Liver and friends Flashcards
Liver tests
ALT/AST
ALP
GGT
Generally associated with hepatocellular damage, ALT more specific for liver
Ratio is important:
AST:ALT = 1 - Ischaemia
AST:ALT > 2.5 - Alcoholic hepatitis
AST:ALT < 1 - High ALT for hepatocellular damage e.g. paracetamol OD with hepatocellular necrosis, viral hepatitis, ischaemic necrosis, toxic hepatitis
Elevated with cholestasis
ALP associated with cholestasis and malignant hepatocellular damage + marker of bone turnover
GGT is sensitive to alcohol ingestion, it is non-specific marker of HC damage
Metabolic causes of liver disease (3)
Hereditary haemochromatosis
Wilson’s disease
Alpha-1 antitrypsin deficiency
Hereditary haemochromatosis
Inheritance
Pathology
Presentation
Autosomal recessive
Increased intestinal absorption of iron leading to accumulation in tissues: liver (fibrosis, cirrhosis, HCC), heart, skin, joints (arthropathy), pancreas (diabetes)
Early: fatigue, weakness, arthralgia, erectile dysfunction
Late: skin bronzing, diabetes, cirrhosis (liver signs), impotence, cardiac arrhythmia, arthropathy 2nd and 3rd metacarpophalangeal joints
Hepcidin
Transferrin
Ferritin
Produced by hepatocytes in response to high iron levels. It blocks iron absorption by blocking ferroportin at enterocytes and reduces iron exit from liver and macrophages (storage sites) in same way
Binds iron reversibly in blood
Stores iron intracellularly, an acute phase protein
Haemochromatosis
Ix
Mx
*Iron studies
-Serum ferritin (high) - lots of iron in cells - low specificity as acute phase pro
-Transferrin saturation (>45%) - lots of iron in blood specific
LFTs
MRI - iron overloaded liver
Liver biopsy with Perl’s stain
ECG/ECHO for cardiomyopathy
Tests for other causes of hyperferritinaemia e.g. inflammation (CRP), alcohol, metabolic syndrome (BP, BMI, glucose, triglycerides
Venesection/phlebotomy 4-500ml weekly
Low Iron diet
Wilsons disease Inheritance Pathology Features: Hepatic/Psychiatric/Neurological/Opthalmological
Autosomal recessive
Disorder of biliary excretion of copper. This is deficient in Wilson’s leading to copper retention in liver and basal ganglia
Acute liver failure, chronic hepatitis and cirrhosis @ younger
Severe depression (50%)
Asymmetrical tremor, ataxia, mask-like facies, clumsiness, excess salivation, choreiform movement - Parkinsonian @ older
Kayser-Fleischer ring (95%) + sunflower cataracts
Wilsons disease
Ix
Mx
Copper studies: low serum caeruloplasmin, high 24 hour urine copper excretion, high free copper, slit-lamp kayser-fleisher, liver biopsy (copper), MRI (density at basal ganglia)
Chelation agents binds copper for excretion in urine- penicillamine (oral)
Stop absorption of copper - zinc compounds
Avoid foods with copper: mushrooms, liver, chocolate, nuts
Monitor hepatic function, renal function, FBC and clotting
Avoid alcohol and hepatotoxic drugs
A1AT deficiency
Inheritance
Pathology
Presentation
Autosomal recessive very common, consider in young person with COPD
A1AT is a glycoprotein produced in the liver. It is a serine protease inhibitor and controls inflammatory cascades and balances the action of neutrophil elastase in the lung (cigs/inflammation). NE will break down elastin leading to alveolar destruction. In A1ATd an abnormal protein is produced which cannot leave, congests in liver cells and causes destruction.
Lung disease at 30s/40s
Dyspnoea, wheezing, cough i.e. COPD (lung bases commonly)
Hepatitis, cirrhosis (HCC), fibrosis
A1AT deficiency
Ix
Mx
Serum A1AT (low) -> phenotyping required
CXR and LuFT
LFT and biopsy
Asymptomatic - smoking and alcohol advice
Lung symptoms - as COPD
Liver disease - regular LFTs , treat cirrhosis, screen for HCC
4 main characteristics of liver failure
Hepatic encephalopathy
Jaundice
Abnormal bleeding - Haematemesis & Melaena - Varices
Ascites
Causes of liver failure (5 groups)
Toxin - Paracetamol, alcohol, medications (co-amoxiclav, cipro, doxy, erythro, methotrexate, gold) Infection - Viral hepatitis, EBV, CMV Neoplastic - HCC Metabolic - Wilson’s A1ATd vascular - Ischaemia, Budd-Chiari AI liver disease
Pathology of hepatic encephalopathy
In liver failure ammonia builds up in circulation and crosses BBB. Astrocytes clear this turning glutamate to glutamine. Glutamine excess causes fluid shift to cells -> cerebral oedema.
- Altered mood, drowsiness, restless, coma
Signs of liver failure
Finger clubbing/fetor hepaticus
Leukonychia
Asterixis (liver flap)
Palmar erythema
Spider naevi/scratch marks
Ascites - Shifting dullness, fluid thrills, due to hypoalbuminaemia
Bleeding - Deficient in: Factor 10, 9, 7, 2 (with vitamin K), fibrinogen (factor 1), 5, 8, 11, 12
Liver failure blood Ix
FBC - Thrombocytopenia LFT - Raised ALT + AST Bilrubin - Raised Ammonia - Raised Glucose - Dangerously low Copper high - ?Wilson’s Paracetamol - ?High Creatinine - Raised at hepatorenal syndrome PT/INR - Raised
Ascites What Causes Ix Management
Collection of fluid in peritoneal cavity
- 1500ml on exam or 500ml on USS
Transudate
Mostly cirrhosis - 50% cirrhosis develop ascites + peripheral oedema + pleural effusions
Decreased albumin (decreased oncotic) and portal hypertension (increased hydrostatic)
15% malignancy - GI tract, ovarian (Meig’s)
Heart failure
Exudate
Nephrotic syndrome - protein lost in urine
Pancreatitis
Peritoneal TB
Albumin levels, WCC, GS&C, amylase.
Treat cause
Restrict salt intake
Diuretics - spironolactone in cirrhosis - beware hyperkalaemia - Aim to lose approx 500ml per day
Spontaneous bacterial peritonitis What Presentation Ix Bacteria causing Mx
Fever, mild abdominal pain, vomiting. Abdominal pain + fever
Triad of peritonism: guarding, rebound tenderness, pain on palpation
FBC - *leuocytosis
LFT, *U+E (renal impairment), blood cultures
*Diagnostic paracentesis - for culture and amylase
Imaging - upright AXR and CXR
E.coli, streptococci, enterococci
IV 3rd generation cephalosporins if >250 cells/mm3
Hepatic encepalopathy
Causes
Ix
Mx
Develops in 50% of patients with cirrhosis and is a feature of decompensated cirrhosis
AKI, infection, constipation, sedatives, diuretics
Arterial/serum ammonia, EEG triphasic waves, MRI/CT for other cause of encephalopathy
Avoid sedatives and diagnose early
Decrease nitrogen load - lactulose removes nitrogen from gut, neomycin (ABX) lowers nitrogen forming gut bacteria
Hepatorenal syndrome
What
Criteria
Mx
A complication of end-stage liver disease (40%) Impaired renal function often precipitated by events lowering BP e.g. spontaneous bacterial peritonitis, GI bleed, pneumonia.
Criteria is a diagnosis of exclusion
Triad - Cirrhosis, ascites, Cr > 133 micromol
+ no shock, no hypovolaemia, no nephrotoxics
General:
Admit to HDU + monitor fluids (urine output), treat infections + stop nephrotoxics/diuretics
Specific:
Splanchnic vasoconstrictors e.g. terlipressin with albumin - increases blood pressure and GFR + TIPS (transjugular intrahepatic shunt) - reduces ascites in portal HTN
Cirrhosis
What
Features
Causes
Diffuse hepatic process characterised by fibrosis and conversion of normal liver architecture to nodules.
Distortion of hepatic vasculature -> increased intrahepatic resistance and portal hypertension (oesophageal varices, hypoperfused kidneys, increased cardiac output)
Hepatocyte damage -> impaired liver function and decreased synthesis clotting factors
Common: alcohol, hep B/C, NAFLD and NASH - non-alcoholic fatty liver/steatohepatitis
Signs and Symptoms of cirrhosis
Fatigue, malaise, anorexia, nausea, weight loss
Advanced/decompensated: oedema, ascites, bruising, poor memory, bleeding varices, SBP
Signs: FLAPS (finger clubbing, leukonychia, asterixis, palmar erythema, spider naevi, scratch (pruritus), jaundice, dupuytren’s
Other - Hepatomegaly, oedema, gynaecomastia (increased production androstenedione by adrenals and conversion to oestrogen), hypogonadism (toxicity of alcohol/iron)
Ix for causes of cirrhosis
AST + ALT raised with hepatocyte damage, GGT raised in alcohol, ALP, bilirubin
Albumin low in advanced cirrhosis
FBC - Bleeding - anaemia, low platelets (hypersplenism), macrocytosis (alcohol abuse)
U&E -Hepatorenal syndrome
Coag- Increased PT in advanced
Ferritin - Raised in HH, low in iron deficiency/blood loss
Viral - Hep B/C
NASH - Fasting glucose, insulin, triglycerides and uric acid levels
AAb screen - Anti-mitochondrial at primary biliary cirrhosis
A1AT level, caeruloplasmin, urinary copper, fasting transferrin saturation
Portal hypertension What Pre hepatic causes Hepatic causes Post hepatic causes
Abnormally high pressure in hepatic portal vein (significant if hepatic venous pressure gradient >10mmHg)
Portal vein thrombosis, splenic vein thrombosis, extrinsic compression e.g. tumour
Cirrhosis, hepatitis, schistosomiasis, granuloma (sarcoid)
Budd-Chiari, RHF/CHF, constrictive pericarditis
Portal hypertension
Signs
Ix
Mx
Ascites, splenomegaly, dilated umbilical veins
*Haematemesis/melaena -> bleeding varices
Signs of cirrhosis/liver failure
AUSS for liver/spleen/ascites Doppler ultrasound - blood flows Spiral CT for portal vasculature Endoscopy for oesophageal varices Portal pressure by hepatic venous pressure gradient (normal < 5, varices > 10)
Treat cause ± liver transplantation
Reduce portal venous pressure (beta blockers ± nitrates or shunts - TIPS (also treatment for big varices)) - Non specific beta blockers e.g. carvedilol
Location of varices in portal hypertension (4)
Gastro-oesophago junction
Anterior abdominal wall
Anorectal junction
Retroperitoneum
Budd-Chiari syndrome
What
Presentation
Rare syndrome with obstruction of hepatic veins
Sudden RUQ pain + rapidly developing ascites + hepatomegaly + jaundice + renal involvement (50%)
Liver cancer Primary vs Secondary occurance Cause Associations Presentation
10% are primary, 90% are secondary cancers (stomach, colon, lung, breast)
90% of primary are HCC, 10% are cholangiocarcinoma (flukes, PSC, biliary cysts, early jaundice)
HepC is the leading cause in the UK
Worldwide - HBV
8x more common in men
Occurs 20 years after initial insult
90-95% of HCC patients have cirrhosis
Alcoholism, HH, PBC, metabolic syndrome
Anorexia, wt loss, night sweats, RUQ pain + symptoms of liver disease/cirrhosis/failure
Liver cancer screening
Screen high risk i.e. HBV ± cirrhosis and HCV/alcoholic cirrhosis
6-12 monthly USS + AFP (alpha fetoprotein levels >400 n.b. If <4cm may be normal)
Steatosis/steatohepatitis What Alcoholic vs non alcoholic distinction Causes (4) Presentation
Accumulation of fat in the liver. If this is associated with inflammation it is called steatohepatitis (or NASH - non-alcoholic steatohepatitis)
Based on alcohol consumption (>2U/day women/ 3U/day men)
Metabolic syndrome, PCOS, alcohol excess, starvation, HBV/HCV, metabolic disorders (Wilson’s, glycogen storage disorder…) medications (amiodarone, tamoxifen, glucocorticoids, methotrexate)
Steatosis generally is asymptomatic (fatigue/RUQ pain). Advanced disease may have cirrhosis symptoms ascites, oedema, jaundice
Hepatomegaly is common
Steatosis/steatohepatitis
Diagnosis
Mx
Biopsy: cells swollen with fat - steatosis at zone 3
Abstinence from alcohol (causes reversal in alcoholic fatty liver) and adequate diet (high protein: calorie)
Weight loss + regular exercise (increases insulin sensitivity) + control comorbidity - BP, diabetes, lipids
Treat cause + prescribe for Delirium tremens
Hep A Spread Who & Incubation Where Presentation Ix Mx
Faeco-oral
Food handlers (hand washing), shellfish, travellers 2-6 weeks
India, Africa, Far East - Travellers should be vaccinated against hepatitis A with live attenuated vaccine
Self limiting, acute, no chronic phase
Prodrome - mild flu (VANFAM, vomiting, anorexia, nausea, fever - uncommon, arthralgia, malaise) + lose taste for cigarettes
Hepatitis/icteric phase - dark urine, pale stools, jaundice, abdominal pain, itch, hepatomegaly
Viral serology: HAV IgM (with onset of symptoms @3W lasts 6 months), HAV IgG (persists years)
LFTs up.
Supportive (fluids, antiemetics, rest), avoid alcohol, for itch cholestyramine - Recovery may take 6 months
Hep E Spread Who & incubation Where Presentation & Mx Ix
Faeco-oral
Heavily associated with pigs, slaughterhouses and vets, contaminated drinking water& 2-9 weeks
India, Asia
Acute and self-limiting
Similar to hepatitis A
Viral serology: HEV IgM, HEV IgG ± viral PCR
Hep B
Spread
Who & Incubation
Where
Parenteral - blood or body fluid
Vertical: up to 90% if HBeAg+ve (10% if negative)
Horizontal: sexual (more than HCV), IVDU, blood products, dialysis, toothbrush
IVDU, health workers, sex workers, prisons *HIGHLY INFECTIOUS & 60 to 90 days
SSAfrica, Asia (may be 10% infected)
Hep B presentation
Ix
Acute:
Prodromal: VANFAM + disinclination to smoke
Hepatic: RUQ pain + hepatomegaly + jaundice (50%) - darkening urine and lightening stools
Occasionally may lead to fulminant hepatic necrosis - marker is increasing INR and requires transplant
Chronic: defined as infection lasting longer than 6 months (HBsAg)
May lead to fibrosis, cirrhosis and *HCC
Fatigue, anorexia, nausea and RUQ pain ?signs of chronic liver disease
Viral serollogy:
HBsAg found at current infection (may be produced as vaccine)
HBsAb indicates immunity post infection/vaccine
HBeAg allows assessment of infectivity
VANFAM
vomiting, anorexia, nausea, fever - uncommon, arthralgia, malaise - Common symptoms in Hepatitis
Heb B Mx
Acute
Chronic
Symptomatic relief, bed rest, antipyretics, fluids, cholestyramine, notification as communicable disease
48 week course of injectable pegylated interferon alpha or second line tenofovir or entecavir oral daily + 6 monthly screen for HCC
Heb C Spread Who & Where Incubation Presentation
RNA virus (flavivirus) + third largest cause of ESLD in UK (alcohol and NAFLD) - 6 genotypes, in UK HCV1 (50%) or HCV2/3 (50%)
Parenteral - blood or body fluid, IV drug use, tattoos, *sexual transfer is much less common as is vertical (6%), blood, transfusion, needlestick (3%)
IVDU, blood transfusion pre 1991, health workers.
6-7 weeks, 9 weeks for seroconversion (may take 9 months)
85% are asymptomatic BUT these are more likely to progress to chronic
15% develop hepatic illness: malaise, nausea, RUQ pain, and jaundice
Chronic infection may be malaise, fatigue, intermittent RUQ pain often unrecognised for 20 years (cirrhosis in 20%)
Heb C
Ix
Mx
HCV serology (anti HCV Ab, IgM or IgG) +ve at 3 months in 90% but may take 9 months
PCR HCV RNA (for ongoing/chronic infection) treat if detectable > 2 months
LFT (AST:ALT < 1) will fluctuate in chronic infection
HIV, HBV testing
Biopsy for degree of inflammation and fibrosis if HCV-PCR+
Prevention: needle exchange, screen blood products, no vaccine, alcohol avoidance
Screen for HCC 6 monthly USS and AFP
SC pegylated interferon alpha + ribavarin
Autoimmune hepatitis What Presnetation Ix Management
Chronic disease of unknown cause characterised by hepatocellular inflammation, necrosis and autoantibodies (association with other AI disease)
N.b. subclinical so many patients have cirrhosis at symptom onset
Generic: Prominent nausea, fatigue, myalgia, anorexia, arthralgias, weight loss
Endocrine: Skin rashes, hirsutism, amenorrhoea, oedema, chest pain (pleuritis),
Liver: Pruritus and jaundice, URQ discomfort
Hepatomegaly, jaundice, splenomegaly, ascites
LFT (elevated 10x)
Raised IgG +ve auto-antibodies (autoantibody screen)
*Liver biopsy = most important diagnostic procedure
Interface hepatitis with portal plasma cell infiltrate
Prednisolone + azathioprine
Liver abscess
Presentation
Mx
RUQ pain (prominent in amoebic), tenderness, hepatomegaly
*Swinging fever (pyogenic may be pyrexia of unknown origin) + night sweats + wt loss
Nausea, vomiting, anorexia
Pain referred to R shoulder, *cough due to diaphragmatic irritation + reactive pleural effusion, jaundice
ABX ± drainage + fluids + pain relief
pyogenic - IV third cephalosporin + metronidazole (anaerobes) for ?12 weeks
Amoebic - metronidazole (good response 72 hours) + diloxanide furoate to clear intestinal amoebae
<5cm = needle aspiration, >5cm = percutaneous catheter drainage
Acute pancreatitis What Causes Presentation Examination signs
Acute inflammation of pancreas releasing exocrine (secrete via ducts) enzymes causing autodigestion of organ. Activation of proenzymes within duct
GETSMASHED gallstones, alcohol, trauma, steroids, mumps, AI, scorpions, hyperlipidaemia/hypothermia/hypercalcaemia, ERCP, drugs
Severe sudden onset epigastric pain (LU) + vomiting + radiate to back relieved by sitting forward (retroperitoneal involvement)
Cullen’s sign (periumbilical bruising)
Grey Turner’s sign (flank bruising) - retroperitoneal haemorrhage
Epigastric tenderness + rigidity (fluid shift to gut and peritoneum)
Tachycardia, fever, hypoxaemia
Jaundice if cause is gallstones/alcohol
SHOCK
Acute pancreatitis
Ix
Imaging
DDx
Serum amylase x3 (also raised in renal failure as renally excreted, DKA, perforated DU), raised serum lipase (more sensitive, pancreas specific) ABG for hypoxaemia
FBC (leukocytosis), CRP (>200 = pancreatic necrosis)
LFT (AST:ALT > 3), raised bilirubin
Hypocalcaemia, hyperglycaemia, raised urea
MODIFIED GLASGOW SCORE
X-RAY FOR ARDS
Plain erect AXR - retroperitoneal shadow = bleed, intestinal obstruction, pancreatic calcif CXR - exclude perforation, shows ARDS CT with contrast is diagnostic USS - swollen pancreas ± gallstones ERCP
*Ruptured or dissecting aortic aneurysm
Acute pancreatitis Mx
Mild
Severe
Pain relief pethidine or buprenorphine ± IV benzodiazepines (morphine spasms ampulla)
IV fluids - Most important
Nil by mouth + NG tube (for severe vomiting) -> stop pancreatic stimulation
No need for CT
Repeat Glasgow score at 24 and 48 hours + daily bloods and obs
Restart food and fluids when symptoms and bloods stabilise + treat gallstones
HDU or ITU + CT for necrosis If evidence of pancreatic necrosis - aspirate peritoneal fluid for culture and target IV antibiotics Enteral nutrition via NG tube Early ERCP for gallstones Give oxygen
Chronic pancreatitis
What
Types
Presentation
Chronic inflammation/fibrosis and calcification of pancreas resulting in irreversible damage, impaired endocrine and impaired exocrine function
Large duct: dilatation and dysfunction of large ducts + diffuse calcification + steatorrhoea. Occurs more in men.
Small duct: not associated with calcification, steatorrhoea. Occurs more in women
Epigastric pain radiating to back relieved by sitting forward - exacerbated by eating
Nausea and vomiting
Exocrine dysfunction: malabsorption, wt loss, diarrhoea, steatorrhoea (pale/loose/offense)
Endocrine dysfunction: diabetes mellitus
Chronic pancreatitis
Ix
Mx
Bloods: FBC, U+E, Cr, LFT, Ca (cause), amylase (normal), glucose, HBa1C (raised)
Secretin stimulation test: causes pancreas to release bicarb to neutralise stomach acid -> +ve result if over 60% exocrine function lost
Malabsorption tests: serum trypsinogen/faecal elastase
Imaging:
CT for atrophy, duct dilatation or calcification
MRCP (magnetic retrograde cholangiopancreatography)
?Endoscopic ultrasound
Manage pain and malabsorption
Pain - simple + opiate (normally tramadol) - risks opioid dependence and gastroparesis
Malabsorption - replace pancreatic enzymes
+ Alcohol advice + low fat diet/gallstones treatment/diabetes treatment
Ca pancreas
Types
Risk factors
Endocrine or exocrine (Most)
95% are adenocarcinoma
Main: Smoking, alcohol, obesity + diet (low fruit veg), diabetes
Precursor: chronic pancreatitis
Family history pancreatic cancer + familial cancer syndromes (BRCA1/2, FAP, Lynch, MEN)
Exocrine Ca of pancreas
Presentation
Ix
Early: vague - epigastric discomfort/dull backache
*painless, progressive, obstructive jaundice (⅔ are in the head of the pancreas)
Pancreatic pain (body/tail)
Obstructive jaundice (dark urine, pale stools, pruritus)
Weight loss, anorexia, steatorrhoea
Palpable gallbladder (from retrograde flow) - Courvoisier’s sign *if it is painless it is unlikely to be gallstones
Stomach/duodenum compression -> gastric outlet obstruction -> nausea/vom (Use Prokinetic antiemetics - metoclopramide)
Advanced disease: rapid wt loss, persistent back pain, ascites, epigastric mass, Virchow’s node
FBC - anaemia of Ca, LFT - for jaundice (bilirubin + ALP + GGT raised), serum glucose - hyperglycaemia
Tumour marker - CA19-9
Imaging: USS liver, bile duct, pancreas -> tumour mass + dilated bile ducts
Abdominal CT for diagnosis and staging
Endocrine Ca pancreas
Insulinoma: confusion, sweating, dizziness, weakness, hypoglycaemia
Gastrinoma: severe peptic ulceration/diarrhoea - Zollinger-Ellison (excess gastrin -> HCl)
VIPoma - profuse watery diarrhoea with hypokalaemia and achlorhydria (no HCl)
Glucagonoma - DM, weight loss, necrolytic migratory erythema
Non-functional (MEN1 - Most) - mass effect e.g. jaundice
Gallstones
Whats in bile
Types
Cholesterol, bile pigments (from Hb), phospholipids
Cholesterol stones (n.b. Ileum absorbs bile salts)
-80% of stones at UK
-Large, solitary, radiolucent
Admirands triangle
Pigment stones 10%
- Small, friable, radiolucent
- Result of haemolytic conditions
Mixed stones 10% faceted - calcium salts + pigment + cholesterol
Admirands triangle
Decreased dietary lecithin
Decreased bile salts (impaired flow)
Increased cholesterol saturation of bile/loss of bile salts (ileal resection/Crohn’s)
Gallstones presentation in: Biliary colic Acute cholecystitis Ascending cholangitis Pancreatitis
RUQ pain
RUQ pain + fever/WCC
RUQ pain + fever/WCC + jaundice - Charcot’s
triad
Jaundice - raised bilirubin, alk phos, GGT
Nb. Most are asymptomatic
Biliary colic
What
Presentation
Ix
Temporary obstruction of cystic or common bile duct (jaundice)
Sudden onset, epigastric/RUQ, radiation to interscapular region, constant lasting 15 minutes- 24 hours, relieved spontaneously or with analgesia
With nausea and vomiting due to GB distension
USS is 90-95% sensitive for stones
Urinalysis, CXR, ECG for exclusion
Acute cholecystitis
What
Presentation
Ix
Second most common presentation of gallstones (95%) or trauma.
Continuous epigastric pain - right shoulder, vomiting, fever, local peritonism (main differences), GB mass
Jaundice if stone moves to common bile duct
Murphy’s +ve - 2 fingers, breathe in, halts inspiration, negative on other side
Raised WCC, abnormal LFT
*USS - *thickened GB wall (>3mm) + fluid or air in the GB, CBD diameter >6mm
ERCP/MRCP
Mx of Gallstones/Acute cholecystitis
Non-surgical
Surgical
Note the patient is probably vomiting NBM (stop CCK release)
Good response of pain to parenteral opioids (pethidine) or ****PR diclofenac
>24 hours admit
Rehydrate IVI
Consider antibiotics IV (3rd gen ceph)
Laparoscopic cholecystectomy for removal of GB
Complications: fat intolerance, injury to bile duct
Ascending cholangitis (infection of bile duct) What Common organisms Causes Charcots triad
Bile normally sterile. If CBD is obstructed, flow of bile is reduced leading to biliary stasis and infection. Infection may also be retrograde flow due to acute cholecystitis or ERCP (1%) - This is a medical emergency
E.coli, klebsiella, enterococci
Obstruction of gallbladder (stones), ERCP, tumours (ca panc, cholangiocarcinoma), bile duct stricture
RUQ + fever/chills + jaundice
Ascending cholangitis
Criteria
Systemic inflammation (A) -Fever/chills/ T>38 -Lab data - elevated WCC or CRP Cholestasis (B) -Jaundice -Abnormal LFT: raised ALP, ALT/AST, GGT Imaging (C) -Biliary dilatation -Evidence of aetiology: stricture, stone, stent (KUB XR + AUSS + contrast CT (best method).
Definite diagnosis if one in A + B + C, suspect if A + B/C
Ascending cholangitis
Mx
Complications (4)
Fluid resuscitation, correct coagulopathy, broad-spec abx
If septic shock O2 + IV fluids + BC + IVABX ?metronidazole + ceftriaxone
Emergency biliary drainage if AKI, shock, DIC etc
Endoscopic biliary drainage
Severe may cause Septic shock AKI All other system dysfunction Liver abscess Liver failure
Primary sclerosing cholangitis
What
Presentation
Ix
Chronic inflammation + fibrosis of intra + extrahepatic bile ducts leading to multifocal biliary strictures
Asymptomatic + abnormal LFT/hepatomegaly
Jaundice/pruritus
RUQ pain
Fever, wt loss, fatigue, sweats
Bloods: LFT (elevated alk phos/GGT, raised transaminase)
Raised immunoglobulins: IgG, IgM, hypergammaglobulinaemia
Autoantibodies: p-ANCA
Imaging: USS may show bile duct dilatation but MRCP is standard
Biopsy for staging
ERCP - Beaded appearance
Child Pugh score
What
Scoring
Criteria (5)
Used to assess the prognosis of chronic liver disease, mainly cirrhosis
Scored 1-3 for each criteria
Total bilirubin Serum albumin Prothrombin time, prolongation (s) OR INR Ascites Hepatic encephalopathy
Primary sclerosing cholangitis
Mx
Symptomwise + treat strictures with balloon dilatation
Pruritus - Colestyramine
Nutrition - With cholestatic disorders supplement fat soluble vitamins DEAK
Prevent progression - Avoid alcohol (risk for cholangiocarcinoma) + ursodeoxycholic acid (secondary bile acid) *little response to immunosuppression
Primary biliary cirrhosis AKA primary biliary cholangitis What Auto antibodies Diagnosis Associations Auto antibodies
Slowly progressive AI disease causing destuction of small interlobular bile ducts (canals of Hering)
AMA - antimitochondrial antibody
Biochemical evidence of cholestasis (raised alk phos)
AMA
Hist evidence of destruction interlobular bile ducts
Heavy association with Sjogren’s (dry eye, dry mouth) + other AI disease e.g. thyroid
Primary biliary cirrhosis AKA primary biliary cholangitis
Mx
Alleviate symptoms + slow disease + only transplant is curative
Pruritus
Sedating antihistamines or colestyramine
Ursodeoxycholic acid slows disease progression
Immunosuppression: methotrexate, steroids
N.b. oestrogens promote cholestasis so avoid COCP
PSC vs PBC Involvement Sex AAb Associations
Both involve primary sclerosis of bile ducts
PSC affects intrahepatic and extrahepatic bile ducts
PBC affects small interlobular bile ducts
PSC occurs more in men, PBC occurs x10 in women
Both have x10 familial association
PSC is an autoimmune condition with pANCA antibodies
PBC is an autoimmune condition with AMA antibodies
The cause of PSC is unclear, but it is associated with UC and colon cancer
PBC is associated with Sjogren’s and thyroid disease
Cholangiocarcinoma aka Klatskin’s tumour What Types Ix Mx
Carcinoma arising in any part of the biliary tree (may be intrahepatic)
90% ductal adenocarcinoma, 10% squamous cell carcinoma
Jaundice early in perihilar tumours, URQ abdo pain + jaundice + cholestasis + pruritus + hepatomegaly + wt loss
LFT: cholestatic picture
Tumour marker CA19-9 and CEA but not AFP
USS/CT, MRI is optimal
To treat it needs removal but only 33% are resectable at presentation
Aggressive surgical resection including liver resection ± liver transplantation
Symptom relief with stents and ERCP
Intrahepatic tumours have worst prognosis
Cholestasis
What
Presentation
Ix
bile cannot flow from the GB to the duodenum. This leads to retention of conjugated bilirubin and regurg to serum, increased serum concentration of unconjugated bilirubin, increased bile salts.
Jaundice - elevated serum conjugated bilirubin
Pale stools and dark urine - no bilirubin to GI tract, reflux of conj bili into blood - excreted in urine
Pruritus - bile salts irritation note this is not histamine mediated and so antihistamines will have no effect therefore use *colestyramine
Cholestasis characterised by elevated serum bilirubin, elevated alkaline phosphatase (>3x), raised GGT compared to transaminase.
Serum concentration of conjugated bilirubin and bile salts
Elevated AST/ALT suggest a hepatocellular picture
Low serum albumin in chronic disease
Hyperlipidaemia if ability to break down cholesterol
Drugs causing jaundice
Haemolysis - antimalarials
Cholestasis - Gold salts, nitrofurantoin, statins, erythromycin, anabolic steroids, oestrogen COCP
Hepatitis - paracetamol, rifampicin, statins
Signs of decompensated liver failure
Oesphageal varacies Encephalopathy Ascites Asterixis Hepato renal syndrome (NO build up causes vasoconstriction in kindeys)
Main complication of pancreatitis
ARDS
Causes of Jaundice
Intra Hepatic
Post Hepatic
Viral hepatits
Drugs
Alcholic hepatits
Autoimmune cholangitis
Gall stones
Ca bile duct/head of pancreas/ampulla
Biliary stricture
Pancreas pseudocyst
Effects of alcohol Cardio Neuro GI Haem Psych
Cardio - Directly toxic = Cardiomyopathy and arrythmias
Neuro - Polyneuropathy, myopathy, cerebellar degeneration, dementia, Wernicke’s/Korsakoff
GI - Liver damage, pancreatits, oesophagitis, oesophageal ca
Haem - Thrombocytopenia, raised MCV, anaemia
Psych - Depression, self harm, dependance
Mx of bleeding varices
Prevention of re bleed
Terliipressin - Restricts portal inflow (CI in IHD - Use Somatostatin)
Somatostatin - Lowers portal pressure
Endoscopy - Band ligation
B Blockers
Band ligation
TIPS
