Drugs to Know 3 Flashcards
Antacids
Preanesthetic Medication
facilitate smooth induction of anesthesia
Anticholinergics
Preanesthetic Medication
facilitate smooth induction of anesthesia;
prevent bradycardia and secretion of fluids into the respiratory tract
Antiemetics
Preanesthetic Medication
facilitate smooth induction of anesthesia;
prevent nausea and possible aspiration of stomach contents
Antihistamines
Preanesthetic Medication
facilitate smooth induction of anesthesia;
prevention of allergic reactions
Benzodiazepines
Preanesthetic Medication; General Anesthetic: IV
facilitate smooth induction of anesthesia
Opioids
Preanesthetic Medication
facilitate smooth induction of anesthesia
Desflurane
General Anesthetic: Inhaled
no specific receptor; interactions with proteins comprising ion channels; some facilitate GABA mediated inhibition and others antagonize the excitatory action of glutamic acid
Isoflurane
General Anesthetic: Inhaled
no specific receptor; interactions with proteins comprising ion channels; some facilitate GABA mediated inhibition and others antagonize the excitatory action of glutamic acid
Nitrous Oxide
General Anesthetic: Inhaled
no specific receptor; interactions with proteins comprising ion channels; some facilitate GABA mediated inhibition and others antagonize the excitatory action of glutamic acid
Sevoflurane
General Anesthetic: Inhaled
no specific receptor; interactions with proteins comprising ion channels; some facilitate GABA mediated inhibition and others antagonize the excitatory action of glutamic acid
Barbiturates
General Anesthetic: Intravenous
exact mechanism of action unknown; thought to be similar to inhaled
Etomidate
General Anesthetic: Intravenous
exact mechanism of action unknown; thought to be similar to inhaled
Ketamine
General Anesthetic: Intravenous
exact mechanism of action unknown; thought to be similar to inhaled
Opioids
General Anesthetic: Intravenous
exact mechanism of action unknown; thought to be similar to inhaled
Propofol
General Anesthetic: Intravenous
exact mechanism of action unknown; thought to be similar to inhaled
Benoxinate
Local Anesthetic: Topical
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
Cocaine
Local Anesthetic: Topical
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
also has alpha adrenergic agonist activity; causes vasoconstriction
Lidocaine
Local Anesthetic: Topical
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
Proparacaine
Local Anesthetic: Topical
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
Tetracaine
Local Anesthetic: Topical
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
Articaine
Local Anesthetic: Injection
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
Bupivicaine
Local Anesthetic: Injection
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
Mepivicaine
Local Anesthetic: Injection
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
Procaine
Local Anesthetic: Injection
bind to a location on the Na channel; alters depolarization (blocks channel); increase recovery time; primarily used to block information about painful stimuli from the point of stimulus to the spinal column
Succinylcholine
Neuromuscular Blocker
produce muscle paralysis; lack CNS activity;
depolarizing agent - reacts with nicotinic receptor to open the ion channel and cause depolarization; muscle fibers remain depolarized because succinlycholine is not metabolized at the synapse; flaccid paralysis results because the muscle fibers can’t repolarize (phase I block)
Cisatracurium
Neuromuscular Blocker
produce muscle paralysis; lack CNS activity;
non-depolarizing agent - competes with acetylcholine for binding site; will also enter and block the ion channel at high doses
Rocuronium
Neuromuscular Blocker
produce muscle paralysis; lack CNS activity;
non-depolarizing agent - competes with acetylcholine for binding site; will also enter and block the ion channel at high doses
Vecuronium
Neuromuscular Blocker
produce muscle paralysis; lack CNS activity;
non-depolarizing agent - competes with acetylcholine for binding site; will also enter and block the ion channel at high doses
Baclofen
Centrally Acting Spasmolytic Drug
reduce spasticity and muscle spasms; CNS depressant; interrupt neuronal communication resulting in sedation and alteration of pain perception
*main effect at GABA receptors; inhibits spinal reflexes
Carisoprodol
Centrally Acting Spasmolytic Drug
reduce spasticity and muscle spasms; CNS depressant; interrupt neuronal communication resulting in sedation and alteration of pain perception
*interrupts neuronal communication; produces sedation and altered pain perception
Cyclobenzaprine
Centrally Acting Spasmolytic Drug
reduce spasticity and muscle spasms; CNS depressant; interrupt neuronal communication resulting in sedation and alteration of pain perception
*main effect at NE and 5HT receptors; increases transmission
Tizanidine
Centrally Acting Spasmolytic Drug
reduce spasticity and muscle spasms; CNS depressant; interrupt neuronal communication resulting in sedation and alteration of pain perception
*main effect at alpha-2 receptors; increase pre-synaptic motor neuron inhibition
Gabapentin
Centrally Acting Spasmolytic Drug
reduce spasticity and muscle spasms; CNS depressant; interrupt neuronal communication resulting in sedation and alteration of pain perception
*thought to bind to a carrier protein at a unique receptor; results in elevated GABA levels in the brain
Dantrolene
Direct Acting Muscle Relaxant
reduces skeletal muscle strength by interfering with excitation-contraction coupling in the muscle fibers; prevents release of calcium by blocking the channel in the sarcoplasmic reticulum; decreases intracellular calcium
Adrenocortioctropic Hormone (ACTH)
Anterior Pituitary Hormone
produced when stimulated by corticotropin hormone; ACTH binds to receptors in the adrenal cortex; stimulates the release of adrenocortiosteroids and adrenal androgens
Growth Hormone (GH)
Anterior Pituitary Hormone
released in response to growth hormone releasing hormone; secretion decreases with age; promotes cell proliferation, bone growth, cartilage synthesis, and others; synthetic GH is used to treat growth failure in children
Luteinizing Hormone (LH)
Anterior Pituitary Hormone- Gonadotropin
regulates gonadal steroid hormones
Follicle Stimulating Hormone (FSH)
Anterior Pituitary Hormone- Gonadotropin
regulates gonadal steroid hormones
Prolactin (PRL)
Anterior Pituitary Hormone
similar in structure to GH; secretion is inhibited by dopamine; primary function is to stimulate and maintain lactation; also involved in reproductive function and immune function
Thyroid Stimulating Hormone
Anterior Pituitary Hormone
Growth Hormone Releasing Hormone
Hypothalamus Hormone
Growth Hormone Inhibiting Hormone
Hypothalamus Hormone
suppress GH and thyroid-stimulating hormone release; also inhibits release of insulin, glucagon, and gastrin
Gonadotropin Releasing Hormone (GnRH)
Hypothalamus Hormone
essential for the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary; must be pulse dose- continuous dose actually inhibits release; synthetic GnRH can be used to suppress production of gonadal hormones; administered continuously
Corticotropin Releasing Hormone
Hypothalamus Hormone
Thyrotropin Releasing Hormone
Hypothalamus Hormone
Oxytocin
Hormone of the Posterior Pituitary
hypothalamus synthesizes the precursors; transported to posterior pituitary and stored;
stimulates uterine contraction and milk injection; used clinically to induce labor
Vasopressin/ADH
Hormone of the Posterior Pituitary
hypothalamus synthesizes the precursors; transported to posterior pituitary and stored;
increases water permeability and reabsorption in the kidney; used clinically to treat diabetes insipidus; also causes constriction of vascular smooth muscle
Iodine and potassium iodide
Drug Affecting the Thyroid
inhibits the production of hormone; mechanism not known
Liothyronine
Drug Affecting the Thyroid
treatment of hypothyroidism
Levothyroxine
Drug Affecting the Thyroid
treatment of hypothyroidism
Methimazole
Drug Affecting the Thyroid
inhibition of thyroid hormone synthesis; inhibit step in production of hormone; have no effect on hormone already stored; may cause delay in effect
Propylthiouracil
Drug Affecting the Thyroid
inhibition of thyroid synthesis; inhibit step in production of hormone; have no effect on hormone already stored; may cause delay in effect
Estradiol
Estrogen
steroid hormones diffuse across cell membrane and bind to estrogen receptors; activated complex interacts with nuclear chromatin to initiate RNA synthesis
most potent estrogen produced by the ovary; principal estrogen in the premenopausal woman
Estrone
Estrogen
steroid hormones diffuse across cell membrane and bind to estrogen receptors; activated complex interacts with nuclear chromatin to initiate RNA synthesis
metabolite of estradiol also produced by the ovary; primary circulating estrogen after menopause
Estriol
Estrogen
steroid hormones diffuse across cell membrane and bind to estrogen receptors; activated complex interacts with nuclear chromatin to initiate RNA synthesis
metabolite of estradiol; produced by the placenta; present in significant amounts during pregnancy
Leuprolide
GnRH Analog
pulse dose causes an increase in the production of FSH and LH; males- stimulate spermatogenesis and testosterone production; females- induce ovulation or treat primary hypothalamic amenorrhea;
chronic administration leads to a decrease in production of FSH and LH; due to a decrease in receptor density; males- treatment of advanced prostate cancer and prostatic hyperplasia; females- treatment of endometriosis, polycystic ovary disease, and other uterine disorders
Gonadorelin
GnRH Analog
pulse dose causes an increase in the production of FSH and LH; males- stimulate spermatogenesis and testosterone production; females- induce ovulation or treat primary hypothalamic amenorrhea;
chronic administration leads to a decrease in production of FSH and LH; due to a decrease in receptor density; males- treatment of advanced prostate cancer and prostatic hyperplasia; females- treatment of endometriosis, polycystic ovary disease, and other uterine disorders
Nafarelin
GnRH Analog
pulse dose causes an increase in the production of FSH and LH; males- stimulate spermatogenesis and testosterone production; females- induce ovulation or treat primary hypothalamic amenorrhea;
chronic administration leads to a decrease in production of FSH and LH; due to a decrease in receptor density; males- treatment of advanced prostate cancer and prostatic hyperplasia; females- treatment of endometriosis, polycystic ovary disease, and other uterine disorders
Raloxifene
Selective Estrogen-Receptor Modulator
interact at estrogen receptors; compete with estrogen for binding in breast tissue; causes regression of some breast tumors; decreases bone resorption and overall bone turnover; little effect on endometrium; lower risk of uterine cancer
Tamoxifen
Selective Estrogen-Receptor Modulator
interact at estrogen receptors; compete with estrogen for binding in breast tissue; causes regression of some breast tumors; decreases bone resorption and overall bone turnover; little effect on endometrium; lower risk of uterine cancer
Clomiphene
Selective Estrogen-Receptor Modulator
interact at estrogen receptors;
Drospirenone
Progestogen
produced in response to LH in both males and females;
in females, promotes development of secretory endometrium; accommodates implantation of embryo; continues to be secreted if conception takes place
Levonorgestrel
Progestogen
produced in response to LH in both males and females;
in females, promotes development of secretory endometrium; accommodates implantation of embryo; continues to be secreted if conception takes place
Medroxyprogesterone
Progestogen
produced in response to LH in both males and females;
in females, promotes development of secretory endometrium; accommodates implantation of embryo; continues to be secreted if conception takes place
Megestrol
Progestogen
produced in response to LH in both males and females;
in females, promotes development of secretory endometrium; accommodates implantation of embryo; continues to be secreted if conception takes place
Norelgestromin
Progestogen
produced in response to LH in both males and females;
in females, promotes development of secretory endometrium; accommodates implantation of embryo; continues to be secreted if conception takes place
Norethindrone
Progestogen
produced in response to LH in both males and females;
in females, promotes development of secretory endometrium; accommodates implantation of embryo; continues to be secreted if conception takes place
Preogesterone
Progestogen
produced in response to LH in both males and females;
in females, promotes development of secretory endometrium; accommodates implantation of embryo; continues to be secreted if conception takes place
Mifepristone
Antiprogestin
progesterone antagonist; partial agonist activity; administration in early pregnancy results in abortion of the fetus
Inhibitor of Adrenocorticoid Biosynthesis or Function
Testosterone
Androgen
bind to specific nuclear receptor; hormone-receptor complex binds to DNA and stimulates synthesis of specific RNAs and proteins
anabolic agent - promotes bone growth and prevents reabsorption, development of internal genitalia, increases muscle mass; androgenic agent- development of male secondary sexual characteristics
Bicalutamide
Antiandrogen
usually combined with GnRH analog to decrease LH and testosterone production
Flutamide
Antiandrogen
blocks action of testosterone in target organs
Nilutamide
Antiandrogen
usually combined with GnRH analog to decrease LH and testosterone production
Aspart
Diabetes - Insulin
insulin tells the cells to absorb and store glucose
Glulisine
Diabetes - Insulin
insulin tells the cells to absorb and store glucose
Lispro
Diabetes - Insulin
insulin tells the cells to absorb and store glucose
Regular Insulin
Diabetes - Insulin
insulin tells the cells to absorb and store glucose
NPH
Diabetes - Insulin
insulin tells the cells to absorb and store glucose
Detemir
Diabetes - Insulin
insulin tells the cells to absorb and store glucose
Glargine
Diabetes - Insulin
insulin tells the cells to absorb and store glucose
Pramlintide
Diabetes - Amylinomimetic
synthetic amylin analog; amylin is a hormone that is secreted along with insulin from beta cells following food intake; delays gastric emptying and decreases glucagon secretion; can be used as adjunct to mealtime insulin
Gliclazide
Diabetes - Sulfonylurea
helps the body secrete more insulin; binds to receptors in the beta cells causing K channels to close; depolarizes membrane; voltage-dependent calcium channels open in response; activates calcium-dependent proteins that control the release of insulin; insulin release is increased
Glimepiride
Diabetes - Sulfonylurea
helps the body secrete more insulin; binds to receptors in the beta cells causing K channels to close; depolarizes membrane; voltage-dependent calcium channels open in response; activates calcium-dependent proteins that control the release of insulin; insulin release is increased
Glipizide
Diabetes - Sulfonylurea
helps the body secrete more insulin; binds to receptors in the beta cells causing K channels to close; depolarizes membrane; voltage-dependent calcium channels open in response; activates calcium-dependent proteins that control the release of insulin; insulin release is increased
Glyburide
Diabetes - Sulfonylurea
helps the body secrete more insulin; binds to receptors in the beta cells causing K channels to close; depolarizes membrane; voltage-dependent calcium channels open in response; activates calcium-dependent proteins that control the release of insulin; insulin release is increased
Nateglinide
Diabetes - Meglitinide
stimulate the pancreas to secrete more insulin; faster acting with shorter duration of action than sulfonylureas; developed to decrease postprandial hyperglycemia; bind to same receptor in beta cells as sulfonylureas; different site; cause similar release of insulin
Repaglinide
Diabetes - Meglitinide
stimulate the pancreas to secrete more insulin; faster acting with shorter duration of action than sulfonylureas; developed to decrease postprandial hyperglycemia; bind to same receptor in beta cells as sulfonylureas; different site; cause similar release of insulin
Metformin
Diabetes - Biguanide
lowers glucose production in the liver and improves body’s sensitivity to insulin; decreases glucose production in the liver; increases hepatic sensitivity to insulin; reduces energy supply for production; decreases the amount of carbohydrate absorbed from intestines; increases insulin sensitivity in all cells and increases uptake in skeletal muscle
Pioglitazone
Diabetes - Thiazolidinediones
improves whole-body insulin sensitivity; agonist at peroxisome proliferator-activated receptor-gamma; results in transcription of a number of insulin-sensitive genes; promotes or enhances the local effects of insulin
Rosiglitazone
Diabetes - Thiazolidinediones
improves whole-body insulin sensitivity; agonist at peroxisome proliferator-activated receptor-gamma; results in transcription of a number of insulin-sensitive genes; promotes or enhances the local effects of insulin
Acarbose
Diabetes - Alpha-Glucosidase Inhibitor
targets the alpha-glucosidase enzymes that break down complex carbohydrates; minimizes upper intestinal digestion and absorption of carbohydrates when taken at the start of a meal; decreases amount of glucose that is absorbed
Miglitol
Diabetes - Alpha-Glucosidase Inhibitor
targets the alpha-glucosidase enzymes that break down complex carbohydrates; minimizes upper intestinal digestion and absorption of carbohydrates when taken at the start of a meal; decreases amount of glucose that is absorbed
Alogliptin
Diabetes - DPP-4 Inhibitor
prolongs the activity of incretin hormones (GLP-1); inhibits DPP-IV; DPP-IV is responsible for inactivation of incretin hormones; prolonging the effect of the enzyme results in an increase in insulin secretion in response to meals and a decrease in glucagon levels; “helps the body continue to make insulin”
Linagliptin
Diabetes - DPP-4 Inhibitor
prolongs the activity of incretin hormones (GLP-1); inhibits DPP-IV; DPP-IV is responsible for inactivation of incretin hormones; prolonging the effect of the enzyme results in an increase in insulin secretion in response to meals and a decrease in glucagon levels; “helps the body continue to make insulin”
Saxagliptin
Diabetes - DPP-4 Inhibitor
prolongs the activity of incretin hormones (GLP-1); inhibits DPP-IV; DPP-IV is responsible for inactivation of incretin hormones; prolonging the effect of the enzyme results in an increase in insulin secretion in response to meals and a decrease in glucagon levels; “helps the body continue to make insulin”
Sitagliptin
Diabetes - DPP-4 Inhibitor
prolongs the activity of incretin hormones (GLP-1); inhibits DPP-IV; DPP-IV is responsible for inactivation of incretin hormones; prolonging the effect of the enzyme results in an increase in insulin secretion in response to meals and a decrease in glucagon levels; “helps the body continue to make insulin”
Dulaglutide
Diabetes - GLP-1 Agonist
GLP-1 is main incretin (responsible for postprandial insulin secretion); binds to GLP-1 receptors and acts as agonist; helps restore activity; results in potentiation of glucose-mediated insulin secretion (may actually increase beta-cell mass), suppression of postprandial glucagon release, and slowed gastric emptying and loss of appetite
Exenatide
Diabetes - GLP-1 Agonist
GLP-1 is main incretin (responsible for postprandial insulin secretion); binds to GLP-1 receptors and acts as agonist; helps restore activity; results in potentiation of glucose-mediated insulin secretion (may actually increase beta-cell mass), suppression of postprandial glucagon release, and slowed gastric emptying and loss of appetite
Liraglutide
Diabetes - GLP-1 Agonist
GLP-1 is main incretin (responsible for postprandial insulin secretion); binds to GLP-1 receptors and acts as agonist; helps restore activity; results in potentiation of glucose-mediated insulin secretion (may actually increase beta-cell mass), suppression of postprandial glucagon release, and slowed gastric emptying and loss of appetite
Lixisenatide
Diabetes - GLP-1 Agonist
GLP-1 is main incretin (responsible for postprandial insulin secretion); binds to GLP-1 receptors and acts as agonist; helps restore activity; results in potentiation of glucose-mediated insulin secretion (may actually increase beta-cell mass), suppression of postprandial glucagon release, and slowed gastric emptying and loss of appetite
Semaglutide
Diabetes - GLP-1 Agonist
GLP-1 is main incretin (responsible for postprandial insulin secretion); binds to GLP-1 receptors and acts as agonist; helps restore activity; results in potentiation of glucose-mediated insulin secretion (may actually increase beta-cell mass), suppression of postprandial glucagon release, and slowed gastric emptying and loss of appetite
Canagliflozin
Diabetes - Sodium-Glucose Transporter 2 Inhibitor
prevents the kidneys from reabsorbing sugar into the blood; glucose is excreted in the urine; sodium-glucose cotransporter 2 is responsible for reabsorbing filtered glucose in the kidney - these drugs inhibit this activity; the result is an increase in urinary glucose excretion; may also reduce blood pressure (not a HTN treatment)
Dapagliflozin
Diabetes - Sodium-Glucose Transporter 2 Inhibitor
prevents the kidneys from reabsorbing sugar into the blood; glucose is excreted in the urine; sodium-glucose cotransporter 2 is responsible for reabsorbing filtered glucose in the kidney - these drugs inhibit this activity; the result is an increase in urinary glucose excretion; may also reduce blood pressure (not a HTN treatment)
Empagliflozin
Diabetes - Sodium-Glucose Transporter 2 Inhibitor
prevents the kidneys from reabsorbing sugar into the blood; glucose is excreted in the urine; sodium-glucose cotransporter 2 is responsible for reabsorbing filtered glucose in the kidney - these drugs inhibit this activity; the result is an increase in urinary glucose excretion; may also reduce blood pressure (not a HTN treatment)
Ertugliflozin
Diabetes - Sodium-Glucose Transporter 2 Inhibitor
prevents the kidneys from reabsorbing sugar into the blood; glucose is excreted in the urine; sodium-glucose cotransporter 2 is responsible for reabsorbing filtered glucose in the kidney - these drugs inhibit this activity; the result is an increase in urinary glucose excretion; may also reduce blood pressure (not a HTN treatment)
Betamethasone
Corticosteroid - Glucocorticoid
binds to specific intracellular cytoplasmic receptors
anti-inflammatory action: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages (not seen with NSAIDs)
promotes normal intermediary metabolism, increases resistance to stress, alters blood cell levels in plasma
Cortisone
Corticosteroid - Glucocorticoid
binds to specific intracellular cytoplasmic receptors
anti-inflammatory action: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages (not seen with NSAIDs)
promotes normal intermediary metabolism, increases resistance to stress, alters blood cell levels in plasma
Dexamethasone
Corticosteroid - Glucocorticoid
binds to specific intracellular cytoplasmic receptors
anti-inflammatory action: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages (not seen with NSAIDs)
promotes normal intermediary metabolism, increases resistance to stress, alters blood cell levels in plasma
may be used in chemo-induced vomiting, usually in combination; mechanism may involve blockade of prostaglandins
Fludrocortisone
Corticosteroid - Mineralocorticoid
binds to specific intracellular cytoplasmic receptors (mineralocorticoid receptors confined to secretory organs and brain)
helps control the body’s water volume and concentration of electrolytes; secretion is increased by angiotensin II and K, especially when Na levels are low
Hydrocortisone
Corticosteroid - Glucocorticoid
binds to specific intracellular cytoplasmic receptors
anti-inflammatory action: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages (not seen with NSAIDs)
promotes normal intermediary metabolism, increases resistance to stress, alters blood cell levels in plasma
Methylprednisolone
Corticosteroid - Glucocorticoid
binds to specific intracellular cytoplasmic receptors
anti-inflammatory action: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages (not seen with NSAIDs)
promotes normal intermediary metabolism, increases resistance to stress, alters blood cell levels in plasma
may be used in chemo-induced vomiting, usually in combination; mechanism may involve blockade of prostaglandins
Prednisolone
Corticosteroid - Glucocorticoid
binds to specific intracellular cytoplasmic receptors
anti-inflammatory action: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages (not seen with NSAIDs)
promotes normal intermediary metabolism, increases resistance to stress, alters blood cell levels in plasma
Triamcinolone
Corticosteroid - Glucocorticoid
binds to specific intracellular cytoplasmic receptors
anti-inflammatory action: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages (not seen with NSAIDs)
promotes normal intermediary metabolism, increases resistance to stress, alters blood cell levels in plasma
Loteprednol
Corticosteroid - Glucocorticoid
*ester-based steroid
binds to specific intracellular cytoplasmic receptors
anti-inflammatory action: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages (not seen with NSAIDs)
promotes normal intermediary metabolism, increases resistance to stress, alters blood cell levels in plasma
Metyrapone
Inhibitor of Adrenocorticoid Biosynthesis or Function
inhibits synthesis of cortisol
Aminoglutheamide
Inhibitor of Adrenocorticoid Biosynthesis or Function
blocks conversion of cholesterol to pregnenolone; inhibits synthesis of ALL steroids
Ketoconazole
Inhibitor of Adrenocorticoid Biosynthesis or Function
at high doses blocks enzyme responsible for steroid production
Spironolactone
Inhibitor of Adrenocorticoid Biosynthesis or Function
blocks aldosterone receptors; also blocks androgen receptor
Eplerenone
Inhibitor of Adrenocorticoid Biosynthesis or Function
blocks aldosterone receptors
Misoprostol
Prostaglandin Analog
PGE1 analog; interacts with prostaglandin receptors on parietal cells; reduces gastric acid secretion; stimulates mucus and bicarbonate production
inhibits secretion of HCl, stimulates secretion of mucus and bicarbonate, deficiency in production may be contributing factor in peptic ulcer development
Iloprost
Prostaglandin Analog
analog of prostacyclin; activates prostacyclin receptors and increases production of cAMP
Latanoprost
Prostaglandin Analog
PGF analog; binds to prostaglandin FP receptors and increases uveoscleral outflow; causes reduction of IOP
Travaprost
Prostaglandin Analog
pro-drug; binds to prostaglandin FP receptors and increases uveoscleral outflow; causes reduction of IOP
Bimatoprost
Prostaglandin Analog
mimics endogenous prostamides; binds to prostaglandin FP receptors and increases uveoscleral outflow; causes reduction of IOP
Aspirin
NSAID
irreversibly inactivates cyclooxygenase; esterases rapidly break down into salicylate; salicylate has anti-inflammatory, antipyretic, and analgesic properties
anti-inflammatory: inhibits cyclooxygenase activity, diminishing the formation of prostaglandins
analgesic: PGE is thought to sensitize nerve endings to inflammatory chemical mediators, repressing sensation of pain
antipyretic: PGE synthesis causes an increase in the set-point of the anterior hypothalamic thermoregulatory center, causing fever; NSAIDs reset the “thermostat” toward normal, with no effect on normal body temp
Indomethacin
NSAID - Acetic and Propionic Acids
inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis
inhibits COX-1 and COX-2; reversible inhibition; does not effect leukotrienes
Ibuprofen
NSAID - Acetic and Propionic Acids
inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis
inhibits COX-1 and COX-2; reversible inhibition; does not effect leukotrienes
Diclofenac
NSAID - Acetic and Propionic Acids
inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis
inhibits COX-1 and COX-2; reversible inhibition; does not effect leukotrienes
Naproxen
NSAID - Acetic and Propionic Acids
inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis
inhibits COX-1 and COX-2; reversible inhibition; does not effect leukotrienes
Ketorolac
NSAID - Acetic and Propionic Acids
inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis
inhibits COX-1 and COX-2; reversible inhibition; does not effect leukotrienes
Meloxicam
NSAID - Oxicam
inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis
preferential for COX-2, non selective at high doses
Peroxicam
NSAID - Oxicam
inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis
Celecoxib
NSAID - COX-2 Specific
inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis
specific for COX-2
Acetaminophen
inhibits prostaglandin synthesis similar to COX-2 specific drugs (higher activity in the CNS); good antipyretic and analgesic; inactivated by chemicals found in inflammatory cells and platelets; poor anti-inflammatory and anti-platelet action; less effect on cyclooxygenase in peripheral tissues (weak anti-inflammatory activity)
Abatacept
Drugs for Arthritis (DMARDs)
inhibits T-cell activation; biologic DMARD
Adalimumab
Drugs for Arthritis (DMARDs)
TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD
Anakinra
Drugs for Arthritis (DMARDs)
IL-1 antagnoist (IL-1 is a pro-inflammatory cytokine); biologic DMARD
Certolizumab
Drugs for Arthritis (DMARDs)
TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD
Hydroxychloroquine
Drugs for Arthritis (DMARDs)
increases pH within inflammatory cells; leads to interference with “antigen processing”; causes decreased stimulation of CD4 cells
Etanercept
Drugs for Arthritis (DMARDs)
TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD
Golimumab
Drugs for Arthritis (DMARDs)
TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD
Infliximab
Drugs for Arthritis (DMARDs)
TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD
Methotrexate
Drugs for Arthritis (DMARDs)
immunosuppressant; inhibits dihydrofolate reductase; impairs DNA synthesis; aids in effectivness for autoimmune disease
Tocilizumab
Drugs for Arthritis (DMARDs)
inhibits IL-6; biologic DMARD
Tofacitinib
Drugs for Arthritis (DMARDs)
regulates immune cell function; biologic DMARD
Beclomethasone
Respiratory Drugs: Anti-Inflammatory
Inhaled Corticosteroid
decreases the inflammatory cascade: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages
reduces the hyperresponsiveness of airway smooth muscle after several months of regular use
Budesonide
Respiratory Drugs: Anti-Inflammatory
Inhaled Corticosteroid
decreases the inflammatory cascade: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages
reduces the hyperresponsiveness of airway smooth muscle after several months of regular use
Ciclesonide
Respiratory Drugs: Anti-Inflammatory
Inhaled Corticosteroid
decreases the inflammatory cascade: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages
reduces the hyperresponsiveness of airway smooth muscle after several months of regular use
Flunisolide
Respiratory Drugs: Anti-Inflammatory
Inhaled Corticosteroid
decreases the inflammatory cascade: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages
reduces the hyperresponsiveness of airway smooth muscle after several months of regular use
Fluticasone
Respiratory Drugs: Anti-Inflammatory
Inhaled Corticosteroid
decreases the inflammatory cascade: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages
reduces the hyperresponsiveness of airway smooth muscle after several months of regular use
Mometasone
Respiratory Drugs: Anti-Inflammatory
Inhaled Corticosteroid
decreases the inflammatory cascade: decreases production of prostaglandins by inhibition of phospholipase A2- blocks release of AA; reduces COX-2 synthesis; interferes with mast cell degranulation; also lowers peripheral lymphocytes and macrophages
reduces the hyperresponsiveness of airway smooth muscle after several months of regular use
Cromolyn
Respiratory Drugs: Anti-Inflammatory
Mast Cell Stabilizer
blocks release of inflammatory mediators
Montelukast
Respiratory Drugs: Anti-Inflammatory
Anti-Leukotriene
blocks effects of leukotrienes
Zafirlukast
Respiratory Drugs: Anti-Inflammatory
Anti-Leukotriene
blocks effects of leukotrienes
Zileuton
Respiratory Drugs: Anti-Inflammatory
Anti-Leukotriene
inhibitor of 5-lipoxygenase; prevents formation of leukotrienes
Albuterol
Respiratory Drugs: Bronchodilators
Short Acting Beta-2 Agonist
Levalbuterol
Respiratory Drugs: Bronchodilators
Short Acting Beta-2 Agonist
Pirbuterol
Respiratory Drugs: Bronchodilators
Short Acting Beta-2 Agonist
Formoterol
Respiratory Drugs: Bronchodilators
Long Acting Beta-2 Agonist
Indacaterol
Respiratory Drugs: Bronchodilators
Long Acting Beta-2 Agonist
Salmeterol
Respiratory Drugs: Bronchodilators
Long Acting Beta-2 Agonist
Ipratropium
Respiratory Drugs: Bronchodilators
Cholinergic Agonist
blocks contraction of airway smooth muscle mediated by vagus nerve; blocks acetylcholine receptors
Tiotropium
Respiratory Drugs: Bronchodilators
Cholinergic Agonist
blocks contraction of airway smooth muscle mediated by vagus nerve; blocks acetylcholine receptors
Theophylline
Respiratory Drugs: Bronchodilators
nonspecific MOA; increases cAMP and antagonizes adenosine receptors
Omalziumab
Respiratory Drugs: Bronchodilators
Immunoglobulin Antagonist
recombinant DNA monoclonal antibody; selectively binds to IgE; decreases release of inflammatory mediators from mast cells and basophils
Codeine
Respiratory Drugs: Antitussives/Expectorants
decreases sensitivity of cough centers in the CNS to peripheral stimuli; decreases mucosal secretion; required doses lower than required for analgesia
Dextromethorphan
Respiratory Drugs: Antitussives/Expectorants
synthetic derivative of morphine; no analgesic effect at antitussive doses; equally effective as codeine
Benzonatate
Respiratory Drugs: Antitussives/Expectorants
local anesthetic; anesthetizes respiratory passage and pleural stretch receptors; reduces cough reflex
Guaifenesin
Respiratory Drugs: Antitussives/Expectorants
expectorant; facilitates the coughing up of mucus; exact MOA unknown; reduces adhesiveness and surface tension of respiratory tract secretions; facilitates expectoration; also reduces frequency of coughing
Cetirizine
Respiratory Drugs: Antihistamines
H1 blockers
Diphenhydramine
Respiratory Drugs: Antihistamines
H1 blockers
Fexofenadine
Respiratory Drugs: Antihistamines
H1 blockers
Loratadine
Respiratory Drugs: Antihistamines
H1 blockers
Amoxicillin
Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents
used in combination with PPIs to eradicate H. pylori
Bismuth Compounds
Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents
used in combination with PPIs to eradicate H. pylori
Clarithromycin
Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents
used in combination with PPIs to eradicate H. pylori
Metronidazole
Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents
used in combination with PPIs to eradicate H. pylori
Tetracycline
Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents
used in combination with PPIs to eradicate H. pylori
Cimetidine
Drugs Used to Treat Peptic Ulcers: H2 Receptor Blockers
competitively block the binding of histamine; reduces secretion of gastric acid; have no effect on H1 receptors; no “regular” antihistamine effect
Famotidine
Drugs Used to Treat Peptic Ulcers: H2 Receptor Blockers
competitively block the binding of histamine; reduces secretion of gastric acid; have no effect on H1 receptors; no “regular” antihistamine effect
Nizatidine
Drugs Used to Treat Peptic Ulcers: H2 Receptor Blockers
competitively block the binding of histamine; reduces secretion of gastric acid; have no effect on H1 receptors; no “regular” antihistamine effect
Ranitidine
Drugs Used to Treat Peptic Ulcers: H2 Receptor Blockers
competitively block the binding of histamine; reduces secretion of gastric acid; have no effect on H1 receptors; no “regular” antihistamine effect
Dexlansoprazole
Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)
binds to the proton pump and prevents secretion of hydrogen ions
Esemoeprazole
Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)
binds to the proton pump and prevents secretion of hydrogen ions
Lansoprazole
Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)
binds to the proton pump and prevents secretion of hydrogen ions
Omeprazole
Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)
binds to the proton pump and prevents secretion of hydrogen ions
Pantoprazole
Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)
binds to the proton pump and prevents secretion of hydrogen ions
Rebeprazole
Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)
binds to the proton pump and prevents secretion of hydrogen ions
Dicyclomine
Drugs Used to Treat Peptic Ulcers: Antimuscarinic Agents
Aluminium hydroxide
Drugs Used to Treat Peptic Ulcers: Antacids
weak bases; react with gastric acid to form water and salt; also reduce pepsin activity; pepsin is inactive at pH >4
Calcium carbonate
Drugs Used to Treat Peptic Ulcers: Antacids
weak bases; react with gastric acid to form water and salt; also reduce pepsin activity; pepsin is inactive at pH >4
Magnesium hydroxide
Drugs Used to Treat Peptic Ulcers: Antacids
weak bases; react with gastric acid to form water and salt; also reduce pepsin activity; pepsin is inactive at pH >4
Constipation Drugs- saline and osmotic laxative
nonabsorbale salts or electrolytes; holds water in the intestine by osmosis
Sodium bicarbonate
Drugs Used to Treat Peptic Ulcers: Antacids
weak bases; react with gastric acid to form water and salt; also reduce pepsin activity; pepsin is inactive at pH >4
Bismuth subsalicylate
Drugs Used to Treat Peptic Ulcers: Mucosal Protective Agents
has antimicrobial actions; inhibits pepsin activity; increases mucous secretion; coats and protects ulcer crater
Drugs Used to Treat Diarrhea: Agents that Modify Fluid and Electrolyte Transport
decreases fluid secretion
Sucralfate
Drugs Used to Treat Peptic Ulcers: Mucosal Protective Agents
complex of aluminum hydroxide and sulfated sucrose; forms complex gel with epithelial cells and covers area of injury (like an artificial mucosal lining); impairs diffusion of HCl; also stimulates prostaglandin secretion
Prochlorperazine
Drugs Used to Treat Chemotherapy-Induced Nausea: Phenothiazines
dopamine antagonist; block dopamine, histamine, and muscarinic receptors in the CTZ; effective against low emetogenic agents (better with higher dose but more side effects)
anti-psychotic
Promethazine
Drugs Used to Treat Chemotherapy-Induced Nausea: Phenothiazines
dopamine antagonist; block dopamine, histamine, and muscarinic receptors in the CTZ; effective against low emetogenic agents (better with higher dose but more side effects)
antihistamine
Droperidol
Drugs Used to Treat Chemotherapy-Induced Nausea:
Butyrophenones
dopamine antagonist; can prolong QT interval; used in patients who do not respond to others
Haloperidol
Drugs Used to Treat Chemotherapy-Induced Nausea:
Butyrophenones
dopamine antagonist; can prolong QT interval; used in patients who do not respond to others
Metoclopramide
Drugs Used to Treat Chemotherapy-Induced Nausea: Substituted Benzamides
dopamine antagonist
Alprazolam
Drugs Used to Treat Chemotherapy-Induced Nausea:
Benzodiazepines
low anti-emetic potency; effectiveness may come from sedative properties; great for anticipatory vomiting
Lorazepam
Drugs Used to Treat Chemotherapy-Induced Nausea:
Benzodiazepines
low anti-emetic potency; effectiveness may come from sedative properties; great for anticipatory vomiting
Dolasetron
Drugs Used to Treat Chemotherapy-Induced Nausea:
5-HT3 Receptor Blockers
serotonin receptor blockers, 5-HT3 specific; effective against all agents and against signals arising from the GI tract; not effective for motion sickness or vertigo
Granisetron
Drugs Used to Treat Chemotherapy-Induced Nausea:
5-HT3 Receptor Blockers
serotonin receptor blockers, 5-HT3 specific; effective against all agents and against signals arising from the GI tract; not effective for motion sickness or vertigo
Ondansetron
Drugs Used to Treat Chemotherapy-Induced Nausea:
5-HT3 Receptor Blockers
serotonin receptor blockers, 5-HT3 specific; effective against all agents and against signals arising from the GI tract; not effective for motion sickness or vertigo
Palonosetron
Drugs Used to Treat Chemotherapy-Induced Nausea:
5-HT3 Receptor Blockers
serotonin receptor blockers, 5-HT3 specific; effective against all agents and against signals arising from the GI tract; not effective for motion sickness or vertigo
Aprepitant
Drugs Used to Treat Chemotherapy-Induced Nausea:
Substance P/Neurokinin-1 Receptor Blocker
targets the neurokinin receptors in the CTZ; very effective for highly emetogenic agents
Diphenoxylate + atropine
Drugs Used to Treat Diarrhea: Antimotility Drugs
have opioid-like actions on the gut; inhibit acetylcholine release and decrease peristalsis; lack analgesic effects at usual dose
Loperamide
Drugs Used to Treat Diarrhea: Antimotility Drugs
have opioid-like actions on the gut; inhibit acetylcholine release and decrease peristalsis; lack analgesic effects at usual dose
Aluminum hydroxide
Drugs Used to Treat Diarrhea: Adsorbents
act by adsorbing intestinal toxins and/or by coating the intestinal mucosa; much less effective than other classes
Methylcellulose
Drugs Used to Treat Diarrhea: Adsorbents
act by adsorbing intestinal toxins and/or by coating the intestinal mucosa; much less effective than other classes
Drugs Used to Treat Constipation: Bulk Laxatives
form gels in the large intestine; cause water retention and intestinal distension; increases peristaltic activity
Bisacodyl
Drugs Used to Treat Constipation: Irritants and Stimulants
stimulates the colon; acts directly on colon nerve cells
Castor oil
Drugs Used to Treat Constipation: Irritants and Stimulants
irritates the stomach and initiates peristalsis
Senna
Drugs Used to Treat Constipation: Irritants and Stimulants
stimulant laxative; causes evacuation of bowels and water/electrolyte secretion
Psyllium
Drugs Used to Treat Constipation: Bulk Laxatives
form gels in the large intestine; cause water retention and intestinal distension; increases peristaltic activity
Magnesium sitrate
Drugs Used to Treat Constipation: Saline and Osmotic Laxatives
nonabsorbable salts or electrolytes; holds water in the intestine by osmosis
Magnesium hydroxide
Drugs Used to Treat Constipation: Saline and Osmotic Laxatives
nonabsorbable salts or electrolytes; holds water in the intestine by osmosis
Polyethylene glycol
Drugs Used to Treat Constipation: Saline and Osmotic Laxatives
nonabsorbable salts or electrolytes; holds water in the intestine by osmosis
Lactulose
Drugs Used to Treat Constipation: Saline and Osmotic Laxatives
nonabsorbable salts or electrolytes; holds water in the intestine by osmosis
Docusate
Drugs Used to Treat Constipation: Stool Softeners
emollients and surfactants; takes longer to be effective; may be used more for prevention
Glycerin suppoistories
Drugs Used to Treat Constipation: Lubricant Laxatives
Mineral oil
Drugs Used to Treat Constipation: Lubricant Laxatives
Lubiprostone
Drugs Used to Treat Constipation: Chloride Channel Activators
activates chloride channels; increases fluid secretion in the intestinal lumen
