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ADAPTATION, INJURY and DEATH of CELLS (Part 1)

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Title: ADAPTATION, INJURY and DEATH of CELLS (Part 1)


1
ADAPTATION, INJURY and DEATH of CELLS (Part 1)
  • Ashley Inman
  • Tom Davis
  • 8-12-2014

2
Lecture 2 Learning Objectives
  • 1. List examples of hypertrophy, hyperplasia,
    atrophy, hypoplasia, metaplasia and dysplasia
  • 2. List examples of reversible and irreversible
    cell injury
  • 3. Diagram abscess, granuloma, renal infarction
    and fat necrosis
  • 4. List consequences of ATP loss
  • 5. List consequences Ca increase and release

3
Pathology the Study of Disease
  • Etiology or cause infection, genetic etc. and
    often mutifactoral
  • Pathogenesis progression of the disease
  • (Molecular and Morphologic Changes)
  • Clinical Manifestations signs and symptoms

4
Cellular Adaptations
  • Hypertrophy
  • Hyperplasia
  • Atrophy
  • Metaplasia
  • Dysplasia

5
HYPERTROPHY
  • Increase in cell size with subsequent increase in
    organ size

6
Causes of Hypertrophy
  1. Increased functional demand
  2. Hormonal stimulation

7
Hypertrophy of Uterus During Pregnancy
8
Hypertrophy of Uterus During Pregnancy
No new cells Cells just bigger
9
  • Hypertrophy can be physiologic or pathologic

10
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11
Cardiac Muscle Hypertrophy and Infarction
12
Results from increased production of cellular
proteins
13
HYPERPLASIA
  • Increase in the number of cells in an organ which
    may then increase organ size.
  • Physiologic or Pathologic

14
PHYSIOLOGIC HYPERPLASIA
  1. Hormonal hyperplasia- female breast at puberty
    and in pregnancy
  2. Compensatory hyperplasia- liver regeneration
    after partial resection

15
Female Breast Tissue after Puberty
16
Lactating breast during pregnancy
17
Causes of Pathologic Hyperplasia
  • Excess hormone- endometrial hyperplasia due to
    estrogens

18
  • Hyperplasia is NOT a neoplastic process, but it
    may be fertlie soil for malignancy
  • Atypical Hyperplasia in the endometrium carries
    an increased risk for development of endometrial
    adenocarcinoma

19
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20
Endometrial Hyperplasia
21
Normal Proliferative Endometrium
22
Endometrial Hyperplasia
23
Benign Prostatic Hypertrophy
24
ATROPHY
  • Decrease in the size of a cell or organ by loss
    of cell substance (both size and number)

25
Physiologic Atrophy
  • Normal development
  • Notochord
  • Thyroglossal duct
  • Uterus following childbirth

26
Causes of Pathologic Atrophy
  1. Decreased workload
  2. Loss of innervation
  3. Decreased blood supply
  4. Inadequate nutrition
  5. Loss of endocrine stimulation
  6. Pressure

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Central skeletal muscle bundle is atrophic
29
Atrophic Brain
Normal Brain
30
Atrophy results from both
  • Decreased protein synthesis
  • Increased protein degradation

31
Protein degradation is important in atrophy
  1. Lysosomes with hydrolytic enzymes
  2. The ubiquitin-proteasome pathway

32
HYPOPLASIA
  • Incomplete development of an organ so that it
    fails to reach adult size

33
Examples of Hypoplasia
Hypoplastic Left Ventricle
Hypoplastic Kidney
34
METAPLASIA
  • A reversible change in which one ADULT cell type
    is replaced by another ADULT cell type

35
Metaplasia
  • Caused by
  • Chronic irritation (cigarette smoke calculi in
    ducts)
  • Vitamin A deficiency
  • Cervix- squamous epithelium of the endocervix
    replaces columnar (dysplasia and squamous CA may
    develop)
  • Barrett esophagus- gastric reflux results in
    columnar epithelium replacing squamous epithelium
    in the esophagus (dysplasia and adenocarcinoma
    may occur)

36
Squamous cells replace columnar cells
37
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38
Esophagus glandular epithelium (R) is
metaplastic
39
Hyperplasia and Metaplasia are not premalignant
changes, however they are fertile fields for
Dysplasia which is a premalignant change
40
DYSPLASIA
  • Atypical proliferative changes due to chronic
    irritation or inflammation
  • Premalignant change

41
DYSPLASIA IN THE CERVIX
Mild dysplasia
Moderate dysplasia
Marked dysplasia
42
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43
CELL INJURY PRINCIPLES
  • The cellular response to injurious stimuli
    depends on the type of injury, its duration and
    its severity.
  • The consequences of cell injury depend on the
    type, state, and adaptability of the injured cell
  • Cell injury results from different biochemical
    mechanisms acting on several essential cellular
    components

44
1. The cellular response to injurious stimuli
depends on the type of injury, its duration and
its severity.
45
Cellular Changes Secondary to Injury
  • REVERSIBLE
  • Cellular swelling
  • Cell membrane blebs
  • Detached ribosomes
  • Chromatin clumping
  • IRREVERSIBLE
  • Lysosomes rupture
  • Dense bodies in mitochondria
  • Cell membrane rupture
  • Karyolysis, karyorrhexis, pyknosis

46
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49
Myocardial Infarction Markers
  • Cardiac specific enzymes and proteins appear in
    serum within 2 hours post infarction
  • Morphologic (light microscopic) changes in 4-12
    hours

50
Normal Myocardium
Coagulation Necrosis at 24-48 hours post MI
51
  • Normal kidney
  • Reversible changes
  • C. Dying Cell

52
Normal Kidney Histology
53
Normal Tubules
54
Tubules Accumulate Water (cloudy swelling)
55
2. The consequences of cell injury depend on the
type, state, and adaptability of the injured cell
56
Cell Proliferation Varies
  • Labile cells continuously dividing (epithelium,
    bone marrow)
  • Stable cells quiescent (in G0 stage
    hepatocytes, smooth muscle, lymphocytes)
  • Permanent cells nondividing (neurons, skeletal
    and cardiac muscle)

57
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58
Susceptibility of Cells to Ischemic Necrosis
High Neurons (3-4 min)
Intermediate Myocardium, hepatocytes, renal epithelium (30 min-2hr)
Low Fibroblasts, epidermis, skeletal muscle (many hours)
59
3. Cell injury results from different
biochemical mechanisms acting on several
essential cellular components
60
Depletion of ATP
  • Na pump fails? Na and water enter and K is
    lost
  • Glycolysis depletes glycogen and lowers pH (loss
    of enzyme activity)
  • Ca pump fails- Ca into cells (toxic)
  • Decreased protein synthesis (ribosomes detach)
  • Unfolded protein response

61
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62
Mitochondrial Damage
  • 3 major consequences
  • Mitochondrial permeability transition (MPT) pore
    opens ? loss of mitochondrial membrane potential
    ? decreased oxidative phosphorylation w/
    decreased ATP
  • Production of reactive oxygen species
  • Leakage of pro-apoptotic proteins

63
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64
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65
Loss of Ca Homeostasis
  • Extracellular Ca is 15X higher than cytosolic
    Ca
  • Loss of ATP increases intracellular Ca
  • Increased Ca activates phospholipases,
    proteases, endonucleases, and ATPases
  • Increased Ca also increases mitochondrial
    permeability triggering apoptosis

66
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67
Free Radical Formation
  • Single unpaired electron highly reactive
  • Normal metabolism produces superoxide anion,
    hydrogen peroxide and hydroxyl ion superoxide is
    produced in neutrophils
  • Reactive oxygen species (ROS) are a type of free
    radical
  • Excess of ROS within cell leads to oxidative
    stress

68
Pathologic Effects of ROS
  • Lipid peroxidation leading to membrane damage
  • Protein damage
  • DNA damage

69
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70
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71
Major Antioxidants
  • Antioxidants block the formation of ROS or
    inactivate them
  • Antioxidant Enzymes superoxide dismutase,
    catalase, glutathione peroxidase
  • Vitamins A, E, ascorbic acid, glutathione

72
Membrane Permeability Defects
  • Plasma membrane
  • Mitochondrial membrane
  • Lysosomal membrane- release of RNases, DNases and
    proteases

73
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74
CAUSES OF CELL INJURY
  • Oxygen deprivation
  • Physical agents
  • Chemical agents and drugs
  • Infectious agents
  • Immunologic reactions
  • Genetic derangements
  • Nutritional imbalances

75
Hypoxia and Ischemia
  • Hypoxia- deficiency of oxygen causes
    cardiorespiratory failure, anemia, CO poisoning
  • Ischemia- loss of blood supply (oxygen and
    nutrients) more rapidly and severely injures
    tissues than does hypoxia alone

76
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77
NECROSIS vs APOPTOSIS
  • Necrosis- death of GROUPS of cells after injury
    usually with inflammation
  • Apoptosis- genetically controlled, ATP and
    enzyme-dependent death of individual cells
    usually no inflammation
  • More details in part 2

78
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79
NECROSIS
  • Morphologic changes in GROUPS of cells that
    follow the death of living tissue cells and PMNs
    leak lytic enzymes
  • CYTOPLASM eosinophilia, vacuoles, calcification,
    myelin figures
  • NUCLEUS pyknosis, karyorrhexis, karyolysis

80
Patterns of Necrosis
  • Coagulative- hypoxic death (except brain)
  • Liquefactive- bacterial infections also
    hypoxic death in brain tissue (infarction)
  • Caseous- tuberculosis
  • Fat- enzymatic or traumatic damage to fatty
    tissue eg. Pancreatitis (enzymatic)
  • Gangrenous- usually involves lower extremities
    and often is a type of coagulative necrosis
  • Fibrinoid- immune complexes in arteries

81
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82
Coagulative Necrosis in Kidney
83
Brain Abscess with Liquefactive Necrosis
84
Abscess/Liquefactive Necrosis
85
Caseous Necrosis of Lung
86
Granulomatous Inflammation with Central Necrosis
87
Fat Necrosis
88
Fat Necrosis (L) and Normal Pancreas (R)
89
Gangrenous Necrosis
90
Fibrinoid Necrosis
91
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