- •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.
Disease, biological and social factors are actual because human being is first of all social creature
1. Animals are influenced by physical, chemical and biological factors. Human beings are also influenced by social factors. These factors are present among diseases reasons and their specific weight is increased and increased.
2. Increased weight of cardiac-vascular diseases and neuroses testify important role of changing conditions of social life (urbanization, informational stress et al.). There are own “human” diseases (myocardial infarction, bronchial asthma) absent in animal world.
3. Disease social side is expressed also in the fact that disease disturbs social life of one person or many people giving material or moral detriment to 1 person and to the society as a whole.
4. Thus, animal’s and human diseases have many things in common (that is why experimental modeling in animals helps greatly in human physiology) and different because integrity of biological and social creates the only picture characterized human disease.
5. Human being depends on nature, nature depends on human being less.
4 Levels of diseases prescription:
fourth level – the highest- disease is an abstract, philosophical uniting (Life under ubnormal conditions – R. Wirhow);
third – disease as typical pathological process;
second – transition from abstract to concrete (pulmonary tuberculosis in human being or sheeps);
first level- concrete level – maximal individualization not only of disease reason, localization, organism type but also organism individuality (representation about disease diagnosis in separate person: inflammation – tuberculosis inflammation – pulmonary tuberculosis - in the patient H. of …years, sex…).
5. Diseases classification principles:
aethiologic – according to it one differentiates hereditary and acquired, infectional and non-infectional diseases;
anatomical-topographical: cardiac-vascular diseases, respiratory organs diseases, kidney diseases et al.;
by age and sex; children’s diseases, diseases of the old, female diseases;
ecological – tropical diseases, diseases of North et al.;
according to injury level – molecular, chromosomal diseases et al.;
social – professional diseases, diseases of military time, “civilization diseases”;
pathogenetic principle – allergic, inflammatory, tumorogenic, metabolic and other diseases;
dependently on structural and functional disorders correlation – organic and functional diseases;
by clinical course – acute, subacute and chronic diseases;
dependently on methods mainly used for the diseases treatment: therapeutic and surgical diseases.
WHO classification of diseases – complete diagnosis (name, stage, period and so on).
6. SHOCK. KINDS. GENERAL HAEMODYNAMICS AND MICROCIRCULATION DISORDERS DEVELOPMENTAL MECHANISMS.
Shock (the term is origined from th French word “choc” – pushing) is hard pathological process which is accompanied by organism vital functions exchaustion and lead the organism to the boarderline between life and death due to capillary circulation critical diminishing in injured organs. Main distinguishing feature of this type of extremal factors is aethiologic factor – epiliminal pathogenic stimuli action to the organism.
Trigger pathogenetic shock mechanism is massive biologic negative afferentation coming to CNS from the area of injuring stimulus action.
Main types:
I According to the reasons of occurrence:
1) haemorrhagic;
2) combustive;
anaphylactic;
haemotransfusional;
cardiogenic;
psychogenic;
turnicet (after turnicet taking off in 4 hours and more after putting it on the extremity);
anhydremic;
pancreatic;
septic;
infectious-toxic and so on.
II According to primary pathogenetic mechanisms:
hypovolemic (haemorrhagic, anhydremic);
shck delt with heart pump function disorder (cardiogenic);
vascular forms (anaphylactic, pancreatic);
noceoceptive delt with circulation central dysregulation (traumatic, combustive).
Main stages:
erectile – neurons generalized, diffused excitement;
torpide – neurons activity generalized inhibiting;
terminal - at complete consciousness loss. It is coma.
General haemodynamics disorders developmental mechanisms:
sympatho-adrenal and hypophyseal-suprarenal influencings activation in erectile stage leading to metabolism modification and physiological systems activation;
at the torpide stage beginning cateholamine and corticosteroids increased level is still present but their action efficacy to the different organs are decreased;
then sympatho-adrenal and hypophyseal-suprarenal system exhaustion and hypoactivity are developed, neurohormones and corticosteroids level in blood became reduced;
tachycardia, arterial hypertension, blood circulation redistribution in erectile phase;
hypotension, minute heart volume and venous return to heart decreasing, increased deponated blood fraction, blood circulating volume reducing; pulse pressure decreasing, pulsus filiformis (thread-like pulse) in torpide phase;
in torpide phase increased acute circulation insufficiency leads (together with respiratory insufficiency) to hard hypoxy which determines the gravity of shock state.
Circulation mechanism disorders at different shock types:
circulating blood volume decreasing:
blood loss (hemorrhagic shock);
blood plasma loosing at generalized excudative inflammation (combustive shock);
liquid outcome from blood vessels at blood vessels permeability generalized increasing (anaphylactic shock);
excicosis (anhydremic shock);
blood redistribution in vascular bed (magistral veins thrombosis and embolism);
heart minute volume decreasing:
heart contractive function disorder (myocardial infarction);
heart tamponade (heart rupture, excudative pericarditis);
arrhythmias (ventricles fibrillation);
common peripheral resistance decreasing - vessels generalized dilation:
arterioles neurogenic tone decreasing (noceoceptive shock);
vessels basal tone decreasing under biologically-active substances action (anaphylactic, pancreatic shock) or toxic substances (traumatic, turnicet, infectious-toxic shock);
blood rheological features disorders:
-disseminated intravascular coagulation syndrome (pancreatic et al.);
formed elements aggregation (septic, infectious-toxic shock);
haemoconcentration (anhydremic shock).
Microcirculation disorders:
They can be developed in erectile phase due to blood circulation redistribution and its reduction in some organs (kidney, liver, intestine). In torpide phase such disorders acquire more diffused character: microvessels perfusion decreasing, blood rheological features deterioration (blood formed elements aggregation, blood hyperviscosity), capillary walls permeability increasing, perivascular oedema. Organs blood circulation volumary velocity is decreased.
Hard shock results are determined by following:
General haemodynamics and microcircualtion disorders are dangerous first of all because of brain, coronary and renal circulation disorders. The result of the mentioned disturbances is vital functions central regulation progressing disorder up to coma development as well as cardiac-vascular and renal insufficiency phenomena. Such pathogenic factors as hypoxy, acidosis and intoxication appearing at this lead to cells generalized and irreversible injury.
7. FUNCTIONAL AND STRUCTURAL DISORDERS UNDER VARIOUS SHOCK STAGES. PHYSIOLOGICALLY-ACTIVE SUBSTANCES AND PRODUCTS OF TISSUES INJURY ROLE IN SHOCK PATHOGENESIS. CNS ROLE IN SHOCK DEVELOPMENT. PHYSIOLOGICAL BASES OF SHOCK TREATMENT AND PROPHYLAXY.
Besides mentioned above disorders of haemodynamics and microcirculation shock is characterized by following changings:
tachypnoe and pulmonary ventilation increasing in erectile phase;
erythrocytosis in erectile phase;
hypoventilation and respiration pathological forms in torpide phase;
toxemia.
Toxemia is obligatory component and pathogenetic factor at shocks of different aethiology. Its appearance velocity, character and role are different dependently on shock type. Multiple biologically-active substances make toxic effect at shocks. They come to the organism internal environement in excessive amount. They are histamine, serotonine, kinines, acetylcholine, catecholamines and others. Denaturated proteins and their decomposition products, lysosomal enzymes toxic products forming in intestine (phenols, scatol et al.), microorganisms and their toxins can be appeared in blood. Metabolites significantly forming in cells as a result of metabolism disorder and coming to blood (lactate, piruvic acid, ketoacids, adenosine, potassium and others ) are important in toxemia development. Kidney and liver dysfunction due to hypoxy and microcirculation disorders lead to bigger blood content changings: ammonia ions accumulation, acidosis, ionic and proteinic dysequillibrium, osmotic and oncotic pressure movement in different organism environmens.
“Circulus vitiosus”: 1) CNS disorders lead to blood circulation and respiration disorders; these vital functions inhibiting causes hypoxy appearance which increases nervous processes disorders.
central haemodynamics and microcirculation disorders lead to liver and kidney dysfunctions; blood content unfavourable changings occurring at this enforce blood circulation disorders.
At definite stage of shock torpide phase haemodynamics disorders can reach such degree that secondary collaps can be developed which gets the patient state worse.
CNS afferent impulsation hyperactivity plays essential role in erectile phase development, CNS inhibiting – in torpide one.
Shock treatment and prophylaxy principles:
pathogenetic and aethiothropic (reason is liquidated by surgical or conservatory method if it is possible);
pain syndrome liquidation - is the most important principle;
toxemia degree diminishing (in parallel to pain decreasing): antidotes, biologically-active substances blockators (of histamine, serotonine), glucocorticoids, haemotransfusion, haemodez, haemosorbtion et al.
hypovolemy and watery balance disorders liquidation – conserved blood, plasma and other liquids transfusioni are used;
electrolyte and acid-alkaline states correction;
blood rheological features (antiaggregants, anticoagulants, plasmine stimulators, rheopolyglukine which reduces blood viscosity);
hypoxy circulatory component weakening;
vital inner organs prevention (first of all lungs and brain) – diuretics (mannitol),
microvessels and cellular membranes permeability getting normal –membranostabilizators such as glucocorticoids, vitamins, calcium drugs;
kidney ishemia prevention and liquidation;
haemodialysis at renal insufficiency.
