GI Flashcards

Question

what is the clinical presentation of dyspepsia?

Answer 1

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

Answer 2

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

Answer 3

- 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

Answer 4

* 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

Answer 5

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

Answer 6

- 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)

Answer 7

* 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

Answer 8

- 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

Answer 9

- 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

Answer 10

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

Answer 11

- 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

Answer 12

- 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

Answer 13

* 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

Answer 14

- 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

Answer 15

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

Answer 16

* 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

Answer 17

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

Answer 18

* 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

Answer 19

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

Answer 20

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

Answer 21

* 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

Answer 22

* 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

Answer 23

- 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)

Answer 24

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

Answer 25

- 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

Answer 26

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

Answer 27

• 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

Answer 28

- 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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

* 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

Answer 33

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)

Answer 34

* 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

Answer 35

- 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

Answer 36

- alcohol and viral cirrhosis | - portal hypertension

Answer 37

thrombosis in portal or splenic vein

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

- cirrhosis - portal hypertension - schistosomiasis infection - alcoholism

Answer 42

- 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

Answer 43

* 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

Answer 44

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

Answer 45

endoscopy to find bleeding source

Answer 46

- 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

Answer 47

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

Answer 48

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

Answer 49

- 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

Answer 50

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

Answer 51

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

Answer 52

- 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

Answer 53

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

Answer 54

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

Answer 55

* 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)

Answer 56

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

Answer 57

- 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

Answer 58

- 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

Answer 59

- vinyl chloride | - silica dust

Answer 60

- 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

Answer 61

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

Answer 62

- barium swallow - CXR - manometry

Answer 63

same as for GORD. e.g. PPIs

Answer 64

- 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

Answer 65

- 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

Answer 66

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

Answer 67

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

Answer 68

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

Answer 69

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

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

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

Answer 74

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

Answer 75

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

Answer 76

- pancreatic insufficiency - defective bile secretion - bacterial overgrowth

Answer 77

- 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

Answer 78

- 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)

Answer 79

* 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

Answer 80

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

Answer 81

* 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

Answer 82

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

Answer 83

- lymphoma | - TB

Answer 84

• 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

Answer 85

gliadin in wheat, hordeins in barley and secalins in rye

Answer 86

- 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

Answer 87

- 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

Answer 88

- 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

Answer 89

- 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

Answer 90

- 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

Answer 91

- 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

Answer 92

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

Answer 93

- low Hb - low B12 - low ferritin

Answer 94

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

Answer 95

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

Answer 96

- 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

Answer 97

- 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

Answer 98

* 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

Answer 99

* 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

Answer 100

- 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

Answer 101

- 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

Answer 102

- 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

Answer 103

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

Answer 104

- 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

Answer 105

- 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

Answer 106

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)

Answer 107

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

Answer 108

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

Answer 109

• 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

Answer 110

- 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

Answer 111

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

Answer 112

* 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

Answer 113

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

Answer 114

- 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

Answer 115

- clubbing - aphthous oral ulcers - erythema nododum - amyloidosis

Answer 116

- fatty change - chronic pericholangitis - sclerosing cholangitis

Answer 117

- blood loss - perforation - toxic dilatation - colorectal cancer

Answer 118

- erythema nodosum | - pyoderma gangrenosum

Answer 119

- ankylosing spondylitis | - arthritis

Answer 120

- iritis - uveitis - episcleritis

Answer 121

- 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

Answer 122

* 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)

Answer 123

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

Answer 124

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

Answer 125

- 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

Answer 126

- sulfalazine - mesalazine - olsalazine

Answer 127

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

Answer 128

glucocorticoids

Answer 129

- hydrocortisone - ciclosporin - infliximab

Answer 130

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

Answer 131

• 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

Answer 132

* 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

Answer 133

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

Answer 134

- 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

Answer 135

- 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

Answer 136

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

Answer 137

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

Answer 138

• 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

Answer 139

* 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

Answer 140

- 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

Answer 141

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

Answer 142

* 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

Answer 143

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

Answer 144

* tenderness of right iliac fossa | * anal examination

Answer 145

* 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

Answer 146

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

Answer 147

- 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

Answer 148

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

Answer 149

controlled release corticosteroids e.g. budesonide

Answer 150

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

Answer 151

* 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

Answer 152

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

Answer 153

* 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

Answer 154

* 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)

Answer 155

- 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

Answer 156

- 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

Answer 157

arrest/blockage of onward propulsion of intestinal contents

Answer 158

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

Answer 159

* simple * closed loop * strangulation * intussusception

Answer 160

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

Answer 161

- Crohn's disease | - diverticulitis

Answer 162

* 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

Answer 163

- 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

Answer 164

- 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

Answer 165

adhesions (80%)

Answer 166

- 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

Answer 167

* 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

Answer 168

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

Answer 169

• 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

Answer 170

- 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

Answer 171

* 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

Answer 172

* ischaemia * necrosis * perforation

Answer 173

- 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

Answer 174

- 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

Answer 175

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

Answer 176

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

Answer 177

* 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

Answer 178

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

Answer 179

- 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

Answer 180

* 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

Answer 181

- 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

Answer 182

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

Answer 183

empty rectum, hard stools, blood

Answer 184

* 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

Answer 185

- 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

Answer 186

clinical picture mimicking obstruction but with no mechanical cause

Answer 187

* 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

Answer 188

patients present with rapid and progressive abdominal distension and pain

Answer 189

X-ray shows a gas-filled large bowel

Answer 190

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

Answer 191

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

Answer 192

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

Answer 193

* 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

Answer 194

* 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

Answer 195

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

Answer 196

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

Answer 197

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

Answer 198

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

Answer 199

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

Answer 200

- 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

Answer 201

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

Answer 202

* 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

Answer 203

- contraceptive pill - nicorandil drug - thrombophilia - vasculitis

Answer 204

- 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

Answer 205

- 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

Answer 206

other causes of acute colitis, e.g. IBD

Answer 207

- 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

Answer 208

- 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

Answer 209

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

Answer 210

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

Answer 211

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

Answer 212

* 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

Answer 213

- 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

Answer 214

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

Answer 215

origin above the dentate line (internal rectal plexus)

Answer 216

- 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

Answer 217

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

Answer 218

- 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

Answer 219

- perianal haematoma - anal fissure - abscess - tumour

Answer 220

- 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

Answer 221

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

Answer 222

* 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

Answer 223

- excisional haemorrhoidectomy | - stapled haemorrhoidopexy

Answer 224

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

Answer 225

- 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

Answer 226

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

Answer 227

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

Answer 228

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

Answer 229

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

Answer 230

- 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

Answer 231

- 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

Answer 232

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

Answer 233

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

Answer 234

- extreme pain especially on defecation | - bleeding

Answer 235

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

Answer 236

- 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

Answer 237

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

Answer 238

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

Answer 239

- painful swellings - tender - discharge

Answer 240

- MRI | - endoanal ultrasound

Answer 241

- surgical excision | - drainage with antibiotics

Answer 242

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)

Answer 243

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

Answer 244

- 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

Answer 245

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

Answer 246

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

Answer 247

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

Answer 248

detected on clinical examination

Answer 249

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

Answer 250

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

Answer 251

- 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

Answer 252

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

Answer 253

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

Answer 254

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

Answer 255

- 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

Answer 256

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

Answer 257

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

Answer 258

• 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

Answer 259

* 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

Answer 260

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

Answer 261

• 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

Answer 262

- 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

Answer 263

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

Answer 264

* education * reassurance * dietary modification

Answer 265

* pharmacotherapy | * psychological treatment

Answer 266

referral to pain treatment centre

Answer 267

``` • 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 ```

Answer 268

* 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

Answer 269

* 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

Answer 270

- 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

Answer 271

antispasmodics e.g. Mebeverine or Buscopan

Answer 272

- 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

Answer 273

anti-motility agents e.g. loperamide

Answer 274

- 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

Answer 275

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

Answer 276

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

Answer 277

presence of diverticula

Answer 278

caused by diverticula that are symptomatic

Answer 279

inflammation of a diverticulum

Answer 280

- 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

Answer 281

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

Answer 282

- low-fibre diet | - over age of 50

Answer 283

* 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

Answer 284

* 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

Answer 285

• 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

Answer 286

* 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

Answer 287

- 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

Answer 288

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

Answer 289

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

Answer 290

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

Answer 291

usually after repeated episodes of acute diverticulitis

Answer 292

- 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

Answer 293

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

Answer 294

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

Answer 295

- polymorphonuclear leucocytosis | - ESR and CRP raised

Answer 296

- 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

Answer 297

may identify obstruction or free air (indicative of perforation)

Answer 298

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

Answer 299

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

Answer 300

* 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

Answer 301

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

Answer 302

affects 2-3% population

Answer 303

* 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

Answer 304

- 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

Answer 305

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

Answer 306

- 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

Answer 307

* faecolith * lymphoid hyperplasia * filarial worms

Answer 308

- 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

Answer 309

- 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

Answer 310

* 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

Answer 311

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

Answer 312

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

Answer 313

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

Answer 314

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

Answer 315

- pregnancy test | - urinalysis to exclude UTI

Answer 316

* 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

Answer 317

• 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

Answer 318

- 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

Answer 319

- 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

Answer 320

- 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

Answer 321

- 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

Answer 322

* 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

Answer 323

- 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

Answer 324

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

Answer 325

- 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

Answer 326

* 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

Answer 327

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

Answer 328

- 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)

Answer 329

* 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

Answer 330

- 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

Answer 331

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

Answer 332

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

Answer 333

• 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

Answer 334

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

Answer 335

to identify extent of pancreatic necrosis

Answer 336

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

Answer 337

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

Answer 338

- 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

Answer 339

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

Answer 340

- 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

Answer 341

systemic inflammatory response syndrome (SIRS)

Answer 342

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

Answer 343

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

Answer 344

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

Answer 345

* 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

Answer 346

- 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

Answer 347

- 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

Answer 348

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

Answer 349

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

Answer 350

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

Answer 351

- 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

Answer 352

- 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

Answer 353

chronic pancreatic inflammation which results from an autoimmune process

Answer 354

high prevalence in Japan

Answer 355

* 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

Answer 356

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

Answer 357

- 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.

Answer 358

- 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

Answer 359

- 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

Answer 360

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

Answer 361

hepatocellular injury

Answer 362

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

Answer 363

most likely due to Gilbert's disease

Answer 364

- 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

Answer 365

- lack of digestive enzymes - decetive intraluminal digestion

Answer 366

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

Answer 367

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.

Answer 368

1. IBS - bowel 2. functional dyspepsia - stomach

Answer 369

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

Answer 370

True linked to hormonal changes

Answer 371

gastric symptoms in the upper abdomen

Answer 372

gastric symptoms in the upper abdomen

Answer 373

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

Answer 374

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

Answer 375

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

Answer 376

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

Answer 377

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

Answer 378

marker of gut inflammation

Answer 379

IBS that occurs after an bout of gastroenteritis.

Answer 380

* 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

Answer 381

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

Answer 382

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

Answer 383

* 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

Answer 384

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

Answer 385

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

Answer 386

the inferior mesenteric artery

Answer 387

* 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

Answer 388

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

Answer 389

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

Answer 390

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

Answer 391

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

Answer 392

* 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**

Answer 393

* 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

Answer 394

* 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

Answer 395

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

Answer 396

* bowel infarction +/or perforation * strictures *

Answer 397

* 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

Answer 398

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

Answer 399

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

Answer 400

* 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

GI Flashcards

(428 cards)