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

tion or compression of the loop and mesosigmoid from the outside similar to strangulation;

b)the main mechanism of the development is trauma of the peritoneum mesothelium;

c)the main mechanism of the development is trauma of the vascular endothelium and the epithelium of the intestinal mucosa;

d)active proliferation of fibroblasts predominates leading to a rapid maturation of the granulation tissue;

e)prevalence of a delayed type of scar formation with partial lysis (substitution).

44.The factors contributing to the development of adhesive intestinal obstruction are all except:

a)abrupt changes in the food regimen;

b)leaving foreign bodies (drains or tampons) inside the abdominal cavity for a long time;

c)inadequate intraoperative hemostasis;

d)instant sharp physical exertion;

e)excessive intestinal stimulation with drugs.

45.Early adhesive intestinal obstruction develops after operations within:

a)5–7 days;

b)30 days;

c)the first three days;

d)45–60 days;

e)14 days.

46.Surgical intervention in adhesive intestinal obstruction can be completed by:

a)colliotomy and naso-intesti- nal intubation;

b)resection of the necrotized part of the intestine with the formation of primary anastomosis;

c)formation of a bypass between the efferent and afferent loops of intestines in a large adhesive mass;

d)subtotal resection of the small intestine in case of a large adhesive mass;

e)surgery with the proximal enterostomy.

47.For the prevention of adhesion recurrence, surgery for adhesive intestinal obstruction is completed by intraoperative administration of:

a)the solution of rheopolyglucin with fibrinolytics and glucocorticoids;

b)highly concentrated solutions of antibiotics or alcohols;

c)cytostatics;

d)biodegradable films (such as Lintex-Mesogel);

e)resorbable collagen repair patches (ColGara).

1.The main features of widespread peritonitis are all except:

a)acute nonspecific inflammation of the peritoneum;

b)acute specific inflammation of the peritoneum;

c)due to various causes or injuries of the abdominal cavity;

d)accompanied by disturbances of the vital functions of the most important organs and systems;

e)a form of local intraabdominal infection.

2.Factors causing the similarity of widespread peritonitis (in the phase of multi-organ failure) and abdominal sepsis are:

a)identical polymicrobial initiating factors;

b)accompanying bacterial in-

testinal translocation;

c)multiple foci of endogenous intoxication;

d)high lethality;

e)the possibility of treatment by both conservative and operational methods.

3.The concept of “intraabdominal infection” typically includes all features except:

a)widespread peritonitis and local abdominal abscesses;

b)the presence of widespread peritonitis in the stage of sepsis only;

c)combination of various pathological processes of the abdominal cavity taking into account a uniform etiopathogenesis;

d)pathological processes of the abdominal cavity having a significant difference in clinical, diagnostic and therapeutic approaches;

e)various pathological processes of the abdominal cavity associated with general principles in clinical, diagnostic and therapeutic approaches.

4.Phases of the course (stages) of peritonitis (K.S. Simonyan, 1971) include all except:

a)reactive;

b)latent;

c)toxic;

d)multiorgan failure;

e)reparative.

5.The forms of local peritonitis are:

a)ascites-peritonitis;

b)delimited peritonitis;

c)multifocal peritonitis;

d)toxic peritonitis;

e)nondelimited peritonitis.

6.The forms of widespread peritonitis include all except:

a)nondelimited;

b)diffuse;

c)general;

d)enzymatic;

e)fecal.

7.In terms of pathogenesis, the following types of widespread peritonitis are distinguished:

a)fecal;

b)primary;

c)secondary;

d)postoperative;

e)tertiary.

8.The development of primary widespread peritonitis is caused by all factors except:

a)extraperitoneal infection;

b)absence of hematogenous, lymphogenic or contact routes of infection;

c)diplococcal inflammation in children;

d)systemic collagens in chil-

dren;

e)presence of specific forms.

9.Secondary widespread peritonitis is caused by:

a)extraperitoneal ingestion of pathogens;

b)primary failure of the body protection against infection;

c)inadequate sanation of the abdominal cavity and accompanying bacterial intestinal translocation;

d)inflammatory destructive processes in the organs of the abdominal cavity;

e)injuries or perforation of the abdominal cavity.

10.Development of tertiary widespread peritonitis is caused by all factors except:

a)improper primary sanation of the abdominal cavity;

b)emergence of new foci of infection in the course of treatment;

c)activation of the process associated with decreased immunoreactivity;

d)failure of the sutures of hollow organs, including failure of “holding” intestinal sutures;

e)inflammatory destructive processes or abdominal injuries.

11.In terms of severity of clinical (septic) manifestations, the following forms of widespread peritonitis are distinguished:

a)toxic;

b)without the signs of sepsis;

c)with severe sepsis;

d)with septic shock;

e)persistent.

12.Toxic stage of widespread peritonitis is characterized by:

a)activation of general and local adaptation reactions;

b)accompanying multiple organ failure;

c)enteral failure with the sequestration of water, toxins, hydrolysis products and electrolytes in the lumen of the small intestine;

d)accompanying the phenomenon of bacterial intestinal translocation;

e)increase in hypoxia, impairment of microcirculation of the peritoneum, small intestine paresis.

13.The terminal stage of a widespread peritonitis is characterized by all features except:

a)accompanying multiple foci of intoxication;

b)accompanying bacterial intestinal translocation;

c)activation of general and local adaptation mechanisms;

d)increasing failure of organs and systems;

e)weakness of anti-infection protection of the body associated with uncontrolled release of proinflammatory mediators.

14.The clinical course of the reactive stage of widespread peritonitis is characterized by:

a)primary localization of the pain syndrome in the projection of the primary destructive focus;

b)diffuse nature of the pain all over the anterior surface of the ab-

dominal wall, beginning with the first hours of the disease;

c)pronounced muscular defense in the region of focus localization and then along the way of the transudate spreading;

d)nausea and vomiting of reflex character;

e)toxic activation of peristalsis and defecation.

15.The clinical course of the stage of multiple organ failure with advanced peritonitis is characterized by:

a)metabolic alkalosis, persistent arterial hypertension associated with persistent bradycardia;

b)acidosis, lactatemia and hy-

poxia;

c)persistent arterial hypotension against tachycardia and tachypnea;

d)dynamic intestinal obstruction associated with an unpronounced defense of the anterior abdominal wall;

e)absence of CNS impairment

signs.

16.Indirect radiographic signs suggesting the widespread peritonitis in the stage of intoxication include all except:

a)pneumatosis and intestinal paresis;

b)dilatation of intestinal loops;

c)multiple Kloiber’s cups and intestinal arcades;

d)presence of pneumoperitoneum under the right dome of the diaphragm;

e)depressions or filling defects along the inner contour of the colon.

17.The ultrasound signs of widespread peritonitis in the stage of intoxication include:

a)multiple Kloiber’s cups and intestinal arcades;

b)intestinal loops stretched and dilated by gas and liquid;

c)exudate accumulation in all parts of the abdominal cavity;

d)increase in intestinal peristalsis in the absence of pneumotosis;

e)low-density areas revealed in the pancreatic tissue or infiltration of parapancreatic mass.

18.Video laparoscopic signs of widespread peritonitis include:

a)presence of purulent exudate or intestinal contents in the abdominal cavity;

b)dilatation of intestinal loops;

c)identification of foci of primary destruction;

d)fibrin deposition on the peritoneum and internal organs;

e)Kloiber’s cups and intestinal arcades.

19.Preoperative preparation in advanced peritonitis is performed for the following groups of patients:

a)all without exception;

b)having the phenomena of sepsis and septic shock;

c)children or patients of advanced age;

d)in the presence of multiple organ failure and severe concomitant pathology;

e)having the total score less than 12 according to SAPS scale.

20.The components of surgical treatment of widespread peritonitis

include all except:

a)examination of the abdominal cavity organs and removal of exudate;

b)radical elimination (less often, delimitation) of the primary focus of peritonitis;

c)sanitation and drainage of the abdominal cavity;

d)nasogastrointestinal intuba-

tion;

e)mandatory removal of unloading enterostomy.

21.Sources of endogenous intoxication with widespread peritonitis are:

a)primary destructive focus of the abdominal cavity;

b)endogenous foci of unsanitary extraperitoneal infection;

c)pathological exudate of the abdominal cavity;

d)toxic content of the small intestine transformed by paralysis;

e)toxic megacolon.

22.To improve the efficiency of intraoperative sanitation of the abdominal cavity in case of widespread peritonitis, locally all remedies are applied except:

a)ozonized solutions;

b)antiseptics in the form of a “pulsating” jet or in a fine-dis- persed state;

c)ultrasonic cavitation;

d)treatment of the abdominal cavity by a defocused laser;

e)highly concentrated solutions of antibiotics.

23.Closing of the abdominal cavity in case of widespread peritonitis can be performed by means of:

a)closing in layers;

b)sewing of a “zipper” into the edges of the wound;

c)laparostomy followed by the covering of intestinal loops with films soaked with water-soluble ointments or the use of absorbent plates;

d)putting in U-shaped approximation stitches through all layers of the abdominal wall or on synthetic pads;

e)open methods without any application of additional protection of intestinal loops.

24.For a full examination and sanation of abdominal organs in case of widespread peritonitis, the optimal type of access is:

a)McBurney’s section;

b)Kocher’s section;

c)lower-median laparotomy according to Pfannenstiel;

d)wide middle-line laparotomy;

e)wide laparophrenothoraco-

tomy.

25.The optimal type of decompression of the small intestine in widespread peritonitis is:

a)nasogastrointestinal intuba-

tion;

b)formation of a jejunostoma;

c)transanal retrograde intubation in children;

d)intubation through enteros-

toma;

e)intubation through appendicostoma.

26.The objectives of naso-intesti- nal intubation in the treatment of widespread peritonitis are all the below mentioned except:

a)decompression and detoxification;

b)creation of an intestinal car-

cass;

c)prevention of failure of the formed anastomoses of the small intestine;

d)nutrition;

e)cytoprotection.

27.To restore the functional activity of the gastrointestinal tract in postoperative treatment of widespread peritonitis, the following procedures are prescribed:

a)prolonged epidural anesthe-

sia;

b)percutaneous stimulation of the intestine;

c)enterosorption;

d)novocaine blockade of the mesentric root;

e)administration of serotonincontaning medicines.

28.To prevent the development of “compartment syndrome”, the postoperative wound in the treatment of widespread peritonitis should be managed in the following way:

a)the wound is closed with a blind suture;

b)a “zipper” is sewn into the edges of the wound;

c)approximation devices-ven- trophils are applied;

d)synthetic films and gauze drains with hydrogels, collagen plates or water-soluble ointments are placed on top of the intestinal loops;

e)NPWT (YAС) – system for the dosed vacuum depression.

29.As the “start” antibacterial therapy in the postoperative period in the widespread peritonitis the following medications are applied:

a)lincosamines;

b)cephalosporins of Class III– IV metronidazole;

c)mono-carbapenems in the presence of multiple organ failure;

d)fluoroquinolones with aminoglycosides (Class III);

e)glycopeptids of Class I–II with fluoroquinolones.

30.The optimal routes of administration of antibiotics in the postoperative treatment of widespread peritonitis are:

a)intravenous;

b)endolymphatic (lymphotropic);

c)intra-arterial;

d)into the abdominal cavity through drains;

e)oral.

31.In case of widespread peritonitis and accompanying severe abdominal sepsis, the “start” immunotherapy should include:

a)preparations of recombinant cytokines;

b)activators of the T-cell component (thymus preparations);

c)activators of monocyte-mac- rophage component;

d)drugs of specific and nonspecific passive immunotherapy (immunoglobulins, plasma);

e)administration of splenoxenoperfuzate.

32.The purpose of infusion-trans- fusion therapy in postoperative

treatment of widespread peritonitis includes everything except:

a)management of immune dis-

oders;

b)management of water-elec- trolyte disorders;

c)management of hypovolemia and colloid osmotic pressure of plasma;

d)management of transmembrane oxygen transport and gas exchange;

e)suppression of a wide range of bacterial microflora.

33.In the treatment of widespread peritonitis complicated by the septic shock the following remedies and procedures are prescribed:

a)preparations of specific passive immunotherapy;

b)ß-adrenoblockers;

c)activators of fibrinolysis;

d)titration of hydrocortisone in combination with vasopressor amines;

e)plasma exchange, multifiltration and other methods of extracorporal detoxification.

34.Prevention of disseminated intravascular coagulation syndrome in postoperative treatment of widespread peritonitis is provided by the administration of all the below mentioned medications except:

a)disaggregants;

b)inhibitors of proteolytic enzymes;

c)synthetic analogue of coagulation factor VII (novoseven);

d)activator of antithrombin III (protein C);

e)thrombolytics.

35.The localized forms of intraabdominal infection include all the below mentioned except:

a)sub-diaphragmatic abscess;

b)subhepatic abscess;

c)abscess of the small pelvis;

d)inter-loop (intestinal) abscess;

e)purulent pyelonephritis.

36.The reasons for the development of intra-abdominal abscesses include:

a)technical intraoperative errors during primary intervention;

b)tactical surgical errors in the postoperative period;

c)unreasonable drug management of the postoperative period;

d)weakened local and general immunoresistance;

e)untreated microflora of the

colon.

37.Predisposing factors for the development of subhepatic (subdiaphragmatic) abscesses include all the below mentioned except:

a)failure of anastomotic stitches or stitches of sutured hollow organs;

b)formation of intra-abdomi- nal hematomas;

c)postoperative bile secretion;

d)encapsulated ascites;

e)perigastritis or periduodenitis due to gastro-stasis.

38.Clinically, the subhepatic

a)pain in the right upper abdomen with irradiation in the right supragastric region or shoulder;

b)febrile fever with intermittent fever;

c)signs of endogenous intoxication;

d)reduction of the respiratory rise of the right lung and reactive pleurisy;

e)bacterial destruction of the

lungs.

39.X-ray findings confirming the presence of subhepatic (sub-dia- phragmatic) abscess are:

a)increased mobility of the right dome of the diaphragm;

b)acute limitation of mobility of the right dome of the diaphragm;

c)the presence of a gas bubble under the diaphragm accompanied by horizontal fluctuations in the liquid level;

d)reactive right-sided pleurisy;

e)intensified shadow of the liver or its reduced clarity.

40.The optimal methods of treatment in case of diaphragmatic (subhepatic) abscesses are:

a)extraperitoneal and extrapleural opening and drainage;

b)shock antibacterial therapy without surgical intervention;

c)puncture and drainage under ultrasound control;

d)physiotherapeutic treatment without surgical intervention;

e)transabdominal or transpleural opening and drainage.

41.The course of abscesses of the small pelvis may have all the below mentioned variants except:

a)rupture into the lumen of the adjacent hollow organ with selfhealing;

b)purulent thrombophlebitis of pelvic veins;

c)rupture into the abdominal cavity accompanied by the development of widespread peritonitis;

d)complete involution without complications;

e)secondary inflammation of the pelvic organs.

42.Clinically abscess of the small pelvis is manifested by:

a)unpronounced pain in the lower abdomen;

b)febrile fever with intermittent fever;

c)pronounced muscular local defense and symptoms of irritation of the peritoneum;

d)addition of dysuric phenomena and intestinal tenesmus;

e)palpable compression with softening in the center (with rectal examination).

43.The optimal type of treatment in case of pelvic abscess is:

a)massive antibacterial therapy without drainage;

b)physiotherapeutic treatment without opening and draining;

c)transabdominal lower-medi- an laparotomy for opening and draining;

d)percutaneous puncture by ultrasound-control;

e)transvaginal (transrectal) opening and draining with a doublelumen PVC-tube.

1.The prolapse of the rectum is characterized by:

a)lifting of the pelvic diaphragm upward;

b)pelvic diaphragm descent;

c)coming out of the sigmoid colon and the distal part of the rectum through the anus;

d)coming out of the distal part of the rectum through the anus;

e)absence of intrarectal outlet of the rectum by means of the formed rectal prolapse.

2.The predisposing factors that cause the development of prolapse of the rectum include everything except:

a)congenital weakness of the ligament apparatus;

b)excessive mobility of the rectum;

c)atony of muscles due to permanent constipation;

d)hereditary predisposition;

e)deep pelvic pocket.

3.The factors that contribute to the development of prolapse of the rectum include:

a)deep pelvic pocket;

b)rough labor;

c)the previous injuries of the rectum and the anal sphincter mechanism;

d)chronic obstructive pulmonary diseases;

e)excess mobility of the rec-

tum.

4.In case of a chronic course of rectal prolapse, the following interventions are used, except:

a)resection of the prolapsed part of the rectum with the putting of the corrugating stitches in the wall;

b)colopexy to the promontory;

c)fixation to the sacrum with a synthetic mesh;

d)pelvic floor plastic surgery with reticular implants;

e)intra-abdominal resections of the proximal parts of the colon with right side hemicolectomy.

5.The pilonidal cyst is characterized by everything except:

a)the canal, represented from the inside by granulation tissue;

b)the canal lined from the inside with epithelium;

c) the fistula, located up to 2 cm from the anal canal in any part of the circumference;

d)the fistula, located in the fat of the sacrococcygeal region along the intergluteal fold;

e)the fistula opening outside with one (more rarely – several) exact orifices.

6.The following clinical variants of pilonidal cyst are distinguished:

a)latent;

b)uncomplicated;

c)acute inflammation in the form of abscess formation;

d)chronic inflammation as infiltrate;