GASTROENTEROLOGY Flashcards
What is HELLP
Haemolysis + hypertension
Elevated liver enzymes
low plateletes
Hepatic manifestation of pre-eclampsia
- Thrombocytopenia occurs due to microangiopathic haemolytic anaemia in liver sinusoids due to HTN
- This gives rise to biliary congestion
- Blockade also causes focal hepatic ischaemia and necrosis
What is Ischaemic Collitis
Ischaemia and necrosis caused by a stenosis or compelte occulsion of flow through the SMA / IMA
Can be chronic or acute
Chronic may present non specifically:
Chronic abdominal pain
weight loss
loose stool
non specific dieficiencies - b12 / folate / fat soluble vitamins
misdagnosed as coeliac / ibs / ibd / anorexia
Acute may present: peritonitis deranged LFTs secondary to ischaemia alongside AAA rupture or AA dissection or Thoracic aorta dissection shock bloody diarrhoea absolute constipation no bowel sounds Gas+++ AXR
CTAP bowel wall gas bowel wall oedema biliary air hepatic necrosis perforation
Causes: vitamin C vascular -Aortic dissection -Post AAA repair -Cardic emobolism / septic embolism -atherosclerotic disease -factor V leiden -antiphospholipid -paradoxical embolism via ASD / VSD
infective:
Water shed from hypovolaemia
TNF-a septic storm
Trauma:
volvulus
interssusseption
autoimmune:
antiphospholipid
metabolic:
Sickle cell
Iatrogenic / drug induced
HIT - heparin induced thrombocytopenia type 2 - IgG mediated platelet depletion and converse hypoercoagulable state
adhesional obstruction
neoplastic:
direct pressure
embolism
Congenital: MEC ileus bowel atresia malrotation - lads bands interssusspetion
How does PBC present
Primary Biliary Cirrhosis
Anti mitochondrial Abs - 90%
AI condition targetting intrahepatic bile ducts ONLY
more common in women especially following pregnancy
presentation 40
4 stages of inflammation leading to cirrhosis
1 - inflammation of bile duct sinusoids
2- extension of inflammatory infiltrate towards liver lobules with increasing fibrosis of local structures
3 - fibrotic septations extend into lobules and begin partitioning liver and reorganising structure
4 - number of immune cells is now reduced. Biliary sinusoids destroyed and fribrosed with limited cellular component. regnertive nodules present
Gradula destruction of intrahepatic bile ducts leading to cholestasis, fibrosis, recurrent cholangitis and hepatic cirrhosis
Px: • Females are most commonly affected, less often males • First disease manifestation following pregnancy • Pruritus • fatigue, reduced performance • xanthelasmata (subcutaneous fat deposits in the eyelids) Keiser fleischer rings jaundice
associated disorders i • Associated rheumatic disorders Joint complaints - RA Hashimoto thyroiditis Sicca syndrome - Exocrine glands • Osteoporosis • Vitamin deficiency • Skin changes typical for cirrhosis (see table 4) • Hepatocellular carcinoma
Causes of bloody diarrhoea
infective: Salmonella Shigella Compylobacter - C.Diff Entamoeba E.Coli
autoimmune
Ulcerative collitis
Miced IBD
vasculitic
wegners granulomatosis and polyangitis
congenital
herediatary haemorrhagic telangiectasia
angiodysplasia
metabolic:
Variceal haemmorhage
Torrential UGIB
Causes of watery diarrhoea
infective:
Cholera
Tropica Sprue - cause unclear - chronic infection?
Cryptosporidium - parasite - Nitazoxanide / praziquantel
Autoimmune
Coeliac
IBS
IgG4 AI pancreatitis
iatrogenic
Abx induced
short bowel syndrome / dumping syndrome
metabolic
Alcohol - pancreatic insufficiency - need creon
chronic pancreatitis
cancer:
Zollinger Ellison - +++ gastrin
What is Coeliac Disease
Autoimmune sensitivity propogated by Il-15 and anti-ttg abs and anti-endomysial abs against the a-gliadin peptide of gluten.
Because of pathophysiology there must be an initial insult to small bowel to allow antigen exposure to vasculature / resident MALT unless this occurs via random sampling by DCs.
Presentation:
abdominal pain - sporadic to gluten containing foods
malabsorption - b12 / folate / fat sol vit a/d/e
wartery diarrhoea
bloating
FTT
Dermatitis herpetiformis is specific for coeliac
- 1cm to widespread vesicular painful and pruritic rash
histology:
flattened villi
shallow crypts
inflammatory infiltrates
treatment
Avoidance rye / wheat / cereals containing gluten
Dapsone for Dermatitis herpetiformis
SULFAPYRIDINE for DH if non responsive - needs monitorinf due to risk of agranulocytosis
What is the pathophysiology of recurrent hydrothorax in cirrhotic liver disease?
Recurrent ascites from raised portal pressures
Typically also causes a right hydrothorax
microdefects in diaphragm allow communication
Lights criteria = transudative - sterile i.e. normal glucose pleural protein / serum protein <0.5 Pleural LDH < 2/3 serum LDH pH >7.35 MCS negative normal CT
Management:
1. Drain if symptomatic
2. TIPS - transjugular intrahepatic portosystemic shunt
60-80% have improvement
3. Chemical pleurodesis - better in malignancy
4. liver transplant
What is PPI induced colitis
Long term use of PPI is associated with lymphocytic collitis
Withdrawal of ppi usually is curative
Dx:
Colonoscopy and biopsy
How does CMV collitis present
Diagnosis:
Colonscopy + biopsy
Biopsy:
Nuclear inclusion bodies
intracytoplasmic inclusion bodies
Who is at risk of CMV collitis
Immunosupressed: ANTI TNFa infliximab / adalimumab / gadalimumab ANTI INTEGRIN A1B4 vedalizumab HIV MTX / azathioprine
Congenital CMV
How is CMV collitis managed
Suppotive only
IV ganciclovir + oral maintenance if immunosupressed
What antibodies are present in PSC and what is it assoicated with
inflammation of bile ducts and sinusoids leading to CLD / fibrosis and cirrhosis via biliary obstruction and inflammation
Abs:
P-ANCA
ANA
and Anti-smooth muscle
Associated with IBD
UC > CD
What anitbodies are present in PBC
Anti-mitochondrial abs
What are the key differences between PBC and PSC
PSC – PRIMARY SCLEROSING CHOLANGITIS
PBC – PRIMARY BILIARY CHOLANGITIS
SEX AGE SMOKING PSC 60%men 40s non smokers
PSC 90% women Typically post partum ?trigger smokers >45
DISEASE SITE:
PSC
Larger Bile ducts inside and outside the liver
Small duct PSC (10-15% of patients) only the small ducts inside the liver are affected
PBC
Small bile ducts inside the liver only
ANTIBODY PROFILE PSC limited anti-smooth muscle ANA P-ANCA +Ve
PBC
Anti-mitochondrial
ANA
DIAGNOSED BY
PSC
MRCP
liver biopsy
PBC
Raised ALP
AMA
diagnostic liver biopsy.
MALIGNANCY RISK:
PSC
increased risk of HCC and colon cancer
PBC
No increased risk
RESPONSE TO URSODEOXYCHOLIC ACID(UDCA)
PSC
Improves liver blood tests in some patients
not conclusively proven to slow disease progression
PBC
Associated with improved prognosis in those individuals who respond well to UDCA
IBD ASSOCIATION
PSC
80% of patients have IBD – mostly UC
PBC
IBD not common
RA / hashimotos and SJORGENS and coeliac are more common
BOTH PRESENT THE SAME:
Itching, fatigue, abdominal pain, cholangitis flares Itching, fatigue, dry eyes and mouth, abdominal pain
PSC FIBROSIS OF MEDIUM AND LARGE BILE DUCTS INSIDE AND OUTSIDE LIVER DIAGNOSIS VIA MRCP MEN AND WOMEN IN 40s most commonly ASSOCIATED UC
INCREASED RISK OF COLON AND HCC
NO CURE - SLOW PROGRESSION ONLY
BLOODS IMPROVED BY URSODEOXYCHOLIC ACID but no change to prognosis
PBC
SMALL INTRAHEPATIC BILE DUCTS ONLY
MAINLY WOMEN 90% WHO SMOKE AND OVER 45
ASSOCIATED RA . HASHIMOTOS . SICCA
DIAGNOSIS VIA BLOODS AND AMA
RESPONSE TO UDCA CORROLATES TO SURVIVAL AND LOWER RISK OF TRANSPLANT
NO ASSOC WITH CANCER or IBD
What is Truelove and Witts Criteria and what is it used for
Used to grade severity of UC presentation 6 areas -Frequency -Blood -Pyrexia -Pulse -Anaemia -ESR
Summary
1-4 stools +/- blood + no fever + normal ESR/CRP
>4 stools + minimal fever / tachycardia
>6 bloody stools with systemic disturbance and ESR>30
Frequency
1-4 stools more than normal
>4 stools more than normal
>6 stools more than normal
Blood
<50% blood
>50% blood
All blood
Pyrexia
no fever
no fever
>38
Pulse
no tachy
no tachy
>tachy
Anaemia
no anaemia
no anaemia
anaemia
ESR
normal ESR
<30
>30
What is measured prior to starting azathioprine / mercaptopurine therapy?
TPMT activity
THIOPURINE METHYL TRANSERASE - changes azathioprine to mercaptopurine
nb xanthine oxidase breaks down mercaptopurine
Low activity = increased risk of BM suppression and toxicity with normal dose of azathioprine or mercaptopurine (toxic compounds hang around longer)
Beware allopurinol - xanthane ox inhibtor - will prevent breakdown of mercaptopurine extending half life and potential toxicity.
Can be used therapeutically to deliver a tiny dose of purine antagonist.
LFT and FBC monitored at 2/4/8/12 weeks
3 monthly thereafter
MMP and TGN levels done at 4 weeks then 12-16 weeks or 4 weeks after dose alteration
ration important as shows appropriate breakdown to avoid toxicity of purine metabolites
What is the best management for fistulating crohns
Primary intervention would be IV hydrocortisone 400mg per day as for UC
Infliximab / adalimumab have the best evidence for fistulating crohns
Fistulas tend to improve within the first 2-3 weeks in 2/3 patients
Need immunoscreen prior:
HBV HCV TB quantiferon / mantoux HAV HEV CMV EBV TPMT
Treatment ladder:
1-IV hydrocort or pred (esp maintenance) +XRay +stool culture
2-elemental diet - mixed evidence
3-rectal and oral enemas of mesalazine - 5’ASA
4-Azathioprine - need TPMT level - steroid sparing agent
Mercaptopurine
5-MTX if intolerant to thiopurines or TPMT low
6-Infliximab
7-adalimumab
8-vedalizumab
9-colectomy
What is Gardener’s Syndrome
Aut Dominant inheritance
COLONIC ADENOMAS
OSTEOMAS
SOFT TISSUE TUMOURS.
Mx:
surveillance colonoscopy
Pancolectomy once polyps appear
Multiple adenomatous polyps throughout large bowel
LESS THAN FAP
INCREASING RISK OF COLONIC CANCER YEAR ON YEAR
7% AT 21
50% AT 39
90% AT 45
What is carcinoid syndrome
Carcinoid tumours secrete serotonin - NEUROENDO
Detected by urinary collection of 5’hydroxyindoleacetic acid
85% CARCINOID: FLUSHING DIARRHOEA NEW MURMUR / CARDIAC INOVLEMENT -RIGHT VALVULAR STENOSIS
DETECTION:
URINARY ANALYSIS OF SEROTONIN METABOLITE AS ABOVE
IMAGING WITH PENTREOTIDE
can be tumours anywhere
COLORECTAL
BRONCHIAL
How does acute porphyria present
Abdominal pain 85-95%
Vomiting 50-90%
Paresis - 40%
Neurological symptoms - seizures 10-30%
- Urine changes colour on standing - due to uro-porphobilinogen
- uro porphobilinogen >300
- photolytic rash
Mx:
avoid triggers
sunlight / alcohol / anti-epileptics / metoclopramide
blood letting in PCT as iron inhibits UROD - UROPORPHYNOGEN DECARBOXYLASE
CHLOROQUINES in PCT
HAEM arginate - replenishes haem and reduces synth
Dextrose - inhibits haem synth and reduces porphyrins
What is the MOA of haem arginate
Replenishes haem store - reduces synthetic drive that causes build up of porphyria
What is oesophagial cancer associated with?
Dermatomyositis
same as bronchial cancer
male smoker barretts achalasia coeliac tylosis pylori - AD keratosis of hands and feet
How Is UC Graded - 2 systems
TRUELOVE AND WITTS Frequency 1-4 / 4-6 / >6 blood <50% / >50% / just blood pyrexia no/ no/ yes tachycardia no/ no / yes anaemia no/ no/ yes ESR no / <30 / >30
MAYO SCORE - 4 areas = x/12 Frequency -1-2 stools > than normal -3-4 stools >than normal ->4 stools than normal per day
Rectal Bleeding
- blood present <50% time
- blood present >50% time
- passing blood alone
Endoscopic Findings
physician’s global assessment - systemic features
GLobal assessment
pyrexia / tachycardia / BP (HD stability)
Not a diagnostic tool
good for assessment
Remission is often defined as a total score of 2 or less with all individual categories ≤1.
Most clinical trials define mucosal healing as an endoscopic score of 0 or 1
How is UC managed
- Score presentation (MAYO / TW) + Xray
- Stool culture + screen TB HAV HEV HBV HCV CMV EBV
- Start IV hydrocort - review after 72 hours
- Oral pentasa / rectal pentasa 2.4g / mesalazine
- left sided tisease mainly rectal preps - Endoscopy to assess + biopsy
- Ciclosporin / tacrolimus for steroid resistant disease
- infliximab
- colectomy
In states of remission can be weaned onto azathioprine or mercaptopurine - may need maintenacne infliximab if this fails
Differential for raised isolated ALT
Viral hepatitis
Blood transfusion - think HCV or HBV
e.g. haemophiliac
What is Achalasia
Failure of LOS relaxation 1/1000 PEOPLE
manometry = failure of peristalsis in distal oesophagus Endoscopy = normal or LOS fails to relax on swallow
intermittent symptoms
hallitosis from residual food
aspiration due to recurrent nocturnal aspiration
How is an acute variceal bleed managed
- Resus - activate major haemorrhage protocol
2 fluids and blood products - urgent variceal banding and commence terlipressin
TERLIPRESSIN / SOMATOSTATIN / OCTREOTIDE
good evidence to support reduced re-bleeding rate and early complications
Sclerotherpay is superior to balloon tamponade but not to banding
How is PBC treated
Remember PBC 90% female with ANTI MITOCHONDRIAL ABS >45 smokers post pregnancy trigger intrahepatic biliary only NO CANCER NO IBD RA / hashimotos + sjorgrens +coeliac
UDCA
Response to UDCA predicts better outcome
failed response add in budesonide / pred
Colestyramine for pruritis (binds bile salts for excretion)
Osteoporosis
Bisphosphonates and exercise
Vit D
Liver transplant
Once jaundiced survival is <2 years
How is PSC treated
Remember PSC Intra or extrahepatic biliary Associated with anti-smooth muscle PR3 - anca (P-ANCA) and ANA 60% men non smokers ASSOC IBD and HCC / COLON
no cure - same as PBC
Treatment
UDCA
bisphosphonates and vit D and diet + oestrogens
Liver transplant
What does Barium swallow show in Achalasia?
what other differentials are raised
Birds beak appearance caused by barium hold up caused by impaired peristalsis and failure of LOS relaxation
Diffs:
Oesophagial Ca - pseudo achalasia
Compressive bronchial cancer
manometry gold standard
progress to endoscopy to visualise
What would achalasia look like on manometry
Raised resting LOS pressure
non propagated lower oesophagial body contractions
How do you monitor for lithium toxicity?
raised GGT
raised lithium levels
