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

a)insufficient intake of iodi-

des;

b)excessive amount of goitrogenic pollutants;

c)genetic factors;

d)long-term use of thyreostatics;

e)radiotherapy courses.

28.Insufficient production of thyroid hormones in case of endemic goiter is accompanied by:

a)stimulation of the thyrotropic hormone production by the pituitary gland;

b)inhibition of the thyrotropic hormone production by the pituitary gland;

c)compensatory tissue proliferation of the thyroid gland;

d)activation of calcitonin production;

e)permanent hypothyroidism.

29.Endemic euthyroid goiter is manifested by all the symptoms except:

a)tightness in the neck;

b)voice hoarseness;

c)difficulty in swallowing;

d)tremor of the hands;

e)ophthalmopathy.

30.For the diagnosis of endemic goiter the following parameters are important:

a)increase in the size of the thyroid gland higher than the second degree;

b)linkage to the area of regional iodine deficiency;

c)parameters of fine acupuncture biopsy;

d)determination of the thyroid hormone levels;

e)thyroid scintigraphy data.

31.Surgical treatment of endemic goiter is recommended in all cases, except:

a)nodal and diffusion-nodal forms;

b)large-sized goiter compressing the trachea or esophagus;

c)diffuse goiter with symptoms of moderate and severe thyrotoxicosis;

d)ineffectiveness of conservative treatment;

e)goiter of substernal localiza-

tion.

32.The main methods of endemic goiter surgical treatment are all mentioned below, except:

a)hemithyroidectomy;

b)subtotal subfascial resection of the thyroid gland;

c)sparing resection of the thyroid gland under ultrasound control;

d)cervical lymph node dissec-

tion;

e)endoscopic operations or operations with video assisstance.

33.There are the following kinds of endemic goiter prevention:

a)by type;

b)group;

c)individual;

d)purposeful;

e)massively.

34.Diffuse toxic goiter has the following characteristics:

a)uniform increase in the thyroid gland size;

b)excessive secretion of the thyroid hormones;

c)endocrine ophthalmopathy;

d)excess of thyroidin;

e)pretybial myxedema.

35.There are the following stages of diffuse toxic goiter except for:

a)neurotic;

b)neurohormonal;

c)multiple organ dysfunction;

d)visceropathic;

e)anabolic.

36.Signs of mild thyrotoxicosis are the following:

a)bradycardia less than 60 beats / minute;

b)tachycardia within the range of 100–120 beats per minute;

c)development of the systemic inflammatory response syndrome;

d)increase in basal metabolism by 10–12%;

e)decrease in body weight by

20%.

37.Severe thyrotoxicosis can be revealed by:

a)dystrophy of the parenchymal organs;

b)atrial fibrillation;

c)increased basal metabolism up to 30%;

d)increased basal metabolic rate up to more than 60%;

e)tachycardia of more than

120beats per minute.

38.Thyrotoxic attack is a complication of thyrotoxicosis due to:

a)a sharp decrease in thyroid hormones;

b)a sharp increase in thyroid hormone levels;

c)increased function of the adrenal cortex;

d)reduced function of the adrenal cortex;

e)a sharp increase in the thyreoliberin level.

39.Laboratory diagnosis of diffuse toxic goiter reveals:

a)decrease in the level of thyroid hormones;

b)increase in the level of thyroid hormones;

c)increased thyroglobulin levels;

d)decrease in the level of thyrotropic hormone of the pituitary gland;

e)decrease in the level of thy- roxine-binding globulin.

40.Conservative treatment of diffuse toxic goiter consists of the following measures, except:

a)use of irradiation of the thyroid gland with radioisotopes I131;

b)use of thyreostatics;

c)use of adrenal cortex hormones;

d)use of serotin drugs;

e)use of anticholesterolemic

drugs.

41.The positive effect of conservative therapy of diffuse toxic goiter reaches:

a)5–7%;

b)50%;

c)50–70%;

d)over 90%;

e)only surgical treatment is indicated.

42.Surgical treatment of diffuse toxic goiter is recommended in case of:

a)inefficiency of conservative therapy;

b)impossibility of using radioisotopes I131;

c)thyrotoxicosis of moderate and severe degrees;

d)compression of the neck or-

gans;

e)nodal and mixed forms.

43.The operation of choice in the treatment of diffuse toxic goiter is:

a)sparing resection of thyroid tissue with nodes;

b)percutaneous injection of sclerosants in the thyroid nodules;

c)extended thyroidectomy with cervical lymphodissection;

d)subtotal subfascial resection of the thyroid gland;

e)lymphodissection with an isthmus.

44.The thyrostatics used in the treatment of diffuse toxic goiter are all mentioned below, except:

a)Mercazolyl;

b)Thymazole;

c)Thymalin;

d)Propyluracil;

e)Sodium Nucleonate.

45.The rapid increase in the absorption curve of iodine-131 radio preparations by 40–70% within 2 hours and the subsequent increase in the scintigraphy curve during 8–10 hours indicates:

a)toxic Plamer’s adenoma;

b)diffuse toxic goiter;

c)autoimmune thyroiditis;

d)Ribel’s fibrosing thyroiditis;

e)impairment in the drug accumulation by the thyroid tissue.

46.To the morphological follicular forms of thyroid cancer belong

the following abnormalities, except:

a)papillary adenocarcinoma;

b)follicular adenocarcinoma;

c)fibrosarcoma;

d)cancer from the AshkinaziGurtle cells;

e)solid cancer with stromal amyloidosis.

47.Cancer of the thyroid gland originating from parafollicular C cells is referred to as:

a)anaplastic;

b)papillary;

c)medullary;

d)neurosarcoma;

e)undifferentiated.

48.The main cell injuries in thyroid cancer are all below except:

a)activation of met oncogenes mutation;

b)restricted activity of growth suppressor genes (p 53);

c)increased expression of proteoglycans (mdm 2);

d)mutations of BRAC-1 BRCA-2 genes;

e)mutations of the K-ras onco-

gene.

49.Clinical manifestations of thyroid cancer are the symptoms associated with:

a)external bleeding;

b)growth of the tumour;

c)invasion to surrounding tis-

sues;

d)appearance of metastases;

e)paraneoplastic disorders.

50.Symptoms associated with the growth of thyroid cancer are attrib-

uted to everything mentioned below, except:

a)rapid growth of nodular goi-

ter;

b)formation of dense or uneven structures in the neck;

c)compression of the sympathetic trunk;

d)appearance of inactive regional lymph nodes;

e)tuberosity of nodes.

51.Symptoms of thyroid cancer associated with the invasion to the surrounding tissues include everything mentioned below, except:

a)limitation of the thyroid gland mobility;

b)difficulty with swallowing and breathing;

c)strengthening of the venous pattern along the front surface of the chest;

d)diarrhea;

e)metastases in the liver.

52.The important tools in the diagnosis of thyroid cancer are the following instrumental methods, except:

a)ultrasound;

b)fine needle aspiration biopsy;

c)scintigraphy of the thyroid

gland;

d)fistulography;

e)identification of the oncomarkers content.

53.Surgical treatment of thyroid cancer depends on:

a)the spread of the process;

b)histological verification;

c)the presence of metastases;

d)the level of oncomarkers;

e)the age of the patient.

54.The best type of surgery in case of thyroid cancer is:

a)hemithyroidectomy with thyroid isthmus;

b)subtotal subfascial resection of the thyroid gland;

c)thyroidectomy with cervical lymphodissection;

d)enucleation of nodes;

e)sclerotherapy of nodes under ultrasound control.

55.The main type of radiation therapy in case of thyroid cancer is:

a)external contact irradiation of the thyroid gland projection;

b)puncture administration of radiopharmaceuticals into the nodes;

c)combination with chemotherapy;

d)use of radioactive iodine-131;

e)lymphotronic drug administration.

56.Follicular thyroid cancer is characterized by the following signs:

a)occurs 9 times more often in women;

b)most often develops at the age of 40–50;

c)lymphogenous metastasis;

d)hematogenous metastasis;

e)histologically contains follicles with invasion to blood vessels.

57.Medullary thyroid carcinoma is characterized by:

a)equal sex ratio;

b)more often revealed at the age of 45–50;

c)calcitonin is a specific marker of tumour cells;

d) histologically represented by cells surrounded by a stroma containing amyloid;

e) characterized by an aggressive course.

58. With highly differentiated forms of thyroid cancer, the life span of 80–90% of patients is:

a)up to 5 years;

b)10–15 years;

c)less than a year;

d)5–10 years;

e)20–25 years.

1.Malformations of mammary glands include:

a)mastopathy;

b)ateliyu;

c)polymathy;

d)macromastia;

e)lythelium.

2.The main complications of breast damage are:

a)hydradenite;

b)erysipelas inflammation;

c)mastitis;

d)formation of external fistula;

e)atelia.

3.Acute inflammatory diseases of mammary glands include:

a)hydradenite;

b)paramastitis;

c)mastitis;

d)external fistulas;

e)micromastia.

4.Chronic inflammatory diseases of the breasts include all except:

a)hydradenite;

b)chronic mastitis;

c)actinomycosis of breast can-

cer;

d)tuberculosis MG;

e)fibrocystic mastopathy.

5.Dyshormonal dysplasia of mammary glands include:

a)chronic mastitis;

b)gynecomastia (in men);

c)lipoma of the MG;

d)fibrocystic mastopathy;

e)cystoadenoma.

6.Benign tumors of mammary glands include all except:

a)fibro-cystic mastopathy;

b)fibroadenoma;

c)phyloid tumor;

d)gynecomastia (in men);

e)macromastia.

7.Special methods for the study of mammary glands include all except:

a)mammography;

b)fine needle aspiration biopsy;

c)trepanobiopsy;

d)phlebography;

e)computer and magnetic resonance imaging.

8.The main tumor cancer markers of malignant processes in the mammary glands include:

a)carcinoembryonic antigen (CEA);

b)cancer antigen CA 19–9;

c)prostate-specific antigen (PSA);

d)antigen squamous cell carcinoma (SCC);

e)cancer antigen CA 15–3.

9.Informative effect of fine-needle aspiration biopsy in neoplasms of MG reaches:

a)more than 95%;

b)40–50%;

c)70–80%;

d)less than 20%;

e)less than 10–15%.

10.The main indications for positron emission tomography for neoplasms of MG are:

a)assessment of the prevalence of the tumor process or its relapse;

b)evaluation of the effectiveness of treatment;

c)search for a primary focus with established metastases;

d)clarification of the prevalence of purulent process;

e)detection of the primary tumor up to 1 cm in diameter in the absence of its clinical manifestations.

11.Localization of the abscess distinguishes the following types of acute mastitis, except:

a)subcutaneous;

b)intramammary;

c)subserosal;

d)subfascial;

e)subareolar.

12.There are the following types of acute purulent mastitis:

a)infiltrative;

b)infiltrative-abscessing;

c)abscessing;

d)phlegmonous;

e)diffuse.

13.The entrance gates for infection in acute mastitis are:

a)hematoma of the MG tissue;

b)cracks and excoriation of the nipples;

c)skin breast damage;

d)Axillary lymph nodes;

e)intracanalicular infection.

14.Factors contributing to the development of acute mastitis are all except:

a)lactostasis;

b)mastopathy in the anamnesis;

c)anatomical features of the structure of MG;

d)cracks of skin in breast feeding or poor personal hygiene;

e)high levels of prolactin before delivery.

15.The main clinical manifestations of acute purulent mastitis are:

a)pain in the MG;

b)hyperemia and increased local temperature;

c)infiltration of tissue with symptoms of fluctuation and softening;

d)itching and change in nipple sensitivity;

e)increase in body temperature to febrile values.

16.By origin, the following types of acute mastitis are distinguished:

a)nonlactational;

b)focal;

c)inductive;

d)lactational;

e)hemorrhagic.

17.The main pathogens of acute mastitis are:

a)epidermal staphylococci;

b)E. coli;

c)protei;

d)streptococci;

e)pseudomonas aeruginosa.

18.In the case of serous-infiltra- tive forms of acute mastitis, treatment includes all except:

a)improvement of milk production;

b)carrying out of the retromemmaral novocain blockade;

c)introduction of broad-spec- trum antibiotics;

d)excision of lesion and conduct of flow-washing drainage;

e)local conduct of FTL.

19.The main principles of surgical treatment of purulent focus in mastitis are all, except:

a)the choice of rational access to preserve the function, the appearance of the MG;

b)radical necrectomy with an adequate way of draining the residual purulent cavity;

c)adequate fasiotomy;

d)early closure of the granulating wound by secondary skin seams or by skin plasty;

e)opening of the abscess with simultaneous application of cutaneous sutures.

20.Surgical treatment of a purulent focus in acute mastitis should be carried out with:

a)serous-infiltrative phase;

b)phase of regeneration;

c)the phase of scar formation and reorganization;

d)purulent-necrotic phase;

e)lactostasis and edema (MG).

21.For the opening of intramammary abscesses in acute mastitis, what incisions are most often used:

a)radial;

b)paraareolar;

c)along the course of the lower transition fold (BardenegarRavinsky);

d)on the lower edge of the breast;

e)axillary.

22.During the surgical treatment of the purulent focus in acute mas-

titis, physical methods of antiseptic are used by:

a)ultrasonic cavitation;

b)local administration of proteolytic enzymes;

c)plasma streams of atmospheric air or argon;

d)local ozone therapy;

e)antiseptics with pulsating jet lavage.

23.Prevention of acute mastitis includes all except:

a)prenatal preparation of breast for feeding;

b)the rational mode of feed-

ing;

c)prevention of postpartum complications;

d)interruption of lactation by parodel (dodonex);

e)preventive administration of antibiotics.

24.The synonym of fibrocystic mastopathy is:

a)Recklinghausen’s disease;

b)Dercum’s disease;

c)Paget-Shreter’s disease;

d)Schimmelbusch’s disease;

e)Madelung’s disease.

25.In the pathogenesis of fibrocystic mastopathy, all are isolated except:

a)combination of proliferative and regressive changes in MG tissue;

b)proliferation of epithelial and connective tissues of MG;

c)hormonal imbalance of female sex hormones;

d)activation of enzyme sys-

tems;

e)activation of anticoagulant properties of blood.

26.Regressive disorders in fibrocystic mastopathy include:

a)atrophy;

b)hyperplasia;

c)fibrosis;

d)formation of cysts;

e)proliferation of lobules and

ducts.

27.The diffuse form of fibrocystic mastopathy proceeds as follow:

a)predominance of the fibrous component;

b)mixed fibrocystic disorders;

c)fibromatosis;

d)adenofibroma;

e)sclerosing adenosis.

28.The nodular form of fibrocystic mastopathy proceeds as follow:

a)adenofibroma;

b)fibroadenoma;

c)adenosis;

d)fibromatosis;

e)the predominance of multiple cysts.

29.Unfavorable factors of the development of fibrocystic mastopathy are all, except:

a)functional disorders of the neuroendocrine system;

b)reproductive disorders;

c)gynecological diseases;

d)genetic predisposition;

e)hemocoagulation disorders.

30.Changes in MG tissue in fibrocystic mastopathy are characterized by:

a)proliferation of ductal epithelium;

b)proliferation of connective tissue with the formation of adenosis;

c)hypervascularization;

d)stromal fibrosis;

e)expansion of the intracanalicular ducts with the formation of cysts.

31.Diffuse form of fibrocystic mastopathy is clinically manifested by:

a)single mobile tumor-like formation decreasing after mensis;

b)diffuse radial traction with multiple tissue seals, depending on the phase of the cycle;

c)pain in palpation of the breast;

d)pain in the MG associated with the menstrual cycle;

e)the appearance of bloody discharge from the nipple.

32.The nodular form of fibrocystic mastopathy is clinically manifested by:

a)diffuse radial traction with multiple tissue seals;

b)single mobile lesion, depending on the phase of the cycle;

c)by the increase in axillary lymph nodes;

d)pain in palpation;

e)pain in the MG associated with the menstrual cycle.

33.The main instrumental methods for diagnosing fibrocystic mastopathy are all except:

a)positron emission tomography;

b)etermination of the proliferation marker for Ki-67 and HER 2-oncogene;

c)ultrasound sonography;

d)rheovasography;

e)magnetic resonance imaging.

34.The basis for treating the diffuse form of fibrocystic mastopathy is all except:

a)elimination of provoking etiological factors;

b)administration of antiestrogens, prolactin inhibitors or gonadotropin activators;

c)prescription of homeopathic medicines and herbal medicine;

d)long-term enzyme therapy;

e)sectoral resection of MG with histological verification.

35.The basis of treatment of the nodular form of fibrocystic mastopathy is:

a)sectoral resection with histological verification;

b)administration of nonsteroidal anti-inflammatory drugs;

c)long-term enzyme therapy;

d)homeopathic remedies and phytotherapy;

e)economical removal of the node with biopsy.

36.Fibroid adenoma of the breast is clinically characterized by:

a)slow growth of the tumor;

b)presence of calcifications in women over the age of 50 years;

c)the presence of a painless tumor of smooth-elastic consistency;

d)growth in pregnancy or lac-

tation;

e)appearance of the symptom of “lemon peel” and umbiliculation.

37.The features of leaf-shaped cystoadenoma of the breast are all except:

a)presence in the structure of connective tissue and epithelium;

b)as a “path” in the form of infiltration to the nipple;

c)rapid growth;

d)malignancy in sarcoma in 10–20% of cases;

e)has the type of erysipelas inflammation.

38.The main features of the structure of breast cancer are:

a)neoplasm of connective tis-

sue;

b)neoplasm of the epithelium;

c)reaches 20–30% of all types of malignant tumors;

d)peak incidenceis on 60–65

years;

e)most frequently the tumor is in women over 45 years of age.

39.Predisposing factors of development of cancer of the mammary gland are all except:

a)late first childbirth;

b)late menopause or early menarche;

c)mastopathy in history;

d)postpartum purulent-septic complications;

e)lactostasis.

40.The genetic factors that affect the development of breast cancer include:

a)genetic predisposition of the mother;

b)the presence of certain HLA antigens (A3-B14);

c)mutation of BRCA type 1

genes;

d)mutation of the genes p53 and oncogene K-ras;