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Lecture 1
Introduction, Cell & Tissue Damage
By Hermizan Halihanafiah
1
Pathology
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)
2
Basic terminology in Pathology
 Disease
 Etiology
 Pathogenesis
 Diagnosis
 Clinical manifestation - Signs and symptoms
 Prognosis
 Epidemiology
3
Disease / dis-ease
 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
4
Etiology
 Refers to the study of the cause of the disease
 General categories of etiological agents; genetic
abnormalities, infective agents, chemical, radiation,
mechanical trauma, malnutrition
5
Pathogenesis
 Is a mechanism of the disease which etiology operates
to produce the pathological and clinical manifestation
 For examples – inflammation, degeneration, immune
response
6
Diagnosis
 Refers to the process of attempting to determine or
identify a possible disease or disorder.
7
Prognosis
• Refers to the expected outcome of a disease.
Complication and sequalae
 Complication – is the onset of the disease in a person
who is already coping with another existing disease.
 Sequalae – unwanted outcomes of having disease or
are the result of trauma
8
Clinical Manifestation
 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
9
Epidemiology
 Is the study of tracking 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.
10
Prefixes and Suffixes and Roots
 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)
11
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)
12
Relationship between Cell Adaptation,
Cells degeneration, Cell Death
13
NORMAL CELLS
CELLS ADAPTATION
CELLS
DEGENERATION
CELLS DEATH
(NECROSIS/APOPTOSIS
Injuries
Injuries
Injuries
Cellular Adaptation
Under normal conditions, cells must constantly adapt to
changes is their environment (physiological,
pathological).
 Atrophy
 Hypertrophy
 Hyperplasia
 Dysplasia
 Metaplasia
14
Atrophy
 Shrinkage of the size of the
cells by the lost of the cells
substance.
 The entire tissue or organs
diminishes in size and
function
 May be due to decrease in
workload, lost of nerve
innervations, Lack of blood
supply, inadequate
nutrition, lost of endocrine
stimulation and aging
process.
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)
16
Hyperplasia
 Increase the number of
cells in an organ or tissue.
(increase rate of cellular
division)
 Hypertrophy and
hyperplasia are closely
related (exp : gravid uterus)
 Can be compensatory
hyperplasia (exp: liver),
hormonal hyperplasia (exp:
uterus, breast) and
pathological (exp:
endometrium)
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 better able to withstand the adverse of environment
18
19
Dysplasia
 Not a true cellular
adaptation
 Atypical hyperplasia
 Abnormal change in the
size, shape and
organization of mature
cells
 Strongly associated with
common neoplastic
growth
 Exp: CIN – cervical
intraepithelial neoplasia,
hip dysplasia
20
21
Cell Injury
 Nonlethal injury - cell degeneration
 Lethal injury – necrosis
22
Cell Degeneration (Nonlethal
Injury)
 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.
23
Necrosis (Lethal Injury)
 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
24
Stages of Necrosis
 Early changes : morphologically normal
 Nuclear changes : pyknosis – chromatin clumps into
coarse strands, nucleus become shrunken
 Cytoplasmic changes : denaturation of cytoplasmic
protein and lost of ribosomes, swelling of
mitochondria and disruption of organelle membranes
and autolysis occur via lysosomes
25
Type of Necrosis
 Different cells shows different morphologic changes
after they undergo necrosis. Base on that necrosis can
be classified into:
1. Coagulative necrosis
2. Liquefactive necrosis
3. Caseous / gummatous necrosis
4. Fat necrosis
5. Gangrenous Necrosis
27
Coagulative Necrosis
 Typically occur in solid organ; heart, kidney, adrenal
glands
 Due to hypoxia (maybe from severe ischemia or chemical)
 Normally, this necrotic cells retains its cellular outline.
 Denaturation of protein albumin causes coagulation.
28
Liquefactive Necrosis
 Normally occurs in CNS
which affects neuron and
neuroglia cells
 Associated with focal
bacterial and fungus
infections
 The affected cells
completely digest by
hydrolytic enzymes thus
changes the tissue into
liquid viscous mass.
29
Caseous Necrosis
 Caseous – cheese like
appearance
 Associated with
tuberculous pulmonary
(TB) infection, esp by
Mycobacterium
Tuberculosis
30
Fat Necrosis
 Occur in pancreas, breast and other abdominal structures
 Caused by lipases enzymes which break down triglycerides
(lipid) into fatty acids and glycerol
 Fatty acids and glycerol then combine with Ca, Mg, Na to
form Calcium Soaps (Saponification)
 The necrotic tissue appears opaque and chalk white.
31
Gangrenous Necrosis (gangrene)
 Extensive tissue necrosis
 Divide into two; dry and wet
 Dry – occurs in extremities as a
results of ischemic coagulative
necrosis due to arterial obstruction
 Wet – occurs in extremities and
internal organ as a results of
liquefactive necrosis due to
bacterial infection.
 Gas – necrotic tissue infected by
clostridium perfringes
32
Causes of Cell Injury
 Oxygen deprivation
 Chemical agents
 Infectious agents
 Immunologic reactions
 Genetic defects
 Nutritional imbalances
 Physical agents
 Aging
33
Oxygen deprivation
 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
34
Chemical agents
 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
35
Infectious agent
 Viruses, bacteria, fungi, parasites, helminths
36
Immunologic Reactions
 Autoimmune disease – immunity against its own
tissues . For examples SLE, Rheumatoid Arthritis etc
37
Genetic Defects
 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
38
Nutritional Imbalance
 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
39
Physical Agents
 Trauma, extremes of temperature, radiation, electrical
shock all have wide ranging effects on cells.
40
Aging
 Aged cells become larger, less able to divide and
multiply
 Lose their ability to functions, or function abnormally.
41

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Lec 1 Intro to Cell & Tissue Damage

  • 1. Lecture 1 Introduction, Cell & Tissue Damage By Hermizan Halihanafiah 1
  • 2. Pathology 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) 2
  • 3. Basic terminology in Pathology  Disease  Etiology  Pathogenesis  Diagnosis  Clinical manifestation - Signs and symptoms  Prognosis  Epidemiology 3
  • 4. Disease / dis-ease  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 4
  • 5. Etiology  Refers to the study of the cause of the disease  General categories of etiological agents; genetic abnormalities, infective agents, chemical, radiation, mechanical trauma, malnutrition 5
  • 6. Pathogenesis  Is a mechanism of the disease which etiology operates to produce the pathological and clinical manifestation  For examples – inflammation, degeneration, immune response 6
  • 7. Diagnosis  Refers to the process of attempting to determine or identify a possible disease or disorder. 7 Prognosis • Refers to the expected outcome of a disease.
  • 8. Complication and sequalae  Complication – is the onset of the disease in a person who is already coping with another existing disease.  Sequalae – unwanted outcomes of having disease or are the result of trauma 8
  • 9. Clinical Manifestation  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 9
  • 10. Epidemiology  Is the study of tracking 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. 10
  • 11. Prefixes and Suffixes and Roots  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) 11
  • 12. 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) 12
  • 13. Relationship between Cell Adaptation, Cells degeneration, Cell Death 13 NORMAL CELLS CELLS ADAPTATION CELLS DEGENERATION CELLS DEATH (NECROSIS/APOPTOSIS Injuries Injuries Injuries
  • 14. Cellular Adaptation Under normal conditions, cells must constantly adapt to changes is their environment (physiological, pathological).  Atrophy  Hypertrophy  Hyperplasia  Dysplasia  Metaplasia 14
  • 15. Atrophy  Shrinkage of the size of the cells by the lost of the cells substance.  The entire tissue or organs diminishes in size and function  May be due to decrease in workload, lost of nerve innervations, Lack of blood supply, inadequate nutrition, lost of endocrine stimulation and aging process. 15
  • 16. 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) 16
  • 17. Hyperplasia  Increase the number of cells in an organ or tissue. (increase rate of cellular division)  Hypertrophy and hyperplasia are closely related (exp : gravid uterus)  Can be compensatory hyperplasia (exp: liver), hormonal hyperplasia (exp: uterus, breast) and pathological (exp: endometrium) 17
  • 18. 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 better able to withstand the adverse of environment 18
  • 19. 19
  • 20. Dysplasia  Not a true cellular adaptation  Atypical hyperplasia  Abnormal change in the size, shape and organization of mature cells  Strongly associated with common neoplastic growth  Exp: CIN – cervical intraepithelial neoplasia, hip dysplasia 20
  • 21. 21
  • 22. Cell Injury  Nonlethal injury - cell degeneration  Lethal injury – necrosis 22
  • 23. Cell Degeneration (Nonlethal Injury)  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. 23
  • 24. Necrosis (Lethal Injury)  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 24
  • 25. Stages of Necrosis  Early changes : morphologically normal  Nuclear changes : pyknosis – chromatin clumps into coarse strands, nucleus become shrunken  Cytoplasmic changes : denaturation of cytoplasmic protein and lost of ribosomes, swelling of mitochondria and disruption of organelle membranes and autolysis occur via lysosomes 25
  • 26.
  • 27. Type of Necrosis  Different cells shows different morphologic changes after they undergo necrosis. Base on that necrosis can be classified into: 1. Coagulative necrosis 2. Liquefactive necrosis 3. Caseous / gummatous necrosis 4. Fat necrosis 5. Gangrenous Necrosis 27
  • 28. Coagulative Necrosis  Typically occur in solid organ; heart, kidney, adrenal glands  Due to hypoxia (maybe from severe ischemia or chemical)  Normally, this necrotic cells retains its cellular outline.  Denaturation of protein albumin causes coagulation. 28
  • 29. Liquefactive Necrosis  Normally occurs in CNS which affects neuron and neuroglia cells  Associated with focal bacterial and fungus infections  The affected cells completely digest by hydrolytic enzymes thus changes the tissue into liquid viscous mass. 29
  • 30. Caseous Necrosis  Caseous – cheese like appearance  Associated with tuberculous pulmonary (TB) infection, esp by Mycobacterium Tuberculosis 30
  • 31. Fat Necrosis  Occur in pancreas, breast and other abdominal structures  Caused by lipases enzymes which break down triglycerides (lipid) into fatty acids and glycerol  Fatty acids and glycerol then combine with Ca, Mg, Na to form Calcium Soaps (Saponification)  The necrotic tissue appears opaque and chalk white. 31
  • 32. Gangrenous Necrosis (gangrene)  Extensive tissue necrosis  Divide into two; dry and wet  Dry – occurs in extremities as a results of ischemic coagulative necrosis due to arterial obstruction  Wet – occurs in extremities and internal organ as a results of liquefactive necrosis due to bacterial infection.  Gas – necrotic tissue infected by clostridium perfringes 32
  • 33. Causes of Cell Injury  Oxygen deprivation  Chemical agents  Infectious agents  Immunologic reactions  Genetic defects  Nutritional imbalances  Physical agents  Aging 33
  • 34. Oxygen deprivation  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 34
  • 35. Chemical agents  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 35
  • 36. Infectious agent  Viruses, bacteria, fungi, parasites, helminths 36
  • 37. Immunologic Reactions  Autoimmune disease – immunity against its own tissues . For examples SLE, Rheumatoid Arthritis etc 37
  • 38. Genetic Defects  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 38
  • 39. Nutritional Imbalance  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 39
  • 40. Physical Agents  Trauma, extremes of temperature, radiation, electrical shock all have wide ranging effects on cells. 40
  • 41. Aging  Aged cells become larger, less able to divide and multiply  Lose their ability to functions, or function abnormally. 41