TEST 1: Cellular Biology Flashcards
Hyperplasia
-Increase in NUMBER of cells
-pathologic: menstruation
-pathophysiologic: BPH, anemia
-only in dividing cells (not in heart or brain)
Metaplasia
-one cell replaces another cell that’s better able to tolerate the environment
(Reversible) usually change isn’t beneficial
-pathological: not normal, no example
-pathophysiologic: lung Ca, GERD
-epithelial cells
Dysplasia
-not a true adaptation
-disorganized cell growth
-can lead to cancer/ pre-cancerous
-from chronic irritation/ inflammation (remove irritant cause)
-no “good” dysplasia
2 ways hypoxic- ischemic injury to cells can occur
- Mitochondrial injury
- Calcium influx injury
Mitochondrial injury that causes ischemic cell damage occurs by
-damage to cytochromes (proteins that are involved in electron transport)
-ATP synthesis fails, which causes failure of ion pumps to function (mitochondria can’t make ATP and thus have no energy)
-endoplasmic reticulum begins to fail (cells are swollen but doesn’t work well in that environment; still reversible)
-if hypoxia continues, structure starts to fail—> swollen, inflamed, cytoskeletal structure breaks down and ATP is lost—> cell death
Mitochondrial damage that is caused by calcium influx injury occurs by
-happens as a result of calcium influx into the cell by loss of function from NA/K and NA/Ca pumps
-more NA and Ca that goes into the cell results in increased cellular edema (potassium increases extracellularly)
-damage to the membrane makes it hard to produce ATP, nucleic acids, and ribonucleic acids
-increase Ca into the cell causes enzyme activation that leads to cell death
How do you know hypoxic injury is occurring
Lysosomes are digesting cytoplasmic and nuclear components, so lysosomes leak acid into the blood, causing:
-increases in lactic acid
-increases in troponin
-increases in transaminases
Reperfusion injury
-when oxygen is reintroduced to cells after hypoxia or ischemia
-huge amount of ATP production to attempt to repair, BUT this huge increase causes excessive oxygen reactive species, which leads to oxidative stress (body can handle only a small amount of ROS at a time)
-ROS damages the cell membrane
Oxidative stress
-associated with: aging, DM, CA, autoimmune disease (chronic inflammation)
-ROS that cause this: hydroxyl radicals, superoxide, hydrogen peroxide, nitric oxide
-you need SOME level of these in normal function in order to signal to cells to regulate enzymes and transcription factors
What are Reactive oxygen species & how to handle them
- AKA “free radicals)
-are electrically charged molecules (that have an unpaired electron) that scavenge for electrons to make to neutral which damages carbs, lipids, proteins, and DNA
-antioxidants neutralize the effect of ROS (Vitamins, C,E, flavonoids, beta carotene)
Cell injury by chemical agents
-damages cell membrane integrity
-membrane either directly affected by the chemical agent or the free radicals that it generates
-can be due to one large injury or multiple small insults over time
Cell injury by chemical agents
-damages cell membrane integrity
-membrane wither directly affected by the chemical agent or the free radicals that it generates
-can be due to one large injury or multiple small insults over time
Cell injury from therapeutic drugs
-Tyelonal OD
-Antibiotics (vanco=renal) (quinolones= tendon rupture & nerve injury)
Cell injury from non- therapeutic drugs
-Arsenic: replaces phosphate in ATP (damaged mitochondrial function + cell death)
-cyanide: deadly after one exposure, blocks intracellular use of oxygen (results in hypoxic injury + cell death)
-Lead: disrupts calcium homeostasis (cells uptake leads instead of key elements)
-Mercury: binds with proteins and lipid soluble aka allows crossing into the BBB and accumulation in the brain
Arsenic
-is naturally found in soils/ water/ products
-used in leukemia treatment
-slow accumulation over time is deadly
-replaces phosphate in ATP and thus damaging mitochondria