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
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