P4 Flashcards
Hydroxocobalamin
A synthetic form of Vitamin B12 (a coenzyme)
MoA: Vitamin B12 acts as a coenzyme for various metabolic functions, including fat and carbohydrate metabolism and protein synthesis. As such it is important in growth, cell proliferation as well as myelin synthesis.
Therefore deficiency of vitamin B12 can cause neurological lesions. Methylcobalamin, however is required for the metabolism of folic acid, deficiency of which leads to reduced DNA synthesis.
Ferrous sulphate
Iron supplement
Use: Ferrous Sulphate is taken in order to replace body iron and therefore maintain red blood cell production. If the patient is lacking iron, this can lead to iron-deficiency anaemia
Folic acid
Member of the vitamin B family (DNA precursor
MoA: Folic acid, is converted to tetrahydrofolic acid and methyltetrahydrofolate by dihydrofolate reductase. Tetrahydrofolic acid and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis, as they are required to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids, methylate tRNA, and generate and use formate
Use: Treatment and prevention of folate deficiencies and megaloblastic anaemia
Azathioprine
Antagonist of purine metabolism
MoA: Probably incorporation of thiopurine analogues into the DNA structure, causing chain termination and cytotoxicity. Its most severe side effect is bone marrow suppression, and it should not be given in conjunction with purine analogues such as allopurinol.
Use: Azathioprine acts to inhibit purine synthesis, and therefore inhibit DNA and RNA synthesis leading to an inhibition of cell proliferation. It is used to treat auto-immune diseases, and also transplant recipients.
Note: Blood tests and monitoring for signs of myelosuppression are essential in long-term treatment with azathioprine
Cyclosporin
An immunosuppressive agent (A cyclophilin binder)
MoA: It binds to cyclophilin, which causes the inhibition of calcineurin, which is responsible for activating the transcription of IL-2. This causes a reversible inhibition of immunocompetent lymphocytes, in the G0 or G1 phase of the cell cycle. T-lymphocytes are preferentially inhibited, with the T1-helper lymphocyte is the main target, although it may also inhibit the T1-suppressor cell
Use: Cyclosporin is used as an immunosuppressive agent, used for the prophylaxis of graft rejection in organ and tissue transplantation
Clopidogrel
P2Y12 antagonist
Clopidogrel is an anti-platelet therapy agent.
It is a prodrug, and requires metabolism by CYP450 enzymes to produce the active metabolite.
MoA: irreversible blocking of the P2Y12 receptor, and thereby blocking the binding site of ADP. ADP is both a direct platelet agonist, and is also secreted by the platelet and acts as a secondary agonist that is critical to complete platelet activation. As a consequence the activation of the GPIIb/IIIa receptor is reduced leading to a reduction in fibrinogen binding and thrombus formation.
Lepirudin
An anti-thrombin agent
MoA: Lepirudin is a recombinant form of hirudin. It is a highly potent, selective agent that forms a stable non-covalent complex with thrombin, preventing fibrinogen cleavage and initiation of the clotting cascade.
Note: It was withdrawn and replaced with Dabigatran (direct thrombin inhibitor) or Apixaban (A factor Xa inhibitor).
Tetanus booster
A vaccination therapy
MoA: The vaccine contains inactive vaccine, which induces a weaker immune response, and as such there is a need for a booster injection.
An inactive vaccine contains virus/bacterial particles which are grown in the lab, but that have been killed using either heat or formaldehyde. In active vaccines can be subdivided into whole virus, split virus or subunit virus vaccinations. In this case the booster should be given every ten years, although can be given within 2 days or the patient’s injury
Warfarin and pregnancy
Warfarin can cross the placental barrier during pregnancy resulting in foetal bleeding, spontaneous abortion, and neonatal death.
Adrenaline
Adrenoreceptor agonist
MoA: Stimulation of alpha, beta-1 and beta-2 adrenergic receptors. Its effects on adrenergic receptors lead to reductions in vasodilation and increased vascular permeability that occurs during anaphylaxis. Its actions on -adrenergic receptors cause bronchial smooth muscle relaxation, and help to alleviate bronchospasm
Chlorphenamine
H1 histamine receptor inverse agonist
MoA: Chlorphenamine binds to the histamine H1 receptor, blocking its activity. Chlorphenamine cometes with histamine for binding to the H1 receptor.
MoA: Temporary relief of the effects of histamine, such as sneezing, watery and itchy eyes, and runny nose due to hay fever
Diclofenac
A COX inhibitor
NSAID
As such it has analgesic due to the inhibition of both COX-1 and COX2 enzymes.
Hydrocortisone
A glucocorticoid nuclear receptor agonist
MoA: Hydrocortisone binds to the cortisol receptor forming a receptor-ligand complex, which translocates to the nucleus, binds to glucocorticoid response elements (GRE) in the promoter region of the target genes, causing the increase in their expression. Corticosteroids are thought to cause the expression of lipocortins, which inhibit phospholipase A2, thereby reducing arachidonic acid synthesis and production of inflammatory mediators.
