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46 terms
Ch1 The Cell; Ch 2 Cellular Adaptation
Prokaryotes vs. Eukaryotes
Organelles
Signal Transduction
Cellular Adaptation
Cellular Injury Mechanisms
Necrosis vs Apoptosis
Prokaryotes
The nucleus is a single, circular chromosome. These include bacteria and cyanobacteria (a type of algae). They lack histones.
Eukaryotes
Animals, plants, fungi, protozoa
Nucleolus
Composed of RNA. Houses most cellular DNA and the processes of DNA replication, repair, & transcription.
RER
Construction team of membranes of cells & organelles by making lipids and proteins.
SER
Contains enzymes to make steroids and talks to Golgi through lysosomes & peroxisomes.
Lysosomes
Originate from the Golgi. They hold 40 types of hydrolases which catalyze proteins, lipids, nucleic acids, and carbs.
They play a role in autodigestion (if the person is starved) to recycle nutrients.
They play a role in autodigestion (if the person is starved) to recycle nutrients.
Peroxisomes
"microbodies". They contain oxidative enzymes like catalase and urate oxidase to break potentially harmful things into harmless products.
Pinocytosis
A non-selective form of endocytosis which requires ATP to function.
Phagocytosis
WBC's engulfing bateria. A form of endocytosis which requires ATP to function.
Potocytosis
Cell uptake via clatharin coated caveolae. A form of endocytosis which requires ATP to function.
Depolarization vs. Repolarization
De - Na+ moves into the cells.
Re - K+ moves out of the cell.
Re - K+ moves out of the cell.
Refractory periods. Absolute vs. Relative
Absolute: refractory period where the K+ channels stay open and too much K+ gets out so the Na+/K+ pump cannot function again.
Relative: Relative to the 1st stimulus, if another stimulus comes along and is greater you could have another AP.
Relative: Relative to the 1st stimulus, if another stimulus comes along and is greater you could have another AP.
Atrophy
Decrease or shrinkage in cellular size. This could be physiological or patho. Thymus shrinkage is fine, muscle disuse is patho.
Hyperplasia
Increase in cell number through an increase in cell division. Ex: hormonal hyperplasia during breast enlargement.
Metaplasia
Replacement of one cell type to another. Ex: normal columnar cells to stratified squamous cells in the respiratory tract.
Dysplasia
"Atypical hyperplasia". Abnormal change in cell size, shape, or organization. Not an adaptive process. Often found adjacent in cancerous cells.
Interphase
Most time spent here.
G1: Growth
S: Duplication of chromosomes
G2: Protein synthesis. Cell sensitivity is the greatest here, just before mitosis.
G1: Growth
S: Duplication of chromosomes
G2: Protein synthesis. Cell sensitivity is the greatest here, just before mitosis.
Cancer
Losing the negative feedback loop of mitosis...= hyperplasia.
Cellular Response of Hypoxic Injury
Decrease in ATP, causing failure of Na+/K+ pump and Na+/Ca+ exchange. Membrane loses selective permeability. ECF and NaCl rushes in. Cellular swelling. Cellular lysis!!
Reperfusion Injury
The reoxygenation and flowback of RBC's and oxygen is too much for the system and causes free radical formation.
ROS
Electrically uncharged atoms or a group of atoms that have an unpaired electron. Highly unstable and can destroy many chemical bonds.
Oxidative Stress
ROS overwhelms antioxidant capacity. Lipid peroxidation, alteration of proteins and DNA occur.
Lipid Peroxidation
Destruction of unsaturated fatty acids with free radicals. This interaction creates peroxides. The peroxides set off a chain rxn resulting in membrane, organelle, and cellular destruction.
Immunologic & Inflammatory Injury
Phagocytic cells (lymphocytes & macrophages).
Histamine, antibodies, lymphokines, complement, enzymes like proteases.
Membrane alterations caused by complement.
Histamine, antibodies, lymphokines, complement, enzymes like proteases.
Membrane alterations caused by complement.
Complement
An immunologic injury caused by the increase in permeability where the ECF comes inside to wash the cell but can ultimately cause lysis. This promotes a loss of K+ from the cell or an influx of water.
Hypothermic Injury
Has long been attributed to disturbances of cellular ion balance or homeostasis, especially of Na balance. Slows cellular metabolic processes and causes the formation and accumulation of free radicals.
Hyperthermic Injury
Heat cramps: water and salt loss from sweat
Heat exhaustion: Excessive sweat loss with hypotension.
Heatstroke: Body temp greater than 106. Life threatening.
Heat exhaustion: Excessive sweat loss with hypotension.
Heatstroke: Body temp greater than 106. Life threatening.
"The Bends"
Rapid release of gases from joints. The gas that is normally dissolved in your blood escapes rapidly upon ascension and can cause a gas embolism.
Ionizing Radiation
Radiation capable of removing orbital electrons from atoms. X-rays, gamma rays, alpha & beta rays.
Result: DNA is directly damaged through ionization or indirectly damage through ionized water.
Result: DNA is directly damaged through ionization or indirectly damage through ionized water.
Necrosis
Cellular dissolution. The sum of all the cellular changes after local cell death and the process of cellular autodigestion or autolysis.
Karyolysis
Nuclear fading. Nuclear dissolution and chromatin lysis during necrosis.
Pyknosis
Nuclear shrinkage or clumping of the nucleus during necrosis.
Karyorrhexis
"Nuclear dust". Fragmentation of the nucleus during necrosis.
Coagulative Necrosis
Occurs in the kidneys, heart, and adrenal glands. Commonly results from hypoxia, protein denaturation results. This hardens albumin and hinders the protein transport system.
Liquefactive Necrosis
Commonly results from ischemic injury to neurons and glial cells in the brain. Hydrolytic enzymes that are normally protected in vesicles are released and can digest the brain tissue. This could be caused by impact.
Caseous Necrosis
Results from Myobacterium TB in the lungs. It's a combination of coagulative and liquefactive necrosis. "Cheese-like"
Fat Necrosis
Occurs in the breasts, pancreas, and other abdominal organs. Lipases break down triglycerides, releasing fatty acids, which then combine with calcium, magnesium, and sodium ions, creating soaps (a process known as soaponification). The necrotic tissue appears opaque and chalk white.
Gangrenous Necrosis
A term commonly used in clinical settings.
Result from sever hypoxic injury, commonly occurring bc of arteriosclerosis, or blockage of major arteries especially in the lower leg.
Result from sever hypoxic injury, commonly occurring bc of arteriosclerosis, or blockage of major arteries especially in the lower leg.
Dry Gangrene
Coagulative necrosis. The skin is dry and shrinks, resulting in wrinkles, and its color changes to dark brown or black.
Wet Gangrene
Liquefactive necrosis. Develops when neutrophils invade the site and try to help but make it worse. Bacterial infection results making it wet. This usually occurs in internal organs causing them to become cold, swollen, and black.
Gas Gangrene
Caused by clostridial myonecrosis. Creates gas bubbles in muscles. It can be fatal if enzymes lyse the membranes of RBCs, destroying their oxygen-carrying capacity.
Somatic Death
Diffuse with no inflammatory response. Death of an entire person.
Algor Mortis
Reduction in body temperature 1-1.5 F per hour. After 24 hours, the body retains the temp of the environment.
Livor Mortis
Gravity causes blood to settle to the lowest tissues which develop a purple discoloration.
Rigor Mortis
After 6 hrs of death there is no ATP left to detach the actin and myosin. This eventually ends due to protein denaturation in aprox 12-14 hrs after death.
Postmortem Autolysis
At a microscopic level, putrefactive changes are associated with the release of enzymes and lytic dissolution.