Ministry of Health of Ukraine

Ukrainian Medical Stomatological Academy

“Approved”

on the meeting of the department

Internal medicine № 3 with

phthisiology

“____” _____________ 20___ yr.

Protocol # _____ from _________

Head of the department

Borzykh O.A. ________________

METHODICAL RECOMMENDATIONS FOR STUDENTS

Educational discipline Basics of internal medicine

Module №1 Basics of internal medicine

Semantic module № 2 Rheumatic medicine. Medicine of organs of digestion.

Theme 18 Chronic hepatitis. Cirrhosis of liver.

Course III

Faculty Foreign students' training, specialty "Dentistry"

Poltava - 2019

Methodical recommendations for practical classes for teachers

Prepared by: doc. Borzykh O.A., as. Khulish K.A.

Methodical recommendations re-approved at the session of the department of internal

medicine № 3 with phthisiology ____________________________________________________________

1. Relevance of the topic: due to the high prevalence of diseases digestive organs, their complications and

the need to care for patients. Therefore, the ability to collect complaints, anamnesis, conduct an objective

examination, the study of the rules of palpation and percussion, the value of laboratory and instrumental

research methods in patients with organ pathology digestion is of great importance in proper diagnosis and

preparation doctors of all specialties, including dentists. Main in diagnostic process - live contact with the

patient, the feeling of the patient, an indication the beginning and subsequent course of the pathological

process for reasons onset of the disease, physical examination - examination, palpation, percussion,

auscultation and others. Laboratory - instrumental methods research should be evaluated in close relation to

other indicators, obtained with the help of 5 doctor's feelings and synthesized in harmony diagnostic

structure.

2. Specific goals:

Analyze: the state of a specific patient with pathology of the digestive system, to note the main syndromes,

to set a specific plan of patient's examination, based on the existing pathological changes.

Explain: palpation, percussion and auscultation of the gastrointestinal tract; major syndromes in

gastroenterology.

Suggest: on an example of clinical examination of a patient with pathology of the digestive system, to be

able to identify the main clinical syndromes.

Classify: to group symptoms in syndrome.

To interpret: laboratory examination methods: gastric juice analysis, duodenal sounding, feces analysis;

clinical blood count and urine tests, biochemical blood test (bilirubin, ALT, AST, blood diastase): methods

of instrumental examination (endoscopic, X-ray, ultrasound, MRI), biopsy.

Draw: Dividing of the anterior abdominal wall to the zones.

Compile: a plan for the examination of patients with diseases of the digestive system.

3. Basic level of preparation

Names of previous disciplines Obtained skills

1. Normal human anatomy Knowledge about the localization of organs and systems of the

human body. Knowledge about the system of digestive organs.

2. Normal human physiology Knowledge about the functions of organs and systems of the

human body. Knowledge about functional features of the

digestive organs system and methods of its research.

3. Biochemistry. Knowledge about laboratory methods and normal biochemical

constants that are used in the examination of the organs of

digestive system.

4. Ethics and deontology Rules of treatment, communication with patients, their

relatives, colleagues.

4.Tasks for independent work during the preparation for the class and on lessons.

4.1.Terminology

Hepatitis - hepatitis;

Cirrhosis; cirrhosis;

4.2.Theoretical questions to the class.

1.What topographic areas are distinguished on the anterior abdominal wall?

To denote the projection of the internal organs of the abdominal cavity on the anterior abdominal wall is

istinguished by the following sections: a) epigastric - the area above the line, which is the lowest point

both costal arches. It is divided by vertical lines running along the outer edges of the right and left rectus

abdominis, the right hypochondrium, proper epigastric and left hypochondrium; b) mesogastric - the vertical

lines mentioned above are separated on the right and left lateral flanks of the abdomen and the umbilical

region; c) hypogastric - the area bounded from above by a line connecting the front upper bones of the iliac

bones, below - the pubis, sides – inguinal pleats. The hypogastrum is divided by vertical lines running along

the outer edges of the right and left rectus abdominis, the right groin, supraorbital and left groin area.

2. What is portal hypertension syndrome and its signs?

Portal hypertension is called increased system pressure portal vein due to stagnation in her blood, which is

caused by mechanical obstructions that impede or stop the flow of blood from the portal vein through the

liver into the inferior vena cava. Often portal hypertension occurs when the connective tissue in the liver

grows with scarring, characteristic of cirrhosis. Clinical portal hypertension syndrome manifested by the

development of:

1) collateral venous mesh - a significant enlargement of the lower veins

parts of the esophagus, anterior abdominal wall (with the formation of the so-called

"Jellyfish heads"), the veins of the rectum due to a significant enlargement in them

blood flow;

2) ascites - the accumulation of free fluid in the abdominal cavity, which

develops when the collateral pathways of blood flow are insufficient for

compensation for stagnation in the portal vein system;

3) enlargement of the spleen, which is largely due to blood stagnation in the

splenic vein.

3. What is mechanical and hemolytic jaundice when they occur?

Mechanical jaundice occurs when impaired bile flow outflow pathways and develops when they are stoned

or swollen. It is characterized by colorless stool, dark urine, hyperbilirubinemia mainly due to conjugated

bilirubin, lack of splenomegaly. Hemolytic jaundice arises from pathologically increased erythrocyte

hemolysis and increased bilirubin production in cells reticuloendothelial system, which occurs in hemolytic

anemia, internal bleeding, hemolytic poisoning. For hemolytic jaundice is characteristic: more intense color

(pleochromia) chairs, hyperbilirubinemia mainly due to non-conjugated bilirubin, a significant plenomegaly.

4. What is bilirubin, talk about its metabolism in the body.

One of the main functions of the liver is the synthesis of bilirubin (up to 300 mg per day). Unconjugated,

direct, free bilirubin is toxic, cannot excreted by the kidneys, 80% of it appears after the breakdown of

erythrocytes in the spleen, bone marrow, liver. It is transported by albumin. In liver cells unconjugated, free

bilirubin is coupled to glucuronic acid and forms a conjugated, straight, bound renal excretory bilirubin is

non-toxic; it is transported into the bile capillary, then into the intestine, where mesobilin is formed, steriline,

urobilin.

5. Tell us about liver function.

The main functions of the liver - metabolic (pigment metabolism, protein, lipid, carbohydrate metabolism);

detoxification, bile function and biliary excretion, cold-forming function, participation in hormone

metabolism.

6. What is jaundice and what are its known species? Give a description parenchymal jaundice.

Jaundice - yellow color of skin, mucous membranes and sclera. Visible jaundice appears at blood bilirubin

levels greater than 30-40 µmol / l per direct fraction score. There are parenchymatous, mechanical and

hemolytic jaundice: Parenchymal jaundice is characteristic of acute and chronic hepatitis, cirrhosis of the

liver. It develops due to swelling of hepatocytes with rupture of their "bottom" and entry into the venous

blood of the conjugated of bilirubin. It is characterized by a decrease in the color intensity of the chair,

urine of dark color, increase of blood bilirubin predominantly by conjugated splenomegaly account.

7. Give a brief description of the methods of objective research liver and biliary tract.

In the examination of the liver and biliary tract the largest The doctor obtains information through percussion

and palpation of the abdominal organs the cavity. Percussion can determine the size of the liver and spleen

stupidity for MG Kurlov, the presence and approximate amount of free fluid in abdominal cavity. By the

method of deep sliding palpation by Obraztsov-Palpation of the palpation begins with the sigmoid colon,

then palpates the blind, end of the colon, the worm-shaped process, transverse colon, then stomach, liver,

pancreas, spleen and kidneys. Keep in mind that the pancreas, spleen and kidneys are in healthy individuals

are not palpable.

8. What additional research methods are most informative at diagnosis of liver diseases and biliary

tract?

Additional research methods: general clinical blood and urine tests, biochemical analysis of blood for

bilirubin and its fractions, residual nitrogen, urea, AST and ALT, creatinine, total protein, sulemic and

thymol samples. Ultrasound and radiological examination of the liver and bile bladder, computed

tomography of the abdomen and duodenal sensing, where three portions of duodental content are evaluated:

"Portion A" consists of intestinal, gastric and pancreatic juices, "Portion B" is gall bladder - dark brown thick

liquid in the amount of 50-60 ml and "portion C" is a clear golden yellow liquid, which is the bile of the

intrahepatic biliary tract.

9. What complaints can patients with liver disease present?

Patients complain of general weakness, fatigue, weight loss, sleep disorders, irritability, poor appetite,

bitterness, bloating abdomen, fever to subfebrile digits pain different intensity and character (from aching to

sharp, cutting) in the right hypochondrium, difficulty in the right hypochondrium, belching or air eaten food,

nausea, sometimes vomiting, heaviness and discomfort in epigastrium, bloating, stool disorders - onstipation

and diarrhea. At jaundice occurs with itching of the skin due to a delay in the blood of the bile acids and

their deposition in the skin.

10.How do liver percussion sizes consistently determine?

Percussion begins with the determination of the upper limit of absolute cardiac stupidity. From level II-III

ribs on the right middle-clavicular line percussion until a dull sound coincides with the upper bound liver

dullness (normal - V rib). Further along the same line, they are percussed from below, from the level of the

navel towards the defined point of the upper boundary to the appearance of dullness that indicates the lower

border of liver dullness. Between defined points I and II the height of liver dullness is 9 - 11 cm. From the

first point lowered perpendicular to the midline of the body and towards this (third) point percussed from the

navel area from the bottom up to the appearance of dullness denoting lower border of hepatic dullness in the

midline (fourth point). Between the third and fourth points determine the second percussion size of the liver

(normally 8 - 10 cm). Then from the bottom up on the left costal arch, percussed to the appearance of

stupidity (fifth point). Between the fourth and fifth points determine third percussion size of the liver

(normally 7 - 10 cm).

11.What is chronic hepatitis? What are the main causes of chronic hepatitis?

Chronic hepatitis is a chronic inflammatory liver disease. If the inflammation of the liver is cured within up

to 6 months, then talk about acute, and with a longer duration of the disease - about chronic hepatitis. The

main etiological factors behind chronic hepatitis are viruses, in particular, hepatitis A, B, C, D, E, F, G

viruses that cause both acute and chronic forms of hepatitis. Chronic hepatitis is most often caused infections

by viruses B, C, D, G. Also causes of chronic hepatitis may be alcohol, radiation exposure, some edications

for long-term use in large doses, autoimmune, hereditary factors and metabolic disorders.

12. What are the complaints about chronic hepatitis?

Typical for chronic hepatitis are complaints of right pain hypochondrium, feeling of heaviness and iscomfort

in the epigastrium and right hypochondrium, general weakness, fatigue, weight loss, sleep disturbance,

irritability, poor appetite, feeling of bitterness in the mouth, bloating, fever up to subfebrile numbers, stool

disorders - diarrhea or constipation.

4.3 PRACTICAL work that is carried out in the classroom:

1. Mastering physical methods of research of patients with pancreatitis, cholecystitis and housing.

2. Establishment of techniques for determining palpation and percussion of the gastrointestinal tract.

3. Diagnosis of patients with pancreatitis, cholecystitis and housing.

4. USG, X-ray examination of the gastrointestinal tract.

5. Contents of the topic.

CHRONIC HEPATITIS

Chronic hepatitis (CH) represents a series of liver disorders of varying causes and severity in which

hepatic inflammation and necrosis continue for at least 6 months. Milder forms are nonprogressive or only

slowly progressive, while more severe forms may be associated with scarring and architectural

reorganization, which, when advanced, lead ultimately to cirrhosis. Several categories of CH have been

recognized. These include chronic viral hepatitis, drug-induced CH, and autoimmune CH. In many cases,

clinical and laboratory features are insufficient to allow assignment into one of these three categories; these

―idiopathic‖ cases are also believed to represent autoimmune CH. Finally, clinical and laboratory features

of CH are observed occasionally in patients with such hereditary/metabolic disorders as Wilson’s disease

(copper overload), α1 antitrypsin deficiency, and nonalcoholic fatty liver disease and even occasionally in

patients with alcoholic liver injury.

Classification of chronic hepatitis Classification of CH is based on (1) its cause; (2) its histologic activity, or grade; and (3) its degree of progression, or stage. Thus, neither clinical features alone nor histologic features—requiring liver biopsy -

alone are sufficient to characterize and distinguish among the several categories of CH.

By cause:

-chronic viral hepatitis, caused by hepatitis B, hepatitis B plus D, or hepatitis C -autoimmune hepatitis, including several subcategories, I and II (perhaps III), based on serologic distinctions-drug-associated chronic hepatitis

-category of unknown cause, or cryptogenic chronic hepatitis

By grade:

-mild

-moderate

-severe

Grade, a histologic assessment of necroinflammatory activity, is based on examination of the liver biopsy.

An assessment of important histologic features includes the degree of periportal necrosis and the disruption

of the limiting plate of periportal hepatocytes by inflammatory cells (so-called piecemeal necrosis or

interface hepatitis); the degree of confluent necrosis that links or forms bridges between vascular structures -

between portal tract and portal tract or even more important bridges between portal tract and central vein -

referred to as bridging necrosis; the degree of hepatocyte degeneration and focal necrosis within the lobule;

and the degree of portal inflammation. Several scoring systems that take these histologic features into

account have been devised, and the most popular are the histologic activity index (HAI), used commonly in

the United States, and the METAVIR score, used in Europe.

By stage:

The stage of CH, which reflects the level of progression of the disease, is based on the degree of hepatic

fibrosis. When fibrosis is so extensive that fibrous septa surround parenchymal nodules and alter the normal architecture of the liver lobule, the histologic lesion is defined as cirrhosis. Staging is based on the degree of

fibrosis as categorized on a numerical scale from 0−6 (HAI) or 0−4 (METAVIR).

Etiology The most common causes are:

1. Hepatitis B virus

2. Hepatitis C virus

3. Nonalcoholic steatohepatitis (NASH) 4. Alcoholic hepatitis

5. Idiopathic (probably autoimmune)

Hepatitis B virus (HBV) and hepatitis C virus (HCV) are frequent causes of chronic hepatitis; 5 to 10% of

cases of HBV infection, with or without hepatitis D virus (HDV) coinfection, and about 75% of cases of

HCV infection become chronic. Rates are higher for HBV infection in children (eg, up to 90% of infected

neonates and 30 to 50% of young children). Although the mechanism of chronicity is uncertain, liver injury

is mostly determined by the patient’s immune reaction to the infection.

Rarely, hepatitis E virus genotype 3 has been implicated in chronic hepatitis.

Hepatitis A virus does not cause chronic hepatitis.

Other causes of CH include nonalcoholic steatohepatitis (NASH) and alcoholic hepatitis. NASH develops

most often in patients with at least one of the following risk factors:

-Obesity

-Dyslipidemia

-Glucose intolerance

Alcoholic hepatitis (a combination of fatty liver, diffuse liver inflammation, and liver necrosis) results from excess consumption. Many cases are idiopathic. A high proportion of idiopathic cases have prominent features of immune-mediated hepatocellular injury (autoimmune hepatitis), including the following: -The presence of serologic immune markers

-An association with histocompatibility haplotypes common in autoimmune disorders (eg, HLA-B1, HLA-B8, HLA-DR3, HLA-DR4) -A predominance of T lymphocytes and plasma cells in liver histologic lesions -Complex in vitro defects in cellular immunity and immunoregulatory functions

-An association with other autoimmune disorders (eg, RA, autoimmune hemolytic anemia, proliferative glomerulonephritis) -A response to therapy with corticosteroids or immunosuppressants Less common causes

Sometimes CH has features of both autoimmune hepatitis and another chronic liver disorder (eg, primary biliary cholangitis). These conditions are called overlap syndromes.

Many drugs, including isoniazid, methyldopa, nitrofurantoin, and, rarely acetaminophen, can cause CH. The

mechanism varies with the drug and may involve altered immune responses, cytotoxic intermediate

metabolites, or genetically determined metabolic defects.

Less often, CH results from α1 antitrypsin deficiency, celiac disease, a thyroid disorder, hereditary

hemochromatosis, or Wilson disease.

Clinical presentation

Clinical features of CH vary widely. About one third of cases develop after acute hepatitis, but most develop

insidiously de novo. Many patients are asymptomatic, especially in chronic HCV infection. However, malaise, anorexia, and

fatigue are common, sometimes with low-grade fever and nonspecific upper abdominal discomfort. Jaundice is usually absent. Often, particularly with HCV, the first findings are:

-Signs of chronic liver disease (eg, splenomegaly, spider nevi, palmar erythema) -Complications of cirrhosis (eg, portal hypertension, ascites, encephalopathy)

A few patients with CH develop manifestations of cholestasis (eg, jaundice, pruritus, pale stools, steatorrhea). In autoimmune hepatitis, especially in young women, manifestations may involve virtually any body system and can include acne, amenorrhea, arthralgia, ulcerative colitis, pulmonary fibrosis, thyroiditis, nephritis, and hemolytic anemia. Chronic HCV is occasionally associated with lichen planus, mucocutaneous vasculitis, glomerulonephritis,

porphyria cutanea tarda, and, perhaps, non-Hodgkin B-cell lymphoma.

About 1% of patients develop symptomatic cryoglobulinemia with fatigue, myalgias, arthralgias,

neuropathy, glomerulonephritis, and rashes (urticaria, purpura, leukocytoclastic vasculitis); asymptomatic

cryoglobulinemia is more common.

Diagnosis

• Liver function test results compatible with hepatitis (serum ALT, AST, alkaline phosphatase, and bilirubin)

• Viral serologic tests

• Possibly autoantibodies, immunoglobulins, alpha-1 antitrypsin level, and other tests

• Usually biopsy Serum albumin, platelet count, and prorhrombin time/international normalized ratio

The diagnosis is suspected in patients with any of the following:

Suggestive symptoms and signs

Incidentally noted elevations in aminotransferase levels

Previously diagnosed acute hepatitis

Liver function tests. Aminotransferase elevations are the most characteristic laboratory abnormalities.

Although levels can vary, they are typically 100 to 500 IU/L. ALT is usually higher than AST.

Aminotransferase levels can be normal during chronic hepatitis if the disease is quiescent, particularly with

HCV. Alkaline phosphatase is usually normal or only slightly elevated but is occasionally markedly high.

Bilirubin is usually normal unless the disease is severe or advanced. However, abnormalities in these laboratory tests are not specific and can result from other disorders, such as

alcoholic liver disease, recrudescent acute viral hepatitis, and primary biliary cirrhosis.

Other laboratory tests If laboratory results are compatible with hepatitis, viral serologic tests are done to exclude HBV and HCV.

Unless these tests indicate viral etiology, further testing is required. The next tests done include:

• Autoantibodies (antinuclear antibody, anti–smooth muscle antibody, antimitochondrial antibody, liver-kidney microsomal antibody)

• Immunoglobulins

• Thyroid tests (thyroid-stimulating hormone)

• Tests for celiac disease (tissue transglutaminase antibody)

• Alpha-1 antitrypsin level

• Iron and ferritin levels and total iron-binding capacity

Biopsy

Unlike in acute hepatitis, biopsy is necessary. Mild cases may have only minor hepatocellular necrosis and inflammatory cell infiltration, usually in portal regions, with normal acinar architecture and little or no

fibrosis. Such cases rarely develop into clinically important liver disease or cirrhosis. In more severe cases,

biopsy typically shows periportal necrosis with mononuclear cell infiltrates (piecemeal necrosis) accompanied by variable periportal fibrosis and bile duct proliferation. The acinar architecture may be

distorted by zones of collapse and fibrosis, and frank cirrhosis sometimes coexists with signs of ongoing hepatitis. Biopsy is also used to grade and stage the disease. In most cases, the specific cause of CH cannot

be discerned via biopsy alone, although cases caused by HBV can be distinguished by the presence of ground-glass hepatocytes and special stains for HBV components. Autoimmune cases usually have a more

pronounced infiltration by lymphocytes and plasma cells. In patients with histologic but not serologic criteria for chronic autoimmune hepatitis, variant autoimmune hepatitis is diagnosed; many have overlap syndromes.

Screening for complications

If symptoms or signs of cryoglobulinemia develop during CH, particularly with HCV, cryoglobulin levels

and rheumatoid factor should be measured; high levels of rheumatoid factor and low levels of complement

suggest cryoglobulinemia.

Patients with chronic HBV infection should be screened every 6 month for hepatocellular cancer with

ultrasonography and serum alpha-fetoprotein measurement, although the cost-effectiveness of this practice is debated. Patients with chronic HCV infection should be similarly screened only if advanced fibrosis or

cirrhosis is present.

Prognosis

Prognosis is highly variable. Chronic hepatitis caused by a drug often regresses completely when the causative drug is withdrawn. Without treatment, cases caused by HBV can resolve (uncommon), progress rapidly, or progress slowly to cirrhosis over decades. Resolution often begins with a transient increase in disease severity and results in seroconversion from hepatitis B e antigen (HBeAg) to antibody to hepatitis B e antigen (anti-HBe). Coinfection with HDV causes the most severe form of chronic HBV infection; without treatment, cirrhosis develops in up to 70% of patients. Untreated chronic hepatitis due to HCV causes cirrhosis in 20 to 30% of patients, although development may take decades and varies because it is often related to a patient's other risk factors for chronic liver disease, including alcohol use and obesity. Chronic autoimmune hepatitis usually responds to therapy but sometimes causes progressive fibrosis and eventual cirrhosis. Chronic HBV infection increases the risk of hepatocellular cancer. The risk is also increased in chronic HCV infection, but only if cirrhosis or advanced fibrosis has developed.

Treatment

• Supportive care

• Treatment of cause (eg, corticosteroids for autoimmune hepatitis, antivirals for HBV and

HCV infection)

There are specific antiviral treatments for chronic hepatitis B (eg, entecavir and tenofovir as first-line therapies) and antiviral treatments for chronic hepatitis C (eg, interferon-free regimens of direct-acting antivirals). General treatment

Treatment goals for chronic hepatitis include treating the cause and managing complications (eg, ascites,

encephalopathy) if cirrhosis and portal hypertension have developed.

Drugs that cause hepatitis should be stopped. Underlying disorders, such as Wilson disease, should be treated. In chronic hepatitis due to HBV, prophylaxis (including immunoprophylaxis) for contacts of

patients may be helpful. No vaccination is available for contacts of patients with HCV infection.

Corticosteroids and immunosuppressants should be avoided in chronic hepatitis B and C because

these drugs enhance viral replication. If patients with chronic hepatitis B require treatment with

corticosteroids, immunosuppressive therapies, or cytotoxic chemotherapy for other disorders, they

should be treated with antiviral drugs at the same time to prevent a flare-up of acute hepatitis B or

acute liver failure due to hepatitis B. A similar situation with hepatitis C being activated or causing

acute liver failure has not been described.

Treatment of NASH aims to:

1. Eliminate causes Control risk factors for NASH

It may involve recommending weight loss, treating hyperlipidemias and hyperglycemia, stopping drugs

associated with NASH (eg, amiodarone, tamoxifen, methotrexate, corticosteroids such as prednisone or

hydrocortisone, synthetic estrogens), and avoiding exposure to toxins (eg, pesticides). Autoimmune hepatitis

- corticosteroids, with or without azathioprine, prolong survival. Prednisone is usually started at 30 to 60 mg

po once/day, then tapered to the lowest dose that maintains aminotransferases at normal or near-normal

levels. To prevent long-term need for corticosteroid treatment, clinicians can transition to azathioprine 1 to

1.5 mg/kg po once/day or mycophenolate mofetil 1000 mg twice/day after corticosteroid induction is

complete and then gradually taper the corticosteroid. Most patients require long-term, low-dose,

corticosteroid-free maintenance treatment.

Liver transplantation may be required for decompensated cirrhosis.

AUTOIMMUNE HEPATITIS

Usually young to middle-aged women.

Chronic hepatitis with high serum globulins and characteristic liver histology.

Positive antinuclear antibody (ANA) and/or smooth muscle antibody in most common type.

Responds to corticosteroids.

Although autoimmune hepatitis is usually seen in young women, it can occur in either sex at any age. The

incidence and prevalence are estimated to be 8.5 and 107 per million population, respectively. Affected younger persons are often positive for HLA-B8 and HLA-DR3; older patients are often positive for HLA-

DR4.

The onset is usually insidious, but up to 40% of cases present with an acute (occasionally fulminant) attack

of hepatitis and some cases follow a viral illness (such as hepatitis A, Epstein-Barr infection, or measles) or

exposure to a drug or toxin (such as nitrofurantoin, minocycline, or infliximab). Exacerbations may occur

postpartum. 34% of patients are asymptomatic. Typically, examination reveals a healthy-appearing young

woman with multiple spider nevi, cutaneous striae, acne, hirsutism, and hepatomegaly. Amenorrhea may be

a presenting feature. Extrahepatic features include arthritis, Sjögren syndrome, thyroiditis, nephritis,

ulcerative colitis, and Coombs-positive hemolytic anemia. Patients with autoimmune hepatitis are at

increased risk for cirrhosis which, in turn, increases the risk of hepatocellular carcinoma (at a rate of about

1% per year).

Treatment. Prednisone with or without azathioprine improves symptoms, decreases the serum bilirubin,

aminotransferase, and γ-globulin levels and reduces hepatic inflammation. Symptomatic patients with

aminotransferase levels elevated tenfold (or fivefold if the serum globulins are elevated at least twofold) are

optimal candidates for therapy, and asymptomatic patients with modest enzyme elevations may be

considered for therapy depending on the clinical circumstances and histologic severity. Prednisone is given

initially in a dose of 30 mg orally daily with azathioprine, 50 mg orally daily, which is generally well

tolerated and permits the use of lower corticosteroid doses than a regimen beginning with prednisone 60 mg

orally daily alone. Preliminary experience suggests that budesonide, 6–9 mg orally daily, may be at least as

effective as prednisone in noncirrhotic autoimmune hepatitis and associated with fewer side effects. The

dose of prednisone is lowered from 30 mg/d after 1 week to 20 mg/d and again after 2 or 3 weeks to 15

mg/d. Ultimately, a maintenance dose of 10 mg/d is achieved. The response rate to therapy with prednisone

and azathioprine is 80%. Nonresponders to corticosteroids and azathioprine (failure of serum

aminotransferase levels to decrease by 50% after 6 months) may be considered for a trial of cyclosporine,

tacrolimus, everolimus, methotrexate, or rituximab.

ALCOHOLIC LIVER DISEASE

Chronic alcohol intake usually exceeds 80 g/d in men and 30–40 g/d in women with alcoholic hepatitis or cirrhosis.

Fatty liver is often asymptomatic.

Fever, right upper quadrant pain, tender hepatomegaly, and jaundice characterize alcoholic hepa- titis, but the patient may be asymptomatic.

AST is usually elevated but usually not above 300 units/L; AST is greater than ALT, usually by a factor of 2 or more.

Alcoholic hepatitis is often reversible but it is the most common precursor of cirrhosis

Excessive alcohol intake can lead to fatty liver, hepatitis, and cirrhosis. Alcoholic hepatitis is characterized

by acute or chronic inflammation and parenchymal necrosis of the liver induced by alcohol. The frequency

of alcoholic cirrhosis is estimated to be 10–15% among persons who consume over 50 g of alcohol daily for

over 10 years. The risk of cirrhosis is lower (5%) in the absence of other cofactors such as chronic viral

hepatitis and obesity. Women appear to be more susceptible than men, in part because of lower gastric

mucosal alcohol dehydrogenase levels. Over 80% of patients with alcoholic hepatitis have been drinking 5

years or more before symptoms that can be attributed to liver disease develop; the longer the duration of

drinking (10–15 or more years) and the larger the alcoholic consumption, the greater the probability of

developing alcoholic hepatitis and cirrhosis. Deficiencies in vitamins and calories probably contribute to the

development of alcoholic hepatitis and its progression to cirrhosis. Many adverse effects of alcohol on the

liver are thought to be mediated by tumor necrosis factor and by the oxidative metabolite acetaldehyde,

which contributes to lipid peroxidation and induction of an immune response following covalent binding to

proteins in the liver.

The clinical presentation of alcoholic liver disease can vary from asymptomatic hepatomegaly to a rapidly fatal acute illness or end-stage cirrhosis. A recent period of heavy drinking, complaints of anorexia and

nausea, and the demonstration of hepatomegaly and jaundice strongly suggest the diagnosis. Abdominal pain and tenderness, splenomegaly, ascites, fever, and encephalopathy may be present. Infection is common in

patients with severe alcoholic hepatitis.

Treatment. Abstinence from alcohol is essential. Fatty liver is quickly reversible with abstinence. Every

effort should be made to provide sufficient amounts of carbohydrates and calories in anorectic patients to

reduce endogenous protein catabolism, promote gluconeogenesis, and prevent hypoglycemia. Nutritional

support (40 kcal/kg with 1.5–2 g/kg as protein) improves liver disease, but not necessarily survival, in

patients with malnutrition. Methylprednisolone, 32 mg/d orally, or the equivalent, for 1 month, may reduce

short-term mortality in patients with alcoholic hepatitis. Pentoxifylline—an inhibitor of tumor necrosis

factor— 400 mg orally three times daily for 4 weeks, may reduce 1-month mortality rates in patients with

severe alcoholic hepatitis, primarily by decreasing the risk of hepatorenal syndrome. It is often used when

corticosteroids are contraindicated.

LIVER CIRRHOSIS

Cirrhosis represents the final common histologic pathway for a wide variety of chronic liver diseases. The term cirrhosis was first introduced by Laennec in 1826. It is derived from the Greek term scirrhus and refers to the orange or tawny surface of the liver seen at autopsy.

Cirrhosis is defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion

of normal liver architecture into structurally abnormal nodules. The progression of liver injury to cirrhosis

may occur over weeks to years. Indeed, patients with hepatitis C may have chronic hepatitis for as long as

40 years before progressing to cirrhosis.

Etiology

Most common causes of cirrhosis are: Chronic viral hepatitis (B or C) Alcoholic liver disease

Non-alcoholic fatty liver disease

Immune

– Primary sclerosing cholangitis

– Autoimmune liver disease Biliary– Primary biliary cirrhosis

– Secondary biliary cirrhosis – Cystic fibrosis

Genetic

– Haemochromatosis – Wilson’s disease

– Alpha1-antitrypsin deficiency

Cryptogenic (unknown—15%)

Chronic venous outflow obstruction Pathophysiology

Many forms of liver injury are marked by fibrosis, which is defined as an excess deposition of the components of the extracellular matrix (ie, collagens, glycoproteins, proteoglycans) in the liver. This

response to liver injury potentially is reversible. By contrast, in most patients, cirrhosis is not a reversible

process. The development of hepatic fibrosis reflects an alteration in the normally balanced processes of extracellular matrix production and degradation. The extracellular matrix, the normal scaffolding for hepatocytes, is composed of collagens (especially types I, III, and V), glycoproteins, and proteoglycans.

Stellate cells, located in the perisinusoidal space, are essential for the production of extracellular matrix.

Stellate cells, which were once known as Ito cells, lipocytes, or perisinusoidal cells, may become activated

into collagen-forming cells by a variety of paracrine factors. Such factors may be released by hepatocytes,

Kupffer cells, and sinusoidal endothelium following liver injury. Distruction of the liver architecture causes

distortion and loss of the normal hepatic vasculature with with the development of portosystemic vascular

shunts and the formation of nodules. Cirrhosis evolves slowly over years to decades, and normally

continues to progress even after removal of etiological agent. Cirrhosis is a histological diagnosis

characterized by diffuse hepatic fibrosis and nodule formation. These changes usually affect the whole liver,

but in primary biliary cirrhosis they can be patchy. Cirrhosis can be classified histologically into two types:

Micronodular cirrhosis, characterized by small nodules about 1 mm in diameter

Macronodular cirrhosis, characterized by larger nodules of various size. Areas of previous collapse of the liver architecture are evidenced by large fibrous scars.

Clinical presentation

The clinical features of cirrhosis result from hepatocyte dysfunction, portosystemic shunting, and portal

hypertension. Patients may have no symptoms for long periods. The onset of symptoms may be insidious or,

less often, abrupt. Weakness, fatigue, disturbed sleep, muscle cramps, and weight loss are common. In

advanced cirrhosis, anorexia is usually present and may be extreme, with associated nau- sea and occasional

vomiting. Abdominal pain may be present and is related either to hepatic enlargement and stretching of

Glisson capsule or to the presence of ascites. Menstrual abnormalities (usually amenorrhea), erectile

dysfunction, loss of libido, sterility, and gynecomastia in men may occur. Hematemesis is the presenting

symptom in 15–25%. Skin manifestations consist of spider angioma (invariably on the upper half of the body), palmar erythema

(mottled redness of the thenar and hypothenar eminences), and Dupuytren contractures. Evidence of vitamin

deficiencies (glossitis and cheilosis) is common. Weight loss, wasting, and the appearance of chronic illness

are present. Jaundice—usually not an initial sign—is mild at first, increasing in severity during the later

stages of the disease. In 70% of cases, the liver is enlarged, pal-pable, and firm if not hard and has a sharp or

nodular edge; the left lobe may predominate. Splenomegaly is present in 35–50% of cases and is associated

with an increased risk of complications of portal hypertension. The superficial veins of the abdomen and

thorax are dilated, reflecting the intrahepatic obstruction to portal blood flow, as do rectal varices. The

abdominal wall veins fill from below when compressed. Ascites, pleural effusions, peripheral edema, and

ecchymoses are late find- ings. Encephalopathy characterized by day–night reversal, asterixis, tremor,

dysarthria, delirium, drowsiness, and ultimately coma also occurs late except when precipitated by an acute

hepatocellular insult or an episode of gastrointestinal bleeding. Fever may be a presenting symptom in up to

35% of patients and usually reflects associated alcoholic hepatitis, spontaneous bacterial peritonitis, or

intercurrent infection.

Portal Hypertension The normal liver has the ability to accommodate large changes in portal blood flow without appreciable

alterations in portal pressure. Portal Hypertension results from a combination of increased portal venous inflow

and increased resistance to portal blood flow. Patients with cirrhosis demonstrate increased splanchnic arterial

flow and, accordingly, increased splanchnic venous inflow into the liver. Increased splanchnic arterial flow is

explained partly by decreased peripheral vascular resistance and increased cardiac output in the patient with

cirrhosis. Nitric oxide appears to be the major driving force for thisphenomenon. Increased resistance across the

sinusoidal vascular bed of the liver is caused by fixed factors (formation of regenerating nodules and, after the

production of collagen by activated stellate cells, deposition of the collagen within the space of Disse) and

dynamic factors (vasoconstriction of the hepatic sinusoid).

The portal hypertension of cirrhosis is caused by the disruption of hepatic sinusoids. However, portal

hypertension may be observed in a variety of noncirrhotic conditions.

Portal hypertension can have prehepatic, intrahepatic, or posthepatic causes. Budd-Chiari syndrome, a posthepatic cause, is characterized by the following symptoms:

Hepatomegaly

Abdominal pain

Ascites

Abdominal distention

Bulging flanks

Shifting dullness

Elicitation of a "puddle sign" in patients in the knee-elbow position

Diagnosis During angiography, a catheter is placed selectively via either the transjugular or transfemoral route into the hepatic vein to measure portal pressure.

Hepatic encephalopathy The symptoms of hepatic encephalopathy may range from mild to severe and may be observed in as many as 70% of patients with cirrhosis. Symptoms are graded on the following scale:

• Grade 0 - Subclinical; normal mental status but minimal changes in memory, concentration, intellectual function, coordination

• Grade 1 - Mild confusion, euphoria or depression, decreased attention, slowing of ability to perform mental tasks, irritability, disorder of sleep pattern (ie, inverted sleep cycle)

• Grade 2 - Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, intermittent disorientation (usually with regard to time)

• Grade 3 - Somnolent, but arousable state; inability to perform mental tasks; disorientation with regard to time and place; marked confusion; amnesia; occasional fits of rage; speech is present but incomprehensible

• Grade 4 - Coma, with or without response to painful stimuli

Diagnosis An elevated arterial or free venous serum ammonia level is the classic laboratory abnormality reported in patients with hepatic encephalopathy. Electroencephalography may be helpful in the initial workup of a patient with cirrhosis and altered mental status, when ruling out seizure activity may be necessary. Computed tomography (CT) scanning and MRI studies of the brain may be important in ruling out intracranial lesions when the diagnosis of hepatic encephalopathy is in question.

Hepatorenal Syndrome This syndrome represents a continuum of renal dysfunction that may be observed in patients with a combination of cirrhosis and ascites. Hepatorenal syndrome is caused by the vasoconstriction of large and small renal arteries and the impaired renal perfusion that results.

Hepatorenal syndrome progression may be slow (type II) or rapid (type I). Type I disease frequently is

accompanied by rapidly progressive liver failure. Hemodialysis offers temporary support for such patients.

These individuals are salvaged only by performance of liver transplantation. Exceptions to this rule are the

patients with fulminant hepatic failure (FHF) or severe alcoholic hepatitis who spontaneously recover liver

and kidney function. In type II hepatorenal syndrome, patients may have stable or slowly progressive renal

insufficiency. Many such patients develop ascites that is resistant to management with diuretics. Diagnosis

Hepatorenal syndrome is diagnosed when a creatinine clearance rate of less than 40 mL/min is present or when a serum creatinine level of greater than 1.5 mg/dL, a urine volume of less than 500 mL/day, and a urine sodium level of less than 10 mEq/L are present. Urine osmolality is greater than plasma osmolality

Diagnosis

Laboratory abnormalities are either absent or minimal in early or compensated cirrhosis. -Anemia, a frequent finding, is often macrocytic; causes include suppression of erythropoiesis by alcohol as well as folate deficiency, hemolysis, hypersplenism, and occult or overt blood loss from the gastrointestinal tract. -The white blood cell count may be low, reflecting hypersplenism, or high, suggesting infection; -thrombocytopenia, the most common cytopenia in cirrhotic patients, is secondary to alcoholic marrow suppression, sepsis, folate deficiency, or splenic sequestration. Prolongation of the prothrombin time may result from reduced levels of clotting factors (except factor VIII). However, bleeding risk correlates poorly with the prothrombin time because of concomitant abnormalities of fibrinolysis, and among hospitalized patients under age 45, cirrhosis is associated with an increased risk of venous thromboembolism. Blood chemistries reflect hepatocellular injury and dysfunction, manifested by modest elevations of AST and alkaline phosphatase and progressive elevation of the bilirubin. Serum albumin decreases as the disease progresses; γ-globulin is increased and may be as high as in autoimmune hepatitis. The risk of diabetes mellitus is increased in patients with cirrhosis, particularly when associated with HCV infection, alcoholism, hemochromatosis, or NAFLD. Vitamin D deficiency has been reported in as many as 91% of patients with cirrhosis. Patients with alcoholic cirrhosis may have elevated serum cardiac troponin I and brain natriuretic peptide levels. Blunted cardiac inotropic and chronotropic responses to exercise, stress, and drugs, as well as

systolic and diastolic ventricular dysfunction (―cir- rhotic cardiomyopathy‖) and prolongation of the QT interval in the setting of a hyperkinetic circulation, are common in cirrhosis of all causes, but overt heart failure is rare in the absence of alcoholism. Relative adrenal insufficiency appears to be common in patients with advanced cirrhosis, even in the absence of sepsis. Liver biopsy may show inactive cirrhosis (fibrosis with regenerative nodules) with no specific features to

suggest the underlying cause. Alternatively, there may be additional features of alcoholic liver disease,

chronic hepatitis, NASH, or other specific causes of cirrhosis. Combinations of routine blood tests (eg, AST,

platelet count), including the FibroSure or FibroMax tests, and serum markers of hepatic fibrosis (eg,

hyaluronic acid, amino-terminal propeptide of type III collagen, tissue inhibitor of matrix metalloproteinase

1) are potential alternatives to liver biopsy for the diagnosis or exclusion of cirrhosis.

Ultrasonography is helpful for assessing liver size and detecting ascites or hepatic nodules, including small

hepatocellular carcinomas. Together with a Doppler study, it may establish patency of the splenic, portal, and hepatic veins. Hepatic nodules are characterized further by contrast-enhanced CT or MRI. Nodules

suspicious for malignancy may be biopsied under ultrasound or CT guidance. Other Examinations Esophagogastroduodenoscopy confirms the presence of varices and detects specific causes of bleeding in the esophagus, stomach, and proximal duodenum. Liver biopsy may be performed by laparoscopy or, in patients with coagulopathy and ascites, by a transjugular approach. In selected cases, wedged hepatic vein pressure

measurement may establish the presence and cause of portal hypertension. Transient elastography, which uses ultrasound to determine liver stiffness, and magnetic resonance elastography are available in a limited number of centers as noninvasive tests for cirrhosis and portal hypertension.

Complications

Upper gastrointestinal tract bleeding may occur from varices, portal hypertensive gastropathy, or

gastroduodenal ulcer. Varices may also result from portal vein thrombosis, which may complicate cirrhosis.

Liver failure may be precipitated by alcoholism, surgery, and infection. Hepatic Kupffer cell (reticuloendothelial) dysfunction and decreased opsonic activity lead to an increased risk of systemic

infection, which increase mortality fourfold. Osteoporosis occurs in 12–55% of patients with cirrhosis. The risk of hepatocellular carcinoma is increased greatly in persons with cirrhosis.

Treatment

The most important principle of treatment is abstinence from alcohol. The diet should be palatable, with adequate calories (25–35 kcal/kg body weight per day in those with compensated cirrhosis and 35–40 kcal/kg/d in those with malnutrition) and protein (1–1.2 g/kg/d in those with compensated cirrhosis and 1.5 g/kg/d in those with malnutrition) and, if there is fluid retention, sodium restriction. In the presence of hepatic encephalopathy, protein intake should be reduced to no less than 60–80 g/d. Vitamin supplementation is desirable. Patients with cirrhosis should receive the HAV, HBV, and pneumococcal vaccines and a yearly influenza vaccine

Specific medical therapies may be applied to many liver diseases in an effort to diminish symptoms and to

prevent or forestall the development of cirrhosis. Examples of such treatments include the following:

• Prednisone and azathioprine - For autoimmune hepatitis • Interferon and other antiviral agents - For hepatitis B and C

• Phlebotomy - For hemochromatosis

• Ursodeoxycholic acid - For primary biliary cirrhosis

• Trientine and zinc - For Wilson disease Once cirrhosis develops, treatment is aimed at the management of complications as they arise. Examples include the following:

• Hepatorenal syndrome - Kidney function usually recovers when patients with cirrhosis and hepatorenal

syndrome undergo liver transplantation; patients with early hepatorenal syndrome may be salvaged by aggressive expansion of intravascular volume with albumin and fresh frozen plasma and by avoidance of

diuretics • Hepatic encephalopathy - Pharmacologic treatment includes the administration of lactulose and antibiotics • Ascites - Treatment can include sodium restriction and the use of diuretics, large-volume paracentesis, and

shunts (peritoneovenous, portosystemic, transjugular intrahepatic portosystemic)

Ascites

Salt restriction is the first line of therapy. In general, patients begin with a diet containing less than 2000 mg of sodium daily. Some patients with refractory ascites require a diet containing less than 500 mg of sodium daily.

Diuretics should be considered the second line of therapy. Spironolactone blocks the aldosterone receptor at

the distal tubule. It is dosed at 50-300 mg once daily. Adverse effects of spironolactone include

hyperkalemia, gynecomastia, and lactation. Other potassium-sparing diuretics, including amiloride and

triamterene, may be used as alternative agents, especially in patients complaining of gynecomastia.

Furosemide may be used as a solo agent or in combination with spironolactone. The drug blocks sodium

reuptake in the loop of Henle. It is dosed at 40-240 mg daily in 1-2 divided doses. Patients infrequently need

potassium repletion when furosemide is dosed in combination with spironolactone. Aggressive diuretic

therapy in hospitalized patients with massive ascites can safely induce a weight loss of 0.5-1kg daily,

provided that patients undergo careful monitoring of renal function. Diuretic therapy should be held in the

event of electrolyte disturbances, azotemia, or induction of hepatic encephalopathy. Albumin may increase

the efficacy and safety of diuretics.

Large-volume paracentesis is thought to be safe in patients with peripheral edema and in patients not

currently treated with diuretics.

Hepatic encephalopathy Lactulose is helpful in patients with an acute onset of severe encephalopathy symptoms and in patients with

milder, chronic symptoms. This nonabsorbable disaccharide stimulates the passage of ammonia from tissues

into the gut lumen and inhibits intestinal ammonia production. Initial lactulose dosing is 30 mL orally once or twice daily. Dosing is increased until the patient has 2-4 loose stools per day. Dosing should be reduced if

the patient complains of diarrhea, abdominal cramping, or bloating. Neomycin and other antibiotics (eg, metronidazole, oral vancomycin, paromomycin, oral quinolones) serve as second-line agents. They work by decreasing the colonic concentration of ammoniagenic bacteria.

Neomycin dosing is 250-1000 mg orally 2-4 times daily. Treatment with neomycin may be complicated by ototoxicity and nephrotoxicity. Other chemicals capable of decreasing blood ammonia levels are L-ornithine L-aspartate and sodium benzoate. Low-protein diets were recommended routinely in the past for patients with cirrhosis. High levels of

aromatic amino acids contained in animal proteins were believed to lead to increased blood levels of the

false neurotransmitters tyramine and octopamine, with resultant worsening of encephalopathic symptoms. In

this author's experience, the vast majority of patients can tolerate a protein-rich diet (>1.2 g/kg daily) that

includes well-cooked chicken, fish, vegetable protein, and, if needed, protein supplements. Protein restriction

is rarely necessary in patients with symptoms of chronic encephalopathy. Many patients with cirrhosis have

protein-calorie malnutrition at baseline; the routine restriction of dietary protein intake increases their risk

for worsening malnutrition.

Zinc deficiency Zinc deficiency commonly is observed in patients with cirrhosis. Treatment with zinc sulfate at 220 mg orally twice daily may improve dysgeusia and can stimulate appetite. Furthermore, zinc is effective in the treatment of muscle cramps and is adjunctive therapy for hepatic encephalopathy.

Pruritus Pruritus is a common complaint in cholestatic liver diseases (eg, primary biliary cirrhosis) and in noncholestatic

chronic liver diseases (eg, hepatitis C). Although increased serum bile acid levels once were thought to be the

cause of pruritus, endogenous opioids are more likely to be the culprit pruritogen. Mild itching complaints may

respond to treatment with antihistamines and topical ammonium lactate.

Osteoporosis Supplementation with calcium and vitamin D is important in patients at high risk for osteoporosis, especially patients with chronic cholestasis or primary biliary cirrhosis and patients receiving

corticosteroids for autoimmune hepatitis.

Liver transplantation Patients should be referred for consideration for liver transplantation after the first signs of hepatic decompensation.

Patient Monitoring

Patients with cirrhosis should undergo routine follow-up monitoring of their complete blood count, renal and liver chemistries, and prothrombin time. The policy is to monitor stable patients 3-4 times per year (surveillance of esophageal varices, surveillance for hepatocellular carcinoma).

6.1. Test tasks on the topic: Chronic hepatitis. Cirrhosis of liver.

1. What biochemical syndromes are typical for chronic hepatitis?

a) Syndrome of cytolysis and hepatic hiperazotemia

b) Syndrome of synthetic liver function deficiency and cytolysis

c) Cholestasis syndrome and immune inflammation

d) All of the mentioned above

e) None of the mentioned above

2. What clinical syndrome is most typical for chronic hepatitis?

a) Pain

b) Articular

c) Fever

d) Asthenovegetative

e) Encephalopathic

3. Etiologic factors of chronic hepatitis are: a) Viruses, bacteria, giardia

b) Smoking, obesity, viruses

c) Viruses, hepatotropic drugs, alcohol

d) Hepatoprotectors, viruses, bacteria

e) Radiation, obesity, protozoa

4. What are the diagnostic criteria for autoimmune hepatitis diagnosis? a) Cholestasis, the efficacy of the choleretics

b) hypergammaglobulinemia, accelerated ESR, the efficacy of glucocorticoids

c) Enlarged liver, elevated transaminases and alkaline phosphatase in the blood

d) Enlarged liver, increased bilirubin, efficacy of hepatoprotectors

e) Efficacy of antiviral drugs, vitamins

5. What causes pain in chronic hepatitis?

a) Stagnation of bile in the bile ducts

b) Stretching of liver capsule

c) Concomitant cholecystitis

d) Concomitant pancreatitis

e) Portal hypertension

6. Which of the listed below factors promote the development of liver cirrhosis?

a) Viruses, alcohol abuse

b) Bacteria, fungi

c) Influence of vitamin supplements

d) Rickettsia, mycoplasma

e) Gallbladder diseases

7. What clinical symptoms are typical for the initial stage of liver cirrhosis? a) Nausea, vomiting, loss of body weight

b) Loss of body weight, meteorism, feeling of heaviness in right hypochondrium

c) Bitter taste in mouth, heartburn

d) Enlargement of a liver, spleen, liver stigmata

e) Xanthelasma, palmar erythema, ascitis

8. What changes in blood are the most typical for liver cirrhosis? a) Iron-deficiency anemia

b) В12- folic acid deficiency anemia

c) Hemolytic anemia

d) None of the listed

e) All of the listed

9. What are the findings on palpation when examining the patient with liver cirrhosis? a) Enlarged, firm, rounded edge

b) Enlarged, doughy, rounded edge

c) Reduced, bumpy, pointy end

d) Enlarged, firm, pointy end

e) Reduced, doughy, rounded edge

10. The syndrome of a portal hypertension is? a) Enlargement of a liver, meteorism, skin itch

b) Enlargement of a liver and a spleen, jaundice

c) Enlargement of a liver, ascites, varicose veins

d) Reduction of a liver, edemas, jaundice

e) Enlargement of a liver, ascitis, edemas, cardiomyopathy

6.2. Situation tasks on the topic: Chronic hepatitis. Cirrhosis of liver.

TASK 1.

The patient A. turned to the doctor with complaints of general weakness, nausea, loss of appetite, aching

pain and heaviness in the right subcostal area. From the anamnesis it is known that the patient abuses

alcohol, badly eats. At examination of the patient there is moderate jaundice, traces of wrinkles, on the skin

of the abdomen - a symptom of the "head of a jellyfish", an increase in the stomach. What disease can be

diagnosed in a patient?

A) mechanical jaundice;

B) chronic pancreatitis;

C) cirrhosis of the liver;

D) gallstone disease

TASK 2.

The patient D. turned to the dentist complaining of a recurrent angular stomatitis, bleeding gums. When

looking at the oral cavity, a yellow-brown plaque on the tongue is found, gums are loose and easy to bleed

(manifestations of avitaminosis). In the corners of the mouth are cracks, the phenomena of inflammation.

When questioning the patient, complaints of aching pain in the right hypochondrium area were found, which

increases with the use of greasy, spicy food; bitterness in the mouth, poor appetite. From history we know

that ill 5 years ago suffered from viral hepatitis A. Over 5 years to the doctor - the therapist not appealed, the

clinical examination is not impressed. What kind of disease of the internal organs in the patient can be

thought of?

A) chronic hepatitis;

B) cholelithiasis;

C) chronic cholecystitis;

D) peptic ulcer disease;

TASK 3.

Patient A., 34 years old. Complaints for persistent aching pain in the area of the right subcostal area,

sometimes nausea, bitterness in the mouth in the morning, constipation. The above complaints periodically

disturbed the patient for about two years. The last deterioration of the condition 2 days ago, after eating a lot

of smoked fish. Five years ago he suffered appendectomy. Objective deviation: on the tongue grayish

plaque, in the area of the right subcostal area, slight tension of the muscles. In the ultrasound examination,

the gall bladder is enlarged, its walls are thickened, and has a constriction. What illness can be assumed in a

patient?

A) cirrhosis of the liver;

B) dyskinesia of the biliary tract;

C) chronic cholecystitis;

D) chronic hepatitis;

TASK 4.

Patient, 18 years old, student. Notices complaints of weakness, dull pain in the liver, long-term, not

associated with the reception of food, periodic light jaundice sclera. Slimming does not notice. He is ill for

about 5 years. The onset of the disease is associated with stay in a hospital about appendectomy. The disease

has a wave-like course. Objectively: an increase (2 cm below the rib arch) and liver densification. In the

biochemical analysis, a slight increase in the activity of AST (aspartate aminotransferase). What illness can

be assumed in a patient?

A) cirrhosis of the liver;

B) dyskinesia of the biliary tract;

C) chronic cholecystitis;

D) chronic hepatitis;

Practical tasks.

1. Supervise patient with CH

2. Interpret the laboratory data.

3. Interpret the data of instrumental methods.

4. Perform differential diagnosis of CH

5. List complications of CH

6. To supervise a patient with LC

7. To give interpretation for the laboratory assays.

8. To give interpretation for the insrtumental methods of study.

9. To perform differential diagnosis of LC

8. Literature:

1. Davidsons “Principles and Practice of Medicine” 21st

edition, Alimentary tract and pancreatic disease, p. 835-919.

2. Current Medical Diagnosis and Treatment, Gastrointestinal disorders, 2014, p. 564-662 3. Harrisons, Principles of Internal Medicine, 19

th edition, Gastoenterology and Hepatology, p.257-398

4. Nair RJ, Lawler L, Miller MR. Chronic pancreatitis. Am Fam Physician. 2007;76:1679-1688.

5. Owyang C. Chronic pancreatitis. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed.

Philadelphia, Pa: Saunders Elsevier; 2007:chap 147. 6. Kumar P, Clark M. (eds.) (2005) Kumar & Clark Clinical medicine. 6th ed. Edinburgh: W B

Saunders. 7. Keim V, Teich N, Moessner J. Clinical value of a new fecal elastase test for detection of

chronic pancreatitis. Clin Lab 2003; 49:209. 8. Schmidt G. Pancreas. Differential diagnosis in ultrasound. A teaching atlas. Georg Thieme

Verlag, Stuttgart, Germany 2006. p.146. 9. Bozkurt T, Braun U, Leferink S, et al. Comparison of pancreatic morphology and exocrine

functional impairment in patients with chronic pancreatitis. Gut 1994; 35:1132. 10. Axon AT, Classen M, Cotton PB, et al. Pancreatography in chronic pancreatitis: international

definitions. Gut 2004; 25:1107. 11. Zuccaro G Jr, Sivak MV Jr. Endoscopic ultrasonography in the diagnosis of chronic

pancreatitis. Endoscopy 1992; 24 Suppl 1:347. 12. Wallace MB, Hawes RH, Durkalski V, et al. The reliability of EUS for the diagnosis of

chronic pancreatitis: interobserver agreement among experienced endosonographers. Gastrointest Endosc 2001; 53:294.

13. Ooi CY, Gonska T, Durie PR, Freedman SD. Genetic testing in pancreatitis. Gastroenterology 2010; 138:2202.

14. Harrison‟s, Principles of Internal Medicine, 19th

edition, Gastoenterology and Hepatology, p.257-398

15. http://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/cholelithiasis. Accessed Oct., 2015

16. http://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/chronic-cholecystitis. Accessed Oct., 2015

17. Functional Hepatobiliary Disease: Chronic Acalculous Gallbladder and Chronic Acalculous Biliary Disease. Ziessman, H.A. Semin Nucl Med. 2006; 36:119-132.

18. Diagnostic Stringency and Healthcare Needs in Patients with Biliary Dyskinesia. Aggarwal, N., Bielfeldt, K. Dig Dis Sci. 2013 Oct; 58(10):2799-808.

19. Utilization of Cholecystokinin Cholescintigraphy in Clinical Practice. Richmond et al. J Am Coll Surg. 2013, Aug;217(2):317-23.

20. Functional Gallbladder and Sphincter of Oddi Disorders. Behar et el. Gastroenterology. 2006 Apr;130 (5):1498-509.