Path 1: Section 1: Part 1 - Cell Injury, Death And Adaptations

Front 1

Three Patterns of Cell response to stress

Back 1

1. Adaptation
2. Cell Injury
3. Cell Death = Irreversible

Front 2

Cell Adaptation

Back 2

Low level stimuli

Front 3

Ideopathic

Back 3

Unknown Cause

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Etiology

Back 4

Start of disease

Front 5

Cell Injury

Back 5

1. Sudden onset w/no time to adapt
2. Reversible up to a point

Front 6

Cell Death

Back 6

Irreversible

Front 7

Hypertrophy - Adaptation

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Increase in size by larger numbers of organelles
- Increased workload
- Hormonal stimulation

Front 8

Morphology

Back 8

Appearance of Disease

Front 9

Physiologic Hypertrophy - Adaptation

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Uterine enlargement during pregnant

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Pathologic Hypertrophy - Adapt

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Hypertension -> Cardiac hypertrophy

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Hyperplasia - Adapt

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Increase in Number of cells

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Physiologic Hyperplasia - Adapt

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Breast proliferation - Hormonal
Compensatory - lost tissue due to removal or disease

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Pathologic Hyperplasia - Adapt

Back 13

Creates fertile soil for neopplastic proliferation of cells
- Endometrial hyperplasia because of excess estrogen

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Atrophy - Only adaptation that may not be reversible

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Shrinkage in size due to loss of substance
- Decreased Workload - immobilization
- Loss of innervation
- Diminished blood supply
- Inadequate Nutrition
- Loss of Endocrine stimulation
- Aging

Front 15

Proteolytic Systems of Atrophy - Adapt

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Ubiquitin - Degrades nucleus and cytosol
Autophagy - Lysosomal enzymes degrade sequestered senescent organelles

Front 16

Metaplasia - Adaptation

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Change from one adult cell type to another.
- Mostly epithelial cells, may be mesenchymal.
- Squamous metaplasia in smokers.

Front 17

Causes of Cell Injury

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1. Oxygen Deprivation - Hypoxia
2. Chemicals
3. Infections
4. Immune reactions
5. Genetic defects
6. Nutritional Imbalances
7. Physical Agents
8. Aging

Front 18

Oxygen Depravation - Hypoxia - Cell Injury

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1. Loss of blood supply = Ischemia = most important
2. Other oxygen shortages

Front 19

Chemical Agents - Cell Injury

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1. Membrane permeability
2. Osmotic homeostasis
3. Mess up enzymes or cofactors

Front 20

Infectious agents - Cell Injury

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Bacteria, viruses, Rickettsiae, fungi, and parasites

Front 21

Genetic Defects - Cell Injury

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Gross chromosomal defect or point mutation

Front 22

Immunologic Reactions - Cell Injury

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1. Reactions to exogenous antigens -> anapphylaxis - Allergies
2. Loss of tolerance -> autoimmune

Front 23

Nutritional Imbalances - Cell Injury

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1. Protein-calorie deficiency
2. Vitamin and mineral deficiencies
3. Nutritional excess

Front 24

Physical Agents - Cell Injury

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Trauma
- Sudden changes in atmospheric pressure - the Benz - pain from nitrogen hypoxia

Front 25

Aging - Cell Injury

Back 25

Wear and tear
or
Genome based - Loss of ability to adapt, replicate and repair.

Front 26

Reversible Injury

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1. Cellular swelling - unable to maintain ionic and fluid hemostasis
- Hydropic and vacuolar degeneration
2. Fatty Change - appearance of fat in cytoplasm
- Hypoxic and toxic injuries.
- Metabolic derangements
- Mostly in cells w/fat metabolism

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Necrosis - Irreversible
- Cytoplasm -> eosinophilic

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1. Enzymatic Digestion of cell
- Autolysis - Hydrolitic enzyme from dead cells
- Heterolysis - From lysosomes of leukocytes
2. Denaturation of proteins -> coagulation

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Karyolysis - Necrosis

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Fading of the nucleus

Front 29

Pyknosis - Necrosis

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Shrinkage or darkening of nucleus - Most common

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Karyorrhexis

Back 30

Fragmentation of the pyknotic nucleus - Rare

Front 31

Coagulative Necrosis

Back 31

From Pknosis - most common
- Denaturation of proteins
- Both lysosomal and structural proteins are denatured -> no autolysis
- Hypoxic death of all tissues cept brain
- Classic is myocardial Infarction
- Kidney starved of blood -> white firm dead chunk

Front 32

Liquefactive Necrosis

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Goes to mush
- Autolysis or heterolysis
- Leaves a defect w/leukocytes
- Mostly focal bacterial infections
- Hypoxic death of CNS

Front 33

Gangrenous Necrosis

Back 33

Mostly in Diabetics and Soldiers

Front 34

Dry Gangrene

Back 34

Coagulative necrosis -> dark and leathery

Front 35

Wet Gangrene

Back 35

Liquefactive Necrosis

Front 36

Caseous Necrosis

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Milk protein - looks like feta cz
- Tuberculosis - Pathoneumonic
- Obliterates Tissue Architecture and outlines

Front 37

Fat Necrosis

Back 37

Pancreas
- Abnormal release of activated pancreatic enzymes
- Fats combine with calcium to produce chalky white areas

Front 38

Fibrinoid Necrosis

Back 38

Immune-related with blood vessels
- Antigen antibodies combine with fibrin to form pink amorphous layer on blood vessel wall
- Only nuclei present are from inflammatory cells

Front 39

Subcellular Responses to Injury

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1. Autophagy
2. Induction of smooth ER
3. Mitochondrial Alterations
4. Cytoskeletal Abnormalities

Front 40

Autophagy response to injury

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1. Organelles -> membrane bound sac
2. Membrane bound sac fuses with lysosomes -> Autophagolysosomes
3. Undigested pigment after intracellular lipid peroxidation = lipofucin pigment (Wear and Tear pigment)
4. Mostly in cells undergoing atrophy

Front 41

Induction of SER response to injury

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Larger SER to keep up with demand
- Barbituate exposures in liver

Front 42

Mitochondrial alteration response to injury

Back 42

Changes in size, number, shape and function of mitochondria

Front 43

Cytoskeletal abnormality response to injury

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1. Defective cell function like locomotion
2. Intracellular accumulation of fibrillar material

Front 44

Cell membrane changes from injury

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Most common change
- Immune molecules, hormone receptors, sites for synthesis

Front 45

Cell Death

Back 45

- Function gone far before death
- Time lag before morphologic evidence
- Ultrastructural and histochemical changes within minutes

Front 46

Apoptosis Morphologies

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1. Eosinophilic Cytoplasm and condensed nuclear chromatin
2. Fragmentation into apoptotic bodies - Surrounded by membrane
3. Chromatin degraded by adjacent phagocytes.

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Mechanism of Apoptosis

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Capase activates - Cystein proteases cleave after aspartic residues
- Breaks don nuclear and extranuclear cell proteins
Takes energy

Front 48

Pathways of Apoptosis

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1. Mitochondrial = Intrinsic
2. Death Receptor = Extrinsic

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GF deprivation apoptosis

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Hormone sensitive cells, lymphocytes
and nurons

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DNA Damage apoptosis

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Prevents neoplastic transformation

Front 51

Accumulation of Misfolded proteins Apoptosis

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Prevents degenerative CNS diseases and diabetes

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Cytotoxic T cells Apoptosis

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Important for target cell killing by CTLs

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Apoptosis of self-reactive lymphocytes

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Prevents autoimmunity

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Storage Disease

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Lacking an enzyme genetically that will remove endogenous substance from cells (Intracellular accumulations)

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Fatty Change = Steatosis
Accumulations

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Reversible if simple fats - always
- Indicator of non-lethal injury

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Cholesterol and Cholesteryl Esters
Accumulations

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Phagocytes overloaded with complex lipids = Foam Cells

Front 57

Russell Bodies

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Protein accumulation in plasma cells

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Alcoholic Hyalin

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Protein accumulation in hepatocytes

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Neurofibrillary Tangle

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Protein accumulation in brain cells = Alzheimer's

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Glycogen storage disease

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Abnormal products collect thru-ought the body.

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Exogenous Pigments

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From outside the body

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Anthracosis

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Carbon in lungs, not harmful. Cept in coal worker's pneumoconiosis.

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Silicosis

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White spots from silicon particles - industrial problems = small population
- Small Amts cause disease

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Siderosis

Back 64

Iron accumulation. Only bad with welders. Redish-brown spots.

Front 65

Amalgam Tattoo

Back 65

NOT REVERSIBLE Atrogenic = caused by HC provider. Use rubber dam

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Endogenous Pigments

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Synthesized inside body

Front 67

Lipofuscin

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Indegestible residues of autophagic vacuoles.
- Brownish Yellow

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Melanin

Back 68

Dark brown normally within melanocytes

Front 69

Adisons

Back 69

Melanin cancer -> bronzing, JFK

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Bilirubin

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Brown-green from hemoglobin.
- Normally in bile

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Jaundice

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Excess biliruben -> yellow skin and sclerae

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Dystrophic Calcification

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From cell death
- Necrotic debris not removed fast enough
- Serum calcium normal

Front 73

Metastatic Calcification

Back 73

Deposition of Ca in vital/alive tissue
- Increased levels of serum Ca = hypercalcemia
- Too Much PTH
- Calcinosis = large areas of metastatic calcification