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Kofi: Surgery + Gastroenterology > Medicine: Gastroenterology Disease > Flashcards

Medicine: Gastroenterology Disease Flashcards

1
Q

How is risk of Acute Upper Gastrointestinal Bleeding assessed?

A

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
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2
Q

What are the factors of the Blatchford Score?

A
  • Urea (mmol/l)
    • 6·5-8 = 2
    • 8-10 = 3
    • 10-25 = 4
    • >25 = 6
  • Haemoglobin (g/l)
    • Men
      • 12-13 = 1
      • 10-12 = 3
      • <10 = 6
    • Women
      • 10-12 = 1
      • <10 = 6
  • 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
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3
Q

What is done with a Blatchford Score of 0?

A

Patients with a Blatchford score of 0 may be considered for early discharge

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4
Q

How is a patient with Acute Gastrointestinal Bleed resuscitated?

A
  • 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
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5
Q

How are Acute Gastrointestinal bleeds investigated?

A

Endoscopy

  • Should be offered immediately after resuscitation in patients with a severe bleed
  • All patients should have endoscopy within 24 hours
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6
Q

How are non-variceal bleeds managed?

A
  • 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
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7
Q

How are variceal bleeds initially managed?

A

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
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8
Q

How are variceal bleeds definitively managed?

A

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
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9
Q

How is Prophylaxis of Variceal Bleed initiated?

A
  • 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.
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10
Q

What are causes of Acute liver failure?

A
  • Paracetamol overdose
  • Alcohol
  • Viral hepatitis (usually A or B)
  • Acute fatty liver of pregnancy
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11
Q

What are features of Acute Liver Failure?

A
  • Jaundice
  • Coagulopathy: raised prothrombin time
  • Hypoalbuminaemia
  • Hepatic encephalopathy
  • Renal failure is common (‘hepatorenal syndrome’)
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12
Q

What is Hepatic Encephalopathy?

A
  • 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.

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13
Q

What are feature of Hepatic Encephalopathy?

A
  • 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)
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14
Q

How is hepatic encephalopathy graded?

A
  • Grade I: Irritability
  • Grade II: Confusion, inappropriate behaviour
  • Grade III: Incoherent, restless
  • Grade IV: Coma
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15
Q

What are some precipitating factors of hepatic encephalopathy?

A
  • Infection e.g. spontaneous bacterial peritonitis
  • GI bleed
  • Post transjugular intrahepatic portosystemic shunt
  • Constipation
  • Drugs: sedatives, diuretics
  • Hypokalaemia
  • Renal failure
  • Increased dietary protein (uncommon)
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16
Q

How is hepatic encephalopathy managed?

A

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
17
Q

What is Coeliac Disease?

A
  • Coeliac disease is an autoimmune condition caused by sensitivity to the protein gluten.
  • Repeated exposure leads to villous atrophy which in turn causes malabsorption.
18
Q

What are conditions associated with Coeliac Disease?

A
  • 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

19
Q

What are clinical features of Coeliac Disease?

A
  • 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
20
Q

How is investigation for Coeliac Disease done?

A
  • 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.
  • 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
21
Q

How is Coeliac Disease managed?

A

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.
22
Q

What are complications of Coeliac Disease?

A
  • 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
23
Q

How is Malnutrition defined?

A
  • 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
24
Q

What is used to screen for Malnutrition?

A

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
25
Q

How is Malnutrition managed?

A
  • 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
26
Q

What is refeeding syndrome?

A
  • 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.
27
Q

What are the metabolic consequences of Re-feeding syndrome?

A

The metabolic consequences include:

  • Hypophosphataemia
  • Hypokalaemia
  • Hypomagnesaemia: may predispose to torsades de pointes
  • Abnormal fluid balance

These abnormalities can lead to organ failure.

28
Q

Which patients are considered high risk for re-feeding syndrome?

A

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
29
Q

How is re-feeding syndrome managed?

A

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.

Kofi: Surgery + Gastroenterology (14 decks)

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