1
Q
The small and large intestine peristalsis is mediated by which types of neural control?
A
intrinsic (myenteric plexus)
extrinsic (autonomic innervation)
2
Q
The myenteric plexus is composed of which nerve plexuses? and where are they located?
A
- Meissener’s plexus: base of the submucosa.
- Auerbach plexus: between the inner circular and outer longitudinal layers of the muscularis propria.
3
Q
Inflammatory bowel disease is a pathological feature of which conditions?
A
- ulcerative colitis.
- Crohn’s disease.
- ischaemic colitis.
- radiation colitis.
- appendicitis.
4
Q
what causes IBD? (not what conditions but the actual mechanism)
A
- strong immune response against normal flora with defects in the epithelial barrier function in genetically susceptible individuals.
5
Q
what areas can Crohn’s disease affect?
A
any part of the GIT from the mouth to the anus
6
Q
what gene mutation is seen in association with Crohn’s disease?
A
NOD2
7
Q
what gene mutation is seen in association with ulcerative colitis?
A
HLA
8
Q
what is the role of intestinal flora in the pathology of IBD?
A
- defects in mucosal barrier could allow microbes access to mucosal lymphoid tissue triggering immune response.
9
Q
the pANCA is present in what % of ulcerative colitis patients?
A
75%
10
Q
the pANCA is positive in what % of Crohn’s disease patients?
A
11%
11
Q
ulcerative colitis (UC) definition
A
a chronic relapsing-remitting inflammatory disease that primarily affects the large bowel.
12
Q
what two peak age groups does UC most commonly occur?
A
20-30 years
70-80 years
13
Q
features of ulcerative colitis?
A
- continuous pattern of inflammation-
- rectum to proximal large bowel.
- pseudopolyps.
- ulceration.
- serosal surface minimal or no inflammation.
14
Q
what will a biopsy show in UC?
A
- loss of goblet cells, crypt abscess and inflammatory cells (predominantly lymphocytes).
- NO GRANULOMAS.
15
Q
what is pancolitis?
A
Pancolitis is a form of ulcerative colitis that affects the entire large intestine or bowel.
16
Q
what are complications of uclerative colitis?
A
- if pancolitis > 10 years > 20-30x higher risk of developing cancer.
- haemorrhage.
- perforation.
- toxic dilatation.
17
Q
in what two age groups does Crohn’s disease peak in?
A
20-30 years
60-70 years
18
Q
what will a colonoscopy with biopsy of Crohn’s disease reveal?
A
- intermittent inflammation (‘skip lesions’).
- cobblestone mucosa (due to ulceration and mural oedema).
- rose-thorn ulcers (due to transmural inflammation) +/- fistulae or abscesses.
- non-caseating granulomas.
19
Q
what are long-term features of crohn’s disease?
A
- small intestine malabsorption > malnutrition.
- strictures.
- fistulas and abscesses.
- perforation.
- increased risk of cancer 5x.
20
Q
NESTS mnemonic in differentiating features of CD from UC
A
- No blood or mucus (less common).
- Entire GI tract affected.
- Skip lesions, strictures and fistulas.
- Terminal ileum most affected and transmural (full thickness) inflammation.
- Smoking is a risk factor.
21
Q
CLOSEUP mnemonic in differentiating between UC and CD
A
- Continuous inflammation.
- Limited to the colon and rectum.
- Only superficial mucosa affected.
- Smoking may be protective.
- Excrete blood and mucus.
- Use aminosalicylates.
- Primary sclerosing cholangitis.
22
Q
What is ischaemic enteritis?
A
inflammation of the small or large intestine or both due to blood vessel occlusion.
23
Q
describe appendicitis?
A
- inflammation of the appendix.
- typically develops due to an obstruction within the appendix.
24
Q
what are complications of appendicitis?
A
- tissue damage.
- pressure-induced necrosis.
- perforation.
- gangrene due to thrombosis in ileocolic artery.
25
what is a dysplasia of the large bowel also called?
adenoma ('polyp')
26
What are the risk factors in developing colorectal adenocarcinoma?
- lifestyle
- family history
- IBD: UC and CD
- Genetics: FAP, HNPCC, Peutz-Jeghers.
27
what are clinical features of right-sided adenocarcinoma of colon?
- exophytic/polypoid (grows outwards from epithelium).
- anaemia (chronic bleeding).
- vague pain.
- weakness.
- obstruction.
28
what are features of left-sided colorectal adenocarcinoma?
- annular (ring-shaped) > napkin ring lesion.
- bleeding > fresh/altered blood PR.
- altered bowel habit.
- obstruction.
29
what side of the large intestine is the site of most bacterial fermentation?
right-side
30
what are the three main short-chain fatty acids produced by microbial fermentation in the large intestine? and how are they used locally?
| baby please aaaaa
- butyrate
- propionate
- acetate
- energy source for gut eptihelial cells.
31
what is the function of butyrate
epithelial cell growth and regeneration
32
what is the function of propionate?
gluconeogenesis in the liver
satiety signalling
33
what is the function of acetate?
transported in blood to peripheral tissues > lipogenesis
34
what is the significance of the pH of the proximal colon?
low pH of 5.5
inhibits pathogems who generally grow optimally at pHs over 6
35
what are the two methods of colonisation resistance in the large intestine?
1. barrier effect
2. active competitive exclusion
36
Describe the barrier effect of colonisation resistance in the large intestine
- the large numbers of the indigenous microbiota prevent colonisation by ingested pathogens and inhibit overgrowth of potentially pathogenic bacteria normally resident at low levels.
37
dysbiosis of the gut microbiota has been linked to which central nervous system conditions?
autistic spectrum disorder
major depressive disorder
multiple sclerosis
38
dysbiosis of the gut microbiota has been linked to which metabolic disorders?
insulin resistance (T2D)
metabolic syndrome
obesity
CVD
39
what are the consequences of antibiotic exposure to the gut microbiota?
- loss of bacterial diversity > opportunity for pathogen colonisation by C.difficile for example which produces toxins.
- bacterial resistance
40
how does fecal microbiotic transplantation (FMT) work? What can it be used to treat?
- faecal sample from screened healthy donor transplanted into recipient with dysbiosis.
- Donor microbiota repopulates large intestine, displaces C.difficile, prevents reinfection.
41
summarise the role of bacteria in the large intestine
- ferment dietary fibre.
- produce metabolites to communicate with other bacteria and the host.
- prime the immune system.
- prevent pathogen colonisation.
42
what external influences can affect the gut microbiota?
diet
antibiotics
probiotics
symbiotic
prebiotics
ageing
disease
43
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44
what are clinical features of IBS?
- abdominal pain > improvement with defecation.
- altered bowel habit.
- abdominal bloating.
- belching wind and flatus.
- passage of mucus.
45
why do we test for calprotectin in stool samples?
- calprotectin is released by inflamed gut mucosa.
- used for differentiating between irritable bowel disease and inflammatory bowel disease.
46
what does treatment for IBS consist of?
- dietary review > cut out irritants.
- drug therapy to treat symptoms:
> painkillers or antidepressants for pain.
> probiotics for bloating.
> laxatives for constipation.
> antimotility agents, FODMAP for diarrhoea.
- PSYCHOLOGICAL INTERVENTIONS.
47
some causes for IBS?
- altered motility.
- visceral hypersensitivity.
- stress, anxiety, depression.
48
describe changes in intestinal motility seen in IBS-D and IBS-C
In IBS-D, muscular contractions may be stronger and more frequent than normal.
In IBS-C, contractions may be reduced.
49
what is inflammatory bowel disease?
chronic, relapsing, remitting inflammation of GI tract.
e.g. CD and UC
50
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51
what are symptoms of UC?
bloody diarrhoea
abdominal pain
weight loss
fatigue
52
what is proctitis?
inflammation of the rectum
53
what are investigations for suspected UC?
- bloods for markers of inflammation- normocytic/microcytic anaemia:
> ^CRP/WCC/Platelets
> decreased albumin.
- stool culture to rule out infection.
- faecal caprotectin > 200ug/g is elevated.
- colonoscopy and colon mucosal biopsies.
54
what will a colonoscopy of UC reveal?
continuous inflammation
erythematous mucosa
loss of haustral markings
pseudopolyps
55
what will a barium enema of UC reveal?
- lead-piping inflammation (secondary to loss of haustral markings).
- thumb-printing (a marker of bowel wall inflammation).
- pseudopolyps.
56
outline the management of acute, severe UC
1. IV corticosteroids first-line.
2. IV ciclosporin.
3. infliximab (Anti-TNF antibody)
4. Surgery
57
what are short-term/acute complications in UC?
Toxic megacolon
massive lower GI haemorrhage.
58
what are long-term complications of UC?
Colorectal cancer
cholangiocarcinoma
colonic strictures
primary sclerosing cholangitis
inflammatory pseudopolyps
59
investigation CD
- bloods > CRP, WCC etc.
- stool culture
- faecal calprotectin
- endoscopy with imaging required for diagnosis.
- MRI for suspected small bowel disease.
- colonoscopy with biopsy.
60
what are symptoms of CD?
symptoms:
- GI symptoms > crampy abdominal pain and diarrhoea.
- systemic symptoms > weight loss and fever.
61
what are signs of CD?
- cachexia.
- paleness (anaemia).
- mouth ulcers.
- abdominal/right lower quadrant tenderness and a right iliac fossa mass.
- perirectal examination may have skin tags, fistulae or perianal abscess.
62
what are the symptoms of perianal crohn's disease?
perianal pain
pus secretion
unable to sit down
63
investigations for perianal crohn's disease?
MRI pelvis
Examination under anaesthetic (EUA)
64
treatment for perianal Crohn's disease?
- surgery to drain abscess and place seton stitch.
- antibiotics.
- biological therapy (anti-TNF).
65
What are some extra-intestinal manifestations of IBD?
- mouth ulcers
- skin: erythema nodosum, pyoderma gangrenosum.
- eyes: anterior uveitis, episcleritis, scleritis.
- musculoskeletal: arthritis, sacro-ilitis, ankolysing spondalitis.
- primary sclerosing cholangitis.
66
discuss the treatment of mild to moderate acute UC
- aminosalicylate (e.g., oral or rectal mesalazine) first-line.
- corticosteroids (e.g., oral or rectal prednisolone) second-line
67
how do aminosalicylates treat UC?
blocking prostaglandins and leukotrienes
68
what is the treatment for maintaining remission in UC?
- aminosalicylate (mesalazine) first-line.
- azathioprine.
- mercaptopurine.
69
discuss the surgical management of UC
Removing the entire large bowel and rectum (panproctocolectomy) will remove the disease. The patient has either a permanent ileostomy or an ileo-anal anastomosis (J-pouch).
70
how is an exacerbation of Crohn's disease treated?
- steroids (e.g., oral prednisolone 40mg or IV hydrocortisone) first-line.
- enteral nutrition as an alternative.
other meds if steroids dont work:
azathioprine
mercaptopurine
methotrexate
infliximab (anti-TNF antibodies)
adalimumab (anti-TNF antibodies)
71
what is the treatment for maintaining remission in CD?
first-line:
azathioprine
mercaptopurine
or methotrexate
72
what are indications for emergency surgery in acute IBD?
1. acute severe colitis not responding to high dose IV steroids =/- anti-TNF biologic 'rescue' therapy.
2. Complications such as perforation, obstruction and abscess.
73
indications for elective surgery for IBD
1. frequent relapses despite medical therapy.
2. not able to tolerate medical therapy.
3. steroid dependent patients.
74
surgical options for CD?
- resection of distal ileum when the disease is isolated to this area.
- treating strictures.
- treating fistulas.
75
what is the overall mortality of acute GI bleeding in the UK?
7%
76
what is the mortality rate if acute GI bleeding in patients admitted to hospital for other reasons?
26%
77
what features is upper GI bleeding associated with?
- haematemesis (vomiting fresh blood).
- melaena (black stools).
- elevated urea (partially digested blood > haem > urea).
- associated with dyspepsia, reflux, epigastric pain.
- NSAID use.
78
what features are associated with lower GI bleeding?
- fresh blood/clots.
- magenta stools.
- normal urea (rarely elevated in proximal small bowel).
- typically painless.
- more common in advanced age.
79
what are some oesophageal causes of upper GI bleeding?
- ulcer
- oesophagitis
- varices
- Mallory Weiss tear
- malignancy
80
what are some gastric causes of upper GI bleeding?
- ulcer
- gastritis
- varices
- malignancy (may be under an ulcer)
- Dieulafoy lesion
- angiodysplasia (tends to be chronic)
81
what are some duodenal causes of upper GI bleeding?
- ulcer
- duodenitis
- angiodysplasia (tends to be chronic)
82
what are the top five most common causes of an acute upper GI bleed?
1. gastric cancer
2. duodenal ulcer
3. mallory-weiss tear
4. oesophagitis
5. oesophageal varices
83
are duodenal or gastric ulcers more common?
duodenal (75%)
84
what are risk factors in developing a peptic ulcer?
- H.pylori infection
- NSAIDs/aspirin
- alcohol excess
- systemic illness- stress ulcers
85
how do NSAIDs cause a peptic ulcer?
- COX-1 and COX-2 inhibition, and topical irritation.
- this causes reduced blood flow, increased leukocyte adhesion and epithelial damage > mucosal injury.
86
what is Zollinger-Ellison syndrome and what does it cause?
gastrin-secreting pancreatic tumour that causes recurrent poor healing duodenal ulcers.
tumour sits underneath ulcer.
87
why does bleeding tend to occur in gastritis and duodenitis?
tend to bleed in context of impaired coagulation:
- medical conditions.
- anti-coagulants (warfarin, LMWH etc.).
- anti-platelets (clopidogrel, ticagrelor).
88
what are some causes of oesophagitis?
- reflux.
- hiatus hernia.
- alcohol.
- biphosphonates (drugs used to treat osteoporosis).
- systemic illness.
89
what are the most common varices that cause GI bleeding?
oesophageal (90%)
gastric (8%)
rectal and spleen (rare)
90
Describe a Mallory-Weiss tear
- linear tear at oesophago-gastric junction
- follows period of retching/vomiting
- up to 10% significant requiring endoscopic treatment.
91
what is a diuelafoy lesion?
- a submucosal arteriolar vessel eroding through mucosa.
- it bleeds in the absence of any abnormality.
- usually found in gastric fundus.
92
what is an angiodysplasia?
- a vascular malformation that can occur anywhere in the GI tract.
- usually causes chronic occult or overt occult bleeding.
- associated with chronic conditions including heart valve replacement.
93
what is haematemesis?
vomiting of blood due to active haemorrhage from the oesophagus, stomach or duodenum.
94
lower GI bleeding accounts for what percentage of acute GI bleeding cases?
25%
95
what are some causes of acute lower GI bleeding?
- diverticular disease.
- haemorrhoids.
- vascular malformation (angiodysplasia, arteriovenous malformation).
- neoplasia (carcinoma or polyps).
- ischaemic colitis.
- radiation enteropathy/proctitis.
- IBD.
96
Describe diverticular disease
- protrusion of the inner mucosal lining through the outer muscular layer forming a pouch.
- diverticulosis - presence.
- diverticulitis - inflammation.
97
what are haemorrhoids?
- enlarged vascular cushions around anal canal.
- painful if thrombosed or external.
98
what are haemorrhoids associated with?
straining/constipation
low fibre diet
99
how is angiodysplasia treated?
Argon phototherapy
100
what is ischemic colitis? what are its complications? and what is the appearance of the mucosa?
- disruption in blood supply to colon.
- gangrene and perforation.
- dusky blue, swollen mucosa.
101
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what investigations are performed when investigating small bowel causes of acute lower GI bleeding?
- CT angiogram
- Meckel's scan (scintigraphy) for Meckel's diverticulum.
- capsule endoscopy
- double balloon enteroscopy
103
when is a blood transfusion indicated in acute GI bleeding?
if Hb < 7g/dl or ongoing active bleeding
104
describe circulatory shock
circulatory collapse resulting in inadequate tissue and oxygen delivery leading to global hypoperfusion and tissue hypoxia.
105
what is the clinical presentation of circulatory shock caused by haemorrhage?
- tachypnoea
- tachycardia
- anxiety or confusion
- cool clammy skin
- low urine output (oliguria)
- hypotension
106
what are risk stratification factors in lower GI bleeding?
- age > occurs most often in elderly.
- co-morbidity > presence of 2 co-morbid conditions doubles the chance of a severe bleed.
- inpatients > 23% mortality compared to 3.6%.
- initial shock.
- drugs > NSAIDS and aspirin.
107
what are the endoscopic therapy options for a peptic ulcer?
- injection > adrenaline 1:10000
- thermal > contact- 'gold probe'
- mechanical > clip
- combo therapy most effective (adrenaline + thermal/clips)
108
what are the management options of peptic ulcers that have ongoing bleeding and are uncontrollable endoscopically?
- angiography with embolisation.
- laparotomy.
109
what are the pharmacological treatments for managing GI bleeding caused by varices?
- terlipressin > vasoconstrictor of splanchnic blood supply > reduces blood flow to portal vein > reducing pressure.
- antibiotics . often systemic infection is recipitant.
- reverse abnormal coagulation.
110
describe endoscopy with endotherapy in treating varices in different areas of GI tract
- oesophageal > band ligation and glue injection.
- gastric > glue injection.
- rectal > glue injection.
111
if varcieal bleeding is ongoing and uncontrollable endoscopically, what are the other options?
- Sengstaken-Blakemore tube.
- Transjugular intrahepatic porto-systemic shunt (TIPSS)..
112
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how does generalised peritonitis occur?
represents failure of localisation and occurs when:
- contamination too rapid.
- contamination persists.
- abscess ruptures.
114
what type of bacteria are highly prevalent in a peritoneal abscess?
anaerobes
115
what conditions should be considered when investigating the acute abdomen?
- peritonitis.
- intestinal obstruction.
- ischaemia.
- non-surgical abdominal pain.
116
what are some routes of peritonitis infection?
- perforation of Gi biliary tract.
- female genital tract.
- penetration of abdominal wall.
- haematogenous spread.
117
what are cardinal features of intestinal obstruction?
depends on site (proximal vs distal) but:
pain
vomiting
distension
constipation
borborygmi (rumbling, gurgling noise)
118
what questions would you ask about abdominal pain?
- character: visceral, somatic, referred.
- site of pain.
- severity.
- systemic upset.
119
how is visceral pain transmitted?
- nociceptors in smooth muscle.
- afferent impulses run with sympathetic fibres accompanying segmental vessels (coeliac trunk, SMA, IMA).
- poorly localised.
120
describe transmission of somatic and referred pain
- receptors in parietal peritoneum or abdominal wall.
- afferent signals pass with segmental nerves (dermatomes).
- accurate localisation but can be referred.
121
what are the complications of peritonitis, ischaemia and obstruction?
fluid loss
sepsis
circulatory collapse
death
122
acute abdomen investigations
- ward tests: urine + bHCG (ectopic pregnancy).
- lab tests: FBC, U + Es, LFTs & amylase.
- radiology: plain, US, axial (CT) ?other.
- laparascopy vs laparotomy
123
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- restore circulating fluid volume (IV fluids).
- enhance tissue perfusion.
- enhance tissue oxygenation.
- treat sepsis.
- decompress gut.
- ensure adequate pain relief.
124
describe coeliac disease
- an autoimmune condition triggered by eating gluten.
125
what other autoimmune conditions are linked with coeliac disease?
- type 1 diabetes.
- thyroid disease.
- primary biliary cholangitis.
126
what is the pathophysiology of coeliac disease?
- autoantibodies are created in response to exposure to gluten.
- these autoantibodies target the epithelial cells of the small intestine, leading to inflammation.
- inflammation affects the small intestine, particularly the jejunum.
127
what antibodies are related to coeliacs?
- anti TTG,
- anti-EMA.
- anti-DGP.
128
what structural changes occur in the small intestine in coeliac disease?
- atrophy of intestinal villa, resulting in malabsorption.
- crypt hypertrophy.
129
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HLA-DQ2
HLA-DQ8
130
what are the symptoms and signs of coeliac disease?
- failure to thrive in young children.
- diarrhoea.
- bloating.
- fatigue.
- weight loss.
- mouth ulcers.
- dermatitis herpetiforms.
- anaemia.
131
what is dermatitis herpetiforms?
an itchy, blistering skin rash, typically on the abdomen, caused by coeliac disease.
132
why can coeliac disease cause anaemia?
occurs secondary to malabsorption and deficiency of iron, B12 or folate.
133
coeliac disease investigations?
first-line:
- total immunoglobulin A levels (to exclude IgA deficiency).
- anti-tissue transglutaminase antibodies (anti-TTG).
second-line:
- anti-endomysial antibodies (anti-EMA).
if + antibody test:
- endoscopy and jejunal biopsy showing crypt hyperplasia and villous atrophy.
134
complications of coeliac disease
- nutritional deficiencies.
- anaemia.
- osteoporosis.
- hyposplenism.
- ulcerative jejunitis.
- enteropathy-associated T-cell lymphoma (EATL).
- non-hodgkin lymhoma.
- small bowel adenocarcinoma.
- oesophageal carcinoma.
135
what is the treatment for dermatitis herpetiforms?
- gluten free diet.
- dapsone.
136
what are functional causes of vomiting?
pregnancy
migraine
alcohol
