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Malaria Is a Very Serious Disease - Assignment Example

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The paper "Malaria Is a Very Serious Disease" describes that antibiotics for example tetracycline and doxycycline are combined with pyrimethamine or quinine for 100% healing. For children under 12 years, pregnant and nursing women doxycycline is contraindicated …
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Malaria Is a Very Serious Disease
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HSC Pharmacology Term Project Malaria is a very serious disease that is present in various regions in the world and it threatens about 40 percent of world’s population killing approximately a million people every year. Quite a number of the affected are young people and migrants. Plasmodium falciparum is the main parasite known to cause severe malaria and it’s carried by the anopheles mosquito. This is a single celled parasite that is neither a virus nor a bacteria but and can survive and multiply both in the gut of the mosquito as well as in the red blood cells of a human being. Several scientists have tried to eliminate the spread of these disease as well as coming up with several ways of treating the infected. The treatment has been somehow demanding due to the fact that P. falciparum develops resistance to any new medicine discovered to treat malaria. Due to this several pharmacological agents have been set in different times to cure malaria. Other plasmodium species that cause malaria are P. vivax, P. Ovale and P. malariae. Chloroquine also known as 4-aminoquinoline has been used to treat malaria caused by falciparum species in the malaria prone areas until this parasite developed a resistant to it. Chloroquine is a weak base that concentrates after mixing with the lysosome of the parasite, probably through parasite-specific drug concentrating mechanism. It’s a weak base and its concentration increases in the lysosome of the parasite probably through parasite –specific drug concentrating mechanism. After infection the parasite digests the hemoglobin forming ferriprotoporphorin IX known as haem which is very toxic to the parasite. However the parasite contains plasmodialhaem polymerase that converts haem to a red pigment associated with malaria referred to as haemozoin, harmless to the parasite. Chloroquine inhibits this enzyme and thus accumulation of haem destroys the parasite by membranolytic action. Moreover chloroquine intercalates in the parasites DNA and also causes fragmentation of its RNA. Chloroquine can be used for clinical cure where it lowers the effect of fever and destroys all the parasites in the blood in 24 hours as well as control method. Chloroquine is only a fundamental treatment for P. falciparum infection and not for P.vivax or P. ovale since the latter contain hypnozoites in the exo-erythrocytic phase that lead to clinical setback attack. However progaunil is combined with it to prevent these relapse in chemoprophylaxis. Due to the resistant nature of P.falciparum maloprim is combined. Apart from malaria Chloroquine is also used for rheumatoid arthritis. Unless in stern attacks where chloroquine is given by continuous intravenous infusion, frequent intramuscular or subcutaneous injection, chloroquine is orally administered. It’s totally absorbed and comprehensively spread throughout the body tissue with slow release from the tissue and later metabolized in the liver and excreted in urine. It has a half-life of about 50 hours despite the fact that 70 percent is excreted as intact drug. The side effects of taking the drug include vomiting, psychoses, rashes, dizziness, blurred vision, headache and nausea and are not present in low doses of chemoprophylaxis (Simooya et al 1998). Irreversible retinopathies could result due to continued usage of high doses. Mefloquine which is in the class of Quinoiline-methanols is another drug used in treatment of malaria. It interrupts the transportation of substances including haemoglobin products to the parasites food vacuole from the human cells (Hellgren et al 1997). To overcome resistance from the parasite mefloqune is combined with other drugs such as chloroquine or quinine. When administered orally it has rapid absorption. It has a slow immediate action but has a long acting with 30 days plasma half-life. The drug is best used for P. falciparum infections resistant to Chloroquine and also as a temporary chemoprophylaxis when moving to regions prone to the resistant parasite. Its unwanted results may include transient, CNS toxicity, giddiness, convulsions, insomnia, neuropsychiatric reactions among others but they are mild in chemoprophylaxis. Another drug in the class of Quinoline-methanols is an alkaloid obtained from cinchona bark known as quinine. It was the first drug used for treatment of malaria discovered before Chloroquine and can be used against all the four species. It’s a powerful schizonticidal drug that was mostly preferred after the parasite developed resistance to Chloroquine. Quinine being an erythrocytic drug (Rimchala et al 196) has no effect on the exo-erythrocytic or gametocytic phase. Its mode of action is similar to that of Chloroquine in that in addition to causing cytoxicity of the parasite through successive accumulation of toxic haem that slows down the action of plasmodialhaem polymerase, it also intercalates in the DNA of the parasite. It’s recommended as a treatment drug where there is resistance to Chloroquine. It’s administered orally as a 7 day course followed by fansidar or tetracycline. However it can be administered parentally to vomiting patients and also in harsh infections. The drug has antipyrexia activity and also clears the blood of parasitaemia. Its absorption in the digestive system is excellent and 80 percent of it sticks to the blood plasma where it has a half-life of 10 hours. It’s excreted in urine in 24 hours after being metabolized in the liver. Quinine has a significant number of side effects that could be incurable. Some of them may include: depressant action on the heart, mild oxytocic effect on the uterus during pregnancy. Hypersensitivity reactions, irritation of the gastric mucosa, nausea, minor blocking action on the neuro muscular junction. Under high doses cardiac dysrhythmias and stern hypersensitivity reactions may be observed. In some cases hypoglycaemia, blood dyscrasias may be observed. Primaquine also known as 8-aminoquinolines is a drug for drastic treatment. Different from the others discussed above primaquinine is a tissue schizonticidal that has no effect on the erythrocytes, sporozoites or hypnozoites but affect the mitochondria of the exo-erythrocytic and gametocytic form of P. falciparum. Due to the above condition it can’t be used in treatment of vivax and ovale malaria. It’s given orally, swiftly absorbed and metabolized. It has a half-life of 3-6 hours and the recommended dose is 15mg/day for 2 weeks. The main side effects result from shortage of glucose 6- phosphate dehydrogenase in the red blood cells. Methaemaglobinaemia with cyanosis haemolysis may also result from large doses. Another blood schizonticidal drug against the erythrocyte P.falciparum that is resistant to Chloroquine is halofantrine (phenantrene-methanol). It also treats P. Vivax but not the hypnozoites. In addition to curing acute form of muitiresistant P. falciparum it also acts as a standby drug incase of failure of chemoprophylaxis. Should be aided by fatty food if taken orally since it’s slowly absorbed. It has a half-life of 1-2 days and is eliminated in feaces. Unwanted results include abdominal pain, gastrointestinal disturbances headache’ slight dysrhythmias sudden cardiac deaths hemolytic anemia and convulsions (Nosten et al 1993, Simooya et al 1998). Drugs that affect the manufacture and utilization of folate are known as folate antagonists. They include pyrimethamine (2, 4 diaminoprimidine) and progaunil that inhibit dihydrofolate reductase that is necessary for tetrahydrofolate that comes in the synthesis of parasite DNA. We also have sulphonamide and sulphones that inhibit folate synthesis by competing for enzyme dihydropteroate synthetase with para- aminobenzoic acid. All these act on erythrocytic P. falciparum but not sporozoites or hypnozotess. These are taken orally, have well but slow absorption, primethamine has a halflife of 4 days, proaunil has 16 hours, dapsone 24-48 hours. They may cause hemolytic anemia and aglanulocytosi when taken in large quantities. Malaria has stood to be a curable disease although it is known to cause mass killing of people especially in times of outbreak. Antibiotics for example tetracycline and doxycycline are combined with pyrimethamine or quinine for 100% healing. For children under 12 years, pregnant and nursing women doxicyclin is contraindicated References David E. Golan. (2008). Principles of pharmacology: The Pathophysiologic Basis of Drug Therapy. Lippincott Williams & Wilkins Hellgren U Berggreb-Palme I., Bergqvist, Y. and Jerling, M. 1997. Enantioselective pharmacokinetics of mefloquine during long-term intake of the prophylactic dose. Br. J. Clin. Pharmacol. 44, 119 -124. Jahangir Moini. (2008). Fundamental pharmacology: For pharmacy technicians. Cengage Learning. 504-505, 531-532. Nosten F., Kuile F. O., Luxemburger C., Woodrow C., Kyle D. E., Siddhi, C. and White, N. J. 1993. Cardiac effects of Antimalarial treatment with halofantrine. The Lancet, 341, w1054 -1056. Oduola O.O, Happi T.C, Gbotosho G.O, Ogundahunsi O.A, Falade C.O, Akinboye D.O et al. (2004). Plasmodium berghei: Efficiency and safety of combinations of chloroquine and promethazine in chloroquine resistant infections in gravid mice. African med sci, 77-81 Sidhu AB, VAlderramos SG, and Fidock DA. (2005). PFmdrl mutations contribute to quinine resistance and enhance Mefloquine and amplification, overexpression and mutation in the P- glycoprotein gene homolog (pfmdr) of plasmodium falciparum in vitro. Am J trop Med Hyg51: 648-658 Simooya,O. O., Sijumbil, G. Lennard, M. S. and Turker, G. (1998) Halofantrine and chloroquine inhibit CY2D6 activity in healthy Zambians. Br. J. Clin. Pharmacol.45, 315 - 317. Rimchala, P., Karbwang J., Sukontason K., Banmairuroi, V., Molunto, P and Na- Bangchang, K.1996. Pharmacokinetics of quinine in patients with chronic renal failure. Eur. J. Clin. Pharmacol. 49, 497-501. Read More
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