What drugs do to the body

1. PHARMACODYNAMICS
Sites of drug action :-
- Understanding of the depth of information of the
drug action is necessary to achieve :
- A suitable comparison of the relative benefits
and risks of alternative drugs on selection .
- A prediction of possible problems in a patient
due to other disease processes or other drugs .
- Drugs may have :
- Non-specific generalized effect via response in
organs with their highest concentrations ( volume of
distribution ) .

2. - Specific-site effects via interactions of drugs with
specific site (s) – one type of receptor families or more-i.e.
selective drugs ( e.g.a β adrenceptive drug has high
affinity for all β adrenergic receptors ) or non selective ( if
it has affinity for all adrenergic receptors ) .It could also
exhibit selectivity amongst the selected receptors (
β1adrenoceptors and not β2 adrenoceptors ) .
- Specifity is reciprocal i.e. individual classes of drugs
bind only to certain targets and individual targets
recognize only certain classes of the drug .
- Specifity may either be :
- Biological ( receptor specifity e.g. ethanol causes
smooth muscle contraction , but relaxation of vascular
smooth muscles ; stimulation of gastric juice secretion ,
but not the salivary secretion ) .
- Chemical due to the chemical of the chemical
struture

3. DRUG SPECIFITY:
I/ BIOLOGICAL ( RECEPTOR-SPECIFITY
):
e.g. ETHANOL PRODUCES INHIBITORY
EFFECT ON MOST CELLS AND TISSUES (
CONTRACTION OF SMOOTH MUSCLES ,
BUT RELAXATION OF THE VASCULAR
SMOOTH MUSCLES AND STIMULATION
OF GASTRIC SECRETION EXCEPT THE
SALIVARY SECRETION.

4. II/CHEMICAL (STEREOSELECTIVITY) :
e.g. HISTAMINE EFFECT BASED ON
MARKED DIFFERENCE BETWEEN
ENANTIOMERIC CHEMICAL STRUCTURE
DUE TO PHARMACOLOGICAL ACTIVITY.
TARGETS FOR DRUG ACTION :
MOST DRUGS ARE EFFECTIVE BECAUSE

5. Drug antagonism :
It is the complete or partial abolishment of a
drug action in the presence of another drug .
It is classified into :
i/ Chemical antagonism :-
This occurs when two substance combine in
solution , so the effect of the active drug is lost (
e.g. inactivation of heavy metals by a chelating
agent like dimercaprol which binds the metal
ion tightly to form an inactive complex .

6. ii/ Pharmacokinetic antagonism :-
This occurs when the antagonist effectively
reduces the concentration of the active drug at
its site of action by :-
a/ Reducing the rate of absorption of the active
drug from the GIT ( e.g. tetracycline and milk ).
b/ Increasing the rate of metabolic degradation
of the active drug ( e.g. reduction of the
anticoagulant effect of warfarin by increasing its
hepatic metabolism by phenobarbitone ) .
c/ Increased renal excretion ( e.g. aspirin and
sodium bicarbonate ) .

7. iii/ Competative Antagonism :-
By receptor-blocking (e.g.for an agonist A and an
antagonist B :
PA = XA / (XA + KA ) = 1- PB ( here B is non
surmountable ) .
iv/ Non-competative antagonism :-
This occurs when the antagonist blocks at some
point of the chain that lead to the production of a
response by the agonist ( e.g. verapamil and
nifedipine prevent the flux of calcium ions through
the cell membrane and hence block the contraction
of smooth muscle produced by other drugs . This
will reduce the slope of the agonist on the DRC .

8. v/ Physiological antagonism :-
This occurs when the interaction of two
drugs in the body tend to cancel each other (
e.g.noradrenaline rises arterial blood
pressure by acting on the heart and
peripheral circulation , while histamine
lowers arterial blood pressure by causing
vasodilation ) .It is not well demarcated
from non-competitive antagonism .