- •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.
79. Haemolytic jaundice.
Total bilirubin level is increased in plasma because of indirect bilirubin. Direct bilirubin is not changed because hepatocytes cytoltsis and cholestasis are absent. Stercobilin increasing in urine and faeces gives them black color. Urine and faeces colour changing is important for making proper diagnosis and for differential diagnostics.
80. Hepato-cellular or parenchymatous jaundice.
Is developed at hepatic failure. Inirect (non-conjugated) bilirubin is increased in plasma because desintoxicational liver function is disturbed. Also direct bilirubin is rised up because of hepatocytes cytolysis.
81. Hepato-portal hypertension. Ascitis.
Hepato-portal hypertension is developed as a result of blood outflow disorders from abdominal cavity organs through portal veins vascular system.
Types dependently on location of obstacle (embol, pressure with tumor) to blood flow:
1) subhepatic – if obstacle is in portal vein stem or large branches (ambols, pressure with tumor);
intrahepatic – obstacle is located inside liver (prolonged spasm of sinusoids smooth-muscular sphincters; small hepatic veins pressure with nodes of regenerating hepatocytes at liver injury, its cirrhosis);
suprahepatic – obstacle is located in extraorganis parts of hepatic veins or vena cava inferior proximally from place of hepatic veins inflow into it. Portal hypertension occurig at pressure increasing in vena cava inferior under conditions of right ventricle insufficieny belongs to the same group.
Main expressions:
collateral circulation switching on determind by porto-caval anastomoses opening. It causes following features development:
a) various dilation of oesophageal veins and the ones of stomach cardia;
b) gastric-intestinal bleedings caused by varicous vins injury;
anterioir thoracical and abdominal wall subcutaneous veins dilation (“jellyfish head”);
blood removal from portal vein to caval veins round liver – it causes intoxication or liver coma in hard cases.
Hepato-lienal syndrome – has 2 main compounds:
a) splenomegaly as a result of blood stagnation;
b) hypersplenism – spleen functional activity increasing - it is expressed in blood formed elements accelerated decomposition; it is characterized by anaemia, leucopenia, thrombocytopenia. Base: linal macrophagues activity enforcement at blood circulation retardation.
Ascitis – see below.
Hepato-lienal syndrome – is expressed in kidney glomerulars filtration
disability at channel epithelium normal function. Reasons: circulating blood volume reducing and vascular hypotony lead to renal circulation diminishing at liver haemodynamic disorders.
Ascitis.
It is free liquid (transsudate as a rule) accumulation in abdominal cavity.
Reasons:
different-origined portal hypertension;
oedemas at chronic cardiac insufficiency, kidney diseases, alimentary dystrophy;
lymph outflow disorders through thoracical duct (its wounding, pressure);
peritoneum injury with tumor or tuberculosis process (ascitis-peritonitis).
Ascitis liquid is usually serose, more seldom – haemorrhagic one.
Pathogenetic factors:
hydrostatic – is connected with blood pressure increasing in portal capillaries;
oncotic – is determined by liver prothein-synthetic function reducing as a result of which hypoproteinemia and hyperoncia are developed;
Na lack in organism due to hyperaldosteronemia and previous renin-angiotensine system activation: blood stagnation in portal vessels→venous return diminishing→heart minute volume decreasing→kidney hypoxy→renin releasing; besides, kidney dysfunction can lead to aldosterone inactivation problems which is equal to its hyperproduction;
lymphogenic – lymphatic flow disorders lead to lymph (rich in protein) transfer in abdominal cavity; it causes abdominal cavity liqud hyperoncy with following water exit from vessels and intersticium.