Cell Pathology

smallest functional unti that an organism can be divided into and return necessary charateristic for life functions.

Larger funtional unit of cells that are grouped together due to their funtion.

Plasma membrane, nucleus, and cytoplasm.

It is a cell membrane that is made up of phospolipids, proteins, and cholesterol. It participates in the generation and conduction of the electrical currents like in nerve and muscle. Also it's semipermeable and seperates environment both intracellular and extracellular.

It can be round or elongated structure. Has a nuclear envelope that has an inner membrane and a outer membrane

contains mostly water. Contains cytoskeleton as well as organelles and fluid (cytocell). Embedded in the cytoplasm which function as organs of the cell are the E.R., golgi aparatus, lysosomes, perioxisomes, proteasesomes, and mitochondria.

Primary site of protein synthesis. Rough E.R- contains ribosome whic can synthesize proteins. Smooth E.R- no ribosomes, no protein synthesis, but synthesis of lipid molecules, steroid hormones, and lipoprotein. Mteabolizes and detoxifies drugs.

Modify substances transported to them into secretory granules or vesicles. Carbohydrate synthesis.

Gigestive organelles of the cell. Breakdown and digest worn out cell parts or foreign bacteria. Lysosomal enzymes are synthesized in the Rough E.R. and transported to the Golgi aparatus where they're chemically modified and packaged for transport.

Degrades peroxides. Breaks down very long chain fatty acids that mitochondrial enzymes can't. In liver, these aid in formation of bile acids Proteasomes.

power plant of the cell. Transform compounds into enerygy. Contain enzymes needed for capturing most of the energy in food and converts it into energy.

Controls the shape and the movement of the cell. Contains microtubules- slender, stiff tubular structures that influence shape. effect the movement of the cilia and of chromosomes during cell division. Contains microfilaments- present in muscle cells. Function or supporting and maintaining the shape of cells.

• change in response to stress- change in cell size, in cell number, in cell type.
• may lead to: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia.

Lower and more effecient level of functioning. Decrease O2 consumption and other functions.

Disuse, denervation, loss of endocrine stimulation, inadequate nutrition, and ischemia or decreased bL. flow.

Increase in cell size w/ amt of functioning tissue mass. Result from increase workload of organ or body part. Increases O2 demand, ATP use.

• Increase number of cells in tissue orin organ. Occurs as a response to an appropriate stimulus and ceases once the stimulus has been removed. Physiologic- hormonal and compensatory.
• Non physiologic- due to excessive hormone stimulation or the effect of growth factors on target tissues.

Reversible change in which one cell type is replaced by another adult cell type. Usually from chronic irritation and inflammation and allows for substitution of cells that are better able to survive.

Derranged cell growth of a specific tissue that results ub cells that vary in size, shape, and organization. Can be chronic irritation and inflammation. Implicated as precursor to cancer but doesn't necessarily lead to cancer.

Build up of substances thats cells can't immediately use or eliminate. Accumulate in the cytoplasm, organelles like lysosomes or nucleus. Genetic disorders that disrupt enzymatic degration.

Abnormal deposits of calcium salts, iron, magnesium, and other minerals.

Dead and dying tissue atheroscerosis cause of organ disfunction.

Occur in normal tissue, increase serum calcium levels. happens in lungs, kidneys, and bl. vessels. Certain cancer, pagets disease, and vit. D intoxication.

Injury from physical agent, radiation injury, chemical injury, injury from biologic agents, and injury from nutritional imbalances

• mechanical forces- split or year tissues, fx bones, injured bl. vessels, and disrupt bl. flow
• Extreme temperatures- heat- vascular injury increases cell metabolism, disrupting cell membrane, and coagulation of bl. vessels.
• cold- increases blood viscosity, vasoconstriction, and capilary stasis.

• Ionizing radiation- used in tx of cancer. clincal manifestation results from acute cell injury.
• UV radiation- increasing energectic rays that are powerful enough to disrupt intracellular bonds.Damages DNA.
• Nonionizing radiation- causes vibration& rotation of atoms and molecules eventually creating thermal energy. Rarely associated w/ skin burns. Infared light, ultrasound, microwaves, and laser energy.

injures cell membrane and other cell structures, block enzymatic pathways, coagulate cell proteins, disrupt osmotic & ionic balance of cells. ex- drugs, lead, and mercury toxicity.

able to replicate and can continue to prduce their injurious effects. virus to bacteria. viruses can enter into the call and become incorporated into its DNA and AIDs.

nutritional excesses and defficiences predispose cells to injury-obesity. Can occur from deficiences like iron,scurvy, ricketts.

• Free radical injury- damage cell which cause unstable & highly reactive molecular bonds.
• Hypoxic cell injury- deprives the cell O2 & interupts oxidative metabolism & generation of ATP.
• Impaired calcium homeostasis- can affect smooth muscle contraction and glycogen breakdown.

impairs cell funtion but doesn't result in death. causes cellular swelling>result of hypoxic cell injury. Fatty change- intracellular accumulation- fat metabolism is impaired during cell injury & fat accumalates in the cell.

balance of cell proliferation and cell death. apoptosis- removes injured or worn out cells and control tissue regeneration. Thought to be responsible for several normal physiologic processes.

Cell death in an organ or tissue that's still part of a living person. Unregulated enzymatic digestion cell components, loss of cell membrane integrity w/ uncontrolled release of products of cell death into intracellular sppace & initiation of inplammatory response.

considerable mass of tissue that undergoes necrosis. ex- dry, moist, or gas.

cell functions decline w/ age- unsure of why.

- limited capacity for replication DNA mutation over time.

gene may determine longevity

damage eventually accumulates to a level suffiecient to result in the physiologic decline associated w/ aging

increase age of onset of aging and increases rates of progression.

• character that doesn't threaten health or life.
• slow, progressive rate of growth.
• benign neoplasms are well differentiated tumors that resemble the tissue of origin but have lost the ability to control cell proliferation, grow by expansion.

• Tending or threatening to produce death, harmful.
• Malignant neoplasms less well differentiated tumors that have lost the ability to control both cell proliferation & differentiation.
• Growth is disorganized and uncontrolled.
• Cell may break loose and travel to different sites to form metastases.

• Genetic and molecular- mechanism that characterize the transformation of normal cells into cancer cells.
• External & more contexual factors- age, heredity, and environmental agents that contribute to its development and progression

• Cancer associated genes:
• Proto oncogenes, loss of tumor, and MicroRNA genes.

overactive genes that become cancer causing if mutated- point of mutation, chromosomal translocation, and gene amplification

• supressor genes- underactive; normal cells have regulatory genetic mechanism that protect them against activated or newly acquired oncogenes.
• tumor supressor has become inactivated which causes unregulated growth to begin.

single RNA strand that regulates gene expression that can undergo rearrangements, deletions, amplifications: can be tumor supressor or oncogenes depending on how its paired.

• involve changes in the patterns of gene expression w/o a change in DNA.
• May silence tumor supressor gene which will still be present but not expressed.

• Defect in DNA repair mechanism caused by chemical, radiation, viruses or inherited.
• Disorders in growth factor signaling pathways which eventually may cause unregulated cell growth & proliferation.

• 3 steps:
• Initiation- exposure of cells to carcinogenic agents.
• promotion- induction of unregulated accelerated growth in already initiated cells by various chemicals and gorwth factor.
• Progression- tumor cells acquire malignant phenotype changes that promote invsiveness, metastatic competence, autnomous growth tendecies, and increased karyotypic instability

heredity, hormones, obesity, immunologic, chemical agents, radiation, viral and microbial agents.

• used to determine the course of disease and aid in selecting appropriated treatment or management plan.
• Microscopic exam of cancer cells to deteremine level of differentaion and # of mitosis.
• Grade scale- I- well differentiation IV- poorly differentiated and display marked anaplasia.

• used to determine the course of disease and aid in selecting appropriate treatment or management plan.
• Helps to estimate prognosis. Size of primary tumor, it extent of local growth, lymph node involvement, and presence of distant metastasis.

• according to grade, stage, and location.
• determined of the extent of disease.
• tumor growth rate and invasiveness.
• if tumor is too small and has well defined margins often the entire tumor can be removed.
• if mor extensive, it will be morew difficult if not impossible to remove.