
Q

What is the management of bowel infarction

A

IV fluids
Broad spectrum ABx
Emergency laparotomy - resection of dead bowel

158
Q

What is diverticular disease

A

A common condition where many diverticula develop in the large bowel. In the west this most commonly affects the SIGMOID colon.
Incidence rises with increasing age. It is known as “arthritis of the bowel”, as it is essentially wear-and-tear.

159
Q

What is the prevalence of diverticular disease

A

50% of over 60s

160
Q

What is a diverticulum

A

A pouch of colonic mucosa that has herniated through the muscularis propria and has come to lie in the sub serosal (pericolic) fat outside the bowel wall. The outer wall of diverticular is supported by just a thin layer of subserosal connective tissue - hence they are prone to obstruction when obstructed/inflamed.

161
Q

What is diverticulosis

A

The presence of diverticula but it is asymptomatic at this stage

162
Q

What is diverticulitis

A

An acutely inflamed diverticulum. This is the most common presentation.

163
Q

What are the 2 important factors in formation of diverticula

A

1) Areas of weakness in the colonic wall - there are natural defects in the wall! Where blood vessels pass through
2) Raised intraluminal pressure - ie due to insufficient dietary fibre.
a. Fibre binds salt and water in the colon resulting in bulky, moist faeces which are easily propelled through the colon
b. If there is low fibre, the faeces are much harder to move through and result in muscle hypertrophy and increased intraluminal pressure. As a consequence, diverticula are more likely to form

164
Q

What is the most commonly affected site in diverticular disease

A

Sigmoid colon
Because the SIGMOID is the part of the large bowel with the smallest diameter it is the site with the highest intraluminal pressure. This is why is is the commonest site of diverticula formation.

165
Q

What are the complications of diverticular disease

A

1) acute diverticulitis
2) abcess formation
3) peritonitis
4) fistulae
5) strictures
6) lower GI bleed

166
Q

How does acute diverticulitis occur in a patient with diverticular disease

A

This occurs when faeces impact and obstruct the neck of a diverticulum. There is consequent bacterial trapping - the bacteria replicate in the occluded lumen = infection + mucosal injury. This injury initiates an acute inflammatory response, causing ACUTE DIVERTICULITIS.

167
Q

How does acute diverticulitis present

A 
Abdominal pain
Malaise
Fever
Localised tenderness
No peritonism
168
Q

How are abscesses formed in diverticulitis

A

The inflammation can extend beyond the site of the diverticulum to the serosal tissue to form a pericolic abcess.

169
Q

What is an abscess

A

An abcess is a localised collection of pus within a newly formed cavity in a tissue

170
Q

What is pus

A

Pus consists of inflammatory cells (neutrophils) admixed with cellular debris, fibrin and oedema fluid.

171
Q

How can diverticular disease result in peritonitis

A

Perforation of pericolic abcess

Perforation of inflamed diverticula –> faecal peritonitis

172
Q

What is a fistula

A

A fistula is an abnormal connection between 2 epithelial surfaces

173
Q

How does a fistula form in diverticulitis

A

As a consequence of the inflammation, a fistula can form between the sigmoid colon and the bladder.
Fistulae can also form to the vagina

174
Q

A 75yr old female presents with faecaluria. She has a PMH of diverticular disease. What is the cause?

A

Fistula - due to diverticulitis

This presents clinically as faecaluria

175
Q

Why do strictures form in patients with diverticular disease

A

Smooth muscle hypertrophy and hyperplasia due to a low fibre diet
Fibrosis around the diverticula (due to the healing process following repeated episodes of inflammation)

Both mechanisms cause a reduction in the size of the lumen

176
Q

72M
4/7 constipation
Vomiting
Abdominal pain

Not sure if passing flatus.

PMH diverticular disease; no past abdominal surgery, no hernias.

What is the cause of his bowel obstruction?

A

Stricture from diverticular disease

177
Q

How does diverticular disease result in a lower GI bleed

A

Small blood vessels stretched over the diverticula can rupture and cause bleeding. This is typically painless and spontaneous.
Usually a small bleed, but occasionally can be massive.

Cellular pathology (8 decks)

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