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Medical Biochemistry > Eicosanoids > Flashcards

Eicosanoids Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the major site of synthesis of PGI2 (prostacyclin)

A

Endothelium of blood vessels

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2
Q

What are the major biological activities of PGI2? (prostacyclin)

A

Vasodilation;
Inhibits platelet aggregation;
Increases formation of cAMP

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3
Q

What is the major site of synthesis of TXA2 (thromboxane A2)?

A

Platelets

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4
Q

What are the major biological activities of TXA2?

A 
Promotes platelet aggregation;
Decreases formation of cAMP;
Vasoconstriction;
Mobilizes intracellular Ca2+;
Contraction of smooth muscle
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5
Q

Within the cell, what part of membrane phospholipids does arachidonic acid predominantly reside?

A

C-2 position

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6
Q

Activation of what releases Arachidonic Acid from the membrane phospholipid?

A

Phospholipase A2

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7
Q

Where are minor eicosanoids derived from?

A

Alpha-linolenic acid

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8
Q

Which enzyme cleaves PIP2 to generate IP3 and DAG?

A

Phospholipase C

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9
Q

Which enzyme cleaves PIP2 to generate Arachidonic acid and Lyso-PIP2?

A

Phospholipase A2;

Note: arachidonic acid released on cytoplasmic side of membrane

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10
Q

What is the rate limiting enzyme in prostaglandin and thromboxane synthesis?

A

Cyclooxygenase

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11
Q

What inhibits Phospholipase A2?

A

Corticosteroids (I.e. cortisol)

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12
Q

How does Asprin inhibit COX?

A

Irreversibly by acetylation

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13
Q

What does Asprin acetylate during inhibition of COX?

A

Serine residue in the active site

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14
Q

Arachidonic acid gets converted to what? By which enzyme? (in the synthesis of prostaglandins and thromboxanes)

A

PGG2;

Cyclooxygenase

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15
Q

PGG2 gets converted to what? By what enzyme?

A

PGH2;

Peroxidase

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16
Q

PGH2 gets acted upon by which enzyme to form TXA2?

A

Thromboxane synthase

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17
Q

PGH2 gets acted upon by which enzyme to form PGI2?

A

Prostacyclin Synthase

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18
Q

What does the drug celecoxib act upon?

A

Selective COX-2 inhibitor use to treat chronic inflammation assoc with some disease.

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19
Q

Why is COX-2 non-constitutive?

A

Because it can be INDUCED

20
Q

What is COX-2 induced in response to?

A

Immune and inflammatory mediators (TNF, Cytokines, tumor promoters, endotoxins)

21
Q

Induction of COX-2 leads to increased prostaglandin synthesis which results in what?

A

Pain, heat, redness, swelling and fever

22
Q

Irreversible inhibition of COX-1 by low dose Asprin results in what two important effects?

A
  • platelet aggregation decrease

- no significant effect on prostacyclin (PGI2) formation in endothelial cells

23
Q

Why does Aspirin cause a platelet aggregation decrease?

A

Reduced synthesis of TXA2

24
Q

When COX-2 is specifically inhibited, how are prostacyclin and thromboxane affected?

A

Less prostacyclin is released from endothelial cells; however thromboxane formation in platelets which only have COX-1 is not inhibited. This leads to increase platlet aggregation, increasing risk of clot formation.

25
Q

What can be used instead of Arachidonic acid for eicosanoid synthesis?

A

Eicosapenaenoic acid (EPA) which is found in fish oil.

26
Q

What is the precursor of eicosanoids?

A

arachidonic acid

27
Q

Phospholipase A2 cleaves what specific phospholipid to release arachidonic acid?

A

phosphatiylinositol -4,5-bisphosphate (PIP2)

28
Q

What are the functions of eicosanoids?

A

A. Inflammatory responses (joints, skin, eyes etc)
B. Affect intensity/ duration of pain / fever
C. Reproductive Fxn (induce labor)
D. Inhibit gastic acid secretion
E. Regulate BP thru vasodilation / constriction
F. Inhibit / activate platlet aggregation / thrombosis.

29
Q

All cells except ______ make eicosanoids.

A

RBC

30
Q

Where is Cox-1 found?

A

in almost all tissues

31
Q

Where is COX-2 found?

A

in liver and macrophages

32
Q

What normal physiological fxns is COX-1 imp for?

A

growth production, decrease acid secretion, maintenance of renal Bl flow, vascular homeostasis, and hemostasis.

33
Q

What is the structure of EPA?

A

20:5, w3

34
Q

What series does the PG and TX from EPA belong to?

A

3 series

35
Q

What series does PG and TX from arachidonic acid belong to?

A

2-series

36
Q

Why does EPA have overall effect of decreasing aggregation / blood clotting when compared to arachidonic acid?

A

TXA3 (from EPA) is less potent than TXA2 in promoting platlet aggregation. PGI3 (from EPA) has the same potency as PGI2 (from arachidonic acid) in inhibiting blood clotting. Therefore net effect of TXA3 and PGI3: decrease blood clotting.

37
Q

In the synthesis of leukotrienes, arachidonic acid is converted to what, by what enzyme?

A

5-Lipoxygenase (LOX) converts arachidonic acid to 5-hyroperoxyeicosatetraeinoic acid (HPETE).

38
Q

What drugs inhibit LOX?

A

Benoxaprofen and Zileuton

39
Q

The intermediate LTA4 in the synthesis of leukotrienes is used by what cells to make LTC?

A

mast cells and eosinophils

40
Q

How is LTC4 formed from LTA4?

A

Add glutathione (GSH)

41
Q

How is LTD4 formed from LTC4?

A

Remove glutamate

42
Q

How is LTE4 formed from LTD4?

A

Remove glycine

43
Q

How is LTF4 formed from LTE4?

A

Add glutamate

44
Q

What are cysteinyl-leukotrienes and why is this important?

A

LTC, LTD, LTE bc they have either peptide or cysteine in their structure. All three increase vascular permeability, bronchoconstriction, vasoconstriction, and lung edema.

45
Q

Cysteinyl-leukotrienes are components of what?

A

slow-reacting substance of anaphylaxis (SRS-A) which is more potent than histamine

46
Q

Asthma treatment targets what?

A

A. The inhibition of leukotriene synthesis (inhibit release of arachidonic acid, inhibit LOX and cysteinyl-leukotriene receptors)
B. Inhibition of leukotriene receptors

bc asthma characterized by
bronchoconstriction and leukotrienes lead to bronchoconstriction.

47
Q

What should be done if a pt has severe asthma crisis (severe shock)?

A

Give steroids to stop everything by inhibiting PLA2.

Medical Biochemistry (35 decks)

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