Structure and Function of cell components
Nucleus: cell division and genetic material
Cytoplasm: fills space between nucleus and plasma membrane—protein
synthesis (protein formation involves transcription [mediated by RNA] and
translation)
ER: synthesis and transport of protein and lipid components
Golgi Ap: processing and packaging proteins into secretory vesicles
Lysosomes: originate in the GOLGI APARATUS, contain digestive enzymes
Nutrient dependent signal transduction
Peroxisome: similar to lysosome but contain several oxidative enzymes
(catalase and urate oxidase)
Mitochondria: energy production, generate most of cell’s ATP
Oxidative proliferation occurs—energy produced from carbs, fats &
proteins by ATP
Desmosomes hold cells together by continuous bands
Gap junctions are clusters of communicating tunnels
Tight junctions are barriers to diffusion and prevent movement of substances
ECM: regulate cell growth and differentiation
Signaling:
Contact dependent
Paracrine: local mediatory that are quickly taken up, destroyed, or immobilized
Hormonal
Neurohormonal
Neurotransmitter
Signal transduction pathways
Transfer signal
Amplify signal
Distribute signal
Modulate signal
Second messenger pathways are cAMP and Ca++
Anabolism: energy using process of metabolism
Catabolism: energy releasing process of metabolism
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,Active transport—uses ATP, passive transport uses osmosis, hydrostatic pressure, and
diffusion
Diffusion: passive movement of solute from HIGH to LOW concentration
Hydrostatic pressure: force of water pushing against cellular membrane
Osmosis: movement of water from LOW to HIGH solute concentration
The amount of hydrostatic pressure required to oppose the osmotic movement of
water is called the OSMOTIC pressure
The overall osmotic effect of colloids (plasma protein) is ONCOTIC or COLLOID
osmotic pressure
Endocytosis: plasma membrane enfolds substances from outside the cell, invaginates,
and separates from plasma membrane forming a vesicle that moves inside the
cell
Pinocytosis: small vesicle formation (Endocytosis)
Phagoyctosis: large vesicles formation (endocytosis) neutrophils &
macrophages engulf cells, debris, foreign mat.
Exocystosis: discharge of secretion of material from intracellular vesicles at the cell
surface
Replacement of portions of the plasma membrane that have been removed, by
endocytosis
Release molecules synthesized by the cells into the ECM
Cell division:
Maturation occurs during INTERPHASE
4 phases:
1. G1 phase: period between M phase and start of DNA synthesis
2. S phase: DNA synthesis in cell nucleus
3. G2 phase: RNA and protein synthesis
4. M phase: (mitosis), nuclear and cytoplasmic division
a. Prophase
b. Metaphase
c. Anaphase
d. Telophase
Cell & Tissue
Function/Dysfunction
Atrophy: decrease in size of
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, cells Hypertrophy: increase
in cell size.
Hyperplasia: increase in number of cells.
Pathologic hyperplasia: abnormal proliferation of normal cells in response
to excessive hormonal stimulation or the effect of growth factors on target
cells
Metaplasia: mature cell type is replaced by a different
mature cell type
Associated with tissue damage, repair, and regeneration
Develops from reprogramming of stem cells in epithelia
or undifferentiated mesenchymal cells in connective
tissue
Dysplasia/Atypical hyperplasia: cells vary in size & shape
within a tissue.
Anaplasia: undifferentiated cells with variable nuclear & cell
structure. Neoplasm: tumor
Cell Damage
Ischemia: oxygen deficit due to respiratory or circulatory
problems. Hypoxia: reduced oxygen in tissue—can lead
to inflammation
MOST COMMON CAUSE OF CELLULAR
INJURY
Reperfusion injury: results from generation of highly
reactive oxygen intermediates or radicals
Oxygen Deficit: decreased energy production, loss of Na pump ↑ intracellular
Na. Temperature: inactivation of some enzymes, damages organelles, protein
coagulation,
disruption of cell membrane.
Micro-organisms
Abnormal Metabolites: caused by genetic disorders or altered
metabolism. Nutritional Deficits
Oxidative stress: activates several intracellular signaling pathways
cuz ROS can modulate enzymes and transcription factors
Can cause lipid peroxidation, alterations of proteins, protein
loss, protein misfolding, and mutations in DNA
Dystrophic calcification: a sign of pathologic change because it
occurs ONLY in injured or dead cells (accumulation of calcium
salts)
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, Metastatic calcification: occurs in uninjured cells in those with
high Ca++
Sensescence: permanent proliferative arrest on cells in respose to
various stressors
Aging—increased levels of cytokines and proinflammatory
markers
Cell Death
Apoptosis:programmed cell death controlled by genetics.
Necrosis:lysis of a cell, cell components leak into blood.
Liquification: dead cells liquefy due to release of enzymes.
Coagulation: cell proteins are altered or denatured causing
coagulation.
Caseous: form of coagulation necrosis, thick, yellowish, cheesy
(TB)
Fat: fatty tissue is broken down into fatty acids
Tissue Damage from Chemicals
Exogenous: from
environment. Endogenous:
from inside the body
Tissue Damage from Physical Agents
Hypothermia: vasoconstriction, ↑ blood viscosity, hypovolemic
shock ↓ blood pressure.
Degenerative changes in cellular myelin sheath are associated
with hypothermic injury
Hyperthermia: causes general vasodilatation, decrease in
circulating blood volume.
Radiation: primarily affects actively dividing
cells Biological Agents
Insects/Animals: direct injection of toxin, transmission of infectious
agent, allergic reaction to insect proteins.
Food
Poisoning
Normal Defenses of the
Body
1st Line Defense
Physical Barriers: unbroken skin, mucous membranes, nasal
hair, clots. Fluids: may contain enzymes or chemicals:
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