Cell Adaptations - Pathology - Lecture Slides, Slides for Pathology. Alagappa University

Pathology

Description: Cell Adaptations, Cell Injury, Cell Death, Concepts of Disease, Concepts of Cellular Growth, Factors of Cell Injury, Free Radicals, Concepts of Apoptosis, Smooth Endoplasmic Reticulum. A lecture from Pathology course to teach you a topic. Key points are given above.
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OBJECTIVES

CELL ADAPTATIONS

CELL INJURY

CELL DEATH

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OBJECTIVES Understand the 3 main anatomic concepts of disease---Degenerative, Inflammatory, Neoplastic

Understand the concepts of cellular growth adaptations---Hyperplasia, Hypertrophy, Atrophy, Metaplasia

Understand the factors of cell injury and death---O2, Physical, Chemical, Infection, Immunologic, Genetic, Nutritional

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OBJECTIVES Understand the pathologic mechanisms at the

SUB-cellular level---ATP, Mitochondria, Ca++, Free Radicals, Membranes

Understand and differentiate the concepts of APOPTOSIS and NECROSIS

Understand SUB-cellular responses to injury--- Lysosomes, Smooth endoplasmic reticulum, Mitochondria, Cytoskeleton

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OBJECTIVES Identify common INTRA-cellular

accumulations---Fat, Hyaline, CA++, Proteins, Glycogen, Pigments

Understand aging and differentiate the concepts of preprogrammed death versus wear and tear.

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PATHOLOGY

Pathos (suffering)

Logos

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PATHOLOGY GENERAL SYSTEMIC

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PATHOLOGY ETIOLOGY (“Cause”) PATHOGENESIS (“Insidious

development”) MORPHOLOGY (ABNORMAL

ANATOMY) CLINICAL EXPRESSION

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ETIOLOGY Cause

vs.

Risk Factors Docsity.com

PATHOGENESIS “sequence of events from the initial stimulus to the ultimate expression of the disease”

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MORPHOLOGY Abnormal Anatomy

Gross Microscopic Radiologic Molecular

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CLINICAL EXPRESSION

Ironically, even though “clinical expression” is not often present in subclinical diseases, it is the “pathos” of pathology.

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Most long term students of pathology, like myself, will strongly agree that the very best way for most minds to remember, or identify, or understand a disease is to associate it with

a morphologic IMAGE. This can be gross, electron microscopic, light microscopic, radiologic, or molecular.

In MOST cases it is at the LIGHT MICROSCOPIC LEVEL.

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CLINICAL/FUNCTIONAL

Rudolph Virchow

1821-1902

The Father of Modern Pathology

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FUNCTIONAL DEFINITION OF DISEASE

HOMEOSTASIS

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CELL DEATH APOPTOSIS (“normal” death) NECROSIS (“premature” or

“untimely” death due to “causes”

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The –plasia brothers • HYPER- HYPO- (A-) • NORMO-

META-

DYS- ANA- • “Frank” ANA-

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HYPO-TROPHY? DE-CREASE IN SIZE OF CELLS?

RARELY

USED

TERM Docsity.com

A-TROPHY? DE-CREASE IN SIZE OF CELLS? YES

SHRINKAGE IN CELL SIZE DUE TO LOSS OF CELL

SUBSTANCE Docsity.com

ATROPHY DECREASED WORKLOAD DENERVATION DECREASED BLOOD FLOW DECREASED NUTRITION AGING (involution) PRESSURE

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METAPLASIA A SUBSTITUTION of one NORMAL CELL

or TISSUE type, for ANOTHER COLUMNAR SQUAMOUS (Cervix) SQUAMOUS COLUMNAR (Glandular)

(Stomach) FIBROUS BONE

WHY?

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CELL DEATH APOPTOSIS vs. NECROSIS What is DEATH? (What is LIFE?)

DEATH is IRREVERSIBLE

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So the question is….

…NOT what is life or death, but what is REVERSIBLE or IRREVERSIBLE injury

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REVERSIBLE CHANGES

REDUCED oxidative phosphorylation

ATP depletion Cellular “SWELLING”

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IRREVERSIBLE CHANGES

MITOCHONDRIAL IRREVERSIBILITY

IRREVERSIBLE MEMBRANE DEFECTS

LYSOSOMAL DIGESTION Docsity.com

REVERSIBLE = INJURY

IRREVERSIBLE = DEATH

SOME INJURIES CAN LEAD TO DEATH IF PROLONGED

and/or SEVERE enough Docsity.com

INJURY CAUSES (REVERSIBLE) Hypoxia, (decreased O2)

PHYSICAL Agents

CHEMICAL Agents

INFECTIOUS Agents Immunologic

Genetic

Nutritional Docsity.com

INJURY MECHANISMS (REVERSIBLE)

DECREASED ATP

MITOCHONDRIAL DAMAGE

INCREASED INTRACELLULAR CALCIUM

INCREASED FREE RADICALS

INCREASED CELL MEMBRANE PERMEABILITY

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What is Death? What is Life?

DEATH is IRREVERSIBLE MITOCHONDRIAL

DYSFUNCTION PROFOUND MEMBRANE DISTURBANCES

LIFE is……..???

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CONTINUUM REVERSIBLE IRREVERSIBLE DEATH EM LIGHT MICROSCOPY GROSS APPEARANCES

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DEATH: LIGHT MICROSCOPY

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NECROSIS BROTHERS: Liquefactive (Brain) Gangrenous (Extremities, Bowel, non-specific)

WET DRY

Fibrinoid (Rheumatoid, non-specific) Caseous (cheese) (Tuberculosis) Fat (Breast, any fat) Ischemic (non-specific) Avascular (aseptic), radiation, organ specific, papillary OneLook lists 153 terms preceding the word “necrosis”:

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EXAMPLES of Cell INJURY/NECROSIS

Ischemic (Hypoxic) Ischemia/Reperfusion Chemical

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ISCHEMIC INJURY

REVERSIBLE IRREVERSIBLE

DEATH (INFARCT)

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ISCHEMIA/RE- PERFUSION INJURY

NEW Damage “Theory”

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CHEMICAL INJURY “Toxic” Chemicals, e.g CCl4 Drugs, e.g tylenol Dose Relationship Free radicals, organelle, DNA

damage

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APOPTOSIS NORMAL (preprogrammed)

PATHOLOGIC (associated with Necrosis)

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“NORMAL” APOPTOSIS Embryogenesis Hormonal “Involution” Cell population control, e.g., “crypts” Post Inflammatory “Clean-up” Elimination of “HARMFUL” cells Cytotoxic T-Cells cleaning up

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“PATHOLOGIC” APOPTOSIS

“Toxic” effect on cells, e.g., chemicals, pathogens

Duct obstruction Tumor cells Apoptosis/Necrosis spectrum

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APOPTOSIS MORPHOLOGY

DE-crease in cell size, i.e., shrinkage IN-crease in chromatin concentration, i.e.,

hyperchromasia, pyknosis karyorhexis karyolysis

IN-crease in membrane “blebs” Phagocytosis

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SHRINKAGE/HYPERCHROMASIA

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APOPTOSIS BIOCHEMISTRY

Protein Digestion (Caspases) DNA breakdown Phagocytic Recognition

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SUB-Cellular Responses to Injury (APOPTOSIS/NECROSIS)

Lysosomal Auto-Digestion • Smooth Endoplasmic Reticulum (SER)

activation

Mitochondrial “SWELLING” • Cytoskeleton Breakdown

– Thin Filaments (actin, myosin) – Microtubules – Intermediate Filaments (keratin, desmin,

vimentin, neurofilaments, glial filaments) Docsity.com

INTRAcellular ACCUMULATIONS

Lipids Neutral Fat Cholesterol

“Hyaline” = any “proteinaceous” pink “glassy” substance

Glycogen Pigments (EX-ogenous, END-ogenous) Calcium Docsity.com

LIPID LAW ALL Lipids are YELLOW grossly and WASHED out (CLEAR) microscopically

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PIGMENTS EX-ogenous--- (tattoo, Anthracosis)

END-ogenous--- they all look the same, (e.g., hemosiderin, melanin, lipofucsin, bile), in that they are all golden yellowish brown on “routine” Hematoxylin & Eosin (H&E) stains

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CALCIFICATION DYSTROPHIC (LOCAL CAUSES)

(often with FIBROSIS)

METASTATIC (SYSTEMIC CAUSES) HYPERPARATHYROIDISM

“METASTATIC*” Disease

*NOT to be confused with “metastatic” calcification Docsity.com

CELL AGING parallels ORGANISMAL AGING

PROGRAMMED THEORY (80%)

vs.

WEAR AND TEAR THEORY (20%)

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