This document discusses symptoms and signs of liver disease. It notes that chronic hepatitis, cirrhosis, cholecystitis and cholangitis are among the most clinically significant liver and bile tract diseases. It describes various complaints patients may report including fatigue, jaundice, abdominal pain, skin itching, and bleeding. Physical exam findings are outlined including signs of liver enlargement (hepatomegaly), ascites, spider angiomas, and other manifestations. Causes, patterns and significance of symptoms are discussed for accurately diagnosing underlying liver conditions.

1. Syndroms of liver
diseases and bile-
excreting tracts

2. Liver’s chronic diffuse - chronic hepatitises and
liver cirrhoses, and also a cholecystitis
(calculous and acalculous) and cholangitis –
have the greatest clinical value among diseases
of a liver and bile-excreting tracts. Besides, it is
necessary to mean (including at differential
diagnostics) real enough possibility focal of liver
- abscesses, echinococcosis and especially
primary tumours of a liver (hepatocellular
carcinoma) and metastasises of tumours in a
liver.

3. A number of genetically caused diseases at
which develops progressive of a liver with
gradual development of cirrhosis among which
are especially important:
• hepatolenticular degeneration (Konovalova -
Wilson's disease), caused by disturbance of
copper metabolism;

4. • hereditary hemochromatosis - disturbance of
ferriferous pigments metabolism with raised
absorption in intestines of iron and its
accumulation in tissue and organs; iron deposit
in a liver can have secondary character at some
anemias, alcoholic illness of a liver;
• Liver at deficiency α- antitrypsin.

5. Revealing of the specified diseases represents
the big practical value, especially under
condition of specification of aetiology or
pathogenetic features of illness. It is important,
for example, for real influence on an aetiology –
use of viricides at chronic virus hepatitises, the
medications removaling from an organism
copper at Konovalova - Wilson's disease, the
termination of use MD, caused hepatitis
development, and, of course, the termination of
alcohol use leading to severe of liver.

6. INSPECTION
Inquiry
• Feature of studying of the anamnesis. Already at
inquiry of patients with diseases of liver and bile-
excreting tracts the constant «etiological
watchfulness» is necessary.
• The epidemiological anamnesis, for example
possibility of infection with hepatitis viruses B, C, D, E
and G is extremely important at blood transfusions
and its components, a donor service, and also at
addicts, homosexuals, medical workers (for example,
employees of department of a chronic hemodialysis,
blood transfusion stations), at operative interventions
including the stomatologic.

7. • In the epidemiological plan it is necessary to specify
the fact of stay of the patient in endemic region of
opisthorchosis, leptospirosis, and a yellow fever.
• The large value has revealing of influence MD. Long
using of nitrofurantoin, tetracycline, some
antihypertensive drugs (methyldopa), antituberculous
drugs (isoniazid, ethambutol) can cause the chronic
drug-induced hepatitis, some psychotropic drugs -
cholestasis, estrogens (including in structure oral
contraceptives) - a syndrome of Badda-Kiari and
formation of stones of a bilious bubble, and also a
jaundice of pregnant women in III trimester of
pregnancy as a result of cholestasis.

8.  Especially attentively it is necessary to ask the
patient concerning alcohol using (it is useful to
use questionnaire CAGE).

9. The important role in diagnostics of diseases of a
liver and bile-excreting tracts is played by
studying of the family anamnesis as a number
of progressing diseases of the liver often found
out already in a stage of far come cirrhosis and
shown by the general hepatic signs, has the
defined genetic features. So, it is important to
reveal hereditary character Konovalov -
Wilson’s disease, hemochromatosis, deficiency
α-antitrypsin; specially single out family benign
hyperbilirubinemia.

10. Complaints
Careful inquiry allows finding out a number signs
of liver disease already at early stages of
disease. For liver and bile-excreting tracts
diseases are most typical following complaints.
• Complaints of the general character: Small
appetites, fatigue, irritability, headaches,
decrease in a potentiality and libido, menstrual
irregularities.

11. • The agonizing itch of a skin amplifying at night
and depriving the patient’s sleep.
• A jaundice (it is frequent at the moment of
survey of a jaundice do not note and it is
possible to reveal it only anamnesticly; in
addition, inquiry allows to estimate character of
a jaundice available for the patient).
• Blood presents in vomit mass or stool.
• Increase in the sizes of abdomen and the
increase of body weight connected with it (for
the account of a collecting liquid).

12. At pathology bile-excreting tracts note also other
complaints in connection with reflux of bile in a
stomach and an oesophagus.
• Unpleasant, usually bitter taste in a mouth.
• Eructation, nausea and vomiting often provoked
by use of fat or fried food.
• Unstable stool (constipations are replaced by
diarrheas), abdomen swelling.

13. • Pains in right hypochondriac region.
• The skin itch is connected with extrahepatic
biliary obstruction.

14. COMPLAINTS of the GENERAL CHARACTER
Usually occurrence of fatigue, irritability and
headaches is connected with an intoxication
arising owing to disturbance of the basic
functions of a liver that is usually shown by
distarbances of activity CNS (hepatic
encephalopathy). At intoxication increase these
signs amplify, sleep disturbance (inversion of
sleep - a night sleeplessness and day
drowsiness), and then loss of consciousness (a
hepatic coma) join.

15. BLEEDINGS
Presence of pure blood at vomit masses usually
testifies to a bleeding from varix dilatations of
an oesophagus or about presence ulcerous
gastritis as displays of a portal hypertensia with
stagnation of blood in portal system, caused by
liver disease. The same origin has occurrence
of scarlet blood in stool (hemorrhoidal
bleedings) and tarry stool (melena). The reason
of bleedings can be also ulcerative esophagitis
and gastritis of alcoholic genesis, a syndrome
Mellory - Veissa.

16. PAINS
Painful sensations patients frequently describe as
weight and pressure in right hypochondrium.
• Pains can be connected with irritation of
peritoneum, covering a liver, at perihepatitis (for
example, in connection with a tumour or a liver
abscess) and pericholecystitis. They usually
have intensive character, irradiate upwards (in
area of the right shoulder), and amplify at
palpation of right hypochondrium.

17. • The stretching of liver capsule in connection with large
liver mass (hepatomegaly) also causes occurrence of
a painful syndrome that most often observe at
stagnation of blood in a liver against the background
of congestive heart failure.
• Painful sensations at patients with diseases of liver
and bile-excreting tracts can be caused also following
conditions.
• - Biliary dyskinesia.
• - Spastic spasm smoothmuscular’s cells of
gallbladder and bile ducts at biliary [hepatic] colic.

18. Last is caused usually by stone advancement in
bile ducts. These pains arise, as a rule,
suddenly, quickly become intolerable, is
frequent irradiate upwards, are accompanied by
a nausea and the vomiting, not bringing to the
patient (unlike other reasons of vomiting)
relieve.

19. - At a chronic inflammation of gallbladder patients
can show complaints on aching or dull aches in
right hypochondrium, amplifying at palpation
gallbladder’s points (a corner between the right
costal arch and external edge of rectus muscle
of abdomen) and point in the regions of a neck
on the right between legs of
sternocleidomastoid muscle - a so-called point
of phrenic nerve (frenikus-symptom). At liver
diseases often accompanying them the chronic
pancreatitis, a gastric ulcer and duodenal ulcer
also can cause belly-aches.

20. Skin itch
This sign relate to typical enough displays of liver
illnesses accompanied cholestasis. Extreme
degree of a skin itch (painful, amplifying at the
night, depriving a sick dream, with a
considerable quantity often infected skin
scratches) observe in the presence of
intrahepatic and extrahepatic biliary obstruction
(cholestasis syndrome), often combined with a
jaundice.

21. JAUNDICE
This is one of the most typical displays of
hepatopathy. For its revealing it is necessary to
ask following questions.

22. • • When there was jaundice and how fast it has
developed? Whether the patient of a belly-ache,
an anorexia, a nausea, vomiting notes?
• • Is there at the patient a fever, shivering, a skin
itch, whether he notes decrease of body
weight?
• • Whether transfused to the patient ever blood,
whether there are for it tattoos?
• • What MD the patient and what purpose uses
for?

23. • What colour of urine and stool?
• • Whether was jaundices at relatives of the
patient and the persons living together with him,
how for a long time?
• • Whether uses sick alcohol? What quantity in,
what frequency with?

24. PHYSICAL METHODS of investigation
The basic method of physical exam of a liver, no
less than other organs of a belly cavity, -
palpation, however should precede it the
general survey, survey abdomen’s area and
percussion, allowing roughly to estimate the
sizes of these organs. Spleen exam usually
carries out after liver exam.

25. The general survey
At the general survey it is necessary to pay
attention to degree of the exhaustion especially
marked at far come (decompensated) cirrhosis
or a cancer of a liver; thus the general decrease
of body weight is often combined with the big
sizes of abdomen for the account ascites. The
great value for understanding genesis of
isolated ascites has revealing of the expanded
veins of a belly wall that with a high probability
allows suspecting presence of a portal
hypertensia as its reason.

26. At it is long existing liver’s cirrhosis of different aetiology
often finding out changes of nail bone of fingers on
type of "clubbed fingers». Some diseases of the liver,
first of all a progressing current (a chronic active
hepatitis and a liver cirrhosis in an active stage), are
accompanied by a number of the general (system)
nonspecific syndromes - not infectious fever (unlike
these illnesses at acute cholecystitis, cholangitis, an
abscess of a liver a fever typically infectious, it is
frequent hectic fever, with chills and profuse sweats),
arthritises, vascular changes with Raynaud's
syndrome (a syndrome of "dead fingers»), a so-called
dry syndrome (Sjögren's sicca [Mikulicz-Sjögren]
syndrome), characterised by insufficient production of
a saliva (xerostomia), eyewater liquid (Sjögren's
[sicca] syndrome), widespread caries of a teeth.

27. Sometimes illness of a liver is shown only by
these signs reminding other disease (for
example, scleroderma, systemic lupus
erythematosus, rheumatoid arthritis), both only
careful studying of the anamnesis and results of
exam of a liver, including biopsy, allow to
diagnose primary disease of a liver with
extrahepatic displays. Nevertheless at the
general inspection of the patient with liver
diseases find out a number of signs (tab.1)
allowing not only to suspect of a liver, but also
to assume an aetiology of this

28. It is important to consider that these signs reveal
at investigation of the most different organs and
systems (cutaneous coverings, face, eyes,
salivary glands, palms and feet, mammaris,
testicles).

29. Small hepatic signs
Relate following changes to small hepatic signs.
• Telangiectasias («vascular spiders»).
• Palmar erythema.
• The hemorrhagic syndrome with occurrence petechias and
ecchymosises on a skin, bleeding of oral cavity and nose
mucous membranes.
• Xanthoma and xanthelasmas.
• Gynecomastia and other signs, characteristic for alcoholic illness
of a liver (a huge parotitis - increase parotics salivary glands,
Dupuytren's contracture - fibrotic -cicatricial sclerosis of palmar
aponeurosis and flexor tendon muscles of fingers, visiable
sclera’s vessels).
• Kaizer – Flaisher’s ring, characteristic for Hepatolenticular
[(progressive) lenticular, Wilson – Konovalov’s] degeneration

30. Telangiectasias or vascular spiders, - local
excessive expansion of capillaries and small
vessels. Their quantity can vary from single to
disseminated in a considerable quantity of
"field" of vascular asterisks). Often
telangiectasias are accompanied by original
strengthening the skin’s vascular [vessel]
pattern reminding by consideration close
drawing of the monetary bank note with
impregnations of colour threads.

31. Telangiectasias
(«vascular spiders»).

32. Telangiectasias
(«vascular spiders»).

33. Liver palms or palmar erythema, - bright red
erythema in the field of thumb and little finger
eminences. Hepatic palms are often combined
with similar changes of feet. The specified
manifestations are caused hyperestrogenemia
(increase of the content of an estrogen in blood
in connection with their lowered destruction in a
liver) and, probably, opening arteriovenous
anastomosis. It testifies first of all to cirrhosis of
a virus and alcoholic aetiology and is rarer -
about an acute hepatitis.

34. Haemorrhagic manifestations - a frequent
variant of changes of the skin characterised by
appearance on a skin punctulate petechias and
ecchymosises; sometimes in places of vascular
changes are formed ulcers. Usually these
phenomena reflect activity of a chronic hepatitis
or cirrhosis and are connected with disturbance
of synthesis in a liver of blood-coagulation
factors (first of all prothrombin) or a
thrombocytopenia.

35. Xanthoma and especially, xanthelasmas with
typical localisation in area of eyelids can testify
about primary biliary [Hanot's] cirrhosis.

36. xanthelasmas

37. xanthelasmas

38. • Gynecomastia and other signs alcohol-
induced liver injury - the enlargement of
mammary glands at the men, caused by the
increased contents of an estrogen, is not
enough metabolizing the injuryed liver; quite
often gynecomastia arises as a sign of alcoholic
illness of a liver (especially at a cirrhosis stage).
To alcoholic cirrhosis also testify a huge
parotitis, and also Dupuytren's contracture. At
alcoholic injurying of a liver sometimes reveal
testicles atrophy.

39. Gynecomastia

40. Gynecomastia

41. Kaizer – Flaisher’s ring is original change of a
cornea in the form of yellowish-green or olive-
brown pigmentation on its periphery caused by
deposits of copper. This sign with high degree
of reliability allows ascertaining the long existing
and genetically caused metabolic disorder of
the copper, leading to cirrhosis development at
Wilson – Konovalov’s illness.

42. Kaizer – Flaisher’s ring

43. The big hepatic signs
The Big hepatic signs include a jaundice and
hepatomegaly, coming to light together with the
big (basics) hepatic syndromes - a portal
hypertensia, hepatocellular failure and a hepatic
encephalopathy, hepatorenal syndrome.

44. • It survey abdomen’s area.
• At survey of liver area it is possible to ascertain its
increase (hepatomegaly) only at the considerable
sizes and a small thickness of a belly wall that is true
also concerning space-occupying s (nodes, tumours,
hepatic hydatid, and the big abscess). In all these
cases attract attention asymmetry of abdomen for the
account bulging of liver and lagging at movement of a
belly wall in right hypochondrium and pit of the
stomach (epigastric region). Also it is possible to see a
pulsation of the enlarged liver for the account of wave
regurgitation blood at tricuspid insufficiency. The
cholecele (at its dropsy, empyema) can cause visible
outpouching.

45. Hepatomegaly
• True large liver mass (hepatomegaly; fig. 2) most
often observe at congestive heart failure, acute and
chronic hepatitis, cirrhosis, tumoral or its metastatic .
Edge of a nutmeg liver usually rounded more off and
painful at palpation, edge cirrotically changed organ
denser, rough, as a rule, the painless. Pressing on the
enlarged liver at congestive heart failure it causes
swelling right jugular vein – easily revealed and very
important sign stagnation of blood on the greater
circulation (reflux – symptom, or hepatojugular reflux).
Hepatocellular carcinoma leads to considerable
consolidation of liver tissues, described as «a liver of
stony density».

46. Palpation of gallbladder
Gallbladder can be palpated at its substantial
enlargement caused by empyema (suppurative
inflammation), dropsy, a chronic cholecystitis, a
cancer. In these cases it is defined in a kind of
sacciform formation of a dense or elastic
consistence in area between a low edge of a
liver and external edge of the right direct
muscle of abdomen. Following specific
symptoms allow estimating a condition of
gallbladder.

47. • Courvoisier's symptom - palpation of
considerably enlarged, with the normal elastic
walls, the tense painless gallbladder filled with
bile in a combination to jaundice at common
biliary obstruction by a tumour of pancreas
head or in the field of major duodenal papilla.
• Murphy's sign - an involuntary breath-holding
on breathe in at palpation areas of right
hypochondrium (especially deep).
• Kehr's symptom - palpatory tenderness of right
hypochondrium at a breath.

48. • Mussy-Georgevsky's symptom (frenikus-
symptom) - painfulness at pressing between
legs of right sternocleidomastoid muscle.
• Ortner's symptom - painfulness at light
tapotement on edge of the right costal arch.
This is symptom usually check, comparing
unpleasant sensations of the patient from both
sides.
These symptoms, with the exception of
Courvoisier’s symptom, are characteristic for a
cholecystitis (acute or aggravations of chronic).

49. Additional analysis
Complete blood count
• Complete blood count can reveal leukocytosis
and increase ESR (often note at acute
cholecystitis and acute alcohol hepatitis), and
also leukopenia and a thrombocytopenia in a
combination with increased ESR (at a chronic
hepatitis of the virus aetiology).

50. Biochemical analysis of blood
Investigation of biochemical analysis of blood in
diagnostics of liver diseases and bile-excreting
ducts belongs to a special place. First of all
definition of one of the main functional index of
a liver-bilirubin is necessary. In detail
metabolism of bilirubin is described more low.
Biochemical to signs and liver s often act
changes of activity of some the enzymes
prodused mainly by tissue of liver.

51. • Transaminase – AST (aspartate aminotransferase) and
ALT (alanine aminotransferase GPT glutamic-pyruvic
transaminase,); increase of their activity in blood
testifies to hepatocytes’s damage (cytolysis).
- the AST contains in many tissues of an organism
(heart, skeletal muscles, a brain, kidneys) mainly in
mitochondrions of cells; considerable increase of
activity is the most typical for damage of liver tissue as
testifies about necrosis of cells. At substantial increase
of level of this enzyme the acute virus or toxic hepatitis
is most probable.

52. - ALT contains in cytoplasms of hepatocytes and
is more specific for hepatic cells, therefore its
activity at a hepatic pathology increases in a
greater degree, than AST, except for cases of
alcohol-induced liver injury, where more
hyperactivity of AST, than ALT.

53. • Activity γ-GGT (gamma glutamyl
transpeptidase) increases at liver, excreting
ducts and a pancreas, leading to cholestasis.
Besides, the increase in activity γ-GGT,
especially in a combination increasing of activity
of AST, acts as a sign of alcohol-induced liver
injury (in some cases change of activity of these
enzymes can be an indirect sign of abusing
alcohol if the patient tries to hide it).

54. • Activity of alkaline phosphatase increases
especially strongly at cholestasis (in the
presence of damage of bilious ducts), and also
at anhepatogenous located tumours
(bronchogenic carcinoma, hypernephroma,
Hodgkin's lymphoma).

55. Besides are bilirubin and enzymes, estimate the
contents of protein and its fractions in blood
serum (investigate with the help electrophoresis
and immunoelectrophoresis) as the liver carries
out also protein synthesis function. At
disturbance correlation of various protein
fractions apply the term « dysproteinemia»;
frequently dysproteinemia is caused by
increase of the relative and absolute contents γ-
globulins, in this case speak about
hypergammaglobulinemia.

56. At a serious pathology of liver the protein content
usually decreases (for account the disturbance
of protein synthesis functions), arises
hypoproteinemia (including hypoalbuminemia)
though in certain cases, for example at
hepatitises with marked autoimmune reactions,
observe hypoproteinemia. By degree of
decrease are albumen’s content, cholesterol
and prothrombin judging the severe of hepatic
insufficiency. High level of cholesterol in blood
find out at a bile delay (cholestasis).

57. Diagnostic value has determination of content
some trace elements in blood, first of all copper
and iron. Increase of these indexs can lead to
liver injury. High level of copper is often
combined with the low content ceruloplasmin
that is usually caused genetically and
characteristic for illness Vilson – Konovalov’s.

58. Immunoassay.
Various immunological methods are apply to
revealing as nonspecific changes (change of
the content of immunoglobulins of different
classes, complement, circulating immune
complexes), and for determination concerning
specific to different diseases of a liver of signs
(high content IgA in blood serum often reveal at
alcoholic injury of a liver, detection of a high
titer antinuclear antibodies and antibody to
SMC is characteristic for autoimmune hepatitis,
antimitochondrion antibody - for primary primary
biliary [Hanot's] cirrhosis).

59. Recently all more widely is applied the methods,
allowing to find out as virus infections of a
hepatitis A, B and C, D, and replication stage
of these viruses (in polymerase chain reaction-
PCR), especially concerning hepatitis B viruses
(НВV) and hepatitis C (HCV). For example, a
stage replication of HBV ascertain on revealing
of such markers, as НВV-DNA
(deoxyribonucleic acid, DNA), DNA-polimeraza,
НВе-Ag, НВс - antibody of IgM class.

60. Now indicators viruses’ infection «virus load» and
determination B and C viruses’ genotypes are
important also. These indicators have essential
value not only for specification of liver disease
aetiology, but also for the decision of a question
on appointment antiviral treatment.

61. Tool methods of investigation.
For diagnostics of liver injury and bile-excreting
ducts use X-ray (contrast), CT-scan,
radionuclide [isotopic] method, ultrasonic scan,
endoscopy, duodenal intubation, laparoscopy
and biopsy.

62. X-ray, radionuclide and ultrasonic methods
Radiological methods with contrast are especially
informative for revealing of esophageal varicose veins
dilatation - the important sign of an elevated pressure
in system of a portal vein. Besides, apply contrast
investigation of bile-excreting ducts – cholegraphy,
when contrast enters inside, parenteral. Also carry out
percutaneous [transdermal, fine needle] transhepatic
cholangiography, PTC - radiological investigation of
bilious channels at which into the general bilious
channel or a bilious bubble enter contrast substance
by means of a puncture through a belly wall and a liver
tissue.

63. In addition to contrast cholegraphy (peroral or
intravenous) apply ascending (retrograde) injection of
contrast substance through an orifice of the common
bile duct at endoscopy (endoscopic retrograde
cholangiopancreatography - ERCPG), allowing to
establish a place and the reason of a bile
hypertension, in particular biliary duct stenosis («the
gold standard» in diagnostics primary sclerosing
cholangitis). Ultrasonics (as the basic routine method
of a liver visualisation), radionuclide and CT-scan are
useful first of all to reveal focals, together with diffuse
changes of hepatic parenchyma (a cirrhosis and fatty
[adipose] degeneration); if necessary of them it is
possible to add a liver angiography.

64. Endoscopical’re methods.
Among these methods is most important FEGDS,
allowing to reveal change of veins of an
oesophagus, a stomach mucous membrane (it
is characteristic for a syndrome of a portal
hypertensia), and also erosive esophagitis
(often observe at alcohol-induced liver injury), a
pathology of a duodenal gut.

65. Duodenal intubation
Duodenal intubation has been very spreaded
until recently, investigation of biliary tracts with
the help duodenal intubation - a method of
investigation by probe introduction in a
duodenal gut for the purpose of its obtaining of
bile contained in different phases. This
investigation is useful at diagnostics of
gallbladder illness and bile-excreting tracts, a
duodenal gut. Now in connection with a wide
spread occurrence endoscopy and ultrasonics
use the given method much less often.

66. Contents of a duodenal gut represent a mix of
bile, a secret of pancreas and duodenal gut with
a small amount of gastric juice. It is many
moment fractional duodenal intubation allows to
receive bile from the general common bile duct,
gallbladder and intrahepatic bile ducts with the
subsequent biochemical and microscopic study.
Besides, this method allows receiving
representation about a functional condition of
gallbladder and bile-excreting tracts.

67. • For carry out of investigation is better the two-
channel probe having on the end a metal olive
with apertures. On a probe put marks,
appropriates to level of enter into stomach of an
olive (subcardial department) and duodenal gut
• Duodenal intubation carries out on an empty
stomach stomach in the morning time.
Duodenal tube enters using active swallowing
movements of the patient.

68. • At carrying out of probing receive some (five)
portions of bile from the common bile duct and
gallbladder (cystic bile) that gives the chance to
estimate a condition of bile-excreting system.
Contents’ investigation of duodenal gut includes
the microscopic and bacteriological analysis.

69. • The most important at microscopic study of bile
can consider detection in one of portions of the
elementaries (lamblias) and helminths’ eggs
(liver fluke [Fasciola hepatica], cat liver fluke
[Opisthorchis felineus]). The leukocytes quickly
lyse by bile acids, therefore them are not often
possible to reveal in bile. At dystrophic and
inflammatory changes in bile-excreting system
observe increase of the content of cylindrical
cells of bile ducts, gallbladder’s epitheliums in
portions B and С

70. • Biochemical indicators, such as cholesterol, bile
acids, have certain value in diagnostics
cholelithiasis. Decreasing of bile acids content
(decrease cholesterol’s coefficient) promotes
falling crystals’ cholesterol and stones’
formation.
• Bacteriological study of bile is necessary for
revealing of bile ducts microflora and definition
of its sensitivity to antibacterial drugs. It is
necessary to notice that duodenal intubation is
counter-indicative at suspicion on cholelithiasis.

71. Laparoscopy and biopsy
In diagnostics of liver and bile-excreting tracts
illnesses the special value have a laparoscopy
and biopsy of liver (apply more often is “blind”,
but under the ultrasonic control, percutaneous
biopsy). Indications for biopsy are following
conditions.

72. • Hepatomegaly unspecified genesis.
• Persistent increase of activity of AST, ALT, γ-
GGT.
• Revealing of virus markers B, C, D in a liver
tissue.
• Medicinal injury of liver.
• Alcohol-induced liver injury.
• Storage diseases.

73. • Infectious and system diseases.
• Inspection patients’ relatives with hereditary
diseases of liver.
• Nidal formation.

74. The laparoscopy allows to specify a stage liver’s
chronic disease (hepatitis or cirrhosis), a
morphological variant of a cirrhosis (small
nodular, large nodular, mixed) to reveal signs of
a portal hypertensia, and also presence of nidal
of liver with morphological study (target biopsy
of liver).

75. The basic clinical syndromes of jaundice
The jaundice (icterus) - is the big hepatic sign
caused by increase of the content in blood of
bilious pigments and shown by colouring in
yellow colour of mucous membranes, scleras
and skin..

76. The basic clinical syndromes of
jaundice
• a jaundice traditionally ascribe to typical
manifestations of liver illnesses though in
some cases it can arise and without its (for
example, at massive haemolysis).
• Colouring of mucous membranes and skin
at jaundice is often accompanied by a skin
itch, in some cases very intensive

77. At jaundice
• the bilirubin content more than 34,2 mkmol/l [2
mg of %] (develop hyperbilirubinemia); thus
there is its accumulation in skin, mucous
membranes and eyes’ scleras.
• Yellow colouring of skin -– can be caused by
using of considerable quantity of the products
• containing carotin (carrots, tomatoes),
• acrichine,
• salts of picric acid;
• a distinctive sign from jaundice in the specified
cases - absence of scleras colouring.

78. jaundice
• At first there is yellowness of scleras,
• further - a mucous membrane of the low
surface of the tongue (frenulum ) and palate,
• then a face skin, palms, soles;
• subsequently there is a yellowness of all
surface of a skin.

79. jaundice
Sometimes it is possible to find out discrepancy between
bilirubin level in blood serum and degree of colouring
of body areas.
• The jaundice is less appreciable at simultaneous
presence of hypostases against the background of
hypoproteinemia, at anaemia, adiposity.
• At thin and brawny patients integuments usually have
more intensive icteric colouring.
• At stagnation of blood in liver against the background
of heart failure (if arises hyperbilirubinemia) yellow
colouring is got by mainly top half of trunk.

80. jaundice
At long hyperbilirubinemia is
• icteric colouring gets a greenish tint (bilirubin
oxidation in a skin with formation biliverdin(e)
[dehydrobilirubin] of green colour) and even
bronze-black.

81. Bilirubin metabolism
Hyperbilirubinemia - a consequence of
disturbance in one or several links of bilirubin
metabolism. Distinguish following fractions of
bilirubin.
• Free, it’s untied, unconjugated [indirect
reacting] bilirubin.
• Connected, it’s conjugated [direct reacting]
bilirubin which is subdivide on
• bilirubin I (monoglucuronid)
• and bilirubin II (diglucuronid); changes of the
last take into attention in clinical practice.

82. Bilirubin metabolism
Indicators of bilirubin metabolism are
• unconjugated bilirubin and
• conjugated bilirubin (diglucuronid) in blood
serum.
• Most part of blood bilirubin (about 85 %) occurs
at disintegration of haemoglobin from
erythrocytes, exposed physiological haemolysis
in cells of the reticuloendothelial system (RES).
• Other bilirubins is formed at destruction of
others hemes’ substances (cytochromes and so
forth).

83. Bilirubin metabolism
• for day in an organism it is formed about 300-
350 mg indirect (unconjugated) bilirubin.
• It quickly and strongly contacts to albumin of
blood serum and circulates in the form of
insoluble in water, and therefore almost not
filtered connection by kidneys.

84. Bilirubin metabolism
• Bilirubin albuminate on hepatocytes’
membrane (at introduction of some medicinal
substances, for example sulfanilamides,
ampicillin, bond between indirect bilirubin and
albumin deteriorates directly in blood vessels),
• and bilirubin is grasped by hepatic cells in
which it is transported in endoplasmic network
where under the influence of enzyme UDP-
glucuronyl transferase (uridine diphosphate
glucuronyl transferase) joins with glucuronic
acid.

85. Bilirubin metabolism
• Conjugated bilirubin - nontoxical and readily
soluble substance in water; the last matters for its
receipt through hepatocyte’s membrane in bile
capillaries by excretion.
• Position that in normal conditions bilirubin transport
through hepatocyte occurs only in one direction
and from blood to bile capillary is very important.
• At damage hepatocyte (necrosis) or an obstacle for
bile passage (at level of bile ducts or more low) it is
possible regurgitation conjugated’s bilirubin, its
movement in the opposite direction - in blood
capillary.

86. Bilirubin metabolism
Through bile-excreting tracts the conjugated
bilirubin gets to intestines - in a thin and thick
gut where by means of bacteria there is
• its transformation in urobilinogen, and then
• by oxidation - in urobilins which are fecal
excretion, giving it brown colour.
Nearby 1 % urobilinogens gets to the general
circulation, being excreted subsequently with
urine.

87. Bilirubin metabolism
• Urobilinogens content increase in urine occurs at
raised their formations in intestines, and also at
disturbance of their removal from blood by hepatic cell
owing to damage of last.
Thus, the bilirubin metabolism in liver, thanks to the
specified functions of hepatocyte is carried out in three
stages:
• capture by hepatocyte of bilirubin from blood,
• connection of the bilirubin with glucuronic acid and
• excretion of the conjugated bilirubin in system of bile
ducts.

88. Reasons of jaundice
The jaundice can be connected with following
conditions:
• Disturbance of bilirubin metabolism at one or
several stages of metabolism; It’s raised
formation in cells of RES;
• Insufficient it’s excreting in bile;
• Disturbance of outflowing of the formed bile.

89. Reasons of jaundice
• At the first stage disturbance of the hepatic’s bilirubin
metabolism seldom accounts for the jaundice reason;
only some are known medicines (for example,
antivermicular) which can interfere to penetration
bilirubin through hepatocyte’s membrane.
• At the second stage of hepatic bilirubin metabolism
the jaundice arises owing to or lowered bilirubin
conjugation because of insufficiency of enzyme
UDP-glucuronyl transferase (hereditary enzymopathy),
or in connection with transport’s defects of indirect
bilirubin in hepatic cell.

90. Reasons of jaundice
• These processes define two kinds of the
hereditary jaundices caused by raised level of
unconjugated bilirubin in blood - Crigler-
Najjar syndrome and Gilbert's syndrome.
• Disturbance of metabolism at the third stage
(excretion by hepatocyte of conjugated bilirubin)
underlies of hereditary jaundice at Dubin-
Johnson syndrome and Rotor's syndrome.

91. Reasons of jaundice
In clinical practice the jaundices have the
greatest value. The jaundice often arises owing
to the change of hepatocyte functions with
disturbance of the
• capture,
• conjugation and
• bilirubin secretions.

92. Reasons of jaundice
• The jaundice can be caused by regurgitation of
conjugated bilirubin in blood capillary - original
endocellular cholestasis which is considered now as
the basic mechanism of all hepatocellulars jaundices.
• Regurgitation of bile also underlies of jaundice
caused by difficulty excreting (owing to obstruction of
bile ducts) of formed conjugated bilirubin which has
already got to bile.
• Mark jaundice out caused by unconjugated
bilirubin at increased haemolysis when normal
hepatocyte cannot transfer all formed in a
considerable quantity unconjugated bilirubin in
conjugated form.

93. Kinds of jaundices
The jaundice arises at increase of content in
blood unconjugated and/or conjugated bilirubin.
In either case mark out hereditary (idiopathic, or
functional), more often benign, and acquired
jaundices.
It is necessary to remember that in all cases a
jaundice - not the self-supporting diagnosis but
only one of graphic evidence of this or that
disease, therefore at its presence diagnostic
actions are necessary for revealing of the
reason and consequently, concrete illness.

94. Kinds of jaundices
• According to the mechanisms named above of
acquired disturbance bilirubin’s metabolism
mark out:
• hemolytic (prehepatic),
• hepatocellular (parenchymatous) and
• mechanical (obstructive, surgical) jaundices.

95. Kinds of jaundices
• The most widespread variant prehepatic
jaundice - hemolytic jaundice,
• hepatocellular - jaundice at acute and
chronic liver diseases with necrosis part of
hepatocytes,
• obstructive - mechanical or cholestatic
jaundice owing to obstruction of intrahepatic
bile ducts or common bile ducts.

96. Hemolytic jaundice
This jaundice is caused by the high content in
blood unconjugated bilirubin. Usually this kind
of jaundice develops at hyperproduction of
indirect bilirubin as a result of erythrocytes
increased disintegration (haemolysis) in
connection with small resistance of erythrocytes
(primary hemolytic jaundice) or from them
haemolysis:

97. Kinds of jaundices
• Because of uneffective erythropoiesis (at
megaloblastic and lead anemias);
• At the big hemorrhages, in and around of
extensive pulmonary infarction;
• At malaria;
• Under action hemolytic poisons (secondary
hemolytic jaundice).
Mark out immune hemolytic anemia arising
usually in the heat of immunological activity of
various serious illnesses, for example systemic
lupus erythematosus.

98. Kinds of jaundices
• At hemolytic jaundice there is no skin itch,
• the spleen is increased (is connected with restoration
of functional activity of spleen as organ of
extramedullary hemopoiesis when marrow not in
condition to cope with the raised and long requirement
of an organism for formation of blood cells);
• anaemia develops,
• stool is painted rather intensively (pleionchroma) that
is caused by formation of a considerable quantity of
bilirubin and its secretion in intestines with the
subsequent transition in stercobilin.

99. Kinds of jaundices
• At hemolytic jaundice in urine there is
considerable quantity urobilin, but there is no
direct bilirubin that is connected with its strong
connection with blood albumin.

100. Hepatocellular jaundice.
• This kind of the jaundice most often meeting at
diseases of liver,
• is caused by hepatocytes injury and
characterised by increase of content in blood as
indirect, and, especially, direct bilirubin,
• decrease urobilin excretion with urine and
stercobilin with stool.

101. Hepatocellular jaundice
The given kind of jaundice observes:
At viral hepatities (acute hepatitises A and B,
chronic hepatitises B, C, D, liver’s cirrhoses of the
virus aetiology);
Alcoholic injuries;
Medicinal injuries;
Autoimmune hepatitises and liver cirrhoses;
At liver’s cirrhoses of other aetiology.

102. Hepatocellular jaundice
• Moderate colouring of integuments is revealing,
• spleen enlargment.
• In urine, as well as at hemolytic jaundice, find
out the increased quantity of the conjugated
bilirubin, for the account of that urine becomes
darker, than usually;
• stool is is more often poorly painted or
decoloured.

103. Mechanical jaundice.
The jaundice is caused by the high content in
blood of the conjugated bilirubin in connection
with it’s regurgitation in blood. Principal causes
of the regurgitation - disturbance of bile
secretion in duodenal gut that observe at:
• Obstruction or compression of hepatic or bile
ducts by stone or tumour, including tumour or
tumour metastasises in liver’s porta;
• Compression of bile ducts orifice by pancreas’s
head tumour;
• Sclerous change of bile ducts at sclerosing
cholangitis.

104. Mechanical jaundice.
• Colouring of integuments at mechanical
jaundice is marked as much as possible; at a
long jaundice the skin gets a dark shade.
• Almost always patients complain of an intensive
itch of skin; at survey on it are visible scratches.
• As well as at hepatocellular jaundice, in urine
find out direct bilirubin (unlike hemolytic
jaundice), but do not reveal urobilin (unlike
hepatocellular jaundice);
• urine at mechanical jaundice of very dark
colour, to its description apply the specific term
«urine of beer colour», dark [black] urine.

105. Mechanical jaundice.
• From all other kinds of jaundices a mechanical
jaundice distinguishes acholic character of the
feces which colour reminds colour of glazier's
putty.
• At investigation of the stool find out is absence
in it stercobilin. Expressiveness of the specified
signs of mechanical jaundice has wavy
character; at their steady increase it is
necessary to conjecture compression of
common bile duct by tumour.

106. Differential diagnostics of jaundices
Sign Jaundice
Hemolytic (prehepatic)
jaundice
Hepatocellular
(parenchymatous) jaundice
Obstructive (mechanical,
surgical) jaundice
Mechanism Increase of bilirubin
formation (indirect)
Hepatocytes’ Obstruction of bile ducts
Aetiology Increased erythrocytes’
haemolysis, Gilbert's
syndrome
Viruses, alcohol, medicinal
preparations and other toxic
influences
Cholelithiasis, pancreas’s
head tumour
Itching no possible pronounced
Skin’s colour lemon Yellow Dark yellow
Colour of urine It is not changed or is
more dark usual (the
urobilinogens’ content in
norm or it is slightly
increased)
Dark (the urobilinogens’
content is raised)
very dark - urine of beer
colour (high concentration of
direct bilirubin, urobilinogens
are not)
Colour of stool Usual or dark (the
content of
stercobilinogens in norm
or is increased)
It’s not changed or decoloured
(the content of
stercobilinogens in norm or is
decreased)
It’s decoloured
(stercobilinogens are not)
Bilirubin in
blood serum
unconjugated mixed reaction, prevails
conjugated
conjugated

107. Jaundice
On features of bilirubin metabolism it is easier to
reveal hemolytic jaundice caused by increase of
the content in blood unconjugated bilirubin.
Among the acquired jaundices at increases
content in blood serum of conjugated bilirubin
the differential diagnostics carry out between
parenchymatous and mechanical jaundices - on
the basis of the anamnesis, the data of
objective and laboratory investigations.

108. Jaundice
• . Rather essential information is made by
definition of activity of some blood enzymes:
increase of level aminotransferases assumes
hepatocytes’ injury, primary increase the
content of alkaline phosphatase – is injury of
bile ducts.
• It is necessary to note possibility of
simultaneous hepatocytes’ injury and bile-
excreting system, as an example of that serves
primary biliary [Hanot's] cirrhosis at which the
content in blood AST, GPT, alkaline
phosphatase and γ-GGT are increased.

109. Jaundice
At suspicion on obstruction of bile-excreting
ducts as the reason of jaundice it is important to
define level of this obstruction first of all by
means of noninvasive methods of investigation
(ultrasonic-test and CT-scan).
• At simultaneous expansion intra- and
extrahepatic ducts the obstruction is localised at
the level of distal part of common bile duct
(tumour of ampoule of common bile duct,
stenosis, stones of gallbladder, pancreas
tumour).

110. Jaundice
• If intrahepatic ducts are expanded only, and the
common bile duct is not changed, it is
necessary to suspect compression of duct (for
example, a tumour) in its bifurcation or an
intrahepatic stone.
• If intrahepatic ducts are not expanded, with the
big share of probability it is necessary to
assume sclerosing cholangitis. Localisation and
character of obstruction can be established
even more precisely if to use percutaneous
transhepatic cholangiography (PTC) or
endoscopic retrograde
cholangiopancreatography (ERCP).