- •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.
58. Anaemias. Erythrocytes regenerative and degenerative forms. Cells of pathological regeneration.
Anaemia – is haematological syndrome or separate disease characterized by erythrocytes number reducing or (and) haemoglobine level in blood volume unit as well as erythrocytes qualitative changings.
Quantitative signs:
erythrocytes content decreasing in blood volume unit (lower than 4x1012 in men and lower than 3,5x1012 in women in 1 l of blood);
haemoglobine level decreasing (lower than 130 g/l in men and lower than 120 g/l in women);
haematocrit level reducing (lower than 43% in men and lower than 40% in women);
colour index reducing (lower than 0,85).
Qualitative features:
erythrocytes regeneratory forms;
degenerative changings in erythroid cells;
cells of pathological regeneration.
Anaemias total clinical manifestations:
hypoxy – syndrome occurring at any anaemia type;
syndromes determined by separate anaemia type distinguishing features (for instance, neurological disorders and alimentary tract dysfunction at B12-B9-deficiency; jaundice at haemolytic anaemia).
Anaemias classification:
Pathogenetically:
posthaemorrhagic (anaemia after acute blood loss);
haemolytic (sircle-celled);
dyseryhtropoietic (iron-deficient).
Aethiologically:
hereditary (thalassemia);
acquired (chronic posthaemorrhagical).
By red bone marrow regenerative ability:
regeneratory (acute posthaemorhagic);
hyperregeneratory (acquired haemolytic anaemia);
hyporegeneratory (iron-deficient anaemia);
aregeneratory (apalastic anaemia).
4) By colour index (CI):
normochromic (CI=0,85-1,0; for instance, acute posthaemorrhagic anaemia during first several days after blood loss);
hypochromic (CI <0,85; for example, iron-deficient anaemia);
hyperchromic (CI >1,0; for instance, B12-B9-deficient anaemia).
5) By haemopoiesis type:
anaemias with haemopoiesis erythroblastic type (iron-deficient anaemia);
anaemias with megaloblastic haemopoiesis (B12-B9-deficient anaemia).
6) Clinically:
acute (anaemia after haemotransfusional shock);
chronic (hypoplastic anaemia).
Regeneratory anaemias features:
in perypheral blood – reticulocytes and polychromatophils amount increasing and normoblasts appearance (erythrocytes regeneratory forms);
in red bone marrow – leuco-erythroid correlation from 3:1 up to 1:1 and even to 1:2 and 1:3.
Cells of pathological regeneration:
megaloblasts;
megalocytes.
Erythrocytes degeneratory changings:
anisocytosis (size diminishing);
poikylocytosis (shape changing);
colour changings (aisochromy);
pathological inclusions:
Zholly’s bodies (nuclear substance derivates);
Kebot’s rings (nuclear membrane residues ring-or 8-shaped);
Basophilic granulation – cytoplasm basophilic substance residues testifying red bone marrow toxic injury.
54. Anisocytosis, poikylocytosis, price-jonce’ curve movements on the right and on the left.
Anisocytosis – presence in blood stains erythrocytes different by their size: with low-sized Er dominance – microcytosis or microanisocytosis (for instance, at iron-deficient anaemia); with large-sized Er dominance - macrocytosis or macroanisocytosis (for instance, at B12-B9-deficient anaemia).
Anisocytosis is present at iron-deficient anaemia both in its initial period and as a result of performed therapy with iron. Er saturated with Hb appeared after therapy are alternated with small Er which were formed before treatment. Anisocytosis is present at diseases characterized by parallel existence of normal and pathologic erythropoiesis; hypoplastic anaemia, paroxysmal night haemoglobinuria, myeloproliferative diseases, thalassemia.
Movement of Price-Jones curve to the left – microcytosis (d<6,5 mcm), to the right – macrocytosis (d>8,0 mcm).
Poykilocytosis – can be observed practically at any anaemia independently on its origin. Doctor should remember that 10-15% of all normal Er can have shape different from discoid. Scientists mention 20-40 different possible Er shapes. Examples: echinocytes (hedgehog), acantocytes (with needles like echinocytes but they are larger and Er can not return to usual shape), stomatocytes or hydrocytes (like boat if to look from the side) drepanocytes (circle-shaped), dacryocytes (like tear), pear-shaphed, spherocytes, elliptocytes and so on.
Only several Er types are specific for separate anaemias. Hereditary spherocytosis – disease of Minkovsky-Shoffar is characterized by microspherocytes, circle-celled anaemia –by drepanocytes. Doctor must differentiate here reversible shapes which can be returned to the normal state (echinocytes, stomatocytes) and irreversibly changed cells (acantocytes, codocytes or target-cells, spherocytes, irreversibly changed stomatocytes).
