Pharmacodynamics Flashcards
Viagra
MOA
Biochem : phosphodiesterase 5 inhibitors
physio: relax vascular smooth muscle
*Penile precapillary sphincters open
*blood engorgrment
*organs effects : penile erection
*indications (registered ) ; ED erectile dysfunction
*ED caused psycho , physio ,patho
*Adverse effects : blue flashing light - retinal PDE
*Side effects :
vasodilation ,headache ,low BP ( by causes venous dilation )
Types of drug classes
- Non-specific physiochemical / physical
* antacids - pH
* general anaesthetics -propofol
- ethanol - Enzyme inhibitors / stimulators
* Acetyl cholinesterase inhibitors
* Proton pum inhibitors
* ACE inhibitors
* COX inhibitors (asprin )
* phosphodiesterase 5 inhibitors - Antimetabilites
* Antimicrobials
* Selective toxicity on bacteria
* resistance
* systemic side effects - Synthesis ,storage ,reuptake ,metabolism ,neurotransmitters
* reuptake inhibitors eg cocain ,antidepressant’s
* Storage release stimulators : amphetamines’
* substrate for endogenous
* neurotransmitters eg levodopa (dopamine for pD)
* Rasigeline : inhibit MOA in dopaminergic neurons - Ligand channel modulators
* Calcium channel blockers - CVs
* Local anesthetics ( Na+ channel block )
* Sulphonylurea - diabetes - Agonists and receptors
interaction
*Ligand -gated receptors( Neuromuscular end plate ,,Ach is released by a presynaptic neuron which stimualte nicotinic receptors ,which is bound to a ER> release Ca2+> binds to troponin > contraction ) drugs like ACh -esterase inhibitors (neostigmine ), Neuromuscular blocker (tuborcurare)
*Nuclear transcription
(linked to slow onset of action of lipophilic hormones , protein enzyme synthesised ,corticosteriods ,thyroid ,vit D)
*Tyrosine kinase
eg insulin
*Second messenger linked to ligand bind receptors .
beta-1- receptors (NE) > GTP activates G protein > adenyl cyclase linked > ATP > increase in cAMP > increase in HR and SV > CO
*Agonists and receptors
> Mimic endogenous hormones’ and neurotransmitters ,with a higher affinity for receptors to bring about physiological changes
Types of antagonists
1.Competitive
*blocks the effect of endogenous agonists
*Where is the receptors located ?
*prevents production of second messengers and stops normal physiological processes .
*They may be reversible by increasing [] of agonists thus overcoming the block of antagonists .
shifts the curve to the right
*maximal efficacy is unchanged
- Non-competitive antagonists
*Binds irreversibly therefore increasing [] does not overcome block .This block of the non-competitive antagonist blocks the effect of the endogenous agonist thus decreasing maximal efficacy and affinity of unbound drug ids the same
> to overcome this , new receptors must be made - Partial agonists
* At low doses simulates receptors and at higher doses acts as an antagonist ,blocking the effect of endogenous agonists .A subminimum second messengers are produced
