The main classes of antibiotics are: penicillins, cephalosporins, aminoglycosides, tetracyclines, macrolides, quinolones, and sulfonamides.

Penicillins inhibit bacterial cell wall synthesis by binding to and inactivating penicillin-binding proteins (PBPs), enzymes involved in the final stages of peptidoglycan synthesis.

Aminoglycosides have low oral bioavailability and are administered parenterally. They are eliminated primarily by glomerular filtration and have a post-antibiotic effect.

Fluoroquinolones inhibit bacterial DNA synthesis by inhibiting the enzymes DNA gyrase and topoisomerase IV, which are involved in DNA supercoiling.

The main classes of antihypertensive drugs are: diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers, and beta-blockers.

ACE inhibitors block the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, thereby reducing blood pressure.

Beta-blockers are well absorbed from the gastrointestinal tract, undergo hepatic metabolism, and are excreted in urine. They have a relatively long half-life.

Proton pump inhibitors irreversibly inhibit the H+/K+ ATPase enzyme system (proton pump) in the gastric parietal cells, blocking the final step of acid production.

The main classes of antidepressants are: selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs).

Selective serotonin reuptake inhibitors (SSRIs) block the reuptake of serotonin into presynaptic neurons, increasing the availability of serotonin in the synaptic cleft.

TCAs are well absorbed from the gastrointestinal tract, undergo hepatic metabolism, and have a relatively long half-life. They can cross the blood-brain barrier.

Benzodiazepines enhance the effects of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) by binding to specific GABA receptors, resulting in sedative, hypnotic, anxiolytic, and muscle relaxant effects.

The main classes of antipsychotics are: typical or first-generation antipsychotics (e.g., chlorpromazine, haloperidol) and atypical or second-generation antipsychotics (e.g., risperidone, olanzapine, quetiapine).

Typical antipsychotics primarily block dopamine D2 receptors in the mesolimbic pathway, leading to a reduction in positive symptoms of schizophrenia such as hallucinations and delusions.

Atypical antipsychotics have improved pharmacokinetic properties compared to typical antipsychotics, including better absorption, longer half-life, and fewer drug interactions.

Statins inhibit the enzyme HMG-CoA reductase, which catalyzes a rate-limiting step in cholesterol biosynthesis, leading to reduced cholesterol levels.

The main classes of anticonvulsants are: sodium channel blockers (e.g., carbamazepine, lamotrigine), GABA analogues (e.g., gabapentin, vigabatrin), and calcium channel blockers (e.g., ethosuximide).

Sodium channel blockers, such as carbamazepine and lamotrigine, inhibit the influx of sodium ions through voltage-gated sodium channels, stabilizing neuronal membranes and reducing the propagation of seizure activity.

GABA analogues like gabapentin and vigabatrin are absorbed via an L-amino acid transport system, are not metabolized, and are eliminated renally.

Opioid analgesics bind to and activate mu, delta, and kappa opioid receptors in the central nervous system, inhibiting the transmission of pain signals and producing analgesia.

The main classes of NSAIDs are: salicylates (e.g., aspirin), propionic acid derivatives (e.g., ibuprofen, naproxen), acetic acid derivatives (e.g., diclofenac, ketorolac), and oxicams (e.g., meloxicam).

NSAIDs inhibit the enzyme cyclooxygenase (COX), which catalyzes the conversion of arachidonic acid to prostaglandins, leading to reduced inflammation and pain.

NSAIDs are well absorbed from the gastrointestinal tract, are highly protein-bound, undergo hepatic metabolism, and are excreted in urine.

Corticosteroids bind to intracellular glucocorticoid receptors, which then translocate to the nucleus and regulate the transcription of genes involved in various physiological processes, including anti-inflammatory and immunosuppressive effects.

The main classes of antineoplastic drugs are: alkylating agents (e.g., cyclophosphamide, cisplatin), antimetabolites (e.g., methotrexate, 5-fluorouracil), plant alkaloids (e.g., vincristine, paclitaxel), and antitumor antibiotics (e.g., doxorubicin).

Alkylating agents form covalent bonds with DNA, leading to DNA strand breaks, crosslinking, and inhibition of DNA replication and transcription, ultimately causing cell death.

Antimetabolites are typically administered intravenously and have a short half-life. They are excreted primarily through the kidneys.

Acyclovir and other nucleoside analogue antiviral drugs inhibit viral DNA polymerase, preventing the replication of viral DNA and the spread of viral infections.

The main classes of antifungal drugs are: polyenes (e.g., amphotericin B), azoles (e.g., fluconazole, itraconazole), and echinocandins (e.g., caspofungin).

Azole antifungals inhibit the enzyme lanosterol 14α-demethylase, which is involved in the biosynthesis of ergosterol, an essential component of the fungal cell membrane.

Echinocandins have poor oral bioavailability and are administered intravenously. They are highly protein-bound and undergo hepatic metabolism.

Chloroquine and other antimalarial drugs accumulate in the acidic food vacuole of the malaria parasite, interfering with the detoxification of heme and leading to the accumulation of toxic heme molecules, which kill the parasite.

The main classes of antiretroviral drugs are: nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), integrase inhibitors, and entry inhibitors.

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) are analogues of the naturally occurring deoxynucleosides and nucleotides, which inhibit the HIV reverse transcriptase enzyme and prevent viral DNA synthesis.

Protease inhibitors (PIs) are generally well absorbed orally, highly protein-bound, and metabolized by the cytochrome P450 system in the liver, leading to potential drug-drug interactions.

Cyclosporine and other calcineurin inhibitors block the production of interleukin-2 (IL-2) by T cells, preventing the activation and proliferation of T cells, leading to immunosuppression.

The main classes of bronchodilators are: beta-2 agonists (e.g., albuterol, salmeterol), anticholinergics (e.g., ipratropium, tiotropium), and methylxanthines (e.g., theophylline).

Beta-2 agonists bind to and activate beta-2 adrenergic receptors on bronchial smooth muscle cells, leading to bronchodilation and improved airflow.

Anticholinergics have poor oral bioavailability and are typically administered via inhalation. They have a relatively long duration of action.

Insulin binds to insulin receptors on target cells, triggering a cascade of intracellular events that lead to increased glucose uptake, glycogen synthesis, and lipogenesis, thereby reducing blood glucose levels.

The main classes of oral hypoglycemic agents are: sulfonylureas (e.g., glipizide, glyburide), biguanides (e.g., metformin), thiazolidinediones (e.g., pioglitazone), alpha-glucosidase inhibitors (e.g., acarbose), and dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g., sitagliptin).

Sulfonylureas stimulate the release of insulin from pancreatic beta cells by binding to and inhibiting the ATP-sensitive potassium channels on the beta cell membrane.

Metformin is not metabolized and is excreted unchanged in the urine. It has a relatively short half-life and requires multiple daily doses.

Diuretics increase the excretion of water and electrolytes by the kidneys, either by inhibiting the reabsorption of sodium and chloride or by increasing the excretion of other ions, leading to decreased blood volume and reduced blood pressure.

The main classes of antihistamines are: first-generation (sedating) antihistamines (e.g., diphenhydramine, chlorpheniramine) and second-generation (non-sedating) antihistamines (e.g., loratadine, fexofenadine).

Antihistamines competitively inhibit the binding of histamine to histamine H1 receptors, preventing the inflammatory and allergic responses mediated by histamine.

Second-generation antihistamines have a longer duration of action, better oral bioavailability, and do not readily cross the blood-brain barrier, reducing sedation and other central nervous system side effects.