10. Coma -

is pathological state characterized by deep inhibiting of CNS functions and expressed by consciousness loss, reflexes absence to external stimuli and organism vital functions dysregulation.

Aethiological classification:

1. exogenic – appear due to environmental pathogenic factors action or as a result of deficiency of factors necessary for organism existence. Exogenic comes examples are he following:

• traumatic (appears at brain injury);

• hypoxic;

• hyperthermic;

• hypothermic;

• exotoxic;

• alimentary-dystrophic (at hard fasting);

2. endogenous – is developed as a result of organism functional systems activity disorders:

-apoplexic – at blood circulation system dysfunctions;

-haemolytic – at blood system dysfunctions;

-uremic – at excretory system dysfunctions;

-hepatic – at liver dysfunctions;

-diabetic (hyperglycemic), hypoglycemic, hypocorticoid, thyreotoxic and others – at endocrinopathies.

Pathogenetic mechanisms:

1. Energetic deficiency – ATP synthesis disorder in CNS neurons leads to neurons generalized dysfunction. Mentioned mechanism is leading one in hypoxic, apoplexic, respiratory, haemolytic, hypoglycaemic, alimentary-dystrophic and exotoxic comas.

2. Synaptic transmittance disorders in CNS –can be connected with:

• neuromediators synthesis, transport, deponating and secretion disorder;

• neuromediators displacement with so-called pseudomediators (unreal mediators);

• inhibitory postsynaptic receptors excessive activation;

• exciting postsynaptic receptors blockade.

The mentioned mechanism is very important in hepatic, uremic and exotoxic comas develelopment.

3. General watery-electrolite disorders. Blood osmotic pressure changings and electrolyte equilibrium disorders are important for its development. This way is dominant in hyperosmolary diabetic coma, hypertermic, hypocorticoid and hypoparathyreoid comas.

4. Acid-alkaline state disorders –they lie on the base of acidotic diabetic, lactateacidemic, chlorhydropenic and some other comas.

5. Intracranial pressure increasing. This mechanism is switched on at brain primary injuries. It is main in comas development at meningitis and encephalitis as well as traumatic coma at cranial-cerebral traumas.

11. Informational aspects of cell injury. Pathology of signalization.

Cell injury ways

1. Disorder of energy consumption of processes occurring in cell:

a) ATP resynthesis process effectiveness or (and) intensivity reducing;

b) ATP energy transport disorder;

c) ATP energy usage disorder;

2. Sygnalization pathology (membrane apparatus and cell enzymatic systems injury):

a) free-radical reactions and peroxidative lipid oxidation excessive intensification;

b) hydrolases (lysosomal, membrane-bounded, free) significant activation;

c) amphyphylic chemicals involvement in membranes lipid phase and their detergent action;

d) membranes injured components resynthesis processes or (and) their synthesis (de novo) inhibiting;

e) prothein, lipoprotheins, phospholipids molecules conformation disorder;

f) swelled cells or (and) their organelles membranes overstretching and rupture.

3. Ions and liquids dysbalance, cell electrophysiologic features changing:

a) separate ions correlation changing in hyaloplasma;

b) ions transmembrane correlation changing;

c) cellular hyperhydration;

d) cellular dehydration.

4. Cell genetic program disorder and (or) mechanisms of its realization:

A. Genetic program disorder:

1. genes biochemical structure changing;

2. pathogenic genes derepression;

3. “vital” genes repression;

4. side DNA fragment (with pathogenic features) involvement in genome.

B. Genetic program realization disorder:

a) mitosis disorder:

-chromosome injury;

-injury of structures providing mitotic cycle;

-cytotomia process injury;

b) meiosis disorder.

5. Cells functions intracellular regulative mechanisms disorder (signal reception disorders):

1. regulatory influencings reception disorder;

2. secondary messengers formation disorder;

3. proteinkinases phosphorylation disorders.

12. PATHOLOGY OF SIGNAL RECEPTION AND SECONDARY MESSENGERS. MOLECULAR MIMICRY.

At a level of biological-active substances (hormones, neuromediators and others) interaction with cells receptors. Sensitivity changing, as well as changing of number or (and) receptor molecules conformation, its biochemical content or lipid surrounding in membrane can modificate essentially cellular answer character to the regulating stimulus. So, peroxidative lipid oxidation toxic products accumulation in myocardiocytes at ishemia determines their membranes (particularly cytolemma) physical-chemical content changing which is accompanied by heart reaction disorder to vegetative nervous system neuromediators noradrenaline and acetylcholine as well as other biologically-active substances.

At a level of cellular or so-called secondary messengers of nervous influencings: cyclic nucleotides – adenosinemonophosphate (cAMP) and guanosinemonophosphate (cGMP), forming as an answer to the action of “first messengers” – hormones and mediators. The example: membrane potential formation disorder in cardiomyocytes at cAMP excessiveness accumulation in them which is particularly one of heart arrhythmias possible developmental reasons.

At a level of metabolic reactions, regulated by cyclic nucleotides or other intracellular factors. So, cellular enzymes activation disorder can greatly change metabolic reactions intensivity and, as a result, lead to cells vital activity disorder.

When receptor can bind 2 different substances than such phenomena is known as molecular mimicry because one substance will change its structure for binding the receptor locus which is usually united only with other substance like “lock and key”.