Gastroenterology Flashcards
Dysphagia- difficulty swallowing liquids and solids from start. Rule out what?
Motility disorder - achalasia or CND or pharyngeal cause
Painful swallowing differentials?
Ulcer
Malignancy, oesophagitis, candida in immune suppressed
Intermittent dysphagia
Oesophageal spasm
Neck bulge or gurgle on drinking
Pharyngeal pouch
What is alchalasia and how does it present?
Loss of coordinated peristalsis and lower oesophageal sphincter fails to relax
Dyshapgia, regurgitation and decreased weight
Investigations and management of achalasia
Manometry or contrast swallow - dilated tapering oesophagus
Treatment - surgical myotomy, endoscopic balloon dilatation. Botulinum toxin injection. Calcium channel blockers may also relax the sphincter
High dose PPI
Dyspepsia Alarm symptoms
Alarm
Anaemia Loss of weight Anorexia Recent onset / progressive Milena/haematemesis Swallowing difficulty
Investigations for dyspepsia
If 55 years old or less - test and treat for H. Pylori - using urea breath test of stool antigen
Positive = PPI and 2 Abx (amoxicillin and clarithromycin)
Negative = PPI and lifestyle modifications
Consider - FBC (anaemia) u/E, CRP
Endoscopy for biopsies or ulcers and rule out malignancy
With repeat endoscopy to see if ulcer healed
ALARM symptoms - urgent referral for endoscopy
Pain a couple of hours after a meal + dyspepsia diagnosis?
Duodenal ulcer
Pain with meal, + dyspepsia. Diagnosis?
Peptic ulcer
What is zollinger Ellison syndrome and its features?
Gastrin-secreting tumour (gastrinoma) usually of pancreatic origin
Results in hypersecretion of gastric acid causing peptic ulceration
Epigastric pain as a result of ulceration and GOTD
Diarrhoea (acid damages pancreatic enzymes)
Causes of upper GI bleed
PUD Inflammation - oesophagitis, gastritis, duodenitis Oesophageal or gastric varices Mallory-weiss tear from sever vomiting Upper GI cancer
Investigations of upper GI bleed
FBC - anaemia
Cross match and coag
Increased urea - absorption and metabolism of blood
LFTs
Erect CXR
Consider CT abdo-chest
Risk assessment - blatchford score, rockall full score
Management of an acute GI bleed
ABCDE Oxygen if hypoxic and able Contact senior staff (surgeon on call) Nill by mouth Insert 2 wide bore cannula IV fluids - o negative blood if appropriate Urinary catheter Transfuse if Hb < 70 g/L Cross match and coag
Urgent endoscopy
If that fails - surgery
PPIs after endoscopy
Management of varicle bleeding
ABCDE
Fluids (treat as GI bleed)
Terlipressin IV 1-2 mg while waiting band ligation
Broad spectrum abx
Endoscopic banding
Sengstaken-blakemore tube to compress varices
Alcoholics - B1 (thiamine)
What causes unconjugated hyperbilirubinaemia?
Over production - haemostasis, ineffective erythropoiesis
Impaired hepatic uptake- drugs (paracetamol), ischaemia hepatitis
Water insoluble so does not enter urine.
What causes conjugated hyperbilirubinaemia?
Post-hepatic causes
Excreted in urine as its water soluble. Urobilinogen is absent in obstructive disease as it doesn’t enter the GI tract, instead leaks into the blood where it cannot be broken down into urobilinogen. Faeces dark (less bile into GI tract)
Causes of cholestasis
PBC, PSC drugs - co-amoxiclav Common bile duct gall stones Pancreatic cancer Compression of the bile duct - cholangiocarcinoma
What can co-amoxiclav cause?
Jaundice - cholestasis / post-hepatic jaundice
Tests in jaundice
Urine - bilirubin, urobilinogen
Bloods - FBF, clotting, reticulocyte count, coombs test, malaria parasites
Chemistry- U+Es (urea up in haemolysis), albumin
US - look at bile ducts, pancreatic mass
ERCP - if bile ducts open
MRCP, LIVER BIOPSY, CT/MRI (MALIGNANCY)
Will you see bilirubin in the urine of pre-hepatic jaundice?
No, as it is un-conjugated and therefore not water-soluble
Bloody diarrhoea differentials
IBD
campylobacter / shigella / colorectal Cancer / colitis
Colonic polyps
Management of diarrhoea
Treat the cause
Oral rehydration unless severe - IV rehydration and electrolyte replacement
Codeine phosphate or loperamide
Avoid Abx unless infection is cause
What is the cause of coeliac disease?
Gladin which is a part of gluten is modified during digestion by the enzyme tissue transglutaminase (tTG)
Autoimmune response to the complex that forms
Anti-tTG antibodies damage intestine and connective tissue in muscles
Presentation of coeliac disease
Young - failure to thrive Diarhhoea / steatorrhoea - mucus Bloating Abdominal pain / discomfort Anaemia Dermatitis herpetiformis Weight loss Malnutrition
Investigations of coeliac
IgA-tTG
Total IgA - are they deficient as an enitrety?
Endomysial antibody
Small bowel histology - gold standard
Consider- FBC, blood smear (iron deficiency)
Vitamin D / calcium / B12 / folate
Management of coeliac disease
Patient education Lifelong gluten free diet Consultation with a dietician Dietary councilling Calcium/ vitamin D supplementation Pneumococcal vaccine (functional hyposplenism)
Annual review
Dexa
What foods contain gluten?
Wheat (bread, pasta)
Barley
Oats
Rye
What is primary biliary cholangitis and its presentation?
Chronic autoimmune disease - progressive destruction of small intrahepatic bile ducts, causing cirrhosis
Female predominance.
Usually 4th-5th decade of life
Fatigue and pruritus - earliest symptoms
Jaundice later
Hepatosplenomegaly
Facial hyperpigmentation and xanthelasmas
Leads to cholestasis as fibrosis of biliary tracts prevents excretion
Cholesterol that is normally metabolised by liver and excreted as bile salts not deposits in eyes and tendons
Investigations of PBC
Obs
Lfts - cholestatic picture
Autoimmune profile - AMA positive in 95%
High levels of IgM are indicative
Imaging - USS of MRCP
Exclude biliary obstruction
Liver biopsy
Management of PBC
Bile acid analogue - urodeoycholic acid
Immunomodulation therapy - prednisolone with azathioprine
Anti-pruritis - colestyramine
Liver transplant for end-stage
What is primary sclerosing cholangitis?
Intrahepatic or extra hepatic ducts become strictured and fibrotic - causes obstruction to bile flow
Causes - combination of genetic and environmental factors
Any age can be affected
60% men
80% of patients have inflammatory bowel disease (UC)
Jaundice
Chronic RUQ pain
Pruritus
Fatigue
Investigstions for PSC
General bloods
LFTs - cholestatic picture
Autoantibodies - non are specific
P-ANCA
ANA
(Not necessarily an autoimmune disease - doesn’t respond to immunomodulation)
MRCP - lesions and strictures to bile ducts
Management of PSC
Observation and lifestyle changes - healthy diet and limit alcohol DEXA Pruritus relief - chloestyramine Urodeocholic acid - slows disease progression Monitor for complications ERCP - dilate and stent strictures Liver transplant Immunomodulation
What is used to prevent oesophagus varices?
Proanolol (non-selective B blocker)
Terlipressin = treat Propranolol = prevent
Who meets referral criteria for urgent dyspepsia?
All with dysphagia
All with upper GI mass
>55 with alarm or persistant symptoms
If stable, what test should be done on patients with upper GI bleed?
Endsocopy within 24h
Harmartomatous polyps in the GI tract and facial freckles is associated with what condition?
What type of genetic condition?
Complications?
Peutz-Jeghers syndrome
Autosomal dominant
BO - intersucseption
GI bleeding
UC presentation
Rectal bleeding (proctitis) Diarrhoea Bloody stool Abdo pain Skin changes Eye problems Arthritis Malnutrition
What are risk factors for UC?
Family history
HLA-B27 association (ankylosing spond)
Extra-abdominal manifestations of IBD
Skin - erythema nordosum, pyoderma gangrenosum
Eyes - anterior uveitis, episcleritis
Joints - arthritis, ank. Spondylitis (UC)
Renal stones
PSC (UC)
Investigations for IBD
Fbc - anaemia, infection U+E - dehydration LFF - low albumin as a marker of severity, PSC CRP ESR
stool mc&s - exclude infection
Faecal calprotectin
AXR - thumb printing, lead pipe, dilatation
Lower GI endoscopy
Serological markers- pANCA (UC)
What is a serological marker likely to be positive in UC?
pANCA
What is a mild flare of UC?
<4 motions a day
Small bleeding
No systemic upset
What is a moderate flare of UC?
4-6 motions a day
Moderate bleeding
Minimal systemic signs
What is a severe flare of UC?
> 6 motions a day
Severe bleeding
Systemic signs
Complications of IBD
Toxic dilatation (UC more common)
VTE
Colon cancer
PSC
SBO (crohns)
Abscess formation
Perforatiin
Malnutrition
Differences in presentation between UC/crohns
Crohns - diarrhoea usually non-bloody. Weight loss more prominent, upper GI symptoms - mouth ulcers, perianal disease. Abdominal mass palpable in RIF
UC - bloody diarrhoea mor common. Abdo pain in Left lower quadrant
Differences in pathology of UC/crohns
Distribution- continous in UC, skip lesions in Crohns
Site - anywhere in crohns, rectal and proximal coclon in UC
Inflammation- confined to mucosa in UC as well as crypt abscesses and goblet cell dysplasia in crohns, transmural involvement, extensive fibrosis and fissures. Granuloma formation
Management of UC
Mild - mesalazine - give PR for distal disease. Topical steroids have a role
Moderate- induce remission with oral pred. Then taper. Maintain on mesalazine.
Severe - admit for IV rehydration, electrolyte replacement, IV steroids
Monitor, assess severity, rehydrate for all
Other therapies- azathioprine if continuous flares also consider biological therapies - inflixamab, adalimumab
Surgery if medical management fails
Managemenr of crohn’s disease
Assess severity. Consider psych input, optimise nutrition
Mild/moderate - prednisolone for 1 week then taper
Sever - admit for hydration/ electrolyte replacement. Iv steroids
VTE prophylaxis
Monitor - if improving, switch to oral pred
If no improvement - biologics have a role
Anti-diarrhoeals
Anti-spasmodics
Osteoperosis
Colonoscopg surveillance
Lifestyle - smoking cessation
Differentials for bloody diarrhoea
Drugs - PPIs, NSAIDs, Abx IBS IBD Gastroenteritis - e. Coli, c. Diff., shigella, campylobacter Cancer Ischaemic colitis Mesenteric ischaemia
What is wilsons disease?
Autosomal recessive condition characterised by error in copper metabolism and accumulation
Pathophysiology of wilsons disease
In Liver, copper is incorporated into caeruloplasmin
In hepatocytes
In wilsons, this process is impaired as well as excretion
Copper accumulates in liver and other organs
Presentation of wilsons disease
Behavioral problems - depression, reduced libido, memory loss Tremor Dysarthria - slurred speech Dystonia Kayser-fleischer rings Children may present with liver disease Young adults - CNS signs
Tests for wilsons disease
Urine 24h copper excretion is high Increased LFTs Serum copper - low Serum caeruloplasmin - low Molecular genetics testing Slit lamp for eye signs Liver biopsy - increased hepatic copper, cirrhosis MRI - degeneration of key areas of brain
Management of wilsons disease
Diet - avoid foods with high copper (liver, chocolate, nuts) Check water sources for copper Drugs - lifelong penicillamine Liver transplantation Screen siblings
What is hereditary haemochromatosis
Autosomal recessive condition that causes the body to absorb too much iron from the diet
Cause - mutation in HFE (protein that regulates iron entry to cells)
Leads to decreased hepcidin synthesis - leads to increased iron absorption
Damage to liver, joints, anterior pituitary, pancreas, heart, thyroid
