Gastro Flashcards
Acute porphyrias
disorders caused by defects in haem synthesis due to alterations in enzyme function or structure.
Acute porphyria types:
Acute intermittent porphyria
Variegate porphyria
ALA deficiency.
Triggers of acute porphyria
Antibiotics - Rifampicin, Isoniazid, Nitrofurantoin Anaesthetic agents - Ketamine, Etomidate Sulfonamides Barbiturates Antifungal agents
Diagnosis of porphyria
Diagnosis can be made on the basis of urinary porphobilinogen levels, which is a product in the pathway of haem metabolism. Urine samples need to be protected from light to prevent the breakdown of PBG.
Management
Treatment of attacks is largely supportive. Haem arginate can also be given intravenously to replenish haem levels.
Indications for inpatient withdrawal
Patients drinking >30 units per day
Scoring over 30 on the SADQ score
High risk of alcohol withdrawal seizures (previous alcohol withdrawal seizures or delirium tremens, or history of epilepsy)
Concurrent withdrawal from benzodiazepines
Significant medical or psychiatric comorbidity
Vulnerable patients
Patients under 18
Management
of alcohol withdrawal
Assisted alcohol withdrawal is required in patients drinking over 15 units per day or in those scoring over 20 on the AUDIT questionnaire.
Chlordiazepoxide prescribed in a reducing regimen in accordance with the CIWA score and local protocol.
In alcohol-withdrawal seizure a patient should be prescribed a rapid-acting benzodiazepine (such as intravenous lorazepam).
Pabrinex (1 pair of ampoules once daily to prevent Wernicke’s encephalopathy).
If there are signs of Wernicke’s encephalopathy (confusion, ataxia, ophthalmoplegia or nystagmus) patients should be prescribed 2 pairs of ampoules TDS.
In delirium tremens (this presents with confusion and visual hallucinations 48-72 hours after abstinence) offer oral lorazepam as first line treatment. If this is declines or symptoms persist offer parenteral lorazepam.
Alpha 1-antitrypsin deficiency
presentation
Alpha 1-antitrypsin deficiency is an inherited condition that affects the lungs, causing emphysema, and the liver, causing cirrhosis and hepatocellular carcinoma.
Presentation
COPD presenting 30-40 years old
Neonatal jaundice at birth
Deranged LFTs in adults with no other identified cause
Alpha 1-antitrypsin deficiency
D and M
investigations
The disease can be tested for with alpha 1 antitrypsin levels, genotyping or liver biopsy (evidence of Periodic acid Schiff positive globules).
Management
The condition has few management options and patients are advised to stop smoking. Intravenous A1AT pooled from human donors is expensive and not widely used. Liver transplant may be required in cases of decompensation.
Causes of a high SAAG in asisties
Cirrhosis Heart failure Budd Chiari syndrome Constrictive pericarditis Hepatic failure A high SAAG (>11g/dL) suggests that the cause of the ascites is due to raised portal pressure.
Causes of a low SAAG (<11g/dL)
Cancer of the peritoneum
Tuberculosis and other infections
Pancreatitis
Nephrotic syndrome
Autoimmune hepatitis
(young middle aged women)
Liver function test results
Liver function test results
Raised ALT and bilirubin with normal/mildly raised ALP. Patients may have an IgG predominant hypergammaglobulinemia.
barrets oesphogous
ass/w GORD
-> leads to a change in the distal oesophagus from the usual squamous epithelium to metaplastic columnar epithelium.
== oesophageal adenocarcinoma.
Cholera treatment
Management
Aggressive fluid replacement: effective therapy can decrease mortality from over 50% to less than 0.2%.
Antibiotics (Doxycycline or co-trimoxazole) decrease volume and duration of diarrhoea by 50% and are recommended for patients with moderate to severe dehydration.
Chronic pancreatitis Clinical Features
Patients present with epigastric pain, classically worse after eating fatty food and relieved by sitting forward.
There may be features of exocrine dysfunction, such as malabsorption and steatorrhoea.
There may be features of endocrine dysfunction (i.e. Type 1 diabetes mellitus) with thirst and polyuria.
On physical examination there may be epigastric tenderness. It is important to check for signs of chronic liver disease (suggestive of alcohol as a cause).
Risk factors for developing CDI
Have been treated with broad-spectrum antibiotics
Common antibiotic risk factors include:
Clindamycin
Ciprofloxacin
Cephalosporins
Penicillins
Have had to stay in a healthcare setting, such as a hospital or care home, for a long time
Are over 65 years old
Have certain underlying conditions, including inflammatory bowel disease (IBD), cancer, or kidney disease
Have a week immune system, as a result of conditions such as diabetes or HIV infection or as side effect of a treatment such as chemotherapy or steroid medication
Are taking a proton pump inhibitor (PPI)
Complications of coeliac
naemia
Hyposplenism (and therefore a susceptibility to encapsulated organisms)
Osteoporosis (a DEXA scan may be required)
Enteropathy-associated T cell lymphoma (EATL; a rare type of non-Hodgkin lymphoma).
The likelhood or aquiring this malignancy is directly proportional to the strength of overall adherence to a gluten free diet - i.e. the more a patient breaks adherence, the more likely they are to get EATL.
Enzyme inducers
Reduce the concentration of drugs metabolised by the cytochrome P450 system
Carbamazepine Rifampicin Phenytoin Griseofulvin Phenobarbitone Alcohol (chronic)
Enzyme inhibitors
Increase the concentration of drugs metabolised by the cytochrome P450 system
Valproate Isoniazid Cimetidine Fluclonazole Erythromycin Omeprazole
Gastroenteritis causes
Bacterial causes
The bacteria most commonly implicated are:
Staphylococcus aureus: usually found in cooked meats and cream products.
Bacillus cereus: mainly found in reheated rice.
Clostridium perfringens: usually found in reheated meat dishes or cooked meats.
Campylobacter
E.coli including E.coli 0157 (which can cause haemolytic uraemic syndrome)
Salmonella
Shigella
Viral causes
Rotavirus: most common cause of infantile gastroenteritis
Norovirus: most common cause of viral infectious gastroenteritis in all ages in England and Wales
Adenoviruses: commonly cause infections of the respiratory system but can also cause gastroenteritis, particularly in children.
Specific antibiotics for Gastroenteriti
Salmonella and shigella are treated with ciprofloxacin.
Campylobacter is treatment with a macrolide, such as erythromycin.
Cholera is treated with tetracycline, to reduce transmission.
Food poisoning is a notifiable disease in the UK.
gastroparesis - d n m
Diagnosis
Diagnosis of gastroparesis can be made with a solid meal gastric scintigraphy (Radionuclide studies of gastric emptying)
Management
Dietary modification - low fibre, smaller/more frequent meals, pureed/mashed food
Domperidone - dopamine receptor antagonist
Metoclopramide or Erythromycin (motility agents)
Treatment of H. Pylori
Amoxicillin, clarithromycin and a PPI twice daily for seven days - so-called triple therapy.
After 4-8 weeks patients can be re-tested for H. Pylori to check it has been eradicated.
If still present, NICE recommend another course of triple therapy with metronidazole or clarithromycin - whichever was not used in the initial course - amoxicillin and a PPI. The importance of adherence should also be discussed with the patient.
If the patient has already had courses of clarithromycin and metronidazole, the recommended treatment is a seven day course of a PPI, amoxicillin and either tetracycline or a quinolone.
main types of hiatus hernias
Sliding hiatal hernia (80%): The gastro-oesophageal junction slides up into the chest. A less competent sphincter results in acid reflux. Treatment is similar as for GORD.
Rolling hiatal hernia (20%): The gastro-oesophageal junction remains in the abdomen but part of the stomach protrude into the chest alongside the oesophagus. This type needs more urgent treatment as volvulus can result in ischemia and necrosis.
Clinical features of hiatus hernias
Symptoms include heartburn, dysphagia, regurgitation, odynophagia, shortness of breath, chronic cough and chest pain.
Hiatal hernias can be diagnosed using barium swallows (upper GI series), which is the most sensitive method, endoscopy and oesophageal manometry.
management of hiatus hernias
Conservative management includes crucial lifestyle changes. Lifestyle advice for patients with hiatal hernia includes
Lose weight
Elevate the head of the bed
Avoid large meals and eat 3-4 hours before bedtime
Avoiding alcohol and acidic foods
Avoid smoking as nicotine relaxes the lower oesophageal sphincter (as can chocolate, peppermint, caffeine, fatty foods, and medications such as calcium-channel blockers, nitrates, and beta-blockers)
Medical management involves PPI use for 4-8 weeks before assessing response.
Surgical management includes Nissen’s fundoplication
Indications for TIPSS
Secondary prophylaxis for oesophageal variceal bleeding
Treatment of refractory ascites
Treating portal hypertension in Budd-Chiari syndrome
Manning criteria for diagnosis of IBS
Abdominal discomfort or pain that is relieved by defecation OR associated with altered bowel frequency or stool form
AND at least 2 of:
Altered stool passage (e.g. straining or urgency)
Abdominal bloating
Symptoms made worse by eating
Passage of mucus
Causes of Prehepatic jaundice
Prehepatic causes of jaundice result in unconjugated hyperbilirubinaemia, which is not water soluble so cannot enter the urine. It is therefore known as acholuric jaundice.
Causes:
Conjugation disorders, such as Gilbert’s disease and Crigler-Naajjar
Haemolysis (such as malaria or haemolytic anaemia)
Drugs, such as contrast or rifampicin
Causes of hepatocelullar dysfunction (‘hepatic jaundice’)
Hepatocellular dysfunction results in a conjugated hyperbilirubinaemia. Causes include:
Viruses (hepatitis, CMV, EBV) Drugs, including paracetamol overdose, halothane, valproate, statins, tuberculosis antibiotics Alcohol Cirrhosis Liver mass (abscess or malignancy) Haemochromatosis Autoimmune hepatitis Alpha-1 antitrypsin deficiency Budd-Chiari Wilson's disease Failure to excrete conjugated bilirubin (Rotor and Dubin-Johnson syndromes)
Causes of post-hepatic jaundice
Impaired excretion of conjugated bilirubin results is cholestasis. Conjugated bilirubin is water soluble, making the urine dark. Less bilirubin reaches the gut, so pale stools also result. Pruritus also suggests an obstructive problem. These so-called post-hepatic causes include:
Primary biliary cirrhosis
Primary sclerosing cholangitis
Common bile duct gallstones or Mirrizi’s syndrome (CBD compression from a gallstone in the cystic duct)
Drugs, including coamoxiclav, flucloxacillin, nitrofurantoin, steroids, sulfonylureas
Malignancy, such as head of the pancreas adenocarcinoma, cholangiocarcinoma
Caroli’s disease
Biliary atresia
Imaging and invasive investigations for cirrhosis
If ascites is present, a peritoneal tap should be taken for microscopy and culture to look for spontaneous bacterial peritonitis.
A Doppler ultrasound would be of use in identifying Budd-Chiari syndrome.
Transient elastography or acoustic radiation force impulse imaging can be used to diagnose non-alcoholic fatty liver disease.
Liver biopsy may be necessary to confirm the underlying diagnosis if still in doubt.
Child-Pugh interpretation
The scores are added and the degree of cirrhosis is classified as Child-Pugh A (<7 points), B (7-9 points) or C (>9 points).
The score can be used as a predictor of mortality, and may also be used to predict the need for a liver transplant.
Management of decompensated liver disease
Good nutrition is essential, with total alcohol abstinence.
Non-steroidal anti-inflammatory drugs, sedatives and opiates should all be avoided.
An ultrasound scan and serum α-fetoprotein every 6 months may be indicated to detect development of hepatocellular carcinoma.
Colestyramine (bile acid sequestrant) can be used to manage pruritus.
Ascites can be managed with fluid restriction (under 1.5L per day) and a low-salt diet. Pharmacological management is with spironolactone; furosemide can be added if necessary. In severe cases, therapeutic paracentesis can be used alongside albumin infusions.
Recurrent episodes of encephalopathy can be reduced in frequency through the use of prophylactic lactulose and rifaximin.
Patients at high-risk of spontaneous bacterial peritonitis (such as those who have had previous episodes, or those with low albumin, a high INR and low ascitic albumin) may be treated with prophylactic antibiotics.
Ultimate treatment is a liver transplant. For cases of chronic liver disease scores such as the Model for End-stage Liver Disease (MELD) and UK End-stage Liver Disease (UKELD) are used to help predict severity of disease.
Four stages of hepatic encephalopathy
Altered mood and behaviour, disturbance of sleep pattern and dyspraxia
Drowsiness, confusion, slurring of speech and personality change
Incoherency, restlessness, asterixis
Coma
King’s College Hospital Criteria for Liver Transplant (paracetamol induced)
The criteria for paracetamol induced liver failure are as follows:
Arterial pH <7.3 24h after ingestion OR
Pro-thrombin time >100s
AND creatinine >300µmol/L
AND grade III or IV encephalopathy.
King’s College Hospital Criteria for Liver Transplant (non-paracetamol liver failure)
Prothrombin time >100s OR Any three of: Drug-induced liver failure Age under 10 or over 40 years 1 week from 1st jaundice to encephalopathy Prothrombin time >50s Bilirubin ≥300µmol/L.
Melanosis coli
Melanosis coli is a finding usually associated with chronic laxative abuse, where colonoscopy reveals the presence of dark brown pigmentation of the macrophages in the lamina propria
Mucosa-associated lymphoid tissue (MALT) lymphoma
Clinical features Abdominal pain Nausea and vomiting Symptoms of anaemia Weight loss
Management
The initial treatment for local and disseminated disease is H. Pylori eradication therapy. This can treat the lymphoma in many cases.
If this fails to eradicate the disease, however, other treatment options are chemotherapy and radiotherapy. These may be considered if the disease is progressive or the patient has high risk features, such as being H. Pylori negative at presentation.
In disseminated disease, chemotherapy and rituximab is recommended if there is a threat to vital organ function. Otherwise, a watch and wait approach can be adopted.
Candida
White patches in the mouth are most commonly caused by a fungal infection with Candida; leucoplakia is a generic way to describe white patches found in the mouth.
Old age Diabetes mellitus Immunosuppression Long term corticosteroids Malignancy Antibiotics
Hairy Leukoplakia
Hairy leucoplakia is a benign condition that does not in itself require any treatment, but may lead to medical and psychological issues for the patient given the likely underlying condition. It is caused by Epstein-Barr virus, and is suggestive of underlying HIV infection.
Oral ulcers
Common deficiencies causing oral ulcers include iron, vitamin B12 and folate, which all lead to anaemia. Crohn’s disease can also cause painful oral ulcers.
