Comprehensive Drugs to Know for Final Flashcards

Question

Cefuroxime

Answer 1

Antimicrobial- antibiotic MOA: 2nd generation cephalosporin; targets transpeptidase in cell wall synthesis Clinical Use: gram positive, some gram negative, anaerobic; intra-abdominal infections Ocular Side Effects: n/a

Answer 2

Antimicrobial- antibiotic MOA: 3rd generation cephalosporin; targets transpeptidase in cell wall synthesis Clinical Use: gram negative; pneumonia Ocular Side Effects: n/a

Answer 3

Antimicrobial- antibiotic MOA: beta-lactamase inhibitor, combined with a penicillin to inhibit breakdown of beta-lactamse in penicillin Clinical Use: combined with penicillin Ocular Side Effects: n/a

Answer 4

Antimicrobial- antibiotic MOA: inhibits bacterial cell wall synthesis by weakening peptidoglycan polymerization Clinical Use: great gram positive coverage, used topically, blepharitis, bacterial corneal ulcers Ocular Side Effects: n/a

Answer 5

Antimicrobial- antibiotic MOA: inhibits bacterial cell wall synthesis by weakening peptidoglycan polymerization Clinical Use: MRSA, very effective against gram positive Ocular Side Effects: n/a

Answer 6

Antimicrobial- antibiotic MOA: tetracycline; inhibits protein synthesis by binding to 30s ribosomal subunit Clinical Use: broad spectrum, 50 mg doxycycline can be used for inflammation Ocular Side Effects: Pseudotumor Cerebri Other Side Effects: Teeth

Answer 7

Antimicrobial- antibiotic MOA: tetracycline; inhibits protein synthesis by binding to 30s ribosomal subunit Clinical Use: broad spectrum Ocular Side Effects: Pseudotumor Cerebri Other Side Effects: Teeth

Answer 8

Antimicrobial- antibiotic MOA: inhibits protein synthesis by binding to 30s ribosomal subunit Clinical Use: broad spectrum, 50 mg doxycycline can be used for inflammation Ocular Side Effects: Pseudotumor Cerebri Other Side Effects: Teeth

Answer 9

Antimicrobial- antibiotic MOA: aminoglycoside; inhibits protein synthesis by binding to 30s ribosomal subunit Clinical Use: gram negative and some gram positive Ocular Side Effects: allergic reactions Other Side Effects: ototoxicity

Answer 10

Antimicrobial- antibiotic MOA: aminoglycoside; inhibits protein synthesis by binding to 30s ribosomal subunit Clinical Use: gram negative and some gram positive Ocular Side Effects: allergic reactions Other Side Effects: ototoxicity

Answer 11

Antimicrobial- antibiotic MOA: aminoglycoside; inhibits protein synthesis by binding to 30s ribosomal subunit Clinical Use: gram negative and some gram positive Ocular Side Effects: allergic reactions Other Side Effects: ototoxicity

Answer 12

Antimicrobial- antibiotic MOA: macrolide; inhibits protein synthesis by binding to 50s ribosomal subunit Clinical Use: good for respiratory infections and chlamydia Ocular Side Effects: n/a

Answer 13

Antimicrobial- antibiotic MOA: macrolide; inhibits protein synthesis by binding to 50s ribosomal subunit Clinical Use: good alternative to PCN, good for gram positive Ocular Side Effects: n/a

Answer 14

Antimicrobial- antibiotic MOA: 2nd generation fluoroquinolone; inhibits DNA replication by interfering with DNA gyrase and topoisomerase IV Clinical Use: Pseudomonas, Anthrax, great gram negative coverage Ocular Side Effects: n/a

Answer 15

Antimicrobial- antibiotic MOA: 2nd generation fluoroquinolone; inhibits DNA replication by interfering with DNA gyrase and topoisomerase IV Clinical Use: Pseudomonas, Anthrax, great gram negative coverage Ocular Side Effects: n/a

Answer 16

Antimicrobial- antibiotic MOA: 3rd generation fluoroquinolone; inhibits DNA replication by interfering with DNA gyrase and topoisomerase IV Clinical Use: very broad spectrum Ocular Side Effects: n/a

Answer 17

Antimicrobial- antibiotic MOA: 4th generation fluoroquinolone; inhibits DNA replication by interfering with DNA gyrase and topoisomerase IV Clinical Use: gram negative, enhanced gram positive Ocular Side Effects: n/a

Answer 18

Antimicrobial- antibiotic MOA: sulfonamide; competes with dihydropteroate synthestase and inhibits folate production Clinical Use: wide spectrum Ocular Side Effects: n/a

Answer 19

Antimicrobial- antibiotic MOA: inhibits dihydrofolate reductase and inhibits folate production Clinical Use: wide spectrum, potent Ocular Side Effects: n/a

Answer 20

Antimicrobial- antibiotic MOA: trimethoprim + sulfamethoxazole; inhibits folate production Clinical Use: broad spectrum, UTIs, respiratory tract infections, pneumocystis jiroveci, MRSA Ocular Side Effects: n/a

Answer 21

Antimicrobial- antimycobacterial MOA: interferes with cell wall synthesis Clinical Use: mycobacteria- TB Ocular Side Effects: optic neuritis

Answer 22

Antimicrobial- antimycobacterial MOA: interacts with bacterial RNA polymerase to block transcription Clinical Use: mycobacteria- leprosy, TB, gram negative and gram positive Ocular Side Effects: secretions will have an orange-red color, including tears

Answer 23

Antimicrobial- antiviral MOA: selectively inhibits neuraminidase enzyme, which is essential to life cycle of the virus; prevents release of new virions Clinical Use: influenza A and B Ocular Side Effects: n/a

Answer 24

Antimicrobial- antiviral MOA: converted to active form by viral enzyme; inhibits DNA polymerase and is incorporated into the viral DNA Clinical Use: herpes virus, herpetic keratitis Ocular Side Effects: n/a

Answer 25

Antimicrobial- antiviral MOA: converted to active form by viral enzyme; inhibits DNA polymerase and is incorporated into the viral DNA Clinical Use: herpes virus, herpetic keratitis Ocular Side Effects: n/a

Answer 26

Antimicrobial- antiviral MOA: inhibits DNA synthesis; also able to incorporate into cellular DNA Clinical Use: herpes virus- restricted to use in the eye, Ocular Side Effects: irritation

Answer 27

Antimicrobial- antiviral MOA: converted to active form by viral enzyme; inhibits DNA polymerase and is incorporated into the viral DNA Clinical Use: herpes virus, herpetic keratitis, CMV Ocular Side Effects: n/a

Answer 28

Antimicrobial- antiviral MOA: nucleotide/nucleoside inhibitor; inhibits reverse transcriptase/RNA polymerase, termination of replication Clinical Use: Hepatitis B/C, HIV Ocular Side Effects: n/a

Answer 29

Antimicrobial- antiviral MOA: non-nucleoside reverse transcriptase inhibitor (NNRTI); highly selective inhibitor of HIV-1 reverse transcriptase, causes conformational change to enzyme Clinical Use: HIV Ocular Side Effects: n/a

Answer 30

Antimicrobial- antiviral MOA: protease inhibitor; inhibits HIV aspartyl protease, prevents maturation of the viral particles Clinical Use: HIV, used as an enhancer of other protease inhibitors (not used on its own), can also be given as a pharmacological booster for hepatic viral infections Ocular Side Effects: n/a

Answer 31

Anticancer MOA: antimetabolite; forms a complex that derives the cell of thymidine, stopping DNA synthesis Clinical Use: topical uses- skin cancer, prevention of scar tissue formation in surgery, some ocular surgeries Ocular Side Effects: n/a

Answer 32

Anticancer MOA: antimetabolite; dihydrofolate reductase antagonist; leads to decreased production of required nucleic compounds; DNA, RNA, and protein synthesis is depressed, leading to cell death Clinical Use: cancer, severe psoriasis, Rheumatoid arthritis, Crohn's disease Ocular Side Effects: n/a

Answer 33

Anticancer MOA: triggers production of specific proteins that reduce cell growth and proliferation Clinical Use: treatment of lymphomas Ocular Side Effects: cataract formation, increased IOP

Answer 34

Anticancer MOA: estrogen antagonist; inhibits RNA synthesis Clinical Use: breast cancer Ocular Side Effects: crystalline retinopathy and other vision problems

Answer 35

Anticancer MOA: monoclonal antibody; antiangiogenesis agent; attaches to and stops VEGF from stimulating the formation of new blood vessels; decreases oxygen supply to tumor cells Clinical Use: cancer, intravitreal for retinal neovascular diseases Ocular Side Effects: n/a

Answer 36

Cardiovascular Agent MOA: thiazide diuretic; inhibits Na/Cl co-transporter in distal convoluted tubule; increased excretion of Na and Cl; reduced peripheral vascular resistance Clinical Use: hypertension, heart failure, hypercalciuria, diabetes insipidus Ocular Side Effects: n/a

Answer 37

Cardiovascular Agent MOA: loop diuretic; major action on ascending limb of loop of Henle; inhibits co-transport of Na/K/2Cl; increased Na and K excretion; increased Ca excretion Clinical Use: drug of choice for reducing acute pulmonary edema of heart failure, useful in emergency situations, useful in treatment of hypercalcemia and hyperkalemia, not as frequently in HTN Ocular Side Effects: n/a

Answer 38

Cardiovascular Agent MOA: carbonic anhydrase inhibitor; inhibits carbonic anhydrase in proximal tubule; decreases the kidney's ability to exchange Na for H; Na is excreted at a higher rate Clinical Use: glaucoma (2-250 mg tablets), treatment of pseudotumor cerebri, mountain sickness Ocular Side Effects: decreases production of aqueous

Answer 39

Cardiovascular Agent MOA: centrally acting alpha 2 agonist; acts in vasomotor center within the medulla; decreases sympathetic outflow; decrease in vascular tone and cardiac output Clinical Use: HTN Ocular Side Effects: n/a

Answer 40

Cardiovascular Agent MOA: vasodilator- calcium channel blocker; block inward movement of calcium; less calcium available to activate contraction in smooth muscle and cardiac muscle; produces reduction in vascular tone; produces dilation of coronary and peripheral arteries; decreases force of contraction and reduces cardiac workload Clinical Use: HTN, some arrhythmias, angina Ocular Side Effects: n/a

Answer 41

Cardiovascular Agent MOA: ACE inhibitor; prevents conversion of angiotensin I to angiotensin II; reduces peripheral vascular resistance; reduce the inactivation of bradykinin (a vasodilator); results in vasodilation as well as decreased sodium and water retention Clinical Use: HTN, diabetic nephropathy, following a heart attack Ocular Side Effects: n/a

Answer 42

Cardiovascular Agent MOA: ACE inhibitor; prevents conversion of angiotensin I to angiotensin II; reduces peripheral vascular resistance; reduce the inactivation of bradykinin (a vasodilator); results in vasodilation as well as decreased sodium and water retention Clinical Use: HTN, diabetic nephropathy, following a heart attack Ocular Side Effects: n/a

Answer 43

Cardiovascular Agent MOA: Angiotensin-Receptor Blocker; antagonist at angiotensin receptor; results in vasodilation, but does not increase bradykinin levels Clinical Use: HTN, diabetic nephropathy, following a heart attack Ocular Side Effects: n/a

Answer 44

Cardiovascular Agent MOA: organic nitrate; enzyme activation of drug causes release of nitric oxide; cause a rapid reduction in myocardial oxygen demand; rapid relief of symptoms; relaxation of smooth muscle in arteries and veins; decreases venous return to the heart; dilate coronary vasculature; increase blood supply to the heart; relieves coronary artery spasm Clinical Use: acute angina from exercise or emotional stress Ocular Side Effects: n/a

Answer 45

Cardiovascular Agent- vasodilator MOA: sodium channel blocker; inhibits the late phase of the sodium current; reduces intracellular sodium and calcium overload; improves diastolic function and improves oxygen supply Clinical Use: used mainly to treat chronic angina Ocular Side Effects: n/a

Answer 46

Cardiovascular Agent MOA: class IA anti-arrhythmic; binds to sodium channels and potassium channels; slows the rate of rise of action potential; slows conduction (phase 0) and slows repolarization (phase 3); increase duration of action potential and refractory period Clinical Use: tachycardia-type rhythms Ocular Side Effects: n/a

Answer 47

Cardiovascular Agent MOA: class III anti-arrhythmic; K channel blocker; diminishes the outward potassium current during repolarization of cardiac cells; prolong the duration of the action potential (phase 3); prolong the effective refractory period; shows class I, II, III, and IV actions Clinical Use: atrial fibrillation, sometimes angina Ocular Side Effects: whorl keratopathy, non-arteritic ischemic optic neuropathy (NAION)

Answer 48

Cardiovascular Agent MOA: type 5 phosphodiesterase inhibitor; potentiates the vasodilative effect of acetylcholine; parasympathetic activation causes release of acetylcholine; acetylcholine activates muscarinic receptors in vascular endothelial cells; increases production and release of NO; type 5 phosphodiesterase breaks down cGMP; these drugs inhibit this step, causing a continuation of vasodilation Clinical Use: erectile dysfunction Ocular Side Effects: mild impairment of color vision, blurry vision

Answer 49

Cardiovascular Agent MOA: type 5 phosphodiesterase inhibitor; potentiates the vasodilative effect of acetylcholine; parasympathetic activation causes release of acetylcholine; acetylcholine activates muscarinic receptors in vascular endothelial cells; increases production and release of NO; type 5 phosphodiesterase breaks down cGMP; these drugs inhibit this step, causing a continuation of vasodilation Clinical Use: erectile dysfunction Ocular Side Effects: mild impairment of color vision, blurry vision (less likely to cause ocular side effects than others)

Answer 50

Cardiovascular Agent MOA: type 5 phosphodiesterase inhibitor; potentiates the vasodilative effect of acetylcholine; parasympathetic activation causes release of acetylcholine; acetylcholine activates muscarinic receptors in vascular endothelial cells; increases production and release of NO; type 5 phosphodiesterase breaks down cGMP; these drugs inhibit this step, causing a continuation of vasodilation Clinical Use: erectile dysfunction Ocular Side Effects: mild impairment of color vision, blurry vision

Answer 51

Cardiovascular Agent MOA: anticoagulant- direct thrombin inhibitor; competitive, reversible inhibitor of thrombin Clinical Use: prevention of stroke in patients with atrial fibrillation Ocular Side Effects: subconjunctival and retinal hemes are possible

Answer 52

Cardiovascular Agent MOA: anticoagulant- factor Xa inhibitor; selectively inhibits only factor Xa Clinical Use: often used in hip or knee surgery as well as prevention of stroke Ocular Side Effects: subconjunctival and retinal hemes are possible

Answer 53

Cardiovascular Agent MOA: anticoagulant- factor Xa inhibitor; selectively inhibits only factor Xa Clinical Use: often used in hip or knee surgery as well as prevention of stroke Ocular Side Effects: subconjunctival and retinal hemes are possible

Answer 54

Cardiovascular Agent MOA: platelet inhibitor- ADP receptor blocker; when ADP binds to platelet, GP receptors are expressed; ADP receptor blockers inhibit expression of GP receptors for fibrinogen by binding to ADP; inhibits platelet function for the life of the platelet Clinical Use: prevention of TIA and strokes in patients with previous event or following heart attack, adjunct with aspirin following coronary stent implantation, decrease thrombotic events in patient with acute coronary syndrome Ocular Side Effects: subconjunctival and retinal hemes are possible

Answer 55

Cardiovascular Agent MOA: platelet inhibitor- ADP receptor blocker; when ADP binds to platelet, GP receptors are expressed; ADP receptor blockers inhibit expression of GP receptors for fibrinogen by binding to ADP; inhibits platelet function for the life of the platelet Clinical Use: prevention of TIA and strokes in patients with previous event or following heart attack, adjunct with aspirin following coronary stent implantation, decrease thrombotic events in patient with acute coronary syndrome Ocular Side Effects: subconjunctival and retinal hemes are possible

Answer 56

Cardiovascular Agent MOA: platelet inhibitor- ADP receptor blocker; when ADP binds to platelet, GP receptors are expressed; ADP receptor blockers inhibit expression of GP receptors for fibrinogen by binding to ADP; does not inhibit platelet for the life of the platelet Clinical Use: prevention of TIA and strokes in patients with previous event or following heart attack, adjunct with aspirin following coronary stent implantation, decrease thrombotic events in patient with acute coronary syndrome Ocular Side Effects: subconjunctival and retinal hemes are possible

Answer 57

Cardiovascular Agent MOA: anticoagulant- vitamin K antagonist; several protein coagulation factors require vitamin K as a cofactor for synthesis; warfarin inhibits vitamin K epoxide reductase; results in the production of clotting factors with diminished activity Clinical Use: blood thinner Ocular Side Effects: subconjunctival and retinal hemes are possible Other Side Effects: extensive drug interactions!

Answer 58

Cardiovascular Agent MOA: HMG CoA reductase inhibitor; inhibit the first committed enzymatic step of cholesterol synthesis; analogs of HMG, a precursor of cholesterol; compete with HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; causes hepatocyte to increase LDL receptors on surface; internalize circulating LDL and prevent release of VLDL Clinical Use: first line therapy for increased LDL, effective in lowering plasma cholesterol levels in all types of hyperlipidemias Ocular Side Effects: n/a

Answer 59

Cardiovascular Agent MOA: HMG CoA reductase inhibitor; inhibit the first committed enzymatic step of cholesterol synthesis; analogs of HMG, a precursor of cholesterol; compete with HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; causes hepatocyte to increase LDL receptors on surface; internalize circulating LDL and prevent release of VLDL Clinical Use: first line therapy for increased LDL, effective in lowering plasma cholesterol levels in all types of hyperlipidemias Ocular Side Effects: n/a

Answer 60

Cardiovascular Agent MOA: HMG CoA reductase inhibitor; inhibit the first committed enzymatic step of cholesterol synthesis; analogs of HMG, a precursor of cholesterol; compete with HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; causes hepatocyte to increase LDL receptors on surface; internalize circulating LDL and prevent release of VLDL Clinical Use: first line therapy for increased LDL, effective in lowering plasma cholesterol levels in all types of hyperlipidemias Ocular Side Effects: n/a

Answer 61

Cardiovascular Agent MOA: bile acid sequestrant; binds bile acids and bile salts in the small intestine (prevents reabsorption into liver); liver must then increase conversion of cholesterol to bile acids; cell surface LDL receptors increase Clinical Use: lower LDL levels, hyperlipidemias Ocular Side Effects: n/a

Answer 62

Cardiovascular Agent MOA: cholesterol absorption inhibitor; inhibits absorption of cholesterol from the small intestine; decreases delivery of intestinal cholesterol to the liver; reduces hepatic cholesterol stores and increases clearance of cholesterol from blood Clinical Use: hyperlipidemia Ocular Side Effects: n/a

Answer 63

CNS Medication MOA: SSRI; blocks reuptake of 5HT; leads to increased concentration in the synaptic gap Clinical Use: depression Ocular Side Effects: n/a

Answer 64

CNS Medication MOA: SSRI; blocks reuptake of 5HT; leads to increased concentration in the synaptic gap Clinical Use: depression Ocular Side Effects: n/a

Answer 65

CNS Medication MOA: SNRI; blocks reuptake of NE and 5HT; non-selective Clinical Use: depression, may be more effective if pain is experienced along with depression Ocular Side Effects: n/a

Answer 66

CNS Medication MOA: atypical antidepressant; weak dopamine and NE reuptake inhibitor Clinical Use: depression, also assists in decreasing the craving and attenuating the withdrawal symptoms for nicotine Ocular Side Effects: n/a

Answer 67

CNS Medication MOA: benzodiazepine; binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effects of GABA; also decreases the release of GABA Clinical Use: anxiety, sedative and hypnotic, anterograde amnesia, anticonvulsant, muscle relaxant, anesthesia, alcohol or opiate physical dependence/addiction (sedates patient during withdrawal) Ocular Side Effects: n/a

Answer 68

CNS Medication MOA: benzodiazepine; binding to receptor increases the affinity of GABA for its receptor; enhances the inhibitory effects of GABA; also decreases the release of GABA Clinical Use: anxiety, sedative and hypnotic, anterograde amnesia, anticonvulsant, muscle relaxant, anesthesia, alcohol or opiate physical dependence/addiction (sedates patient during withdrawal) Ocular Side Effects: n/a

Answer 69

CNS Medication MOA: benzo-like; high affinity for the benzodiazepine binding site of GABA receptors; mimic effect of BZDs Clinical Use: sleep problems Ocular Side Effects: n/a

Answer 70

CNS Medication MOA: benzo-like; high affinity for the benzodiazepine binding site of GABA receptors; mimic effect of BZDs Clinical Use: sleep problems Ocular Side Effects: n/a

Answer 71

CNS Medication MOA: second generation antipsychotic; dopamine and 5HT receptor antagonist; have activity at more dopamine receptors than first generation; also called "atypical" antipsychotics; do not produce movement disorders Clinical Use: effective control of positive and negative signs, antiemetic effects, adjunct treatment of depression or a treatment of bipolar disorder Ocular Side Effects: n/a

Answer 72

CNS Medication MOA: second generation antipsychotic; dopamine and 5HT receptor antagonist; have activity at more dopamine receptors than first generation; also called "atypical" antipsychotics; do not produce movement disorders Clinical Use: effective control of positive and negative signs, antiemetic effects, adjunct treatment of depression or a treatment of bipolar disorder Ocular Side Effects: n/a

Answer 73

CNS Medication MOA: anti-Parkinson drug; boosts DA synthesis; increases content of DA vesicles; increases amount of DA released; increased activation of postsynaptic receptors Clinical Use: Parkinson's Ocular Side Effects: n/a

Answer 74

CNS Medication MOA: anti-Parkinson drug; given along with levodopa to inhibit PNS conversion to dopamine; allows therapeutic levels of levodopa to reach the CNS at a lower dose; essentially makes levodopa more bioavailable Clinical Use: Parkinson's Ocular Side Effects: n/a

Answer 75

CNS Medication MOA: antiviral; also used for Parkinson's, but MOA is not known; possibly more than usual DA-containing vesicles in the axon terminal are induced to release contents into the synapse Clinical Use: Parkinson's, influenza A Ocular Side Effects: n/a

Answer 76

CNS Medication MOA: NMDA receptor antagonist; binds to glutamine receptors on the post-synaptic neuron; prevents binding of glutamine; theory is that blockage of NMDA receptors reduces cytotoxic effects on neurons caused by Ca influx across the plasma membranes Clinical Use: Alzheimer's Disease Ocular Side Effects: n/a

Answer 77

CNS Medication MOA: cholinesterase inhibitor; binds reversibly to acetylcholinesterase; leads to an increase in acetylcholine in the synapse Clinical Use: Alzheimer's Disease, Myasthenia Gravis Ocular Side Effects: n/a

Answer 78

CNS Medication MOA: amphetamine; is a substrate for the enzyme responsible for reuptake of NE and DA; is not metabolized by MAO and is instead stored in neurotransmitter storage vesicles (leaves NE and DA out); causes release of intracellular stores of neurotransmitter via a reversal of the reuptake enzyme; also inhibits MAO to a certain extent Clinical Use: ADHD, narcolepsy Ocular Side Effects: n/a

Answer 79

CNS Medication MOA: amphetamine; is a substrate for the enzyme responsible for reuptake of NE and DA; is not metabolized by MAO and is instead stored in neurotransmitter storage vesicles (leaves NE and DA out); causes release of intracellular stores of neurotransmitter via a reversal of the reuptake enzyme; also inhibits MAO to a certain extent Clinical Use: ADHD, narcolepsy Ocular Side Effects: n/a

Answer 80

Opiate MOA: opioid agonist Clinical Use: pain control and in conjunction with general anesthesias; analgesic, sedative, respiratory depressant, antitussive, antidiarrheal, miotic Ocular Side Effects: pupillary constriction (withdrawal = dilation)

Answer 81

Opiate MOA: opioid agonist Clinical Use: treatment of opioid addiction- eases cravings, does not produce high; analgesic, sedative, respiratory depression, and antitussive effects Ocular Side Effects: pupillary constriction (withdrawal = dilation)

Answer 82

Opiate MOA: opioid agonist Clinical Use: pain control, in conjunction with general anesthesia; analgesic, sedative, respiratory depressant, antitussive, antidiarrheal, miotic Ocular Side Effects: pupillary constriction (withdrawal = dilation)

Answer 83

Opiate MOA: partial opioid agonist Clinical Use: antitussive action at doses that do not produce analgesia (some OTC preparations), analgesic Ocular Side Effects: pupil constriction

Answer 84

Opiate MOA: partial opioid agonist Clinical Use: pain control, in conjunction with general anesthesia; analgesic, sedative, respiratory depressant, antitussive, antidiarrheal, miotic Ocular Side Effects: pupil constriction

Answer 85

Opiate MOA: binds to opioid receptor and weakly inhibits reuptake of NE and serotonin Clinical Use: moderate to moderately severe pain Ocular Side Effects: pupil constriction

Answer 86

Opiate MOA: opioid antagonist; reverse all effects of agonist except induction of coma Clinical Use: opiate overdose; allows stabilization prior to transportation to an emergency center Ocular Side Effects: n/a