Cellular Pathology, TBP Flashcards by CM L

4 basic types of cellular adaptations

1) Hyperplasia
2) Hypertrophy
3) Atrophy
4) Metaplasia

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Increase in number of cells

Hyperplasia

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Permanent cells (do not undergo hyperplasia) (3)

1) Cardiac cells
2) Neurons
3) Skeletal muscle cells

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Increase in size of cell

Hypertrophy

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T/F: Hyperplasia and hypertrophy can be distinguished grossly

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Physiologic vs pathologic, hyperplasia vs hypertrophy: Increase in size of breast during pregnancy

Physiologic hyperplasia

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Physiologic vs pathologic, hyperplasia vs hypertrophy: Adrenal enlargement due to pituitary adenoma

Pathologic hyperplasia

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Physiologic vs pathologic, hyperplasia vs hypertrophy: Skeletal muscle enlargement during exercise

Physiologic hypertrophy

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Physiologic vs pathologic, hyperplasia vs hypertrophy: LVH

Pathologic hypertrophy

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Physiologic vs pathologic, hyperplasia vs hypertrophy: Increase in thickness of endometrium during menstrual cycle

Physiologic hyperplasia

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Physiologic vs pathologic, hyperplasia vs hypertrophy: Endometrial proliferation due to prolonged estrogen stimulus

Pathologic hyperplasia

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Physiologic vs pathologic, hyperplasia vs hypertrophy: Liver growth after partial resection

Physiologic hyperplasia

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Mechanisms by which hyperplasia and hypertrophy can occur (2)

1) Up regulation or down regulation of receptors

2) Induction of new protein synthesis

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New proteins induced (3)

1) Transcription factors
2) Contractile proteins
3) Embryonic proteins

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Decrease in size of cell that has once been of normal size

Atrophy

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Physiologic vs pathologic atrophy: Decrease in size of uterus after pregnancy

Physiologic

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Stimuli for pathologic atrophy (7)

1) Loss of blood supply
2) Loss of nerve supply
3) Loss of endocrine stimulation
4) Disuse
5) Mechanical compression
6) Decreased workload
7) Aging

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Organ that is small in size and was never normal in size

Hypoplasia

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Eccentric vs concentric cardiac hypertrophy: Pressure overload

Concentric

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Eccentric vs concentric cardiac hypertrophy: Volume overload

Eccentric

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Change in epithelium from one type to another

Metaplasia

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Metaplasia: Barrett esophagus

Glandular metaplasia

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Metaplasia: Smoker’s lung

Squamous metaplasia

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Occurs when cells cannot adapt to new environment

Cell injury

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2 common sources of cellular injury

1) Ischemia | 2) Hypoxia

Ischemia vs hypoxia: Much more damaging

Ischemia

T/F Cellular injury always results in cell death

4 cellular systems especially vulnerable to cellular injury

1) DNA 2) Cell membranes 3) Protein generation 4) ATP production

Mechanisms of cellular injury (4)

1) Hypoxia 2) Generation of oxygen-derived free radicals 3) Chemical injury 4) Increased mitochondrial cytosolic calcium

Mechanisms of cellular injury: Decrease in O2 results in decreased

ATP production

Mechanisms of cellular injury: ATP is required by (2)

1) Na/K ATPase pump | 2) Ca pump

Mechanisms of cellular injury: Entry of calcium into cells cause

Activation of endonucleases, proteases, phospholipases, and DNAses that damage cells

Mechanisms of cellular injury: Decrease in O2 results in increased

Anaerobic respiration resulting in accumulation of lactic acid, decreasing cellular pH

Mechanisms of cellular injury: Decrease in intracellular pH results in

Disaggregation of ribosomes from RER

Mechanisms of cellular injury: A molecule with an unpaired electron in the outer orbit

Free radical

Mechanisms of cellular injury: Another term for free radical

ROS

Mechanisms of cellular injury: Normal physiologic reactions that generate free radicals

Redox reactions

Mechanisms of cellular injury: Damage by free radicals (3)

1) Lipid peroxidation 2) DNA fragmentation 3) Protein cross-linking

Mechanisms of cellular injury: Methods to prevent formation of ROS (4)

1) Catalase 2) Superoxide dismutase 3) Glutathione 4) Vitamin ACE

Mechanisms of cellular injury: Action of catalase

Degrades hydrogen peroxide

Mechanisms of cellular injury: Action of superoxide dismutase

Converts superoxide to hydrogen peroxide

Mechanisms of cellular injury: Action of glutathione

Catalyzes breakdown of hydroxyl radicals

Mechanisms of cellular injury: Toxic metabolite of ethylene glycol (antifreeze)

Oxalic acid

Mechanisms of cellular injury: Toxic metabolite that directly inactivates cytochrome oxidase, impairing formation of ATP

Cyanide

Mechanisms of cellular injury: Increased mitochondrial cytosolic calcium leads to (3)

1) Lipid peroxidation 2) Formation of mitochondrial permeability transition 3) Release of cytochrome c

Mechanisms of cellular injury: Mitchondrial permeability transition

Nonselective pore that dissipates proton gradient

Mechanisms of cellular injury: Action of cytochrome c

Activates apoptosis

Light microscopic findings of reversible cellular injury

1) Cellular swelling | 2) Fatty change

Ligt microscopic findings of irreversible cellular injury

1) Nuclear karyolysis 2) Nuclear pyknosis 3) Nuclear karyorrhexis

2 most important factors determining irreversible cell damage

1) Membrane distrubances | 2) Inability to reverse mitochondrial dysfunction

Loss of nuclear basophilia

Karyolysis

Shrinkage of nucleus

Pyknosis

Electron microscopic findings of reversible injury

1) Cellular blebs | 2) Small mitochondrial densities

Electron microscopic findings of irreversible injury

1) Ruptured lysosomes 2) Myelin figures 3) Lysis of ER 4) Large calcium rich mitochondrial densities

Myelin figures indicate

Phospholipid precipitation

2 forms of cell death

1) Apoptosis | 2) Necrosis

Cell death: Occurs in response to damage to DNA

Apoptosis

Cell death: Occurs in response to injurious stimuli

Necrosis

Phases of apoptosis

1) Initiation | 2) Execution

Phases of apoptosis: In which caspases become catalytically active

Initiation

Phases of apoptosis: In which caspases causes death of cell

Execution

Mechanisms of apoptosis

1) Extracellular | 2) Intracellular

Mechanisms of apoptosis: Initiation of extracellular pathway

Fas ligand binds to Fas receptor of the TNF family (Fas-Fas ligand binding)

Mechanisms of apoptosis: Action of Fas receptor

Activates FADD

Mechanisms of apoptosis: Action of FADD

Activates caspases

Mechanisms of apoptosis: Initiation of intracellular pathway

Release of cytochrome c from mitochondria

Mechanisms of apoptosis: Cytochrome c combines with __ to activate caspases

Apaf-1

Mechanisms of apoptosis: Action of caspases

Cleave DNA in a coordinated manner

Mechanisms of apoptosis: DNA cleavage in necrosis

Uncoordinated

Mechanisms of apoptosis: Necrosis vs apoptosis, generates inflammatory response

Necrosis

Mechanisms of apoptosis: Expressed by cell fragments in apoptosis that are recognised by macrophages and engulfed without generating an inflammatory reaction

Phosphatidyl serine

Mechanisms of apoptosis: Microscopic key feature of apoptosis

Chromatin condensation and fragmentation

Necrosis: 2 main types

1) Coagulative | 2) Liquefactive

Necrosis: Protein denaturation is more prominent than enzymatic breakdown

Coagulative

Necrosis: Microscopic morphology of coagulative necrosis

1) Increased eosinophilia of cytoplasm | 2) Decreased basophilia of nucleus

Necrosis: Type wherein general cellular architecture is identifiable

Coagulative

Necrosis: Organs with high fat content

Coagulative followed rapidly by liquefactive

Necrosis: Enzymatic breakdown is more prominent that protein denaturation in organs that lack a substantial protein-rich matrix or have a high concentration of proteolytic enzymes

Liquefactive

Necrosis: Microscopic morphology of liquefactive necrosis

Sheets of lipid-laden/foamy macrophages

Necrosis: Chalky deposits due to combination of fat and calcium

Fat necrosis

Necrosis: Cheesy-looking due to granulomatous disease process

Caseous

Necrosis: Infection commonly associated with caseous necrosis

Tuberculosis

Necrosis: T/F Coagulative and liquefactive necrosis are mutually exclusive

Necrosis: Morphologic vs functional change, first appreciated

Functional

Intracellular accumulations: Product of lipid peroxidation and free radical injury that accumulates as the cell ages

Lipofuscin

Intracellular accumulations: Lipofuscin accumulates in what organelle

Lysosome

Lipofuscin: Most common organs of accumulation

Heart and liver

2 forms of calcium deposition

1) Metastatic | 2) Dystrophic

Calcium deposition, metastatic: Calcium level

Elevated

Calcium deposition, metastatic: Tissue of accumulation

Normal or abnormal

Calcium deposition, sarcoidosis: Metastatic vs dystrophic

Metastatic

Calcium deposition, sarcoidosis: Increase serum calcium by

Activating vitamin D precursor

Calcium deposition, dystrophic: Calcium level

Normal

Calcium deposition, dystrophic: Tissues affected

Abnormal

Calcium deposition: Organs most commonly affected

1) Vasculature 2) Kidneys 3) Lungs

Protein accumulation: Often involve what type of filaments

Intermediate filaments

Protein accumulation: Liver

Mallory hyaline

Protein accumulation: Alzheimer disease

Neurofibrillary tangles

Iron accumulation: Without resulting side effects

Hemosiderosis

Iron accumulation: With resulting side effects

Hemochromatosis

Iron accumulation, hemosiderosis: Found within

Macrophages

Iron accumulation: Aggregates of ferritin micelles

Hemosiderin

Iron accumulation: (+) Prussian blue stain

Hemosiderosis

Iron accumulation, hemochromatosis: Found within

Parenchymal cells

Iron accumulation, hemochromatosis: Common side effects

1) CHF 2) DM 3) Cirrhosis

Iron accumulation, hemochromatosis: Hereditary vs acquired

Both

Iron accumulation, hemochromatosis: Most common organs affected

1) Heart 2) Pancreas 3) Liver 4) Skin

Fat accumulation: Most common organs affected

1) Liver 2) Kidney 3) Heart 4) Skeletal muscle

Fat accumulation: 1 fat vacuole per cell

Macrovesicular steatosis

Fat accumulation: Many vacuoles per cell

Microvesicular steatosis

Protein accumulation: Most commonly associated with alcohol use

Mallory hyaline in the liver

Iron accumulation: Macrophages of the liver

Kupffer cells

Iron accumulation: In the liver, represents

Extravascular hemolysis

Cholesterol accumulation: Organs affected

1) Blood vessels | 2) Sites of hemorrhage

Glycogen accumulation: Glycogen storage disorder

McArdle syndrome

Glycogen accumulation: Most common organs affected

1) Liver | 2) Skeletal muscle

Common exogenous pigment accumulation (2)

1) Tattoos | 2) Anthracotic pigment

Common endogenous pigment accumulation (2)

1) Melanin | 2) Bilirubin

Intracellular accumulations: Gross, brown atrophy

Lipofuscin

Intracellular accumulations: Microscopic, finely granular, yellow-brown pigment that often surrounds the nucleus

Lipofuscin

Intracellular accumulations: Gross, hard yellow nodules

Calcium

Intracellular accumulations: Microscopic, chunky, smooth, purple granules

Calcium

Intracellular accumulations: Microscopic, chunky, yellow-brown granules

Iron

Intracellular accumulations: Microscopic, ropy, eosinophilic condensation within a cleared-out hepatocyte

Mallory hyaline

Intracellular accumulations: Finely stippled black appearance in interstitial and alveolar macrophages

Anthracotic pigment

TTAGGG repeats

Telomeres

Protects the ends of chromosomes and shorten with cell division

Telomeres

Telomere too short is interpreted as

Broken DNA

Enzyme present in immortal cells (germ and stem cells) allowing cell's lifespan to continue indefinitely

Telomerase

Action of telomerase

Adds telomeres to the end of the chromosome

Syndrome of premature aging

Werner syndrome

Mutation in Werner syndrome

Defective DNA helicase