- •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.
44. Inflammation stages, main signs and types.
Main signs:
oedema – tumor; 2) reddish (rubor); 3) heat, ardour, fever –calor; 4) pain – dolor; 5) dysfunction – functio laesa. These features are known as pentade of Cels-Galen.
Stages:
alteration;
microcirculation disorders with exsudation and emigration;
proliferation.
Doctor must remember that these stages are not always consequent and can interfere one another.
Inflammation types (continuation).
I. Dependently on exsudate character:
haemorhagic;
purulent;
decoy;
serose et al.
II. Dependently on sepsis development:
septic;
aseptic.
45. Primary and secondary alteration.
Primary alteration – tissue injury due to flogogenic agents direct action.
Secondary alteration – tissue injury which occurs due to action of factors being formed as primary alteration result.
Secondary alteration developmental factors:
Inflammation mediators (lyzosomal factors, activated complement, lymphokines-lymphotoxins).
Free radicals and peroxides.
Hypoxy occurring as a result of circulation local disorders.
Local acidosis.
Osmotic and oncotic pressure increasing in inflammation locus (as a result of protein level increasing, its dispersity and hydrophyly).
Hyperiony – accumulation such ions as K+, Cl-, HPO4-, Na+.
Dysiony.
46. Mediators and antimediators.
According to the source:
Cellular:
From polymorphic-nuclear leucocytes, mainly neutrophils and basophils:
highly-active lysosomal hydrolases;
cationic proteins;
prostaglandines;
leucotriens;
interleukines;
biogenic amines.
Eosinophils participate in oxidants and leucotriens detoxication. They play essential role in inflammation allergy component.
From mononuclears (lymphocytes, monocytes, tissular macrophags):
lymphokines;
monokines;
neutral proteases;
estherases;
acid phosphatases and others.
From platelets:
adhesive proteins;
ADP;
serotonine;
lysosomal enzymes;
Willebrand’s factor.
From labrocytes (adipocytes):
biogenic amines;
platelet activation factor;
leucotriens (C4 and D4) are compounds of anaphylaxy slow-reacting substance (ASRS);
eosinophilic chemotactic factor;
neutrophilic chemotactic factor;
heparine and others.
Other cells of injured tissue:
lysosomal enzymes;
prostaglandines;
lipids peroxidative oxidation products et al.
Plasmic – from blood:
complement system components;
kinines;
blood coagulation system factors.
According to mediators nature:
Biogenic amines:
histamine;
serotonine and others.
Active polypeptides and proteins:
kinines (bradykinine, kallydine, methyonyl-lysyl-bradykinine);
complement system components;
enzymes (mainly lysosomal);
leucocytic proteinic factors (cationic proteins, interleukine-1, monokines, lymphokines).
Polysaturated fatty acids (arahidonic, linolic) derivates:
prostaglandines (E, I2 or prostacycline);
thromboxanes;
leucotrienes;
lipids free-radical peroxidative oxidation products.
Antimediators – 1) glucocorticoids decrease alteration, arachidonic acid and its derivation synthesis (decreasing of exsudation and leucocytes emigration, microcirculation disorders weakening); cellular division and protein biosynthesis inhibiting by glucocorticoids leads to proliferation decreasing in inflammation focus;
proteases inhibitors;
histaminase – it is in eosinophils (it decomposes histamine released from basophils)…
