cirrhosis and portal hypertension in children
TRANSCRIPT
I, caudate lobe; II-IV the I, caudate lobe; II-IV the left-; V-VIII the right left-; V-VIII the right hemiliverhemiliver
Functional unit: Functional unit: acinus acinus PT: PT: PV, arteriole, bile PV, arteriole, bile
ductuleductule
Zone 1 Zone 1 is well O2; more is well O2; more resistant than zone 3. resistant than zone 3.
Sinusoids Sinusoids lack BM; have lack BM; have fenestrated endoth. Bile fenestrated endoth. Bile
canaliculi join to form canaliculi join to form bile ductulesbile ductules
BM: basement membrane
THV: terminal hepatic venule
PT: Portal triad
Cirrhosis & Portal Cirrhosis & Portal HypertensionHypertension
Cirrhosis: OverviewCirrhosis: Overview L. processes nutrients & filter blood; controls BGL & L. processes nutrients & filter blood; controls BGL &
cholesterol, & makes coagulantscholesterol, & makes coagulants It can regenerate: large portion can be removed. But if the It can regenerate: large portion can be removed. But if the
damage is chr., repair fails & scars: damage is chr., repair fails & scars: cirrhosiscirrhosis It cannot be reversedIt cannot be reversed Goal: stop progress, by Rx underlying causeGoal: stop progress, by Rx underlying cause
Cirrhosis have serious complications like PH & Cirrhosis have serious complications like PH & hepatopulmonary syn. It can also increase risk of HCChepatopulmonary syn. It can also increase risk of HCC
In children d. of biliary tract & inherited d. are the most In children d. of biliary tract & inherited d. are the most common. Adults: alcoholcommon. Adults: alcohol
DefinitionDefinition
Chr. liver d.: Chr. liver d.: progressive damage & regen. of progressive damage & regen. of liver parenchyma lasting liver parenchyma lasting >6mo. >6mo. It canIt can lead to lead to cirrhosis. cirrhosis. Causes:Causes: inf., metabolic, genetic, drugs, ., metabolic, genetic, drugs, idiopathic, idiopathic, structural d., HCC & AIDstructural d., HCC & AID
Cirrhosis: Cirrhosis: scarring of Liver from injury/long-term d. scarring of Liver from injury/long-term d.
blocking BF: blocking BF: HC failure & HC failure & Portal HTNPortal HTN
Chr. Hepatitis: Chr. Hepatitis: chr. inflam. inchr. inflam. inliver leading to cirrhosisliver leading to cirrhosis& liver failure; persistent & liver failure; persistent for a period of 6mofor a period of 6mo
BF: blood flow. D: disorder/diseaseBF: blood flow. D: disorder/disease
At the end we will learnAt the end we will learn
>100 liver diseases>100 liver diseases CLD is rare in children (1/5000)CLD is rare in children (1/5000) CLD may be CLD may be idiopathicidiopathic Most CLD are preventableMost CLD are preventable Commonest c/of PH is cirrhosisCommonest c/of PH is cirrhosis Commonest c/of HCC is HBVCommonest c/of HCC is HBV HCV is curableHCV is curable
CLD: chr. liver d. PH: portal HTN. HCC: HC CaCLD: chr. liver d. PH: portal HTN. HCC: HC Ca
Etiology of Cirrhosis/CLD & PHEtiology of Cirrhosis/CLD & PH
InfectionsInfectionsLiver disorders: Liver disorders: Bile ductal blockages: Bile ductal blockages: Drugs & toxins: Drugs & toxins:
Liver disorders:Liver disorders: – Autoimmune hepatitis:Autoimmune hepatitis:– Chr. Chr. alcoholismalcoholism– Hereditary:Hereditary:
HemochromatosisHemochromatosis αα1-antitrypsin deficiency1-antitrypsin deficiency GSDGSD GalactosemiaGalactosemia Cystic FibrosisCystic Fibrosis Fructose intoleranceFructose intolerance TyrosinemiaTyrosinemia Wilson DWilson D
– Indian childhood cirrhosisIndian childhood cirrhosis
Autoimmune Liver DiseasesAutoimmune Liver DiseasesBy autoantibodies; rare in children: By autoantibodies; rare in children: 2% of LD in 2% of LD in specialized pediatric L. centersspecialized pediatric L. centersBroad clinical spectrum. Broad clinical spectrum. Quickly responds to steroids Quickly responds to steroids
& immunosuppressants& immunosuppressantsCommon Common SS: SS: tiredness & unwellness, anorexia, school tiredness & unwellness, anorexia, school deterioration. deterioration. HSM, abnormal LFT, HSM, abnormal LFT, autoantibodiesautoantibodies, , characteristic liver characteristic liver biopsybiopsy
Dx Dx is often by is often by exclusionexclusion. Anti-sm Ab, anti-liver kidney . Anti-sm Ab, anti-liver kidney microsome type 1 Ab, ANA. Biopsy may be necessary microsome type 1 Ab, ANA. Biopsy may be necessary for for type & severity of L. damagetype & severity of L. damage2 types: 2 types: AIH & AI sclerosing cholangitisAIH & AI sclerosing cholangitis
Inherited liver diseasesInherited liver diseases
2 common are 2 common are haemochromatosis & alpha-1 antitrypsin d.haemochromatosis & alpha-1 antitrypsin d.
Haemochromatosis: Haemochromatosis: excess Fe is absorbed & deposited. excess Fe is absorbed & deposited. The commonest is hereditary. 2y HC occurs in The commonest is hereditary. 2y HC occurs in
hemolytic a. Genetic HC affects M x5. As F hemolytic a. Genetic HC affects M x5. As F menstruate, are unlikely menstruate, are unlikely to show SS till >10y after to show SS till >10y after MP. MP. More in N Europe More in N Europe
SS: SS: HM, joint p, fatigue, wt loss, darkening of skin HM, joint p, fatigue, wt loss, darkening of skin ("bronzing“), AP, loss of libido. DM & heart d. may ("bronzing“), AP, loss of libido. DM & heart d. may dev.; also cirrhosis, HCC, testicular atrophy. Blood Fe dev.; also cirrhosis, HCC, testicular atrophy. Blood Fe is is confirmatory. HC DNA confirmatory. HC DNA test is done for screeningtest is done for screening
Rx.Rx. of haemochromatosis of haemochromatosis
Goal: Goal: remove excess Fe. Fe is removed by phlebotomy: ½L remove excess Fe. Fe is removed by phlebotomy: ½L blood is removed/w for 2-3y until Fe is reduced; then blood is removed/w for 2-3y until Fe is reduced; then less frequentlyless frequently
Avoid dietary Fe, most commonly offal, fortified BF Avoid dietary Fe, most commonly offal, fortified BF cereals, Fe medicinescereals, Fe medicines
Limit Limit vitamin Cvitamin C No alcoholNo alcohol If HC has caused cirrhosis, the risk If HC has caused cirrhosis, the risk
of HCC is higherof HCC is higherScreening/6moScreening/6mo
Alpha-1 antitrypsin d.Alpha-1 antitrypsin d.
an imp. liver protein A1AT, an imp. liver protein A1AT, is lacking/low. Pts. can is lacking/low. Pts. can make it; make it; but, the disease prevents entrance to blood & it but, the disease prevents entrance to blood & it
accumulates in liveraccumulates in liver
A1AT A1AT protects lungs from damage. protects lungs from damage. The lungs become The lungs become damaged: SoBdamaged: SoB
1% COPD have it. Risk of cirrhosis is high 1% COPD have it. Risk of cirrhosis is high
SS: SS: first symptoms appear usually in lungs: COPD: first symptoms appear usually in lungs: COPD: SoB/ SoB/
wheezing, unexplained wt loss & barrel-shaped chest wheezing, unexplained wt loss & barrel-shaped chest As As it progresses, SS of cirrhosis may appear it progresses, SS of cirrhosis may appear
A1AT in blood will confirm A1AT in blood will confirm
Rx.: Rx.: No cure. Replacement has been triedNo cure. Replacement has been tried
Rx COPD & cirrhosis: ABT, inhaled medications. DiureticsRx COPD & cirrhosis: ABT, inhaled medications. Diuretics
& other measures to reduce edema& other measures to reduce edema No alcohol, smokingNo alcohol, smoking Healthy dietHealthy diet Flu & pneumonia vax.Flu & pneumonia vax. Treat inf. Treat inf. asapasap. Occasionally the lungs or liver deteriorate . Occasionally the lungs or liver deteriorate
despite Rx. Lung/liver transplant may be neededdespite Rx. Lung/liver transplant may be needed With appropriate Rx A1AT is usually not fatal. But, With appropriate Rx A1AT is usually not fatal. But,
complications a/with them can be fatalcomplications a/with them can be fatal It is v. imp. that people with inherited LD do all they can It is v. imp. that people with inherited LD do all they can
to stay healthyto stay healthy
Wilson DWilson D AR; 1/30,000; typically in 2AR; 1/30,000; typically in 2ndndD (neurological 3D (neurological 3rdrd D) D) Mutations in ATP7B Cu translocase, a protein mainly Mutations in ATP7B Cu translocase, a protein mainly
expressed by the hepatocyte to regulate Cu. ATP7B expressed by the hepatocyte to regulate Cu. ATP7B synthesize ceruloplasmin. Cu accumulates within L. The synthesize ceruloplasmin. Cu accumulates within L. The severity of L damage: asymptomatic - cirrhosis. 2/3severity of L damage: asymptomatic - cirrhosis. 2/3rdrd show show hemolysis., coagulopathy, & renal failure. 6% WD have ac. hemolysis., coagulopathy, & renal failure. 6% WD have ac. LD. KF rings are seen in 50%. 50% show psychiatric- LD. KF rings are seen in 50%. 50% show psychiatric- psychotic SS. Rx can now effectively treat & gene therapy is psychotic SS. Rx can now effectively treat & gene therapy is effective in animal modelseffective in animal models
Low S. ceruloplasmin & high urine Cu help to perform the Low S. ceruloplasmin & high urine Cu help to perform the Dx in most cases, some false negatives are describedDx in most cases, some false negatives are described
Severe mutations (nonsense, frameshift) are a/with the Severe mutations (nonsense, frameshift) are a/with the most severe d, while missense mutations (60%) show a most severe d, while missense mutations (60%) show a variable severity & outcome. Liver biopsy is now used in variable severity & outcome. Liver biopsy is now used in cases with ambiguous biochemical parameters & to cases with ambiguous biochemical parameters & to evaluate liver Cu levelsevaluate liver Cu levels
Bile ductal blockagesBile ductal blockages
– Cong.: biliary atresia Cong.: biliary atresia – Sclerosing cholangitis– Gallbladder surgeryGallbladder surgery
Drugs & toxinsDrugs & toxins– Paracetamol. arsenic, INH Paracetamol. arsenic, INH
– MethotrexateMethotrexate
– Excess vitamin A, ironExcess vitamin A, iron
– Afla toxinAfla toxin
InfectionsInfections– Hepatitis B, C, DHepatitis B, C, D– Schistosomiasis, brucellosisSchistosomiasis, brucellosis
– Echinococcosis, advanced or cong. syphilisEchinococcosis, advanced or cong. syphilis
Indian Childhood CirrhosisIndian Childhood Cirrhosis
a CLD of children (1–3y) due to deposition of Cu in liver. a CLD of children (1–3y) due to deposition of Cu in liver. It is It is a non-Wilsonian Cu overload by ingested Cu occurs in a non-Wilsonian Cu overload by ingested Cu occurs in genetically susceptible infantsgenetically susceptible infants
It had a v. high CFR before but has eventually become It had a v. high CFR before but has eventually become preventable, treatablepreventable, treatable
Now rareNow rare
CLD: chr liver d. CFR: case fatality rateCLD: chr liver d. CFR: case fatality rate
The commonest The commonest surgicalsurgical c/of cirrhosis in c/of cirrhosis in childhood is biliary atresiachildhood is biliary atresia
The commonest The commonest medicalmedical causes are causes are– infectionsinfections
– alpha-1- antitrypsin Dalpha-1- antitrypsin D
– metabolic LDmetabolic LD
C.F. of C.L.D/CirrhosisC.F. of C.L.D/Cirrhosis
Often asymptomatic in early! Often asymptomatic in early! Start with L. failure. Start with L. failure. Severity depends on damageSeverity depends on damage
– Early: Early: fatigue, weakness, AN, AP, fatigue, weakness, AN, AP, wt. losswt. loss
– Later: Later: jaundice, jaundice, dark urinedark urine, itching, edema, ascites, , itching, edema, ascites, poor healing, drug toxicity, testicular atrophy, poor poor healing, drug toxicity, testicular atrophy, poor hair, hair, hepatic facies, hepatic facies, easy bruising; esophageal, easy bruising; esophageal,
stomach & anal varices; stomach & anal varices;
kidney failure, gall stoneskidney failure, gall stones
A small number get A small number get liver cancerliver cancer
CF have 2 componentsCF have 2 components
SS of Hepatocellular failureSS of Hepatocellular failure– pallor, edema, pallor, edema, fatigue, fatigue, jaundice,jaundice, itchy skin, dark urine, itchy skin, dark urine,
ANVANV, , wt. loss, palmar erythemawt. loss, palmar erythema
– AP & swelling, pale stool, hepatic facies, spider nevi, AP & swelling, pale stool, hepatic facies, spider nevi, pigmentationpigmentation
– testicular atrophy, poor hair, gynecomazia, poor libidotesticular atrophy, poor hair, gynecomazia, poor libido
SS of Portal HypertensionSS of Portal Hypertension– ascites, distended vein (caput medusa), splenomegaly, ascites, distended vein (caput medusa), splenomegaly,
varices at PS junctions: hematemesis, varices at PS junctions: hematemesis, bloody/tar-bloody/tar-colored stoolcolored stool
Muehrcke nails Muehrcke nails
Terry nailsTerry nails
Kayser–Fleischer ring Kayser–Fleischer ring at limbus: deposition at limbus: deposition of Cu in Descemet m.: of Cu in Descemet m.: characteristic in most characteristic in most
neuro-Wilson & 50% of neuro-Wilson & 50% of hepatic WDhepatic WD
Arcus senilis
Xanthomatosis Xanthomatosis
Mechanism of Ascites in CirrhosisMechanism of Ascites in Cirrhosis
Portal hypertension: Portal hypertension: commonestcommonest Hepatic arterial vasodilatationHepatic arterial vasodilatation HypoalbuminemiaHypoalbuminemia 2y hyperaldosteronism2y hyperaldosteronism Raised ADHRaised ADH
Complications of CirrhosisComplications of Cirrhosis
Palmar erythemaPalmar erythema HypogonadismHypogonadism Darkening of skinDarkening of skin GynecomaziaGynecomazia HypersplenismHypersplenism Spider neviSpider nevi Caput medusaCaput medusa Ascites, edemaAscites, edema
Varices: hgeVarices: hge Itching Itching Abdominal infx.Abdominal infx. EencephalopathyEencephalopathy Raised drug toxicityRaised drug toxicity Liver cancerLiver cancer
Spider naevi (arterial spider, vascular spider, naevus araneus, naevus
arachnoidius, spider angioma
DiagnosisDiagnosis
LFTLFT CT, USG, laparoscopy CT, USG, laparoscopy BiopsyBiopsy Others: Others:
– FibroscanFibroscan
– Measuring the amount of caffeine in the salivaMeasuring the amount of caffeine in the saliva
– Measuring the pressure within the liver vein Measuring the pressure within the liver vein
– Ascitic fluid analysisAscitic fluid analysis
TreatmentTreatmentNothing cures scarNothing cures scar
Goals:Goals:– Rx underlying causesRx underlying causes
– Preventing further damagePreventing further damage
– Rx symptoms & complicationsRx symptoms & complications Fight inf. Vax. flu, pneumonia, hepatitisFight inf. Vax. flu, pneumonia, hepatitis Cut down absorption of wastes/toxinsCut down absorption of wastes/toxins FEB. Salt restriction FEB. Salt restriction HemostasisHemostasis
Liver transplant SOSLiver transplant SOS No hepatotoxic drugsNo hepatotoxic drugs No alcoholNo alcohol Diet: extra calories & a generous protein to help Diet: extra calories & a generous protein to help
liver regenerateliver regenerate If cirrhosis is advanced limit proteinIf cirrhosis is advanced limit protein
PORTAL HYPERTENSIONPORTAL HYPERTENSION
Portal vein: Portal vein: SV with SMV: carries 70% of liver blood. SV with SMV: carries 70% of liver blood. Ends in sinusoidsEnds in sinusoids
Double capillariesDouble capillaries Raised pressure in PV >Raised pressure in PV >11mmHg 11mmHg or a splenic pulp or a splenic pulp
pressure of >16mmHg. Clinically this is not measured pressure of >16mmHg. Clinically this is not measured directly until a TIPS is decideddirectly until a TIPS is decided
SV: splenic vein. SMV: superior mesenteric vein. PH: portal hypertensionSV: splenic vein. SMV: superior mesenteric vein. PH: portal hypertension
TIPS: transjugular intrahepatic portosystemic shuntTIPS: transjugular intrahepatic portosystemic shunt
PH: PH: splenomegaly splenomegaly & & porto-systemic shunts at:porto-systemic shunts at:
Lower end of Lower end of eophagus eophagus via GE veins: via GE veins: hemat./malenahemat./malena Anal Anal veins: veins: hemorrhoidshemorrhoids Umbilical Umbilical veins: veins: caput medusacaput medusa Abdominal wall & retroperitoneum: Abdominal wall & retroperitoneum: distended veinsdistended veins
GE: gastroesophagealGE: gastroesophageal
Eesophageal varicesEesophageal varices
• Gastroesophageal junction to 15cm upGastroesophageal junction to 15cm up
• Slow oozing or sudden severe hgeSlow oozing or sudden severe hge
Gastric varicesGastric varices
Extension of esophageal varices or varices in Extension of esophageal varices or varices in fundus & upper body. Can occur alonefundus & upper body. Can occur alone
Rectal varices:Rectal varices: hemorrhoidshemorrhoids
Gastric varicesGastric varices
Rectal varicesRectal varices
Aetiology of Portal HTNAetiology of Portal HTN• IntrahepaticIntrahepatic:: 80% 80%
• CirrhosisCirrhosis is the commonest; scar tissue blocks BF & is the commonest; scar tissue blocks BF & slows liver functionsslows liver functions
•Schistosomiasis, cong. hepatic fibrosis, etc.Schistosomiasis, cong. hepatic fibrosis, etc.
• PrehepaticPrehepatic:: 20%20%•PV thrombosis:PV thrombosis:
• extension of obliterative process of umb. veinextension of obliterative process of umb. vein• omphalitis (in newborn)omphalitis (in newborn)
• PosthepaticPosthepatic (rare): cons. pericarditis, tricuspid (rare): cons. pericarditis, tricuspid incompetence, incompetence, Budd-Chiari syn. Budd-Chiari syn. (occlusion of HV)(occlusion of HV)
Cong. hepatic fibrosis: Cong. hepatic fibrosis: hematemesis, normal LFTs, hematemesis, normal LFTs, hepatomegaly. May have polycystic disease & other hepatomegaly. May have polycystic disease & other renal D. Etiology is unknownrenal D. Etiology is unknown
Hepato-portal sclerosis: Hepato-portal sclerosis: thickening of intrahepatic PV thickening of intrahepatic PV obstructs BF: leads to collateral veins in porta hepatisobstructs BF: leads to collateral veins in porta hepatis
Suprahepatic obstruction Suprahepatic obstruction c/by a web in the IVC or c/by a web in the IVC or Budd-Chiari syn. Extremely rare. CF may mimic Budd-Chiari syn. Extremely rare. CF may mimic
constrictive pericarditis. DD by echo-, venographyconstrictive pericarditis. DD by echo-, venography
CF of portal hypertensionCF of portal hypertension
may not always be specificmay not always be specific Splenomegaly (hypersplenism: pancytopenia)Splenomegaly (hypersplenism: pancytopenia) Caput medusaCaput medusa Hematemesis, melena or PR bleedHematemesis, melena or PR bleed AscitesAscites Encephalopathy: poor liver function & diversion of blood Encephalopathy: poor liver function & diversion of blood
away from liveraway from liver
DD of uncommon CLDDD of uncommon CLD
ConditionsConditions PresentationPresentation
Budd-Chiari SynBudd-Chiari Syn AscitesAscites
Primary sclerosing Primary sclerosing Cholangitis (PSC)Cholangitis (PSC)
Abnormal LFT/jaundice Abnormal LFT/jaundice
Primary bil. cirrhosis (PBC)Primary bil. cirrhosis (PBC) Abnormal LFT, malaise, Abnormal LFT, malaise, lethargy, itchinglethargy, itching
Caroli diseaseCaroli disease Abdominal pain/sepsisAbdominal pain/sepsis
Simple liver cystSimple liver cyst Pain/coincidental findingsPain/coincidental findings
Polycystic liver diseasePolycystic liver disease Pain/hepatomegalyPain/hepatomegaly
Diagnosis: Diagnosis: by detecting CLD, encephalopathy, ascites, by detecting CLD, encephalopathy, ascites,
varices.varices. Investigations: Investigations: esophagoscopy, Ba-swallow, esophagoscopy, Ba-swallow, USG, celiac axis angiogramUSG, celiac axis angiogram
PV Thrombosis: PV Thrombosis: Dx is difficultDx is difficult
may present within 5y age as hematemesis with only may present within 5y age as hematemesis with only splenomegaly & low plateletsplenomegaly & low platelet
• H/of umbilical V cannulation & abdo. sepsis (40%), or H/of umbilical V cannulation & abdo. sepsis (40%), or trauma/pancreatitis. PVT is mainly congenital. LFTs in trauma/pancreatitis. PVT is mainly congenital. LFTs in these these are normal. USG may confirm PVT: collateral veins are normal. USG may confirm PVT: collateral veins in the in the porta hepatis replacing the PVporta hepatis replacing the PV
TreatmentTreatmentEsophageal variceal bleeding:Esophageal variceal bleeding:
By the time pt. reaches ERBy the time pt. reaches ER
- 1/31/3rdrd – stopped bleeding – stopped bleeding
- 1/31/3rdrd – still oozing – still oozing
- 1/31/3rdrd – still bleeding heavily – still bleeding heavily
Initial measures: ICUInitial measures: ICU- BT: up to 10 unitsBT: up to 10 units- LFT: coagulation profileLFT: coagulation profile- If <50,000, platelet transfusion- If <50,000, platelet transfusion- Endoscopic evaluation & treatment- Endoscopic evaluation & treatment
• Encephalopathy: may need ventilatorEncephalopathy: may need ventilator
• Bronchial aspiration – a frequent complicationBronchial aspiration – a frequent complication
• If profuse bleed prohibits endoscopy:If profuse bleed prohibits endoscopy:
• Insert Sengstaken – Blakemore tube & tamponade; Insert Sengstaken – Blakemore tube & tamponade; deflate after 12h to avoid pressure necrosisdeflate after 12h to avoid pressure necrosis
Endoscopic sclerotherapyEndoscopic sclerotherapy
- Ethanolamine oleate- Ethanolamine oleate
- Sodium tetradesyl sulphate- Sodium tetradesyl sulphate
- 5% phenol in Almond oil- 5% phenol in Almond oil
- Butyl cyanoacrylate- Butyl cyanoacrylate
DrugsDrugs
• I/V Vasopressin. SE: Abdo. crampsI/V Vasopressin. SE: Abdo. cramps
• I/V Octreotide (Somatostatin analogue): Equally I/V Octreotide (Somatostatin analogue): Equally
effective, safeeffective, safe
TIPSSTIPSS (transjugular intrahepatic portosystemic stent) (transjugular intrahepatic portosystemic stent)
revolutionized the Rx. Main Rx for drug revolutionized the Rx. Main Rx for drug resistant cases or in endoscopic Rx failureresistant cases or in endoscopic Rx failure
Surgical shuntSurgical shunt
(Replaced by TIPSS & liver transplant)(Replaced by TIPSS & liver transplant)
Surgical shunts:Surgical shunts:
• splenorenalsplenorenal
• portocaval portocaval
SE: encephalopathy (40%)SE: encephalopathy (40%)
No benefit for pts. who have no bleedingNo benefit for pts. who have no bleeding
C.I. C.I. of Liver transplantof Liver transplant
• Age >65 yAge >65 y
• H/o IHD, HF, Chr. Respiratory diseaseH/o IHD, HF, Chr. Respiratory disease
• Previous Surgical shunts (relative C.I.)Previous Surgical shunts (relative C.I.)
Rx of Ascites of CLDRx of Ascites of CLD
• Salt restrictionSalt restriction
• DiureticsDiuretics
• ParacentesisParacentesis
• Peritoneovenous shuntingPeritoneovenous shunting
• TIPSSTIPSS
• Liver transplantLiver transplant
MCQMCQ
Hepatitis A & E are common c/of CLDHepatitis A & E are common c/of CLD Vaccines for HBV protects against HDVVaccines for HBV protects against HDV Haemorrhoids in cirrhosis are due to HC failureHaemorrhoids in cirrhosis are due to HC failure Palmer erythema is normal in pregnancyPalmer erythema is normal in pregnancy Commonest c/of PHT is cirrhosisCommonest c/of PHT is cirrhosis
MCQMCQ
Commonest surgical c/of cirrhosis in children is Commonest surgical c/of cirrhosis in children is biliary atresiabiliary atresia
Edema in CLD starts in legsEdema in CLD starts in legs CLD may be idiopathicCLD may be idiopathic Autoimmune LD have good prognosisAutoimmune LD have good prognosis A1AT protects lungsA1AT protects lungs Aflatoxin can cause cirrhosis Aflatoxin can cause cirrhosis
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