- •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.
32. Ishemia
Ishemia is organ or tissue locus blood filling decreasing as a result of arterial blood inflow limiting or complete stoppage. Ishemia is also called as local anaemia.
Features:
organ part pale colour;
local hypothermia;
sensitivity disorders (dumning, paresthesias et al.);
pain syndrome;
blood stream velocity decreasing in organ;
organ volume reducing;
blood pressure decreasing in locus located below to obstacle;
oxygen tension decreasing in ishemia locus;
tissular liquid hypoproduction and tissular turgor decreasing;
organ or tissue dysfunction.
Compressive ishemia occurs as a result of arteria pressure outside with ligature, scar, tumor, side body.
Obturational – is a result of arteries particular constriction or complete occlusion with atherosclerotic plaque, thrombus or embolus.
Angiospastic – appears due to arterial spasm caused by emotional influencing (fear, worrying, anger), physical stimuli (coldness, trauma, mechanical irritation), chemical stimuli, biological factors (bacterial toxins) and others. Nervous reflectory mechanisms or stimuli direct action to vessels smooth muscles (vasopressine, angiotensine II, endotheline).
Factors influencing on metabolic, functional and structural disorders at ishemia:
hypoxy degree which, in turn, depends on developmental speed and ishemia type, its duration, location, collateral circulation character as well as organ or tissue functional state;
ishemia at complete vessel obturation (occlusion) causes harder changings than at angiospasm;
rapid ishemia and prolonged one has harder course comparatively to slow and short-termed one;
vital organs (brain, heart) ishemia has harder results than the one of kidney, lungs, spleen and the ishemia of the latest ones – harder comparatively to ishemia of skeletal muscular, osseal or cartillageous tissue;
brain and heart are characterized by energy metabolism high level but at the same time their collateral vessels can’t compensate functionally circulation disorders; on the contrary, skeletal muscles and connective tissue especially are more resilient under ishemic conditions due to energy metabolism lower level;
arterial blood inflow retardation at organ hyperactivity (overloading) is more dangerous than under rest conditions.
Pathogenesis consequent stages:
energy metabolism disorders –are expressed in Krebs’ cycle and tissular respiration activity reducing and as final result – creatinephosphate and ATP level decreasing in cells; energy formation disorder in ishemia locus is delt with oxygen and substrates (necessary for oxidation) insufficient consumption, enzymes activity and synthesis dcreasing, enzymes exit from injured cells as well as oxidation and phosphorylation dissociation;
energy-dependent processes disturbances in cells caused by energy production decreasing; such cells specific functions as contractive, secretory one as well as substances active transport mechanisms (particularly ionic pumps activity) are disturbed; non-collagenic proteins biosynthesis is decreased; final result – cell injury and necrobiotic changings which can be ended in infarction (in the most difficult cases);
connective tissue components biosynthesis enforcement such as collagen, glycosamines, glyoproteins – they are basement for ishemized locus sclerosis.
