- •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.
55. Blood loss.
Blood loss – pathological process occurring as a result of bleeding which is characterized by significant complex of pathological disturbances and compensatory reactions directed to circulating blood volume reducing and hypoxy caused by blood respiratory function inhibiting.
Aethilogical factors;
vessels integrity disorder at wounding or injury with pathological process (atherosclerosis, tumor, tuberculosis);
vascular wall permeability increasing (acute radiational disease);
blood coagulation decreasing (haemorrhagical diatesis).
Protective-compensatory reactions:
By term:
urgent;
non-urgent.
By direction:
directed to vascular bed volume decreasing;
directed to circulating blood volume increasing;
directed to blood content restoration;
directed to protection from hypoxy.
Circulating blood volume increasing:
tissular liquid transfer to vessels;
water and Na ions reabsorbtion enforcement by kidney (vasopressine, renine-angiotensine system, sympathy-adrenale system acyivation);
blood exit from depot to vascular bed.
Blood content restoration:
Circulatory (circulating blood volume reducing) and haemic (anaemic) hypoxy causes kidney hypoxy and, in turn, erythropoietin synthesis activation by juxta-glomerular apparatus.
Pathological changings at blood loss:
Systemic hamodynamics disorders (circulating blood volume diminishing, arterial pressure decreasing) and local circulation (microcirculation) disturbances up to shock development.
Acute post-haemorrhagic anaemia.
Hypoxy – first it is circulatory, then haemic (anaemic).
Non-gas acidosis - caused by hypoxy and lactate coming to blood.
Kidney excretory function disorder: hypotony leads to glomerular filtration inhibiting and finally acute renal insufficiency,oligo- and anuria, intoxication (azotemia or nitrogenemia).
56. Acute and chronic posthaemorrhagic anaemias.
Acute – is developed after rapid massive blood loss at vessels injury or their injuries with pathological process.
Characteristics:
Pathogenetically |
Posthaemorrhagic |
Aethiologically |
Acquired |
By red bone marrow regeneratory ability |
Regeneratory |
By colour index |
First normochromic, then hypochromic |
By haemopoiesis type |
Erythroblastic |
By clinical course |
Acute |
Blood picture:
In course of several hours after blood loss:
Hb – N; b) Er- N; c) CI – N; d) Ht- N.
From several hours up to several days after acute blood loss:
Hb - ↓; b) Er - ↓; c) CI - N; d) Ht - ↓.
From several days to 1-2 weeks:
Hb - ↑; b) Er - ↑; c) CI - ↓; d) Ht - ↑.
Chronic anaemia – is developed as a result of repeated blood losses caused by vessels injury at several pathological conditions (menstrual cycle disorders, stomach ulcer disease, haemorrhoids) as well as vascular-platelet and coagulational haemostasis disorders (haemorrhagical diatesis). Iron loss at frequent bleedings gives this anaemia iron-deficient character.
Blood picture:
Hb decreasing;
CI decreasing;
Er degenerative forms (micro- and poikylocytosis, hypochromy);
Er number and Ht can be without changing.
Characteristics:
Pathogenetically |
Posthaemorrhagic |
Aethiologically |
Acquired |
By red bone marrow regeneratory ability |
Hypoegeneratory |
By colour index |
Hypochromic |
By haemopoiesis type |
Erythroblastic |
By clinical course |
Chronic |
