• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/9

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

9 Cards in this Set

  • Front
  • Back
Blank
Blank
Describe in general the formation of eicosanoids including prostaglandins, thromboxanes and leukotrienes
Initiated by hormones, proteases or histamine and tissue injury. PLA2 releases arachidonic acid, a precursor of eicosanoids. Tissue injury and inflammation triggers arachidonate release and eicosanoid synthesis.
1. Phospholipase A2 makes Arachidonate out of a phospholipid
2. Cyclic endoperoxides are made from arachidonate in the COX (cyclooxegenase) pathway.
3. Each eicosonoid is made from PGH2 by its enzyme
- Prostacylcin (PGI2) - prostacyclin synthase
- Prostaglandins (PGD, PGE, PGF) - Reductase or isomerase
- Thromboxanes (TX) - Thromboxane synthetase

- OR -
2. Leukotrienes and lipoxins are made in the LOX (lipoxygenase) pathway.
Discuss the role of cortisol in eicosanoid synthesis
It inhibits Phospholipase A2 from making Arachidonate.
Describe the two enzyme activities of prostaglandin H synthase and cycloxygenase (COX)
Prostaglandin H2 synthase catalyzes the commited step of prostaglandin synthesis.

COX-1: responsible for normal physiological production of PGs
COX-2: present in low levels in inflammatory cells. induced by inflammatory responses such as cytokines, mitogens and endotoxins.
COX-3: expressed in heart and brain tissue
Differentiate between COX-1 and COX-2 and discuss their inhibition by NSAIDs
Aspirin (NSAID) irreversibly inhibits COX by acetylizing the SER530 OH group. This prevents PGH2 transcription.
The anti-inflammatory effects are due to COX-2 inhibition whereas the side-effects are due to COX-1 inhibition.
Indicate the eicosanoids formed from EPA and their biomedical activity compared to series-2 eicosanoids
Series 2, made from arachidonic acid, are pro-inflammatory.

Series 3, made from EPA, are far less biologically active and are anti-inflammatory.
Describe the synthesis of leukotriene LTA and the following change to LTB and LTC
Leukotriene A4 (LTA4) is formed from 5-HPETE in mast cells and leukocytes. It is unstable and immediately degrades to LTB4 and LTC4.
Describe the synthesis of components and actions of the slow-reacting substance of anapylaxis (SRS-A)
SRS-A is a mixture of LTC4, LTD4 and LTE4. They are secreted by mast cells during an anaphylactic reaction, inducing inflammation. The work primarily as bronchoconstrictors in asthma. They prolong the effects of leukotrienes. They are made from LTA4.
Discuss the biochemical basis for using corticoids, LOX-inhibitors or inhibitors of CysLT receptors in the management of asthma.
Corticosteroids inhibit phospholipase A2 (turns phospholipids into arachidonic acid). They prevent the brochoconstriction of leukotrienes as well as inducing the release of phosphorylated annexin-1.