Gastro Flashcards
Management of alcoholic hepatitis?
Prednisolone
What is the management of Clostridium difficile?
Gram positive rod
1. Oral metronidazole
2. Oral vancomycin
3. Fidaxomicin if not responding (useful for recurrence)
Life threatening: Oral vancomycinc and IV metronidazole
‘For severe infection in patients with multiple co-morbidities who are receiving treatment with other antibacterials, or for second or subsequent episode of infection, fidaxomicin can replace vancomycin’
What can cause a raised faecal calprotectin?
IBD Bowel malignancy Coeliac disease Infectious colitis NSAIDs
Systemic sclerosis
What is the LES pressure?
As well as oesophageal dysmotility the lower oesophageal sphincter (LES) pressure is decreased.
Pathophysiology of Achalasia?
Failure of oesophageal peristalsis and of failure to relax lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus
What is paracentesis induced circulatory dysfunction?
Occurs in large volume paracentesis (>5 L)
Associated high rate of ascites recurrence, hepatorenal syndrome, dilutional hyponatraemia, mortality
How is colorectal cancer screened in UK?
Faecal Immunochemical Test (FIT)
Every 2 years age 60-74
Age 74+ can request
If abnormal result, offered colonoscopy
Complications and prognosis of eosinophilic oesophagitis?
Complications:
Strictures, impaction, mallory-weiss tears
Prognosis:
Chronic condition
How is paracentesis induced circulatory dysfunction diagnosed in lab tests?
PICD is definitively diagnosed through laboratory results, with increases of more than 50% of baseline plasma rennin activity to > 4 ng/mL/h on the days 5-6 following paracentesis
What should you do for decompensated liver disease?
Investigate and exclude causes of decompensation
Enhance nitrate clearance with phosphate enemas aiming for minimum three loose stools per day and lactulose to enhance binding of nitrate in the intestine.
What are the three pictures of drug induced liver disease and can you name some causes?
hepatocellular, cholestatic or mixed
The following drugs tend to cause a hepatocellular picture: paracetamol sodium valproate, phenytoin MAOIs halothane anti-tuberculosis: isoniazid, rifampicin, pyrazinamide statins alcohol amiodarone methyldopa nitrofurantoin
The following drugs tend to cause cholestasis (+/- hepatitis):
combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine
Diagnosis of Colorectal cancer?
- Colonoscopy
2 Double contrast barium enema - CT colongraphy
Staging:
CTTAP
Pelvic - MRI scan
CEA used for follow up (correlate roughly with disease burden)
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
Management of diffuse oesophageal spasm?
calcium channel blockers are optimal for those presenting primarily with chest pain
dysphagia resistant to pharmacological therapies require more invasive or surgical treatments
Test for malabsorption?
D-xylose test.
Xylose is a sugar that does not require enzymes to be digested. Patient’s drink a set volume of D-xylose, and then levels of D-xylose are measured in the blood and urine. If no D-xylose is present that the small bowel is not absorbing properly, and it is not a problem of enzymatic function.
Investigation for small bowel bacterial overgrowth?
- Hydrogen breath test
- Small bowel aspiration and culture (gold standard)
- -> more than 100,000 bacteria per ml
Management of alcoholic hepatitis?
Prednisolone
AST: ALT >2:1
MDS >32 associated with 50% mortality
Pentoxifylline reduce mortality in hepatorenal syndrome
How do you investigate eosinophilic oesophagitis?
Endoscopy and biopsy
PPI Trial - persistence of oesinophilia and no improvement of symptoms
Investigation of Achalasia?
- Manometry: excessive LOS tone which doesn’t relax
- Barium Swallow - birds beak and fluid level, expanded oesophagus
- CXR - wide mediastinum
How should you investigate dysphagia?
- UGI endoscopy
- Fluoroscopy (if motility)
- FBC
- Ambulatory oesophageal pH and manometry if achalasia/GORD awaiting surgery
Colorectal Cancer Screening with IBD.
Low Risk:
Extensive colitis with no inflammation
OR left sided colitis
OR Crohn’s colitis <50% colon
Screen every 5 years
How is ascites grouped into categories?
serum-ascites albumin gradient (SAAG) <11 g/L or a gradient >11g/L
What is paracentesis induced circulatory dysfunction?
Occurs in large volume paracentesis (>5 L)
Associated high rate of ascites recurrence, hepatorenal syndrome, dilutional hyponatraemia, mortality
increases of more than 50% of baseline plasma rennin activity to > 4 ng/mL/h on the days 5-6 following paracentesis
SAAG <11g/L
Peritoneal carcinomatosis Tuberculous peritonitis Pancreatic ascites Bowel obstruction Biliary ascites Postoperative lymphatic leak Serositis in connective tissue diseases
Acute Pancreatitis causes?
Popular mnemonic is GET SMASHED
Gallstones
Ethanol
Trauma
Steroids
Mumps (other viruses include Coxsackie B)
Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
Scorpion venom
Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)
Treatment of Achalasia?
- Nifedipine or nitrates
- Intra-sphincteric injection of botulinum toxin
- Heller cardiomyotomy
- Pneumoatic balloon dilation
What is the presentaiton of eosinophilic oesophagitis?
Dysphagia, strictures, fibrosis, food impaction, regurgitation, anorexia, weight loss
Management for small bowel bacterial overgrowth?
- Rifaximin
Also effective results with co-amoxiclav or metronidazole
What is dumping syndrome?
Early and Late
early: food of high osmotic potential moves into small intestine causing fluid shift
late (rebound hypoglycaemia): surge of insulin following food of high glucose value in small intestine - 2-3 hours later the insulin ‘overshoots’ causing hypoglycaemia
Symptoms of Carcinoid Tumours?
Flushing Diarrhoea Bronchospasm Hypotension Right Heart Valvular stenosis
Is Azathioprine safe in Pregnancy if on it for Crohn’s Disease?
Yes, better than relapse of Crohn’s disease
Management of Acute UGI bleed?
Resuscitation:
- RBC if < 70
- Platelets if <50
- FFP if Fibrinogen < 1 or PT/APPT > 1.5x normal
- Prothrombin complex if warfarin and active bleeding
Endoscopy:
- Immediately if severe bleed
- Within 24 hours otherwise
Non-Variceal Bleeds:
- No PPI before endoscopy
- Further bleed after endoscopy - repeat endoscopy/IR/surgery
Variceal Bleeds:
- Terlipressin and prophlactic antibiotics before
- Band ligation > sclerotherapy
- Transjugular intrahepatic portosystemic shunts (TIPS) if not controlled
What is management for maintaining remission in Crohn’s Disease?
- Stop smoking
- Azathioprine/Mercaptopurine
If macroscopic resection, 3/12 azathioprine and metronidazole
SAAG > 11g/L
Indicates portal hypertension
Cirrhosis Alcoholic hepatitis Cardiac ascites Mixed ascites Massive liver metastases Fulminant hepatic failure Budd-Chiari syndrome Portal vein thrombosis Veno-occlusive disease Myxoedema Fatty liver of pregnancy
Symptoms of Carcinoid Tumours?
Flushing Diarrhoea Bronchospasm Hypotension Right Heart Valvular stenosis (or triscupid regurg) - endocardial plaques of fibrous tissue
Complications of gastrectomy?
Dumping syndrome (early and late) Weight loss, early satiety
Iron-deficiency anaemia
Osteoporosis/osteomalacia
Vitamin B12 deficiency
Other complications
increased risk of gallstones
increased risk of gastric cancer
What is the test for Bile Acid Malabsorption?
SeHCAT
Scan at 7 days apart
SeHCAT is bile acid analogue which can be detected by a nuclear medicine scan. The SeHCAT test involves a baseline scan, and then a 7 day scan. A 7-day SeHCAT retention value of less than 15% is generally considered indicative of bile salt malabsorption
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
What is alkaptonuria?
rare autosomal recessive disorder of phenylalanine and tyrosine metabolism caused by a lack of the enzyme homogentisic dioxygenase (HGD) which results in a build-up of toxic homogentisic acid. The kidneys filter the homogentisic acid (hence black urine) but eventually it accumulates in cartilage and other tissues.
Alkaptonuria is generally a benign and often asymptomatic condition. Possible features include:
pigmented sclera
urine turns black if left exposed to the air
intervertebral disc calcification may result in back pain
renal stones
Treatment
high-dose vitamin C
dietary restriction of phenylalanine and tyrosine
Autoimmune Hepatitis Markers
Type 2
LKM1 (anti-liver/kidney microsomal type 1 antibodies)
Affects children only
What is eosinophilic oesophagitis?
Allergic inflammation of the oesophagus. Likely an allergic reaction to ingested food
Autoimmune Hepatitis features and risk factors:
- chronic liver disease
- acute hepatitis: fever, jaundice etc (only 25% present in this way)
- amenorrhoea (common)
- ANA/SMA/LKM1 antibodies, raised IgG levels
- liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
Risk Factors:
- autoimmune history
Hypergammaglobulinaemia
- HLA B8, DR3
Management of eosinophilic oesophagitis?
Dietary modification
- Elemental diet
- Exclusion of six food groups
- Targeted elimination
Combine with topical steroids (fluticasone/budesonide) if dietary modification fails
Oesophageal dilation
Colorectal Cancer Screening with IBD.
Moderate Risk:
Extensive colitis with inflammation (mild)
OR post-inflammatory polyps
OR family history of colorectal cancer first degree >50 years
Screen every 3 years
Dubin-Johnson syndrome - tell me about it
Benign
Autosomal recessive
Hyperbilirubinaemia (conjugated, present in urine)
What is management for inducing remission in Ulcerative Colitis?
- Topical (rectal) aminosalicylate
- Add oral aminosalicylate if >4 weeks and no effect
- If no remission, add oral steroid
N.B. there is some variation between proctitis, proctosigmoiditis and extensive disease
Severe
IV steroids or IV ciclosporin if contraindicated
If no improvement in 72 hours, add IV ciclosporin or surgery
Tell me about HNPCC
Autosomal dominant
Proximal colon or endometrial cancer
Amsterdam criteria help in diagnosis
What is management for inducing remission in Crohn’s Disease?
- Steroids (budesonide if need low S/E profile)
- 5-ASA (unless severe)
- Azathioprine/Mercaptopurine (if 2+ exacerbation in 12 months)
- Infliximab or Adalimumab (refractory or fistulating disease)
N.B. Metronidazole for isolated peri-anal disease
Autoimmune Hepatitis Markers
Type 1
ANA
SMA (anti-smooth)
Affects adults and children
Management of Ascites?
- Reduce dietary sodium
- If Na <125, fluid restrict
- Spironolactone +/- Loop diuretic
- Drainage if tense. If large volume, give albumin cover
- Prophylactic antibiotics (Ciprofloxacin or norfloxacin if protein <15g and cirrhosis)
- Consider TIPS
Colorectal Cancer Screening with IBD.
High Risk:
Extensive colitis with inflammation (severe)
OR stricture in past 5 years
OR dysplasia in past 5 years declining surgery
OR PSC/transplant for this
OR family history cancer in first degree relative <50 years
Screen every 1 year
Acute Upper GI Bleed. Which scoring system and for when?
Blatchford - first assessment
Rockall score - after endoscopy
What is management for maintaining remission in Ulcerative Colitis?
- Topical aminosalicylate
- Oral and topical aminosalicylate
- Oral aminosalicylate
(Any one of the above)
If severe exacerbation or 2+ in one year:
1. Azathioprine or Mercaptopurine
When is capsule endoscopy used?
The SIGN guidelines for occult bleeding recommend OGD and colonoscopy. If they are both normal they recommend either repeat OGD or capsule endoscopy. If the capsule is negative then either a second capsule or enteroscopy is indicated.
What is the triad in Budd-Chiari Syndrome?
Abdominal pain (sudden onset, severe)
Ascites
Tender hepatomegaly
Management of eosinophilic oesophagitis?
Dietary modification
- Elemental diet
- Exclusion of six food groups
- Targeted elimination
Combine with topical steroids (fluticasone/budesonide) if dietary modification fails
Oesophageal dilation
Radiological evidence of diffuse oesophageal spasm?
barium swallow demonstrates a ‘corkscrew appearance’
Tell me about FAP
Autosomal dominant APC defect (tumour suppressor) TOtal colectomy with ileo-anal pouch formation age 20
What is dumping syndrome?
Early and Late
early: food of high osmotic potential moves into small intestine causing fluid shift (colicky abdominal pain, diarrhoea and nausea)
late (rebound hypoglycaemia/postprandial hyperinsulinemic hypoglycaemia): surge of insulin following food of high glucose value in small intestine - 2-3 hours later the insulin ‘overshoots’ causing hypoglycaemia
Complications of gastrectomy?
Dumping syndrome (early and late)
Weight loss
early satiety
Iron-deficiency anaemia
Osteoporosis/osteomalacia
Vitamin B12 deficiency
risk of gallstones
risk of gastric cancer
Bile gastritis
Afferent loop syndrome
Efferent loop syndrome
What is characteristically seen on histology of gastric cancer?
Signet cells.
Large vacuole of ucin which displaces nucleus to one side
WHat associations are there with gastric cancer?
H. Pylori Group A Blood Gastric adenomatous polyps Pernicious anaemia Smoking Salty, spicy, nitrates in diet
How do you investigate and stage gastric cancer?
Diagnosis with endoscopy and biopsy
Stage with endoscopic ultrasound
May also stage with CTTAP and laparoscopy to identify occult peritoneal disease
PET CT (for junctional tumours)
How do you classify gastric cancer?
Type 1 - true oesophageal cancer (may be associated with barraetts)
Type 2 - carcinoma of cardia. Arise from cardiac type epithelium or short segments with intestinal metaplasia at the oesophagogastric junction
Type 3 - sub cardial cancers that spread across the junction. Involve similar nodal stations to gastric cancer
How do you treat gastric cancer?
Proximal disease 5-10cm from OG junction- subtotal gastrectomy
<5cm from OG junction - total gastrectomy
Type 2 tumours (extending into oesophagus) - oesophageogastrectomy
Early disease confined to mucosa (<2cm, no ulceration, no lymphovascular involvement) - endoscopic sub mucosal resection
GI parasitic infections:
Signs and symptoms and treatment
Enterobiasis (threadworm)
Enterobius vermicularis
pruritus ani (esp. at night)
placing scotch tape at the anus, this will trap eggs that can then be viewed microscopically
mebendazole
GI parasitic infections:
Signs and symptoms and treatment
Ancylostoma duodenale
Hookworms that anchor in proximal small bowel
Most asymptomatic
iron deficiency anaemia
Larvae may be found in stools left at ambient temperature, otherwise infection is difficult to diagnose
infects by cutaneous penetration, migrates to lungs, coughed up and then swallowed
mebendazole
GI parasitic infections:
Signs and symptoms and treatment
Ascariasis
roundworm Ascaris lumbricoides
Infections begin in gut following ingestion, then penetrate duodenal wall to migrate to lungs, coughed up and swallowed
Diagnosis is made by identification of worm or eggs within faeces
mebendazole
GI parasitic infections:
Signs and symptoms and treatment
Strongyloidiasis
Strongyloides stercoralis
Rare in west
nematode living in duodenum of host
skin penetration. They then migrate to lungs and are coughed up and swallowed. Then mature in small bowel are excreted
An auto infective cycle where larvae will penetrate colonic wall
asymptomatic,
respiratory disease
skin lesions
Diagnosis is usually made by stool microscopy
mebendazole
GI parasitic infections:
Signs and symptoms and treatment
Cryptosporidium
Protozoal infection
cysts which are excreted
diarrhoea and cramping abdominal pains. worse if immunosuppressed
Cysts may be identified in stools
metronidazole
GI parasitic infections:
Signs and symptoms and treatment
Giardiasis
Diarrhoeal infection
Giardia lamblia (protozoan)
Ingestion of cysts
abdominal pain, bloating and passage of soft or loose stools
Diagnosis is by serology or stool microscopy
metronidazole
Gilbert’s Syndrome
Autosomal recessive
Defective bilirubin conjugation
Deficiency in UDP glucuronosyltransferase
Ix: Rise in bilirubin following prolonged fast or IV nicotinic acid
Which features of haemochromatosis are reversible (4), some improvement (3) and which are irreversible (2)?
Reverisble: Cardiomyopathy, skin pigmentation (also transaminitis and fatigue)
Some improvement:
diabetes mellitus, hypogonadotrophic hypogonadism, arthralgia
Irreversible:
Liver cirrhosis, arthropathy
Who do you genetic test for hereditary haemochromatosis?
Elevated serum ferritin (> 300 microgram / L in males; > 200 microgram / L in females)
Elevated transferrin saturation (> 45 %)
First degree relative with haemochromatosis
Management of H. Pylori?
Management - eradication may be achieved with a 7 day course of
a proton pump inhibitor + amoxicillin + clarithromycin,
or
a proton pump inhibitor + metronidazole + clarithromycin
Management of hepatic encephalopathy ?
- Lactulose
2. Rifaximin (secondary prevention)
Grading of hepatic encephalopathy?
Grading of hepatic encephalopathy Grade I: Irritability Grade II: Confusion, inappropriate behaviour Grade III: Incoherent, restless Grade IV: Coma
What are the risks of hepatitis D superinfection?
fulminant hepatitis, chronic hepatitis status and cirrhosis.
Symptoms and signs of cholangiocarcinoma
Persistent biliary colic symptoms, associated with anorexia, jaundice and weight loss. A palpable mass in the right upper quadrant (Courvoisier sign), periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
Symptoms and signs of amoebic liver abscess?
Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.
Investigation and treatment of hepatocellular carcinoma?
Ix:
Screen with USS and alpha-fetoprotein if high risk
Management: Surgical resection (early disease) Liver transplant Radiofrequency ablation Transarterial chemoembolisation Sorafenib (multikinase inhibitor)
Types of hepatorenal syndrome and pathophysiology?
Thought to be caused by splanchnic vasodilation causing underfilling kidneys with RAAS activation, but this isn’t enough to counter balance.
Type 1
Rapidly progressive
Doubling of serum creatinine to > 221 µmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks
Very poor prognosis
Type 2
Slowly progressive
Prognosis poor, but patients may live for longer
Management of hepatorenal syndrome?
Terlipressin
20% albumin
Transjugular intrahepatic portosystemic shunt
Symptoms, management and complications of hydatid cysts?
Caused by Echinococcus granulosus.
Form a fibrous outer capsule
Cysts are allergens and cause Type 1 hypersensitivity reaction
Symptoms:
90% in liver and lung
Asympomatic or symptoms if >5cm
Morbidity if cyst bursts, infection or organ dysfunction
Treatment:
Surgery (do not rupture walls of cyst!)
Symptoms and management of hyperemesis Gravidarum
Symptoms:
5% pre-pregnancy weight loss
Dehydration
Electrolye imbalance
Management: Cyclizine Ondansetron/metoclopramide 2nd line IV hydration Thiamine if severe
Complications of hyperemesis gravidarum?
Wernicke's encephalopathy Mallory-Weiss tear central pontine myelinolysis acute tubular necrosis fetal: small for gestational age, pre-term birth
What are the four types of inherited jaundice? Separate by conjugation or not.
Unconjugated:
Gilbert’s
Crigler-Najjar
Conjugated
Dubin-Johnson (black liver)
Rotor (benign)
List inherited glycogen storage disease (four)
Von Gierke’s disease (type I)
Glucose-6-phosphatase Hepatic glycogen accumulation. Key features include hypoglycaemia, lactic acidosis, hepatomegaly
Pompe’s disease (type II)
Lysosomal alpha-1,4-glucosidase
Cardiac, hepatic and muscle glycogen accumulation. Key features include cardiomegaly
Cori disease (type III)
Alpha-1,6-glucosidase (debranching enzyme)
Hepatic, cardiac glycogen accumulation. Key features include muscle hypotonia
McArdle's disease (type V) Glycogen phosphorylase (myophosphorylase) Skeletal muscle glycogen accumulation. Key features include myalgia, myoglobinuria with exercise
List inherited lysosomal storage dsisease (six)
Gaucher’s disease
Beta-glucocerebrosidase
Most common lipid storage disorder resulting in accumulation of glucocerebrosidase in the brain, liver and spleen. Key features include hepatosplenomegaly, aseptic necrosis of the femur
Tay-Sachs disease
Hexosaminidase A
Accumulation of GM2 ganglioside within lysosomes. Key features include developmental delay, cherry red spot on the macula, liver and spleen normal size (cf. Niemann-Pick)
Niemann-Pick disease
Sphingomyelinase
Key features include hepatosplenomegaly, cherry red spot on the macula
Fabry disease
Alpha-galactosidase-A
Accumulation of ceramide trihexoside. Key features include angiokeratomas, peripheral neuropathy of extemeties, renal failure
Krabbe’s disease
Galactocerebrosidase
Key features include peripheral neuropathy, optic atrophy, globoid cells
Metachromatic
leukodystrophy Arylsulfatase A
Demyelination of the central and peripheral nervous system
List inherited mucopolysaccharidoses diseases (two)
Hurler syndrome (type I)
Alpha-1-iduronidase
Accumulation of glycosaminoglycans (heparan and dermatan sulfate). Key features include gargoylism, hepatosplenomegaly, corneal clouding
Hunter syndrome (type II) Iduronate sulfatase Accumulation of glycosaminoglycans (heparan and dermatan sulfate). Key features include coarse facial features, behavioural problems/learning difficulties short stature, no corneal clouding
What increases and what reduces iron absorption?
Increased with:
Vitamin C
Gastric Acid
Reduced with: PPI Tetracycline Gastric achlorhydria Tannin (tea)
Management of IBS
Pain
Constipation
Diarrhoea
Pain - anti-spasmodic
Constipation - laxative (avoid lactulose). If not improvement after 12 months, linaclotide
Diarrhoea - loperamide
Second Line:
Low dose TCA
CBT
Third Line:
SSRI
IBS dietary advice
Regular meals Avoid missing meals Plenty of fluid Restrict coffee, alcohol and fizzy drinks Limit high fibre food Limit fresh fruit 3 potion
What features of ischaemic hepatitis?
Due to acute hypoperfusion
Inciting event
Increase in aminotransferase levels >1000 or 50x normal
Contraindications to percutaneous liver biopsy?
deranged clotting (e.g. INR > 1.4) low platelets (e.g. < 60 * 109/l) anaemia extrahepatic biliary obstruction hydatid cyst haemoangioma uncooperative patient ascites
Who should be screened for liver cirrhosis? How?
If cirrhosis, what then?
People with hepatitis C
Men with 50+ units alcohol
Women 35+ units alcohol
Alcohol-related liver disease
Screen with transient elastography
Upper endoscopy for varicies
Liver USS every 6 months (+/- alpha-feto protein)
Causes of malabsorption (separate into three types)
Intestinal causes of malabsorption coeliac disease Crohn's disease tropical sprue Whipple's disease Giardiasis brush border enzyme deficiencies (e.g. lactase insufficiency)
Pancreatic causes of malabsorption
chronic pancreatitis
cystic fibrosis
pancreatic cancer
Biliary causes of malabsorption
biliary obstruction
primary biliary cirrhosis
Other causes
bacterial overgrowth (e.g. systemic sclerosis, diverticulae, blind loop)
short bowel syndrome
lymphoma
When should metoclopramide be avoided and when may it be helpful?
Metoclopramide should be avoided in bowel obstruction, but may be helpful in paralytic ileus.
Adverse effects extrapyramidal effects: oculogyric crisis. This is particularly a problem in children and young adults hyperprolactinaemia tardive dyskinesia parkinsonism
What is microscopic colitis?
Name some risk factors:
chronic inflammatory condition of the gut.
Risk factors
smoking
drugs: NSAIDs, PPIs and SSRIs
Features of microscopic colitis?
Watery diarrhoea Faecal urgency and incontinence Abdominal pain Constitutional symptoms Mild anaemia RF or ANA positive occasionally Raised inflammatory markers
Features and associated factors for non-alcoholic fatty liver disease
Associated factors obesity type 2 diabetes mellitus hyperlipidaemia jejunoileal bypass sudden weight loss/starvation
Features usually asymptomatic hepatomegaly ALT is typically greater than AST increased echogenicity on ultrasound
Management of NAFLD
ALT >AST
No evidence to screen. Only manage incidental findings
- Enhanced liver fibrosis scan and blood tests
- Lifestyle changes (lose weight, normal alcohol)
- pioglitazone or vitamin E can be used
A score of > 10.51 suggests severe fibrosis.
Repeat ELF blood test every 3 years if <10.51
Investigation and management of oesophageal cancer
- UGI endoscopy
- Contrast swallow if motility disorder, but not for tumours
- Staging with CT TAP
- If no metastasis, local endoscopic USS
Management
Ivor-Lewis Oesophagectomy
Triad in Plummer Vinson syndrome?
Dysphagia - oesophageal webs
Glossitis
Iron deficiency anaemia
Oesophageal webs are premalignant for SCC
Freuquently webs improve with iron replacement
Dilation may be required
Add in PPI for reflux
Investigation of pancreatic cancer
- USS (60-90% sensitivity)
2. High resolution CT if diagnosis suspected
What is peutz-jeghers syndrome?
Autosomal dominant
Numerous hamartomatous polyps in GI tract
Associated pigmented freckles on lips, face, palms and soles
Causes of jaundice in pregnancy?
Intrahepatic cholestasis of pregnancy
- rx ursodeoxycholic acid with weekly liver function tests. Induce at 37 weeks
Acute fatty liver of pregnancy
- sx abdo pain, N&V, headache, jaundice, hypoglycaemia, ALT 500+
- rx supportive
HELLP
Primary Biliary Cirrhosis (cholangitis) features?
Associated with sjogrens syndome, RA, systeic sclerosis, thyroid diseae
AMA (98%)
Anti-smooth (30%)
raised serum IgM
Fatigue, pruritus, cholestatic jaundice, hyperpigmentation, RUQ pain, xanthelasmas
Management and complications of primary biliary cholangitis (cirrhosis)
Management: Cholestyramine Fat soluble vitamin supplementation Ursodeoxychoic acid Liver transplant
Complications Cirrhosis Osteomalacia Osteoprosis Malabsorption Portal HTN Hepatocellular cancer
Adverse effects of PPIs
Hyponatraemia Hypomagnasaemia Osteoprosis Microscopic colitis C. Difficile
What is pseudomyxoma Peritonei
Rare mucinous tumour most commonly arising from appendix
Treat with cytoreductive surgery and peritonectomy
Management of pyogenic liver abscess?
drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin
Pyogenic liver abscess organisms?
Staphylococcus aureus in children
Escherichia coli in adults.
Refeeding Syndrome - metabolic consequences?
hypophosphataemia
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance
Patients at high risk of refeeding syndrome are:
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)
NICE recommend that 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.
How is H. Pylori tested?
CLO (Campylobacter-Like Organism) at OGD
Uses a reagent on biopsy sample
What is small bowel bacterial overgrowth syndrome? Name some risk factors
Excessive amounts of bacteria in small bowel leading to GI symptoms.
Risk factors:
Neonates with congenital GI abnormalities
Scleroderma
Diabetes
Features of small bowel bacterial overgrowth syndrome?
Chronic diarrhoea
Bloating
Flatulence
Abdominal Pain
Low B12, normal folate (usually)
Diagnosis of small bowel bacterial overgrowth syndrome?
Hydrogen breath test
Small bowel aspiration and culture (gold standard)
Treatment of small bowel bacterial overgrowth syndrome?
Rifaximin
Which people with ascites should be given prophylacctic antibiotics?
Episode of SBP
FLuid protein <15g/L and child pugh score 9+ or hepatorenal syndrome
Oral ciprofloxacin or norfloxacin
Diagnosis and management of SBP?
Diagnosis
paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli
Management
intravenous cefotaxime is usually given
Management of acute variceal haemorrhage?
- Terlipressin
- Prophylactic antibiotics (quinolones)
- Endoscopy (band ligation > sclerotherapy)
Do not give PPI
Sengstaken-Blakemore tube if uncontrolled haemorrhage
Transjugular intrahepatic portosystemic shunt (TIPSS)
Prophlaxis of variceal haemorrhage?
Propranolol
isosorbide mononitrate if beta-blocker contra-indicated
Endoscopic variceal band ligation at 2 weekly intervals
‘Offer endoscopic variceal band ligation for the primary prevention of bleeding for people with cirrhosis who have medium to large oesophageal varices.’
How to manage blood products in variceal haemorrhage?
Platelets if <50
Hb if <70
Vit K and FFP if >1.5x INR/APTT/PT
Fibrinogen if < 1g
Management of varicies in cirrhosis?
No varices - Rescope 2-3 years
Grade 1 varices -Rescope 1 year
Grade 2 or 3 varices or signs of bleeding - Non-cardio selective beta blocker
Contraindications for TIPSS?
Absolute contraindications:
Severe and progressive liver failure (Child-Pugh score >12 is associated with a high risk of early death) Uncontrolled hepatic encephalopathy Right-sided heart failure Uncontrolled sepsis Unrelieved biliary obstruction
Relative contraindications:
Severe uncorrectable coagulopathy (INR >5) Thrombocytopenia <20 * 109/l Portal and hepatic vein thrombosis Pulmonary hypertension Central hepatoma
What are villous adenomas?
Colonic polyps with potential for malignant transformation.
Secrete large amounts of mucous. May have electrolyte disturbances
non-specific lower gastrointestinal symptoms
secretory diarrhoea may occur
microcytic anaemia
hypokalaemia
Conditions of thiamine deficiency (b1)?
Wernicke’s encephalopathy: nystagmus, ophthalmoplegia and ataxia
Korsakoff’s syndrome: amnesia, confabulation
dry beriberi: peripheral neuropathy
wet beriberi: dilated cardiomyopathy
Causes and consequences of B6 deficiency?
Causes of vitamin B6 deficiency
isoniazid therapy
Consequences of vitamin B6 deficiency
peripheral neuropathy
sideroblastic anemia
Signs and symptoms of scurvy?
Follicular hyperkeratosis and perifollicular haemorrhage
Ecchymosis, easy bruising
Poor wound healing
Gingivitis with bleeding and receding gums
Sjogren’s syndrome
Arthralgia
Oedema
Impaired wound healing
Generalised symptoms such as weakness, malaise, anorexia and depression
What is Whipple’s disease? What are the signs?
Tropheryma whippelii infection
HLA-B27 positive and in middle-aged men.
malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus
Investigation and management of Whipple’s disease?
Investigation
jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules
Management
guidelines vary: oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin
Features of Wilson’s disease?
Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea:
liver: hepatitis, cirrhosis
neurological: basal ganglia degeneration, speech, behavioural and psychiatric problems are often the first manifestations. Also: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
Diagnosis of Wilson’s disease?
Diagnosis
reduced serum caeruloplasmin
reduced serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
increased 24hr urinary copper excretion
Management of Wilson’s disease?
Management
penicillamine (chelates copper)
trientine hydrochloride is an alternative chelating
What is Zollinger-Ellison Syndrome?
gastrin secreting tumour usually of the duodenum or pancreas
30% are MEN Type 1
Features
multiple gastroduodenal ulcers
diarrhoea
malabsorption
Diagnosis
fasting gastrin levels: the single best screen test
secretin stimulation test
Management of pouchitis in UC reconstruction?
Presentation?
his presents with increased stool frequency, urgency, incontinence and nocturnal seepage.
Management
metronidazole or ciprofloxacin.
In 5 % of cases, pouchitis can become chronic, ultimately leading to pouch failure and requiring pouch excision.
What are elastase levels?
Normal > 200
100-200 - mild
<100 insufficiency
Vitamin D/Ca/Po Results and their diseases
Paget’s disease Ca - N, Po - N, ALP - H
Primary Osteoporosis Ca - N, Po - N, ALP - N
Primary hyperparathyroidism Ca - H, Po - L, ALP - H
Secondary hyperparathyroidism Ca - L, PO - H, ALP - H
Vitamin D deficiency Ca - L, PO - L, ALP - H
What can you give to someone with small bowel obstruction due to cancer?
Steroids and bowel rest
Following UGI bleed, what should you do with the anti-platelets??
If UGI controlled and no bleed:
Aspirin can continue if for secondary prevention
How to differentiate secretary diarrhoea
Very large daily stool weight indicates organic pathology
Maintenance of large stool weight on fasting suggests secretory diarrhoea
Osmotic diarrhoea diarrhoea is reduced with fasting
How does VIP cause diarrhoea?
VIP is a hormone that stimulates the secretion and inhibits the absorption of sodium, chloride, potassium and water within the small intestine and increases bowel motility. These actions lead to a secretory diarrhoea, hypokalaemia, and dehydration.
Pellegra is see in which syndrome?
Carcinoid syndrome
Histology of autoimmune hepatitis?
interface hepatitis (inflammation with lymphocytic infiltrate at the junction between hepatocytes and portal tracts).
What are the Dukes scales?
A - confined to mucosa and submucosa
B - extends through muscularis propria
C - regional lymph node involvement
D - distal spread
Management of hyponatraemia in liver cirrhosis?
Sodium 126-135 mmol/L with normal creatinine - Continue normal diuretic regimen and observe, do not fluid restrict the patient.
Sodium 121-125 mmol/L with normal creatinine - International opinion is to continue diuretics, however, the British Society of Gastroenterology recommend a more cautious approach, and suggest either stopping diuretics or reducing the dose.
Sodium 121-125 mmol/L with raised creatinine (>150 mmol/L or >120 mmol/L and rising) - Stop diuretics and volume expand with human albumin solution 4.5%, gelofusine, or haemaccel
Sodium <121 mmol/L - Incredibly controversial, but the British society of gastroenterology suggest stopping diuretics and volume expanding with human albumin solution 4.5%, gelofusine, or haemaccel (which all contain sodium concentrations similar to that of normal saline).
Colonoscopic surveillance of adenomas?
Low Risk - every 5 years (adenoma < 10mm in size)
Intermediate - every 3 years
High risk - every year
