GI

Question 1

what is the clinical presentation of GORD?

Answer 1

• heartburn
• belching
• food/acid brash (food, acid or bile regurgitation)
• water brash (increased salivation)
• odynophagia (painful swallowing)

Question 2

what is heartburn? what are some features of it?

Answer 2

• burning chest pain that is aggravated by bending, stooping and lying down which promotes acid exposure and may be relieved by antacids
• worse with hot drinks or alcohol
• seldom radiates to the arms

Question 3

what is odynophagia?

Answer 3

painful swallowing

Question 4

what are extra-oesophageal clinical presentations of GORD?

Answer 4

• nocturnal asthma
• chronic cough
• laryngitis (hoarseness and throat clearing)
• sinusitis

Question 5

what are differential diagnoses of GORD?

Answer 5

• ACS
• Stable angina
• peptic ulcer disease
• malignancy

Question 6

when can GORD be diagnosed without investigation?

Answer 6

• when there are no alarm bell signs, e.g. weight loss, haematemesis, dysphagia >55
• patients under 55 can safely be treated initially without investigation

Question 7

what is used to investigate and diagnose GORD?

Answer 7

• endoscopy

- barium swallow may show hiatus hernia

Question 8

what are the aims of investigations of GORD?

Answer 8

assess oesophagitis (inflammation of oesophagus) and hiatal hernia by endoscopy:
- if there is oesophagitis or Barrett’s oesophagus then reflux is confirmed

document reflux by intraluminal monitoring:

• 24hr oesophageal pH monitoring is helpful in diagnosing GORD when endoscopy is normal or just prior to surgery to confirm reflux
• also helpful if there is no response to proton-pump inhibitors

Question 9

what classification is used to assess GORD?

Answer 9

use Los Angeles classification of GORD/Oesophagitis when doing endoscopy to gauge extent of damage

Question 10

what lifestyle changes can be used to treat GORD?

Answer 10

• encourage weight loss
• smoking cessation
• small, regular meals
• avoid; hot drinks, alcohol, citrus fruits and eating less than 3 hours before bed

Question 11

what drugs are used to treat GORD? how do they work?

Answer 11

• antacids e.g. magnesium triscilicate mixture: relieves symptoms by forming a gel or ‘foam raft’ with gastric contents to reduce reflux, note: side effect of magnesium containing antacids is diarrhoea
• alginates e.g. gaviscon; relieves symptoms
• proton pump inhibitor (PPI) e.g. lanzoprazole to reduce gastric acid production
• H2 receptor antagonists e.g. cimetidine

Question 12

what surgery can be used to treat GORD? when is it used?

Answer 12

nissen fundoplication; aims to laparoscopically increase the resting LOS pressure

• only in severe GORD
• use when not responding to therapy
• complications include dysphagia and bloating

Question 13

what are complications of GORD?

Answer 13

peptic stricture and Barrett’s oesophagus

Question 14

what is peptic stricture? what is its clinical presentation and treatment?

Answer 14

• oesophagitis resulting from gastric (peptic) acid exposure resulting in the narrowing and stricture of the oesophagus
• usually occurs in patients over 60
• presents as gradually worsening dysphagia
• treat with endoscopic dilatation and long term PPI therapy

Question 15

what is barrett’s oesophagus? what is its clinical presentation?

Answer 15

• GORD may induce barrett’s oesophagus
• distal oesophageal epithelium undergoes metaplasia from squamous to columnar epithelium
• always a hiatus hernia present
• risk of progressing to oesophageal cancer; is premalignant for adenocarcinoma of the oesophagus

Question 16

what is a Mallory-Weiss tear? what is its epidemiology?

Answer 16

• this is a linear mucosal tear occurring at the oesophagogastric junction and is produced by a sudden increase in intra-abdominal pressure
• often follows a bout of coughing or retching and is classically seen after alcoholic ‘dry heaves’
• most common in males
• seen mainly in age 20-50

Question 17

what are risk factors for Mallory-Weiss tears?

Answer 17

• alcoholism
• forceful vomiting
• eating disorders
• male
• NSAID abuse

Question 18

what are clinical features of Mallory-Weiss tears?

Answer 18

• vomiting
• haematemesis after vomiting
• retching
• postural hypotension
• dizziness

Question 19

what are differential diagnoses of Mallory-Weiss tears?

Answer 19

• gastroenteritis
• peptic ulcer
• cancer
• oesophageal varices

Question 20

what is used to diagnose Mallory-Weiss tears?

Answer 20

endoscopy to confirm

Question 21

what is the treatment of Mallory-Weiss tears?

Answer 21

• most bleeds are minor and heal in 24 hours
• haemorrhage may be large but tends to stop spontaneously
• if surgery is required then it involves the oversewing of the tear but this is rarely needed

Question 22

what is dyspepsia?

Answer 22

one or more of the following:

• postprandial fullness
• early satiation
• epigastric pain or burning for more than 4 weeks

an inexact term used to describe a number of upper abdominal symptoms such as heartburn, acidity, epigastric pain or discomfort, fullness or belching

Question 23

what is the epidemiology of dyspepsia?

Answer 23

• dyspepsia is a common complaint affecting up to 25% of the population each year
• patients may say it’s indigestion

Question 24

what are causes of dyspepsia?

Answer 24

• disorders of the GI tract - the most common is functional dyspepsia that affects around 75% with no known cause
• other causes are peptic ulcers

Question 25

what is the clinical presentation of dyspepsia?

Answer 25

- reflux when lying flat - heartburn - acid taste due to reflux - bloating - indigestion

Question 26

what are red flag alarm symptoms in dyspepsia for cancer?

Answer 26

- unexplained weight loss - anaemia - evidence of GI bleeding e.g. melaena (dark tar like black stools) or haematemesis - dysphagia - upper abdominal mass - persistent vomiting

Question 27

what is the history/differentials of dyspepsia?

Answer 27

- heartburn/regurgitation/cough: possibly GORD - alarm symptoms or family history can be an indicator of possible malignancy - onset; acute vs. chronic - age; over 55 is a red flag and thus means increased risk of cancer - relationship to food

Question 28

what is the relationship to food of dyspepsia?

Answer 28

* early postprandial pain - could be due to gastritis, GORD or gastric carcinoma * postprandial pain could be due to a gastric ulcer * pain that is relieved by milk could also be a sign of gastric ulcer

Question 29

what is the management of dyspepsia?

Answer 29

- reassurance - dietary review - antidepressants e.g. SSRIs - look for Helicobacter pylori using faecal antigen testing or breath test - endoscopy

Question 30

what is the structure of the mucosal lining of the stomach?

Answer 30

- can stretch in size with feeding - the greater curvature of the undistended stomach has thick folds called rugae - the mucosa of the upper two thirds of the stomach contain: • parietal cells - secrete HCl • chief cells - produce pepsinogen and thus initiate proteolysis - the digestion of proteins • enterochromaffin-like (ECL) cells - releases histamine (stimulates acid release)

Question 31

what cells does the antral mucosa of the stomach contain?

Answer 31

* mucus secreting cells - secrete mucin (protects gastric mucosa) and bicarbonate * G cells - secrete gastrin which stimulates acid release * D cells - secrete somatostatin which suppresses acid secretion

Question 32

what is the mucosal barrier of the stomach? what is its structure and function?

Answer 32

- is made up of the plasma membranes of the mucosal cells and the mucus layer (made up of mucin), protects the gastric epithelium from damage by acid and, for example, alcohol, aspirin, NSAIDs and bile salts - prostaglandins stimulate the secretion of mucus and their synthesis is inhhibited by aspirin and NSAIDs, which inhibit cyclo-oxygenase

Question 33

what is the structure/function of the duodenal mucosa?

Answer 33

- has villi like the rest of the small bowel and also contains Brunner’s glands which secrete alkaline mucus - this, along with the pancreatic and biliary secretions, helps to neutralise the acid secretion from the stomach when it reaches the duodenum

Question 34

what is a peptic ulcer?

Answer 34

consists of a break in the superficial epithelial cells which penetrates down to the muscularis mucosa of either the stomach or the duodenum; there is a fibrous base and an increase in inflammatory cells

Question 35

where are duodenal and gastric peptic ulcers often seen?

Answer 35

- duodenal ulcers most commonly seen in duodenal cap | - gastric ulcers most commonly found on the lesser curve of the stomach but can be found anywhere in the stomach

Question 36

what is the epidemiology of peptic ulcer disease?

Answer 36

- duodenal ulcers affect around 10% of the adult population and are 2-3 times more common than gastric ulcers - more common in the elderly - more common in developing countries due to Helicobacter pylori - ulcers due to NSAID use is increasing - decline in incidence in men and increasing in women

Question 37

what are the main causes of peptic ulcer disease?

Answer 37

* Helicobacter pylori infection * drugs e.g. NSAIDs (including aspirin), steroids and SSRIs * increased gastric acid secretion (minor) * smoking (minor) * delayed gastric emptying * blood group O

Question 38

what is the pathophysiology of peptic ulcer disease?

Answer 38

- ulcers result in gastritis - usually the gastric mucosa is protected by a layer of mucin that is produced by gastric cells - NSAIDs e.g. naproxen and aspirin - Helicobacter pylori - ischaemia of the gastric cells - too much acid production - alcohol has a direct toxic effect on gastric cells in high concentrations

Question 39

how can NSAIDs lead to peptic ulcer disease?

Answer 39

e.g. naproxen and aspirin • mucous secretion is stimulated by prostaglandins (in inflamed tissue, prostaglandin triggers inflammatory response thus inhibition = less inflammation) • cyclo-oxygenase 1 is needed for prostaglandin synthesis • NSAIDs inhibit cylclo-oxygenase 1 • thus reduced mucosal defence

Question 40

how can Helicobacter pylori lead to peptic ulcer disease?

Answer 40

* highly adapted to the stomach environment and exclusively colonises gastric epithelium and inhabits the mucous layer/just beneath it * causes major destruction to the protective mucin layer * causes decrease in duodenal HCO3- thereby increasing the acidity of the stomach as there will be less alkali to buffer the acid * secretes urease, splitting urea into CO2 and ammonia * ammonia + H+ = ammonium * ammonium is toxic to gastric mucosa resulting in less mucous produced * secreted proteases, phospholipase and vacuolating cytotoxin A can then begin attacking the gastric epithelium further reducing mucous production * results in an inflammatory response and less mucosal defence * also increases gastrin release, causing more acid secretion from parietal cells and also triggering the release of histamine which further increases acid secretion * also increases parietal cell mass meaning more acid production * also decreases somatostatin release (which reduces acid secretion) resulting in increased acid release * increased acidity overwhelms the protective mucin layer resulting in mucosal damage and ulceration

Question 41

what are the overall effects of H. pylori?

Answer 41

- inflammation e.g. antral gastritis - gastric cancer - peptic ulcers

Question 42

how can ischaemia of the gastric cells lead to peptic ulcer disease?

Answer 42

* causes gastric cells to produce less mucin resulting in less protection from acid, meaning acid is able to damage mucosa and cause an ulcer * caused by low blood pressure or atherosclerosis

Question 43

how can too much acid production lead to peptic ulcer disease?

Answer 43

* too much acid overwhelms mucin and results in ulceration * stress can result in increased acid production * PPIs and H2 blockers used to treat this

Question 44

what is the clinical presentation of peptic ulcer disease?

Answer 44

- recurrent burning epigastric pain - nausea may accompany the pain - anorexia and weight loss, particularly with gastric ulcers

Question 45

what are features of recurrent burning epigastric pain in peptic ulcer pain?

Answer 45

* if patient points with a single finger to the epigastrium as the site of pain, then this is strongly suggestive of peptic ulcer disease * pain of duodenal ulcers classically occurs at night (as well as during the day) and is worse when the patient is hungry * pain in both gastric and duodenal ulcers can be relieved by antacids

Question 46

what are complications of peptic ulcers?

Answer 46

* in duodenal ulcers, the ulcer can get deeper and deeper until it hits an artery, most commonly the gastroduodenal artery, which can result in massive haemorrhage, presents as an emergency * can result in peritonitis as acid enters peritoneum; will see air under diaphragm on erect X-ray * can result in acute pancreatitis if the ulcer hits the pancreas

Question 47

what is the diagnosis of peptic ulcer disease?

Answer 47

- if patients is under 55 then carry out non-invasive testing e.g. serological test, breath test or stool antigen testing, if test is positive then start eradication immediately - usually an endoscopy is not necessary, but if found to have a gastric ulcer then re-scope 6-8 weeks later to ensure there is no malignancy - endoscopy is essential is all red flag patients and those who are over 55 - non-invasive H. pylori testing (serology, C-urea breath test, stool antigen test)

Question 48

how is serology used as a non-invasive H. pylori test for peptic ulcer disease?

Answer 48

detects IgG antibodies - not useful for confirming eradication or presence of current infection since IgG takes 1 year to fall by 50%

Question 49

how is a C-urea breath test used as a non-invasive H. pylori test for peptic ulcer disease?

Answer 49

- quick and reliable test for H.pylori - measures CO2 in breath after the ingestion of C-Urea - used to monitor infection after eradication - highly sensitive and specific - no antibiotics or proton-pump inhibitors (PPIs) before test

Question 50

how is a stool antigen used as a non-invasive H. pylori test for peptic ulcer disease?

Answer 50

- immunoassay using monoclonal antibodies for detection of H. pylori - monitors the efficacy of eradication therapy - patients should be off PPIs for 2 weeks before

Question 51

how is biopsy used as an invasive H. pylori test for peptic ulcer disease?

Answer 51

• histology - direct visualisation of H.pylori, reduced if on PPIs • biopsy urease test: - H. pylori produces urease - splits urea to release ammonia which will raise pH of the solution and causes a rapid colour change of yellow to red - no PPIs or antibiotics should be used before since this will give false negatives

Question 52

what is the treatment of peptic ulcer disease?

Answer 52

- lifestyle adjustments (reduce stress, avoid irritating foods, reduce smoking) - stop NSAIDs - H.pylori eradication (7-14 days) - H2 antagonists to reduce acid release - surgery if complications arise such as haemorrhage

Question 53

how is H. pylori eradication confirmed? how long does it take?

Answer 53

- 7-14 days | - confirmed by urea breath or faecal antigen test

Question 54

what is used for H. pylori eradication?

Answer 54

triple therapy - PPI for acid suppression e.g. lansoprazole or omeprazoel - plus 2 of: metronidazole, clarithromycin, amoxicillin, tetracycline, bismuth - note: amoxicillin and tetracycline have low resistance, and clarithromycin has high resistance - quinolones e.g. ciprofloxacin, furozolidone and rifabutin are used when standard regimens have failed as rescue therapy

Question 55

what is a varice?

Answer 55

dilated vein which is at risk of rupture resulting in haemorrhage and can result in GI bleeding

Question 56

what is the function of the hepatic portal vein?

Answer 56

* carries nutrient rich blood from the GI tract, gallbladder, pancreas and spleen to the liver * rich in nutrients that have been extracted from food and the liver processes these nutrients; it also filters toxins that may have been ingested alongside the food * the blood leaves the liver to the heart in the hepatic veins via the IVC

Question 57

what is the normal pressure of the hepatic portal vein?

Answer 57

5-8mmHg

Question 58

how is portal hypertension classified? what are the classifications?

Answer 58

according to the site of obstruction - pre-hepatic; blockage of the hepatic portal vein before the liver - intra-hepatic; distortion of the liver architecture, either pre-sinusoidal (e.g. schistosomiasis) or post-sinusoidal (e.g. cirrhosis) - post-hepatic; venous blockage outside the liver (rare)

Question 59

how are varices formed within the systemic venous system?

Answer 59

* as portal pressure rises above 10-12mmHg, the compliant venous system dilates and varices form within the systemic venous system * these can form at the gastro-oesophageal junction, rectum, left renal vein, diaphragm and the anterior abdominal wall via the umbilical vein * gastro-oesophageal varices are superficial and tend to rupture, resulting in GI bleeding, usually when pressure exceeds 12mmHg

Question 60

what is the epidemiology of gastro-oesophageal varices? where do they tend to develop?

Answer 60

- around 90% of patients with cirrhosis will develop gastro-oesophageal varices over 10 years, but only a third of these will bleed - bleeding is likely to occur with large varices, or those with red flag signs at endoscopy and in severe liver disease - varices tend to develop in the lower oesophagus and gastric cardia

Question 61

what are the main causes of gastro-oesophageal varices?

Answer 61

- alcohol and viral cirrhosis | - portal hypertension

Question 62

what are causes of pre-hepatic portal hypertension?

Answer 62

thrombosis in portal or splenic vein

Question 63

what are causes of intra-hepatic portal hypertension?

Answer 63

* cirrhosis (commonest cause in UK) * schistosomiasis (commonest cause worldwide) * sarcoid * congenital hepatic fibrosis

Question 64

what are causes of post-hepatic portal hypertension?

Answer 64

* Budd-Chiari syndrome (hepatic vein obstruction by tumour or thrombosis) * right heart failure * constrictive pericarditis

Question 65

what is Budd-Chiari syndrome?

Answer 65

hepatic vein obstruction by tumour or thrombosis | - causes post-hepatic portal hypertension

Question 66

what are risk factors for gastro-oesophageal varices?

Answer 66

- cirrhosis - portal hypertension - schistosomiasis infection - alcoholism

Question 67

what is the pathophysiology of gastro-oesophageal varices?

Answer 67

- following liver injury and fibrogenesis, the contraction of activated myofibroblasts (mediated by endothelin, nitric oxide and prostaglandins) contributes to increased resistance to blood flow - this leads to portal hypertension → splanchnic vasodilation → drop in BP → increased cardiac output to compensate for BP drop → salt and water retention to increase blood volume and compensation → hyperdynamic circulation → formation of collaterals between the portal and systemic systems → gastro-oesophageal varices develop once portal pressure is above 10mmHg - can occur rapidly and result in major haemorrhage

Question 68

what is the clinical presentation of a ruptured gastro-oesophageal varices?

Answer 68

* haematemesis * abdominal pain * shock - if major blood loss * fresh rectal bleeding - associated with shock in acute massive GI bleed * hypotension and tachycardia * pallor * suspect varices as the cause of GI bleeding if there is alcohol abuse or cirrhosis

Question 69

what is the clinical presentation of gastro-oesophageal varices?

Answer 69

- signs of rupture - signs of chronic liver damage e.g. jaundice, increased bruising and ascites - splenomegaly - ascites - hyponatraemia

Question 70

what is used to diagnose gastro-oesophageal varices?

Answer 70

endoscopy to find bleeding source

Question 71

what is the treatment of gastro-oesophageal varices?

Answer 71

- resuscitate until haemodynamically stable - if anaemic then do blood transfusion aiming to get Hb to 80g/L - correct clotting abnormalities with vitamin K and platelet transfusion - vasopressin e.g. IV terlipressin or somatostatin - prophylactic antibiotics - variceal banding - balloon tamponade to reduce bleeding - transjugular intrahepatic portoclaval shunt (TIPS); a shunt between the systemic and portal systems which reduces sinusoidal and portal vein pressure

Question 72

what is TIPS?

Answer 72

transjugular intrahepatic portoclaval shunt - artificial channel within the liver that establishes communication between the inflow portal vein and the outflow hepatic vein - uses endoscope - jugular vein is usual entry site - used to treat varices

Question 73

how can gastro-oesophageal varices be prevented?

Answer 73

* non-selective beta-blockade to reduce resting pulse rate to decrease portal pressure * variceal banding repeatedly * liver transplant

Question 74

what is the epidemiology of achalasia?

Answer 74

- characterised by oesophageal aperistalsis and impaired relaxation of the lower oesophageal sphincter - the lower oesophageal pressure is elevated in more than half of patients - incidence is 1 in 100,000 and is equal in both males and females - occurs at all ages but rare in childhood - patients usually have a long history of intermittent dysphagia characteristically for both liquids and solids from the onset - cause is unknown

Question 75

what is achalasia?

Answer 75

failure of smooth muscle fibres in the oesophagus to relax, which can cause the LOS to remain closed

Question 76

what is the pathophysiology of achalasia?

Answer 76

the LOS fails to relax due to degeneration of the | mesenteric plexus of the oesophagus, with reduction of ganglion cell numbers

Question 77

what is the clinical presentation of achalasia?

Answer 77

- dysphagia for fluids and solids - regurgitation of food particularly at night and aspiration pneumonia is a complication - substernal cramps - weight loss (usually minimal) - spontaneous chest pain occurs due to oesophageal ‘spasm’; may be misdiagnosed as cardiac pain

Question 78

how is achalasia diagnosed?

Answer 78

CXR • dilated oesophagus • may be fluid level behind/above the heart barium swallow • shows lack of peristalsis • lower end shows a ‘birds beak’ due to failure of sphincter to relax manometry • confirms diagnosis • shows aperistalsis of the oesophagus and failure of relaxation of the LOS CT and oesophagoscopy used to rule out carcinoma at the lower end of the oesophagus which can produce a similar x-ray appearance

Question 79

what is treatment of achalasia?

Answer 79

- relief of symptoms - medical treatment to relax the LOS e.g. nifepidine, nitrates or sildenafil - surgery

Question 80

what is the surgical treatment of achalasia?

Answer 80

* endoscopic balloon dilation to open sphincter * Heller’s cardiomyotomy - the surgical division of the lower oesophageal sphincter and then PPIs * botox injection into sphincter to relax it (effects wear off)

Question 81

what are complications of treatment of achalasia?

Answer 81

there is a slight increase in the incidence of squamous carcinoma of the oesophagus in both treated and untreated cases

Question 82

what is scleroderma?

Answer 82

- group of autoimmune disease that may result in changes to skin, blood vessels, muscles, and internal organs - increased synthesis of collagen, damage to small blood vessels, activation of T lymphocytes and production of altered connective tissues - multi-system disease

Question 83

what is the epidemiology of scleroderma/systemic sclerosis?

Answer 83

- more common in females than males - peak incidence is between 30 and 50 - rare in children - there is oesophageal involvement in almost all patients with this disease

Question 84

what are risk factors for scleroderma/systemic sclerosis?

Answer 84

- vinyl chloride | - silica dust

Question 85

what is the pathophysiology of scleroderma/systemic sclerosis?

Answer 85

- diminished peristalsis and oesophageal clearance due to the replacement of the smooth muscle by fibrous tissue - LOS pressure is decreased thereby allowing GORD with consequent mucosal damage - strictures may develop

Question 86

what is the clinical presentation of scleroderma/systemic sclerosis?

Answer 86

- initially there are no symptoms - dysphagia and heartburn occur as the oesophagus becomes more severely involved

Question 87

how is scleroderma/systemic sclerosis diagnosed?

Answer 87

- barium swallow - CXR - manometry

Question 88

what is the treatment of scleroderma/systemic sclerosis?

Answer 88

same as for GORD. e.g. PPIs

Question 89

what is gastritis? what does gastropathy indicate?

Answer 89

- inflammation of the lining of the stomach - may occur as a short episode or have long duration - inflammation that is associated with mucosal injury - gastropathy indicates epithelial cell damage and regeneration without inflammation; commonest cause is mucosal damage associated with aspirin/NSAIDs

Question 90

what are causes of gastritis?

Answer 90

- Helicobacter pylori infection - autoimmune gastritis - viruses e.g. cytomegalovirus and herpes simplex - duodenogastric reflux, where bile salts enter stomach and damage mucin protection, resulting in gastritis - specific causes e.g. Crohn’s (more common in children than adults) - mucosal ischaemia; reduced blood supply to mucosal cells can mean less mucin produced so acid can induce gastritis - increased acid; can overwhelm mucin resulting in gastritis, stress can increase acid production - aspirin and NSAIDs - alcohol

Question 91

what is the pathophysiology of gastritis caused by H. pylori?

Answer 91

* most common cause * causes severe inflammatory response * gastric mucus degradation and increased mucosal permeability, which is directly cytotoxic to the gastric epithelium

Question 92

what is the pathophysiology of autoimmune gastritis?

Answer 92

affects the fundus and body of the stomach leading to | atrophic gastritis and loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia

Question 93

what is the pathophysiology of gastritis caused by aspirin and NSAIDs?

Answer 93

NSAIDs will inhibit prostaglandins (which stimulate mucus production) via the inhibition of cyclo-oxygenase resulting in less mucus production and thus gastritis

Question 94

what is the clinical presentation of gastritis?

Answer 94

- nausea or recurrent upset stomach - abdominal bloating - epigastric pain - vomiting - indigestion - haematemesis

Question 95

what are differential diagnoses of gastritis?

Answer 95

- peptic ulcer disease (PUD) - GORD - non-ulcer dyspepsia - gastric lymphoma - gastric carcinoma

Question 96

how is gastritis diagnosed?

Answer 96

- endoscopy - biopsy - H.pylori urea breath test - H.pylori stool antigen test

Question 97

what is the treatment of gastritis?

Answer 97

- remove causative agents - reduce stress - H. pylori eradication (7-14 days) - H2 antagonists and PPIs to reduce acid release - antacids

Question 98

what is malabsorption?

Answer 98

the failure to fully absorb nutrients due to the destruction of epithelium or due to a problem in the lumen meaning food cannot be digested

Question 99

what are disorders of the small intestine that result in malabsorption?

Answer 99

- coeliac disease - tropical sprue - Crohn’s - parasite infection

Question 100

what are causes of malabsorption?

Answer 100

- defective intraluminal digestion - insufficient absorptive area - lack of digestive enzymes - defective epithelial transport - lymphatic obstruction

Question 101

how can defective intraluminal digestion cause malabsorption?

Answer 101

- pancreatic insufficiency - defective bile secretion - bacterial overgrowth

Question 102

how can pancreatic insufficiency cause defective intraluminal digestion causing malabsorption?

Answer 102

- pancreas produce majority of digestive enzymes such as amylase - pancreatitis causes damage to most of the glandular pancreas meaning less or no enzymes are released - cystic fibrosis results in the blockage of the pancreatic duct due to excess mucus, meaning enzymes are not released

Question 103

how can defective bile secretion cause defective intraluminal digestion which causes malabsorption?

Answer 103

- lack of fat solubilisation - biliary obstruction - ileal resection (bile salts are reabsorbed in the terminal ileum so if removed then bile salt reuptake will be decreased)

Question 104

how can insufficient absorptive area cause malabsorption?

Answer 104

* essentially anything that damages microvilli and villi thereby reducing absorptive surface area and thus absorption potential * Coeliac disease * Crohn’s * giardia lamblia * surgery for small bowel infarction

Question 105

how can giardia lamblia cause insufficient absorptive area which causes malabsorption?

Answer 105

- extensive surface parasitisation of the villi and microvilli - parasites coat the surface of the villi thus food cannot be absorbed

Question 106

how can lack of digestive enzymes cause malabsorption?

Answer 106

* disaccharidase deficiency (lactose intolerance) - cannot break down the lactose in milk into glucose which can then be absorbed. the undigested lactose passes into the colon where it is then eaten up by bacteria and CO2 is released leading to wind and diarrhoea * bacterial overgrowth resulting in brush border damage

Question 107

how can defective epithelial transport cause malabsorption?

Answer 107

* abetalipoproteinaemia - lack of transporter protein to transport lipoprotein across cell * primary bile acid malabsorption - mutations in bile acid transporter protein

Question 108

how can lymphatic obstruction cause malabsorption?

Answer 108

- lymphoma | - TB

Question 109

what is Coeliac disease?

Answer 109

• condition in where there is inflammation of the mucosa of the upper small bowel that improves when gluten is withdrawn from the diet and relapses when gluten is reintroduced • T-cell mediated autoimmune disease of the small bowel in which prolamin (alcohol-soluble proteins in wheat, barley, rye and oats) intolerance causes villous atrophy and malabsorption

Question 110

what are types of prolamins?

Answer 110

gliadin in wheat, hordeins in barley and secalins in rye

Question 111

what is the epidemiology of Coeliac disease?

Answer 111

- around 1% of population affected - occurs at any age but peaks in infancy and 50-60yrs - affects males and females equally - 10% risk in 1st degree relatives and 30% risk in siblings

Question 112

what are risk factors for Coeliac disease?

Answer 112

- other autoimmune diseases: type 1 diabetes, thyroid disease, Sjorgrens - IgA deficiency - breast feeding - age of introduction to gluten into diet - rotavirus infection in infancy increases risk

Question 113

what is the pathophysiology of Coeliac disease?

Answer 113

- in wheat and in gluten the prolamin a-gliadin is toxic and resistant to digestion by pepsin and chymotrypsin because of their high glutamine and proline content, and it remains in the intestinal lumen thereby triggering immune responses - the gliadin peptides pass through the epithelium and are deaminated by tissue transglutaminase, which increases their immunogenicity - the gliadin peptides bind to antigen-presenting cells which interact with CD4+ T cells in the lamina propria via HLA class II DQ2 or DQ8 - these two HLA class II molecules DQ2 (95%) or DQ8 (5%) activate the gluten-sensitive T cells - these T cells produce pro-inflammatory cytokines and initiate an inflammatory cascade - the cascade releases metalloproteinkinases and other mediators, which contribute to the villous atrophy, crypt hyperplasia and intraepithelial lymphocytes that are typical of the disease and result in malabsorption - proximal small bowel mucosa is predominantly affected - this mucosal damage means that B12, folate and iron cannot be absorbed resulting in anaemia - mucosal damage decreases in severity towards the ileum as gluten is digested into small ‘non-toxic’ fragments

Question 114

what HLA molecules contribute to Coeliac disease?

Answer 114

- HLA class II molecules DQ2 or DQ8 - these two HLA class II molecules DQ2 (95%) or DQ8 (5%) activate the gluten-sensitive T cells - these T cells produce pro-inflammatory cytokines and initiate an inflammatory cascade

Question 115

what is the clinical presentation of Coeliac disease?

Answer 115

- 1/3 are asymptomatic and only detected on routine blood tests (raised MCV) - stinking stools/fatty stools (steatorrhoea) - diarrhoea - abdominal pain - bloating - nausea and vomiting - angular stomatitis - weight loss - fatigue - anaemia - osteomalacia; softening of bones due to impaired bone metabolism due to lack of phosphate, calcium and vitamin D leading to osteoporosis (40-60% risk in untreated patients leading to fracture risk) - dermatitis hepetiformis; red raised patches, often with blisters that burst on scratching, commonly seen on elbows, knees and buttocks

Question 116

what is dermatitis hepetiformis?

Answer 116

- chronic autoimmune blistering skin condition - characterised by blisters filled with watery fluid - itchy - cutaneous manifestation of Coeliac disease - red raised patches - commonly seen on elbows, knees and buttocks

Question 117

how can Coeliac be diagnosed?

Answer 117

- should maintain gluten for at least 6 weeks before testing to get true results - duodenal biopsy is gold standard for diagnosis - serum antibody testing

Question 118

what is seen on an FBC in Coeliac disease?

Answer 118

- low Hb - low B12 - low ferritin

Question 119

what is seen on a duodenal biopsy in Coeliac disease?

Answer 119

* see villous atrophy, crypt hyperplasia and increased intraepithelial WCC * all reverse on gluten free diet

Question 120

what are indications for serum antibody testing to detect Coeliac disease?

Answer 120

- persistent diarrhoea - folate or iron deficiency - family history of Coeliac disease or associated autoimmune disease

Question 121

what is serum antibody testing for Coeliac disease?

Answer 121

- 95% sensitive unless patient is IgA deficient - endomysial antibody (EMA) - tissue transglutaminase antibody (tTG) - both are IgA antibodies - these correlate with the severity of mucosal damage and can thus be used for dietary monitoring

Question 122

what is the treatment of Coeliac disease?

Answer 122

- lifelong gluten free diet; use serum antibody testing for monitoring - correction of vitamin and mineral deficiencies e.g. B12, folate, iron, calcium and vitamin D - DEXA scan to monitor osteoporotic risk

Question 123

what are features of lifelong gluten free diets used to treat Coeliac disease?

Answer 123

* eliminate wheat, barley and rye; see results in days/weeks * poor compliance is main reason for recurrent issues * oats usually tolerated unless contaminated with flour during production * meat, dairy product, fruits and vegetables are all gluten-free

Question 124

what are complications of treatment of Coeliac disease?

Answer 124

* a few patients do not improve on a strict diet and are said to have non-responsive coeliac disease * anaemia * secondary lactose intolerance * T-cell lymphoma * increased risk of malignancy (gastric, oesophageal, bladder, breast and brain) due to increased cell turnover * osteoporosis

Question 125

what is tropical sprue?

Answer 125

- malabsorption disease commonly found in tropical regions, marked with abnormal flattening of the villi and inflammation of the lining of the small intestine - severe malabsorption of two or more substances accompanied by diarrhoea and malnutrition

Question 126

what is the epidemiology of tropical sprue?

Answer 126

- the term tropical sprue is reserved for severe malabsorption (of two or more substances) accompanied by diarrhoea and malnutrition - occurs in residents or visitors to tropical areas where the disease is endemic; most of Asia, some Caribbean islands, Puerto Rico and parts of South America - cause is unknown but is likely to be infective because the disease occurs in epidemics and patients improve on antibiotics

Question 127

what is the pathophysiology of tropical sprue?

Answer 127

- villous atrophy with malabsorption - onset is acute and occurs either a few days or many years after being in the tropics - epidemics can break out in villages, affecting thousands of people at the same time

Question 128

what is the clinical presentation of tropical sprue?

Answer 128

- diarrhoea - anorexia - severe malabsorption - weight loss - abdominal distension - the onset can also be insidious with chronic diarrhoea and evidence of nutritional deficiency

Question 129

how is tropical sprue diagnosed? how is it different from Coeliac disease?

Answer 129

- exclude acute infective causes of diarrhoea e.g. Giardia intestinalis, which can produce similar symptoms - bloods: anaemia due to malabsorption of B12, folate and iron - jejunal biopsy: jejunal mucosa is abnormal showing partial villous atrophy

Question 130

what is the treatment/prognosis of tropical sprue?

Answer 130

- leave area - folic acid daily and antibiotics for up to 6 months - severe cases require resuscitation with fluids and electrolytes for dehydration and nutritional deficiencies should be corrected and B12 given - excellent prognosis - mortality is only associated with water and electrolyte depletion particularly in epidemics

Question 131

what are the two forms of inflammatory bowel disease?

Answer 131

both autoimmune conditions: - ulcerative colitis (UC), which affects only the colon - crohn’s disease (CD), can affect any part of the GI tract (mouth to anus)

Question 132

what is the epidemiology of inflammatory bowel disease?

Answer 132

jewish people are more prone to IBD than any other ethnic group

Question 133

when does IBD occur?

Answer 133

IBD occurs when the mucosal immune system exerts an inappropriate response to luminal antigens, such as bacteria, which may enter the mucosa via a leaky epithelium

Question 134

what is ulcerative colitis? what areas can it affect?

Answer 134

• relapsing and remitting inflammatory disorder of the colonic mucosa • it may affect just the rectum; proctitis (50%) • it may affect the rectum and left colon; left-sided colitis (30%) • it may affect the entire colon (entire large bowel) up to the ileocaecal valve; pancolitis/extensive colitis • it never affects proximal to the ileocaecal valve

Question 135

what is the epidemiology of ulcerative colitis?

Answer 135

- highest incidence and prevalence in Northern Europe, UK and North America - higher incidence than Crohn’s per year - affects males and females equally - presentation mostly at 15-30 years - is 3 times more common in non/ex-smokers; symptoms may relapse on cessation - cause is unknown - 1 in 6 will have a first degree relative with UC - an appendicectomy appears to be protective against the development of UC, especially if performed for appendicitis before 20yrs. It also leads to a lower incidence of colectomy and reduced need for immunosuppressive therapy

Question 136

what are risk factors for UC?

Answer 136

- family history - NSAIDs - chronic stress and depression triggers flares

Question 137

what is the macroscopic pathophysiology of UC?

Answer 137

* affects only the colon up to the ileocaecal valve * begins in the rectum and extends * circumferential and continuous inflammation - no skip lesions * mucosa looks reddened and inflamed and bleeds easily (friability) * ulcers and pseudo-polyps (regenerating mucosa) in severe disease

Question 138

what is the microscopic pathophysiology of UC?

Answer 138

* mucosal inflammation; inflammation does not go deeper e.g. transmural * no granulomata (rare) * depleted goblet cells * increased crypt abscesses

Question 139

what is the clinical presentation of UC?

Answer 139

- remissions and exacerbations - restricted pain usually in lower left quadrant - episodic or chronic diarrhoea with blood and mucus - cramps - bowel frequency linked to severity - in acute UC there may be fever, tachycardia and tender distended abdomen - in acute attack patients have bloody diarrhoea (passing 10-20 liquid stools per day), diarrhoea also occurs at night, with urgency and incontinence that is severely disabling - extraintestinal signs; clubbing, aphthous oral ulcers, erythema nodusum and amyloidosis

Question 140

what are extraintestinal signs of UC?

Answer 140

- clubbing - aphthous oral ulcers - erythema nododum - amyloidosis

Question 141

what are complications of UC in the liver?

Answer 141

- fatty change - chronic pericholangitis - sclerosing cholangitis

Question 142

what are complications of UC in the colon?

Answer 142

- blood loss - perforation - toxic dilatation - colorectal cancer

Question 143

what are complications of UC in the skin?

Answer 143

- erythema nodosum | - pyoderma gangrenosum

Question 144

what are complications of UC in the joints?

Answer 144

- ankylosing spondylitis | - arthritis

Question 145

what are complications of UC in the eyes?

Answer 145

- iritis - uveitis - episcleritis

Question 146

how can UC be diagnosed?

Answer 146

- blood tests - stool samples to exclude C. diff and Campylobacter etc - faecal calprotectin; indicates IBD but not specific - colonoscopy with mucosal biopsy - abdominal X-ray

Question 147

what is seen on blood tests in UC?

Answer 147

* WCC and platelets raised in moderate/severe attacks * iron deficiency anaemia * ESR and CRP raised * liver biochemistry may be abnormal * hypoalbuminaemia is severe disease * pANCA may be positive (in Crohn's it's negative)

Question 148

how can colonscopy be used to diagnose UC?

Answer 148

* gold standard for diagnosis * allows for assessment of disease activity and extent * can see inflammatory infiltrate, goblet cell depletion, crypt abscesses and mucosal ulcers

Question 149

what is seen on an abdominal X-ray in UC?

Answer 149

* done in all patients suffering acute severe attacks to exclude colonic dilatation * useful when UC too severe for colonoscopy

Question 150

what is the treatment of UC?

Answer 150

- aim is to induce remission - aminosalicylate which acts topically in the colonic lumen - the active component of these drugs is 5-aminosalicylic acid (5-ASA) which is absorbed in the small intestine - the aminosalicylate preparations are designed to deliver the active 5-ASA to the colon by binding to something else - commonly prescribed 5-ASA aminosalicylates are sulfalazine, mesalazine or olsalazine

Question 151

what are the commonly prescribed 5-ASAs in UC?

Answer 151

- sulfalazine - mesalazine - olsalazine

Question 152

what is treatment of mild/moderate UC?

Answer 152

* oral 5-ASA; first line for left sided/extensive * rectal 5-ASA for proctitis * glucocorticoid if no response to 5-ASA

Question 153

what is treatment of severe UC?

Answer 153

glucocorticoids

Question 154

what is treatment of severe UC with systemic features e.g. liver, skin, eye involvement?

Answer 154

- hydrocortisone - ciclosporin - infliximab

Question 155

what is treatment to maintain remission of UC?

Answer 155

* 5-ASA | * azathioprine, for patients who relapse despite 5-ASA treatment or are ASA intolerant

Question 156

when is surgery used to treat UC? what type is used?

Answer 156

• indicated for severe colitis that fails to respond to treatment • colectomy with ileoanal anastomosis: - whole colon removed and rectum fused to ileum - terminal ileum is used to form a reservoir ‘pouch’ to store faeces and patients remain continent • panproctocolectomy with ileostomy: - whole colon and rectum are removed and the ileum brought out on to the abdominal wall as a stoma

Question 157

what is Crohn's disease? how does it differ from UC?

Answer 157

* a chronic inflammatory GI disease characterised by transmural (goes deep into mucosa) granulomatous inflammation affecting any part of the gut from mouth to anus (especially in the terminal colon and the proximal colon) * unlike in UC, there is unaffected bowel between areas of active disease; these are skip lesions

Question 158

what are skip lesions?

Answer 158

- occur in Crohn's disease and not in UC | - unaffected bowel between areas of active disease

Question 159

what is the epidemiology of Crohn's disease?

Answer 159

- highest incidence and prevalence in Northern Europe, UK and North America - lower incidence than UC per year - prevalence is less if asian - affects females more than males - cause is unknown - smoking increases risk by 3-4 x - 1 in 5 patients with Crohn's have a first-degree relative with the disease - presentation mostly at 20-40 yrs

Question 160

what are risk factors for Crohn's disease?

Answer 160

- genetic association is stronger in CD than in UC: • mutations on NOD2 (CARD 15) gene on chromosome 16 increases risk - smoking - NSAIDs may exacerbate disease - family history - chronic stress and depression triggers flares - good hygiene - those who live in poor hygiene families have a lower risk of developing CD - appendicectomy may increase the risk of CD development

Question 161

what is a genetic risk factor for Crohn's disease?

Answer 161

mutations on NOD2 (CARD 15) gene on chromosome 16 increases risk

Question 162

what is the pathophysiology of Crohn's disease?

Answer 162

- transmural granulomatous inflammation affecting any part of gut from mouth to anus - in particular the terminal ileum and proximal colon is affected

Question 163

what is the macroscopic pathophysiology of Crohn's disease?

Answer 163

• not continuous i.e. there are skip lesions/patchy areas where there is a gap between affected and unaffected mucosa • involved bowel is usually thickened and is often narrowed • cobblestone appearance due to ulcers and fissures in mucosa • affects any part of GI tract

Question 164

what is the microscopic pathophysiology of Crohn's disease?

Answer 164

* inflammation extends through all layers of the bowel * increase in chronic inflammatory cells and there is lymphoid hyperplasia * granulomas present in 50-60% - these are non-caseating epithelioid cell aggregates with Langerhans’s giant cells * goblet cells are present * less crypt abscesses than UC

Question 165

what is the clinical presentation of Crohn's disease?

Answer 165

- diarrhoea with urgency (need to go 5-6 times in 45 mins), bleeding and pain due to deification - abdominal pain can present as an emergency with acute right iliac fossa pain mimicking appendicitis - weight loss - malaise - lethargy - anorexia - abdominal tenderness/mass - perianal abscess - anal strictures - extraintestinal signs; aphthous oral ulcerations, clubbing, skin, joint and eye problems

Question 166

what are extraintestinal signs of Crohn's disease?

Answer 166

- aphthous oral ulcerations - clubbing - skin - joint and eye problems

Question 167

what are complications of Crohn's disease?

Answer 167

* perforation and bleeding are major * fistula formation * anal; skin tags, fissure, fistula (between loops of bowel) * malabsorption * small bowel obstruction as grossly dilated * toxic dilatation of colon * colorectal cancer * venous thrombosis * amyloidosis

Question 168

what are differential diagnoses of Crohn's disease?

Answer 168

- alternative causes of diarrhoea should be excluded e.g. Salmonella spp, Giardia intestinalis and rotavirus - chronic diarrhoea

Question 169

how can Crohn's be diagnosed by examination?

Answer 169

* tenderness of right iliac fossa | * anal examination

Question 170

what is seen in bloods in Crohn's disease?

Answer 170

* anaemia is common due to malabsorption and thus deficiency of iron and folate * however, despite terminal ileal involvement, B12 anaemia is not unusual * raised ESR and CRP * raised white cell count and platelets * hypoalbuminaemia present in severe disease as part of an acute phase response to inflammation associated with a raised CRP * liver biochemistry may be abnormal * negative pANCA

Question 171

how is colonoscopy used to diagnose Crohn's disease?

Answer 171

biopsy to confirm; will see skip lesions and granulomatous transmural inflammation

Question 172

how is Crohn's disease diagnosed?

Answer 172

- examination - bloods - stool sample to exclude C.difficile and Campylobacter - faecal calprotectin; indicates IBD but not specific - colonoscopy: biopsy to confirm will see spot lesions and granulomatous transmural inflammation - upper GI endoscopy: to exclude oesophageal and gastroduodenal disease

Question 173

what is treatment of Crohn's disease?

Answer 173

- smoking cessation | - anaemia due to iron, B12 or folate should be treated with replacement

Question 174

what is the treatment of mild attacks in Crohn's disease?

Answer 174

controlled release corticosteroids e.g. budesonide

Question 175

what is treatment of moderate to severe attacks in Crohn's disease?

Answer 175

glucocorticoids; reduce dose every 2-4 weeks if symptoms resolve

Question 176

what is treatment of severe attacks in Crohn's disease?

Answer 176

* IV hydrocortisone * treat rectal disease using hydrocortisone per rectum * antibiotics e.g. IV metronidazole for perianal disease (inflammation at or near the anus) and abscesses * if there is improvement then transfer to oral prednisolone

Question 177

what is the treatment of severe attacks in Crohn's disease if there is no improvement?

Answer 177

if no improvement then switch to anti-TNF antibodies e.g. infliximab or adalimumab: - can reduce disease activity by countering neutrophil accumulation and granuloma formation, and activating complement - also causes cytotoxicity to CD4+ T cells thereby clearing cells which drive the immune response

Question 178

what is treatment of Crohn's disease to maintain remission?

Answer 178

* azathioprine - side effects; bone marrow suppression, acute pancreatitis and allergic reactions * methotrexate if intolerant of azathioprine * anti-TNF antibodies to induce remission if resistant to corticosteroids, immunosuppression then maintains it e.g. infliximab or adalimumab

Question 179

how is surgery used to treat Crohn's disease?

Answer 179

* 80% require surgery at some point * avoided and only minimal resection * indicated in medical therapy failure, failure to thrive (in children) and perianal sepsis * temporary ileostomy to allow time for affected areas to rest * resection at worst areas, but can result in short bowel syndrome (leading to diarrhoea and malabsorption)

Question 180

what areas are affected in Coeliac disease, UC and Crohn's disease?

Answer 180

- Coeliac: duodenum - UC: colon; starts at rectum and goes up, stops at ileocaecal valve - Crohn's: whole GI tract: mouth to anus, affects other places more often than UC

Question 181

what are histological features of Coeliac, UC and Crohn's?

Answer 181

- Coeliac: jejunal biopsy via endoscopy; flattened villi and deeper crypts - UC: no skip lesions, circumferential and continuous inflammation, not transmural - Crohn's: cobblestoning of mucosa, skip lesions, scattered inflammation, transmural

Question 182

what is the definition of intestinal obstruction?

Answer 182

arrest/blockage of onward propulsion of intestinal contents

Question 183

how is intestinal obstruction classified?

Answer 183

- according to site - extent of luminal obstruction (partial or complete) - according to mechanism (mechanical, true or functional) - according to pathology

Question 184

how can intestinal obstruction be classified according to pathology?

Answer 184

* simple * closed loop * strangulation * intussusception

Question 185

what can cause lumen obstruction which can lead to intestinal obstruction?

Answer 185

* tumour: carcinoma or lymphoma * diaphragm disease * meconium ileus - in neonates, content of bowel is sticky = blockage * gallstone ileus; gallstone within lumen of small bowel

Question 186

what inflammatory diseases can cause intestinal obstruction?

Answer 186

- Crohn's disease | - diverticulitis

Question 187

what is diverticulitis? how can it cause intestinal obstruction?

Answer 187

* usually occurs in the sigmoid colon * diverticula forms at gaps in the wall of the gut where blood vessels penetrate * in a low fibre diet, the colon must push harder to move things along (fibre helps gut motility) so pressure increases * this pressure increases, pushes the mucosa through the gaps which results in a diverticula or outpouching * this can get inflamed or burst resulting in acute peritonitis and possible death

Question 188

what is Hirschprung's disease? how can it cause intestinal obstruction?

Answer 188

- birth defect in which nerves are missing from parts of the intestine • neonates are born without complete innervation of colon to rectum • results in gut dilatation and the filling of faeces which remains since there are no ganglion cells to result in peristalsis and movement of contents; results in obstruction

Question 189

what are adhesions? how can they cause intestinal obstruction?

Answer 189

- sticking together of abdominal structures to one another, bowel loops, omentum, other solid organs or the abdominal wall by fibrous tissue - commonly occurs after surgery - in the intestines, the loops of the small and large intestines can normally move around freely within the abdominal cavity - when adhesions form, the intestines are no longer able to move around freely because they become tethered to each other, the abdominal wall or to other abdominal organs - at the sites where the adhesions occur, the intestine can twist on itself, resulting in the obstruction of blood supply or the normal movement of the contents of the intestines, the small intestine in particular

Question 190

what is the most common cause of intestinal obstruction?

Answer 190

adhesions (80%)

Question 191

what is volvulus? how can it cause intestinal obstruction?

Answer 191

- a twist/rotation of segment of bowel which is on a long mesentery can twist on itself, resulting in obstruction - always occurs at the part of bowel with a mesentery - type of closed loop bowel obstruction

Question 192

what are features of intestinal obstruction?

Answer 192

* most intestinal obstruction is due to a mechanical block * intestinal obstruction is one of the most common causes of hospital admission * tinkling bowel sounds and tympanic percussion is typical of obstruction

Question 193

what are causes of small bowel obstruction?

Answer 193

- accounts for 60-75% of intestinal obstruction - majority is caused by previous surgery (60%) - Crohn’s disease is also a significant cause (25%)

Question 194

what are the main causes of small bowel obstruction?

Answer 194

• adhesions (60%): - usually secondary to previous abdominal surgery - increased incidence in; pelvic, gynaecology and colorectal surgery • hernia: - abnormal protrusion of an organ or tissue out of the body cavity in which it normally lies - particularly in the developing world - untreated can result in strangulation • malignancy • Crohn’s disease

Question 195

what is the pathophysiology of small bowel obstruction?

Answer 195

- mechanical obstruction is most common e.g. adhesions, hernia and Crohn’s - obstruction of the bowel leads to bowel distension above the block with increased secretion of fluid into the distended bowel - also leads to proximal dilatation above the block

Question 196

what does proximal dilatation caused by small bowel obstruction lead to?

Answer 196

* increased secretions and swallowed air in the small bowel * more dilatation results decreased absorption and mucosal wall oedema * increased pressure with the intramural vessels becoming compressed resulting in ischaemia and or perforation

Question 197

what can untreated small bowel obstruction lead to?

Answer 197

* ischaemia * necrosis * perforation

Question 198

what is the clinical presentation of small bowel obstruction?

Answer 198

- pain; initially colicky (starts and stops abruptly) then diffuse, pain is higher in the abdomen than in LBO - profuse vomiting that follows pain; vomiting occurs earlier in SBO compared to LBO - less distension compared to LBO (since the more distal the obstruction, the greater the distension) - nausea and anorexia - tenderness suggests strangulation and urgent surgery is required - constipation with no passage of wind occurs late in SBO - increased bowel sounds

Question 199

how is small bowel obstruction diagnosed?

Answer 199

- abdominal X-ray: • shows central gas shadows that completely cross the lumen and no gas in the large bowel • distended loops of bowel proximal to obstruction • fluid levels seen - examination of hernia orifices and rectum - FBC - CT: gold standard to localise lesion accurately

Question 200

what is the treatment of small bowel obstruction?

Answer 200

- aggressive fluid resuscitation - bowel decompression - analgesia and antiemetics - antibiotics - surgery to remove obstruction done by laparotomy

Question 201

what is the epidemiology of large bowel obstruction?

Answer 201

less common, accounting for only 25% of all intestinal obstruction

Question 202

why does presentation of LBO differ from SBO?

Answer 202

* large bowel has a larger lumen as well as circular and longitudinal muscles thus the ability of the large bowel to distend is much greater thus symptoms present slower and later than in SBO * about 5 days of symptoms

Question 203

what are the main causes of large bowel obstruction?

Answer 203

* 90% due to colorectal malignancy in US/Europe | * in African countries the cause is more likely to be volvulus

Question 204

what is the pathophysiology of large bowel obstruction?

Answer 204

- the colon dilates proximal to the obstruction - there is increased colonic pressure and decreased mesenteric blood flow resulting in mucosal oedema; transudation of fluid and electrolytes from the lumen - this can compromise the arterial blood supply and also cause mucosal ulceration resulting in full thickness necrosis as well as perforation - bacterial translocation can also occur resulting in sepsis

Question 205

what is the pathophysiology of large bowel obstruction in colonic volvulus?

Answer 205

* there is axis rotation off of mesentery and a 360 degree twist results in a closed loop obstruction * fluid and electrolytes shift into the closed loop * this results in increased pressure and tension in the loop causing impaired colonic blood flow * ischaemia, necrosis and perforation of the loop of the bowel soon follows if untreated

Question 206

what is the clinical presentation of large bowel obstruction?

Answer 206

- abdominal pain that is more constant than in SBO - abdominal distension - bowel sounds normal then increased then quiet later - palpable mass e.g. hernia, distended bowel loop or caecum - late vomiting which is more faecal like; suggestive of LBO - vomiting may be absent - constipation - fullness/bloating/nausea

Question 207

how is large bowel obstruction diagnosed?

Answer 207

- digital rectal exam - FBC essential: see low Hb as a sign of chronic occult blood loss - abdominal X-ray - CT

Question 208

what is seen on a digital rectal exam in large bowel obstruction?

Answer 208

empty rectum, hard stools, blood

Question 209

what is seen on an abdominal X-ray in large bowel obstruction?

Answer 209

* peripheral gas shadows proximal to the blockage e.g. in caecum but not in the rectum, unless PR examination done (this is always essential) * caecum and ascending colon distended

Question 210

what is the treatment of large bowel obstruction?

Answer 210

- aggressive fluid resuscitation - bowel decompression - analgesia and antiemetics - antibiotics - surgery to remove obstruction is done by laparotomy • obstruction due to malignancy requires colorectal stents followed by elective surgery

Question 211

what is pseudo-obstruction?

Answer 211

clinical picture mimicking obstruction but with no mechanical cause

Question 212

what conditions can cause pseudo-obstruction?

Answer 212

* intra-abdominal trauma * pelvic, spinal and femoral fractures * postoperative states e.g. abdominal, pelvic, cardiothoracic, orthopaedic and neuro * intra-abdominal sepsis * pneumonia * drugs e.g. opiates, antidepressants * metabolic disorders e.g. electrolyte disturbances, malnutrition, diabetes mellitus and Parkinson’s disease

Question 213

what is the clinical presentation of pseudo-obstruction?

Answer 213

patients present with rapid and progressive abdominal distension and pain

Question 214

how is pseudo-obstruction diagnosed?

Answer 214

X-ray shows a gas-filled large bowel

Question 215

what is the treatment of pseudo-obstruction?

Answer 215

- treat underlying problem e.g. withdrawal of opiate analgesia - IV neostigmine

Question 216

what are the 3 main types of bowel ischaemia?

Answer 216

- acute mesenteric ischaemia - chronic mesenteric ischaemia - ischaemic colitis (aka chronic colonic ischaemia)

Question 217

what is the epidemiology of acute mesenteric ischaemia?

Answer 217

- usually seen in those over 50 | - almost always involves the small bowel

Question 218

what are causes of acute mesenteric ischaemia?

Answer 218

* superior mesenteric artery (SMA) thrombosis; commonest cause * superior mesenteric artery (SMA) embolism (e.g. due to AF); rarer now * mesenteric vein thrombosis; common in younger patients with hypercoagulable states and tends to affect small lengths of bowel * non-occlusive disease; occurs in low flow states and reflects poor cardiac output

Question 219

what is the classical clinical triad seen in acute mesenteric ischaemia?

Answer 219

* acute severe abdominal pain; tends to be constant, central or around the right iliac fossa * no abdominal signs * rapid hypovolaemia resulting in shock; pale skin, weak rapid pulse, reduced urine output, confusion * note: the degree of illness is often far out of proportion with clinical signs

Question 220

what is seen in bloods in acute mesenteric ischaemia?

Answer 220

* raised Hb due to plasma loss * raised WCC * persistent metabolic acidosis

Question 221

what is seen on an abdominal X-ray in acute mesenteric ischaemia?

Answer 221

* used to rule out other pathology | * see gasless abdomen

Question 222

how are laparatomy and CT/MRI angiography used to diagnose acute mesenteric ischaemia?

Answer 222

- laparotomy: • to make diagnosis • may see necrotic bowel if not treated quickly - CT/MRI angiography: • provides non-invasive alternative to simple arteriography

Question 223

what is the treatment of acute mesenteric ischaemia?

Answer 223

- fluid resuscitation - antibiotics e.g. IV gentamicin and IV metronidazole - IV heparin to reduce clotting - surgery to remove dead bowel

Question 224

what are complications of treatment of acute mesenteric ischaemia?

Answer 224

* septic peritonitis * systemic inflammatory response syndrome (SIRS) progressing into a multi-organ dysfunction syndrome, mediated by bacteria translocation across the dying gut wall

Question 225

what is ischaemic colitis?

Answer 225

- medical condition in which inflammation and injury of the large intestine result from inadequate blood supply - usually follows low flow in the inferior mesenteric artery (IMA) territory and ranges from mild ischaemia to gangrenous colitis

Question 226

what is the epidemiology of ischaemic colitis?

Answer 226

- older age group usually - related to underlying atherosclerosis and vessel occlusion - in young population is associated with women taking contraceptive pill, thrombophilia and vasculitis

Question 227

what are the main causes of ischaemic colitis?

Answer 227

* thrombosis * emboli * decreased cardiac output and arrhythmias * drugs e.g. oestrogen, antihypertensives, vasopressin * surgery e.g. cardiac bypass, aortic dissection and repair, aortoiliac reconstruction * vasculitis e.g. SLE, sickle cell disease and polyarthritis nodosa (hep B and C) * coagulation disorders * idiopathic

Question 228

what are risk factors for ischaemic colitis?

Answer 228

- contraceptive pill - nicorandil drug - thrombophilia - vasculitis

Question 229

what is the pathophysiology of ischaemic colitis?

Answer 229

- occlusion of branched of the superior mesenteric artery (SMA) or inferior mesenteric artery (IMA), often in the older age group - the anatomy of the vascular supply to the colon results in a watershed area at the splenic flexure, which is thus the most common site affected

Question 230

what is the clinical presentation of ischaemic colitis?

Answer 230

- sudden onset lower left side abdominal pain - passage of bright red blood with/without diarrhoea - may be signs of shock (pale skin, weak rapid pulse, reduce urine output, confusion) and evidence of underlying cardiovascular disease

Question 231

what are differential diagnoses of ischaemic colitis?

Answer 231

other causes of acute colitis, e.g. IBD

Question 232

how is ischaemic colitis diagnosed?

Answer 232

- urgent CT scan to exclude perforation - flexible sigmoidoscopy: biopsy shows epithelial cell apoptosis - colonoscopy and biopsy - gold standard: • only done after patient has fully recovered to exclude stricture formation at the site of disease and confirm mucosal healing - barium enema: thumb printing of submucosal swelling at splenic flexure

Question 233

what is the treatment of ischaemic colitis?

Answer 233

- most patients settle on symptomatic treatment - fluid replacement - antibiotics to reduce infection risks due to translocation of bacteria across possibly dying gut wall - most recover but strictures are common

Question 234

what are features and treatment of gangrenous ischaemic colitis?

Answer 234

* presenting with peritonitis and hypovolaemic shock * requires prompt resuscitation followed by surgical resection of the affected bowel and stoma formation * high mortality

Question 235

what is the definition of haemorrhoids (piles)?

Answer 235

disrupted and dilated anal cushions masses of spongy vascular tissue due to swollen veins around the anus - the anus is lined by discontinuous masses of spongy vascular tissue (the anal cushions) which contribute to anal closure

Question 236

what is the epidemiology of haemorrhoids?

Answer 236

- prevalence increases with age with a peak in 45-65 year olds - equally common in both males and females

Question 237

what are the main causes of haemorrhoids?

Answer 237

* constipation with prolonged straining is a key factor * diarrhoea * effects of gravity due to posture * congestion from a pelvic tumour, pregnancy, portal hypertension * anal intercourse

Question 238

what is the pathophysiology of haemorrhoids?

Answer 238

- the normal/healthy anus is lined by discontinuous masses of spongy vascular tissue (anal cushions), which contribute to anal closure - they are attached by smooth muscle and elastic tissue but are prone to displacement and disruption, either singly or together - the effects of gravity (erect posture), increased anal tone (possibly due to stress) and the effects of straining when defecating may make them become both bulky and loose, and protrude to form piles - they are vulnerable to trauma (e.g. from hard stools) and bleed readily from the capillaries of the underlying lamina propria - since blood loss is from capillaries, it is bright red - since there are no sensory fibres above the dentate line (squamomucosal junction), piles are not painful unless they thrombose when they protrude and are gripped by the anal sphincter, blocking venous return - there is a vicious circle; the vascular cushions protrude through a tight anus → become more congested and hypertrophy → protrude again more readily - these protrusions may then strangulate

Question 239

what may make anal cushions become bulky and loose, and protrude to form piles?

Answer 239

- effects of gravity (erect posture) - increased anal tone (possibly due to stress) - effects of straining when defecating

Question 240

what are internal haemorrhoids?

Answer 240

origin above the dentate line (internal rectal plexus)

Question 241

what are the 4 degrees of internal haemorrhoids?

Answer 241

- 1st: remain in rectum - 2nd: prolapse through the anus on defecation but spontaneously reduce - 3rd: prolapse but can be reduced manually - 4th: remain persistently prolapsed

Question 242

what are external haemorrhoids?

Answer 242

- originate below the dentate line (internal rectal plexus) - may be visible externally - extremely painful since there is sensory nerve supply below the dentate line

Question 243

what is the clinical presentation of haemorrhoids?

Answer 243

- bright red rectal bleeding (since there is blood from the capillaries) that often coats stools, seen on tissue or drips into toilet - mucus discharge and pruritus ani (itchy bottom) - severe anaemia may occur - weight loss and change in bowel habit should prompt thoughts of pathology

Question 244

what are differential diagnoses of haemorrhoids?

Answer 244

- perianal haematoma - anal fissure - abscess - tumour

Question 245

how are haemorrhoids diagnosed?

Answer 245

- abdominal examination to rule out other disease - PR (per rectum) exam: • prolapsing piles are obvious • internal haemorrhoids are not palpable - proctoscopy to see internal haemorrhoids - sigmoidoscopy to see rectal pathology higher up

Question 246

what is the 1st degree of treatment of haemorrhoids?

Answer 246

* increase fluid and fibre | * topical analgesic and stool softener

Question 247

what are 2nd and 3rd degree treatments of haemorrhoids?

Answer 247

* rubber band ligation: cheap, produces an ulcer to anchor the mucosa (side effects are bleeding, infection and pain) * infra-red coagulation: locally coagulates vessels and tethers mucosa to subcutaneous tissue

Question 248

what is the 4th degree treatment of haemorrhoids?

Answer 248

- excisional haemorrhoidectomy | - stapled haemorrhoidopexy

Question 249

what is treatment of prolapsed or thrombosed piles?

Answer 249

* treated with analgesia, ice packs and stool softeners | * pain usually resolved in 2-3 weeks

Question 250

what is an anal fistula?

Answer 250

- chronic abnormal communication between the epithelialised surface of the anal canal and usually the perianal skin - narrow tunnel with its internal opening in the anal canal and its external opening in the skin near the anus - blockage of deep intramuscular gland ducts is thought to predispose to the formation of accesses, which discharge to form the fistula

Question 251

what are the main causes of anal fistulas?

Answer 251

* perianal sepsis * abscesses * Crohn’s * TB * diverticular disease * rectal carcinoma

Question 252

what is the clinical presentation of anal fistula?

Answer 252

- pain - discharge (blood or mucus) - pruritus ani - systemic abscess if it becomes infected

Question 253

how are anal fistulas diagnosed?

Answer 253

MRI: • to exclude sepsis • to detect associated conditions e.g. Crohn’s or TB endoanal ultrasound: • to determine track location and underlying causes

Question 254

what is the treatment of anal fistula?

Answer 254

- fistulotomy and excision | - drain abscess with antibiotics if infected

Question 255

what is an anal fissure?

Answer 255

- a break or tear in the skin of the anal canal | - painful tear in the sensitive skin-lined lower anal canal, distal to the dentate line resulting in pain on defecation

Question 256

what is the epidemiology of anal fissure?

Answer 256

- 90% are posterior - anterior ones follow childbirth - females affected more than males - can be an isolated primary problem in young middle-aged adults or can occur in associated with Crohn’s or ulcerative colitis

Question 257

what are the main causes of anal fissure?

Answer 257

* hard faeces * spasm may constrict the inferior rectal artery resulting in ischaemia which makes healing difficult and exacerbates the problem

Question 258

what are rare causes of anal fissure?

Answer 258

- syphilis - herpes - trauma - Crohn’s - anal cancer

Question 259

what is the clinical presentation of anal fissure?

Answer 259

- extreme pain especially on defecation | - bleeding

Question 260

how is anal fissure diagnosed?

Answer 260

- can usually be made on history alone - confirmed on perianal inspection - rectal examination is often not possible due to pain and sphincter spasm

Question 261

what is the treatment of anal fissure?

Answer 261

- increase dietary fibre and fluids to make stools softer - lidocaine ointment + GTN ointment or topical diltiazem - botulinum toxin injection (2nd line) - surgery if medication fails

Question 262

what is a perianal abscess?

Answer 262

abscess (collection of pus that has built up within the body) adjacent to the anus

Question 263

what is the epidemiology of perianal abscess?

Answer 263

2/3 times more common in gay sex and in those who have anal sex

Question 264

what is the clinical presentation of perianal abscess?

Answer 264

- painful swellings - tender - discharge

Question 265

how is perianal abscess diagnosed?

Answer 265

- MRI | - endoanal ultrasound

Question 266

what is the treatment of perianal abscess?

Answer 266

- surgical excision | - drainage with antibiotics

Question 267

what is a pilonidal sinus/abscess?

Answer 267

hair follicles get stuck under the skin in the natal cleft resulting in irritation and inflammation leading to small tracts which can become infected (abscess)

Question 268

what is the epidemiology of pilonidal sinus/abscess?

Answer 268

- much more common in males than females | - commonly presents between 20-30 yrs

Question 269

what are risk factors for pilonidal sinus/abscess?

Answer 269

- obese caucasians and those from Asia, Middle East and Mediterranean are at increased risk - large amount of body hair - sedentary job - occupation involving sitting or driving - family history

Question 270

what is the pathophysiology of pilonidal sinus/abscess?

Answer 270

the ingrowing of hair triggers a foreign body reaction and may cause secondary tracks to open laterally with or without abscesses, with foul-smelling discharge

Question 271

what is the acute clinical presentation of pilonidal sinus/abscess?

Answer 271

* painful swelling over days * pus filled with foul smell from abscess * systemic signs of infection

Question 272

what is the chronic clinical presentation of pilonidal sinus/abscess?

Answer 272

* 4 in 10 have repeated recurrent pilonidal sinus | * infection never clears completely

Question 273

how is pilonidal sinus/abscess diagnosed?

Answer 273

detected on clinical examination

Question 274

what is the treatment of pilonidal sinus/abscess?

Answer 274

- surgery: • excision of the sinus tract and primary closure and pus drainage • pre-op antibiotics - hygiene and hair removal advice (near sinus)

Question 275

what is irritable bowel syndrome?

Answer 275

a mixed group of abdominal symptoms without any evidence of underlying damage/organic cause

Question 276

what is the epidemiology of IBS?

Answer 276

- age of onset is under 40 - more common in females than males - common, in western world around 1 in 5 report symptoms consistent with IBS - symptoms are exacerbated by stress, food, gastroenteritis or menstruation

Question 277

what are the main causes of IBS?

Answer 277

* depression, anxiety * psychological stress and trauma * GI infection * sexual, physical or verbal abuse * eating disorders

Question 278

what are the types of IBS?

Answer 278

IBS-D: diarrhoea IBD-C: constipation IBS-M: diarrhoea and constipation IBS-U: neither diarrhoea nor constipation are common

Question 279

what are the risk factors for IBS?

Answer 279

- female - previous severe and long diarrhoea - high hypochondrial anxiety and neurotic score at time of initial illness

Question 280

what is the pathophysiology of IBS?

Answer 280

- altered gut microbiota - abnormal gut motility - autonomic nervous dysfunction - visceral hypersensitivity - genetic factors - mood/stress/psychological morbidity - dysfunction in the brain-gut axis results in disorder of intestinal motility and/or visceral hypersensitivity

Question 281

what are some non-intestinal symptoms of IBS?

Answer 281

* painful period * urinary frequency, urgency, nocturia and incomplete emptying of bladder * back pain * joint hypermobility * fatigue

Question 282

what is ABC in relation to IBS?

Answer 282

A: abdominal pain or discomfort B: bloating C: change in bowel habit

Question 283

when should IBS be considered?

Answer 283

• abdominal pain that is either relieved by defecation or is associated with altered stool form or bowel frequency (constipation and diarrhoea may alternate) AND: • there are 2 or more of: - urgency - incomplete evacuation - abdominal bloating/distension - mucous in stool - worsening symptoms after food • other symptoms: nausea, bladder symptoms and backache • symptoms are chronic (more than 6 months) and exacerbated by stress, menstruation or gastroenteritis (post-infection IBS) • general abdominal tenderness

Question 284

what are some red flag symptoms in IBS?

Answer 284

* unexplained weight loss * PR bleed/blood in stool * family history of bowel or ovarian cancer * change in bowel habit and aged over 50 * nocturnal symptoms * rectal or abdominal mass * anaemia * raised inflammatory markers * if any found then refer to secondary care for further investigations

Question 285

what are some differential diagnoses of IBS?

Answer 285

- coeliac disease (5% of IBS patients) - lactose intolerance (esp. in IBS-D) - bile acid malabsorption - IBD - colorectal cancer

Question 286

how are bloods used to diagnose IBS?

Answer 286

• FBC to look for anaemia • ESR and CRP to look for inflammation • coeliac serology testing for endomysial antibody (EMA) and tissue transglutaminase antibody (tTG) - if either positive then there is a high chance of coeliac disease

Question 287

what is used to diagnose IBS?

Answer 287

- since there is nothing physical to be found, diagnosis is made by ruling out the differentials - bloods - faecal calprotectin is raised in IBD - colonoscopy to rule out IBD or colorectal cancer - Rome III diagnostic criteria

Question 288

what is Rome III diagnostic criteria for IBS?

Answer 288

recurrent abdominal pain or discomfort at least 3 days a month in the past 3 months, associated with two or more of the following: - improvement with defecation - onset associated with a change in frequency of stool - onset associated with a change in form (appearance) of stool

Question 289

what is the treatment of mild IBS?

Answer 289

* education * reassurance * dietary modification

Question 290

what is the treatment of moderate IBS?

Answer 290

* pharmacotherapy | * psychological treatment

Question 291

what is the treatment of severe IBS?

Answer 291

referral to pain treatment centre

Question 292

what is the dietary/lifestyle modification for IBS?

Answer 292

``` • regular or small frequent meals • plenty of fluids (8 cups/day) • reduce/avoid caffeinated drinks, alcohol and fizzy drinks • for IBS-D and bloating, reduce/avoid: - insoluble fibre intake - fruit intake to 3 portions/day • for wind and bloating, increase soluble fibre intake • fibre ```

Question 293

what are features of soluble fibre for IBS?

Answer 293

* good for constipation (IBS-C) * dissolves in water and is broken down by bacteria * softens stool * slows down sugar release * e.g. barley, oats, beans, prunes, figs

Question 294

what are features of insoluble fibre for IBS?

Answer 294

* makes IBS-D worse so should be cut down * not dissolved in water * passes through the gut mostly unchanged * absorbs water and bulks up faeces * increases gut motility * e.g. cereals, whole-wheat bread, lentils, apple, avocado

Question 295

what is a low FODMAP diet?

Answer 295

- fermentable - oligosaccharides - disaccharides - monosaccharides - and - polyols - all produce a lot of gas, bloating, diarrhoea and pain - e.g. apple, artichoke, cottage cheese, baked beans, cow milk

Question 296

what is pharmacological therapy for pain/bloating in IBS?

Answer 296

antispasmodics e.g. Mebeverine or Buscopan

Question 297

what is pharmacological therapy for constipation in IBS?

Answer 297

- laxative e.g. mavicol, sodiumdocusate or senna - linaclotide only used for constipation lasting for more than 12 months and not relieved by 2 different classes of max dose laxatives - can also use 5-HT4 receptor agonist e.g. prucalopride

Question 298

what is pharmacological therapy for diarrhoea in IBS?

Answer 298

anti-motility agents e.g. loperamide

Question 299

what is pharmacological therapy for IBS patients that haven't responded to other drugs?

Answer 299

- tricyclic antidepressants e.g. amitriptyline or nortriptyline - but warn about drowsiness - need to take it for 4-6 weeks to take effect - not to treat depression but to dampen down gut sensitivity - if not tolerated then move to SSRI - can also use psychological therapy in conjunction

Question 300

what are differences between IBD and IBS?

Answer 300

IBS: - normal investigation results - persistant/fluctuating symptoms - wouldn't really get fever - no symptoms outside GI tract - no blood in stool - no melaenea - food triggers - no weight loss - no mouth ulcers - constipation more common - exacerbated by stress - bloating IBD - abnormal investigation results - persistent/fluctuating symptoms - more likely to get fever - symptoms outside GI tract - blood in stools - melaena (black stool) - food triggers - weight loss - mouth ulcers - constipation but less common than in IBS - can be exacerbated by stress - bloating much less common than in IBS

Question 301

what is a GI diverticulum?

Answer 301

a GI diverticulum is an outpouching of the gut wall, usually at sites of entry of perforating arteries

Question 302

what is a diverticulosis?

Answer 302

presence of diverticula

Question 303

what is diverticular disease?

Answer 303

caused by diverticula that are symptomatic

Question 304

what is diverticulitis?

Answer 304

inflammation of a diverticulum

Question 305

what is the epidemiology of diverticular disease and diverticulitis?

Answer 305

- frequently found in the colon and occur in 50% of patients over the age of 50 yrs - they are most frequent in the sigmoid colon, but can be present throughout the whole colon - diverticula can be acquired or congenital and may occur elsewhere but the most important are acquired colonic diverticula - rare in the young - 95% are asymptomatic

Question 306

what are the main causes of diverticular disease and diverticulitis?

Answer 306

``` • low fibre diet: - commonly eaten in developed countries - rare in rural Africa • obesity • smoking • NSAIDs ```

Question 307

what are risk factors for diverticular disease and diverticulitis?

Answer 307

- low-fibre diet | - over age of 50

Question 308

what is the pathophysiology of diverticula formation?

Answer 308

* diverticula form at gaps in the wall of the gut where blood vessels penetrate * in a low fibre diet, the colon must push harder to move things along (fibre helps gut motility) so pressure increases * this pressure increase results in pouches of mucosa being extruded through the muscular wall through weakened areas near blood vessels leading to diverticula formation * there is also thickening of the muscle layer

Question 309

what is the pathophysiology of acute diverticulitis?

Answer 309

* occurs when faeces obstruct the neck of the diverticulum, causing stagnation and allowing bacteria to multiply and produce inflammation * this can then lead to bowel perforation (peridiverticulitis), abscess formation, fistulae into adjacent organs, haemorrhage and generalised acute peritonitis and possibly death

Question 310

what is the clinical presentation of diverticular disease?

Answer 310

• asymptomatic in 95% of cases and is usually detected incidentally on colonoscopy or barium enema examination • in symptomatic cases: - intermittent left iliac fossa pain - erratic bowel habit • in severe cases: - severe pain and constipation due to luminal narrowing

Question 311

what is the clinical presentation of acute diverticulitis?

Answer 311

* most commonly affects diverticula in the sigmoid colon * severe pain in the left iliac fossa * fever and constipation * symptoms are similar to those of appendicitis but are located on the left side

Question 312

what is the presentation of acute diverticulitis on examination?

Answer 312

- febrile - tachycardia - abdominal examination: • tenderness, guarding and rigidity on the left side of the abdomen • a palpable tender mass is sometimes felt in the left iliac fossa

Question 313

what are complications of diverticular disease?

Answer 313

- perforation - fistula formation - intestinal obstruction - bleeding - mucosal inflammation

Question 314

what are features of perforation as a complication of diverticular disease?

Answer 314

- usually occurs in association with acute diverticulitis - can lead to paracolic or pelvic abscess or generalised peritonitis - rurgery may be required

Question 315

what are features of fistula formation as a complication of diverticular disease?

Answer 315

fistula formation into: - the bladder resulting in dysuria or pneumaturia (gas or air in urine resulting in bubbles) - the vagina resulting in discharge

Question 316

what are features of intestinal obstruction as a complication of diverticular disease?

Answer 316

usually after repeated episodes of acute diverticulitis

Question 317

what are features of bleeding as a complication of diverticular disease?

Answer 317

- sometimes this is massive - in most cases the bleeding stops and the cause is established by colonoscopy and sometimes angiography - in some cases emergency segment colectomy is required

Question 318

what are features of mucosal inflammation as a complication of diverticular disease?

Answer 318

occurs in areas of diverticula, giving the appearance of Crohn’s on endoscopy

Question 319

how is diverticular disease diagnosed?

Answer 319

in the absence of clinical signs of acute diverticulitis (i.e. excluding this) then colonoscopy is best option

Question 320

what is seen on blood tests in acute diverticulitis?

Answer 320

- polymorphonuclear leucocytosis | - ESR and CRP raised

Question 321

what is seen on a CT colonography in acute diverticulitis?

Answer 321

- best for diagnosis - will show colonic wall thickening and diverticula - also pericolic collections and abscesses - findings above are diagnostic for acute diverticulitis and differ from those of malignant disease - sigmoidoscopy or colonoscopy are not performed during an acute attack

Question 322

what is seen on an abdominal X-ray in acute diverticulitis?

Answer 322

may identify obstruction or free air (indicative of perforation)

Question 323

what is seen on a barium enema in acute diverticulitis?

Answer 323

can clarify diagnosis in patients with abdominal pain and altered bowel habit

Question 324

what is the treatment of diverticular disease?

Answer 324

in uncomplicated symptomatic disease a well-balanced high fibre diet with smooth muscle relaxants i.e. antispasmodics e.g. mebeverine is recommended

Question 325

what is the treatment of acute diverticulitis?

Answer 325

* mild attacks can be treated with oral antibiotics e.g. ciprofloxacin and metronidazole * those with signs of systemic upset (fevers, tachycardia) and significant abdominal pain require bowel rest, IV fluids and IV antibiotics * surgical resection is occasionally required

Question 326

what is Meckel's diverticulum?

Answer 326

- true congenital diverticulum - slight bulge in the small intestine present at birth - vestigial remnant of the omphalomesenteric duct

Question 327

what is the epidemiology of Meckel's diverticulum?

Answer 327

affects 2-3% population

Question 328

what is the clinical presentation and treatment of Meckel's diverticulum?

Answer 328

* usually symptomless * in 50% of cases, the distal ileum contains gastric mucosa that secretes HCL, meaning peptic ulcers can occur which may bleed or perforate; causes GI pain * acute inflammation of the diverticulum also occurs and is clinically indistinguishable from acute appendicitis * treatment is surgical removal of diverticula, often laparoscopically

Question 329

what is acute appendicitis? where is it located?

Answer 329

- acute inflammation of the appendix - should be considered for all right sided pain if appendix is present in patient - located at McBurney’s point which lies 2/3 of the way from the umbilicus to the anterior superior iliac spine

Question 330

what is McBurney's point?

Answer 330

lies 2/3s of the way from the umbilicus to the anterior superior iliac spine

Question 331

what is the epidemiology of acute appendicitis?

Answer 331

- most common surgical emergency - more common in males than females - can occur at any age although highest incidence is between 10-20 yrs - rare before age of 2 since appendix is cone shaped with a larger lumen

Question 332

what are the main causes of acute appendicitis?

Answer 332

* faecolith * lymphoid hyperplasia * filarial worms

Question 333

what is the pathophysiology of acute appendicitis?

Answer 333

- occurs when the lumen of the appendix becomes obstructed by lymphoid hyperplasia, filarial worms or a faecolith (most common) resulting in the invasion of gut organisms into the appendix wall - this leads to oedema, ischaemia, necrosis and perforation as well as inflammation - if the appendix ruptures then infected and faecal matter will enter the peritoneum resulting in life threatening peritonitis

Question 334

what is the clinical presentation of acute appendicitis?

Answer 334

- pain in the umbilical region that migrates to the right iliac fossa, specifically McBurney’s point after a few hours - anorexia is important - nausea and vomiting and occasionally diarrhoea can occur - constipation is usual - examination of abdomen reveals tenderness in the right iliac fossa with guarding due to localised peritonitis - may be a tender mass in the right iliac fossa - patient is pyrexic

Question 335

why does pain occur in acute appendicitis?

Answer 335

* this is because the internal organs and the visceral peritoneum have no somatic innvervation, so the brain attributes the visceral signals to a physical location whose dermatome corresponds to the same entry level in the spinal cord; importantly, there is no laterality to the visceral unmyelinated C-fibre pain signals, which enter the cord bilaterally and at multiple levels * early inflammation irritates the structure and walls of the appendix, so a colicky pain is referred to the mid-abdomen around the umbilical area known as periumbilical pain * as the inflammation progresses and irritates the parietal peritoneum (especially on examination and palpation) the somatic, lateralised pain settles at McBurney’s point

Question 336

what are differential diagnoses of acute appendicitis?

Answer 336

- acute terminal ileitis due to Crohn’s - ectopic pregnancy - UTI - diverticulitis - perforated ulcer - food poisoning

Question 337

what is seen on blood tests in acute appendicitis?

Answer 337

* raised white cell count with neutrophil leucocytosis | * elevated CRP and ESR

Question 338

what is seen on ultrasound in acute appendicitis?

Answer 338

can detect inflamed appendix and can also indicate an appendix mass or other localised lesion

Question 339

how is CT used to diagnose acute appendicitis?

Answer 339

* highly sensitive and specific - gold standard for diagnosis * reduces risk of removal of a healthy appendix

Question 340

what is used to exclude differential diagnoses in acute appendicitis?

Answer 340

- pregnancy test | - urinalysis to exclude UTI

Question 341

what is the surgical treatment of acute appendicitis?

Answer 341

* laparascopic appendicectomy * IV antibiotic pre-op to reduce wound infections e.g. IV metronidazole and IV cefuroxime * if appendix mass is present, the patient is usually treated with IV fluids and antibiotics until mass disappears over a few weeks; appendicectomy is recommended later to prevent further acute episodes

Question 342

what are complications of acute appendicitis? how are they treated?

Answer 342

• perforation: commoner if faecolith present and in young children • appendix mass: - when an inflamed appendix becomes covered in omentum (thus forming a mass); ultrasound or CT can help diagnose - treat with antibiotics and then surgery to remove appendix later to prevent further event • appendix abscess: - results if appendix mass fails to resolve but instead enlarges and the patient gets more unwell - treat by draining appendix - antibiotics

Question 343

what is the structure of the exocrine pancreas?

Answer 343

- no ducts, secreted directly at site of action, secrete enzyme, short term activity - functional unit of the exocrine pancreas comprises of an acinus and its draining ductule - a ductule from the acinus drains into interlobar (intercalated) ducts, which in turn drain into the main pancreatic ductal system - the main pancreatic duct itself joins the common bile duct to enter the duodenum as a short single duct at the ampulla of Vater

Question 344

what do pancreatic acinar cells do?

Answer 344

- acinar cells are responsible for the production of digestive enzymes e.g. amylase, lipase, colipase, phospholipase and the proteases (trypsinogen and chymotrypsinogen) - these enzymes are released by acinar cells and are then transported into the duodenum via pancreatic secretions

Question 345

what are features of the endocrine pancreas?

Answer 345

- ductless, released directly into blood, secrete hormones, long term activity - endocrine component is scattered through the gland in the form of pancreatic islets of Langerhans

Question 346

what do endocrine pancreatic cells secrete?

Answer 346

- alpha cell: glucagon production - beta cells: insulin production - D cells: somatostatin (inhibits acinar enzyme secretion) production - PP cells: pancreatic polypeptide (inhibits acinar enzyme secretion) - enterochrommaffin cells: serotonin production

Question 347

what is acute pancreatitis?

Answer 347

* process that occurs on the background of a previously normal pancreas and can return to normal after resolution of the episode * sudden inflammation of the pancreas

Question 348

what is the epidemiology of acute pancreatitis?

Answer 348

- syndrome of inflammation of the pancreatic gland initiated by any acute injury - recurrent episodes if untreated - in most severe form (10% of all cases) mortality is 40% - 80%: • extensive pancreatic and peripancreatic necrosis • haemorrhage - difficult to differentiate between chronic and acute

Question 349

what are the main causes of acute pancreatitis? what is a mneumonic to remember this?

Answer 349

I GET SMASHED - Idiopathic - Gallstones (majority - 60%) - Ethanol (30%) - Trauma - Steroids - Mumps - Autoimmune - Scorpion venom - Hyperlipidaemia - ERCP (endoscopic retrograde cholangiopancreatography) - Drugs e.g. azathioprine, furosemide (diuretics), corticosteroids, NSAIDs, ACE inhibitors - also pregnancy and neoplasia

Question 350

what is the pathophysiology of acute pancreatitis?

Answer 350

- acute pancreatitis is caused by the destructive effect of premature activation of pancreatic enzymes which causes self-perpetuating pancreatic inflammation by enzyme-mediated autodigestion - there are many mechanisms by which this can occur, with the majority being caused by gallstones and alcohol

Question 351

what is the pathophysiology of gallstone acute pancreatitis?

Answer 351

* accumulation of enzyme-rich fluid within the pancreas due to obstruction of the pancreatic duct by gallstones * intracellular Ca2+ increases and causes the early activation of trypsinogen * in this situation, trypsinogen is cleaved (by cathepsin B) to trypsin, and trypsin degradation (by chymotrypsin C) is impaired and overwhelmed leading to a buildup of trypsin and thus increased enzymatic digestion of the pancreas and inflammation leading to extensive acinar damage

Question 352

what is the pathophysiology of alcohol-induced acute pancreatitis?

Answer 352

alcohol is shown to interfere with Ca2+ homeostasis in increased stimulation of enzyme secretion and obstruction of the duct due to contraction of the ampulla of Vater

Question 353

what can prematurely activated enzymes in acute pancreatitis lead to?

Answer 353

- the prematurely activated enzymes also cause leaky vessels by digesting vessel walls in the pancreas leading to the leakage of fluid into the tissues causing oedema, inflammation and hypovolaemia (as extracellular fluid is trapped in the gut, peritoneum and retroperitoneum) - destruction of blood vessels by enzymes causes haemorrhage - destruction of the adjacent islets of Langerhans can result in hyperglycaemia as beta cells will be destroyed resulting in less insulin - lipolytic enzymes cause fat necrosis, which can result, if extensive and involving the anterior abdominal wall, in skin discolouration (Grey Turner’s sign)

Question 354

what can fat necrosis in acute pancreatitis lead to?

Answer 354

* the released fatty acids bind to Ca2+ ions, forming white precipitates in the necrotic fat * if this is very severe, it can result in hypocalcaemia, presenting with tetany

Question 355

what is the clinical presentation of acute pancreatitis?

Answer 355

- acute pancreatitis is a differential diagnosis in any patient with upper abdominal pain - gradual or sudden severe epigastric or central abdominal pain that radiates to the back; sitting forward may relieve this - anorexia, nausea and vomiting - tachycardia - fever - jaundice - dehydration - hypotension - abdominal guarding and tenderness on examination - Cullen's sign - Grey Turner's sign

Question 356

what is Cullen's sign?

Answer 356

``` periumbilical ecchymosis (skin discolouration due to blood under the skin due to bruising) - seen in acute pancreatitis ```

Question 357

what is Grey Turner's sign?

Answer 357

left flank bruising (skin discolouration due to blood under the skin due to bruising) - seen in acute panreatitis

Question 358

what is seen on blood tests in acute pancreatitis?

Answer 358

• raised serum amylase - 3-fold the upper limit of normal - note: may be normal even in severe pancreatitis as levels fall after 3-5 days of acute event and other things can cause raised amylase e.g. upper GI perforation • raised urinary amylase; may be diagnostic as levels remain elevated over long time period • raised serum lipase; more sensitive and specific for pancreatitis than amylase • CRP level for monitoring severity and prognosis

Question 359

what is seen on erect CXR in acute pancreatitis?

Answer 359

* essential to exclude gastroduodenal perforation, which also raises serum amylase * may show gallstones or pancreatic calcification

Question 360

what is seen on a contrast enhanced CT in acute pancreatitis?

Answer 360

to identify extent of pancreatic necrosis

Question 361

what is seen on an MRI in acute pancreatitis?

Answer 361

* identifies degree of pancreatic damage | * useful in differentiating fluid and solid inflammatory masses

Question 362

what are the different pancreatic scoring systems?

Answer 362

- used as a predictor of severity and prognostic tool - Glasgow and Ranson scoring systems - APACHE II (Acute Physiology And Chronic Health Evaluation)

Question 363

what is the Glasgow and Ranson scoring system for acute pancreatitis?

Answer 363

- uses various factors such as; age, neutrophils, calcium and blood glucose etc to predict a severe attack - 80% sensitive, although only after 48 hours from presentation

Question 364

what is the APACHE II score for acute pancreatitis?

Answer 364

Acute Physiology And Chronic Health Evaluation - used to assess severity - based on common physiological and laboratory values, age and presence/absence of chronic conditions e.g. obesity - has a high sensitivity and can be applied as early as 24 hours after symptom onset

Question 365

what is the treatment of acute pancreatitis?

Answer 365

- severity assessment is essential - nil by mouth - nasogastric tube for dietary supplements (as less pancreatic enzymes are released so need to support patients nutritionally!) to decrease pancreatic stimulation - urinary catheter - analgesia e.g. IM pethidine or IV morphine - drainage of collections may be required - prophylactic antibiotics e.g. cefuroxime or metronidazole to reduce risk of infected pancreatic necrosis

Question 366

what is a complication of acute pancreatitis?

Answer 366

systemic inflammatory response syndrome (SIRS)

Question 367

what is SIRS?

Answer 367

systemic inflammatory response syndrome - proinflammatory state - any two of: tachycardia, tachypnoea, pyrexia with temp >38, high WCC

Question 368

what is chronic pancreatitis?

Answer 368

debilitating continuing inflammatory process of the pancreas resulting in progressive loss of exocrine pancreatic tissue which is replaced with by fibrosis

Question 369

what is the epidemiology of chronic pancreatitis?

Answer 369

- worldwide prevalence is around 4-5% - males affected more than females - median age of presentation is 51

Question 370

what are the main causes of chronic pancreatitis? what is the most common cause?

Answer 370

* commonest cause in the developed world is long-term alcohol excess (60-70%) * chronic kidney disease * hereditary: defects in the trypsinogen gene or cystic fibrosis * autoimmune pancreatitis - raised IgG4 (seen in many autoimmune disorders) triggers pancreatitis * idiopathic * trauma * recurrent acute pancreatitis

Question 371

what is the pathophysiology of chronic pancreatitis?

Answer 371

- obstruction or reduction in bicarbonate secretion, which produces an alkaline pH which in turn stabilises trypsinogen, leads to the activation of trypsinogen as pH rises making it more unstable and causing its activation into trypsin which leads to pancreatic tissue necrosis with eventual fibrosis - abnormalities of bicarbonate excretion can be the result of functional defects at the level of the cellular wall e.g. cystic fibrosis or mechanical as in trauma - increased intrapancreatic enzyme activity leads to the precipitation of proteins within the duct lumen in the form of plugs - these plugs then become calcified resulting in ductal obstruction and further pancreatic damage - alcohol increases trypsinogen activation and also causes proteins to precipitate in the ductal structure of the pancreas leading to local pancreatic dilatation and fibrosis - note: the vast majority of people drinking excess alcohol do not develop pancreatitis - this suggests that the disease process is a complex interaction of different mechanisms

Question 372

what is the clinical presentation of chronic pancreatitis?

Answer 372

- epigastric pain that ‘bores’ through to the back: • can be episodic or unremitting; can be relieved by sitting forward • exacerbated by alcohol - nausea and vomiting - decreased appetite - exocrine dysfunction - endocrine dysfunction

Question 373

what is the pain like in chronic pancreatitis?

Answer 373

epigastric pain that bores through to the back • can be episodic or unremitting; can be relieved by sitting forward • exacerbated by alcohol

Question 374

what does exocrine dysfunction caused by chronic pancreatiits lead to?

Answer 374

malabsorption (presenting feature in absence of pain) with: - weight loss - diarrhoea - steatorrhoea (pale, loose, fatty, foul smelling stools that float) - protein deficiency

Question 375

what are differential diagnoses of chronic pancreatitis?

Answer 375

pancreatic malignancy - lots of common symptoms should be thought of especially when there is a short history and pancreatic mass

Question 376

how is chronic pancreatitis diagnosed?

Answer 376

- serum amylase and lipase: may be elevated, but in advanced disease, there may not be sufficient residual acinar cells to produce elevation - faecal elastase will be abnormal in majority of patients with moderate-severe disease - abdominal ultrasound and contrast-enhance CT: • detects pancreatic calcification and a dilated pancreatic duct to confirm diagnosis - MRI with MRCP to identify more subtle abnormalities

Question 377

what is the treatment of chronic pancreatitis?

Answer 377

- alcohol cessation - abdominal pain: • NSAIDs • opiates e.g. oral tramadol • tricyclic antidepressants e.g. amitryptiline - duct drainage - shock wave lithotripsy to fragment gallstones in the head of pancreas - steatorrhea: • pancreatic enzyme supplements • PPIs help supplement pass stomach - diabetes: insulin

Question 378

what is autoimmune chronic pancreatitis?

Answer 378

chronic pancreatic inflammation which results from an autoimmune process

Question 379

what is the epidemiology of autoimmune chronic pancreatitis?

Answer 379

high prevalence in Japan

Question 380

what is the clinical presentation of autoimmune chronic pancreatitis?

Answer 380

* presentation is very similar to normal chronic pancreatitis * there are elevated levels of serum gammaglobulins and immunoglobulin G (IgG) levels - IgG4 * autoantibodies such as antinuclear cytoplasmic antibody (ANCA) and rheumatoid factor may also be elevated

Question 381

what is the treatment of autoimmune chronic pancreatitis?

Answer 381

this condition is steroid responsive with glucocorticoid therapy e.g. oral prednisolone for 4-6 weeks

Question 382

what is the ALT/AST ratio? what is it like in different conditions?

Answer 382

- the ALT/AST ratio is a useful clinical indicator. - in viral hepatitis, ALT > AST unless cirrhosis is present, when AST > ALT. - in alcoholic liver disease and steatohepatitis the AST is often greater than the ALT. - thus in patients with viral hepatitis, an AST/ALT ratio > 1 indicates cirrhosis, and in patients without cirrhosis in whom AST > ALT, alcohol or obesity should be considered the most likely cause.

Question 383

how can the origin of alkaline phosphatase be determined?

Answer 383

- the origin can be determined by electrophoretic separation of isoenzymes or bone-specific monoclonal antibodies. - however, if the γ-GT is also abnormal, the ALP is presumed to come from liver

Question 384

what is gamma-glutamyl transpeptidase? when is its activity induced? when is it raised?

Answer 384

- this is a microsomal enzyme present in liver and many other tissues. - activity can be induced by drugs such as phenytoin, warfarin and alcohol. - if the ALP is normal, a raised serum γ-GT can be a useful guide to alcohol intake. - however, mild elevation of γ-GT is common, even with minimal alcohol consumption, but it is raised in fatty liver disease. - in the absence of other liver function test abnormalities, a slightly raised γ-GT can safely be ignored

Question 385

what are total proteins and globulin fraction levels like in liver disease?

Answer 385

the globulin fraction is often raised in autoimmune hepatitis and a fall indicates successful therapy.

Question 386

what does a predominant elevation of serum aminotransferases indicate?

Answer 386

hepatocellular injury

Question 387

what does elevation of serum bilirubin and alkaline phosphatase in excess of aminotransferases indicate?

Answer 387

indicates a cholestatic disorder such as primary biliary cirrhosis, primary sclerosing cholangitis or extrahepatic bile duct obstruction

Question 388

what does an isolated rise in bilirubin indicate?

Answer 388

most likely due to Gilbert's disease

Question 389

what are the first steps for patients with a persistent elevation of serum aminotransferases?

Answer 389

- careful history (alcohol consumption, exposure to hepatotoxic drugs, risk factors for chronic liver disease) - physical examination (features of chronic liver diseases) - simple laboratory tests (viral hepatitis, metabolic and autoimmune liver disease) - ultrasound

Question 390

causes of malabsorption

Answer 390

- lack of digestive enzymes - decetive intraluminal digestion

Question 391

causes of defective intraluminal digestion

Answer 391

- pancreatic insufficiency - pancreatitis + - defective bile secretion - bile obstruction + ileal reesection - bacterial overgrowth

Question 392

pathophysiology of coeliac disease

Answer 392

gliadin in wheat presented to APC -\> formation of toxic T cells + gliadin antibodies --\> enterocyte injury -\> loss of epithelial cells --\> malabsorption due to loss of absorptive area.

Question 393

what are the 2 most common functional gut disorders

Answer 393

1. IBS - bowel 2. functional dyspepsia - stomach

Question 394

what is a functional gut disorder

Answer 394

chronic GI symtpoms in the absence of organic disease to explain the symptoms

Question 395

T/F women are more likely to have functional gut disorders

Answer 395

True linked to hormonal changes

Question 396

define dyspepsia

Answer 396

gastric symptoms in the upper abdomen

Question 397

define dyspepsia

Answer 397

gastric symptoms in the upper abdomen

Question 398

symptoms of IBS

Answer 398

- chronic frequent abdo pain - altered bowel habit - bloating communly associated

Question 399

T/F IBS pts should also be tested for coeliac disease

Answer 399

True - IBS symptoms are v similar to coeliac, so should be ruled out

Question 400

IBS differentials

Answer 400

- ovarian - Ca-125 test - coeliac TTA/G??

Question 401

what are the ALARM features of gastric disorders

Answer 401

1. Age \>45 years 2. Short history of symptoms 3. Documented unintentional weight loss 4. Nocturnal symptoms 5. Family history of Gl cancer/IBD 6. GI Bleeding 7. Palpable abdominal mass or lymphadenopathy 8. Evidence of iron deficiency anemia on blood testing 9. Evidence of inflammation on blood/stool testing

Question 402

T/F IBS + IBD symptoms do not wake pts up from their sleep

Answer 402

FALSE IBD pts will experience symptoms all through the night while IBS pts won't as its a disorder linking the brain and the gut so one the brain sleep so does the gut

Question 403

what is faecal calprotectin

Answer 403

marker of gut inflammation

Question 404

what is post-infectious IBS

Answer 404

IBS that occurs after an bout of gastroenteritis.

Question 405

IBS criteria

Answer 405

* abdominal pain at least 1 day per week with 2 or more of these symptoms: * symptoms related to defecation * associated with change in frequency of stools * associated with change in forms of stools

Question 406

risk factors of oesophageal cancer

Answer 406

* alcohol * tobacco use * Barretts oesophagus * obesity * acid reflux * physical activity.

Question 407

what GI conditions are associated with pain

Answer 407

Question 408

what GI conditions are associated with difficulty swallowing

Answer 408

Question 409

what GI conditions are associated with haematemesis

Answer 409

Question 410

what is achalasia and what causes it?

Answer 410

* oesophageal motility disorder where there is no peristalsis in the oesophagus + the lower oesophageal sphincter is unable to relax in response to swallowing.

Question 411

key features of achalasia

Answer 411

* non-progressive dysphagia - difficulty swallowing solids + liquids * chesty retro-sternal pain * cough caused by regurgitation * cough when laying down * weight loss due to reduced intake

Question 412

treatment for achalasia

Answer 412

initially: CCBs and nitrates to help lower pressure around LOS - usually ineffective and just while pt waits for definitive tx: 1. surgery 2. endoscopic balloon stent

Question 413

what is ischaemic colitis?

Answer 413

ischamia of the colon's arterial supply → colonic inflammation due to hypoperfusion

Question 414

which vessel is most likely to be affected in ischaemic colitis

Answer 414

the inferior mesenteric artery

Question 415

causes of ischaemic colitis and which one is most common

Answer 415

* non-occlusive: reduced perfusion = **most common** * heart failure due to reduced cardiac output * septic shock * PVD * cocaine use * recent CABG * occlusive * thrombus * embolus * tumour, volvulus, hernia

Question 416

symptoms of ischaemic colitis

Answer 416

* transient LLQ pain * bright bloody stool * may have signs of hypovolaemic shock

Question 417

gold standard + other diagnostic tools for ischaemic colitis

Answer 417

GS = colonoscopy + biopsy other: AXR= not diagnostic but may show ‘thumbprinting

Question 418

treatment for ischaemic colitis

Answer 418

depends on presentation but usually * non-occlusive cause improves with supportive management * IV fluids * ABX * nil by mouth + NG tube * treatment of underlying cause. * occlusive causes may need **surgery** * gangrene → surgery

Question 419

what is mesenteric ischaemia and what types can you get?

Answer 419

* ischamia of the small intestine caused by thrombus or embolus blocking the superior mesenteric artery. * types: * acute → acute attack * chronic → lasts over months

Question 420

components + blood supply of the foregut, midgut and hindgut

Answer 420

* Foregut * Stomach and part of duodenum, biliary system, liver, pancreas * **Celiac artery** * Midgut * Duodenum to 1st half of transverse colon * **Superior mesenteric artery** * Hindgut * 2nd half of transverse colon to rectum * **Inferior mesenteric artery**

Question 421

signs and symptoms of mesenteric ischaemia

Answer 421

* symptoms * abdominal pain * Acute ischaemia: severe, out of proportion to abdominal signs * Chronic ischaemia: colicky, intermittent, post-prandial and described as ‘intestinal angina’. * N+V * diarrhoea * fever * signs * NO abdominal signs e.g. guarding or rebound tenderness. * severe pain not proportional to clinical findings * hypotension + tachycardia - rapid hypovolemic shock. * bleeding on rectal exam

Question 422

mesenteric ischaemia diagnostic tools: which one is gold standard

Answer 422

* CT angiogram = gold standard: shows the site of occlusion + the extent of necrosis and ischeamia. * ECG: as AF is the most common cause of acute mesenteric ischaemia. * FBC + ABG: looking for anaemia + persistent metabolic acidosis

Question 423

management of mesenteric ischaemia

Answer 423

* chronic = management of CVD risk +/or elective procedures * acute * initial management * fluid resus, ABX, IV heparin * definitive management * surgery: especially for infarcted/ necrotic bowel

Question 424

complications of ischeamic colitis and mesenteric colitis

Answer 424

* bowel infarction +/or perforation * strictures *

Question 425

difference between internal and external haemorrhoids

Answer 425

* internal originate **above** the rectal plexus [**dentate line**] * ∴ less painful as there is much less sensory supply. * may feel tenesmus * external originate **below** the dentate line * ∴ extremely painful as there is more innervation. * pts struggle to sit

Question 426

haemorrhoid symptoms

Answer 426

* bright red PR blood * PAIN * mucus discharge * itching * swelling

Question 427

what are haemorrhoids

Answer 427

swollen veins around the anus disrupting the anal cushions and potentially causing prolapse of anal cushions through the anal passage.

Question 428

treatment of haemorrhoids

Answer 428

* 1st degree / mild * **Increase fibre and fluid intake** * **Stool softeners** * **Topical analgesia** * **Topical steroids** for short periods * 2nd/ 3rd degree / definitive tx * non-surgical = rubber band ligation * surgery