Pemicu 2

Vicky
405110230
 LO 1

Menjelaskan radang pada hati /

hepatitis
 Liver disease
Hepatocellular disease
viral hepatitis or alcoholic liver disease
Features liver injury, inflammation, and
necrosis predominate
Cholestatic disease
Mixed
 Typical presenting symptoms
Jaundice
Fatigue
Itching
RUQ pain
Abdominal distention
Poor apetite
Malaise
Dark urine & light stools
 Anamnesis
Evaluation
establishing the etiologic diagnosis
estimating the disease severity (grading)
establishing the disease stage (staging)
 Physical examination
Icterus Spider angiomata
Hepatomegaly acute and chronic liver
cirrhosis, venoocclusive disease
disease, infiltrative superficial, tortuous
disorders such as arterioles and, unlike
amyloidosis, metastatic or simple telangiectases (fill
primary cancers of the from the centers outwards
liver, and alcoholic arms, face, and upper
hepatitis torso
Splenomegaly Palmar erythema
Hepatic tenderness acute and chronic liver
disease
Advanced disease

Muscle wasting Male + alcohol

Ascites Hyperestrogenemia
Gynecomastia
Edema
Testicular atrophy
Dilated abdominal veins Loss of male patern hair
Hepatic fetor distribution

Asterixis
Mental confusion
Stupor
Coma
Laboratory testing
 Diagnostic imaging
US & CT fatty liver, biliary duct dilatation,
obstructive jaundice
MRCP
ERCP
MRI
Diagnosis & algorithm of liver disease
Grading & staging for cirrhosis
 Management
Abstinence from alcohol
Vaccination for hepatitis virus
Influenza and pneumococcal vaccination
careful in use of any medications, other than
the most necessary
Varices beta blockers or offered endoscopic
obliteration
 LO 1.1
Menjelaskan drug-induced hepatitis
 Toxic and Drug-Induced Hepatitis

inhalation, ingestion, or parenteral

administration of a number of pharmacologic
and chemical agents liver injury

Etiology
industrial toxins (e.g., carbon tetrachloride,
trichloroethylene, and yellow phosphorus)
heat-stable toxic bicyclic octapeptides of certain
species of Amanita and Galerina (hepatotoxic
mushroom poisoning)
pharmacologic agents used in medical therapy
Some examples of drugs
 Pathophysiology
Drug & its metabolite
distort cell membranes or other cellular molecules
bind covalently to intracellular proteins,
endogenous bile acids
injure the liver, to accumulate
necrosis of hepatocytes
injure bile ducts cholestasis
block pathways of lipid movement
inhibit protein synthesis
mitochondrial oxidation of fatty acids lactic
acidosis and intracellular triglyceride accumulation
(microvesicular steatosis)
 drug metabolites sensitize hepatocytes to
toxic cytokines
Drug hepatotoxicity immunologically
mediated liver injury
Drug activation of nuclear transporters
(constitutive androstane receptor (CAR))
induction of drug hepatotoxicity
 2 major type of hepatotoxicity

Direct toxic type

Idiosyncratic type
result from differences in metabolic reactivity to
specific agents
 Drug induced cholestasis
bland cholestasis with
limited hepatocellular
injury
(e.g., estrogens, 17,-
substituted androgens)
inflammatory cholestasis
(e.g., phenothiazines,
amoxicillinclavulanic acid,
oxacillin, erythromycin
estolate)
sclerosing cholangitis
(e.g., after intrahepatic
infusion of the
chemotherapeutic agent
floxuridine for hepatic
metastases from a primary
colonic carcinoma)
disappearance of bile
ducts, "ductopenic"
cholestasis
(e.g., carbamazepine,
chlorpromazine, tricyclic
antidepressant agents)
 Treatment
largely supportive, except in acetaminophen
hepatotoxicity
fulminant hepatitis resulting from drug hepatotoxicity
liver transplantation (life saving)
Withdrawal of the suspected agent
Glucocorticoids for drug hepatotoxicity with allergic
features
silibinin for hepatotoxic mushroom poisoning
ursodeoxycholic acid for cholestatic drug hepatotoxicity
have never been shown to be effective and are not
recommended
 Acetaminophen Hepatotoxicity
direct toxin
most common culprit among patients
presenting with acute liver failure
Fatal fulminant disease (ingestion of 25 g)

Blood levels of acetaminophen severity of

hepatic injury (levels > 300 g/mL 4 h after
ingestion are predictive of the development of
severe damage)
 Pathophysiology
a small proportion of acetaminophen
phase 1 reaction by cytochrome P450 CYP2E1
N-acetyl-benzoquinone-imine (NAPQI) :
hepatotoxic metabolite

detoxified by binding to "hepatoprotective"

glutathione to become harmless
water-soluble mercapturic acid, which
undergoes renal excretion
 binding of acetaminophen to hepatocyte
macromolecules hepatocyte necrosis

Complications chronic hepatitis and

cirrhosis

Risk factors
alcohol, phenobarbital, isoniazid, or other drugs
conditions that stimulate the mixed-function
oxidase system
starvation that reduce hepatic glutathione levels
 Treatment
gastric lavage
supportive measures
oral administration of activated charcoal or
cholestyramine to prevent absorption of
residual drug
Routine use of N-acetylcysteine reduced
the occurrence of fatal acetaminophen
hepatotoxicity
 Halothane Hepatotoxicity
Idiosyncratic Reaction
structurally similar to chloroform severe
hepatic necrosis

Risk factors
Adults (rather than children)
obese people
women
 Clinical manifestations
1st week Fever, moderate leukocytosis, and
eosinophilia
Jaundice is usually noted 710 days
Nausea and vomiting
Hepatomegaly is often mild, but liver tenderness
is common
aminotransferase levels are elevated
 Treatment
Methoxyflurane should not be used after
halothane reactions
Use later-generation halogenated
hydrocarbon anesthetics
 Methyldopa Hepatotoxicity
Toxic and Idiosyncratic Reaction
<1% of patients, acute liver injury resembling
viral or chronic hepatitis or, rarely a cholestatic
reaction 1 2 weeks

Sign & symptoms

Fever, anorexia, malaise jaundice
Rash, lymphadenopathy, arthralgia, and
eosinophilia rare
 Serologic markers
autoimmunity are detected infrequently
<5% of patients have a Coombs-positive hemolytic
anemia

Other antihypertension agent (ACE-1, ARB

rare)
 Isoniazid Hepatotoxicity
Toxic and Idiosyncratic Reaction
illness develops that is indistinguishable from
viral hepatitis
occur within the first 2 months of treatment

Risk factors
Age (increasing substantially after age 35; the
highest frequency is in patients over age 50, the
lowest under the age of 20)
 Precipitation factors alcohol, rifampin, and
pyrazinamide

Pathophysiology
Metabolite of INH (acetylhydrazine) liver injury
slow acetylators more severe hepatotoxicity

Clinical manifestations
Fever, rash, eosinophilia, and other manifestations of
drug allergy are distinctly unusual
 Sodium Valproate Hepatotoxicity

Toxic and Idiosyncratic Reaction

anticonvulsant useful in the treatment of
petit mal and other seizure disorders

Risk factors mitochondrial enzyme

deficiencies

Pathophysiology
Metabolite of sodium valproate (4-pentenoic acid)
hepatic injury
 Clinical manifestations
Asymptomatic elevations of serum
aminotransferase levels
jaundice, encephalopathy, and evidence of hepatic
failure are found liver tissue : microvesicular fat
and bridging hepatic necrosis
 Phenytoin Hepatotoxicity
Idiosyncratic Reaction
Pathophysiology
Phenytoin + cyp 450 highly reactive
electrophilic arene oxides + epoxide hydrolase
finish metabolism
defect of epoxide hydrolase in cytochrome P450
to metabolites highly reactive electrophilic arene
oxides hepatic injury
 Sign & symptoms
Striking fever
Lymphadenopathy
rash (Stevens-Johnson syndrome or exfoliative
dermatitis)
Leukocytosis
Eosinophilia
Asymptomatic elevations of aminotransferase and
alkaline phosphatase levels
 Amiodarone Hepatotoxicity
Toxic and Idiosyncratic Reaction
may persist for months after the drug is stopped
Pathophysiology
Desethylamiodarone accumulate in hepatocyte
lysosomes and mitochondria and in bile duct
epithelium
Sign & symptoms
elevations in aminotransferase levels
pseudoalcoholic liver injury steatosis, to alcoholic
hepatitis-like neutrophilic infiltration and Mallory's
hyaline, to cirrhosis
 Erythromycin Hepatotoxicity
Cholestatic Idiosyncratic Reaction
associated with erythromycin estolate
usually begins during the first 2 or 3 weeks of
therapy

Signs & symptoms

nausea, vomiting, fever, right upper quadrant
abdominal pain, jaundice, leukocytosis, and
moderately elevated aminotransferase levels
Trimethoprim-Sulfamethoxazole Hepatotoxicity

Idiosyncratic Reaction
relatively uniform latency period of several
weeks

Sign & symptoms

eosinophilia, rash, and other features of a
hypersensitivity reaction
tissue eosinophilia and granulomas
 Others
Oral Contraceptive Total Parenteral Nutrition
Hepatotoxicity (Steatosis, Cholestasis)
(Cholestatic Reaction) "Alternative and
17,-Alkyl-Substituted Complementary
Anabolic Steroids Medicines
(Cholestatic Reaction) (Idiosyncratic Hepatitis,
HMG-CoA Reductase Steatosis)
Inhibitors (Statins) (HAART) for HIV Infection
(Idiosyncratic Mixed (Mitochondrial Toxic,
Hepatocellular and Idiosyncratic, Steatosis;
Cholestatic Reaction) Hepatocellular, Cholestatic,
and Mixed)
 LO 1.2
Menjelaskan hepatitis virus akut
 Acute viral hepatitis
a systemic infection affecting the liver
predominantly

Etiology
hepatitis A virus (HAV), hepatitis B virus (HBV),
hepatitis C virus (HCV), the HBV-associated delta
agent or hepatitis D virus (HDV), and hepatitis E
virus (HEV)
Other transfusion-transmitted agents hepatitis
G" virus and "TT" virus
Features of hepatitis viruses
Hepatitis A

LO 1.2
 Hepatitis A
This agent is transmitted almost exclusively by
the fecal-oral route
enhanced by poor personal hygiene and
overcrowding person to person
transmission
more symptomatic in adults

Pathology cholestasis
 Serologic test
Hepatitis A
Hepatitis B

LO 1.2
 Hepatitis B
Percutaneous inoculation major route of
transmission

High risk group

acutely infected persons
sexually promiscuous persons
health care workers exposed to blood
persons who require repeated transfusions especially with
pooled blood product concentrates
residents and staff of custodial institutions for the
developmentally handicapped, prisoners, and, to a lesser
extent, family members of chronically infected patients
 Pathogenesis
nucleocapsid proteins (HBcAg and possibly
HBeAg) present on infected hepatocyte cells
membrane invite cytolytic T cells
destroy HBV-infected hepatocytes liver
injury
precore genetic mutants of HBV more
severe outcome
 Pathology
Acute HBV infection large hepatocytes with
a ground-glass appearance of the cytoplasm
contains HBsAg
 Serologic test
Hepatitis B
 Wild type chronic hepatitis B
Hepatitis C

LO 1.2
 Hepatitis C
Egypt, United States, African Americans and
Mexican Americans
transmitted by other percutaneous routes
(injection drug use), exposure to blood
Symptoms may arise 20 30 years after
infected
 Pathogenesis
HCV infection of lymphoid cells immune
responses (Intrahepatic HLA class Irestricted
cytolytic T cells) nucleocapsid, envelope,
and nonstructural viral protein antigens
virus-activated CD4 helper T cytokines
HCV-specific CD8 cytotoxic T cells liver
injury
HCV proteins interfere with innate
immunity blocking of type 1 interferon
 Pathology
relative paucity of inflammation
marked increase in activation of sinusoidal
lining cells
lymphoid aggregates
the presence of fat increased to fibrosis
bile duct lesions biliary epithelial cells
appear to be piled up without interruption of
the basement membrane
 Serologic test
Hepatitis C
Hepatitis D

LO 1.2
 Hepatitis D
Northern Africa, southern Europe, the Middle East
co-infections with acute hepatitis B or of
superinfections in those already infected with HBV

Transmissions
blood and blood products
primarily injection drug users
Hemophiliacs

Pathology microvesicular steatosis

Hepatitis E

LO 1.2
 Hepatitis E
India, Asia, Africa, the Middle East, and
Central America ~ hepatitis A
enteric mode of spread
person-to-person transmission rare

Pathology cholestasis
Sign & symptoms of viral hepatitis
Prodromal phase
Constitutional symptoms anorexia, nausea and
vomiting, fatigue, malaise, arthralgias, myalgias,
headache, photophobia, pharyngitis, cough, and
coryza
Icteric phase
clinical jaundice + prodromal phase diminish +
hepatomegaly & tender RUQ discomfort
Spider angiomas
Recovery phase
constitutional symptoms disappear, liver
enlargement and abnormalities in liver
biochemical tests evident
Laboratory features of viral hepatitis
 Prognosis
hepatitis A recover completely from their
illness with no clinical sequelae
acute hepatitis B, 9599% of previously
healthy adults have a favorable course and
recover completely
Hepatitis C is less severe during the acute
phase than hepatitis B and is more likely to be
anicteric; fatalities are rare, but the precise
case-fatality rate is not known
HDV superinfection of a person with chronic
hepatitis B fulminant hepatitis
 Complications & sequelae
relapsing hepatitis
Hepatitis A cholestatic hepatitis
chronic hepatitis C and is part of a spectrum of B
cell lymphoproliferative disorders B cell
lymphoma
Fulminant hepatitis (B, D, E)
Cerebral edema, brainstem compression,
gastrointestinal bleeding, , respiratory failure,
cardiovascular collapse, and renal failure are
terminal events
 Chronic hepatitis, if:
lack of complete resolution of clinical symptoms of
anorexia, weight loss, and fatigue and the
persistence of hepatomegaly
the presence of bridging/interface or multilobular
hepatic necrosis on liver biopsy during protracted,
severe acute viral hepatitis
failure of the serum aminotransferase, bilirubin,
and globulin levels to return to normal within 612
months after the acute illness
the persistence of HBeAg for >3 months or HBsAg
for >6 months
 Differential diagnosis
Viral diseases such as infectious
mononucleosis (cytomegalovirus, herpes
simplex, and coxsackieviruses)
Toxoplasmosis
Leptospira, Candida, Brucella, Mycobacteria,
and Pneumocystis
genetic or metabolic liver disorders
nonalcoholic fatty liver disease
 Treatment
Severe acute hepatitis B
nucleoside analogue (lamivudine)
Hepatitis C
interferon
long-acting pegylated interferon plus the nucleoside
analogue ribavirin
Fulminant hepatitis
support the patient by maintenance of fluid balance
support of circulation and respiration, control of
bleeding
correction of hypoglycemia
Protein intake should be restricted, and oral lactulose
or neomycin administered
Prevention
 LO 1.3
Menjelaskan hepatitis kronik
Autoimmune hepatitis

LO 1.3
 Autoimmune hepatitis
continuing hepatocellular necrosis and
inflammation, fibrosis cirrhosis and liver
failure
Untreated 6-month mortality of as high as
40%
 Pathogenesis
Abnormalities of immunoregulatory control over
cytotoxic lymphocytes (impaired regulatory
CD4+CD25+ T cell influences) may play a role as well

In the liver, the histopathologic lesions are composed

predominantly of cytotoxic T cells and plasma cells
circulating autoantibodies (nuclear, smooth muscle,
thyroid, etc.; see below), rheumatoid factor, and
hyperglobulinemia are common
other autoimmune disorders
histocompatibility haplotypes associated with
autoimmune diseases
responsive to glucocorticoid/immunosuppressive
therapy
 Clinical features
Fatigue, malaise, anorexia, amenorrhea, acne,
arthralgias, and jaundice
arthritis,
maculopapular eruptions (including cutaneous
vasculitis),
erythema nodosum,
colitis,
pleurisy,
pericarditis,
anemia, azotemia, and
sicca syndrome (keratoconjunctivitis, xerostomia)
 Laboratory features
normal serum bilirubin, alkaline phosphatase,
and globulin levels
minimal aminotransferase elevations
Advanced disease hypoalbuminemia
Hypergammaglobulinemia
Rheumatoid factors
ANA
Liver biopsy Necroinflammatory activity
 Diagnostic criteria
hyperglobulinemia, autoantibodies, and
characteristic histologic features
Factor that weigh favor
female gender;
predominant aminotransferase elevation;
presence and level of globulin elevation;
presence of nuclear, smooth muscle, LKM1, and
other autoantibodies;
concurrent other autoimmune diseases;
characteristic histologic feature;
HLA DR3 or DR4 markers;
response to treatment
 Differential diagnosis
acute viral hepatitis
Postnecrotic or cryptogenic cirrhosis
primary biliary cirrhosis
rheumatologic disorders (RA & SLE)
autoimmune biliary disorders (primary biliary
cirrhosis, primary sclerosing cholangitis, or,
even more rarely, mitochondrial antibody-
negative autoimmune cholangitis)
 Treatment
high-dose glucocorticoid monotherapy (60 mg
daily)
glucocorticoid (30 mg daily) plus high-dose
azathioprine (150 mg daily)
liver transplantation
Chronic viral hepatitis

LO 1.3
 Chronic hepatitis
series of liver disorders of varying causes and
severity in which hepatic inflammation and
necrosis continue for at least 6 months

Classification based on
Caused
Histologic activity / grade
Its degree of progression / stage
Classification by cause
Classification by grade
Classification by stage
 Chronic hepatitis B
associated with clinically silent acute infection
90% chronic
progression to more severe chronic hepatitis
and cirrhosis has been observed in more than
a quarter of cases

Clinical features
Fatigue, persistent / intermittent jaundice,
malaise, anorexia
 Laboratory features
Aminotransferase elevations
aminotransferase (ALT) tends to be more elevated
than aspartate aminotransferase (AST)
Cirrhosis AST tends to exceed ALT
alkaline phosphatase activity tend to be normal or
only marginally elevated
Classification & treatment

Oral agents : lamivudine, adefovir, entecavir

 Complication
Ascites
Edema
Bleeding gastroesophageal varices
Encephalopathy
Coagulopathy
Hypersplenism
 Chronic hepatitis D
follow acute co-infection with HBV but at a
rate no higher than the rate of chronicity of
acute hepatitis B
HDV superinfection occurs in a person who is
already chronically infected with HBV
worsening of the liver disease

Serologic features anti-LKM3 (liver kidney

microsomes)
 Treatment
high-dose IFN- (9 million units three times a
week)
IFN is likely to become a more convenient
replacement for standard IFN
lamivudine, adefovir, entecavir
transplantation
 Chronic hepatitis C
return to normal in aminotransferase levels
after acute hepatitis C chronic (85%)
quarter of cases cirrhosis

Clinical features ~ chronic hepatitis B

Laboratory features ~ chronic hepatitis B

aminotransferase levels tend to fluctuate more &
to be lower
presence of autoantibodies
Treatment
 LO 1.4
Menjelaskan penyakit hati karena alkohol
 Alcoholic liver disease
Pathology 3 major lesions
Fatty liver
Alcoholic hepatitis
Cirrhosis

Comorbid factors gender, heredity,

immunity
 Etiology
wine, beer, or spirits, and pattern of drinking
are less clear
Chronic infection with hepatitis C
progression alcoholic liver disease cirrhosis
Risk factors
Pathogenesis
 Clinical features
unsuspected hepatomegaly

Fever, spider nevi, jaundice, and abdominal

pain
Portal hypertension, ascites, or variceal
bleeding can occur in the absence of cirrhosis
Laboratory features
Treatment
 LO 1.5
Menjelaskan sirosis hati
 Sirosis hati
Definisi Epidemiologi
sirkulasi mikro, anatomi Laki-laki : wanita = 1,6 : 1
pembuluh darah besar dan Rata-rat 30-59 tahun
seluruh sitem arsitektur hati dengan puncaknya 40-49
mengalami perubahan tahun
menjadi tidak teratur dan
terjadi penambahan
jaringan ikat (fibrosis)
disekitar parenkim hati yang
mengalami regenerasi
 Etiologi
Virus hepatitis (B,C,dan D)
Alkohol
Kelainan metabolic :
1. Hemakhomatosis (kelebihan beban besi)
2. Penyakit Wilson (kelebihan beban tembaga)
3. Defisiensi Alphal-antitripsin
4. Glikonosis type-IV
5. Galaktosemia
6. Tirosinemia
 Kolestasis
Sumbatan saluran vena hepatica
Sindroma Budd-Chiari
Payah jantung
Gangguan Imunitas (Hepatitis Lupoid)
Toksin dan obat-obatan (misalnya :
metotetrexat, amiodaron,INH, dan lainlain)
Operasi pintas usus pada obesitas
Kriptogenik
Malnutrisi
Indian Childhood Cirrhosis
 Patofisiologi
Irreversible chronic injury of the hepatic
parenchyma
Extensive fibrosis - distortion of the hepatic
architecture
Formation of regenerative nodules
 Clinical Manifestations
Spider angiomas Asterixis
Palmar erythema Pigment gallstones
Nail changes Parotid gland
Muehrcke's nails enlargement
Terrys nails Cruveilhier-Baumgarten
Gynecomastia murmur
Testicular atrophy Hepatomegaly
Fetor hepaticus Splenomegaly
Jaundice Caput medusa
 Clinical Manifestations
Muehrcke's nails Terrys nails
 Klasifikasi
Secara Morfologi Fungsional
1. Mikronodular 1. Kompensata :
2. Makronodular Laten Sirosis hati. Pada
stadium kompensata ini belum
3. Campuran (yang terlihat gejala-gejala yang
memperlihatkan nyata. Ditemukan pada saat
gambaran mikro-dan pemeriksaan screening
makronodular) 2. Dekompensata
Active Sirosis hati.Stadium ini
biasanya gejala-gejala sudah
jelas, mis: ascites, edema dan
ikterus
 Morphologic Classification
Micronodular cirrhosis
Nodules less than 3 mm in diameter
Believed to be caused by alcohol,
hemochromatosis, cholestatic causes of
cirrhosis, and hepatic venous outflow
obstruction
 Macronodular
cirrhosis

Nodules larger
than 3 mm
Believed to be
secondary to
chronic viral
hepatitis
Evaluation of Cirrhosis
 Complications
Ascites
Spontaneous Bacterial Peritonitis
Hepatorenal syndrome
Variceal hemorrhage
Hepatopulmonary syndrome
Other Pulmonary syndromes
Hepatic hydrothorax
Portopulmonary HTN
Hepatic Encephalopathy
Hepatocellular carcinoma
 Ascites
Accumulation of fluid within the peritoneal
cavity
Most common complication of cirrhosis
Two-year survival of patients with ascites is
approximately 50 percent
D/ : USG
T/ :
underlying cause of the hepatic disease
ascitic fluid itself
combination of single morning oral doses of
Spironolactone and Furosemide
Tujuan:
Overly rapid removal of fluid
Progressive electrolyte imbalance
 Ascites
Assessment of ascites
Grading
Grade 1 mild
Grade 2 moderate; Moderate symmetrical distension
of the abdome
Grade 3 large or gross asites with marked abdominal
distension
Older system -subjective
1+ minimal, barely detectable
2+ moderate
3+ massive, not tense
4+massive and tense
What do I want to order ?
 Spontaneous Bacterial Peritonitis

Infection of ascitic fluid

Almost always seen in the setting of end-
stage liver disease
The diagnosis is established by
A positive ascitic fluid bacterial culture
Elevated ascitic fluid absolute
polymorphonuclear leukocyte (PMN) count (
>250 cells/mm3)
Clinical manifestations:
Fever
Abdominal pain
Abdominal tenderness
 Hepatorenal syndrome
acute renal failure+advanced hepatic disease (due to
cirrhosis/less often metastatic tumor/severe alcoholic hepatitis)
characterized by:
Oliguria
benign urine sediment
very low rate of sodium excretion
progressive rise in the plasma creatinine concentration
Reduction in GFR often clinically masked
Prognosis: poor, unless: hepatic function improves
Nephrotoxic agents and overdiuresis can precipitate HRS
 Variceal hemorrhage
Occurs in 25 to 40 percent of patients with
cirrhosis
Prophylactic measures
Screening: upper GI endoscopy
T/: nonselective beta blocker, which reduces
the risk of variceal bleeding
Hepatopulmonary syndrome
Hepatopulmonary syndrome (HPS) triad:
Liver disease
Increased alveolar-arterial gradient while
breathing room air
Evidence for intrapulmonary vascular
abnormalities, referred to as intrapulmonary
vascular dilatations (IPVDs)
Cirrhotic patients lacking HPS, mild
hypoxemia is common and is presumably
caused by ascites, with resulting
diaphragmatic elevation and
ventilation/perfusion mismatch
 Hepatic Hydrothorax
Pleural effusion in a patient with cirrhosis and no
evidence of underlying cardiopulmonary disease
Movement of ascitic fluid into the pleural space through
defects in the diaphragm, and is usually right-sided
Diagnosis -pleural fluid analysis
reveals a transudative fluid
serum to fluid albumin gradient greater than 1.1
Confirmatory study:
Scintigraphic studies demonstrate tracer in the chest
cavity after injection into the peritoneal cavity
Treatment options:
diuretic therapy
periodic thoracentesis
TIPS
 Portopulmonary HT
Refers to the presence of pulmonary
hypertension in the coexistent portal
hypertension
Prevalence in cirrhotic patients is
approximately 2 percent
Diagnosis:
Suggested by echocardiography
Confirmed by right heart catheterization
Hepatic Encephalopathy
 Hepatic Encephalopathy
Monitoring for events likely to precipitate HE
[i.E.- variceal bleeding, infection (such as SBP), the
administration of sedatives, hypokalemia, and
hyponatremia]
Reduction of ammoniagenic substrates
Lactulose / lactitol
Dietary restriction of protein
Zinc and melatonin
 References
Fauci. Braunwald. Dkk. Harrisons Principles of
Internal Medicine. 17th edition. United State:
The McGraw-Hills; 2008