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Summary Bradykinin explained

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I want to help you get through all the different drug classes in Pharmacology. I have found that students struggle to get through the amount of work. These summaries helped me get through my Honours Degree. I will soon graduate with my Masters of Science in Neurogenetics. You got this!

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  • June 19, 2019
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  • 2014/2015
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PRINCIPLE 1: BINDING
 Specific targets of drug action
 Drug action is explained in terms of CONVENTIONAL
CHEMICAL INTERACTIONS
 Low [D] still involve large numbers of molecules
 Avogadro’s number = number of molecules found in 1 mole
of a substance
 1 drop of a [D] = 10-10 mol/l contains 1010 drug molecules

 Drug molecules must get so CLOSE to other molecules
that they exert a CHEMICAL INFLUENCE on them

 Drug distribution = at random,
interaction (with particular cellular molecule) = negligble
D/R INTERACTION:
 Depends on [D] and [R]
 D-R amount determines the RESPONSE MAGNITUDE
 Threshold: minimum number of D-R complexes 
response
↑ [D]  ↑D-R  ↑ EFFECT
SATURATION = NO FURTHER ↑R
 LAW OF MASS ACTION APPLIES TO D-R INTERACTION
 A DRUG WILL NOT WORK UNLESS IT IS BOUND!!

, TARGETS OF DRUG ACTION:
1) SIMPLE CHEMICAL NEUTRALISATION - antacid
2) ENZYME INHIBITORS – antibiotics
o Inhibitor  normal reaction INHIBITED
o False substrate  ABNORMAL METABOLITE produced
o Pro-drug  ACTIVE drug produced
3) R OCCUPYING DRUGS – related to NTs
o Agonist  direct  ion channel OPENING/CLOSING
o Agonist  transduction  Enzyme +/-, ion channel
modulation, DNA transcription

o Antagonist  NO EFFECT, endogenous mediators BLOCKED

4) MODULATORS OF CERTAIN TRANSPORT SYSTEMS –
Na+/K+-ATPase

o NORMAL TRANSPORT
o Inhibitor  transport BLOCKED
o False substrate  ABNORMAL COMPUNDS accumulate

5) ION CHANNEL INTERACTION – local anesthetics

o Blockers  permeation BLOCKED
o Modulators  ↑/↓ opening

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