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

e)generalized vasodilation of blood vessels.

35.Adaptive reactions of the body to acute gastroduodenal bleeding (over 25% of GCB) are characterized by:

a)transition to hypo-dynamic type of hemodynamics;

b)transition to hyper-dynamic type of hemodynamics;

c)progression of metabolic acidosis;

d)cell hydration;

e)activation of anaerobic glycolysis.

36.Depending on the volume of GCB deficit acute gastroduodenal bleeding is divided into:

a)latent (up to 5%);

b)mild (up to 10–20%);

c)moderate (up to 21–30%);

d)moderate (up to 30–35%);

e)severe (more than 31–40%).

37.Early signs of acute gastroduodenal bleeding are the following except:

a)dizziness;

b)tachycardia;

c)hypotension;

d)fainting;

e)tarry stool (melena).

38.Late manifestations of acute gastroduodenal bleeding are:

a)“coffee grounds” vomiting;

b)fainting;

c)“flickering flies” in the eyes;

d)liquid bulky stool with blood;

e)hypotension.

39.Objective criteria of examining patients with acute gastroduodenal bleeding are:

a)state of the shock index of Algovera-Buri;

b)orthostatic test;

c)gastric aspirate composition;

d)composition of the punctate of bile ducts;

e)character of feces.

40.Additional instrumental methods for detecting acute gastroduodenal bleeding include the following except:

a)esophagogastroduodenoscopy;

b)endoscopic ultrasonography;

c)irrigoscopy;

d)ultrasound of the abdominal cavity organs;

e)vide laparoscopy.

41.Pathophysiological features of hemostasis in acute gastroduodenal hemorrhage are:

a)adaptive hypervolemia on the 2nd day with increased blood and plasma volume;

b)hypervolemia on the 2nd day due to decreased blood and plasma volume;

c)oligocythemic volemia on the 6th–7th day;

d)oligocythemic vollemia on the 3rd–5th day;

e)restoration of the globular volume on the 6th–7th day.

42.Urgent medical and diagnostic measures in acute gastroduodenal bleeding begin with:

a)urgent laparotomy with gas- tro-duodenotomy and final hemostasis;

b)endoscopic hemostasis;

c)replenishment of acute blood loss;

d)elimination of etio-pathoge- netic mechanisms of peptic ulcer;

e)correction of the initial wa- ter-electrolyte state and cellular metabolism.

43.Endoscopic hemostasis in acute gastroduodenal bleeding is achieved by the following methods except:

a)injection;

b)mechanical and thermal;

c)titration of vasopressors;

d)application;

e)embolization of the blood vessels supplying ulcer.

44.For injection endoscopic hemostasis in acute gastroduodenal bleeding the following substances are used except:

a)1–3% ethoxysclerol;

b)70% ethanol;

c)hypertonic sodium chloride solution with epinephrine;

d)2% novocaine with ethanol and norepinephrine;

e)1% solution of nitroglycerin.

45.For thermal endoscopic hemostasis in acute gastroduodenal bleeding the following methods are used except:

a)clipping of bleeding vessel;

b)monoand bipolar diathermocoagulation;

c)tachocomb applications;

d)laser photocoagulation;

e)argon-plasma coagulation.

46.The following preparations are used for embolization of blood vessels supplying the ulcer to per-

form highly selective celiacography except:

a)autologous blood clots;

b)preparations of absorbed ge-

latin;

c)preparations of oxidized cellulose;

d)tachocomb;

e)metal spirals.

47.The main types of surgical interventions performed in acute gastroduodenal hemorrhages are:

a)gastro-, duodenotomy with suturing bleeding vessels;

b)excision of ulcerative infiltrate with primary pyloric-duode- noplasty;

c)various types of vagotomy with excision of ulcer and pyloroduodenoplasty;

d)distal resection of the stom-

ach;

e)exploratory laparotomy.

48.For ulcerative pyloroduodenal stenosis the following features are characteristic except:

a)organic narrowing of the pyloroduodenal area;

b)functional compression of the lumen from the outside;

c)stomach evacuation disturbances;

d)disorders of water-electro- lyte and acid-base balance;

e)toxic diarrhea.

49.The stages of ulcerative pyloroduodenal stenosis are distinguished according to motor-evacu- ation disorders:

a)latent (asymptomatic);

d)weakening of peristalsis in sub-compensation;

e)reinforcement of peristalsis in decompensation.

56.The main laboratory changes in decompensated pyloroduodenal stenosis are:

a)dysproteinemia;

b)development of metabolic alkalosis;

c)azotemia (uremia);

d)hypocalcemia;

e)hypokalemia.

57.The following instrumental methods are used to confirm the degree of pyloroduodenal stenosis except:

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

b)esophagogastroduodenoscopy;

c)endoscopic ultrasonography;

d)computer electrogastemyog-

raphy;

e)highly selective goalography.

58.Medical treatment for pyloroduodenal stenosis includes:

a)fractional aspiration of gastric contents;

b)active antiulcer (antisecretory) treatment;

c)correction of water-electro- lyte and protein disorders;

d)activation of motor activity of the stomach;

e)enteral probe feeding (via the nipple probe beyond the level of organic narrowing).

59.The operation of choice in sub-compensated pyloroduodenal ulcer stenosis is:

a)anterior gastroenterostomy;

b)various types of vagotomy in combination with pyloroduodenoplasty;

c)stem (selective) vagotomy with antrumectomy;

d)distal gastrectomy;

e)gastrostomy.

60.In pyloroduodenal stenosis the acid-base state changes toward:

a)metabolic alkalosis;

b)metabolic acidosis;

c)hyperkalemia;

d)respiratory alkalosis;

e)does not change.

61.The operation of choice in ulcerative decompensated pyloroduodenal stenosis is:

a)gastrostomy;

b)anterior gastro-enterostomy;

c)various types of vagotomy with gastro-duodenostomy according to Jabulei;

d)types of distal resections of the stomach;

e)stem vagotomy with an-

trum-resection.

1. The abdominal hernia is characterized by all signs except:

a)exit of inner organs through an acute defect in the musculoaponeurotic layer;

b)presence of acute defects in the parietal peritoneum or skin;

c)preservation of the integrity of internal or external membranes;

d)exit of organs covered by the peritoneum through natural physiological openings;

e)exit of inner organs through natural defects (openings) in the musculoaponeurotic layer.

2.Abdominal hernias protruding under the skin are called:

a)internal;

b)complicated;

c)strangulated;

d)external;

e)subcutaneous.

3.Abdominal hernias protruding through the pockets or windows of the peritoneum are called:

a)internal;

b)external;

c)uncomplicated;

d)irreducible;

e)strangulated.

4.The anatomical components of the external abdominal hernias are all ones except:

a)hernial orifice;

b)hernial sac;

c)hernial contents;

d)external hernial membranes;

e)natural physiological openings.

5.Eventration means:

a)exit of internal organs through natural physiological openings;

b)natural openings in the muscular aponeurotic layer;

c)inner pockets or peritoneal openings;

d)acute defects in the muscu- lar-aponeurotic layer;

e)acute bone defects.

6.Prolapse (or prolapse) refers to the exit of internal organs covered with the peritoneum through:

a)acute defects in the muscular aponeurotic layer;

b)acute bone defects;

c)natural physiological holes;

d)natural openings in the mus- culo-aponeurotic layer;

e)internal pockets or windows of the peritoneum.

7.The characteristic features of the hernial orifice are all ones except:

a)openings in anatomically “ready-made” areas of the anterior abdominal wall;

b)aponeurotic structural type;

c)muscular-aponeurotic structural type;

d)periosteal-muscular-aponeu- rotic structural type;

e)channel of a spiral direction.

8.The characteristic features of sliding hernia are all ones except:

a)parietal peritoneum is part of hernial sac;

b)the wall of the sliding hernia is a portion of the greater omentum or small intestine;

c)the organs whose wall is part of the hernia are more often sigmoid, cecum or urinary bladder;

d)most often irreducible;

e)hernial sac cannot be represented by internal organs covered with a parietal peritoneum.

9.The main signs characterizing the hernial contents are:

a)presence of mobile organs in the sac;

b)presence of the organs fixed by parietal peritoneum constituting the sac wall;

c)the size depends on the volume and mobility of the included organs;

d)the contents differ in the number of included organs;

e)the contents do not depend on the number of included organs.

10.By their origin acquired abdominal hernias are subdivided into:

a)uncomplicated;

b)traumatic (accidental);

c)postoperative;

d)dystrophic;

e)postnecrotic.

11.Internal abdominal hernias include all the following types except:

a)true;

b)hernia of bursa omentalis;

c)retroduodenal;

d)diaphragmatic;

e)of the intestine mesentery openings.

12.By the clinical course, the following types of abdominal hernias are distinguished:

a)irreducible;

b)uncomplicated (free);

c)complicated;

d)false;

e)internal.

13.Abdominal hernia complications include all the following types except:

a)coprostasis;

b)Richter’s hernia;

c)gangrenous;

d)inflammation of the hernial

sac;

e)strangulation.

14.By the mechanism of formation the following types of strangulated abdominal hernias are distinguished:

a)false;

b)elastic;

c)fecal;

d)combined;

e)mixed.

15.By the anatomical and clinical features, the following types of strangulated abdominal hernias are distinguished:

a)false;

b)Littre’s (Meckel’s diverticu-

lum);

c)retrograde (Maydle’s);

d)parietal (Richter’s);

e)true.

16.The main etiological factors in the onset of congenital hernias are

all ones except:

a)unfinished embryogenesis in the course of formation of various areas;

b)teratogenic effects;

c)ontogenetic deficiency of the mother’s hormones regulating the differentiation of the mesenchyma;

d)trauma of a particular anatomical area;

e)underdeveloped muscularaponeurotic layer.

17.Local causes of acquired abdominal hernias are:

a)accidental or intentional in-

juries;

b)teratogenic effects in ontogenesis;

c)distortion of gene informa-

tion;

d)anatomical disorders of postnatal tissue development;

e)areas of passage of anatomical structures through the abdominal wall.

18.General predisposing causes of acquired abdominal hernias are all ones except:

a)certain sex-age characteris-

tics;

b)distorted gene transforma-

tion;

c)muscle atrophy;

d)general dysplastic constitu-

tion;

e)diseases accompanied by a sharp increase in intra-abdominal pressure.

19.Factors contributing to the development of abdominal hernias include all ones except:

a)constipation and difficulty urinating;

b)age involution of tissues;

c)chronic processes associated with muscle atrophy;

d)physical exercises associated with a sharp increase in intraabdominal pressure;

e)general dysplastic constitu-

tion.

20.Pathogenesis of abdominal hernias is based on:

a)reduction of the parietal peritoneum;

b)stretching and displacement of the parietal peritoneum;

c)dilatation of anatomically ready-made areas of the abdominal wall;

d)fibrous thickening of the parietal peritoneum in the neck portion;

e)formation of fissures between the walls of the hernial sac and internal organs.

21.The factors fostering the irreducibility of hernia contents include all ones except:

a)fibrous thickening of the sac

neck;

b)cystic fibrotic proliferation within the sac;

c)formation of fissures between the walls of the sac and internal organs;

d)scar tissue changes in the area of the hernia orifice;

e)acute impairment (obstruction) of the intestinal passage.

22.Characteristic features of reducible (uncomplicated) abdominal hernias are all ones except:

a)the onset of pain syndrome after intense physical exertion or coughing;

b)the onset of pain syndrome at night or after meals;

c)reduction of the “hernial” bulging in the horizontal position;

d)absence of “cough push” symptom;

e)purple-cherry skin color over the area of hernial bulging.

23.Techniques applied for additional diagnosis of uncomplicated abdominal hernias include all ones except:

a)diaphanoscopy;

b)thermography;

c)celiacography;

d)ultrasound examination of soft tissues;

e)X-ray of the intestine with dynamic assessment of the passage.

24.When assessing contraindications to planned herniotomy in patients with a high operational risk, it is necessary to take into account:

a)results of spirometry;

b)findings of stress functional

tests;

c)readings of treadmill test or Master’s test;

d)readings of acid-base state;

e)readings of local tissue oxi-

metry.

25.Special preoperative preparation in case of large abdominal hernias should include all procedures except:

a)long-time dosed repositioning of internal organs followed by

retention with the help of abdominal bandage;

b)compensation of concomitant pathology;

c)sanation of endogenous foci of infection;

d)selective decontamination of the colon;

e)sanation of the area of anticipated operational access.

26.The main surgical principles for the treatment of abdominal hernias are all except:

a)dissection of the external hernial membranes;

b)isolation and treatment of the hernial sac;

c)plastics of the hernial orifice (hernioplasty);

d)naso-intestinal intubation;

e)external hernial membranes.

27.Autohernioplasty with local tissues in abdominal hernias includes all the following types except:

a)fascial;

b)muscular;

c)aponeurotic;

d)muscular-aponeurotic;

e)osteo-fascial.

28.Fascial-muscular-aponeurotic autohernioplasty is carried out by means of:

a)applying cryopreserved tissues to close the hernial defect;

b)combining previously mobilized edges;

c)creating a duplicate of sutured tissues;

d)using muscular aponeurotic flaps displaced on a wide base;

e)suturing autologous tissues taken at a distance from the primary hernial defect.

29.Xenoplasty with abdominal hernia is carried out by applying:

a)cadaveric cryopreserved tis-

sues;

b)synthetic implants of various materials;

c)autologous tissues taken at a distance from the primary hernial defect;

d)tissues sutured after mobilization over the hernial orifice;

e)biodegradable endoprosthe-

ses.

30.In case of tension-free hernioplasty synthetic mesh implants are placed:

a)on the side of the abdominal cavity along the margins of the hernial defect (“inlay”);

b)onto the loops of the intes-

tine;

c)between the aponeurosis and the parietal peritoneum;

d)under the aponeurosis and the muscles of the anterior abdominal wall (“sublay”);

e)over the sutured edges of the muscles (“onlay”).

31.Indications for the use of synthetic mesh implants (tension-free hernioplasty) include all ones except:

a)hernial orifice of a large size with abdominal wall atrophy;

b)giant hernias with a high risk of developing the “compartment syndrome”;

c)repeatedly recurring hernias of various localizations;

d)postoperative hernias with multiple hernial orifice;

e)presence of the focus of infection of soft tissues in the area of the intended plastics.

32.When performing videolaparoscopic hernioplasty (inguinal hernia), the synthetic mesh implant may be inserted in the following positions:

a)transabdominal position over the intestinal loops;

b)transabdominal preperitoneal (TAPP);

c)totally extraperitoneal (TEP);

d)subcutaneous;

e)over the aponeurosis.

33.The main advantages of performing videolaparoscopic hernioplasty are:

a)lengthening of the recovery period;

b)absence of pain syndrome;

c)reduction of the recovery pe-

riod;

d)minimal cosmetic defect;

e)increased tissue injury during intervention.

34.Strangulated hernia is characterized by all signs except:

a)sudden compression of the contents in the hernia orifice;

b)gradual compression of the contents in the hernia orifice associated with chronic intestinal passage disorder;

c)impairment of blood circulation in the strangulated organ only

when it is turned more than 270 degrees;

d)absence of circulatory impairment in the strangulated intestinal loop;

e)necrosis of the strangulated

organ.

35.Factors contributing to the development of strangulation include:

a)wide hernia orifice;

b)narrow orifice with the development of fibrosclerosis of the edges;

c)abrupt one-time heavy lift-

ing;

d)severe cough;

e)difficulty urinating or performing an act of defecation.

36.Factors contributing to the development of elastic strangulation include all ones except:

a)gradual increase in intra-ab- dominal pressure;

b)sudden increase in intra-ab- dominal pressure;

c)dilatation of narrow hernial orifice;

d)compression of displaced internal organs with the contracted tissues in the hernial orifice;

e)compression (strangulation) of the mobile internal organs with the development of rapid ischemic necrosis.

37.The following factors contribute to the development of fecal strangulation:

a)sudden increase in intra-ab- dominal pressure in the absence of coprostasis;