Jon Pharm

Benzodiazepine – Sedative hypnotic anxiolytic: enhance inhibitory effects of gamma-aminobutyric acid (GABA) in CNS, relief occurs rapidly; T: Seizure disorders, insomnia, muscle spasms; alcohol withdrawal, anesthesia

Nonbarbiturate – Atypical anxiolytic: Unknown – binds to serotonin and dopamine receptors; T: Panic disorder, OCD, social anxiety disorder, PTSD

SSRI – Antidepressant: selectively inhibits serotonin reuptake; T: Generalized Anxiety Disorder, panic disorder, OCD, social anxiety disorder, PTSD, depressive disorders, effects = 4 wks

TCA - Tricyclic Antidepressant – block reuptake of norepinephrine and serotonin – intensifying these neurotransmitters; T: Depression, depressive episodes of bipolar disorder (BD), chronic pain, enuresis*

SSRI: - selectively block reuptake of monoamine neurotransmitter serotonin in synaptic space T: Major depression, OCD, bulimia nervosa, premenstrual dysphoric disorders, PTSD

MAOI – Monoamine Oxidase Inhibitor: block MAO-A in brain = increases norepinephrine, dopamine, & serotonin T: atypical depression, bulimia nervosa, OCD

Atypical Antidepressant: inhibiting dopamine uptake; T: Depression, aid to quit smoking, SAD (seasonal affective disorder) prevention Alternative to SSRI for sexual function

Mood Stabilizer: neurochemical changes, serotonin receptor blockade, decrease in neural atrophy and/or neural growth; T: Bipolar disorder, acute mania, prevention, suicidal, alcoholism, bulimia, schizophrenia

AED – Mood-Stabilizing Antiepileptic Drug: slows entrance of Na & Ca back into neuron (slows return to action state), potentiates inhibitory effects of GABA, inhibits glutamic acid (glutamate) à suppressing CNS excitation; T: manic & depressive episodes, prevention, esp – rapid cycling

AED: slows entrance of Na & Ca back into neuron (slows return to action state), potentiates inhibitory effects of GABA, inhibits glutamic acid (glutamate) à suppressing CNS excitation; T: manic & depressive episodes, prevention, esp – rapid cycling

AED: slows entrance of Na & Ca back into neuron (slows return to action state), potentiates inhibitory effects of GABA, inhibits glutamic acid (glutamate) à suppressing CNS excitation; T: manic & depressive episodes, prevention, esp – rapid cycling

Antipsychotic – Conventional: Block dopamine (D2), acetylcholine, histamine, and norepinephrine (NE) receptors in brain & periphery; T: acute & chronic psychosis, Schizophrenia, Bipolar disorder, Tourette’s, delusional & schizoaffetive disorders, dementia, prevention of nausea & vomiting in trigger zone – medulla; 2-4 wks for affect

Antipsychotic – Atypical: works by blocking serotonin & some dopamine receptors; also block receptors for NE, histamine, and ACh; T: Schizophrenia, psychosis by levodopa therapy, relief of psychotic behavior ie bipolar

SSRI: - selectively block reuptake of monoamine neurotransmitter serotonin in synaptic space T: Major Depression, bulimia nervosa, panic, school phobia, separation anxiety disorder, PSTD, OCD, ADHD

TCA - Tricyclic Antidepressant – block reuptake of norepinephrine and serotonin – intensifying these neurotransmitters; T: Depression, depressive episodes of bipolar disorder (BD), Autistic disorder, ADHD, Panic school phobia, separation anxiety disorder, PTSD, OCD

Nonbarbiturate – Atypical anxiolytic: Unknown – binds to serotonin and dopamine receptors No Sedation; T: Panic disorder, OCD, social anxiety disorder, PTSD

CNS Stimulants: Raise the levels of NE, serotonin, & dopamine in CNS T: ADHD, Conduct disorder

Norepinephrine Selective Reuptake Inhibitor: block reuptake of NE, not stimulant! T: ADHD

Antipsychotic – Atypical: works by blocking serotonin & some dopamine receptors; also block receptors for NE, histamine, and ACh; T: Schizophrenia, psychosis by levodopa therapy, relief of psychotic behavior ie bipolar

Detox: Alcohol Withdrawal; Benzodiazepines: maintenance of client’s vital signs within normal limits; decrease risk of seizures, Decrease in intensity of symptoms

Detox: Alcohol Adjunct Withdrawal Meds:

Carbamazepine: decrease in seizures

Clonidine & Propanolol: depression of autonomic response (BP, HR, diaphoresis

Propanolol: decrease in cravings

Maintenance: Alcohol Abstinenc: daily oral med, aversion (behavioral) therapy

Pure Opioid Antagonist: suppresses craving and pleasurable effects of alcohol also used in opioid withdraw

Decreases unpleasant effects resulting from abstinence – anxiety, restlessness

Substition – Oral Opioid Agonist: replaces opioid addiction, prevent abstinence syndrome, withdrawal and long-term maintenance, still has dependence

Suppresses autonomic hyperactivity, does not reduce cravings

Agonist-Antagonist Opioids: decrease feelings of craving and adherence

Decreases nicotine craving and symptoms of withdrawal

Nicotine replacements are substitutes for cigarettes or chewing tobacco

Cholinesterase Inhibitor: prevents cholinesterase (ChE) from inactivating acetylcholine (ACh) /| ACh in brain; T: treatment and reversal of myasthenia gravis

Dopaminergic: precursor crosses b-b barrier & taken up by dopaminergic nerve terminals à more DA; T: 1st line med for Parkinson’s Disease (PD)

Dopaminergic Augment – decreases amount of levodopa converted to DA in intestines and periphery; T: PD

Dopamine Agonist: Act directly on DA receptors; T: PD for early onset w/ younger pts b/c hypotension & drowsy

Central Acting Cholinergic: block acetylcholine at muscarinic receptors, maintains DA & ACh balance; T: PD

Antiviral: stimulate DA release, prevent dopamine reuptake, may block cholinergic & glutamate receptors; T: PD

Barbiturates: suppresses seizures by potentiating the effects of GABA, binds to GABA receptors causing receptor to respond more intensely to GABA = CNS depression; T: partial* & generalized* seizures EXCEPT absence* seizures

Antiepileptic Drugs (AED) - Hydantoins: slows entrance of Na & Ca back into neuron (slows return to action state), à suppressing CNS excitation; T: ALL seizures EXCEPT absence; IV route for status epilepticus

AED - Benzodiazepines: Sedative hypnotic anxiolytic: enhance inhibitory effects of gamma-aminobutyric acid (GABA) in CNS, relief occurs rapidly; T: status epilepticus

AED - Benzodiazepines: slows entrance of Na & Ca back into neuron (slows return to action state), à suppressing CNS excitation T: partial & tonic-clonic seizures

AED - Benzodiazepines: suppresses neurons in thalamus responsible for generating absence seizures (low-threshold calcium currents) T: absence seizures

AED – Suppression of high-frequency neuronal firing by blocking Na channels, suppresses Ca influx in T-type channels, augments inhibitory factors of GABA; T: partial, generalized & absence seizures – GOOD

AED – Unknown, analog of GABA, but does not directly affect GABA receptors, may enhance release of GABA, increasing GABA-mediated inhibition of neural firing; T: single agent for partial seizures

Beta Adrenergic Blockers – decrease intra-ocular pressure by decreasing amount of aqueous humor produced T: primarily for POAG

Alpha2 Adrenergic Agonists – decrease production & outflow of aqueous humor; T: 1st line long term med for POAG

Prostaglandin Analog: increases aqueous humor outflow through relaxation of ciliary muscle; T: for ocular hypertension & POAG

Osmotic Agent: Decrease intraocular pressure rapidly drawing fluid from anterior chamber of eye; T: treat rapid progression of closed-angle glaucoma to prevent blind

Carbonic Anhydrase Inhibitor (systemic): Reduces production of aqueous humor by causing diuresis through renal effects; T: last resort, non-antimicrobial sulfonamide for emergency acute angle closure glaucoma – also, seizures, heart failure, acute mountain sickness

Antimicrobial: eradication of infection; T: otitis media & bacterial infections of body

Fluoroquinolone Antibiotic + Steriod: decrease pain, edema, and erythema in ear canal; T: treat otitis externa

Depolarzing Neuromuscular Blocker: mimics ACh, binds to cholinergic receptors at neuromuscular junction, blocking ACh, causes sustained depolarization of muscle = muscle paralysis; do no cross b-b barrier, no loss of consciouness or pain; T: general anesthesia – muscle relaxation, spontaneous resp. movement w/ mechanical vent., seizure control w/ electroconvulsive therapy, endotrach intubation and endoscopy

Nondepolarzing Neuromuscular Blocker: Block ACh from binding w/ cholinergic receptors at motor end plate. Muscle paralysis occurs b/c inhibited nerve depolarization & muscle contraction

Centrally Acting Muscle Relaxants: acts in CNS to enhance GABA & produce sedative effects & depress spasticity of muscles T: muscle spasm, anxiety, panic, insomnia, status epilepticus, EHOH withdrawal, anesthesia induction

Peripherally Acting Muscle Relaxant: acts directly on spastic muscles and inhibits muscle contraction by preventing release of calcium in skeletal muscles; T: relief of spasticity – cerebral palsy, spinal cord injury, multiple sclerosis, malignant hyperthermia

Muscarinic Agonist: stimulation of muscarinic receptors of GU tract = relaxation of trigone & sphincter muscles & contraction of detrusor muscle; T: Nonobstructive urinary retention – postop or postpartum

Muscarinic Antagonist (M3 receptor selective): inhibiting muscarinic receptors of detrusor muscle of bladder – prevent contraction & urge to void; T: overactive bladder

Benzodiazepine: enhance action of gamma-amino butyric acid (GABA) in CNS T: anxiety, seizure, insomnia, muscle spasm, alcohol withdrawal, panic disorder, induction to anesthesia

Nonbenzodiazepine: enhance action of GABA in CNS – prolonged sleep duration, decreased awakenings; NOT antianxiety, muscle relaxant, antiepileptic T: management of insomnia

Melatonin Agonist: activation of melatonin receptors; T: management of insomnia; 30 min before bedtime on empty stomach

Intravenous Anesthetics: Barbituate, Benzodiazepine 2x, Opioid; loss of consciousness & elimination of response to painful stimuli; T: induction & maintenance of anesthesia

Beta2-Adrenergic Agonist: selectively activates Beta2-receptors in the bronchial smooth muscle – bronchodialation = histimine release inhibited; ciliary motility increased; Salmeterol = long term

Methylxanthine: causes relaxation of bronchial smooth muscle; T: Orally for long-term chronic asthma; IV or oral - emergency

Inhaled Anticholinergics: block muscarinic receptors of bronchi = bronchodialation T: bronchospasm w/ COPD; allergen induced / exercise induced asthma

Glucocorticoids: Inhalation, prevent inflammation, suppress airway mucus production, & promote B2 receptor response in bronchial trees; not immediate; \/ frequency & severity of exacerbations & acute attacks T: short term status asthmaticus, acute asthma attack; chronic asthma;

Glucocorticoids: Oral, prevent inflammation, suppress airway mucus production, & promote B2 receptor response in bronchial trees; not immediate; \/ frequency & severity of exacerbations & acute attacks T: short term status asthmaticus, acute asthma attack; chronic asthma;

Mast Cell Stabilizer (Anti-Inflammatory): stabilize mast cells, à inhibits release of histamine & other inflam. Mediators; suppress inflam. Cells (eosinophils & macrophages); T: chronic asthma, allergen-induced attack; allergic rhinitis

Leukotriene Modifier: prevent effects of leukotrienes à suppressing inflammation, bronchoconstriction, airway edema, & mucus production; T: long-term asthma therapy; prevent exercise-induced bronchospams

Beta2-Adrenergic Agonist: selectively activates Beta2-receptors in the bronchial smooth muscle – bronchodialation = histimine release inhibited; ciliary motility increased; Salmeterol = long term

Methylxanthine: causes relaxation of bronchial smooth muscle; T: Orally for long-term chronic asthma; IV or oral - emergency

Inhaled Anticholinergics: block muscarinic receptors of bronchi = bronchodialation T: bronchospasm w/ COPD; allergen induced / exercise induced asthma

Glucocorticoids: Inhalation, prevent inflammation, suppress airway mucus production, & promote B2 receptor response in bronchial trees; not immediate; \/ frequency & severity of exacerbations & acute attacks T: short term status asthmaticus, acute asthma attack; chronic asthma;

Glucocorticoids: Oral, prevent inflammation, suppress airway mucus production, & promote B2 receptor response in bronchial trees; not immediate; \/ frequency & severity of exacerbations & acute attacks T: short term status asthmaticus, acute asthma attack; chronic asthma;

Mast Cell Stabilizer (Anti-Inflammatory): stabilize mast cells, à inhibits release of histamine & other inflam. Mediators; suppress inflam. Cells (eosinophils & macrophages); T: chronic asthma, allergen-induced attack; allergic rhinitis

Leukotriene Modifier: prevent effects of leukotrienes à suppressing inflammation, bronchoconstriction, airway edema, & mucus production; T: long-term asthma therapy; prevent exercise-induced bronchospams

High Ceiling Loop Diuretic: block reabsorption of Na & Cl & prevents reabsorption of H2O in ascending limb of loop of Henle; cause extensive diuresis even w/ severe renal failure; T: emergent mobilization of fluid, pulmonary edema, hypertension, hypercalcemia w/ kidney stone

Thiazide Diuretic: in early distal convoluted tubule, blocks reabsorption of Na & Cl & prevents reabsorption of H2O, promote diuresis w/ no renal failure; T: 1st line med for hypertension; edema of mild-moderate heart failure/ liver & kidney disease

Potassium-Sparing Diuretic: block action of aldosterone (sodium & water retention) = secretion of Na & H2O; T: heart failure, hyperaldosteronism

Osmotic Diuretics: reduce intracranial pressure & intraocular pressure by raising serum osmolarity & drawing fluid back into vascular & extravascular space; T: renal failure w/ hypovolemic shock, severe hypotension, intracranial pressure, intraocular pressure; promote sodium retention & water excretion w/ hyponatremia & fluid volume excess

ACEI: block the production of angiotensin II = vasodialation (mostly arteriole); excretion of Na & H2O, retention of K in kidneys; reduces pathology of blood vessels from angiotensin II & aldosterone; T: hypertension, heart failure, myocardial infaction, diabetic & nondiabetic nephropathy

ARB: block angiotensin II in body = vasodialation, excretion of Na & H2O, retention of K; T: hypertension, heart failure, stroke prevention, delay progress of diabetic nephropathy

Calcium Channel Blocker: Blocking of calcium channels in blood vessels = vasodialation (primarily arterioles) of peripheral arterioles & arteries/arterioles of heart; T: agina pectoris, hypertension

Calcium Channel Blocker: Blocking of calcium channels in blood vessels = vasodialation (primarily arterioles) of peripheral arterioles & arteries/arterioles of heart & in myocardium, SA node, AV node = decreased force of contraction, heart rate, & slowing of rate of conduction through AV node; T: angina, hypertension, & cardiac dysrhytmias – atrial fib, flutter, svt

Alpha Adrenergic Blockers (Sympatholytics): selective alpha-1 blockade = venous & arterial dilation, smooth muscle relaxation of prostatic capsule & bladder neck; T: primary hypertension, decrease symptoms of benign prostatic hypertrophy (urgency, frequency, dysuria)

Centrally Acting Alpha2 Agonist: within CNS, \/ sympathetic outflow = \/ stimulation of adrenergic receptors of heart & peripheral vascular system = bradycardia & \/ cardiac output; vasodialation = \/ blood pressure; T: primary hypertension, severe cancer pain

Beta Adrenergic Blockers (Sympatholytics): selective B1-adrenergic block in myocardium & electrical conduction of heart = \/ heart rate, contractility, rate of conduction through AV node; T: primary hypertension, angina, tachydysrhythmias, heart failure, myocardial infarction

Beta Adrenergic Blockers (Sympatholytics): B1 & B2-adrenergic block in myocardium & electrical conduction of heart = \/ heart rate, contractility, rate of conduction through AV node; T: primary hypertension, angina, tachydysrhythmias, heart failure, myocardial infarction

Hypertensive Crisis Med: direct vasodilation of arteries and veins resulting in rapid reduction of blood pressure (decreased preload & afterload); T: hypertensive emergencies

Cardiac Glycoside: increased force of myocardial contraction (inotropic); decreased heart rate (chronotropic); T: heart failure, dysrhythmias

Catecholamine: Alpha 1 receptor – vasocontriction (slows abs. Of local anesthetics), Beta 1 receptor - /\ heart rate, myocardial contractility, rate of conduction through AV node (AV block & Cardiac arrest), Beta 2 receptor – bronchodialation (Asthma)

Catecholamine: Low Dose – Dopamine receptors – renal blood vessel dilation; Moderate - & Beta 1 - /\ heart rate, myocardial contractility, rate of conduction through AV node; High - & Alpha 1 – vasocontriction; T: shock, heart failure

Catecholamine: Beta 1 - /\ heart rate, myocardial contractility, rate of conduction through AV node

Organic Nitrates: dilates veins & decreases venous return (preload), à \/ oxygen demand, also prevents or reduces coronary artery spasm à /\ O2 supply; T: acute angina, preventing chronic & variant angina

Antianginal Agent: lowers cardiac oxygen demand à improves exercise tolerance & \/ pain; T: chronic stable angina in combo w/ amlodipine (Norvasc) – beta adrenergic blocker or an organic nitrate

Class IA Sodium Channel Blocker: \/ electrical conduction, rate of polarization & /\ automaticity; T: supraventricular & ventricular tachycardia, atrial flutter & fibrillation

Class IB Sodium Channel Blocker: \/ electrical conduction & automaticity; /\ rate of repolarization; T: short-term use only for ventricular dysrhythmias

Class IC Sodium Channel Blocker: \/ electrical conduction & excitability & /\ rate of depolarization; T: Severe ventricular dysrythmias

Class II Beta-Adrenergic Blocker: \/ heart rate, slow conduction rate through SA node; \/ atrial ectopic stimulation; T: atrial fib. & flutter, paroxysmal SVT, hypertension, angina

Class III Potassium Channel Blocker: \/ rate of repolarization, electrical conduction, contractility, automaticity; T: conversion of atrial fibrillation – oral; recurrent ventricular fib or ventricular tachycardia

Class IV Calcium Channel Blocker: \/ force of contraction, heart rate, slow rate of conduction through AV node; T: paroxysmal SVT, Wolf-Parkinson-White syndrome

Class IV: \/ electrical conduction through AV node

Class IV:\/ electrical conduction through AV node, /\ myocardial contraction

Fibrates: \/ triglyceride levels (/\ in VLDL secretion), /\ HDL levels by promoting production of precursors; T: \/ of plasma triglycerides (VLDL); /\ levels of HDL

HMG COA Reductase Inhibitors: \/ manufacture of LDL cholesterol, very low-density lipoproteins, /\ manufacture of High-density lipoproteins; promotion of vasodilation, \/ plaque site formation & risk of thromboembolism; T: primary hypercholesterolemia, prevents coronary events, MI & stroke w/ diabetes,

Cholesterol Absorption Inhibitor: inhibits absorp. Of cholesterol secreted in bile & from food; T: adjunct to lower LDL cholesterol, alone or combo as statin med

Bile-Acid Sequestrants: \/ LDL cholesterol; T: adjunct w/ HMG CoA reductase inhibitor & dietary measures

Decrease LDL cholesterol & triglyceride levels; T: For pts w/ risk for pancreatitis & elevated triglyceride levels; \/ LDL & triglyceride levels & /\ HDL leels

Anticoagulants/Parental: prevent bleeding by interaction of thrombin formation and factor Xa, resulting in inhibition of the formation of fibrin; T: prompt anticoagulant activity (stroke, dvt, etc); open heart surgery, renal dialysis; prophylaxis against post op veinous thrombosis

Low Molecular Weight Heparin Anticoagulants/ Parental: prevent bleeding by interaction of thrombin formation and factor Xa, resulting in inhibition of the formation of fibrin; T: esp treating acute myocardial infarction

Activated factor X (Xa) inhibitory - Anticoagulants/ Parental: prevent bleeding by interaction of thrombin formation and factor Xa, resulting in inhibition of the formation of fibrin; T: esp treating disseminated intravascular coagulation

Anticogulant/Oral: antagonizes vitamin K, thereby preventing synthesis of four coagulation factors: factor VII, IX, X and prothrombin; T: venous thrombosis, thrombus formation w/ atrial fib, or prosthetic heart valves; recurrent myocardial infarction, transient ischemic attacks

Antiplatelets / Salicylic: prevent platelets from clumping together by inhibiting enzymes & factors that normally lead to clotting; inhibit aggregation at onset of clotting process; T: Acute myocardial infarction & prevention; stroke prevention

Antiplatelets / Glycoprotein inhibitor: prevent platelets from clumping together by inhibiting enzymes & factors that normally lead to clotting; inhibit aggregation at onset of clotting process; T: esp – acute coronary syndromes

Antiplatelet / Adp inhibitor: prevent platelets from clumping together by inhibiting enzymes & factors that normally lead to clotting; inhibit aggregation at onset of clotting process; T: Acute myocardial infarction & prevention; stroke prevention

Antiplatelet / Aterial vasodilator: prevent platelets from clumping together by inhibiting enzymes & factors that normally lead to clotting; inhibit aggregation at onset of clotting process; T: esp – intermittent claudication (muscle pain)

Thrombolytic: dissolve clots already formed, converts plasminogen to plasmin, which destroys fibrinogen & other clotting factors; T: acute MI, DVTs, massive pulmonary emboli, ischemic stroke (alteplase especially)

Erythropoietic Growth Factor: acts on bone marrow to /\ production of red blood cells; T: anemia related chronic renal failure, use of zidovudine (Retrovir) – HIV-infection, chemotherapy, & elective surgery

Leukeopoietic Growth Factor: stimulates bone marrow to increase production of neutrophils; T: \/ risk of infection in pts w/ neutropenia (cancer)

Granulocyte Macrophage Colony Stimulating Factor: acts on bone marrow to /\ production of wbcs (neutrophils, monocytes, macrophages, eosinophils); T: hastens bone marrow function post bone marrow transplant; treats failed bone marrow transplant

Thrombopoietic Growth Factors: /\ production of platelets; T: \/ thrombocytopenia & need for platelet transfusions in pts receiving chemotherapy

Increases circulating volume; T: replacement therapy for acute blood loss; volume extesion in pts w/ extensive burn injury, dehydration, shock

Increases number of RBCs; T: severe symptomatic anemia, hemoglobinopathies, medication-induced hemolytic anemia, erythroblastosis fetalis

Increases platelet counts; T: thrombocytopenia, aplastic anemia, chemotherapy-induced bone marrow suppression; active bleeding

Replaces coagulation factors; T: active bleeding, massive hemorrage, extensive burns, shock, disseminated intravascular coagulatin, Antithrombin deficiency, Thrombotic thrombocytopenic purpura, reversal of anticoagulation effects of warfarin, replacement therapy for coagulation factors II, V, VII, IX, X, and XI

Replaces neutrophils/ granulocytes; T: Severe neutropenia, life-threatening bacterial/fungal infection not responding to antibiotics, neonatal sepsis, neutrophil dysfunction

Expands circulating blood volume by exerting oncotic pressure; T: hypovolemia, hypoalbuminemia, burns, adult respiratory distress, severe nephrosis, cardiopulmonary bypass surgery, hemolytic disease of the newborn

Antibiotics: Eradication of H. pylori; T: Combination of 2 or 3 antibiotics for 14 days

Histamine2-Receptor Antagonist: Suppress secretion of gastric acid by selectively blocking H2 receptors in parietal cells lining the stomach; T: gastric & peptic ulcers, GERD, hypersecretory conditions – Zollinger-Ellison syndrome; w/ antibiotics to treat H. Pylori ulcers

Proton Pump Inhibitor: reduce gastric acid secretion by irreversibly inhibiting enzyme that produces gastric acid; reduce basal & stimulated acid production; T: gastric & peptic ulcers, GERD, & hypersecretory conditions – Zollinger-Ellison syndrome

Mucosal Protectant: Acid changes sucralfate into thick substance that sticks to ulcer, protects ulcer from further injury from acid & pepsin; sticks to ulcer for upto 6 hrs; T: duodenal ulcers & maintanence, gastric ulcers, GERD

Antacid: Neutralize gastric acid & inactive pepsin; protection may occur by antacid’s ability to stimulate production of prostaglandins; T: peptic ulcer disease (PUD), symptomatic relief of GERD

Prostaglandin E Analog: acts as an endogenous prostaglandin in GI tract to \/ acid secretion, /\ secretion of bicarbonate & protective mucus, & promote vasodilation to maintain submucosal blood flow; T: prevention for long-term NSAID use, Induces labor

Glucocorticoid: Unknown; T: combo w/ other antiemetics for chemotherapy-induced nausea & vomiting (CINV)

Substance P/Neurokinin1 Antagonist: inhibits Substance P/Neurokinin1 in brain; T: combo w/ glucocorticoid or serotonin antagonist, extended duration – can be used for immediate & delayed response

Serotonin Antagonist: prevents emesis by blocking serotonin receptors in chemoreceptor trigger zone (CTZ) & antagonizing serotonin receptors on afferent vagal neurons that travel from upper GI tract to CTZ; T: prevents emesis w/ chemotherapy, radiation therapy, & postop recovery

Dopamine Antagonist (subset of phenothiazine): blockade of dopamine receptors in the CTZ; T: prevents emesis w/ chemotherapy, opioids, & postop recovery

Cannabinoid: Unknown; T: controls CINV & /\ appetite in clients who have AIDS

Anticholinergic: Interferes w/ transmission of nerve impulses traveling from vestibular apparatus of inner ear to vomiting center (VC) in brain; T: motion sickness

Antihistamine: blocks muscarinic & histaminergic receptors in nerve pathways that connect inner ear & VC; T: treats motion sickness

Bulk-forming Laxative: Softens fecal mass & increases bulk (just like dietary fiber); T: \/ diarrhea in pts w/ diverticulosis & IBS; control stool w/ ileostomy or colostomy; promote defecation

Surfactant Laxative: lower surface tension of stool to allow water penetration; T: constipation, painful elimination, prevent straining, \/ risk of fecal impaction in immobile pts & promote defecation

Stimulant Laxative: stimulation of intestinal peristalsis; T: treat short-term constipation by high-dose opioid; presurgery prep (colonoscopy)

Osmotic Laxative: draw water into intestine to /\ mass of stool – stretching musculature = peristalsis

Antidiarrheal: activate opioid receptors in GI tact to \/ intestinal motility & /\ absorption of fluid & sodium in intestines; T: provides symptomatic treatment of diarrhea

Prokinetic Agent: controls N/V by blocking dopamine & serotonin receptors in CTZ, augments action of acetylcholine à /\ in upper GI motility; T: control postop & chemo-induced N/V (CINV), GERD, gastroparesis

Med for Irritable Bowel Syndrome w/ Diarrhea (IBS-D): Selective blockade of 5-HT3 receptors, which innervate viscera & result in /\ firmness in stool & \/ in urgency & frequency of defecation; T: female clients w/ IBS w/ diarrhea that has last > 6 months resistant to conventional therapy

Med for Irritable Bowel Syndrome w/ Constipation (IBS-C): /\ fluid secretion in intestine to promote intestinal motility; T: IBS w/ constipation, chronic constipation

5-Aminosalicylates: decrease inflammation by inhibiting prostaglandin synthesis; T: IBS: Crohn’s disease, ulcerative colitis

Iron Preparations: provide iron needed for RBC development & O2 transport to cells (normally poorly absorped = high doses); T: iron deficiency anemia (Iron sucrose & SFGC – solely for dialysis)

Vitamin B12-Cyanocobalamin: necessary to convert folic acid from inactive to active – DNA production; T: Vitamin B deficiency, megaloblastic (macrocytic) anemia

Essential in production of DNA & erythropoiesis (RBC, WBC, & platelets); T: megaloblastic anemia, prevention of neural tube defects during pregnancy, malabsorption syndrome (sprue)

Potassium Supplements: essential for conducting nerve impulses, maintaining electrical excitability of muscle & regulation of acid/base balance; T: hypokalemia (Lasix), vomiting, diarrhea, GI fistulas

Activates many intracellular enzymes & helps regulating skeletal muscle contractility & blood coagulation; T: hypomagnesemia, stop preterm labor

See Addendum Below

Rapid-acting: promotes cellular uptake of glucose, converts glucose à glycogen, moves K into cell (w/ glucose); T: glycemic control of diabetes mellitus;
O: <15 min; P: 0.5-1hrs; D: 3-4hrs

Short-acting: promotes cellular uptake of glucose, converts glucose à glycogen, moves K into cell (w/ glucose); T: glycemic control of diabetes mellitus
O: 0.5-1hr; P: 2-3hrs; D: 5-7hrs

Intermediate-acting: promotes cellular uptake of glucose, converts glucose à glycogen, moves K into cell (w/ glucose); T: glycemic control of diabetes mellitus
O: 1-2hr; P: 4-12hrs; D: 18-24hrs

Long-acting: promotes cellular uptake of glucose, converts glucose à glycogen, moves K into cell (w/ glucose); T: glycemic control of diabetes mellitus
O: 1hr; P: none; D: 10.4-24hrs

Oral Hypoglycemic, Sulfonylurea: insulin release from pancrease; T: control blood glucose levels w/ type 2 DM

Oral Hypoglycemic, Sulfonylurea: Insulin release from the pancreas; T: control blood glucose levels w/ type 2 DM

Oral Hypoglycemic, Meglitinide: Insulin release from the pancreas; T: control blood glucose levels w/ type 2 DM

Oral Hypoglycemic, Biguanide: Reduces production of glucose w/in liver through suppression of gluconeogenesis, /\ muscle’s glucose uptake & use; T: control blood glucose levels w/ type 2 DM, & treats polycystic ovary syndrome (PCOS)

Oral Hypoglycemic, Thiazolidinedione: /\ cellular response to insulin by \/ insulin resistance, /\ in glucose uptake & \/ glucose production; T: control blood glucose levels w/ type 2 DM

Oral Hypoglycemic, Alpha Glucosidase Inhibitor: slows carbohydrate absorption & digestion; T: control blood glucose levels w/ type 2 DM

Oral Hypoglycemic, Gliptin: Augments naturally occurring incretin hormones à promote release of insulin & \/ secretion of glucagon; lowers fasting & postprandial blood glucose levels; T: control blood glucose levels w/ type 2 DM

Amylin Mimetic: reduction of postprandial glucose levels from \/ gastric emptying time & inhibition of section of glucagon, /\ in sensation of satiety à \/ calorie intake; T: Supplemental glucose control w/ insulin or oral agent – i.e. metformin or slufonylurea

Incretin Mimetic: mimics glucagon-like peptide-1, promotes release of insulin, \/ secretion of glucagon, slows gastric emptying, lowers fasting & postprandial blood glucose leves; T: Supplemental glucose control w/ insulin or oral agent – i.e. metformin or slufonylurea

Hyperglycemic Agent: /\ blood glucose levels by increasing breakdown of glycogen into glucose, \/ glycogen synthesis enhances synthesis of glucose; T: emergency of hypoglycemic reactions; \/ in gastrointestinal motility in pts w/ radiological procedures of stomach & intestines

Antimetabolites, Folic Acid Analog: S-phase specific, stops cell reproduction by inhibiting folic acid conversion; T: choriocarcinoma, solid tumors (breast & lung, head & neck sarcomas, acute lymphocytic leukemia, non-Hodgkin’s lymphoma

Antimetabolites, Pyrimidine Analog: S-phase specific, inhibits RNA & DNA synthesis of cancer cells; T: acute myelogenous leukemia, solid tumors (breast & colon)

Antimetabolites, Purine Analog: S-phase specific, interrupts RNA & DNA synthesis of cancer cells; T: acute lymphocytic leukemia, acute non-lymphocytic leukemias

Antitumor Antibiotics, Anthracycline: Nonspecific cell cycle phase, binds to DNA, altering its structure; T: solid tumors – lung, bone, stomach, & breast, Hodgkin’s & non-Hodgkin’s lymphomas

Antitumor Antibiotics, Nonanthracycline: Nonspecific cell cycle phase, binds to DNA, altering its structure; T: Wilm’s tumor, rhabdomyosarcoma, choriocarcinoma, Ewing’s sarcoma & Kaposi’s sacroma

Antimitotics, Vinca Alkaloid: M-Phase specific; useful in combo treatment, stops cell division during mitosis, not bone marrow toxic; T: acute lymphocytic leukemia, Wilms tumor, rhabdomycosarcoma, solid tumors (bladder & breast cancers, Hodgkin’s and non-Hodgkin’s lymphomas

Antimitotics, Taxanes: Stop cell division during mitosis; T: ovarian, non-small cell lung tumors, & Kaposi’s sarcoma

Alkylating Agent, Nitrogen Mustard: Nonspecific cell cycle phase, kills rapid growing cells by interrupting DNA & RNA synthesis; T: acute lymphomas, solid tumors (head, neck, & breast; Hodgkin’s & non-Hodgkin’s lymphomas)

Alkylating Agent, Nitrosoureas: Nonspecific cell cycle phase, kills rapid growing cells by interrupting DNA & RNA synthesis; crosses blood brain barrier; T: brain tumors, Hodgkin’s & non-Hodgkin’s lymphomas, & multiple myeloma

Alkylating Agent, Platinum Compounds: Nonspecific cell cycle phase, kills rapid growing cells by interrupting DNA & RNA synthesis; T: bladder, testicular, & ovarian cancers

Topoisomerase Inhibitors, : S-specific cell cycle phase, kills cancer cells by interrupting DNA synthesis; T: ovary & small cell lung tumors

Other Antineoplastic Agents: G1-specific cell cycle phase, kills cancer cells by interrupting DNA synthesis in leukemia cells; T: acute lymphocytic leukemia

Other Antineoplastic Agents: S-specific cell cycle phase; kills cancer cells by interrupting DNA synthesis, may cross blood-brain barrier; T: Chronic myelogenous, leukemia, ovarian & squamous cell cancers

Other Antineoplastic Agents: Non-specific cell cycle phase, kills cancer cells by interrupting DNA and RNA synthesis, may cross blood-brain barrier; T: brain tumors, Hodgkin’s & non-Hodgkin’s lymphomas

Non-cytotoxic, Hormonal Agent, Gonadotropin-Releasing Hormone Agonist: Testes stop producing testosterone; T: prostate cancer

Non-cytotoxic, Hormonal Agent, Androgen Receptor Blocker: blocks testosterone at receptor site, used w/ gonadotropin-releasing hormone agonist, to block androgen receptors & suppress growth of prostate cancer

Non-cytotoxic, Hormonal Agent, Estrogen Receptor Blocker: stops growth of breast cancer cells, which are estrogen-dependent cancers; T: to treat & prevent breast cancer

Non-cytotoxic, Hormonal Agent, Aromatase Inhibitor: stops growth of cancer cells by blocking estrogen; T: to treat breast cancer in postmenopausal women

Non-cytotoxic, Hormonal Agent, Monoclonal Antibody: targets breast cancer cells, prevents cell growth & causes cell death; T: used to treat metastatic breast cancer, may be used alone or in conjunction w/ paclitaxel

Biological Response Modifier: /\ immune response & \/ production of cancer cells T: to treat or prevent hairy cell leukemia, chronic myelogenous leukemia, malignant melanoma, & AIDS-related Kaposi’s sarcoma

Targeted, EGRF-tyrosine Kinase Inhibitor: Antibody that stops cancer cell growth & /\ cell death; T: cancers that are EGFR positive (colorectal & solid tumors of head & neck)

Targeted BCR-ABL Tyrosine Kinase Inhibitor: stops cancer growth by inhibiting intracellular enzymes; T: chronic myeloid leukemia

Targeted CD20-Directed Antibodies: Antibody that stops cancer cell growth & /\ cell death; T: non-Hodgkin’s lymphoma

Targeted Angiogenesis Inhibitor: Antibody that stops cancer cell growth & /\ cell death; colorectal & lung cancers

Antimicrobial, anti-inflammatory, analgesic – topically; cathartic properties – ingested; T: soothes pain & inflammation of burn, softens skin, laxative

Acts as estrogen substitute, mechanism unknown; T: symptoms of menopause

Stimulates immune system, \/ inflammation, /\ phagocytosis; /\ T-lymphocyte, tumor necrosis factor, & interferon production; T: Oral – common cold (no research); topical – skin disorders, wounds, burns

Possibly blocks factor necessary to cause migraine, stops release of arachidonic acid in thrombcytes à block platelet aggregation; T: \/ number & severity of migraines, not existing migraines

Crushed garlic cells = enzyme allicin = blocks cholesterol synthesis in liver, suppresses platelet aggregation & coagulation; acts a vasodilator; T: lower cholesteral, LDL & triglycerides, slightly /\ HDL; may \/ BP

Unknown mechanism, acts on areas of brain that cause Nausea, /\ intestinal motility & gastric production; \/ GI spasms, inhibits prostaglandins & leukotrienes to produce anti-inflammatory effects, suppresses platelet aggregation; T: \/ nausea, morning & motion sickness, \/ pain & stiffness of rheumatoid arthritis

Promotes vasodialation, suppresses platelet aggregation & bronchospasm; T: mental ability, erectile dysfunction, pain, \/ risk of thrombosis & bronchospams

Antiseptic, suppresses inflammation, may stimulate immune system, /\ bile secretion; T: treat infections, \/ gall bladder inflammation

Unknown; possibly acts on GABA receptors in CNS; T: insomnia, anxiety, & muscle relaxation w/ decreased concentration

May activate alpha & beta adrenergic receptors to constrict arterioles, /\ HR, bronchodialation, & suppress appetite; stimulates CNS; T: colds, influenza, & allergies, wt loss, /\ athletic abilities

Affects serotonin, NE, dopamine, & GABA uptake to produce antidepressant effects; T: mild depression

Unknown, may \/ conversion of testosterone into dihydrotestosterone (DHT) in prostate; T: \/ symptoms of BPH

/\ GABA to prevent insomnia; may be similar to benzodiazepines; T: promotes sleep; w/ increased effect of time