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 Basices of internal medicine

Module №1 Basiecs of internal medicine

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

Theme 17 Pancreatitis. Cholecystitis.

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

Pancreatitis pancreatitis

Cholecystitis cholecystitis

Cholelithiasis gallstone disease

4.2.Theoretical questions to the class.

1. What are the main complaints of patients with software disorders.

Pain, dyspeptic symptoms (loss of appetite, nausea, vomiting, diarrhea, flatulence), jaundice, general weakness,

weight loss.

2. What are your knowledge of laboratory and instrumental research methods patients with software

diseases?

Coprological examination, study of pancreatic juice, enzymes in the blood, urine, ultrasound software,

computed tomography, endoscopic retrograde pancreatocholangiography and gland angiography,

esophagogastroduodenoscopy, examination radiographic image of abdominal organs.

3. Define the terms "polyfecal", "steatorrhea", "creatorrhea", Amylorea. Polyfecal increase in the

frequency of feces.

Steatorrhea - increased amount of neutral fat in feces.

Creatoria - Increased amount of muscle fibers in the stool.

Amilorrhea - an increase in the amount of starch in the stool.

4. Describe the features of the structure of the pancreas.

The pancreas is behind the stomach, it is isolated head, body, tail. The outer gland is covered by a connective

tissue capsule, the tissue of which penetrates between the lobules of the gland. Anterior body and tail gland

covered with parietal peritoneum. Through all departments of a pancreas passes outlet duct, which is formed by

merging midline and intertidal channels. Pancreas consists of exocrine and endocrine compartments. The

exocrine part produces a complex secret - pancreatic juice, which is excreted through the duct system into the

duodenum. - The endocrine part of the organ produces a number of hormones that get into directly into the

vascular bed and play an important role in regulation carbohydrate and fat metabolism in the body.

5. What is the exocrine function of the software?

The pancreas secretes digestive enzymes and the rare part of the secretion. The enzyme amylase promotes the

digestion of complex starch carbohydrates and glycogen almost to disaccharides. Lipase, phospholipase 2 and

carboxylesterase is hydrolyzed to fatty acids and fatty acids of monoglycerides. Trypsin, chymotrypsin,

elastase, carboxypeptidase A and B hydrolyze proteins. These enzymes are secreted by iron in inactive form.

6. What is the endocrine function of the software?

The pancreas secretes by specialized beta cells The hormone insulin involved in various types of metabolism, in

particular, reduces blood glucose levels, translating it into glycogen. A-cells are secreted glucagon, which

increases blood glucose, stimulating breakdown glycogen. D-cells secrete somatostatin, which regulates

secretion insulin and glucagon. F-cells form a pancreatic polypeptide that inhibits secretion of water,

bicarbonates, enzymes in software.

7. Define chronic pancreatitis (CP). Etiology and pathogenesis.

CP is an inflammatory, progressive process in the software that is accompanied destruction of the tissue of the

gland and the gradual replacement of its connective tissue cloth. Etiological factors: alcohol abuse (mainly in

men), gallbladder and biliary tract diseases (mainly in women), eating with sharply restricted protein and fat,

single use alcohol and fatty foods, hyperparathyroidism, hyperlipidemia, chemical effects substances, drugs

(hypothiazide, furosemide, estrogens, sulfonamides, antibiotics, corticosteroids), hormonal and circulatory

disorders, uremia, infections, injuries, including postoperative surgery. Noted hereditary predisposition (more

often women suffer) and more frequent addiction disease in persons with blood group 0 (I). The main

pathogenetic mechanism for the development of CP is self-digestion as a result of activation of their own

proteolytic enzymes (trypsinogen, chymotrypsinogen, proelastases and phospholipase A), which causes the

development of edema, coagulation necrosis and tissue fibrosis. Soluble protein - calcium associates are

formed, which block intra-pancreatic ducts. The output of pancreatic enzymes in the blood leads to destructive

changes of organs and tissues (in the kidneys, lungs, central nervous system) and fat necrosis. Activation plays

an important role in the development of CP enzymes of pancreatic juice as a result of regurgitation into the

ducts of bile bile from the duodenum.

8. Classification of chronic pancreatitis (CP).

According to the Marseille - Roman classification, which is accepted in the European countries (1989),

distinguish the following forms of CP:

- chronic calcifying pancreatitis

- chronic obstructive pancreatitis

- chronic fibro-inducing pancreatitis

- chronic cysts and software pseudocysts.

9. What are the main clinical manifestations and complications of CP.

The clinical picture in most cases consists of an abdominal pain, indigestion, signs of diabetes. Abdominal pain

associated with the use of food or alcohol with localization in the left hypochondrium with irradiation in the

back, heart characterized by a "girdle" pain, eliminated by analgesics, antispasmodics. Manifestations external

secretory software failure is characterized by a violation digestive and absorption processes, the development of

excess microbial growth in the small intestine.

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 PANCREATITIS

Chronic pancreatitis is commonly defined as a continuing, chronic, inflammatory process of the pancreas,

characterized by irreversible morphologic changes. This chronic inflammation can lead to chronic

abdominal pain and/or impairment of endocrine and exocrine function of the pancreas. By definition,

chronic pancreatitis is a completely different process from acute pancreatitis. In acute pancreatitis, the

patient presents with acute and severe abdominal pain, nausea, and vomiting. The pancreas is acutely

inflamed (neutrophils and edema), and the serum levels of pancreatic enzymes (amylase and lipase) are

elevated. Full recovery is observed in most patients with acute pancreatitis, whereas in chronic pancreatitis,

the primary process is a chronic, irreversible inflammation (monocyte and lymphocyte) that leads to

fibrosis with calcification.

Epidemiology

In population studies, males are affected more commonly than females. Rates in males peak between ages

45 and 54 years and then decline; female rates reach a plateau, which remains stable after age 35 years. Alcohol-induced illness is more prevalent in males, idiopathic and hyperlipidemic-induced pancreatitis is

more prevalent in females, and equal sex ratios are observed in chronic pancreatitis associated with hereditary pancreatitis.

Etiology

Causes of chronic pancreatitis („TIGAR-O‟:)

Toxic-metabolic Alcohol

Tobacco Hypercalcaemia

Chronic renal failure

Idiopathic Tropical Early/late

onset types

GeneticHereditary pancreatitis (cationic trypsinogen mutation) SPINK-1 mutation

Cystic fibrosis

AutoimmuneIsolated or as part of multi-organ problem

Recurrent and severe acute pancreatitis Post-necroticRecurrent acute pancreatitis

ObstructiveDuctal adenocarcinoma Intraductal papillary mucinous neoplasia Pancreas divisum Sphincter of Oddi stenosis

Chronic pancreatitis occurs most often in patients with alcoholism (45–80% of all cases). The risk of chronic

pancreatitis increases with the duration and amount of alcohol consumed, but pancreatitis develops in only 5–

10% of heavy drinkers. Tobacco smoking is a risk factor for idiopathic chronic pancreatitis and has been

reported to accelerate progression of alcoholic chronic pancreatitis. About 2% of patients with

hyperparathyroidism develop pancreatitis. In tropical Africa and Asia, tropical pancreatitis, related in part to

malnutrition, is the most common cause of chronic pancreatitis. A stricture, stone, or tumor obstructing the

pancreas can lead to obstructive chronic pancreatitis. Autoimmune pancreatitis is associated with

hypergammaglobulinemia (IgG4 in particular) and often with autoantibodies and other autoimmune diseases

and is responsive to corticosteroids. Between 10% and 30% of cases of chronic pancreatitis are idiopathic, with

either early onset (median age 23) or late onset (median age 62). Genetic factors may predispose to chronic

pancreatitis in some of these cases and include mutations of the cystic fibrosis transmembrane conductance

regulator (CFTR) gene, the pancreatic secretory trypsin inhibitory gene (PSTI, serine protease inhibitor,

SPINK1), and possibly the gene for uridine 5-diphosphate glucuronosyltransferase.

Pathophysiology

The cause of chronic pancreatitis usually is metabolic in nature. The proposed pathologic mechanisms of chronic pancreatitis are as follows:

3. Intraductal plugging and obstruction - Eg, ethanol (ETOH) abuse, stones, tumors 4. Direct toxins and toxic metabolites - These act on the pancreatic acinar cell to stimulate the release of

cytokines, which stimulate the stellate cell to produce collagen and to establish fibrosis; cytokines also act to

stimulate inflammation by neutrophils, macrophages, and lymphocytes (eg, ETOH, tropical sprue) 5. Oxidative stress - Eg, idiopathic pancreatitis

6. Necrosis-fibrosis - Recurrent acute pancreatitis that heals with fibrosis 7. Ischemia - From obstruction and fibrosis; important in exacerbating or perpetuating disease rather than

in initiating disease 8. Autoimmune disorders - Chronic pancreatitis has been found in association with other autoimmune

diseases, such as Sjögren syndrome, primary biliary cirrhosis, and renal tubular acidosis. 9. Secondary forms of autoimmune chronic pancreatitis are associated with primary biliary cirrhosis,

primary sclerosing cholangitis, and Sjögren syndrome. 10. While alcohol greatly influences the understanding of its pathophysiology because it is the most

common etiology (60-70%), approximately 20-30% of cases are idiopathic and 10% of cases are due to rare diseases.

Whatever the etiology of chronic pancreatitis, pancreatic fibrogenesis appears to be a typical response to injury. This involves a complex interplay of growth factors, cytokines, and chemokines, leading to deposition of extracellular matrix and fibroblast proliferation. In pancreatic injury, local expression and release of transforming growth factor beta (TGF-beta) stimulates the growth of cells of mesenchymal origin and enhances the synthesis of extracellular matrix proteins, such as collagens, fibronectin, and proteoglycans.

Clinical presentation

Clinically, the patient experiences intermittent attacks of severe pain, often in the midabdomen or left upper

abdomen and occasionally radiating in a bandlike fashion or localized to the midback. The pain may occur

either after meals or independently of meals, but it is not fleeting or transient and tends to last at least several

hours. Unfortunately, patients often are symptomatic for years before the diagnosis is established; the average

time from the onset of symptoms until a diagnosis of chronic pancreatitis is 5 years. The delay in diagnosis is

even longer in people without alcoholism, in whom the average time is 7 years from onset of symptoms to

diagnosis. The natural history of pain in chronic pancreatitis is highly variable. Most patients experience intermittent

attacks of pain at unpredictable intervals, while a minority of patients experience chronic pain. In alcohol-induced disease, eventual cessation of alcohol intake may reduce the severity of pain. Pain is due to a combination of increased pressure within the pancreatic ducts and direct involvement of

pancreatic and peripancreatic nerves by the inflammatory process. Pain may be relieved by leaning forward.

Weight loss is common and results from a combination of anorexia, avoidance of food because of postprandial

pain, malabsorbtion and/or diabetes. Steatorrhea occurs when more than 90% of the exocrine tissue had been

destroyed; protein malabsorption only develops in the most advanced cases.

In most instances, the standard physical examination does not help to establish a diagnosis of chronic pancreatitis; however, a few points are noteworthy. During an attack, patients may assume a characteristic position in an attempt to relieve their abdominal pain (eg, lying on the left side, flexing the spine and drawing the knees up toward the chest). Occasionally, a tender fullness or mass may be palpated in the epigastrium, suggesting the presence of a

pseudocyst or an inflammatory mass in the abdomen. Patients with advanced disease (ie, patients with

steatorrhea) exhibit decreased subcutaneous fat, temporal wasting, sunken supraclavicular fossa, and other

physical signs of malnutrition.

Diagnosis

Tests to establish the diagnosisUltrasound CT (may show atrophy, calcification or ductal dilatation) Abdominal X-ray (may show calcification) Magnetic Resonance Cholangiopancreatography (MRCP) Endoscopic ultrasound

Tests of pancreatic functionCollection of pure pancreatic juice after secretin injection (gold standard but invasive and seldom used) Fecal pancreatic elastase

Tests of anatomy prior to surgeryMRCP

Blood tests Serum amylase and lipase levels may be slightly elevated in chronic pancreatitis; high levels are found only

during acute attacks of pancreatitis. In the later stages of chronic pancreatitis, atrophy of the pancreatic parenchyma can result in normal serum enzyme levels because of significant fibrosis of the pancreas, resulting

in decreased concentrations of these enzymes within the pancreas. While low concentrations of serum trypsin are relatively specific for advanced chronic pancreatitis, they are not

sensitive enough to be helpful in most patients with mild to moderate disease.

Laboratory studies to identify causative factors of chronic pancreatitis include serum calcium and triglyceride levels. When common etiologies are not found, research protocols are available to test for genetic mutations in cationic trypsinogen and CFTR. Fecal tests Because maldigestion and malabsorption do not occur until more than 90% of the pancreas has been destroyed, steatorrhea is a manifestation of advanced chronic pancreatitis. Neither qualitative nor quantitative fecal fat analysis can detect early disease. Assays of fecal chymotrypsin and human pancreatic elastase-1 have the same limitations but are useful in

confirming advanced chronic pancreatitis with exocrine insufficiency. These tests allow to determine or to rule out pancreatic exocrine insufficiency and its degree. The study of elastase-1 in stool allows to determine

pancreatic insufficiency of moderate and severe cases is 95-100%. Pancreatic Function Tests Direct tests These tests are the most sensitive and can be used to detect chronic pancreatitis at its earliest stage; however,

they are somewhat invasive, labor intensive, and expensive.

- Determination in duodenal aspirates- Determination in pancreatic juice Indirect testsNoninvasive tests of pancreatic function have been developed for detecting chronic pancreatitis. In principle,

these tests work via oral administration of a complex substance that is hydrolyzed by a specific pancreatic

enzyme to release a marker substance. The intestine absorbs the marker, which then is measured in the serum or

urine. These tests are capable of detecting moderate to severe chronic pancreatitis. The presence of renal,

intestinal, and liver disease may interfere with the accuracy of these tests.

Respiratory pancreatic tests: 13

C-triglyceride breath test - determines pancreatic lipase activity in the lumen of the intestine and can differentiate pancreatic steatorrhea from enteric steatorrhea.

Protein breath test with 13

C-marked egg white - reduced in case of CP - lack of trypsin.

Amylase (13

C-corn-starch) breath test – allows to detect deficiency of pancreatic amylase in duodenum (normal

– in the end of 4th hour - 10-30%). Neither currently is freely available.

Imaging Plain films show calcifications due to pancreaticolithiasis in 30% of affected patients. CT may show

calcifications not seen on plain films as well as ductal dilatation and heterogeneity or atrophy of the gland.

Occasionally, the findings raise suspicion of pancreatic cancer (“tumefactive chronic pancreatitis”). Endoscopic

retrograde cholangiopancreatography (ERCP) is the most sensitive imaging study for chronic pancreatitis and

may show dilated ducts, intraductal stones, strictures, or pseudocyst, but the results may be normal in patients

with so-called minimal change pancreatitis. MRCP (including secretin-enhanced MRCP) and endoscopic

ultrasonography (with pancreatic tissue sampling) are less invasive alternatives to ERCP.

Differential diagnosis

• Ampullary carcinoma

• Cholangitis

• Cholecystitis

• Chronic gastritis

• Crohn disease

• Mesenteric Artery Ischemia

• Myocardial infarction

• Pancreatic cancer

• Peptic ulcer disease

Complications

Pseudocysts and pancreatic ascites, which occur in both acute and chronic pancreatitis Extrahepatic obstructive jaundice due to a benign stricture of the common bile duct as it passes through the

diseased pancreas Duodenal stenosis Portal or splenic vein thrombosis leading to segmental portal hypertension and gastric varices Peptic ulcer

Diabetes mellitus

Treatment

No curative treatment for chronic pancreatitis exists. Medical therapy is determined primarily by symptoms. If no anatomic explanation for abdominal pain can be found, medical therapy can be attempted. This therapy

includes pain control with analgesic agents and a trial of noncoated pancreatic enzymes. The goals of medical treatment are as follows:

• Modify behaviors that may exacerbate the natural history of the disease

• Enable the pancreas to heal itself

• Determine the cause of abdominal pain and alleviate it

• Detect pancreatic exocrine insufficiency and restore digestion and absorption to normal

• Diagnose and treat endocrine insufficiency

Cessation of alcohol consumption and tobacco smoking are important. In early stage alcohol-induced chronic

pancreatitis, lasting pain relief can occur after abstinence from alcohol, but in advanced stages, abstinence does not always lead to symptomatic improvement. Patients continuing to abuse alcohol develop either marked

physical impairment or have a death rate 3 times higher than do patients who abstain.

A diet low in fat and high in protein and carbohydrates is recommended, especially in patients with steatorrhea.

The degree of restriction depends on the severity of fat malabsorption; generally, an intake of 20 g/day or less is

sufficient. Patients who continue to suffer from steatorrhea following fat restriction require medical therapy.

Malabsorption of the fat soluble vitamins (A, D, E, and K) and vitamin B-12 may also occur. Oral

supplementation of these enzymes is recommended.

Opioids should be avoided if possible. Preferred agents for pain are acetaminophen, nonsteroidal anti-

inflammatory drugs (naproxen, diclofenac, ketorolac, ibuprofen) and tramadol, along with pain-modifying

agents such as tricyclic antidepressants (amitriptyline hydrochloride), selective serotonin uptake inhibitors, and

gabapentin or pregabalin. Steatorrhea is treated with pancreatic supplements that are selected on the basis of

their high lipase activity. A total dose of 40,000 units of lipase in capsules is given with meals. Higher doses

may be required in some cases. The tablets should be taken at the start of, during, and at the end of a meal.

Concurrent administration of a H2-receptor antagonist (eg, ranitidine, 150 mg orally twice daily), a proton

pump inhibitor (eg, omeprazole, 20–60 mg orally daily), or sodium bicarbonate, 650 mg orally before and after

meals, decreases the inactivation of lipase by acid and may thereby further decrease steatorrhea. In selected

cases of alcoholic pancreatitis and in cystic fibrosis, enteric-coated microencapsulated preparations may offer an

advantage. However, in patients with cystic fibrosis, high-dose pancreatic enzyme therapy has been associated

with strictures of the ascending colon. Pain secondary to idiopathic chronic pancreatitis may be alleviated in

some cases by the use of pancreatic enzymes (not enteric-coated) or octreotide, 200 mcg subcutaneously three

times daily. Micronutrient therapy to correct electrophilic stress on key macromolecules in the pancreas by toxic

metabolites has shown promise in early studies.

Associated diabetes mellitus should be treated. Autoimmune pancreatitis is treated with prednisone 40 mg/d

orally for 1–2 months, followed by a taper of 5 mg every 2–4 weeks.

CHRONIC CHOLECYSTITIS

Cholecystitis is inflammation of the gallbladder that occurs most commonly because of an obstruction of the

cystic duct by gallstones arising from the gallbladder (cholelithiasis). Uncomplicated cholecystitis has an

excellent prognosis; the development of complications such as perforation or gangrene renders the prognosis

less favorable. Ninety percent of cases involve stones in the gallbladder (ie, calculous cholecystitis), with the

other 10% of cases representing acalculous cholecystitis.

Chronic inflammation of the gallbladder wall is almost always associated with the presence of gallstones and is

thought to result from repeated bouts of subacute or acute cholecys titis or from persistent mechanical

irritation of the gallbladder wall by gallstones. The presence of bacteria in the bile occurs in >25% of patients

with chronic cholecystitis (CC). The presence of infected bile in a patient with CC undergoing elective

cholecystectomy probably adds little to the operative risk. CC may be asymptomatic for years, may progress to

symptomatic gallbladder disease or to acute cholecystitis, or may present with complications.

Epidemiology

An estimated 10-20% of Americans have gallstones, and as many as one third of these people develop acute

cholecystitis. Cholecystectomy for either recurrent biliary colic or acute cholecystitis is the most common major

surgical procedure performed by general surgeons. The incidence of cholecystitis increases with age. Gallstones

are 2-3 times more frequent in females than in males, resulting in a higher incidence of calculous cholecystitis

in females. Elevated progesterone levels during pregnancy may cause biliary stasis, resulting in higher rates of

gallbladder disease in pregnant females. Acalculous cholecystitis is observed more often in elderly men.

Etiology Main etiological factor for persistent inflammation of gallbladder is opportunistic pathogenic infections (E.coli, coccal flora), sometimes – other microbial causes (Proteus, Pseudomonas aeruginosa, etc.). Bacteria can get to

gallbladder by contact path from the small intestine, or by hematogenic and lymphogenic path from any site of chronic inflammation.

Risk factors for calculous cholecystitis mirror those for cholelithiasis and include the following:

1. Female sex

2. Certain ethnic groups (people of Scandinavian descent, Pima Indians, and Hispanic populations)

3. Obesity or rapid weight loss

4. Drugs (especially hormonal therapy in women)

5. Pregnancy

Increasing age

Acalculous cholecystitis is related to conditions associated with biliary stasis, and include the following: - Critical illness

- Major surgery or severe trauma/burns

- Sepsis

- Long-term total parenteral nutrition (TPN)

- Prolonged fasting

2. Cardiac events, including myocardial infarction

3. Sickle cell disease

4. Salmonella infections

5. Diabetes mellitus

Patients with AIDS who have cytomegalovirus, cryptosporidiosis, or microsporidiosis

Patients who are immunocompromised are at an increased risk of developing cholecystitis from a number of different infectious sources. Idiopathic cases exist.

Pathophysiology Development of CC is gradual. Entry of microbial flora against a background of GB hypotonia causes catarrhal

inflammation of mucosa. Inflammation progresses to submucosa and muscular layer of GB, where it causes

infiltration and activation of connective tissue. These processes lead to deformation of gallbladder and

pericholecystitis development.

Calculous cholecystitis is caused by obstruction of the cystic duct, leading to distention of the gallbladder. As

the gallbladder becomes distended, blood flow and lymphatic drainage are compromised, leading to mucosal

ischemia and necrosis. Although the exact mechanism of acalculous cholecystitis is unclear, several theories

exist. Injury may be the result of retained concentrated bile, an extremely noxious substance. In the presence of

prolonged fasting, the gallbladder never receives a cholecystokinin (CCK) stimulus to empty; thus, the

concentrated bile remains stagnant in the lumen.

Clinical presentation

Chronic cholecystitis may be asymptomatic for years. Dull pain in right upper quadrant (RUQ) and epigastrium

and feeling of fullness may be present, can last for hours, increase after fatty, fried, spicy food, eggs, wine, beer.

Pain radiates to right scapula or shoulder. Upper abdominal tenderness may be present, but usually fever is not.

Fever suggests acute cholecystitis. However, subfebrile body temperature may be present. Once episodes begin,

they are likely to recur. Bitter taste in mouth sometimes is present in the morning. Nausea, belching, bloating

are often reported. Bowel movement disorders – alternation of constipations and diarrheas.

The absence of physical findings does not rule out the diagnosis of cholecystitis. Many patients present with

diffuse epigastric pain without localization to the RUQ. Patients with chronic cholecystitis frequently do not have a palpable RUQ mass secondary to fibrosis involving the gallbladder.

Diagnosis

1) Ultrasonography.

Ultrasonographic criteria of inflammation in gallbladder:

Thickness of wall of GB > 4 mm in the absence of liver and kidney pathology, and congestive heart failure; Increase of gallbladder size over 5 cm above the normal for the corresponding age;

Presence of sonographic Murphy's sign;

Presence of paracystic hypoechogenic limbus (edema of gallbladder wall).

2) Cholecystography.

The following symptoms are characteristic for patients with CC:

1) Absence of gallbladder shadow;

2) Derangements of concentration ability and motility of gallbladder (delayed emptying);

Deformation of gallbladder wall.

1) Duodenal intubation – can be conducted only if gallstones are absent! Helps to access motor function of gallbladder. Provides 3 portions of bile for further studying of bile characteristics: • Microscopy – signs of inflammation and lithogenicity of bile;

• Culture – determination of bacterial flora;

•Biochemical analysis – determination of cholesterol, bile acids, phospholipids in bile.

Treatment

Treatment of cholecystitis depends on the severity of the condition and the presence or absence of

complications. Uncomplicated cases can often be treated on an outpatient basis. Antibiotics may be

given to manage infection.

Treatment: phase of exacerbation.

Antibiotics. Indications for antibiotic therapy: presence of clinical and laboratory signs of inflammation, positive results of bile culture, cholangitis.

Ciprofloxacin 500 mg 2/d per os, course 5 days

Cefotaxime 1 g 2/d i/m Doxycycline 100 mg 2/d per os, course 5 days

Amoxicillin 500 mg 3-4/d

Tinidazole 4 pills per os once (if Lamblia is a causative agent) Symptomatic therapy: Prokinetic agents – domperidone 10 mg or itoprid 50 mg 3/d 30 min prior to meals

Spasmolytics: mebeverine 200 mg 2/d, course 3-4 weeks

drotaverine (No-Spa) 40 mg 3/d before meals

papaverine hydrochloride 2% - 2,0 i/m

Bile-expelling medications (cholagogues): Preparations that stimulate cholepoietic function of liver (choleretics):

Preparations of bile acids: cholenzym, liobilum

Synthetic preparations: oxaphenamide, cyclovalone

Preparations of herbal origin: strawflower extract, peppermint extract, corn stigmas

Preparations that improve secretion of bile by increasing of its aqueous component (hydrocholeretics) – mineral waters Preparations that stimulate biliary excretion:

- Cholekinetics (inrease tonus of GB and decrease tonus of bile ducts): xylite, sorbite, magnesium sulfate - Cholespasmolytics: anticholinergic drugs, aminophylline.

3. UDCA – 8-10 mg/kg/day (if microlites and/or stagnation of bile are present);

4. Herbal hepatoprotectors with bile-expelling properties. Treatment: phase of remission. Diet – meals 5-6 times a day, exclude fatty, fried, spicy, smoked food, pickles,

alcohol. Phytotherapy. Mineral water. Physiotherapy. Exercise therapy.

4. Self-control materials:

4.1. Tests for self-control.

4.2. Tasks for self-control on the topic: "Pancreatitis. Cholecystitis. Cholelithiasis. Clinic. Diagnosis.

Treatment".

4.1. Tests for self-control on the topic: "Pancreatitis. Cholecystitis. Cholelithiasis. Clinic. Diagnosis.

Treatment".

1. Acute pancreatitis is most likely confirms: a) urine amylase b) blood glucose c) coagulogram d) urine sediment e) blood test 2.For the treatment of chronic cholecystitis used: a) Inderal, Nitroglycerin

b) novokainamid, izoptyn

c) almagel, ranytydin

d) alochol, nospanum

e) sulfokamfokayin, kordiamin

3. Changes in the oral mucosa in chronic pancreatitis seen as a result of: a) secondary vitamin deficiencies

b) violation of metabolism c) dysproteinemia d) hyperglycemia e) hypoglycemia 4. What is the main laboratory parameters in the diagnosis of exacerbation of chronic pancreatitis: a) hyperglycemia b) aminotransferase levels c) leukocytosis d) phosphatase level meadow e) amylase blood and urine 5. Ultrasound signs of cholecystitis include: a) increasing consolidation and spleen b) sealing the capsule of the pancreas, it outlines inequality c) consolidation of the gallbladder wall d) the presence of inclusions with acoustic shadow in the renal pelvis e) significant increase in liver size 6. For the treatment of exacerbation of cholelithiasis and "hepatic colic" is used: a) antacids, proton pump inhibitors b) hepatoprotectors, enzymes c) cardioprotectors, calcium antagonists d) antispasmodics, is needed - surgery e) hinidine drugs, nitrates 7. At what disease "fatty feces" are determined? a) cholecystitis b) hepatitis c) pancreatitis d) colitis e) gastritis 8. The main pathogenetic mechanisms of acute pancreatitis: a) microbial aggression b) coagulopathy c) nautoimmune aggression d) activation of enzymes, followed by autolysis of the pancreatic tissue e) decrease of venous outflow of pancreas 9. The main direction of pathogenetic therapy of acute pancreatitis: a) reduction of exocrine pancreatic function b) fight infection c) correction fluid and salt balance d) fight with hypovolemia e) prevention of pulmonary complications 10. In acute cholelithiasis and "hepatic colic" pain often irradiating to: a) the left arm, jaw b) in the left iliac area

c) under the left shoulder d) the right shoulder e) the lumbar and inguinal area

4.2. Tasks for self-control on the topic: "Pancreatitis. Cholecystitis. Cholelithiasis. Clinic. Diagnosis.

Treatment".

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.

The patient turned to the doctor with complaints about abdominal pain, nausea, heaviness in the epigastrium,

diarrhea. Feeling acutely, after eating acrid foods, alcoholic beverages, overeating. When looking at the oral

cavity, there is a lack of 6 teeth, common caries. The tongue is covered with a grayish-white patch; the tongue

nipples are smoothed. What illness can be assumed in a patient?

A) chronic cholecystitis;

B) alimentary gastritis;

C) peptic ulcer disease;

D) alcoholic cirrhosis of the liver;

TASK 4.

The patient appealed to the doctor with complaints of pain in the right subcostal area, nausea, bitterness in the

mouth. He suffers from chronic cholecystitis for about two years, the condition has worsened after consuming

fatty food, psycho-emotional stress. On examination, oral patient has a yellowish coating on the tongue,

palpation - pain at the point of the gallbladder, positive symptoms Ortner, Kerala. What illness can be assumed

in a patient?

A) chronic hepatitis;

B) cholelithiasis;

C) alimentary gastritis;

D) chronic cholecystitis;

TASK 5.

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 6.

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;

4.3. Practical Tasks:

1. Supervise patients with chronic pancreatitis.

2. Interprete the obtained laboratory data. 3. Interprete the obtained data of instrumental study. 4. Write a prescription for the chronic pancreatitis treatment

5. To perform physical examination of patient with biliary tract diseases.

6. To interpret the received data of laboratory tests.

7. To interpret the received data of instrumental tests.

8. To write recipes for the treatment of GD.

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.