Lectures 4

Lectures 4.

 

Wounds classification. Surgery process. Purulent wounds.
Necrosis, necrosis, gangrene, ulcers, fistulas.
Fundamentals of Clinical Oncology.

 

Wound – any mechanical damage to the body, which is accompanied by breach of integrity covering tissue – of skin or mucous membranes.

Classification of wounds:

1. On the mechanism of operating, random (combat).

2. The nature of damage: sliced, chopped, minced, slaughter, crushed, torn, bitten, poisoned, fire, mixed.

3. The degree of infection: aseptic, bacterial contaminated, infected.

4. In the course of wound channel: blind, continuous, tangent.

5. In relation to body cavities: penetrating, non-penetrating.

6. On the complexity: simple, complex.

7. On complication: complicated, uncomplicated.

8. In the area of ​​injury: wounds of the head, neck, torso, limbs, etc..

9. Combined wounds – mechanical damage, coupled with the effect of high or low temperatures, chemicals, radioactive substances and others.

 

Physico-chemical and biochemical changes in the wound.

Underlying biological processes is cell death, breakdown of proteins, the prevalence of anaerobic glycolysis over aerobic accumulation of biologically active substances – histamine, serotonin, kinins and others., Microcirculation disturbances, accumulation of toxic products of disintegration of tissues, metabolism and death of microorganisms.

Formation in anaerobic glycolysis and lactic pyruvic acid accumulation of carbon dioxide due to microcirculation disturbances, leading to the development of disorders of acid-base balance in inflammation, with development initially compensated, and decompensated acidosis. Acidosis causes exudative changes in the wound increases the penetration of capillaries. The migration of leukocytes, macrophages begin the shear pH to the acid side. Phagocytosis begins when a difference in pH in the wound and blood. Increasing the wound extracellular potassium increases the degree of acidosis.

Is changing the part of the colloids. The transition from a state of colloids in sol gel causes rupture cell membranes, destroying cells and the development of secondary necrosis in the wound. This in turn causes accumulation of free radicals, increased osmotic pressure violation circulation, increasing exudation and cellular infiltration, which leads to the development of “vicious circle” that determines the course of the inflammatory process in the wound.

In the inflammatory phase of wound healing process in the wound dominated catabolic processes over anabolic and a phase dominated by the regeneration of anabolic processes. In the course of the wound healing process affecting biologically active substances, which contributes to the accumulation of acidosis, active proteolysis, catabolic processes. Histamine, serotonin, heparin, bradikinin, kinins, prostaglandins cause effects on the processes of inflammation, vascular penetration and migration of leukocytes. A role in inflammation play enzymatic processes, as they are lysed necrotic tissue, accelerate wound cleaning.

 

Phases of wound healing process.

Currently, the most widely used classification phases of wound healing by M.I.Kuzinym (1977), according to which in the motion of wound healing process emit:

I phase – the phase of inflammation (1-5 days). It distinguished between vascular changes and period cleaning the wound of necrotic tissue;

Fig.1. Phase inflammation

–         II phase – the phase of regeneration (6-14 days);

Fig.2. phase of regeneration

 

–         III phase – the phase formation and reorganization of the scar and epithelialization (15 days).

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–        

Fig.3. phase formation and reorganization of the scar

I. Phase inflammation.

1. Period vascular changes characterized initially short spasm and then steady expansion paretic microvessels, under the influence of biogenic amines. Deficiency of blood in the affected area causes changes in trophic tissues with the development of acidosis and tissue edema. There exudation of plasma and lymph output and migration of leukocytes into the wound site, degranulation of mast cells, which creates conditions for cleaning wounds.

2. Period cleaning the wound of necrotic tissue. This process is implemented through phagocytosis with subsequent extracellular proteolysis, proteolytic enzymes by macrophages, tissue and bacterial enzymes and immune responses.

II. Phase regeneration.

In wound there are two main processes – kolahenizatsiya wounds and intense growth of blood and lymphatic vessels with the formation of granulation tissue. Formation of new blood vessels occurs through brunkuvannya old vessels (straight type formation of blood vessels), as well as directly in the tissues without regard to previous vessels (the second type of tumor vessels). Formation of granulation tissue occurs in the endothelial cells of capillaries. Granulation tissue includes a large number of fibroblasts – the main function of the formation of collagen fibers that provides maturation of granulation tissue and scar formation.

III. Phase formation and scar regeneration and epithelialization.

In this phase, the synthetic activity of fibroblasts and other cells ceases and the basic processes reduced to strengthen scar by constructing a grid of elastic fibers and the appearance of lumbar links between collagen bundles. both processes go epithelialization.

Factors that affect healing.

– Age of the patient;

– Nutritional status and weight of the patient;

– Overall health (comorbidity, circulatory disorders, infectious diseases, anemia, diabetes, etc.);

– The degree of infection of the wound;

– The state of the blood supply in the area of ​​destruction;

– Disruption of water and electrolyte balance of protein, carbohydrate and fat metabolism;

– Immune status of the body;

– Hormonal and immunosuppressive effects.

Types of wound healing.

There are three classic types of healing.

1. Healing by primary intention.

2. Healing by secondary intention.

3. Healing under the crust.

Healing by primary intention is the most economical and functionally beneficial, it is a short time to form a thin, relatively lasting scar. The primary intention healing surgical wounds when the wound edges touch each other.

To wound healed by primary intention to:

– Lack of wound infection;

– Dense matching edges of the wound;

– Absence of hematoma and foreign bodies in the wound;

– Absence of necrotic tissue;

– Satisfactory reactivity of the patient.

Healing by secondary intention is due to suppurating wounds caused by:

– Significant microbial contamination;

– Large-sized defect of skin;

– Presence of foreign bodies, hematoma;

– Presence of necrotic tissue;

– Reducing the overall reactivity of the patient.

Healing under the crust occurs when small injuries by type osadnen skin damage epidermis abrasions, superficial burns and others. In place of the lesions formed crust, which acts as a “biological dressing”. When crust is rapid regeneration of the epidermis and scab yourself away.

The difference in the types of healing is not qualitative but quantitative. That passes all three phases of the wound healing process, but in varying degrees of severity.

Clinical signs of wound.

1. Pain, which depends on the location of the wounds, damaged nerve trunks, character traumatizing agent, neuro-psychiatric condition the patient’s body.

2. Bleeding – which is determined by the nature and the diameter of the damaged vessel, the nature of traumatic factor, hemodynamic and coagulation system.

3. Ziyannya wounds by reducing the elastic fibers of the skin (lines of Langer).

Treatment of wounds.

General principles of treatment and problems in the treatment of wounds:

– Providing qualified first aid;

– Struggle with early complications;

– Prevention and treatment of infection in the wound;

– Achieve healing by primary intention in the shortest time;

– Full restoration of function of damaged tissues and organs.

First Aid aims to eliminate early life-threatening complication of the wound and prevent further infection of the wound. The most severe complications of early wound is bleeding, development of traumatic shock, damage to vital organs, fighting what is considered appropriate topics. Prevention of further infection is made by removing foreign objects from wounds and eliminating contamination of the skin around the wound, leather processing alcohol antiseptic solutions and overlay aseptychnoyipov’yazky.

Further wound (depending on the nature, location, volume and damage limitation) subject to the primary surgical treatment (PST) to prevent the development of septic complications and to create conditions for healing by primary intention.

PST – the first surgery, which is performed in compliance with the rules of asepsis and antisepsis in pain relief and includes the following sequential actions.

1. Dissection wounds – for a full audit of wound damage under direct vision.

2. Revision of the wound channel – under direct vision, finger, tools.

3. Excision edges, sides and bottom of the wound – to remove necrotic tissue, foreign bodies, infected surfaces.

4. Hemostasis – for prevention of bruising and bleeding secondary.

5. Restorative phase – restoration of damaged nerves, blood vessels, tendons, bones, etc. connections.

6. Closure of wound (with or without drainage drainage) or open of the wound.

 

Fig. 4 primary surgical treatment of the wound

 

The main types of PST.

1. Early PST – conducted in time to 24 hours from the time of the wound.

1. Deferred PST – held from 24 to 48 hours after application of the wound.

2. Late PST – is performed within 48 hours after application of the wound.

Indications for PST.

Fore be all random wound within 48-72 hours after their application.

Pho is made with:

– Superficial wounds, scrapes and osadnennyah;

– Small wounds on the edges of the difference is less than 1 cm;

– Multiple small wounds without damaging deep-lying tissues (eg shot wound);

– Puncture wounds without damage to internal organs, nerves, blood vessels;

– In some cases through-ball soft tissue injuries.

Contraindications for PST is the development of signs Purulent processes and the critical condition of the patient (terminal condition, shock IV st).

Types of stitches.

Primary overlapping sutures the wound to the development of granulation tissue, and the wound healed by primary intention.

There are:

– Primary suture – applied to the wound immediately after surgery;

– Primary delayed suture – applied for 1-5 days after Pho wounds in the absence of suppurative inflammation. A variety of data is provisionally stitches stitches – after surgery wound overlapping seams, but the thread tied 1-5 days at reduction inflammation.

Secondary overlapping sutures for granulating wound when there is no danger of suppurating wounds. A variety of data stitches are:

– Early secondary sutures – superimposed on the 6-21 day for granulating wound;

– Late secondary seams – imposed after excision of scar tissue wound edges (within 21 days).

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Fig. 5 provisionally suture

 

Purulent wound – a wound which developed infectious process due to hit and the development of microorganisms. Depending on the etiological factor suppurating wounds can be caused by gram-positive, gram-negative flora, anaerobic spore-forming microorganisms and asporogenous and specific microflora (syfylis, diphtheria, and others). Development of infection in the wound alter the course of wound healing process causes a variety of complications and delays wound healing.

 

 

Terms. contributing to the development of infection in the wound.

General:

– Reducing the total resistance of the body;

– Immunosuppressive conditions;

– Comorbidities (diabetes mellitus, systemic disease);

– Shock, bleeding, hypothermia and others.

Local:

– Violation of regional blood flow in the wound;

– The nature of the wound defect;

– The number of microorganisms in 1 g of tissue in the wound;

– Anatomic location of the wound;

– Reduction of the phagocytic activity of leukocytes;

– The presence of hematoma, nonviable tissue, foreign bodies in the wound, and so on.

“Critical microbial count” is 10⁵ organisms per 1 g of tissue. Such bacterial contamination of the wound leads to development of inflammatory process.

Clinical picture.

Local body reaction in the wound:

a) swelling (tumor);

b) redness (rubor);

c) pain (dolor);

d) increase in local temperature (color);

e) dysfunction (fundctiolaesa);

e) in some cases of wound “are purulent discharge.

Total body reaction manifested clinical symptoms of intoxication (fatigue, fever, headache, disturbance of water and electrolyte balance, carbohydrate and protein metabolism, acid-base balance, dysfunction of organs and systems, etc.)

Severity of local and general manifestations of purulent wounds depends on the reactivity of the organism and the immune system, the number and virulence of pathogens, character, localization and Purulent processes.

Healing festering wounds is the type of secondary tension with pronounced phase course of wound healing process.

Complications of septic wounds.

1. Secondary bleeding.

2. Purulent resorptive fever

3. Sepsis

4. Hypertrophic and keloid scars.

Treatment of purulent wounds

I. Surgical treatment:

Radical surgical treatment:

– Disclosure of purulent focus and pockets

– Necrectomy radical excision of nonviable tissue, removal of foreign bodies

– Drainage of the wound (passive, active)

Improved debridement

– Pulsating jet

– Vacuum processing

– Ultrasonic cavitation

– Laser

– Cryotherapy

II. Local treatment of purulent wounds

1. phase inflammation: the use of water-soluble antiseptics (furatsillin, chlorhexidine, dioxidin, Khlorophilipt, iodinol, etc.) and ointments on the water-soluble basis (levosyn, Levomekol, dioksydynova ointment, etc.), proteolytic enzymes sorbents.

 

 

Fig.6. Options for setting the active drainage

2. phase regeneration – preparations ointment base, preventing injury granulation tissue (sintomitsinovoy, tetracycline, etc.), stimulating substances (metyluratsylova ointment Solcoseryl, actovegin) compound ointment containing anti-inflammatory, antibacterial stimulating the means and stimulate regeneration (pantestin, Streptonitol and others.).

3. phase reorganization scar and epithelialization.

Used air “ties with indifferent and stimulating drugs and physiotherapy (UHF, UV, electrical phonophoresis, etc.).

Treatment in a controlled environment abacterial by vehicles Ata-3, Ata-5.

 

Fig. 7. The device is controlled abacterial environment and container to it

 

III. General treatment

1. Antibiotic therapy based on the characteristics of microbial pathogens and their sensitivity to antibiotics. Compliance with antibiotic therapy.

2. Detoxification therapy:

– Infusion of salt solution;

– Forced diuresis;

– The use of detoxification;

– Extracorporeal detoxification methods.

3.Imunokorehuyucha therapy – specific and non-specific.

4. Anti-inflammatory therapy.

5. Increasing the total resistance of the organism

6.Symptomatychna therapy.

 

 

Necrosis, necrosis, gangrene, ulcers, fistulas.

 

Necrosis

 

Necrosis is not an independent disease entities, but is a process that occurs in many diseases.

 

A) Terminology.

 

a) Necrosis (nekros – dead) – necrosis, uncontrolled cell death and tissue in a living organism under the influence of pathogenic factors.

 

b) apoptosis (apoptosis – programmed cell death) – genetically controlled process by which internal or external factors lead to the death of the old worn-out cells and their effective removal of tissue

 

– The process of apoptosis is a physiological and sustainable regeneration of cells;

 

– Morphologically evident apoptosis deaths single, randomly located cells, accompanied by the formation of rounded, surrounded by a membrane cells (“apoptotic ¬ til this”), which phagocytose immediately surrounding cells;

 

– While reducing apoptosis is an accumulation of cells (eg tumor growth), while increasing apoptosis observed a progressive decrease in the number of cells in the tissue (eg, atrophy).

 

c) infarction (infarctus) – necrosis of cells in organs that do not collide with the environment.

 

d) Gangrene (gangraena) – necrosis of tissue in contact with the external environment.

 

B) causes necrosis:

 

– Individuals (gunshot wounds, radiation, electricity, low and high temperatures – from ¬ morozhennya and burn).

 

– Toxic (acids, alkalis, salts of heavy metals, enzymes, drugs, ethanol and others., Such as chemical burns: the impact of acid – dry necrosis when exposed to alkali-moist necrosis).

 

– Biological (bacteria, viruses, protozoa, etc.)..

 

– Allergic (endo-and ekzoantyheny such as fibrinoid necrosis in infectious-allergic and autoimmune diseases, Arthus phenomenon).

 

– Vascular (necrosis resulting embolism, thrombosis, damage or compression of vessels, for ¬ example, myocardial infarction, gangrene of the lower extremities in obliterating endarteritis or atherosclerosis).

 

– Trofonevrotychni (pressure ulcers, sores that do not heal).

 

B) The pathogenesis of necrosis:

 

– Necrosis appears different clinical and morphological changes that depend on the structural and functional features of organs and tissues, speed and type of necrosis, and the reasons for its emergence and development conditions.

 

– Damage to cell membranes impairs their transport function and leads to an influx of calcium ions into the cell. Calcium activates endonuclease (hydrolysis, DNA cleavage), phospholipase (Bursting) and protease (destruction and digestion of the cytoskeleton).

 

– Chromatin condenses dead cells in large clumps and the core becomes smaller in volume, wrinkled (piknoz) and dense. Piknotychne core can burst into numerous small particles (karyorhexis) or subjected to dissolution (kariolisis).

 

– Cell digested by enzymes that are released from their lysosomes (autolysis) in the cytoplasm coagulate proteins, variable course of kollikvatsii.

 

– The intercellular substance evolving fibrinoid necrosis (collagen, elastic fibers and retikulin converted into dense, homogeneous mass that may be subjected fragmentation and disintegration or lysis). Rarely there kolikvatsiynyy necrosis (swelling, lysis and mucilaginized fibrous structures).

 

– After exposure pathogenic factor in 1 -3 hours there are changes that can be recognized by electron microscopy, after 6-8 hours – changes detected by light microscopy, and only after 12-24 hours and later developing macroscopic changes.

 

D) Classification of necrosis:

 

a) On the mechanism of action of pathogenic factors:

 

– Direct necrosis caused by the direct action of the factor (traumatic, toxic and biological necrosis);

 

– Indirect necrosis that occurs indirectly via vascular and neuro-endocrine system (allergic, vascular and trofonevrotychni necrosis).

 

b) The clinical and morphological forms:

 

• coagulation (dry) necrosis: coagulation of cytoplasmic proteins makes them resistant to the action of lysosomal enzymes, slowing their discharge and dead cells retain their shape for a few days.

 

Location: bodies, rich in proteins and poor fluids (kidney, myocardium, adrenal glands, spleen).

 

Causes: lack of blood flow and anoxia, the effect of physical, chemical, toxic agents and Nonbacterial bacterial origin.

 

Examples of coagulatioecrosis:

 

– Myocardial (most frequent type of necrosis) – a kind of vascular (ischemic) necrosis of internal organs (except the brain);

 

– Cheesy (caseous) necrosis specific tuberculosis, syphilis, leprosy and chlamydia;

 

– Waxy or tsenkerovskyy necrosis (necrosis of muscle in severe infections – tifah typhoid and typhus, cholera);

 

– Fibrinoid necrosis – the type of tissue necrosis observed in allergic and autoimmune diseases (eg rheumatoid arthritis, rheumatoid arthritis and systemic lupus erythematosus);

 

– Fat necrosis (enzymatic fat necrosis in acute pancreatitis and pancreatic injuries and nefermentnyy fat necrosis with injuries of the breast, or subcutaneous adipose tissue).

 

• Wet necrosis is characterized by fusion of dead tissue resulting from the action of its own enzymes (autolysis).

 

Location: tissue relatively poor in protein and rich in fluids, where there are favorable conditions for hydrolytic processes. Examples wet kolikvatsiynoho necrosis:

 

– Fireplace gray softening (ischemic infarction) of the brain;

 

– Necrosis of soft tissues of extremities against diabetic angiopathy.

 

D) Clinical manifestations of necrosis.

 

The severity of clinical manifestations depends on the type of necrosis, its location, the amount of damaged tissue on the total of the amount of safety features of tissue remaining:

 

a) Complaints:

– Pain in the affected area that the most intense in the development of irreversible nekrobiotychnyhzmin, which entail the death of nerve endings.

 

b) History:

– Traumatic injuries;

– Pathology of cardiovascular, neuroendocrine and other systems.

 

c) Objective data:

– Fever (due to the release of pyrogenic substances from necrotic cells and tissues);

– Tachycardia;

– Depending on the localization of necrosis: lower AT, arrhythmias, collapse in acute myocardial necrosis, impaired consciousness, sensation and movement in myocardial brain and others.

 

g) Review:

– In the areas of coagulatioecrosis necrosis of dry, dense, friable, white, yellow or black, practically odorless;

– When kolikvatsiynomu necrosis necrosis wet areas, with edema of surrounding tissues and an unpleasant odor.

 

e) palpation, percussion and auscultation reveal functional organ failure, which is localized necrosis:

 

– Acute heart failure as a result of extensive necrosis (myocardial) infarction;

– Impaired respiratory function in lung gangrene;

– Impaired excretory function with necrosis in the kidney;

– Impaired brain function in myocardial brain;

– Dynamic intestinal obstruction and peritonitis myocardial intestine.

 

E) Laboratory findings:

 

– When you connect to an acute inflammatory response occurs neutrophilic leukocytosis with a shift leukocyte formula;

– With biochemical studies may increase the level of enzymes necrotic cells that enter the bloodstream (eg, increased creatine kinase-MB isoenzyme characteristic of myocardial necrosis, because this enzyme is found only in myocardial cells, and increased transaminases characteristic necrosis of liver cells);

– In late term necrosis can be detected signs of toxic damage and organ failure.

 

G) Instrumentation Research:

 

The method of the research and its results depend on the localization of foci of necrosis:

 

– ECG myocardial infarction;

– Computed tomography myocardial brain;

– Doppler ultrasound or angiography in circulatory disorders of the extremities;

– X-ray in pulmonary infarction;

– Fibergastroduodenoscopy ulcers;

– Laparoscopy myocardial intestine.

 

F) Treatment of necrosis:

 

a) conservative treatment in case of myocardial infarction, brain, lung;

b) in the case of surgical treatment of bowel infarction, gangrene of the lower extremities.

 

Types of operations:

 

– Nekrotomiya – cut necrotic tissue to tissue fluid outflow and reduce swelling and progression of necrosis (eg circular burns of the extremities, chest);

 

– Necrectomy – once removing dead tissue delineated by dry necrosis due to various injuries or gradually as clear signs of non-viability (eg, frostbite, burns);

 

– Amputation of a limb or segment – running with gangrene at healthy tissue, the blood supply of sufficient healing of the stump;

 

– Resection or removal (hysterectomy) is performed in organ urgently with necrosis of the abdominal cavity;

 

c) conservative local treatment according to the principles of wound treatment;

 

d) improving trophic tissue to reduce the area of ​​tissue loss and improve wound healing (reduction in oxygen demand of tissues – limb immobilization, antioxidants, improve microcirculation – antispasmodics, Antiplatelet, anticoagulant, HBO).

 

3) The consequences of necrosis:

 

Necrosis – an irreversible process and its outcome can be favorable and unfavorable.

 

Favorable outcome:

 

– Replacement of connective tissue necrosis: around gangrenous tissue inflammation occurs jet demarcation that separates necrotic tissue demarcation zone.

Then there hyperemia and edema, there is a large number of leukocytes which melted necrotic masses and macrophages that resolving them. In place of the necrotic areas connective tissue cells proliferate and form scar (eg scar in place of a myocardial infarction).

 

– Encapsulation of necrotic – fouling connective tissue.

 

– Calcification (petrification) foci of necrosis – the deposition of calcium salts in dead weight when dry necrosis.

 

– Ossification – bone formation at the site of necrosis.

 

– Formation of cavities (cysts) in the area of ​​necrosis (usually found in moist necrosis and often – in the brain).

 

Unfavorable outcome:

 

– Necrosis of vital organs, especially large areas of them, often leading to death (myocardial infarction, ischemic necrosis of the brain, kidney cortex necrosis, progressive hepatic necrosis, acute pancreatitis that was complicated by pancreatic necrosis).

 

Purulent (septic) melt pockets necrosis occurs when you connect to a secondary infection.

 

Sequestration – the formation of areas of dead tissue that undergoes autolysis is not replaced by connective tissue and is freely among the living tissues (eg, osteomyelitis).

 

Variety sequestration – mummification (rejection of all fingers).

 

Development of severe complications (rupture of the heart in miomalyatsiyi, paralysis in hemorrhagic and ischemic stroke, infection with massive bedsores, intoxication due to exposure to the organism tissue decay products, such as limb gangrene, etc.)..

 

 

Gangrene

 

A) Terminology: Gangrene (gangraena – fire) – a necrosis of tissue in contact with the environment and change under its influence, often complicated by secondary bacterial infection.

 

B) The etiology of gangrene:

 

– Ischemic necrosis of tissue coagulation resulting in slowly progressive circulatory problems, burns acids;

– Accession of infection, which, under the influence of enzymes of microorganisms (heterolizys) a secondary kollikvatsii;

– Kolikvatsiynyy tissue necrosis resulting from rapid circulatory disorders (thrombosis, embolism, injury to blood vessels), alkali burns, necrotic forms of infectious inflammation.

 

 

B) Pathogenesis of gangrene:

 

a) Dry gangrene:

 

– In dry, wrinkled fabrics not penetrate microorganisms and white blood cells, so they prac ¬ cally not amenable to lysis and symptoms of intoxication are not expressed;

 

– On the verge of emerging leukocyte necrosis, and granulation demarcation shaft;

 

– Possible self rejectioecrosis with the formation of granulating tissue defects (wounds, ulcers).

 

b) Wet gangrene:

 

– Necrotic tissue containing normal or excess fluid and subjected to microbial contamination of putrid decay dead tissue;

 

– Demarcation shaft is not expressed, which promotes absorption of toxins and microbial degradation products in the blood and tissues of severe intoxication;

 

– In the surrounding tissue edema, capillary stasis, hypoxia, because wet gangrene tends to spread.

 

D) Classification of gangrene:

 

For clinical and morphological manifestations:

 

– Dry gangrene – coagulatioecrosis of tissue in contact with the external environment that runs without microorganisms. For example, limb gangrene in atherosclerosis and thrombosis of arteries (atherosclerotic gangrene) obliterating endarteritis, with frostbite or burns, gangrene of fingers in Raynaud’s disease or vibration disease, gangrene of the skin with typhus and other infections;

 

– Wet gangrene – the result of deposition oecrotic tissue changes of severe bacterial infection. For example, diabetic gangrene of the lower extremities, gangrene of bowel obstruction mesenteric arteries (thrombosis, embolism), pulmonary gangrene as a complication of pneumonia (influenza, measles).

 

In frail infection (usually measles) children can develop wet gangrene of the soft tissues of cheeks, perineum, which is called nomoyu (from the Greek. Pote – water cancer);

 

– Gas gangrene occurs when infected wounds anaerobic flora (eg, Clostridium perfringens and other microorganisms that group) is characterized by extensive necrosis of tissue and the formation of gas as a result of enzymatic activity of bacteria. D) Clinical gangrene:

 

 

 

The clinical picture depends on the type of gangrene and its localization.

 

a) Complaints:

 

– Pain in the localization of gangrene, the intensity of which decreases significantly after necrosis of tissue and increases when joining secondary infection;

– Sometimes fever;

– Complaints caused localized necrosis (hemoptysis in pulmonary infarction, delayed emptying and intestinal gases myocardial et al.).

 

b) History of the disease:

 

– The availability of chronic vascular diseases (atherosclerosis, occlusive disease, Raynaud’s disease, and others.)

– Infectious Diseases;

– Diabetes.

 

c) Objective data:

 

– Condition is more moderate or severe, especially in wet gangrene when pronounced manifestations of endogenous intoxication;

– Hyperthermia;

– Tachycardia.

 

g) Review:

 

– Pale skin;

– Active movement in the joints, which are in the localization of gangrene, sharply limited or impossible;

– The initial stage of necrosis of the skin occurring areas in dark blue, can be formed epidermal blisters filled with hemorrhagic fluid in their flaking exposing purplish-bluish dermis;

 

– In dry gangrene limbs black necrotic tissue (change colors through re ¬ making hemoglobin, in the presence of hydrogen sulfide in iron sulfide), dried (formed scab or mummification), practically odorless, clearly distinguished from viable tissue, on the border with them – the demarcation inflammation, lip skin is absent, mild swelling;

 

– With wet gangrene limb necrotic area swollen, red and black, with a large decay of dead tissue from the fetid exudate, crust is formed, inflammation is not clearly separated from the adjacent healthy tissue, spread it in the form of congestion, limfanhiyitu, thrombophlebitis, lymphadenitis .

 

e) Palpation:

 

– With gangrene limb pain at the site of inflammation, necrotic painless, they lack all kinds of sensitivity;

– In dry gangrene resulting from vascular disease limb below the cold of obliteration, in wet diabetic gangrene – ending heat, cold only in the area of ​​necrosis;

– In dry gangrene resulting from vascular disease pulsation vessels below the obliteration reduced or absent in wet diabetic gangrene – pulsation vessels, usually maintained, can be eased on the foot;

– With gas gangrene crepitus in the soft tissues;

– Myocardial intestine stomach pain, tense all over, gradually symptoms of peritonitis.

 

g) Percussion and auscultation show signs of dysfunction of internal organs in their necrosis.

 

E) Laboratory Methods:

 

– Neutrophilic leukocytosis with a left shift, lymphopenia;

– Signs of endogenous intoxication: hypoproteinemia, anemia, electrolyte imbalance, etc..

 

E) Treatment of gangrene – surgical removal of the gangrenous tissue

 

– With gangrene resulting frostbite benchmark is the demarcation line (¬ tion to form a clear demarcatioecrectomy not met);

– In wet diabetic gangrene amputation urgently away from the zone of necrosis and inflammation (eg, gangrene toes amputation at the middle third of the thigh);

– In dry gangrene resulting from vascular disease amputation zone satisfactory blood supply sufficient for next healing stump;

– With gangrene of the abdominal cavity – emergency resection or removal of the body as part of surgery for peritonitis.

 

 

Bedsores

 

A) Definition: bedsore (decubitus) – necrosis of superficial parts of the body (skin, soft tissue) that are squeezing.

 

B) The etiology of pressure ulcers:

 

– Compression of soft tissue between the bed and the bone in bedridden patients or with prolonged bed rest and lack of care;

– Prolonged compression plaster cast;

– Pressure on the supporting surface stump prosthesis.

 

B) The pathogenesis of pressure ulcers:

 

– Bedsore – it trofonevrotychnyy necrosis as compressed nerves and blood vessels, increasing trophic tissue disorders in critically ill, suffering from cardiovascular diseases, cancer, infectious and neurological diseases;

– There is tissue ischemia, then skiecrosis and subcutaneous tissue;

– Necrotic ulcer is long and almost no tendency to healing.

 

D) Localization of bedsores:

 

Pressure sores often appear in patients lying in the sacrum, spinous processes of the vertebrae, large swivel femur p’yatok, elbows, shoulder blades, back.

 

D) Clinical bedsores:

 

a) Complaints:

 

– While maintaining sensitivity pain in the bedsores.

 

b) Review:

 

– Initially appears pale skin in places long pressure that varies redness, and cyanosis (bluish color);

– Joins the swelling of the skin and there are blisters filled with fluid yellowish and later sukrovatoho color after opening formed erosion;

– If the action etiological factor is not removed, there is necrosis of tissue with the formation of the ulcer with necrotic bottom, which tends to spread depth and breadth;

– The treatment and proper care for patients on the spot erosion may form a dark brown or black scab.

 

c) Palpation:

 

– Tenderness tissues around bedsores.

 

d) Percussion and auscultatioot informative.

 

E) Laboratory and instrumental methods for the diagnosis of pressure ulcers are not used.

 

 

Fig.2 Bedsores

 

 

E) Preventing pressure ulcers:

 

– Frequent changes in body position in bed (up to 8-10 times a day except sleep time);

– Regular change of bedding and underwear and eliminate folds formed;

– Washing of places that are most susceptible to the formation of pressure ulcers, with warm soapy water and rubbing alcohol camphor, cologne, dusting talc;

– Planting under the pelvis, heels, elbows, neck rubber circles of linen pillowcase or use ¬ tions making use of special mattresses.

 

F) Treatment of pressure ulcers:

 

– It is desirable to exclude the patient lying on the side of the formation of bedsores;

– With the appearance of redness – rubbing alcohol camphor, cologne, a solution of potassium permanganate, quartz exposure of the skin;

– With blisters the skin treated with 70% alcohol or a solution of brilliant green;

– The appearance of erosions – measures aimed at reducing maceration: processing iodine antiseptics, ultraviolet irradiation, application of dressings sorbents;

– With deep ulcers – treatment similar to treatment of purulent wounds.

 

3) The consequences of pressure ulcers:

 

– There are long term, often heal only after eliminating etiological factor {for example, the transition to the active mode after prolonged bed regime);

– Addition of secondary infection from which the patient may die.

 

 

Fistula

 

A) Definition: Voles (fistula) – a pathological passage that connects the cavity, hollow organs

or pathological focus with each other or with the environment.

 

Artificial external fistula called stoma (Gastrostomy, epitsystostoma, tsekostomata al.). Artificial internal fistulas called anastomosis (hastroyeyunoanastomoz, ileotransverzo-anastomosis et al.). B) The etiology of fistula:

 

– Defects of embryonic development (median and lateral neck fistula, resulting from the infi ¬ forging medial and lateral neck cysts, which are pathological substrate remains rudimentary);

– Injury (intestinal fistula after injury);

– Trophic disorders (holetsystoduodenalna fistula resulting from bedsores gallbladder wall stone);

– Infection (chronic osteomyelitis, osteo-articular tuberculosis and others.)

– Collapse neoplasms (vesico-uterine fistula in cancer uterine or gastrocolic fistula gastric cancer);

– Therapeutic measures (artificial healing fistula or ligature postoperative fistula.

 

B) The pathogenesis of fistula:

 

– As a result of injury or inflammation of the disintegration of tissues;

– In parallel with the collapse occurs bonding, splicing together located near organs and tissues with connecting their clearance or clearance with skin;

– If distinguishing pathological focus and not marked fistula is formed, there are other complications: peritonitis, cellulitis, abscesses;

– Prevent fistula healing: constant leakage pathological contents (pus, bile, feces, etc.)., It clusters in the cavity, which is its source, or in the arms of fistulas course, the destruction of granulation tissue aggressive fluids (the contents of the small intestine, pankrea ¬ understanding that both policy juice etc.)., scar regeneration wall fistulas course;

 

D) Classification of fistula:

 

a) By origin:

 

– Congenital {eg fistula in the region of the navel as a result of cleft urahusa – urinary fistula or ductus omphalo-entericus – enteric fistula, rectal fistula with urinary ¬ genital system);

– Values:

 

♦ pathological – resulting from trauma, inflammation, tumors decay;

 

♦ artificial – formed by surgery to remove obstruction of the gastrointestinal tract (eg, syhmostoma in tumors that obturuye in the rectum), or feeding the patient (eg, Gastrostomy with esophageal cancer) on a permanent or temporary period.

 

b) the surface of the body:

 

– External – combined with the surface of the body;

 

– Internal – not connected with the body surface.

 

c) By lining fistulas move:

 

– Granulating – fistulas move paved with granulation tissue and can shut yourself or conservative treatment (often Acquired fistulas);

 

– Epithelial – fistulas course lined epithelium, which goes directly into the epidermis, so the fistula alone caot close (usually congenital and shtuchninorytsi);

 

– Mixed – fistulas course partially lined epithelium, and partly hranulyatsiynoyutkanynoyu.

 

d) According to the structure:

 

– Tubular fistula – organ cavity connected with skin fistulas course;

 

– Hubopodibni fistula – mucosal epithelium goes directly to the skin and fistulas channel is actually a hole hollow body (often artificial fistula, do not close yourself);

 

– Simple – have a channel without branches;

 

– Complex – with a complex extended structure of the channel.

 

e) The nature of content that stands out from the fistula:

 

– Urinary;

– Salivary;

– Excrement;

– CSF;

– Pus.

 

D) Clinical manifestations of fistula:

 

Clinical manifestations depend on the location and size of the fistula, the type and amount of content that stands out:

 

a) Complaints:

 

– With external fistulas – the presence of fistulas hole with content that is allocated to the fistula;

 

– Pain and skin irritation around the fistulas hole if the content has an aggressive nature (duodenal, and pancreatic fistula yeyunalni);

 

– With internal fistulas complaints caot be, or complaints caused by organ dysfunction (eg, diarrhea, weight loss and fecal burp at gastrocolic fistula, fecal discharge from the vagina with vaginal-rectal fistulas, income and output air through the hole fistulas during breathing bronchial fistulas).

 

b) History of the disease:

 

– Indication of inflammation, cancer of internal organs, or performed before surgery.

 

c) Objective data:

 

– With little loss of fistula condition is satisfactory, with more losses, especially at high fistulas of the gastrointestinal tract (stomach, duodenum and small intestine) – serious condition due to dehydration, electrolyte disorders and protein metabolism;

 

– Body temperature normal;

 

– In severe cases – tachycardia, hypotension, electrolyte disturbances with – seizures.

 

g) Review:

 

– A significant loss of fistula may decrease body weight (sometimes to the point of cachexia), pale skin, dry;

– With external fistulas: a hole in the skin from which released the contents of the organ and which begins with fistula;

– In the localization of the external opening of the fistula – perifocal dermatitis (edema, bright red color of the skin, lack of epidermis, soak increased bleeding), including the formation of ulcers.

 

e) Palpation:

 

– In the presence of perifocal dermatitis – pain in his area;

– With internal fistulas can palpate infiltrates, tumor formation.

 

g) Percussion and auscultation informative.

 

E) Laboratory findings:

 

– With fistulas with minor discharge pathological changes are not detected;

– A significant loss of intestinal contents and high fistulas developing hypo-and dysproteinemia, electrolyte imbalance, anemia.

 

E) These instrumental methods:

 

a) sensing fistulas move to set its depth and direction;

b) fistulography – X-ray study of the introduction of contrast medium through the external fistulas move. Allows you to set the length and direction of fistulas course, the presence of cavities, the connection fistula to the internal organs;

c) fistuloskopiya – endoscopy fistulas course that besides its characteristics, to assess the extent of epithelial lining;

d) contrast radiography of the gastrointestinal tract, bronchial tree, urinary tract reveals internal fistulas and install them topical diagnosis;

e) endoscopic study of hollow organs to determine the location and size of fistulas move from body to body.

 

F) Treatment of fistula:

 

a) conservative therapy:

 

– Removal of foci of chronic inflammation and the factors that support the operation: granulating fistula may contribute to its self-closing (eg, removal of foreign objects, ligatures);

 

 Local treatment: careful skin care, protecting it from the irritant action fistulas content using protective pastes and ointments;

 

– General treatment: nutrition, compensation fluid and electrolyte and protein loss, stimulation of repair processes;

 

b) surgical treatment is shown in epithelial hubopodibnyh fistulas.

 

Types of surgery:

 

– Cutting fistulas progress with removing its source (eg, cutting ligature fistula soft tissue);

– Disconnection or resection of internal organs in fistulas (eg, separation holetsystoduodenalnoyi fistula with cholecystectomy);

– Sealing fistulas course (eg, external pancreatic fistulas);

– Reduction surgery for external hubopodibnyh fistulas, which consist in mobilizing walls of hollow organs and stitching holes in it, or stitching of its walls to restore the continuity of the organ.

 

3) Complications fistulas:

 

The most common complication is joining secondary infection, which could lead to the closure of the external opening fistulas and abscess formation.

 

Fig.3. Trophic ulcer of leg

 

Ulcers

 

A) Definition: Ulcer (ulcus) – a defect of the skin and mucous membranes of the spread on hlybokolezhachi tissue that developed as a result of rejection of necrosis and stored for a long time as a result of failure of regeneration processes.

 

B) The etiology of ulcer:

 

a) tissue necrosis:

 

– Skin lesions at specific infectious diseases (such as syphilis, tuberculosis ¬ kuloz, leprosy);

– The collapse of malignant tumors of the skin or internal organs;

– Chronic disorders of blood and lymph circulation;

 

b) failure or breach of reparative processes in the body:

 

– Large amount of tissue necrosis;

– Hypoproteinemia, anemia, hypoxia as a result of exhaustion, vitamin deficiencies, metabolic diseases, systemic diseases;

– A disease of the arteries or veins, microcirculation failure;

– Organic diseases of the nervous system, reducing its trophic function (paralysis, syringomyelia, amyotrophic sclerosis, neyrosyfilista etc.).

– Long course of wound infection with degeneration of connective tissue results in disturbed microcirculation;

– The development of autoimmune processes, violation of protective properties of the mucous membranes, neuroendocrine regulation of organ function ( peptic ulcer).

 

B) The pathogenesis of ulcer:

 

– A leading factor in causing ulcers is a violation of trophic tissues, causing tissue defect after rejection or removal necrosis does not heal;

 

– While maintaining expressed violations trophic ulcer defect gradually increases as the area and deep into tissues, which can cause various complications ( arrosive bleeding ulcer perforation or penetration of hollow organs);

 

– With external ulcers, infection by attachment, it becomes chronic, recurrent course;

 

– Long-existing trophic ulcers turn into sores with blackout corned edges.

 

G) The clinical picture depends on the localization of ulcers, especially its origin and complications developed:

 

a) Complaints:

 

– With external localization – in the presence of ulcers, when you connect to infection – pain and swelling in the area of ​​ulceration;

– With internal localization – abdominal pain, dyspeptic disorders (nausea, vomiting, heartburn, belching, bloating, etc.)..

 

b) History:

 

– The presence of cardiovascular, neurological and other diseases, injuries.

 

c) Objective data:

 

– Condition of satisfactory to the plight that occurs with metabolic disturbances and wound cachexia or development of complications.

 

g) Review:

 

– With external localization: defect leather flat character, the bottom of which – granulation tissue pale pink or cyanotic color with patina and small fibrinous exudation. Granulation dull, badly bleeding. The walls and bottom of the ulcer scar sealed, fixed, marginal epithelization is not expressed, the surrounding skin may be hyper-pigmented, compacted. In the long edges of existing ulcers dense pidryti may protrude above the surface of the skin;

 

– The localization of ulcers on the lower extremities are often components of varicose veins or trophic skin changes (thinning, discoloration, hair reduction, etc.)..

 

e) Palpation:

 

– With external localization – slight tenderness and induration around the ulcer, skin warm;

 

– With internal localization – may be local pain stomach ulcers in the projection.

 

g) Percussion and auscultation informative.

 

D) Laboratory findings:

 

– Changes usually do not show;

– For the continued existence of large ulcers may develop anemia, dis-and hypoproteinemia;

– In the bacteriological examination of the ulcer may allocate specific or infectious agent.

 

E) Instrumental methods:

 

Choice of methods depends on the localization of ulcers and reasons that it caused:

 

– Anhioscaning or duplex Doppler in the pathology of blood vessels;

– Radiographic and endoscopic methods for the localization of ulcers in the gastrointestinal tract;

– When ulcers and localization of ulcers in the stomach biopsy tissue binding of ulcers.

 

E) Treatment of ulcers:

 

a) Pathogenetic treatment:

 

– Aimed at eliminating the causes that led to the formation of ulcers (eg, removal of varicose veins of the lower extremities with the elimination of abnormal reflux of blood from the deep veins in the leg trophic ulcer, eradication Helycobacter pylori in peptic

ulcer);

– Pathogenetic approaches difficult to be realized in systemic diseases and organic lesions of the nervous system.

 

b) symptomatic treatment:

 

– Cleaning the ulcer surface of necrotic tissue and elimination of infection (the use of proteolytic enzymes cutting necrosis);

– Improving the trophic tissue (nutrition, stimulants reparations such as pentoxyl, methyluracil and others., Vitamins, Antiplatelet, HBO);

– Local treatment (inhibition of infection, stimulation of repair, if indicated – plastic skin);

– Physiotherapy.

 

F) Effect of ulcers.

 

Treatment of ulcers – a lengthy process. Failure to eliminate the underlying disease that led to the occurrence of ulcers, cause their recurrence or treatment failure.

 

 

SUBJECT AND METHODS STUDY OF ONCOLOGY

 

 

Oncology (from the Greek. Onsos – inflation, logos-science) – the science that studies the causes, development mechanisms and clinical manifestations of tumors and developing methods of their diagnosis, treatment and prevention.

 

Tumor process as other typical pathological processes may develop in any organ or tissue. Factors that cause the development of tumors, frequently in production, the environment, the home. Because the tumor is a special kind of pathology, knowledge of the causes and mechanisms of development and required for the formation of medical thinking.

The tumor is a typical violation tissue growth, manifested in uncontrolled multiplication of cells, which are characterized atypical or anaplasia.

 

Etiology of tumors. Carcinogenic agents and their interaction with cells.

 

Found that tumors can be caused by physical, chemical and biological agents called carcinogens.

 

Over 75% of cancers in humans caused by environmental factors, especially – chemical compounds. The first experimental evidence of carcinogenicity of chemicals were experiments Yamahiva and Ishikawa (1915). They managed to induce skin cancer bunny ears by applying coal tar for 15 months.

 

Chemical carcinogens are very common in the environment, most of them have anthropogenic origin. However, we should not hyperbolize their role in human pathology, because only about 100 compounds and manufacturing processes considered carcinogenic to humans.

 

The chemical structure carcinogens are divided into several groups. The most important are polycyclic aromatic hydrocarbons, aromatic amines and amides, nitrosamines and nitrozamidy.

 

The first group owns more than 200 substances with three or more benzene rings. Only one of them – namely, 3,4-benzpyrene credited to those that can cause cancer in humans. Other causes tumors only in experimental animals. Carcinogens that group most in tobacco smoke, vehicle exhaust gases, smoke in blast furnaces, asphalt, waste chemical productions, dried and overcooked foods.

 

Substances with polycyclic structure exhibit predominantly local carcinogenic effect. If the experiment they applied to the skin, there is a cancer, if you enter under the skin, there’s sarcoma. Polycyclic aromatic hydrocarbons extracted from various organs of the body, and there are tumors of these organs: kidneys, skin, mammary glands.

 

The second group of carcinogens – is mostly azo dyes, which are characterized by the presence of two or more azohrup (monoazobenzol, 2-naphthylamine, benzidine). These substances are used for coloring natural and synthetic fibers in the printing industry, cosmetics, color photographs, for the synthesis of medicinal substances, insecticides. Carcinogenic effects of amines and amides appears when you enter them into the digestive canal, under the skin or in the skin lubrication. Tumors occur in organs remote from the site of injection, usually – in the liver, bladder, intestines, kidneys.

 

Nitro compounds (nitrosamines and nitrozamidy) are characterized by having an alkyl radical. They are used as antioxidants, pesticides, solvents, paints, intermediates in the synthesis of dyes, drugs and polymers. Carcinogenicity them to humans is not proven, but the experimental data cause cancer wary. The possibility of synthesis of nitro compounds in the gastrointestinal tract of man and nitrites, nitrates, oxides of nitrogen. Nitrites are widely used as food preservatives.

 

Almost all the chemicals themselves are not carcinogenic. They acquire these properties once get into the body and undergo metabolic transformations. It formed an idea of ​​the so-called final carcinogens that can interact with macromolecules of cells – DNA, RNA, proteins. Given the role of DNA in the transfer of genetic information, most attention is paid to the binding of carcinogens is with this acid. It was discovered a number of products that allow decipher subtle mechanisms of end carcinogens to DNA. They mainly metylyuyut guanine and violate complementarity purine bases – instead of the normal combination of guanine-cytosine formed parametylovanyy guanine-thymine. So carcinogens causing point mutations in certain positions of DNA. If these mutations are related to transforming gene, ie an oncogene, it starts a chain of events that lead to malignancy.

 

Radiation carcinogenesis. The physical carcinogens include ionizing and less – ultraviolet rays. Ionizing rays are not directly but through the formation of highly active free radicals that break DNA structure. Ultraviolet rays preventing its repair.

 

Viral carcinogenesis. There are many biological factors that are able to induce tumor growth. The largest group of viruses. These irrefutable evidence of viral origin of many tumors in animals – Routh sarcoma in chickens, fibroma and papilloma Shopa in rabbits breast cancer in mice (virus transmitted through milk). Number of presently known tumors in people who have undoubtedly caused by viruses are small – Berkita lymphoma, nasopharyngeal cancer, cancer of the cervix.

 

Viruses that cause tumors, called oncogene. They are divided into two groups depending on the molecular structure of the genome – RNA-containing and DNA-containing. The main group consists RNKomni oncogenic viruses that belong to a group of retroviruses. Their common characteristic is that they have a gene in a single-stranded RNA and enzyme RNA-dependent DNA polymerase (reverse transcriptase, revertazu). Essence virusindukovanoho carcinogenesis is to ensure that oncogenic viruses in infected cells make their genome, which includes transforming gene – a viral oncogene. Product of its activity (onkobilok) begins transforming cells and supports it in a transformed state.

 

Retroviruses – not the main cause of human cancer, but they point the way to understanding the major mechanism that underlies the disease. They acted as a model system by which received the latest data on thin molecular distortions that occur during cell transformation.

 

All this leads to the radical conclusion: the tumor begins with DNA damage. This mechanism is required for all tumors, regardless of what they are caused by carcinogens – chemical, physical or biological. All of them are carcinogenic precisely because that can disrupt the genetic apparatus. Chemical agents give mostly point mutations, ionizing radiation – mostly chromosomal, and retroviruses vklynyuyut in DNA cells additional genes, among which are oncogenes. Thus, DNA damage can be regarded as the molecular basis of these processes that transform normal cells into transformed. In other words, DNA damage – a common denominator, which reduces the effect of all known carcinogens.

 

 

 The pathogenesis of tumors. Molecular basis of carcinogenesis.

 

Stages of carcinogenesis. The emergence and development of tumors – a multistage process. Main stage three – transformation (initiation), promotion and progression. Activation of proto ends the first stage – the stage of initiation. The properties, which comes as a result of cell transformation in proto oncogene – a immortalizatsiya, ie its ability to potentially unlimited division to immortality. However, an active oncogene – is only potential to expression. A cell with an active oncogene years may be in a latent (drowsy) condition does not manifesting itself. Required additional impacts immortalizovanu cell, which would have brought it from the latent state and fueled rampant division.

 

Risk factors for tumor growth. These triggers may be additional doses of chemical or physical carcinogens retroviral superinfection, as well as a variety of agents, which in themselves do not cause tumors, but are able to bring immortalizovanu cell from the latent state. Hence the old idea of ​​the extraordinary bahatoprychynnist tumor growth, although in reality an absolute majority of the factors which attributed etiologic role should be attributed to predisposing conditions that cause expression of latent, potentially cancerous cells. Factors that activate precancerous cells are called promoters. Under their influence transformed cells are moving into a new stage of development – the stage of promotion, which is characterized by expression of cellular oncogenes.

 

If the involvement of oncogenes in carcinogenesis have no doubt that their mechanism of action remains a mystery. It was found that oncogenes encode specific proteins (onkobilky), most of which has tyrozynaznu activity. Then it turned out that onkobilky that cause uncontrolled growth of cancer cells similar to normal growth factors – platelet growth factor, epidermal growth factor, insulin-like growth factors. Iormal conditions, growth factors entering into the cell from the outside, it makes it dependent on the body. Tumor cells are characterized by the fact that they themselves produce growth factors. Some of them are designed to maintain their own proliferation (autocrine secretion), and some – for other types of cells (paracrine secretion).

 

Progression-last phase of tumor development. This term realize stable, irreversible qualitative changes of the tumor toward malignancy. For example, the hormone was hormoneindependent tumor, tumor responded to medication effects, ceased to respond. Progression – the last and longest stage of tumor development, which continues until the death of the body.

 

The most important clinical and pathological manifestations of tumor growth.

 

 The relationship between the tumor and the body. The negative impact of the tumor on the body depends on its type (benign or malignant), localization, growth and metastasis directions. Tumor directly damages the body in which it develops, disrupting its structure and function. Surrounding bodies undergo atrophy and deformation of hollow lumearrowing. Because chronic intoxication decay products and malnutrition develops cachexia. Depression hematopoiesis, excessive hemolysis and chronic bleeding leading to anemia.

 

If the tumor is composed of hormonally active cells, then there are diseases associated with hyper appropriate hormone or paraneoplastic syndromes: endocrinopathies, neurological manifestations (dementia, neuropathy), skin manifestations, hematologic effects (increased blood clotting, anemia, thrombocytopenia, polycythemia). Pheochromocytoma (tumor of adrenal medulla, which produces epinephrine) leads to the development of hypertension, insulinoma (tumor cells – islets of Langerhans) causes hypoglycemia, hastrynoma (tumor of the pancreas, which produces gastrin – a stimulant of gastric secretion) causes stomach ulcers.

 

The structure of tumors. For macro-and microscopic structure of various tumors. External their appearance may resemble a mushroom, cauliflower, node or swelling. Tumors of the cut mostly white, gray and pink colors. Often they are hemorrhage, necrosis and cyst cavity are written in mucus or bloody mass. Some tumors have a brown color, such as melanoma.

 

Dimensions tumors depend mainly on their origin, location and duration of growth. In some cases they can reach gigantic proportions (fibroids), in others they can be found only through a magnifying glass or microscope (mikrokartsynomy). Tumors localized near the vital centers are usually small in size.

 

Consistency tumors determined, above all, the original type of tissue and the ratio between the stroma and parenchyma. Tumors of bone, cartilage and fibrous connective tissue with a dense texture. Malignant tumors of the epithelium, which is slightly developed stroma, and flabby in texture reminiscent of newborn brain (cancer-mozkovyk).

 

Microscopically determined in each tumor stroma and parenchyma. Parenchyma – is a specific part of it, which is represented by tumor cells and determines the location of the tumor in histological classification. Even in tumors that originate from the mesenchyme, the cells that produce intercellular substance (collagen fibers, the basic substance of cartilage or bone), should also be attributed to the parenchyma. Stroma – a mechanically-trophic skeleton that includes connective tissue, blood and lymph vessels and nerves.

 

Most tumors in structure resembling a body that should parenchyma and fully expressed stroma. These tumors are called orhanoyidnymy. In undifferentiated tumors dominated parenchyma and stroma developed poorly. They are called histioyidnymy. They easily occurs circulatory failure, and therefore – necrosis. Along with this there are tumor, poor on parenchymal elements and rich stromal such fibrotic cancer or skir, stomach. These tumors give complications due zmorschennya stroma. They deform the body or constrict its lumen.

 

Tumors corresponding structure body in which it is localized, called homologous, and when its structure differs from the structure of the body, such a tumor is defined as heterologous. If the tumor develops from the cells of the body where it originated – is homotopically tumor. In cases where it arises from embryonic cells displacement (heterotopia), it is called heterotopic, for example, a tumor of the bone tissue in the uterus.

 

Tumor (neoplasm, tumor, neoplasm, blastoma) – a typical pathological process in the form of overgrowth of tissue in which there was a change of the genetic apparatus, characterized by infinite potential and nerehulovanistyu growth and atypical structural elements.

 

Biology of tumor growth. Universal and compulsory feature of all tumors – benign and malignant – is their ability for unlimited growth. This is a fundamental feature of any tumor. Uncontrolled excessive proliferation of tumor cells does not mean that they share rather than homologous cells of healthy tissue. On the contrary, some healthy tissue grow much faster than nayzloyakisnisha tumor, such as embryonic stem cells, the rate of regeneration of the liver. So, not speed division and growth, and the nature of his distinguished proliferation of tumor and normal cells.

 

Infinity growth of tumor cells is that they are not able to exhaust the resource division. It is shown that each cell is embedded genetic program that limits the number of its divisions. Tumor cells due to gene somatic mutation loses this program and begins bounding share “infinitely” avoiding aging, until the death of the host organism. If such cells from a living organism to move to another of the same species, they take root again and will share the death of the body of the recipient. If these cells are transferred to culture medium, and there they will share an infinite number of times, they become immune to the rule Heyflika. This ability of tumor cells to the unlimited division dominantly transmitted to subsequent cell generations.

 

Tumor cells is another characteristic feature – nerehulovanist growth. At the level of the whole organism cell growth is controlled by the nervous and endocrine systems, and at the local level – and mitogen keylonamy. Tumor cells gets out of control, that exhibits autonomy, independence growth. It is clear that this autonomy is not absolute, but to some extent characteristic of all tumors. If the tumor is partly retains the ability to undergo the controlling influence of hormones, then it is called a hormone, and if it completely loses this ability – hormoneindependent. Autonomy does not mean that the tumor has lost any connection with the body. These relationships have changed. They can be described as the relationship between the organism and the host-parasite tissue.

 

The third feature of cancer cells – anaplasia, which refers to rack their dedifferentiation, loss characteristic of normal cells ability to form specific tissue structures or produce specific substances. In other words, a return to the embryonic state, a simplified structural and chemical organization.

 

The tumor arises from a single mother cell that undergoes genetic mutation. From the common ancestor of normal tumor cells differ in many ways. This difference is related to the structure of cells and their organelles, metabolism, specific properties and functions. Therefore isolated morphological, biochemical, physical, chemical, immunological and functional anaplasia.

 

Description of morphological anaplasia reduced until the tissue, cellular and subcellular atypovosti. Tumor cells characteristic polymorphism – as they become smaller and larger sizes, as well as unusual forms of normal cells. The ratio between the nucleus and cytoplasm is shifted in favor of the nucleus due to its increase. There is a multi-core, giperhromatoz nuclei due to the accumulation of these nucleic acids, increasing the number of nucleoli and their migration into the cytoplasm. With major changes in subcellular structures undergo mitochondria. The number and size of their declining membrane thinner, Christie also become thinner and disappear. At the tissue level observed changes in the size and shape of the structures formed by tumor cells. This applies, for example, glandular follicles in adenocarcinomas and lesions skosteninnya in osteosarcoma. Sometimes the tumor completely loses morphological features that would indicate its origin from a differentiated tissue.

 

Biochemical anaplasia – it features the metabolism of tumor cells caused by changes in their genetic apparatus. Carcinogens caot only disrupt the process of mitosis and launch mechanisms unlimited division, but also inhibit or rozhalmovuvaty other genes. Because this is another enzyme spectrum of tumor cells. There intracellular dysfermentoz – some enzymes are inhibited, but others are activated and begin to synthesize entirely new substance, which in normal cells was not.

 

It was found that all tumors undergoing progression starting to become similar to one another by an enzyme set, no matter from which they are derived cells. Unification isozyme spectrum of tumors irrespective of their histogenesis – very typical manifestation ozloyakisnennya.

 

We know that every tissue synthesizing enzymes specific to it, each enzyme represented strictly specific set of isozymes. In tumors, this specificity is lost. Developing so-called Monotonization or isozyme simplification – the number of isozymes decreases, and their set is approximately the same for tumors of any origin. Isozyme restructuring goes towards increasing those enzymes that are inherent in embryonic tissues.

 

Most characteristic biochemical features of tumor cells for the exchange of proteins and carbohydrates. Protein synthesis predominates over their breakup. To build your own protein tumor carries amino acids from other organs (“tumor – a trap for nitrogen”).

 

Significantly different from normal carbohydrate metabolism and energy tumor cells. In aerobic conditions, normal cells provide themselves with energy mostly due to more favorable cleavage of glucose in the Krebs cycle and in anaerobic conditions forced passes to glycolysis. If oxygen is enough, glycolysis is inhibited respiration (Pasteur effect).

 

Tumor cells also provides its energy needs through glycolysis and respiration, but these processes repeatable value otherwise. Features Energy tumors: a) activation of anaerobic glycolysis and enzymes that provide it – pyruvate, hexokinase, fruktokinazy b) the presence of aerobic glycolysis, which normal cells caot (exceptions – white blood cells, sperm cells of the retina), c) inhibition respiration glycolysis (Krebtri effect), rather powerful system glycolytic enzymes intercept substrates – inorganic phosphorus, coenzymes.

 

Among the physico-chemical characteristics of tumor cells should provide the following: acidosis due to accumulation of lactic acid, intracellular hydration accumulation of potassium ions, increased conductivity, reducing the viscosity of colloids, increasing the negative charge of membranes, reducing their surface tension.

 

Antitumor immunity. In immunocompromised anaplasia understand changes antigenic properties of tumor cells. These changes – the result of the restructuring of protein metabolism. We know that every tissue synthesizes its specific set of antigens. In this set of tumors varies.

 

Antigens of tumors. There antigenic simplification and antigenic complications. Antigenic simplification characterized by the fact that the number of antigens produced by the tumor cell, reduced several times.

 

Antigenic complexity manifests antigenic divergence and antigenic reversion. Antigenic divergence is that the tumor cells begin to synthesize not peculiar to the corresponding healthy cells antigens, these antigens synthesized by other cells. For example, liver tumors can synthesize antigens spleen or kidneys. Antigenic reversion called tumor antigen synthesis. Cancer human liver synthesizes alpha-fetoprotein, which serves as a test for its diagnosis. As she begins ozloyakisnennya tumors synthesize antigens characteristic of all the earlier stages of fetal development.

 

The body is vulnerable to carcinogens and transformed (mutant) cells. It features a powerful defense mechanisms that prevent cancer or slow its progression. This includes a system of neutralization of carcinogenic compounds and removing them through the kidneys, digestive tract and skin. From mutant cells the body is cleared by immune surveillance function inherent in T-lymphocytes. There is also a system endonucleases, which provides repair damaged oncogenes and stops synthesis encoded onkobilkiv. On the growth of tumors also affect hormones – insulin, epinephrine, pituitary tropic hormones, thyroid hormones and gonads. This effect is not unique and depends on its combination with other mechanisms antyblastomnoho protection.

 

Functional anaplasia manifest loss or distortion performed cell function. In the tumor cells of the thyroid gland can decrease or increase the synthesis of thyroid hormones until the emergence of myxedema or hyperthyroidism. In hepatoma stops kon’yuhuvatysya bilirubin. In some cases, tumors begin to synthesize non-core products. For example, tumors of the lungs and bronchi can produce hormone-like substances.

 

Secondary changes in the tumor. In tumors may develop secondary metabolic disorders as mucilaginized, hyalinosis, obesity, calcification. For malignant tumors characterized by functional failure, since parenchyma always grows faster than the stroma. In addition, blood vessels often trombovani, which promotes the development of necrosis, on which there are sores, bleeding, and perforation.

 

 

Benign and malignant tumors.

 

From a clinical standpoint tumors are not equivalent. Depending on the degree of differentiation, speed and character growth, propensity for metastasis and recurrence, secondary changes in tumors, their effects on the body, they are divided into benign, malignant and destructive local growth.

 

Benign or mature, tumor cells are constructed from, the structure is always possible to determine from which tissue they grow. If they are not placed near the vital centers, the apparent local changes and slightly affect the body. However, these tumors may become malignant in – malihnizuvatys.

 

Malignant (immature) tumors constructed with little or undifferentiated cells lose their structural similarity to the cells from which they originate. Unlike benign tumors, they give metastasis, relapse, local changes occur and affect the entire body, not moving in differentiated form.

 

Tumors with local destructive growth occupy an intermediate position between benign and malignant. They are signs of infiltrative growth, but do not metastasize. These are cavernous hemangioma, desmoyid.

 

The main distinctive features of benign and malignant tumors

 

 Benign                                                                                                     Malignant

 

Have a slight deviation from the maternal tissue                                      Expressed atipizm: tissue and cellular

Expansive growth                                                                                     Infiltrative growth

Grow masse                                                                                              Grow rapidly

Attains a large size                                                                                    rarely reach large sizes

Rarely undergo forging expression                                                           often undergo ulceration

Do not give metastases                                                                             give metastases

Relapse is characterized                                                                            by frequent relapse

Not violate the general condition of the patient                                        have a significant effect on the entire body

 

The growth and spread of tumors in the degree of differentiation orhanizmi.Zalezhno distinguish expansive, apozytsiynu and infiltrative (invasive) form of tumor growth. The first form is characterized by benign tumors, second and third – malignant.

 

The tumor that grows expansively, increases in a node, pushing the surrounding tissue. Cells that surround it, atrophy and stroma collapse, which leads to the formation of pseudocapsule and crisp boundaries of the tumor.

 

Aposition height – intermediate between expansive and infiltrative. The tumor grows from multiple points of growth – focal proliferations that comprise “tumor field.” Neoplastic transformation (malignancy) sequentially from the center to the periphery and ends merger foci of malignancy in a single node.

 

 Infiltrative growth is characterized by the fact that the tumor elements are distributed in the direction of least resistance and grow into surrounding tissue, destroying them. The boundaries of the tumor in this case is not clear, erased.

 

In relation to the cavity body isolated endophytic and exophytic growth. As a form of considering peredinvazyvnyy or intraepithelial cancer. Histology revealed dysplasia, atipizm disappears posharovist its normal, but the basement membrane is not damaged.

Tumors that grow expansively, not extending beyond the body. In the case of infiltrative tumor growth extends not only to the body but also beyond. There are continuous contact tumor spread and metastasis.

 

Continuous distribution – is sprouting tumors in adjacent organs. In infiltrative growth of tumor cells can reach serosa, where there is reactive inflammation and fluid organization completes the formation of Unification with neighboring authorities. A Unification tumor invades these organs (eg, stomach cancer invades the liver or pancreas). When spliced ​​hollow bodies, the result of continuous proliferation and necrosis, the formation of fistulas (fistulas). Fistula colon, for example, observed in cancer of the stomach or gall bladder.

 

Metastasis – is the transfer of tumor cells from the primary lesion in remote areas with subsequent engraftment and formation of secondary foci. There are several ways metastasis – hematogenous, lymphogenous perineural, grafting, mixed.

 

Hematogenous metastases occur when tumor cells get into the bloodstream and move with the flow of venous or arterial blood. Spread across the veins – the most common way of metastasis. Thus there are two possible directions: the first – through the vena cava, when tumor cells from the primary lesion (uterus, kidneys, bones) are transferred to the lungs, the second – through the portal vein when the tumors of the stomach, intestines, pancreas metastasize to the liver . Sometimes possible paradoxical and retrograde metastases. Arterial road metastasis concerned primarily primary lesion localized in the lungs. This gives rise to metastases in the brain, bone marrow, liver and other organs. Hematogenous metastasis most peculiar way sarcoma.

 

Lymphogenic metastasis-carrying tumor cells in the regional and later – in distant lymph nodes. Subsequently, tumor cells through the thoracic lymphatic duct enter the circulatory system.

 

Perineural metastasis properly be regarded as an example of a continuous distribution. Cells were distributed through the cracks perynevriyu.

 

Implantation metastasis of tumors called spread through serous cavities or natural channels. When serosa invades tumor cells, they may come off and dissipate in serous cavities. Under favorable conditions, they take root and there are new pockets – Implantation metastasis. Macroscopically these metastases appear as white patches or bumps. Thus there hemorrhagic inflammation. Implantation metastases should be distinguished from lymphogenic metastases (carcinomatosis pleura, peritoneum) when these mounds are formed over the course of the lymphatic vessels. Rarely seen intrakanalikulyarne distribution. For example, cancer cells bronchus, esophagus, pharynx implanted in the lining of the small bronchi, stomach, intestines and cause the appearance of new tumors. Before implantation metastases also include perescheplenyy metastasis (transfer of tumor cells from the hands of a surgeon and instruments) and pin metastasis (transfer from one body to another, such as the upper lip to the bottom).

 

Cells metastases have the structure and function of the parent tumor. The intensity of metastasis depends on the degree of differentiation of the tumor and immunological reactivity. Relationship between tumor size and intensity absent metastases. Malignant tumor has the ability to metastasize from inception. Often metastasis size larger than the parent tumor. Most cells are carried to another place dies, metastases may long remain latent.

 

Recurrence of the tumor – a re-emergence of the same on the basis of the tumor in place treated or removed. Recurs as benign and malignant tumors, the latter – often.

 

The clinic isolated Precancer conditions (diseases in which increased risk of tumor development) and pre-cancerous changes (histological “abnormal” tissue). They are classified by the following types: a) abnormal regeneration, examples of which can be chronic bronchitis with epithelial metaplasia, mucosal leukoplakia, chronic atrophic gastritis, chronic stomach ulcers, skin ulcer with a slow course, and b) a chronic productive inflammation, especially gastric polyps and colon c) hormonal disease – proliferative breast disease, glandular endometrial hyperplasia, endocervicoses, prostatic hypertrophy, c) defects tissues – teratoma, liver and birthmarks.

 

Precancer processes caot be likened to etiology. The presence of precancerous changes does not mean that their background must arise tumor. Therefore, the degree of the threat of cancer, they are divided into optional (in which cancer occurs rarely) and obligate (in which cancer occurs quite often).

 

In practical work it is important to know, which is derived tumor tissue, ie clarify its histogenesis. If the tumor is constructed from differentiated cells that retain similarity to the parent, can accomplish this relatively easily. When dominated by undifferentiated cells determine histogenesis causes difficulties and sometimes even becomes impossible.

 

 

Classification of tumors. Terminology.

 

Modern classification is based on the principle Histogenetic considering morphological structure, localization, structure features in certain organs (orhanospetsyfichnosti), purity or malignancy. Title tumors ending in “Oma” (myoma, fibroma). Malignant epithelial tumors are called “cancer-cancer”, mesenchymal – “sarcoma” tumor of embryonic tissues – “blastoma” of several germ layers “teratoma.” Some tumors are called surnames, which they described – Kaposi’s sarcoma (angiosarcoma), Wilms tumor (nefroblastoma). Most common tumor used international system TNM, where T (tumor) – characteristics of the tumor, N (nodus) – presence of metastases in the lymph nodes, M (metastasis) – the presence of distant hematogenic metastases. By building the following types of tumors:

 

 a) epithelial tumor without specific localization (orhanonespetsyfichni);

 

b) organ epithelial tumors;

 

c) mesenchymal tumors;

 

d) tumor tissue from melaninoutvoryuyuchoyi;

 

 Nomenclature and morphological characteristics of the tumor tissues derived from mesenchyme.

 

Mesenchymal tumors – tumors that grow from the tissue derived mesenchymal: connective, adipose, mya “zova, vascular, bone, cartilage, synovial and serous membranes. These tumors have organ specificity, are less common than epithelial tumors.

 

Benign tumors of connective tissue:

 

fibroma (solid, m “position) – is found in the skin, uterus, ovaries, legs (everywhere where there is connective tissue) grows povino, expansively;

 

 fibrous histiocytoma or dermatofibroma – found in the skin, subcutaneous tissue;

 

fibromatosis (desmoyid) that are locally destruyuyuchyy infiltrative growth, but do not give metastases arise over the course of fascia, aponeurosis.

 

Benign tumors of adipose tissue:

 

lipoma (fibrolipoma, anhiolipoma, miyelolipoma) (Fig. 6)

 

hibernoma – a tumor of brown fat.

 

Fig. 6. Lipoma of chest

 

 

Benign tumors of muscle:

 

leiomyoma – a tumor of smooth mya’ziv more common in the uterus;

 

rhabdomyoma – tumor of striated muscle occurs mainly in children; granular cell tumor or tumor Apricot, localized in the tongue, skin, esophagus.

 

Benign tumors of blood vessels:

 

hemangiomas, which include angio capillary, cavernous angio, angio glomus (tumor Barre-Masson) – found on the toes or hands; benign hemanhioperytsytomu; chylangioma.

 

Tumors synovium

 

presented synoviomamy that most authors refer to malignant regardless of morphological structure.

 

Among the mesothelial tissue tumors more common fibrous mesothelioma.

 

In bone tumors include osteoma spongy and compact, benign osteoblastoma, osteoyid-osteoma.

 

Tumors of cartilage – chondroma are two options: ekhondromy and enhondromy and benign Chondroblastoma.

 

In tumors of mesenchymal origin also include giant cell tumor.

 

Malignant tumors of mesenchymal origin

 

called sarcomas from the Greek word sarcos-meat rare. In the context of the tumor with whitish-gray color, recalling “fish meat” these tumors usually metastasize through hematogenous. Since connective tissue fibrosarcoma occurs, which, depending on the degree kataplaziyi can be differentiated and poorly differentiated and malignant histiocytoma. Malignant tumor of adipose tissue – liposarkoma and malignant hibernomy grow slowly and for a long time does not give metastases. There are highly differentiated, miksoyidni, kruhloklitynni, polimorfnoklitynni liposarkoma. (Fig.7).

 

Fig.7. Pathomorphology tumor

 

 

Since muscles arise malignant leiomyoma, malignant tumor and rhabdomyosarcoma zernystoklitynna. Malignant tumors of vessels – from developing angiosarcoma endothelial and pericyte – malignant hemanhioendotelioma, hemangiopericytoma, limfanhioendotelioma, Kaposi’s sarcoma. In joints are malignant synoviomy in the peritoneum, pleura, pericardium – malignant mesothelioma. In developing bones osteoblastychni and osteolytic osteosarcoma, Ewing’s sarcoma, and cartilage – chondrosarcoma. (Fig. 8, 9).

 

 

Fig. 8. Breast Cancer                                         Fig.9. Squamous cell carcinoma.

 

 

Tumors of the nervous tissue. Tumors of the nervous tissue have several clinical features: in its course, they almost all malignant, irrespective of their morphological characteristics, as pressure on the adjacent areas of the brain, is spread within the nervous tissue without distant hematogenic metastases. Tumors of the nervous tissue is divided into neuroectodermal and meninhosudynni.

 

Neuroectodermal tumors are divided into astrocytic, oligodendroglial, ependymal tumors and horioyidnoho epithelial, neuronal, and embryonic poorly.

 

Astrocytic tumors may be benign – astrocytoma (fibrillary, protoplazmatychna, fibrillar-protoplazmatychna) and malignant – astroblastoma and occur in any part of the brain.

 

Oligodendroglial tumors presented oligodendroglioma and olihodendrohlioblastomamy.

 

By ependymal tumors include ependymoma, ependymoblastomy, horioyidpapilomy and horioyidkartsynomy. Among neuronal tumors secrete hanhlionevromu or hanhliotsytomu, hanhlioneyroblastomu, neuroblastoma. In poorly and embryonic tumors include meduloblastomu (usually found in the cerebellum and children) and glioblastoma (occurs in adults in the white matter of the brain, the second frequency is growing rapidly and lead to death).

 

Meninhosudynni tumors develop from the meninges and meningiomas presented and meningeal sarcomas. Meningioma (Fig. 10) are arahnoyidendotelialnymy and fibrous. Meningeal sarcoma by histological picture resembles fibrosarkomu.

 

Fig.10. Meningioma

 

Separately identify a group of tumors of the peripheral nervous tissue that develop mainly covers nerves. These include neuromas (shvanomy), neurofibromas, neurofibromatosis (Recklinghausen’s disease) and neurogenic sarcoma.

 

 The degree of proliferation of the malignant process is now generally accepted international classification of the TNM system. It operates in three main categories: T (tumor) characterizes the spread of the primary tumor, N (nodulus) displays the status of regional lymph nodes, M (metastasis) indicates the presence or absence of distant metastases.

 

Primary tumor classification is characterized by specified symbols TX, T0, Tis, T1, T2, T3, T4.

 

TX is used when the size and local spread of the tumor is difficult to assess. This situation occurs when tumors of internal organs when surgery is not possible with the audit result or distribution process, or refusal of surgery.

 

T0 – a primary tumor is not defined. In oncology, this situation sometimes occurs. So, according to some researchers, among patients with metastases in the lymph nodes of the neck in 8% of cases caot detect the primary location.

 

Tis – peredinvazyvnyy cancer or carcinoma in situ. This is the initial stage of the tumor without evidence of invasion through the basement membrane. These tumors are often diagnosed as finding patohistoloha that explores precancerous pathology (polyps, ulcers, erosion).

 

T1, T2, T3, T4 – symbols that define the character of growth, the degree of germination of the primary tumor into the surrounding tissue and organs. For different locations of tumors, these characters may be unequal. For example, breast tumors up to 2 cm is defined as T1, 2 to 5 cm – T2, over 5 m as T3.

 

Status of regional lymph nodes define categories NH, N0, N1, N2, N3.

 

NH – insufficient data to assess the lymph nodes often observed in tumors of visceral localizations.

 

N0 – no clinical and histological signs of metastases in the lymph nodes.

 

N1, N2, N3 – Displays information about the different degrees of metastatic lesions in regional lymph nodes.

 

For each localization characteristics of these different characters.

 

MX M0, M1 – characterize the presence or absence of distant metastases.

 

MX – not enough data to identify distant metastases. This situation arises when their presence caot be verified by special methods of investigation.

 

M0 – no signs of distant metastases.

 

M1 – have distant metastases.

 

Histopathological differentiation

 

In most cases, additional information relating to the primary tumor can be marked as follows:

 

G-histopathologic differentiation

 

(EX degree of differentiation caot be established. GI high degree of differentiation. G2 Average degree of differentiation. G3 low degree of differentiation. G4 undifferentiated tumors

 

Note. G3 and G4 in some cases may be combined as «G3-4 low differentiated or undifferentiated.”

 

Additional symbols classification

 

In some cases, the definition of TNM or pTNM used characters in, r, a, m. While these characters and do not affect the group on stage, they emphasize the need for a separate analysis of the case. Using additional characters not required.

 

in character. Used in cases where the classification is determined during and after the application of different treatments. TNM or pTNM category defined in the symbol.

 

g. Tumor recurrence defined symbol g

 

a Symbol. Indicates that the classification is first determined at autopsy.

 

m symbol. Used in cases of multiple primary tumors.

 

 

Optional characters

 

L – Invasion of lymphatic vessels

 

LX invasion of lymphatic vessels caot be estimated

 

LO invasion of lymphatic vessels absent

 

L1 is an invasion of lymphatic vessels

 

V – Invasion of veins

 

VX venous invasion caot be assessed

 

VO invasion veins absent

 

VI are microscopic venous invasion

 

V2 are macroscopic venous invasion

 

Note. Macroscopic involvement wall veins (without the presence of tumor tissue within the vein) is classified as V2.

 

 

C-factor

 

C-factor, or “level of security” reflects the reliability of classification based diagnostic methods used. Its use is not mandatory. C-factor is divided into:

 

C1 Data standard diagnostic methods (clinical research, x-ray, endoscopy)

 

C2 Data obtained by using special diagnostic techniques (x-ray in special projections, tomography, computed tomography, ultrasound, scintigraphy, mammography, magnetic resonance, endoscopy, angiography, biopsy, cytology)

 

C3 Data only trial of surgery, including biopsy and cytology

 

C4 Data obtained after radical surgery and operational research drug

 

C5 Data section

 

For example, the degree of applicable to T, N and M categories. You can describe a particular case as follows: TZS2, N2C1, MOS’2.

 

Thus, the clinical TNM classification for treatment meets C1, C2, C3 with equal degree of reliability, pTNM equivalent to C4.

 

Residual tumor (R classification)

 

The presence or absence of residual tumor after treatment is denoted by R. Its use is not mandatory. Classification TNM and pTNM describe the anatomical distribution of cancer without treatment applied. Classification can be supplemented R classification associated with the state of the tumor after treatment. This reflects the efficacy, impact on future therapeutic procedures and significantly affects the prognosis.

 

RX is insufficient data to determine the residual tumor

 

RO residual tumor absent

 

R1 residual tumor determined microscopically

 

R2 residual tumor determined macroscopically

 

There are four stages in the course of malignant tumors:

 

I Stage – small tumors without metastases;

 

II Stage – a tumor of considerable size, but within the affected organ, with metastases to regional lymph nodes;

 

III Stage – a tumor that went beyond the organ in which they arise, with multiple metastases in the lymph nodes and infiltration of tissues;

 

Stage IV – very advanced tumors with regional and distant metastases.

 

The most effective treatment of patients in stages I and II, in stage IV applies symptomatic treatment.

 

 

No less important in clinical oncology is the classification of patients with malignant tumors in clinical groups.

 

IA clinical group – patients with suspected malignant tumor. Within 10-14 days so ill install or remove a malignant tumor diagnosis.

 

IB clinical group – patients with benign tumors or precancerous conditions.

 

IIA clinical group – patients who diagnosed as “malignant tumor” and subject to radical treatment.

 

II clinical group – patients who are subject to special treatment.

 

III clinical group – patients who are subject to radical treatment and practically healthy persons.

 

IV clinical group – patients to be symptomatic treatment.

 

 

Clinical manifestations of tumors

 

Tumors are characterized by asymptomatic. Therefore, in the initial stages of tumor diagnosis is difficult and requires a thorough examination of patients and the use of special methods (fluoroscopy and radiography, endoscopy, cytology discharge, etc.)..

 

In connection with asymptomatic tumors important for early detection of a preventive checkups and health education among the population.

 

Benign and malignant tumors in areas accessible inspection and palpation, svoyechasnishe diagnosed than tumors of internal organs.

 

For the diagnosis of tumors of internal organs are very important special methods. Thus, for the diagnosis of tumors of the alimentary canal, lungs, pleura, bones and others. critical x-ray.

 

When tumors of the bladder conduct endoscopy with cystoscopy. Important role played by cytological analysis of sputum in lung cancer. Widely used term histological study sites of tumor or its metastases (biopsy).

 

Malignant tumors cause disturbance of the general condition. Patients complain of general weakness, fatigue, loss of appetite, weight loss.

 

Due to the growing tumor disorder marked bodies. Thus, gastric cancer is significantly reduced gastric secretion, in cancer liver function is disturbed it develops jaundice etc.

 

Tumors impair normal patency, compressing the lumen of various organs. Thus, in esophageal cancer disturbed patency food until complete cessation of her stomach. In cancer pyloric difficult passage of gastric contents into the intestine, with intestinal tumors resulting obturation lumen develops intestinal obstruction. For tumors of the prostate is typical dysuria until the complete urinary retention.

 

One of the characteristic symptoms of malignant tumors is bleeding that occurs due to destruction of their vessel wall. Yes, hemoptysis and pulmonary hemorrhage observed in lung cancer, gastrointestinal – gastric cancer, uterine – cancer of the uterus. Isolation of blood in the urine (hematuria) is characteristic of renal tumors and bladder.

 

In the hospital diagnosis of tumors, especially in the early stages, can cause some difficulties, despite thorough clinical examination and the use of special diagnostic methods. In these cases, conduct prompt diagnosis to direct inspection and palpation of the body (stomach, intestines, etc.).. In doubtful cases resort to urgent histological examination (biopsy).

 

 

             Methods of test. In the diagnosis of cancer is very important medical history and life. Good collected history can sometimes detect early stages of the disease, as well as a precancerous condition. Hereditary predisposition also has significance for diagnosis.

 

         Physical examination includes examination of the patient, with special attention to the lymph nodes. When the feeling of the tumor to determine its boundary, mobility, communication with surrounding organs and tissues, tenderness and consistency. All women h cancer should be subjected bimanual gynecological examination to exclude pathology of the female genital lesions and secondary tumors of the pelvis. In the diagnosis of malignant diseases is important laboratory research. Hidden blood in secretions (feces, mochyvshy, sputum) is often a symptom of cancer.

 

Radiological research plays an important role in tumors of many organs. Conducted fluoroscopy, radiography (Fig. 11) and imaging studies, which provides a layering images Authority.

 

Fig. 11. Kartsinoma lungs. X–ray study

 

Computed tomography (CT) is one of the methods of cancer diagnosis that uses special x-ray equipment to obtain images of the body section. Getting any X-ray image based on the different densities of organs and tissues through which the X-rays (Fig.12, 13.14). This procedure is also called “axial computed tomography.”

 

 

Fig. 12. Apparatus for computer tomography.

 

Fig. 13. Apparatus for magnetic resonance imaging.

 

Fig.14. Tumor of Spinal cord.

 

Significant place in oncology occupy endoscopy. It is now widely used esophagogastroduodenoscopy (Fig. 15.16), laparoscopy, bronchoscopy, rektoskopiya, cystoscopy, colposcopy, etc. With these methods it is possible not only to examine the eye tumor, but also take swab zmyvshy and biopsy. Taken biopsy material sent to the laboratory with a note, which stated the name of the patient, his initials, year number, month of birth, number of medical history or medical card, from which the body is taken a piece of fabric and alleged diagnosis. At the direction of unacceptably inaccurate documentation, as it may lead to serious errors in treatment, because the results of histological examination tactics determine further treatment.

 

Fig. 15. Fibrogastroscopy

 

Fig. 16. Tumor restenosis, which developed 6 months after papillosphincterotomy

 

Widely used puncture biopsy performed thick needle or trocar (tumors of the soft tissues, bones). Column material obtained while subjected to the usual microscopic study. The results of microscopic examination determine the extent of surgery. For example, all breast tumors are resection with urgent biopsy. If confirmed cancer performed radical mastectomy (removal of the breast). Tsytolohychne research was of great use in the diagnosis of malignant tumors. Conduct research punctates of tumors, tumor-like formations, lymph nodes and internal organs (liver, spleen, kidneys, etc.), and various secretions and excreta. Puncture is made in compliance with all the rules of asepsis. From the material obtained by puncture, preparing smear, which is dried, paint and examined under a microscope (Fig. 17.18).

 

Fig. 17. Biopsy of brain

 

Fig.18. Light microscope on the stage which is a piece of glass with colored histological pattern.

 

There are also studies of prints from the surface wounds, tumors, washouts mucous membranes, wound surfaces.

 

 

General principles of treatment of tumors

 

         Treatment of the patient, who diahnozovano malignant novoutvir defined biological, general and pathologic criteria.

 

  Local biological criteria include: histological structure (degree of differentiation) of the tumor, its form of growth, spread (stage process), and the dependence of growth on the level of certain hormones.

 

   Common biological criteria include status:

 

– General immunity

 

– Antitumor immunity

 

– Hormone metabolism in the body of the patient,

 

– General metabolic processes in the body.

 

By pathophysiological criteria include:

 

– Age of the patient,

 

– The functional state of the cardiovascular, respiratory and excretory systems

 

– Comorbidities.

 

 

 Principles of treatment of malignant tumors.

 

In oncology, there are three basic methods of independent special treatment: surgery, radiation and chemotherapy. The effectiveness of treatment depends on the degree rozpovsyudzhenennya tumor histological its structure, localization, individual patient, including the degree of intensity of its immunity. The above methods are often used in certain combinations and in combination with other treatments. In addition to the basic techniques, there are additional or Adjuvant, which themselves do not stop cancerous growth, but increase the efficiency of the basic methods or eliminate or reduce the negative impact of the past on the body. Such methods include immune, hormonal, local hyperthermia, methods synchronization of cell division, baro-, magnet and more.

 

Combined treatment – the use of two or three main methods in any order or simultaneously. For example, preoperative radiotherapy, surgery, postoperative chemotherapy.

 

Complex method – application along with the main methods of adjuvant. For example, preoperative chemotherapy, surgical treatment, postoperative hormone and immunotherapy.

 

In the early stages of the disease usually is enough to use one of the methods of treatment, usually surgery or radiation. In common malignant tumors need combined or complex treatment.

 

For most malignancies cardinal method of treatment is surgery, which is used either alone or in combination with others. It has its own characteristics, which partly distinguishes onkohirurhichni approaches from zahalnohirurhichnyh.

 

When radical surgery (Fig. 19, 20) in oncology understand this, which involves removal of the tumor within healthy tissue in one block the paths of regional metastasis. For example, surgery for cancer of the breast is removed from the mammary gland tumor, large and small pectoral muscles, tissue from lymph nodes axillary and subclavian chuck plots. The concept of “radical surgery” is purely clinical. This does not mean that all cancerous cells removed from the body. Therefore, even after radical surgery possible extension of the disease and in most cases Adjuvant therapies reduce the risk of recurrence and metastases.

 

Fig. 19. Gastric leiomyoma on the operation

 

 

Fig. 20. Leiomyoma stomach – macropreparation.

 

 

In oncosurgery great importance is ablation and antyblation.

 

Ablation – a set of measures aimed at the prevention of dissemination of malignant cells in the wound. They are:

 

1) Prevention of trauma tumor during surgery;

2) removal of the tumor within healthy tissue;

3) removal of the tumor in one block of the regional lymph nodes;

4) primary operations in early ligation of blood vessels coming from the body, which is to be removed to prevent hematogenous metastasis;

5) isolating wipes tumor if it sprouted in serous membrane and contact with other tissues;

6) the use of a laser scalpel diathermocoagulation and cryodestruction that destroy cancer cells and blocking their way to the surface tissues;

7) periodic hand washing, replacement of gloves and instruments during surgery;

8) neoadjuvant (preoperative) course of radiation or chemotherapy, thus reducing the possibility of metastasis during a surgical trauma.

 

Antyblation – a set of measures aimed at the destruction of the scattered field in the operating cell tumor. They are:

 

1) 96⁰ ethanol processing areas where there is contact with the tumor;

2) debridement solution chlorhexidine and dioxidin;

3) Use long-acting forms of chemotherapy that immobilized on polymetilsyloksani or liposomes.

 

For antyblation also offer short-radiotherapy on wound and laser irradiation after previous administration photosensitizing.

 

Fig.21. Removal of retroperitoneal tumors.

 

Among surgery on tumors distinguish radical that can be made when the operable tumor and the absence of distant metastases (Fig. 21), and palliative care, which prevents the patient from suffering inflicted tumor that grows, and partially or fully restore the function of the affected body. For example, in some tumors, stomach, impeding the passage of food, overlay bypass spivustya between the stomach and small intestine saves the patient from vomiting and starvation.

 

Metastatic pleurisy, which often occurs in inoperable tumors of the lung and breast cancer, an indication for pleural puncture and drain fluid from the pleural cavity in order to alleviate the suffering of the patient.

 

Preparing cancer patients to palliative surgery is no different from preparing for difficult zahalnohirurhichnyh operations. However, patients with tumors often exhausted and time on their training and examination is limited. Therefore of particular importance for these patients with blood transfusion regimen enhanced food, long son.Hvori with recurrences, metastases, which are not subject to surgical and radiation treatment, are symptomatic (medical) treatment aimed at reducing the suffering of the patient and mainly pain. Treatment in most cases is carried out at home, since the life expectancy of some patients with common forms of cancer that are not subject to radical treatment, sometimes up to 1 to 3 years. Therefore, symptomatic treatment and organized medical staff caring for such patients should be designed to more or less long term and aimed at improving the overall condition, fighting pain, insomnia and bleeding from the tumor, decaying, while maximizing protect the psyche of the patient and maintaining hope for recovery. Regular visits to the patient to perform assignments (subcutaneous injections, dressings, etc.)., Holding control over its content and power necessary for the implementation of symptomatic treatment. Widespread rehabilitation of cancer patients, especially in diseases and defects of the musculoskeletal system. The essence of rehabilitation is to restore lost or weakened functional or psychological abilities of the patient, the development of compensatory mechanisms by surgical, medical and spa treatments.

 

Vocational rehabilitation is to teach people that lost efficiency, new professions available to them for health reasons. During rehabilitation of rational means of employment.  

 

Authores- doc.L.Yu. Ivashchuk