hepatology mrcp1

7/27/2019 hepatology MRCP1

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Hepatology


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Functions of the Liver

Main functions include: Metabolism of CHO, protein, fat

Storage/activation vitamins and minerals

Formation/excretion of bile Detoxifier of drugs/alcohol

Action as (bacteria) filter and fluid chamber

Conversion of ammonia to urea


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Generally LFTs reflects 2 patterns of liverdisease;

1. Cholestatic Alk P, GGT.

2. Hepatocellular AST, ALT.

Factors favouring hepatic origin of Alk P;1. GGT.

2. 5-nucleotidase.


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Route of

transmission

fecal-oral percutaneous

permucosal

percutaneous

permucosal

percutaneous

permucosal

fecal-oral

Chronic

infection

no yes yes yes no

Prevention pre/post-

exposure

immunization

pre/post-

exposure

immunization

blood donor

screening;

risk behavior

modification

pre/post-

exposure

immunization;

risk behavior

modification

ensure safe

drinking

water

Type of HepatitisA B C D E


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Is an RNA enterovirus Incubation period:Average 30 days ( 2 - 6 wks )

Complications: Fulminant hepatitis.Cholestatic hepatitis.

Relapsing hepatitis

Prevention;

- Immune Globulin IM,0.02 mL/kg- Pre-exposure (travelers to endemic regions/4-6months) &- Post-exposure (within 2-4 wks)

- HepatitisA vaccines .- for persons > 2 years old .- provides long-lasting protection (20 years).- (Havrix) use 3 doses at 0, 1, 6 months).

TTT; bed rest, symptomatic ttt e.g. antiemetics, avoid hepatotoxic

drugs.

Hepatitis A - Clinical Features


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Hepa DNA virus.

Mode of transmission; Bl, sexual, perinatal. Incubation period: Average (2 -6 ms).

Chronic infection: 30%-90%.

Association/ complications of HBV;

- Aplastic anemia.- Arthralgia/itis.- PAN.

- Glomerulonephritis; membranous., MP.

- HCC. - urticaria, acrodermatitis.

Hepatitis B - Clinical Features


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Symptoms

HBeAg anti-HBe

Total anti-HBc

IgM anti-HBc anti-HBsHBsAg

0 4 8 12 16 20 24 28 32 36 52 100

Acute Hepatitis B Virus Infection with Recovery

Typical Serologic Course

Weeks after Exposure

Titre


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Di i


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Diagnosisserological tests ;

HBsAg - used as a general marker ofactive infection, persistance

> 6 m= chronic infection. HBsAb - used to document recovery and/or immunity to HBV

infection.

HBc Ag is not detected in the blood.

anti-HBc IgM - marker of acute infection, may be the onlymarker in the window period.

anti-HBc IgG - past or chronic infection. It can distinguish pastinfection from previous vaccine.

HBeAg - indicates active replication of virus and thereforeinfectiveness.

Anti-Hbe - virus no longer replicating= no longer infectious .

HBV-DNA - indicates active replication of virus, more accuratethan HBeAg


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HBsAg +ve

Repeat HBs Ag after 6 m to confirm,

if HBs Ag become -veresolved

if HB sAg still +ve

HBe Ag -veALT =n

=carrier

HBe Ag +ve

=chractive

biopsy & TTTobserve


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HBsAg +ve

+ve HBc Ig M=acute

+ve HBc IgG=chronic

-ve=resolved

+ve=chronic

HBsAg after 6 months

1. If acute symptomatic ttt2. If HBsAg +ve after 6 mths, HBeAg +ve or -ve, HBeAb _ve,

PCR>105,enzymes >2folds antiviral ttt.3. If HBsAg +ve after 6 mths, HBeAg gray zone or normal enzymes

biopsy hepatitis activity index > 4 antiviral ttt.4. If HBeAg-ve, HBeAb +ve, PCR+ve,normal enzymes Carrier

(no ttt).

5. Liver cirrhosis nucleozide analogue only.

TTT of HBV


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Treatment Interferon

- Peg INF 2a (high mw, long life)

- Mechanism; immune distruction of virally infected cells clear thevirus.

- Dose; 180 Ug/wk

- Duration; 6 mth for eAg +ve, 12 mths for eAg _ve (mutant form)- Indications; chr hepatitis

- NB; not for normal biopsy or LC (lead to decompensated liver)

- Response rate is 30 to 40%.

- Side effects;

common; flu like S, N, V, wt loss, loss of hair, depression, mildBM suppression.

less common; thyroiditis, BM suppression, seizures, retinopathy,

tinitus, teratogenic.


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# to IFN therapy;

Asolute;

Poorly controlled medical condition, DM

Anaemia, thrombocytopenia.

Poor medication compliance.

Alcohol, IV drug abuse, Severe depression.

Relative;

Autoimmune dis (SLE, Rh, IBD, psoriasis)

Neuropathy.

Thyroiditis.


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Nucleotide analogues; Lamivudine, Adefovir, entecavir, tenofovir

Mechanism; reverse transcriptase inhibitorinhibit viralreplication, decrease enzymes but does not clear the virus.

Adv; oral, no hep decompensation, delay the progression of LC& HCC.

Disadv;relapse , drug resistance mutant strains, no viral

clearance.

Duration; 1-3 yrs.

NB; there are 8 genotypes for HBV (AH).better response with A

&B.HBe Ag-ve mutant forms are more drug resistant but less HCC,

common in Egypt.


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Response to ttt;

1) virologic;

- Early response (12 wks)

- End of ttt response (at 24 or 48 wk)- Sustained response (after 6 mths)

- Non responder (at the end)

- Breakthrough (reappear while on ttt)

- Relapse (-ve at the end but +ve during FU).2) biochemical(normal ALT).

3) Histologic(>2 Hist. A ct. Ind improvement).

Predictors of good response;

Viral; genotype, titre.

Liver; minimal fibrosis, moderate enzymes.

Patient; female, Caucasian, lean, compliant, not IC, no alcohol, no otherCLD.

P ti


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Prevention

Vaccination

- highly effective recombinant vaccines.- given to those who are at increased risk ; health

care workers, neonates.

HBIGpost exposure to hepatitis B. It isparticular efficacious within 48 hours, toneonates whose mothers are HBsAg and

HBeAg positive.

Other measures - screening of blood donors,blood and body fluid precautions, All pregnantwomen.


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Natural History of HCV

Incubation period: Average 6-7 wks (2-6 ms) Chronic HCV----------Cr-------HCC

20-30 y 5-10 y The rule of 20;

- 20% of pts with acute infection aresymptomatic.- 20% of pts with acute infection clear thevirus.

- 20-40% with chronic HCV develop C after20 yrs.- Crr---20%--HCC

- 20%-55% of Chronic who receive IFN willobtain a sustained rresponse.


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Extrahepatic manifestation of HCV

1. PCT.

2. Cryo.3. Leukocytic vasculitis.

4. MPGN.

5. Thyroiditis.

6. Sjogrens.

7. Lichen planus.

8. Vitiligo.

9. IGT (type II DM).

10. B cell lymphoma.


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Laboratory Diagnosis

HCV antibody (by EIA or RIBA; more

sensitive) appear at least 4 weeks after

infection.

HCV-RNA( in the acute phase), (monitoring

the response to antiviral therapy).

EIA detect anti-HCV by 4- 10 wks ofexposure, while PCR as early as 1-2wks.


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HCV RNARIBAEIAALTCategory

__+NFalse +veEIA

_++NResolvedinfection

+++NHCV carrier

Diagnostic tests for HCV

If a low risk patients with normal LFTs has a +ve EIA Only30-40% will be RIBA +ve.However, in high risk individuals, PPV of ELISA> 95%.


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HCV genotypes

6 genotypes.

Genotype 1 most common in US, lowresponse rates to TTT, 30% 1 year.

Genotype 2,370% response after 6 ms.


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RecommendationPt ccc

INF+ ribavirinPCR +ve, ALT, liverbiopsy with inflammation,

bridging necrosis

INF+ ribavirin or do liverbiopsy

PCR +ve, ALT,

Observe.Normal ALT

Observe, consider TTTCompensated CConsider transplantationdecompensated C

TTT guidelines for HCV


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Treatment

Interferon - may be considered for patients withchronic active hepatitis. The response rate is

around 50% but 50% of responders will relapseupon withdrawal of treatment.

Ribavirin- combination of interferon and ribavirinis more effective than interferon . progression

even in absence of viral response; side effect;teratogenic, hemolysis esp in renalinsufficiency..


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Coinfection with HBV

severe acute disease.

low risk of chronic infection.

Superinfection

usually develop chronic HDV infection.

high risk of severe chronic liver disease.

may present as an acute hepatitis.

Hepatitis D - Clinical Features


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Incubation period: As HCV

Pregnant women Illness severity: Increased with age

Chronic sequelae: None identified

Hepatitis E - Clinical Features


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Alcoholic Liver Disease, Alcoholichepatitis, and Cirrhosis

Diseases resulting from excessive alcoholingestion characterized by fatty liver (hepaticsteatosis), hepatitis, or cirrhosis .

Prognosis depends on degree of abstinenceand degree of complications

C/P; N/V, anorexia, abd pain, wt.

Malnutrition often an issue in these patients TTT; abstinence, good nutrition.


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Lab;

GGT.

MCV (macrocytosis).

AST/ALT > 2/1. Ig A.

Mallory bodies; dense perinuclear esinophilicfragments in hepatocytes (DD; PBC, wilson).

thrombocytopenia. Blood alcohol

Bleeding tendency in alcoholicCirrhosis;1. synthesis of coagulation factors.

2. Plat. Function defect.

3. Thrombocytopenia ( hyperslenism, BMsuppression).


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NAFLD Spectrum; steatosis, NASH, cirrhosis.

Etiology;

- 1ry; obese, DM, hyperlipidemia.

- 2ry;

drugs; amiodarone, tamoxifen, steroid, tetracyclin

rapid wt loss, malnutrition, jej bypass, TPN.

Inv; U/S, MRI, AST/ALT


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Autoimmune liver disease

Autoimmune

Hepatitis(AIH)

Primary Biliary Cirrhosis

(PBC)

Primary SclerosingCholangitis (PSC)

Autoimmune

Cholangitis (AIC)

Overlap

Syndromes

The diagnosis requires: exclusion of major causes of liverdamage, including alcoholic, viral, drug- and toxin-induced,hereditary metabolic, andNAFLD.


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Auto immune Hepati t is Young women (10-20 yrs)

Typically present with malaise, artharalgia, tenderhepatomegaly, 2 ry amenorrhea,.

Patients may be asymptomatic

AIH may present as acute hepatitis, chronic hepatitis,

or well-established cirrhosis , Investigation. Type 1,ASMA,ANA ,Anti-actin, Type 2,Anti-LKMA

nti-liver-kid., Type 3, Anti-Soluble liver- antigen , globulins,

Without therapy, most patients die within 10 years ofdisease onset.

With TTT,10 yrs survival = 93%.

TTT=steroids + aza for pt with or withoutCirrhosis70% remission in 2 yrs.

Relapse after remission=50% at 6 ms, 80% at 3 yrs.


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Primary Biliary Cirrhosis

Middle aged females

C/P; pruritis,Jaundice, steatorrhea( 2ry to cholestasis),hyperpigmentation, xanthelasma.

PBC frequently is associated with other autoimmunedisorders , such as Sjgren syndrome, Hashimotothyroiditis, AIHA, arthritis.

Criteria for the diagnosis include:(1) A cholestatic serum enzyme pattern, Alk. Phosph.

(2) Presence of AMAs antimitochondrial.

(3) Elevated serum IgM,

(4) bile duct lesion of mid-sized IHBD(1),(2) & a compatible histologyare regarded asmandatory for the diagnosis of PBC.

Liver biopsy lymphocytic portal infiltration.

TTT; UDCA, colchicine, transplant.


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Primary Sclerosing Cholangitis Criteria for the diagnosis :1- RUQ pain , jaundice , pruritis & wt loss

A cholestatic enzyme pattern;

2- histologically ., large bile duct (intra & extrahepatic)stenosis & dilatations without prior bile duct surgery or2ry SC ; mild to moderate portal infiltration.

3- concomitant IBD ( before, during, after UC mainly) in70 % of the patients, detected by asympt Alk P.

but in case of UC, 3% have PSC.

4- presence of pANCAs in > 70% of patients.

MRCP, ERCP beading of intra & extrahepatic bile duct.

risk ofcholangiocarcinoma, retroperitoneal fibrosis.

TTT; supportive (UDCA, colchicine), , transplantation.


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Autoimmune Cholangitis

AIC (AMA ve PBC) shares many features with PBC

including :

1- F>M,

2- fatigue and pruritus,

3- a cholestatic serum enzyme pattern,4- bile duct lesions (histology), &

5- a slowly progressive course leading to

fibrosis and cirrhosis of the liver.

Patients with AIC are by definition AMA -ve

& often present with serum ANA and/or ASMA.


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AICPSCPBCAIHCriteria

9:11:29:14:1F : M

ALP, -GTALP, -GTALT, AST(1-3 times)

ALP (6-10times), -GT

ALT, AST(7-10 times)

ALP

(1-3 times)

Predominantliver test

ANA, ASMAp ANCAAMA

AMA-M2

ANA, ASMA,

LKM, SLA,

Auto

antibodies

Florid bile

duct lesionFibrosing bileduct lesion

Florid bile ductlesion

interfacehepatitis

Histology

Cholestatic

AMA-ve, ANAor ASMA +ve,

histologycompatible

with PBC

BD st./dilat.(choigraphy),

cholestaticenzymepattern,

IBD, p ANCA

AMA-M2,cholestatic

enzymepattern,

compatible

histology

Hepatocellularenzymepattern,

Diagnosis


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Overlap Syndromes

Patients with overlap syndromes present with

both hepatitic and cholestatic biochemical andhistological features of AIH, PBC, and/or PSC,and usually show a progressive course towardliver cirrhosis .

AIH-PBC overlap syndromes ...reported inalmost 10% of adults with AIH or PBC.

AIH-PBC Overlap Syndrome

AIH-PSC Overlap Syndrome AIH-AIC Overlap Syndrome

Coexistence of PBC and PSC

Coexistence of AIH and Chronic HCV


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Wilsons Disease AR.

Genetic defect in copper transport ( ATP7Bgene on ch 13) hepatic excretion Cu organdeposition.

Presentations :

Hepatic, chronic hepatitis, macronodular C, mallorybodies.

Neurological;(BG) flapping, chorea, dysarthria, tremorsparkinsonism

Kayser Fleicher ringRenal; RTA

Haematological; coombsve HA.

Endocrinal; hypoparathyroidism

pseudogout.


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Wilsons Disease

Inv;

1. Low serum ceruloplasmin

2. High urinary copper.

3. Liver biopsy with orcein stain.

TTT;

- penicillamine for life + pyridoxine, oral Zn

- Transplantation- Family screening with ceruloplasmin.


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KF ring


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Hemochromatosis AR, mutation of HFE gene on chr 6. Homozygous C282Y or hetero C282Y/ H63D. Exessive Fe absorption & deposition in various organs;

- heart restrictive cardiomyopathy,- pancreas DM,- pituitary hypogonadism,- joints pseudogout,- skin bronzed colour.

risk of malignancy HCC. Cause of death; HCC, restrictive cardiomyopathy.

Lab;1. screening by TSAT > 60% in males & 50% in females.2. Ferritin > 5003. Fe, TIBC.

4. Hepatic iron conc (HIC), hepatic iron index (HII), MRI.5. Liver biopsy staining with prussian blue.

6. Genetic study.

TTT; phlebotomy/1-2 wks for 2-3 yrs to Hb


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1 antitrypsin

Inhibit neutrophil elastase, itsabsenceemphysema &LC.

AR, Pi ZZ phenotype

Inv; PAS +ve globules in periportalhepatocytes.

Ttt; hepatic transplantation, stopsmoking.


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Drug induced liver diseaseAcute hepatitis.acetaminophen

Budd chiari.EstrogenCholestasis.Amoxiclave, chlorpromazine,

erythro, OCP,

Hepatic granuloma.Amiodarone,allopurinol

Adenomas +/- intraperitoneal

rupture.

Cholelithiasis, cholestasis

HV thrombosis

Peliosis hepatis

OCP,

CAH.Methyl dopa, INH, nitrofurantoin

Cryptogenic C.MeThotreX, amiodarone, vit A

Massive ischemic necrosisCocaine

Peliosis hepatisAnabolic steroids , OCP

Ci h i


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CirrhosisTTTDiagnosisEtiology

AbstinenceGGT, MCV, AST/ALTAlcoholic C.

INF-2b

Lamivudine

serologyHBV

INF

ribavirin

serologyHCV

Phlebotomy,desferroxamine

TSAT, Ferritin, hepaticFe index, HFE gene

Hemochromatosis

Prednisone,azathioprine

ASMA, anti LKM, SLA,ANA

AIH

ursodiolAMAPBC

D-penicillamine, ZnSerum& urine Cu,ceruloplasmin

wilson

Enzyme replacement,

transplantation

1 antitrypsin level1 antitrypsin

Fulminant Hepatic Failure


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Fulminant Hepatic Failure - Def; Rapid, severe acute liver injury with

encephalopathy

within 8 weeks in someone with a previouslynormal liver.

- pathology; massive necrosis, severe fattydegeneration.

- Causes; HEV in pregnancy, Reyes, IVtetracycline, paracetamol toxicity, ecstasy,halogenated anathesia, wilson, viral, Alcohol,mushroom poising, shocked liver.

- C/P; enceph, hypoglycemia, Na, bleeding tendency,

renal failure.- Ttt; as hep. enceph.

- Poor prognostic factors;

- Paracetamol; Ph300, PT>100, grade3,4

enceph.


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Reyes Syndrome

It is acute encephalopathy + fattydegeneration of the liver

Pathogenesis: loss of mitochondrial function. Disturbed FAO + carnitine def

Clinical picture: Acute fulminant hepatitis.age 4-12 yrs

URTI or chicken pox

Mortality 50% Ttt; supportive

The Child Turcotte Pugh Classification


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The Child-Turcotte-Pugh Classification


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Complications of LC;1. Portal HTN ov, hypersplenism, ascites.2. Ascites3. HCC4. Hep encephlopathy5. HRS6. Malnutrition

7. Coagulopathy8. Endocrinal; amenorrha, testicular

atrophy.


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Portal hypertensionDef; PV pressure > 12 mmhg.Types

According to site of obstructionPrehepatic eg PVT

Hepatic: presinusoidal eg CHFsinusoidal eg Cir,

postsinusoidal eg VOD

Posthepaticeg Budd Chiari synd

Clinical Picture

Hematemesis Melena Splenomegaly Hypersplenism Dilated abdominal wall veins Ascites

Encephalopathy

GIT bl di


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upper GIT bleeding;

1. Ulcers;- high risk ulcers= active bleeding, visible vessel, adherent clot.

- Hospitalization for 3 days.- PPI infusion- endoscopy electrocoag, heater probe, injection of absolutealcohol or 1: 10.000 epin.

2. Mallory Weiss; self limiting.

3. Esoph. Varices;- octoreotide-ligation better than injection sclerotherapy- quinolone Ab- chronic non selective BB

- decompressive surgery as distal splenorenal shunt in class A & Blower rate of intervension than TIPS.- TIPS; less bleeding, equal mortality but more encephalopathythan endoscopy.

4. Others; gastric or esophageal erosions, malignancy

M t


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Management

A) Of an acute attack of hematemesis

1-Resuscitation2-anti shock measures; IV cannula, line, Ryle, IV crystalloids,

colloids, Blood, FFP.3- hemostatic drugs; Vit K, tranexamic acid, ethamsylate.4- PPI infusion in PU.

5- Octreotide for esophageal varices.6- anticoma measures; lactulose, metronidazole, enemas.

7- UGIE for band ligation or injection sclerotherapy + quinolone.

8- sengestaken-blackmore tube for massive uncontrolledbleeding from OV.9-if still uncontrolled TIPS for high risk,, emergency surgery

for low risk.10- if massive bleeding, source unknown (obscure)

enteroscopy or angiography.

B) IN between the attacks;1- PPI for PU2- non selective BB; propranolol, quinolone for prophylaxis from

SBP, UGI Band ligation or injection sclerotherapy for OV.

L GI bl di


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Lower GI bleeding

SI bleeding

Causes;1. Hemorroids2. Anal fissure3. Adolescent IBD, jej. Polyp4. Adult diverticula5. Elderly vascular ectasia, malignancy6. Others; dysentry, ischemia, vasculitis, intussuception.

C/P;- If facial, oral telangectasia HHT- Acanthosis nigricans Malignancy- Perioral pig spots PJS. Investigation;- UGIE

- Colonoscopy- Push enteroscopy- Videocapsule enteroscopy- TC labelled RBC scan (during bleeding)- Angiography (tumour, Vs malformation)


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Occult bl in stool;

- benzidine, guaiac tests

False +ve; meat, NSAIDs

Falseve; vit C, cauliflower(peroxidase containing)

Iron darken the test.


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PVT

Aetiology: intra abdominal infection

umbilical catheterization

hypercoagulable state

invasion by tumorsidiopathic

Clinical picture: splenomegaly

no hepatomegaly

normal LFTs


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Veno occ lusive disease

Thickening and fibrosis ofsmallhepatic venules and centrilobularveins

Aetiology: * Herbs.

* toxins (aflatoxin).

* drugs . Azathiprine

* bone marrow tx


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Budd Chiar i Syndrome

Obstruction of the main hepatic veinsor IVC : Acute onset of abd. Pain&ascites , jaundice with no LL oedema.

Risk factors;1. Chemotherap

2. Irradiation

3. alkaloids

Hepatic Encephalopathy


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Hepatic Encephalopathy

Def; neuropsychiatric S that may complicateCLD, fulminant LCF & portosystemic shunts.

Pathogenesis; protein in the colon bactflora neurotoxins e.g. NH3, mercaptans,

false neurotransmitors as octopamine &tyramine dt aromatic & branched chain aa, GABA.

Role of ammonia;

1. Bind glutamic acid glutamine - CNS.

2. Bind ketoglutarateCNS energy.

Ttt by binding to lactic acid.


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Drugs

Benzodiazepines

Narcotics

Alcohol

Increased Ammonia Production,

Absorption or Entry Into the BrainExcess Dietary Intake of Protein

GI Bleeding

Infection

Electrolyte Disturbances (ie., hypokalemia)

Constipation

Metabolic alkalosis

Dehydration

Vomiting

Diarrhea

Hemorrhage

Diuretics

Large volume paracentesis

Primary Hepatocellular Carcinoma

Precipitants of Hepatic Encephalopathy


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neurologic symptoms

Cognitive impairment

Inverted sleep rhythm

Neuromuscular disturbance

Altered consciousness


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Stages of Hepatic Encephalopathy

Stage Symptoms

I Apathy Slow mentation(Mild Confusion, agitation, irritability, sleep

disturbance, decreased attention)

IIlethargy

Easy arousable, disorientation, inappropriatebehavior, drowsiness

III stupor Somnolent but difficult arousal by vigorous stimuli;pain & voice, slurred speech, confused, aggressive

IV coma Light Coma; respond to pain only

Deep coma; no response


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DD of flapping tremor;

1. Hepatic Encephalopathy.

2. Wilsons dis.

3. Uremia.4. CO2 narcosis.

DD of irritable coma;

1. Hypoglycemia

2.

Subdural hematoma3. Acute alcohol intoxication

4. Delerium tremens; dt balcohol withdrawal, visual hallucinations,paranoid psychosis, tremors, agitation, pyrexia, tachycardia,sweating, dilated pupil within 3-1 wks, ttt; sedation that GABA asBDZ.

5. Wernickes encephalopathy6. Drug intoxication

7. Meningitis

8. wilson


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Treatmen t of Hepatic Encephalopathy

1. Control precipitating factors.

2. Lactulose

3. Antibiotics

4. Enema/4 hr

5. Protein restriction6. BCAA supplementation

7. Flumazenil (Anexate) BDZ receptor antagonist.

8. Ldopa or bromocriptine ; dopamine agonist; improve NMtransmission.

9. Zinc10. Artificial liver support (hemoperfusion, artificial liver device.

11. Liver transplantation


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AscitesDefinition


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DefinitionThe presence of free fluid in the peritoneal cavity.

Differential diagnosis F F F.

Causes :1. Portal HTN; SAAG> 1.1g/dlPrehepatic eg PVTHepatic:

presinusoidal eg CHF, constrictive pericarditis, TIsinusoidal eg Cirrhosis,metastasis, fibrosis, AFL.postsinusoidal eg VOD

Posthepatic eg Budd Chiari synd

2- Hypoalbuminemia. SAAG< 1.1g/dl- nephrotic, protein loosing entero, malnutrition.

3- Local causes; SAAG< 1.1g/dlDiseased peritoneum;malignant as P carcinomatosus, mesotholioma,infections as TB, fungal, bact,others; FMF, vasculitis as HSP,

granulomatous, esinophilic. Normal peritoneum pancreatic,chylous, myxedema, Meigs S.

Paracentesis


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ParacentesisExudatesTransudates

> 3 g< 3 gAscitic protein

> 200 0.6 0.5


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Serum-Ascitic Albumin gradient ( SAAG ratio);

SAAG >1.1

= portal HTN mediated

SAAG


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Mechanism of hepatic ascites;- Hypoalb- PHT- Renal Na retension- Lack of distruction of Est, aldosterone, ADH- Complicated; PVT, SBP, HCC, HRS. TTT of ascites- Dietary Na restriction; 2 g/d

- Oral diuretics.- Fluid restriction is not necessary unless serum sodium is 500/mm3with lymphocyte predominance

Chylous ascites -TG in ascites > serum(usually > 200mg/dL)- milky, clear by ether- sudan staining- dt intestinal lymph e.g.TB,

filaria, nephrotic, ectasia,Mucinous - dt pseudomyx perit,

Pancreatic ascites Amylase in ascites > serum(often > 1000 U/L)


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TIPS

Indications1. Resistant, recurrent refractory

ascites.

2. Recurrent variceal bleeding. contraindications of TIPS

1. HV thrombosis.

2. SBP3. Mild to moderate ascites.

SBP


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SBPdef; An infection of the peritoneal fluid in the absence of a

known or suspected intra-abdominal surgical source of the

infection.

Risk factors;GI hemorrhage.previous SBP.ascitic fluid TP < 1gm/dL,S. bilirubin > 3.2 mg/dLlow platelet count < 98,000 cells/mm.fulminant hepatic failure.

diagnosis;1. C/P; fever, abd pain, tenderness, ascites2. a PNL in ascites 250 cells/mm (or WBCs >500/mm3).

3. a positive ascitic fluid culture (usually of a single organism;enterobacteriaceae 63%, step pneum 15%, enterococci 6-10%) but often cultureve.

of SBP


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Treatment

empiric antibiotic therapy, e.g., 2g of

cefotaxime i.v. every 8 hours,or other 3rd Gceph or Amoxacillin-clavulonate

or quinolone if not on quinolone prophylaxis

for 5 days

1.5g albumin/kg BW within 6 hours of

detection and 1g/kg on day 3.

Prophylaxis;Oral norfloxacin 400mg 1x2

1ry or 2ry prevention for high risk patients for

short term (7d) as 1ry prophylaxis,

long term for 2ry prophylaxis

o S

Variants of ascitic fluid infection


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according to ascitic fluid characteristics

Category Ascitic fluid analysis

S B P PMN 250/mm Single

Culture-negative neutrocyticascites

PMN 250/mm Negative

culture

Secondary bacterial peritonitis PMN 250/mm Multiple

Count Organism(s)

Jaundice


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Jaundice Isolated unconjugated hyperbil (direct 4 times)- extrahepatic; U/S dilated bile ducts CT, ERCP. e.g. malignancy,

stones, stricture, PSC, parasitic as ascaris, AIDS cholangiopathy.

- Intrahepatic serology, biopsy.e.g.viral, alcoholic, PBC, PSC,GVHD, infiltrative dis as TB, lymphoma, sarcoid, amyloid, drugs as

OCP, anabolic steroids (pure cholestasis), erythromycin (cholestatichepatitis).


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Gilberts

1 ry cause of isolated indirect bili.

Usually caused by fasting states

Nicotinic acid test delay & high peak of

biliribin ( 3 hrs).


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DD

Cholestasis in ICU shock liver, sepsis, TPN. Jaundice after BM transplantation

venoocclusive dis, GVHD.

AIDS cholangiopathy;- Picture of PSc. Cholangitis.

- Dt infection with CMV or cryptosporidia.

- ALK =800 but bil often normal.

GGT in alcohol, phenytoin,, pancreatitis, cholestasis.

Cholestasis; Alk P fractionate, 5nucleotidase, GGT.


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DD of jaundice in 3rd trimester of pregnancy

1. Viral hepatitis (hep E).2. Herpes hepatis.3. HELPS.4. Acute fatty liver of pregnancy5. Intrahepatic cholestasis.

Pruritis gravidarum;dt intrahepatic cholestasis.Ttt;- mild reassurance .- Severe cholestyramine, ursodeoxycholic

acid.

HCC


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HCC Predisposing factors;- LC esp hemochromatosis & alcoholic C.- HBV, HCV- Aflatoxin (fungal metabolite in food)- Androgenic steroids & rarely OCP. Fibrolamellar carcinoma; a microscopic variant consisting of large

polyclonal cells arranged in trabiculae separated by parallel bundlesof collagen, in young females, of better prognosis.

Inv; AFP>400 ng/ml, carboxyprothrombin, spiral CT.

TTT;1. Surgery; resection, transplantation if < 3 cm, good liver function2. Percutaneous ttt; if < 5cm or 3


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Liver transplantation

Elevated liver enzymes aftertransplantation;

Early few wks to ms

1. Allograft rejection.

2. Drug toxicity.

3. Art. Thrombosis.

After 1st yr recurrence of initialdis

HRS


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HRS

P t h l t t S


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Post-cholecystectomy S; Causes;

1. Oesophagitis, pancreatitis, radiculopathy2. Functional BD (hepatic flexure S)3. Stone in CBD, stricture CBD, FB granuloma4. Sphincter iof odd dysfunction Management;1. Liver FTs2. Abd U/S3. UGI endoscopy.4. Biliary manometry5. Biliary scan TTT;1. If LFTs , abd U/S normal symptomatic pain releif.2. If LFTs abnormal, U/SCBD dilatationERCP with

manometry or sphincterotomy.

Acute PANCREATITIS


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Acute PANCREATITIS

Causes;

1. Gall stones 50%; 75% of pt with unexplainedpancreatitis has microlithiasis(microscopic stonedis).

2. Alcoholism3. Infections; Coxsackie, mumps, ECHO & hep

viruses4. Tumours5. Drugs; PD FAST VET (pentamidine, didanosine,

frusemide, azathioprine, steroids, sulfa, thiazide,valproate, OCP, tetracyclin)

6. Hypertrigyceridemia7. Hypercalcemia8. Iatrogenic e.g. ERCP9. Idiopathic.

C/P;Abd pain N V


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- Abd pain, N, V.- MOF, shock Cullen's sign (periumbilical discolouration) Grey Turner's sign (flank discoloration)Inv;1. s. amylase 4 times,levels does not correlate with the

severity, macroamylasemia (bound to Ig), urinaryamylase/creat.

2. s. lipase; specific, remain high for long time (10d)

3. s trypsin4. Leuckocytosis, AST, ALP, Ca.5. Imaging; CT Scan

TTT;1. Bowel rest2. Analgesic; pethidine3. Antibiotics; tienem, 3rd G ceph.4. Correct fluid & electrolytes.5. Somatostatin IV6. Plat activating Fact antagonist (lexipafant)


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poor prognostic indicators in acute pancreatitis:During 48 hrs Ransons BASline BUNdle Sure Can Help

Out- Base deficit > 4 meq/l- BUN > 5 mmol/l

- Sequestration of fluid>6L- Calcium < 2.0 (10%

- PaO2


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Complications of acute pancreatitis;1. Plegmon; a mass of inflamed pancreatic tissue.2. Pseudocysts.3. Hypocalcemia4. Pancreatic abcess; 2-4 wks after

5. ARDS.6. MOF.7. Splenic or portal vein thrombosis varices--.

Hematemesis.8. DM, exocrine pancreatic insufficiency.

Pseudocysts;- Fluid collections.- In 15 % of acute panc.- Body & tail- Do not have epithelial lining.

- resolve spontaneously within wks


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Causes of a raised amylase are: acute/chronic pancreatitis pancreatic cysts and carcinoma perforated duodenal ulcer ovarian carcinoma . ectopic pregnancy gallstones salivary tumour adenitis ,mumps diabetic ketoacidosis

Chronic Pancreatitis


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Causes;1. Alcohol2. Cystic fibrosis3. Hemochromatois4. Others; traumatic, autoimmune, Hypertrigyceridemia5. Hypercalcemia

C/P;abd. Pain.

Steatorrhoea, B12 deficiency, trypsin is required in the processingof dietary B12 which enables absorption . DM

Inv; CT calcifications. ERCP (of choice)..... Chain of lakes

Test for exocrine pancreatic functions;- therapeutic test with pancreatic enzymes- secretin test (most sens)- fecal elastase, chemotrypsin- serum trypsinogen.

TTT: analgesics, DM, steatorrhea.

P ti


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Pancreatic cancer Risk factors;

1. Smoking, advanced age, male gender, blackrace.

2. Type I DM, chronic pancreatitis.3. Familial pancreatitis

4. Industrial exposure to petroleum components& leather tanneries.

Pathology; adeno, 80& in the head. C/P; cachexia, obst jaundice with palpable

GB (courvoisier law), ascites, abd pain,thrombophlebitis ( trousseau sign) Inv; CT, MRI., ERCP. TTT; whipple radical surgery or palliative

hepatology mrcp1

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