Hepatology, Mhu, Mbbs Iv

Front 1

Childs-Pugh Score Cirrhosis

Back 1

Front 2

Child's pugh interpretation + survival

Back 2

Front 3

Hepatorenal syndrome def

Back 3

Dev. renal failure in px with advanced chronic liver disease + sometimes fulminant hepatitis. Caused by portal HTN.

~40% of patients with cirrhosis and ascites will develop HRS during the natural history of their disease

Front 4

hepatorenal patho

Back 4

stressor eg. infection, gastrointestinal hemorrhage, or major surg + liver failure inc. NO,and other factors=>systemic vasodilation=> dec. Renal perfusion pressure=>Activation of renal SNS=> vasoconstriction ofthe afferent renal arterioles + inc. Synth renal vasoactive mediators => dec. renal perfusion + GFR =>Na+ retention + Impaired free H2O excretion + poor urine output, inc BUN and creatinine

Front 5

Prognosis and tx hepatorenal syndrome

Back 5

- Median survival of only 2 weeks in the rapid-onset form and 6 monthswith the insidious-onset form

- Treatment = liver transplantation.

Front 6

Cirrhosis sequale

Back 6

- Hepatorenal

- Oedema: dec albumin prod,

- Bleeding/low platelets: dec. TPO, dec vit K dep clotting factors 2, 7, 9, 10

- Hypoglycaemia: dec gluconeogenesis

- Macrocytic anaemia: dec vit B12 storage

- Gyenecomastia, shrunken testes, spider naevae, palmar erythema: dec. steroid clearance=>inc oestrogen

- Confusion, encephalopathy, asterixis: dec metabolism of toxins (esp. ammonia)

- Varices: portal HTN

- Splenomegaly: portal backflow=>sequestration red cells + haemolytic anaemia

- Ascites: Portal HTN, low albumin, Na retention, systemic vasodilation

Front 7

Cirrhosis s/s

Back 7

Skin:includejaundice, spider angiomata, skin telangiectasias ("paper moneyskin"), palmar erythema, white nails, disappearance of lunulae, clubbing

Systemic: Fatigue,weakness, weight loss, ascites, pruritis, hepatosplenomegaly, bruising, shifting dullness, fluid thrill, altered mental status (d/t portosystemic encephalitis), hepatic fetor (portosystemic shunting)

Oestrogen: loss of secondary sexual hair, gyenecomastia or breast atrophy(women), testicular atrophy, dec libido

Albumin: leg oedema, muscle wasting,

Immunity: inc infections

Platelet dysfunction: Bleeding

Front 8

Steatosis definition and causes

Back 8

Accumulation of lipid within hepatocytes, most common histologicresponse to hepatotoxic stimuli, reversible

- Causes: excessive alcohol intake, starvation, certain drugs and toxins,acute fatty liver of pregnancy,

Front 9

Steatohepatitis definition and causes

Back 9

Liver cell damage (includes ballooning degeneration and apoptosis), variable degrees of fibrosis, steatosis and inflammatory cell infiltrate (neutrophils mainly)

- Causes: Alcohol ingestion (alcoholic hepatitis), obesity, DM, dyslipiaemia, certain drugs

Front 10

NASH

Back 10

- Hepatocyte injury that may progress to cirrhosis in 10-20% cases

- Strongly associated with obesity/insulin resistance/dyslipidemia/hyperinsulinemia

- Main components: Hepatocyte ballooning, Lobular inflammation, Steatosis, With progressive disease, fibrosis develops

Front 11

NASH pathogenesis

Back 11

Genetics + environmental factors cause: (May include: insulin resistance & inc beta cell secretion of insulin =>dec. lipolysis in liver & inc. storage of TAG by hepatocytes=> adipose tissue releases inflammatory mediators) Hepatic fat accumulation + oxidative stress => lipid peroxidation and the release of lipid peroxides => reactive oxygen species= ballooning degeneration& apoptosis=>Progression of necroinflammatory and fibrotic processes=>cirrhosis

Front 12

NASH histology

Back 12

- Steatosis and multifocal parenchymal inflammation, mainly neutrophils, Mallory (Denk) bodies, hepatocyte death (both ballooning degeneration and apoptosis), and sinusoidal fibrosis.

- Fibrosis also occurs within portal tracts and around terminal hepatic venules (sim to alcoholic hepatitis)

- Progression of necroinflammatory and fibrotic processes=> cirrhosis

Front 13

Steatosis histology

Back 13

Usually involves more than 5% of the hepatocytes and sometimes more than 90%. Large (macrovesicular) and small (microvesicular) droplets of fat, predominantly triglycerides, accumulate within hepatocytes No appreciable hepatic inflammation, hepatocyte death, or scarring, despite persistent elevation of serum liver enzymes

Front 14

Acute liver failure

Back 14

- Acute liver injury with an encephalopathy within 6months

- “Fulminant” if the encephalopath <2 weeks of jaundice onset & sub-fulminant if in <3months

- Caused by massive hepatic necrosis

- Most often after poisoning with toxins or drugs

- Paracetamol causes 50%, other:mushroom poisoning, rifampin, isoniazid, MAO inhibs, industrial chemicals eg.carbon tetrachloride, Hep A (4%) and B (8%). Hep C is a rare cause

Front 15

Hepatic encephalopathy epi, path

Back 15

- Subtle in 70% cirrhosis px

- Overt in 30-45%

- Neurotoxins accumulate=>damage astrocytes=>BBB damage=>toxins (eg. ammonia) can enter brain

- Also episodic subtype

Front 16

Hepatic encephalopathy s/s. epi

Back 16

Mood disturbances like euphoria or depression, insomnia or hypersomnia, motor disturbances eg. Asterixis or ataxia, somnolence, confusion, which may be followed by unconsciousness or coma. Hyper-reflexia, nystagmus, clonus,hemiplegia,

1 in 200-500 people

Front 17

Haemochromotosis s/s

Back 17

Most common autosomal recessive genetic disorder. Adult onset

- Asymptomatic in 75%/presents in a generalisedway with severe fatigue, impotence and arthralgias

- OR hepatomegaly, skin pigmentationand arthritis, DM, cardiomyopathy, amennorrhoea/impotence/hypogonadism, Koilonychia, hair loss, oseteopoenia/porosis

Front 18

Haemochromotosis path

Back 18

Errorof iron metabolism =>inappropriately high iron absorption=>progressive iron overload=> creation free radicals=>inflammation and fibrosis of liver,heart, pancreas, pituitary, joints, and skin

HFE mutations responsible (C282Y, H63D)

Front 19

Haemochromotosis ix and mgmt

Back 19

- Genetic testing:Examination of HFE mutations (C282Y, H63D) is pivotal for diagnosis ofhemochromatosis

- Transferrin saturationlevels

- Serum ferritin studies

- Hepatic iron concentration

MGMT: phlebotomy and chelation, organ transplant

Front 20

Primary biliary cirrhosis epi

Back 20

- Presumed autoimmune

- Female predominance

- Onset in 40s-60s

- Progressive cholestasis and ESLD

Front 21

Primary biliary cirrhosis s/s

Back 21

Fatigue, Pruritus, Right upper quadrantdiscomfort.

PE (advanced disease):- Hepatomegaly/spleno, Hyperpigmentation, Jaundice, Xanthelasmas(10%) + stigmata of ESLD

Front 22

Primary Biliary Cirrhosis patho

Back 22

CD4/8+ lymphocytes aberrantly activated and destroy small & medium bile ducts +bile duct epithelial cells+ hepatocytes display inc. HLA-II(easily targeted by lymphocytes)=> unable to regenerate=> cholestasis=>deposition of toxins (eg. bile acids and copper)=>more destruction of bile ducts &hepatocytes=>

Front 23

Primary biliary cirrhosis, ix

Back 23

• inc ALP, γ-glutamyl transpeptidase (GGTP), & immunoglobulin levels(mainly IgM): (Usually the most prominent findings)

• antimitochondrialantibodies (AMAs) in serum. AMAs found in 90-95%, specificity 98%

• inc ALT and AST

• inc lipid and cholesterol levels, with an inc HDLfraction

• inc ESR

• inc bilirubin level, prolonged prothrombin time, & inc albuminlevel:progression to cirrhosis

• Thrombocytopenia: portal HTN

• Antinuclear antibodies(ANAs): Can be identified in 20-50% of patients with PBC

Front 24

PBC mgmt

Back 24

• Ursodeoxycholic acid (UDCA)slows progression disease (a bile acid, it's activated by intest bact)

• Methotrexate improves biochemical and histologic findings

• Corticosteroids alleviate sympts + improve biochem and histo

- Antihistamines for pruritis, but contraindicated in encephalopathy

Front 25

Wilson's Disease path

Back 25

• Mutationin gene that codes for binding protein that binds copper=>copper secretd into bile + Copperaccumulates in liver and other areas including the brain, eyes, kidneys =>cirrhosis, arthropathy,

Front 26

Wilson's disease s/s

Back 26

- Chronicactive hepatitis=>Cirrhosis(the most common initial presentation), Fulminanthepatic failure, jaundice, pruritis, thrombocytopoenia

- Ataxia, Mask facies, hand clumsiness, personality change

- Osteopenia• Arrhythmias• Keyser-Fleischerrings• Urolithiasis/Haematuria

Front 27

Wilson's disease tx

Back 27

- Will eventually require liver transplant

Front 28

HCC s/s

Back 28

In past: advanced stage, RUQ pain, weightloss, early satiety, signs of decompensated liver disease.

Now, routine surveillance of cirrhosis px, asymptomatic when picked up

Front 29

HCC ix

Back 29

- CBE: microcytic anaemia (d/t potential varicealbleeds)/thrombocytopenia (d/t portal HTN)

- Metabolic panel: inc urea (hepatorenal), low Na (diuretic use or vol overload)

- LFTs: inc transaminases, inc bilirubin, inc ALP, dec. albumin

- PTT/INR normal/inc

- a- fetoprotein: inc. in 75%, esp. advanced disease.Mild inc. in chronic hepatitis

- Liver ultrasound

- Viral hepatitis panel

Front 30

HCC tx

Back 30

- Resection if early stage(Comps: Postoperativehaemorrhage and liver failure)

- Liver transplant with transarterial chemo embolization(TACE) or radiofrequency ablation (RFA can damage large areas of liver+cause hepatic failure in patients with decompensatedcirrhosis or large tumour.)

as a bridging tx while waiting for a liver

- Percutaneous ethanol injection

- Sorafenib (chemo agent for advanced disease)

Front 31

Wilson's disease tx

Back 31

- Zinc (binds intestinal copper&stops absorption)

- Trientine 6 mnths (chelator, enhances urinary excretion of copper. SE bone marrow suppression, drug-induced lupus, proteinuria, neurological worsening in 25%)

- Liver transplant

- Avoid Cu rich foods (shellfish, liver)

Front 32

Primary Sclerosing Cholangitis def

Back 32

Autoimmune characterized by a progressive course of cholestasis with inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts=>cirrhosis

Front 33

PSC associated conditions

Back 33

Strongly assoc. w IBD,mainly UC, and is often complicated by cholangiocarcinoma. A inc. risk of colorectal cancer exists in UC px with PSC.

Front 34

PSC s/s

Back 34

- age in 40s or 50s

- abdo pain, pruritus, fatigue, weight loss, fever, jaundice, steatorrhoea, splenomegaly, ascites, encephalopathy. Stigmata cirrhosis

Front 35

PSC ix

Back 35

- Transaminase elevation

- Low albumin

- Raised bilirubin (mostly conjugated)

- CBE: thrombocytopaenia ± anaemia, leukopaenia (d/t liver synthetic fcn disturbance)

- PTT can be prolonged

- Abdo USS

- MRCP (if suspected no intervention needed) or ERCP: dominant biliary stricture (40-50% over time), intrahepatic and extrahepatic duct involvement in 50% to 70% of cases. There is intrahepatic duct-only involvement in 15% to 25% of cases. There is extrahepatic duct-only involvement in <5% of cases

Front 36

PSC tx

Back 36

- Lifestyle + obs if asympt (weight, diet, alcohol)

- Colon ca. screening if concominant UC

- Pruritis control w rifampicin

- Corticosteroids for immunosupp.

- ERCP for strictures (balloon + stent)

- Liver transplant for ESLD

Front 37

Alph-1 antitrypsin deficiency epi

Back 37

-1-5% of px with COPD

- Common in whites (1 in 1600)

- 1 in 3000-5000 worldwide

- m=f

- Emphysema in 4th dec life smokers, 5th non-smokers, jaundice in babies, liver failure in kids

Front 38

Alph-1 antitrypsin deficiency

Back 38

Mutation in SERPINA1=>malformed alpha1-antitrypsin + can't release from hepatocytes=> dec serum A1A=> low alveolar conc.=> can't protect against proteases (eg. neutrophil elastase)=> protease excess=> destroy alveolar walls=>emphysema.

- Accumulation of A1A in hepatocytes=>destruction=>cirrhosis

Front 39

Alph-1 antitrypsin deficiency s/s

Back 39

Productive cough, SOB on exertion, hepatomegaly, ascites, confusion, wheezing, chest hyperinflation, scleral icterus/jaundice, asterixis

s/s emphysema/cirrhosis

Front 40

Alph-1 antitrypsin deficiency ix

Back 40

- Dec AAT in serum

- CXR - PFTs - LFTs

Front 41

Alph-1 antitrypsin deficiency tx

Back 41

- Avoid smoke/occupational fumes/alcohol

- Hep A and B, flu vaccines

- Normal cirrhosis and emphysema tx

- Alpha1-proteinase inhibitor

Front 42

Acute hepatitis definition, presentation

Back 42

- Lasts <6 months

• most are subclinical

• flu-like prodrome may precede jaundice by 1-2 wk

- N/V, anorexia, taste/smell disturbance, headaches, fatigue, myalgia, low-grade fever arthralgia and urticaria (especially HBV)

• Some progress to icteric phase, lasting days-weeks

- Pale stools and dark urine 1-5 d prior to icteric phase

- Hepatomegaly and RUQ pain

- Splenomegaly and cervical lymphadenopathy (10-20% of cases)

Front 43

Hep A, s/s

Back 43

- RNA virus fecal-oral transmission

- incubation period 4-6 wk diagnosed by elevated transaminases, positive anti-HAV IgM

- In children: characteristically asymptomatic in

- adults: fatigue, nausea, arthralgia, fever, jaundice

- can cause acute liver failure and subsequent death (<1-5%) can relapse, but never becomes chronic

Front 44

Hep B seroconversion

Back 44

- Loss of HBeAg and appearance of anti-HBe

- occurs as early as 2 weeks in acute infection or may take years in chronic infection

- Assoc w a lower level of HBV DNA or a low replicating state of the virus

- Implies clinical improvement and can help predict long-term clearance of the virus.

- Can be used to monitor response to treatment and possible remission of the disease (HBV PCR is an earlier sign)

Front 45

ddx hepatomegaly

Back 45

- Congestive (right heart failure, Budd-Chiari syndrome: thrombotic or nonthrombotic obstruction of the hepatic venous outflow)

• Infiltrative

* Malignant (primary, secondary, lymphoproliferative, leukemia)

* Benign (CHAFE: cysts, hemochromatosis, amyloid, fatty liver, extramedullary hematopoiesis, )

• Proliferative

* Infectious (viral, tuberculosis, abscess, echinococcus, malaria)

* Inflammatory (granulomas [sarcoid], histiocytosis X)

Front 46

4 Stages Hep B

Back 46

1. Immune tolerance

Extremely high HBV DNA, HbeAg pos, normal ALT/AST b/c little immune control=>little immune mediated liver damage (incubation period)

2. Immune Clearance

Falling HBVDNA, HBeAg pos, immune attack on virus=>immune mediated liver damage=>increasing fibrosis=>cirrhosis if not stopped

3. Immune control

Low HBVDNA <20,000 (other stages all >20K), HBeAg neg, anti-HBe pos, ALT/AST normal d/t immune control + less damage, risk of reactivation to stage 2 esp w. immunosuppression

4. Immune escape

Elevated HBVDNA (>20K), HBeAg neg b/c of pre-core or core gene mutation, anti-HBe pos, ALT/AST high=> progressive disease w/o tx=>fibrosis=>cirrhosis=>HCC

Front 47

HBe mutations explained

Back 47

There is a high error rate associated with the reverse transcription step in HBV replication. As a consequence, HBV has a mutation rate 10-fold higher than that of other DNA viruses. The most potent selective force during the natural course of HBV infection is the host immune response. As a consequence of the development of anti-HBe and the reduction in HBV viremia, "escape" mutants of anti-HBe are selected. Because HBeAg expression is not essential for virus replication, the virus can evade anti-HBe immunity by turning off or reducing HBeAg expression.

- Respond poorly to IF-a

- Lamivudine, entecavir, and adefovir are regarded as safe and efficacious, but they usually require treatment over several years.

Front 48

Hep D

Back 48

- Requires HBsAg for entry into hepatocyte, therefore px must have HBV;

=> more aggressive disease

- coinfection: acquire HDV and HBV at the same time better prognosis than superinfection (acute HDV infection on pre-existing HBV infection)

- HDV can present as ALF and/or accelerate progression to cirrhosis

Front 49

Hep C chronicity rates

Back 49

- 80% become chronic, 20% of these get cirrhosis

Front 50

Spontaneous clearance rates hep

Back 50

~25% clear spontaneously

- clearance rates are even higher in symptomatic patients (up to 40%), young females, and patients with favourable IL28B polymorphisms.

Front 51

RFs for cirrhosis progression from Hep C

Back 51

- alcohol consumption

- obesity

- type 2 diabetes

- older age at infection

- male sex

- longer duration of infection

- co-infection with hepatitis B, HIV or schistosomiasis

- inflammation on liver biopsy

- heavy cannabis use

- tobacco use

Front 52

Extrahepatic manifestations of Hep C

Back 52

● Hematologic diseases such as cryoglobulinemia & lymphoma

● Autoimmune disorders such as thyroiditis

●Renal disease

●Dermatologic: lichen planus & porphyria cutanea tarda

Front 53

Hep C genotype prevalance in aus

Back 53

Genotype 1 (54%) and genotype 3 (37%) with genotype 2 accounting for around 5%.

Front 54

Autoimmune Hep presentation, mortality

Back 54

- Can present as acute (fever, hepatic tenderness, and jaundice) or chronic hep, well established cirrhosis, rarely fulminant hepatic failure.

- Mostly insidious onset

- S/s assoc diseases

- 40% mortality at 6 mo without treatment

- Diagnosis of exclusion rule out viruses, drugs, metabolic, or genetic causes

Front 55

Diseased assoc w autoimmune hep

Back 55

- Pretty much everything autoimmune

- IBD, Raynaud’s, RA, thyroiditis, Sjögren’s,

hypergammaglobulinemia,

Front 56

Cirrhosis morphology

Back 56

- Bridging fibrous septa

- Parenchymal nodules

*Hepatocytes encircled by fibrosis *Results from cycles of scarring and repair * Can vary in size (micro/macronodular)

- Disruption of entire liver architecture - Type I and III collagen layed down in space of disse(where it is usually type IV and type I and III are concentrated in the portaltracts and around the central veins). This aberrant collagen creates thefibrous septae tracts

- Collagen layed down by stellate cells that haveproliferated and become myofibroblasts through signals from Kupffer cells andlymphocytes (eg. TGFb and metalloproteases), plus direct stimulation by toxins, chronic inflamm,lipid peroxidation products, disruption of the ECM etc

- Loss of fenestration in the sinusoids + angiogenesisalong the newly fibrotic tracts shunting blood away from parenchyma => decrease exchangebetween hepatocytes and plasma

- Myofibroblasts are contractile cells => constrictsinusoidal vascular channels=> inc. vascular resistance

- Viable cells are encouraged to regenerate as nodules=> fibrotic, nodular liver

- Delivery of blood + secretory ability of liver very much impaired

- Biliary tracts can be obliterated=>jaundice

Front 57

Ascites mechanism cirrhosis

Back 57

1. Sinusoidal hypertension, altering Starling forces+ hypoalbuminemia. =>drives fluid intothe space of Disse=>
removed by hepatic lymph=>Percolation of hepatic lymph into the peritonealcavity. Heptic lymph flow exceeds thoracic duct capacity so stays in peritoneum. Hepatic lymph is richin proteins and low in triglycerides=>protein inthe ascitic fluid. 


2. Splanchnic vasodilation + hyperdynamic circulation (mediated by NO triggered by decreased bacterial DNA clearance)

* Arterial vasodilation=>reduce arterial blood pressure=> CO unable to maintain the BP=>triggers RAAS+ADH=>portal HTN+ vasodilation + sodium/water retention =>inc. perfusion pressure of interstitial capillaries, causing extravasation offluid into the abdominal cavity.

Front 58

Porto-systemic shunt mech

Back 58

Portal HTN => flow reversed by dilation of collateral vessels + development of newvessels=>Venous bypasses develop wherever the systemic and portal circulationshare common capillary beds.

Causes haemorrhoids, caput medusae, varices, splenomegaly

Front 59

Hepatorenal

Back 59

Systemic vasoldilation & NO release=>dec. BP=>activation RAAS=>retention of Na+ H2O=>more ascites.

All the while low BP=> dec renal perfusion=>constriction afferent arteriole in order to inc GFR=>

- dec urine output

- Urea&creatinine

- rapid development of renal failure if there's precipitatingstress eg. infection, GI hemorrhage, majorsurgical procedure.

o Median surviva 2 weeks in the rapid-onset form and 6 monthswith the insidious-onset form

Front 60

Hepatopulmonary

Back 60

inc NO=>systemic vasodilation=>V/Q mismatch (more perfusion, normal V w inhibited hypoxic vasoconstriction)=>oxygenation defect

Clinically: - Dyspnoea (worse of sitting up - platypnoea) anddefects of saturation

Front 61

1o Biliary Cirrhosis. def, presentation, s/s

Back 61

- Presumed autoimmune

- Female predominance

- Onset in 40s-60s

- Progressive cholestasis and ESLD

- 25% are incidentally diagnosed during a routine bloodevaluation.

Front 62

s/s 1o biliary cirrhosis

Back 62

- Fatigue (65% of patients): The first reported symptom

- Pruritus (55%)

- Right upper quadrant discomfort (8-17%)

- Advance disease s/s cirrhosis + sicca sx

• Hepatomegaly (25%) • Hyperpigmentation (25%)

• Splenomegaly (15%)

• Jaundice (10%)

Front 63

1o bil cirrhosis patho

Back 63

Continuous destruction of small+med bileducts, mediated by CD4 and CD8=> chronic cholestasis=> no bile flow, deposition of toxins (eg. bile acids, copper)=>2o destruction bile ducts + hepatocytes (which have inc. expression HLAII)

- Ducts cannot regenerate

Front 64

Alcoholic hepatitis epi

Back 64

-Occurs in 35% alcoholics, usually reversible w tx

- Mech:

*ETOH increases gut perm=>inc bact. translocation

*ETOH binds to hepatocytes=>immune rxn

*ETOH metab=>hypoxia zone III liver=>necrosis

*ETOH metab reduces NAD+ to NADH=>inc. NADH=>dec. ATP in liver=I lipolysis=>fatty acids/TAGs in liver

Front 65

Alcoholic hepatitis histology

Back 65

- Ballooning

- Mallory-Denk bodies, surrounded by neutrophils

- Large fat globules

- Fibrosis of space of Disse and perivenular

Front 66

Alcoholic hepatitis s/s

Back 66

Fatty liver:

- Mildly tender hepatomegaly, jaundice rare

- mildly inc transaminases <5x normal Alcoholic hepatitis

- Mild: stops drinking because feels unwell, resumes when feeling better, potentially mild jaundice, mildly elevated INR)

- Severe: stops drinking but feels unwell, low grade fever, RUQ discomfort, inc WCC

ddx: RLL pneumonia, cholecystitis

Front 67

Alcoholic hepatitis mortality

Back 67

- Immediate: 30%-60% in the first 6 mo if severe - With continued alcohol: 70% in 5 yr

- With cessation: 30% in 5 yr

Front 68

1o sclerosing cholangitis def, epi, aetiology

Back 68

- Narrowing of biliary tree (intra and extrahepatic bile ducts from scarring)=>cirrhosis

- Thought to be autoimmune

- Mostly primary

*assoc w IBD (70% UC px - usually male)

* one of the most common indics for liver transplant

- Secondary

*Long term choledocholithiasis

*cholangiocarcinoma

*surgical trauma/post ERCP

*HIV

Front 69

1o sclerosing cholangitis s/s

Back 69

• Often insidious, may present with fatigue and pruritus

• May present with signs of episodic bacterial cholangitis secondary to biliary obstruction

- 10-15% increase cholangiocarcinoma risk, difficult to tx

Front 70

Cholangitis

Back 70

- Charcot's triad: fever, jaundice, and RUQ pain

- Infection biliary tract, most respond to abx, but some may need urgent biliary drainage