GI Flashcards
1
Q
List all the layers of the GIT
A
Mucosa Submucosa Muscularis Propria Subserosa Serosa
2
Q
Which layer of the GIT is the only one to change through different organs?
A
Mucosa
3
Q
What is the function of the oesophagus?
A
Transit tube
4
Q
What is the function of the stomach?
A
Storage and digestion
5
Q
What is the function of the small intestine?
A
Nutrient absorption (+ digestion)
6
Q
What is the function of the colon?
A
Water absorption
7
Q
What is the mucosa of the oesophagus?
A
Stratified squamous
8
Q
What is the mucosa of the stomach?
A
Thick glandular (columnar)
9
Q
What is the mucosa of the small intestine?
A
Glandular with villi
10
Q
What is the mucosa of the large intestine?
A
Glandular with crypts
11
Q
What is GORD
A
Regurgitation of acidic gastric contents into the lower oesophagus
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)
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
14
Q
What is a hiatus hernia
A
The protrusion of the upper part of the stomach into the thoracic cavity.
15
Q
What is the cause of a hiatus hernia
A
A combination of diaphragmatic weakening and increased intraabdominal pressure
16
Q
How does a hiatus hernia result in GORD
A
Weakens the LOS
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)
18
Q
What complication of GORD occurs in 10% patients
A
Barrett’s oesophagus
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
20
Q
How does Barrett’s oesophagus present
A
Asymptomatic
Often identified when patients undergo OGD due to other symptoms
21
Q
What is the metaplastic change that occurs in Barrett’s oesophagus?
A
Squamous mucosa –[reflux of gastric acid]–> glandular mucosa
22
Q
What percentage of patients with Barrett’s oesophagus progress to dysplasia and then to invasive adenocarcinoma?
A
2%
23
Q
What is the most common demographic diagnosed with oesophageal cancer?
A
50-70yr old men
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
25
What are the investigations for oesophageal cancer
Endoscopy and biopsy.
The biopsy will tell you the type of cancer and the grade
26
What is the most common type of oesophageal cancer in the UK?
Adenocarcinoma
27
How does oesophageal cancer typically arise
Due to Barrett's oesophagus most often
28
What is the 2nd most common type of oesophageal carcinoma in the UK?
Squamous cell carcinoma (most common type in Japan/China)
29
How is oesophageal cancer staged
TNM
30
What is the curative management option for oesophageal cancer
Surgery
31
What are the palliative management options for oesophageal cancer
Dilation
Stenting
Radiotherapy
32
What is the prognosis of oesophageal cancer
5 year survival is 5-10%
33
What are the 2 most important causes of gastritis?
NSAIDs
| H Pylori infection
34
Is H. Pylori a gram positive or gram negative organism?
Gram negative
35
How does H. Pylori spread
Faecal-oral or oral-oral transmission
36
How does H Pylori survive in the stomach
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.
37
List the consequences of H Pylori infection
(1) Minority develop symptomatic gastritis (<20%)
(2) Minority develop peptic ulcer
(3) Small minority develop gastric carcinoma
(4) Very small minority develop gastric lymphoma
38
What is a peptic ulcer
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.
39
What are the most common sites for a peptic ulcer
Gastric antrum / proximal duodenum.
40
What are the most common causes of peptic ulcers
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
```
41
What are the most common causes of oesophageal ulcers?
GORD
42
How do peptic ulcers illustrate chronic inflammation
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
43
How does H Pylori cause peptic ulcers
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
44
How do NSAIDs cause peptic ulcers
It overcomes the defence mechanisms: epithelial cell defences
45
How do curling ulcers occur
Acute ulcers (ie. CURLING) occur in clinical states of shock and affect the mucosal blood flow
46
What is Zollinger-Ellison syndrome and how does it cause peptic ulceration
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.
47
What are the complications of peptic ulcers
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.
48
If a gastric ulcer is found on endoscopy what should be done?
Biopsy should be taken to exclude cancer
49
If a duodenal ulcer is found on biopsy what should be done?
Nothing - duodenal cancer is very rare and hence biopsy of these ulcers is rare.
50
What demographic is most often diagnosed with gastric cancer?
50yr old males
51
What are risk factors for gastric cancer
```
H. Pylori infection
Cigarette smoking
Alcohol
Diet - food with nitrates/nitrite components or salt-based preservatives
Autoimmune gastritis
```
52
How does gastric cancer present
```
new-onset dyspepsia (>55 especially)
unintentional weight loss
progressive dysphagia
vomiting
trousers sign = enlarged virchow's node
```
53
How do you investigate suspected gastric cancer
Endoscopy and biopsy
| Biopsy tells you type of cancer and grade.
54
How is gastric cancer staged
TNM
55
How do gallstones form
Cholesterol is normally soluble in bile but if there is an imbalance of either, the excess will precipitate and form a gallstone
56
What are the types of gallstones
```
Cholesterol stones (20%) = large, yellow coloured stones
Bilirubinate stones (5%) = small, pigmented stones
Mixed (75%) = Ca salts, bile pigment and cholesterol
```
57
List risk factors for gallstones
5Fs: Female, fat, forty, fertile, family history
Crohn's
Haemolytic anaemia
58
How does Crohn's disease cause gallstones
Malabsorption of bile salts from the terminal ileum = can't maintain the cholesterol dissolved in bile
59
How does haemolytic anaemia cause gallstones
RBCs being broken down = increase in bilirubin = too much bile salt compared to cholesterol
60
How would you investigate a suspected gallstone
USS of gallbladder
| LFTs - to assess liver function
61
What is Charcot's triad
RUQ pain
Fever
Jaundice
62
How does biliary colic present
RUQ pain which can radiate to shoulder
63
Where will the gallstone be to cause biliary colic
Cystic duct
Gallstone impacts in and obstructs the cystic duct / neck of gallbladder. The gallbladder will contract against the acutely obstructed duct
64
How does acute cholecystitis present
RUQ pain which can radiate to shoulder
| Fever
65
How do gallstones cause acute cholecystitis
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.
66
What is acute acalculous cholecystitis
Cholecystitis without gallstones
67
What causes acute acalculous cholecystitis
Ischaemia - this can occur as the cystic artery is an end artery
eg. if patient has Infection / hypotension / major trauma
68
How does ascending cholangitis present
RUQ pain which can radiate to shoulder
Fever
Jaundice
69
Where is the stone in ascending cholangitis
CBD
70
What is the pathogenesis behind ascending cholangitis
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
71
How will ascending cholangitis present if not treated
Can progress up to the liver and result in abcesses / sepsis
72
What is the most common cause of acute pancreatitis
Gallstones
73
Where is the obstruction when gallstones cause acute pancreatitis
Ampulla of vater
74
How do gallstones cause pancreatitis
Blocked ampulla of vater which causes a reflux of pancreatic secretions and consequent autodigestion of the pancreas --> pancreatitis
75
What is the second biggest cause of pancreatitis
Alcohol
76
What is gallstone ileus
A gallstone causing mechanical SBO
77
How does gallstone ileus present
Colicky abdominal pain; vomiting; abdominal distension; absolute constipation
78
How can gallstones cause bowel obstruction
A fistula forms between the inflamed wall of the gall bladder and SI
79
What is Courvoisier's law
The presence of a palpable gallbladder means jaundice is unlikely to be caused by gallstones impacted in the biliary system
80
In a jaundiced patient, what is a palpable gallbladder most likely to indicate?
Pancreatic cancer (head of pancreas)
81
What are the functions of the pancreas
Endocrine - secreting hormones eg. Insulin / glucagon directly into the blood
Exocrine - secreting digestive enzymes into the pancreatic duct system
82
What is the most common type of pancreatic cancer
Adenocarcinoma
83
What cells are most likely to be affected in pancreatic cancer
Glandular duct cells
84
What part of the pancreas is most commonly affected in pancreatic cancer
Head
85
What is the most common demographic to be affected in pancreatic cancer
Elderly males who smoke
86
What are the risk factors for pancreatic cancer
Smoking
87
How does pancreatic cancer present
Obstructive jaundice
Weight loss
Mid-epigastric pain (radiates to the back)
88
What is the prognosis of pancreatic cancer
Overall 5yr survival is 5%
89
What is the palliative management of pancreatic cancer
Chemo
Stenting CBD
Symptom control
90
What is the curvative management of pancreatic cancer
Whipple's procedure
91
When can Whipple's procedure be done
If the tumour is confined to the pancreas WITHOUT lymph node involvement
92
What does Whipple's procedure remove
Consists of removal of the distal stomach, gallbladder, CBD, head of pancreas, duodenum, proximal jejunum, regional lymph nodes
93
What is the prognosis of pancreatic cancer after Whipple's procedure
5 year survival is 20-40%
94
What is coeliac disease
Intolerance to gluten - in particular GLIADIN (the alcohol-free fraction of gluten)
95
What food is gluten found in
Wheat, barley, rye
96
What are the genetically susceptible haplotypes in coeliac disease
HLA-DQ2 and HLA-DQ8
97
Explain the pathogenesis of coeliac disease
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
In coeliac disease, what features can be seen on duodenal biopsy
Crypt hyperplasia
Intraepithelial lymphocytes
Villous atrophy
99
What antibodies are generated by the humeral immune response in coeliac disease
Antigliadin, antiendomysial and antiTTG antibodies.
100
What is the presentation of coeliac disease
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
What condition does dermatitis herpetiformis indicate?
Coeliac disease
102
What must be true for the investigations for coeliac disease to be accurate?
Patient is consuming a gluten diet during the testing period
103
What are the investigations for coeliac disease
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
How is coeliac disease managed
Life long gluten free diet
105
What are the complications of coeliac disease
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
What is peritonism
The inflammation of the peritoneum
107
What is the peritoneum
A thin layer of cells that cover the external surfaces of the abdominal organs and pelvic organs
108
What are the clinical features of peritonitis
```
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
What are the causes of peritonitis
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
How will peritonitis progress without treatment
LEFT UNTREATED IT WILL PROGRESS TO SEPSIS, SEPTIC SHOCK AND DEATH.
111
What are the investigations for peritonitis
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
What is the management of peritonitis
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
What is intestinal obstruction
A restriction to the normal passage of intestinal contents along the intestines.
114
What are the clinical features of intestinal obstruction
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
How will a SBO present differently to a LBO
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
What are the 2 types of intestinal obstruction
Mechanical / paralytic ileum
117
How can you classify mechanical obstruction
Speed of onset - acute
Anatomical site - SBO
Compromise of blood supply - strangulating
Loop - closed-loop
118
What is ischaemia
Tissue dysfunction due to interference with blood flow
| It is reversible
119
What is infarction
```
Tissue death (necrosis) due to interference of blood flow
It is irreversible
```
120
What is necrosis
Cell death due to a pathological process
121
What is gangrene
Infarction with a superimposed bacterial invasion and putrefaction of the tissue
122
What is the mechanism behind strangulating bowel obstruction
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
How will strangulation progress if not treated
If not treated strangulation will progress to ischaemia, bowel infarction, perforation, peritonitis and then death.
124
List the signs of strangulation
Toxic appearance - tachycardia and fever
Colicky pain - becomes continuous as peritonitis develops
Tenderness, guarding and rebound tenderness
Absent bowel sounds
125
Describe the difference between an open and closed loop bowel obstruction
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
What is paralytic ileus
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
List the main causes of mechanical SBO
```
Adhesions
Hernias
Intussusception
Volvulus
Crohn's Disease - stricture
```
128
List the main causes of mechanical LBO
Colorectal cancer
Diverticular disease - strictures
Sigmoid volvulus
129
What is the most common cause of intestinal obstruction in the UK
Adhesions
130
What is the most common cause of intestinal obstruction worldwide
Abdominal hernias
131
What is an adhesion
A band of fibrous (scar) tissue binds together two anatomical structures which are usually separate.
132
How do adhesions cause SBO
They cause SBO by pushing in from the outside - they can kink, twist and pull the intestine out of place.
133
Do adhesions cause LBO and why
They rarely cause LBO because the colon is mostly retroperitoneal.
134
What is a hernia
Abnormal protrusions of peritoneal-lined sacs through defects in the abdominal wall
135
What type of bowel obstruction can hernias often lead to
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
What are the common sites for hernias
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
What is intussusception
A segment of small bowel invaginates within the immediately adjoining bowel
138
What is the most common site for intussusception
Ileocaecal valve
139
What age group does intussusception most commonly occur in
Infants and young children
140
What type of obstruction does intussusception result in
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
What is volvulus
An abnormal twisting of a segment of bowel around its mesentery
142
What type of obstruction does volvulus result in
Closed loop obstruction - and can result in strangulation if the vessels are occluded in the twisting.
143
What are the common sites of volvulus
Sigmoid colon, caecum, small intestine
144
What are some of the precipitating factors for volvulus
Long sigmoid loop
Short mesenteric attachment
Attachment - via adhesions to the apex
Constipation
145
How do you manage sigmoid volvulus
Insert a flatus tube
146
How does Crohn's disease result in bowel obstruction
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
What type of bowel obstruction does Crohn's disease cause
Crohn's disease most commonly affects the terminal ileum and so results in SBO rather than LBO
148
What percentage of CRC presents with bowel obstruction
20%
149
In order for CRC to cause obstruction, what side is it usually on
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
Is gallstone ileus a mechanical / paralytic form of bowel obstruction?
Mechanical
151
Describe the general principles of management for bowel obstruction
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
List the causes of paralytic ileus
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
What is bowel infarction
Tissue necrosis due to interference with the blood supply
154
What are the main causes of bowel infarction
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
How does acute bowel infarction present compared to gradual
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
What is the textbook clinical presentation of bowel infarction
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
What is the management of bowel infarction
IV fluids
Broad spectrum ABx
Emergency laparotomy - resection of dead bowel
158
What is diverticular disease
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
What is the prevalence of diverticular disease
50% of over 60s
160
What is a diverticulum
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
What is diverticulosis
The presence of diverticula but it is asymptomatic at this stage
162
What is diverticulitis
An acutely inflamed diverticulum. This is the most common presentation.
163
What are the 2 important factors in formation of diverticula
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
What is the most commonly affected site in diverticular disease
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
What are the complications of diverticular disease
1) acute diverticulitis
2) abcess formation
3) peritonitis
4) fistulae
5) strictures
6) lower GI bleed
166
How does acute diverticulitis occur in a patient with diverticular disease
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
How does acute diverticulitis present
```
Abdominal pain
Malaise
Fever
Localised tenderness
No peritonism
```
168
How are abscesses formed in diverticulitis
The inflammation can extend beyond the site of the diverticulum to the serosal tissue to form a pericolic abcess.
169
What is an abscess
An abcess is a localised collection of pus within a newly formed cavity in a tissue
170
What is pus
Pus consists of inflammatory cells (neutrophils) admixed with cellular debris, fibrin and oedema fluid.
171
How can diverticular disease result in peritonitis
Perforation of pericolic abcess
| Perforation of inflamed diverticula --> faecal peritonitis
172
What is a fistula
A fistula is an abnormal connection between 2 epithelial surfaces
173
How does a fistula form in diverticulitis
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
A 75yr old female presents with faecaluria. She has a PMH of diverticular disease. What is the cause?
Fistula - due to diverticulitis
| This presents clinically as faecaluria
175
Why do strictures form in patients with diverticular disease
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
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?
Stricture from diverticular disease
177
How does diverticular disease result in a lower GI bleed
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.
