Transcript LIVER DISEASES

LIVER DISEASES
Symptoms. Signs. Syndroms. Diseases.
Part I
Do you know that …
• Liver is a depot for 13% of blood in every given
moment
• Liver receives blood from 2 vessels
-oxygenated blood from a. hepatica
- blood with nutrients and metabolic products from
v. porta
• Venous blood enters through v. porta and leaves
liver via v. hepatica
• Liver may lost ¾ of hepatocytes before hepatic
failure develops
• Liver is the unique human organ that can
regenerate it self
Liver structure v. portae system
Liver
• Stores sugar needed for energy
• Absorbs good nutrients
• Breaks down poisons (toxins) and
drugs
• Makes important proteins that help
build new tissue and repair broken
tissue
• Produces bile, which helps remove
waste from the body
Liver functions
• Synthetic
- synthesis of albumin, coagulation factors, fibrinogen,
cholesterol, compliment, binding proteins for iron,
copper, vit. A and other
• Detoxification and excretion
- products of metabolism (proteins, steroids,
prostaglandins, drugs, alcohol, bilirubin, urea,
ammonium and so on)
• Accumulation (deposition)
- glycogen, lipids, iron, copper, vitamins А,В12,D,Е,К
• Secretion
- secretion of bile
Major risk factors for liver disease
• alcohol use
• medications (including herbal compounds, birth
control pills, and over-the-counter medications)
• personal habits
• sexual activity
• injection drug use
• recent surgery
• remote or recent transfusion with blood and blood
products
• occupation
• familial history of liver disease
Symptoms of liver disorders
Constitutional symptoms
Liver-specific symptoms
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Fatigue*
Weakness
Nausea
Poor appetite
Malaise
Jaundice*
Dark urine*
Light stools*
Itching
Ascites*
Abdominal pain
Liver pain
Bloating
Fatigue
• The most common and most characteristic
symptom of liver disease.
• It is variously described as lethargy,
weakness, listlessness, malaise,  need for
sleep, lack of stamina, and poor energy.
• Typically arises after activity or exercise
Jaundice
– A yellow discoloration of the skin or sclera
is a manifestation of hyperbilirubinemia
and can be congenital or acquired.
– It may be also classified as:
• hemolytic (sickle cell anemia)
• hepatocellular (viral hepatitis)
• and obstructive (carcinoma of bile duct or
head of the pancreas).
Jaundice or icterus
• Jaundice is the hallmark symptom of liver disease and
perhaps the most reliable marker of severity.
• Occurs only in the presence of serum hyperbilirubinemia
and is a sign of either liver disease or, less often, a
hemolytic disorder.
• Slight increases in serum bilirubin are best detected by
examining the sclera which have a particular affinity for
bilirubin due to their high elastin content.
• Patients usually report darkening of the urine before they
notice scleral icterus.
• Jaundice is rarely detectable with a bilirubin level less
than 43 umol/L (2.5 mg/dL)
• The presence of scleral icterus indicates a serum bilirubin
of at least 3.0 mg/dL. The ability to detect scleral icterus is
more difficult if the examining room has fluorescent
lighting.
Jaundice: major types
• Prehepatic or unconjugated hyperbilirubinaemia
• Hepatic hyperbilirubinemia
– Hepatocellular disease
– Intrahepatic cholestasis
• Extrahepatic cholestasis
Causes of jaundice
• Prehepatic or unconjugated hyperbilirubinaemia
• haemoiytic anaemias
• Gilbert's syndrome
• Hepatocellular disease
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viral hepatitis (types A, B, C, D and E)
alcoholic hepatitis
autoimmune hepatitis (lupoid)
Drug-induesed hepatitis (halothane, paracetamol)
decompensated cirrhosis
• Intrahepatic cholestasis
• cholestatic hepatitis
• Primary biliary cirrhosis
• Extrahepatic cholestasis
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Darkening of the Urine
• Sensitive indicator of S bilirubin
• Is due to the renal excretion of conjugated
bilirubin.
• Patients often describe their urine as tea or
cola colored.
• Bilirubinuria indicates an  of the direct
Sbilirubin fraction and therefore the presence
of liver disease.
Pale (light) Stools
• Suggest biliary obstruction either
intrahepatic or extrahepatic.
– Degradation of bilirubin in the intestine imparts
the normal yellow-brown color to the stool.
– Failure of bilirubin to reach the intestine renders
the stool pale and grayish.
Liver Pain
• Right upper quadrant discomfort or ache
occurs in many liver diseases and is usually
marked by tenderness over the liver area.
• The pain arises from stretching or irritation of
Glisson's capsule, which surrounds the liver
and is rich in nerve endings.
• Severe pain is most typical of gall bladder
disease, liver abscess
Ascites
• Definition: free fluid in the abdomen
• Clinical manifestations:
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Distended abdomen
Fullness in flanks
Umbilicus everted
Distended veins, striae
Dullness (requires at least 2 liters), sonogram or CT best
diagnostic tools for smaller amounts
Ascites
– In most cases ascites appears as part of a wellrecognized illness that is, cirrhosis, CHF, nephrosis,
or disseminated carcinomatosis
– Diagnostic paracentesis (50 to 100 mL) should be
part of the routine evaluation of the patient with
ascites.
– The fluid should be examined for its gross
appearance; protein content, cell count, and
differential cell count should be determined
Stigmata of chronic liver disease
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spider nevi,
palmar erythema
dilated superficial abdominal veins
Gynecomastia
parotid gland enlargement
Dupuytren’s contracture
white nails (leukonychia)
Симптомы и синдромы заболеваний печени
Etiology of Dupuitren contracture
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Chronic alcohol intoxication
Manual labor
Trauma
Diabetes mellitus
Epilepsy (drugs?)
Elderly persons
Etiologic factors of gynecomastia
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Chronic hepatitis and liver cirrhosis
Chronic alcohol intoxication
Drugs
Hyperthyreosis
Uremia
Initial hypogonadism
Portal hypertension
Clinical picture
 Collateral blood circulation (portocaval anastomosis)
- esophageal varicose veins dilatation
- caput Medusae
- upper haemorrhoidal varicose veins dilatation
 Ascites
 Splenomegaly
 Dilation of v. рortae on ultrasound (more then 12 mm)
Possible levels of block in portal hypertension
Causes of portal hypertension
 Suprahepatic block
- Occlusion of hepatic veins
- Budd-Chiari syndrome
- Acute increase of CVP
 Intrahepatic block
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Liver cirrhosis (viral, alcoholic, primary biliary)
Wilson disease
Acute alcoholic hepatitis
Chronic viral hepatitis
Primary sclerotic cholangitis
 Subhepatic block
-occlusion of v. porta (thrombosis, tumor compression, compression
with enlarged lymph nodes, sarcoidosis)
Esophagogastroscopy
Esophageal varicose veins dilatation
Dilation of v. рortae and vv. hepaticae
норма
Hepatocellular cytolisis
• Enzymes that Reflect Damage to Hepatocytes
• The aminotransferases (transaminases) are sensitive
indicators of liver cell injury and are most helpful in
recognizing acute hepatocellular diseases such as
hepatitis.
• They include the aspartate aminotransferase (AST)
and the alanine aminotransferase (ALT).
• AST is found in the liver, cardiac muscle, skeletal
muscle, kidneys, brain, pancreas, lungs
• продолжение
Cholestasis syndrom
• Cholestatic Conditions
• When the pattern of the liver tests suggests a cholestatic
disorder, the next step is to determine whether it is intra- or
extrahepatic cholestasis.
• Distinguishing intrahepatic from extrahepatic cholestasis may
be difficult
• Ultrasonography rarely identifies the site or cause of
obstruction because of overlying bowel gas
• Appropriate next tests include computed tomography and
endoscopic retrograde cholangiopancreatography
• Extrahepatic cholestasis
• Intrahepatic cholestasis
CHOLESTASIS
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Intrahepatic cholestasis
drugs (phenothiazines)
primary billiary cirrhosis
primary sclerosing cholangitis
Extrahepatic cholestasis
bile duct stricture (benign and malignant)
common duct stone
cancer of the head of the pancreas
Hepatocellulare failure
• Clinical picture: jaundice, encephalopathy,
decreased size of liver, brain edema
• Hyperbilirubinemia
• Decreased levels of protrombine, coagulation
factors
• Hypoalbuminemia
• Hypocholesterolemia
Causes of hepatocellular failure
• Alcohol
• Viral hepatitis
(viruses of hepatitis, herpes, CMV and other)
• Drugs (paracetamol, estrogens, antidepressants,
NSAID, antibiotics, anti tuberculous)
• Poisoning (mushrooms, CCl4
• Liver ischemia (cardiogenic shock,)
• Wilson disease
• Acute fatty liver
Syndrome of hepatocellular
Damaged function
Sintetic
 Coagulation factors
 Albumin
Detoxication/excreation
Ammonium
Feature
 protrombin, fibrinogen,
hemorrhages
Hypoalbuminemia, edema,
ascites
Liver fetor
Encephalopathy
estrogens
Spiders nevi, palmar erytema,
gynecomastia
[B1]No tick box requrired?
Hepatic encephalopathy
Hepatic encephalopathy is a clinical diagnosis
Stage 0
Minimal
hepatic
encephalopathy
(previously
known
as
subclinical
hepatic
encephalopathy). Lack of detectable changes in personality or behavior. Minimal
changes in memory, concentration, intellectual function, and coordination. Asterixis
is absent.
Stage 1
Trivial lack of awareness. Shortened attention span. Impaired addition or subtraction.
Hypersomnia, insomnia, or inversion of sleep pattern. Euphoria, depression, or
irritability. Mild confusion. Slowing of ability to perform mental tasks. Asterixis can be
detected.
Stage 2
Lethargy or apathy. Disorientation. Inappropriate behavior. Slurred speech. Obvious
asterixis. Drowsiness, lethargy, gross deficits in ability to perform mental tasks,
obvious personality changes, inappropriate behavior, and intermittent disorientation,
usually regarding time.
Stage 3
Somnolent but can be aroused, unable to perform mental tasks, disorientation about
time and place, marked confusion, amnesia, occasional fits of rage, present but
incomprehensible speech
Stage 4
Coma with or without response to painful stimuli
Hepatorenal syndrome I and II type
Features of liver damage:
 Hepatocellulare failure
 Portal hypertension
Arterial hypotension
ARF (oliguria, anuria, GFR,)
No primary renal pathology
Pathogenesis of hepatorenal syndrome
• Develops in presence of hepatocellular insufficiency
and portal hypertension (acsites)
• Decrease of GFR and renal blood flow
• Activation of RAAS and renal vasoconstriction
• Increase of fluid reabsorbtion and plasma volume
• No morphological changes in renal parenchima
Types of hepatorenal syndrome
• Type 1
- Doubling of serum creatinine > 2.5 mg/dl
during < 2 weeks
• Type 2
- More slow increase of serum creatinine > 2.5 mg/dl
Provocative factors for hepatorenal syndrome
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Alcoholic excess
Bleeding
Excess of diuretics and massive diuresis
Drugs (NSAID, aminoglycosides)
Paracentesis
Hypersplenism
• Anemia (normo- or macrocytic)
• Leucopenia with granulocytopenia and
lymphopenia
• Thrombocytopenia
• Commonly is associated with splenomegaly
• Hemorrhagic syndrome may be present
FibroScan®
•No need to be fasting
• Duration of investigation – 5 min
•10 measurements
•Mean value = True value
• Result is given in kPa
•Contraindication: ascitis
FibroScan
Intensity of fibrosis during liver fibroscanning
Wave velocity is associated with elasticity of liver tissue and level of
fibrosis
Depth (мм)
Elasticity = 3× density × velocity2