USU Pharm Lec 61-62 Word Scramble
|
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
| Question | Answer |
| Iodoquinol* is used to treat what | E. histolytica, only useful in treatment of intestinal amebiasis |
| Mechanism of action of Iodoquinol* | liberates iodine which is the active amebicide |
| What is the pharmacology of Iodoquinol* | not readily absorbed from GI tract so it is effective in treating intestinal infections |
| Side effects of Iodoquinol* | Low dose: headache, diarrhea, nausea, vomiting, skin rashes, anal puritis, and slight thyroid enlargement in some. High dose: causes loss of visual acuity, optical atrophy and blindness |
| What is Paromomycin* used to treat | useflul only in the treatment of intestinal amebiasis and some intestinal cestode infections |
| What is the mechanism of action of Paromomycin* | It acts on protein synthesis by binding to the 16S ribosomal RNA of the 30S ribosomal subunit, it is an aminoglycoside antibiotic |
| What is the pharmacology of Paromomycin* | Poorly absorbed from the intestine. |
| What are the side effects of Paromomycin* | Main side effects are diarrhea and abdominal pain, and sometimes nausea or dizziness. It can also alter bowel bacteral population and a GI superinfection can be a problem. |
| Drugs used to treat asymptomatic or mild intestinal only amebiasis | Iodoquinol*, Paromomycin* |
| Drugs used to treat Mixed amebicides | Metronidazole* for the systemic infection, with Diloxanide furoate or Iodoquinol* to treat the intestinal infection. |
| What is used to treat Cryptosporidium: a water-borne coccidian protozoan that causes diarrhea | Nitazoxanide* is about 80% effective and is approved for treatment of children over 12 months. |
| What is used to treat Cyclospora cayetanensis: causes diarrhea in AIDS patients | Trimethoprim-sulfamethoxazole (TMP/SMX)* |
| What is used to treat Giardia lamblia: cause of traveler's diarrhea from water contamination | Metronidazole*, 85-90% effective (Not FDA apporved). Nitazoxanide* is available in a pediatric liquid suspension. Paromomycin* should be used to treat pregnant women. |
| What is used to treat Isospora belli: tropical cause of diarrhea | Trimethoprim-sulfamethoxazole (TMP/SMX)* |
| What is used to treat Trichomonas vaginalis: The common pathogen of the urogenital tract | Metronidazole*. periodic vinegar douches in women can restore the protective acidic environment of the vagina (T vaginalis can't survive a pH below 4.9) |
| Metronidazole* is used to treat what | E. histolytica, T. vaginalis, G. lamblia, and anaerobic bacteria such as Clostridia and Bactreoides |
| What is the mechanism of action of Metronidazole* | It acts as electron sink to prevent the terminal electron transport system from re-oxidizing NADH and NADPH in anaerobic and microaeorophilic organisms. Once reduced Metronidazole is toxic and can introduce DNA strand modifications |
| What is the pharmacology of Metronidazole* | well absorbed by the GI tract, extensively metabolized (metabolite are mutagenic), eliminated by the kidneys |
| What are the side effects of Metronidazole* | GI upset, metallic taste. DISULFIRAM-like effect if taken within 24 hrs of EtOH consumption. Rarely,nervous system toxicities: weakness, paresthesias, vertigo, and ataxia. Avoid in pregnancy carcinogenic/teratogenic in animals mutagenic in bacteria |
| What is Nitazoxanide* used to treat | FDA approved to treat giardiasis and cryptosporidiosis in kids over 1. May be effective against other intestinal parasites including helminths. Good for Metronidazole resistant organism because it has a different mechanism |
| What is the mechanism of action of Nitazoxanide* | Inhibits parasties' pyruvate-ferredoxin oxidoreductase, which is essential in anaerobic energy metabolism. |
| What is the pharmacology of Nitazoxanide* | it is given in 3 oral doses, absorbed for GI tract and 1/3 of oral dose excreted in urine, 2/3 in feces. the active species is its metabolite tizoxanide which is liberated by hydrolysis in blood. |
| What is Tizoxanide | The active metabolite of Nitazoxanide* liberated by hydrolysis in the blood |
| What are the side effects of Nitazoxanide* | Very mild, not significantly different from placebo. No known drug interactions. Safety in pregnant or lactating women not proven. |
| What are the common diseases in AIDS patients | cryptosporidiosis, cyclosporiasis, isosporiasis, microsporidiosis, pneumocystis, toxoplasmosis |
| What is the treatment of choice for toxoplasmosis infections: can cause encephalitiis especially in HIV patients | Pyrimethamine* with sulfadizine*. (leucovorin to prevent pyrimethamine induced bone marrow suppression). Pregnant women should not take pyrimethamine*. |
| All patients on pyrimethamine* treatment must also take this | Leucovorin a folinic acid supplement to prevent bone marrow suppression. |
| What prophylactic treatment can be given for toxoplasma seropositive HIV patients with low CD4 counts | TMP/SMX* or Pyrimethamine*+Dapsone+Leucovorin. |
| What is the treatment for Pneumocystis jiroveci (PCP): which presents as a respiratory illness in immunocompromised individuals | TMP/SMX*, AIDS paitents have high rates of adverse reactions to this. Pentamidine isethionate* is a second line choice for those intolerant of TMP/SMZ* and have a mild illness. |
| What is the Prophylactic treatment of PCP | TMP/SMX* or inhalation of aerosolized Pentamidnie* |
| What is the mechanism of action of pyrimethamine* | Folate antagonist: blocks reduction of Dihydrofolic acid to Tetrahydrofolic acid |
| What is Atovaquone used to treat | Second line treatment of PCP, toxoplasmosis, and babesiosis. Also used for microsporidiasis in AIDS patients. |
| What is the mechanism of Atovaquone | An inhibitory analog of ubiquinone which interferes with mitochondrial electron transport and related processes |
| What is the pharmacology of Atovaquone | Not well absorbed so it is given with fat to aid absorptions. Half life is 2-3days. It isn't metabolize and is excreted unchanged. 99% is bound to plasma proteins. |
| What are the side effects of Atovaquone | Few which include: rash, fever, vomiting, and headache |
| What are 3 drugs that interfere with Folate and where do they act | Sulfonamides: Block the conversion of Pteridine*+PABA to dihydropteric acid, a precursor of dihydrofolic acid. Trimethoprim and Pyrimethamine* block the reduction of dihydrofolic acid to tetrahydrofolic acid |
| What are the sources of Folate | Food-> Folic acid-> Dihydrofolic acid-> Tetrahydrofolic acid. or Pteridine+PABA-> Dihydropteric acid-> Dihydrofolic acid-> Tetrahydrofolic acid |
| What is Pentamidine Isethionate* used to treat | Trypanosomiasis gambiense, Leishmania donovani (kala azar), Pneumocystis jiroveci |
| What is the mechanism of Pentamidine Isethionate* | Causes selective breaks in the kinetoplast mini-circle DNA of trypanosomes which disrupts DNA replication |
| What is the pharmacology of Pentamidine Isethionate* | Given i.m. or i.v., NOT well absorbed from the gut. Stored in tissues and excreted unchanged |
| What are the side effects of Pentamidine Isethionate* | Immediate effects: hypotension, tachycardia, dizziness, fainting, headaches and vomiting. Reversible renal and hepatic damage seen. Also, selectively toxic to pancreatic beta cells, causing insulin release and hypoglycemia, and eventually irreversible DM |
| What is the treatment for Babesia microti: transmitted by deer tick presents as hemolytic anemia with fever, weakness, jaundice, and hepatosplenomegaly | clindamycin and quinine |
| What is the treatment of African Trypanosomiasis (sleeping sickness): transmitted by tsetse fly | T. brucei gambiense(W. Africa): inital stage Pentamidine*, late stage Melarsoprol or Eflorinithine*. T. brucei rhodesiense(E. Africa): initial stage Suramin, late stage Melarsoprol |
| What is the treatment of choice for Trypanosomiasis meningoencephalitis | Melarsoprol because it crosses the blood brain barrier (But it is extreamly toxic so don't use if CNS uninfected) |
| What is the treatment of American Trypanosomiasis (Chagas Disease) caused by T. Cruzi: transmitted by blood-sucking triatomid bugs and causing cardiac myopathy and chronic GI disease | Nifurtimox and Benznidazole are used to treat acute infection and prevent chronic disease, but neither drug is effective against chronic infection. |
| What is the treatment of Leishmaniais: transmitted by the sandfly causing either visceral leishmaniasis, cutaneous leishmaaniasis, or mucocutaneous leishmaniasis | In the US Sodium Stibogluconate is the first line choice. Amphotericin B is a good second line drug for mucocutaneous or visceral leishmaniasis. Pentamidine* is a good second line choice for visceral leishmaniasis resistant to antimony. |
| What is Eflornithine* used to treat | Late stage trypanosomiasis |
| What is the mechanism of Eflornithine* | Suicide inhibitor of ornithine decarboxylase(key enzyme of polyamine biosynthesis and a requisite for DNA synthesis and cell replication). It has a 10 fold greater affinity for the parasite enzyme than for the host enzyme |
| What is the pharmacology of Eflornithine* | associated with the disappearance of trypanosomes from body fluids, sometimes within one day |
| What are the side effects of Eflornithine* | Generally well-tolerated but can cause diarrhea, abdominal pain, and anemia. |
| What is Melarsoprol used for | Used only for the meningoencephalitic stages of sleeping sickness becuase of toxicity and because it's class is the only one that can cross the blood brain barrier |
| What is the mechanism of Melarsoprol | reacts with sulfhydryl groups in proteins, inactivating a wide variety of enzymes |
| What is the the pharmacology of Melarsoprol | Given by slow i.v injection and very irritating |
| What are the side effects of Melarsoprol | Very toxic: hypertension, abdominal pain, vomiting, proteinuria, peripheral neuropathy, rashes. The most serious, common and potentially fatal side effect is reactive encephalopathy. |
| What is Nifurtimox used for | Active against the amastigote and the extracellular mastigote stages of T. Cruzi |
| What is the mechanism of Nifurtimox | converted to nitrofuran radical and then to a superoxide radical and a peroxide. All 3 forms toxic to the parasite |
| What is the pharmacology of Nifurtimox | Well absorbed from the GI and extensively metabolized |
| What are the side effects of Nifurtimox | High incidence: CNS disturbances with transitory convulsive episodes, stiffness, and weakness in the limbs |
| What is Sodium Stibogluconate used for | Treatment of all three forms of Leishmaniasis |
| What is the mechanism of Sodium Stibogluconate | It is a prodrug which is converted to a trivalent form that may inhibit the parasite's phosphofructokinase, the rate-limiting step in glycolysis |
| What are the side effects of Sodium Stibogluconate | Highly toxic. Common adverse side effects: muscle pain, joint stiffness, nausea,flattend T wave. Occasional: weakness, liver damage and radycardia. Also: myocardial and renal damage, shock or sudden death |
| What is Suramin used for | Treats early infections of T. gambiese and rhodesiense. Can be combined with Diethylcarbamazine to treat O. volvulus infection |
| What is the mechanism of Suramin | Doesn't diffuse across mammalian cell membranes, selectively endocytosed by parasites. Inhibits large numbers of enzymes, specific target unknown |
| What is the pharmacology of Suramin | Administered by slow i.v. binds tightly to serum proteins which cause it to remain in circulation for prolonged periods. Small test doses administered first |
| What are the side effects of Suramin | Serious idiosyncratic reaction possible: shock, coma (small test doses given first). Also causes nervous system disorders: paresthesias, hyperesthesias, peripheral neuropathy, and photophobia. Nephrotoxic resulting in proteinuria |
Created by:
MCHess
Popular Pharmacology sets