Bioavailability and AUC Bioavailability is the portion of a drug dose that reaches the systemic circulation in an active form. It impacts the drug's effectiveness and can vary for oral medications due to absorption and first-pass metabolism.

AUC (Area Under the Curve) in pharmacokinetics signifies the drug exposure over time, reflecting the total amount of unchanged drug reaching systemic circulation.

Bioavailability can be calculated using the formula: F = (AUCoral/AUCiv) * (Doseiv/Doseoral).

AUC helps assess bioavailability, compare drug formulations, and design dosage regimens for desired effects with no toxicity.

Bioavailability is influenced by several factors including:

• Drug's physicochemical properties such as solubility and stability
• Formulation factors like disintegration, dissolution rate, and excipients
• Physiological factors like GI tract pH, gastric emptying time, and intestinal motility
• Biological factors like first-pass metabolism, transport proteins, and enzymatic activity
• Pathological conditions like diseases and impaired liver function
• Drug interactions with food and other medications

Therapeutic Index and Therapeutic Range Therapeutic Index (TI) is the ratio of a drug's toxic dose to its effective dose. A larger TI signifies a safer drug due to a wider gap between effective and toxic doses. The therapeutic range is the drug concentration producing the desired effect without toxicity.

Benefits of a wide TI include enhanced safety, dosing flexibility, improved patient compliance, and lesser risk of overdose. Examples of narrow TI drugs are Warfarin, Digoxin, and Lithium, requiring vigilant monitoring. Penicillin, Ibuprofen, and Acetaminophen are wide TI drugs, offering flexible dosing with lesser toxicity risks.

Competitive drugs, like Propranolol and Ibuprofen, fight with natural substrates for receptor binding. Increasing substrate concentration can overcome their effect. Non-competitive drugs, such as Phenoxybenzamine and Omeprazole, bind elsewhere, altering receptor function. Their effect can't be negated by increasing substrate concentration.

Ephedrine elevates blood pressure by directly stimulating adrenergic receptors and promoting norepinephrine release.

1. Repeated ephedrine use can lead to reduced responses due to receptor desensitization, norepinephrine depletion, and physiological adaptation.