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VET YEAR ONE > FORM & FUNCTION (Eicosanoid) > Flashcards

FORM & FUNCTION (Eicosanoid) Flashcards

1
Q

Eicosanoid:

A

-modified 20 carbon polyunsaturated fatty acids
-3 major classes
-synthesized from dietary fats (Omega-3 and Omega-6)
-mediate several processes

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2
Q

3 major classes:

A

-prostaglandins (PGs)
-thromboxanes (Txs)
-Leukotrienes (LTs)

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3
Q

Eicosanoids mediate

A

several processes:-inflammatory response
-production of pain and fever
-regulation of blood pressure
-induction of blood clot
-induction of labor
-etc.

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4
Q

Eicosanoids AND. hormones:

A

-induce profound physiological effects at extremely low concentrations
-bind to GPCR to initiate a signal transduction cascade (cAMP)

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5
Q

Eicosanoids different from hormones:

A

-are not transported in the blood to their site of action
-produced by all mammalian organ cells except RBC
-very unstable and rapidly degraded
-promotes local and cell specific actions

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6
Q

Palmitic acid:

A

-generated from lipid biosynthesis
-further modified to form other lipids

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7
Q

Animals can’t make omega-3 and omega-6:

A

-missing desaturases that form the double bonds past the 9th carbon

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8
Q

Double bonds in omega-3 and omega-6:

A

-double bond is 3 C away from the terminal group: omega-6
-double bond is 6C away from the terminal group: omega-3

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9
Q

Dietary supplement:

A

-plant oil (flaxseed) or fish oil
-fish omega-3 comes from their dietary consumption of microalgae

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10
Q

How are omega-3 and omega-6 stored?

A

-as a phospholipids
*important for cell membranes

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11
Q

Omega-3 family breakdown:

A
  1. Alpha-linolenic acid
  2. Eicosapentaenoic acid (EPA)
  3. Docosahexaenoic acid (DHA)
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12
Q

Omega-6 family breakdown:

A
  1. Linoleic acid
  2. Arachidonic acid (AA)
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13
Q

Delta-6 desaturase:

A

-enzyme that converts:
>alpha-linolenic acid to EPA
>linoleic acid to AA

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14
Q

AA, EPA, DHA:

A

-precursors to:
>prostaglandins
>thromboxanes
>leukotrienes

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15
Q

Omega-3 and omega-6 generally produce eicosanoids:

A

-omega-6: associated with pro-inflammatory
-omega-3: with anti-inflammatory response

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16
Q

Healthy diet:

A

-low omega-6/omega-3 ratio is recommended

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17
Q

Cats and omega-3/6 processing:

A

-lack delta-6 desaturase activity
-must obtain EPA, DHA, or AA from other animal organs or via transport

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18
Q

Eicosanoid synthesis:

A

-omega-3/6 are stored in the cell membrane
-phospholipase A2 cleaves AA, EPA, DHA to get them in active form
-2 pathways

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19
Q

Phospholipase A2 activated by:

A

-greater [Ca2+]
-physical trauma
-immunoglobulins
-microbial products

20
Q

Phospholipase A2 inhibited by:

A

-anti-inflammatory signals (glucocorticoids)

21
Q

2 pathways: eicosanoid synthesis:

A
  1. Cyclooxygenase (COX-1 and COX-2)
  2. Lipooxygenase
    *compete for the same substrates
    *oxidation reaction
22
Q

Cyclooxygenase (COX-1 and COX-2):

A

-prostanoids
>prostaglandins
>thromboxane

23
Q

Lipooxygenase:

A

-leukotrienes

24
Q

Prostanoids:

A

-COX-1 is constitutively expressed
-COX-2 is inducible by inflammation stimuli
-different prostaglandins are produced by specific cell types to regulate local responses

25
Q

Different prostaglandins local responses:

A

-control muscle function (vessel constriction and dilation)
-regulate CNS activity (pain reception)
-mediate cytokine production for inflammation response

26
Q

NSAIDS:

A

-nonsteroidal anti-inflammatory drug
*inhibit COX-1 and COX-2
>side effects

27
Q

NSAIDS used to:

A

-reduce pain
-decrease fever
-decrease inflammation
-commonly used to treat prescribed (arthritis)

28
Q

COX-1:

A

-constitutive enzyme that generates the signal ligand for homeostatic intracellular signaling

29
Q

COX-2:

A

-inducible enzyme with increased activity accompanying acute and chronic inflammatory conditions

30
Q

NSAIDS block PGE2 production:

A

-PGE2 normally inhibits gastric secretion
-inhibition consequences:
>increase HCl secretion (can’t control how much HCl is in mucous)
>decrease mucous secretion (barrier) in the stomach
>GI bleeding

31
Q

NSAIDS: PGI2

A

-vasodilators that increase renal perfusion
-inhibition consequence:
>reduced afferent blood flow that can lead to acute kidney injuries

32
Q

COX-2 specific inhibitor:

A

-developed to treat acute and chronic inflammations
-reduce side effects of GI bleeding and kidney necrosis
*not used in humans
-effective in reducing prostaglandins, but increase the ration of thromboxane that regulates clotting

33
Q

COX-2 specific inhibitor examples:

A

-Firocoxib (Equioxx)
-Previcox (used to treat canine arthritis and tumors)

34
Q

Don’t use COX-2 specific inhibitors in humans:

A

-can lead to 40% increase in risk for cardiovascular complications

35
Q

Thromboxanes:

A

-synthesized primarily in platelets (thrombocytes)
-activated by damage to the arterial wall

36
Q

Activated Thromboxanes:

A

-induce platelet aggregation and vascular muscle contraction

37
Q

Normal conditions thromboxanes:

A

-PGI2 and nitric oxide cause vasodilation to inhibit thromboxanes

38
Q

Increased Thromboxanes from COX-2 inhibtion:

A

-constricted vessel
-platelet aggregation
*increase risk of heart attacks

39
Q

Leukotrienes:

A

-synthesized by the enzyme lipoxygenase (LO)
-primarily act as inflammatory mediators
-various biologic responses
>bind to receptors on individual cells

40
Q

Lipoxygenase (LO):

A

-synthesizes leukotrienes
-primarily found in leukocytes

41
Q

Leukotrienes biologic responses:

A

-pro-inflammatory action
-bronchoconstriction (10-100x more potent than histamine)
-mucus secretion
-edema in airways

42
Q

Leukotrienes and asthma:

A

-elevated leukotrienes levels (chronic inflammation, allergies) lead to asthma in humans and similar in cats

43
Q

Asthma:

A

-characterized by increased mucous production and bronchoconstriction
-laboured breathing and wheezing

44
Q

Asthma treatment:

A

-with bronchodilator (beta-agonist) or corticosteroid (reduce inflammation)

45
Q

Leukotriene receptor agonist:

A

-blocks leukotriene binding in target cells (montelukast & zafirlukast)
-promising anti-inflammatory agents
*need further validation in vet med

VET YEAR ONE (108 decks)

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