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
How is ALD monitored
AST: ALT ratio
ALD = AST x2 : ALD i.e. ratio >2 abdo USS Na recurrent ascites HCV/HBV status ALC liason nurse
What is Peutz Jeghers syndrome
Autosomal dominant condition more common in Ashkenazi Jews
MUTATION IN serine threonine kinase 11
Significant risk of malignant tranformation
almost 50% with PJ develop cancer and die by age 57
STOMACH / COLON / PANC / BREAST
- macular oral pigmentation crossing vermillion border
(mucocutaenous melanocytic macules) - hamartomatous polyps
Mx:
yearly mammography / uss
endoscopy yearly
abdo uss
What is Plummer Vinson Syndrome
Triad:
Iron def
Oesophagial webs + Dysphagia
Angular chelitis
RF for SCC of oesophagus
What is Tropical Sprue
Diagnosis of exclusion for state of malabsorption on returning from abroad
Typically thought to be due to floral imbalance
Common caribbean and far east
small intestinal malabsorption due to infection
See villous atrophy
crypt hypertrophy
megaloblastic / macrocytic anaemia due to folate and b12
fat malabsorption
Rx: abx for 6/12
Tetracyclin
ampicillins
b12 and folate replacement
What is Pellagra
Deficiency of niacin or tryptophan (precursor)
A) Primary deficiency
B) Secondary
- malabsorption state e.g. tropical sprue / coeliac
-consumptive state - carcinoid tumours use native tryptophan and convert this to serotonin. This prevents production of niacin and thus pellagra
diarrhoea dementia dermatitis death
confusion / inattention / memory loss / thick skin
Substrate for serotonin production
deficiency = dementia
replace with nicotinic acid
How can boehaaves present?
Spontaneous oesophagial rupture secondary to vomiting
- Epigastric pain radiating to back
- dyspnoea
- pleural effusion
- empyema
- surgical emphysema of neck
What are side effects of ileal resection
SBS -chronic malabsorption of b12 / folate (IF binds b12 for absorption ileum) - macrocytic anaemia - Dermatitis (no linoleic acid absorption) -chronic diarrhoea + dehydration -dumping syndrome -weight loss - bile salt malabsorption - fatty stools Abnormal 14C glycolate test (also seen in bacterial overgrowth and H.Pylori) - can also be done with 13C
Rx: Parenteral nutrition loperamide codeine teduglutide = GLP-2 agonist which slows gastric transit and after 6 months reduces TPN top up requirments by 20-100%
What is Zollinger Ellison syndrome
Heightened Gastrin production - GASTRINOMA
- FASTING GASTRIN LEVEL ON 3 SEP DAYS
-release is pulsatile
3 normal = gastrinoma unlikely - secretin stimulation test
- basal acid output
Treatment:
Excision
ocreotide
IFN / chemo
What are the extra GI manifestations of CD
- PSC (anti smooth muscle / malignancy / UDCA / >men)
- seronegative spondyloathropathy or RA like
- Uveitis or episcleritis
- PYODERMA GANGRENOSUM (failed wound healing / stoma ulcers / new ulcers - TOPICAL TAC / oral/ IV pred or inflix or tac)
- Gall stones- Bile acid malabsorption and Bact overgrow
- erythema nodosum
What mutation is the most common in the HFE gene
C282Y
What is the treatment for NASH
weight loss
What causes MALT lymphoma?
B cell lymphoma associated with H.Pylori infection.
Urease 13/14 breath test
drink radio-labelled compound
detect radio-isotope in expired breath only if h.pylori present
treat anyway due to incidence of fa;se negative
Treatment:
1 H.Pylori eradication = remission in 75% of cases
if not - chemo and resect
What is Whipple’s disease?
Whiipples = coeliac+ mulitsystem + wobbly and fatal
Rare multi system disorder caused by T.Whippelei.
- cardiac / pericarditis / endocard / conduction defects
- Diarrhoea
- weight loss
- cerebellar ataxia / seizures / CN lesions
- pleurisy / fibrosis
- pigmentation
- fatty stool
- lymphadenopathy
Diag:
histology
Acid Schiff positive mcrophages in small intestine mucosa
flattened villi - Coeliac / tropical sprue
Treat abx
30% relapse
What are the sequelae of entamoeba hystolica infection?
Fever abdominal pain weight loss malabsorption watery diarrhoea
liver abscess - usually single right lobe
mutliple left sided abscesses also possible
Rx:
trophozoite is susceptible to metronidazole
10 day course
When should diarrhoea be treated with antibiotics?
Conditions:
Pyrexia
>6 stools per day without improvement after 72 hours or worsening symptoms
HD compromise
no history of IBD
What medications are used in liver transplant?
Immunosuppressive therapy options following liver transplantation • Cortisone preparations (e. g. prednisolone or prednisone) • Cyclosporin A • Tacrolimus • Azathioprine • Mycophenolate Mofetil • Combination of the above medications
What are the sequelae of C. Diff
PSEUDOMEMBRANOUS COLLITIS
Yellow plaques on flexi-sigmoidoscopy
Mort in elderly = 10%
Rx:
Vancomycin - oral = 0 absorption so good for gut treatment
Metronidazole
Cholestyramine may be useful to reduce diarrhoea
How does fatty liver of pregnancy present?
Late onset in gestation
DIC
raised wcc
Raised ALT
Nausea and vomiting
low albumin
prolonged PT indicating abnormal synthetic function
encephalopathy if enters decoompensated liver disease
May need ITU admission
May also require FFP / cryo precipitate
protein restriction to reduce ammonia
laxatives
Intrahepatic cholestasis of pregnancy
Bile acid transporter defect
Last trimester
Prutiris
jaundice
prolonged PT due to vit K deficiency
Selective B12 deficiency with normal folate
B12 is coupled to IF for absorption in TI Therefore a) ileal disease Crohns ileal resection TB
b) Pernicious anaemia
c) b12 excess utilisation with little to absorb bacterial overgrowth diverticula fistulae radiation enteritis systemic sclerosis
How does Haemochromatosis present and how is it managed?
Iron storage disoder leading to iron overload and deposition in organs causing systemic dysfunction and CLD.
- weakness
- fatigue
- bronze diabetes
- impotence
- depression
- Cardiomyopathy
- Signs of CLD
Most common mutation
C282Y = HFE mutation
Diagnosis
1) transferrin saturation >55%
2) genotyping
3) biopsy if remains unclear
RX:
Weekly venesection until transferrin <16%
Aim ferritin <50%
Desferoxamine iron chelation
What are the causes of acute pancreatitis and how is it graded?
Glasgow criteria for pancreatitis:
PANCREAS - >3 = severe
Pa02 <8 Age >55 Neutrophils >15 Calcium <2 (norm 2.25-2.5 mmol/l) Renal Urea >16 Enzymes - LDH>600 or ASt>2000 Albumin <32 Sugar >10
Causes: I GET SMASHED
IDIOPATHIC
GALL STONES
ETOH
TRAUMA or Mechanical - sphincter of Odi dysfunction
STEROIDS
MUMPS
AUTO IMMUNE IGG4
SCORPION STINGS
HEREDITARY and hypercalcaemia and hypertrigyceridaemia - CF / PRIMARY CILIARY DYSK / AIH
ERCP
DIURETICS - THIAZIDE / THIAZIDE LIKE / LOOPS
What is a sensitive marker for measuring lithium toxicity?
GGT
What LFT ratio is common in ALD?
AST:ALT
2:1
OGD confirms low grade dysplasia - next step?
6 monthly OGDs
Oral omeprazole 40mg OD or equiv
How is bacterial overgrowth syndrome managed?
How might it present?
What is it associated with?
Associations:
SBS post small bowel
- crohns
- obstruction / mechanical / ischaemic /
Dumping syndrome in Ziehl Niehsson gastrinoma
Systemic sclerosis
Wartery diarrhoea
malabsorption
Fatty vitamin dieficiency - prolonged INR / steatthorhoea / offensive stool / b12 def - mixed motor and sensory neurop / folate def = macrocytic anaemia / iron def anaemia (normocytic or micro) / bile salt malaborption
Test:
Increased hydrogen on H breath test
Acute management of UGIB?
A BLATCHFORD AT PRESENTATION ROCKALL POST ENDOSCOPY 1. Massive transfusion protocol + /- sengstaken tube 2.PLT transfusion only if - PLT<50 - active bleeding 3. FFP if PT is x1.5 4. Reverse Warfarin with PTC / berryplex 5. Prep endoscopy
What is the blatchford score used for?
Stratify patients based on risk of mortality into intervention tiers
- Hb
- urea
- BP
- M/F
- HR>100
- meleana?
- syncope?
- liver disease?
- HF?
0 = likely no need for intervention
>0 = itervention
higher scores corrolate with mortality
Management of Variceal bleed?
A BLATCHFORD AT PRESENTATION ROCKALL POST ENDOSCOPY 1. Massive transfusion protocol + /- sengstaken tube 2.PLT transfusion only if - PLT<50 - active bleeding 3. FFP if PT is x1.5 4. Reverse Warfarin with PTC / berryplex 5. IV Terlipressin for 5 days 6. Neomycin or rifaximin 5. Prep endoscopy
Oesophageal varices
- band ligation
- Transjugular intrahepatic portosystemic shunts (TIPS)
Gastric varices
- endoscopic injection of N-butyl-2-cyanoacrylate
- TIPS ifnot controlled by N-butyl-2-cyanoacrylate.
What is the evidence behind PPI use in UGIB?
Reduces rebleed risk by 50% and surgical intervention by 40% - meta-analysis of 21 RCTs
H2 inhibitors (ranitidine) are less effective
Note for PPI post stabilisation!
HCV is associated with what renal problem?
Can be associated with a mixed cryoglobulinaemia
can present at ay time
Associated with systemic vasculitis and purpuric presentation
This may result in nephritic presentation
Treatment is focused on the reduction of systemic viraemia which is though to drive the process
Note there may be crossover in HIV
HIV associated nephropathy is an FSGS pattern and associated with heavy heavy proteinurea
GORD management
History sodium alginate lansoprazole omeprazole -both associated with lymphocytic colitis and hyponatraemia -omeprazole can also interfere with cyt p450 OGD h.pylori eradication
What is pyoderma gangrenosum associated with?
Crohns
treat with topical tac
oral pred
iv hydrocort if widespread
How can SBS be managed?
Parenteral nutrition Creon loperamide codeine teduglutide = GLP-2 agonist which slows gastric transit and after 6 months reduces TPN top up requirments by 20-100%
How can NASH be managed?
diet weight loss Liraglutide - reduces hepatic steatosis - aids weight loss -stabilises glycaemia TIPS / banding / terlipressin
Evidence of decompensated CLD
Ascites
Asterixis
Altered GCS
Causes hepatomegally x3
Alcohol related liver disease
Congestive cardiac failure
Metastases
Plus
Infection
Auto immune (PSC PBC AIH)
Infiltrative (amyloid CML)
Cirrhosis investigation
Liver screen HAV HBV HCV CMV EBV HIV A1 ANTI TRYPSIN AFP Ferritin if >500 HFE AND IN 30s Caeruloplasmin and Copper AIH - antimitochondrial
Plus
INR AND ALB for synthetic function LFTs Liver biopsy Liver USS with Dopplers ERCP (PSC brushings )
Malignancy Ix
CXR AND CT PET LIVER BIOPSY MDT RESECTION RFA
Complications of Cirrhosis
Hepatic Encephalopathy G1 disorientated G2 Confused G3 fluctuant GCS cannkt fimmow commands G4 Flat and depressed GCS and death SBP Wcc >250 on tap Variceal haemorrhage
Child Pugh score
Prognostic indicator of mortality 1 year Encephalopathy Ascites Inr and albumin Br
<6 100%survival 1 year
7-9 81% survive 1 year
10-15 45% survive 1 year
Treatment ascites
Drain Pleurex (palliative) Abstinence Low salt and nitrogen diet Spironolactone Transplant
Causes splenomegally
Massive >8cm
Myelofibrosis or myeloproloferative (P rubra vera) and CML CLL or Non hodgkins or hairy cell lymphoma
Malaria and Leishmaniasis
Moderate >4cm Myelofibrosis or proliferative Haemolysis Chronic Infectious hepatitis or EBV Gaucher amyloid sarcoid TV
Minor Tip
ITP / AIHA /Haemolysis
Portal HTN
Infection acute Hav hev hbv hcv ebv htlv
Myeloproliferative or lymphoproliferative CML / MYELOFIBROSIS Infectious Malaria/ TB/ Leishmaniasis Haemolysis B THAL / ITP /Autoimmune /sickle cell Infiltrative Gaucher / amyloid/ sarcoid
Splenomegally screen
FBC - raised wcc - raised plt - raised rbc / rdw Calcium and ACE LFTS BNP Viral screen ABDO USS FILM nuclear inclusions / blasts - myeloprololif Smear +ve old small wcc - CLL Tear drop poikilocytosis high basophil and eosonophil myeloproliferative
Hb electrophoresis
SPECIAL JAK 2 for Polycythaemia rubra vera BCR ABL for CML Protein elec and IGs for MGUS SMG MM MPL for myelofibrosis Malaria screen thick and thin film trophozoites
Reasons for liver transplant
CIRRHOTIC LIVER DISEASE -ALD NAFLD SARCOID AMYLOID Acute liver failure -PCT OD and Viral hep plus PBC PSC HCC -HFE / viral hep / etc
Causes Gum Hypertrophy
Ciclosporin Nifedipine Phenytoin Scurvy AML Pregnancy Familial
Transplant skin signs
Bcc and Melanoma X 10 Scc X 100 Acitinic keratosis Viral warts Cellulitis
Transplant side effects
Immunosuppression -PCP / CMV / viral hep or TB Side effects -Tac tremor and HTN Ciclosporin gumnhypertrophy and nephro tox -Chronic Rejection Minor HLA incompatibility Recurrence of original disease Skin malignancy Other malignancy or lymphoma
Liver transplant causes
CIRRHOSIS
ALF
HCC