Gastrointestinal Medicine Flashcards
Inflammatory bowel disease most common presentation?
Most patients with IBD will present with a change in bowel habit, often diarrhoea. It is important to clarify what patients mean when they describe their bowel habit and also relate this to what their usual habit would be.
UC vs Crohns features?
See table in workbook
Change in bowel habits investigations.
When thinking about the investigation of patients with a change in bowel habit you should use a surgical sieve approach and consider what you are looking for with each test:
Blood Tests
FBC – may be anaemic, or have a raised platelet count
U&E – may have deranged electrolytes or AKI due to GI losses
CRP – inflammatory marker, but a normal CRP doesn’t exclude IBD
Stool Tests
Stool Cultures – important to exclude infective colitis
Faecal Calprotectin – usually raised in active disease and negative in
irritable bowel or IBD in remission, but not specific to IBD and shouldn’t be used if blood is present as the presence of blood requires further investigation
Simple Imaging
AXR – used less often now but should be requested if there is a clinical
suspicion of toxic megacolon & can be useful to assess for proximal
constipation
Endoscopy
Flexible sigmoidoscopy – safest test in bloody diarrhoea
Colonoscopy – needed to look for more proximal disease
Capsule endoscopy – useful to view the small bowel mucosa
Cross Sectional imaging
CT abdomen when looking for acute complications
MRI enterography when looking for small bowel crohn’s, fistulas or to
map the extent of small bowel crohn’s
MRI Rectum to image perianal crohn’s
IBD treatment?
Patient in hospital - give IV Hydrocortisone 1oomg qds
If not responding:
For UC: ciclosporin, biologics or surgery.
Crohns; biologics or surgery.
Maintenance treatment for UC?
Mesalazine.
If fails escalate to azathioprine and biologics,
Maintenance treatment for Crohn’s?
Azathioprine and Biologics.
For perianal or fistulating Crohns; biologics are first line
Coeliac disease classic Presentation?
The presentation is varied & may include loose stools, bloating, wind, abdominal cramps, weight loss or dermatitis herpetiformis. There may be no symptoms and it can be found incidentally when investigating iron deficiency anaemia or due to a family history of coeliac disease (first degree relatives of someone with the condition have a 1/10 chance of also having coeliac disease).
Risks of untreated coeliac disease?
In untreated coeliac disease there is an increased risk of small bowel lymphoma, small bowel cancer, osteoporosis and neurological complications such as gluten ataxia and neuropathy.
Tests for Coeliac?
tTG (tissue transglutaminase) is raised in most cases of coeliac disease, but is not a diagnostic test in adult patients
OGD and duodenal biopsies is the diagnostic test, and histologically you will see villous atrophy and intra-epithelial lymphocytosis
Coeliac treatment?
Dietitians are key as treatment is a lifelong gluten free diet. Gluten is found in Barley, Rye, Oats and Wheat although some patients are able to reintroduce oats into their diet.
Dysphagia? Oesophageal Dysphagia
Either a physical obstruction or neuromuscular problem is present. Obstruction may be a tumour, a benign (peptic) stricture or inflammation from oesophagitis. Neuromuscular problems include achalasia, dysmotility and presbyoesophagus. OGD is usually needed to exclude an obstructive cause first and barium swallow or oesophageal manometry will look for neuromuscular problems. Treatment depends on the cause; dilatation for benign strictures and surgery or stenting for cancers.
Oreo-pharyngeal Dysphagia
Difficulty getting the food to leave the mouth is usually due to problems coordinating the muscles that move the food bolus to the back of the mouth, as a result of neurological disease such as stroke. It is important to examine the patient’s cranial nerves and obtain a speech therapy assessment of the safety of their swallow. A video-fluoroscopy may be helpful, and if their swallow remains unsafe with altered consistencies of food and fluid an enteral feeding tube may be necessary.
Functions of the liver?
Nutrition/metabolic
Bile salts
Bilirubin
Clotting factors
Detoxification
Immune function
Proteins
Diagnosis for ALT >500
Viral
Ischaemia
Toxic drugs
Autoimmune
ALT 100-200?
NASH
Autoimmune hepatitis
Chronic viral hepatitis
Drug induced liver injury
Cholestatic disease (dilated ducts) blood
Gallstones
Malignancy
Cholestatic (non-dilated ducts)
Alcoholic hepatitis
Cirrhosis
Drug induced liver injury
Things to screen in the liver
Hepatitis B&C Serology (in acute liver disease consider Hep A & E if marked ALT rise)
Iron studies (Ferritin & transferrin saturation)
Autoantibodies (AMA & SMA) and immunoglobulins
Consider caeuruloplasmin if age under 30 years
Alpha-a-antitrypsin
Coeliac serology
TFTs, lipids & glucose
Chronic liver disease causes?
There are many different aetiologies of chronic liver disease that can subsequently lead to cirrhosis if not treated. The commonest conditions are alcoholic liver disease, Non-alcoholic steatohepatitis and viral hepatitis (B&C). There are a number of less common conditions that it is important to consider:
Commoner in women: autoimmune hepatitis & primary biliary cholangitis (PBC)
Commoner in men: Primary sclerosing cholangitis (PSC) which is associated with IBD
Occurs earlier in men: haemachromatosis
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Occurs only in adolescents & young adults: Wilsons disease & Anti LKM autoimmune hepatitis
Treatment of chronic liver disease is based on removing the underlying aetiology (stopping drinking, weight loss, antivirals, venesection etc) to prevent further liver damage and progression to cirrhosis.
Liv cirrhosis
Cirrhosis is the end pathology of any cause of chronic liver disease and as such the monitoring, treatment and complications are the same irrespective of the underlying aetiology.
You should suspect cirrhosis in any patient with chronic liver disease who has thrombocytopenia or clinical stigmata of chronic liver disease. Imaging can be suggestive of cirrhosis (splenomegaly, coarse texture and nodularity) but a fibroscan is quicker and more specific than other imaging modalities and can be performed in the clinic room. The presence of varices on endoscopy in a patient with chronic liver disease would also be diagnostic of cirrhosis. Liver biopsy is rarely needed, and by the time cirrhosis has developed it is unlikely that this will give you any clue as to the underlying aetiology.
It is important to screen for varices in all patients with cirrhosis as primary prophylaxis can decrease the risk of bleeding significantly. Ascites develops in many patients with cirrhosis and is treated with spironolactone or, if tense, paracentesis. In the longer term patients with cirrhosis are at risk of Osteoporosis and they should have a DEXA scan.
Hepatocellular carcinoma is a type of primary liver tumour that can develop in patients with cirrhosis and patients should be screened using alpha-fetoprotein and USS every 6 months as early diagnosis is associated with better prognosis.
It is also important that any additional insult to the liver can cause further damage or decompensation and so wherever possible the aetiology of the liver disease should be tackled and patients advised to avoid all alcohol.
GI bleeding score systems?
ROCKALL score - simple score that predicts risk of death and rebleeding from an upper GI bleed.
Splint into a pre and post Endoscopy score. High er the score the higher the chance of death from a GI bleed.
Blatchford scores predicts the need for intervention (blood transfusion or therapeutic endoscopy) and requires blood tests. It is most useful in deciding if a patient needs admitting to hospital or not.
GI bleed investigations
In acute Upper GI bleeding your management and investigations will proceed at the same time as each other. Alongside your A-E approach you need to request
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investigations that will help assess the severity and cause of the bleeding and also help with your management.
The following investigations will be helpful:
FBC – to check the level of Haemoglobin and platelet count (thrombocytopenia may be suggestive of chronic liver disease and platelets will need replacing if low and bleeding)
U&E – a raised urea supports your diagnosis of upper GI bleeding
Clotting – abnormal clotting should be corrected in order to help control the
bleeding
Group and Save (Cross Match if haemodynamically unstable) – you may
need to give a blood transfusion
LFTs – remember however that normal liver function tests do not exclude
chronic liver disease
Venous Blood gas – this is a quick way to get a haemoglobin result
GI bleed variceal management
Variceal bleeding is a medical emergency and most often presents with fresh
haematemesis +/- melaena.
Initial action: gain IV access. Fluid resuscitation if haemodynamically compromised (followed by blood) but remember the systolic blood pressure is often low in patients with cirrhosis
Prescription: IV Terlipressin (if no ischaemic heart disease or peripheral vascular disease) AND IV antibiotics
Definitive treatment: refer urgently to the GI team for Upper GI endoscopy
The definitive treatment of variceal bleeding is a mechanical obstruction to the flow of blood through the varices. This is usually by means of endoscopic banding, but if this does not control the bleeding a Linton or Sengstaken tube may be required as a temporary measure, or a TIPSS (trans-jugular intrahepatic porto-systemic shunt) procedure.
Non-variceal bleeding treatment
Non-variceal bleeding covers a whole range of conditions, most commonly ulcer disease but also various vascular malformations such as angiodysplasia and dieulofoys. These conditions are more likely to stop bleeding on their own than variceal bleeds, and it is important to ensure that the patient is as haemodynamically stable as possible before their endoscopy in order to decrease the risks of this procedure and to increase the likelihood of definitive intervention being possible.
-Initial action: gain IV access. Fluid resuscitation if haemodynamically compromised (followed by blood)
-Prescription: there is no evidence for giving PPI before the endoscopy, but this may be indicated post-endoscopy
-Definitive treatment: Discuss with the gastroenterology team. Dependent on the pathology found there are various different endoscopic treatments possible. If the bleeding cannot be stopped by endoscopy, radiological embolization or surgery may be possible. The Endoscopist will advise on the need for any medications (such as PPI to treat ulcers) after the endoscopy.
