Medicine: Gastroenterology Disease Flashcards
How is risk of Acute Upper Gastrointestinal Bleeding assessed?
Use the Blatchford score at first assessment
- Predicts need for intervention
ROCKALL Score: Predicts Mortality
- Pre-Endoscopy Rockall Score before endoscopy
- Full Rockall score after endoscopy
What are the factors of the Blatchford Score?
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Urea (mmol/l)
- 6·5-8 = 2
- 8-10 = 3
- 10-25 = 4
- >25 = 6
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Haemoglobin (g/l)
- Men
- 12-13 = 1
- 10-12 = 3
- <10 = 6
- Women
- 10-12 = 1
- <10 = 6
- Men
-
Systolic blood pressure (mmHg)
- 100-109 = 1
- 90-99 = 2
- <90 = 3
-
Other markers
- Pulse >=100/min = 1
- Presentation with melaena = 1
- Presentation with syncope = 2
- Hepatic disease = 2
- Cardiac failure = 2
What is done with a Blatchford Score of 0?
Patients with a Blatchford score of 0 may be considered for early discharge
How is a patient with Acute Gastrointestinal Bleed resuscitated?
- ABC, 2 wide-bore intravenous access
- Platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
- Fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a PT (INR) or APTT greater than 1.5 times normal
- Prothrombin complex concentrate to patients who are taking warfarin and actively bleeding
How are Acute Gastrointestinal bleeds investigated?
Endoscopy
- Should be offered immediately after resuscitation in patients with a severe bleed
- All patients should have endoscopy within 24 hours
How are non-variceal bleeds managed?
- Endoscopy indicated
- Mechanical: Clips with/without adrenaline
- Thermocoagulation with adrenaline
- Fibrin or Thrombin with Adrenaline
- IV PPIs should be given to patients with
- Non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
- If further bleeding then options include repeat endoscopy, interventional radiology and surgery
How are variceal bleeds initially managed?
At presentation:
- ABC: patients should ideally be resuscitated prior to endoscopy
- Correct Clotting: FFP, vitamin K
- Vasoactive agents
- 1st Line: Terlipressin to prevent re-bleeding
- 2nd Line: Octreotide
-
Prophylactic antibiotics
- Quinolones typically used
How are variceal bleeds definitively managed?
Endoscopy
- Oesophageal Varices
- Band ligation
- TIPSS
- Sengstaken-Blakemore tube if uncontrolled haemorrhage
- Gastric Varices
- Injections of N-butyl-2-cyanoacrylate
- Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail
How is Prophylaxis of Variceal Bleed initiated?
- Propranolol: reduced rebleeding and mortality compared to placebo
- Endoscopic variceal band ligation (EVL) is superior to endoscopic sclerotherapy. It should be performed at two-weekly intervals until all varices have been eradicated.
- Proton pump inhibitor cover is given to prevent EVL-induced ulceration.
What are causes of Acute liver failure?
- Paracetamol overdose
- Alcohol
- Viral hepatitis (usually A or B)
- Acute fatty liver of pregnancy
What are features of Acute Liver Failure?
- Jaundice
- Coagulopathy: raised prothrombin time
- Hypoalbuminaemia
- Hepatic encephalopathy
- Renal failure is common (‘hepatorenal syndrome’)
What is Hepatic Encephalopathy?
- Hepatic encephalopathy may be seen in liver disease of any cause.
- Aetiology is thought to include excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut.
- Associated with Acute liver failure but can occur in chronic liver failure
buildup of ammonia in the blood, a substance that is normally removed by the liver.
What are feature of Hepatic Encephalopathy?
- Confusion, altered GCS
- ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
- Constructional apraxia: inability to draw a 5-pointed star
- Triphasic slow waves on EEG
- Raised ammonia level (not commonly measured anymore)
How is hepatic encephalopathy graded?
- Grade I: Irritability
- Grade II: Confusion, inappropriate behaviour
- Grade III: Incoherent, restless
- Grade IV: Coma
What are some precipitating factors of hepatic encephalopathy?
- Infection e.g. spontaneous bacterial peritonitis
- GI bleed
- Post transjugular intrahepatic portosystemic shunt
- Constipation
- Drugs: sedatives, diuretics
- Hypokalaemia
- Renal failure
- Increased dietary protein (uncommon)
How is hepatic encephalopathy managed?
Treat any underlying precipitating cause
-
1st line: Lactulose + Rifaximin
- Lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
- Rifaximin are thought to modulate the gut flora resulting in decreased ammonia production for secondary prophylaxis
- Other options include embolisation of portosystemic shunts and liver transplantation in selected patients
What is Coeliac Disease?
- Coeliac disease is an autoimmune condition caused by sensitivity to the protein gluten.
- Repeated exposure leads to villous atrophy which in turn causes malabsorption.
What are conditions associated with Coeliac Disease?
- It is strongly associated with HLA-DQ2 and HLA-DQ8 (80%).
- Autoimmune thyroid disease
- Dermatitis herpetiformis
- Irritable bowel syndrome
- Type 1 diabetes
- First-degree relatives (parents, siblings or children) with coeliac disease
Coeliacs DID’T know they cant eat gluten
What are clinical features of Coeliac Disease?
- Chronic or intermittent diarrhoea
- Failure to thrive or faltering growth (in children)
- Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
- Prolonged fatigue (‘tired all the time’)
- Recurrent abdominal pain, cramping or distension
- Sudden or unexpected weight loss
- Unexplained iron-deficiency anaemia, or other unspecified anaemia
How is investigation for Coeliac Disease done?
- If patients are already taking a gluten-free diet they should be asked, to reintroduce gluten for at least 6 weeks prior to testing.
- Villous atrophy and immunology normally reverses on a gluten-free diet.
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Immunology
- Tissue Transglutaminase (TTG) antibodies (IgA) are first-choice
- endomyseal antibody (IgA)
- anti-casein antibodies are also found
-
Gold standard imaging: OGD and Duodenal biopsy
- Villous atrophy
- Crypt hyperplasia
- Increase in intraepithelial lymphocytes
- Lamina propria infiltration with lymphocytes
How is Coeliac Disease managed?
Management of coeliac disease involves a gluten-free diet.
- Gluten containing cereals include: wheat (bread, pasta, pastry), barley (beer), Rye, oats**
- Some notable foods which are gluten-free include: rice, potatoes, corn (maize)
- Tissue transglutaminase antibodies may be checked to check compliance with a gluten free diet.
- Patients with coeliac disease often have a degree of functional hyposplenism so all patients with coeliac disease are offered the pneumococcal vaccine.
What are complications of Coeliac Disease?
- Anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
- Hyposplenism
- Osteoporosis, osteomalacia
- Lactose intolerance
- Enteropathy-associated T-cell lymphoma of small intestine
- Subfertility, unfavourable pregnancy outcomes
- Rare: oesophageal cancer, other malignancies
How is Malnutrition defined?
- Body Mass Index (BMI) of less than 18.5; or
- Unintentional weight loss greater than 10% within the last 3-6 months; or
- BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
What is used to screen for Malnutrition?
Screening for malnutrition done using MUST (Malnutrition Universal Screen Tool).
- Should be done on admission to care/nursing homes and hospital, or if there is concern. For example an elderly, thin patient with pressure sores
- Takes into account BMI, recent weight change and the presence of acute disease
- Categorises patients into low, medium and high risk
How is Malnutrition managed?
- Dietician support if the patient is high-risk
- ‘food-first’ approach with clear instructions (e.g. ‘add full-fat cream to mashed potato’), rather than just prescribing oral nutritional supplements (ONS) such as Ensure
- If ONS are used they should be taken between meals, rather than instead of meals
What is refeeding syndrome?
- Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation.
- It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism.
What are the metabolic consequences of Re-feeding syndrome?
The metabolic consequences include:
- Hypophosphataemia
- Hypokalaemia
- Hypomagnesaemia: may predispose to torsades de pointes
- Abnormal fluid balance
These abnormalities can lead to organ failure.
Which patients are considered high risk for re-feeding syndrome?
Patients are considered high-risk if one or more of the following:
- BMI < 16 kg/m2
- unintentional weight loss >15% over 3-6 months
- little nutritional intake > 10 days
- hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
If two or more of the following:
- BMI < 18.5 kg/m2
- Unintentional weight loss > 10% over 3-6 months
- Little nutritional intake > 5 days
- History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids
How is re-feeding syndrome managed?
if a patient hasn’t eaten for > 5 days, aim to re-feed at no more than 50% of requirements for the first 2 days.
