Pharm Exam 3: Drug Moa By Group

Front 1

Inhibits cough reflex by direct effect on brainstem cough center

Back 1

Antitussive

Front 2

Bind to alpha 1 receptors located on the blood vessels of the nasal mucosa and stimulate vasoconstriction

Back 2

Decongestant

Front 3

-Block H1 histamine subtype receptor thus blocking the effects of histamine during allergic reactions and the like
-May have some effect on the H3 receptor (sedation)

Back 3

Antihistamine

Front 4

Bind to beta-2 receptor resulting in relaxation of bronchiole smooth muscle → bronchodilation

Back 4

Beta 2 Agonist

Front 5

-Inhibit production of proinflammatory products while increasing the production anti-inflammatory proteins
-Decrease vascular permeability
-Inhibit migration of neutrophils and monocytes

Back 5

Respiratory Glucocorticoid

Front 6

-Block muscarinic cholinergic receptors to prevent acetylcholine-induced bronchoconstriction

Back 6

Anticholinergic Drugs

Front 7

-Block receptor for leukotriene on respiratory tissue to decrease inflammation

Back 7

Leukotriene Inhibitors

Front 8

-Base combines with excess hydrogen ions in the stomach to increase intragastric pH

Back 8

Antacid

Front 9

-Selectively bind to H2 receptors without activating it to prevent acid release

Back 9

H2 Blocker

Front 10

-Irreversibly block the H+, K+, -ATPase enzyme that secretes acid into the stomach
-Must be activated when drug in at site of action (i.e. take with food)

Back 10

Proton Pump Inhibitor

Front 11

-Decrease GI motility and reduce fluid loss
-Bind to neuronal receptors (mu) on enteric nerve plexus

Back 11

Antidiarrheal (Loperamide)

Front 12

-Stimulate water and electrolyte reabsorption from lower GI tract
-Anti bacterial effects
-Antacid effects

Back 12

Antidiarrheal (Bismuth)

Front 13

-Absorb water and swell within lower GI tract→ increased size stretches the bowel stimulating intestinal movement

Back 13

Bulk forming laxatives

Front 14

-Precise MOA: unknown
-May activate peristalsis by direct irritant effect on the intestinal mucosa or stimulating nerve plexus within gut wall

Back 14

Stimulant laxatives

Front 15

Osmotically active substances produces a gradient the draw water into the bowel→ stimulates peristalsis

Back 15

Hyperosmotic laxative

Front 16

-Facilitate entry of water into the fecal mass→ stool softens→ easier defecation

Back 16

Lubricant/ stool softener laxative

Front 17

-1) Alteration in protein synthesis: steroid enters cell and binds to receptor in cytosol→ complex enters the nucleus and binds to specific DNA gene segment that controls inflammation (inhibits transcriptions)
-2) Binding to cell surface proteins that changes membrane permeability and enzyme activity

Back 17

Adrenocorticosteroid Glucocorticoid

Front 18

-Binds to receptors in epithelial cells of the distal tubule of the nephron

Back 18

Mineralocorticoid (Fludrocortisone)

Front 19

-1) Mineralocorticoids bind to receptors in tubular epithelial cell to create an activated hormone-receptor complex→ complex travels to the nucleus→ initiates transcription of mRNA→ makes proteins→ proteins help open sodium channels→ sodium goes out f cell
-2) Mineralocorticoids bind to receptors on epithelial cell membrane that increase the activity of existing sodium channels and pumps

Back 19

Mineralocorticoid Antagonist

Front 20

-Inhibits thyroid peroxidase enzyme (which helps prepare iodide for addition to tyrosine residue)
-Blocks conversion of T4 to T3

Back 20

Hyperthyroid Drugs

Front 21

-Give synthetic thyroid hormone to replace natural hormone that is deficient

Back 21

Hypothyroid Drug

Front 22

-Provide addition calcium source to prevent calcium depletion and encourage bone formation
-Doesn’t prevent osteoporosis
-Useful in combination with other agents

Back 22

Bone Drugs (Calcium)

Front 23

-Enhance bone formation by increasing the absorption and retention of calcium and phosphate in the body
-Useful for treating disorders caused by vitamin D deficiency
-Helps osteoporosis but limited data on fracture prevention

Back 23

Bone Drugs (Vitamin D)

Front 24

-Block excessive bone resorption and formation
-Used to normalize bone turnover and prevent hypercalcemia
-Absorb calcium crystals in bone and prevent breakdown
-Prevents fractures and increases bone mineral density
-Needs to be taken on an empty stomach

Back 24

Bone Drugs (Bisphosphonates)

Front 25

-Mimic effects of endogenous calcitonin and increase bone formation
-Reduces fractures but less so than bisphosphonates
-Comes in nasal spray

Back 25

Bone Drugs (Calcitonin)

Front 26

-Helpful in preventing fractures
Stabilize bone turnover and promote bone mineralization in women that lack endogenous estrogen production (e.g. following menopause or ovariectomy)
-SERMS such as raloxifene are better

Back 26

Bone Drugs (Estrogen)

Front 27

-Synthetic insulin acts like normal insulin to help metabolize glucose

Back 27

Diabetes Drugs (Insulin)

Front 28

-Increase insulin secretion from pancreatic beta cells→ helps reduce blood glucose by increasing glucose storage in muscle and by inhibiting hepatic glucose production

Back 28

Diabetes Drugs (Sulfonylureas)

Front 29

-Act directly on liver to decrease hepatic glucose production
-Increase sensitivity of peripheral tissues to insulin

Back 29

Diabetes Drugs (Metformin)

Front 30

-Inhibit sugar breakdown in the intestines and delay glucose absorption from the GI tract (reduces peak glucose level

Back 30

Diabetes Drugs (Alpha-glucosidase Inhibitor)

Front 31

-Increase sensitivity of peripheral tissue to insulin
-Not similar to metformin

Back 31

Diabetes Drugs (Thiazolidinediones)

Front 32

Similar to sulfonylureas

Back 32

Diabetes Drugs (Benzoic Acid Derivative)