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Basic pathophysiology.pptx

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DrirFaisalHasan

This document discusses cell and tissue damage from various causes and their effects. It begins by explaining prefixes, suffixes, and roots used in medical terminology. It then defines pathology and discusses basic terminology like disease, etiology, pathogenesis, diagnosis, and prognosis. Various types of cellular adaptation and degeneration are described, including atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia. Necrosis, or lethal cell injury, is defined and the stages are outlined. Various causes of cell injury are provided like oxygen deprivation, chemicals, infections, immunological reactions, genetics, nutrition, physical agents, and aging.

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Cell /Tissue Damage & Nutritional effect By Assoc.Prof.dr.Faisal 1 Basic Pathophysiology
Prefixes and Suffixes and Roots 2  Root- the foundation of the word  Prefix – place before the root to modify its meaning  Suffix – places after root to modify and give essential meaning to the root 1. Hyperlipoproteinemia  Prefix : hyper (higher)  Roots : lipoprotein  Suffix : -emia (blood condition)
2. Hepatosplenomegaly  Root : hepato (hepar), spleno (spleen)  Suffix : -megaly (enlargement) 3. Meningitis  Root : mening (meninges)  Suffix : - itis (inflammation) 4. Tachycardia  Root : cardia (heart)  Prefix : tachy – (fast/rapid) 3
Pathology 4 Definition  Pathology is the study (logos) of suffering/diseases (pathos)  Involves basic medical sciences and clinical practice to investigates of the causes (etiology) of the diseases and the mechanism (pathogenesis)
Basic terminology in Pathology 5  Disease  Etiology  Pathogenesis  Diagnosis  Clinical manifestation - Signs and symptoms  Prognosis  Epidemiology
Disease / dis-ease 6  Disease is a condition in which the presence of an abnormality of the body causes a loss of normal health  Idiopathic – no identifiable causes  Iatrogenic – occur as a result from medical treatment  Congenital – disease existing at birth or before birth, involves in the development of fetus  Acquired - develops post –fetally  Nosocomial – due to being in a hospital environments
Etiology 7  Refers to the study of the cause of the disease  General categories of etiological agents; genetic abnormalities, infective agents, chemical, radiation, mechanical trauma, malnutrition
Pathogenesis 8  Is a mechanism of the disease which etiology operates to produce the pathological and clinical manifestation  For examples – inflammation, degeneration, immune response  Complication – is the onset of further diseases in a person who is already suffering from another existing disease.
Diagnosis 9  Refers to the process of attempting to determine or identify a possible disease or disorder. Prognosis • Refers to the expected outcome of a disease.
Clinical Manifestation 10  Are the signs and symptoms or evidence of disease  Signs – objective alteration that can be observe or measured by another person; pulse rate, blood pressure, Temperature…. etc  Symptoms – subjective experiences reported by the person, complains such as pain, nausea, vomiting …..etc
Epidemiology 11  Is the study of patters of disease occurrence and transmission among populations and by geographic areas.  Incidence of a disease– is the number of new cases occurring in specific time of period  Prevalence of a disease – is the number of existing cases within a populations during the specific time of period.
Relationship between Cell Adaptation, Cells degeneration, Cell Death NORMAL CELLS CELLS ADAPTATION CELLS DEGENERATION CELLS DEATH (NECROSIS/APOPTOSIS Injuries Injuries Injuries 12
Cellular Adaptation 13 Under normal conditions, cells must constantly adapt to changes is their environment (physiological, pathological).  Atrophy  Hypertrophy  Hyperplasia  Dysplasia  Metaplasia
Atrophy  The entire tissue or organs diminishes in size and function  May be due to decrease in workload, lost of nerve stimulating, Lack of blood supply, inadequate nutrition, lost of endocrine stimulation and aging process. 14
Hypertrophy  Increase the size of the cells and consequently the size of the organs.  Increased the synthesis of structural protein and organelles.  Can be physiologic (ex;increase workload during exercise, uterine myometrium during pregnancy) and pathologic (hypertrophy of myocardium – hypertension/aortic valve disease) and adiposity of adipose tissue. 15
Hyperplasia  Increase the number of cells in an organ or tissue. (increase rate of cellular division)  Hypertrophy and hyperplasia are closely related  Can be compensatory hyperplasia (exp: liver), hormonal hyperplasia (exp: uterus, breast) and pathological (exp: endometrium) 16
Metaplasia  Is a reversible change in which one adult cell type is replaced by another cell type.  Adaptation of cells that sensitive to particular stress to cell types and the adverse of environment 17
Dysplasia  Atypical hyperplasia  Abnormal change in the size, shape and organization of mature cells  Strongly associated with common neoplastic growth 18
Cell Injury 19  Nonlethal injury - cell degeneration  Lethal injury – necrosis
Cell Degeneration (Nonlethal Injury) 20  Nonlethal injury may produce cell degeneration  Manifested as a abnormality of biochemical function, structural changes or combination.  Its reversible but may become irreversible (necrosis/apoptosis)  May produce clinical disease.
Necrosis (Lethal Injury) 21  Definition – unprogrammed cell death and living tissues. (opposite to apoptosis)  Irreversible  Accompanied with by biochemical and morphological changes  Due to hypoxia, chemical substances, free radical, immunologic response, infections ….etc
Stages of Necrosis 22  Early changes : morphologically normal  Nuclear changes : Pyknosis – is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.  Cytoplasmic changes : denaturation of cytoplasmic protein and lost of ribosomes, swelling of mitochondria and disruption of organelle membranes and autolysis occur via lysosomes.
Causes of Cell Injury 23  Oxygen deprivation  Chemical agents  Infectious agents  Immunologic reactions  Genetic defects  Nutritional imbalances  Physical agents  Aging
Oxygen deprivation 24  Hypoxia – oxygen deficiency  Due to ischemia – lost/lack of blood supply (due to arterial blockage or reduce venous drainage)  Hypoxia also can occurs via:  Lack of oxygen inside blood  Reduction in oxygen carrying capacity in RBC (anemia)  Carbon monoxide poisoning
Chemical agents 25  Most of the chemical substances can cause cell injury  For example : poisons, air pollutants, insecticides, CO, asbestos, ethanol, therapeutics drugs etc  This agents can cause cell death by:  Altering membrane permeability’  Altering osmotic homeostasis  Altering integrity of an enzyme
Infectious agent 26  Viruses, bacteria, fungi, parasites, helminths
Immunologic Reactions 27  Autoimmune disease – immunity against its own tissues . For examples SLE, Rheumatoid Arthritis etc
Genetic Defects 28  Abnormalities to the genomes - mutation  This chromosome anomaly is associated with missing, or irregularities or extra in portion of chromosomal DNA  Syndrome Down, Alzheimer's Disease, Huntington’s Disease etc
Nutritional Imbalance 29  Cause by directly or indirectly lack of essential nutrients (malnutrition)  Or it maybe related to excessive of food intake (Diabetic Mellitus)  For example protein deficiency – Kwashiorkor, Marasmus  Calcium deficiency – osteoporosis  Vitamin C - Scurvy
Physical Agents 30  Trauma, extremes of temperature, radiation, electrical shock all have wide ranging effects on cells.
Aging 31  Aged cells become larger, less able to divide and multiply  Lose their ability to functions, or function abnormally.
References - Understanding Pathophysiology, 7th Edition by Sue E. Huether. - Story, L. (2012). Pathophysiology: A Practical Approach (2nd ed.). Burlington, MA: Jones & Bartlett Learning. - Hubert, R. J., & Van Meter, K. C. (2018). Gould’s pathophysiology for the health professions (6th ed.). St. Louis, MO: Elsevier Saunders.

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Basic pathophysiology.pptx

  • 1. Cell /Tissue Damage & Nutritional effect By Assoc.Prof.dr.Faisal 1 Basic Pathophysiology
  • 2. Prefixes and Suffixes and Roots 2  Root- the foundation of the word  Prefix – place before the root to modify its meaning  Suffix – places after root to modify and give essential meaning to the root 1. Hyperlipoproteinemia  Prefix : hyper (higher)  Roots : lipoprotein  Suffix : -emia (blood condition)
  • 3. 2. Hepatosplenomegaly  Root : hepato (hepar), spleno (spleen)  Suffix : -megaly (enlargement) 3. Meningitis  Root : mening (meninges)  Suffix : - itis (inflammation) 4. Tachycardia  Root : cardia (heart)  Prefix : tachy – (fast/rapid) 3
  • 4. Pathology 4 Definition  Pathology is the study (logos) of suffering/diseases (pathos)  Involves basic medical sciences and clinical practice to investigates of the causes (etiology) of the diseases and the mechanism (pathogenesis)
  • 5. Basic terminology in Pathology 5  Disease  Etiology  Pathogenesis  Diagnosis  Clinical manifestation - Signs and symptoms  Prognosis  Epidemiology
  • 6. Disease / dis-ease 6  Disease is a condition in which the presence of an abnormality of the body causes a loss of normal health  Idiopathic – no identifiable causes  Iatrogenic – occur as a result from medical treatment  Congenital – disease existing at birth or before birth, involves in the development of fetus  Acquired - develops post –fetally  Nosocomial – due to being in a hospital environments
  • 7. Etiology 7  Refers to the study of the cause of the disease  General categories of etiological agents; genetic abnormalities, infective agents, chemical, radiation, mechanical trauma, malnutrition
  • 8. Pathogenesis 8  Is a mechanism of the disease which etiology operates to produce the pathological and clinical manifestation  For examples – inflammation, degeneration, immune response  Complication – is the onset of further diseases in a person who is already suffering from another existing disease.
  • 9. Diagnosis 9  Refers to the process of attempting to determine or identify a possible disease or disorder. Prognosis • Refers to the expected outcome of a disease.
  • 10. Clinical Manifestation 10  Are the signs and symptoms or evidence of disease  Signs – objective alteration that can be observe or measured by another person; pulse rate, blood pressure, Temperature…. etc  Symptoms – subjective experiences reported by the person, complains such as pain, nausea, vomiting …..etc
  • 11. Epidemiology 11  Is the study of patters of disease occurrence and transmission among populations and by geographic areas.  Incidence of a disease– is the number of new cases occurring in specific time of period  Prevalence of a disease – is the number of existing cases within a populations during the specific time of period.
  • 12. Relationship between Cell Adaptation, Cells degeneration, Cell Death NORMAL CELLS CELLS ADAPTATION CELLS DEGENERATION CELLS DEATH (NECROSIS/APOPTOSIS Injuries Injuries Injuries 12
  • 13. Cellular Adaptation 13 Under normal conditions, cells must constantly adapt to changes is their environment (physiological, pathological).  Atrophy  Hypertrophy  Hyperplasia  Dysplasia  Metaplasia
  • 14. Atrophy  The entire tissue or organs diminishes in size and function  May be due to decrease in workload, lost of nerve stimulating, Lack of blood supply, inadequate nutrition, lost of endocrine stimulation and aging process. 14
  • 15. Hypertrophy  Increase the size of the cells and consequently the size of the organs.  Increased the synthesis of structural protein and organelles.  Can be physiologic (ex;increase workload during exercise, uterine myometrium during pregnancy) and pathologic (hypertrophy of myocardium – hypertension/aortic valve disease) and adiposity of adipose tissue. 15
  • 16. Hyperplasia  Increase the number of cells in an organ or tissue. (increase rate of cellular division)  Hypertrophy and hyperplasia are closely related  Can be compensatory hyperplasia (exp: liver), hormonal hyperplasia (exp: uterus, breast) and pathological (exp: endometrium) 16
  • 17. Metaplasia  Is a reversible change in which one adult cell type is replaced by another cell type.  Adaptation of cells that sensitive to particular stress to cell types and the adverse of environment 17
  • 18. Dysplasia  Atypical hyperplasia  Abnormal change in the size, shape and organization of mature cells  Strongly associated with common neoplastic growth 18
  • 19. Cell Injury 19  Nonlethal injury - cell degeneration  Lethal injury – necrosis
  • 20. Cell Degeneration (Nonlethal Injury) 20  Nonlethal injury may produce cell degeneration  Manifested as a abnormality of biochemical function, structural changes or combination.  Its reversible but may become irreversible (necrosis/apoptosis)  May produce clinical disease.
  • 21. Necrosis (Lethal Injury) 21  Definition – unprogrammed cell death and living tissues. (opposite to apoptosis)  Irreversible  Accompanied with by biochemical and morphological changes  Due to hypoxia, chemical substances, free radical, immunologic response, infections ….etc
  • 22. Stages of Necrosis 22  Early changes : morphologically normal  Nuclear changes : Pyknosis – is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.  Cytoplasmic changes : denaturation of cytoplasmic protein and lost of ribosomes, swelling of mitochondria and disruption of organelle membranes and autolysis occur via lysosomes.
  • 23. Causes of Cell Injury 23  Oxygen deprivation  Chemical agents  Infectious agents  Immunologic reactions  Genetic defects  Nutritional imbalances  Physical agents  Aging
  • 24. Oxygen deprivation 24  Hypoxia – oxygen deficiency  Due to ischemia – lost/lack of blood supply (due to arterial blockage or reduce venous drainage)  Hypoxia also can occurs via:  Lack of oxygen inside blood  Reduction in oxygen carrying capacity in RBC (anemia)  Carbon monoxide poisoning
  • 25. Chemical agents 25  Most of the chemical substances can cause cell injury  For example : poisons, air pollutants, insecticides, CO, asbestos, ethanol, therapeutics drugs etc  This agents can cause cell death by:  Altering membrane permeability’  Altering osmotic homeostasis  Altering integrity of an enzyme
  • 26. Infectious agent 26  Viruses, bacteria, fungi, parasites, helminths
  • 27. Immunologic Reactions 27  Autoimmune disease – immunity against its own tissues . For examples SLE, Rheumatoid Arthritis etc
  • 28. Genetic Defects 28  Abnormalities to the genomes - mutation  This chromosome anomaly is associated with missing, or irregularities or extra in portion of chromosomal DNA  Syndrome Down, Alzheimer's Disease, Huntington’s Disease etc
  • 29. Nutritional Imbalance 29  Cause by directly or indirectly lack of essential nutrients (malnutrition)  Or it maybe related to excessive of food intake (Diabetic Mellitus)  For example protein deficiency – Kwashiorkor, Marasmus  Calcium deficiency – osteoporosis  Vitamin C - Scurvy
  • 30. Physical Agents 30  Trauma, extremes of temperature, radiation, electrical shock all have wide ranging effects on cells.
  • 31. Aging 31  Aged cells become larger, less able to divide and multiply  Lose their ability to functions, or function abnormally.
  • 32. References - Understanding Pathophysiology, 7th Edition by Sue E. Huether. - Story, L. (2012). Pathophysiology: A Practical Approach (2nd ed.). Burlington, MA: Jones & Bartlett Learning. - Hubert, R. J., & Van Meter, K. C. (2018). Gould’s pathophysiology for the health professions (6th ed.). St. Louis, MO: Elsevier Saunders.