General Pathology Summary for
the Exam
Rachel Presser
Third Year Medicine
, Contents
1. Introduction to pathology - subject, objectives and methods in pathology.
2. Etiology and pathogenesis. Types of damaging factors. General pathological processes.
3. Reversible cell injury - cellular edema, initiation mechanisms.
4. Necrosis - nature, types, exit.
5. Death – clinical and biological; signs of death.
6. Infarction – pathogenesis and morphology; types.
7. Apoptosis - nature, causes and mechanisms.
8. Cellular accumulations - abnormal intracellular accumulations of products, disproteinoses.
9. Lipid metabolism disorders - lipid degeneration, lipomatosis, lipoidosis.
10. Cumulative diseases – thesaurismoses.
11. Intercellular matrix disorders - connective tissue degeneration and fibrinoid deposition.
12. Elastin and collagen content and synthesis disorders.
13. Hyalinosis - causes, mechanisms for development. Types of hyalin.
14. Amyloidosis - causes, mechanisms for development, classification.
15. Calcium metabolism disorders - types of calcification. Concrement formation.
16. Mineral metabolism disorders - potassium, copper etc. Urate deposition.
17. Pigment metabolism disorders – hemosiderosis, hemochromatosis.
18. Pigment metabolism disorders - bilirubin. Types of jaundice.
19. Pigment metabolism disorders - melanin, exogenous pigments.
20. General principles of adaptations. Hypertrophy and hyperplasia.
21. Adaptational processes - atrophy, metaplasia, hystologic accommodation.
22. Regeneration (repair) – general characteristics. Disorders in the process of regeneration.
23. Regeneration (repair) of various tissues and organs.
24. Fibrosis - causes and mechanisms for development.
25. Circulatory disorders - anemia, hyperemia, stasis, hypostasis.
26. Hemorrhages - causes, types, mechanisms for development. Exit.
27. Tissue fluids balance disorders – dehydration. Edema – causes, types, mechanisms for development.
28. Hemostasis and thrombosis - pathogenesis, morphological characteristics, exit.
29. Embolism - types and morphological characteristics.
30. Disseminated intravascular coagulation - subject, pathogenesis, morphological
characteristics.
31. Shock - types and morphological characteristics.
32. Inflammation - general principles, pathogenesis and morphogenesis. Mediators of
inflammation.
33. Morphological characteristics of the acute inflammation. Types.
34. Chronic productive inflammation. Diffuse and granulomatous inflammation.
35. Immunopathology - morphological characteristics of immune reactions.
36. Hypersensitivity reactions - types, morphological characteristics. Bronchial asthma.
37. Autoimmune diseases - types, morphological characteristics.
38. Immunodeficiency syndromes. AIDS.
39. Immunology of transplantation - types of transplantation, main principles of tissue compatibility.
40. Immunology of transplantation –types of reactions of transplant rejection.
41. General Features of tumor growth, definition and terminology.
42. Etiology of tumors. Tumor genesis theories.
43. Morphological characteristics and classification of tumors. 44. Molecular basis of the tumor growth.
45. Biology of tumor growth - paraneoplastic syndromes.
46. Biology of tumor growth - staging and grading. Metastases.
47. Benign and malignant tumors – general characteristics.
48. Epithelial tumors – morphological characteristics.
49. Mesenchymal tumors - morphological characteristics.
50. Pigment tumors - types, morphological characteristics.
51. Teratomas - types, morphological characteristics.
52. Precancerous lesions. Displasia.
53. General principles of the infectious process - pathogenetic mechanisms and morphological manifestations.
54. Respiratory infections and tuberculosis - morphological characteristics.
55. Gastrointestinal infections - morphological characteristics.
56. Diseases caused by parasites - morphological characteristics.
57. Infectious diseases in the childhood – general characteristics.
58. Sexually transmitted infections - general characteristics.
59. Morphological signs of the physical and the chemical injuries.
60. Professional diseases.
61. Nutritional disorders - general characteristics, types, morphological manifestations.
62. Nutritional disorders – obesity.
63. Nutritional disorders. Avitaminoses.
64. Cell aging. Aging of the organism.
65. Developmental disorders - teratogenic factors, types of malformations.
66. Genopathies and blastopathies – types.
67. Embryopathies – types, morphological manifestations.
68. Fetopathies – types, morphological manifestations.
,1.Introduction to pathology - subject, objectives and methods in pathology.
Pathology is the study of disease, it involves the investigation of the causes and the associated changes at the level of
cells, organs, systems, etc, which in turn give rise to the presenting signs and symptoms of the patient.
It is divided into general or cellular and clinical or special pathology. General pathology studies the basic reactions of
cells and tissues to abnormal stimuli of the external and internal environment, whereas clinical pathology focuses on
specific responses of specified tissues and organs to harmful stimuli.
The objective of pathology is to understand how the disease occurs and develops. The main aspects that form its core
are etiology, pathogenesis, molecular and morphologic changes, clinical significance and pathomorphosis.
There are 3 basic methods in pathology: necropsy (autopsy), biopsy and experiment.
Necropsy: its aim is to provide an explanation of signs and symptoms noted during the patient’s illness. It consists of
gross description, dissection, microscopic observation and concluding about the cause of death, the mechanism of
pathogenesis, effect of treatment and discrepancies between the findings and the clinical diagnosis.
Biopsy: medical test involving the removal of cells or tissues for microscopic examination. It can be:
- incisional or core biopsy: only a sample of tissue is removed
- excisional biopsy: when the entire lump or suspicious area is removed
- pinch biopsy: is done with biopsy forceps and is the most commonly used form of tissue
- needle aspiration biopsy: a sample of tissue or fluid is removed with a needle
- citology: smears, brush, effusions, washings, FNAB. It gives us info about morphological diagnosis (etiological
agent, grading and staging of neoplasm, follow up the results of treatment, evaluation of the quality of surgical
treatment, etc)
Experiment via tissue processing and morphological methods.
- Tissue processing: fixation, paraffin embedment, sections and staining (HE- haematoxyllin eosin)
- Morphological methods: gross examination and microscopic observation (light microscopy – ordinary light
source, fluorescent light, laser light and polarised light \ electron microscopy – TEM, SEM
The aim of pathology is to study the structural basis of disease at different levels:
• Organism, system, organ, tissue, cell, organelles and molecules.
2.Etiology and pathogenesis. Types of damaging factors. General pathological
processes.
Defining etiology and pathologenesis of disease not only is essential for understanding a disease but also the basis for
developing rational treatments. Thus, by explaining the causes and development of disease pathology provides the
scientific foundation for the practice of medicine.
Etiology: origin of disease, including the underlying causes and modifying factors. Understanding the genetic and
environmental factors underlying diseases is a major theme of modern medicine. Aka why the disease happened.
Major etiologic factors
Intrinsic or genetic: results from abnormalities in the DNA which forms the genome. It may develop during fetal life or
postnatal life.
Acquired
Endogenous: genetic disorders, hormonal disturbances, immune factors and allergies.
, - Exogenous: deficiencies (O2...), physical factors (trauma, temperature (high and low), electricity, radiation),
chemicals (including drugs), biological factors (prions, viruses, helmiths, protozoa, bacteria…) immunological factors,
psychogenic factors
Etiological categories: congenital, vascular, neoplasmic, infectious, toxic, atrophic or degenerative, metabolic, traumatic,
autoimmune, dietary, iatrogenic, idiopathic.
Pathogenesis: refers to the steps in the development of disease. It describes how etiologic factors trigger cellular and
molecular changes that give rise to the specific functional and structural abnormalities that characterize the disease.
Whereas etiology refers to why a disease arises, pathogenesis describes how a disease develops. It is the link between
the etiologic factor and the structural damage and functional failure. Aka how the disease developed.
There are 6 mechanisms of cell injury:
• ATP depletion
• Mitochondrial damage
• Ca influx
• Oxygen derived free radicals
• Membrane damage
• Damage to DNA and proteins
3. Reversible cell injury - cellular edema, initiation mechanisms
The stage of cell injury in which the deranged function and morphology of the injured cells can return back to normal if
the damaging stimulus is removed.
The two main morphological correlates of reversible cell injury are:
• Cellular swelling –
o commonly seen in cell injury associated with increased permeability of the plasma membrane.
o causes pallor as a result of compression of capillaries,
o increased turgor and an increase in organ weight.
§ Microscopic examination may show distended and pinched off segments of the endoplasmic
reticulum. This pattern of nonlethal injury is sometimes called hydrophobic change or vacuolar
degradation.
• Fatty change –
o this is manifested by the appearance of triglycerde containing lipid vacuoles in the cytoplasm. It is
principally encountered in organs involved in lipid metabolism so the liver.
General changes
• The cytoplasm of injured cells may also become redder (eosinophilia)
• Plasma membrane alterations – such as blebbing, bluting or distortion of microvilli and loosening of cellular
attachments.
• Mitochondrial changes - such as swelling and the appearance of phospholipid rich amphorous densities
• Dilation of the ER - with detachment of the ribosomes and dissociation of the polysomes.
• Nuclear alterations – such as clumping of chromatin
• myelin figures (collections of phospholipids resembling myelin sheaths that are derived from damaged cellular
membranes) may appear in the cytoplasm
• injurious insults can induce specific alterations in the cellular organelles such as the ER.
o The smooth ER is involved in the metabolism of various chemicals and cells exposed to these chemicals
show hypertrophy of the ER as an adaptive response that may have important functional consequences.
With persistent or excessive noxious exposures, cells pass a nebulous point of no return and undergo cell death.
There are two types of cell death, these are apoptosis and necrosis.
• With severe disturbances such as loss of oxygen, the cell cannot withstand the changes and undergoes a
random sequence of uncontrollable events, leading to cell death. This is necrosis.
• With less severe disturbances or when a cell has to elimate cells in normal biological processes, they activate a
precise set of molecular pathways that culminate in death. This is apoptosis. Or controlled cell death.
the Exam
Rachel Presser
Third Year Medicine
, Contents
1. Introduction to pathology - subject, objectives and methods in pathology.
2. Etiology and pathogenesis. Types of damaging factors. General pathological processes.
3. Reversible cell injury - cellular edema, initiation mechanisms.
4. Necrosis - nature, types, exit.
5. Death – clinical and biological; signs of death.
6. Infarction – pathogenesis and morphology; types.
7. Apoptosis - nature, causes and mechanisms.
8. Cellular accumulations - abnormal intracellular accumulations of products, disproteinoses.
9. Lipid metabolism disorders - lipid degeneration, lipomatosis, lipoidosis.
10. Cumulative diseases – thesaurismoses.
11. Intercellular matrix disorders - connective tissue degeneration and fibrinoid deposition.
12. Elastin and collagen content and synthesis disorders.
13. Hyalinosis - causes, mechanisms for development. Types of hyalin.
14. Amyloidosis - causes, mechanisms for development, classification.
15. Calcium metabolism disorders - types of calcification. Concrement formation.
16. Mineral metabolism disorders - potassium, copper etc. Urate deposition.
17. Pigment metabolism disorders – hemosiderosis, hemochromatosis.
18. Pigment metabolism disorders - bilirubin. Types of jaundice.
19. Pigment metabolism disorders - melanin, exogenous pigments.
20. General principles of adaptations. Hypertrophy and hyperplasia.
21. Adaptational processes - atrophy, metaplasia, hystologic accommodation.
22. Regeneration (repair) – general characteristics. Disorders in the process of regeneration.
23. Regeneration (repair) of various tissues and organs.
24. Fibrosis - causes and mechanisms for development.
25. Circulatory disorders - anemia, hyperemia, stasis, hypostasis.
26. Hemorrhages - causes, types, mechanisms for development. Exit.
27. Tissue fluids balance disorders – dehydration. Edema – causes, types, mechanisms for development.
28. Hemostasis and thrombosis - pathogenesis, morphological characteristics, exit.
29. Embolism - types and morphological characteristics.
30. Disseminated intravascular coagulation - subject, pathogenesis, morphological
characteristics.
31. Shock - types and morphological characteristics.
32. Inflammation - general principles, pathogenesis and morphogenesis. Mediators of
inflammation.
33. Morphological characteristics of the acute inflammation. Types.
34. Chronic productive inflammation. Diffuse and granulomatous inflammation.
35. Immunopathology - morphological characteristics of immune reactions.
36. Hypersensitivity reactions - types, morphological characteristics. Bronchial asthma.
37. Autoimmune diseases - types, morphological characteristics.
38. Immunodeficiency syndromes. AIDS.
39. Immunology of transplantation - types of transplantation, main principles of tissue compatibility.
40. Immunology of transplantation –types of reactions of transplant rejection.
41. General Features of tumor growth, definition and terminology.
42. Etiology of tumors. Tumor genesis theories.
43. Morphological characteristics and classification of tumors. 44. Molecular basis of the tumor growth.
45. Biology of tumor growth - paraneoplastic syndromes.
46. Biology of tumor growth - staging and grading. Metastases.
47. Benign and malignant tumors – general characteristics.
48. Epithelial tumors – morphological characteristics.
49. Mesenchymal tumors - morphological characteristics.
50. Pigment tumors - types, morphological characteristics.
51. Teratomas - types, morphological characteristics.
52. Precancerous lesions. Displasia.
53. General principles of the infectious process - pathogenetic mechanisms and morphological manifestations.
54. Respiratory infections and tuberculosis - morphological characteristics.
55. Gastrointestinal infections - morphological characteristics.
56. Diseases caused by parasites - morphological characteristics.
57. Infectious diseases in the childhood – general characteristics.
58. Sexually transmitted infections - general characteristics.
59. Morphological signs of the physical and the chemical injuries.
60. Professional diseases.
61. Nutritional disorders - general characteristics, types, morphological manifestations.
62. Nutritional disorders – obesity.
63. Nutritional disorders. Avitaminoses.
64. Cell aging. Aging of the organism.
65. Developmental disorders - teratogenic factors, types of malformations.
66. Genopathies and blastopathies – types.
67. Embryopathies – types, morphological manifestations.
68. Fetopathies – types, morphological manifestations.
,1.Introduction to pathology - subject, objectives and methods in pathology.
Pathology is the study of disease, it involves the investigation of the causes and the associated changes at the level of
cells, organs, systems, etc, which in turn give rise to the presenting signs and symptoms of the patient.
It is divided into general or cellular and clinical or special pathology. General pathology studies the basic reactions of
cells and tissues to abnormal stimuli of the external and internal environment, whereas clinical pathology focuses on
specific responses of specified tissues and organs to harmful stimuli.
The objective of pathology is to understand how the disease occurs and develops. The main aspects that form its core
are etiology, pathogenesis, molecular and morphologic changes, clinical significance and pathomorphosis.
There are 3 basic methods in pathology: necropsy (autopsy), biopsy and experiment.
Necropsy: its aim is to provide an explanation of signs and symptoms noted during the patient’s illness. It consists of
gross description, dissection, microscopic observation and concluding about the cause of death, the mechanism of
pathogenesis, effect of treatment and discrepancies between the findings and the clinical diagnosis.
Biopsy: medical test involving the removal of cells or tissues for microscopic examination. It can be:
- incisional or core biopsy: only a sample of tissue is removed
- excisional biopsy: when the entire lump or suspicious area is removed
- pinch biopsy: is done with biopsy forceps and is the most commonly used form of tissue
- needle aspiration biopsy: a sample of tissue or fluid is removed with a needle
- citology: smears, brush, effusions, washings, FNAB. It gives us info about morphological diagnosis (etiological
agent, grading and staging of neoplasm, follow up the results of treatment, evaluation of the quality of surgical
treatment, etc)
Experiment via tissue processing and morphological methods.
- Tissue processing: fixation, paraffin embedment, sections and staining (HE- haematoxyllin eosin)
- Morphological methods: gross examination and microscopic observation (light microscopy – ordinary light
source, fluorescent light, laser light and polarised light \ electron microscopy – TEM, SEM
The aim of pathology is to study the structural basis of disease at different levels:
• Organism, system, organ, tissue, cell, organelles and molecules.
2.Etiology and pathogenesis. Types of damaging factors. General pathological
processes.
Defining etiology and pathologenesis of disease not only is essential for understanding a disease but also the basis for
developing rational treatments. Thus, by explaining the causes and development of disease pathology provides the
scientific foundation for the practice of medicine.
Etiology: origin of disease, including the underlying causes and modifying factors. Understanding the genetic and
environmental factors underlying diseases is a major theme of modern medicine. Aka why the disease happened.
Major etiologic factors
Intrinsic or genetic: results from abnormalities in the DNA which forms the genome. It may develop during fetal life or
postnatal life.
Acquired
Endogenous: genetic disorders, hormonal disturbances, immune factors and allergies.
, - Exogenous: deficiencies (O2...), physical factors (trauma, temperature (high and low), electricity, radiation),
chemicals (including drugs), biological factors (prions, viruses, helmiths, protozoa, bacteria…) immunological factors,
psychogenic factors
Etiological categories: congenital, vascular, neoplasmic, infectious, toxic, atrophic or degenerative, metabolic, traumatic,
autoimmune, dietary, iatrogenic, idiopathic.
Pathogenesis: refers to the steps in the development of disease. It describes how etiologic factors trigger cellular and
molecular changes that give rise to the specific functional and structural abnormalities that characterize the disease.
Whereas etiology refers to why a disease arises, pathogenesis describes how a disease develops. It is the link between
the etiologic factor and the structural damage and functional failure. Aka how the disease developed.
There are 6 mechanisms of cell injury:
• ATP depletion
• Mitochondrial damage
• Ca influx
• Oxygen derived free radicals
• Membrane damage
• Damage to DNA and proteins
3. Reversible cell injury - cellular edema, initiation mechanisms
The stage of cell injury in which the deranged function and morphology of the injured cells can return back to normal if
the damaging stimulus is removed.
The two main morphological correlates of reversible cell injury are:
• Cellular swelling –
o commonly seen in cell injury associated with increased permeability of the plasma membrane.
o causes pallor as a result of compression of capillaries,
o increased turgor and an increase in organ weight.
§ Microscopic examination may show distended and pinched off segments of the endoplasmic
reticulum. This pattern of nonlethal injury is sometimes called hydrophobic change or vacuolar
degradation.
• Fatty change –
o this is manifested by the appearance of triglycerde containing lipid vacuoles in the cytoplasm. It is
principally encountered in organs involved in lipid metabolism so the liver.
General changes
• The cytoplasm of injured cells may also become redder (eosinophilia)
• Plasma membrane alterations – such as blebbing, bluting or distortion of microvilli and loosening of cellular
attachments.
• Mitochondrial changes - such as swelling and the appearance of phospholipid rich amphorous densities
• Dilation of the ER - with detachment of the ribosomes and dissociation of the polysomes.
• Nuclear alterations – such as clumping of chromatin
• myelin figures (collections of phospholipids resembling myelin sheaths that are derived from damaged cellular
membranes) may appear in the cytoplasm
• injurious insults can induce specific alterations in the cellular organelles such as the ER.
o The smooth ER is involved in the metabolism of various chemicals and cells exposed to these chemicals
show hypertrophy of the ER as an adaptive response that may have important functional consequences.
With persistent or excessive noxious exposures, cells pass a nebulous point of no return and undergo cell death.
There are two types of cell death, these are apoptosis and necrosis.
• With severe disturbances such as loss of oxygen, the cell cannot withstand the changes and undergoes a
random sequence of uncontrollable events, leading to cell death. This is necrosis.
• With less severe disturbances or when a cell has to elimate cells in normal biological processes, they activate a
precise set of molecular pathways that culminate in death. This is apoptosis. Or controlled cell death.
