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Systemic Pharmacology II > Drugs to Know 3 > Flashcards

Drugs to Know 3 Flashcards

1
Q

Antacids

A

Preanesthetic Medication

facilitate smooth induction of anesthesia

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2
Q

Anticholinergics

A

Preanesthetic Medication

facilitate smooth induction of anesthesia;
prevent bradycardia and secretion of fluids into the respiratory tract

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3
Q

Antiemetics

A

Preanesthetic Medication

facilitate smooth induction of anesthesia;
prevent nausea and possible aspiration of stomach contents

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4
Q

Antihistamines

A

Preanesthetic Medication

facilitate smooth induction of anesthesia;
prevention of allergic reactions

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5
Q

Benzodiazepines

A

Preanesthetic Medication; General Anesthetic: IV

facilitate smooth induction of anesthesia

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6
Q

Opioids

A

Preanesthetic Medication

facilitate smooth induction of anesthesia

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7
Q

Desflurane

A

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

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8
Q

Isoflurane

A

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

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9
Q

Nitrous Oxide

A

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

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10
Q

Sevoflurane

A

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

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11
Q

Barbiturates

A

General Anesthetic: Intravenous

exact mechanism of action unknown; thought to be similar to inhaled

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12
Q

Etomidate

A

General Anesthetic: Intravenous

exact mechanism of action unknown; thought to be similar to inhaled

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13
Q

Ketamine

A

General Anesthetic: Intravenous

exact mechanism of action unknown; thought to be similar to inhaled

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14
Q

Opioids

A

General Anesthetic: Intravenous

exact mechanism of action unknown; thought to be similar to inhaled

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15
Q

Propofol

A

General Anesthetic: Intravenous

exact mechanism of action unknown; thought to be similar to inhaled

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16
Q

Benoxinate

A

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

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17
Q

Cocaine

A

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

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18
Q

Lidocaine

A

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

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19
Q

Proparacaine

A

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

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20
Q

Tetracaine

A

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

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21
Q

Articaine

A

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

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22
Q

Bupivicaine

A

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

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23
Q

Mepivicaine

A

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

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24
Q

Procaine

A

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

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25
Q

Succinylcholine

A

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)

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26
Q

Cisatracurium

A

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

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27
Q

Rocuronium

A

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

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28
Q

Vecuronium

A

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

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29
Q

Baclofen

A

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

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30
Q

Carisoprodol

A

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

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31
Q

Cyclobenzaprine

A

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

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32
Q

Tizanidine

A

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

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33
Q

Gabapentin

A

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

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34
Q

Dantrolene

A

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

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35
Q

Adrenocortioctropic Hormone (ACTH)

A

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

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36
Q

Growth Hormone (GH)

A

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

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37
Q

Luteinizing Hormone (LH)

A

Anterior Pituitary Hormone- Gonadotropin

regulates gonadal steroid hormones

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38
Q

Follicle Stimulating Hormone (FSH)

A

Anterior Pituitary Hormone- Gonadotropin

regulates gonadal steroid hormones

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39
Q

Prolactin (PRL)

A

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

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40
Q

Thyroid Stimulating Hormone

A

Anterior Pituitary Hormone

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41
Q

Growth Hormone Releasing Hormone

A

Hypothalamus Hormone

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42
Q

Growth Hormone Inhibiting Hormone

A

Hypothalamus Hormone

suppress GH and thyroid-stimulating hormone release; also inhibits release of insulin, glucagon, and gastrin

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43
Q

Gonadotropin Releasing Hormone (GnRH)

A

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

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44
Q

Corticotropin Releasing Hormone

A

Hypothalamus Hormone

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45
Q

Thyrotropin Releasing Hormone

A

Hypothalamus Hormone

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46
Q

Oxytocin

A

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

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47
Q

Vasopressin/ADH

A

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

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48
Q

Iodine and potassium iodide

A

Drug Affecting the Thyroid

inhibits the production of hormone; mechanism not known

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49
Q

Liothyronine

A

Drug Affecting the Thyroid

treatment of hypothyroidism

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50
Q

Levothyroxine

A

Drug Affecting the Thyroid

treatment of hypothyroidism

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51
Q

Methimazole

A

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

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52
Q

Propylthiouracil

A

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

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53
Q

Estradiol

A

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

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54
Q

Estrone

A

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

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55
Q

Estriol

A

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

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56
Q

Leuprolide

A

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

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57
Q

Gonadorelin

A

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

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58
Q

Nafarelin

A

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

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59
Q

Raloxifene

A

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

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60
Q

Tamoxifen

A

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

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61
Q

Clomiphene

A

Selective Estrogen-Receptor Modulator

interact at estrogen receptors;

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62
Q

Drospirenone

A

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

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63
Q

Levonorgestrel

A

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

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64
Q

Medroxyprogesterone

A

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

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65
Q

Megestrol

A

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

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66
Q

Norelgestromin

A

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

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67
Q

Norethindrone

A

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

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68
Q

Preogesterone

A

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

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69
Q

Mifepristone

A

Antiprogestin

progesterone antagonist; partial agonist activity; administration in early pregnancy results in abortion of the fetus

Inhibitor of Adrenocorticoid Biosynthesis or Function

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70
Q

Testosterone

A

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

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71
Q

Bicalutamide

A

Antiandrogen

usually combined with GnRH analog to decrease LH and testosterone production

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72
Q

Flutamide

A

Antiandrogen

blocks action of testosterone in target organs

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73
Q

Nilutamide

A

Antiandrogen

usually combined with GnRH analog to decrease LH and testosterone production

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74
Q

Aspart

A

Diabetes - Insulin

insulin tells the cells to absorb and store glucose

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75
Q

Glulisine

A

Diabetes - Insulin

insulin tells the cells to absorb and store glucose

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76
Q

Lispro

A

Diabetes - Insulin

insulin tells the cells to absorb and store glucose

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77
Q

Regular Insulin

A

Diabetes - Insulin

insulin tells the cells to absorb and store glucose

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78
Q

NPH

A

Diabetes - Insulin

insulin tells the cells to absorb and store glucose

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79
Q

Detemir

A

Diabetes - Insulin

insulin tells the cells to absorb and store glucose

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80
Q

Glargine

A

Diabetes - Insulin

insulin tells the cells to absorb and store glucose

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81
Q

Pramlintide

A

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

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82
Q

Gliclazide

A

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

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83
Q

Glimepiride

A

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

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84
Q

Glipizide

A

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

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85
Q

Glyburide

A

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

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86
Q

Nateglinide

A

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

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87
Q

Repaglinide

A

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

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88
Q

Metformin

A

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

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89
Q

Pioglitazone

A

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

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90
Q

Rosiglitazone

A

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

91
Q

Acarbose

A

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

92
Q

Miglitol

A

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

93
Q

Alogliptin

A

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”

94
Q

Linagliptin

A

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”

95
Q

Saxagliptin

A

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”

96
Q

Sitagliptin

A

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”

97
Q

Dulaglutide

A

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

98
Q

Exenatide

A

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

99
Q

Liraglutide

A

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

100
Q

Lixisenatide

A

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

101
Q

Semaglutide

A

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

102
Q

Canagliflozin

A

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)

103
Q

Dapagliflozin

A

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)

104
Q

Empagliflozin

A

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)

105
Q

Ertugliflozin

A

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)

106
Q

Betamethasone

A

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

107
Q

Cortisone

A

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

108
Q

Dexamethasone

A

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

109
Q

Fludrocortisone

A

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

110
Q

Hydrocortisone

A

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

111
Q

Methylprednisolone

A

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

112
Q

Prednisolone

A

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

113
Q

Triamcinolone

A

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

114
Q

Loteprednol

A

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

115
Q

Metyrapone

A

Inhibitor of Adrenocorticoid Biosynthesis or Function

inhibits synthesis of cortisol

116
Q

Aminoglutheamide

A

Inhibitor of Adrenocorticoid Biosynthesis or Function

blocks conversion of cholesterol to pregnenolone; inhibits synthesis of ALL steroids

117
Q

Ketoconazole

A

Inhibitor of Adrenocorticoid Biosynthesis or Function

at high doses blocks enzyme responsible for steroid production

118
Q

Spironolactone

A

Inhibitor of Adrenocorticoid Biosynthesis or Function

blocks aldosterone receptors; also blocks androgen receptor

119
Q

Eplerenone

A

Inhibitor of Adrenocorticoid Biosynthesis or Function

blocks aldosterone receptors

120
Q

Misoprostol

A

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

121
Q

Iloprost

A

Prostaglandin Analog

analog of prostacyclin; activates prostacyclin receptors and increases production of cAMP

122
Q

Latanoprost

A

Prostaglandin Analog

PGF analog; binds to prostaglandin FP receptors and increases uveoscleral outflow; causes reduction of IOP

123
Q

Travaprost

A

Prostaglandin Analog

pro-drug; binds to prostaglandin FP receptors and increases uveoscleral outflow; causes reduction of IOP

124
Q

Bimatoprost

A

Prostaglandin Analog

mimics endogenous prostamides; binds to prostaglandin FP receptors and increases uveoscleral outflow; causes reduction of IOP

125
Q

Aspirin

A

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

126
Q

Indomethacin

A

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

127
Q

Ibuprofen

A

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

128
Q

Diclofenac

A

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

129
Q

Naproxen

A

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

130
Q

Ketorolac

A

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

131
Q

Meloxicam

A

NSAID - Oxicam

inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis

preferential for COX-2, non selective at high doses

132
Q

Peroxicam

A

NSAID - Oxicam

inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis

133
Q

Celecoxib

A

NSAID - COX-2 Specific

inhibits the synthesis of prostaglandins; inhibits cyclooxygenase enzymes, leading to decreased prostaglandin synthesis

specific for COX-2

134
Q

Acetaminophen

A

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)

135
Q

Abatacept

A

Drugs for Arthritis (DMARDs)

inhibits T-cell activation; biologic DMARD

136
Q

Adalimumab

A

Drugs for Arthritis (DMARDs)

TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD

137
Q

Anakinra

A

Drugs for Arthritis (DMARDs)

IL-1 antagnoist (IL-1 is a pro-inflammatory cytokine); biologic DMARD

138
Q

Certolizumab

A

Drugs for Arthritis (DMARDs)

TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD

139
Q

Hydroxychloroquine

A

Drugs for Arthritis (DMARDs)

increases pH within inflammatory cells; leads to interference with “antigen processing”; causes decreased stimulation of CD4 cells

140
Q

Etanercept

A

Drugs for Arthritis (DMARDs)

TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD

141
Q

Golimumab

A

Drugs for Arthritis (DMARDs)

TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD

142
Q

Infliximab

A

Drugs for Arthritis (DMARDs)

TNF inhibitor (TNF is a pro-inflammatory cytokine); biologic DMARD

143
Q

Methotrexate

A

Drugs for Arthritis (DMARDs)

immunosuppressant; inhibits dihydrofolate reductase; impairs DNA synthesis; aids in effectivness for autoimmune disease

144
Q

Tocilizumab

A

Drugs for Arthritis (DMARDs)

inhibits IL-6; biologic DMARD

145
Q

Tofacitinib

A

Drugs for Arthritis (DMARDs)

regulates immune cell function; biologic DMARD

146
Q

Beclomethasone

A

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

147
Q

Budesonide

A

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

148
Q

Ciclesonide

A

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

149
Q

Flunisolide

A

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

150
Q

Fluticasone

A

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

151
Q

Mometasone

A

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

152
Q

Cromolyn

A

Respiratory Drugs: Anti-Inflammatory
Mast Cell Stabilizer

blocks release of inflammatory mediators

153
Q

Montelukast

A

Respiratory Drugs: Anti-Inflammatory
Anti-Leukotriene

blocks effects of leukotrienes

154
Q

Zafirlukast

A

Respiratory Drugs: Anti-Inflammatory
Anti-Leukotriene

blocks effects of leukotrienes

155
Q

Zileuton

A

Respiratory Drugs: Anti-Inflammatory
Anti-Leukotriene

inhibitor of 5-lipoxygenase; prevents formation of leukotrienes

156
Q

Albuterol

A

Respiratory Drugs: Bronchodilators

Short Acting Beta-2 Agonist

157
Q

Levalbuterol

A

Respiratory Drugs: Bronchodilators

Short Acting Beta-2 Agonist

158
Q

Pirbuterol

A

Respiratory Drugs: Bronchodilators

Short Acting Beta-2 Agonist

159
Q

Formoterol

A

Respiratory Drugs: Bronchodilators

Long Acting Beta-2 Agonist

160
Q

Indacaterol

A

Respiratory Drugs: Bronchodilators

Long Acting Beta-2 Agonist

161
Q

Salmeterol

A

Respiratory Drugs: Bronchodilators

Long Acting Beta-2 Agonist

162
Q

Ipratropium

A

Respiratory Drugs: Bronchodilators
Cholinergic Agonist

blocks contraction of airway smooth muscle mediated by vagus nerve; blocks acetylcholine receptors

163
Q

Tiotropium

A

Respiratory Drugs: Bronchodilators
Cholinergic Agonist

blocks contraction of airway smooth muscle mediated by vagus nerve; blocks acetylcholine receptors

164
Q

Theophylline

A

Respiratory Drugs: Bronchodilators

nonspecific MOA; increases cAMP and antagonizes adenosine receptors

165
Q

Omalziumab

A

Respiratory Drugs: Bronchodilators
Immunoglobulin Antagonist

recombinant DNA monoclonal antibody; selectively binds to IgE; decreases release of inflammatory mediators from mast cells and basophils

166
Q

Codeine

A

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

167
Q

Dextromethorphan

A

Respiratory Drugs: Antitussives/Expectorants

synthetic derivative of morphine; no analgesic effect at antitussive doses; equally effective as codeine

168
Q

Benzonatate

A

Respiratory Drugs: Antitussives/Expectorants

local anesthetic; anesthetizes respiratory passage and pleural stretch receptors; reduces cough reflex

169
Q

Guaifenesin

A

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

170
Q

Cetirizine

A

Respiratory Drugs: Antihistamines

H1 blockers

171
Q

Diphenhydramine

A

Respiratory Drugs: Antihistamines

H1 blockers

172
Q

Fexofenadine

A

Respiratory Drugs: Antihistamines

H1 blockers

173
Q

Loratadine

A

Respiratory Drugs: Antihistamines

H1 blockers

174
Q

Amoxicillin

A

Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents

used in combination with PPIs to eradicate H. pylori

175
Q

Bismuth Compounds

A

Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents

used in combination with PPIs to eradicate H. pylori

176
Q

Clarithromycin

A

Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents

used in combination with PPIs to eradicate H. pylori

177
Q

Metronidazole

A

Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents

used in combination with PPIs to eradicate H. pylori

178
Q

Tetracycline

A

Drugs Used to Treat Peptic Ulcers: Antimicrobial Agents

used in combination with PPIs to eradicate H. pylori

179
Q

Cimetidine

A

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

180
Q

Famotidine

A

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

181
Q

Nizatidine

A

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

182
Q

Ranitidine

A

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

183
Q

Dexlansoprazole

A

Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)

binds to the proton pump and prevents secretion of hydrogen ions

184
Q

Esemoeprazole

A

Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)

binds to the proton pump and prevents secretion of hydrogen ions

185
Q

Lansoprazole

A

Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)

binds to the proton pump and prevents secretion of hydrogen ions

186
Q

Omeprazole

A

Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)

binds to the proton pump and prevents secretion of hydrogen ions

187
Q

Pantoprazole

A

Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)

binds to the proton pump and prevents secretion of hydrogen ions

188
Q

Rebeprazole

A

Drugs Used to Treat Peptic Ulcers: Proton Pump Inhibitors (PPIs)

binds to the proton pump and prevents secretion of hydrogen ions

189
Q

Dicyclomine

A

Drugs Used to Treat Peptic Ulcers: Antimuscarinic Agents

190
Q

Aluminium hydroxide

A

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

191
Q

Calcium carbonate

A

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

192
Q

Magnesium hydroxide

A

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

193
Q

Sodium bicarbonate

A

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

194
Q

Bismuth subsalicylate

A

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

195
Q

Sucralfate

A

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

196
Q

Prochlorperazine

A

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

197
Q

Promethazine

A

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

198
Q

Droperidol

A

Drugs Used to Treat Chemotherapy-Induced Nausea:
Butyrophenones

dopamine antagonist; can prolong QT interval; used in patients who do not respond to others

199
Q

Haloperidol

A

Drugs Used to Treat Chemotherapy-Induced Nausea:
Butyrophenones

dopamine antagonist; can prolong QT interval; used in patients who do not respond to others

200
Q

Metoclopramide

A

Drugs Used to Treat Chemotherapy-Induced Nausea: Substituted Benzamides

dopamine antagonist

201
Q

Alprazolam

A

Drugs Used to Treat Chemotherapy-Induced Nausea:
Benzodiazepines

low anti-emetic potency; effectiveness may come from sedative properties; great for anticipatory vomiting

202
Q

Lorazepam

A

Drugs Used to Treat Chemotherapy-Induced Nausea:
Benzodiazepines

low anti-emetic potency; effectiveness may come from sedative properties; great for anticipatory vomiting

203
Q

Dolasetron

A

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

204
Q

Granisetron

A

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

205
Q

Ondansetron

A

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

206
Q

Palonosetron

A

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

207
Q

Aprepitant

A

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

208
Q

Diphenoxylate + atropine

A

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

209
Q

Loperamide

A

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

210
Q

Aluminum hydroxide

A

Drugs Used to Treat Diarrhea: Adsorbents

act by adsorbing intestinal toxins and/or by coating the intestinal mucosa; much less effective than other classes

211
Q

Methylcellulose

A

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

212
Q

Bisacodyl

A

Drugs Used to Treat Constipation: Irritants and Stimulants

stimulates the colon; acts directly on colon nerve cells

213
Q

Castor oil

A

Drugs Used to Treat Constipation: Irritants and Stimulants

irritates the stomach and initiates peristalsis

214
Q

Senna

A

Drugs Used to Treat Constipation: Irritants and Stimulants

stimulant laxative; causes evacuation of bowels and water/electrolyte secretion

215
Q

Psyllium

A

Drugs Used to Treat Constipation: Bulk Laxatives

form gels in the large intestine; cause water retention and intestinal distension; increases peristaltic activity

216
Q

Magnesium sitrate

A

Drugs Used to Treat Constipation: Saline and Osmotic Laxatives

nonabsorbable salts or electrolytes; holds water in the intestine by osmosis

217
Q

Magnesium hydroxide

A

Drugs Used to Treat Constipation: Saline and Osmotic Laxatives

nonabsorbable salts or electrolytes; holds water in the intestine by osmosis

218
Q

Polyethylene glycol

A

Drugs Used to Treat Constipation: Saline and Osmotic Laxatives

nonabsorbable salts or electrolytes; holds water in the intestine by osmosis

219
Q

Lactulose

A

Drugs Used to Treat Constipation: Saline and Osmotic Laxatives

nonabsorbable salts or electrolytes; holds water in the intestine by osmosis

220
Q

Docusate

A

Drugs Used to Treat Constipation: Stool Softeners

emollients and surfactants; takes longer to be effective; may be used more for prevention

221
Q

Glycerin suppoistories

A

Drugs Used to Treat Constipation: Lubricant Laxatives

222
Q

Mineral oil

A

Drugs Used to Treat Constipation: Lubricant Laxatives

223
Q

Lubiprostone

A

Drugs Used to Treat Constipation: Chloride Channel Activators

activates chloride channels; increases fluid secretion in the intestinal lumen

Systemic Pharmacology II (4 decks)

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