- •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.
65. Cardiac insufficiency.
Cardiac insufficiency – is a pathological condition determined by heart non-ability to provide blood supply for organs and tissues according to their needs. It is a state when load to heart is higher than its ability to perform activity. It is expressed in following: heart can not transfer all blood to vascular bed coming to it through veins.
Types:
1) By clinical course:
acute;
chronic.
2) By clinical manifestations expression:
compensated (hidden);
b) visible (decompensated).
3) Dependently on primary dysfunction:
left-ventricular;
right-ventricular;
total.
4) By pathogenesis:
from overloading;
myocardial;
extramyocardial.
Cardiac failure from overloading is developed as a result of very big loads (with resistance or volume) action to healthy heart, id est when resistance to cardiac charge is increased or blood flow to heart separate chamber is rised up. Reasons: heart vices, large or small circulation circles hypertension, arterio-venous shunts or at very hard physical load performance. Excesive recquirements are given to the heart with normal contractive ability.
2 Overloads types:
Overload with volume – occurs when increased blood volume comes to heart or its separate chambers; heart or this chamber under overloading must transport increased blood volume in arterial system; t is reached by heart minute volume increasing correspondingly to increased venous return. There are 3 main cases:
venous blood return increasing to heart – particularly at hypervolemy or veins hypertony (venous system capacity decereasing);
heart vices- its valves insufficiency; left ventricle overloading is developed at aortal and mitral valves insufficiency; right ventricle – at pulmonary artery and tricuspid valve insufficiency.
Overload with resistance – occurs when heart or its separate parts have to perform work against increased resistance which prevents all blood transfer in arteries. Heart must save its minute volume despite increased resistance to blood exile. Cases:
arterial pressure increasing (peripheral vascular resistance rising up); left ventricle has overload at large circle hypertension; right one – of small circle;
heart vices – valvular foramens stenosis: at aorta foramen stenosis - left ventricle overload, mitral valve foramen – left atrium, pulmonary artery foramen stenosis – right ventricle, tricuspidal valve foramen - right atrium
Compensatory mechanisms at overloads action:
Urgent:
heterometric mechanism;
homeometric mechanism;
chronoinothropic mechanism;
catecholamines inotropic action.
2) Hypertyhrophy of myocardium - long-termed adaptation.
Heart and vessels work in complicated functional interrelations. Besides, heart has its own (myogenic) regulative mechanisms. One of them – heterometric – is performed as answer to myocardium fibres length change (Starling’s law). Such cardiac regulative mechanism can provide circulatory insufficiency compensation and its anomalies. It is characterized by very high sensitivity. It may be observed at introduction of 1-2 % of all circulating blood mass in magistral veins.
Second myogenic regulative mechanism type is homeometric. Myocardial fibres ending dyastolic stretching degree is not important for its realizing. The most important is correlation between cardiac contractions and aortal pressure (Anrep’s effect): aortal pressure increasing causes initial heart systolic volume decreasing and then – heart contractions force increasing and cardiac discharge stabilizing at new contractions level.
Thus, heart activity myogenic regulational mechanisms may permit its contraction significant changes.
Besides, heart has sympathetic and parasympathetic innervation like vessels. At tone dominance of one of them heart and vessels activity will be different.
Efferent nerves tone support is provided by cardiac-vascular regulation center. Heart-vascular regulative center – is a rather complicated structure in which dominant importance has its “working” part, located in medulla oblongata. It was there where neurons are located from which excitement are transmitted on effector ways (parasympathetic and sympathetic) while reaching heart and vessels. That’s why their reflectory regulation is always performed simultaneousely. When sympathetic nervous system tone is dominant (hypersympaticotony) than heart activity is increased:
its contraction freaquency is rised up – positive chronotropic effect;
contraction force is increased – positive inotropic effect;
excitability is increased – positive bathmotropic effect;
conductance is rised up - positive dromotropic effect.
