Quick revision ↓ Medical Dictionary
Deep Learning — Module 17
Read this section in sequence. It moves from drug targets to therapeutic effects, adverse reactions and safe use.
Tuberculosis principles
Mycobacterial biology, slow growth and resistance risk require combination treatment guided by current susceptibility and national protocols. Isoniazid interferes with mycolic-acid synthesis and can cause neuropathy and liver injury; pyridoxine is used for neuropathy prevention in appropriate patients. Rifampicin inhibits RNA polymerase, induces many metabolic pathways and may discolor body fluids orange. Pyrazinamide can contribute to hepatotoxicity and hyperuricemia. Ethambutol can impair optic function, requiring attention to vision. Drug-resistant disease needs specialized regimens rather than simply extending an ineffective combination.
Leprosy and additional antimycobacterials
Leprosy is treated with multidrug therapy to reduce resistance and relapse. Dapsone inhibits folate synthesis and can produce hemolysis or methemoglobinemia, with additional risk in G6PD deficiency. Clofazimine can cause marked skin pigmentation. Drug-resistant TB medicines such as bedaquiline target different bacterial processes and require careful interaction and cardiac monitoring. The aim is to understand why agents are combined and what must be monitored, not to substitute a fixed classroom list for changing national regimens.
Antifungal targets
Amphotericin B binds ergosterol and disrupts fungal membranes; nephrotoxicity and infusion reactions limit use. Azoles inhibit ergosterol synthesis through a fungal cytochrome enzyme and can produce substantial drug interactions. Echinocandins inhibit beta-glucan cell-wall synthesis. Flucytosine is converted in susceptible fungi to metabolites that disrupt nucleic-acid synthesis, and is generally used in combinations because resistance can emerge. Site, species, host immunity and susceptibility determine choice; superficial and invasive fungal disease are different therapeutic problems.
Antiviral selectivity
Viruses depend on host cells, limiting selective targets. Aciclovir is preferentially activated in infected cells by viral thymidine kinase and inhibits viral DNA polymerase; renal toxicity and dose adjustment can matter. Ganciclovir is useful against CMV in selected settings but may suppress bone marrow. Oseltamivir inhibits influenza neuraminidase. Antiretroviral combinations target reverse transcriptase, integrase, protease or entry pathways. Durable suppression requires adherence and resistance-aware combinations; these drugs do not act on bacteria.
Integrated monitoring
Check organ function and all co-medications before long antimicrobial courses. Rifampicin can lower concentrations of interacting medicines; azoles may increase them through inhibition. Visual symptoms with ethambutol, neuropathy with isoniazid and renal changes with amphotericin need timely review. Viral hepatitis therapies are selected according to virus, disease stage and current guidance. A negative symptom report does not replace planned laboratory monitoring, and an abnormal laboratory value must be interpreted with timing and alternative causes.
High-Yield Revision
- Combination therapy protects effectiveness but does not eliminate adherence needs.
- Match visual, hepatic, renal and hematologic monitoring to the drug.
- Fungal cell-wall and membrane targets are different.
Common Exam & Concept Pitfalls
- Never assume a historical TB regimen covers resistant disease.
- Antiviral activity is virus specific, not universal.
Sources & Further Reading
Curriculum scope checked 23 September 2026. These original study notes summarize established principles; current institutional guidance and product information govern clinical use. Faculty review is pending.
