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45 Cards in this Set
- Front
- Back
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What is Selective Toxicity? |
• Directly target specic structures/processes of the pathogen • Produgs which are activated by pathogens • Drugs which are inactivated by host cells |
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Explain Red squill rodenticides as an example of Antiratties |
Red squill rodenticides as a cardiac glycoside is toxic to all mammals. Because rats cannot vomit, they are susceptible to the toxic effect. |
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Explain sulphanilamide as an example of antibiotics. |
Sulphanilamide is the precursor of p-aminobenzoic acid(PABA) .It works better when combined with trimethoprim It inhibits essential bacterial metabolismby inhibiting bacterial synthesis of folic acid. Selective due to bacterial synthesis of folic acid is different from human's. |
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Explain the mechanism of Penicillin(antibiotic), and why it is selective to bacteria. |
binds(inhibit) D-alanine of transpeptidase, and thereby inhibiting synthesis of bacterial cell walls The Selectivity is due to: • No cell walls in humans • No transpeptidase-like enzymes in humans • no D-amino acids present in humans, only L-amino acids. |
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Whata are some side effects of penicillin? |
•relatively few because of high selectivity • GI disturbances mediated by its primary action (i.e. on-target) • Excitatory in high concentrations in CNS (off-target) • Sometimes allergenic (off-target) |
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What are some shortcomings of penicillin? |
1. Poorly absorbed after oral administration 2. Short half life, due to actively secreted in urine. 3. Resistance developed by bacteria.( by mechanisms such as enzyme cleaving the drug, extra penecillin binding sites and impermeant wall) |
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Explain how β-lactamase (penicillinase) as an examle of bacterial resistance to penecillin. |
β-lactamase cleave penecillin into penicillonic acid(inactive) This enzyme can be inhibited by clavuanic acid(i.e. amaoxycillin + clavulanate) |
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Explain the mechanism of chloramphenicol(antibiotic), and why is it selective |
Interferes with protein synthesis, by binding to 50S ribosomes and prevents tRNA binding The selectivity is due to human are 80S and 70S ribosomes |
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What are some shortcomings of chloramphenicol? |
1. Interfere action of penecillin 2. Can inhibit mammalian mitochondrial protein synthesis(particularly bone marrow) 3. Unwanted actions limit its use |
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What does Insecticides try to target? |
the order Hemiptera, true bugs
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Explain the mechanism of insecticides? |
Increase opening of insect Na+ channels |
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What are some examples of insecticides? |
DDT, chlordane, dieldrin |
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What are some side effects of insecticides? |
1. High lipid solubility, stay in food chain 2. Disappearance of songbirds, due to reduced insect population 3. Loos of fish-eating birds, due to thinning of eggshells. This thinning is induced by altered steroid hormone metabolsim |
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What is acyclovir, and what happens when it enter the cell. (also explain how the selectivity is achieved) |
Acyclovir is a guanosine derivatived antiviral targeting antiviral.(espically for herpes viruses) When enter the cell, it will be phosphorylated by thymidine kinase. Selectivity is achieved since only infected cells has thymidine kinase for initial conversion for virus. |
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What is the mechanism of acyclovir? |
Resembles a nucleoside triphosphate →acyclovir triphosphate inhibits DNA polymerase |
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Explain what happens to zidovudine when it enters infected cell, and the mechanism of action. |
It is phosphorylated to triphosphate Resembles a nucleoside triphosphate, and incorporate into proviral DNA by viral reverse transcripase. |
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How is the selectivity of zidovudine achieved? |
Used by viral reverse transcriptase rather than host DNA polymerase. Note that mitochondrial DNA polymerase is sensitive as well(side effect) |
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Explain the mechanism of squinavir. |
targets HIV cleavage of poly-proteins into separate capsid proteins and viral enzymes.(maturation) |
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How is the selectivity of squinavir achieved? |
target proteases with distinct Phe-Pro turn substrate requirement, which is absent in mammalian enzymes |
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What side effect does squinavir, and how is it special? |
changes in fat distribution (buffalo hump) It is unrelated to primary action |
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What is amphotericin, and how does it work |
ring-shaped molecule binds to and forms pores in ergosterol cell membranes, and used to treat systemic fungal infections |
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How is the selectivity of amphotericin achieved? |
mammalian membranes containing cholesterol instead of ergosterol |
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Explain the mechanism of ketoconazole. |
inhibits CytP34, inhibiting ergosterol synthesis Fungistatic, thereby do not kill the fungi(long action) |
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What are the side effcts of ketoconazole. |
Cannot be used systemically as will target human Cyt families Relatively toxic and interacts with many drugs |
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Explain the mechanism of terbinafine. |
inhibits fungal enzyme squalene epoxidase, Squalene accumulation results in fungal cell death (much fater action in comparsion to ketoconazole) |
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Explain the mechanism of glyphosate herbicide. |
herbicidal analogue of glycine which inhibits amino acid synthesis Very safe and effective as toxicity expressed slowly |
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How is the selectivity of glyphosate herbicide achieved? |
amino acid synthesis essential in plants as they are autotrophic - no dietary amino acids Human can eat these amino acids |
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Explain the mechanism of paraquat herbicide |
non-selective herbicidal prodrug activated by reduction to radical form, producing ROS which destroy cell membranes via lipid peroxidation Activation via electron transfer from photosynthetic electron transport pathway to paraquat Each paraquat molecule can be repeatedly activated |
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What are some side effects caused by paraquat herbicide. |
electron transport chain present in mammalian cells, making them susceptible Selective uptake by alveolar epithelial cells results in lung damage |
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Explain the mechanism of metyorexate, and how is the selectivity achieved? |
inhibits dihydrofolate reductase, disrupting DNA synthesis Selectivity: actively dividing cells which undergo more frequent folate metabolism |
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Explain the mechanism of Paclitaxel, and how the selectivity is achieved. |
binds to polymerised tubulin, preventing disassembly of microtubules Leads to failure of cell division and cell death Selectivity: actively dividing cells, as these have large quantities of polymerised tubulin! |
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Explain the mechanism of Tamoxifen, and how the selectivity is achieved. |
partial agonist/antagonist of oestrogen Reduces expression of oestrogen - useful in treatment of oestrogen-dependent cancers (e.g. breast cancer) electivity: cells which utilise oestrogen |
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Explain the mechanism of Imatinib, and how the selectivity is achieved. |
Inhibits BCR-ABL, a faulty tyrosine kinase which causes chronic myeloid leukemia Selectivity: non-selective binding to mutant tyrosine kinases, able to be utilised in the treatment of many cancers |
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What is venom, and what is it usually mixture of? |
Biological substance made by specialised glands of animals( i.e.salivary glands, skin secretory glands ) , and delivered by specialised apparatus. Usually complex mixture of proteins or peptides |
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How is posion different from venom? |
poison is not produced by specialised gland and doesn't delivered by specialised apparatus |
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Which kind of species has a distictive microbiologic toxins? |
Marine |
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What do venoms and poisons both contain of? |
Venoms and poisons can all contain toxins |
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What can venoms be used for |
Defence - Immobilize prey - Digestion |
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Are toxins new versions of genes? |
No. Many toxins represent mutated versions of otherwise common endogenous genes |
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What are some effects caused by venom? |
Pain Inflammation Paralysis/neurologic dysfunction Coagulation disturbance Cardiovascular effects Tissue destruction (skin, muscle) |
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Do venom toxins have high MW? |
May be high or low molecular weight |
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Do venom toxins act specifically?
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May be broadly acting or very specific |
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Describe the mechanism of action of venom toxins, and give 3 examples. |
May be enzymatic in action or a simple receptor agonist/antagonist or have multiple actions - Prothrombin activators: eg Oscutarin from taipan venom - NAchR antagonists: eg Death Adder short chain neurotoxins acting post-junctionally - Notexin (tiger snake) and Taipoxin (taipan) = Phospholipases: PPLA2, which hydrolyses cell membrane phospholipids acting both presynaptically and on tissues (myolysis) |
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How to manage a snakebite? |
First Aid: Pressure-Immobilisation bandaging - Transfer to facility with: Laboratory, Adequate antivenom supplies, Physician and facilities capable of treating envenoming and anaphylaxis |
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How to Diagnose snakebite? |
SVDK Varies corresponding antibodies in the wells in the kits, put in sample of solutions of bite sites or urine, detection of free venoms, cross linking, colour changes |
