cellular physiology Flashcards
what is arachidonic pathway
A acid is a polyunsaturated fatty acid, produces different types of eicosanoids (chemical messangers produced)
-initially, membrane phospholipid is covered into arachidonic acid (mediated by enzyme phospholipase A2)
different eicosanoids we need to know
- protstaglandins
- thromboxanes
- leukotrienes
two pathways arachidonic pathway can go
cyclooxygenase pathway and lipooxygenase pathway
cyclooxygenase pathway
produces endoperoxides (protaglandins and thromboxanes)
lippxygenase pathway
produces leukotrienes
prostaglandins
vascular actions, inflammation
thromboxanes
blood clotting and other vascular actions
leukotrienes
mediated allergic and inflammatory reactions
eicosanoids (what they do)
they are not stored, they act locally and are released immediately
What does NSAID do?
NSAIDs inhibit cyclooxygenase, and therefore blocks the synthesis of cyclic endoperoxides, prostaglandins, and thromboxanes
What do adrenal steroids do?
Adrenal steroids inhibit phospholipase A2 and thus block all eicosanoids
Point of CAMP?
second messengers activate protein kinases, which phosphorylate a variety of proteins (all have diff functions) and amplification
-regulates glycogen breakdown into glucose, as well as sugar and lipid metabolism
Calcium
you can effect it directly (cellular response, doesn’t need second messanger), can help activate CAMP, muscle contraction, transcription, etc….
What happens to Na/K when ATP levels fall
-decreased production of ATP -> Na/K+ pump stops working -> sodium enters the cell -> water enters -> cellular and organelle swelling. Cell switches from aerobic to anaerobic respiration, decreasing pH. If ATP is produced again, the Na/K+ pumps start working and pH will be corrected!
examples of irreversible cell injury
- membrane disturbances
- inability to reverse mitochondrial dysfunction
cellular injury related to free radicals
- lipid peroxide in membranes
- DNA fragmentation
- lesions in DNA
lipid peroxide in membranes
Oxidative degradation of lipids where free radicals steal electrons from lipids in a cell membrane, which damages the cell membrane
DNA fragmentation
The separation or breaking of DNA strands into pieces. DNA is vulnerable to radical attack do to its double bonds and other characteristics.
protein cross linking
when attachments are formed along the protein’s three dimensional structure in abnormal places, disrupting the protein’s function which result in increased degradation and decreased activity.
ischemia
decreased blood supply
anoxia
complete deprivation of O2 due to no blood supply to tissue - leads to infarct
induction (of cell injury)
- PM loses permeability
- Na and H2O into cell, K out of cell
- cell swells and Ca enters cell
induction (of cell death)
- influx of Ca
- membrane disruption leads to hydrolyzing of proteins and DNA cleavage
- feedback mech leads to death
effector
-molecules which selectively bind to cells in process of apoptosis to induce degradation by phase for macrophages
Degredation
Breakdown of unnecessary or dysfunctional cellular components by lysosymes.
degeneration
a breakdown that leaves some loss of function
regeneration
replacement of lost cells and tissue whose function is so similar to the original lost cells that the replacements may be considered identical.
Apoptosis
- single cell
- programmed cell death
- no inflame response
- cell shrinkage
- membrane blebbing
- cell breaks into several apoptotic bodies, organelles still functional
necrosis
- affects groups of neighboring cells
- significant inflamm response
- cell swelling, die and burst, spilling contents all over neighbors
coagulative necrosis
changing liquid to solid (think egg whites, proteins denature), due to sudden death of tissue by blockage in arterial blood supply (thrombus or embolism)
-well defined, firm and pale
liquefactive necrosis
changing solid to liquid, usually result of the digestion of tissues by granulocytes, abscess forms (surrounding tissue intact)
caseous necrosis
turning “cheese like”, IE tuberculosis or fungal infections
fat necrosis
when fat is digested by digestive enzymes, flecks of yellow material, releases fatty acids and calcium. IE Pancreatitis
gummatous necrosis
- pink and dusty red nodules or plaques
- most commonly affect skin and mucous membranes
- form of granuloma
- tertiary syphillis
hemorrhagic necrosis
dying tissue leading to bleeding, TNF (cross section of bowel showed with spots on it)
fibrinoid necrosis
cell loses outline and become homogeneous and pink, fibrin like appearance (seen in blood vessels of people with autoimmune diseases like lupus)
fat saponification
chalk white areas within fat due to breakdown of fat into fatty acids and precipitation of Ca (X-ray of precipitated Ca mass in breast tissue)
wet gangrene
appears swollen, dark red and liquefied, foul odor and obscured border between dead and viable tissue (bacterial infection) -> diabetes (mmm food…sugar)
dry gangrene
appears black, dry and shriveled with sharp demarcation from viable tissue (atrophy)
-decrease in size or number of cells due to aging, disuse or reduced/absent blood supply, hormonal stim or neural stim (frost bite)
hypertrophy
increase in size of cell (increase in bulk without multiplication of parts)
hyperplasia
increase in numbers of cells (not size) in tissue or organ (not cancer)
metaplasia
normal transformation of tissue from one type to another (think of gerd, tissue gets hard and when gerd gone, tissue changes back) -> reversible
dysplasia
abnormal development of an organ or part of the body, including congenital absence (cells change) -> can be reversible
anaplasia
follows dysplasia
-loss of structural differentiation within cell or group of cells (invade other tissues) -> cannot be reversed
