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

d)phlegmasia alba dolens;

e)phlegmasia cerulea dolens.

9.Ileofemoral phlebothrombosis is characterized by everything except:

a)pronounced severe pain in the affected extremity;

b)edema of the affected extremity upto the inguinal fold;

c)presence of trophic ulcers of the lower leg;

d)skin cyanosis of the affected extremity, which increases in an upright position;

e)coldness of the affected extremity associated with pale color of the skin and disappearance of peripheral pulsations.

10.Conservative treatment of ileofemoral phlebitrombosis includes everything except:

a)local thrombolytic therapy;

b)anticoagulants;

c)antiplatelet agents;

d)venotonics;

e)vasoprostan.

11.Surgical treatment of ileofemoral phlebothrombosis includes:

a)emergency phlebectomy with crossectomy;

b)open thrombectomy with restoration of venous outflow;

c)bandaging or plication of the inferior vena cava, iliac and femoral veins;

d)endovascular interventions;

e)ligation of the tibial veins.

12.Phlegmasia alba dolens is caused by:

a)marked lymphatic edema of the affected extremity;

b)anemia of the affected extremity;

c)marked edema of the tissues of the affected extremity;

d)spasm of the homonymous artery of the affected extremity;

e)unstable hemodynamics.

13.Phlegmasia cerulea dolens is caused by:

a)angina of the vessels of the affected extremity;

b)interruption of outflow through perforator veins;

c)complete occlusion of the femoral, iliac or inferior vena cava;

d)Floating thrombus;

e)acute violation of lymphatic outflow.

14.The main cause of PE development is:

a)mitral heart defects;

b)atrial fibrillation;

c)varicothrombophlebitis;

d)phlebothrombosis;

e)arterial spasm of the vessels of the small circle of blood circulation.

15.The main method of PE (main trunk) treatment is:

a)catheter local thrombolysis;

b)emergency thrombemboctomy;

c)pulmonectomy;

d)emergency installation of a cava filter;

e)plication of the inferior vena

cava.

16.In the event of the recurrent form of PE, the most effective treatment methods are all except:

a)catheter local thrombolysis;

b)administration of indirect anticoagulants;

c)wearing compression garments;

d)emergency thrombembocto-

my;

e)formation of arteriovenous fistulas.

17.Thrombosis of the common femoral vein is manifested in:

a)quick-spreading bottom-up swelling of the lower leg and thigh;

b)secondary lymphangeitis and lymphadenitis;

c)local temperature increase of the affected extremity;

d)intensification of the subcutaneous venous pattern;

e)skin cyanosis of the affected extremity intensifying in the distal direction.

1.CVI is a pathological symptom complex:

a)caused by an individual disease of the venous system;

b)resulting in gradual disruption of venous drainage;

c)accompanied by local trophic disorders in the tissues;

d)which is a consequence of the disease course of autoimmune prosesses;

e)which is an outcome of chronic lymphostasis.

2.The main reasons for the development of CVI are:

a)obliterating thromboangiitis;

b)Paget-Shreter’s disease;

c)varicose veins;

d)postthrombophlebitic disease;

e)disorders of hemocoagulation properties of blood.

3.Varicose disease is:

a)a chronic disease of the lower extremities;

b)a chronic disease of the upper extremities;

c)an acute process of venous wall change;

d)irreversible changes of venous valve apparatus;

e)a reversible transformation of the venous wall.

4.The following pathogenic varieties of varicose veins are distinguished:

a)latent;

b)primary;

c)secondary;

d)tertiary;

e)slowly progressing.

5.The most common causes of secondary varices are all except:

a)postthrombophlebitic dis-

ease;

b)chronic lymphostasis;

c)presence of functioning arteriovenous fistulas;

d)congenital tibial vein occlu-

sion;

e)obliterating thromboangiitis.

6.The etiological factors of varicose disease include:

a)hereditary factors of impared relationship of collagen type I and type II;

b)reduction in the function of musculo-venous pump of lower extremities;

c)inheritance of the anatomical structure of the venous valves;

d)female gender;

e)constant increase in the hydrostatic pressure of the lower extremities.

7.The pathogenesis of varicose veins includes all except:

a)increase in intravenous pres-

sure;

b)activation of platelet-aggre- gation properties of blood;

c)reduction of the perfusion pressure of oxygen in the tissues lower than 30 mm Hg;

d)failure of venous valves;

e)retrograde venous reflux.

8.The forms of varicose disease include everything except:

a)ascending;

b)latent;

c)small saphenous vein system;

d)both venous pathways;

e)atypical.

9.Venous reflux develops due to valve failure of:

a)saphenofemoral junction;

b)saphenopopliteal junction;

c)perforated veins of the lower extremity;

d)deep veins;

e)perforated veins of the femur.

10.The III degree of chronic venous insufficiency is characterized by:

a)transient tibia edema;

b)resistant tibia edema;

c)hyperpigmentation and cel-

lulitis;

d)presence of the open or healed trophic ulcer;

e)all of the above.

11.Complications of varicose veins include everything except:

a)arrosive bleeding;

b)varicothrombophlebitis;

c)acute phlebothrombosis;

d)trophic ulcers;

e)Paget-Shretter’s syndrome.

12.To assess the state of the valve apparatus of perforated tibial and femoral veins the following methods are used:

a)Schwartz-McKeling’s test;

b)Pratt-2 test;

c)three tourniquets test of Sheinis;

d)Troyanov-Brodie-Trende- lenburg’s test;

e)Talman’s test.

13.The main noninvasive methods of assessment of venous reflux are:

a)radiocontrast phlebography;

b)CT with the contrast injection in the vein;

c)duplex (triplex) venous angiography;

d)percutaneous oximetry;

e)selective celiacography.

14.The surgical treatment of varicose veins includes all except:

a)endovasal laser coagulation;

b)combined phlebectomy;

c)cross femoro-femoral venous shunting;

d)tibial veins resection;

e)deep vein valve correction.

15.Subfascial ligation of perforated veins of the lower extremity is called the operation of:

a)Cocket;

b)Linton;

c)Varadi;

d)Muller;

e)crossectomy.

16.Suprafascial ligation of perforated veins is called the operation of:

a)Linton;

b)Varadi-Muller;

c)Cocket;

d)Narath;

e)crossectomy.

17.The main effect of endovasal laser coagulation (EVLC) includes all except:

a)active endothelial growth;

b)freezing of endothelium to the cryoprobe;

c)vaporization effect of endothelium;

d)primary obliteration of the lumen by thrombus formation;

e)secondary fibrosis of the venous wall with lumen obliteration.

18.EVLC of varicose veins is recommended in case(s) of:

a)a straight type of varicose veins with an expansion of less than

10mm in its external diameter;

b)a “friable” type of varicose;

c)the saccular venous transformation with an increase in the external diameter of the vein over 11 mm;

d)cosmetic removal of intradermal varicose;

e)recurrence of varicose in particular branches of the saphenous veins.

19.Sclerotherapy of varicose veins is recommended in case(s) of:

a)the presence of horizontal and vertical venous pathological reflux;

b)saccular transformation of the venous wall with an increase in the external diameter of the vein over 11 mm;

c)intradermal type of varicose

veins;

d)telangiectasias;

e)varicose veins recurrence in particular parts of saphenous veins.

20.Operations for correcting deep vein valves include:

a)tibial resection;

b)concentric luminal narrowing from the inside (in the projection of the valve);

c)extravasal valvuloplasty;

d)crossectomy;

e)combined phlebectomy.

21.Postthrombophlebitic disease (PTD) is:

a)a form of chronic venous insufficiency;

b)venous system disease that develops nine months after acute phlebothrombosis;

c)venous system disease caused by thromboangiitis obliterans;

d)a disease, that develops 2−3 months after acute phlebothrombosis;

e)a disease arising after the varicose disease of the saphenous veins.

22.The following pathological mechanism(s) form the basis of PTFB pathogenesis, except:

a)infiltration of the vein wall;

b)intimal fibroblast proliferation;

c)increased intravenous pres-

sure;

d)activation of blood hemocoagulation properties;

e)valve inconsistency of perforated veins.

23.To diagnose PTD the following methods are applied, except:

a)Doppler ultrasound;

b)ultrasonic duplex angiography of veins;

c)radionuclide flebostsintiog-

raphy;

d)radiocontrast CT angiography;

e)antegrade lymphography.

24.For surgical treatment of PTD the following is applied, except:

a)phlebectomy of saphenous veins with secondary modifications;

b)cross femoro-femoral venous shunting;

c)ligation of incompetent perforated veins of the lower extremity;

d)foam sclerotherapy;

e)endovasal plastics with possible endostenting.

25.For conservative treatment of PTD the following is applied, except:

a)medical compression stock-

ings;

b)phlebotonics;

c)drugs for cell metabolism improvement;

d)antihypoxants;

e)antispasmodics.

1.Chronic lymphostasis of the extremities (CLE) is a pathological symptom complex, caused by:

a)acute disorder of lymphatic outflow;

b)gradual disorder of lymphatic outflow;

c)persistent limb edema;

d)an increase in the limb it size;

e)fibrosis of the skin and subcutaneous tissue.

2.To the acquired reasons for the development of CLE include:

a)inflammatory changes in lymphatic structures;

b)transferred interventions with the removal of subcutaneous tissue or regional lymph nodes;

c)growing neoplasms on the

limbs;

d)endolymphatic administration of antibiotics;

e)sessions of local radiotherapy.

3.The pathogenesis of CLE is based on:

a)discrepancy of the volume of lymphatic outflow to the level of lymphogenesis of this region;

b)reduction of pumping function and motor function of lymphangia;

c)irreversible disorders of the structure and contractile function of lymphangia;

d)irreversible changes in the valve apparatus of the venous wall due to acute phlebothrombosis;

e)perivennous fibrosis of tis-

sues.

4.The local status of fibredema is characterized by:

a)persistent dense swelling of the limb;

b)difficulty in forming the symptom of skin fold;

c)appearance of a trace reaction – “pits” after palpation of the limb;

d)cold extremities due to edema;

e)lack of a trace “fossa” after palpation of the limb.

5.One of the most common complications of CLE is:

a)PTFB;

b)chronic arterial insufficiency;

c)chronic venous insufficiency;

d)relapses of erysipelas;

e)transformation of the venous

wall.

6.Surgical treatment of CLE includes everything, except for operations aimed at:

a)dissociation of arteriolo-ve- nous fistulas;

b)discharge of lymph into the venous bed;

c)excision of fibrous tissues;

d)creation of a vein-venous cross femoral-femoral bypass;

e)resection of the tibial veins.

7.The lymphovenous interventions for CLE include all except:

a)anastomosing the lymphatic vessels of the thigh and branches of the (GSV) LSV;

b)dermatofascioectomy;

c)conducting the finiteness of a full-blown musculoskeletal transplant on feeding vessels;

d)anastomosing the veins and arteries of the lower leg;

e)lateral lymphonodulovenous anastomosis.

8.Lymphoscintigraphy for the diagnosis of CLE is carried out lymphotropically by introducing an albumin labeled with Tx 99 isotopes in:

a)the main shin collector;

b)inguinal lymphonodus of Pirogov-Rosenmuller;

c)the first interdigital interval of the foot;

d)prevenous;

e)anterior tibial artery.

9.Complex conservative treatment of CLE is effective at the stage of:

a)formation of fibredema;

b)presence of trophic ulcers of the foot or lower leg;

c)the stage of compensation;

d)with significant functional and structural damage to lymphangia;

e)presence of pulsations of the arteries of the rear of the foot and shin.

10.Enzyme therapy drugs prescribed for the treatment of CLE have an effect:

a)anti-inflammatory;

b)antihypoxic;

c)decongestant;

d)fibrinolytic;

e)activation of peripheral vasodilation.

1. A-cells of the parenchyma of the thyroid gland are called:

a)thyrocytes;

b)Gurtle-Ashkinazi cells;

c)stomata;

d)follicular cells;

e)cells of the neuroendocrine system.

2. B-cells of the thyroid gland parenchyma participate in:

a)synthesis of thyroid hormones;

b)synthesis of biogenic hormones;

c)synthesis of calcitonin;

d)synthesis of vaso-intestinal peptides;

e)production of glucagon.

3.The cells of the thyroid gland parenchyma are the cells:

a)synthesizing biogenic amines;

b)synthesizing calcitonin;

c)synthesizing thyroid hormones;

d)called parafollicular;

e)synthesizing phosphorus and calcium.

4.The main structural and functional unit of the thyroid gland is:

a)respiron;

b)thyrocyte;

c)thyroglobulin;

d)pancreocyte;

e)thyrotropin-releasing hor-

mone.

5.Which thyroid hormone is considered to be a more active form:

a)thyroxine (T4);

b)triiodothyronine (T3);

c)calcitonin;

d)thyroglobulin;

e)thyrosine.

6.What is the ratio of the more active thyroid hormone (triiodothyronine) to thyroxine (T4) after its deiodization:

a)1:20;

b)1:2;

c)1:10;

d)10:1;

e)20:1.

7.Thyroid hormones have the effect on everything mentioned below, except:

a)stimulation of water-salt metabolism;

b)stimulation of fat metabo-

lism;

c)stimulation of carbohydrate metabolism;

d)activation of oxidation-re- duction processes;

e)reinforcement of the phosphates absorption and reducion of calcium reabsorption.

8.Congenital thyroid gland position anomalies include:

a)aplasia;

b)ectopia;

c)hypoplasia;

d)dystopia;

e)dysplasia.

9.Dystopia is a congenital anomaly of the thyroid gland position when:

a)thyroid tissue is present in its anatomical area;

b)thyroid tissue is absent in its anatomical area;

c)there are additional areas of thyroid tissue in a number of organs located nearby;

d)there are thyroid tissue areas in distant organs;

e)thyroid tracts are sclero-

tized.

10.There are the following types of thyroiditis, except:

a)acute;

b)fulminant;

c)latent;

d)persistent;

e)chronic.

11.Subacute types of thyroiditis include:

a)fibrosing (Riedel);

b)autoimmune (Hashimoto);

c)granulomatous;

d)viral;

e)Kervena-Krail’s thyroiditis.

12.Hashimoto’s disease is a manifestation of:

a)Kervena-Krail’s thyroiditis;

b)actinomycotic lesion;

c)autoimmune lesion;

d)endemic goiter;

e)diffuse toxic goiter.

13.Hashimoto’s thyroiditis occurs clinically with:

a)transient thyrotoxicosis at the onset of the disease;

b)slowly increasing hypothyroidism;

c)progressive increase in the thyroid gland size;

d)tissue atrophy and a decrease in the thyroid gland size;

e)toxic adenoma.

14.The main indication for surgical treatment of Hashimoto’s thyroiditis is:

a)progressive hypothyroidism;

b)progressive thyrotoxicosis;

c)compression of surrounding tissues;

d)decrease in the level of procalcitonin;

e)metastasis in the axillary lymph nodes.

15.The basis of Riedel’s thyroiditis is:

a)lymphocytic infiltration of the thyroid tissue;

b)proliferation of connective tissue in the thyroid gland;

c)autoimmune changes;

d)purulent melting of the thyroid tissue;

e)appearance of pseudo-giant multinucleate cells in the thyroid tissue.

16.The outcome of Riedel’s thyroiditis progression is the development of:

a)diffuse toxic goiter;

b)Hashimoto’s goiter;

c)hypothyroidism;

d)purulent melting of thyroid

tissue;

e)Horner-Bernard’s syndrome (ptosis, miosis, enophthalmus).

17.Treatment of Riedel’s thyroiditis includes:

a)use of iodine preparations;

b)use of cytotoxic agents;

c)use of glucocorticoids and non-steroid anti-inflammatory drugs;

d)surgical operation;

e)replacement hormone therapy with L-thyroxine.

18.The course of Kerven-Krail’s subacute thyroiditis is accompanied by the change of the following successive phases:

a)thyreotoxic;

b)latent;

c)cachectic;

d)euthyroid;

e)hypothyroid.

19.Treatment of Kerven-Krail’s subacute thyroiditis consists of:

a)prescription of glucocorti-

coids;

b)prescription of radio iodine preparations;

c)surgical removal of the damaged thyroid tissue;

d)administration of nonsteroid anti-inflammatory drugs;

e)conducting contact gamma therapy.

20.Hypothyroidism is a syndrome caused by:

a)hyperproduction of thyroid hormones;

b)decreased synthesis of thyroid hormones;

c)decreased secretion of the pituitary gland thyroid hormone;

d)decreased secretion of thyroliberin;

e)decreased sensitivity of tissue receptors to thyroid hormones.

21.The causes of acquired hypothyroidism are all below, except:

a)post-traumatic effect;

b)post-radiation lesion;

c)cytostatic effects;

d)development of follicular adenoma;

e)neoplastic lesion of the thyroid gland.

22.Development of tertiary hypothyroidism is based on:

a)damage to the pituitary

gland;

b)damage to the hypothalamus;

c)decrease in thyroliberin production;

d)immunity of tissue receptors to thyroid hormones;

e)treatment with serotonin.

23.Thyrotoxicosis is a syndrome caused by all the factors below, except:

a)hyperproduction of thyroid hormones;

b)destruction of the thyroid gland follicles;

c)medication stimulation;

d)trophoblastic postpartum chan-

ges;

e)hereditary causes of thyroid hormones deficiency.

24.Clinically the following forms of thyrotoxicosis are distinguished, except:

a)subclinical;

b)torpid;

c)latent;

d)manifested;

e)complicated.

25.Among the characteristic laboratory indicators of thyrotoxicosis are the following:

a)decreased level of thyroid hormones;

b)increased level of thyroid hormones;

c)increased level of thyroidstimulating hormone of the pituitary gland;

d)decreased level of calcitonin;

e)decreased level of thyroidstimulating hormone of the pituitary gland.

26.According to the morphological features there are the following forms of endemic goiter, except:

a)parenchymatous;

b)undifferentiated;

c)parafollicular;

d)colloidal;

e)vascular.

27.Among the etiological factors of endemic goiter are all below, except: