- •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.
8. Collapse. Comparative characteristics with shock. Aethiology and pathogenesis. Role of nervous and humoral mechanisms
Collapse –(crash, failure) – one of forms of acute vascular insufficiency occurring as a result of normal correlation disorder between vascular bed capacity and blood circulating volume.
Types (by I.R.Petrov):
Infectious-toxic (vessels and heart injury at infections).
Hypoxemic.
Orthostatic (at body position changing from horizontal one to vertical one).
Haemorrhagic (some scientists consider it shock state).
Peptonic (only experimental).
Hystaminic (only under experimental conditions).
Pancreatic (metabolic products come from pancreas to blood and arterial pressure is reduced).
Enterogenic (at demping-sysndrome).
This classification is based on aethiologic principle.
Pathogenesis. Vascular tone rapid decreasing and (or) circulating blood mass reducing lead to venous flow (return) reducing to heart, arterial and central venous pressure reducing, brain hypoxy and organism vital functions inhibiting.
Comparative characteristics
Parameters |
Shock |
Collapse |
1. Term, process essence |
Nozologic unit |
Syndrom, it is not separate nozologic unit |
2. Aethiology |
Shock is “collapse from trauma” as a result of exteroreceptors irritation |
Collapse is “shock without trauma”; it is caused by intoxication as a result of interoreceptors irritation |
3. Existence and dominance of the main in pathogenesis |
Changings is CNS are primary |
Acute weakness of vessels and heart are primary, changings in CNS are secondary ones. |
4. Course peuliarities |
Phasic, with rapid development |
Phases absence, relatively slow development |
5. Gravity dependence on arterial pressure reducing |
Without direct dependence |
Direct dependence, arterial pressure decreasing is shock gravity criterium |
6. Consciousness state |
It is preserved or darkened |
Lost or darkened |
7. Circulating blood volume changing |
Blood volume is decreased, blood is deponated |
Blood volume is normal or reduced |
8. Narcosis and anaesthesia |
They have preventive significance in shock initial stage |
They influence negatively on collapse course |
9. Protective-compensatory reactions |
First of all – from CNS side, then all organism is involved |
Dyspnoe, tachycardia, haemopoietic organs functions stimulation, blood mobilization from depot |
Shock and collapse similarity- in development:
vascular insufficiency;
respiratory insufficiency;
hypoxy;
compensatory and pathological reactions.
Collapse humoral causative agents:
histamine;
NO;
prostaglanine I2 or prostacycline;
noradrenaline acting through beta-2-adrenoreceptors and causing excessive vasodilation.
9. Crash-syndrome -
is a syndrome of prolonged pressure- pathological process developing in the injured as a result of long-termed (4-8 h and more) pressuring of soft tissues of extremities with parts of destroyed buildings, ground blocks et al.
3 periods: 1) early – up to 3 days – with shock phenomena dominance; 2) intermediate – 3-12 days – with renal insufficiency dominance; 3) late- (from 8-12 days up to 1-2 months), or recovery period, with local symptoms dominance.
3 main pathogenetic factors:
noceoceptive irritation;
traumatic toxemia caused by tissues autolysis toxic products absorbtion from injury locus;
plasma and blood loss delt with oedema and haemorrhagias in a zone of pressured or ishemized tissues (for long).
