Chronic cholecystitis

June 3, 2024
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Зміст

Diseases of a liver and bile ducts. Chronic hepatitis, liver cirrhosis. Ethiology. Clinical pattern. Daignostics. Complications. Principles of treatment.

Chronic cholecystitis

Chronic cholecystitis may develop after acute cholecystitis but in most cases it develops gradually as an independent disease.

         Etiology: 1. Bacterial infection diseases: nasopharyngeal infection (chronic tonsillitis, sinusitis); diseases of oral cavity (stomatitis, paradontosis); urinary tract diseases (prostatitis, uretritis); gynecological diseases; intestinal infection; viral affection of the liver.The most typical microbiological agents are: E. Coli, Enterococci, Staphylococci, Streptococci.

2. Нelmintic invasion: opistorchosis, asckaridosis, lambliosis.

3. Duodenal-billiary reflux (regurgitation of pancreatic juice or duodenal content to the gall bladder)

4. Cholecistitis of toxic or allergic nature.

5. Chronic inflammatory  diseases of alimentary tract

6. Acute cholecystitis.

 Predisposing factors:

1. Bile congestion coursed by: dyskinesia of bile ducts; obesity; pregnancy; psycho emotional stresses; non-observation of dietary mode, fatty and fried food; rare meals; food poor in dietary fibers; inactive mode of life; congenital defects of bile ducts or gall bladder.

2. Reflectory influences from other internal organs.

3. Dysbacteriosis.

4. Metabolic disorders (obesity, diabetes mellitus, podagra)

5. Hereditary predisposition.

 Pathogenesis. Infection may enter to the gall bladder by following ways: enterogenic (from the intestine, in the case of reflux); haematogenic; lymphogenic.

Inflammation in the gall bladder develops only in the case when infection contamination is combined with bile congestion, changes of bile properties, dystrophy of gall bladder walls or immunodepression.

Classification of chronic cholecystitis

1.     By etiological agent, it is caused by: E. Coli, Enterococci, Staphylococci, Streptococci, Pneumococci, Salmonella ets.

2.     By degree of severity: mild form, moderate and heavy form.

3.     By the course of the disease: recurrent, monotonous, and intermittent.

4.     Phases of the disease: exacerbation, relapse.

5.     Complications: non-complicated; complicated (pericholecystitis, cholangitis, pancreatitis ).

Clinical picture: Complaints:

   Pain in the right hypochondrium;

   dyspeptic syndrome (bitter or metallic taste in the mouth; regurgitation (belching), nausea, abdominal flatulence, diarrhea or constipation);

  psyсhoemotional disorders;

  the temperature is often subfebrile;

  skin itching.

Objective signs: The appearance of the patient and his nutrition are usually normal. Moderate obesity is sometimes observed.

   obesity (in many cases); Moderate obesity is sometimes observed.

   flatulence of abdomen; Examination of the abdomen can reveal its flatulence

   yellowish tint of the skin;

  data of palpation: sensitivity or mild pain; sometimes pronounced tenderness in the region of gall bladder projection.

De Mussy-Georgievsky, Ortner’s, Obraztsov-Murphy, and Vasilenko’s symptoms are positive.

1.     Vasilenko`s symptom – sharp pain in the region of the gall bladder when it is tapped over at the height of inspiration.

2.     Obraztsov-Murphy symptom – sharp pain in the right hypochondrium when the examiner` hands press the gall bladder at the height of inspiration.

3.     Ortner`s symptom – pain during tapping over the right costal arch by the edge of the hand.

4.     The de Mussy-Georgievsky symptom – tenderness at the point of the phrenic nerve, between the heads of the sterno-cleidomastoid muscle.

Liver: usually is of normal sizes, but becomes enlarged in complications (hepatitis, cholangitis).

The gall bladder is impalpable.

 Laboratory and instrumental examination:

1. Blood count: moderate leucocytosis; mildly increased ESR.

2. Biochemical blood analysis: increased content of seromucoid, fibrin, α2-globulines, γ-globulines.

3. Duodenal probing:

Signs of inflammation (mucus, leucocytes, desquamated epithelium) can be found in B bile.

Portion B bile is sometimes impossible to obtain (this indicate disordered contractility of the gall bladder). Bacteriological studies of B bile reveal microbial flora.

4. X-Ray study. There are following methods: cholecystography, cholangiography, endoscopic (retrograde) cholangiopancreatography.

Cholecystography shows changes in the configuration of the gall bladder and the absence of its distinct contours. This indicates upset concen¬trating capacity of the gall-bladder mucosa.  After taking of stimulators of contraction (like egg yolk or magnesium sulfate) the gall bladder contracts insufficiently.

5.     Sonographyc signs of chronic cholecystitis :

         thickening of gall bladder walls more then 2 mm;

         induration of walls;

         uneven and deformed contour of the gall bladder, enlargement or diminishing of its dimensions; adhesions;

         decreased or absent mobility of the organ in respiratory phases;

         non-homogeneous content of the gall bladder; „ bile sediments.”

6. Computer tomography: gives possibility to estimate location, dimensions, shape of the gall bladder, thickness  of its walls, gallstone presence.

7.     Thermography: reveals local deviation of temperature up to 0,3 – 2ŸC, the zone of the gall bladder looks more light.

 Treatment:

Stage of exacerbation:

1.     bed mode during 7 – 10 days;

2.     diet № 5a, warm drink; food intake 5 – 6 time a day by small portions;

3.     elimination of pain: M-cholinolitics (atropine sulfate, metacin, plathyphyllin, gastrocepin). Spasmolitics ( papaverin, no-spa ). Analgetics (analgin, baralgin);

4.     improvement of bile excretion: cholagoges (sunflower oil, allochol, cholenzyme, cholagone, liobile, nicodine, cholagogic species). This group of preparations is contraindicated in gallstones;

5.     antibioticotherapy (broad-spectrum antibiotics – erythromicin, ampicillin, oxacyllin, lyncomicin, tetracyclin, oletetrin, ceftriaxon );

6.     detoxication(wild-rose decoction, mineral water, intravenous infusion of Hemodes, 5% Glucose solution, ISS  ets.);

7.     physiotherapy.

In the period of relapse: anti- exacerbation courses of treatment 1-2 times a year: periodical duodenal probing, cholagogues in 3-4 week courses (e.g. allochol per os, 1-2 tablets 3 times a day after meals, cholagogic species in the form of infusions, 10—20:200 ml, half-glass 3 times a day, 30 minutes before meals). Sanatorium and health-resort therapy is also indicated.

 Prophylaxis.

The  disease  and  recurrent  exacerbations  should   be prevented by taking measures to control bile congestion (exercises, walks and trips, regular and frequent meals with certain restriction) and treatment of focal infections.

 

Cholangitis

Cholangitis is the inflammatory process of bile ducts. Acute and chronic cholangitis are distinguished. Inflammatory process may be catarrhal and purulent.

Acute cholangitis often occurs in obstruction of common bile duct and it is one of the most typical complications of cholelithiasis. Ascending cholangitis very often is observed in acute cholecystitis.

Purulent cholangitis is characterized by high  body temperature, chills and sweating (this is so-called “Charcot’s triad” or “intermittent hepatic fever”). Chills with following profuse sweating can repeat several times a day. Jaundice  can develop as well. Liver is enlarged and painful. Sometimes splenomegaly occurs. Signs of intoxication become more and more pronounced in the dynamics.

In the blood analysis there are: neutrophil leukocytosis, accelerated ESR (erythropcytes sedimentation rate), elevation of alkaline phosphatase and aminotransferase levels.

The course of chronic cholangitis may be latent, recurrent or prolonged with septic component.

Clinical manifestation of chronic cholangitis resembles clinical pattern of acute cholecystitis. The main symptoms are: sensation of heaviness or dull pain in the right hypochondrium which occur if the patient doesn’t observe dietary mode, in jolt riding or in physical loading. The pain irradiates toward the right shoulder blade.

Dyspeptic syndrome manifests by bitter taste in the mouth, disgust to fatty food, nausea after food intake or even in inhalation of the smell of such a food. Other symptoms: skin itching (it can occur in limited zone of the skin), asthenodepressive syndrome (weakness, rapid fatigability), prolonged periods of not-motivated subfebrile fever with periodical chills. By inspection yellowish tint of mucous coats may be revealed. The liver is enlarged, mild and painful.

Blood analysis results: neutrophil leukocytosis, accelerated ESR. Activity of alkaline phosphatase rises. Duodenal probing results: inflammatory changes in all portions of bile.

Prognosis: it is serious in obstruction to bile outflow. In this case the disease manifests as severe sepsis with formation of plural  cholangiolithic abscesses in the liver; very often subdiafragmatic abscess develops. Wen urgent operative treatment is impossible the complex therapy of sepsis is carried out.

Treatment. Diet N 5a, antibiotics and cholagoges.  Sometimes surgical treatment is necessary.

Prophylaxis: effective treatment of acute cholecystitis and cholelithiasis.

 

Cholelithiasis

Cholelithiasis is characterized by formation of stones in the gall bladder Or, less frequently, in the bile ducts. The incidence of the disease is rather high. According to the data of postmortem examination, stones are found in the gall bladder of every tenth patient who dies from various causes. At

the same time, clinical signs of cholelithiasis are only found in 10 per cent of carriers of stones, mainly in women aged 30—55.

Aetiology and pathogenesis. The disease is underlain by general metabolic disorders which provoke formation of stones. Infection and bile congestion are also important. Upset cholesterol metabolism with hyper¬cholesterolaemia attended by the increased bile cholesterol content is decisive because most stones contain cholesterol. This is also confirmed by the fact that cholelithiasis often concurs with atherosclerosis, diabetes mellitus, obesity, and other conditions attended by hypercholesterolaemia. Frequent formation of pigmented stones in the presence of excess bilirubin in bile in haemolytic anaemia (haemolytic jaundice) is explained in a similar way. At the same time, blood cholesterol is not increased in all pa¬tients with cholelithiasis. There is no parallelism between cholesterol level of bile and blood.

The main components of stones are cholesterol, bilirubin, and calcium. These are contained in bile in the form of unstable colloidal solutions. Cholesterol is retained in bile mainly by bile acids. When cholate level in the bile decreases, cholesterol precipitates as crystals. The ratio between salts of bile acids (cholates) and cholesterol iormal bile is 15:1; in  cholelithiasis this ratio decreases to 6:1. Disorders in the physico-chemical composition of bile are believed to be decisive for stone formation.  Hepatocyte dysfunction decreases the formation of bile acids which may be the cause of dyscholia. The importance of the infectious factor consists in that protein-rich exudate of inflamed gall bladder upsets the normal colloidal and chemical  composition of bile to precipitate bilirubin, cholesterol and calcium, and to cause formation of mixed stones typical for infectious diseases of the gall bladder.

Bile congestion in the gall bladder provides conditions for stone formation because it promotes concentration of bile and stimulates an increase (10-12 times) in cholesterol concentration in the bile, while gradual absorption of bile acids decreases their content in the bile. Moreover, bile congestion can provide favourable conditions for development of infection. Disordered neurohumoral regulation of contractility of the gall bladder and bile ducts (dyskinesia), as well as the anatomical changes in the bile passages (bends, adhesions, scars), are essential factors provoking bile congestion. Factors interfering with normal emptying of the gall bladder are also    important:    increased    intra-abdominal    pressure    (e.g.    during pregnancy),   ptosis   of  the  internal   organs,   persistent   constipations,  hypodynamia, and rare meals are among these factors.

Hereditary predisposition is also very important. Stones often occur in several generations of one family (especially among women). Excessive, food rich in fats and calories causes hypercholesterolaemia and stimulates formation of gall stones. Pathological anatomy. There exist three major groups of gall stones. Purely cholesterol stones are white or yellowish concretions which are found in the gall bladder. They usually develop as single round or oval concretions. The stones are light (float on the surface of water) and burn with a bright flame. The section of a stone shows its radial structure (crystals of cholesterol). Pigment stones consist of bilirubin and calcium. Their shapes vary. Usually pig¬ment stones are small and multiple. Their colour is black with a greenish tint; the stones are dense but brittle. Stones consisting of only calcium carbonate rarely occur. Mixed stones con¬sisting of cholesterol, calcium, and pigment occur most frequently. They are heavier than water and burn with difficulty. A section reveals laminar structure. The shape and size of mixed stones vary but they are usually small and multiple. If stones are tightly packed in the gall bladder, their surfaces become facetted (from mutual pressure).

The mucosa of the gall bladder can be affected with inflammation in the presence of stones. Prolonged presence of stones in a non-inflamed gall bladder can cause atrophy and sclerosis of the bladder wall or (in very rare cases) decubitus and perforation of its walls.

Clinical picture. Pain attacks in the right hypochondrium (the so-called biliary colic) are the most characteristic symptom of cholelithiasis. Colics are usually provoked by small stones as they move in the region of the neck of the gall bladder, its isthmus, or directly in the cystic duct. Pain is caused by spastic contractions of the gall bladder and the ducts which develop as a result of a sudden distension of the gall bladder and increased pressure in¬side it due to a mechanical obstruction to bile outflow. The pain develops also by the reflex mechanism, as a response to irritation of the cystic duct receptors by stones. A gall-bladder colic can be provoked by physical or nervous strain, jolting motion, ingestion of much fat, etc.

A gall-stone colic develops suddenly. The pain is first diffuse and is felt in the entire right hypochondrium. Later it localizes in the region of the gall bladder or in the epigastrium. Pain is piercing and so severe that cannot be tolerated without pain-relieving preparations. The patient groans and tosses in bed vainly seeking for a convenient posture. The pain can specifically radiate upwards, to the right posteriorly, to the right shoulder, neck, the jaw, and into the right subscapular region. Pain can radiate also into the heart to provoke an attack of angina pectoris.

Pain can continue from several minutes to a few hours and even days, Periodically subsiding and strengthening. Intensified contractions of the gall bladder promote further propulsion of the stone (not more than 1.5 cm in diameter) from the neck or the cystic duct into the common bile duct. Sometimes, after relaxation of the spasm the stone may return back to the silent” zone (the fundus of the gall bladder). In both cases, the pain attack ^continues as suddenly as it begins. The patient’s condition rapidly im¬proves. The attack can often be alleviated by applying warmth or giving

spasmolytics (atropine sulphate, 16 ml of a 0.1 per cent solution, or papaverine hydrochloride, 2 ml of a 2 per cent solution subcutaneously). This is a valuable differential-diagnostic sign: these remedies fail to relieve pain in acute cholecystitis, while warmth (e.g. a hot-water bottle) is con-traindicated because warmth intensifies blood inflow and the inflam¬matory process.

If the colic is long-standing, jaundice may develop at the end due to a spasm of the common bile duct. The jaundice usually is not intense and is only transient (2 to 3 days).

Gall-stone colic is usually attended by nausea and recurrent vomiting. The reflex mechanism explains the fever which often attends the pain at¬tack. The fever ends with the attack. If fever persists, it indicates its con¬nection with inflammatory complication of cholelithiasis. This is confirm¬ed by an increase in leucocytosis, ESR, and a sharp deterioration of the pa¬tient’s general condition. ;

The patient may sometimes be obese, with xanthomatous plaques “. (cholesterol deposits) on the upper eyelids (less frequently on the other parts of the skin). The abdomen is distended; surface palpation reveals ten¬sion of the anterior abdominal wall, especially in the region of the right hypochondrium, and also excessive tenderness of this region. As pain is abated, the muscular tension subsides, and the tender edge of the liver can then be palpated. The gall bladder can sometimes be palpated as an oval or pear-shaped elastic body.

Tender points and sites of hyperaesthesia can sometimes be determined on the body according to Zakharyin and Head (Fig. 100). These are as follows: (1) the region of the gall bladder (its projection on the skin); (2) epigastrium; (3) pancreato-biliary-cystic point; (4) shoulder zone; (5) point of the scapular angle; (6) paravertebral points to the right of the 8th to 11th thoracic vertebra; (7) phrenic nerve site (tender to pressure in the region between the anterior heads of the right sternocleidomastoid muscle (phrenic symptom, or de Mussy-Georgievski symptom).

Some laboratory and instrumental studies reveal signs of cholelithiasis in the full absence of its symptoms. Blood test shows an increased cholesterol content. Duodenal probing (carried out in remission) can sometimes reveal fine stones (microliths) and a large quantity of cholesterol crystals. The most important diagnostic technique in cholelithiasis is con¬trast roentgenography (cholecysto- or cholangiography and echographу studies). These techniques help reveal stones in the gall bladder and the bile ducts.

Course and complications. The course of cholelithiasis is quite varied-Non-complicated cholelithiasis can manifest itself by only one attack of gall-stone colic. The attacks however are usually recurrent. Rare cases are known when the patient recovers spon¬taneously with the discharge of a small stone into the intestinal lumen. Long-standing cholelithiasis is usually attended by infection. The main disease is then aggravated by symptoms of cholecystitis or cholangitis.

Obstruction of the gall-bladder neck is a complication of the disease. It can cause hydrops. Obstruction is manifested by a most severe pain attack. Following several weeks, an enlarged gall bladder can be palpated. It is elastic and painless. In the absence of gall-bladder adhesion to the neighbouring organs (due to pericholecystitis) the bladder can easily be displaced together with the liver during deep respiration and by palpation. In hydrops, the gall bladder is filled with a yellowish or colourless fluid (white tole) which is formed due to absorption of bile elements in the gall¬bladder walls and effusion of serous exudate from the gall-bladder roucosa. If an infection joins, empyema of the gall bladder develops and

patient’s condition is sharply deteriorated. The patient feels chills; the temperature is high; pain in the right hypochondrium develops again.

The common bile duct is obstructed completely when a mechanical closure (by a stone) combines with a spasm and inflam¬matory oedema of mucosa of the bile duct (cholangitis) that hinder bile outflow. The gall bladder does not usually increase despite congestion because its walls are affected by the attending inflammation and are no longer distended (Courvoisier-Terrier syndrome).

Bile outflows to the duodenum when stones move from the narrow to the wider part of the common bile duct (valve stones), or during transient relaxation of the gall-bladder walls. Jaundice intensity thus increases and decreases periodically; the colour of faeces changes accordingly.

Another complication of the disease is perforation of the gall bladder (less frequently of the common bile duct) with development of the outer or inner vesico-intestinal passages and sometimes bile peritonitis. Long presence of stones in the gall bladder can cause cancer, and prolonged obstruction of the common bile duct with bile congestion and infection of the bile ducts often provoke biliary (cholestatic) cirrhosis of the liver.

Investigations

Blood test shows an increased cholesterol content. Duodenal probing (carried out in remission) can sometimes reveal fine stones (microliths) and a large quantity of cholesterol crystals.

1.     Ultrasound

1.     It is the method of choice for diagnosis of gall stone

2.     It shows dilated extra – and intra hepatic ducts when common bile duct is obstructed

2.     Endoscopic retrograde cholangiography (ERSP)

  It determines the cause of common bile duct obstruction. Stones can be removed from common bile duct during this procedure.

1.     X-ray abdomen

Plain x-ray abdomen shows gallstones in 10-20% of cases only. Therefore, this is not useful investigation for diagnosis of gallstones.

         Treatment of gallstones

        Cholecystectomy – open or laparoscopic

         Bile acids – chenodeoxycholic or ursodeoxycholic

        Contact dissolution

        Lithotripsy

        Endoscopic sphincterotomy   

 Conservative treatment provides better outflow of bile and decreases the tendency to further formation of stones. The patient is recommended to lead a more active life, and prescribed frequent meals with restricted intake of cholesterol-containing foods, mineral water, and cholagogues. Various antispastic and pain removing preparations are prescribed (atropine, papaverin, warmth, etc).

Surgical treatment of cholelithiasis is indicated in the presence of hydrops or empyema of the gall bladder, obturation of the common bile duct with obstructive jaundice, perforation of the gall bladder with development of Fistulae or bile peritonitis, or in the presence of frequent at¬tacks of gall-stone colics that fail to be removed by conservative treatment. Prophylaxis consists in removal of metabolic disorders and causes of bile congestion. The patient is recommended regular meals, exercises, active mode of life, rational diet, and measures to prevent constipation.

 

Chronic Hepatitis

Chronic Hepatitis  is a chronic diffuse or focal inflammatory affection of the liver.

 Classification:

1.     Authoimmune hepatitis

2.     Viral hepatites –  B (HBV), C (HCV) and D (HDV) occupy  more than 80% of all hepatites.

3.     Nondefined chronic viral hepatitis

4.     Medicamentous hepatitis

5.     Criptogenic hepatitis.

 Main etiological factors:

1.     Viruses of hepatitis B, C and D.

2.     Alcohol abuse.

3.     Usage of some medicines (aminazine, tubasid, paracetamol, sulfa-drugs, metotrexat, aspirin, aldomet ets in prolonged usage)

4.     Rarely – some metabolic disorders, influence of hepatotrophic agents. Toxic hepatitis may be caused by industrial, domestic and food chronic poisoning by hepatotropic toxic substances (chloroform, trinitrotoluene, lead compounds, etc); metabolic hepatitis arises due to metabolic disorders in the liver, associated with protein-vitamin deficiency, and also in fat dystrophy and amyloidosis.

The most common causative agent is hepatitis B virus (HBV) independently or in combination with viruses C (HCV) or D (HDV).

 Pathogenesis. 

1. Toxic lesions of hepatocites. Progressive affection of hepatocytes by hepatotropic toxic substances, (to necrobiosis) with secondary inflammatory reaction of the liver mesenchyma.

2. Hepatitis of virus nature is probably associated with persistence of the virus in the liver cells and with the progressive cytopathic effect of this virus, which kills the hepatocytes to cause inflammatory reaction of the connective tissue.

3. Autoimmune processes arise in response to the primary affection of the liver tissue by any aetiological factor.

4. Obstructed bile excretion and bile congestion, cholangitis and cholangiolitis (with subsequent extension of inflammation onto the liver tissue), and also some medicamentous poisonings (phenothiazine derivatives) are decisive in the pathogenesis of the so-called cholestatic hepatitis.

Clinical picture.

I.                   Data of anamnesis.  Ask the patient about:

         probably acute viral hepatitis in the past (or cases of jaundice),

         transfusions of blood and blood substitutes;

         plural injections, vaccinations,

         donors;

         operations and other invasive manipulations;

         comtact with patients with hepatitis (jaundice);

         the same disease in relatives,

         usage of hepatotoxic drugs,

         industrial and domestic hazards.

II.                Main clinical syndromes

1.     Jaundice. Clinical symptoms: yellow colour of the skin and sclera, changes of colour of urine and feces, skin itching.

2.     Portal hypertension. This is elevation of blood pressure in the bassein of V.Portae. Clinical symptoms: dilatation of portocaval anastomoses (dilatation of esophageal and hemorrhoidal veins, pointed venous pattern of the anterior abdominal and chest wall – “caput medusae”), ascites, splenomegaly. Bleeding from dilated collaterals.

3.     Hepatolienal syndrome. This is simultaneous enlargement of both liver and spleen becouse of primary lesion of one of these organs.

4.     Hemorrhagic syndrome. Clinical symptoms:  nasal and gingival bleeding, hemorrhagic rash on the skin. Changes in the blood: decreased amount and functional activity of tyhrombocites, II, V and VII factors of serum coagulation.

5.     Hepatirenal syndrome – involvement of kidneys into the systemic process.

6.     Cholestasis. Clinical symptoms: darc colour of skin, skin itching, jaundice. Xanthelasmes – yellow-colour plaques on palms, eyeleads, external surfaces of elbows and knee joints. Elevation of body temperature, chills. Changes in the blood: increased level of conjugated bilirubin, cholesterol, b-lipoptoteids, g-glutamiltransferase. Urine is dark as beer, feces are light.

7.     Hepatocellular insufficiency – disorders of liver’s functions cause gross disorders of homeostasis, functions of internal organs and central nervous system.

8.     Dyspeptic syndrome. Clinical symptoms: nausea, vomiting, regurgitation, pyrosis, deranged appetite.

9.     Pain in the right hypochondrium. Moderate enlargement and induration of the liver and the spleen by palpation and percussion.

But the clinical picture and also the course of each clinical-morphological form of hepatitis have their special features.

 Chronic autoimmune hepatitis

Young females of 10-30 years old are mostly affected, less frequently the disease is observed in menopausal period. Female/male ratio is 3/1.

Onset of the disease is manifested with general weakness, anorexia (complete absence of appetite), diacherge of dark urine  and following jaundice.  Onset is possible also with extrahepatic signs:  fever, involvement of joints (hepatitis under the mask of rheumatic fever or lupus eritema tosus).

Later subfebrile fever develops as well as arthralgias. Large joints are involved: knee, elbow, shoulder, joints of spinal cord. Lesion of joints means change of their  configuration  because of periarticular inflammation.

Skin lesions are possible in the form of hemorrhagic rash. (recidiving purpura). Rash spots don’t disappear  when to press on them, after resolution pigmentation develops instead of petechia. Other types of rash are possible: erythema, erythema nodosa, psoriasis, sclerodermia.

Endocrine disorders: amenorrhea, hirsutismus (accessive growth of hair including atypical places). Jaundice moderatelly rises in exacerbation. The liver is enlarged, painful by palpation, of solid consistence. Sometimes spleen also is enlarged and ascites develops.

 Chronic authoimmune hepatitis is systemic disease (systemic desintegration of connective tissue because of production of antibodies hepatitis virus to antigrens which also act to own patient’s tissues. Affection of skin, mucous membranes, internal organs are possible. In the patient may develop pleuricy, myocardidts, pericarditis, ulcerous colitis, glomerulonephritis as well as generalised lymphadenopathy, hemolitic anemia. Course is progressing.

In the blood: hyperbilirubinemia, increased activity of aminotransferases, hypergammaglobulinemia, hypoalbuminemia, positive timol test, slowing of bromsulfalein excretion.Signs of hypersplenism are posssibl (thrombocytopenia, leucopenia). Serological tests: positive LE-reaction and antinuclear factor, reaction of complement consumption, high (1:160-1:320) tytres of antibodies to smoth muscles (pathognomonic sign of liver injury).

Chronic viral hepatitis

Chronic persistance of HV in the liver with possible periodical replication in exacerbation stage.

It is manifested with:

         repeated jaundice and asthenovegetative syndrome (non-specific symptoms like rapid fatigue, decreased working capacity, ipochondria, loosing of body weight (on 3-10 kg);

         pain in right hypochondrium (dull boring, mostly intensive. Pain becomes more pronounced after physical loading. Pain develops due to infiltration of liver stroma and capsule. Equivalent of pain may be heaviness in right hypochondrium;

         dyspeptic syndrome: chande of taste to differrent kind of food, permanent nausea more pronounced after meals;

         “minor signs of liver insufficiensy” – bleedings, transitory jaundice, ascites – develops iecrosis of hepatocites;

         cholestasis: skin itching, increased content of bilirubin, cholesterol, alkaline phosphatase, gammaglutamiltralsferase in blood serum;

         extrahepatic signs: arthralgias, myalgias, amenorrhea, gynecomastia, decreased libido, spidedrs angiomata, red palms;

         hepatomegalia: lower liver border is 5-7 cm below costal arch, liver is painful at palpation, of moderatelly increased density, margin is acute. Spleen also may be enlarged. In remission sizes of liver and spleen diminish.

         The course of the disease is relapsing.

         Blood. in exacerbation following findings are possible: hypergammaglobulinemia, hypoalbuminemia, positive timol test, increased activity of aminotransferases, hyperbilirubinemia, increased protein content. In remission these chenges dimin ish but don’t come back to the norm.

         Laparoscopic examination: liver is enlarged, its colour is red, surface is tuberous), capsule is sickened, pointed vascular pattern is visible.

         Ultrasonic examination reveales moderate enlargement of liver, lower margin is rounded, density is increased .

 Chronic HBV hepatitis

In 10-20 % of cases it is a result of acute viral infection. Main serological markers are of virus replication : HBV-DNA, DNA-polimerase, Hbe-Ag, antiHBc of IgM class. These findings are present in patients with chronic HBV pathology and they testify about active process).  HBs-Ag appearance in the blood suggrsts about persistence of virus.

 Chronic HCV-infection in 20-50 % of cases transforms to liver cirrhosis. Viral replication is possible not only in liver but also in monomuclear phagocites. Thet is why this disease manifests with signs of polyorganic lesions 9idiopathic thrombocytopenia, aplastic anemia, uveitis, injury of thyroid gland, systemic vasculitis ets).

 HDV-infection is mixt-infection. It is combined with HBV becouse HD virus nedds HBs-Ag for replication. HDV-infection aggravates course of HBV hepatitis.

 Chronic medicamentous hepatitis

It is in spire of view becouse progressive increaseing of medicamentous preparations amount, their uncontrolled usage and polypragmasia. Injury of liver may be realized in authoimmune and toxic reactions. Hepatotoxic agent can cause necrosis of hepatocites evven in moderate dosage (chloroform, muscarine ets). Influence of other drugs is realized by idiosyncrasia (individual hypersensitivity to certain preparation). In this case effect doesn’t depend on the dosage (aminasin, phthorothan, isoniaside, erythromycine, tetracycline, anabolic steroids). This action manifests in metabolic and immune disorders.

Clinical signs of chronic medicamentous hepatitis resembles chronic viral one.

 Criptogenic hepatitis

This diagnosis is put to a patient when ethoiligy of hepatitis is not identified. It may be because undersensitivity of modern serological tests to sone types of viruses, mutation of viruses ets.

 Prognosis – in most cases is favorable especially when it is possible to remove ethiological agent.

 Prophylaxis: early diagnostics, anequate treatment of acute viral liver infection, dyspancery observation, prevention of different industrial, domestic and medicamentous poisonings.

Treatment. The cause of chronic hepatitis should be removed in the first instance: exclusion of hepatоtoxic influences, complete discontinuation of taking alcohol or exposure to harmful substances, etc.

Limitation of heavy physical loading.Avoiding of drugs which are metabolized in liver (trankvilisators, sedative agents, analgethics ets). Prohibition of physiotherapeutical treatment in the zone of right hypochondrium, balneotherapy.

Diet N 5.Meals 4-5 times a day by small portions.

Medicamentous treatment:

         antoiviral preparations: interfearone intramuscullary in HBV infection – 5-10 millions of MU 3 times a week during 4-6 months, in HCV infection course of treatment lasts for 18 months, in HDV infection – for 12 months;

         immunostimulators (levamisolum, timalin ets).

         Hepatoprotectors (essentiale, vitamins C, B), antioxidants and membranostabilisators.

         In autoimmune hepatitis – glucocorticoids and immunodepressants.

 

Cirrhosis of the Liver

Cirrhosis of the liver is a chronic progressive disease characterized by increasing hepatic insufficiency in connection with dystrophy of the liver cells, cicatricial cirrhosis, and structural reconstruction of the liver.

Etiology.

 Cirrhosis of the liver is a polyaetiological disease. It may develop due to (1) infection (virus of epidemic hepatitis); (2) alcoholism; (3) protein- and vitamin-deficient diet; (4) toxico-allergic factor; (5) cholestasis. Of the mentioned aetiological factors, the leading role in this country belongs to the virus of epidemic hepatitis. Cirrhosis caused by the virus is probably explained by its long persistence in the liver cells.

Chronic alcoholic poisoning is also a very important etiological factor. It affects absorption of vitamins and proteins in the intestine to provoke cirrhosis of the liver. It also acts directly and specifically on metabolism of the liver cells. The alimentary factor (malnutrition, mainly protein- and vitamin deficit) is a frequent cause of liver cirrhosis in some developing countries. In this country the alimentary factor (malnutrition) is only of en¬dogenous origin: deranged absorption of proteins and vitamins (in grave chronic diseases of the gastro-intestinal tract, in patients with total resection of the stomach, resection of the intestine, chronic pancreatitis, and in some other cases). Toxic cirrhosis of the liver arises in repeated and chronic exposure to carbon tetrachloride, compounds of phosphorus or arsenic, in food poisoning (inedible mushrooms, seeds of heliotrope). Toxic-allergic cirrhosis of the liver includes also affections connected with hypersensitivity (autoallergy) to various drugs (aminazine, chloroform, some antibiotics, sulpha preparations, etc); hypersensitivity can cause dystrophy and necrosis of the liver parenchyma.

Obturation of intra- and extrahepatic bile ducts and their inflammation cause congestion of bile and cholestasis, and are important factors in the development of biliary cirrhosis.

The aetiological factor does not always determine the way of develop¬ment of liver cirrhosis. One and the same factor can cause various mor¬phological variants of cirrhosis (portal, postnecrotic, and biliary); at the same time various aetiological factors can cause similar morphological changes.

 

Pathogenesis. The pathogenesis of liver cirrhosis is closely connected with   morphogenesis.   The  greatest  importance  in  the  developmental mechanism of liver cirrhosis belongs to recurrent necrosis of the liver cells which is provoked by aetiological factors and cause collapse of the reticulin framework of the liver, formation of cicatrices, and derangement of cir¬culation in the adjacent portions of the preserved liver parenchyma. Intact hepatocytes or lobe fragments begin their intense regeneration under the effect of growth stimulants supplied from the necrotic focus. The formed large nodes of regenerated tissue compress the surrounding tissue with the invested vessels; the hepatic veins are compressed especially strongly. The   1 blood outflow becomes upset to provoke portal hypertension and forma¬tion of anastomoses between the branches of the portal and hepatic veins; that facilitate intrahepatic circulation. Blood now bypasses the liver paren-   chyma to impair drastically its blood supply, to cause new ischemic    necroses, and to stimulate the progress of cirrhosis even in the absence of  the primary etiological factor. Collagenous connective tissue grows intensively: connective tissue partitions (septa) grow into the parenchyma from; the periportal fields to cause fragmentation of the liver lobules. These false   j lobules can later become the source of nodular regeneration. Chronic   direct exposure to certain toxic hepatotropic substances, and also auto-   I immune and some other mechanisms are important in the pathogenesis of   I certain forms of cirrhosis.

Pathological anatomy. Three main morphological variants of liver cirrhosis are distinguished: portal (septal), postnecrotic, and biliary.

Portal (septal) cirrhosis of the liver is usually the result of alimentary insufficiency and alcoholism; less frequently it is secondary to Botkin’s disease (virus hepatitis). Us development is underlain by formation of connective-tissue septa interconnecting periportal fields with the central zone of the lobule and causing its fragmentation. Macroscopically the liver may be enlarged or diminished. Small nodes of regenerated tissue, circumscribed by narrow septa of connective tissue, are distributed uniformly over the entire surface of the liver. The nodes are almost equal in size. The microscopic picture: marked fatty infiltration of the liver cells is observed in alimentary or alcoholic cirrhosis; these changes may be absent in cirrhosis that develops after virus hepatitis. “False bile ductules”, leucocytes infiltration, and compress¬ed small veins are found in the stroma between the nodes of regenerated tissue.

Postnecrotic cirrhosis of the liver develops as a result of submassive and massive necrosis of the liver cells due to virus and (less frequently) toxic hepatitis. Macroscopic picture is characterized by irregular changes in the liver, which is usually diminished in size. Nodes of various form and size can be seen on the liver surface. Microscopy shows irregular nodes of regenerated tissue and intact portions of the parenchyma. Broad fields of collapsed collagenized stroma with closely running portal tracts, venues, and cell infiltrates can be found between the nodes of the regenerated tissue. Inflammatory infiltration is marked.

Biliary cirrhosis of the liver has two variants. Primary biliary cirrhosis (pericholangiolitic) arises after epidemic hepatitis or toxico-allergic action of some medicinal preparations. Its development is underlain by obstruction of fine intrahepatic bile ductules which accounts for bile congestion. Macroscopy: the liver is enlarged and consolidated and is dark-green or olive in colour; it is microgranular. Extrahepatic bile ducts are patent. Microscopy is characterized by the presence of intralobular and periportal cholestases. The periportal fields are broad, with fibrosis around proliferating cholangioles; intralobular fibrosis develops around in¬tralobular cholangioles with dissociation of the liver cells and their groups. Secondary biliary cirrhosis arises as a result of prolonged obstruction of extrahepatic bile ducts by stones, tumors, etc. It provokes dilation of the bile ducts, development of cholangitis, and pericholangitis; cirrhosis of the liver develops if these changes progress.

In addition to the described variants of cirrhosis, they may also be mixed: morphological signs of other variants may join the main variant. Activity of cirrhosis is characterized by the presence of new dystrophic and regenerative processes in the parenchyma, intense inflam¬matory infiltrations in the stroma, proliferation of cholangioles, indistinct borders betweeodular parenchyma and internodular stroma. A neglected cirrhotic process is characterized °y replacement of liver tissue by nodes of regenerated tissue, markedly pronounced portal hypertension, large quantity of vascular connective-tissue septa growing into the parenchyma (portohepatic anastomoses). According to the morphological picture, fine- and large-nodular cirrhosis is distinguished. Mixed variants also occur.

 Clinical picture.

Portal cirrhosis of the liver occurs mostly between the ages of 40 and 60. The incidence in men is twice higher than in women. Postnecrotic and biliary cirrhosis of the liver develop in younger patients, mostly in women.

Clinical manifestations of liver cirrhosis depend on the degree of affec¬tion of the liver cells and the associated hepatic dysfunction and portal hypertension, on the stage of the disease (compensated or decompensated), and also on the activity of the process. The following symptoms of the disease are most characteristic of the majority of patients with various forms of liver cirrhosis.

Pain in the region of the liver, in the epigastrium, or diffuse pain in the whole abdomen is usually dull and boring, intensifying after meals,

especially after fatty food, ample drinking and physical exercise. Pain is usually associated with enlargement of the liver and distension of the cap¬sule, or with necrotic foci located near the capsule, with perihepatic symp¬toms, and also concurrent inflammatory affections of the bile ducts.

Dyspepsia in the form of decreased appetite to complete anorexia, the feeling of heaviness in the epigastrium after meals, nausea, vomiting, meteorism and dyspeptic stools (especially after fatty meals) depend mainly on deranged secretion of bile and hence defective digestion. But they can also be associated with the attending dyskinesia of the bile ducts or alcoholic gastroenteritis.

Decreased work capacity, general weakness, fatigue and insomnia are often observed in cirrhosis of the liver. Fever is usually irregular and sometimes of the undulant type. It often attends postnecrotic cirrhosis of the liver and is explained by necrotic destruction of the liver cells. Marked fever is characteristic of the active period and infectious cirrhosis.

A haemorrhagic syndrome is observed in 50 per cent of patients with cirrhosis of the liver. Profuse bleeding from varicose veins of the esophagus and the stomach can often be early signs of portal cirrhosis; they are caused by increased pressure in the veins of the esophagus and the stomach. In other variants of cirrhosis nasal, gum, uterine and skin hemorrhages develop in marked decompensation. They depend on the decreased coagulability of blood due to liver dysfunction.

Signs of cirrhosis are as follows. Cachexia is especially characteristic of patients with portal cirrhosis of the liver. In long-standing disease the sub¬cutaneous fat disappears along with atrophy of muscles, especially of the upper shoulder girdle. The appearance of such patients is quite specific: the face is very thin with grey or subicteric skin; the lips and the tongue are bright-red; the cheek bone region is affected by erythema; the extremities are thin and the abdomen is large (due to ascites, enlarged liver and spleen);  the subcutaneous veins of the abdominal wall are dilated, the legs are edematous. Malnutrition is usually associated with disordered digestion   and assimilation of food, and impaired synthesis of proteins in the affected  liver. Jaundice   (except   the  cases  with   biliary  cirrhosis)   is   a  sign  of   hepatocellular insufficiency associated with necrosis of the liver cells. The affected hepatocytes partly lose their capacity to capture bilirubin from  blood and to bind it with glucuronic acid. Bilirubin excretion into bile is disordered as well. Free (indirect) and bound (direct) bilirubin of blood  serum therefore also increases. Jaundice is usually characterized by partial; decolouration of faces and by the presence of bile in the duodenal contents. Jaundice is often attended by skin itching. Jaundice associated with biliary cirrhosis resembles obstructive jaundice; severe skin itching ‘s observed. The intensity of jaundice varies from light subicteric to marked jaundice (depending on the degree of obstruction of the bile ducts). In pro¬longed obstruction of the extrahepatic duct the skin acquires a greenish tint which depends on oxidation of bilirubin to biliverdin. Moreover, brown pigmentation of the skin may also be observed. It depends on accumula¬tion of melanin.

“Minor” signs of cirrhosis can also be revealed during examination of the patient. These signs are as follows: (1) spider angiomata (they may develop years before marked symptoms of the disease develop); their number increases and the colour intensifies during exacerbation of the disease; (2) erythema of the palms; (3) red lustrous lips, scarlet mucosa of the mouth, scarlet (lacquered) tongue; (4) gynaecomastia (increased mam¬mary glands) and other female sex characters developing in men (decreas¬ing growth of hair on the face, chest, abdomen, and the head); (5) xan-thomatous plaques on the skin (observed in patients with biliary cirrhosis of the liver); (6) Hippocrates fingers with hyperaemic skin at the nail beds. Inspection of the abdominal skin can reveal dilation of the veins that can be seen through the thinned skin of the abdominal wall (caput medusae). Collateral venous system can be seen on the chest as well. Haemorrhoidal veins are often dilated.

Ascites is the most characteristic sign of portal cirrhosis. Ascites may develop slowly and the abdomen grow to huge size; the patient develops dyspnoea. Oedema may develop; hydrothorax may also occur in some cases. In other variants of cirrhosis, ascites develops at later stages of the disease.

Enlarged liver can be palpated in 50—75 per cent of patients with cir¬rhosis. The enlargement can be insignificant, only determinable by percus¬sion, or considerable when the liver occupies the entire left part of the ab¬dominal cavity. The liver is firm, the surface is sometimes irregular, and the lower edge sharp. Enlargement of the spleen is often attended by its in¬creased activity (hypersplenism).

Laboratory findings.

An active cirrhotic process is characterized by anaemia, leucopenia, thrombocytopenia, and increased ESR. Anaemia can per due to hypersplenism and gastro-intestinal hemorrhage, hepatocellular sufficiency, and often increased haemolysis, which is accompanied by reticulocytosis of the peripheral blood.

The blood serum bilirubin content becomes considerable only in the anal stage of the disease. At the same time, the affection of the excretory function of the cirrhotic liver can be assessed by the presence of the con¬jugated fraction of bilirubin (bound bilirubin). Its content increases ior-Jttal and increased total bilirubin. The free bilirubin content increases in the lood serum as a result of upset conjugation of bilirubin in the liver cell

and haemolysis. The blood serum bilirubin content varies in biliary cir¬rhosis of the liver from 26 to 340^0101/1 (1.5-20mg/100 ml), mostly at the expense of bound bilirubin.

The presence of much urobilin in the urine indicates liver insufficiency. The amount of urobilin in the urine and stercobilin in the faeces decreases in the presence of pronounced jaundice when a small amount of bilirubin enters the intestine. Bilirubin is found in the urine of patients with jaun¬dice.

The upset excretory function of the liver is manifested by retention of bromsulphthalein in the blood (during its intravenous administration) and also by radioisotopic hepatography and scanning of the liver.

Affection of liver cells is manifested by characteristic changes in the protein indices: decreased concentration of serum albumins and hypergam-maglobulinaemia which in turn decreases the albumin-globulin coefficient. Activation of the inflammatory process in the liver involves an increase in the a2-globulins, while jaundice causes an increase in /3-globulins. During remissions, all these changes become less pronounced. The blood level of • lipids and cholesterol also increases considerably in the presence of biliary ; cirrhosis. A sensitive index of liver dysfunction is the decreased activity of cholinesterase. Transaminase activity increases in exacerbation of liver cir¬rhosis. Activity of alkaline phosphatase also increases in biliary cirrhosis.

The decreased prothrombin content (which is synthesized by the liver cells), increased antithrombin coagulative activity and decreased total coagulative activity of plasma are important in the aetiology of haemor-rhagic diathesis in liver cirrhosis. ;

Laparoscopy and especially biopsy of the liver help reveal intravital morphological signs of each variant of liver cirrhosis. Varicose veins of the esophagus are revealed by X-rays.

It is not always possible to differentiate between all variants of liver cirrhosis from the data of clinical and instrumental methods of examination, nevertheless, by comparing the mentioned signs, one can notice that the symptoms of portal hypertension in portal cirrhosis of the liver are often revealed long before the functional insufficiency develops. Hepatic insuffi¬ciency only develops at a later stage of the disease. But in the presence of postnecrotic cirrhosis of the liver, the symptoms of hepatic insufficiency develop early. They largely determine the entire clinical picture of the disease. Chronic jaundice (obstructive type) prevails in the clinical picture of biliary cirrhosis along with satisfactory general condition of the patient, who suffers from skin itching, sometimes fever (associated with chills); the blood alkaline phosphatase and cholesterol content increases. Transcutaneous cholangiography is used to determine the cause of cholestasis. The procedure is done when indicated.

Complaints of patients with compensated liver cirrhosis are not serious. The disease is often revealed accidentally during examination (enlarged liver and spleen). Remissions may be long (measured by years). Decompensated active cirrhosis is characterized by marked symptoms of the disease and rapid progressive course.

Course.

The course of the disease is usually progressive. The overall term of the disease is usually 3 to 5 years; in rare cases the disease may last 10 years and even longer (usually in biliary cirrhosis of the liver).

The terminal period of the disease, irrespective of the form of cirrhosis, is characterized by gastro-intestinal haemorrhage and progressive signs of functional insufficiency of the liver, with finally developing coma. These are two most frequent direct causes of death of patients with liver cirrhosis. Gastro-intestinal haemorrhage (blood vomiting and melaena) is caused by the rupture of varicose nodes in the lower third of the oesophagus or, less frequently, in the stomach. A direct cause of varicose haemorrhage is physical strain or local affection of the mucosa (e.g. by coarse food). Pro¬fuse haemorrhage (if it does not cause death) can cause anaemia with subsequent impairment of the function of the liver cells and accelerated development of hepatic coma.

Treatment.  Treatment Cirrhosis of the liver in the compensation stage is treated by preventing its further affection with alcohol, toxic substances, etc., and also by rational organization of work regimen and nutrition (high-calorie diet rich in protein and vitamins). During decompensation stage, hospital treatment is required. Glucocorticosteroid hormones are given in the active process (except cases complicated by dilation of the oesophageal veins); syrepar (hydrolysate of cattle liver), essential (a complex preparation con¬taining essential phospholipids), and vitamins are also prescribed. Patients with ascites are prescribed a diet restricted in salt and diuretics (periodical¬ly). If ascites cannot be cured by diuretics, the fluid is released by Paracentesis.

In order to decrease the lipid content of the serum in primary biliary cir¬rhosis, lipoic acid preparations are prescribed. Skin itching is removed by cholestyramine (preparation binding fatty acids). Surgical treatment is in¬dicated in cases with secondary biliary cirrhosis of the liver, e.g. in obstruc¬tion of the bile duct by a stone.

 

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