Хирургические болезни. Практикум = Surgical diseases. Practice book. Учебное пособие

b)malignant tumors of extrahepatic bile ducts;

c)malignant tumors of the head of the pancreas;

d)malignant tumors of the large duodenal papilla;

e)gallbladder cancer.

40.The main laboratory signs of mechanical jaundice are all except:

a)hyperbilirubinemia due to direct fraction;

b)hyperbilirubinemia due to indirect fraction;

c)increased level of alkaline phosphatase;

d)absence of bile pigments in

urine;

e)stercobilin in the feces.

41.For instrumental diagnostics of mechanical jaundice all methods are applied except:

a)ultrasound of the abdominal cavity;

b)endoscopic retrograde cholangiopancreatography;

c)MR-cholangiography;

d)double balloon enteroscopy;

e)irrigoscopy.

42.The main objectives of treatment of mechanical jaundice are:

a)relief of spasm of Oddi’s sphincter;

b)restoration of bile outflow;

c)elimination of biliary hypertension;

d)elimination of the main cause of the process;

e)prevention of choledocholithiasis.

43.The operations aimed at decompression of the bile ducts in case of mechanical jaundice include:

a)cholecystectomy;

b)percutaneous transhepatic cholecystostomy;

c)percutaneous transhepatic cholangiostomy;

d)endoscopic papillosphincterotomy with nasobiliary drainage of the bile ducts;

e)pancreatosequestrectomy.

44.Minimally invasive interventions in patients with mechanical jaundice and decompensated concomitant pathology include:

a)formation of biliodigestive anastomoses;

b)resection of bile ducts with tumor and formation of choledochojejunoanastomosis;

c)percutaneous transhepatic cholecystostomy;

d)endoscopic papillosphincterotomy with nasobiliary drainage;

e)endoscopic duodenobiliary prosthesis.

45.Biliodigestive interventions for mechanical jaundice contributing to the recovery of bile outflow include:

a)choledochoduodenostomy;

b)choledocho-(hepatico)-jeju- nostomy;

c)gastrocholecystostomy;

d)cholecystoenterostomy;

e)external drainage of the bile

ducts.

46.The main causes of the development of bacterial (purulent) cholangitis are all except:

a)choledocholithiasis;

b)cicatricial strictures of the bile ducts;

c)stenosis of the major duodenal papillum;

d)thrombosis of splenic and portal veins;

e)virsungolithiasis.

47.Charcot’s triad in case of purulent cholangitis is characterized by:

a)pain syndrome in the right hypochondrium;

b)absence of pain syndrome;

c)progressive mechanical jaundice;

d)hyperthermia with chills and sweating;

e)arterial hypotension.

48.Reynold’s pentad in purulent cholangitis is characterized by:

a)impaired consciousness;

b)hyperthermia with chills and sweating;

c)arterial hypotension;

d)increasing mechanical jaun-

dice;

e)pain in the right hypochondrium.

49.The main causes of secondary cicatricial strictures of bile ducts are:

a)purulent cholangitis;

b)choledocholithiasis;

c)spread of inflammation from nearby organs;

d)postoperative damage to the

ducts;

e)cardioesophageal reflux dis-

ease.

50.Early clinical manifestations of cicatricial strictures of bile ducts are:

a)mechanical jaundice;

b)cholangitis;

c)arterial hypotension;

d)achlorhydria;

e)developing external biliary fistula.

51.Courvoisier’s sign is defined as:

a)pain syndrome with rapidly progressive mechanical jaundice;

b)a pain-free form with gradually progressive mechanical jaundice;

c)shrunken gallbladder;

d)painful infiltration in the projection of the gallbladder;

e)enlarged palpable painless gallbladder.

52.Methods of intraoperative diagnosis of strictures of the bile ducts include:

a)intravenous cholangiography;

b)videocholangoscopy;

c)debitocholangiomanometry;

d)intraoperative cholangiography;

e)selective celiacography.

53.Biliodigestive interventions used for long strictures of the bile ducts include all except:

a)choledochoduodenostomy;

b)hepaticojejunostomy;

c)hemihepatectomy;

d)transduodenal biliary prosthetics;

e)transduodenal papillosphincteroplastics.

1.Acute pancreatitis is characterized by everything below except:

a)acute primary-aseptic process in the pancreas;

b)primary destructive-purulent process in the pancreas;

c)auto-enzymatic necrobiotic changes and intracellular activation of enzymes with autolysis of acini;

d)development of secondary endogenous infection;

e)subsequent involvement of the tissues of the retroperitoneal space.

2.The main etiological factors in the development of acute pancre-

atitis are all below except:

a)diseases of extrahepatic biliary tract;

b)diseases of the duodenum and the major duodenal papilla;

c)alimentary-toxic factors;

d)acute and chronic microcirculatory disorders;

e)diseases of the rectum and paracola tissue.

3.The main diseases of biliary tract that cause the development of acute pancreatitis are:

a)choledocholithiasis;

b)acute calculous cholecystitis;

c)diverticula of choledochus and major duodenal papilla;

d)penetrating ulcer of the duodenum;

e)constant spasm of Oddi sphincter.

4.Acute biliary pancreatitis is most frequently revealed:

a)in men over 80 years;

b)in men aged 30–50 years;

c)in women aged 25–40 years;

d)in women aged 50–60 years;

e)in teenagers or children.

5.Acute pancreatitis due to ali- mentary-toxic factors is most frequently detected:

a)in women before 30–40 years;

b)in women older than 50 years;

c)in men over 60;

d)in men aged 35–50 years;

e)in adolescents.

6.To activate trypsinogen in the development of acute pancreatitis of greatest importance is the following:

a)intracellular increase in the concentration of calcium ions;

b)triggering the production of intracellular cytokinase by pancreatocytes;

c)inhibition of cytokinase production by pancreatocytes;

d)edema of the gland, accompanied by acidosis and hypoxia of the acini;

e)edema of the gland against the background of alkalosis.

7.The main pathological mechanisms of activated trypsin formation which contributes to the development of acute pancreatitis are:

a)activation of kallikrein-kinin system;

b)activation of pancreatic enzymes;

c)inhibition of the synthesis of pancreatic enzymes;

d)inhibition of kinin synthesis;

e)development of platelet activation factor.

8.Trypsin activated pancreatic enzymes in case of acute pancreatitis are caused by everything except:

a)proteolysis of protein substances;

b)destruction of the walls of vessels and interstitial connective tissue structures;

c)destruction of cell membranes;

d)hydrolysis of intracellular triglycerides to fatty acids;

e)inhibition of plasmin, thrombin systems and cytokinogenesis.

9.The main mechanisms of action of activated pancreatic enzymes in case of acute pancreatitis are:

a)general effect on pancreatic tissue through the blood system;

b)local effect on pancreatic tissue and parapancreatic tissue;

c)effect on the activation of cytokinogenesis;

d)activation of synthesis of acute phase proteins by the liver;

e)enzyme toxemia.

10.The 3rd-order aggression factors in case of acute pancreatitis include:

a)activated trypsin, phospholipase, elastase and carboxypeptidase;

b)pathogenic kinins;

c)producers of activation of plasmin and thrombin systems;

d)proteins of the acute phase of inflammation;

e)proinflammatory and antiinflammatory cellular mediators.

11.The most frequent microbial pathogens of purulent-septic complications of acute pancreatitis are:

a)escherichia coli;

b)enterobacteria and strepto-

cocci;

c)pseudomonas aeruginosa and staphylococci;

d)anaerobic nonclostridial microfl ora;

e)noncandidous mucotic (fungal) infection.

12.Edematous (interstitial) form of acute pancreatitis is characterized by:

a)extensive hemorrhages and hemorrhagic impregnation of tissues;

b)the appearance of multiple foci of steatonecrosis and hemorrhages;

c)parapancreatic infiltration of gland tissue and closely located organs;

d)single small focal areas of sterile tissue necrosis;

e)purulent diffuse impregnation of pancreatic tissue and retroperitoneal tissue.

13.There are the following types of infected necrosis of the pancreas and the surrounding tissue in acute pancreatitis, except:

a)the right-sided retroperitoneal phlegmon;

b)the central type phlegmon with the involvement of the mes-

entery of the transverse and small intestine;

c)the left-sided phlegmon with the involvement of the tail of the gland, colon and peripheral tissue on the left;

d)total retroperitoneal phleg-

mon;

e)acute fluid formations (pseudocysts).

14.According to the modern classification (Atlanta, USA, 1992), the following forms of acute pancreatitis are distinguished:

a)edematous;

b)sterile (aseptic) pancreatic necrosis;

c)pseudocysts;

d)infected pancreatic necrosis;

e)pancreatogenic abscesses.

15.The period of formation of necrosis in acute pancreatitis lasts:

a)from 3–5 days to 2 weeks;

b)more than 14 days;

c)the first 24–36 hours due to intense exudation into the abdominal cavity;

d)36–48 hours due to thrombosis and the formation of a coagulated hematoma;

e)over 1.5 months due to the appearance of pseudocysts or fistulous pancreas.

16.The phase of sequestration in acute necrotizing pancreatitis lasts:

a)up to 36–48 hours;

b)more than 14 days;

c)3–5 days to 2 weeks;

d)more than 1.5–2 months;

e)more than 3–6 months.

17.Purulent-septic complications of acute pancreatitis include all, except:

a)arrosive late bleeding;

b)pancreatogenic abscess;

c)enzymatic peritonitis;

d)mechanical jaundice;

e)infected pseudocysts.

18.Pain syndrome in acute pancreatitis is caused by:

a)mediated reflex disorders;

b)stretching the capsule of the gland due to swelling;

c)intoxication;

d)hypertension inside the

ducts;

e)repeated vomiting.

19.The main characteristic features of pain syndrome in acute pancreatitis are:

a)intensive permanent character contributing to the development of pancreatogenic shock;

b)appearance after drinking alcohol or eating fatty food;

c)encircling character;

d)relief with analgesics and antispasmodics within 24 hours;

e)lack of effect from the administration of analgesics and antispasmodics.

20.The peculiarities of the onset of peritoneal syndrome in different periods of acute pancreatitis include:

a)appearance of aseptic fermentative transsudate within 24–

48hours;

b)occurrence of purulent exudate during the first 24–48 hours;

c)occurrence of purulent exudate on the 4th–7th day due to the development of enterogenous infection;

d)appearance of purulent exudate on the 14th–30th day due to the development of purulent-septic complications;

e)appearance of aseptic fermentative transsudate within 7–20 days.

21.The positive symptom of Voskresensky in acute pancreatitis is interpreted as:

a)increasing pain syndrome when the patient’s position changes;

b)bloating in the epigastric

area;

c)detection of painful transverse resistance of the muscles of the anterior abdominal wall 6–7 cm above the navel;

d)occurrence of multiple petechial hemorrhages in the navel;

e)disappearance of pulsation of the abdominal aorta due to parapancreatic infiltrate.

22.The positive symptom of Korte in acute pancreatitis is regarded as:

a)occurrence of cyanosis of the face;

b)detection of painful transverse resistance of the muscles of the anterior abdominal wall 6–7 cm above the navel;

c)disappearance of pulsations of the abdominal aorta due to parapancreatic infiltrate;

d)growing pain on palpation in the area of the gallbladder projection;

e)reflex interruption of the patient’s breath on palpation of the right hypochondrium.

23.The positive symptom of Mayo-Robson in acute pancreatitis is regarded as:

a)disappearance of pulsation of the abdominal aorta due to parapancreatic infiltrate;

b)detection of painful transverse resistance of the muscles of the anterior abdominal wall 6–7 cm above the navel;

c)appearance of yellowishcyanotic spots around the navel;

d)appearance of tenderness in the area projected to the left ribiliac angle;

e)gradual shift of pain from epigastric to the right iliac area.

24.Parapancreatic infiltrate in acute pancreatitis is characterized by everything below except:

a)appearance within the period of 3 to 14 days;

b)is caused by focal necrosis of pancreatic tissue;

c)represents a conglomerate of enlarged pancreas and the surrounding organs;

d)is a form of suppurative omentobursitis;

e)is the outcome of the previous aseptic fermentative peritonitis.

25.With the development of puru- lent-septic complications of acute pancreatitis the following is revealed except:

a)symptoms of softening and fluctuation of parapancreatic infiltrate;

b)appearance of pastosity in the lumbar areas;

c)the hectic nature of the temperature with chills and increased sweating;

d)appearance of hematuria;

e)arterial hypotension.

26.Informative laboratory indicators that confirm the diagnosis of acute pancreatitis are all except:

a)reduced levels of trypsin, elastase, phospholipase against the background of increased levels of trypsin inhibitor;

b)increased level of pancreatic

lipase;

c)reduced levels of trypsin inhibitors (α1-antitrypsin, α2-macro- globulin);

d)increased levels of trypsin, elastase and phospholipase;

e)increased levels of general proteolytic activity of blood serum.

27.The following laboratory findings indicate pancreatogenic destruction in acute pancreatitis:

a)increased levels of transaminidase, elastase and methem-albu- min;

b)hypocalcemia and increased levels of procalcitonin and C-reac- tive protein;

c)hypoalbuminemia and persistent hyperglycemia;

d)hypercalcemia and a decreased level of procalcitonin;

e)hypoamylasemia.

28.Instrumental methods of diagnosing acute pancreatitis include everything except:

a)ultrasound examination of the abdominal cavity organs;

b)fibrogastroduodenoscopy;

c)videolaparoscopy;

d)irrigoscopy;

e)CT – with contrast enhancement (angio-CT).

29.The videolaparoscopic signs of acute pancreatitis include everything except:

a)“glass” edema of tissue;

b)stearin plaques and fatty ne-

crosis;

c)hemorrhagic tissue inhibition;

d)purple-black sections of the swollen loops of the small intestine;

e)tension of the gallbladder wall.

30.The methods that help suppress the exocrine function of the pancreas in the treatment of acute pancreatitis include:

a)invasive or artificial external hypothermia;

b)administration of synthetic somatostatin analogues;

c)administration of cytostatics and ribonuclease;

d)administration of protease inhibitors;

e)administration of fat emulsions with heparin.

31.Absolute indications for surgical treatment for acute pancreatitis are all except:

a)presence of pancreatogenic abscesses;

b)concomitant destructive cholecystitis;

c)septic phlegmon of retroperitoneal tissue;

d)purulent peritonitis;

e)virsungolithiasis.

32.Minimally invasive interventions performed in acute pancreatitis include:

a)videolaparoscopic sanation and drainage of the abdominal cavity in fermentative peritonitis;

b)percutaneous puncture of infected pseudocysts and abscesses;

c)mini-access operations using special equipment;

d)left-sided lumbotomy with drainage of retroperitoneal space;

e)laparotomy, pancreato-necro- sequestrectomy with the formation of external omentopancreatobursostoma.

33.Indications for the surgical treatment of acute pancreatitis in the stage of purulent-septic complications include everything except:

a)removal of necrotic tissues;

b)removal of infected peritoneal exudate;

c)reduction of hypertension in the pancreatic duct;

d)providing regional lavage and adequate outflow of the contents;

e)internal drainage by the formation of pancreatojejunoanastomosis.

34.The main types of regimes for repeated operations in acute pancreatitis in the phase of purulentseptic complications are:

a)planned sanation of the destruction zones within 48–72 hours;

b)relaparotomy for draining the pancreatic duct;

c)relaparotomy “on demand” due to developed complications;

d)recurrent percutaneous sanation puncture interventions due to the occurrence of common complications;

e)planned interventions for long-term complications.

35.“Closed” drainage interventions in the phase of purulent-sep- tic complications of acute pancreatitis include:

a)active drainage and aspiration under conditions of restoring the anatomical integrity of the omental bursa and abdominal cavity;

b)the use of videolaparoscopic techniques for the formation of omentopancreatobursostoma;

c)percutaneous drainage of limited cystic fluid formations and ulcers under ultrasound control;

d)necrosequestrectomy with the introduction of gauze drainage;

e)videolaparoscopic sanation and drainage of the abdominal cavity.

36.The “semi-open” draining operations in the phase of purulentseptic complications of acute pancreatitis include all except:

a)videolaparoscopic sanation and drainage of the abdominal cavity;

b)interventions with the creation of active drainage and aspiration under conditions of restoring the anatomical integrity of the omental bursa and abdominal cavity;

c)percutaneous drainage of limited abscesses under ultrasound control;

d)videolaparoscopic interventions with the formation of omepopancreatobursostoma;

e)laparotomy or lumbotomy followed by necrectomy and gauze swabs.

37.Toxic complications of acute pancreatitis include:

a)toxic megacolon;

b)pancreatogenic shock;

c)exudative pleurisy;

d)toxic dystrophy of the liver and kidneys;

e)pancreatogenic encephalopathy.

38.Postnecrotic complications of acute pancreatitis include:

a)formation of postnecrotic

cysts;

b)parapancreatic infiltrate;

c)pancreatogenic shock;

d)purulent omentobursitis;

e)thrombosis of the branches of the portal vein.

1.Chronic pancreatitis is characterized by everything except:

a)chronic inflammatory degenerative dystrophic process in the pancreatic tissue;

b)chronic destructive purulent lesion of the pancreatic tissue;

c)obstruction of the pancreatic ducts with proliferative fibrosis and tissue calcification;

d)atrophy of the acini with impaired exoand endocrine function of the pancreas;

e)purulent fusion of the tissue of retroperitoneal space.

2.The main etiological factors in the development of chronic pancreatitis are all, except:

a)chronic alcoholism;

b)congenital or acquired diseases of the biliary tract, leading to the development of complications;

c)autoimmune diseases, accompanied by fibrotic sclerotic processes;

d)hereditarily defects in the secretion of trypsinogen;

e)direct damage to the tissue of the pancreas.

3.The most important exogenous factors contributing to the development of chronic pancreatitis include:

a)protein deficiency or prevalence of protein food;

b)a long term use of glucocorticoids, cytostatics or estrogens;

c)lack of food antioxidant substances (zinc, copper, selenium);

d)a viral infection which the patient suffered;

e)cystic fibrosis, hyperparathyroidism, chronic renal failure in the medical history.

4.The fibro-sclerotic autoimmune processes contributing to the development of chronic pancreatitis include:

a)primary sclerosing cholangitis;

b)systemic scleroderma;

c)systemic atherosclerosis;

d)autoimmune thyroiditis;

e)cystic fibrosis of the pancreas.

5.The most important mechanisms of the pathogenesis of chronic pancreatitis include all, except:

a)protein precipitation and occlusion of the acini;

b)development of local autocatalytic processes of trypsinogen activation;

c)the presence of specific granulomas in the tissue;

d)progressive intraductal hypertension;

e)deposits of calcium salts and ossificates in the tissue.

6.Activation of trypsinogen and enzymes in chronic pancreatitis is accompanied by:

a)autodigestion of tissue;

b)intraductal hypertension;

c)autosensibilization;

d)inflammatory fibrous degener-

ation;

e)atrophy and depletion of inhibitors.

7.Intraductal hypertension and tissue ossification in chronic pancreatitis is accompanied by: