Reasons why patients might respond differently to medicines
Disease Interactions Renal/Liver Function Age Resistances Genetics Ethnicity
***DO NOT MEMORISE AT ALL
Polymorphisms
Discontinuous genetic variation resulting in the occurrence of genes/bases
- Single Nucleotide Polymorphism
- Mutations leading to aa substitutions
Activation and Deactivation Drugs
Deactivation - Drugs to inactivate metabolite
Activation - Pro-drug to activate metabolite
Codeine on those with Chinese ethnicity
Chinese patients are more likely to be unable to metabolise codeine into its active form morphine since the drug requires metabolic conversion - patients do not benefit
Effects of metabolism on Tamoxifen
It is a drug to treat lower oestrogen levels (I think)
In poor metabolisers, impaired conversion to active agonist may be noticed and the drug does not do much
Resistance to Clopidogrel
Patients with heterozygous variant may need higher dose while those of homozygous of certain allele entirely do not respond
Anti-platelet med
Risk of clopidogrel’s poor metabolism
It is used in stenting to prevent the formation of a thrombus, so if it is ineffective, a thrombus is more likely to form
Why is warfarin dosage so individual to the patient
There are two competing genetic variations/polymorphisms so clearance is so significantly affected that it cannot be easily standardised
DONT WORRY ABOUT THIS LECTURE, ITS MORE IMPORTANT TO BE VAGUELY AWARE OF THE CONTENT THAN TO ACTUALLY DEEP THE CONTENT
