- •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.
Urine relative density (weight) (in morning portion)
Urine relative weight in a healthy person depends on many factors but mainly on daily diuresis – the more is diuresis the lower is urine relative density which is measured with urometer.
In healthy people sum of 2 first ziphras in 24-houred diuresis and 2 latest ziphras in urine relative weight is 30. For instance, at 24-houred diuresis equal to 1100 ml, relative weight is 1019 g/l, than 11+19=30.
Isosthenuria – urine releasing with constant density level, protein-free blood plasma part density equal indexes (primary urine relative weight is 1010…1011g/l) testify to kidney concentrational function complete loss.
Hypersthenuria – urine relative weight is more than 1025 g/l:
Oedemas increasing:
acute glomerulonephritis;
circulation insufficiency.
Significant extrarenal liquid losses:
diarrhea;
vomiting;
bleeding;
spread burnings;
oedemas formation;
abdomen traumas;
intestinal obturation (impermeability).
Appearance in urine big quantity of glucose, protein, medicines and their metabolites (3,3% of protein in urine increases its relative weight on 0,001).
Taking:
mannitole;
dextran;
drugs used at X-ray examination.
Toxicosis of the pregnant.
Hyposthenuria – urine relative weight decreasing less than 1015 g/l main reasons:
renal channels acute injure;
diabetes unmellitus;
chronic renal insufficiency;
malignant hypertension.
Pathophysioogists tell about 3 main polyurias types:
1) Water diuresis – is determined by water facultative (non-obligatory) reabsorbtion decreasing. It appears at watery load, diabetes unmellitus. Urine is hypotonic because it ontains little amoun of osmotically-ative substances.
2) Osmotic diuresis (saluresis) is connected with increasing of non-reabsorbed asmotically-active substances in urine which leads to water reabsorbtion secondary disorder; reasons: electrolytes reabsorbtion disorders; threshold substances (glucose at diabetes mellitus) increasing in urine; exogenic substances action with weak reabsorbtion (mannitol) or the ones which disturb electrolytes reabsorbtion (saluretics); uroreleasing can reach 40% of glomerular filtration level under maximal diuresis conditions.
Hypertensive diuresis – is developed at arterial hypertension when blood velocity is increased in kidney medulla vasa recti (straight vessels) (these vessels come in parallel to Genle loop genuses). Na, Cl, urea are gone away from intersticium by active transport which leads to extracellular liquid hypoosmy and in turn to water reabsorbtion weakening in Genle loop descendent genus and polyuria.
83. Urine pathological components. Protein
Normal value: absent or traces (0,025-0,1 g/day).
Proteinuria is often non-specific symptom of kidney pathology. According to its value, one can tell about non-massive (proteins loss up to 3 g/day) and massive (more than 3 g/day) proteinuria. At renal proteinuria proteins can be detected both in morning and evening urine. Proteinuria is often combinated with cylindruria, erythrocyteuria, leucocyteuria.
Benz-Jons´ protein – low-molecular protein which is detected in urine at malignant new-formations in course of B-cells dysfunctions (myelomic disease).
Myoglobinuria – myoglobine appearance in urine – occurs at its level in plasma more than 0,15 g/l. Myoglobinuria can be primary and secondary. Primary one is hereditary determined in the biggest cases. It occurs due to muscular necroses and irreversible kidney changings combination. Such conditions are known as myorenal syndrom.
hereditary muscles pathology;
hard physical loadings (paroxysmal paralytic myoglobinuria);
without hard physical loadings (idiopathic myoglobinuria);
muscles necroses;
muscles traumas;
their long-termed ischemia;
poisoning substances action.
Urine is dark brown at myoglobinuria.
Haemoglobinuria – free haemoglobine appearance in urine as the result of its content increasing in blood plasma up to 1,2 g/l. Reason – erythrocytes haemolysis.
Mostly often proteins loss with urine occurs due to albumines. Alpha-globulins can appear in urine at nephroses. Beta- and gamma-globulins are excreted with urine at primary amyloidosis and myelomic disease; alpha-2-macroglobulins and beta-lipoproteids - at proliferative and membranous glomerulonephritis.
