Medications and Their Uses: A Comprehensive Review
Retinoids
Mechanism of Action (MOA)
Retinoids are derivatives of vitamin A that regulate gene expression by binding to nuclear retinoic acid receptors (RARs and RXRs). They influence cellular processes like differentiation, proliferation, and apoptosis, affecting skin cell turnover.
Types of Retinoids
- Topical Retinoids (e.g., Tretinoin, Adapalene): Used for acne and photoaging.
- Oral Retinoids (e.g., Isotretinoin): Primarily for severe acne and psoriasis.
Indications
- Acne vulgaris (mild to severe).
- Psoriasis, photoaging, vitamin A deficiency, acute promyelocytic leukemia (APL).
Adverse Effects
- Skin irritation (redness, peeling).
- Teratogenic (contraindicated in pregnancy).
- Dryness (skin, eyes, mucous membranes).
- Hyperlipidemia (with oral isotretinoin).
Key Points
- Topical for mild acne, oral for severe acne.
- Avoid in pregnancy due to teratogenicity.
- Monitor for side effects like dry skin, lipid changes, and liver function (with oral use).
Anti-TB Regimen
First-Line Drugs
- Isoniazid (INH): Inhibits mycolic acid synthesis in bacterial cell walls.
- Rifampicin (RIF): Inhibits DNA-dependent RNA polymerase, preventing RNA synthesis.
- Pyrazinamide (PZA): Disrupts mycobacterial cell membrane and energy production.
- Ethambutol (EMB): Inhibits arabinosyl transferase, affecting cell wall synthesis.
- Streptomycin: An aminoglycoside that inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit.
Regimen
- Initial phase (2 months): INH, RIF, PZA, EMB.
- Continuation phase (4-6 months): INH and RIF (can be extended in resistant cases).
Indications
Active tuberculosis (TB), including pulmonary and extrapulmonary TB.
Adverse Effects
- Isoniazid: Hepatotoxicity, peripheral neuropathy.
- Rifampicin: Hepatitis, orange-red urine.
- Pyrazinamide: Hepatotoxicity, hyperuricemia.
- Ethambutol: Optic neuritis.
- Streptomycin: Ototoxicity, nephrotoxicity.
Key Points
- Directly Observed Therapy (DOT) is recommended for adherence.
- Monitor liver function and vision during treatment.
Cephalosporins
Mechanism of Action (MOA)
Cephalosporins are beta-lactam antibiotics that inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs). This leads to cell wall disruption and bacterial lysis.
Generations and Spectrum
- 1st Generation (e.g., Cefazolin, Cephalexin): Effective against Gram-positive bacteria (e.g., Staphylococcus, Streptococcus).
- 2nd Generation (e.g., Cefuroxime, Cefoxitin): Broader spectrum, including some Gram-negative bacteria.
- 3rd Generation (e.g., Ceftriaxone, Ceftazidime): More effective against Gram-negative bacteria and meningitis.
- 4th Generation (e.g., Cefepime): Broad spectrum against Gram-positive and Gram-negative bacteria, including Pseudomonas.
- 5th Generation (e.g., Ceftaroline): Effective against MRSA and other resistant Gram-positive bacteria.
Indications
- Infections like pneumonia, UTIs, skin infections, and meningitis.
- Surgical prophylaxis (1st and 2nd generations).
Adverse Effects
- Hypersensitivity reactions (rash, anaphylaxis).
- Gastrointestinal disturbances (nausea, diarrhea).
- Nephrotoxicity (especially with higher doses).
Key Points
- Broad-spectrum antibiotics with varying generation-specific coverage.
- Generally well tolerated but should be used cautiously in patients with penicillin allergy.
Low Molecular Weight Heparin (LMWH)
Mechanism of Action (MOA)
LMWHs, such as enoxaparin and dalteparin, are derived from unfractionated heparin. They primarily inhibit Factor Xa by binding to antithrombin III. This reduces thrombin generation, preventing clot formation. LMWHs have less effect on thrombin (Factor IIa) compared to unfractionated heparin, making them more predictable in their action.
Indications
- Prevention and treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE).
- Acute coronary syndromes (ACS), including unstable angina and NSTEMI.
- Prophylaxis of thromboembolism in surgical and immobilized patients.
Administration
- Administered subcutaneously, typically once or twice daily.
- No routine monitoring is required for most patients, unlike unfractionated heparin.
Adverse Effects
- Bleeding (less frequent than with unfractionated heparin).
- Thrombocytopenia (rare but can lead to heparin-induced thrombocytopenia (HIT)).
- Osteoporosis (with long-term use).
Key Points
- More predictable and safer than unfractionated heparin.
- Preferred for outpatient management of DVT, PE, and ACS.
- Does not require regular coagulation monitoring.
Artesunate
Mechanism of Action (MOA)
Artesunate is a water-soluble derivative of artemisinin. It works by reacting with heme in the parasite’s food vacuole, generating free radicals that damage parasitic proteins, lipids, and membranes, leading to the destruction of the malaria parasite.
Indications
- Severe malaria, particularly caused by Plasmodium falciparum.
- First-line treatment for uncomplicated and severe malaria (often used in combination with other antimalarials like mefloquine or lumefantrine).
Administration
- Administered parenterally (IV or IM) in cases of severe malaria.
- It is converted to artemether in the body.
Adverse Effects
- Short-term effects: Fever, nausea, vomiting, dizziness.
- Long-term effects: Potential for hepatotoxicity, though rare.
- Hemolysis and QT prolongation in some patients.
Key Points
- Fast-acting; used for life-threatening malaria.
- Preferred for severe cases due to its rapid onset and effectiveness.
- Combination therapy improves efficacy and reduces resistance development.
Adenosine in PSVT
Mechanism of Action (MOA)
Adenosine is a naturally occurring nucleoside that works by binding to A1 adenosine receptors in the AV node, leading to a transient block of AV node conduction. This causes a temporary interruption in the reentrant circuit, which restores normal sinus rhythm in PSVT.
Indications
- First-line treatment for acute conversion of PSVT to normal sinus rhythm.
- Effective in reentrant arrhythmias involving the AV node, including AV nodal reentrant tachycardia (AVNRT) and AV reciprocating tachycardia (AVRT).
Administration
- Given as a rapid IV bolus (6 mg initially, followed by 12 mg if needed).
- Short half-life (~10 seconds), so its effects are rapid and transient.
Adverse Effects
- Transient asystole (brief pause in heart rate).
- Flushing, chest discomfort, shortness of breath, and dizziness.
Key Points
- First-line agent for acute PSVT management.
- Short-acting, with minimal long-term side effects.
- Often effective in restoring sinus rhythm in a single dose.
Cotrimoxazole
Composition
Cotrimoxazole is a combination of trimethoprim (a folate antagonist) and sulfamethoxazole (a sulfonamide), used to enhance the antimicrobial effect.
Mechanism of Action (MOA)
Trimethoprim inhibits dihydrofolate reductase, preventing the conversion of dihydrofolic acid to tetrahydrofolic acid, which is required for bacterial DNA synthesis. Sulfamethoxazole inhibits dihydropteroate synthetase, preventing the conversion of para-aminobenzoic acid (PABA) to dihydropteroic acid, a precursor to folic acid. Together, they block two sequential steps in the folate pathway, leading to synergistic bactericidal action.
Indications
- Urinary Tract Infections (UTIs): Effective against common pathogens like E. coli.
- Respiratory Tract Infections: Including bronchitis and pneumonia (e.g., Pneumocystis jirovecii in immunocompromised patients).
- Gastrointestinal Infections: For enteric infections caused by Shigella and Salmonella.
- Other Infections: Toxoplasmosis, nocardiosis, and prophylaxis for Pneumocystis jirovecii pneumonia in HIV/AIDS.
Adverse Effects
- Allergic reactions: Rash, fever, and, rarely, Stevens-Johnson syndrome.
- Hematologic: Leukopenia, thrombocytopenia, and anemia (due to folate inhibition).
- Gastrointestinal: Nausea, vomiting, and diarrhea.
- Hepatotoxicity: Elevation of liver enzymes.
- Renal: Crystalluria, especially with inadequate hydration.
Contraindications
- Pregnancy (especially in the first trimester) and infants under 2 months due to the risk of kernicterus.
- Severe hepatic or renal impairment.
Key Points
- Broad-spectrum antibiotic with synergistic action.
- Commonly used for UTIs, respiratory, and GI infections.
- Monitor renal and hepatic function during prolonged use.
Vitamin K
Mechanism of Action (MOA)
Vitamin K is essential for the activation of vitamin K-dependent clotting factors (II, VII, IX, X) in the liver by gamma-carboxylation. This process enables these clotting factors to bind calcium, which is necessary for their participation in the coagulation cascade. Vitamin K also activates protein C and protein S, natural anticoagulants that help regulate clotting.
Forms of Vitamin K
- Vitamin K1 (Phytonadione): Found in leafy green vegetables, the primary dietary source.
- Vitamin K2 (Menaquinone): Found in fermented foods and produced by gut bacteria.
- Vitamin K3 (Menadione): Synthetic form, rarely used clinically due to potential toxicity.
Indications
- Vitamin K deficiency: To treat or prevent bleeding disorders (e.g., in neonates or individuals with malabsorption syndromes).
- Anticoagulant reversal: In patients on warfarin (oral or parenteral vitamin K).
- Neonatal hemorrhagic disease: Administered to newborns to prevent bleeding due to low vitamin K levels at birth.
Adverse Effects
- Hypersensitivity reactions: Rarely, allergic reactions with parenteral vitamin K.
- Hypercoagulability: Excessive doses can promote thrombus formation (rare).
- Pain or irritation at injection site (for parenteral use).
Key Points
- Vitamin K is essential for normal coagulation.
- Used in warfarin reversal and in cases of vitamin K deficiency-related bleeding.
- Deficiency can lead to bleeding disorders, including easy bruising and excessive bleeding.
Loop Diuretics
Mechanism of Action (MOA)
- Inhibit the Na⁺/K⁺/2Cl⁻ symporter in the thick ascending limb of the loop of Henle.
- Prevent Na⁺, Cl⁻, and water reabsorption → potent diuresis.
- Increase calcium and magnesium excretion.
Examples
Furosemide, Torasemide, Bumetanide, Ethacrynic acid.
Indications
- Pulmonary edema, heart failure.
- Hypertension with renal impairment.
- Hypercalcemia, acute renal failure.
Adverse Effects
- Hypokalemia, hyponatremia, hypocalcemia.
- Ototoxicity (dose-dependent).
- Dehydration, hypotension.
- Hyperuricemia (can trigger gout).
Key Points
- Most potent diuretics, effective even in renal impairment.
- Short duration of action; commonly used in acute conditions.