Gastroenterology Flashcards
Histology of Ulcerative Colitis
Superficial inflammation with chronic inflammatory cells infiltrating the laminate proprietary with crypt abscesses, with little involvement of the muscularis mucosa and with reduction of goblet cells.
Imaging for Ulcerative Colitis
Barium enema/CT/MRI - loss of normal haustral pattern with shortening of the large intestine; bowel appears like a smooth tube (hosepipe appearance). Undermined ulcers and pseudo polyps may be seen. Stricture formation or carcinoma produces fixed areas of narrowing.
AXR - acute dilatation when present; bowel gas may outline mucosal ulceration.
During acute dilatation, barium enema may produce perforation.
DDx of Ulcerative Colitis
Colon carcinoma (bloody diarrhoea) Infective enteritis Antibiotic-associated pseudomembranous colitis Acute ischaemic colitis Irritable bowel syndrome
Medical management of Ulcerative Colitis
Oral 5-aminosalicyclic acid (5-ASA) compounds - induce remission in mild/moderate colitis
- sulfasalazine (5-ASA + sulfapyridine)
- mesalazine
- olsalazine
If 5-ASA ineffective or severe colitis, treat with steroids (oral; or rectal in proctitis), consider azathioprine for steroid-sparing
Short-term anti-TNF agent infliximab if refractory to 5-ASA and steroids
If severe colitis, admit for IV steroids and fluids
Taper treatment once remission is achieved
Histology of Crohn’s Disease
Submucosal inflammation, less marked than in UC, and numerous fissures down to the sub mucosa with or without chronic granulation tissue.
Imaging for Crohn’s Disease
Barium enema - rose thorn appearance of spikes of barium entering deep into the bowel wall if mucosal ulceration is deep; skip lesions; coarse cobblestone appearance of the mucosa; (later) fibrosis causing narrowing (string sign) with proximal dilatation
Small-bowel enema - mucosal ulceration, luminal narrowing or pooling of barium in irregular clumps at the site of an inflammatory mass
Contrast CT/MRI
Indium-labelled white cell scanning to localise active disease
Complications of Crohn’s Disease
Fever Anaemia Weight loss Hypoalbuminaemia Fistulae Peri-anal fissures Sepsis
Medical management of Crohn’s Disease
Aminosalicyclates and corticosteroids to induce remission.
Mesalazine suppositories can be used in localised rectal disease.
Budesonide that is formulated to be released in the terminal ileum and colon can be effective with fewer side-effects than conventional steroids.
Anti-TNF treatment with infliximab, adalimumab or certolizumab pegol are usually reserved for patients who do not enter remission with mesalazine or steroids.
Methotrexate or ciclosporin may be useful in refractory disease.
Correct nutritional deficiencies and electrolyte imbalances.
Antibiotics (ciprofloxacin and metronidazole) are widely used for the treatment of fistulas; azathioprine and anti-TNFs may also help.
Causes of upper GI bleeding
Peptic ulcer Gastric ulcer Mallory-Weiss tear Oesophagitis Oesophageal ulcer Oesophageal varices GI malignancy (Concurrent NSAIDs/aspirin + SSRIs)
Management of upper GI bleeding
Admit to hospital
Resuscitate if evidence of intravascular volume loss
Management of variceal bleeding
Upper GI endoscopy within 24hrs (and as early as condition allows)
Local diathermy or injection of a sclerosis that may arrest bleeding
If bleeding continues/recurs, surgery may be necessary
PPIs reduce mortality, rebleeding and the need for surgical intervention
-IV bolus followed by continuous infusion of PPI should be considered in high-risk patients
Causes of lower GI bleeding
Haemorrhoids Fissure Ulcerative colitis Crohn’s disease Ischaemic colitis Rectal, colonic, and caecal carcinoma Diverticular disease Meckel’s diverticulum Polyps Endometriosis
Vitamin B12 deficiency causes…
…megaloblastic anaemia
Vitamin D/calcium deficiency causes…
…osteomalacia/rickets
Vitamin B deficiency causes…
…glossitis and angular stomatitis
Vitamin K deficiency causes…
…deficient coagulation
Potassium deficiency causes…
…muscle pain, weakness, abnormalities of cardiac rhythm
Investigations for coeliac disease
Anti-tissue transglutaminase and anti-endomysial antibodies
Duodenal biopsy
Histology of coeliac disease
Villus atrophy
Causes of malabsorption
Coeliac disease
Bile salt deficiency (carcinoma of head of pancreas /gallstones /primary biliary cirrhosis /bile duct stricture -> obstructive jaundice -> malabsorption of fat -> steatorrhoea)
Pancreatic enzyme deficiency (chronic pancreatitis /carcinoma of pancreatic ducts/ cystic fibrosis/ pancreatic calculi/ benign pancreatic cystadenoma)
Post-surgical (gastrectomy /gastroenterostomy /small bowel resection)
Crohn’s disease
Investigations for malabsorption
Bloods - anaemia, low folate, low iron, low transferrin, hypoalbuminaemia, prolonged PT, hypocalcaemia, hypophosphataemia, hypomagnesaemia, raised alkaline phosphatase
Measure faecal fat excretion over 3-5 days
Small intestinal barium meal - flocculation and segmentation of barium as evidence of excess mucus secretion; widening of the small intestinal calibration and decreased distance between adjacent bowel loops, indicating thickening of the intestinal wall; detection of diverticula, fistulae or Crohn’s
Most common pancreatic cancer type
Adenocarcinoma
Imaging for pancreatic cancer
USS or CT may show the tumour
ERCP may comfort diagnosis and allows palliative stunting of obstructed common bile duct to relieve pruritis and jaundice
Management of pancreatic cancer
Resection is the only curative treatment, but less than 10% of patients are suitable for surgery.
Adjuvant chemotherapy may be of benefit.
Differential diagnoses for acute pancreatitis
Cholecystitis Acute myocardial infarction Dissecting aortic aneurysms Mesenteric vascular occlusion Intestinal perforation
Investigations for acute pancreatitis
Bloods:
Serum amylase - usually very high (>1000u/ml) within 24h of onset, can fall rapidly.
Serum calcium may fall
Leukocytosis
AXR - may show gallstones; pancreatic calcification (indicating previous inflammation); distended loop of jejunum or transverse colon (if close to inflamed pancreas)
CT - exclude other pathology
Management of acute pancreatitis
Pain relief
IV fluid to correct electrolyte imbalance and maintain circulating volume, whilst monitoring central venous pressure
Nutritional support - enteral/parenteral
Monitor blood glucose
Renal support with haemodialysis or haemofiltration may be required
Monitor SaO2 and give O2 if needed
If pancreatitis severe or causing organ dysfunction, manage in HDU/ICU
If extensive (>30%) or infected necrosis of pancreas, drainage is required
Conditions associated with chronic pancreatitis
Cystic fibrosis
Haemochromatosis
Hyper parathyroid is
Investigations for chronic pancreatitis
Serum amylase is unhelpful
Imaging can be helpful, but may be normal (early disease) or difficult to distinguish between an inflammatory or malignant mass (later disease)
Investigate for malabsorption and exocrine pancreatic function, diabetes mellitus, and obstructive jaundice, if relevant.
Management of chronic pancreatitis
Treat pancreatic malabsorption with a low-fat diet, fat-soluble vitamins, calcium and pancreatic enzymes (e.g. Pancrex V, Creon)
Treat diabetes mellitus
Remove gallstones if present
Consider sphincterotomy or pancreatectomy if recurrent attacks
Completely avoid alcohol
Management of acute cholecystitis
Bed rest, analgesia (pethidine) and antibiotics according to local protocol
Early laparoscopic cholecystectomy
Charcot’s triad
Fever + jaundice + upper abdominal pain -> ascending cholangitis
Investigations for gallstones
USS will reveal most stones; CT or MRI provide alternative imaging modalities
Management of gallstones
Remove if causing symptoms.
If stones removed include pigment stones, investigate for haemolysis.
In elderly patients or if surgery is contraindicated, sphincterectomy via ERCP may release the stones if they are in the common bile duct.
Ursodeoxycholic acid may prevent formation of stones and dissolve radiolucent stones if they are <2cm in diameter and if the gallbladder is functioning
