- •Pathophysiology tasks:
- •General doctrine of disease. Basic concepts of general pathology: norm, health. Definition by who. Disease.
- •Disease.
- •Conception of pathological process, pathological state, pathological reaction. Definition of typical pathological processes.
- •Typical pathological processes are the processes which are developed by similar laws, independently on reasons, localization, animals type and organism individual peculiarities.
- •Disease difference from health
- •3 Points of view:
- •Disease, biological and social factors are actual because human being is first of all social creature
- •4 Levels of diseases prescription:
- •5. Diseases classification principles:
- •8. Collapse. Comparative characteristics with shock. Aethiology and pathogenesis. Role of nervous and humoral mechanisms
- •9. Crash-syndrome -
- •10. Coma -
- •11. Informational aspects of cell injury. Pathology of signalization.
- •13. Programmed cell death (pcd)
- •3 Apoptosis phases:
- •14. Outcomes of apoptosis inhibiting and activation.
- •Classification.
- •4 Main types.
- •Classification.
- •16. The concept of primary and secondary alteration. Molecular mechanisms of cell injury. Lipid mechanisms role in alteration pathogenesis.
- •17. Free radicals and their role in pathological processes development.
- •19. Antioxidant mechanisms of cells. Antioxidant insufficiency.
- •19. Apoptosis and necrosis comparative characteristics.
- •20. Reactivity. Types. Dependence on sex.
- •23. Resistance. Passive and active resistance. Resistance and reactivity relationship.
- •25. Constitution, role in pathology, types classification.
- •26. Diatheses.
- •27. Stress, general adaptation syndrome.
- •28. Stress-inducing and stress-limiting systems. Diseases of adaptation.
- •29. Concept of “local microcirculatory disorders”. Some mechanisms.
- •30. Arterial hyperemia
- •2 Subtypes:
- •31. Venous hyperemia
- •32. Ishemia
- •33. Reperfusion syndrome
- •34. Stasis.
- •Variants:
- •35. Thrombosis and embolism. Thrombosis characteristics.
- •3 Main factors encouraging thrombi formation (Wirhow’s triad):
- •36. Embolism.
- •37. Embolism of pulmonary, systemic and portal circulation.
- •38. Microcirculation disorders typical forms:
- •39. Intravascular circulation disorders: rheological changings and changings of blood flow.
- •41. Microvascular tone disorders.
- •42. Extravascular disorders.
- •43. Concept of inflammation. Aethiology.
- •44. Inflammation stages, main signs and types.
- •Inflammation types (continuation).
- •45. Primary and secondary alteration.
- •46. Mediators and antimediators.
- •47. Circulatory changings during inflammation.
- •48. Fever aethiology. Pyrogens classification.
- •49. Fever stages. Fever reactions types.
- •50. Fever comparative characteristics with exogenous overheating and hyperthermia other forms.
- •50. Edemas. Classification. Oncotic and hydrostatic mechanism.
- •58. Anaemias. Erythrocytes regenerative and degenerative forms. Cells of pathological regeneration.
- •54. Anisocytosis, poikylocytosis, price-jonce’ curve movements on the right and on the left.
- •55. Blood loss.
- •56. Acute and chronic posthaemorrhagic anaemias.
- •57. Hereditary hemolytic anaemias.
- •3 Groups:
- •58. Acquired haemolytic anaemias.
- •59. Dyserythropoietic anaemias.
- •60. Aplastic and hypoplastic anaemias. Metaplastic anaemia. Myelophthysis.
- •2 Groups of factors:
- •2 Main pathogenetic mechanisms:
- •61. Cardiac arrhythmias.
- •62. Concept of arterial hypo- and hypertension.
- •63. Primary arterial hypertension.
- •2 Pathogenetical conceptions:
- •64. Secondary arterial hypertension.
- •65. Cardiac insufficiency.
- •2 Overloads types:
- •66.Heart failure myocardial form.
- •67. Coronary cirulation disorders. Reperfusion syndrome. Calcium paradox. Oxygen paradox.
- •68. Respiratory failure.
- •Probes which allow to determine one or another disorders type:
- •69. External respiratory failure. Dyspnea.
- •70. Hypoxies.
- •71. Appetite disturbance.
- •2 Main mechanisms:
- •72. Caries.
- •73. Periodontitis and parodontosis.
- •74. Hypo- and hypertonic gastric dyskinesias.
- •75. Heartburn, eructation, nausea, vomiting.
- •76. Hepatic failure. Classification. Functional hepatic tests.
- •77. Hepatic failure hepatic-vascular form.
- •78. Liver excretory function disorders. Jaundices. Liver functions
- •Proteinic exchange
- •Carbohydrates metabolism
- •Lipid metabolism
- •Pigment metabolism
- •Jaundices differentiated diagnosis
- •79. Haemolytic jaundice.
- •80. Hepato-cellular or parenchymatous jaundice.
- •81. Hepato-portal hypertension. Ascitis.
- •82. Urine amount qualitative and quantitative changings.
- •Urine relative density (weight) (in morning portion)
- •83. Urine pathological components. Protein
- •Leucocytes:
- •Cylinders
- •84. Proteinuria.
- •85. Renal acid-alkaline balance disorders
- •86. Adrenal glands pathology. Cortex acute and chronic insuffieiency.
- •87. Thyroid hypofunction.
- •88. Hypothyroidism.
- •89. General regularities in occurrence and development cns disorders. Pathological processes classification.
- •90. Pathological excitement and inhibiting in nervous centers.
- •I. Of pathological excitement:
- •II. Of pathological inhibiting:
- •91. Ephaptic effects.
- •92. Pain.
20. Reactivity. Types. Dependence on sex.
Reactivity is an organism and his structures respond to environmental factors action with vital activity changings.
Role: it defines organism interaction with surrounding world. It influences greatly on diseases development and course.
Examples at different organizational levels (to question N.22):
molecular – oxyhaemoglobine dissociation curve movement to the right under acidosis caused by hypoxy (Bor’s effect);
cellular – microbic phagocytosis with leucocytes;
tissular – inflammation development after injuring factors action;
organic – heart beating rate increasing at blood temperature increasing;
systemic- external respiration, blood circulation reaction in blood at oxygen fasting;
organismic –complex oriented reactions as answer to sound and light signals action.
Reactivity types:
1) Species – is a characteristics of all individuals belonging to a given species;
2) group – of individuals belonging to 1 group;
3) individual – of 1 separate organism.
1) Non-specific (primary, simple) –is expressed at different factors influencing on organism; its base is answer genetically-programmed standard variants (example – protective-compensatory reactions at high and low temperatures action, at oxygen fasting, phagocytosis);
2) specific – immunological reactivity.
3. 1) Physiological – is actual in healthy organism;
2) pathological – qualitatively changed reactivity at pathogenic factors action.
4. 1) Increased (hyperergia);
2) decreased (hypoergia).
Factors influencing on reactivity:
Age – children have low reactivity; it is gradually is increased up to adult age, then is decreased in the old people.
Sex.
Heredity.
Functional state of nervous, endocrine, immune systems and connective tissue.
Environmental factors – climate, feeding character, social conditions et al.
Reactiveness main indexes:
Non-specific reactivity: 1.Irritability.
2.Excitability.
3.Sensitivity (to pain, heating, coldness, of sense organs et al.).
4.General adaptation syndrome development speed and intensivity (it is considered that men are more resistant to acute stress, women – to chronic one).
5.Ability to respond to the stimulus action with adrenaline secretion enforcement, tachycardia, hypertension (is higher in men comparatively to women).
Specific reactivity:
Antibodies formation velocity and intensivity (according to several data, it is higher in men than in women).
Immunoglobulines types.
23. Resistance. Passive and active resistance. Resistance and reactivity relationship.
Resistance is an organism resistance to pathogenic factors action.
Types:
Passive – non-sensitivity to pathogenic factor action, imperceptibility to them. It appears when organism interaction with pathogenic factor is impossible or hardened (complicated). Passive resistance is energy-independent. It can be determined by following mechanisms:
barriers existence for pathogenic factor interaction with organism structures (biological barriers);
absence or decomposition of organism structures capable to interact with pathogenic factor (for instance, receptors absence to pathogenic viruses);
pathogenic factor destroying with mechanisms which are not delt with organism reaction to the action of this factor (for example, cholera vibrion decomposition with gastric juice);
pathogenetic mechanisms realization retardation when these ways are triggered by organism interaction with pathogenic factor (for example, passive resistance increasing at hypothermia).
Active – resistance provided by complex of protective-compensatory reactions directed to pathogenic factor destroying as well as results of its action. This resistance is energy-dependent. Reactivity mechanisms are its base (for example, phagocytosis, antibodies production, cellular immunity reactions).
Reactivity and resistance interrelations (variants):
1. Reactivity increasing causes active resistance rising up. For example, at body temperature increasing antibodies synthesis is activated which increases active resistance to the infections.
2. Reactivity increasing causes active resistance decreasing. So, antibodies production increasing can be allergy reason at which organism resistance is decreased to antigens action.
3. Reactivity decreasing leads to active resistance decreasing. For instance, antibodies synthesis decreasing reduces active resistance to the infections.
4. Reactivity reducing is accompanied by passive resistance increasing. So, at hypothermia passive resistance to the infections, intoxications and other pathogenic factors action is increased (for instance, at winter anabolism in animals).
24. NON-SPECIFIC RESISTANCE MECHANISMS. CELLS UNDERACTIVITY. NON-SPCIFIC RESISTANCE PHYSICAL AND CHEMICAL FACTORS.
Mechanisms of non-specific resistance providing organism resistance to infectious agents action
Cellular areactivity.
Physical and physical-chemical factors.
Biological barriers.
Antagonistic interrelations between normal and pathogenic microflora.
Connective tissue physiological system functioning.
Non-specific resistance humoral factors.
Phagocytosis.
Inflammation.
Cellular areactivity – cells non-ability to interact with infectious agent. It can be determined by:
absence of receptors to viruses on cellular surface;
absence of receptors to bacterial toxins in cells;
toxin binding with cells receptors which are non-resistant to its action (receptors scanning).
Physical and physical-chemical factors of non-specific organism resistance to infections:
Temperature – temperature level in birds provides their resistance to anthrax causative agent. At body temperature increasing reproduction of many viruses is disturbed and they die.
Environment pH level – many causative agents of infectious diseases (particularly vibrio cholerae) die in stomach acid environment. Hydrogen ions high concentration is created in inflammation focus. It causes microorganisms injury here.
Oxygen tension in tissues. PO2 is so under normal conditions that prevents anaerobic infections development.
