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Pathophysiology > cellular physiology > Flashcards

cellular physiology Flashcards

1
Q

what is arachidonic pathway

A

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)

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2
Q

different eicosanoids we need to know

A
  • protstaglandins
  • thromboxanes
  • leukotrienes
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3
Q

two pathways arachidonic pathway can go

A

cyclooxygenase pathway and lipooxygenase pathway

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4
Q

cyclooxygenase pathway

A

produces endoperoxides (protaglandins and thromboxanes)

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5
Q

lippxygenase pathway

A

produces leukotrienes

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6
Q

prostaglandins

A

vascular actions, inflammation

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7
Q

thromboxanes

A

blood clotting and other vascular actions

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8
Q

leukotrienes

A

mediated allergic and inflammatory reactions

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9
Q

eicosanoids (what they do)

A

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

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10
Q

What does NSAID do?

A

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

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11
Q

What do adrenal steroids do?

A

Adrenal steroids inhibit phospholipase A2 and thus block all eicosanoids

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12
Q

Point of CAMP?

A

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

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13
Q

Calcium

A

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

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14
Q

What happens to Na/K when ATP levels fall

A

-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!

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15
Q

examples of irreversible cell injury

A
  • membrane disturbances

- inability to reverse mitochondrial dysfunction

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16
Q

cellular injury related to free radicals

A
  • lipid peroxide in membranes
  • DNA fragmentation
  • lesions in DNA
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17
Q

lipid peroxide in membranes

A

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

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18
Q

DNA fragmentation

A

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

19
Q

protein cross linking

A

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.

20
Q

ischemia

A

decreased blood supply

21
Q

anoxia

A

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

22
Q

induction (of cell injury)

A
  • PM loses permeability
  • Na and H2O into cell, K out of cell
  • cell swells and Ca enters cell
23
Q

induction (of cell death)

A
  • influx of Ca
  • membrane disruption leads to hydrolyzing of proteins and DNA cleavage
  • feedback mech leads to death
24
Q

effector

A

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

25
Q

Degredation

A

Breakdown of unnecessary or dysfunctional cellular components by lysosymes.

26
Q

degeneration

A

a breakdown that leaves some loss of function

27
Q

regeneration

A

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

28
Q

Apoptosis

A
  • single cell
  • programmed cell death
  • no inflame response
  • cell shrinkage
  • membrane blebbing
  • cell breaks into several apoptotic bodies, organelles still functional
29
Q

necrosis

A
  • affects groups of neighboring cells
  • significant inflamm response
  • cell swelling, die and burst, spilling contents all over neighbors
30
Q

coagulative necrosis

A

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

31
Q

liquefactive necrosis

A

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

32
Q

caseous necrosis

A

turning “cheese like”, IE tuberculosis or fungal infections

33
Q

fat necrosis

A

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

34
Q

gummatous necrosis

A
  • pink and dusty red nodules or plaques
  • most commonly affect skin and mucous membranes
  • form of granuloma
  • tertiary syphillis
35
Q

hemorrhagic necrosis

A

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

36
Q

fibrinoid necrosis

A

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

37
Q

fat saponification

A

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)

38
Q

wet gangrene

A

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

39
Q

dry gangrene

A

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)

40
Q

hypertrophy

A

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

41
Q

hyperplasia

A

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

42
Q

metaplasia

A

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

43
Q

dysplasia

A

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

44
Q

anaplasia

A

follows dysplasia

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

Pathophysiology (7 decks)

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