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21 fall: Biochem > Test 3: 64-65 > Flashcards

Test 3: 64-65 Flashcards

1
Q

inflammation mediators derived from eicosanoids are ___

A

postaglandins and leukotreines

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2
Q

eicosanoids contribute to mediating and ___ inflammation

A

resolution (stopping inflammation)

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3
Q

how do eicosanoids stop inflammation

A

neutrophils- short lived cells, do their job then die

Macrophages switch what arachidonic acid is produced from leukotrienes to lipoxins, anti-inflamatory cytokines, TGFB and IL10, stop TNFa production

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4
Q

___ are a family of oxygenated natural lipid products

A

eicosanoids

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5
Q

Eicosanoids are formed from PUFAs by pathways involving at least one step of dioxygen-dependent oxidation by ___

A

cycloocygenases, lipocygenases and cytochrome P450

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6
Q

Eicosanoids are typically not stores in tissues but rather formed ___ by liberation of precursor ___ forms of fatty acids

A

on demand

esterified

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7
Q

Numerous enzymes metabolize eicosanoids into ___ products that possess divers biologic activities

A

secondary

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8
Q

major function of eicosanoids

A

modulators of inflammation:

pro inflammatory, anti-inflammatory/resolution of inflammation

vascular tone and platelet function

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9
Q

eicosanoids play a role in reproductive and perinatal processes by ___

A

patent ductus arteriosus

preeclampsia

estrus synchronization

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10
Q

eicosanoids play a role in cardiovascular effects by ___

A

vascular homeostasis

platelet aggregation

atherosclerosis/ myocardial infarct/ stroke

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11
Q

eicosanoids play a role in bone marrow by __

A

endosteal niche

hematopoiesis

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12
Q

example of PUFA that is used as precursor to eicosanoids

A

arachidonic acid AA

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13
Q

archidonic acid is an example of a ___ used as a precursor to eicosanoids.

A

PUFA

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14
Q

arachidonic acid is an omega-6 fatty acid with four double bonds in the cis configuration

is it a ___ associated fatty acid

A

membrane phospholipid

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15
Q

phospholipase A2s is triggered by mechanical trauma, ischemia, other physical perturbations, pathogens or paracrine factors such as chemotactic factors, cytokines, growth factors and certain ___

A

eicosanoids

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16
Q

___ esterase activity releases ω-6 and ω-3 fatty acids bound in ester linkage to the SN2 position of membrane PLs

A

PLA2 (phospholipase A2)

breaks PUFAs into unesterified fatty acid chain (free AA) and phospolipid side chains

the free AA will either by re-esterified or acted upon by COX, LOX or cytochrome P450.

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17
Q

arachidonic acid is the principal substrate for ___synthesis in animal tissues

A

eicosanoid

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18
Q

arachidonic acid is an essential fatty acid derived from the diet - directly or following synthesis from dietary ___

A

linoleic acid

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19
Q

arachidonic acid is stored in ___ form in the phospholipid fraction of cell membranes

A

esterified

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20
Q

arachidonic acid is released from membrane phospholipids by the acyl hydrolase ___

A

PLA2 (phospholipase A2)

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21
Q

when arachidonic acid is broken into free AA (un-esterified fatty acid chain) by PLA2 it is either immediately re-esterified or acted upon by ___

A

COX, LOX and cytochrome P450 pathways to make eicosanoids

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22
Q

cyclooxygenase take ___ and turn it into prostaglandins, thromboxanes and prostacyclins

A

arachidonic acid

forms eicosanoids

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23
Q

COX-1 which turns arachidonic acid into prostaglandins, thromboxanes and prostacyclins works by ___

A

constitutive active enzyme to make eicosanoids that are involved in homeostatic processes

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24
Q

COX2 is an ___ enzyme that is associated with pro inflammatory processes

A

inducible

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25
Q

____ is a constitutive active enzyme to make eicosanoids that are involved in homeostatic processes

A

COX1

one of the PUMA used to make eicosanoids from arachidonic acid

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26
Q

what type of eicosanoids do cycloocygenases make ___

A

prostaglandin, thromboxanes, prostacyclins

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27
Q

arachidonic acid (lipoxygenase)=

A

–Hydroxyeicosatetraenoic acids (HETEs)

–Leukotrienes (LT)

–Eoxins

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28
Q

eicosanoids can have a potent and often opposing effects on eg, smooth muscle (vasculature and myometrium), platelets, inflammatory cells, etc. e.g. PG12 vs ___

A

PGI2

Thromboxane A2

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29
Q

omega-6 series of eicosanoids derived from dihomo-gamma-linolenic acid give rise to ___

A

TXA2

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30
Q

omega-3 series of eicosanoids derived from eicosanpenteanoic acid give rise to ___

A

resolvins of the E series

RvE1, 183 Rv E1, RvE2 and RvE3

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31
Q

eicosanoids that have a pro-inflammatory response are ___

A

leukotriene B4 and C4

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32
Q

Eicosanoids that have an anti- inflammatory response are ___

A

resolvins and protectins

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33
Q

COX-1 or COX-2 converts aracidonic acid to prostaglandin G2 which is rapidly converted to prostaglandin H2 via COX and ___

A

peroxidase activity

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34
Q

prostaglanins are oxygenated ___ containing a cyclopentane ring

A

PUFAs

polyunsaturated fatty acids

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35
Q

COX1 is a ___ enzyme made at ___ levels used for house keeping functions such as ___

A

constitutive

constant (low level prostaglandin production)

platelet regulation (blood clotting), kidney function, stomach acid regulation

36
Q

COX2 is a ___ enzyme that makes ___ to maintain inflammation response such as ___

A

inducible (needs inflammatory stimuli)

acute high level prostaglandin production (transient gets stimulated, makes something then stops)

pain, heat, swelling

37
Q

prostaglandin H2 (___) = prostaglandin E2

A

prostaglanin E2 synthase

38
Q

three types of prostaglandin E2 synthase

A

mPGES-1 (membrane)

mPGES-2 (mitochondrial)

cPGES (cytoplasmic)

39
Q

prostaglandin E2 binds to __ receptors

40
Q

the function of prostaglanin E2 is

A

pro-inflammatory response: fever, pain perception

parturition

41
Q

___ inhibit prostaglandin E2’s productions to reduce inflammation, fever and pain

42
Q

___ if given in very high doses or early in gestation can cause abortion

A

PGF2 alpha

43
Q

PGH2 (____) =PGD2

A

prostaglandin D2 synthase

44
Q

what receptors does PGD2 act on?

A

prostaglandin DP1 and DP2 receptors

45
Q

prostaglandin D2 functions to regulate ___

A

allergic reactions

46
Q

steps of spontaneous dehydration of PGD2

A

PGD2→ PGJ2→ Δ12-PGJ2 → 15-deoxy-Δ12,14-PGJ2

47
Q

___ are derived from cyclopentenone PGs

48
Q

15-deoxy-Δ12,14-PGJ2 which is derived form ___ can bind to ___ receptors and functions to ___

A

PGD2

PPAR gamma, PGDP2 receptors

inhibit inflammation and cell growth

(inhibits diverse inflammatory responses in animal models)

49
Q

___ made from PGD2 inhibits inflammation and cell growth

A

15-deoxy-Δ12,14-PGJ2

50
Q

clinical relevance of 15-deoxy-Δ12,14-PGJ2

A

inhibits diverse inflammatory responses in animal models

51
Q

PFH2 (____) = PGI2

A

prostacyclin synthase

52
Q

how can you detect PGI2 levels

A

PGH2 → PGI2 → 6-keto PGF1 alpha

this can be detected and easily measured

53
Q

PGH2 (___) = TxA2 →

A

thromboxane synthase

TxB2

54
Q

function of PGI2

A

anti platelet activation

vasodilator

counteracts thromboxane A2

55
Q

iloprost and cisaprost

A

(synthetic prostacylins (PGI2))

56
Q

synthetic prostacylins (PGI2) such as ___ and ___ are used as a vasodilatorin severe ___or ischemiaof a limb

57
Q

___ is used to treat pulmonary hypertension

A

iloprost, cisaprost (syntheic prostacyclin PGI2)

58
Q

Thromboxane synthase converts ___ into TXA2

59
Q

thromboxane A2 (TXA2) binds to ___ receptors and functions to regulate ___

A

thromboxane receptors alpha and beta

blood platelet aggregation, blood clotting and allergic reaction

60
Q

How do NSAIDs effect thromboxane A2

A

inhibits production to reduce incidence of strokes and MI

(thromboxane A2= clotting)

61
Q

cyclooxygenase pathway and how NSAID effects it

62
Q

why does aspirin prevent platelet aggregation?

A

aspirin = NSAID

blocks both COX1 and CoX2

Prostacyclin (PGI2= anti clot) concentrations however, recover much faster than thromboxane levels (TXA2= clot), so aspirin administration eventually prevents platelet aggregation

Why the difference in recovery?

PGI2 is primarily produced by endothelial cells that over time with aspirin treatment, increase their production of COX enzymes to catalyze the formation of PGI2.

In contrast, TXA2 is released primarily by platelets, which as anucleated cells, are unable to respond to COX inhibition with increased transcription of the COX genes and therefore irreversibly inhibits TXA2 production.

63
Q

lipoxygenase pathway

arachidonic acid (___) = HPETE

A

lipoxygenase

5, 15, 12 sometimes 8

64
Q

aracidonic acid (5 lipoxygenase) =

A

arachidonic acid (5-LOX)= 5 HPETE

which is metabolized to

leukotrienes LTA4 which turns into LTB4 or LTC4,

LTC4→ LTD4 → LTE4

also

Arachidonic acid (5 LOX) = lipoxins A and B

65
Q

arachidonic acid (15 LOX) =

A

15 HPETE → 15 HETE → lipoxins A and B

66
Q

arachidonic acid (12 LOX)=

A

12 HPETE → 12 HETE

67
Q

arachidonic acid (8 LOX) =

68
Q

5 LOX need ___ to do their jobs

A

FLAP (co-factor)

69
Q

15 LOX is found in ___ and acts on ___ to make ___. the cofactors needed are ___

A

reticulocytes, macrophages (cytokine-induced)

Arachidonic acid (and others)

15 HPETE, lipoxins, resolvins and protectins

12-HETE, 8-15 diHETE, Eoxin A4

70
Q

FLAP is a cofactor that helps ___

A

5-LOX

AA (5LOX)(FLAP)= primary source of leukotreines

(5HETE, LTA4, LTC4, LTD4, LTE4 and LTB4 as well as lipoxins A and B)

71
Q

LTB4 is made from ___ and its major function is ___

A

arachidonic acid (5 LOX) → HPETE → LTA4 → LTB4

chemotactic factor for and activator of leukocytes, inflammation

72
Q

___ are formed by ___ and its major function is vascular permeability, vascular smooth muscle contraction, allergy

A

LTC4 and LTD4

arachidonic acid (5 LOX) → HPETE → LTA4 → LTC4 → LTD4

73
Q

___ are antagonists of CYSLTR1 used in ___ as well as other allergic and allergic- like reactions

A

LTC4 and LTD4

asthma

74
Q

____ primary function is increased vascular permeability and airway mucin secretion

A

LTE4

arachidonic acid (5 LOX) → HPETE → LTA4 → LTC4 → LTD4→ LTE4

75
Q

___ contributes to asthma as well as other allergic and allergic like reactions

76
Q

___ and ___inhibits functions of pro- inflammatory cells

A

lxA4 and LxB4

(lipoxins A and B)

77
Q

___ are specialized pro- resolving mediators class of inflammatory reaction suppressors

A

lipoxins A and B (Lx A4 and LxB4)

78
Q

___ and ___ inhibits function of pro-inflammatory cells

A

RvE1 and RvE2

(resolvins 1 and 2)

79
Q

lipoxins are ___ mediators

A

anti-inflammatory

80
Q

__ counteract the pro-inflammatory pathway of lipoxygenases

A

lipoxins and resolvins

81
Q

glucocorticoids (steroids) will inhibit ___ in the formation of eicosanoids

A

phospholipase A2

(1st step) stops membrane phospholipid from breaking down into arachidonic acid

82
Q

NSAIDs are used to block what part of eicosanoid production

A

COX 1 and COX2

arachidonic acid → prostaglandins, prostacylins (PGI2) and Thromboxanes (TXA2)

83
Q

COX-2 specific NSAIDs are used to ___

A

prevent inflammation instead of preventing COX1 which leads to homeostatic pathways

84
Q

____ inhibits LOX

A

zileton

arachidonic acid (LOX) → HETEs, leukotrienes, lipoxins

85
Q

montelukast is meant to block ___

A

leukotrienes

arachidonic acid (LOX) → HETEs, leukotrienes, lipoxins

21 fall: Biochem (44 decks)

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