gastro Flashcards
CMV colitis flare investigation
Cytomegalovirus may be a cause of a colitis flare and should be suspected in patients with steroid refractory disease. The presence of multiple intranuclear inclusion bodies on colonic biopsy is highly indicative.
PBC
Pruritus and lethargy are the classical presenting symptoms of primary biliary cirrhosis (PBC). Patients may have associated autoimmune conditions such as thyroid disease, Raynaud’s and Addison’s diseases.
Clinical features include:
Stigmata of chronic liver disease
Excoriations due to pruritus, and
Xanthelasma.
Blood results show elevated ALP and GGT with mildly elevated transaminases. A rise in bilirubin is usually a late sign. Prothrombin time may also be elevated due to impaired synthetic function or vitamin K malabsorption. IgM will be raised. AMA autoantibodies are positive in 95% of cases.
Abdominal ultrasound must be performed in all cases to exclude biliary duct dilatation. The need for liver biopsy is debated as it rarely affects the management but it is indicated in cases of diagnostic uncertainty.
PBC increases the risk of hepatocellular carcinoma but often focal liver lesions are seen on ultrasound in cases of HCC.
grading encephalopathy
Pruritus and lethargy are the classical presenting symptoms of primary biliary cirrhosis (PBC). Patients may have associated autoimmune conditions such as thyroid disease, Raynaud’s and Addison’s diseases.
Clinical features include:
Stigmata of chronic liver disease
Excoriations due to pruritus, and
Xanthelasma.
Blood results show elevated ALP and GGT with mildly elevated transaminases. A rise in bilirubin is usually a late sign. Prothrombin time may also be elevated due to impaired synthetic function or vitamin K malabsorption. IgM will be raised. AMA autoantibodies are positive in 95% of cases.
Abdominal ultrasound must be performed in all cases to exclude biliary duct dilatation. The need for liver biopsy is debated as it rarely affects the management but it is indicated in cases of diagnostic uncertainty.
PBC increases the risk of hepatocellular carcinoma but often focal liver lesions are seen on ultrasound in cases of HCC.
small bowel bacterial overgrowth
Steatorrhoea and flatulence are classic presenting features of small bowel bacterial overgrowth.
At risk groups are those with:
absent gastric acid secretion
small bowel diverticulae
fistulae between the small and large bowel
small bowel strictures
diabetic neuropathy, and
adhesions.
Biochemically there is classically a low vitamin B12 level and normal or elevated folate level as a result of bacterial metabolism of B12 to folate.
Bile salt malabsorption
Bile salt malabsorption causes secretory diarrhoea (watery) and is a result of failure of bile salt reabsorption due to disease of the terminal ileum.
Melanosis coli
Melanosis coli is found in patients who use and abuse anthraquinone laxatives. Melanosis coli is a histological diagnosis made from rectal biopsy material which shows numerous macrophages filled with brown pigment within the lamina propria. This phenomenon is seen in over 70% of persons who use anthraquinone laxatives (for example, cascara sagrada, senna, and frangula) within several months of use.
The condition is benign and reversible on stopping the laxatives.
The macroscopic appearance varies from deep black pigmentation to reticulated brown discolouration.
Melanosis coli may involve the entire large intestine, but can be segmental.
The discolouration is caused by deposits of lipofuscin rather than true melanin deposition.
Anthraquinone cathartics induce apoptosis of epithelial cells of the large intestine. The apoptotic bodies are taken up by epithelial macrophages and they are converted to lipofuscin.
hyponatremia and DLD
The British Society of Gastroenterology guidelines suggest that where the serum sodium is ≤120 mmol/L diuretic therapy should be stopped and patients should receive volume expansion with colloid or normal saline.
These guidelines also advise that fluid restriction should only be used in patients who are clinically euvolaemic, not on diuretics and have severe hyponatraemia with a normal serum creatinine.
Bloody ascitic fluid
Bloody ascitic fluid with a Gram stain revealing Gram negative bacilli and Gram positive cocci is suggestive of bowel perforation.
Anti-mitochondiral antibodies
Anti-mitochondiral antibodies are positive in 95% of cases of primary biliary cirrhosis.
Autoimmune gastritis
Autoimmune gastritis is associated with anti-gastric parietal cell antibodies, with or without pernicious anaemia.
Anti-liver kidney microsomal antibodie
Anti-liver kidney microsomal antibodies are found in autoimmune chronic hepatitis.
coeliac antibodies
Anti-endomysial and anti-tissue transglutaminase antibodies are found in patients with coeliac disease.
Bartter’s syndrome
hypokalaemic metabolic alkalosis with urinary potassium wasting characteristic of Bartter’s syndrome.
Bartter’s syndrome usually presents in childhood with polyuria, nocturnal enuresis and growth retardation.
Bartter’s syndrome is associated with hyperplasia of the juxtaglomerular apparatus.
haemochromatosis
Clinical signs of haemochromatosis include hepatomegaly, cirrhosis and splenomegaly. Patients may have cardiomyopathy and endocrine complications including diabetes mellitus, hypogonadism, panhypopituitarism and testicular atrophy. The term ‘bronze diabetes’ comes from the skin pigmentation which is seen in these patients. Chondrocalcinosis and arthritis may also develop. Hepatocellular carcinoma should be excluded especially in those with cirrhosis with three to six monthly alpha fetoprotein and ultrasound.
wilsons disease
Wilson’s disease presents between the ages of three and 40 years. Acute hepatitis, acute liver failure and decompensated cirrhosis are all recognised with Wilson’s disease.
Neuropsychiatric features are common in adolescence and early adulthood with behavioural change, parkinsonism and cognitive impairment.
Kayser-Fleischer rings are seen in patients with neurological disease.
Primary sclerosing cholangitis
Primary sclerosing cholangitis is associated with inflammatory bowel disease. Patients often present with pruritus, intermittent jaundice and right upper quadrant pain. Features of cholangitis (fever, pain and jaundice) usually occur subsequent to instrumentation such as endoscopic retrograde cholangiopancreatography (ERCP). Examination reveals signs of chronic liver disease and signs of portal hypertension may be present.
GORD management
In endoscopically determined gastro-oesophageal reflux disease or oesophagitis full-dose proton pump inhibition for one month will typically result in healing in 76%, continuation for a further month increases this by a further 14%. In those failing to respond to two months of full dose therapy doubling the dose of proton pump inhibitor increases response rate.
In those failing to respond to a double dose of proton pump inhibition an H2 receptor antagonist may be added or substituted in treatment or a prokinetic agent added to treatment. Simply extending the duration of proton pump inhibitor therapy beyond two months without any additional change is not recommended.
Repeat gastroscopy is not recommended in the absence of new or emergent symptoms or where there is severe resistance to therapy.
It is also the latter group in whom referral for consideration of acid reflux reduction surgery might be considered.
GORD management
In endoscopically determined gastro-oesophageal reflux disease or oesophagitis full-dose proton pump inhibition for one month will typically result in healing in 76%, continuation for a further month increases this by a further 14%. In those failing to respond to two months of full dose therapy doubling the dose of proton pump inhibitor increases response rate.
In those failing to respond to a double dose of proton pump inhibition an H2 receptor antagonist may be added or substituted in treatment or a prokinetic agent added to treatment. Simply extending the duration of proton pump inhibitor therapy beyond two months without any additional change is not recommended.
Repeat gastroscopy is not recommended in the absence of new or emergent symptoms or where there is severe resistance to therapy.
It is also the latter group in whom referral for consideration of acid reflux reduction surgery might be considered.
iron deficiency investigations
The serum ferritin is the most powerful marker of iron deficiency in the absence of inflammation, should there be inflammation transferrin saturation should be used.
IBS investigations
Abdominal bloating, alternating diarrhoea and constipation, abdominal pain relieved by defecation and urgency are all classical features of irritable bowel syndrome. Adequate history must be taken to exclude red flag symptoms such as weight loss. Coeliac disease must be excluded as a possible alternative diagnosis.
NICE guidelines on the diagnosis and management of Irritable bowel syndrome (CG61) state that in the presence of a history classical for irritable bowel syndrome (and the absence of red flag symptoms such as weight loss) the following are sufficient to exclude other causes of bowel symptoms:
A normal full blood count
C-reactive protein
Erythrocyte sedimentation rate, and
Negative anti-tissue transglutaminase antibodies.
Risk factors for toxic megacolon in UC
management of ulcerative colitis identify the following as risk factors for the precipitation of toxic colonic dilatation:
Hypokalaemia Hypomagnesaemia Under-treatment Purgative bowel preparations for colonoscopy Non-steroidals Opioids Anti-cholinergics, and Anti-diarrhoeal agents.
gastric vs duodenal ulcer
Patients with gastric ulceration tend to suffer from anorexia and weight loss while those with a duodenal ulcer maintain or gain weight.
Although weight gain may be suggestive of duodenal ulceration the characteristic clinical feature which aids the diagnosis is abdominal pain which is relieved by eating. Endoscopy should be performed to confirm ulceration.
Risk factors for peptic ulceration include Helicobacter pylori (H. pylori) infection, non-steroidal anti-inflammatory drug (NSAID) use, cigarette smoking and genetic factors - Lewis blood group antigens facilitate H. pylori attachment to the mucosa.
medication that cause dyspepsia
The following drugs are recognised as causing dyspepsia:
Steroids Calcium channel blockers Theophyllines Nitrates Bisphosphonates, and Non-steroidal anti-inflammatory drugs. This is either due to irritation of the mucosa (for example, bisphosphonates, steroids) or relaxation of the lower oesophageal sphincter increasing reflux (for example, calcium channel blockers, nitrates).
SAAG
<11 exudate
>11 transudate
SAAG = Serum albumin − Ascites albumin
Transudative: Cirrhosis Alcoholic Hepatitis Cardiac Ascites "Mixed Ascites" Massive Liver Metastasis Fulminant Hepatic Failure Budd-Chiari Syndrome Portal Vein Thrombosis Veno-Occlusive Disease Myxedema Fatty Liver of Pregnancy Nephrotic syndrome
Exudative: Peritoneal Carcinomatosis Tuberculous Peritonitis Pancreatic Ascites Bowel Obstruction Biliary Ascites Nephrotic Syndrome Posteroperative Lymphatic Leak Serositis in Connective Tissue Disease
Mangement of hepatic encephalopathy
- Correction of hypoglycaemia - 10% dextrose can be used but 20-50% may be required if the hypoglycaemia is severe.
- A full septic screen is essential including an ascitic tap if appropriate - ideally before starting empirical antibiotic therapy. Patients may be critically ill and signs of sepsis may be absent. There is also a potential role for the use of antibiotics in reducing the concentration of ammoniagenic bacteria in the gut.
Rifaximin, a non-absorbable form of rifampicin, has been licensed for and is used in the treatment of hepatic encephalopathy.
- IV fluids. Ensure adequate plasma expansion. Good hydration is important in preventing renal failure.
- Bowel cleansing reduces ammonia-producing substrates from the gut.
- Patients should be commenced on lactulose 30-50 ml qds orally or via nasogastric tube.
PBC
This presentation is typical of primary biliary cirrhosis:
pruritus
lethargy
evidence of lipid derangement, and
obstructive pattern of liver function test abnormalities (alkaline phosphatase and gamma-GT raised in excess of transaminases).
Ursodeoxycholic acid is used in the management of primary biliary cirrhosis. It is safe and improves liver function tests, however its effect on disease progression and transplant-free survival is debated.
chelating agents
Iron chelation with desferrioxamine is sometimes required in haemochromatosis when venesection is not tolerated.
Doxycycline is very effective if given in the early stages of leptospirosis (Weil’s disease).
Penicillamine with pyridoxine causes urinary copper excretion in Wilson’s disease and zinc may be used for maintenance treatment.
glasgow score
A PTC would not be indicated in this setting unless there was cholangitis and failure of ERCP to decompress the biliary system.
Glasgow score for Pancreatitis:
PaO2 <7.29 kPa Glucose >10 mmol/L Age >55 years WBC >15 Calcium <2.0 mmol/L Urea >16 mmol/L LDH >600 IU/L Albumin <32 g/L The presence of three or more of these criteria within the first 48 hours is indicative of severe pancreatitis.
If the score ≥3, severe pancreatitis is likely Referral to the HDU/ICU is suggested in this case. If the score <3, severe pancreatitis is unlikely.
a score greater than three which is predictive of severe disease. In patients with gallstone pancreatitis when the disease is predicted to be severe ERCP and endoscopic stone extraction should be performed within 72 hours of the onset of pain.
Aortic -enteric fistual presentation
Aortic-enteric Fistula formation often occurs in the setting of infection of prosthetic material, such as endovascular repair and results in massive gastrointestinal haemorrhage.
Fistula formation often occurs in the setting of infection of prosthetic material (more frequently in open than endovascular repairs) and the pyrexia and raised inflammatory markers in this case may indicate this.
Presents with malena and haemodynamically unstable
Criteria for liver transplant in fulminant failure in non-paracetamol cases
Criteria for liver transplant in fulminant failure in non-paracetamol cases include INR greater than 6.7 or prothrombin time greater than 100 seconds, or any three of the following:
Aetiology that is not due to hepatitis A, hepatitis B or a drug reaction
Age less than 10 years or more than 40 years
Jaundice more than seven days before encephalopathy
INR greater than 4 or prothrombin time greater than 50 seconds, and
Bilirubin greater than 300 µmol/L.
Criteria for liver transplant in fulminant failure in cases of paracetamol overdose
Criteria for liver transplant in fulminant failure in cases of paracetamol overdose include arterial pH lower than 7.3 or all of the following:
Prothrombin time greater than 100 seconds
Creatinine greater than 300 µmol/L, and
Grade 3-4 encephalopathy.
Guidelines for referral to a liver unit following paracetamol overdose include
An arterial pH <7.3 INR >3 (or prothrombin time >50 seconds) Oliguria Creatinine >200 µmol/L, or Hypoglycaemia.
short bowel and renal stones
Hyperoxaluria occurs both in patients with an ileal resection and in patients with a short bowel who have had a distal small bowel resection (for example, Crohn’s disease, infracted bowel). It is caused by increased absorption of oxalate by the colon.
Bile salts in the colon increase oxalate absorption.
Hyperoxaluria is associated with renal stone formation and the propensity to form stones is reduced when citrate intake is increased.
Radio-opaque renal stones:
Calcium oxalate Calcium phosphate Triple phosphate (calcium, magnesium, ammonium Cysteine (semi-opaque). Radio-lucent renal stones:
Urate.
features of IBS
Clinical features supporting a diagnosis of irritable bowel syndrome (IBS) include:
A long history with a relapsing and remitting course
Exacerbations triggered by life events
Symptoms aggravated by eating, and
Coexistence of anxiety and depression.
Revised rome criteria
diffuse oesophageal spasm; the manometry findings
Manometry reveals prolonged, repetitive and high amplitude contractions. The lower oesophageal sphincter pressure is increased and there is incomplete relaxation of the sphincter.
Achalasia
Achalasia typically causes absence of peristalsis in the body of the oesophagus.
rockall score
Score 0 Score 1 Score 2 Score 3
Age <60 60-79 >80 -
Shock No shock Pulse >100 Systolic blood pressure <100 mmHg -
Co-morbidity Nil major CCF, IHD, major morbidity Renal or liver failure, metastatic cancer
Diagnosis Mallory-Weiss tear All other diagnoses GI malignancy -
Evidence of bleeding None - Blood, adherent clot, spurting vessel -
British Society of Gastroenterology (BSG) guidance on endoscopic surveillance of Barrett’s oesophagus
2013 British Society of Gastroenterology (BSG) guidance on endoscopic surveillance of Barrett’s oesophagus recommends that endoscopy should be performed every three to five years for patients with a <3 cm segment of Barrett’s without dysplasia. For longer segment Barrett’s (>3 cm) without dysplasia the recommended interval between endoscopies is shorter (two to three years).
Patients with low grade dysplasia should have high dose acid suppression and endoscopy six monthly until dysplastic change resolves (then as per no dysplasia) or high grade dysplasia is noted.
Patients with high grade dysplasia should be discussed in an MDT for consideration of more aggressive treatment endoscopically (for example, EMR) or even surgically.
main causes of dyspepsia
The main causes of dyspepsia are
Gastro-oesophageal reflux disease (GORD) (15 - 25%)
Gastric and duodenal ulcers (15 - 25%) and
Stomach cancer (2%).
The remaining 60% are classified as non-ulcer dyspepsia (NUD).
main causes of dyspepsia
The main causes of dyspepsia are
Gastro-oesophageal reflux disease (GORD) (15 - 25%)
Gastric and duodenal ulcers (15 - 25%) and
Stomach cancer (2%).
The remaining 60% are classified as non-ulcer dyspepsia (NUD).
GIST
CD117 (c-KIT) positivity implies a gastrointestinal stromal tumour (GIST) and therefore, staging investigations with a view to surgery should be performed. Ninety-five percent of GISTs stain positive for CD117 and the majority occur in the stomach.
CT and endoscopic ultrasound allow tumour staging to plan further management.
Rome III criteria describe functional GI diagnoses.
Pain must be randomly spaced and be in episodes of >30 minutes to fulfil Rome III criteria. There should be no relieving manoeuvre such as postural change or defecation.
The Rome III criteria for functional gall bladder pain are as follows:
episodes lasting 30 minutes or longer
recurrent symptoms occurring at different intervals (not daily)
the pain builds up to a steady level
the pain is moderate to severe enough to interrupt the patient’s daily activities or lead to an Emergency Department visit
the pain is not relieved by bowel movements
the pain is not relieved by postural change
the pain is not relieved by antacids, and
exclusion of other structural disease that would explain the symptoms.
The pain may present with one or more of the following supportive criteria:
associated with nausea and vomiting
radiates to the back and/or right infra subscapular region, and
awakens from sleep in the middle of the night.
Gorlin syndrome
causes gastric hamartomas, basal cell carcinomas, mandibular bone cysts, and intracranial calcification, as well as pits on the palms and soles.
Familial adenomatous polyposis (FAP
Familial adenomatous polyposis (FAP) is caused by a mutation in the APC gene and is associated with the formation of multiple adenomatous polyps in the colon. By the age of 35, around 95% of patients with FAP have polyps and, without colectomy, colon cancer is effectively inevitable. Extra-colonic manifestations are variable and include polyps of the gastric fundus and duodenum, osteomas, dental anomalies, and congenital hypertrophy of the retinal pigment epithelium (CHRPE).
Juvenile polyposis syndrome
Juvenile polyposis syndrome is characterised by a tendency to form hamartomatous polyps throughout the GI tract. Juvenile refers to a particular type of polyp rather than the age of the patients at the onset of polyp formation (though most have polyps by the age of 20). Inheritance is autosomal dominant. There is an increased risk of GI cancer mostly attributable to an excess of colon cancer. Estimates of lifetime risk of GI cancer are variable and range from 9-50%.
Peutz-Jehgers syndrome
Peutz-Jehgers syndrome is characterised by the association of hamartomatous GI polyps and mucocutaneous hyperpigmentation. PJS-type hamartomas are most frequently found in the small bowel but also occur in the stomach, colon, and nasal passages. Patients with PJS are increased risk of both stomach and colon cancers arising from adenomas in addition to other cancers such as pancreatic, breast, and ovarian malignancy.
Cowden’s syndrome
Cowden’s syndrome is one of the PTEN hamartoma tumour syndromes. There is widespread development of hamartomas with mucocutaneous lesions being pathognomonic. Criteria for making the diagnosis are complex. Breast and thyroid carcinomas are frequent (and major criteria for making the diagnosis) and formation of GI hamartomas is one of the minor diagnostic criteria.
medication that lowers pressure of oesophageal sphincter
Theophylline lowers the pressure of the lower oesophageal sphincter.
indication for TIPS
Intractable ascites is an indication for a transjugular intrahepatic portosystemic shunt.
acute dysphagia
Consider food impaction as a cause of acute dysphagia and vomiting with those with pre-existing stents and acute symptoms.
alarn symptoms
Epigastric mass Any sign of chronic gastrointestinal bleeding Progressive unintentional weight loss Dysphagia Persistent vomiting Iron deficiency anaemia, and suspicous barium meal
whipples disease
Whipple’s disease is caused by Tropheryma whippelei, a Gram positive bacterium. The typical presentation is of a wasting illness with arthralgia, arthritis, fever, and diarrhoea. Malabsorption is common. If the disease affects the small intestine, patients may also have steatorrhea.
Early symptoms include fever, malaise, and lymphadenopathy may precede the onset of GI symptoms by 1-10 years. The clinical manifestations of the disease are thought to be caused by infiltration of tissues by T. whippelei and the uptake of these organisms into tissue macrophages. The CNS and cardiovascular system may also be involved.
Many of the physical signs in Whipple’s disease are due to malabsorption:
Cachexia
Abdominal distention
Glossitis
Angular cheilitis
Chvostek’s or Trousseau’s signs (secondary to hypocalcaemia)
Gingivitis (secondary to vitamin C deficiency)
Night blindness (secondary to vitamin A deficiency).
There may be perioral and malar hyperpigmentation. Depending on the site of involvement patients with CNS disease may develop meningoencephalitis, ataxia and clonus (cerebellum) or loss of inhibition (frontal). Cardiac complications include pericarditis, myocarditis, and left-heart valve lesions. The patient may have finger clubbing.
Whipple’s disease is most common in white males aged 40-50 years and rarely is described in women (M:F ratio 9:1). There is an association with the HLA-B27 haplotype. The diagnosis is made by demonstrating the presence of T. whippelei DNA in tissue by PCR.
Treatment is with an initial two week course of parenteral penicillin and streptomycin; followed by a prolonged course (one year) of tetracycline. Untreated, patients have a poor prognosis.
management of dyspepsia after trial of PPI
NICE guidelines on the management of dyspepsia advise that patients over the age of 55 with persistent and unexplained dyspepsia of recent onset should be referred for urgent endoscopy as suspected cancer. Persistent is defined as beyond the time frame of a self-limiting illness, typically four to six weeks, unexplained would be considered to be a new episode in the absence of any known aggravating factors.
Haemochromatosis diagnostic investigations
Haemochromatosis is an autosomal recessive condition.
Two mutations of the HFE gene (C282Y and H63D) account for over 90% of cases in Europeans.
The disease is also associated with HLA-A3 and HLA-B14.
Ferritin
elevated level of iron and transferrin saturation
treatment of IBS
- dietary, laxative, anti-motility e.g.loperamide, buscopan
- Although not licensed in the UK, tricyclic antidepressants are a recognised second line agent in irritable bowel syndrome.
Hpylori investigations
if a rapid urease (for example, CLO) test is negative this does not exclude Helicobacter pylori infection. Although rapid urease testing has a sensitivity of 93-97% the false negative rate increases significantly in the context of recent gastrointestinal haemorrhage, acid suppression therapy and recent antibiotic treatment. Serological markers would indicate the likelihood of Helicobacter pylori infection and are unaffected by the factors mentioned above.
types of choledocal cysts
Choledochal cysts are usually diagnosed in the neonatal period but a few are delayed until adulthood. The Todani classification is used to define these:
Type 1 - a fusiform dilation of the common hepatic duct (CHD)
Type 2 - a diverticulum of the CHD
Type 3 - a choledochcele
Type 4 - describes extension into the intrahepatic ducts
Type 5 - intrahepatic cystic disease only.
Type 1 is the most common and Type 4 the second most common.
Resection and reconstruction is advised to prevent recurrent cholangitis, pancreatitis, and malignant change.
types of DILI
Dose-depent: eg. paracetamol
Dose-independent (usually immune mediated): - eosinophilis and rash
Types of heptatic involvement:
1) hepatitis (rasied ALT) - paracetamol, aspirin; does-independent: NSADIS, isoniazid
2) Cholestatic (rasied ALP and bili) - rifampicin, oestrogen, anabolic steroids; dose-independent - NSAIDS, chlorpromazine, co-amox, clari, fluclox, carbimazole
3) microsteatosis - aspirin, valrpoate, tetracyclines
4) macrosteatosis - amiodraone, methotrexate
antibodies/liver screen
PBC: IgM and AMA
PSC (associated with UC): pANCA, ANA
AIH: type 1 - ASMA, ANA, adults type 2: children progress to cirrhosis, LKM1 type 3: SLA, adults
Haemochromatosis: high ferrtin, high transferrin sats, high iron, low TIBC
Wilsons: low copper, low caeroplasmina
HCC: AFP
HBV: HbsAg, HbeAg, HbcAg, and antiboides, viral load
HBC: core antigen and viral load, IgM, IgG
a1 anti trypsin
unconjugated bili - gilberts and criglar nijjar
conjugated - dubin-johnson and rotar syndrome
