Gastro 3 Flashcards
Who is FIT screen offered to?
the NHS now has a national screening programme offering screening every 2 years to all men and women aged 60 to 74 years in England, 50 to 74 years in Scotland. Patients aged over 74 years may request screening
a type of faecal occult blood (FOB) test which uses antibodies that specifically recognise human haemoglobin (Hb)
Outcomes of colonoscopy following FIT screening?
5 out of 10 patients will have a normal exam
4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
1 out of 10 patients will be found to have cancer
Clincial features of acute upper GI bleeeding?
Haematemesis
coffee gorund vomit
Melena
raised urea
features associated with a particular diagnosis e,g,
oesophageal varices: stigmata of chronic liver disease
peptic ulcer disease: abdominal pain
Oesophageal causes for UGIB?
Gastric causes of upper GI Bleed?
Duodenal causes of upper GI bleed?
Risk assessment in UGIB?
the Glasgow-Blatchford score at first assessment
helps clinicians decide whether patients can be managed as outpatients or not
the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality
includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage
Management of upper GI bleed?
Reusciation - A-E
IV access
Endoscopy -if svere bleed immediately after resusitation, all other patients within 24 hours
Management of non-variceal bleeding
NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected variceal upper gastrointestinal bleeding although 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
Management of variceal bleeding
terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
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 prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal
prothrombin complex concentrate to patients who are taking warfarin and actively bleeding
management of Upper GI bleed when endoscoic magement has failed?
Refer to surgeons
causes of threadworms?
Enterobius vermicularis,
Symptoms of thread worms?
perianal itching, particularly at night
girls may have vulval symptoms
Management of threadworms?
CKS recommend a combination of anthelmintic with hygiene measures for all members of the household
mebendazole is used first-line for children > 6 months old. A single dose is given unless infestation persists
causes of dysphagia?
Drug indiced liver disease
causes of hepatocellular picture?
paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin
Drug indiced liver disease
causes of cholestasis picture?
combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine
causes of drug induced liver cirrhosis?
methotrexate
methyldopa
amiodarone
what is microscopic colitis?
Microscopic colitis is a chronic inflammatory condition of the gut. It is approximately as common as the ‘classic’ inflammatory bowel diseases (ulcerative colitis and Crohn’s disease) and is considered a separate entity.
causes of microscopic colitis?
smoking
drugs: NSAIDs, PPIs and SSRIs
what are the two types of microscopic colitis?
Collagenous colitis (CC)
Lymphocytic colitis (LC)
For both types of MC, there is an increased number of intraepithelial and lamina propria lymphocytes seen on microscopy. In CC specifically, there is a thickened subepithelial collagen band.
Features of microscopic colitis?
Diarrhoea (watery, non-bloody)
Abdominal pain
Faecal urgency and incontinence
Bloating and flatulence
weight loss
noctural diarrhoea
Extraintestinal manifestations of microscopic collitis?
Joint pain: Arthralgia or arthritis may occur in patients with microscopic colitis, particularly in those with underlying autoimmune disorders.
Dermatological manifestations: Skin conditions such as erythema nodosum and pyoderma gangrenosum have been reported in association with microscopic colitis.
Autoimmune diseases: There is an increased prevalence of concomitant autoimmune disorders including celiac disease, thyroid dysfunction, rheumatoid arthritis, and type 1 diabetes mellitus among patients with microscopic colitis.
Investigations for microscopic colitis?
Guidelines written by the British Society for Gastroenterology advise that when microscopic colitis is suspected, patients should be referred for colonoscopy even before assessing faecal calprotectin levels.
Microscopic colitis can only be diagnosed by histology examination of biopsied tissue taken during colonoscopy. Macroscopic changes are not usually seen unlike in other types of IBD. The characteristic microscopic findings are:
Lymphocytic colitis: increased number of intraepithelial and lamina propria lymphocytes (>20 per 100 cells)
Collagenous colitis: as above, along with a thickened collagenous band in the subepithelial layer (>10µm)
Management of microscopic colitis?
Lifestyle factors that can exacerbate MC should first be addressed. These include:
Stopping smoking, Stopping medications such as NSAIDs, PPIs and SSRIs where possible
Decreasing caffeine intake, Decreasing dairy intake (in patients with lactose intolerance)
Decreasing alcohol consumption
if lifestyle fails
mid cases - trial of loperamide
Budenoside - shown to be effective in the induction and maintenance of remission. A typical dosage is 9mg daily for 8 weeks and the medication then stopped to assess response. If symptoms recur, then re-initiation of budesonide may be necessary.
In patients who do not respond to budesonide, other medications that may be tried include immunomodulators (e.g. azathioprine) and biologics (e.g. anti-TNF-alpha drugs).
mechanism of action of PPI?
Proton pump inhibitors (PPI) cause irreversible blockade of H+/K+ ATPase of the gastric parietal cell.
adverse effects of PPI?
hyponatraemia, hypomagnasaemia
osteoporosis → increased risk of fractures
microscopic colitis
increased risk of C. difficile infections
What is intrahepatic cholestasis of pregnancy?
A liver disease occurring in around 1% of pregnancies, typically in the third trimester.
What are the common features of intrahepatic cholestasis of pregnancy?
- Pruritus, often in the palms and soles
- No rash (skin changes may be present due to scratching)
- Raised bilirubin
What is the primary management for intrahepatic cholestasis of pregnancy?
- Ursodeoxycholic acid for symptomatic relief
- Weekly liver function tests
- Induction at 37 weeks
What is a significant complication of intrahepatic cholestasis of pregnancy?
Increased rate of stillbirth.
Is intrahepatic cholestasis of pregnancy associated with increased maternal morbidity?
No, it is not generally associated with increased maternal morbidity.
What is acute fatty liver of pregnancy?
A rare complication that may occur in the third trimester or immediately after delivery.
What are the features of acute fatty liver of pregnancy?
- Abdominal pain
- Nausea & vomiting
- Headache
- Jaundice
- Hypoglycaemia
- Severe disease may result in pre-eclampsia
What laboratory finding is typically elevated in acute fatty liver of pregnancy?
ALT is typically elevated, e.g., 500 u/l.
What is the management approach for acute fatty liver of pregnancy?
Support care and delivery once stabilized.
What syndromes may be exacerbated during pregnancy?
Gilbert’s and Dubin-Johnson syndrome.
What does HELLP stand for?
Haemolysis, Elevated Liver enzymes, Low Platelets.
What is Whipple’s disease?
Whipple’s disease is a rare multi-system disorder caused by Tropheryma whippelii infection. It is more common in those who are HLA-B27 positive and in middle-aged men.
Features of Whipple’s disease?
malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus
Inestigations for Whipples disease?
jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules
Managment of Whipple’s disease?
guidelines vary: oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin
What is Peutz Jeghers syndrome?
Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don’t have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.
genetics in Peutz jeghers syndrome?
autosomal dominant
responsible gene encodes serine threonine kinase LKB1 or STK11
Features of Peutz Jeghers syndrome?
hamartomatous polyps in the gastronintestinal tract (mainly small bowel)
small bowel obstruction is a common presenting complaint, often due to intussusception
gastrointestinal bleeding
pigmented lesions on lips, oral mucosa, face, palms and soles
what is Pseudomembranous colitis?
This condition is characterised by the presence of multiple white plaques or pseudomembranes on the gastrointestinal mucosa, typically as a result of overgrowth of the bacterium Clostridium difficile following antibiotic use.
what are the two types of oesophageal cancer?
The majority of adenocarcinomas are located near the gastroesophageal junction whereas squamous cell tumours are most commonly found in the upper two-thirds of the oesophagus.
Features of oesophageal cancer?
dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough
How is oesophageal cancer diagnosed?
Upper GI endoscopy with biopsy is used for diagnosis
Endoscopic ultrasound is the preferred method for locoregional staging
CT scanning of the chest, abdomen and pelvis is used for initial staging
FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans.
Laparoscopy is sometimes performed to detect occult peritoneal disease
why does TIPs procedure lead to increased risk of hepatic encephalopethy?
The hepatic vein is cannulated percutaneously via the internal jugular vein, using a needle under radiological guidance. A connection is created and a stent is inserted through the liver from the hepatic to the portal vein, thereby reducing portal pressure and reducing the risk of a bleed. Encephalopathy is found in up to 25% of cases as blood normally detoxified in the liver, now bypasses this stage and toxins are delivered in greater quantity to the cerebral circulation.
Features of NAFLD?
usually asymptomatic
hepatomegaly
ALT is typically greater than AST
increased echogenicity on ultrasound
Pathophysiology - H.pylori?
Helicobacter pylori has 2 main mechanisms to survice in the acidic gastric environment:
chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells underneath
secretes urease → urea converted to NH3 → alkalinization of acidic environment → increased bacterial survival
pathogenesis mechanism:
Helicobacter pylori releases bacterial cytotoxins (e.g. CagA toxin) → disruption of gastric mucosa
what is assoicated with H.pylori?
peptic ulcer disease
95% of duodenal ulcers
75% of gastric ulcers
gastric cancer
B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
atrophic gastritis
The role of H pylori in Gastro-oesophageal reflux disease (GORD) is unclear - there is currently no role in GORD for the eradication of H pylori
Managament of H.pyloir?
eradication may be achieved with a 7-day course of
a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
Primary biliary cholangitis - the M rule
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
Serology testing in coeliac?
tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE
endomyseal antibody (IgA)
needed to look for selective IgA deficiency, which would give a false negative coeliac result
anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE
anti-casein antibodies are also found in some patients
Biopsy findings in coeliac?
the ‘gold standard’ for diagnosis - this should be performed in all patients with suspected coeliac disease to confirm or exclude the diagnosis
traditionally done in the duodenum but jejunal biopsies are also sometimes performed
findings supportive of coeliac disease:
villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes
side effects of sulphasalazine?
many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis
other side-effects are common to 5-ASA drugs (see mesalazine)
side effects of mesealazine?
ulphapyridine side-effects seen in patients taking sulphasalazine are avoided
mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis
*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
most common causes of HCC?
Hepatocellular carcinoma
hepatitis B most common cause worldwide
hepatitis C most common cause in Europe
Management of pyogenic liver abscess?
drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin
What is the most appropriate test for post eradication therapy for hypyloria?
the only recommended test for H. pylori post-eradication therapy, is urea breath test. The others are either too invasive, remain positive, or are not sensitive and specific enough.
Indicators of severe pancreatitis?
age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST
what is plummer vinson syndrome?
Triad of:
dysphagia (secondary to oesophageal webs)
glossitis
iron-deficiency anaemia
Treatment includes iron supplementation and dilation of the webs
What are the causes of increased ferritin?
We can split the causes of increased ferritin levels into 2 distinct categories
The best test to see whether iron overload is present is transferrin saturation. Typically, normal values of < 45% in females and < 50% in males exclude iron overload.
Management of IBS?
First-line pharmacological treatment - according to predominant symptom
pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line
Second-line pharmacological treatment
low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg) are used in preference to selective serotonin reuptake inhibitors
psychological interventions - if symptoms do not respond to pharmacological treatments after 12 months and who develop a continuing symptom profile (refractory IBS), consider referring for cognitive behavioural therapy, hypnotherapy or psychological therapy
Dietary advice in IBS?
have regular meals and take time to eat
avoid missing meals or leaving long gaps between eating
drink at least 8 cups of fluid per day, especially water or other non-caffeinated drinks such as herbal teas
restrict tea and coffee to 3 cups per day
reduce intake of alcohol and fizzy drinks
consider limiting intake of high-fibre food (for example, wholemeal or high-fibre flour and breads, cereals high in bran, and whole grains such as brown rice)
reduce intake of ‘resistant starch’ often found in processed foods
limit fresh fruit to 3 portions per day
for diarrhoea, avoid sorbitol
for wind and bloating consider increasing intake of oats (for example, oat-based breakfast cereal or porridge) and linseeds (up to one tablespoon per day).
Associations of pancreatic cancer?
increasing age
smoking
diabetes
chronic pancreatitis (alcohol does not appear an independent risk factor though)
hereditary non-polyposis colorectal carcinoma
multiple endocrine neoplasia
BRCA2 gene
KRAS gene mutation
Features of pancreatic cancer?
classically painless jaundice
pale stools, dark urine, and pruritus
cholestatic liver function tests
the following abdominal masses may be found (in decreasing order of frequency)
hepatomegaly: due to metastases
gallbladder: Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
epigastric mass: from the primary tumour
many patients present in a non-specific way with anorexia, weight loss, epigastric pain
loss of exocrine function (e.g. steatorrhoea)
loss of endocrine function (e.g. diabetes mellitus)
atypical back pain is often seen
migratory thrombophlebitis (Trousseau sign) is more common than with other cancers
Investigations for pancreatic cancer?
ultrasound has a sensitivity of around 60-90%
high-resolution CT scanning is the investigation of choice if the diagnosis is suspected
imaging may demonstrate the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
Management for pancreatic cancer?
less than 20% are suitable for surgery at diagnosis
a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas. Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
adjuvant chemotherapy is usually given following surgery
ERCP with stenting is often used for palliation
what test can be used to check for H.pylor eradication?
Urea breath test
What is Achalasia?
Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated. Achalasia typically presents in middle-age and is equally common in men and women.
Clinical features of Achalsia?
dysphagia of BOTH liquids and solids
typically variation in severity of symptoms
heartburn
regurgitation of food
may lead to cough, aspiration pneumonia etc
malignant change in small number of patients
Investigations for Achalasia?
oesophageal manometry
excessive LOS tone which doesn’t relax on swallowing
considered the most important diagnostic test
barium swallow
shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance
chest x-ray
wide mediastinum
fluid level
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Treatment for achalaisa?
pneumatic (balloon) dilation is increasingly the preferred first-line option
less invasive and quicker recovery time than surgery
patients should be a low surgical risk as surgery may be required if complications occur
surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk
drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects
Investigations for pancreatitis?
Serum amylase
Serum lipase (more sensitive and specific)
USS
Contast CT
what is Purtscher retinopathy?
Rare features associated with pancreatitis:
ischaemic (Purtscher) retinopathy - may cause temporary or permanent blindness
Pathophysiology of pancreatitis?
autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis
What is Cholestyramine?
When is it used?
Cholestyramine is a bile acid sequestrant used in the management of hyperlipidaemia. It decreases bile acid reabsorption in the small intestine, therefore upregulating the amount of cholesterol that is converted to bile acid. The main effect it has on the lipid profile is to reduce LDL cholesterol. It is also occasionally used in Crohn’s disease for treatment diarrhoea following bowel resection.
Adverse effects of Cholestyramine?
Adverse effects
abdominal cramps and constipation
decreases absorption of fat-soluble vitamins
cholesterol gallstones
may raise level of triglycerides
Common features of bowel ischaemia?
abdominal pain - in acute mesenteric ischaemia this is often of sudden onset, severe and out-of-keeping with physical exam findings
rectal bleeding
diarrhoea
fever
bloods typically show an elevated white blood cell count associated with a lactic acidosis
Common predisposing features to bowel ischaemia?
increasing age
atrial fibrillation - particularly for mesenteric ischaemia
other causes of emboli: endocarditis, malignancy
cardiovascular disease risk factors: smoking, hypertension, diabetes
cocaine: ischaemic colitis is sometimes seen in young patients following cocaine use
Features of chronic pancreatitis?
epigastric pain
radiates to the back
typically worse 15 to 30 minutes following a meal
may be relieved by sitting forward
steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
diabetes mellitus develops in the majority of patients. It typically occurs more than 20 years after symptom begin
What is MALT Lymphoma?
Overview
associated with H. pylori infection in 95% of cases
good prognosis
if low grade then 80% respond to H. pylori eradication
Features
paraproteinaemia may be present
causes of hepatosplenomegaly?
Causes of hepatosplenomegaly
chronic liver disease - with portal hypertension
infections: glandular fever, malaria, hepatitis
lymphoproliferative disorders
myeloproliferative disorders e.g. CML
amyloidosis
Indications for OGD in GORD?
Indications for upper GI endoscopy:
age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss
If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)
what is haemochromatosis?
Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6*. It is often asymptomatic in early disease and initial symptoms often non-specific e.g. lethargy and arthralgia
Presenting features in haemochromastosis?
early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
‘bronze’ skin pigmentation
diabetes mellitus
liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
cardiac failure (2nd to dilated cardiomyopathy)
hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
arthritis (especially of the hands)
Inital presenting symptoms for UC?
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
extra-intestinal features - arthritis, erythema nodosum, episcleritis, pyoderma gangrenosum, clubbing, primary sclerosing cholangitis
What does endoscopy show in UC?
red, raw mucosa, bleeds easily
no inflammation beyond submucosa (unless fulminant disease)
widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
inflammatory cell infiltrate in lamina propria
neutrophils migrate through the walls of glands to form crypt abscesses
depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent
What would a barium enema show in UC?
loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’
what is the method ofaction of Terlipressin?
Terlipressin - method of action = constriction of the splanchnic vessels
metabolic consequences of refeeding syndrome?
- hypophosphataemia (this is the hallmark of refeeding syndrome - may result in heart failure and respiratory failure)
- hypokalaemia
-hypomagnesaemia
pathophysiology of refeeding syndrome?
Shift from Fat to Carbohydrate Metabolism: In refeeding syndrome, the reintroduction of carbohydrates leads to a shift from fat to carbohydrate metabolism. This switch activates insulin secretion, which in turn increases cellular uptake of glucose.
Intracellular Movement of Phosphate: Insulin and increased glucose uptake stimulate the intracellular movement of phosphate, which is used in the synthesis of ATP and 2,3-diphosphoglycerate in erythrocytes. This intracellular shift reduces serum phosphate levels.
Decreased Phosphate Stores: Patients with chronic malnutrition often have depleted phosphate stores, although their serum phosphate levels may initially be normal. When refeeding starts, the sudden demand for phosphate in anabolic processes exceeds the supply, leading to hypophosphatemia.
what are the clinical consequences of hypophosphataemia?
- cardiac dysfunction 0 can impair myocardial contractility
- resp failure (Phosphate is essential for ATP production, necessary for respiratory muscle function)
- Neurological complications - confusion/seizure.coma - attributable to disturbed ATP metabolism in the central nervous system
- haematological effects - Reduced 2,3-diphosphoglycerate levels in erythrocytes affect oxygen release from haemoglobin, leading to tissue hypoxia. Hypophosphatemia can also result in hemolysis.
- rhabdo - Phosphate depletion impairs ATP production in muscles, which can lead to muscle breakdown and rhabdomyolysis.
How to identify patients at risk of 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
hereditary non-polyposis colorectal cancer (HNPCC) due to a defect in the MSH2 gene. What is the function of this gene??
The MSH2 gene is involved in the process of DNA mismatch repair, which is essential for maintaining genomic stability.
What drug can be given to prevent c.diff recurrence?
Bezlotoxumab
This is a drug that acts as a monoclonal antibody which targets Clostridium difficile toxin B. It is listed as an option in the BNF as an option for prevention of the recurrence of Clostridium difficile in those at high risk of recurrence but has not yet received NICE approval.
What is the first marker of hep B infection?
surface antigen (HBsAg) is the first marker to appear and causes the production of anti-HBs
What does HBsAg suggest?
HBsAg normally implies acute disease (present for 1-6 months)
if HBsAg is present for > 6 months then this implies chronic disease (i.e. Infective)
What does Anti-HBs imply?
Anti-HBs implies immunity (either exposure or immunisation). It is negative in chronic disease
What does Anti-HBc imply?
Anti-HBc implies previous (or current) infection. IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months. IgG anti-HBc persists
What does HBeAg imply?
HbeAg results from breakdown of core antigen from infected liver cells as is, therefore, a marker of infectivity. Marker of HBV replication and infectivity
What would be seen in hep B immunisation?
Previous Hep be infection, not a carrier?
Previous Hep b infection now a carrier?
previous immunisation: anti-HBs positive, all others negative
previous hepatitis B (> 6 months ago), not a carrier: anti-HBc positive, HBsAg negative
previous hepatitis B, now a carrier: anti-HBc positive, HBsAg positive
HBsAg = ongoing infection, either acute or chronic if present > 6 months
anti-HBc = caught, i.e. negative if immunized
what are the brush border enzymes?
maltase: cleaves disaccharide maltose to glucose + glucose
sucrase: cleaves sucrose to fructose and glucose
lactase: cleaves disaccharide lactose to glucose + galactose
What disease is most strongly associated with primary biliary colangitis?
Sjogren’s syndrome (seen in up to 80% of patients)
What is Dubin-Johnson syndrome?
Dubin-Johnson syndrome is a benign autosomal recessive disorder resulting in hyperbilirubinaemia (conjugated, therefore present in urine). It is due to a defect in the canillicular multispecific organic anion transporter (cMOAT) protein. This causes defective hepatic bilirubin excretion
Dubin-Johnson syndrome results in a conjugated hyperbilirubinaemia
VIPoma
Where does it arise from?
symptoms?
VIP (vasoactive intestinal peptide)
source: small intestine, pancreas
stimulation: neural
actions: stimulates secretion by pancreas and intestines, inhibits acid and pepsinogen secretion
VIPoma
90% arise from pancreas
large volume diarrhoea
weight loss
dehydration
hypokalaemia, hypochlorhydia
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