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Pharmacology > Itches, scratches and sneezes / Prostaglandins and leukotrienes > Flashcards

Itches, scratches and sneezes / Prostaglandins and leukotrienes Flashcards

1
Q

What is the allergic response (to pollen)?

A

1.) pollen
2.) White blood cells
3.) Memory cells
4.Engulf and digest (re-exposure)
5.) Release inflammatory mediators

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2
Q

What happens when mast cells are stimulated?

A
  • Mast cells stimulated by the binding of pathogens/ allergens?
  • Mast cell degranulates and releases its components into cells
  • Releases histamines, prostaglandins and leuukotrienes , cytokines
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3
Q

What are some of the functions of mast cells?

A
  • Epithelian permeability secretion (histamine LTC4, PGD2)
  • Blood flow vascular permeability coagulation (histamine LTC4)
  • Neuroimmune interactions, perisatalsis, bronchoconstrictio, pain (histamine proteases PGD2)
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4
Q

What are some pharmacological strategies for allergy prevention?

A
  • Immunotherapy
  • Prevent the release of mediators from mast cells
  • Block actions of mediators (receptor antagonist)
  • Inhibit synthesis of mediators
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5
Q

What is an example of a drug used to prevent the release of mediators from mast cells?

A
  • Ammi visnaga = toothpick plant
  • Khellin = active ingredient
  • Cromoglicate stabilises mast cells which inhibits degranulation
  • dry powder inhaler
    Used in :
  • eye drops
  • nasal spray
  • asthma
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6
Q

What are eicosanoids?

A
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6
Q

What are some other inhibitors of mast cell release?

A
  • Tyrosine kinase inhibitors:
  • Imatinib (Gilvec)
  • used in GI tumors but not for inflammation
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7
Q

What are actions of histamine?

A
  • epithelial permeability secretion and blood flow vascular permeability coagulation can lead to runny nose, wheezing and flare and wheal
    **- H1 receptor subtype **: contraction of smooth muscle (ileum, bronchi, uterus) , vasodilation, plasma exudation

H2 receptor subtype- increase gastric acid secretion and mucus secretion
H3 receptor subtype - inhibit release of neurotransmitters

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8
Q

What are 1st generation antihistamines?

A
  • Histamine receptor antagonist
  • Cyclizine : anti-emetic in space-sickness
    -     Diphenhydramine, dimenhydrinate     : cross blood brain barrier, have other non- histamine actions
  • prevent motion sickness
  • **Chlorpherniramine (Piriton) **- crosses BBB sedation, effective allergy treatment
  • Promethazine - sedation
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9
Q

What are 2 and 3rd generation antihistamines?

A
  • Terfenadine : non-sedating antihistamine
  • can cause arrhythmias (withdrawn)
  • Fexofenadine, cetirizine, loratadine ( non-sedating)
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10
Q

How are prostaglandins and leukotrienes synthesised?

A
  • Membrane phospholipids - phospholipase A2- arachidonic acid :
  • FOR PROSTAGLANDINS:
  • cyclooxygenase COX
  • Prostaglandins
  • prostacyclin (PGI2), PGF 2a, PGD2, PGE2, thromboxane (TXA2)
  • Lipoxyhenase - (leukotrienes, LTC4, LTD4, LTE4)
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11
Q

What are analgesics?

A
  • Anti-inflammatory drugs such as aspirin, ibruprofen, diclofenac, naproxen
  • Cyclooxygenase inhibitors = NSAIDS (NON-STEROIDAL ANTIINFLAMMATORY DRUGS)
  • Antipyretic anlgesics (e.g. Paracetamol)
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12
Q

What is the action of PGI2 (prostacyclin)?

A
  • generating cell: endothelium
    -IP receptor:
  • vasodilator
  • pain
  • cough
  • inhibits platelet aggregation ( blood clots forming)
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13
Q

prostaglandin

What is the action of PGF2A?

A

FP receptor
- Broncho-constrictor
- myometrial contraction
- cough

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14
Q

What is the action of PGD2?

A
  • generating cell = Mast cells
    DP receptor
  • vasodilator
  • broncho-constriction / allergic asthma (DP1)
  • chemotaxis (DP2)
  • inhibits platelet aggregation
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15
Q

What is the action of PGE2?

A

Generatign cell(s) : many cells
-EP receptor
- vasodilator
- pain (EP1 , neurons)
- fever ( EP3 neurons)
- cough
- Bone resporption ( EP4)
- mucus secretion (EP1)

16
Q

What is the action of TXA2?

A
  • generating cell: platelets
  • TP receptor
  • Vasoconstrictor
  • Increases platelet aggregation
17
Q

How do COX inhibitors work?

A
  • Inhibit COX production from arachidonic acid
  • Therefore no prostaglandinds secreted
  • Anti-inflammatory : vasodilation, plasma exudation
  • analgesics
  • COX inhibition
  • inflammed tissue contains prostaglandins whixh increases the pain signal
  • antipyretic - inhibition of prostaglanding production in hypothalamus
  • Paracetamol - not very anti-inflammatory
  • Indomethacin/ piroxicam - not very antipyretic
18
Q

How is leukotirene secretion inhibited?

A
  • Inhibited by antagonists :
  • Zarifirlukast (accolate)
  • montelukast (Singulair)
  • Lipoxygenase secretion inhibited (promotes inflammatory response)
19
Q

What are the actions of LTC4, LTD4 and LTE4?

A
  • bronchoconstriction, increased microvascular permeability
20
Q

What is the action of LTB4?

A
  • chemoattractant for neutrophils
  • stimulates release of lysosmal enzymes from macrophages
21
Q

What are some effects of glucorticoids ?

A
  • Decrease inflammatory response ( adverse = increase susceptibility to infection)
  • Decrease immunological response ( adverse: increase susceptibility to infection)
  • increase gluconeogenesus and glucosse output from liver. Decreases utilisation ( could lead to diabetes)
  • Increased protein catabolism (neg = muscle wasting)
  • Increased bone catabolism ( neg - osteoporosis)
  • Increased gastric acid and pepsin ( neg = peptic ulcer)
  • Increase Na reabsorption, K, H excretion ( neg = hypertension, hypokalaemia, muscle weakness)
22
Q

Why is the route of synthetic glucocoticoids adminstration varied?

A
  • To limit adverse effects
  • eg asthma — as aerosol — beclomethasone, budenoside
  • eg eczema — topical
  • eg rheumatoid arthritis — intra-articular injection of
  • triamcinolone
    eg enema in ulcerative colitis
    sometimes get rebound after withdrawal
23
Q

What are eicosanoids?

A
  • 20 carbon fatty acids (i.e. Prostaglandins, Thromboxane’s, Leukotrienes, Lipoxins (LX)
    • Not stored and very unstable - get broken down quickly
    • Synthesised and act locally
      Play an important role in everyday housekeeping physiology and inflammation
24
Q

Where do eicosanoids come from?

A
  • Membrane phospholipids : arachidonic acid
    • Arachidonate is released by specialised phospholipase A2
      Then production of eicosanoids
25
Q

What are the types of COX?

A
  • COX 1
  • Physiological roles
  • Stomach
  • Kidney
  • Constitutive
    -COX 2 :
  • inflammatory roles
  • Induces during inflammation
26
Q

What happens when Aspirin binds to COX?

A

-irreversible binding to COX
-Platelets :
- Express COX-1 , produce TXA2. Non nuclei
-TP receptors on vascular smooth muscle
Endothelial cells :
- Express COX-2 upon inflammation
- Produce PGi2
- Have nuclei
- IP receptors on vascular smooth muscle - vasodilation
- IP receptors on platelets = platelet disaggregation

27
Q
A

Pharmacology (14 decks)

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