21 topics with concise breakdowns: definitions, key facts, and class questions.
This section is dedicated to the pharmacology of drugs used to combat parasitic infestations. Traditionally in this study block, we combine agents against protozoa (causative agents of malaria, amoebiasis, leishmaniasis, trypanosomiasis, giardiasis) and a broad group of anthelmintic drugs for the treatment of intestinal and extraintestinal lesions.
Here you will analyze the mechanisms of action of classic and modern antimalarials (quinine, artemisinin, primaquine, atovaquone), and the specifics of therapy for Chagas disease and sleeping sickness. A separate important body of knowledge covers the criteria for selecting anthelmintics: from basic mebendazole and pyrantel for the treatment of nematodes to praziquantel and niclosamide.
In colloquia and exams, examiners are most strict about the connection between the malaria parasite's life cycle and the drug targets (tissue and erythrocyte schizontocides). Also, be prepared for clinical case studies on the rational selection of anthelmintics depending on the parasite's localization, and questions regarding specific toxicity (e.g., complications associated with emetine).
Why is malignant tertian malaria more severe than other forms?
The causative agent of malignant tertian malaria (Plasmodium falciparum) increases erythrocyte adhesion to the endothelium. This causes vascular thrombosis, which can lead to severe complications, including cerebral malaria.
What raw material is used to obtain quinine?
Quinine is a natural alkaloid obtained from the bark of the cinchona tree.
Why is the drug selectively toxic only to the malaria parasite and not to human cells?
Selectivity is due to the fact that the drug purposefully accumulates inside the parasite itself. It is there that it reacts with iron, leading to the local formation of destructive free radicals.
Why is primaquine strictly contraindicated during pregnancy?
The drug easily crosses the placental barrier. Due to the physiologically low activity of the G6PD enzyme in the fetus, the drug's metabolites cause fatal hemolysis of its red blood cells.
Why does atovaquone disrupt DNA replication if its primary target is located in the mitochondria?
The drug blocks electron transport in mitochondria, depriving the plasmodium of energy. This energy is critically essential for the de novo synthesis of pyrimidines. Without pyrimidine nucleotides, the synthesis of a new DNA strand becomes impossible, so replication halts.
Why are antifolate drugs lethal to the malaria parasite but safe for humans?
The human body cannot synthesize folic acid and obtains it ready-made from food. The drugs block the de novo folate synthesis enzymes, which are vital for parasites, while human metabolism is unaffected.
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