- •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.
17. Free radicals and their role in pathological processes development.
Peroxidative lipid oxidation – non-saturated fatty acids free-radical oxidation. These fatty acids are cellular membranes phospholipids compounds.
Free radicals are PLO triggers. The most important are following: *O2 _ or (HO2*) – superoxide radical; OH* - hydroxile radical; H+ - hydrogen radical; *O2 – singlet (excited) oxygen.
Singlet oxygen is formed at light quant absorbtion by triplet oxygen. It can be produced in the cell at reactions catalized by peroxidases, catalazes. It can be free-radical oxidation (FRO) trigger in cholesterol and non-saturated fatty acids peroxidative oxidation, inhibit microsomic oxidation enzymes, cause DNA ruptures, serve as mutagen. Its inhibitors are: water, cholesterol, hystidine, methionine, beta-carotine, tocopherol, asorbate.
Ozone is formed in atmosphere at electrical spark. It is similar to biradical. It initiates poly-saturated fatty acids autooxidation. Its action to human organism is similar to NO action to it. It causes the hardest injuries in lungs.
Superoxideanionradical - is produced in mitochondria, at methaemoglobine appearance (particularly nitrate intoxication), in microsomes, in iron- and copper-containing systems. Superoxidedismutase (SOD) is its major inhibitor. This radical actively induces and contiunues PLO chain as well as modifies membraines fluidity. SOD, probably, participates in proliferation regulating.
Hydroxile radical –is produced at water radiolysis and is lipids FRO main trigger. Its inhibitors are alpha-tocopherol, bioflavonoids, beta-carotine, ascorbate, reducted glutathione.
Hydrogen peroxide is produced at flavin-, copper- and haem-containing peroxidases functioning. Catalase and peroxidases eliminate hydrogen peroxide. This free radical participates in gene expression, in nuclear membrane decomposition and renewal.
Reactions which are on the base of lipids peroxidative oxidation.
Primary radical (A*) which appeared in the cell interacts with non-saturated fatty acid molecule (RH), as the result of which this acid free radical (R*) is formed as well as reaction molecular product (HA):
A*+RH=R*+HA.
Fatty acid free radical after its formation interacts with molecular oxygen which is present always in the cell – peroxide radical of this acid appears as a result of this (ROO*).
R*+O2=ROO*
Peroxide radical, in turn, interacts with non-saturated acid new molecule. Hydroperoxide (ROOH) and new free radical is formed in course of this reaction:
ROO*+RH=ROOH+R*
PLO main peculiarities:
reactions chain character: free radicals are not destroyed during PLO but new and new molecules of non-saturated fatty acids are involved in the process;
branched character: free radicals are appeared in increasing amount the source of which are PLO intermediate products themselves; example of this is free radicals formation from lipids hydroperoxides while their interaction with metals of changing covalence: ROOH+Fe3+=RO*+OH-+Fe3+.
Since free radicals little quantity is formed constantly in normal biochemical reactions in organism there is constant danger in organism of POL activation. But it doesn’t occur under physiological conditions because any cell possesses powerful antioxidant mechanisms.