GI Flashcards

Question

symptoms of Acute Upper GI Bleed

Answer 1

* Haematemesis – coffee-ground vomit indicates less severe * Malaena – offensive, black tarry stool; always indicates a significant bleed * Fresh red bleeding PR = massive upper GI bleed * Faintness/dizziness - shock * Collapse +/- cardiac arrest * Dark blood and clots w/o shock: lower GI bleed * Acute massive upper GI bleeding may present with rectal bleeding  almost always in association with shock

Answer 2

* Cold/clammy and sweating – peripherally shut down * Capillary refill <2 sec – peripherally shut down * Hypotensive/decreased JVP * Postural drop * Sudden tachycardia * Weak pulse * Rapid breathing * Decreased or no urine output * Signs of shock – confusion or lack of alertness

Answer 3

• Lower GI bleed – fresh blood PR

Answer 4

* Upper GI: FBC, LFTs, U&E’s, clotting screen and ‘group and save’ * Both: IV fluids whilst examination and history are undertaken, Rockall risk score – assess risk of rebleeding or death, abdo exam +/- PR, Glasgow-Blatchford bleeding score (GBS) – assess need for intervention e.g. endoscopy, transfusion

Answer 5

• Determine site of bleeding through history (vomiting preceding the haematemesis suggests Mallory-Weiss tear) • Establish IV access i.e. cannula (central line if brisk bleed) • Give IV fluids • Give blood transfusion/colloid if necessary, indications are: - SHOCK – cold nose, pallor, systolic BP <100mmHg, >100 b.p.m - HAEMOGLOBIN - <10g/dL in patients with recent or active bleeding • Give oxygen PRE-ENDOSCOPY: • Stop aspirin, NSAIDs and warfarin and INR reversed • PPIs given to high risk patients who cannot have an endoscopy immediately • Abx given to pateitns with suspected variceal haemorrhage • 85% of bleeding stops on its accord but if not then suggest surgery for thermal therapy

Answer 6

• Mortality remained same for past years at 5-12% due to ↑ elderly with co-morbidities

Answer 7

• Massive bleeds are rare and usually due to diverticular disease or ischaemic colitis; small bleeds = haemorrhoids or anal fissures

Answer 8

* Peptic ulceration - commonest cause (50%) * Oesophageal varices (10-20%) * Oesophagitis/Gastritis (5-10%) * Mallory-Weiss syndrome/tear (5-10%) - haematemesis from a tear in the mucosa of the oesophagus, brought on by prolonged vomiting; linear mucosal tear at the oesophagogastric junction and produced by sudden ↑ in intra-abdo pressure: after bout of coughing or retching; most bleeds are minor and stop spontaneously * Oesophageal/gastric cancer (uncommon) * Swallowed blood from nosebleed * Bleeding after Percutaneous Coronary Inetrvention (PCI)

Answer 9

* Alcohol abuse * Chronic liver disease - bleeding associated with liver disease is often from varices * NSAID use - can produce ulcers and anticoagulation = bigger bleed) * H. Pylori * Oral steroid use * Anticoagulant use * Evidence of co-morbidity (HF, IHD, renal disease, malignant disease)

Answer 10

* Fresh blood PR, brisk bleeding – medical emergency * Mixed blood and stool – bleeding proximal to sigmoid colon * Blood around stool – more distal bleed * Blood on toilet paper/in pan – anal bleeding e.g. haemorrhoids/anal fissure

Answer 11

* Cold/clammy and sweating – peripherally shut down * Capillary refill <2 sec – peripherally shut down * Hypotensive/decreased JVP * Postural drop * Sudden tachycardia * Weak pulse * Rapid breathing * Decreased or no urine output * Signs of shock – confusion or lack of alertness

Answer 12

* Lower GI: proctoscopy to look for anorectal disease (e.g. Piles), sigmoidoscopy or colonoscopy for IBD, polyps, colon cancer, diverticula disease, ischaemic colitis, vascular esions, angiography for vascular abnormality (e.g. angiodysplasia) * If patient is <45 y/o and isolated bleeding, DRE and flexibile sigmioidoscopy only required as probability of a significant proximal lesion is very low unless a strong Fx of CRC at young age

Answer 13

* Most acute lower GI bleeds start and stop spontaneously * If they don’t stop and patient is haemodynamically unstable then follow immediate steps as for acute upper GI bleed * Surgery is rarely required

Answer 14

• Upper GI bleed – haematemesis, melaena

Answer 15

* Chronic inflammatory disease characterized by transmural granulomatous inflammation affecting any part of the gut from mouth to anus (especially terminal ileum in approx. 70%) * Unlike UC, there is unaffected bowel between areas of active disease

Answer 16

* 10-20/100 000, typically presents 20-40yrs of age * World-Wide distribution but more in northern Europe, UK and North America * Increased likelihood in Hispanic, Asians, Jewish races * Equal distribution between males and females * Common in smokers

Answer 17

* Genetic Susceptibility: genetic association is strong in CD, familial aggregation of the disease, concordance rates are higher in monozygotic (58%) than dizygotic (4%), CARD15(NOD2) gene on chromosome 16 confer susceptibility * Environment: smoking is associated with a two-fold increased risk, stress and depression may precipitate relapses in IBD, altered enteric microflora, appendicectomy may result in more aggressive, NSAIDs, oral contraception * Host Immune Response: IBD results from a defective mucosal immune system producing an abnormal response to luminal antigens such as bacteria which enter the intestine via a leaky epithelium, E. coli, more anaerobic bacteria, disrupted toll like receptor signalling

Answer 18

``` Genes, Smoking Stress Depression Appendectomy NSAIDs Oral Contraceptives Fx ```

Answer 19

* Affects: all GI tract – especially terminal ileum and ascending colon, rectum involved in 50% of cases, lesions are patchy (unaffected areas between areas of disease) * Macroscopic: small bowel thickened, deep ulcers and fissures in mucosa, cobblestone appearance, fistulae and abscesses in colon, aphthoid ulceration is an early features * Microscopic: granulomas present in 50-60% non-caseating epithelioid cell aggregates with Langhans’ giant cells * Inflammation: transmural/deep * Strictures: common * Crypt Abscesses: uncommon * Goblet Cells: present

Answer 20

• SYMPTOMS DEPEND ON THE REGIONS OF INVOLVED BOWEL - Commonest site is ileocecal (40% of patients) - Small Bowel = pain, weight loss, steatorrhoea - Terminal Ileal Disease = acute abdomen with right iliac fossa pain mimicking appendicitis (uncommon) - Colonic Disease = diarrhoea, bleeding and pain related to defecation - Perianal Disease = anal tags, fissures, fistulae an abscess formation, full thickness of wall is inflamed - Extra Intestinal Manifestations = iritis, arthritis, erythema nodosum and pyoderma gagrenosum

Answer 21

* Mouth Ulcers * Signs of systemic illness – anorexia, fatigue, malaise, fever and clubbing * Anal or peri-anal skin tag fistula or abscess * Abdominal pain and tenderness – with tenderness or a mass in lower right quadrant * Aphthous ulcers * Joint arthritis * Conjunctivitis/uveitis * Pyoderma gangrenosum * Fatty liver * Malnutrition

Answer 22

* Infective colitis – systemic Sx; following travel/infection risk * IBS – diagnosis of exclusion; alternating diarrhoea and constipation; related to certain foods * Coeliac disease – malnutrition; related to certain foods * Diverticulitis – affects elderly * Endometriosis * Intestinal ischaemia

Answer 23

1. 1st LINE: - FBC – thrombocytosis is a useful marker of active inflammation, leucocytosis associated with acute or chronic inflammation, abscess or corticosteroid treatment, anaemia can be due to chronic inflammation - IRON STUDIES – serum iron, serum ferritin, total iron binding capacity, transferrin saturation - SERUM VIT B12 AND SERUM FOLATE - CMP – comprehensive metabolic panel - CRP AND ESR - STOOL TESTING - YERSINIA ENTERCOLITICA SEROLOGY – pathogen which causes an acute ileitis, should be negative in crohns - ABDO X-RAY, CT ABDO, MRI ABDO/PELVIS - COLONOSCOPY – shows disease extent, allows for biopsy, first line investigation for diagnosis • RECTAL BIOPSY – diagnosis usually made from this, can differentitate between UC and CD

Answer 24

* Lifestyle – smoking cessation, nutrition * Screening – screen for CRC, ensure the risk of osteoporosis is managed * Pain – manage with analgesics, paracetamol preferred * Corticosteroids – topical preferred to systemic, only used for induction of remission * Immunosupressant’s – azathioprine, merceptopurine and methotrexate OR cyto-line modulating drugs such as infliximab and adalimumab * Treatment is not always needed in mild Crohn’s (18% entered remission with a placebo)

Answer 25

INDUCTION OF REMISSION: • Glucocorticoids useful in moderate-severe attacks of CD (oral prednisolone 30-60mg/day) • Enteral nutrition; efficacy independent of nutritional status; low fat diets best • Infliximab: anti-TNF-α monoclonal Ab induces remission in corticosteroid/immunosuppressive resistant pts and helps maintain it; infusion reactions may occur via host Ab against infliximab Ab. MAINTENANCE OF REMISSION: • Azathioprine, 6-mercaptopurine, methotrexate, mycophenolate mofetil; rate of relapse on discontinuation of drugs is ~70%! SURGERY: • ~80% patients will require surgery at some point of their disease but should be avoided if possible as recurrence in 15%/year is inevitable • Panproctocolectomy and end-ileostomy (remove rectum, colon and attach ileum to skin surface of stomach) may be needed => ileostomy is lifelong and has its own problems

Answer 26

* Prognosis is poorer if steroids required at diagnosis, early presentation, perianal or structuring disease, weight loss >5kg. * Relapses and remissions are unpredictable and vary. Many will have lots of relapses at beginning.

Answer 27

* Strictures * Fistulae * Perforation * Haemorrhage * Colorectal cancer * Toxic megacolon * Anaemia – iron or B12/folate * Osteoporosis- due to steroid therapy * Renal disease – due to obstruction of right ureter by ileocaecal disease

Answer 28

* Relapsing and remitting inflammatory disorder of the colonic mucosa * May affect just the rectum (proctitis, as in around 30%) or extent to involve part of the colon (left sided colitis, in 40%) or the entire colon (pancolitis, in 30%) * Never spreads proximal to the ileocaecal valve (except for backwash ileitis)

Answer 29

* World-Wide distribution but more in northern Europe, UK and North America * Increased likelihood in Hispanic, Asians, Jewish races * Equal distribution between males and females * Common in smokers

Answer 30

* Genetic Susceptibility: genetic association is stronger in CD than UC, familial aggregation of the disease * Environment: smoking halves the risk of UC, stress and depression may precipitate relapses in IBD, altered enteric microflora, appendicectomy may result in more aggressive, NSAIDs, oral contraception * Host Immune Response: IBD results from a defective mucosal immune system producing an abnormal response to luminal antigens such as bacteria which enter the intestine via a leaky epithelium, E. coli, more anaerobic bacteria, disrupted toll like receptor signalling

Answer 31

• Genes, Smokng, Stress, Depression, Appendectomy, NSAIDs, Oral Contraceptives and Fx

Answer 32

* Affects: rectum is always involved, colon, appendix, and terminal ileum (in backwash ileitis), continuous rather than patchy * Macroscopic: mucosa is reddened, inflamed and bleeds easily, ulcers may be present if severe with adjacent mucosa appearing as inflammatory polyps * Microscopic: mainly mucosal, with inflammatory cells in lamina propria, no granulomas * Inflammation: superficial * Strictures: uncommon * Crypt Abscesses: common * Goblet Cells: depletion

Answer 33

* Diarrhoea – often containing blood and mucus, may be persistent, relapses, remissions or severe fulminant colitis * Faecal Urgency with Nocturnal Defecation * Tenesmus – persistent, painful urge to pass stool even when rectum is empty * Abdominal Pain – particularly in the lower left quadrant * Pre-Defecation Pain – relieved upon passage of stool

Answer 34

* Extra-intestinal Manifestations – uveitis, irits, inflammatory arthritis, erythema nodosum, pyoferma gangrenosum, fatty liver, mouth ulcers * Weight Loss – faltering growth in children, anorexia, malnutrition * Signs of Systemic Illness – fatigue, malaise, fever and clubbing

Answer 35

* Infective colitis – systemic Sx; following travel/infection risk * IBS – diagnosis of exclusion; alternating diarrhoea and constipation; related to certain foods * Coeliac disease – malnutrition; related to certain foods * Diverticulitis – affects elderly * Endometriosis * Intestinal ischaemia

Answer 36

• 1st LINE: - STOOL STUDIES: faecal calprotectin – elevated when there is bowel inflammation - FBC: may show leucocytosis, thrombocytosis and anaemia - CMP – LFTs - ESR AND CRP - PLAIN ABDO RADIOGRAPH - FLEXIBLE SIGMOIDOSCOPY - COLONOSCOPY – indicated in patients with UC who are not responding well to treatment in order to rule out infections - BIOPSIES

Answer 37

DRUGS: - Aminosalicylate/mesalazine; released in terminal ileum when right pH; mechanism unknown but induce remission in mild-moderate and maintain remission in all forms of disease - If moderate-severe flare ups in the past 3 years, consider starting azathioprine SURGERY: - May be life-saving, curative and eliminates cancer risk; subtotal colectomy with end-ileostomy is common procedure

Answer 38

* Lifestyle – smoking cessation, nutrition * Screening – screen for CRC, ensure the risk of osteoporosis is managed * Pain – manage with analgesics, paracetamol preferred * Corticosteroids – topical preferred to systemic, only used for induction of remission * Immunosupressant’s – azathioprine, merceptopurine and methotrexate OR cyto-line modulating drugs such as infliximab and adalimumab * Treatment is not always needed in mild Crohn’s (18% entered remission with a placebo)

Answer 39

Prognosis is poorer if steroids required at diagnosis, early presentation, perianal or structuring disease, weight loss >5kg. • Relapses and remissions are unpredictable and vary. Many will have lots of relapses at beginning. ``` complications: • Strictures • Fistulae • Perforation • Haemorrhage • Colorectal cancer • Toxic megacolon • Anaemia – iron or B12/folate • Osteoporosis- due to steroid therapy • Renal disease – due to obstruction of right ureter by ileocaecal disease ```

Answer 40

• IBS is a functional bowel disorder – means that symptoms occur in the absence of any demonstrable abnormalities in the digestion and absorption of nutrients, fluid and electrolytes and no structural abnormality can be identified in the GI tract • Denotes a group of abdominal symptoms for which no cause can be found • It can be classified as: - IBS-D – diarrhoea predominated - IBS-C – constipation predominated - IBS-A – alternating stool pattern - Pain-predominant IBS - IBS-PI – post-infective • Co-exists with chronic fatigue syndrome, fibromyalgia, temporomandibular joint dysfunction

Answer 41

* Prevalence 10-20% * Most common functional gastrointestinal disorder (FGID) * Up to 1 in 5 patientss report symptoms suggestive of IBS – only 50% of which will consult doctors and up to 30% of these will be referred to hospital

Answer 42

* 20-30 years of age most common * Twice a scommon in F vs M  due to higher anxiety and depression in women - gut more sensitive; women more focussed on internal events; food and eating have more psychological significance; pelvic region carries more significance (defecation, urination, sexuality AND pregnancy, childbirth, menstruation); women more likely to seek medical attention anyway.

Answer 43

• The cause is unknown but it is thought to be due to biopsychosocial interactions that may interact to cause dysregulation of brain-gut function

Answer 44

* Affective disorders: depression, (hypochondrial) anxiety * Psychological stress and trauma, life events * GI infection * Ax therapy * Sexual, physical, verbal abuse * Pelvic surgery * Eating disorders * Female! * Severity and duration of diarrhoea

Answer 45

• Abdominal Pain – described as crampy, relieved by defecation or the passage of wind • Altered Bowel Habit – sensation of incomplete evacuation (tenesmus), abdominal bloating and distention are common symptoms • Morning Rush – urgent need to defecate in the morning and several times through breakfast • Subtypes can be identified corrding to the predominant stool pattern - IBS-D – diarrhoea predominated - IBS-C – constipation predominated - IBS-A – alternating stool pattern - Pain-predominant IBS - IBS-PI – post-infective • Psychological Problems - anxiety, depression • Extra-intestinal Symptoms - headache, asthma, backache, lethargy, dyspareunia, urinary frequency and urgency, dysmenorrhoea • Signs may be few and non-specific e.g. tenderness

Answer 46

* IBD – no constipation; aphthous ulcers; blood/mucous in stools * Coeliac disease * Gastroenteritis – acute; no constipation; could be infective trigger for IBS * Colorectal carcinoma – older presentation; red flag symptoms

Answer 47

• No investigations to confirm – rectal biopsy shpuld be taken (if frequency of defecation is a feature) to exclude IBD • 1st LINE: - FBC – if anaemic or FBC count is raised, other diagnoses should be considered - STOOL STUDIES – performed if the patient has diarrhoea - ANTI-ENDOMYSIAL ANTIBODIES – may be ordered if the patient has a diarrhoea component and/or weight loss and coeliac disease is suspected - ANTI-tTG Abs – may be ordered if the patient has a diarrhoea component and/or weight loss - PLAIN ABDO X-RAY - FLEXIBLE SIGMOIDOSCOPY - COLONOSCOPY – should be performed if the patient is >50 years or has a FX of a firstdegree relative with a colon neoplasm <60yrs but is not nexessary in younger pts • Manning and Rome II criteria to help establish a diagnosis

Answer 48

Referral: • If diagnosis unsure • If changing symptoms in ‘known IBS’ • To surgeon if rectal mucosal prolapse • To dietician if food intolerance • To psycho/hypno-therapist if stress of depression or refactory symptoms • To gynaecologist If cyclical pain, dyspareuinia, dysmennorhoea as endometriosis can mimic IBS • To dermatologist if co-existing atopy • To pain clinic if chronic pain overlap syndromes (fibromyalgia, chronic fatigue, chronic pelvic pain)

Answer 49

NUTRITION: • Explore dietary triggers • High fibre diet and fibre supplements for constipation – refer to dietician and prescribe ISPAGHULA HUSK DRUGS: • Antidiarrhoeal drugs for bowel frequency – loperamide, codeine, co-phenotrope • Smooth muscle relaxants for pain - mebeverine hydrochloride, dicycloverine hydrochloride, peppermint oil • Antidepressants - clomipramine in functional diarrhoea, TCAs (amitriptyline) in IBS-D, SSRIs (paroxetine) in IBS-C

Answer 50

* In 50% Sx go or improve after 1 year. * More than 50% will continue to have Sx after 5 years. * <5% worsen.

Answer 51

* Infection of the stomach and intestinal tract that involves some sort of combination of diarrhoea, vomiting and abdominal pain and cramping * It is also referred to as infectious diarrhoea, gastro, stomach bug and stomach virus

Answer 52

* Most common form of acute GI infection, causing diarrhoea +/- vomiting * Especially in developing world; 2.25 million still die/year despite oral rehydration programmes * Less common and less likely to cause death in Western world * Major cause of morbidity in elderly though * Travellers to developing countries, homosexual men, infants in day care facilities are also at risk

Answer 53

* Viral - common cause of D+V in young children; rarely seen in adults unless an outbreak in hospital; norovirus is the most common * Bacterial - most common cause of significant adult gastroenteritis; can cause watery diarrhoea or dysentery (severe and mixed with blood and mucous) * Parasitic – protozoa; most commonly giardia lamblia; also entamoeba histolytica cryptosporidium MECHANISMS – cannot distinguish bacterial/viral based on clinical evidence alone - Mucosal Adherence – most bacteria must adhere to specific receptors in the gut mucosa e.g. pili, fimbriae, may be the prelde to invasion or toxin production though EPEC causes diarrhoea just by binding - Mucosal Invasion – penetration of intestinal mucosa e.g. shigella, EIEC, campylobacter, entrty helped by ‘invasins’ which disrupt the cell’s cytoskeleton, destruction of cells causes the symptoms of dysentery: low volume bloody diarrhoea and abdominal pain - Toxin Production – enterotoxins: bacteria bind to intestinal epithelium, induce excessive fluid secretion into bowel lumen causing watery diarrhoea w/o damage to cell (so no blood) e.g. cholera, ETEC, cytotoxins: damage intestinal mucosa and vascular endothelium sometimes too TYPES OF BACTERIAL/VIRAL INFECTION CAUSES: - Salmonella: commensals in bowels of livestock (esp poultry) and in oviducts of chickens (which is why eggs can be infected); produce enterotoxins and invade mucosa - Campylobacter (jejuni): bowel commensal of livestock; worldwide; childhood gastroenteritis; undercooked meat - Shigella: (S. dysenteriae, S sonnei, S flexneri); spread by poor hygiene - ETEC: enterotoxins; common in developing countries so cause of travellers’ diarrhoea - EHEC (usually O157: H7 serotype): also known as verotoxin producing E coli (VTEC); associated with cattle; outbreaks (Scotland, Japan) associated with contaminated food; secretes Shiga-like toxin 1 affecting vascular endothelial cells in gut and kidney; after some days pts may develop thrombotic thrombocytopenic prupura or haemolytic uraemic syndrome; treatment is supportive - Bacillus cereus: 2 toxins; one produces watery diarrhoea, the other is preformed in food and causes severe vomiting (‘fried rice poisoning’) - Staph A: some strains produce heat stable (enterotoxin B); due to poor food hygiene; as toxin is preformed in contaminated food onset of symptoms is rapid - C diff: causes Abx-associated diarrhoea, colitis and pseudomembranous colitis; G+ve, anaerobic, spore-forming bacillus; found in normal bowel flora of 3-5% of pop and up to 20% of hospital pts; produces 2 toxins: toxin A (enterotoxin), toxin B (cytotoxic = bloody diarrhoea); all Abx but esp with quinolones (ciprofloxacin); begin with 2-30 days of starting Abx; symptoms mild diarrhoea to watery haemorrhagic colitis and abdo pain; colonic mucosa inflamed and ulcerated and can be covered by an adherent membrane-like material (psurodmembranous colitis); can lead to death; detect toxins A or B in stools by ELISA; metronidazole 400mg TDS or vancomycin 125mg QDS; isolation of pts!, need CT/X-ray to exclude toxic megacolon

Answer 54

* Poor personal hygiene * Lack of sanitation * Immunocompromisation * Achlorydhia (when acid production in stomach is absent or low) * Increased age or very young * Poorly/un-cooked food * Food left at room temperature for too long * Insufficient reheating of food – even if reheating kills all bacteria enterotoxins are not destroyed

Answer 55

* Diarrhoea – watery or mixed with blood/mucous (dysentery) – blood means more likely bacterial * Vomiting * Abdominal pain/cramps * Fever – usually viral infections * Fatigue – usually viral infections * Headache – usually viral infections * Muscle pain – usually viral infections signs • Usually none apart from maybe abdo tenderness or pyrexia.

Answer 56

* IBD – chronic; aphthous ulcers; no vomiting * IBS – chronic; no vomiting; constipation * Coeliac disease – chronic; no vomiting * Colorectal cancer – elderly; red flag Sx * UTI – urinary Sx * Chest infections in elderly – resp Sx * Malaria

Answer 57

• 1st LINE: - STOOL CULTURE: positive for causative bacteria - STOOL MICROSCOPY: presence of RBCs and neutrophils

Answer 58

• 1ST LINE: Adequate hydration - ADJUNCT: antimotolity agents such as loperamide  other than those with bloody diarrhoea or fever • Antibiotic therapy is not usually given as the illness is self-limiting - Abx are actively avoided in patients with suspected ENTEROHAEMORRHAGIC E.COLI INFECTION - Only given in immunocompromised, pregnant women and those with symptoms lasting over a week - May increase the risk of HUS (haemolytic uraemic syndrome) • Empirical Abx therapy = ciprofloxacin and metronidazole  given to patients with severe symptoms or bloody diarrhoea, pending the results of the stool sample

Answer 59

* Oral rehydration solutions (ORS) * Abx if systemically unwell, elderly, immunocompromised * For severe symptoms (but not dysentery) give antiemetics (prochlorperazine) and antidiarrhoeals (codeine or loperamide) * Shigella, Campylobacter and Salmonella: ciprofloxacin 500mg/12hrs PO * Cholera: tetracycline reduces transmission * Food poisoning is a notifiable disease in the UK

Answer 60

* Usually a self-limiting disease with spontaneous recovery. * In children, acute gastroenteritis has a ↑ mortality due to dehydration; death and serious morbidity are less common but can still occur esp in developing countries and elderly.

Answer 61

* Dehydration * IBS * Haemolytic uraemic syndrome – rare; usually affects young children and elderly

Answer 62

* This is acute inflammation of the pancreas, releasing exocrine enzymes that cause autodigestion of the organ * There may be involvement of local tissues and distant organs - this is not to be confused with chronic pancreatitis

Answer 63

* UK incidence = 150-420 cases per million and rising. | * There is significant geographical variation - much higher in Scandinavia and USA

Answer 64

I GET SMASHED - gallstones and alcohol account for majority of cases - Idiopathic - Gallstones - account for majority of cases; block the bile duct causing back pressure in the main pancreatic duct and increased cytosolic calcium - Ethanol/alcohol - account for majority of cases; seems to be reason for geographic variation in prevalence; changes calcium homeostasisi in pancreatic acinar cells - Trauma – blunt trauma - Steroids - Mumps (Coxsackie B) - Autoimmune (+ tumour) - Scorpion stings - Hyperlipidaemia/hypercalcaemia - ERCP (post-endoscopic retrograde cholangiopancreatography) - Drugs - azathioprine, diuretics, oestrogens, corticosteroids, didanosine

Answer 65

* Epigastric/central abdominal pain – gradual or sudden severe (tpical) * Radiates to back * May be relieved by sitting forward/foetal position and worsens with movement * Vomiting * May be generalised with peritonism if peritonitis is suspected

Answer 66

* Abdominal tenderness - varies from mild tenderness in the upper abdomen to generalised peritonitis, rebound tenderness, and guarding in more severe attacks. * Abdominal distention - common in attacks of acute pancreatitis. Caused by a leakage of fluid into the retroperitoneum in an effort to dilute pancreatic enzymes, causing abdominal contents to be pushed forward. * A bluish discoloration - around the umbilicus (Cullen’s sign); or the flank (Grey-Turners sign) is sometimes associated with haemorrhagic pancreatitis (a late, serious complication) caused by blood vessel autodigestion and retroperitoneal haemorrhage, suggest necrotising pancreatitis

Answer 67

* Any acute abdomen pain | * Ruptured/dissecting AAA – unzipping pain; hypotension; shock

Answer 68

1st LINE: - SERUM AMYLASE: sensitive, 3x than upper limit of normal when measured within 24hrs of onset of pain, raised amylase may also be caused by cholecysits, mesenteric infarction, GI perforation, renal failure (as it is excreted renally), amylase will fall back to normal within 3-5 days so late presentation may result in false –ve diagnosis - SERUM LIPASE: more sensitive, preferred to amylase, increased - CRP – assess disease severity and prognosis - OTHER BASELINE LEVELS – FBC, U&E’s, glucose, LFT, Plasma Ca, ABG - CXR – mandatory to exclude gastroduodenal perforation which increases serum amylase, may also see gllastones or pancreatic calcification - ABDO USS – screening test to identify biliary (gallstone) cause, distal bile duct obstruction difficult to detect but there will be dilated intrahepatic ducts, stones in GB cannot be used to diagnose gallstone-related pancreatitis - CONTRAST-ENHANCED SPIRAL CT – essential in all except mild attacks of pancreatitis, do it after 72hrs to assess extent of pancreatic necrosis and prognosis info and complications - MRI – assess degree of pancreatic damage and identifies gallstones in biliary tree - ERCP – treatment measure to remove bile duct stones in gallstone-related pancreatitis • Majority of cases of pancreatitis are mild, but 25% run into complications  haemodynamic instability and multiple organ failure, early clinical assessment is not sensitive enough to predict severity MODIFIED GLASGOW CRITERIA – FOR PREDICTING SEVERITY OF PRANCREATITIS: • Have been validated for prancreatitis caused by gallstones and alcohol • Within 48hrs • Could also do RANSON’S CRITERIA for ALCOHOL INDUCED PANCREATITIS – only valid after 24hr ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION II (APACHE II) SCORE: • Used to predict severity in a number of diseases and is adjusted for age and other chronic health problems • Very sensitive even within first 24hrs for presentation

Answer 69

• Similar regardless of cause; score pts within 24hrs and again at 72hrs VACCINES - Vital signs monitoring (O2) - determine need for O2 therapy; give anticoagulant too - Analgesia/Abx - pethidine and tramadol for immediate post-presentation pain control, or pt-controlled system (eg fentanyl); morphine/diamorphine best avoided as theoretically could ↑ pancreatic ductular hypertension by causing Sphincter of Oddi contraction; prophylactic broad-spectrum Abx (cefuroxime) ↓ risk of infective complications and are given from the outset - Catheter/calcium gluconate - if necessary - Cimetidine (H2 receptor) - IV access and fluids - NBM/Nutrition - total parenteral needed as ↓ chance of oral feeding for a few weeks - Empty gastric contents (nasogastric tube) - nasogastric suction prevents abdominal distension and vomitus so the risk of aspiration pneumonia - Surgery if required/Senior review * If gallstone-related pancreatitis and bile duct obstruction, sphincterotomy and stone extraction best * If no evidence of bile duct obstruction, then perform only if severe pancreatitis * If less severe then ? MRCP

Answer 70

* 80% have mild disease and recover without complications. * Progression to chronic pancreatitis occurs only in 6%. * Severe cases may have pancreatic insufficiency for a couple of years following. * 5% mortality in mild cases; 30% in severe cases.

Answer 71

PAIN: - Peripancreatic fluid collections/Pseudocyst - peripancreatic fluid collections are common but most resolve spontaneously; if fluid collection surrounded by granulation tissue = pseudocyst and are not fully formed until 6/52 after onset of illness; small <6cm pseudocysts resolve spontaneously but bigger ones may cause infection, intraperitoneal bleeding or gastric outlet obstruction => endoscopic drainage - Abscesses – usually present several months after an attack and require surgery - Infection - biggest concern; may develop into sepsis so hence prophylactic Ax; may require surgical resection of necrotic pancreas as well as IV Ax - Necrosis – infection occurs in most cases; needs surgical debridement

Answer 72

• Chronic pancreatitis is long-standing inflammation which leads to irreversible damage to the pancreas and can present with recurrent acute inflammations in a previously damaged pancreas, chronic inflammation with pain or malabsorption.

Answer 73

* Worldwide prevalence is 4-5%. * Male:Female 4:1. * Median age 51y.

Answer 74

• The causes are the same as for acute pancreatitis but the mechanism is not fully understood. - The most common thought is that there is obstruction or reduction of bicarbonate excretion - this in turn leads to activation of pancreatic enzymes, 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, as in cystic fibrosis, or mechanical, such as trauma. - Alcohol causes proteins to precipitate in the ductular structure of the pancreas - This leads to local pancreatic dilatation and fibrosis - This is not seen in patients with recurrent attacks of acute pancreatitis associated with alcohol use - There may be direct toxic effects of alcohol on the pancreas  noted that patients who drink 'normal' amounts of alcohol can also develop chronic pancreatitis, ie a dose-response relationship does not exist. - It may be that there is excessive free radical formation which leads to pancreatic damage - some trials have looked at the role of antioxidants (e.g. selenium and methionine) and pain relief with promising results. • Some Other Causes: - Tropical chronic pancreatitis - children and young adults; aetiology unknown - Hereditary chronic pancreatitis - autosomal dominant, variable penetrance; trypsinogen gene mutations => 100x ↑ risk of cancer - Autoimmune chronic pancreatitis - middle-aged men; anti-nuclear factor and ↑ IgG4. - Cystic fibrosis - almost all pts with CF usually from birth - Tumours - benign/malignant

Answer 75

• Suspect it in anyone with chronic or recurrent upper or generalised abdominal pain, particularly if they have a history or clinical features of alcohol misuse. Pain is present in 20% of people with chronic pancreatitis, when present it is usually: - Deep, severe, and dull in the epigastric region. It may radiate to the back, or may be localised to the right or left upper quadrants. - May be intermittent, constant, or with superimposed acute flares - Sitting upright and leaning forward may relieve it - May be associated with nausea and vomiting • Ask about other symptoms: bloating, abdominal cramps, excessive flatulence, weight loss, malnutrition, steatorrhea, diabetes mellitus, impaired glucose regulation, jaundice, steatorrhoea

Answer 76

* Signs of Chronic Liver Disease – for alcohol misuse * Epigastric Tenderness * Jaundice – concomitant liver disease or mechanical obstruction of the extrahepatic bile duct by a mass in the head of the pancreas or pseudocyst * Abdominal Distention – pseudocyst, pancreatic ascites or pancreatic cancer * Firm Skin Nodules – due to a disseminated fat necrosis * SOB – due to fluid leaking from a ruptured duct or pseudocyst and tracking to the pleural space

Answer 77

• Pancreatic malignancy - consider if short history and localised ductular abnormality

Answer 78

• In a patient with known alcohol abuse and typical pain, few investigations are needed INVESTIGATIONS: - Serum Amylase and Lipase – rarely raised if chronic pancreatitis - Faecal Elastase – abnormal in the majority of patients with moderate-severe pancreatitis, due to malabsorption - Transabdo USS/Contrast-Enhanced Spiral CT – in presence of pancreatic calcification, a dilated pancreatic duct is characteristic of chronic pancreatitis, helps to exclude other conditions e.g. gallstones - LFTs – may be abnormal if there is coexistent liver disease or compressionof the intra-pancreatic bile duct (e.g. pseudocyst or fibrosis)

Answer 79

LIFESTYLE: • Don’t smoke or drink • Low fat diet – due to inability to digest DRUGS: • Analgeisa – pain relief • Pancreatic enzyme supplementation (Creon) and fat soluble vitamins (A, D, E, K) • Treatment of hypertriglycaemia or hypercalcaemia • Treatment of diabetes mellitus secondary to chronic pancreatitis SCREENING: • Diabetes mellitus • Osteoporosis • REFER IMMEDIATELY IF UNEXPLAINED PROGRESSIVE WEIGHT LOSS AS WELL SURGERY: • For unremitting pain, narcotic abuse or decreased weight – pancreatectomy or pancreacticojejunostomy

Answer 80

• 1/3 patients will die within 10 years – increased mortality and morbidity.

Answer 81

* Pancreatic pseudocyst - a fluid collection surrounded by granulation tissue * Diabetes * Biliary obstruction * Local arterial aneurysm * Pancreatic carcinoma * Intra-or retroperitoneal cyst rupture - bleeding or cyst infection may occur

Answer 82

Crystalline concretions formed within the gallbladder by accretion of bile components. Also called cholelithiasis.

Answer 83

• 15% of people in adult Western world develop gallstones.§

Answer 84

5F’s: | - Fair, Fat, Fertile, Female and Forty

Answer 85

TWO TYPES OF GALLSTONES: • CHOLESTEROL GALLSTONES: - MOST COMMON - Due to cholesterol crystallisation into stones and depends on cholesterol supersaturation of bile relative to bile salts and phospholipids, crystallisation-promoting factors in bile and motility of GB • BILE PIGMENT STONES: - Small and ark - Comprise of bilirubin and calcium salts found in bile - Black = calcium bilirubinate and calcium carbonate/phosphate; seen in 40-60% of patients with haemolytic conditions e.g. sickle cell anaemia and hereditary spherocytosis - Brown = calcium salts of fatty acids and calcium bilirubinate, almost always found in the presence of bile stasis and/or biliary infection; common cause of recurrent stones • MIXED STONES: - Usually contain cholesterol, calcium salts and pigment - Because of their calcium content they are often radiographically visible

Answer 86

* Increasing age * Female * Family history * Obesity * Sudden weight loss * Loss of bile salts – e.g. ileal resection, terminal ileitis * Diabetes – as part of metabolic syndrome * Oral contraception – especially in younger women; increases cholesterol in bile and decreases gallbladder movement * Smoking * Parity * Crohn’s * Higher levels of serum triglycerides and lower levels of high density lipoprotein

Answer 87

• 90% ARE ASYMPTOMATIC – INCREASINGLY DETECTED INCIDENTALLY • CAN PRESENT IN SEVERAL WAYS: - BILIARY/GALLSTONE COLIC: o Epigastric/RUQ pain - due to temporary obstruction of cystic duct or common bile duct by a stone migrating from the GB o Pain radiates round to back in interscapular region o Normally severe and crescendo-like o Jaundice – obstructive due to blockage of common bile duct o High fatty food intake o Common during mid-evening/early hours of morning o Nausea and vomiting if severe attack - ACUTE CHOLECYSTITIS – stones cause 95% of cases – MOST COMMON: o Obstruction results in ↑ GB secretions = ↑ GB distension = compromise vascular supply = inflammatory and immune response o Epigastirc/RUQ pain o Referred to the right shoulder/tip of scapula o Vomiting – main difference between biliary colic; peritonism o Fever – main difference between biliary colic; peritonism o Jaundice – if stone moves to block common bile duct; obstructive - CHOLANGITIS – bile duct infection o Bile duct infection causing RUQ pain, jaundice, rigors

Answer 88

• MURPHY’S SIGN - place 2 fingers on RUQ, ask pt to breathe in, causes pain and stops breathing as inflamed GB impinges on fingers, only +ve if not present in LUQ

Answer 89

• Peptic ulcer disease, gastritis, IBS, GORD, pancreatitis from other causes, tumours of the liver, gallbladder, stomach, gut and pancreas. Acute hepatitis, IBD, bile duct stricture. These may also occur at the same time as gallstones

Answer 90

• BLOODS – CRP ↑, CBD obstruction/cholangitis: ↑ ESR, CRP, serum bilirubin with mikd ↑ in ALP, y-GT, AST, ↑ prothrombin time due to loss of Vit K absorption • INVESTIGATIONS – urinalysis, ECG, CXR – help to exclude other causes o AXR – only shows about 10% of gallstones o USS – 90-95% sensitive, best way to look for stones, can only pick up half of stones in in CBD, if negative but suspicion still high then repeat USS

Answer 91

* Analgesia – morphine or pethidine * Antibiotics – cefuroxime IV for acute cholecystitis followed by lap cholecystectomy * Laparoscopic Cholecystectomy - for all with symptomatic GB stones, converted to an open laparotomy in 5% cases if perforation * Post-cholecystectomy Syndrome - RUQ pain months after operation; related to functional bowel disease with hepatic spasm or hypertension of Sphincter of Oddi * Stone Dissolution and Shock Wave Lithotripsy - infrequently used unless pt is not fit for operation, dissolution if pure cholesterol stones but high recurrence rate and poor efficacy * If Suspect CBD Obstruction - if LFTs worsening, can do MRCP, but ERCP with sphincterotomy offers therapeutic option, then ?cholecystectomy

Answer 92

* Obstructive jaundice – CBD stones * Cholangitis – treat with cefuroxime and metronidazole IV * Gallstone ileus – stone erodes through GB into duodenum ad might obstruct terminal ileum * Pancreatitis * Mucocele/empyema – obstructed GB fills with mucous * Silent stones * Mirizzi’s syndrome – a stone in GB presses on bile duct causing jaundice * Gallbladder perforation – rare because of dual blood supply from hepatic artery via cystic artery and smaller branches of hepatic artery

Answer 93

* Hepatitis is inflammation of the liver caused by infection, medications, toxins and autoimmune disorders * Viral hepatitis can be caused by HAV, HBV, HCV, HDV or HEV. HAV, HBV and HCV can all result in acute illness with symptoms of nausea, abdominal pain, fatigue, malaise, and jaundice * HBV and HCV can also lead to chronic infection.

Answer 94

* HEPATITIS A - most common acute viral hepatitis; levels decreaseing in UK due to vaccination; more prevelant in less developed countries; endemic in Africa and South America so common in travellers. * HEPATITIS B - is most common cause of hepatitis; estimated 350 million people worldwide; high prevalence in sub-saharan Africa, Asia and Pacific Islands. * HEPATITIS C - affects around 216000 people in UK; large number of undiagnosed cases; deaths, transplants and hospital admissions continue to rise. * HEPATITIS D - 5% of HBV carriers have HDV co-infection; can only replicate in presence of HBV * HEPATITIS E - is being recognised as an increasingly important cause of acite hepatitis; epidemics can occur

Answer 95

PATHOLOGY FOR ACUTE HEPATITIS: • Most changes are v similar regardless of the cause. • Hepatocytes show degenerative changes (swelling, cytoplasmic granularity, vacuolation), undergo necrosis (becoming shrunken, eosinophilic Councilman bodies) and are rapidly removed. • Extent of damage variable amongst individuals with same aetiology: single and small groups of hepatocytes die (spotty or focal necrosis), or multiacinar necrosis involving a substantial part of the liver (massive hepatic necrosis) resulting in fulminant hepatic failure. HEP A: RNA VIRUS: • Faecal-oral spread or shellfish • Humans are only reservoir • Picornavirus, replicates in the liver, excreted in the bile and then faeces for ~2wks before onset of symptoms and for 7 days after HEP B: DNA VIRUS: • Hepadnavirus • Reverse transcriptase activity • HBV not directly cytopathic – damage is caused by host rather than HBV (via T cells and HLA class I molecules) • Transmission via infectious blood or bodily fluids containing blood HEP C: RNA VIRUS: • Transmission via infectious blood or bodily fluids containing blood • Flavivirus HEP D: INCOMPLETE RNA VIRUS: • Activated by the presence of HBV so it is unable to replicate on its own HEP E: RNA VIRUS: • Similar to HAV • Spread via faecal-oral route

Answer 96

* IVDU * Alcohol abuse * Poor hygiene * Contaminated water/sewage workers * Travel * Bleeding disorders/blood transfusions * MSM (men who have sex with men) * Sexual promiscuity * Pregnancy and breastfeeding * Needlestick injury/healthcare workers

Answer 97

``` HEP A: • Prodrome of flu-like symptoms: Fever, Malaise, Anorexia, Nausea • RUQ pain • Arthralgia and skin rash • Jaundice – develops after 1-2 weeks • Dark urine • Pale stools – intrahepatic cholestasis • Hepatosplenomegaly • Adenopathy • Distaste for cigarettes! ``` HEP B: • Resembles Hep A but arthralgia and urticaria are commoner • Subclinical in many cases HEP C: • Most are asymptomatic • 10% have mild flu-like illness with jaundice and a ↑ in aminotransferases • Most will develop silent chronic infection

Answer 98

* Other causes of hepatitis – drugs, alcohol, autoimmune disorders, other infections * Any other cause of jaundice – biliary colic, pancreatitis * Any other cause of RUQ pain – cholecystitis, biliary colic

Answer 99

HEP A: • Bloods – LFTs: ↑ AST/ALT (within a couple of weeks) and bilirubin - AST and ALT remain high for upto 6months after jaundice subsided, FBC: leucopenia with relative lymphocytosis, PT prolonged in severe cases, increased ESR • Viral Markers – antibodies to HAV: IgM = recent infection, IgG detectable for life HEP B: • Bloods – LFTs: ↑ AST/ALT (within a couple of weeks) and bilirubin - AST and ALT remain high for upto 6months after jaundice subsided, FBC: leucopenia with relative lymphocytosis, PT prolonged in severe cases, increased ESR • Viral Markers – Abs to HBV: - HBsAg (surface antigen) is present 1-6 months after exposure - HBeAg (e antigen) is present 1.5-3 months after acute illness and implies high infectivity - Antibodies to HBcAg (anti-HBc) imply past infection - Antibodies to HBsAg (anti-HBs) alone imply vaccination HEP C: • Screening recommended for any unexplained abnormal LFTs and people in high-risk groups • Bloods - AST: ALT <1:1 until cirrhosis develops • Test for anti-HCV – positive 3 months after exposure but could take up to 9 months HEP D: • Viral markers - antibodies to HDV: anti-HDV AB

Answer 100

HEP A: • Treatment – mainly supportive with treatment of symptoms, avoid alcohol • Active Immunisation – most frequent vaccine preventable disease in travellers, an inactivated protein derived from HAV, given to people travelling to endemic areas, pts with CLD, haemophiliacs, AB persist for 1 year, immunity for 10 years so need a booster injective • Passive Immunisation – normal Ig is used if exposure to HAV <2wks HEP B: • Treatment – mainly supportive with treatment of symptoms, avoid alcohol, avoid all sexual intercourse/contact, immunise sexual contacts • Active Immunisation – uses a recombinant yeast vaccine produced by insertion of a plasmid containing the gene of HBsAg into a yeast. 3 injections (at 0, 1 and 6 months) are given into the deltoid muscle; this gives short-term protection in over 90% of patients, immunisation of contacts after high-risk exposure with passive immunisation with specific anti-HBV immunoglobulin HEP C: • Treatment - Weekly peginterferon-α SC, daily ribavirin, combincation therapy can achieve sustained virological response in approx. ½ patients, can also add boceprevir and tolaprevir for those with genotype 1 chronic HCV HEP D & E: • Mainly supportive treatment, Hep D can also be treated with pegylated interferon alpha and liver transplantation which can be curative

Answer 101

HEP A: • Normally self-limiting • Most make a complete recovery • Mortality in young adults is 0.1% but ↑ with age • Death is due to fulminant hepatitis necrosis HEP B: • Majority of pts recover completely, with fulminant hepatitis occurring in 1% • Some go on to develop chronic hepatitis, cirrhosis, HCC or inactive HBV infection • Complete eradication of HBV is probably rare HEP C: • 90% develop CLD • Cirrhosis develops in 20–30% within 10–30 years and of these patients between 7% and 15% will develop hepatocellular carcinoma. HEP D: • Complicated by super or co-infection with HBV. Fulminant hepatitis can follow.

Answer 102

* Chronic hepatitis * Cirrhosis * Chronic liver disease * Hepatocellular carcinoma

Answer 103

• Sudden inflammation of the appendix and is a surgical emergency

Answer 104

* Most common surgical emergency. * Most common cause of acute abdomen. * Lifetime incidence = 6% * Highest incidence between 10-20y but can occur at any age. * Rare before 2yo because appendix is coe chaped and larger. * Not commoner in pregnancy but ↑ fetal mortality * Frequent Abx users (a balance of microbial gut flora is important for prevention of infection and digestion)

Answer 105

* Most commonly occurs when lumen of appendix becomes obstructed with faecolith – HARD MASS OF FAECAL MATTER (can also become obstructed due to lymphoid hyperplasia or filarial worms). * Gut organisms then invade the appendix wall. * The appendix becomes filled with mucous and swells. * Pressure increases in the lumen and walls and occludes the small vessels causing ischaemia followed by necrosis. * As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). * The end result of this cascade is appendiceal rupture (a 'burst appendix') causing peritonitis, which may lead to septicemia and eventually death.

Answer 106

• Classical presentation (which is what is described as follows) appears in only about 50% of people • Abdominal pain – periumbilical which then localises to RIF - Typicallythe person will describe a peri-umbilical or epigastric pain that worsens during the first 24 hours (becoming constant and sharp) and migrates to the right iliac fossa - The pain is worsened by movement (such as coughing or driving over speed bumps) - Ask children to hop, they will refuse to due to the pain • Nausea • Vomiting – profuse vomiting may indicate development of peritonitis • Anorexia – this is almost always present • Constipation - although diarrhoea may occur • Temperature (pyrexia)

Answer 107

• General Abdominal Tenderness – worsened on percussion • Guarding – muscular rigidity at the RIF • Rebound Tenderness • McBurney’s sign – 2/3 from umbilicus to right ASIS, maximal site of tenderness, pain, guarding, + rebound tenderness • Tachycardia • Furred Tongue (halitosis) • Low Grade Fever (not more than 38) • Facial Flushing • Dry Tongue • Coughing Hurts • Shallow Breaths • Less Common Peritoneal Signs Include: - Rovsing’s Sign – palpation of the left lower quadrant increases the pain in the right lower quadrant - Psoas Sign – extending the right thigh with the person in the left lateral position elicits pain in the right lower quadrant - Obturator Sign – internal rotation of the flexed right thigh elicits pain in the right lower quadrant

Answer 108

* GI: Gastroenteritis, intestinal obstruction, intussusception, acute cholecystitis, perforated peptic ulcer, diverticulitis, pancreatitis, terminal ileitis * Urological causes: Right uteric colic, right pyelonephritis, UTI * Gynaecological causes: Ectopic pregnancy, ruptured ovarian follicle, torted ovarian cyst, salpingitis, pelvic inflammatory disease * Other: Pneumonia, mesenteric adenitis, rectus sheath haematoma, diabetic ketoacidosis, shingles and porphyria.

Answer 109

• No single investigation to rule out appendicitis, however there are some tests to rile out differentials: - Pregnancy test - Urine dipstick test – excludes UTI (but this may be abnormal in about 50% of people with acute appendicitis) - FBC and CRP to rule out infection – neutrophil predominant leucocytosis is present in about 80-90% of people • Alvardo Scoring System – scoring system for appendicitis, not very good - Migration of Pain, Nausea/Vomiting, Anorexia, Rebound Pain, Temp >37.3, Neutrophil Count >75%  1 Point - RIF Tenderness, WCC >Q0X109/L  2 Points - 5-6 = Possible, 7-8 = Probable, >9 = Very Probable • USS – detects an inflamed appendix or mass, not always visualised though • CT – highly sensitive and specific, decreased appendicectomies, delays possible in emergency

Answer 110

SURGERY: • Appendicectomy by open or commonly laparoscopically • IV Ax pre-op reduces wound infections (metronidazole and cefuroxime)

Answer 111

* Appendicectomy is relatively safe. | * Mortality is 20% in >70s but this is due to delay in diagnosis and treatment.

Answer 112

* Perforation - does not appear to cause infertility in women; perforation is commoner with ↓ age reflecting diagnostic difficulty = can lead to localised abscess or generalised peritonitis * Appendix mass - when an inflamed appendix becomes covered with omentum; do US/CT to exclude a colonic tumour which can present as early as in 40s; treat conservatively with Abx and NBM first then interval (i.e. delayed) appendicectomy * Appendix abscess - occurs if appendix mass fails to resolve; signs = mass ↑ size and ↑ pain, temp, pulse, WCC; treat by drainage

Answer 113

• A mechanical or functional obstruction of the intestines preventing the normal transit of the products of digestion. It can occur at any point distal to the duodenum and is a medical emergency.

Answer 114

MECHANICAL: • Obstruction is either: - Simple = 1 point - Closed Loop (volvulus) - Strangulated (blood supply compromised and patient more ill than you expect) • Caused by: - Adhesions – most common, usually post-surgery - Constipation, tumours, hernias, sigmoid/caecal volvulus, diverticular stricture, foreign body, gallstone ileus, intussusception (when part of intestine invaginates into another part)] FUNCTIONAL – ADYNAMIC BOWEL DUE TO THE ABSENCE OF NORMAL PERISTALTIC CONTRACTIONS: • Occurs with a Paralytic Ileus – ofte seen in the post-operative stage of peritonitis or of major abdominal surgery, or in association with opiate treatment (acute colonic pseudo-obstruction, Ogilvie’s syndrome) • Occurs when the nerves or msucles of the inestines are damage, causing pseudo-obstruction • Caused by: - Abso surgery, pancreatitis, spinal surgery, hypokalaemia, hyponatraemia, uraemia, drugs (tricyclics) PSEUDO-OBSTRUCTION: • Like mechanical but with no cause found • Acute colonic pseudo-obstruction = Olgilvie’s syndrome • Predisposing factors: puerperium, pelvic surgery, trauma

Answer 115

MECHANICAL: • Patient complains of colicky abdo pain • Associated with vomiting (occurs earlier with small bowel obstruction and compared to large bowel) • Absolute constipation (occurs earlier in large bowel obstruction) FUNCTIONAL: • Pain is often no present BOTH: • Colic - seen in early obstruction and may be absent in long-standing obstruction • Constipation/no flatus - proximal obstruction = may not be absolute, distal obstruction = absolute • Abdominal distension - ↑ with progression of problem; distension is above the obstruction

Answer 116

MECHANICAL: • Tinkling sound and distention FUNCTIONAL: • Decreased bowel sounds BOTH: • Abdominal distention • Tenderness • Resonant to percussion

Answer 117

* Gastroenteritis – diarrhoea; flatus | * Gut perforation – pneumoperitoneum on AXR/CXR; sepsis/shock

Answer 118

* AXR - distended loops of bowel proximal to the obstruction, gas can be seen throughout the bowel in functional obstruction * Water-soluble (Gastrografin) enema - may help to demonstrate the site of the obstruction * CT - can localize the lesion accurately and is the investigation of choice = dilated, fluid-filled bowel * Colonoscopy - may induce a perforation

Answer 119

* Incomplete small bowel obstruction can be treated conservatively initially with fluids, analgesia, correction of electrolyte imbalance * Large bowel obstruction or strangulation require surgery, emergency if strangulation. Stenting can be used * Sigmoid volvulus can be ‘un-kinked’ with flexible sigmoidoscopy.

Answer 120

* In patients with small bowel obstruction, the mortality is 25% if surgery is delayed beyond 36 hours; under 36 hours this drops to 8%. * 50% of sigmoid volvulus will recur in the following two years.

Answer 121

* Perforation and bowel ischaemia  peritonitis and septicaemia * Fluid and electrolyte imbalance  AKI

Answer 122

• The protrusion of a viscus or part of a viscus through a defect of the wall of its containing cavity into an abnormal position (any structure passing through another so ending up in the wrong place). • Classified as: - Irreducible: part of bowel that cannot be pushed back into the right place (this does not mean they are necessarily obstructed or strangulated) - Incarceration: contents of hernia sac are stuck inside by adhesions. - Obstructed: when GI contents cannot pass through = classic obstruction symptoms and signs appear! - Strangulated: if ischaemia occurs. • There are many types of hernia according to location: - Inguinal – pass through the internal inguinal ring - Femoral – bowel enters femoral canal

Answer 123

* Inguinal hernia - most common hernia. * Indirect more common than direct. * Age groups: femoral > common in middle aged to elderly females. * Inguinal hernias affect mainly males. Femoral affect mainly females (elderly)

Answer 124

INGUINAL HERNIAS: • Indirect: pass through the deep/internal inguinal ring and if large extend through the superficial/external inguinal ring, can strangulate. • Direct: push directly forward through the posterior wall of the inguinal canal into a defect. Rarely strangulate FEMORAL HERNIA: • Bowel enters the femoral canal, presenting as a mass in the upper thigh, or above inguinal ligament where it points down the leg whereas an inguinal hernia points towards the groin • Likely to be irreducible and strangulate due to canal’s borders. Frequently strangulate.

Answer 125

* Male for inguinal hernias – due to larger inguinal canal which transmitted testes in development and accommodates structures of spermatic cord * Female for femoral hernias – due to wider bone structure of female pelvis * Chronic cough * Constipation * Urinary obstruction * Heavy lifting * Ascites * Past abdominal surgery

Answer 126

* Swelling in groin – may appear with lifting * May be accompanied with sudden pain – indirect inguinal hernias more prone to cause pain and dragging sensation in scrotum * Impulse palpable on coughing * May be reducible * Lower abdominal pain if incarcerated

Answer 127

* Examine patient both sittin and standing * Ask them to cough or strain * Palpate for cough impulse * Try to reduce lump if visible – beware of reduction en massewhere you push strangulated bowel and hernia sac back into abdominal cavity giving appearance of succesul reduction * Distinguish between direct and indirect hernias by occluding inguinal ring after reducing and ask the patient to cough or stand – if it pope out it is direct, if it doesn’t it is indirect – of no clinical use as surgical repair is exactly the same * Souldn’t be able to get your fingers above or behind hernia

Answer 128

* Hydrocele – can get fingers above and behind; luminates with light * Lymph node swelling – firm; non-reducible * Abscess painful; non-reducible * Saphena varix – cough impulse; bluish tinge; disappears on lying down; associated with varicose veins; detectable on USS * Varicocoele * Undescended testes

Answer 129

• Diagnosis is usually clinical (often missed though due to lack of thorough abdo exam) however if doubt USS can be used. Imaging can also be useful.

Answer 130

* Lose weight and stop smoking * If inguinal hernia is small, then it could be left but have to monitor for risk of strangulation – if pain or tender then treatment needed SURGICAL REPAIR: • INGUINAL HERNIAS - Mesh techniques (Lichtenstein repair) is most popular and has low recurrence rate – mesh inserted to reinforce abdominal wall - Laparoscopic repair is usually reserved for recurrances or bilateral hernias – TAPP (transabdominal pre-peritoneal) or TEP (totally extraperitoneal) methods - Surgery is usually day case - Return to work and driving after ≤2wks if all is well • FEMORAL HERNIAS - All femoral hernias should be repaired due to risk of strangulation. - Herniotomy = ligation and excision of the sac - Herniorrhapy = repair of hernia defecit

Answer 131

* Recurrence rates are low. | * Operative mortality for strangulated hernia is 10%.

Answer 132

• Strangulation leading to ischaemia. Obstruction.

Answer 133

• Mucosal lesions that originate in the epithelial cells lining the oesophagus

Answer 134

* Adenocarcinoma: ↑ Incidence in Western world. M:F 5:1 * Squamous carcinoma: Slightly reducing incidence in western world M:F 3:1 * Rhabdomyosarcoma: Malignant tumour of skeletal muscle wall of the oesophagus. Very Rare * Lipoma and gastrointestinal stromal tumour: Rare

Answer 135

* Oesophageal cancer arises in the mucosa of the oesophagus * It then progresses locally to invade the submucosa and the muscular layer and may invade contiguous structures such as the tracheobronchial tree, the aorta, or the recurrent laryngeal nerve * Metastasis typically occurs to the peri-oesophageal lymph nodes, liver and lungs * Adenocarcinoma: associated with dietary nitrosamines, GORD, and Barret’s metaplasia, typically occurs in the lower half of the oesophagus * Squamous carcinoma: associated with smoking, alcohol intake, diet poor in fresh fruit and veg, chronic achalasia, chronic caustic strictures, HPV  may occur anywhere in oesophagus

Answer 136

* AC: GORD and Barrett’s oesophagus, hiatus hernia, obesity, dietary nitrosamines * SCC: tobacco use, alcohol use, Fhx of oesophageal, stomach, oral or pharyngeal cancer, non-white race, high-temperature beverages and food, drinking maté * Male * Low-SES * Low intake of fresh fruit and vegetables

Answer 137

* Presence of RFs * Dysphagia – most common presenting sympptom of oesophageal cancer, usually only occurs after there is obstruction of more than two thirds of the lumen * Odynophagia – pain on swallowing is one of the signs of a locally advanced tumour * Weight loss * Hoarseness – involvement of the recurrent laryngeal nerve * Hiccups – prhenic nerve involvement can trigger hiccups * Postprandial/paroxysmal cough – may indicate the presence of an oesophagotracheal or oesphagobronchial fistula result from local invasion by a tumour

Answer 138

* Cervical lymphadenopathy | * Hepatomegaly

Answer 139

* Benign stricture * Achalasia * Barret’s oesophagus

Answer 140

• 1st LINE: - OESOPHAGOGASTRODUODENOSCOPY (OGD) WITH BIOPSY: first test in pts with severe dysphagia, odynophagia or weight loss, differentiates oesophageal cancer from benign causes of dysphagia  mucosal lesion, histology shows squamous carcinoma or adenocarcinoma - COMPREHENSIVE METABOLIC PROFILE: should be performed in cases with near or complete oesophageal obstruction  advanced cases: hypokalaemia, elevated creatinine and serum urea/nitrogen

Answer 141

• 1ST LINE: - NO OBVIOUS LESION: endoscopic resection with or without resection (1st), oesophagectomy (2nd line) - TUMOUR INVASION: oesophageactomy (1st line if surgical candidate), chemo/radiotherapy (1st line if not surgically viable)

Answer 142

• One of the most lethal of all malignancies w/o aggressive tx

Answer 143

• Postoperative pneumonia, post-resection oesophageal reflux, aspiration pneumonia

Answer 144

* Neoplasm that can develop in any porton of the stomach and may spread to the lymph nodes and other organs * Most tumours are adenocarcinomas

Answer 145

• Adenocarcinoma: Commonest age of incidence >50 M:F 3:1

Answer 146

* Several events at the molecular level have been implicated in the development and progression of gastric cancers * Gastric cancers can involve loss of the tumour suppressor gene p53 * Several proto-onocgenes such as rac, c-myc and erbB2 (HER2/neu) have been shown to be over-expressed in gastric cancers * H. pylori has been associated with molecular events that could lead to gastric cancer such as an increase in p53 mutations

Answer 147

* Pernicious anaemia * H. pylori * N-ntiroso compounds

Answer 148

* Presence of RFs * Abdominal pain – tends to be epigastric and vague in early-stage disease * Weight loss * Lymphadenopathy – vrichow’s node, sister mary jospehs nodule or irish node

Answer 149

* Peptic ulcer disease * Benign oesophageal stricture * Achalasia

Answer 150

• 1st LINE: | - UPPER GI ENDOSCOPY WITH BIOPSY: ulcer or mass or mucosal changes

Answer 151

• 1st LINE: - SURGERY CANDIDATE: surgery resection - NON-SURGERY CANDIDATE: radiotherapy

Answer 152

• 5-year relative survival rates

Answer 153

• Malnutrition, gastric obstruction, GI bleeding

Answer 154

• Pancreactic cancer refers to primary pancreatic ductal adenocarcinoma which accounts for >85% of all pancreatic neoplasms

Answer 155

• 3% of all new cancer cases in Europe

Answer 156

* Pancreatic cancer is a disease of older people, with a peak incidence in people 65-75 years of age * The only consistenly reported exogenous risk factor for pancreatic cancer is cigarette smoking * It is estimated that 5-10% of all pancreatic cancer patients have an inherited component * Inherited cancer syndromes associated with pancreatic cancer are hereditary pancreatitis, PJ-syndrome, familial atypical mutilple mole melanoma, familial breast cancer syndrome and HNPCC syndrome * About 65% of tumour are located within the head of the pancrease, 15% are in the body, 10% are in the tail and 10% are multifocal

Answer 157

* Smoking * Fx of pancreatic cancer * Other hereditary cancer syndromes * Chronic sporadic pancreatitis * Diabetes mellitus * Obesity * Dietary factors

Answer 158

* Presence of risk factors * Jaundice – suggests biliary obstruction or varey rarely hepatic or hilar nodal metastases * Non-specific upper abdo pain or discomfort – uneplained, non-specific upper abdo pain is usually one of the first symptoms and may be overlooked by pts and physicians, persistent back pain is associated with retroperitoneal metastases * Weight loss and anorexia – other signs of advanced disease include weight loss and anorexia, rapid weight loss is usually associated with unresectability * Steatorrhoea – extensive pancreatic infiltration or obstruction of the major pancreatic ducts will also cause exocrine dysfunction, resulting in malabsorption and steatorrhoea * Thirst, polyuria, nocturia and weight loss * Nausea, vomiting and mid-epigastric pain

Answer 159

* Hepatomegaly – sign of advanced disease * Positive Courvoisier’s sign – sign of advanced disease (indicated by painless palpable gallbladder and jaundice) * Petechiae, purpura, bruising – signs of disseminated intravascular coagulation in advanced disease * Trousseau’s sign – because pts with pancreatic cancer have an increased risk of thromboembolic disease, venous thrombosis or migratory thrombophlebitis (Trousseau’s sign) could also be a first prsentation of pancreatic cancer

Answer 160

* Chronic pancreatitis * Bile duct stones * Ampullary carcinoma * Cholangiocarcinoma * Autoimmune pancreatitis

Answer 161

• 1ST LINE: - ABDOMINAL USS: USS of pancreas, bile duct and liver  pancreatic mass, dilated bile ducts, liver mets - PANCREATIC PROTOCOL CT: may demonstrate a mass in the pancreas and the extent of local or distant spread - LFTs: bilirubin, alkaline phosphatase, and gamma glutamyl transpeptidase elevated in obstructive jaundice, aminotransferases (alanine aminotransferase) normal or slightly elevated

Answer 162

• 1st LINE: - STAGE 1 AND 2: surgical resection - STAGE 3 AND 4: endoscopic stent insertion or palliative surgery

Answer 163

* Poor prognosis | * Duodenal obstruction, pancreatic leaks and fistula, cholangitis

Answer 164

* Majority of CRCs are adenocarcinomas derived from epithelial cells * 71% of CRCs arise in the colon and 29% in the rectum * Less common types of malignant CR tumours are carcinoid tumours, GI stromal cell tumours and lymphomas

Answer 165

• Third most common cancer in the western world

Answer 166

* CRCs arise from dysplastic adenomatous polyps in the majority of cases * There is a multistep process involving the inactivation of a variety of tumour suppressor and DNA repair genes, along with simultaneous activation of oncogenes * This confers a selective growth advantage to the colonic epithelial cell and drives the transformation from normal colonic epithelium to adenomatous polyp to invasive CRC * Germline mutations underlie the well-described inherited colon cancer syndromes, whereas sporadic cancers arise from a step-wise accumulation of somatic genetic mutations * A single germline mutation in the APC tumour suppressor gene is responsible for the dominantly inherited FAP * Spread of CRC is to local lymph nodes, via enteric venous drainage to the liver and haematogenously to the lungs and less commonly to bone and brain

Answer 167

* Increasing age * APC mutation * Lynch syndrome * MYH-associated polyposis * Hamartomatous polyposis syndromes * IBD * Obesity * Acromegaly * Limited physical activity * Lack of dietary fibre

Answer 168

* Presence of risk factors * Increasing age * Rectal bleeding: usually due to benign disease but is a common symptom * Change in bowel habit: increased frequency or looser stools, particularly combined with rectal bleeding, is common in left-sided cancers * Rectal mass: palpable rectal mass * Positive FHx * Abdominal mass: usually abdo exam is normal, mass may be felt in advanced disease * Anaemia * Abdo pain * Weight loss and anorexia * Abdo distension

Answer 169

• Palpable lymph nodes: indicates advanced disease

Answer 170

* IBS * Ulcerative colitis * Crohn’s disease * Haemorrhoids * Anal fissure * Diverticular disease

Answer 171

• 1ST LINE: - FBC: anaemia - LFTs: normal, often even when liver mets present - RENAL FUNCTION: normal, except if advanced pelvic disease is compressing ureters - COLONOSCOPY: ulcerating or exophytic mucosal lesion that may narrow the bowel lumen - DOUBLE-CONTRAST BARIUM ENEMA: mass lesion in the colon and/or as a characteristic ‘apple core’ lesion - CT COLONOGRAPHY: appearances similar to conventional colonoscopy, with an ulcerating exophytic mucosal lesion that may narrow the bowel lumen - CT SCAN OF THORAX, ABDOMEN AND PELVIS

Answer 172

• 1ST LINE: | - SURGICAL RESECTION: only curative Rx, pre-op chemo may also be used

Answer 173

* Cirrhosis is the pathological end-stage of any chronic liver disease and most commonly results from chronic hep b and C, alcohol related liver disease and NAFLD * Characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules

Answer 174

• Third biggest cause of premature mortality in the UK

Answer 175

* Cirrhosis can derive from any chronic liver disease * The most common causes of cirrhosis in the western world are alcohol-related liver disease, NAFLD and chronic viral hepatitis * Hepatic fibrosis occurs in most pts with any type of chronic liver injury and may ultimately evolve into cirrhosis with nodule formation * Central event in hepatic fibrosis is the activation of hepatic stellate cells, which are the major source of extracellular matrix * This leads to an accumulation of collagen tupes 1 and 3 in the hepatic parenchyma and space of Disse * The result of collagen deposition in the space of Disse is termed ‘capillarisation’ of the sinusoids, a process in which the hepatic sinusoids lose their characteristic fenestration, thereby altering the exchange between hepatocytes and plasma * With activation, hepatic stellate cells become contractile, which may be a major determinant of increased portal resistance during liver fibrosis and cirrhosis

Answer 176

* Alcohol abuse * IV drug use * Unprotected intercourse * Obesity * Country of birth * Blood transfusion * Tattooing

Answer 177

* Presence of RFs * Abdominal distension – symptom of decompensated cirrhosis secondary to ascites in portal hypertension * Jaundice and pruritus – suggestive of decompensated cirrhosis secondary to reduced hepatic excretion of conjugated bilirubin into the biliary tree, pruritius is secondary to impaired bile secretion * Haematemesis and malaena – symptoms of decompensated cirrhosis secondary to GI haemorrhage from G-O varices in portal hypertension

Answer 178

* Constructive pericarditis * Budd-chiari syndrome * Portal vein thrombosis * Splenic vein thrombosis * IVC obstruction

Answer 179

* Leukonychia, palmar erythema, spider naevi, clubbing, xanthomata * Facial features – telangiectasia, spider naevi, jaundiced sclera * Abdominal features – collateral circulation, hepatosplenomegaly, distension (shifting dullness and fluid thrill), loss of secondary sexual hair and testicular atrophy, hepatic bruit (may be present with a vasular hepatoma)

Answer 180

• 1st LINE: - TX OF UNDERLYING CHRONIC LIVER DISEASE AND PREVENTION OF SUPERIMPOSED HEPATIC INSULT: oral directing ARTs are first line for chronic hep c virus infection, superimposed hepatic insult may be prevented through the avoidance of alcohol and other hepatotoxic drugs - SODIUM RESTRICTION AND DIURETIC THERAPY FOR ASCITES: spironolactone • 2nd LINE: - LIVER TRANSPLANTATION: suruvival benefit fromm undergoing liver transplantation is seen when the MELD socre is >15

Answer 181

• Median survival rate is approx. 10 years

Answer 182

• Ascites, G-O varices, hepatocellular carcinoma, bleeding and thrombosis

Answer 183

• 1ST LINE: - LFTs: AST and ALT levels increase with hepatocellular damage, total bilirubin may be normal in pts with compensated cirrhosis but as the cirrhosis progresses, serum levels generally rise - GGT: increase in this liver enyme representgs enzyme activation, which can be induced by alcohol and certain drugs  elevated - SERUM ALBUMIN: reduced - SERUM SODIUM: reduced - PROTHROMBIN TIME: prolonged - PLATELET COUNT: reduced - ANTIBODIES TO HEP C VIRUS: present - HEP B SURFACE ANTIGEN: present

Answer 184

• Fluid in the peritoneal cavity

Answer 185

5 Fs • TRANSUDATE: - Portal hypertension, hepatic outflow obstruction, Budd-Chiari syndrome, hepatic veno-occlusive disease, cardiac failure, tricuspid regurgitation, constrictive pericarditis, meig’s syndrome (triad of benign ovarian fibroma, ascites and pleural effusion) • EXUDATE: - Peritoneal carcinomatosis, peritoneal TB, pancreatitis, nephrotic syndrome, lymphatic obstruction (chylous ascites) • Cirrhosis is the commonest cause - In cirrhosis, peripheral arterial vasodilation (mediated by nitric oxide and other vasodilators) leads to reduction in effective blood volume with activation of sympathetic NS and RASS, thus promoting salt and water retention, all encouraged by hypoalbuminemia and mainly localized to the peritoneal cavity

Answer 186

* Alcohol abuse | * Chronic liver disease - bleeding associated with liver disease is often from varices

Answer 187

* Fullness in the flanks, with shifting dullness * Tense ascites is uncomfortable and produces respiratory distress * Pleural effusion (usually right sided) * Peripheral oedema

Answer 188

• 1st LINE: - DIAGNOSTIC ASPIRATION: take 20ml of ascetic fluid and test it o Albumin conc >11g/L suggests a transudate, if below then an exudate, check neutrophil count, gram stain and culture, cytology for malignant cells and mayluase to exclude pancreatic ascites

Answer 189

• 1st LINE: - DEPENDS ON THE CAUSE - DIURETICS: restrict sodium, oral spirolactone, furesomide is added if response is poor, aim to los 500g of body weight per day - PARACENTESIS: usually done if the ascites is tense or are resistant to standard medical therapy, the perforation of a cavity of the body or of a cyst or similar outgrowth, especialy with a hollow needle to remove fluid or gas

Answer 190

* Very common in hospitals | * Common in obesity

Answer 191

* DISEASES COMMONLY COMPLICARED BY MALNUTRITION INCLUDE: anorexia, carcinoma of the oesophagus or stomach, post-op states, dementia * Malnutrition can be a protein-energy malnutrition, vitamin deficiencies or both * Protein-energy malnutrition frequently coexists with infections * The infections may exacerbate this deficiency

Answer 192

* In children  Kwashiorkor (swollen ankles, scaly skin, swollen abdomen, depigmented beair, Marasmus (hair loss, wrinkled skin, severe wasting) * Cachexia

Answer 193

* Any organ with an abnormal opening * Viscus technically means a hollow organ found inside the body * Pleural viscera are used if multiple organs have been perforated

Answer 194

* Blunt abdominal trauma * Stab and gunshot wounds * Infections can lead to them

Answer 195

* Spilling of materials from GI organs inside the abdomen usually happens in the presence of a perforated abdominal viscus * These materails are often toxic inside the body cavity and can place the life of a patient in danger * Bacteria often reach the blood system in most of these cases thus immediate medical attention and effective treatment generally are needed in such situations

Answer 196

* Fever * Low BP * Tachycardia * Abdo pain – feels rigid or board-like when touched * Nausea * Vomiting * Abdominal distension

Answer 197

• Upper GI bleed – haematemesis, melaena

Answer 198

• 1St LINE: | - OPEN SURGERY

Answer 199

* Systemic autoimmune disease triggered by dietary gluten peptides found in wheat, rye, barley and related grains * Immune activation in the small intestine leads to villous atrophy, hypertrophy of the intestinal crypts, and increased numbers of lymphocytes in the epithelium and lamina propria * Locally lead to GI symptoms and malabsorption

Answer 200

• Common, affecting up to 1% of the general population

Answer 201

* Coeliac disease is a systemic autoimmune disorder triggered by gluten peptides from grains including wheat, rye, and barley * Almost all people with coeliac disease carry one of two MHC class-2 molecules (Hla-DQ2 or DQ8) that are required to present gluten peptides in a manner that activates an antigen-specific T-cell response * The requirement for DQ2 or DQ8 is a major factor in the genetic predisposition to coeliac disease * However, most DQ2 or DQ8 positive people never develop coeliac disease despite daily exposure to dietary gluten * Additional environmental or genetic factors that are required for loss of immune tolerance are unknown

Answer 202

* Fx * Immunoglobulin A deficiency * Type 1 diabetes * Autoimmune thyroid disease * Downs, sjogrens syndrome * IBD * Primary biliary cirrhosis

Answer 203

* IgA deficiency – lack of secretory IgA and Peyer’s patch malfunction allow for increased free gluten peptides in the submucosa * Diarrhoea – pts may present with chronic or intermittent diarrhoea * Bloating – long-standing or refractory abdo symptoms should be screened for coeliac disease * Abdo pain/discomfort – pts may present with recurrent abdo pain, cramping or distension * Iron deficiency * Dermatitis herpetiformis – intensely pruritic paulovesicular lesions that occur symmetrically over the extensor surfaces of the arms and legs, as well as on the buttoclks, trunk, neck and scalp

Answer 204

* Peptic duodenitis * Crohn’s * Giardiasis * Tropical sprue * Post-gastroenteritis

Answer 205

• 1ST LINE: - FBC AND BLOOD SMEAR: iron deficiency is the most common clinical presentation in adults  low Hb and microcytic red cells - IgA-Ttg: titre above normal range for lab, order this in any pt with suspected coeliac disease - EMA: more expensive alternative to IgA-tTG, perform initially if IgA-tTG is unavailable  elevated titre - SKIN BIOPSY: granular deposits of IgA at the dermal papillae of lesional and perilesional skin by direct immunofluorescence - IgG DGP or IgA/IgG DGP: elevated titre - SMALL BOWEL – MACROSCOPIC: atrophy and scalloping of mucosal folds, nodularity and mosaic pattern of mucosa - SMALL BOWEL – HISTOLOGY: gold standaed and is essential to confirm the diagnosis  presence of intra-epitehlial lymphocytes, villous atrophy and crypt hyperplasia

Answer 206

• 1ST LINE: - GLUTEN FREE DIET - After diagnosis pts should bec checked for common deficiencies such as Vit D or iron, all pts with coeliac disease should take calcium and Vit D supplements

Answer 207

``` prognosis is good complications - Osteoporosis/osteopenia, dermatitis herpetiformis, malignancy, pneumococcal infection ```

GI Flashcards

(231 cards)