Science / Dr. Smith's Final Drugs

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

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

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