cellular physiology

Question 1

what is arachidonic pathway

Answer 1

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)

Question 2

different eicosanoids we need to know

Answer 2

• protstaglandins
• thromboxanes
• leukotrienes

Question 3

two pathways arachidonic pathway can go

Answer 3

cyclooxygenase pathway and lipooxygenase pathway

Question 4

cyclooxygenase pathway

Answer 4

produces endoperoxides (protaglandins and thromboxanes)

Question 5

lippxygenase pathway

Answer 5

produces leukotrienes

Question 6

prostaglandins

Answer 6

vascular actions, inflammation

Question 7

thromboxanes

Answer 7

blood clotting and other vascular actions

Question 8

leukotrienes

Answer 8

mediated allergic and inflammatory reactions

Question 9

eicosanoids (what they do)

Answer 9

they are not stored, they act locally and are released immediately

Question 10

What does NSAID do?

Answer 10

NSAIDs inhibit cyclooxygenase, and therefore blocks the synthesis of cyclic endoperoxides, prostaglandins, and thromboxanes

Question 11

What do adrenal steroids do?

Answer 11

Adrenal steroids inhibit phospholipase A2 and thus block all eicosanoids

Question 12

Point of CAMP?

Answer 12

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

Question 13

Calcium

Answer 13

you can effect it directly (cellular response, doesn’t need second messanger), can help activate CAMP, muscle contraction, transcription, etc….

Question 14

What happens to Na/K when ATP levels fall

Answer 14

-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!

Question 15

examples of irreversible cell injury

Answer 15

• membrane disturbances

- inability to reverse mitochondrial dysfunction

Question 16

cellular injury related to free radicals

Answer 16

• lipid peroxide in membranes
• DNA fragmentation
• lesions in DNA

Question 17

lipid peroxide in membranes

Answer 17

Oxidative degradation of lipids where free radicals steal electrons from lipids in a cell membrane, which damages the cell membrane

Question 18

DNA fragmentation

Answer 18

The separation or breaking of DNA strands into pieces. DNA is vulnerable to radical attack do to its double bonds and other characteristics.

Question 19

protein cross linking

Answer 19

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.

Question 20

ischemia

Answer 20

decreased blood supply

Question 21

anoxia

Answer 21

complete deprivation of O2 due to no blood supply to tissue - leads to infarct

Question 22

induction (of cell injury)

Answer 22

• PM loses permeability
• Na and H2O into cell, K out of cell
• cell swells and Ca enters cell

Question 23

induction (of cell death)

Answer 23

• influx of Ca
• membrane disruption leads to hydrolyzing of proteins and DNA cleavage
• feedback mech leads to death

Question 24

effector

Answer 24

-molecules which selectively bind to cells in process of apoptosis to induce degradation by phase for macrophages

Question 25

Degredation

Answer 25

Breakdown of unnecessary or dysfunctional cellular components by lysosymes.

Question 26

degeneration

Answer 26

a breakdown that leaves some loss of function

Question 27

regeneration

Answer 27

replacement of lost cells and tissue whose function is so similar to the original lost cells that the replacements may be considered identical.

Question 28

Apoptosis

Answer 28

- single cell - programmed cell death - no inflame response - cell shrinkage - membrane blebbing - cell breaks into several apoptotic bodies, organelles still functional

Question 29

necrosis

Answer 29

- affects groups of neighboring cells - significant inflamm response - cell swelling, die and burst, spilling contents all over neighbors

Question 30

coagulative necrosis

Answer 30

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

Question 31

liquefactive necrosis

Answer 31

changing solid to liquid, usually result of the digestion of tissues by granulocytes, abscess forms (surrounding tissue intact)

Question 32

caseous necrosis

Answer 32

turning “cheese like”, IE tuberculosis or fungal infections

Question 33

fat necrosis

Answer 33

when fat is digested by digestive enzymes, flecks of yellow material, releases fatty acids and calcium. IE Pancreatitis

Question 34

gummatous necrosis

Answer 34

- pink and dusty red nodules or plaques - most commonly affect skin and mucous membranes - form of granuloma - tertiary syphillis

Question 35

hemorrhagic necrosis

Answer 35

dying tissue leading to bleeding, TNF (cross section of bowel showed with spots on it)

Question 36

fibrinoid necrosis

Answer 36

cell loses outline and become homogeneous and pink, fibrin like appearance (seen in blood vessels of people with autoimmune diseases like lupus)

Question 37

fat saponification

Answer 37

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)

Question 38

wet gangrene

Answer 38

appears swollen, dark red and liquefied, foul odor and obscured border between dead and viable tissue (bacterial infection) -> diabetes (mmm food...sugar)

Question 39

dry gangrene

Answer 39

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)

Question 40

hypertrophy

Answer 40

increase in size of cell (increase in bulk without multiplication of parts)

Question 41

hyperplasia

Answer 41

increase in numbers of cells (not size) in tissue or organ (not cancer)

Question 42

metaplasia

Answer 42

normal transformation of tissue from one type to another (think of gerd, tissue gets hard and when gerd gone, tissue changes back) -> reversible

Question 43

dysplasia

Answer 43

abnormal development of an organ or part of the body, including congenital absence (cells change) -> can be reversible

Question 44

anaplasia

Answer 44

follows dysplasia | -loss of structural differentiation within cell or group of cells (invade other tissues) -> cannot be reversed