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18 Cards in this Set
- Front
- Back
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Why for a normal person do you not want to enhance immunity |
Autoimmunity and hypersensitivity of immune system |
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What strategies do we use for immunosuppresion |
False metabolites Alkylating agents Inhibitors of nucleotide synthesis |
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What’s responsible for transplant rejection, whats our target |
T cells; so we want at cell proliferation to stop So cytotoxic- kill the cells |
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Most strategies are targetted at what |
DNA replication step If the cell cant replicate DNA it will die |
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What are some of the effects of using non specific immunosuppression and why? |
Putting a cytotoxic drug into the cell it wont just kill cells you want i.e fast replicating cells Hair loss-hair follicles have a high turnover Gastrointestinal damage- length of the gut has cells with high turnover Skin damage- skin cells have high turnover |
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Example of a false metabolite |
Azathioprine(imuran) Cant do anything but the conversion of it to 6-mercaptopurine |
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What is a pro drug |
Biologically inactive compound which can be metabolised in the body to produce a drug |
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Why is azathioprine a pro drug |
Take azathioprine orally, so when taken the first cells in the gut arent exposed to cytotoxic compound. Why we can tolerate azathioprine and its converted into 6-mercaptopurine in the blood |
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Pathway of 6-mercaptopurine into cell death |
6-mp in blood can be incorporated into purine synthesis which is a false metabolite and lead to cell death |
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What else can happen to 6-mercaptopurine |
The metabolic pathway can make xanthine oxidase which will metabolise 6-MP to thiobarbituric acid which is highly polar so going to the kidney and gets excreted through urine very quickly In order to keep 6-MP up you give patients allopurinol which inhibits xanthine oxidase and keeps 6-MP In the blood |
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Explain cyclophosphamide |
Alkylating agent Nitrogen mustard, two chloride atoms at the end of the molecule- chlorine is highly reactive because it has high electronegativity |
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What part of cyclophosphamide gets converted and how does it get to active form |
Front ent of drug gets converted Liver metabolises cyclophosphamide into 4-OH-cpa , this spontaneous converts and opens up to active form that’s highly reactive- aldophosphamide Aldophosphamide can become inactive form and its excreted |
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What does aldophosphamide do |
As DNA is unwinding the reactive chloride centres become expose and its what chloride binds to the two N7 nitrogej in the guanosine covalently binds to the chloride and stops it from seperating because the net charge on the nitrogen is positive and negative chloride ion reacts with it |
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What is mycophenolic acid |
Inhibitors of nucleotides |
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What is mycophenolic acid delivered as |
Pro drug mycophenolate mofetile. Given to patients and then its broken down and hydrolysed into MPA which is the active inhibitor of nucleotide synthesis |
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How does mycophenolic acid work |
Non competitive enzyme inhibitor Allosteric regulator of activity |
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What is mycophenolic acids target and what does this mean |
Usually inosine binds to IMP dehydrogenase making guansosine to make DNA. Mycophenolic acids blocks imp dehydrogenase enzyme(target) so no guanosine can be made to make dna |
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Where does mpa bind wnd what does this do |
Binds to allosteric site as its a allosteric regulator of activity It regulated the shape of active site and when it binds it changes the active sites shape so it cant bind |
