Dr. Bill's Science Information Site.
Immunoglobulins
Immunoglobulins = antibodies
In pharmacology we are interested in IgA, IgM, IgG, and IgE.
IgA is found in all body secretions and excretions.
IgM and IgG are involved in two major reactions:
- immune complex or toxic complex
- cytolytic or cytotoxic reactions
Immune Complex reactions involved IgG or IgM interacting with the antigen - precipitating - and producing crystals that can damage linings of blood vessels and crystallize in joints.
Cytolytic reactions involve the antigen becoming part of a cell - IgG or IgM interact with the antigen - causing the cell to lyse.
If a drug is the antigen, the following statement type will be presented in the PDR.
This drug may cause thrombocytopenia, agranulocytosis or hemolytic anemia. Referring to lysis of platelets, white blood cells and red blood cells respectively.
The IgE reaction sequence is referred to as anaphylaticoid reactions. They can produce skin reactions, asthma, or migrane headaches.
The antigen interacts with either mast cells or the circulating mast cells - the basophils. When IgE interacts with the antigen the mast cells and/or basophils release various mediators of inflammation.
The best known mediator of inflammation is histamine but there are many others including:
SRS-A = slow releasing or reacting substance of anaphylaxis;
ECF-A = eosinophil chemotactic factor of anaphylaxis;
BK-A = basophil kallikrein of anaphylaxis - forms bradykinin;
PAF = platelet activating factor of anaphylaxis;
NCF-A = neutrophil chmotactic factor of anaphylaxis.
Platelets can be activated by PAF - causing them to release a form of prostaglandin called thromboxane TxA2.
Prostaglandins
PGE versus PGF were first major types of prostaglandins developed from research of U.S. von Euler.
They typically produce opposite effects:
PGE - relaxes bronchial tree muscles; vasodilates; relaxes uterine muscle
while
PGF - constricts bronchial tree muscles; vasoconstricts; contracts uterine muscle.
The other two major prostaglandins are thromboxane or TxA2 (produced by platelets) and prostacyclin or PGI 2 produced by blood vessel walls.
arachidonic acid produces an endoperoxide PGH 2 via enzyme cyclooxygenase.
PGH 2 in platelets under influence of the enzyme thromboxane synthetase is converted into thromboxane (TxA2).
PGH 2 in blood vessel walls under influence of the enzyme prostacyclin synthetase is converted into prostacyclin (PGI 2 or PGX).
Thromboxane:
- increases cyclic GMP
- decreases cyclic AMP
- promotes platelet aggregation
- vasoconstricts blood vessels
Prostacyclin:
- decreases cyclic GMP
- increases cyclic AMP
- decreases platelet aggregation
- vasodilates blood vessels
Thromboxane can be picked up by blood vessel walls and is converted into prostacyclin.
Steroids - like cortisone - inhibit formation of TxA 2 = anti inflammatory and anti platelet aggregation actions.
Aspirin and other NSAID's inhibit cyclooxygenases and prostacylcin synthetase.
Dipyridamole (Persantine) potentiates PGI 2 action and inhibits phosphodiesterase which increases cyclic AMP and this results in actions of decreased platelet aggregation, vasodilation, bronchial relaxation.
