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What questions should be asked in a history investigating suspected IBD?
- Stool frequency, consistency, urgency and blood
- Abdominal pain,
- Malaise, fever or weight loss
- Extraintestinal symptoms
- Family history
What lab investigations are useful when diagnosing IBD?
- FBC (Anaemia, WBC, platelets)
- ESR, CRP
- U+Es (dehydration)
- Stool cultures + C.Diff toxin
- Faecal calprotectin (stool WCCs)
What is seen on colonoscopy in Crohn's and ulcerative colitis?
- Crohn's: Ulceration and inflammation
- Ulcerative colitis: Granular mucosa, reduced blood vessels
What criteria define an acute exacerbation of an IBD?
- Bowel movements >6 daily
- PR blood frequent
- Raised temperature
- HR >90
- Haemoglobin <10
- ESR >30
What treatments are used in acute exacerbation of an IBD?
- Prophylactic LMW heparin
- IV hydrocortisone
- If no improvement >72hrs, infliximab > ciclosporin
- Surgery if immunosuppression contraindicated/refractory
Outline the use of steroids in controlling an IBD
- Indicated if severe systemic symptoms
- IV hydrocortisone/methylprednisolone
- Allow remission, but not maintenance (maximum course 1 week)
What immunosuppressive drugs can be used in the management of IBDs
- Effective in active and maintenance therapy of both IBDs
What is the biologic treatment of IBD and when is it used?
- Anti-TNF monoclonal antibody
- Used in very severe UC or fistulating Crohn's
- Allergy common/Expensive
Outline the use of surgery in the management of the IBDs
- Ulcerative colitis: Surgery curative; ileo-anal pouch or ileostomy
- Crohn's: Indicated in strictures, perforations or fistulations. Remission can still occur, so used sparingly
What is the cause of Whipple's disease, and what are its clinical features?
- Tropheryma whipplei infection when patient has a lack of immunity
- Weight loss, arthralgia, diarrhoea, abdominal pain
Describe some complications of acute appendicitis
- Acute inflammation of mucosa = ulceration and transmural inflammation
- Gangrene can cause perforation, generalised peritonitis or abscess
Define ulcerative colitis, its presentation and complications
- Chronic inflammation of the mucosa and submucosa of the large intestine and rectum (no granulomas)
- Onset 15-25, with gradual onset of chronic bloody diarrhoea
Define Crohn's disease, its presentation and complications
- Chronic transmural inflammation in any part of gut (usually ileum and anus) causing garnulomas and 'fissuring ulcers'
- Common in smokers, 15-25yoa, with cramps, abdominal pain, vomiting, mouth ulcers, weight loss and bleeding
- Fistulas, stenosis, abscess and inflammation cause 'knots' in bowel. Greatly increased cancer risk.
What is 'indeterminate colitis'?
When a diagnosis of colitis is between Crohn's and UC
What is 'microscopic colitis'?
- Profuse watery diarrhoea
- Colonoscopy normal
- Abnormal histology; either collagenous or lymphocytic (relates to inflammatory cells in lamina propria)
- May be associated with drug treatment, e.g. PPIs, statins
Outline the pathophysiology of ischaemia affecting the gut
- Extreme problem, with certain death if not operated upon
- Mucosal/transmural infarction, coagulative necrosis and gangrene
Outline the presentation of acute and chronic gut ischaemia
- Acute: abdominal pain and bloody stool
- Chronic: Pain when eating, with weight loss (abdominal angina)
Outline some causes of gut ischaemia
- Hypotension (watershed infarction)
- Strangulated hernia
- Mesenteric artery/vein thromboembolism
- Volvulus (sigmoid colon twisting)
Outline the pathogenesis of cholesterol stones
- Excessive secretion of cholesterol or decrease secretion of bile salts
- Precipitation occurs
- Example is Crohn's, reducing bile salt recycling
Outline how Crohn's is different from UC
- Usually involves terminal ileum and anus, but not the rectum.
- The areas of inflammation are patchy, not continuous.
- Deep ulceration, may even be transmural
- Stenosis is common
Outline the pathogenesis of bile stones
- Excessive bile secretion (e.g. haemolytic anaemia)
- Causes bile precipitation after concentration in the gall bladder
Describe chronic cholecystitis, its pathogenesis and its clinical features
- May be a progression from acute cholecystitis, with gallstones virtually always present
- Inflammation due to chemical damage from supersaturated bile, not bacterial infection
- Ulceration, fibrosis and macrophage/lymphocyte infiltration
How does a bladder mucocoele occur?
- Gallstone becomes stuck in Hartmann's pouch of gallbladder
- Reduces bile entry, but mucin still secreted
- No inflammation, but distension
How does a gallstone ileus occur?
- Fistula develops between gallbladder and duodenum from inflammation/necrosis
- Allows entry of a large stone into terminal ileum, and air into biliary tree
What is the link between painless obstructive jaundice and carcinoma of bile ducts/pancreas?
- Cancer growth compresses bile duct
- Back up of bile prevents excretion from liver
- Bilirubin builds up in blood, causing jaundice
How does cystic fibrosis affect the GI tract?
- Mucous can block the bile ducts, preventing bile salt transportation to the GI
- Bile salts needed by some pancreatic enzymes = reduction in digestions efficiency
- Hepatic cirrhosis can occur, causing ascites, varicosities and splenomegaly
- Pancreatic scarring can also occur
Describe an insulinoma
- Commonest functional tumour of the pancreas
- Presents with hypoglycaemia
- Usually benign, but even malignant have much better prognosis
What important points should be remembered about the bilirubin cycle when assessing plasma bilirubin?
- Increased unconjugated bilirubin = increased haemolysis OR liver damage (produced more or conjugated less)
- Bile duct obstruction leads to conjugated biliruin in plasma
- Urobilinogen created in GI tract - if bilirubin transport obstructed, urine doesn't contain urobilinogen
Briefly outline the anatomy of teeth
- Central chamber of tooth has stroma and vessels
- Surrounded by dentine (tubular connective tisuse) with enamel surface (calcium)
- Attached by ligaments to mandible and by connective tissue fibres to gums.
What is oral leukoplakia?
- Treated as pre-malignant squamous dysplasia, with keratosis
- Change in histology, with mild cytological atypia
- Behaves like any dysplasia; may become more atypical, then carcinoma in situ
- Usually found on floor of mouth (chemical pooling) or soft palate
- HPV and smoking common causes
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