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Classes of Drugs
Different drug classes
| Question | Answer |
|---|---|
| ACE Inhibitors | Inhibits the enzyme that converts angiotensin I to angiotensin II called ACE |
| Angiotensin II receptor blocker (ARB) | Directly inhibits angiotensin II by blocking angiotensin II from interacting with its receptor |
| Beta-blockers | Blocks beta receptors on the heart which increase blood pressure when stimulated. |
| DHP calcium channel blocker (CCB) | Inhibits calcium influx on the peripheral arteries |
| non-DHP-calcium channel blocker (non-DHP-CCB) | Inhibits calcium influx on the cardiac muscle and large, systemic arteries in the heart |
| Diuretics | Reduce blood volume by working in the kidneys to increase the amount of water and electrolytes excreted. |
| Alpha blockers | Blocks alpha receptors on the smooth arteries from being stimulated and causing the arteries to constrict. |
| Alpha-2 agonist | Decreases the sympathetic input by stimulating alpha-2 receptors which are receptors that detect the amount of NE or sympathetic tone. |
| HMG-CoA reductase inhibitors | Inhibits the enzyme responsible for making the precursor for cholesterol synthesis called HMG-CoA reductase. |
| Cholesterol absorption inhibitors | Blocks the absorption of dietary cholesterol in the intestines |
| Bile acid sequestrants | Binds bile acids in the gut leading to the excretion of bile acid which are normally used to make bad cholesterol. Therefore more bad cholesterol in broken down to make bile acids. |
| Fibrates | Inhibits the enzyme responsible for synthesizing triglycerides called lipoprotein lipase. |
| Sulfonylurea | Stimulates pancreatic beta cells to produce more insulin (increases insulin secretion) |
| Meglitinides | Stimulates pancreatic beta cells to produce more insulin (increases insulin secretion) |
| Biguanides | Increases sensitivity to insulin especially in the liver |
| Thiazolidinediones (TZDs) | Increases sensitivity to insulin especially in skeletal muscle and fat cells |
| Alpha-glucosidase inhibitors | Inhibits the enzyme that breaks down sucrose and other large sugars to reduce the amount of sugars that are absorbed in the body. |
| Dipeptidyl peptidase IV inhibitors (DPP-IV inhibitor) | Inhibits the enzyme that breaks down incretins, which increase insulin secretion in the presence of elevated glucose levels |
| Incretin mimetic | Synthetic incretins which increase insulin secretion in the presence of elevated glucose levels |
| Inhaled corticosteroids (ICS) | Blocks or prevents the late phase of allergic reactions by inhibiting the substances that cause allergic reactions such as histamine, leukotrienes, prostaglandins, and bradykinin. |
| Long-acting beta agonists (LABA) | Stimulate beta-2 receptors in the lungs, which causes the bronchioles to relax or dilute to improve breathing. Long onset. |
| Short-acting beta agonists (SABA) | Stimulate beta-2 receptors in the lungs, which causes the bronchioles to relax or dilute to improve breathing. Short onset. |
| Mast cell stabilizer | Prevents the release of histamine and other inflammatory antigens from mast cells (allergen-containing cells) to prevent bronchiole constriction during allergic reactions |
| Methylxanthines | Reduces the airway's responsiveness to histamine and other antigens |
| Leukotriene receptor antagonists | Binds to the cysteinyl leukotriene receptor in the lungs to block the activity of leukotriene D4 receptor which causes bronchiole constriction |
| Leukotriene formation inhibitors | Inhibit 5-lipogenase which is an enzyme responsible for forming leukotrienes |
| Oral corticosteroids | Systemic antiinflammatory agent that increases the number and sensitivity of beta-2 cells in the lungs, reduces mucus production, and prevents and reverses airway remodeling |
| Antacids | Neutralize stomach acid to decrease heartburn and raise the stomach pH preventing the release of pepsinogen |
| Histamine-2 antagonists (H2As) | Reversibly inhibits histamine from interacting with histamine-2 receptors on parietal cells |
| Proton pump inhibitors (PPI) | Inhibits the proton pump in parietal cells resulting in decreased acid secretion |
| Aspirin | Inhibits COX-1 and COX-2 centrally and peripherally to inhibit the formation of the inflammatory mediator prostaglandins. |
| Acetaminophen | Inhibits COX-1 and COX-2 centrally to increase the pain threshold. |
| Non-steroidal anti-inflammatory drugs (NSAIDs) | Inhibits COX-1 and COX-2 centrally and peripherally to prevent the formation of prostaglandins |
| Cyclooxygenase 2 inhibitors (COX-2-I) | Inhibits COX-2 centrally and peripherally |
| Narcotic analgesics | Work by stimulating the mu receptor in the CNS which changes the way people perceive pain. Also target kappa and delta receptors to produce analgesia. |
| Non-narcotic analgesics | Stimulates the mu receptor in the CNS and also inhibits the reuptake of serotonin and NE in the CNS which inhibits pain transmission in spinal cord. |
| Oral contraceptive pills | Progestin component prevents the LH surge to prevent ovulation while estrogen prevents follicle stimulating hormone |
| Selective serotonin reuptake inhibitors (SSRI) | Improves chemical imbalance in the brain by inhibiting the reuptake of serotonin. |
| Tricyclic antidepressants (TCAs) | Improves the chemical balance in the brain by inhibiting the reuptake of norepinephrine+/-sertonin. |
| Serotonin and norepinephrine reuptake inhibitors (SNRIs) | Improves the chemcial balance in the brain by inhibiting the reuptake of serotonin and norepinephrine. |
| Alpha-2 antagonists | Make the brain think that not enough norepinephrine has been released so the brain releases more norepinephrine and serotonin. |
| Psychotropic antidepressants | Improves the chemical balance in the brain by inhibiting the reuptake of dopamine and norepinephrine. |
| Nefazodone | Inhibits serotonin type 2 (5-HT2) receptors which are responsible for increasing depression. |
| monoamine oxidase inhibitors (MAOIs) | Inhibits monoamine oxidase which is responsible for metabolizing and inactivating neurotransitters (NE, serotonine, dopamine) |