Liver & Friends Flashcards
Arteries of the foregut
Celiac trunk
- Left gastric
- Splenic
- Common hepatic
What does ALT test show
Assoc with hepatocellular damage
e.g. paracetamol OD with hepatocellular necrosis, viral hepatitis, ischaemic necrosis, toxic hepatitis
AST:ALT ration
If over 1 = Ischaemia
If over 2.5 Alcoholic hepatitis
GGT
Sensitive to alcohol ingestion
ALP
Elevated with
- Cholestasis
- Malignant hepatocellular damage
- Marker of bone turnover (Paget’s)
Metabolic liver diseases:
Hereditary haemochromatosis (Deficiency of iron regulatory hormone hepcidin)
Wilson’s (accumulation of copper at tissues)
A1AT deficiency (Lungs and liver, enzyme not able to leave liver)
Hereditary haemochromatosis
- Inheritence
- Mechanism
- Organs affected
- Gene
Autosomal recessive
Inc intestinal absorption of iron leading to tissue accumulation. Hepcidin deficient (blocks iron absorption when high levels detected)
- Liver: fibrosis, cirrhosis, HCC,
- Heart
- Skin (bronzing)
- Joints (arthropathy)
- Pancreas (DM)
HFE (Chr 6)
Hereditary haemochromatosis
- Symptoms
- Age of onset
- TIBC
Early: fatigue, weakness, arthralgia, erectile dysfunction
Late: bronzing, diabetes, cirrhosis, arrhythmia, arthropathy
TIBC dec, Ferritin inc, Transferrin saturated (over 45%)
Hereditary haemochromatosis Investigations
Iron studies (high ferritin, Transferring over 45% saturated) HFE genetic testing LFTs MRI: iron overload Liver biopsy with Perls stain (blue)
Rule out Ddx: CRP (other cause of high ferritin - acute phase protein)
Treatment Hereditary haemochromatosis
Venesection/phlebotomy (4-500ml weekly)
Liver transplant in decompensation
Monitor ferritin
Wilson’s
- Hepatic features
- Psychiatric features
- Neuro features
- Opthalmological features
Liver failure, hepatitis,
Severe depression
Asymmetrical tremor, ataxia, clumsiness
Kayser-Fleisher ring
Wilson’s investigations
Copper studies:
- low serum caeruloplasmin
- high 24 hour urine copper
- high free copper
slit lamp: Keyser-Fleisher
Liver biopsy: copper
MRI: density in BG
Wilson’s Treatment
Chelation agents (Penicillamine) binds copper to excrete in urine
Stop copper absorption: Zinc
Avoid copper dense food: mushrooms, liver, chocolate, nuts
Monitor: LFTs, Renal functionalists, FBC
Avoid alcohol and hepatotoxics
A1At deficiency
- Inheritence
- Mechanism
- Consider when…
Autosomal recessive
A1AT is glycoprotein in the liver which controls inflammatory cascades and balances neutrophil elastase in the lung. Deficiency = alveolar destruction
Abnormal A1AT can not leave liver, congesting liver cells.
Young person with emphysema
A1At deficiency
- Hepatic features
- Lung features (Presenting factors)
Hepatitis, cirrhosis, HCC
Dyspnoea wheeze, cough, COPD
A1At deficiency
- Investigations
- Tx
Serum A1AT low
CXR and Lung functions (Peak flow and spirometry)
Smoking and alcohol advice
Treat like COPD (LABA)
Regular LFTs, screen for HCC
A1At deficiency
- Investigations
- Tx
Serum A1AT low
CXR and Lung functions (Peak flow and spirometry)
Smoking and alcohol advice
Treat like COPD (LABA)
Regular LFTs, screen for HCC
4 Things seen with Liver failure
Jaundice
Ascites
Abnormal Bleeding (dec clotting and varices)
Hepatic Encephalopathy
(when liver loses ability to regenerate)
Toxins causing Liver failure
Paracetamol,
Alcohol,
Medications (co-amoxiclav, Abx - cipro, doxy, erythro, methotrexate, gold)
Infective liver failure
Viral hepatitis (A, B, C, E) EBV, CMV
Neoplastic liver failure
Primary HCC
Secondary
Metabolic liver failure causes
Haemochromatosis
Wilson’s
A1ATd
Vascular Liver failure causes
Ischaemia (Atherosclerosis)
Budd-Chiari (hepatic vein thrombosis - triad 1) Abdo pain, 2) Ascites, 3) Hepatomegaly)
Inflammatory Liver failure
Autoimmune hepatitis
Hepatic encephalopathy pathophys + presentation + Tx
In liver failure ammonia builds up in circulation and crosses BBB causing cerebral oedema.
Altered mood, Drowsiness, Restlessness, Coma
Lactulose (removes Nitrogen from gut), Neomycin (lower nitrogen forming bacteria)
Signs of chronic liver disease
Finger clubbing
Fetor hepaticus
Leukonychia (white nails/milk spots)
Asterixis (flap)
Spider naevi
Hypoalbuminaemia = Ascites: shifting dullness, fluid thrills
Bleeding (Factor 1972 Fit K), Fibrinogen deficiency too
In Liver failure:
FBC LFT Billirubin Ammonia Glucose Copper Paracetamol Creatinine INR Viral serology Doppler USS
FBC: Thrombocytopenia LFT: ALT + AST raised Billirubin: Raised Ammonia: Raised Glucose: Dangerously low Copper: High in Wilsons Paracetamol: high in OD Creatinine: hepatorenal syndrome = Raised INR: Raised Viral serology: viral hep, EBV, CMV Doppler USS: Budd Chiari occlusion?
Liver cirrhosis severity Classification & Markers
Child-Pugh classification
BRAIN: Bilirubin (high) Refractory ascites Albumin low < 28 INR > 1.7 eNcephalopathy
Class A = least severe
Class C = Most severe
Consider transplant early
Liver failure management
- If OD
- Ammonia
- Raised ICP (Hep encephalopathy)
- AKI (hepatorenal)
- Bleeding
- Glucose
- Ascites
- If OD (para): N-Acetylecysteine
- Ammonia: Lactulose
- Raised ICP (Hep encephalopathy): IV mannitol
- AKI (hepatorenal): Haemodialysis
- Bleeding: FFP, Pts, Vit K
- Glucose: IV glucose
- Ascites: Diuretics, low salt
Liver transplant complications
Hepatorenal syndrome
Infection/sepsis - spontaneous bacterial peritonitis
Cerebral oedema
Haemorrhage form oesophageal varices
Ascites:
- Def
- Complications
- Cause (4)
- Presentation
Fluid collection in peritoneal cavity due to low oncotic pressure (hypo albumin)
Infection (SBP), Hepatorenal syndrome
75% cirrhosis (dec oncotic, portal hypertension - inc hydrostatic)
15% malignancy (GI tract, ovarian)
Heart failure
Nephrotic syndrome
Abdo distension + Umbilical herniation, dyspnoea (impaired lung function), weight gain.
Ascites:
- Investigation
- Management
- Complications
- Examination: Shifting dullness, fluid thrill (large ascites)
- LFT: look for cirrhosis
- Abdo USS (Ca Ovary, Liver mets)
- CXR (HF, pleural effusion)
Tx cause
Diuretics: Spironolactone (beware hyperkalaemia)
Paracentesis (symptom relief)
TIPS (transjug intraheaptic shunt)
SBP, Hepatorenal syndrome
Spontaneous bacterial peritonitis
- Def
- Symp
- Investigations
- Organism
- Tx + prevention
Intrabdo sepsis with 20% mortality
Fever, abdo pain (peritonism: gourding, rebound tenderness, pain on palpation), vomiting.
FBC (leukocytosis), LFT, U&E (hepatorenal), blood cultures.
Diagnostic paracentesis (culture and amylase)
Imaging: AXR (upright) and CXR
E.coli, Strep, enterococci
IV 3rd gen cephalosporin.
Prophylactic Abx
Precipitants for hepatic encephalopathy
AKI Infection Constipation Sedatives Diuretics
Hepatorenal syndrome
- Assoc
- Precipitants
- Pathophys
End-stage liver disease with ascites.
Events lowering BP e.g. SBP, GI bleeding.
Splanchnic Vasodilation drops BP, activates SNS and RAAS
Hepatorenal syndrome Diagnostic criteria
Cirrhosis with ascites
Creatinine over 133 micro mol
No nephrotixics
Hepatorenal syndrome management
Admit to HDU, monitor urine output, stop diuretics
Splanchnic vasoconstrictors e.g. terlipressin with albumin
TIPS - reduces ascites in portal HTN
Cirrhosis
- Def
- Complications
- Causes
Fibrosis converting Liver architecture to nodules
hepatic/portal HTN (oesophageal varices), dec synthesis (clotting factors, albumin)
Common: Alcohol, Hep B/C, NAFLD, NASH (Non-Alp steatohepatitis
Uncommon: AI hep, PBC, PSC, sarcoidosis, Haemochromatosis
Cirrhosis
- RF
- Pathophysiology
Alcohol, Hepatitis, Obesity, T2DM
Cytokines activate stellate cells i space of disse
Normal Liver replaced with collagen
Loss of fenestration/sinusoid = imparted function Blood flow
Signs (FLAPS) and symptoms Cirrhosis
& Decompensated
Occur when 80% parenchyma destroyed - may be asymptomatic
Fatigue, malaise, anorexia, weight loss, gynaecomastia (inc oestrogen conversion as testosterone synthesis drop)
Signs: FLAPS: finger clubbing, Leukonychia, Asterixis, Palmar erythema, spider naevi)
Decompansated: Oedema, ascites, bruising, poor memory, Variceal bleeding, SBP
Portal HTN signs
Ascites, splenomegaly, caput medusae (veins from umbilicus), hematemisis
Investigating Cirrhosis
- general
- for cause (Viral, Alc, NASH, Metabolic, AI)
LFT: AST + ALT raised, GGT in alc, ALP + Bilirubin (PBC, PSC)
Albumin: low
FBC: Macrocytosis (alc)
U&E: Hig Cr - Hepatorenal
Imaging: USS, CXR (pleural effusion from ascites)
Biopsy: Gold standard for diagnosis (nodular, bridging fibrosis)
Viral screen: Hep B/C
Alc: GGT, MAcrocytosis, Carbohydrate deficient transaminase
NASH: fasting glucose
Metabolic: AIAT, Caeruloplasmin, transferrin sats (TIBC)
AAb screen - antimitochondrial
Cirrhosis management
Delay progress, treat cause and complications
Alcohol abstinence
Antihistamines (pruritus)
Prophylactic ciprofloxacin (SBP)
Monitor Oesophageal varies and HCC
Transplant is the only cure
Portal HTN
- Def
- Causes
Abnormally high hepatic portal vein pressure
Pre-hepatic: Portal thrombosis, Compression (e.g. tumour)
Hepatic: Cirrhosis, hepatitis, Sarcoid granuloma
Post-hepatic: Budd-Chiari, RHF/Congestive HF,
Portal HTN pathophysiology
Complication
Risk of TIPS
Due to either inc vascular resistance or inc blood flow
Pressure goes back to veins draining into portal vein
Causes varices e.g. in Gastro-oesophageal vein
May cause encephalopathy due to toxins bypassing liver
Portal HTN signs
Ascites, splenomegaly, dilated umbilical veins, signs of liver failure
Haematemisis, melaena (bleeding varices)
Portal HTN investigations
Abdo USS (liver, spleen, ascites) Doppler USS Endoscopy for varices
Portal HTN Tx & Complicatios
Treat cause ± transplant
Beta-blockers (Carvedilol) ± nitrates ± TIPS to reduce portal venous pressure
Variceal bleeding, Ascites complications (Hepatorenal, SBP)
Oesophageal/Gestirc varices
- Why important
- Ix
- Tx
Most common SE of portal HTN
Life threatening
Early endoscopy
1) Terlipressin at presentation + emergency endoscopy
2a) Oesophageal - band ligation, TIPs if not effective
2b) Gastric - Injection of surgical glue then TIPS
Budd Chiari syndrome
- Incidence
- Def
- Assoc
- Pres
Rare
Obstruction of Hepatic veins
Myeloproliferative disorders, Hypercoagulable state (TB, Tumour, Preg)
Sudden RUQ pain, rapid ascites, hepatomegaly, jaundice
Budd Chiari syndrome
- Ix
- Tx
Doppler USS
Begin Warfarin, treat ascites e.g. TIPS
Liver:
- Types
- Common causes
90% secondary (Stomach, colon, lung, breast)
10% primary (HCC - 90%, Cholangiocarcinoma e.g. PSC - 10%)
90% have chronic liver cirrhosis
HCV leading cause in the UK (HBV worldwide commonest)
Liver Ca
- Pres
- Screening (who&how)
- Ix & Diagnosis
Anorexia, weight loss, night sweats, RUQ pain, symptoms of liver failure
HBV/HCV ± cirrhosis, Alc cirrhosis
USS + AFP (over 2cm mass + raised AFP)
Liver Ca Tx
Prognosis
Surgical resection
Radiofrequency ablation
Systemic chemo.
Transplant - according to Milan criteria
6month median survival. death from cachexia, variceal bleeding.
Liver Ca prevention
HBV vaccine
Reduced alcohol
Screen those with cirrhosis
What enzyme converts alcohol and what to?
Alcohol dehydrogenase converts alcohol to acetaldehyde
How doe alcohol cause liver damage?
Inc in NADH(from acetaldehyde) = Oxidative stress = hepatocyte injury
Inhibited gluconeogenesis, carb/protein metabolism
+ Inc Lipogenesis = Fatty liver
Steatosis
- Def
- Types
- When inflamed
Fat accumulation in Liver
Alcohol related fatty liver and non-alcohol fatty liver
Assoc with inflammation (steatohepatitis, NASH if non-alcoholic)
Fatty liver pathophys
Accumulation of triglycerides and lipids in hepatocytes
Defective fatty acid metabolism, excess intake, mitochondrial damage
Steatosis causes
Metabolic syndrome, PCOS, Excess alcohol, HBV/HCV, starvation, Wilson’s, Meds (amiodarone, tamoxifen, glucocorticoids, methotrexate)
Steatosis Presentation
Generally asymptomatic.
Fatigue, RUQ pain, Hepatomegaly
Advanced disease have cirrhosis symptoms (Jaundice, oedema, ascites)
Steatosis Ix and Diagnosis
Biopsy = Definitive
- cells swollen with fatty inclusions
- mallory bodies (eosinophilic cytoplasmic inclusions)
Liver USS echogenic liver
FBC (macrocytes in alcohol)
LFTs raised, ALT>AST
Ddx: viral studies, caerulopasmin, AI (ANA)
Steatosis/Steatohepatitis
Management
Complications
Abstain from alcohol will cause reversal
Weight loss + exercise (inc insulin sensitivity)
Progression to cirrhosis, liver failure, HCC
Triad in alcohol hepatitis/NAFLD
Fever + Mallory bodies + Steatosis
Architecture of liver
Hepatocytes are arranged in Hexagonal lobules with central vein and portal triad (Vein artery and biliary ductiles) at each point of hex.
Sinusoids Connect portal vein and hepatic artery to central vein.
Zone 1-3 going from outer lobule edge –> central vein
Viral hepatitis mechanism
Replication of virus in hepatocytes and secretion into bile
Liver inflammation and necrosis caused by immune response
Hep A
- Type of virus
- Spread
- Area
- Course
- Clinical pres
- Ix
- Tx + Prevent
RNA virus
Faeco-oral (hand-washing, shellfish)
India, Africa, Far East
Self limiting, acute. May take 6 months to recover.
Flu like prodrome.
Hepatitis: Dark urine, pale stool, jaundice, abdo pain, hepatomegaly, pruritus
Viral serology: IgM for Hep A- lasts 6M. IgG produced after 3w and persist years
LFT: rise in ALT, AST, ALP and bilirubin
Vaccinate travellers (live attenuated) Supportive manage (fluids, antiemetics, rest, avoid alcohol, cholertyramine for itch)
Hep E
- Virus type
- Spread
- Prev + Tx
RNA virus
Faeco-oral (heavily assoc with pigs)
Supportive Tx.
Good hygiene, no vaccine exists
Hep B
- Virus
- Spread
- RF
DNA virus (commonest form of hepatitis in world)
Paraenteral (blood or body fluid)
- Vertical: high (90%) if HbeAg +ve
- Horizontal: Sexual, IVDU, Blood prods.
IVDU, sex workers, prisons, healthworkers
HBsAg
HBsAb
HBcAb
HbeAg
HBsAg - Current infection
HBsAb - Shows clearance of infection
HBcAb - Shows immune response to infection. Could be acute/chronic/cleared
HbeAg - In those who are infective
Hep B
- Clinical course
- Pres (acute & chronic)
- Ix
Acute, if persists after 6m = Chronic
Acute
- Prodrome (VANFAM - vomiting, anorexia, nausea, fever, arthralgia, malaise)
- Hepatic: RUQ pain, hepatomegaly, jaundice, darki urine/light stools,
- Occasionally fulminant necrosis (inc INR, need transplant)
Chronic (over 6m)
- Fibrosis, Cirrhosis and HCC
- fatigue, anorexia, nausea, RUQ pain
PCR for HBV, HBV serology
LFT
Screen for liver cancer
HBV serology in:
- Acute
- Chronic
- Cleared
- Vaccinated
Positive for HB core antigen IgM and IgG antibod. HB surface antigen positive and high HBVDNA
Same as acute but no IgM, just IgG
There is anti-HBs (surface antigen) and IgG to core antigen (rest is cleared)
Just positive for antibody for HB surface antigen (Anti-HBs). There is no core antigen in vaccine
Hep B prevention
Blood prod screening, Safe sex
Vaccination at risk (inc children)
Hep B Tx
Acute: Bed rest, fluids, antipyretics, cholestyramine
Chronic: 48 wk injectable interferon alpha (1st line).
2nd line = tenofovir
Screen HCC 6 monthly
Hep B complications
Fulminant hepatic failureRelapseCirrhosisHCCConcurrent HCV/HIV (increases progression to cirrhosis)
Hep C
- Virus
- Spread
- At risk
RNA
Parenteral: Blood, body fluids
sex, IVDU, tattoos, blood transfusion, needle-stick
IVDU, pre 1991 blood transfusion, needle stick
Hep c
- Clinical course
- Symptoms
Acute or chronic
Acute is often asymptomatic
malaise, nausea, RUQ pain, jaundice
Quicker disease progression in viral hepatitis:
Coinfection Hep B/C
Alc
HIV co-infection
Chances of end-stage liver disease in Hep C
⅓ at 25 years, ⅓ after, ⅓ never
Hep C
- Ix
- Tx
PCR Hep C RNA
LFT (AST:ALT over 1)
Degree of fibrosis (if PCR+Ve): Fibroscan, Biopsy
Pegylated interferon alpha + Ribavarin (for 6m)
Aim of Tx to prevent cirrhosis and HCC
AI hepatitis:
- Types of Ab
- Pres
- Ix
- Tx
ANA, ASMA (anti smooth muscle), Anti-liver-kidney-microsomal
Prominent nausea, pruritus and jaundice. URQ discomfort.
Hepatomegaly, splenomegaly, ascites
LFT elevated, autoantibodyscreen (IgG polyclonal hypergammaglobulinaemia)
Prednisolone + Azathioprine
Will need transplant if end stage liver disease
AI hepatitis assoc diseases
IBD, coeliac, proliferative glomerulonephritis, Grave’s, AI thyroiditis, T1DM
Immunosuppression
Liver cysts:
- Causes
- Pres
- Ix
- Tx
Bacterial: Klebsiella, enterococcus
Amoebic: entamoeba histolytica
Polycytic liver disease (ADPKD assoc)
If large: RUQ pain, bloating
USS/CT/MRI, abnormal LFTs
Spontaneous resolution, aspirate
Abx: 3rd gen ceph + metronidazole (just met for amoeba)
ADPKD manage PKD
Acute pancreatitis:
- def
- Causes
Acute inflammation of pancreas. Exocrine enzyme release = autodigestion of organ
GETSMASHED
Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hyperlipid/Hypotherm/Hypercalcaemia, ERCP, Drugs
Acute pancreatitis:
- Presentation
- Signs
Severe, sudden onset epigastric pain + vomiting
Pain radiates to back, relieved by sitting forward
Cullen’s signs: periumbilical bruising
Grey-Turner’s sign: Flank bruising - Retroperitoneal haemorrhage
Epigastric tenderness, Tachycardia, fever, hyperaemia, Jaundice (if cause is gallstones)
Acute pancreatitis:
- Tx
- Imaging
- Ddx
Seruma amylase (also rated in renal fail as renaly excreted), Serum lipase more specific
FBC (leukocytosis), CRP (pancreatic necrosis)
Raised bilirubin
CT w contrast = diagnostic
USS - swollen pancreas ± gallstones
ERCP
Abdo Xray - Retroperitoneal shadow = bleed, Pancreatic calcification
Dissecting AAA
Acute pancreatitis:
- Tx (mild)
- Tx (severe
Pain: buprenorphine ± IV benzodiazepines
IV fluids, Nil by mouth (Stops pancreas stimulation)
HDU/ITU
NG enteral nutrition
ERCP for gallstones
IV antibiotics if evidence of necrosis
Acute pancreatitis: severity criteria
Modified Glasgow score
Complications of Acute pancreatitis:
DIC, Shock, Hypovolaemia, Hypocalcemia/hypoglycaemia
Renal dysfunction
ARDS, pleural effusions
Chronic pancreatitis
- Def
- Typical Patient
- Cause
Chronic inflammation/fibrosis and calcification of pancreases. impaired endocrine and exocrine functions
40y.o. drinker
GETSMASHED
Chronic pancreatitis Presentation
Nausea and vomiting
Exocrine: malabsorption, wt loss, diarrhoea, steatorrhoea (pale, loose, offensive)
Endocrine: diabetes mellitus
Chronic pancreatitis
- Ix
- Tx
Secretin stimulation test - Causes bicarb secretion by pancreas. 60% function loss = +ve result
Malabrosption: Serum trypsinogen, faecal elastase
Imaging: CT (atrophy), MRCP
Manage pain (tramadol) and malabrosption (replace enzymes)
Retroperitoneal structures:
SADPUCKER
Suprarenal Aorta/IVC Duodenum (2+3) Pancreas Ureter Colon Kidney Esophagus Rectum
Pancreatic cancer
- Types
- Better when..
- Worry
- RF
Endocrine or Exocrine
95% Adenocarcinoma, most exocrine
Periampullary present early with obstructive jaundice (better prog)
High mortality, early mets, late pres.
Smoking, alcohol, obese, diabetes, FH, Syndromes (BRCA1/2, FAP, Lynch, MEN)
Exocrine Pancreatic cancer
- Pres
- Ix
Early = Vague - epigastric discomfort, dull backache Painless obstructive jaundice (dark urine, pale stools, pruritus) Epigastric pain (for tail lesions) Gastric outlet obstruction (nausea/vom) Rapid weight loss, Virchow's nod
LFT: Bilirubin, ALP, GGT = jaundice picture
Tumour marker: C19-9
USS liver
Abdo CT (diagnosis and staging)
Pancreatic cancer Tx
Only 10% resectable (often metastatic)
Whipples procedure (proximal pancreaticoduodenectomy)
Adjuvant chemo: 5-FU
Palliation: stent in bile duct for pruritus/jaundice
Chemo/radiotherapy
Endocrine Pancreatic cancer (3% of all)
- Prognosis
- Types and pres
Neuroendocrine tumours
Better prognosis than exocrine tumours
Mainly insulinoma (sweating, dizzy, hypoglycaemia) or Gastrinoma (severe peptic ulcer/diarrhoea due to high HCL)
Gallstones:
- Presentation
- Typical person
- Types of stone
Biliary colic, Acute cholecystitis
Fair, Fat, Fertile, Female, Forty
Cholesterol: 80%
Pigment: 10%, seen in haemolytic conditions
Mixed: 10%, Calcium salts + pigment + Cholesterol
Result of Gallstones. how do they present?
- Biliary colic
- Acute cholecystitis
- Ascending cholangitis
Pancreatits (can be seen with distal CBD stone)
RUQ pain
RUQ pain + fever/WCC, Murphys sign, fatty meals = worse
Charcot’s triad: Jaundice, RUQ pain, Fever
Jaundice, Raised bilirubin/Alk phos/GGT
Biliary colic
- Mech
- Pres
- Ix
- When does Jaundice occur
Temporary obstruction of Cystic/Common bile duct
Sudden onset RUQ pain, radiates to inter scapular region. Lasts 15 min-24hr
Can cause vomitng (GB distension)
USS 90-95% sensitive
When stone moves to CBD (obstruction of outflow)
Acute Cholecystitis
- Cause
- Pres
- Ix
Gallstones (95%), trauma and subsequent inflammatory response to retained bile
Continuous epigastric/RUQ -> R shoulder pain, fever and peritnoism. Fat stimulates CCK = inc pain
Murphy’s sign +ve
Raised WCC, abnormal LFT
USS - Thickened GB wall
ERCP/MRCP
Managing Gall stone complications
Non-surgical:
NBM = stop CCK release
Pain - Parentral opioids or declofenac (NSAID)
Surgical:
Laparoscopic cholecystectomy to remove GB (this is now done early in cholecystitis)
Ascending cholangitis:
- Pres
- Mech
- Organism
- Causes
Charcot’s triad: Fever, RUQ pain, Jaundice
If CBD obstruction flow of bile reduced = biliary stasis and infection.
E.coli, klebsiella, enterococci
Obstruction of GB/CBD: stones, ERCP, tumours (Ca pancreases, Cholangicarcinoma)
This is medical emergency
Ascending cholangitis: Ix and diagnosis
Systemic inflammation:
Temp over 38
Elevated WCC or CRP
Cholestasis: Jaundice (high bilirubin), Abnormal LFT (ALP/ASt/ALT/GGT raised)
Imaging: AUSS, CT, MRCP (evidence stricture/stone, biliary dilatation)
U&E, amylase and blood cultures (worry about complications: pancreatitis, Sepsis, AKI)
Ascending cholangitis Tx
Fluid resus, broad spec Abx
Metroenidazole + Ceftriaxone
If AKI, Shock, DIC –> Endoscopic biliary drainage
Primary sclerosing cholangitis:
- Def
- Assoc
- Pres
Chronic inflammation + fibrosis of intra/extrahepatic bile ducts.
Gives multifocal biliary strictures
Inflammatory bowel (UC), HCC
Abnormal LFT, Jaundice, pruritus, RUQ pain, Fever, Wt loss, Fatigue
Primary sclerosing cholangitis Ix
LFT (alk phos, GGT, raised transaminase), Imaging (USS shows bile duct dilatation and strictures)
Biopsy for staging (onion skin fibrosis)
Primary sclerosing cholangitis Tx
Complications
Baloon dilatation to treat strictures
Colestyramine (pruritus)
Supplement fat soluble Vits (low bile to emulsify fats in intestine)
Portal HTN (Varices) Cholangiocarcinoma
Primary biliary cirrhosis
- Def
- Pres
- Assoc
- Antibody
Slow progressive AI disease with destruction of small interlobular bile ducts
Fatigue, pruritus, RUQ pain, Cholestatic jaundice
Sjogren’s and other AI (thyroid)
Antimitochondiral antibody
Primary biliary cirrhosis Ix
AMA, LFT (raised alk phos), MRCP, Liver biopsy (granulomatous infiltration of portal triad)
Only transplant is curative
Colestyramine (pruritus), Immunosuppression (MTX, Steroids)
PSC Vs PBC
- AAb
- Assoc dis
- Affected vessels
PBC - AMA antibodies
PSC - pANCA antibodies
PBC - Sjogrens and thyroid
PSC - UC and colon cancer
PBC - interlobular ducts
PSC - extra hepatic and intra hepatic ducts
Cholangiocarcinoma
- Type of tumour
- Pres
- Tumour markers
- Ix
- Tx
90% ductal adeno
URQ abdo pain + jaundice + cholestasis + pruritus + hepatomegaly + wt loss
Ca19-9 and CEA
MRI best. AlsoUSS/CT
Surgery but only 33% resectable.
Palliative: stent and ERCP
Cholestasis symptoms mech
Bile cannot flow from GB (stored) to Duodenum.
Conjugated bilirubin regurgitation to serum (inc conc)
Pale stools/Dark urine: urobilinogen can not be formed in gut. High conjugated bilirubin is excreted in urine (dark)
Pruritus (Bile salt irritation)
What is diff between prehepatic and post hepatic jaundice
Unconjugated bilirubinaemia higher in pre hepatic
Conjugate higher in post hepatic
Bilirubin product excreted in gut and in kidneys
Gut = Stercobilin
Kidneys = Urobilin
Types of Jaundice
Pre-hepatic: haemolytic (unconjugated hyperbilirubinaemia e.g. malaria, sickle cell, thalassaemia, G6PDD)
Hepatic: Hepatitis, fibrosis/cirrhosis, Para/rifampicin/statins
Post-hepatic: Cholestasis, Anabolic steroids
