- •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.
28. Stress-inducing and stress-limiting systems. Diseases of adaptation.
Adaptation diseases- diseases dominant role in the development of which has excessive stress and so-called stressor injuring mechanisms. Stress at its big intensivity and duration can be transformed from adaptation mechanism to dysadaptation and even pathogenesis mechanism. Adaptation diseases:
psycho-somatic diseases:
heart ishemic disease;
hypertonic disease;
stomach and duodenum ulcer disease;
substances exchange diseases (diabetes mellitus);
allergic and inflammatory diseases:
bronchial asthma;
rheumatism.
Stress-triggers or stressors:
trauma;
coldness;
pain;
emotions (negative ones);
bleeding;
physical loading;
hypoglycaemia;
infections.
These stressors cause excitement of the highest nervous regulatory centers and hormones big amount releasing determined by this. Such excitement can be realized through homeostasis disorders.
Stress-realizing processes:
activation of hypothalamic-adenohypophyseal system – ACTH, STH, TTH releasing which stimulate (correspondingly) secretion of glucocorticoids, somatomedines, thyroid hormones;
vegetative nervous system activation (sympathetic and parasympathetic) – is accompanied by catecholamines, insuline, glucagons passage to blood;
aldosterone-vasopressine system activation which leads to angiotensine, aldosterone, ADH content increasing in blood.
Stress-limiting systems:
endogenic opiates;
lovely job;
active sexual life;
joy from life and so on.
29. Concept of “local microcirculatory disorders”. Some mechanisms.
Mai local microcirculatory disorders:
arterial hyperemia;
venous hyperemia;
ishemia;
stasis;
thrombosis;
embolism.
Endotheline is considered “maestro of blood circulation” because it plays one of the most essential role in hypertonic disease (together with atrial sodium-uretic factor). Endotheline is synthesized by endotheliocytes. Endothelium is considered now whole separate endocrine gland because all endotheliocytes weight is approximately 5 kg in 1 organism and because is a source of about 50-100 different substances influences on vessels tone, haemostasis, transcapillary exchange (and, thus, inflammation development). Endotheline is very powerful vasoconstrictor and proaggregant.
NO is its antagonist because it is vasodilator and antiaggregant. It is also can be produced by endothelicytes.
Inreased hyperemia can be caused by NO hyperproduction. Endotheline hypersecretion and hyperactivity can lead to ishemia and stasis (as a result of vasoconstriction), thrombosis (as a result of hyperaggregation). NO is also named as endothelial relaxation factor. It acts to vascular wall smooth myocytes and causes their hyperpolarization (endothelin causes depolarization) that lead to vessel basal tone decreasing and vasodilation at blood pressure action (edotheline action leads to vessel basal tone increasing and vasoconstriction). NO is origined from arginine. Both NO and endothelines act through cAMP (more endotheline) and cGMP (more NO).
30. Arterial hyperemia
Arterial hyperemia – organ or tissue blood filling increasing due to blood excessive passage to arterial vessels.
Functional features:
shine arteries, veins and capillaries dilation;
blood stream acceleration in them;
shine arteries and capillaries pulsation;
increasing the amount of vessels visible with eyes;
pressure increasing in arterioles, capillaries and veins.
As the result of these functional changings one can see visual expressions:
dispersed (disseminated) rubor (reddish colour);
local temperature increasing;
hyperemized locus volume increasing;
tissular turgor increasing;
metabolism and organ function enforment.
Reasons:
physical factors;
chemical factors;
biological factors;
loading increasing to the organ or tissue locus;
psychogenic actions.
Physiological hyperemia – occurred under usual physiological stimuli (loading increasing to organ, psychogenic stimuli) action.
