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IHO Week 6 > Regal- Prostaglandins, Thromboxane and NSAIDS > Flashcards

Regal- Prostaglandins, Thromboxane and NSAIDS Flashcards

1
Q

How are leukotrienes synthesized?

A

Phospholipase A2 cleaves membrane phospholipids into AA

5 LPO converts AA to 5HPETE then LTA4

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2
Q

What do LTC4 synthase or glutathione S transferase do to LTA4? What converts LTE4 to LTB4?

A 
LTA4>
LTC4
LTD4
LTE4-->LTA hydrolase
LTB4
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3
Q

Where does LT synthesis occur?

A

Many cells and tissues

Predominately synthesized in leukocytes

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4
Q

What enzyme is associated w/ mast cells and basophils and what to they primarily make?

A

LTC4 synthase

peptido LTs

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5
Q

What enzyme is associated with endothelial cells and smooth muscle cells?

A

Glutathione S transferase

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6
Q

What are the 2 (4) types of leukotrienes?

A

LTB4

Peptidoleukotrienes
LTC4, LTD4, LTE4

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7
Q

How is LTB4 degraded?

A

Oxidized to inactive compound by enzymes in PMNs and others

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8
Q

What are the biological effects of LTB4?

A

Chemotactic for neutrophils
enhanced leukocyte adhesion

Decreased pain threshold–> hyperalgesia

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9
Q

What receptors does LTB4 target?

A

Non mentioned specifically but they’re distinct from peptide LTs

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10
Q

How is LTE4 degraded?

A

It is excreted in urine or acetylated and excreted in bile

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11
Q

LTC4, LTD4, LTE4 act on what receptor?

A

Cys LTR1

Cyst LTCR2

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12
Q

Interaction of peptido leukotriens w/ LTR1 leads to…

A

increased vascular permeability-> swelling
chemotactic for eosinophils and cytokine secretion
bronchoconstriction
increased mucous production
DC maturation and migration
smooth muscle proliferation

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13
Q

Interaction of peptido leukotrienes w/ LTR2 leads to…

A

endothelial cell and macrophage activation

fibrosis

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14
Q

What two peptido leukotrienes are important in asthma?

A

LTC4

LTD4

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15
Q

What drugs are leukotriene modifiers?

A

Zileuton
Zafirlukast
Montelukast

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16
Q

What is the therapeutic use of leukotriene modifiers?

A

bronchial asthma

CHRONIC not acute

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17
Q

What is the MOA of zileuton?

A

Inhibits 5-LPO

prevents synthesis of LTB4 and peptido LT

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18
Q

How is zileuton eliminated?

A

M: cyp450

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19
Q

What are the toxicities associated with zileuton?

A 
drug interactions
hepatic toxicity (req monitoring)
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20
Q

What is a unique property of zileuton related to asthma?

A

It can decrease the need for beta agonists in asthma

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21
Q

What is the MOA of zafirlukast and montelukast?

A

LTR antagonists (cys LTR1)

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22
Q

What is a toxicity associated w/ zafirlukast?

A

inhibits cyp450–> drug interactions

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23
Q

What is a unique property of montelukast?

A

it can be administered once daily w/out regard to meals

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24
Q

What are prostanoids?

A 
PGD2
PGE2
PGF2
PGI2- prostacylcin
TXA2
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25
Q

How are prostanoids synthesized?

A

Phospholipase A2 cleave membrane bound phospholipids into AA>
Cox acts on platelets to form products

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26
Q

What cells produce cos?

A

numerous cells in response to different stimuli

27
Q

Where is COX1 found?

A

platelets

constitutively expressed in most cells and is thought to protect mucosa

28
Q

Where is cox 2 found? What products is it more involved inmaking?

A

not in platelets
inducible
more involved in production of PG and TXA in inflammation

29
Q

How does enzyme expression of PG synthases influence the type of PG produced?

A

Platelets–> thromboxane (vasoconstrictor)

Endothelium–> prostacylcin (vasodilator)

Mast cells–> PGD2 (bronchoconstrictor)

30
Q

How are prostanoids degraded?

A

spontaneous chemical hydrolysis or rapid enzyme degradation

31
Q

What type of molecules are prostanoids, do they have a long or short t1/2?

A

unstable molecules

short t 1/2

limited systemic effects

32
Q

What does PGD2 do?

A

Bronchoconstriciton

33
Q

What receptor does PGD2 act on?

34
Q

What does PGE2 do?

A

vasodilation> redness and heat
increased vascular permeability> swelling
decreased pain threshold, sensitize pain receptors, synergy w/ other receptors > pain
fever

35
Q

What receptors does PGE2 act on?

A

EP subtypes

EP1-4

36
Q

What receptors does PGF2 act on?

37
Q

What does prostacyclin (PGI2) do?

A
  1. Vasodilation → redness & heat & opposes platelet aggregation
  2. increased vascular permeability → swelling
  3. increased pain threshold, sensitize pain receptors, synergy w/ other mediators→ pain
38
Q

What receptors does PGI2 act on?

39
Q

What does TXA2 do?

A
  1. Vasoconstriction → platelet aggregation
40
Q

What receptor does TXA2 act on?

41
Q

What drugs are NSAIDS?

A

acetylsalicylate
ibuprofen
naproxen

ketorolac
idomethacin
sulindac
petoprofen
piroxicam
42
Q

What is the MOA of NSAIDS?

A

Inhibit COX

43
Q

How are NSAIDS eliminated?

44
Q

What are toxicities associated w/ NSAIDS?

A 
Gastric ulcers
prolonged gestation
impaired renal function
increased bleeding
aspirin hypersensitivity
45
Q

What is the generic name for acetylsalicylate and it’s MOA?

A

Aspirin

irreversibly inhibits COX 1 and 2

46
Q

What are SE associated w/ aspirin?

A

reye syndrome
fatty liver
tinnitus
low TI

47
Q

What are SE associated w/ ibuprofen?

A

Fewer GI SE than aspirin

48
Q

What is a unique property associated with naproxen?

A

Primary algesia

anti-inflammatory

49
Q

What is a toxicity associated w/ indomethacin?

A

severe frontal lobe head ache

50
Q

What is the most potent NSAID?

A

indomethacin

51
Q

What is a SE associated w/ piroxicam?

A

Dose related GI bleeding

52
Q

What is the only cox inhibitor?

53
Q

What is the MOA of celecoxib?

A

selective cox 2 inhibitor

54
Q

What are toxicities associated w/ celecoxib?

A

Increased risk of thrombotic vascular events
Gastric ulcer (less likely than for NSAIDS)
Altered renal function
Hypersensitivity (less likely)

55
Q

What is the MOA of acetaminophen?

A

Weak inhibitor of COX

56
Q

How is acetaminophen distributed?

A

D: highly effective on COX in brain, but not inflammatory sites

57
Q

What is a SE of acetaminophen?

A

Overdose>

serious hepatic injury

58
Q

What MUST you know about acetaminophen?

A

It is NOT anti-inflammatory

used as anti-pyretic and analgesic

59
Q

What are the two types of kinins?

A

bradykinin

kalldin

60
Q

Where are kinins synthesized?

A

extracelluar in blood or interstitial fluid

61
Q

How is kinase I degraded?

A

carboxypeptidase N or anaphylatoxin inactivator removes carboxy terminal arg–> des arg kinins

62
Q

How is kinase II degraded?

A

Angiotensin converting enzyme (ACE) OR

dipeptide hydrolase

63
Q

What kinins act on B-2 receptor and what does that do?

A

kallidin & braykinin more active

  1. Vasodilation → redness & heat
  2. VERY strong vasodilators → hypotension
  3. increased vascular permeability → swelling, edema
  4. cause pain
  5. Bronchoconstriciton
  6. Release catecholamines & PGs
64
Q

What kinins act on the B1 receptor? and what effect does that have?

A

des-arg kinins (lack terminal ARG) more active

  1. chronic inflammatory effects
  2. induced after trauma
  3. cytokine production & long term effects
  4. hypotension & pain

IHO Week 6 (14 decks)

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