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

Test 3: 64-65 Flashcards

(85 cards)

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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
\_\_\_\_ is a constitutive active enzyme to make eicosanoids that are involved in **homeostatic processes**
COX1 one of the PUMA used to make eicosanoids from arachidonic acid
26
what type of eicosanoids do cycloocygenases make \_\_\_
prostaglandin, thromboxanes, prostacyclins
27
arachidonic acid (lipoxygenase)=
–Hydroxyeicosatetraenoic acids (HETEs) –Leukotrienes (LT) –Eoxins
28
eicosanoids can have a potent and often opposing effects on eg, smooth muscle (vasculature and myometrium), platelets, inflammatory cells, etc. e.g. PG12 vs \_\_\_
PGI2 Thromboxane A2
29
omega-6 series of eicosanoids derived from dihomo-gamma-linolenic acid give rise to \_\_\_
TXA2
30
omega-3 series of eicosanoids derived from eicosanpenteanoic acid give rise to \_\_\_
resolvins of the E series RvE1, 183 Rv E1, RvE2 and RvE3
31
eicosanoids that have a pro-inflammatory response are \_\_\_
leukotriene B4 and C4
32
Eicosanoids that have an anti- inflammatory response are \_\_\_
resolvins and protectins
33
COX-1 or COX-2 converts aracidonic acid to prostaglandin G2 which is rapidly converted to prostaglandin H2 via COX and \_\_\_
peroxidase activity
34
prostaglanins are oxygenated ___ containing a cyclopentane ring
PUFAs polyunsaturated fatty acids
35
COX1 is a ___ enzyme made at ___ levels used for house keeping functions such as \_\_\_
constitutive constant (low level prostaglandin production) platelet regulation (blood clotting), kidney function, stomach acid regulation
36
COX2 is a ___ enzyme that makes ___ to maintain inflammation response such as \_\_\_
inducible (needs inflammatory stimuli) acute high level prostaglandin production (transient gets stimulated, makes something then stops) pain, heat, swelling
37
prostaglandin H2 (\_\_\_) = prostaglandin E2
prostaglanin E2 synthase
38
three types of prostaglandin E2 synthase
mPGES-1 (membrane) mPGES-2 (mitochondrial) cPGES (cytoplasmic)
39
prostaglandin E2 binds to __ receptors
PTGER 1-4
40
the function of prostaglanin E2 is
pro-inflammatory response: fever, pain perception parturition
41
\_\_\_ inhibit prostaglandin E2's productions to reduce inflammation, fever and pain
NSAID
42
\_\_\_ if given in very high doses or early in gestation can cause abortion
PGF2 alpha
43
PGH2 (\_\_\_\_) =PGD2
prostaglandin D2 synthase
44
what receptors does PGD2 act on?
prostaglandin DP1 and DP2 receptors
45
prostaglandin D2 functions to regulate \_\_\_
allergic reactions
46
steps of spontaneous dehydration of PGD2
PGD2→ PGJ2→ Δ12-PGJ2 → 15-deoxy-Δ12,14-PGJ2
47
\_\_\_ are derived from cyclopentenone PGs
PGD2
48
15-deoxy-Δ12,14-PGJ2 which is derived form ___ can bind to ___ receptors and functions to \_\_\_
PGD2 PPAR gamma, PGDP2 receptors **inhibit inflammation and cell growth** **(inhibits diverse inflammatory responses in animal models)**
49
\_\_\_ made from PGD2 inhibits inflammation and cell growth
15-deoxy-Δ12,14-PGJ2
50
clinical relevance of 15-deoxy-Δ12,14-PGJ2
inhibits diverse inflammatory responses in animal models
51
PFH2 (\_\_\_\_) = PGI2
prostacyclin synthase
52
how can you detect PGI2 levels
PGH2 → PGI2 → 6-keto PGF1 alpha this can be detected and easily measured
53
PGH2 (\_\_\_) = TxA2 →
thromboxane synthase TxB2
54
function of PGI2
anti platelet activation vasodilator counteracts thromboxane A2
55
iloprost and cisaprost
(synthetic prostacylins (PGI2))
56
synthetic prostacylins (PGI2) such as ___ and ___ are used as a [_vasodilator_](https://en.wikipedia.org/wiki/Vasodilator)in severe \_\_\_[](https://en.wikipedia.org/wiki/Raynaud%27s_phenomenon)or [_ischemia_](https://en.wikipedia.org/wiki/Ischemia)of a limb
iloprost and cisaprost [_Raynaud's phenomenon_](https://en.wikipedia.org/wiki/Raynaud%27s_phenomenon)
57
\_\_\_ is used to treat pulmonary hypertension
iloprost, cisaprost (syntheic prostacyclin PGI2)
58
Thromboxane synthase converts ___ into TXA2
PGH2
59
thromboxane A2 (TXA2) binds to ___ receptors and functions to regulate \_\_\_
thromboxane receptors alpha and beta blood platelet aggregation, blood clotting and allergic reaction
60
How do NSAIDs effect thromboxane A2
inhibits production to reduce incidence of strokes and MI (thromboxane A2= clotting)
61
cyclooxygenase pathway and how NSAID effects it
62
why does aspirin prevent platelet aggregation?
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, i**ncrease 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
lipoxygenase pathway arachidonic acid (\_\_\_) = HPETE
lipoxygenase 5, 15, 12 sometimes 8
64
aracidonic acid (5 lipoxygenase) =
arachidonic acid (5-LOX)= 5 HPETE [which is metabolized to](https://en.wikipedia.org/wiki/5-HPETE) leukotrienes LTA4 which turns into [LTB4](https://en.wikipedia.org/wiki/Leukotriene_B4) or [LTC4](https://en.wikipedia.org/wiki/Leukotriene_C4), LTC4→ LTD4 → LTE4 **also** Arachidonic acid (5 LOX) = lipoxins A and B
65
arachidonic acid (15 LOX) =
15 HPETE → 15 HETE → lipoxins A and B
66
arachidonic acid (12 LOX)=
12 HPETE → 12 HETE
67
arachidonic acid (8 LOX) =
8 HPETE
68
5 LOX need ___ to do their jobs
FLAP (co-factor)
69
15 LOX is found in ___ and acts on ___ to make \_\_\_. the cofactors needed are \_\_\_
reticulocytes, macrophages (cytokine-induced) Arachidonic acid (and others) **15 HPETE, lipoxins,** resolvins and protectins 12-HETE, 8-15 diHETE, Eoxin A4
70
FLAP is a cofactor that helps \_\_\_
5-LOX AA (5LOX)(FLAP)= primary source of leukotreines (5HETE, LTA4, LTC4, LTD4, LTE4 and LTB4 as well as lipoxins A and B)
71
LTB4 is made from ___ and its major function is \_\_\_
arachidonic acid (5 LOX) → HPETE → LTA4 → LTB4 chemotactic factor for and activator of leukocytes, **inflammation**
72
\_\_\_ are formed by ___ and its major function is vascular permeability, vascular smooth muscle contraction, allergy
LTC4 and LTD4 arachidonic acid (5 LOX) → HPETE → LTA4 → LTC4 → LTD4
73
\_\_\_ are antagonists of CYSLTR1 used in ___ as well as other allergic and allergic- like reactions
LTC4 and LTD4 asthma
74
\_\_\_\_ primary function is increased vascular permeability and airway mucin secretion
LTE4 arachidonic acid (5 LOX) → HPETE → LTA4 → LTC4 → LTD4→ LTE4
75
\_\_\_ contributes to asthma as well as other allergic and allergic like reactions
LTE4
76
\_\_\_ and \_\_\_inhibits functions of pro- inflammatory cells
lxA4 and LxB4 | (lipoxins A and B)
77
\_\_\_ are specialized pro- resolving mediators class of inflammatory reaction suppressors
lipoxins A and B (Lx A4 and LxB4)
78
\_\_\_ and ___ inhibits function of pro-inflammatory cells
RvE1 and RvE2 | (resolvins 1 and 2)
79
lipoxins are ___ mediators
anti-inflammatory
80
\_\_ counteract the pro-inflammatory pathway of lipoxygenases
lipoxins and resolvins
81
glucocorticoids (steroids) will inhibit ___ in the formation of eicosanoids
phospholipase A2 (1st step) stops membrane phospholipid from breaking down into arachidonic acid
82
NSAIDs are used to block what part of eicosanoid production
COX 1 and COX2 arachidonic acid → prostaglandins, prostacylins (PGI2) and Thromboxanes (TXA2)
83
COX-2 specific NSAIDs are used to \_\_\_
prevent inflammation instead of preventing COX1 which leads to homeostatic pathways
84
\_\_\_\_ inhibits LOX
zileton arachidonic acid (LOX) → HETEs, leukotrienes, lipoxins
85
montelukast is meant to block \_\_\_
leukotrienes arachidonic acid (LOX) → HETEs, leukotrienes, lipoxins

21 fall: Biochem (44 decks)

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