Dr. Smith's Final Drugs

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Can you name the Dr. Smith's Final Drugs?

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DescriptionDrug
Blocks electron flow from cytochrome bH to ubiquinone.
the committed step of its reaction is the inhibition of the conversion of PRPP into PR-amine
Side effects: gastrointestinal problems due to fermentation of carbohydrates in large intestines and water holding capacity of the disaccharides.
Suicide inhibitor; is converted into FdUMP and forms a covalent intermediate with thymidylate synthase that cannot be reversed
Has a modified sugar which has 2 fluorine atoms at the 2' position rather than 2 hyrdogens. Can be twice phosphorylated by deoxycytidine kinase and then dCMP kinase and acts as a s
structure similar to dihydrofolate, thus can be a competitive inhibitor of dihydrofolate reductase.
Binds bacterial/protozoal dihydrofolate reductase proteins 10^5 more tightly than human DHFR
converted to the deoxynucleotide, which inhibits cell division.
Used in treatment of inflammatory bowel disease.
decrease efficiency of fat-soluble vitamin absorption due to their effect on bile acids.
Phosphorylated by viral encoded thymidine kinase but not human thymidine kinase. Only infected cells efficiently phosphorylate the drugs, which then inhibit DNA replication
It catalyzes the conversion of arachidonic acid to prostaglandins
inhibits cell division in a similar manner as 6-mercaptopurine and is also inactivated by thiopurine methyltranserfase
competitively inhibiting HMG CoA reductase to inhibit endogenous cholesterol synthesis
Anticoagulant, similar to warfarin, which prevents the formation to carboxyglutamate in prothrombin.
Common treatment for methemoglobinemia
If this drug is dosed >7mg/kg, then it becomes an oxidant
a prodrug of mycophenolic acid (MPA)
Inhibits cyclooxygenase by acetylating the serine residue that lies along the path to the active site and blocks the channel
Anticancer and rheumatoid arthritis agent that affects both DNA synthesis and de novo purine synthesis
Inactivated by xanthine oxidase and thiopurine methyltransferase (TPMT).
Relieves symptoms of gout
Bind bile acids, thus decrease absorption of exogenous (dietary) cholesterol.
Inhibits inducible nitric oxide synthase
DescriptionDrug
similar structure to vitamin K and competitively inhibits carboxylase.
Large, bulky molecules;unable to bind to COX-1
Combined antibiotic - sulfamethoxazole and trimethoprim
Inhibits TMP production by preventing the regeneration of methylene-THF; used as an anticancer agent and in the treatment of rheumatoid arthritis
Increases cytochrome b5 reductase
Associated with inflammation, cancer, colitis, and arthritis
Its mechanism is to increase glutathione levels by supplying cysteine for the synthesis of glutathione
Inhibits the electron flow from the Fe-S centers of Complex I to ubiquinone, thus blocking oxidative phosphorylation
Converted to alloxanthine which binds tightly with xanthine oxidase, which decreases urate production and xanthine and hypoxanthine concentrations rise
Anti-coagulant, binds to ant-thrombin which leads to a conformation change allowing anti-thrombin to bind to thrombin, which inactivates it, inhibiting the activation of fibrinogen
Nucleotide analog of deoxcycytidine used in treatment of pancreatic cancer
Inhibits bacterial synthesis of folate
Antibiotic that directly binds to ATP synthase and inhibits both ATP synthesis and the transfer of electrons through the electron transport chain
Drug used to treat sickle cell disease
Anti cancer drug, can block the synthesis of thymidylate
It binds to the toxic metabolite (forming mercapturic acid) for excretion in the urine
Works by increasing the blood concentration of fetal hemoglobin
An alpha-glucosidase inhibitor. It delays carbohydrate digestion in the small intestines and thus decreases blood glucose in Diabetics (type II)
Binds at ubiquinone binding site that is close to cytochrome bH on the matrix side membrane
prodrug of 6-mercaptopurine
cytostatic against lymphocytes which almost entirely lack purine salvage and depend on de novo pathway for purines
Marketed by Roche as CellCept(R)
Induces hemolysis in patients with glucose 6-phosphate dehydrogenase deficiency
Inhibits the production of prostaglandins;irreversible inhibitor
DescriptionDrug
Inhibits alpha-amylase, alpha-dextrinase, maltase, and sucrase
can also inhibit folate absorption by preventing the excess glutamates from being cleaved off
Herpes treatment
inhibits IMP dehydrogenase (IMP --> XMP [de novo pathway])
used as an immunosuppressant in organ transplants and in patients with inflammatory bowel disease
Inhibits oxidative phosphorylation by binding to one of the ubiquinone binding sites on Complex III
non-prescription form of Orlistat
An anti-inflammatory drug metabolized in the colon by intestinal bacteria to produce 5-aminosalicylic acid
Competitively inhibits dihydrofolate reductase and prevents the regeneration of tetrahydrofolate
Covalently binds to transpeptidase thus prevents synthesis of bacterial cell walls. Suicide inhibitor.
Inhibitor of pancreatic lipase, side effects are GI problems
Vasodilator which releases NO
Suicide inhibitor of xanthine oxidase
Phosphorylated by human kinases but selectively interfere with viral replication. Both have modified sugars that lack 3; OH group and in effect terminates DNA synthesis
Carboxylation of glutamate to carboxyglutamate in prothrombin requires the enzyme ________ and cofactor _________
Selective COX-2 inhibitor
Is converted to fluorodeoxyuridylate (has a similar structure to deoxyuridylate), which irreversibly inhibits thymidylate synthase - suicide inhibition.
prevents the necessary 1,3 hydride shift to reduce the CH2 to CH3 on methylenetetrahyrdofolate
peroxynitrite [ONOO-] scavenging compound
inhibitor of pancreatic lipase
Used to treat acetaminophen overdose
Analog of uracil used to treat breast and colorectal cancer.

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