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

a)stimulation of exocrine function;

b)inflammation of perineural sympathetic fibers;

c)stenosis of the major duodenal papilla;

d)secondary duodenal obstruc-

tion;

e)endoand exocrine insufficiency.

8.According to the clinical classification the following forms of chronic pancreatitis are distinguished:

a)chronic calcifying;

b)chronic obstructive;

c)chronic retentional;

d)chronic fibro-indurative;

e)chronic cysts and pseudo-

cysts.

9.The following forms of chronic pancreatitis are distinguished by the nature of the morphological changes:

a)regional;

b)parenchymatous;

c)ductal (retentional);

d)fibrous calculous;

e)pseudotumorous.

10.The following types of complications of chronic pancreatitis are distinguished, except:

a)mechanical jaundice;

b)duodenal obstruction;

c)pseudocysts;

d)internal and external fistula;

e)ulcerative colitis.

11.The clinical picture of chronic pancreatitis includes the following varieties of its course with:

a)recurrent or continuous pain syndrome;

b) predominance of exoand endocrine insufficiency;

c) mechanical (obstructive) jaundice and duodenosis;

d)formation of cysts;

e)development of pancreatic fistulas.

12.Characteristic features of the clinical course of recurrent pain syndrome in chronic pancreatitis are:

a)lack of connection with the secretory activity of the pancreas;

b)the presence of connection with increased secretion of the pancreas and intraductal pressure;

c)connection with the intake of fatty foods or alcohol;

d)sitophobia (fear of eating);

e)absence of direct correlation with the severity of morphological changes.

13.Secondary endocrine insufficiency in chronic pancreatitis is manifested by:

a)increased tolerance to glu-

cose;

b)malabsorption disorders;

c)flatulence;

d)steatorrhea;

e)secondary latent diabetes mellitus.

14.Pancreatic cysts of large sizes are clinically manifested by:

a)cramping pain in the abdo-

men;

b)permanent, increasing pain syndrome;

c)the presence of a palpable smooth elastic formation (lump) in the epigastrium;

d)secondary duodenostasis and mechanical jaundice;

e)subfebrile temperature and inflammatory syndrome in case of suppuration development.

15.Complications of large pancreatic cysts are all except:

a)suppuration;

b)bleeding into the cavity;

c)metastasis to distant organs;

d)spontaneous perforation into the abdominal cavity;

e)development of hematogenous infection.

16.To assess the exocrine function of the pancreas in chronic pancreatitis, we apply everything except:

a)stimulating tests with secretin;

b)inhibitory test with methacin;

c)oral pancreatolaurin test;

d)Shilling’s dual radioisotope

test;

e)coprological analysis.

17.To assess the endocrine function of the pancreas in chronic pancreatitis, we apply:

a)Shilling’s dual radioisotope

test;

b)determination of blood glu-

cose;

c)determination of the level of glycated hemoglobin;

d)determination of the activity of proteolytic and lipolytic enzymes of the pancreas;

e)test for glucose tolerance.

18.The main areas of conservative treatment in the uncomplicated course of chronic pancreatitis are:

a)elimination of pain syndrome;

b)elimination of spasm of the sphincter of the major duodenal papilla;

c)correction of exocrine and endocrine insufficiency;

d)the use of choleretic drugs and pepsin;

e)nutritional therapy.

19.Indications for surgical treatment of chronic pancreatitis are all except:

a)complications of large cysts;

b)virsungolithiasis and ductal hypertension;

c)suspected malignant tissue transformation;

d)prolonged failure to control the pain syndrome with drugs;

e)high secretory activity of the pancreas.

20.The following groups of surgical interventions are distinguished for chronic pancreatitis:

a)performed on the autonomic nervous system;

b)eliminating the causes contributing to the development of the disease;

c)correcting endocrine insufficiency;

d)correcting exocrine insufficiency;

e)eliminating hypertension in the ductal pancreatic system.

21.The operations on the autonomic nervous system in chronic pancreatitis include:

a)cholecystectomy with the formation of biliodigestive anastomoses;

b)transduodenal papillosphincterotomy;

c)resection of the abnormal areas of the pancreas;

d)longitudinal pancreaticojejunostomy;

e)resection of celiac ganglia and nerves (sympatosplahectomy).

22.Operations aimed at eliminating the causes of chronic pancreatitis include:

a)resection of celiac ganglia and nerves (sympatosplahectomy);

b)cholecystectomy with the formation of biliodigestive anastomoses;

c)transduodenal papillovirusungoplastics;

d)longitudinal pancreaticojejunostomy;

e)resection of abnormal areas of the pancreas.

23.The operations aimed at the elimination of hypertension in the duct system in case of chronic pancreatitis include:

a)longitudinal pancreaticojejunostomy;

b)resection of the altered tissue of the head of the pancreas with preservation of duodenum;

c)cholecystectomy with the formation of biliodigestive anastomoses;

d)pancreatoduodenal resection;

e)caudal (distal) resection of the pancreas.

24.In pseudotumorous chronic pancreatitis with the involvement of the head the operations of choice are:

with preservation of duodenum and the formation of pancreaticojejunostomy;

d)pancreatoduodenal resec-

tion;

e)caudal (distal) resection of the pancreas.

25.Pancreatic cysts are divided into:

a)latent;

b)congenital;

c)acquired;

d)true;

e)false (pseudocysts).

26.Acquired pancreatic cysts depending on the causes of their formation are divided into:

a)degenerative;

b)ossifying;

c)proliferative;

d)retentional;

e)parasitic.

27.Specific features of true pancreatic cysts are:

a)the absence of epithelial lin-

ing;

b)the presence of epithelial

lining;

c)represented by cystadenoma in case of acquired character and retentional origin;

d)the consequence of previous inflammatory-degenerative processes;

e)more often congenital in na-

ture.

c)absence of epithelial lining inside;

d)absence of a formed wall;

e)presence of necrotic tissues with an increased amount of amylase.

29.Clinically uncomplicated large pancreatic cysts are characterized by everything except:

a)duodenostasis;

b)gastrostasis;

c)colonic (large intestine) obstruction;

d)mechanical jaundice;

e)sepsis and septic shock.

30.Complications of large pancreatic cysts are:

a)suppuration of the contents;

b)rupture into the abdominal cavity with the development of peritonitis;

c)hemorrhage into the cavity;

d)erosive reflux esophagitis;

e)formation of external and internal fistulas.

31.Among the instrumental methods for diagnosing pancreatic cysts everything is important, except for:

a)multispiral CT with intravenous contrast;

b)mesentericography;

c)identification of oncomarkers – PSA and osfetoprotein;

d)identification of tumor (onco) markers (CA 19-9 and CEA);

e)double balloon enterography.

32.There are the following groups of surgical interventions in case of the formed pancreatic cysts:

a)resectional with the removal of the portion of the altered tissue with the cyst;

b)eliminating the contributing causes;

c)traditionally draining;

d)minimally invasive draining;

e)radiovascular.

33.The traditional draining interventions used in case of the formed pancreatic cysts include:

a)resection of the pancreatic tissue with the cyst;

b)formation of anastomoses between the cyst and the loop of the jejunum, stomach or duodenum;

c)marsupilization of the cyst;

d)selective angiography with vascular embolization;

e)internal drainage with the installation of internal endoprostheses (stents).

34.Minimally invasive drainage interventions used in the formation of the pancreatic cysts include:

a)resection of the pancreatic tissue with the cyst;

b)formation of anastomoses between the cyst and the loop of the jejunum, stomach or duodenum;

c)percutaneous drainage;

d)transpapillary (through the major duodenal papilla) drainage;

e)transgastric (transduodenal) internal drainage with the installation of endoprostheses (stents).

35.In unformed cysts of the pancreas (less than 5–6 cm in diameter), the optimal method of the treatment is:

a)dynamic observation;

b)endoscopic methods of drainage with the installation of endoprostheses (stents);

c)laparotomy with internal drainage interventions;

d)laparotomy with marsupilization (external drainage);

e)percutaneous puncture under ultrasound control.

36.The external drainage (marsupilization) in case of false cysts of

the pancreas is performed when there is:

a)development of the subhepatic form of portal hypertension;

b)suspected malignancy;

c)development of duodenosta-

sis;

d)bleeding into the cyst cavity;

e)abscess formations of the contents.

1. There are the following types of chronic pylori-duodenal ulcers (according to Johnson):

a)the body of the stomach (mesogastric);

b)symptomatic;

c)combined stomach and duodenum;

d)pre-pyloric;

e)cardiac.

2.The main pathogenetic mechanisms for the development of gastric ulcers include everything except:

a)reverse diffusion of hydrogen ions from the lumen into the wall of the stomach;

b)reduction in the production of protective gastric factors;

c)prevalence of the intestinal phase of acid formation;

d)atrophy of the glands of the stomach body;

e)gastroesophageal reflux dis-

ease.

3.The main pathogenetic mechanisms for the development of combined ulcers of the stomach and duodenum are:

a)deformation of the pyloricbulbar area;

b)secondary insufficiency of the pylorus;

c)prevalence of the intestinal phase of acid formation;

d)reverse diffusion of hydrogen ions along the small curvature of the stomach;

e)long-term use of nonsteroidal anti-inflammatory drugs or glucocorticoids.

4.The main pathogenetic mechanisms for the development of prepyloric ulcers of the stomach include the following except:

a)long-term use of nonsteroidal anti-inflammatory drugs or glucocorticoids;

b)reverse diffusion of hydrogen ions along the small curvature of the stomach;

c)high acid-forming activity of gastric secretion;

d)Gastroesophageal reflux dis-

ease;

e)reduction of the production of local protective mechanisms.

5.According to the size gastroduodenal ulcers are divided into:

a)tiny (up to 0.5 cm);

b)medium (0.5–1 cm);

c)small (up to 1 cm);

d)large (2–3 cm);

e)giant (more than 3 cm).

6.According to the localization gastroduodenal ulcers are divided into those involving:

a)cardiac area;

b)sub-cardiac area;

c)body or angle of the stom-

ach;

d)antral area;

e)pyloric canal.

7.Complications of gastroduodenal ulcers include everything except:

a)perforation;

b)penetration;

c)malignancy;

d)gastroduodenitis;

e)acute gastroduodenal hemorrhages.

8.The main types of gastroduodenal motor disorders in peptic ulcer disease are:

a)duodenogastric reflux;

b)dysfunction of the bile duct or gastroesophageal valve;

c)acceleration of the peristalsis and tone of the pylorus;

d)asynchronous contractions;

e)decreased peristalsis and

tone.

9.Predisposing (genetically determined) factors of peptic ulcer disease include everything except:

a)excess number of major and gastrin-producing cells;

b)absence of antigens responsible for the production of glycoproteins of gastric mucus;

c)inheritance of a special type of pepsinogen;

d)the first (O (I)) blood group;

e)increase in the activity of α1-antitrypsin.

10.Causative factors for the development of peptic ulcer disease include everything except:

a)alimentary (digestive) disor-

ders;

b)long-term use of nonsteroidal anti-inflammatory drugs or glucocorticoids;

c)reduction in the production of protective gastroduodenal factors;

d)presence of persistent Helicobacter pylori infection;

e)excess number of major, oxyntic and gastrin-producing cells.

11.Factors of local gastroduodenal aggression contributing to the development of ulcers are the fol-

lowing except:

a)excess synthesis of hydrochloric acid and pepsin;

b)reverse diffusion of hydrogen ions from the lumen of the stomach intothe wall;

c)disorders of secretory and motor activity;

d)presence of excessive amounts of bile acids and lysolecithin in the lumen of the duodenum;

e)increased production of mucosal prostaglandins.

12.Prolonged helicobacter infection is accompanied by a damaging effect on the gastroduodenal mucosa by means of:

a)direct aggressive effect of enzymes (urease, protease, phospholipase);

b)enhanced secretion of hydrochloric acid;

c)desquamation of protective layer of epithelial cells;

d)production of cytotoxic protein (CadA) and polypeptide (p 130) leading to the iflammation of the mucosa;

e)activation of microcirculation in the stomach wall.

13.Morphological signs of chronic gastroduodenal ulcer are the following except:

a)progressive sclerosis of the

edges;

b)insufficiency of granulation and fibrous tissue in the center;

c)occurrence of secondary destruction (necrosis) in the center;

d)spread of the pathologic process to the serous coat or beyond it;

e)rapid regeneration of the defect within 3–4 weeks.

14.Malignant chronic ulcer (early gastric cancer) is characterized by the following features:

a)all layers of the stomach are damaged;

b)spread within the mucosalsubmucosal layer;

c)the presence of metastases in closely located peripheral lymph nodes;

d)the absence of metastases in closely located peripheral lymph nodes;

e)high percentage of cure after timely surgical treatment.

15.For early detection of malignancy signs of chronic gastroduodenal ulcers the following procedures are used except:

a)chromogastroscopy;

b)narrow spectral double-cavi- ty endoscopy;

c)laser-scanning endoscopy;

d)endoscopic coherent tomog-

raphy;

e)computer electrogastroenteromyography.

16.Indications for emergency surgical treatment of peptic ulcer are the following except:

a)perforation of ulcers;

b)profuse gastroduodenal blee-

ding;

c)lack of funds for regular drug treatment;

d)decompensated pyloric-duo- denal stenosis;

e)malignancy confirmed by the biopsy.

17.The arbitrary-absolute indications for surgical treatment of peptic ulcer include:

a)compensated pyloric-duode- nal stenosis with evacuation disturbances;

b)callous or penetrating ulcers with the absence of the therapeutic effect within 3 months;

c)callous or penetrating ulcers with the absence of the therapeutic effect within 4–6 months;

d)a combination of gastric and duodenal ulcer with a high acidproducing function;

e)recurrent gastroduodenal bleeding in the presence of recurrence factors.

18.The operations of choice for the treatment of complicated gastric and duodenal ulcer are:

a)gastro-duodenotomy with the excision of ulcerative defect;

b)selective proximal vagotomy with gastric drainage operations;

c)distal resection of 2 / 3 of the stomach;

d)selective vagotomy with antrumectomy;

e)formation of gastro-jejuno- anastomosis.

19.In perforation of gastroduodenal ulcers the following clinical periods are distinguished:

a)latent (painless);

b)neuro-reflex disorders (pain shock);

c)development of irreversible disorders;

d)“imaginary well-being”;

e)diffuse peritonitis.

20.Predisposing factors of perforation of gastroduodenal ulcers are the following except:

a)previous exacerbation of the process with the wall destruction;

b)sharp intra-abdominal pressure increase after physical exertion;

c)excessive mental stress;

d)long-term use of glucocorti-

coids;

e)auto-activation of trypsinogen and kinin.

21.The clinical picture of typical perforated gastroduodenal ulcer is characterized by:

a)acute pain in the whole abdomen due to the absence of muscle defensiveness;

b)“stabbing pain” in the upper abdomen;

c)“wooden” muscles of the anterior abdominal wall;

d)disappearance of hepatic dullness during examination;

e)positive symptoms of irritation of the peritoneum.

22.The course of the “imaginary well-being” period in perforated gastroduodenal ulcer is characterized by:

a)intensification of pain manifestations;

b)reduction of symptoms of endogenous intoxication;

c)reduction of pain manifesta-

tions;

d)increase in endogenous intoxication symptoms;

e)increase in dynamic intestinal obstruction phenomena.

23.The duration of the “imaginary well-being” period after perforation of gastroduodenal ulcers is:

a)up to 12 hours;

b)up to 6–8 hours;

c)up to 20–24 hours;

d)over 24 hours;

e)up to 2 hours.

24.The period of diffuse peritonitis after perforation of gastroduodenal ulcers occurs within:

a)6–8 hours;

b)12–16 hours;

c)16–24 hours;

d)72 hours;

e)8–12 hours.

25.The main instrumental methods for diagnosing perforated gastroduodenal ulcers are the following except:

a)pneumogastrography;

b)esophagogastroduodenos-

copy;

c)radiography of the abdominal cavity;

d)videolaparoscopy;

e)gastro-electromyography.

26.Localizations of gastroduodenal ulcers that cause the development of atypical perforations are the following except:

a)cardiac portion of the stomach;

b)posterior wall of the duode-

num;

c)posterior wall of the stom-

ach;

d)anterior wall of the stomach or duodenum;

e)anterior wall of the stomach or duodenum against the background of the existing adhesions.

27.Clinical manifestations of atypical perforations of gastroduodenal ulcers are:

a)pronounced pain syndrome with clear localization;

b)moderate pain syndrome without clear localization;

c)unexpressed muscular de-

fense;

d)decreased duration of the “imaginary well-being” period;

e)increased duration of the “imaginary well-being” period.

28.Palliative interventions performed in case of perforated gastroduodenal ulcers include:

a)suturing of the perforation;

b)excision of the edges of ulcerous perforated defect with transverse suturing;

c)stypage (tamponade) of the perforation with a strand of greater omentum;

d)pyloric-antrumectomy with stem vagotomy;

e)distal resection of 2 / 3 of the stomach body.

29.Radical interventions performed in perforation of gastroduodenal ulcers include:

a)videolaparoscopic suturing of the perforation;

b)various types of distal resections of the stomach;

c)perforation suturing in combination with vagotomy (stem, selective proximal, combined);

d)excision of perforated ulcer with pyloric (duodenum) plasty and vagotomy;

e)pyloroantrumectomy in combination with stem vagotomy.

30.Radical interventions in combination with vagotomy in perforated gastroduodenal ulcers are indicated in case of:

a)callous meso-gastric ulcers of the stomach;

b)decompensated pyloric-duo- denal stenosis;

c)combination of duodenal and stomach ulcers;

d)presence of duodenal stasis;

e)deficiency of the closing function of the pyloric pulp.

31.Factors contributing to the development of acute gastroduodenal hemorrhage include:

a)presence of chronic callous

ulcer;

b)localization of ulcers in the region of small curvature or the posterior wall of the duodenum;

c)low acid-producing activity due to the increase in local protective mechanisms;

d)high acid-producing activity due to the reduction in local protective mechanisms;

e)chronic persistence of Helicobacter pylori infection.

32.Local causes of gastroduodenal bleeding include:

a)progression of ulcerative de- structive-inflammatory process;

b)exposure of the vessels of the bottom of the ulcerative defect;

c)active granulation and epithelization of the ulcer niche;

d)rupture of vessels in the region of ulcer edges;

e)aneurysmal dilatation of ulcer vessels (towering above the bottom).

33.Concomitant pathological processes that contribute to the development of acute gastroduodenal bleeding include the following except:

a)dishormonal disorders;

b)long-term use of glucocorti-

coids;

c)extensive burns;

d)massive blood loss;

e)hereditary-genetic predispo-

sition.

34.Adaptive reactions of the body to acute gastroduodenal bleeding (up to 20% of GCB) is characterized by the following except:

a)closure of nonfunctional ar- terio-venous shunts;

b)venous deposition of GCB;

c)centralization of blood circulation;

d)auto-hemodilution;