GI presenting symptoms 2

Question 1

Diarrhoea

Answer 1

Increased stool water hence increased stool volume e.g. >200 mL daily which increases stool frequency and causes the passage of liquid stool.

If it is the fat content of the stool which is increased then use the term steatorrhoea – pale, malodourous stool that is difficult to flush.

Both should be distinguished from faecal urgency which suggests rectal pathology e.g. malignancy.

Question 2

Diarrhoea - Classification

Answer 2

• Is this small or large bowel problem? – large bowel symptoms – watery stool ± blood and mucus, pelvic pain relieved by defecation, tenesmus and urgency. Small bowel symptoms – periumbilical or right iliac fossa pain not relieved by defecation, watery stool or steatorrhoea.
• Acute or chronic – if acute suspect gastroenteritis – ask about travel, change in diet and contact history. Chronic diarrhoea alternating with constipation suggests irritable bowel syndrome. Anorexia, weight loss, nocturnal diarrhoea or anaemia suggests an organic cause of diarrhoea.

Question 3

Diarrhoea - Contents

Answer 3

• Bloody diarrhoea – can be caused by Salmonella, Shigella, Campylobacter, E coli, amoebiasis, UC, Crohn’s, malignancy, colonic polyps, pseudomembranous colitis or ischaemic colitis.
• Mucus – can occur in irritable bowel syndrome, colorectal cancer and colonic polyps.
• Pus – suggests inflammatory bowel disease, diverticulitis, a fistula or an abscess.

Question 4

Diarrhoea - Non-GI Causes

Answer 4

• Drugs – antibiotics, proton pump inhibitors, cimetidine, propranolol, cytotoxics, NSAIDs, digoxin, alcohol or alcohol abuse.
• Medical conditions – thyrotoxicosis, autonomic neuropathy, Addison’s disease and carcinoid syndrome.

Question 5

Diarrhoea - Examination

Answer 5

Look for weight loss, clubbing, anaemia, oral ulcers, rashes and abdominal scars.

Assess severity of dehydration – dry mucous membranes, decreased skin turgor and capillary refill >2 seconds.

Palpate for an enlarged thyroid or an abdominal mass and perform a rectal examination to look for masses (rectal carcinoma) or impacted faeces (overflow diarrhoea).

Also test for faecal occult blood.

Question 6

Diarrhoea - Investigations

Answer 6

• Bloods – FBC (for iron deficiency or raised MCV in coeliac disease, alcohol abuse or ileal Crohn’s due to decreased B12 absorption), U+Es (for hypokalaemia), ESR (raised in malignancy or IBD), CRP (raised in infection or IBD), TSH (low in thyrotoxicosis) or coeliac serology.
• Stool – test for pathogens and Clostrisium difficile toxin (Pseudomembranous colitis). Test for faecal fat excretion or 13C-hiolein breath test (a much nicer test for measuring pancreatic exocrine function) if symptoms of pancreatitis, malabsorption or steatorrhoea.
• Rigid sigmoidoscopy – with biopsy of both normal and abnormal looking mucosa.
• Colonoscopy ± barium enema – to look for malignancy or colitis but avoid during acute attacks.

Question 7

Diarrhoea - Management

Answer 7

Treat the cause where possible.

Practical issues – food handlers must not work until stool samples and negative and if there is an outbreak hospital wards may need to be closed.

Oral rehydration is better than IV but if impossible give 0.9% saline with 20mmol potassium per litre. In addition 30mg Codeine phosphate QDS or 2mg Loperamide after each loose stool (up to 16mg per day) can help reduce stool frequency.

Avoid antibiotics except in infective diarrhoea that is causing systemic illness due to the risk of antibiotic resistance.

Question 8

C Diff - Definition and Toxin

Answer 8

A gram positive superbug whose spores are contagious - faecal-oral or from the environment where spores can live for extended periods and are difficult to eradicate.

Toxins – tissue culture, ELISA and PCR help detect the Clostridium difficile toxins.

Question 9

C Diff - Signs and Carriage

Answer 9

• Signs – pyrexia, colic, diarrhoea ranging from mild to severe bloody diarrhoea with systemic upset – raised CRP and WCC, low albumin and colitis (with yellow, adherent plaques on inflamed non-ulcerated mucosa = the pseudomembrane) and possible multi-organ failure.
• Asymptomatic carriage – occurs in 1-3% of adults – risk factors are old age, being in hospital, >80% bed occupancy and antibiotic use (especially broad spectrum or IV antibiotics).

Question 10

C Diff - Management

Answer 10

Stop the causative antibiotics where possible and if symptomatic give 400mg Metronidazole TDS for 10 days or 125mg Vancomycin QDS for severe disease.

In very severe cases e.g. toxic megacolon or raised lactate dehydrogenase a colectomy may be performed.

Question 11

C Diff - Reoccurence and Spread

Answer 11

• Recurrent disease – repeat metronidazole once (overuse causes irreversible neuropathy). Probiotics can help prevent reoccurrences (not for immunosuppressed or if CVP line in situ).
• Preventing spread – meticulous cleaning, use of disposable gloves, not using rectal thermometers, hand washing and ward protocols e.g. bare below elbows.

Question 12

Constipation - Definition and Criteria

Answer 12

Infrequent bowel movements (<3 times weekly) or passing stool less frequently than the patients normal habit or with difficult, straining or pain. Ask the patient exactly what they mean by constipation as bowel habits vary greatly between individuals and according to diet.

The Rome criteria – constipation is the presence of 2 or more of following during >25% of bowel movements – straining, lumpy or hard stools, sensation of incomplete evacuation, sensation of anorectal obstruction, manual manoeuvres needed to facilitate and <3 bowel movements per week.

Question 13

Constipation - Causes

Answer 13

• General – poor diet, lack of exercise, dehydration, irritable bowel syndrome, old age, post-operative pain, hospital environment (e.g. lack of privacy) or distant or squalid toilets.
• Anorectal disease – anal fissure or stricture, rectal prolapse, mucosal ulceration or neoplasia or functional anorectal pain syndromes – proctalgia fugax and levator ani syndrome.
• Intestinal obstruction – colorectal carcinoma, strictures in Crohn’s disease, pelvic mass e.g. fetus or fibroids, diverticulosis (usually presents with bleeding) or pseudo-obstruction.
• Metabolic or endocrine cause – hypercalcaemia, hypothyroidism, hypokalaemia or porphyria.
• Drugs – opiates, tricyclic antidepressants, iron, antacids, diuretics e.g. furosemide and CCBs.
• Neuromuscular – slow transit from decreased propulsive activity – spinal or pelvic nerve injury, aganglionosis (Chagas’ or Hirschsprung disease), systemic sclerosis or diabetic neuropathy.
• Other – chronic laxative abuse, idiopathic slow transit, idiopathic megacolon or psychological.

Question 14

Constipation - Features

Answer 14

Ask about frequency, nature and consistency of stools, whether there is mucus or blood present, does diarrhoea alternate with constipation, has there been a recent change in bowel habit, is there any pain and has there been a recent change in diet or medication?

A PR examination is essential!

Refer if there are atypical symptoms e.g. weight loss, abdominal pain or anaemia.

Question 15

Constipation - Investigations

Answer 15

Indications for investigations are >40 years, change in bowel habit or associated symptoms – weight loss, PR mucus or blood or tenesmus.

Perform bloods – FBC, ESR, U+Es, Ca2+ and TFTs, sigmoidoscopy and biopsy of abnormal mucosa or is there is suspicion of colorectal malignancy perform colonoscopy or barium enema.

Question 16

Constipation - Management

Answer 16

Often increased fluid intake and diet and exercise advice is all that is needed. A high fibre diet is often advised but can caused increased bloating without helping the constipation. Only progress to medication where above measures fail and try to use them for a limited period of time.

Medication options - bulking agent, stimulent or osmotic laxatives or stool softeners.

Question 17

Constipation - Bulking Agents

Answer 17

Increase faecal mass so stimulate peristalsis. They must be taken with lots of fluid and can take a few days to take effect.

Contraindications – difficulty in swallowing, GI obstruction, colonic atony or faecal impaction.

Examples – bran powder (3.5g added to 2-3 meals per day – can inhibit absorption of trace elements if used with every meal), ispaghula husk e.g. Fybogel (3.5g sachet taken with water after meals), methycellulose e.g. Celevac (3-6 500mg tablets BD taken with >300mL water) or sterculia e.g. Normacol (10mL granules sprinkled onto food daily).

Question 18

Constipation - Stimulent Laxatives

Answer 18

Increase intestinal motility so must not be used in intestinal obstruction or acute colitis. Avoid prolonged use as they can cause colonic atony, hypokalaemia or side effects such as abdominal cramps.

Examples – pure stimulant laxatives e.g. biscodyl (5-10mg at night) or senna (2-4 tablets per night) or mixed stimulant laxative and stool softener e.g. Docusate sodium.

In addition Sodium picosulphate (5-10mg 12 hours prior to procedure) can be used for rapid bowel evacuation.

Question 19

Constipation - Osmotic Laxatives

Answer 19

Retain fluid in bowel.

Examples – lactulose (30-50mL BD causes osmotic diarrhoea of low faecal pH that discourages growth of ammonia producing organisms – so useful in hepatic encephalopathy), magnesium salts (e.g. magnesium hydroxide or sulphate are useful when rapid bowel evacuation is required) or phosphate enemas can be used for evacuation prior to procedures.

Question 20

Constipation - Stool Softeners

Answer 20

Particularly useful in the management of painful anal condition e.g. an anal fissure.

Examples – Arachis oil enemas lubricate and soften impacted faeces.

Question 21

Vomiting - Investigations

Answer 21

Do bloods – FBC, Us and Es, LFTs, Ca2+ and amylase.

Also do ABG as a metabolic alkalosis (hypochloraemic) can result from loss of gastric contents – pH >7.45 and raised HCO3- indicates severe vomiting.

Request a plain abdominal x-ray if you suspect bowel obstruction and an upper GI endoscopy if vomiting is prolonged and consider a CT head if you suspect raised ICP.

Question 22

Vomiting - Management

Answer 22

Try to use pre-emptive therapy e.g. pre-operatively for post op symptoms. Try the oral route where possible but around a third of patients will require a 2nd line anti-emetic.

If patients are dehydrated also give IV fluids with potassium replacement and monitor electrolytes and fluid balance.

Question 23

Anti-emetics

Answer 23

H1 antagonists - cyclizine or cinnarizine.

D2 antagonists - metoclopramide, domperidone or prochlorperizine.

5-HT3 antagonist - ondansetron.

Question 24

Jaundice - Definition

Answer 24

Yellow pigmentation of the skin, sclerae and mucosa due to increased plasma bilirubin – visible at >35 μmol/L but not always easy to spot when mild.

Jaundice can be classified by the site of the problem – pre-hepatic, hepatocellular or obstructive (cholestatic) or by the type of circulating bilirubin – conjugated or unconjugated.

Kernicterus – this is seen in infants and involves deposition of unconjugated bilirubin in the basal ganglia which causes opisthotonus – hyperextension and spasticity.

Question 25

Bilirubin Metabolism

Answer 25

Bilirubin is formed from haemoglobin breakdown and its metabolism has 3 steps – hepatic uptake, conjugation and excretion.

In the liver bilirubin is conjugated with glucuronic acid by hepatocytes making it water soluble. Conjugated bilirubin is secreted into the bile and passes out into the gut.

Some is taken up by the liver via enterohepatic circulation and the rest is converted to urobilinogen by gut bacteria. Urobilinogen is then reabsorbed, excreted or converted to stercobilin.

Question 26

Unconjugated Hyperbilirubinaemia - Causes

Answer 26

• Overproduction – in haemolysis or ineffective erythropoiesis.
• Impaired hepatic uptake – drugs (contrast media or rifampicin) or congestive cardiac failure.
• Impaired conjugation – glucuronyl transferase deficiency - Gilbert’s or Crigler-Najjar syndrome.
• Physiological neonatal jaundice – a combination of the above mechanisms – red blood cell lifespan is short and the process of bilirubin conjugation is not completely developed.

Question 27

Conjugated Hyperbilirubinaemia - Causes

Answer 27

• Hepatocellular dysfunction – viruses (hepatitis, CMV or EBV) drugs (see below), alcoholic hepatitis, cirrhosis, liver metastases or abscess, haemochromoatosis, autoimmune hepatitis, septicaemia, leptospirosis, α1-antitrypsin deficiency, Budd-Chiari or Wilson’s disease.
• Impaired hepatic excretion – primary biliary cirrhosis, primary sclerosing cholangitis, extrinsic compression of the bile duct, drug induced cholestasis, common bile duct gallstones, pancreatic malignancy, lymph nodes at the porta hepatis or biliary atresia.

Question 28

Drugs Causing Jaundice

Answer 28

There are a number of mechanisms:

• Haemolysis – antimalarials e.g. dapsone
• Hepatitis – paracetamol overdose, isoniazid, rifampicin, pyrazinamide, monoamine oxidase inhibitors, sodium valproate, halothane or statins e.g. somatostatin.
• Cholestasis – flucloxacillin (occurs weeks after use), fusidic acid, co-amoxiclav, nitrofurantoin, steroids (anabolic or the OCP), sulfonylureas, prochlorperazine or chlorpromazine.

Question 29

Jaundice - Clinical Features

Answer 29

Ask about blood transfusions, IV drug use, body piercings, tattoos, sexual activity, travel abroad, jaundiced contacts, family history, alcohol consumption and all medications.

Question 30

Jaundice - Examination

Answer 30

For signs of chronic liver disease, encephalopathy, lymphadenopathy, hepatomegaly, splenomegaly, ascites and a palpable gall bladder (which with painless jaundice suggests a cause other than gallstones – Courvoisier’s sign).

Pale stool and dark urine are found in cholestatic jaundice.

Question 31

Jaundice - Investigations

Answer 31

Perform screening tests for chronic liver disease, urine (bilirubin is absent in pre-hepatic causes and urobilinogen is absent in obstructive jaundice), blood (FBC, clotting, blood film and reticulocyte count), biochemistry (U+Es and LFTs), ultrasound (are the bile ducts dilated >6mm, are there gallstones, hepatic metastases or a pancreatic mass), ERCP (if bile ducts are dilated and LFTs are not improving), MRCP (if conventional ultrasound shows gallstones but no common bile duct stones), liver biopsy (if the bile ducts are normal) and consider abdominal CT or MRI (for malignancy).

Question 32

Upper GI Bleeding - Definition and Causes

Answer 32

Haematemesis – vomiting of blood which may be bright red or coffee grounds. Malaena – means black motions, often tar like and has a characteristic smell of altered blood. Both indicate upper GI bleeding.

Causes – duodenal ulcer (30%), gastric ulcer (20%), acute erosions or gastritis (20%), Mallory-Weiss tear (10% - due to vomiting), oesophageal varices (5%), oesophagitis (5%) or malignancy (<3%).

Question 33

Upper GI Bleeding - History and Examination

Answer 33

• History – ask about previous GI bleeds, dyspepsia, known peptic ulcers, liver disease or varices, dysphagia, vomiting or weight loss. Check current medication and alcohol use. Are there any serious co-morbidities e.g. cardiovascular or respiratory disease, hepatic or renal impairment or metastases.
• Examination – look for signs of chronic liver disease and perform a PR to check for melaena. Is the patient shocked - cool and clammy to touch, delayed capillary refill, altered GCS, pulse >100 bpm, systolic BP <100mmHg, postural BP drop of >20mmHg on standing and urine output <30mL/h.

Question 34

Upper GI Bleeding - Rockall Risk Score

Answer 34

The pre-endoscopy criteria make up the initial Rockall score and the post-endoscopy criteria make up the final Rockall score. An initial score >6 is said to be an** ** but the decision is usually more complex.

Pre-endoscopy:

• Age - <60 years, 60-79 years, >80 years.
• Shock - Pulse <100 bpm, Pulse >100 bpm or SBP <100 mmHg.
• Comorbidity - Nil major, HF or IHD, RF or LF or Metastases.

**Post-endoscopy: **

• Diagnosis - Mallory Weiss, All other dx or GI malignancy.
• Haemorrhage - Dark red spot or Blood or vessel.

Question 35

Upper GI Bleeding - Mx if Not Shocked

Answer 35

Insert 2 large bore cannulae and start a slow saline IVI to keep lines patent. Check bloods and monitor vital signs and urine output. Aim to keep Hb >8 g/dL at all times.

Question 36

Upper GI Bleeding - Mx if Shocked

Answer 36

• Protect the airway, give high flow oxygen and keep the patient nil by mouth.
• Insert 2 14G cannulae and take bloods – FBC, Us+Es, LFTs, glucose, clotting, cross match (4 units).
• Start a rapid crystalloid infusion up to a maximum of 1L.
• If the patient remains shocked start blood transfusion otherwise start slow saline infusion.
• Correct clotting abnormalities with vitamin K, FFP or platelet concentrate and give IV PPI.
• Set up a CVP line to guide fluid replacement and catheterise to monitor urine output.
• Monitor vital signs every 15 minutes and perform emergency endoscopy for diagnosis.

Question 37

Upper GI Bleeding - Endoscopy

Answer 37

Should be arranged after resuscitation, within 4 hours of a suspected variceal haemorrhage or when bleeding is ongoing within 24 hours of admission.

It can be used to identify the site of bleeding, to estimate the risk of rebleeding and to administer treatment – preferably 2 of adrenaline, sclerotherapy, variceal banding or argon plasma coagulation (for superficial lesions).

Question 38

Upper GI Bleeding - Rebleeding

Answer 38

Risk can be assessed during endoscopy – 80% if there’s active arterial bleeding, 50% if there’s a visible vessel and 30% if there’s visible clots or black dots.

40% of those who rebleed will die of complications so high risk patients need to be identified and closely monitored. Give an IV infusion of Omeprazole and get a surgeon if haematemesis with melaena or any signs of shock are present.

Question 39

Oesophageal Varices

Answer 39

Portal hypertension causes dilated collateral veins at sites of porto-systemic anastomosis. They most commonly occur in the lower oesophagus but also in the stomach around the umbilicus (caput medusae) and in the rectum. Varices usually develop once portal pressure is >10 mmHg.

Question 40

Portal Hypertension - Causes

Answer 40

• Pre-hepatic – portal or splenic vein thrombosis.
• Intra-hepatic – cirrhosis (causes 80% of cases - most common in the UK), schistosomiasis (most common worldwide), sarcoidosis, myeloproliferative disorders or congenital hepatic fibrosis.
• Post-hepatic – Budd-Chiari syndrome, RHF, constrictive pericarditis or veno-occlusive disease.

Question 41

Upper GI Bleeding - Prophylaxis

Answer 41

Treatment reduces the risk of varices in a cirrhotic patient bleeding from 30% to 15%. Should give 40-80mg Propanolol BD and/or endoscopic banding ligation but 80% will re-bleed within 2 years.

Resistant cases can be given a TIPSS – transjugular intrahepatic portosystemic shunt.

Question 42

Acute Oesophageal Variceal Bleeding

Answer 42

Resuscitate until haemodynamically stable (but do not give 0.9% saline), correct clotting abnormalities with vitamin K and FFP, start an IVI of Terlipressin – 2mg bolus followed by 1-2mg/4 hours for <3 days. Endoscopic banding or sclerotherapy should then be attempted.