Gastroenterology and hepatology Flashcards
how do the areas of the GI tract affected by Crohn’s and UC differ?
Crohn’s- can affect anywhere from mouth to anus, transmural inflammation but discontinuous= skip lesions, commonly affects terminal ileum and prox colon
UC- always affects the rectum, and extends proximally, continuous distribution, although may not look this way as result of local tment, superficial inflammation (mucosa and SM) so no fissures, fistulae or strictures.
what term is used to diagnose ptnts in whom it is impossible to distinguish between UC and isolated colonic Crohn’s?
indeterminate colitis
microscopic appearance of Crohn’s?
non-caseating granuloma- differentiate from caseous in colonic TB, and TNF has major role
lymphoid hyperplasia and neutrophil aggregates
goblet cells present
transmural inflammation
microscopic appearance of UC?
crypt abscesses
goblet cell depletion
chronic inflammatory cell infiltrate in lamina propria
superficial inflammation
macroscopic appearance of UC?
erythematous and inflamed mucosa, bleeds easily (very friable)
mucus discharge
ulceration continuous
3 key features of colitis?
bloody diarrhoea (includ. nocturnal)
urgency- ?ptnt exerience of incontinence, not making toilet in time
tenesmus
macroscopic appearance of Crohn’s disease?
skip lesions
thickened bowel wall with strictures, repeated healing attempts cause extensive fibrosis and TGF-beta has key role.
deep ulcers and fissures, ulcers may appear as apthous ulcers- white spots
cobblestone appearance due to linear ulceration which is separated by normal mucosa
why do ptnts with UC experience urgency?
solid stools irritate inflamed mucosal lining producing pain, so rapid transit, BUT ptnts can have proximal constipation for which a laxative may have to be used as proximal transit slowed despite rapid transit distally in L sided disease (below splenic flexure), and relief may allow remission of L sided disease.
AXR appearance of UC?
thickened white line of bowel wall due to oedema, increasing distance between bowel loops
white protrusions of bowel- inflammatory ulcers and assoc. oedema, thick haustra= thumb printing due to mucosal thickening
lead pipe sign=featureless colon in longstanding UC with loss of normal haustral markings, so just air filled bowel
incidence of UC?
10-20 per 100,000 per year
prevalence= 100-200 per 100,000
how is severity of UC classified?
mild= less than 4 stools per day, no systemic upset moderate= 4 to 6 stools per day, minimal disturbance severe= more than 6 stools per day, with blood and systemic disturbance.
Truelove and Witts criteria:
mild=less than 4 motions per day, small amount rectal bleeding, apyrexial, HR less than 70, Hb more than 11g/dL, ESR less than 30mm/hr
moderate=4-6 motions, moderate PR bleeding, temp 37.1-37.8, HR 70-90, ESR less than 30, Hb 10.5-11
severe=more than 6 motions/day, large PR bleeding, temp more than 37.8, HR more than 90, Hb less than 10.5, ESR more than 30.
why do an AXR in suspected UC?
look for toxic megacolon
look at extent, absence of solid stool in inflamed colon
look for proximal constipation
define toxic megacolon
transverse colon more than 6cm in diameter with loss of haustration
indications for colonoscopy in UC?**
performed at later date to determine proximal extent, and screen for colorectal Ca
surveillence colonscopy starts after 10 yrs of disease
require yearly colonscopy if co-existing primary sclerosing cholangitis-non-malignant, non-bacterial inflammation, fibrosis, and strictures of intra- and extrahepatic bile ducts, due to higher risk of CR Ca.
what is important in management of ptnts with UC and primary sclerosing cholangitis?
must have yrly colonscopy as higher risk of bowel Ca development
PSC= cholestatic liver disease with biliary stricturing and dilatation
extra-intestinal manifestations of IBD related to disease activity?
erythema nodosum
apthous ulcers
episcleritis
acute arthropathy
why is LMWH given to pts with IBD?
IBD= pro-thrombotic state- risk of DVT and PE
and may treat colitis as helps with microvascular occlusion
why must frequent Us and Es be taken for ptnts given mesalazine as maintenance of remission in UC?
risk of interstitial nephritis
why can azathioprine not be used in acute flares of UC?
takes at least 6 wks for onset of action
MOA of ciclosporin?
calcineurin inhibitor- a protein required in activation of T cells which mediate an inflammatory response
a patient presents complaining of bleeding per rectum. what qns should be asked regarding the bleeding to differentiate between UC, colorectal Ca and diverticular disease?
pain?- all are painless, pain in diverticular disease only if acute diverticulitis, and in Ca if distally placed in rectum or in anal canal, causing tenesmus
blood relation to stools- mixed in with loose stools+mucus=UC, large volume in pan= diverticular disease, mixed in with stool, espec. if prox. tumour in Ca.
colour, volume
bleeding PR: timings, prev.episodes,progression?volume?colour?relation to stools?pain?other assoc. symptoms e.g. tenesmus, urgency, constipation.
assoc with diarrhoea-?mucus and waking up at night to open bowels-UC
Ca-?weight loss, tenesmus, diarrhoea and/or constipation
presentation of oesophageal hypermotility disorders e.g. Nutcracker oesophagus?
retrosternal chest pain, possible radiation to back, and persisting discomfort following acute episodes
dysphagia
heartburn
how are all oesophageal hypermotility disorders diagnosed?
manometry-pressure evaluation
definition of classical Barrett’s oesophagus?
columnar mucosa extending 3 or more cm into tubular oesophagus
=metaplasia=reversible change from 1 differentiated cell type to another fully differentiated cell type
incidence of adenocarcinoma of oesophagus in pts with barrett’s oesophagus?
1 in 100 pt yrs
definitive diagnosis of barrett’s oseophagus?
oesophageal biopsy via endoscopy
tment of barrett’s oesophagus?
lifestyle advice: lose weight, stop smoking, avoid alcohol, raised head of bed at night, eat small regular meals, avoid hot drinks, alcohol and eating within 3 hrs of going to bed, avoid drugs that affect oesophageal motility or damage the mucosa e.g. anticholinergics, nitrates, NSAIDs, bisphosphonates
LT PPI therapy
aspirin
must try and prevent progression to adenocarcinoma-5% lifetime risk in men and 3% in women, 40-50% of those with barrett’s and severe dysplasia go on to develop adenocarcinoma within 5 years.
when no dysplasia, if surveillence considered appropriate should be every 2-5 years depending on length of affected segment and presence if intestinal metaplasia
?over whether medical or surgical intervention can result in clinically meaningful regression of the barrett’s epithelium or reduce risk of subsequent malignancy.
low-grade dysplasia-after confirmation by 2 pathologists, surveillence every 6 months. may consider endoscopic radiofrequency ablation or photodynamic therapy. should allow regrowth of squamous epithelium.
photodynamic therapy- with laser +/- photosensitising agents to ablate dyslastic epithelium is being used, due to high mortality of surgery-7%.
Consider using radiofrequency ablation or photodynamic therapy alone for flat high-grade dysplasia.
Consider using endoscopic mucosal resection alone for localised lesions, use circumferential endoscopic mucosal resection with care because of the high incidence of stricture formation and consider following with an additional ablative therapy.
if suitable for surgery and wish to have this, oesophagectomy indicated in high grade dysplasia and intramucosal Ca.
if residual or recurrent disease, offer EMR or ablative therapy or both.
complication of achalasia?
squamous cell carcinoma of oesophagus, thought to be due to food stasis and mucosal irritation
aetiology of achalasia?
may be related to viruses or AI
known that myenteric plexus ganglion cells are reduced, and the non adrenergic non cholinergic inhibitory innervation to LOS, mainly via NO to cause relaxation, is impaired.
clinical features of achalasia?
dysphagia- both solids and liquids
regurgitation
weight loss
chest pain- linked to oesophageal spasm
findings of radiological investigation of achalasia?
CXR- may see air-fluid level due to dilated oesophagus
barium swallow- dilated oesophagus with reduced peristalsis
why is endoscopy performed in suspected achalasia?
to exclude mucosal pathology and pseudo-achalasia
what does oesophageal manometry reveal in achalasia?
raised LOS pressure and incomplete/absent sphincter relaxation
what is pseudo-achalasia?
oesophageal dilatation and dysphagia, usually due to malignant obstruction
complications of surgical myotomy for achalasia?
reflux
this is also a complication of endoscopic dilatation, which also poses the risk of perforation
define irritable bowel syndrome
a common recurrent chronic illness, characterised by abdominal pain/discomfort and disturbed bowel habit, but no recognised pathology or specific cause.
what are the Rome II diagnostic criteria for IBS?
at least 12 wks of abdo discomfort/pain in preceding yr with 2 or more of: relief by defecation, onset assoc. with change in stool frequency, onset assoc. with change in stool appearance.
symptoms supporting a diagnosis= abnormal stool frequency abnormal stool form difficulties in evacuation mucus passage bloating or feelings of distension
clinical features supporting IBS diagnosis?
Rome II criteria
long history with relapsing and remitting course
exacerbations triggered by life events
coexistence of anxiety or depression
assoc with symptoms in other organ systems
symptoms aggravated by eating
clinical features suggesting organic disease other than IBS?
onset in old age progressive deterioration fever weight loss rectal bleeding steatorrhoea dehydration
investigations in suspected IBS?
routine hamatology/BC
sigmoidoscopy with rectal biopsy (if diarrhoea)
if diarrhoea persistnet, serum B12, folic acid, iron studies, TFTs, coeliac Abs, LFTs, and stool microscopy
consider colonoscopy to exclude microscopic colitis
faecal urgency or incontinence suggest need for anorectal manometry
examples of alternative therapy in IBS tment?
physical therapy e.g. massage, acupuncture, reflexology, to work on tension release
meditation and hypnotherapy- produce focused relaxation which may facilitate cognitive behavioural change.
drugs used in IBS management?
antispasmodics for abdo pain e.g. mebeverine-synthetic anticholinergic, hyoscine butylbromide (buscopan)- anticholinergic/anti-muscarinic, MR peppermint oil capsules-local effect of colonic relaxation, and inhibits smooth muscle activity via interference with Ca2+, alverine citrate-spasmolytic.
antidiarrhoeal e.g. loperamide-synthetic opioid, and colestyramine-bile acid sequestrant
anticonstipation e.g. macrogols-osmotically acting laxative
antidepressants e.g. TCAs, SSRIs
considerations in management of diet in IBS pt?
pt may keep a food diary to detect food intolerance and eliminate these from diet, and speak to a dietician
exclusion diet- start off with bland diet for few days, slowly introd. favourite foods to identify a precipitating food.
illnesses which overlap with IBS?
fibromyalgia
chronic fatigue syndrome (ME)
how does recent rise in incidence of Crohn’s disease support role of enviromental factors in disease pathogenesis?
part. importance of smoking and diet
diet= some pts may have problems handling saturated FA
and smoking worsens disease possibly due to effect on microvasculature.
how do clinical features of Crohn’s differ from those of UC?
Crohns typically abdo pain and diarrhoea, may be weight loss, anorexia and fever, gross rectal bleeding and acute haemorrhage uncommon.
colonic crohn’s may present with bloody diarrhoea, but tenesmus less common than in UC as rectum less commonly affected.
gastroduodenal crohns can present as H.pylori -ve peptic ulcer disease.
EI manifestations of Crohn’s?
Eyes- scleritis, episcleritis, anter. uveitis
Joints- enteropathic arthritis assoc. with HLA-B27 and AS, typically large joints e.g. sacroileitis.
Skin- apthous ulceration, erythema nodosum, pyoderma gangrenosum-responds well to topical steroids and infliximab
metabolic bone disease- osteopenia with disease and as result of steroid tment of disease
venous and arterial VTE
GSs, fatty liver, AI hepatitis and primary sclerosing cholangitis
renal oxalate stones
when is MRI used in Crohn’s?
for imaging perianal or pelvic fistulating disease
micro and macroscopic evaluation favouring Crohn’s over UC?
transmural, granulomas, small-bowel disease, mainly R sided colonic disease, rectal sparing, fistulae (can be seen on US), perianal disease.
aim of crohn’s disease management?
NO CURE, so induce and maintain remission
indications for surgery in Crohn’s disease pts?
haemorrhage intra-abdominal masses obstruction as fibrotic strictures medically intractable fistulae toxic megacolon cancer
MOA of azathioprine?
pro-drug activated to 6-MP, which is a purine antagonist
elimination requires TPMT, so activity must be measured before commencing tment.
NICE recommendations for induction of remission in Crohns?
glucocorticosteroid e.g. prednisolone if 1st pres. or single inflammatory exacerbation in a yr
consider enteral nutrition as alternative in young if worried about growth retardation
consider adding azathioprine or 6-MP if 2 or more inflammatory exacerbations in 1 yr or can’t reduce steroid dose.
consider MTX if can’t take azathioprine or 6-MP
consdier infliximab or adalimumab if severe active disease not responding to conventional tments
NICE recommendations for remission maintenance in Crohns?
azathioprine or mercaptopurine
MTX considered only if needed to induce remission, or didn’t tolerate azathioprine or mercaptopurine for remission, or have CIs to these.
NICE recommendations for remission maintenance in Crohn’s after surgery?
azathioprine or mercaptopurine if adverse prognostic factors e.g. >1 resection, or previously debilitating/complicated disease e.g. abscesses, fistualising disease.
5-ASA tment may be considered e.g. mesalazine (pentasa).
investigations in Crohn’s?
FBC-?anaemia, leucocytosis, raised platelets-reactive to inflammation
iron, total iron binding capacity (TIBC), B12, folate
CRP-raised
LFTs- INR and albumin-lowered
low Ca2+, Mg2+, zinc- zinc important in tissue healing
Stools culture for C. difficile toxin and infectious cause of colitis
endoscopy-colonoscopy-allows mucosal biopsy and balloon dilatation of strictures
barium follow through- evaluate small bowel
USS- thickened bowel, fistulae and abscesses
CT- extraluminal features, blood flow
MRI- perianal or pelvic fistulating disease
NICE guidance for inducing remission in UC with proctitis and proctosigmoiditis?
proctitis and proctosigmoiditis: mild to mod 1st pres. or inflam. exacerbation, offer topical ASA alone- suppository or enema, or add an oral ASA to topical, or oral ASA alone although not as effective as 1st 2 options.
if unable to have aminosalicylate, consider topical corticosteroid or oral pred
if subacute pre, consider oral pred
NICE guidance for inducing remission in UC with L sided and extensive UC?
high induction dose of an oral ASA, and consider adding a topical ASA or oral beclometasone dipropionate
same for children and young people, but not high induction dose of oral ASA
oral pred if decline ASA/CI, or subacute UC
step 2 therapy in treating mild to mod UC?
consider adding oral pred to ASA in remission induction if no improvement within 4 wks, or worsening. stop becl dipro if adding pred.
consider adding oral tacrolimus to oral pred. if inadequate response to oral pred. after 2-4wks
NICE guidence for remission induction in acute severe UC?
IV corticosteroids, and assess likelihood for needing surgery
if not steroids, consider IV ciclosporin or surgery
NICE guidence for maintenance of remission in proctitis and proctosigmoiditis in UC?
topical ASA alone (daily or intermittent) or plus an oral ASA or just oral ASA although not as effective
NICE guidence for maintenance of remission in L sided and extensive in UC?
low maintenance dose of an oral ASA in adults
oral ASA in children and young adults
consider pt pref, ADRs and cost
oral ASA consider once daily dosing for increased effectiveness, but may be more ADRs.
when is oral azathioprine or mercaptopurine considered in UC?
as maintenance of remission after 2 or more inflammatory exacerbations in 12 mnths that require tment with systemic corticosteroids
or if remission not maintained by ASAs
also considered after single episode of acute severe UC for remission maintenance- consider ASAs if these are CI, not tolerated or declined.
difference between a suppository and enema for ASA administration in inducing remission in proctitis in UC?
suppository= solid placed into rectum, slowly dissolves enema= liquid or gas injected into rectum
MOA of mesalazine (an aminosalicylate)?
intestinal anti-inflammatory drug
inhibits leucocyte chemotaxis and cytokine prod. and scavengers for free radicals.
ADRs of mesalazine?
common= GI= diarrhoea, abdo pain, N+V, general=headaches, and skin= rash rare= leucopenia, thrombocytopenia, peripheral neuropathy, pancreatitis, lupus erythematosus type reactions, renal failure.
ADRs of azathioprine?
myelosuppression-leucopenia, anaemia, thrombocytopenia, neutropena nausea neoplasma e.g. NH lymphoma cholestasis-raised ALP, jaundice, LFT deterioration, liver impairment interstital nephritis hair loss myalgia arthralgia
why should pts with PSC have yrly abdo ultrasound
due to risk of malignant GB polyps/GB cancer e.g. cholangiocarcinoma- cancer of CBD.
azathioprine drug class?
antiproliferative immunosuppressant
symptoms and signs of toxic megacolon?
those assoc. with exacerbations of crohns and UC include abdo pain abdo tenderness diarrhoea, repeat, bloody distension fever tachycardia shock dehydration
define severe active Crohn’s disease necessitating anti TNF tment?
very poor general health and 1 or more of the following: severe abdominal pain, fever, weight loss and usually frequent (3-4) stools daily.
Crohn’s disease activity index (CDAI) of 300 or more, or a Harvey-Bradshaw score of 8-9 or above.
what is the Glasgow alcoholic hepatitis score (GAHS) used for?
to help in prognosticating pts with alcoholic liver disease predicts mortality based on age WCC blood urea nitrogen (BUN) bilirubin PT PT lab normal
9 or more is a predictor of mortality
(75% mortality at 28 days?, and anyone with alcoholic hepatitis 50% mortality at 28 days?)
components of tment in alcoholic liver disease (ALD)?
alcohol withdrawal
abstinence
nutrition- enteral preferred, parenteral- line sepsis, line thrombosis, electrolyte imbalance, mechanical trauma. also shouldn’t restrict protein despite fear over hepatic encephalopathy.
glucocorticoids- block inflammatory and cytotoxic pathways in alcoholic hepatitis
anti TNF alpha e.g. pentoxifylline, with elevated TNFalpha levels found to be predictive of poor survival in alcoholic hepatitis pts.
liver transplantation in decompensation
medications used for hepatic encephalopathy?
Rifaximin (antimicrobial) is recommended as an option for reducing the recurrence of episodes of overt hepatic encephalopathy in adults.
?metronidazole?
what is calcineurin (inhibited by ciclosporin used in UC tment)?
a protein phosphatase involved in T cell activation
aim of a low residue diet in Crohn’s disease pts?
may help in inducing and maintaining remission as involves a diet that avoids high fibre foods as fibre can cause cramping, and lower fibre means less residue (undigested portion of food) so less stools.
Pts should avoid legumes, most raw fruit and veg, potato skins, milk, caffeine, most whole grain foods e.g. bread and pasta.
ideal marker of liver synthetic disruption to help determine timing/need for orthotopic liver transplantation?
PT
so do not correct elevated PT e.g. with FFP, unless pt actively bleeding.
indications for liver transplantation in CLD?
refractory ascites, hepatic encephalopathy and variceal bleeding (not effectively controlled by medical/endoscopic therapy) after 1st episode of SBP, as predoicts 50% 2 yr mortality. poor QOL e.g. pruritis, severe fatigue in cholestatic liver disease e.g. PBC Child-Pugh score >7= score of 1-3 given for 5 variables, with 3 being most severe=total bilirubin, serum albumin, PT, ascites and hepatic encephalopathy, with class C=score 10-15, with 45% 1 yr survival, and MELD score (model for endstage liver disease- determines % mortlaity in CLD without transplant)= indicators for need of referral.
other than low PLTs, why do many pts in hospital have some degree of abdominal bruising?
result of SC VTE prophylaxis injections e.g. dalteparin
contraindications to liver transplantation?
active sepsis
advanced CP disease
extrahepatic/extensive intrahepatic malignancy
active alcohol dependency or substance abuce- most programmes require 6 mnths abstinence prior to transplantation for alcoholic cirrhosis.
psychosocial factors that impair pt’s ability to comply with immunosuppressive tment
HIV was previously but now improved ART and comparable graft survival so may be considered, although reduced post transplant outcomes.
what does a Glasgow Alcoholic Hepatitis Score (GAHS) of 9 or more indicate?
50% mortality at 28 days
indicates need for steroids to treat hepatits
if score less than this, consider general factors in pt management- alcohol abstinence, adequate E + D, fluid intake, education on alcohol withdrawal and abstinence, ref to alcohol liason team, discuss need for physio/OT if necessary.
common drug now used to prevent recurrent episodes of overt hepatic encephalopathy?
rifaximin from rifamycin class of antibacterials, and inhibits RNA polymerase. may inhibit division of urea-deaminating bacteria, so reducing NH3 production.
excreted in the faeces
post liver transplant complications?
rejection- hyperacute- treat with re-transplant, acute- hgih dose IS, chronic- adjust IS but graft failure usual.
technical problems- VC thrombosis, haemorrhage, anastamotic leak
drug effect- increase infections, and ISs can cause hepatotoxic effects
INFECTION e.g. EBV reactivation
what is pabrinex?
indicated for severe depletion or malabsorption of water soluble vitamins B and C part. in alcoholism
(Parenteral thiamine)
how is hepatic encephalopathy assessed for?
hepatic flap?
AMT: is pt orientated to person, time and place
are there symptoms of drowsiness, confusion, or is pt unresponsive?
Pt may have positive Babinski test- big toe DF and fanning of the toes.
characteristic appearance on biopsy of primary sclerosing cholangitis?
onion skin fibrosis around the bile ducts
risk factors for non-alcoholic fatty liver disease?
obesity
HTN
hyperlipidaemia
type 2 DM
considered the liver component of the metabolic syndrome, and insulin resistance is universal.
management of NAFLD?
weight loss
good BP, lipid and diabetes control
exercise
pts most at risk of NAFLD progression following assoc. inflammation?
diabetics
how is NAFLD diagnosis confirmed?
fatty liver on USS
how is liver fibrosis enhanced by insulin resistance?
induces connective tissue GF
give 2 reasons for thrombocytopenia in liver disease?
reduced thrombopoietin prod which is dependent on functional liver cell mass and is required for platelet production
and portal hypertension leads to splenomegaly, causing sequestratioin of platelets by the spleen.
causes of cirrhosis and CLD?
alcoholic liver disease (ALD) hepatitis B hepatitis C primary sclerosing cholangitis primary biliary cirrhosis drugs e.g. MTX- so ensure review of pt's medications metabolic liver diseases NAFLD haemochromatosis AI hepatitis Wilson's disease alpha 1 antitrypsin deficiency-*emphysema Budd-Chiari syndrome secondary biliary cirrhosis cryptogenic
what must pts with liver cirrhosis be monitored for?
HCC- 3-6mnthly alpha fetoprotein and USS
osteoporosis-bone densitometry-DEXA, Ca2+ and vit D supplements
PH complications e.g. bleeding varices, so carry out OGD- if moderate to large varices seen can give primary prophylaxis to prevent bleed with non-selective beta blocker propranolol which reduces portal pressure
hepatitis infection- test immunity adn vaccinate as appropriate to reduce risk of decompensation following additional liver insult
malnourishment- give thiamine 100mg OD PO
what is Budd-Chiari syndrome (BCS)?
obstruction of main heaptic veins by thrombus
causes= thrombophilia e.g. myeloproliferative disorder, factor V leiden deficiency, HCC, chronic infection, IVC anomalies.
presentation of budd-chiari syndrome?
abdominal pain, ascites and hepatomegaly developing over several months.
Acute liver failure may rarely occur.
Variable jaundice.
How is Budd-Chiari diagnosed.
Doppler US or contrast CT
Site of hepatic vein obstruction can be defined with venography and venous pressure measurement.
May see caudate lobe hyper trophy due to separate drainage into IVC.
Ascitic fluid often an exudate-serum to ascites albumin gradient (SAAG) less than 11g/L (?more than?)
Do thrombophilia screen to identify underlying cause.
Management of budd-chiari syndrome?
Acute: thrombosis and subsequent anticoagulation
Liver transplant in acute liver failure.
Percutaneous tranche patio balloon angioplasty.
May do liver transplant in chronic syndrome, or transjugular intrahepatic portosystemic shunt.
Trent of bleeding oesophageal varices?
Variceal band ligation
Can follow with non selective beta blocker propranolol.
If bleeding not controlled with ligation then consider transjugular intrahepatic portosystemic shunts.
Trent of bleeding gastric varices?
Offer endoscopic injection of N-butyl-2-cyanoacrylate (a haemostatic glue) to patients with upper gastrointestinal bleeding from gastric varices.
TIPS if bleeding not controlled by injection.
How is endoscopic therapy used in tment of bleeding peptic ulcer?
Can inject adrenaline
How is Wernicke’s encephalopathy prevented in pts addicted to alcohol?
Prophylactic oral thiamine should be offered to harmful or dependent drinkers:
if they are malnourished or at risk of malnourishment or
if they have decompensated liver disease
or
if they are in acute alcohol withdrawal
or
before and during a planned medically assisted alcohol withdrawal.
Tment of Wernicke’s encephalopathy?
Parenteral thiamine (pabrinex) for minimum of 5 days, followed by oral thiamine.
NICE recommended interventions for harmful drinking and mild alcohol dependence?
Offer a psychological intervention (such as cognitive behavioural therapies, behavioural therapies or social network and environment-based therapies) focused specifically on alcohol-related cognitions, behaviour, problems and social networks.
Nalmefene is recommended as an option for reducing alcohol consumption, for people with alcohol dependence who have a high drinking risk level.
Drug regimen for assisted alcohol withdrawal?
BZD e.g. Chlordiazepoxide or diazepam
Consider lorazepam which has limited liver metabolism in pts with liver impairment, start on a reduced dose and monitor LFTs carefully.
Tment for acute alcohol withdrawal?
Consider offering a benzodiazepine or carbamazepine.
Offer oral lorazepam as first-line treatment for delirium tremens. If symptoms persist or oral medication is declined, give parenteral lorazepam, haloperidol or olanzapine.
For people with alcohol withdrawal seizures, consider offering a quick-acting benzodiazepine (such as lorazepam) to reduce the likelihood of further seizures.
When should liver transplantation be considered in de compensated liver disease?
still have decompensated liver disease after best management and 3 months’ abstinence from alcohol and
are otherwise suitable for transplantation.
What is the discriminant function in ALD?
Helps determine prognosis in severe acute alcoholic hepatitis
If 32 or more ? Corticosteroid tment
Importance of laxatives in liver cirrhosis?
Reduce risk of encephalopathy exacerbated by constipation.
grading of ascites that is not infected and not asssoc. with hepatorenal syndrome?
1=mild, only detectable by USS
2=moderate, moderate symmetrical abdo distension
3=large, marked abdo distension
2 types of refractory ascites?
diuretic-resistant-refractory to dietary Na+ restriction and intensive diuretic theray for at least 1 wk.
diuretic-intractable- refractory to diuretic tment due to development of diuretic induced complications so unable to use effective dose of diuretic.
causes of ascites?
liver cirrhosis malignancy-GI tract, ovary-Meig's syndrome, lymphoma, metastatic, often very painful heart failure nephrotic syndrome TB pancreatitis hypothyroidism protein losing enteropathy
presentation of a pt with ascites?
abdo distension weight gain abdo discomfort increasing dyspnoea nausea and loss of appetite
consider RFs for liver disease e.g. alcohol, chronic hep B or C, history of jaundice, and those assoc. with non-alcoholic steatohepatitis e.g. obesity, hyperlipidaemia and type 2 DM.
how much ascitic fluid must be present for shifting dullness to be positive?
1.5L
investigations in ascites?
UBIX:
Us and Es
FBC, LFTs, clotting screen, TFTs
USS- assess extent of ascites, and identify underlying pathology e.g. metastatic liver disease or carcinoma of ovary, CXR-pleural effusion, HF, pulmonary metastases
MRI if USS failed to reveal cause
ascitic tap- WCC, RCC-microscopy, culture, sensitivity, gram stain, cytology?
management of ascites?
salt restriction
diuretics- spironolactone 1st line in cirrhosis, 100mg/day can grad be increased to 400, must monitor K+.
furosemide can be used alongside if max doses of spironolactone reached, start with 40mg/day, must monitor for electrolyte disturbance e.g. hyponatraemia.
paracentesis if large or refractory, and give HAS if 5L or more being drained to expand plasma.
TIPS can be used if refractory ascites requiring more than 3 drainages per month
ascites complications?
hyponatraemia on diuretics
SBP-treat with 3rd gen cephalosporin
pleural effusions-dyspnoea
investigations following an ascitic tap
microscopy- WCC-neutrophils more than 250 cells per mm cubed diagnostic of SBP, RCC- usually less than 1000, but higher levels suggest underlying malignancy e.g. HCC. gram staining culture and sensitivity albumin or protein amylase
contraindications to performing an ascitic tap?
skin infection at proposed puncture site uncooperative pt pregnancy severe bowel distension coagulopathy e.g. DIC
features of post-paracentesis circulatory dysfunction?
hyponatraemia
AKI
increased plasma renin activity
why is an immunosuppressant given alongside and anti-TNF tment in Crohn’s disease?
It is thought that immunosuppressants may extend the inter-treatment interval and reduce development of antibodies to infliximab that in turn reduce efficacy and increase adverse effects.
define fulminant hepatic failure
severe hepatic failure in which encephalopathy develos in under 2 wks in a pt with a previously normal liver.
e.g. due to hep A, B, D, drugs, AI hepatitis, Budd-Chiari, Wilson’s disease.
what are the 2 types of cirrhosis that have been identified?
micronodular and macronodular
micro seen in ongoing alcoholic damage and biliary tract disease, regenerating nodules less than 3mm in size and liver involved uniformly, whereas macro= nodules of variable size and normal acini may be seen, often seen following chronic viral hepatitis.
best indicators of liver function?
serum albumin
prothrombin time
how is severity of liver disease assessed?
liver function- serum albumin and prothrombin time, albumin less than 28g/L=poor prognosis
liver biochemistry-usually elevation in ALP and aminotransferases, all deranged if decompensated disease
serum electrolytes- low Na+ indicates severe disease due to defect in free water clerance or excess diuretic therapy.
serum creatinine- if more than 130 micromol/L, then worse prognosis indicated.
serum alpha fetoprotien more than 200ng/ml, strongly suggests HCC.
how can type of cirrhosis be determined?
viral markers serum autoantibodies serum Igs total iron binding capacity and ferritin- hered haemochromatosis alpha 1 antitrypsin copper
what can imaging reveal in liver cirrhosis?
USS- increased echogenecity if fatty liver and fibrosis, marginal nodularity, HCC
CT-hepatosplenomegaly, dilated collaterals in CLD and HCC
endoscopy- for detection and tment of oesopaheal varices and portal hypertensive gastropathy
MRI-tumours
what is usually necessary to confirm severity and type of liver disease?
biopsy
only dietary restriction in pts with compensated cirrhosis?
reduce salt intake
major diseases in which LT survival is inhibited by disease recurrence after liver transplantation?
PSC
HCC
Hep C
medications which can cause gastric reflux?
NSAIDs alendronate Ca2+ caffeine Ca2+ ion channel blockers GTN
components of the glasgow alcoholic hepatitis score?
age BUN/urea bilirubin INR/PT WCC
what is faecal calprotectin?**
substance released into intestines when inflammation present
can be measured in stools sample to distinguish between IBS and IBD
if less than 50 micrograms/gram of stool, then likely to be IBS, and if 150 -200 micrograms/gram of stool or more then likely to be IBD.
lactoferrin also raised in active colonic disease in IBD.
blood tests in Crohn’s?
FBC- anaemia- normochromic normocytic anaemia of chronic disease, or hypochromic microcytic anaemia of Fe deficiency PLT-raised WCC- raised ESR-raised CRP-rasied low albumin blood cultures if sepsis suspected LFTs may be abnormal immunological- pANCA negative
blood tests required in pts on azathioprine?
FBC-Hb decrease, WCC decrease with myelosuppression
LFTs
TPMT
amylase-?pancreatitis
most common cause of acute liver failure in the UK?
paracetamol (acetaminophen) overdose
what criteria can be used to determine which pts following paracetamol overdose should be immediately referred for liver transplant?
King’s College Criteria
include arterial pH, PT, serum creatinine and grade 3 or 4 encephalopathy
components of a confusion screen?
CXR urine dipstick CT head LFTs?, blood NH3- hepatic encephalopathy- note attacks often precipitated by infection or constipation, laxatives of Abx can suppress toxic substance prod. in intestine TFTs Ca2+ MMSE blood cultures
define nutcracker oesopahgus
also known as hypertensive peristalsis
motility disorder of oesophagus characterised by smooth muscle contractions of oesophagus in normal sequence but excessive amplitude or duration.
in case where contractions are so intense- known as jackhammer oesophagus
achalasia also a motility disorder, and oesopageal dysmotility also seen in limited form of systemic sclerosis (scleroderma.)
markers of severity in paracetamol overdose?
encephalopathy ALT more than 1000 IU/L clotting screen-PT/INR creatinine- *renal function glucose- hypo common with hepatic necrosis ABG-acidosis
what paracetamol ingestion is significant?
> 75mg/kg/24hr
what medication might be given to a Crohn’s disease pt to maintain remission if had previous episodes of pancreatitis?
methotrexate
as azathioprine often used but can cause pancreatitis
which pts are classed as high risk when determining frequency of colonoscopic surveillence in IBD?
pts with extensive ulcerative or crohn’s colitis with moderate or severe active inflammation as confirmed endoscopically or histologically
primary sclerosing cholangitis
colonic stricture in past 5 yrs
any grade of dysplasia in last 5 yrs
colorectal Ca FH in 1st degree relative aged under 50
frequencies of colonoscopies in IBD surveillence for colorectal Ca in low, intermediate and high risk pts?
low risk=at 5 yrs
intermediate=at 3 yrs
high= at 1 year
surveillence offered in those whose symptoms started 10 yrs ago and have UC (not proctitis alone) or crohn’s colitis involving more than 1 segment of colon.
use chromoscopy- use of dyes
what can faecal elastase be used to diagnose or exclude?
pancreatic exocrine insufficiency e.g. result of chronic pancreatitis, gallstones, DM, pancreatic tumour, CF and chronic IBD.
what is thought to initiate hepatorenal syndrome?
this occurs typically in pt with advanced cirrhosis, portal hypertension, ascites and jaundice.
initiator= extreme peripheral vasodilatation, possible due to NO, causing extreme decrease in effective blood volume and hypotension.
this activates RAAS, NA and ADH, causing renal vasculature vasoconstriction, increasing preglomerular vascular resistance, reducing GFR and plasma renin remains high, so salt and water are retained.
also CO decrease inappropriate to degree of systemic vasodilatation.
PGs may also be involved, as syndrome precipitated by inhibitors of PG synthase e.g. NSAIDs.
best option for hepatorenal syndrome?
liver transplant
most common infecting organisms in SBP?
E coli
klebsiella
enterococci
prehepatic causes of portal hypertension?
portal vein thrombosis e.g. congenital portal venous abnormalities or neonatal sepsis of umbilical vein, or prothrombotic condition e.g. factor V leiden- where variant form of factor V cannot be inactivated.
intrahepatic causes of portal hypertension?
presinusoidal- schistosomiasis, sarcoidosis, primary biliary cirrhosis
sinusoidal-cirrhosis, partial nodular transformation
postsinusoidal-veno-occlusive disease, budd-chiari syndrome
posthepatic causes of portal hypertension?
R heart failure
constrictive pericarditis
IVC obstruction
vasoconstrictor drugs given for emergency bleeding control in varices while waiting for endoscopy and in combination with it?
terlipressin
somatostatin if terlipressin contraindicated
agents restrict portal inflow by splanchnic arterial vasoconstriction.
definition and aetiology of primary biliary cirrhosis?
chronic disorder in which progressive destruction of the small bile ducts occurs, eventually leading to cirrhosis.
immunological mechanisms involved, including anti-mitochondrial antibodies (AMA), cytotoxic CD4+ and CD8+ T cells directly produce biliary epithelium damage. IgM raised, maybe as failure to switch to IgG synthesis.
clinical features of primary biliary cirrhosis?
hepatomegaly pruritus jaundice fatigue pigmented xanthelasma
disorders assoc. with primary biliary cirrhosis?
sjogrens scleroderma thyroid renal tubular acidosis keratoconjunctivitis sicca coeliac disease interstitial pneumonitis
investigations in primary biliary cirrhosis?
bloods: LFTs- high ALP
immunology- AMA-antimitochondrial antibody, high serum IgM
high serum cholesterol
imaging: USS- diffuse alteration to liver architecture
liver biopsy- portal tract infiltrate of lymphocytes and plasma cells, loss of small bile ducts, portal tract fibrosis sometimes granuloma- also seen in TB, sarcoidosis, schistosomiasis, drug reactions.
PBC tment?
ursodeoxycholic acid-displaces endogenous bile acids from enterohepatic circulation
Vit A, D E and K supplementation
bisphosphonates for OP
cholestyramine for pruritus
what blood test may differ between crohns and UC?
pANCA- may be +ve in UC whereas often -ve in crohn’s.
what complicates all procedures used to treat achalasia?
reflux oesophagitis
aetiology of coeliac disease (gluten-sensitive enteropathy)
gluten=entire protein content of cereals wheat, barley and rye. Prolamins=proteins which are part of gluten in these cereals, and are damaging factors as resistant to digestions by pepsin and chymotrypsin as high glutamine and proline content, so remain in intestinal lumen where trigger immune responses.
coeliac disease=intolerance to prolamin which causes a T cell mediated AI response producing villous atrophy and malabosorpton.
mucosa of proximal small bowel typically affected, as closer towards ileum, gluten is digested into smaller non toxic fragments.
HLA association, increased disease incidence within families
environmental factors important: breast-feeding and age of introduction of gluten into diet.
rotavirus infection in infancy
coeliac disease clinical features?
symptoms very variable and non specific
peak in adults is females in their 50s
often asymptomatic, and come to attention due to routine blds showing raised MCV or Fe deficiency
tiredness and malaise
diarrhoea or steatorrhoea, abdo pain and weight loss suggest more severe disease
mouth ulcers and angular stomatitis frequent
infertility
neuropsychiatric symptoms- anxiety and depression
rare complications= tetany, osteomalacia, gross malnutrition with peripheral oedema. Paraesthesia, ataxia, muscle wkness or a polyneuropathy can occur.
increased incidence of AI disease e.g. thyroid, type 1 DM and sjrogen’s.
characteristics of enteropathic arthritis assoc. with IBD?
seronegative spondyloarthropathy-RF negative, HLA-B27
positive, enthesitis-achilles tendonitis, plantar fasciitis, costochondritis
asymmetrical, large joint oligoarthritis or monoarthritis
axial arthritis-spine and sacroiliac joint pathology
lower-limb joints
symptoms may predate IBD diagnosis
UC remission or total colectomy usually leads to remission of joint disease but arthritis can persist
NSAIDs help, but worsen diarrhoea
monoarthritis can be treated with IA corticosteroid inections
sulfasalazine can treat IBD and joint arthritis, as can the anti TNF infliximab
long term problems in coeliac disease?
osteoporosis- occurs even if pt on long term gluten free diet.
gold standard investigation for coeliac disease diagnosis?
small bowel biopsy
4-6 taken from second part of duodenum due to disease sometimes being patchy
endoscopic signs= mucosal fold scalloping, absence of mucosal folds, mosaic pattern of surface.
histological appearance of coeliac disease?
villous atrophy
crypt hyperplasia
enterocytes cuboidal, lymphocyte and plasma cell infiltration into LP
increase in intraepithelial lymphocytes in mild disease
indications for Ab testing as suspecting coeliac disease?
persistent diarrhoea
Fe or folate deficiency
FH of coeliac disease
assoc AI disease e.g. thyroid, type 1 DM
most sensitive tests of serology in coeliac disease?
anti-tissue transglutaminase Abs (anti-TTG)
anti endomysial antibodies (AEA)
can be used for dietary monitoring as correspond with mucosal damage
investigations in coeliac disease?
bloods: FBC- mild or moderate anaemia, increase MCV as macrocytosis with folate deficiency, decrease MCV with Fe deficiency as malabsorption and increased loss of desquamated cells, so may be normocytic anaemia with increased red cell distribution width (RDW), blood film may show micro and macrocytes, hypersegmented neutrophils and Howell-Jolly bodies-basophilic nuclear remnant (DNA cluster) inside erythrocytes due to splenic atrophy (hyposplenism).
autoantibodies-anti TTG and anti EMA
biochemistry, LFTs: low Ca2+ and high PO43 if severe with osteomalacia, and low albumin.
HLA typing-HLA-DQ2, HLA-DQ8
barium follow through: small bowel dilatation with slow transit, thicker folds.
DXA: as OP risk, OP diagnosed with T score of -2.5 or less.
capsule endoscopy if complications suspected to look for gut abnormalities.
duodenal biospy
small bowel disorders causing malabsorption?
crohn's disease coeliac disease intestinal resection radiation enteropathy dermatitis herpetiformis bacterial overgrowth whipple's disease parasite infection e.g. giardia intestinalis
components of tment of coeliac disease?
conservative measures e.g. smoking cessation, to reduce risk of complications patient susceptible to e.g. osteoporosis- risk even when on gluten free diet, and malignancy-gastric, oesophageal, bladder, breast, brain
replace vit and min stores e.g. Ca2+, Vit D, Fe, folic acid
Gluten free diet
Pt support organisations as info sources e.g. the coeliac society, national health services may subsidise food
pneumococcal vacinations 5 yrly due to risk of splenic atrophy.
complications of coeliac disease?
OP GI T cell lymphoma ulcerative jejunitis-fever, abdo pain, bleeding and perfo. small bowel adenocarcinoma oesophageal carcinoma gastric Ca, breast Ca, brain Ca, bladder Ca myopathies neuropathies aneamia secondary lactose intolerance
incidence of malignancies reduced by gluten-free diet
what do the markers faecal calprotectin and lactoferrin indicate?
inflammation
surgery of choice in presentation of acute UC requiring emergency operation e.g. toxic megacolon refractory to treatment, fulminant attack refractory to medical treatment, uncontrolled colonic bleeding or colonic perforation?
subtotal colectomy (part of colon removed or entire colon leaving the rectum behind) with end ileostomy and rectum preservation.
at a later date, the rectum can be removed and an ileo-anal pouch formed, aswell as a loop ileostomy.
the ileostomy can then be closed later
problems associated with formation of an ileo-anal pouch after subtotal colectomy in UC?
pouchitis- pouch mucosa inflammation with diarrhoea, bleeding, fever and sometimes extra-intestinal manifestations.
incidence twice as high in those with PSC, and +ve ANCA and backwash ileitis prior to surgery.
Tment of pouchitis in cases following ileo-anal pouch formation in UC surgery?
Abx-metronidazole and or ciprofloxacin
Steroids may be required
Probiotics may help prevent onset and maintain remission.
Where does calprotectin originate from?
Neutrophils
New Rome III criteria for IBS?
Recurrent abdo pain or discomfort on at least 3 days each month over last 3 months with 2 or more of:
Improvement with defecation
Onset assoc with change in stool appearance
Change in stool frequency
And symptoms which cumulatively support diagnosis are:
Bloating
Mucus passage
Urgency or tenesmus or straining
Abnormal frequency BO either more than 3 times daily or less than 3 times wkly.
Abnormal stools appearance
Why should ALD pts avoid being constipated?
Can precipitate hepatic encephalopathy as urea accumulation in bowel**
Main differentials in pts with gastrointestinal symptoms e.g. Abdo pain and change in bowel habit?
Coeliac disease-anti endomysial and tissue transglutaminase ABs, and biopsy
Food intolerance-food challenge test
Disaccharide intolerance-breath test and disaccharide challenge
IBD-faecal calprotectin
IBS
Diverticular disease of colon
Colorectal cancer-FOB and colonoscopy
Bile acid induced diarrhoea-check medicosurgical history and liver function
Bacterial overgowth or infection-culture faeces and breath test
Scar in liver transplant pt?
Mercedes Benz- bilateral roof top incision with sterna extension.
Features of chronic diverticular disease?
Can mimic local clinical features of colon cancer
Change in bowel habit with diarrhoea alternating with constipation
Large bowel obstruction with vomiting, colicky abdo pain and abdo distension and constipation.
Blood and mucus per rectum.
LIF tender on examination and often thickened mass in region of sigmoid colon which may also be felt per rectum.
What is angiodysplasia and how is it investigated and treated?
1 or multiple mucosal or SM vascular malformations, usually dilated vein or sheaf of veins, caecum and ascending colon most usually involved, but can be found anywhere in small or large bowel.
Only symptom is bleeding, can be anaemia or recurrent acute dark or bright red rectal haemorrhage.
Can do colonoscopy-bright red lesions
Or mesenteric angiogram where contrast leaks into bowel lumen.
May need blood transfusion
Colonoscopic electro coagulation or argon plasma coagulation may cure
Resection sometimes required.
ADRs of ciclosporin?
Leucopenia Hyperlipidaemia Tremor Headache Hypertension GI symptoms Abnormal hepatic function Hirsuitism Myalgia Nephrotoxicity Lymphoma Thrombocytopenia Infections
why is diazepam CI in severe hepatic insufficiency?
elimination t1/2 may be prolonged as metabolism takes place by the liver
why is peppermint oil used in IBS patients?
Antispasmodic
Enteric coating delays opening of the capsule until it reaches the distal small bowel. Peppermint oil then slowly released along the gut and exerts a local effect of colonic relaxation and a fall of intra-colonic pressure.
Inhibitory effect on gastrointestinal smooth muscle is thought to be by interference with the mobilisation of Ca2+.
what can the drug linaclotide (constella) be used to treat?
constipation in moderate to severe IBS
it is a guanylate cyclase C receptor agonist, which increases cGMP EC and IC, reducing visceral pain fibre activity and increasing fluid secretion into bowel lumen and transit respectively.
reasons for massive intestinal resection causing short-bowel syndrome?
Crohn’s disease
mesenteric vessel occlusion
radiation enteritis
trauma
major problem with a shortened small intestine ending at a terminal small bowel stoma?
sodium and fluid depletion
can increase salt intake, restrict hypotonic fluids and give oral glucose-electrolyte mixture with 90mmol/L sodium conc.
somatostatin analogue octreotide and a PPI, loperamide and codeine can increase jejunal transit itme and reduce stomal effluent loss.
problems with shortened small intestine in continuity with colon?
unabsorbed fat impairs colonic fluid and electrolyte absorption, so pts should be on low fat diet.
high carb intake also advised as unabsorbed carb met anaerobically to short chain FA which are absorbed and stimulate fluid and electrolyte absorption in colon and act as energy source.
cholestyramine can reduce diarrhoea and colonic oxalate absorption.
effects of resection of ileum?
bile salt induced diarrhoea
steatorrhoea and GS formation
oxaluria and urinary oxalate stones as bile salts in colon increase oxalate absorption
B12 deficiency
what is dermatitis herpetiformis?
disorder of small intestine that can cause malabsorption, and is characterised by a blistering subepidermal eruption of skin assoc. with a gluten sensitive enteropathy.
Inheritence and immunological abnormalities same as for coeliac disease, but morphological abnormalities of jejunum less severe.
skin condition responds to dapsone- an anti leprosy drug which is active against bacteria and inhibits folic acid synthesis.
gluten free diet advised for long term benefit, improving skin lesions and the enteropathy.
differences between mesenteric ischaemia and ischaemic colitis?**
ischaemic colitis- investigated with unprepeared f,exible sigmoidoscopy, and usually responds to symptomatic tment.
describe what is meant by steatosis/fatty change in the liver?
often result of alcohol- metabolism invariably produces fat in liver with NAD consumption and subsequent inability for beta oxidation of FA to occur but there is increased hepatic FA synthesis, which is then esterified to glycerides.
Fat mainly produced in zone 3 around central vein. No liver cell damage occurs and stopping alcohol reverses fatty changes. Fat also deposited in NAFLD.
Collagen may be laid down around central hepatic veins (perivenular fibrosis) which can progress to cirrhosis without a preceding hepatitis. Alcohol directly affects stellate cells, transforming them into collagen-producing myofibroblast cells.
often asymptomatic, but may be heaptomegaly
Microscopic features of alcoholic hepatitis?
neutrophil infiltration and hepatocyte necrosis in zone 3 surrounding hepatic venules where oxygenation poor, IL-8 involved in neutrophil chemotaxis.
Mallory bodies and giant mitochondria in hepatocytes. mallory bodies=eosinophilic hyaline inclusions in hepatocytes.
what on an FBC often indicates heavy drinking?
an elevated MCV
results of investigations in alcoholic hepatitis?
FBC: leucocytosis-neutrophilia, macrocytic anaemia suggestive of alcohol excess, thrombocytosis or thrombocytopenia may be present, cytosis-as reactive response to inflammation, or cytopenia due to PH and splenic sequestration of PLTs.
CRP raised
raised urea?
LFTs: elevated serum bilirubin, AST, ALT, ALP and PT. Usually, AST moderately elevated whilst ALT only mildly elevated or in reference range. AST/ALT ratio more than 1. raised GGT confirms alcoholism. May be low serum albumin due to decreased hepatic synthetic function and protein-energy malnutrition.
clotting studies-raised PT due to coagulopathy affecting mainly extrinsic pathway. raised INR-should measure daily*
marked aminotransferase levels should raise suspicion of viral hepatitis or drug hepatotoxicity, espec. in alcoholics who can develop severe liver necrosis in response to therapeutic doses of paracetamol.
USS-hepatomegaly and diffusely hyperechoic.
28 day mortality in pts with GAHS of >9?
75%
at less than 9 it is 50%.
poor prognostic indicators in cirrhosis?
bloods: low albumin less than 28g/L
low serum Na+ less tahn 125mmol/L
prolonged PT more than 6s above normal value
raised creatinine more than 130 micromol/L
clinical: persistent jaundice failure of response to therapy ascites haemorrhage from varices neuropsychiat. complications small liver persistent hypotension aetiology e.g. alcoholic cirrhosis and pt continues drinking.
how can GI symptoms be investigated using the hydrogen breath test?
Hydrogen only produced in body by colonic anaerobic bacteria when exposed to unabsorbed food, especially sugars e.g. lactose, and carbs. It is absorbed into blood and travels to lungs for expiration. Significantly more hydrogen may be produced and expired in pts with a high amount of unabsorbed food in colon e.g. in lactose intolerance pts, and if colonic bacteria move back into small intestine where food not yet able to be have been absorbed-bacterial overgrowth of small bowel-a cause of malabsorption-symps include diarrhoea, steatorrhoea, weight loss, anaemia
red flag indicators in suspected IBS which may indicate IBD or underlying malignancy?
unintentional and unexplained weight loss
rectal bleeding
change in bowel habit to looser or more frequent stools, persisiting for more than 6 wks in person over 60yrs old
abdominal mass
rectal mass
anaemia
FH of bowel or ovarian cancer
inflammatory markers for IBD e.g. faecal calprotectin
what is the Montreal classification of Crohn’s disease?
classified based on predominant phenotypic elements:
age at diagnosis: 16 or below (A1), 17-40 (A2) and over 40 (A3)
disease location: just ileum (L1), isolated to large bowel (L2), both (L3)
behaviour: no structuring or perforation (B1), strictures (B2), perforations (B3)
usefulness of montreal classification in crohn’s?
**
drugs used in IBD with risk of nephrotoxicity?
ciclosporin-may be used in acute severe UC, IV, monoclonal immunoassay can be used to monitor ciclosporin levels
mesalazine
most common manifestations of renal or urinary problems in IBD patients?
kidney stones-calcium oxalate or uric acid. oxalate stones formed as increased oxalate intestinal absorption due to bile salts in colon
enterovesical fistulae
ureteral obstruction
why is it important to check Mg2+ levels in pt on ciclosporin?
ciclosporin enhances clearance of Mg2+, and hypomagnesaemia can cause problems such as neurological disturbance e.g. seizures, and arrhythmias.
a pt has been suffering from chronic abdominal pain, thought to be due to chronic pancreatitis. O/E, the presence of reticulated erythema on the abdomen is nored. What name is given to this and why does it occur?
Erythema ab igne
result of long term exposure to heat e.g application of a hot water bottle for abdominal pain.
components of a full liver screen and why would one be formed?**
deranged LFTs-bilirubin, ALT,ALP of unknown cause
Viral screen-Hep A, B, C, D, E, CMV, EBV
Cu and serum caeruloplasmin, alpha 1 antitrypsin, serum Fe, transferrin sat, serrum ferritin, alpha fetoprotein, serum Igs-IgG raised in AI hepatitis and IgM in PBC.
autoantibodies: AMA-PBC, anti-nuclear, actin, liver/kidney microsomal Ab-AI hepatitis, ANCA-PSC.
HFE gene- hereditary haemochromatosis.
common cause of Vit K deficiency and hence of an elevated PT?
biliary obstruction as inability of bile salts to travel into the small bowel for fat absorption and subsequent absorption of fat-soluble vitamins-A, D, E and K.
when are highest levels of ALP seen?
hepatic metastases
primary biliary cirrhosis
how is meropenem administered?** e.g. for treating a severe pneumonia?
always IV
why are TFTs performed in pt suspected of IBS?
IBs symtpoms of constipation and diarrhoea can be result of underactive thyroid- constipation, and overactive thyroid-diarrhoea, due to thyroid hormones influence of neurotransmitter receptor synthesis in the bowel affecting gut motility*
cause of black stools other than upper GI bleed-malaena?
Fe tablets e.g. ferrous fumarate
NICE recommended tment of high grade dysplasia or intramucosal cancer in Barrett’s oesophagus?
EMR (endoscopic mucosal resection)- must use with care as high risk of stricturing, consider following with additional ablative therapy e.g. argon plasma coagulation (APC) to remove residual flat dysplasia completely
ablative therapy e.g. radiofrequency ablation (also used in varicose vein tment*) or photodynamic therapy, NOT APC if ablative therapy being used alone
oesophagectomy
how can a pt be assessed for GORD post history?
24hr intraluminal pH monitoring- NG tube inserted to 2 inches above lower oesophageal sphincter and pH measured over 24hr period, recording made of reflux episodes, excessive if pH less than 4 for more than 4% of the time, and there should be a good correlation between reflux and symptoms.
OGD can assess oesophagitis and hiatus hernia, if oesophagitis or barrett’s then reflux confirmed
unless alarm features e.g. dysphagia, then can safely treat initially without investigating once clinical diagnosis made without investigating
aetiology of wilson’s disease?
autosomal recessive
molecular defect in a copper-transporting ATPase
failure of both incorporation of copper into procaeruloplasmin in hepatocytes, resulting in low serum caeruloplasmin, and biliary excretion of copper.
tment of wilson’s disease?
lifelong tment with penicillamine-chelates Cu
avoid eating foods with high Cu content e.g. chocolate, mushrooms, liver, nuts
liver transplantation if severe liver disease
presentation of wilson’s disease?
children-hepatic problems, young adults- more neurological problems e.g. tremor, dysarthria, involuntary movements and eventually dementia.
liver disease-acute hepatitis, ALF, chronic hepatitis and cirrhosis
specific sign=kayser-fleischer ring- Cu deposition in Descemet’s membrane in iris, appears as greenish brown pigment at corneoscleral junction.
blue lunulae (nails)
polyarthritis
hypermobile joints
grey skin-also seen in haemochromatosis, amiodarone tment
abortions
hypoparathyroidism
results of investigations in wilson’s disease?
low serum Cu and caeruloplasmin
increased urinary copper-24hr excretion more than 100micrograms
high Cu in liver, although this also found in cholestasis
haemolysis and anaemia
liver biopsy-increased hepatic copper content
MRI-basal ganglia degeneration, with or without frontotemporal, cerebellar and brainstem atrophy.
mechanism of damage in hereditary haemochromatosis?
autosomal recessive, apart from ferroportin overload-dominant
iron taken up by mucosal cells inappropriately exceeding binding capacity of transferrin
reduced expression of hepcidin gene which control fe absorption facilitates liver iron overload.
classic triad in haemochromatosis?
bronze skin pigmentation due to melanin deposition
hepatomegaly
diabetes mellitus
nost common endocrine feature of haemochromatosis?
hypogonadism secondary to pituitary dysfunction e.g. testicular atrophy
results of investigations in haemochromatosis?
serum Fe elevated, reduction in toal iron binding capacity and transferrin sat more than 45%
serum ferritin elevated
liver biochemistry often normal
tment of haemochromatosis?
twice weekly venesection for up to 2 yrs
then 3 or 4 per year to prevent Fe reaccumulation
amino acid to which most bile acids are conjugated to?
glycine
where does most fat absorption take place?
proximal jejunum
define alcohol dependence
a physical dependence on or addiction to alcohol. with a pattern of repeated self-administration that causes tolerance, withdrawal and compulsive drug-taking, with continued alcohol use despite significant alcohol-related problems.
symptoms of alcohol dependence?
missing meals morning drinking morning retching and vomiting memory lapses/blackouts restless without a drink trembling after drinking the day before sweating excessively at night withdrawal fits hallucinations, frank delirium tremens
what are delirium tremens (DTs)?
most serious alcohol withdrawal state where pts are disorentated, agitated and have a marked tremor and visual hallucinations e.g. insects coming menacingly towards them.
signs= sweating, fever, tachycardia, tachypnoea.
complications= wernicke-korsakoff syndrome, infection, hepatic disease, dehydration
what condition could meaningfully link a psychiatric disorder with LFTS showing mildly raised ALT,AST,ALP and GGT?
wilson’s disease
can be further investigated with serum copper, serum ceruloplasmin, 24hr urinary collection for copper, slit lamp examination of eyes to look for copper deposition (fleisher rings), and liver biopsy.
why is it important to know if a pt with suspected coeliac disease is IgA deficient?
anti-endomysial (EMA) antibodies are 95% specific for coeliac disease, unless pt Ig-A deficient as anti-EMAs are are type of IgA antibody.
prognosis in wilson’s disease?
no clear indicators
pre-cirrhotic liver disease reversible
neurological damage less reversible
death occurs from liver failure, variceal haemorrhage or infection
