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

c)primary liquefaction or autolysis of tissues;

d)paraosseous phlegmon;

e)paresis of the gastrointestinal tract.

16.Which of the presented methods are not used in the treatment of pressure sores:

a)resection of bony prominence (large trochanter and ishial tuberosity) in the absence of osteomyelitis;

b)staged necretomy with excision of decubitus and its capsules;

c)passive (spontaneous) clearance of defects;

d)nonfree plastic surgery by local tissues with rotational or moved flaps;

e)plastic dermal fascial muscular flap on the feeding vascular pedicle.

17.The peculiarities of trophic ulcer formation include:

a)defect of the skin (mucous membranes) due to rejection of necrotic tissues;

b)absence of active perifocal regenerative processes;

c)tendency to spontaneous healing;

d)the time period of healing repair is less than 8–10 weeks;

e)slightly pronounced granulations of pale pink color or cyanosis with fibrinous coating.

18.What factors prevent the healing of granulating fistulas:

a)presence of fibrillation of the fistula epithelium on the skin;

b)containing bacterial toxins;

c)chemically active ingredients of digestive secretions of the gastrointestinal tract;

d)constant expiration of exudate from the pathological focus;

e)accumulation of the fistula in the fistula cavity or in its branches.

19.What factors prevent healing of epithelial fistulas:

a)transition of infection beyond the fistula;

b)incompleteness of reparative processes;

c)defect of the skin;

d)transition of the fistula epithelium directly to the epidermis;

e)presence of excess scar tissue around the fistulous passage.

20.The pathological fistula in Latin is called:

a)vulnus;

b)ulcus;

c)fisura;

d)fistula;

e)stoma.

21.Diagnosis of fistula is based on:

a)clinical manifestations;

b)performing shunting of the fistulous passage;

c)fistulography data combined with gastrointestinal tract, bronchial tree or urinary tract contrasting;

d)thermography data of soft tissues;

e)character of fistulous discharge (microflora, presence of atypical cells, defining of specific enzymes).

1.The main causes of acute arterial obstruction are:

a)embolism;

b)phlebothrombosis;

c)traumatic artery disease;

d)vascular spasm;

e)ligation of the artery.

2.Arterial thrombosis is a form of acute arterial insufficiency caused by:

a)compression by hematoma from the outside;

b)prolonged tourniquet leaving on the limb segments;

c)finger physical examination;

d)in vivo formation of a blood clot in the arterial bed;

e)postmortem blood clot formation.

3.Embolism is a form of acute arterial insufficiency, caused by everything except:

a)presence of mitral malformation;

b)myocardial infarction with rhythm disturbances;

c)fragmentation of atherosclerotic plaque;

d)entering air bubbles or fat particles into the arterial blood stream;

e)lifelong formation of blood clots in the bloodstream.

4.Acute arterial insufficiency at the stage of functional disorders (nonthreatening ischemia) is characterized by:

a)limb flexion contracture;

b)paralysis of the limb with no active movements;

c)acute pain in the limb;

d)numbness and parasthesia by the “stocking” type;

e)dullness of pulse distal to the level of occlusion.

5.In acute arterial insufficiency at the stage of irreversible changes growth (threatening ischemia), everything is typical, except:

a)distal contracture;

b)purulent inflammation of soft tissues;

c)paresis and paralysis;

d)tissue necrosis;

e)subfascial edema.

6.Acute arterial insufficiency at the stage of irreversible (necrotic) changes is characterized by:

a)reactive hyperemia and cya-

nosis;

b)muscular contracture;

c)subfascial edema;

d)decrease in any type of sensitivity and paresis of the affected limb;

e)tissue necrosis.

7.The most important instrumental methods to examine acute arterial obstruction are:

a)ultrasound duplex angioscan-

ning;

b)MRI – angiography with visualization of vascular structures;

c)ascending phlebography;

d)ultrasound Doppler study;

e)radiopaque angiography.

8.For catheter thrombolysis, in treatment of AAO, the following treatment is used:

a)preparations of low molecular weight heparin (clexane, fragmine, fraxiparin);

b)antispasmodics with myotropic effect;

c)direct anticoagulants;

d)antiplatelet agents and drugs improving microcirculation;

e)activators of fibrinolysis (atelplase, celiaz, streptokinase).

9.Atelplase belongs to:

a)antiplatelet agents;

b)nonsteroidal anti-inflamma- tory drugs;

c)anticoagulants;

d)fibrinolytics (activators of fibrinolysis);

e)phlebotonics.

10.Performing catheter thrombolysis is the most effective during:

a)the first 2 hours;

b)the first 4–6 hours;

c)the first 8 hours;

d)the first 12 hours;

e)the first 24–48 hours.

11.Gangrene of the limb with AAO develops:

a)only with progressing of its course;

b)with rapid progression;

c)with slowly progressing form;

d)always, in any forms;

e)does not develop.

1.The main outcomes of CAO are:

a)myocardial dystrophy;

b)phlebothrombosis;

c)occlusion of the artery;

d)vascular spasm;

e)stenosis (narrowing) of the lumen.

2.When the arteries of the lower extremities are affected and the development of CAO is observed, in the pathological process, most often involved:

a)femoropopliteal segment;

b)aorto-iliac;

c)tibial arteries;

d)artery toes stop;

e)deep femoral artery.

3.The absolute majority of occlusive diseases of the lower extremi-

ty vessels are the consequence of:

a)myocarditis;

b)diabetic angiopathy;

c)obliterating atherosclerosis;

d)nonspecific aortoarteritis;

e)obliterating thrombangiitis.

4.Functional diseases of arteries include everything, except of:

a)Reynaud syndrome;

b)erythromelalgia;

c)blue phlegmace;

d)cold erythrocyanosis;

e)“syndrome” trench foot.

5.The symptom of “intermittent claudication” is manifested by:

a)visible atrophy of calf mus-

cles;

b)paresthesia of a transient nature;

c)skin pallor;

d)the need to stop walking for relieving pain in the calf muscles;

e)persistent lower leg lymphostasis.

6.The main complaints in case of chronic arterial insufficiency are the following except:

a)the symptom of “intermittent claudication”;

b)seizures and paresthesias;

c)sensitivity to cold and fatigue of muscles while walking;

d)hypertrophy of calf muscles;

e)swelling of the ankles, worsening by the evening.

7.The I stage of chronic arterial insufficiency of the extremities is characterized by:

a)pain at rest;

b)ulcerative-necrotic changes;

c)the symptom of “intermittent claudication” while walking for more than 800−1000 meters;

d)coldness and paresthesia;

e)development of lymphedema.

8.The II-A stage of chronic arterial insufficiency of the lower limbs, other symptoms are typical, except:

a)“intermittent claudication”, arising at a walking distance of up to 200 meters;

b)pain at rest;

c)atrophy of the calf muscles;

d)“intermittent claudication” while walking a distance of 200−1000 meters;

e)ulcerative-necrotic changes of feet.

9.The III-A stage of chronic arterial insufficiency of the lower extremities is characterized by:

a)ulcerative-necrotic manifestations;

b)absence of ischemic edema;

c)pain at rest or while passing a distance of less than 50 meters;

d)atrophy of the lower leg muscles;

e)pain at rest or while passing a distance of more than 50 meters.

10.For the III-B stage of chronic arterial insufficiency of the lower limbs the following symptoms are typical, except:

a)ulcerative-necrotic manifestations;

b)pain at rest and at night;

c)development of ischemic edema;

d)impossibility of keeping the foot in the horizontal position for more than 2 hours;

e)“intermittent claudication” while walking the distance of 50–

200 meters.

11.The IV stage of chronic arterial insufficiency is characterized by:

a)ischemic edema;

b)atrophy of the lower leg muscles;

c)“intermittent claudication” less than 50 meters;

d)ulcerative-necrotic manifestations;

e)pain at rest.

12.The symptoms of “plantar ischemia” include everything except:

a)Oppel;

b)Samuels;

c)Moshkovich;

d)Pratt;

e)Troyanov-Trendelenburg.

13.The Goldflam’s symptom, characterized by rapid fatigability of the affected lower limb while performing 20−30 movements in the ankle, is typical for:

a)acute venous insufficiency;

b)acute arterial insufficiency;

c)plantar ischemia;

d)postthrombotic disease;

e)lymphostasis.

14.“Plantar” tests of Oppel and Samuels show:

a)compensation of arterial blood circulation;

b)decompensation of venous outflow;

c)lymphatic insufficiency;

d)decompensation of the distal arterial blood flow;

e)decompositions of central hemodynamics.

15.Noninvasive techniques to assess macrohemodynamics in chronic arterial insufficiency of the lower extremities include:

a)ascending phlebography;

b)duplex angioscanning;

c)rheovasography;

d)oscillography;

e)ultrasound Dopplerography with the definition of the anklebrachial index.

16.Invasive methods to assess macrohemodynamics in chronic arterial insufficiency of the lower extremities include:

a)radiocontrast angiography;

b)duplex angioscanning;

c)computer tomography angiography in the SCT mode;

d)transcutaneous oximetry;

e)magnetic resonance angiography with contrast enhancement (gadolinium).

17.To assess microhemodynamics in chronic arterial insufficiency of the lower extremities everything is applied except:

a)rheovasography;

b)transcutaneous oximetry;

c)laser Doppler flowmetry;

d)video capillaroscopy;

e)radiocontrast angiography.

18.Critical ischemia of the lower limbs means:

a)permanent pain at rest for more than 2 weeks;

b)the need to prescribe narcotic analgesics;

c)reduction of the ankle-bra- chial index by less than 0.4 conv. units;

d)reduction of oxygen tension in the foot tissues by less than 30 mm Hg;

e)ulcerative and necrotic tissue changes.

19.Synthetic analogue of prostaglandin (vasaprostan), used in treatment of chronic arterial insufficiency of the lower extremities belongs to the group of:

a)phlebotonics;

b)antiplatelet agents;

c)direct anticoagulants;

d)ganglioblockers central action;

e)peripheral vasodilators.

20.In complex treatment of obliterating atherosclerosis everything

is applied except for drugs from the group of:

a)statins;

b)3; 6 – unsaturated fatty acids;

c)α-lipoic acid;

d)cytostatics;

e)inhibitors of serotonin.

21.In complex treatment of obliterative thrombangiitis everything is applied, except for drugs from the group of:

a)cytostatics;

b)glucocorticoids (pulse-ther-

apy);

c)statins;

d)serotonin inhibitors;

e)preparations of α-lipoic acid.

22.The stages of pathogenesis of obliterating atherosclerosis include all except:

a)lipoidosis;

b)thrombungiita;

c)phlebitis;

d)liposclerosis;

e)complications (of fibrosis and atherocalcinosis).

23.The clinical forms of obliterating atherosclerosis include all except:

a)latent;

b)stable;

c)prodromal;

d)slowly progressing;

e)acute.

24.Development of “critical ischemia” syndrome with chronic arterial obstruction of the lower limbs dictates the need for:

a)intensive conservative the-

rapy;

b)urgent amputation of the limb;

c)urgent restoration of the main blood flow;

d)planned X-ray-vascular intervention;

e)planned restoration of the blood flow.

25.Operative interventions for obliterating atherosclerosis of the lower extremities include everything except:

a)direct reconstruction-recon- structive;

b)indirect vasculitis;

c)minimally invasive X-ray;

d)operations on the lumbar ganglia;

e)operations to restore venous outflow.

26.Restorative operations performed with obliterating atherosclerosis of the lower extremities include:

a)thrombembolecomy;

b)intimendarterectomy;

c)stenting;

d)resection of posterior tibial

veins;

e)percutaneous balloon dilata-

tion.

27.Reconstructive operations performed with obliterating atherosclerosis of the lower extremities include:

a)intimendarterectomy;

b)different types of prosthetics of the arteries;

c)shunt interventions;

d)profundoplasty;

e)arterial veins of the legs and

feet.

28.Operations for indirect vascularization of the ischemic lower

limb in CAO are recommended in case of:

a)impossibility to perform surgery to restore the direct blood flow;

b)presence of severe concomitant pathology;

c)presence of ischemic edema;

d)development of ulcerative necrotic changes;

e)distal or multilevel lesions of peripheral arteries.

29.The operations for indirect vascularization of the ischemic lower limb in CAO include:

a)resection of posterior tibial

veins;

b)microvascular transplantation of the epiploon / omentum onto the lower limb;

c)micro-osteotrepanation of the lower leg bones;

d)autotransplantation of soft tissue grafts;

e)arterialisation of tibial veins.

30.Minimally invasive X-ray-vas- cular interventions in CAO include all except:

a)transluminal balloon angioplasty;

b)endostenting (endoprosthetics) of blood vessels;

c)lumbar sympathectomy;

d)laser endovascularization;

e)rotational atheroectomy.

31.Takayasu’s disease (nonspecific aorto-arteritis) refers to vascular diseases, the leading component of which is:

a)dysplastic;

b)metabolic;

c)noninfectious;

d)autoimmune;

e)hemocoagulation.

32.The etiological factors of Takayasu’s disease (nonspecific aorto-arteritis) include everything except:

a)autoimmune processes, accompanied by an increase in the titer of antimedial and anti-aortic antibodies;

b)genetic predisposition with the inheritance of certain histocompatibility antigens;

c)inflammatory diseases accompanied by a productive process;

d)tumor diseases of arteries;

e)age under 40 in females.

33.Clinical types of nonspecific aorto-arteritis include all except:

a)isolated type of lesion of the aorta arch;

b)lesions of the thoracoviscelal segment of the aorta;

c)combined lesion of the aorta arch and visceral branches;

d)previously presented variants with lesions of the pulmonary artery branches;

e)pathology of the deep femoral artery.

34.Surgical treatment of nonspecific aorto-arteritis must begin at the stage of:

a)irreversible changes in pulmonary vessels;

b)occlusion of the lumen;

c)aneurysm transformation;

d)stenosis of different aortic

sites;

e)development of compartment syndrome.

35.Obliterating thromboangiitis is:

a)chronic arterial wall disease;

b)occlusive lesions of arteries and veins small and medium in the diameter;

c)a process being autoimmune by nature;

d)a disease that occurs more often in women under 40;

e)a disease that occurs in men aged 30–50.

36.Previously obliterating thrombonagiitis was known as:

a)spontaneous gangrene;

b)Raynaud-Frindlander-Vinivar- ter-Burger disease;

c)obliterative atherosclerosis of the lower extremities;

d)obliterative endarteritis;

e)diabetic angiopathy.

37.Etiopathogenetic theories of obliterating thromboangiitis include all except:

a)neurovegetative;

b)chronic nicotine intoxica-

tion;

c)autoallergic;

d)oncological;

e)metabolic.

38.The basis of obliterative thrombangiitis pathogenesis is:

a)hyperactivation of sympathetic regulation;

b)resistant primary angiospasm of the arteries of the limb distal segments;

c)desolation of vasa vasorum;

d)hypertrophy and sclerosis of the muscle layer of small arteries;

e)disorders of the thrombusforming and anti-coagulant components of hemostasis.

39.In the clinical course of obliterating thrombangiitis the following stages are distinguished except:

a)spastic;

b)arterial obliteration;

c)necrotic (gangrenous);

d)neurocircular;

e)embolic.

40.Reconstructive and restorative operations on the main arteries with obliterative thrombangiitis can be performed in:

a)50–60% of cases;

b)10−20% of cases;

c)5–7% of cases;

d)only for life-saving indica-

tions;

e)in case of critical limb isch-

emia.

41.In obliterative thrombangiitis, the following types of surgical interventions are used except:

a)resection of the occluded site with the restoration of patency with the help of prostheses;

b)shunting the site of the obliterated artery;

c)aneurysm resection with aorto-bifemoral shunting;

d)indirect revascularization interventions;

e)extravascular interventions on sympathetic ganglia.

1.The main causes of acute venous insufficiency are:

a)venous thrombosis;

b)embolism;

c)vascular spasm;

d)compression of the vein wall (from outside);

e)intraoperative vein ligation.

2.The central types of thrombosis localization include:

a)ileocaval;

b)femoral;

c)subclavian vein;

d)projections of superior vena

cava;

e)jugular veins.

3.The Paget-Schroetter Syndrome includes cases of thrombosis in:

a)VSM system;

b)superficial veins of the arm and veins of the thorax;

c)deep veins of the lower leg and thigh;

d)system of the inferior vena

cava;

e)innominate, jugular or subclavian veins.

4.A thrombus attached to an unchanged venous wall is called:

a)thromboembolism;

b)thrombophlebitis;

c)phlebothrombosis;

d)angiospasm;

e)obliterating thrombangiitis.

5.Pathogenic formation of thrombus in the region of the initially inflamed venous wall is called:

a)thrombophlebitis;

b)phlebothrombosis;

c)venous stasis;

d)Paget-Schroetter syndrome;

e)obliterating thrombangiitis.

6.In the development of venous thrombosis, everything matters except:

a)Virchow’s triad;

b)prolonged bed regime;

c)congenital deficiency of antithrombin III or proteins S and C;

d)hormonal drugs and smok-

ing;

e)impairment of lymphatic outflow.

7.Clinically, thrombophlebitis of the superficial veins of the legs is manifested in:

a)edema of the lower leg;

b)local temperature increase;

c)the appearance of pain on compression of the calf muscle forwards against the tibia;

d)the presence of a palpable painful infiltrate along the subcutaneous vein;

e)minor edema of perivenous tissues.

8.Among the clinical manifestations of ileofemoral phlebothrombosis we distinguish everything except:

a)prodromal stage;

b)latent stage;

c)clinical manifestation stage;