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

a)formation of bronchopleural fistula;

b)prolonged atelectasis of the

lung;

c)dysplasia of the pulmonary epithelium;

d)destruction of the lung tissue with the formation of largescale sequestration;

e)elevated levels of electrolytes in the blood.

54. In case of total atelectasis of one lung it is recommended to carry out:

a)puncture of the pleural cavity;

b)videothoracoscopy;

c)bronchoscopy with tracheobronchial pathways sanation;

d)adequate antibiotic therapy;

e)respiratory hypoxia treat-

ment.

1. The following clinicomorphological forms of acute appendicitis are distinguished except:

a)superficial (catarrhal);

b)phlegmonous;

c)gangrenous;

d)empyema of the appendix;

e)serous-indurative.

2. Primary changes in acute appendicitis are revealed:

a)in the mucosa;

b)in the serous layer (visceral peritoneum);

c)in the plexus of the muscular layer;

d)in the Bauhin’s valve;

e)in the vessels of the mesen-

tery.

3.In the pathogenesis of acute appendicitis the following mechanisms are distinguished except:

a)obstruction of the lumen and development of stagnant contents;

b)enterogenous initiation against the background of local immune resistance disorders;

c)development of vascular response accompanied by a prolonged reflex spasm;

d)activation of microcirculation in the wall of the appendix;

e)decrease in pressure within the lumen of less than 85 mm Hg.

4.The main clinical syndromes of acute appendicitis are:

a)painful;

b)toxicoallergic;

c)pseudo-peritoneal;

d)peritonial;

e)inflammatory.

5.The main features of the pain syndrome in acute appendicitis are:

a)constant increase in intensity up to pain shock;

b)double-phase character causing epigastric and visceral phase of pain;

c)triple-phase character causing the development of the phase of “imaginary well-being”;

d)pain which is spasmodic in character and arrested by spasmolytics;

e)pain appearing only in case of perforation.

6.The migrating character of the pain syndrome from epigastrium to the right iliac region is called:

a)Kummel;

b)Volkovich-Koher;

c)Sitkovsky;

d)Bartomier-Michelson;

e)Stchetkin-Blumberg.

7.Varieties of the anatomical location of the appendix are all except:

a)pelvic;

b)retrocecal;

c)medial;

d)lateral;

e)subdiaphragmatic.

8.Characteristic features of the inflammatory syndrome in acute appendicitis are as follows:

a)tachycardia in case of high (hectic) temperature;

b)severe tachycardia in case of subfebrile temperature;

c)severe leukocytosis (more than 20x1000 / l) with a shift of white blood count to the “left”;

d)moderate leukocytosis (up to 12–15x1000 / l) with a shift of white blood count to the “left”;

e)the temperature in the rectum exceeding that in the armpit by more than 1 °C.

9.The main objective manifestations of acute appendicitis are:

a)symptom of Hippocrates;

b)symptom of StchetkinBlumberg;

c)local tenderness and muscular defense in the right iliac region;

d)symptom of “shirt” (Voskresensky’s symptom);

e)Rovsing’s symptom.

10.The main features of the clinical picture of acute appendicitis in the elderly are:

a)absence of marked epigastric phase;

b)development of dynamic obstruction;

c)moderate leukocytosis with a shift to the left even in case of destruction;

d)prevalence of general intoxication symptoms;

e)decreased muscular defense intensity.

11.Specific features of the clinical picture of acute appendicitis in the last trimester of pregnancy are:

a)displacement of localization (upward and laterally) of the appendix;

b)rapid development of destructive forms;

c)increased pain on examination in the left lateral decubitus;

d)increased pain on examination in the ventral decubitus or right lateral decubitus;

e)slow growth of the inflammatory syndrome.

12.In case of typical localization of the appendix the following surgical access is applied:

a)Koher-Fedorov;

b)Lenander;

c)lower-middle (inferomedia) laparotomy;

d)McBurney (Volkovich-Koher);

e)Pirogov’s extraperitoneal.

13.The main features of typical appendectomy are all except:

a)isolation of the appendix;

b)exteriorization of the appendix into the wound;

c)bandaging the mesentery of the appendix at the base;

d)electrocoagulation or clipping of mesentery vessels;

e)ligature method of treatment of the appendix.

14.The intraoperative complications of typical appendectomy are all except:

a)bleeding;

b)damage to the abdominal cavity organs;

c)infection of the abdominal cavity;

d)eventration development;

e)acute adhesive intestinal obstruction.

15.Complications of the postoperative period after appendectomy include:

a)seroma or haematoma of the postoperative wound;

b)eventration;

c)secondary early or late (delayed) bleeding;

d)infiltrate and abscess of the abdominal cavity;

e)acute adhesive intestinal obstruction.

16.Specific features of periappendicular infiltrate are all except:

a)forms of localized peritoni-

tis;

b)it is formed after 3–5 days from the onset of the disease;

c)it is formed after 7–14 days from the onset of the disease;

d)the main tactics in case of the diagnosed process without abscess formation is conservative;

e)the main tactics in case of the diagnosed process without

abscess formation is emergency appendectomy.

17.After the involution of periappendicular infiltrate planned appendectomy is performed:

a)3 weeks after discharge from hospital;

b)in 1 year;

c)in 3 months;

d)is not performed;

e)only in the presence of the clinical picture of acute appendicitis.

18.Appendicular abscess is characterized by everything except:

a)sharp tenderness over the projection of the expanding borders of theinfiltrate;

b)local symptoms of irritation of the peritoneum;

c)signs of softening of the infiltrate;

d)appearance of fluctuation signs of the palpable infiltrate;

e)unassisted resolution of endogenous intoxication signs.

19.The confirmed diagnosis of appendicular abscess is an indication for:

a)planned operation;

b)continuation of conservative treatment;

c)emergency surgery;

d)delayed surgical interven-

tion;

e)surgery in case of the development of diffuse peritonitis.

20.The appendicular abscess is opened by:

a)McBurney’s (VolkovichKocher’s) access;

b)inferomedian laparotomic access;

c)Lenander’s access;

d)extraperitoneal Pirogov’s access;

e)lumbotomic on the right.

21.The diagnosis of appendicular abscess is clarified on the basis of:

a)ultrasound of the ileac region;

b)local liquid-crystal thermog-

raphy;

c)hemogram showing increased intoxication indices;

d)rectal examination;

e)irrigoscopy with double filling.

22.Pelvic abscess after appendectomy is a consequence of:

a)suppuration of intraperitoneal hematoma;

b)suppuration of the postoperative wound;

c)suppuration of a localized accumulation of uneliminated exudate;

d)insufficiency of the stitches of the appendicular stump;

e)eventration of the postoperative wound.

23.The optimal opening of the pelvic abscess after appendectomy is:

a)inferomedian access;

b)extraperitoneal access according to Pirogov;

c)McBurney’s (VolkovichKocher) access;

d)Lenander’s access;

e)access through the front wall of the rectum (posterior vaginal vault).

24.Everything is typical of appendicular infiltration except:

1.Cholelithiasis is characterized by all features except:

a)abnormal amount of cholesterol, lecithin and bile acids;

b)impairment of water-salt metabolism;

c)formation of stones in the bile ducts;

d)impairment of purine metabolism;

e)formation of stones in the intrahepatic bile ducts.

2.There are the following forms of uncomplicated cholelithiasis:

a)residual;

b)latent;

c)acute calculous cholecysti-

tis;

d)hepatic colic;

e)chronic calculous cholecys-

titis.

3.The clinical course of uncomplicated cholelithiasis has the following forms:

a)acute calculous cholecysti-

tis;

b)chronic calculous cholecys-

titis;

c)empyema and edema of the gallbladder;

d)Mirizzi’s syndrome;

e)choledocholithiasis.

4.The contributing factors for the development of cholelithiasis include all except:

a)hereditary type of obesity and hyperglyceridemia;

b)previous vagotomies and by-pass operations on the small intestine;

c)history of hemolytic jaundice;

d)female gender and changes in hormonal status;

e)alcohol abuse.

5.The predisposing factors for the development of cholelithiasis in women are:

a)actinomycosis;

b)pregnancy and childbirth;

c)changes in hormonal status;

d)taking contraceptive estrogenic drugs;

e)sedentary lifestyle and obe-

sity.

6.Factors of genetic predisposition to the development of cholelithiasis include:

a)hereditary type of obesity and hypercholesterolemia;

b)hereditary defect characterized by a decrease in the activity of enzymes involved in the synthesis of bile acids;

c)presence of positive antigens A3 and B14 of the HLA complex;

d)hereditary increase in mucosassociated lymphoid tissue (MALT) of the digestive system;

e)hereditary increase in hepatic cell receptors accompanied by hypersecretion of cholesterol.

7.In the pathogenesis of gallstones the following main factors are distinguished:

a)decreased perfusion pressure in the tissues of the gallbladder, less than 30 mm Hg;

b)increased bile lithogenicity;

c)activation of the mechanisms of primary nuclei formation of cholesterol crystallization;

d)reduction of the contractility of the gallbladder;

e)increased tonus of the gallbladder.

8.Increased lithogenesis of bile in the course of cholelithiasis is caused by all the factors except:

a)cholesterol in the bile in the form of micelles (bile acids);

b)increase in the concentration of biliary phospholipids (lecithin);

c)decrease in the concentration of biliary phospholipids (lecithin);

d)increase in the concentration of bile acids;

e)decrease in the cholesterol concentration.

9.Reduction of the contractility of the gallbladder in cholelithiasis is caused by:

a)decrease in the reabsorption of sodium and water;

b)decrease in bile concentra-

tion;

c)activation of reabsorption of water and sodium salts;

d)more than 10 times increase in bile concentration;

e)alkaline pH in the gallblad-

der.

10.Characteristic features of hepatic colic are all except:

a)the pain syndrome is provoked by the ingestion of fatty foods and is controlled by antispasmodics;

b)cramp-like pains associated with stretching or contraction of the gallbladder wall;

c)characteristic pain irradiation to the right shoulder or under the scapula;

d)accompanying severe inflammatory syndrome;

e)absence of inflammatory syndrome.

11.Chronic calculous cholecystitis is manifested by:

a)repeated attacks of hepatic

colic;

b)accompanying moderate inflammatory syndrome;

c)absence of inflammatory syndrome;

d)wall thickening of more than 3 mm and a “double contour” according to the ultrasound findings;

e)absence of acute inflammation according to the ultrasound findings: thickening of the wall under 3 mm, no double contour or obturation.

12.Acute calculous cholecystitis is manifested by:

a)an attack of intractable hepatic colic lasting for 4–6 hours;

b)presence of local protective muscular tension and tenderness in the right hypochondrium;

c)presence of local protective muscular tension and tenderness all over the anterior abdominal wall;

d)accompanying pronounced inflammatory syndrome;

e)ultrasound readings of acute inflammation of the gallbladder: thickening of the wall of more than 3 mm and an increase in volume of more than 150 ml.

13.In patients of senile age with severe concomitant pathology the methods used for the treatment of uncomplicated forms of cholelithiasis are as follows:

a)dynamic observation;

b)cholelitholysotherapy;

c)percutaneous transrenal methyl tert-butyl lysis;

d)extracorporal lithotripsy;

e)urgent cholecystectomy.

14.The development of acute acalculous cholecystitis is caused by:

a)obturation of the excretory duct and gall bladder with mucus or parasites;

b)atherothrombosis of the cystic artery;

c)secondary enzyme effects on the mucosa;

d)blockage of outflow due to hypertrophy of perivesical lymph nodes;

e)obturation of the common bile duct (choledochus).

15.A characteristic feature of the chemical structure of GB cholesterol stones is:

a)the cholesterol content is more than 50%;

b)stones are lighter than bile and float on the surface;

c)rounded shape and smooth surface;

d)absence of radioopacity;

e)stones are dissolvable under certain conditions.

16.A characteristic feature of the chemical structure of GB pigmentary stones is:

a)presence of various bilirubin salts, evenly distributed per stone volume;

b)presence of various bilirubin salts distributed in the form of cells;

c)predominance of black and brown forms, depending on the severity of bile infection;

d)stones are lighter than bile and float on the surface;

e)stones are heavier than bile.

17.A characteristic feature of the chemical structure of calcium stones is:

a)up to 20–40% content of calcium carbonate salts;

b)more than 50% content of calcium carbonate salts;

c)stones are heavier than bile;

d)crystalline form of stones;

e)radioopaque stones.

18.By the nature of morphological changes the following forms of acute calculous cholecystitis are distinguished:

a)superficial;

b)catarrhal;

c)phlegmonic;

d)gangrenous;

e)primary chronic.

19.The diseases contributing to the development of acute acalculous cholecystitis include:

a)hypomotor dyskinesia of the bile ducts;

b)stem vagotomy in the past history;

c)duodenostasis;

d)diabetes;

e)atherosclerosis of peripheral branches of the celiac trunk.

20.The main types of complications of acute calculous cholecystitis include everything except:

a)perforation of the wall;

b)perivesical infiltration;

c)empyema and edema of the gallbladder;

d)purulent cholangitis;

e)perforated ulcer of the gastroduodenal area.

21.The main microflora favoring inflammation of the gallbladder wall in acute calculous cholecystitis is:

a)aerobic gram-positive bacteria;

b)aerobic gram-negative bacteria;

c)aerobic gram-positive cocci;

d)anaerobic clostridial bacteria;

e)nonclostridial anaerobes.

22.The main way of penetration (entry) of microflora into the gallbladder in acute cholecystitis is:

a)contact with the peritoneum;

b)hematogenous;

c)postoperative;

d)lymphogenous;

e)enterogenic.

23.Ultrasound readings confirming acute calculous cholecystitis are all except:

a)decrease in linear size and volume of the gallbladder;

b)more than 4 mm thickening of the wall of the bladder;

c)up to 1.5–2 mm thickening of the wall of the bladder;

d)a 4-layer wall contour;

e)a 2-layer wall contour.

24.Specific signs of acute cholecystitis are:

a)Murphy’s sign;

b)Ortner-Grekov’s sign;

c)Kerr’s sign;

d)Volkovitch-Kocher’s sign;

e)Mussi-Georgievsky’s sign.

25.Emergency surgery for acute calculous calcite is recommended in case of:

a)accompanying diffuse peritonitis;

b)resolution of acute process;

c)accompanying mechanical jaundice;

d)no effect of conservative therapy during 48–72 hours;

e)development of edema of the gallbladder.

26.Planned surgical treatment in acute calculous cholecystitis is recommended in case of:

a)3 months after the resolution of acute inflammation;

b)the first 3 weeks after the resolution of the acute process;

c)mechanical jaundice;

d)accompanying cholangitis;

e)accompanying acute pancrea-

titis.

27.The appearance of destruction in the gallbladder in acute cholecystitis is characterized by:

a)increased pain in the right upper quadrant;

b)decrease in the intensity of pain in the right hypochondrium;

c)Grekov-Ortner’s sign;

d)local signs of irritation of the peritoneum;

e)increasing inflammatory syndrome.

28.Highly informative methods for the diagnosis of acute calculous cholecystitis include:

a)X-ray of the stomach with barium suspension;

b)endoscopic retrograde pancreaticocholangiography;

c)videolaparoscopy;

d)ultrasound of the abdominal cavity;

e)magnetic resonance imaging.

29.Videolaparoscopic findings of acute cholecystitis are all except:

a)shrunken and reduced gallbladder;

b)enlarged and tense gallblad-

der;

c)fibrin overlays on the wall of the gallbladder and turbid effusion along the right lateral canal;

d)signs of inflammation (infiltration) of the surrounding tissues;

e)stagnant, “Muscat” type of

liver.

30.The main surgical method used for treating acute calculous cholecystitis is:

a)cholecystostomy;

b)external drainage of the bile

ducts;

c)cholecystectomy;

d)diagnostic videolaparoscopy with biopsy and drainage of the abdominal cavity;

e)cholecystectomy and formation of biliodigestive anastomoses.

31.Methods of intraoperative diagnosis of the bile ducts pathology include all except:

a)intraoperative examination and palpation of bile ducts;

b)intraoperative cholangiography;

c)videocholangioscopy;

d)instrumental revision by the Dollyoti bougies;

e)selective celiacography.

32.The main cause of choledocholithiasis is:

a)migration of stones from the gallbladder to choledochus;

b)obturation of the cervix of the gallbladder with a concrement;

c)development of Mirrizi’s syndrom (internal fistula between GB and the common bile duct or duodenum);

d)undiagnosed bile duct stones after previous interventions;

e)chronic calcifying pancreati-

tis.

33.Choledocholithiasis is clinically manifested by:

a)choledocholitic colic;

b)mechanical jaundice;

c)purulent cholangitis;

d)severe duodenal obstruction;

e)reflux-esophagitis.

34.Complications of choledocholithiasis include all except:

a)biliary pancreatitis;

b)stenosis of the major duodenal papillum and terminal section of the choledchus;

c)gastroesophageal reflux dis-

ease;

d)cholangiogenic liver abscesses;

e)cholangiogenic sepsis.

35.Methods applied for endoscopic treatment of choledocholithiasis include:

a)papillosphincterotomy;

b)extraction of stones using Dormia’s basket;

c)extraction of stones using balloon Fogarty catheter;

d)contact laser or shock wave lithotripsy;

e)intraluminal methyl-tert- butyl choledocholysis.

36.After choledocholithotomy the operation can be finished with:

a)the blind suturing of the choledochus;

b)suturing of choledochus with simultaneous external drainage;

c)formation of bioliodigestive anastomosis;

d)transduodenal papillosphincteroplastics;

e)installation of a catheter for methyl tert-butyl choledocholysis.

37.Mechanical (obturational) jaundice is characterized by all symptoms except:

a)skin itching;

b)yellowish skin, sclera and mucous membranes;

c)fecal discoloration;

d)spleen dilatation;

e)absence of itching.

38.Benign diseases causing the development of mechanical jaundice include:

a)choledocholithiasis with the insertion of a stone into the major duodenal papillum;

b)pseudotumorous pancreatitis;

c)scar stricture of the bile

ducts;

d)marked nonspecific pericholangial lymphadenitis;

e)primary sclerosing cholangi-

tis.

39.Malignant diseases causing the development of mechanical jaundice include:

a)shrunken gallbladder;