Pharmacology: Exam 3 and Drug Name
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177 terms
Terms | Definitions |
|---|---|
 Order of Antibacterial | 1. Blood Culture and Sensitivity 2. Start Broad Spectrum Antibacterial 3. Get Cultures Identified 4. Switch to Narrow Spectrum Antibacterial |
| Types of Antibacterials (4) | Cell Wall Synthesis Inhibitors, Protein Synthesis Inhibitors, DNA Synthesis Inhibitors, Metabolism Inhibitos |
| Cell Wall Synthesis Inhibitors MOA (3) | 1. Bind to cell wall proteins (bricks) 2. Inhibit bacterial enzyme (glue) 3. Activate autolysins to create holes in cell wall |
| Penicillin | - Suffix: -cillin - MOA: Cell Wall Synthesis Inhibitors - Expected Effect: Bacteriacidal - For: Narrow and Broad Spectrum, G+ and G-, infections (staph, e coli, salmonella, syphilis) - Side Effects: allergies, GI upset - Adverse Effects: bleeding, kidney damage, Stephen Johnson Syndrome - Pregnancy/Lactating: okay for pregnant but excreted through breastmilk |
| Cephalosporins (beta-lactam) | - Suffix: -cef-, ceph-, kef- - MOA: Cell Wall Synthesis Inhibitors - Expected Effect: Bacteriacidal - For: Narrow but mostly Broad Spectrum ---1st Gen: G+ (strep/staph) ---2nd Gen: G+ and G- (strep/flu) ---3rd Gen: G+ but mostly G- (penetrate CNS) ---4th Gen: Both G+ and G- (penetrate CNS, resistant to beta-lactamase -Side Effects: low toxicity, GI upset, allergy, bleedin, cross reaction with penicllin - Adverse Effects: interfere w/vitamin K, excessive bleeding, - DON'T: drink alcohol (disulfiram reaction), uricosis (prevents elimination of cephalosporin), take warfarin |
| Carbapenems (Beta-Lactams) | - Suffix: -enem - MOA: Cell Wall Synthesis Inhibitors - For: IV Broad Spectrum G+ and G-, resistant to Beta-lactamase, Anaerobic and Aerobic - Adverse Effects: CNS changes (confusion, seizures), kidney damage, Steven Johnson Syndrome - DON'T: use first, only a second line drug; cross reactive with penicillin |
| Vancomycin | - MOA: Cell Wall Synthesis Inhibitors - For: Very serious G+ Infection (MRSA, CDAD, VRSA, VRE) resistant to Beta-lactams - Expected Effect: Bacteriacidal - Side Effect: GI upset - Adverse Effect: Allergies, ototoxicity, red man syndrome, nephrotoxicity, thrombophlebitis, cardiac - DON'T: give too fast, give too much (narrow therapeutic index), take with food, iron, or antacid - Monitor: BP, IV site, skin and toxicity |
| Protein Synthesis Inhibitor Subtypes | Aminoglycosides, Tetracyclines, Macrolides |
| Aminoglycosides | - Suffix: -micin or -mycin - MOA: Protein Synthesis Inhibitor - For: Narrow Spectrum G- (not for gut) - Expected Effect: Bacteriacidal - Side Effect: GI upset, rash, fever, lethargy - Adverse Effect: ototoxicity, neuromuscular blockade, nephrotoxicity - DON'T: use with penicillin - Pregnancy/Lactation: avoid |
| Macrolides | - Suffix: -mycin - MOA: Protein Synthesis Inhibitor - For: Oral and IV Broad Spectrum G+ and G-, Strep/pneumoniae/chlamydia/gonorrhea, aerobic - Expected Effect: Bacteriacidal or Bacteriostatic (dependent of blood level/bacteria type) - Side Effect: GI upset, loss of appetite, abdominal pain, photosensitivity - Adverse Effect: ototoxicity, hepato/cardiac disorders, decrease metabolism of other drugs - DON'T: take with loop diuretic |
| Tetracycline | -Suffix: -cycline - MOA: Protein Synthesis Inhibitor - For: Broad Spectrum G+ and G-, People with healthy immune system , peptic ulcer due to H. pylori, acne, anthrax, chlamydia, gonorrhea - Expected Effect: Bacteriostatic - Side Effect: GI upset, bleeding, sore tongue, rash, photosensitivity - Adverse Effect: increased intracranial pressure (CNS toxic), kidney and liver dysfunction - DON'T: give to kids (retards bone growth), take with food, dairy, antacid, iron, or milk of magnesium - Pregnancy/Lactation: avoid (passes into breast milk) |
| Clindamycin | - MOA: Protein Synthesis Inhibitor - For: G+, acne, pneumonia, peritonitis, cellulitis (staph. a) - Expected Effect: bacteriacidal or bacteriostatic depending on dose - Side Effect: site irritation, thrombophlebitis - Adverse Effect: decreased liver function, decreased WBC, shock/cardiac arrest |
| Linezolid | - MOA: Protein Synthesis Inhibitor - For: Severe and Life-threatening G+ infections (VRE, VSRA, MRSA) or diabetic ulcers - Side Effect: GI upset, hypertension - Adverse Effect: Serotonin Syndrome (it is a MAOI), decrease RBC, damage to optic nerve, hypertension - DON'T: eat food with tyramine or take an MAOI |
| DNA Synthesis Inhibitor | Fluoroquinolones and Metronidazole |
| Fluoroquinolones | - Suffix: -floxacin - MOA: DNA Synthesis Inhibitor - For: Broad Spectrum G+ and G-, Skin infections, UTI, GI infection, prevent and treat anthrax - Expected Effect: Bacteriacidal - Side Effect: GI upset, Rash, Abdominal pain, headache, dizziness, burning urination, change BS - Adverse Effect: dysrhythmia, hypokalemia, neurotoxicity, peripheral neuropathy, Steven Johnson Syndrome, photosensitivity, tendon rupture - DON'T: take with caffeine, theophylline effects (seizure, cardiac arrest), antacid, levaquin, iron, vitamins, warfarin, give to kids - Pregnancy/Lactation: avoid |
| Metronidazole | - MOA: DNA Synthesis Inhibitor - For: Pelvic Inflammatory Disease, anaerobic, CDAD, vaginitis - Expected Effect: GI upset, metallic taste in mouth - Adverse Effect: leukopenia, neutropenia, peripheral neuropathy, CNS toxicity, bone marrow suppression - DON'T: |
| Metabolism Inhibitors | - MOA: Stop bacteria making folic acid - Drugs: Sulfamethoxazole, trimethoprim, bactrim, silver sulfadiazine - For: Broad Spectrum G+ and G- (some nonbacterial infections) - Side Effect: GI upset, photosensitivity, headache, fever, skin rash, itchiness - Adverse Effect: renal or kidney failure, bone marrow suppression, blood disorders, Steven Johnson Syndrome, hepatitis or liver failure, bleeding - DON'T: take with warfarin or hypoglycemic agents, go tanning, give to kids (kernicterus), take with thiazide diuretics - Monitor: G6PD deficiency, fluid intake - Pregnancy/Lactation: avoid |
| Antihistamines | - Suffix: -amine, -adine, -tadine, -izine - MOA: Block histamine release at H1 receptor - For: allergies, anaphylaxis, blood transfusion, motion sickness - Expected Effect: decrease inflammation - Side Effect: anticholinergic effects (Oh 5 Can'ts) - Adverse Effect: coma (first generation), confusion, hypotension, seizure - DON'T: allergies, acute asthma, hepatic disorder, live/kidney, glaucoma, prostate hypertrophy, alcohol, depressants, ketoconazole, erythromycin, MAOI's, give to kids - Monitor: vitals and urine output |
| Non-Steroidal Decongestants | - Suffix: -ephrine, -zoline, -edrine - MOA: Increase alpha-adrenergic response (increase sympathetic) - For: allergies, hay fever, surgeries - Side Effects: restlessness, hypertension, increased HR, photosensitivity, increased BS - Adverse Effect: cardiac disorders, dysrhythmia, rebound - DON'T: caffiene, prescription hypertension, abuse, use more than 5 days - Monitor: vitals |
| Steroidal Decongestants | - Suffix: -sone, -lone - MOA: decrease inflammation - For: allergies - Side Effect: epitaxis, dry nose/throat - DON'T: dexamethasone for more than 30 days |
| Antitussives | - MOA: Opioids (CNS) vs. Nonopioid (local) - For: nonproductive, dry, irritating cough - Expected Effect: stop coughing - Side Effect: Opioid: sedation, GI upset, lightheadedness; Nonopioid: dizziness headache, drowsiness, sedation, GI upset - Adverse Effect: emphysema, asthma - DON'T: mix with other CNS depressants, don't drink liquid for 30 min |
| Expectorants | - MOA: add water content to respiratory mucus (making it easier to remove) and cause irritation of the GI tract (loosening and thinning of respiratory tract fluid) - For: productive cough associated with asthma, bronchitis, COPD - Expected Effect: removes mucus, reduce the viscosity and thin secretions - Side Effect: GI upset, dizziness, drowsiness, headache - Adverse Effect: dermatitis, GI upset - DON'T: if you have respiratory failure, elderly |
| Mast Cell Stabilizer: Intranasal Cromolyn | NasalCrom: - A mast cell stabilizer, suppressing release of mediators from mast calls to prevent inflammation - For prevention and not treatment - Takes a long time to work and can cause epitaxis |
| Asthma Management | - Acute Asthma (rescue therapy) vs. Chronic Asthma (control/maintenance) |
| Classes of Chronic Asthma (4) | 1. Intermittent 2. Mild persistent 3. Moderate persistent 4. Severe persistent |
| Anti-Inflammation Leukotriene Receptor Antagonist | - MOA: block leukotrienes from binding to receptors on the cells in the lungs - For: chronic asthma (not first line for acute asthma) - Expected Effect: improve asthma symptoms - Side Effects: GI upset, dizziness, nasal congestion, cough, pharyngitis - Adverse Effects: Heart Attack, liver dysfunction |
| Anti-Inflammation: Steroids | - MOA: decrease edema, decrease mediators, increase bronchial beta-adrenergic stimulation - For: chronic asthma or bronchospastic disorders - Expected Effect: suppress inflammation - Side Effect: --- Inhalers: coughing, dry mouth, oral fungal infection ---Oral/Injection: hyperglycemia, peptic ulcer disease, growth suppression, mood swings, increased appetite - Adverse Effect: adrenal suppression, osteoporosis, bone loss, cataracts/glaucoma - Contraindications: psychosis, fungal infections, AIDS, TB |
| Mast Cell Stabilizer | - MOA: inhibit mast cells from releasing inflammatory mediators after exposure to a specific antigen - For: preventing asthma (chronic asthma) - Side Effects: cough, bad taste, rebound bronchospasm |
| Monoclonal Antibody: Omalizumab | - MOA: antagonism of IgE - For: allergy mediated asthma (second line drug) - Side Effects: URI, viral infection, pharyngitis, sinusitis, headache - Adverse Effects: malignancy and anaphylaxis |
| Mucolytics | - MOA: liquefies and loosens thick mucus secretions by breaking down the mucus proteins - For: cystic fibrosis, bronchitis, emphysema - Use: five minutes after bronchodilator - Side Effects: GI upset, bad taste, bronchospasm, aspiration pneumonia |
| Bronchodilators: Adrenergic | - MOA: binding and activating beta2 receptors > cAMP > relaxes smooth muscle in the airway > bronchodilation and increased airflow and suppress histamine release in lung and increase ciliary motility - Three Types: ---Nonselective: stimulate alpha, beta1, and beta2 receptors (epinephrine) ---Nonselective Beta-adrenergics: stimulate both beta1 and beta2 receptors ---Selective Beta2: stimulate only beta2 receptors - For: acute and chronic asthma, bronchospasm and bronchitis - Expected Effect: sympathomimetic or adrenergic agonist reducing bronchoconstriction and restore normal flow - Side Effect: insomnia, restlessness, anxiety, heart attack, tremor, dizziness, palpitation, increased BP, anorexia, hyperglycemia, constipation, dry mouth, dry skin, flushing (1 OH and 5 can'ts) - Adverse Effects: angina, hypertension, urinary retention, tachycardia, dysrhythmia |
| SABA: Short Acting Beta2 Adrenergic | Rescue Drug (Albuterol) |
| LABA: Long Acting Beta Agonist | Fixed Schedule (Formoterol or Salmeterol) |
| Bronchodilators: Anticholinergic | - MOA: prevent bronchoconstriction and keep airway open by blocking ACh > blocking the increase in mucus (drying) - For: emphysema or chronic bronchitis - Expected Effect: parasymatholytics or cholinergic antagonist - Side Effect: blurred vision, dry mouth, nasal congestion, palpitations, GI upset, urinary retention, heart attack, anxiety - Adverse Effect: allergy, acute bronchospasm - Contraindication: narrow angle glaucoma, acute asthma attack - NOT FOR ACUTE ASTHMA |
| Bronchodilators: Xanthine Derivatives | - MOA: inhibit phosphodiesterase > inhibit the breakdown of cAMP > increase cAMP > relax smooth muscle > bronchodilation and increased airflow, increased force of contraction and increased heart rate/cardiac output, and increased blood flow to the kidneys - Side Effects: GI upset, gastroesophageal reflux during sleep, palpitations, transient increased urination, nervousness, restlessness - Adverse Effects: GI bleeding, tachycardia, dysrhythmias, hypotension, cardiorespiratory collapse, CNS excitation (heart attack, insomnia, irritability, dizziness and lightheadedness), hepatotoxicity, seizures (narrow therapeutic index) - Contraindications: peptic ulcer disease, GI disorders, cardiac/renal/liver disease, seizure - DON'T: take with ABX, erythromycin, cimetidine, oral contraceptives, allopurinol, fluoroquinolones, take with fatty meals or caffeine |
| Non-opioids: Acetaminophen | - MOA: change the perception of pain by increasing the pain threshold in the brain - For: mild pain to moderate pain - Adverse Effect: permanent liver or kidney damage, acetylcystein is the antidote - Pediatric: toxic to liver/kidneys (dependent on weight) |
| Non-opioids: NSAIDS | - MOA: suppress inflammation-induced pain at the injury site - For: mild to moderate pain for bone, cancer, soft tissue trauma - Side Effect: decrease clot formation (aspirin) > increased risk of bruise and bleeding, GI upset/irritation, water/salt retention > high blood pressure and heart failure - Adverse Effect: induced asthma, salicylate poisoning (fever, rapid heart rate, rapid respirations, GI upset, confusion, tinnitus, acidosis, seizures, coma, and death - Monitor: hypertension, chronic heart failure, peptic ulcer disease, GERD, bleeding/bruising - DON'T: Take on an empty stomach or take with warfarin, give to children (reye's syndrome, mental retardation, death), give to pregnant children |
| Opioid Analgesics (Narcotics) | - MOA: Bind to opioid receptor sites in brain, altering perception of pain and reducing anxiety (opioid receptor agonist) - For: Moderate to severe pain - Expected Effect: reduce pain - Side Effects: GI upset, drowsiness, sedation, mental confusion, orthostatic hypotension, dizziness, skin pruritus, urticaria, urinary retention, miosis - Adverse Effects: respiratory depression (opioid blocker, narcan - antidote), addiction, dependence, tolerance, withdrawal (nausea, vomiting, abdominal cramping, sweating, delirium, seizures - Pediatric Consideration: addiction/withdrawal - DON'T: breastfeed |
| Adjuvant drugs: Anticonvulsants | - MOA: change the way sodium and calcium travel across the surface of sensory nerve cells in the brain (fewer pain signals) - For: chronic pain, cancer - Expected Effect: reduce pain - Side Effects: drowsiness, confusion, blurred vision, clumsiness, muscle aches, weakness, ataxia - Pregnancy/Pediatric Consideration: cause aggressive/suicidal behavior, benefits must outweigh risk - DON'T: breastfeed |
| Adjuvant Drugs: Antidepressants | - Types: TCAs (-triptyline) or SNRIs - MOA: reduce pain signals transmitted to the brain (pain dose < depression dose) - For: chronic pain, cancer pain - Side Effects: Anticholinergic Effects (1 OH and 5 CAN'Ts), GI upset, heart attack, sexual dysfunction, urinary retention, intraocular pressure, orthostatic hypotension, hand tremor, sedation - Pregnancy/Pediatric Consideration: suicidal behavior, avoid breastfeeding - Older Adult Consideration: heart block, increase urinary retention, increase glaucoma, pupil dilate, orthostatic hypotension |
| Types of drugs for Insomnia (4) | 1. Benzodiazepine receptor agonists (non-benzo) 2. Benzodiazepines: anxiety, addictive 3. Antihistamines 4. Antidepressants |
| Insomnia: nonbenzodiazepine | - MOA: act of the GABA-A receptor sites - For: insomnia - Expected Effect: induce sleep - Side Effect: drowsiness, dizziness, fatigue, headache, GI upset, sleep-related behavior - Pregnancy: Categories B and C |
| Insomnia: Benzodiazepine Hypnotics | - Suffix: -pam, -lam - MOA: act of the GABA-A receptor in the brain - For: insomnia - Expected Effect: induce sleep - Side Effect: respiratory depression, daytime sleepiness, memory loss, sleep-related behaviors - Adverse Effect: dependence, withdrawal, rebound insomnia - Pregnancy: Categories D and X |
| Insomnia: Antihistamines | - Suffix: -mine, -zine, -tine, -tadine - MOA: H1 blocker - For: insomnia - Expected Effect: mild sleep inducer - Side Effect: next day drowsiness, unrestful sleep, daytime sleepiness, cognitive impairment, dizziness, blurred vision, dry mouth, may cause increased excitement (pediatrics) - DON'T: use for pts. w/angina, heart arrhythmias, glaucoma, urinary retention |
| Insomnia: Antidepressants | - MOA: SNRI - For: secondary insomnia caused by depression |
| -actone | potassium-sparing diuretics |
| -afil | phosphodiesterase inhibitor |
| -ane | general anesthetics |
| -ase | thrombolytics |
| -azole | antifungals |
| -azosin | alpha blockers (adrenergic antagonists) |
| -bicin | antineoplastic |
| -barbital | barbiturate (sedative hypnotics) |
| -caine | local anesthetic |
| cef-, ceph- | cephalosporin antibacterial |
| -calci- | calcium & vitamin D supplements |
| -ciclovir, -cyclovir | antiviral |
| -cillin | cell wall synthesis inhibitors (antibacterials) |
| Cole-, Chole- | antilipidemic drugs |
| -cox- | NSAIDS, COX 2 inhibitors |
| cort | orticosteroid |
| -curium | neuromuscular blockers |
| -curonium | neuromuscular blockers |
| -cycline | tetracycline antibiotics |
| -dopa | anti-parkinsons |
| -dazole | anthelmintic, antibiotic, antibacterial |
| -dipine | calcium channel blocker |
| -ergot- | ergotamines (anti-migraine) |
| -fenac | NSAID |
| -fibr- | antilipidemic drugs |
| -floxacin | fluoroquinolone antibiotic |
| -gliptin | antidiabetic; inhibitor of the DPP-4 enzyme |
| -glitazone | antidiabetic; thiazolidinedione |
| -ine | stimulants |
| -iramine, -mine | antihistamine |
| -lam | benzodiazepine (anxiolytics) |
| -limus | immunosuppressant |
| -lol, -olol | beta blockers (adrenergic antagonist) |
| -lone, -olone | corticosteroids (anti-inflammatory) |
| -luk, -leu | leukotriene modifiers/inhibitors |
| -mab | monoclonal antibody |
| -mustine | alkylating agent (antineoplastic) |
| -mycin, -micin | antibiotic/antibacterial |
| -nacin | antimuscarininic/ anticholinergic |
| -navir | HIV/AIDS antivirals |
| -nazole | antifungal |
| -nib | antineoplastic |
| -pamil | calcium channel blockers |
| -pram | SSRI antidepressant |
| -oxetine | SSRI atidepressant |
| -prazole | proton pump inhibitor |
| -pam | benzodiazepine (anxiolytic) |
| -aparin-, -parin | antithrombotic; anticoagulant |
| -phylline | xanthine derivative (bronchodilator) |
| -pred- | corticosteroid |
| -pril | ACE inhibitor |
| -profen | NSAID |
| -quine | antiparasitics |
| rifa- | antituberculars |
| -sartan | angiotensin II receptor antagonist ARB |
| -semide | loop diuretic (water pill) |
| -setron | serotonin receptor antagonist |
| -setron | antiemetic and antinauseant |
| -sone | corticosteroid |
| -stigmine | cholinergics |
| -stine | antineoplastics (anti-tumor) |
| -statin | HMB-CoA reductase inhibitor; statins |
| -tadine | H1 blocker (H1 antagonist or antihistamine) |
| -tadine | antiviral; anti-influenza-A |
| -terol | beta agonist; bronchodilator |
| -thiazide | thiazide diuretic (water pill) |
| -tidine | H2 receptor antagonists (anti-ulcer) |
| -trate | antianginals |
| -trel | female hormone (progestin) |
| -tretin- | retinoid; dermatologic agent; form of vitamin A |
| -triptan | antimigrain; selective serotonin receptor agonist |
| -tropium | anticholinergic; bronchodilators |
| -triptyline | tricyclic antidepressants (TCA) |
| -tyline | tricyclic antidepressant (TCA) |
| -vastatin | antilipemics (anti-cholesterol) |
| -vir | antiviral; anti-HIV; anti-herpes; anti-hepatitis; anti-CMV; anti-flu |
| -vudine | antiviral; nucleoside analogues |
| -zepam | benzodiazepine |
| -zine | phenothiazines (antipsyctics, antiemetics) |
| -zoline | nasal decongestants |
| -zosin | alpha blocker |
| Anti-Inflammatory Drugs | NSAIDS: -fenac, -profen Steroids: -sone, -solone Antihistamines: -mine, -zine, -dine Leukotriene Inhibitor: n/a |
| Pain drugs | Opioids: -codone, -phine, -tanyl, -morphone NSAIDS: -fenac, -profen Acetaminophen: n/a Antidepressants: -line, -tine, -xine Anticonvulsants: -zepine, -zepam |
| Insomnia drugs | Benzodiazepine Receptor Agonist (nonbenzo): n/a Benzodiazepine: -pam Antihistamine: -mine, -zine, -dine Antidepressants: -line, -tine, -xine |
| Antibacterial: Cell Wall Synthesis Inhibitors | Penicillins: -cillin Cephalosporins: cef-, ceph- Carbapenems: -apenem Others: -mycin |
| Antibacterial: Protein Synthesis Inhibitors | Aminoglycosides: -micin, -mycin Macrolides: -mycin Tetracyclines: -cyclines Others: -mycin |
| Antibacterial: Metabolism Inhibitors | Sulfonamides: n/a Trimethoprim: n/a Combination: n/a |
| Antibacterial: DNA synthesis inhibitors | Fluoroquinolones: -floxacin |
| Antidepressants | SSRIs: -pram, -mine, -tine, -line TCAs: -line, -mine, -pine MOAIs: -line, -mine, -zine SARIs: -done SNRIs: -xine, -tine NDRIs: n/a |
| Mood Stabilizers (Euthymics) | Antimania: n/a Anticonvulsants: n/a Atypical Antipsychotics: n/a Benzodiazepine: -lam, -pam Calcium Channel Blockers: -pine, -mil |
| Antianxiety and Sedative | Benzodiazepine: -lam, -pam Sedative-hypnotics: -lam, -pam Antihistamins: -mine, -dine, -zine Antidepressants: SSRIs: -pram, -mine, -tine, -line Non-Benzodiazepine: n/a Barbituates: -barbital Beta Blocker: -olol, -lol Alpha 2 blocker: n/a others: n/a |
| Antipsychotics | Typical: n/a Atypical: n/a |
| Antiemetric Drugs | Phenothiazines: -azine Anticholinergics: -mine Antihistamines (H1): -zine, -mine, -dine Dopamine antagonists: n/a |
| Drugs for constipation | Bulk forming laxatives: n/a Osmotic laxaties: n/a Lubricants: n/a Stool Softener: n/a Stimulants: n/a |
| Antidiarrheal Drugs | Antimotility: n/a Adsorbent/Absorbent: n/a |
| Peptic Ulcer/GERD Drugs | Histamine H2 Blockers: -dine Proton Pump Inhibitors: -prazole Antacids: n/a Cytoprotectives: n/a |
| Respiratory Drugs | Antitussives: n/a Decongestants: -rine, -line Antihistamines: -mine, -dine, -zine Steroids: -sone, -nide, -solone Expectorants: n/a Mucolytics: n/a SABA Bronchodilators: -terol LABA Bronchodilators: -terol Anticholinergic Bronchodilators: -tropium Xanthine Bronchodilators: n/a Leukotriene Inhibitors: -luk-, -leu- Mast Cell Stabilizers: n/a |
| Antidiabetic Drugs | Oral Insulin Secretagogues: -Sulfonylureas: -ride, -zide -Meglitinides: -nide Biguanide: n/a Thiazolidinedione (TZD): -glitazone Alpha Glucosidase Inhibitors: n/a Glucagon like peptide or Incretin: n/a DPP-4 Inhibitors: n/a |
| Antilipidemic Drugs | Statins: -statin Bile Acid Suestrants: cole-, chole- Nicotinic Acid Agents: nia- Fibric Acid: fibr- cholesterol absorption inhibitors: n/a |
| Cardiovascular Drugs | Diuretics: -Thiazides -Loop -Aldosterone Blocker -Potassium Sparring Beta blockers: -non-selective beta -selective beta -beta-alpha blockerrs Vasodilators: n/a ACE Inhibitors: -pril ARB: -sartan Calcium Channel Blockers: n/a Antianginals: -Short Acting Nitrates -Long Acting Nitrates Antiplatelets: n/a Anticoagulants: n/a |
| Alzheimer's Disease Drugs | Cholinesterase/AChE Inhibitors: -pezil, -stigmine NMDA Blocker (glutamate): n/a |
| Parkinson's Disease Drugs | Dopaminergic: -dopa Dopamine agonist: n/a COMT Inhibitors: -capone MAO-B Inhibitors: n/a Anticholinergics: n/a |
| Nicotine: Pharmacokinetics | Nicotine is faster absorbed into the blood via lungs and more slowly through the buccal mucosa in chewing and the nasal mucosa in snuffing. Nicotine passes freely into breast milk, leading to toxicity in the nursing infant. It is metabolized in liver and eliminated in urine. T1/2=1-2 hours. |
| Nicotine: MOA | In the CNS, nicotine rapidly acts on the reward system of the brain, promoting the relapse of dopamine and mimicking the effects of cocaine & other addictive stimulants. |
| Nicotine: Side Effects | cardiovascular disease, chronic lung disease, and cancers, leukemia, cataracts, and abdominal aortic aneurysm. CNS stimulant, causing tremors, increased alertness and arousal. VERY STRONG PSYCHOLOGICAL DEPENDENCE. |
| Nicotine: Treatment | 1st line: Nicotine replacement therapy (NRT), Bupropion (Zyban), Varenicline (Chantix). 2nd line: Nortriptyline (Pamelor) & Clondine (Catapres), Not FDA approved. |
| Cocaine: Pharmakokinetics | Smoking and IV methods result in the fastest absorption and the highest "rush." Intranasal use or snuffing produces the longest effects. It crosses the placenta in pregnant women and accumulates in the fetal circulation. Long-term user can develop tolerance. Cocaine is metabolized by the liver. T 1/2 = 50-80 min |
| Cocaine: MOA | It increases dopamine action in the brain reward system, leading to magnified pleasures and rapid dependence. It increases norepinephrine action in blood vessels and heart, producing intense vasoconstriction and cardiovascular stimulation. |
| Cocaine: Side Effects | Euphoria, increased energy and alertness; hallucinations, adrenaline-like actions, impaired concentration and memory, irritability and mood swings, paranoia, and depression. Stimulant psychosis: paranoid delusions, visual and tactile hallucinations, Symptoms of skin excoriations, ↑BP, HR, temp, RR help differentiate a stimulant psychosis from schizophrenia. Acute cocaine toxicity: cardiac palpitations, tachycardia, increased respiratory rate, and fever. Overdose: seizures, hypertension, and dysrhythmias or MI, leading to death. The client experiences restlessness, paranoia, agitated delirium, confusion, their behavior becomes bizarre, erratic, and violent. Physical dependence and withdrawal: dysphoria, fatigue, depression, and hypersomnia, cocaine-seeking behavior, and indefinite craving. |
| Cocaine: Treatment | No specific antidote for cocaine toxicity. Cognitive-behavioral therapies are often the only effective approach to cocaine addiction. |
| Acetaminophen: Pharmacokinetics | More rapid effects are obtained by smoking, snorting and IV, longer half-life and more intense effect than cocaine |
| Acetaminophen: MOA | Similar to cocaine, increase the action of dopamine and norepinephrine in CNS, increase dopamine response in the brain reward system, leading to euphoria and increased self-confidence |
| Acetaminophen: Side Effects | Initial: ↑alertness, improved performance, relief of fatigue, and anorexia, ↑HR, BP, RR and temp (cardiovascular stimulation). Chronic use: irritability, anxiety, paranoia, and hostile, violent behaviors, tooth decay, dermatologic deterioration. Psychosis: similar to cocaine. Acute toxicity: paranoia, seizures, and death. Physical dependence and withdrawal symptoms: dysphoria, fatigue, depression, and hypersomnia, meth-seeking behavior, and craving. |
| Acetaminophen: Treatment | No specific drug therapy is indicated to help maintain abstinence, primarily treat symptoms |
| Caffeine: MOA | CNS stimulant, diuretic and myocardial stimulant (↑HR, cardiac contraction and oxygen demands), leading to ↑cardiac workload. It relaxes smooth muscle and promotes peripheral vasodilation (reduced BP) and cerebral vasoconstriction (used to treat migraine headache). |
| Caffeine: Side Effects | Use < 500mg/day: elevate mood, produce insomnia, increase irritability, cause anxiety, and offset fatigue. Use >500mg/day: nervousness and panic, insomnia, gastric hyperacidity, muscle twitching, confusion, chest pain, tachycardia, and cardiac dysrhythmias. Withdrawal symptoms: headache, irritability, drowsiness, and fatigue. |
| Caffeine: Pharmacokinetics | Absorbed from the GI tract and reaches peak plasma levels in approximately (1) hour |
| Caffeine: Treatment | Managed symptomatically; control HTN; dysrythmias, and seizures; assist with reduction or stopping of intake; substitute decaffeineted beverages as tolerated; provide general food/drink list with caffeine dosage amount |
| Alcohol: Pharmacokinetics | Faster absorption occurs when alcohol is mixed with carbonated liquids. It crosses the placenta and can affect fetal development. Alcohol is primarily metabolized in the liver. Women have have higher blood alcohol levels than men after the same amount of alcohol intake. |
| Alcohol: MOA | CNS depressant, increase dopamine responses in brain reward system, promoting the addiction. Potentiation and cross-tolerance with other CNS depressants. |
| Alcohol: Side Effects | Acute over dose: malaise, N/V, HA, thirst, fatigue, coma, and respiratory depression, hypotension, leading to renal failure and cardiogenic shock and associated death. Chronic alcohol use: Wernicke's encephalopathy, Korsakoff's psychosis, and cirrhosis of the liver. Alcohol withdrawals: gross tremors, seizures, hallucinations and alcohol withdrawal delirium (disorientation, visual or auditory hallucinations, and increased hyperactivity without seizures). Death may be caused by hyperthermia, peripheral vascular collapse, or cardiac failure. |
| Alcohol: Treatment | For acute alcohol toxicity: basic principles of airway, breathing, and circulation (ABCs). No antidote for alcohol is available, and stimulants should not be given. Thiamine should be started before glucose in all clients with alcoholism to treat Wernicke's encephalopathy. For alcohol withdrawal: benzodiazepines such as chlordiazepoxide (Librium), or lorazepam (Ativan) if the person has liver dysfunction. For maintaining abstinence: cognitive-behavioral therapy, and drug therapy, including disulfiram (Antabuse) and Naltrexone (ReVia, Depade, Vivitrol). You must educate the patients that consumption of any alcohol, including use of alcohol-based mouthwash, while taking disulfiram can cause a severe, potentially fatal reaction. |
| Sedative Hypnotic: MOA | Benzodiazepines enhance the effects of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the brain. Barbiturates not only enhance the inhibitory effect of GABA, but they can directly mimic the actions of GABA. |
| Sedative Hypnotic: Side Effects | Initial: euphoria and intoxication similar to that of alcohol. Chronic use: Rapid development of tolerance to the sedative effect NOT to respiratory depression. It develops cross-tolerance to other CNS depressants such as alcohol, benzodiazepines, and general anesthetics NOT opioids. Overdose: hypotension and respiratory depression, leading to coma and death. Withdrawal symptoms: anxiety, tremors, weakness, nausea, vomiting, muscle cramps, and increased reflexes, delirium, grand mal seizures, respiratory and cardiac arrest. |
| Sedative Hypnotic: Treatment | Overdose of Benzodiazepine treated with Flumazenil (Romazicon) No antagonists are known to counteract the effects of barbiturates or other sedative-hypnotic drugs, so emergency life support measures must be taken in cases of overdose Treat withdrawal: Gradual withdrawal of the drug; Use Phenobarbital to control withdrawal symptoms in patients using barbiturates; Then gradually withdraw Phenobarbital when the patients are stable; Hospitalization is recommended during drug withdrawal. |
| Opioid: Pharmacokinetics | IV use can cause effects within seconds and peaks in about 20 min. The onset of most opioids is rapid and may last for up to 24 hours. Smoking or sniffing produces a longer onset and effect. Opioids are metabolized by the liver, crosses placenta; is excreted in urine and breast milk. T1/2= ½ to 3 hours. |
| Opioid: MOA | Opioids activate the brains reward system increasing likelihood of addiction. In addition, opioids bind to the opioid receptor sites in the brain and other areas activating receptors which decrease pain and increase the feeling of well-being. They act similarly to endophins and enkephalins. |
| Opioid: Treatment | For overdose: opioid antagonist, naloxone (Narcan). For withdrawal syndrome: opioid agonist, Methadone (Dolophine) and alpha2-adrenergic agonist, clonidine (Catapress). For long-term management: 1. opioid agonists. Methadone is the most commonly used opioid agonist. Methadone is an addictive drug, so its treatment is managed through agencies approved by the FDA and state authorities. 2. opioid antagonists, Naltrexone (oral ReVia, injectable Vivitrol). 3. mixed opioid agonist-antagonists, Buprenorphine (Subutex or Suboxone when combining with naloxone). |
| Marijuana: Pharmacokinetics | When smoked effects occur usually in 20-30 min and can last up to 7 hrs. THC is stored in body fat, so it is eliminated slowly, half life is 2-7 days. Orally, it's almost completely absorbed but undergoes extensive first-pass metabolism. |
| Marijuana: MOA | Stimulate the dopamine pathways in the pleasure areas of the brain. THC affects cannabinoid receptors in the brain and may act in part through the same reward system as opioids and cocaine. |
| Marijuana: Side Effects | Low to moderate dose: euphoria, sedation, relaxation, enhanced sensory perception, distortion of time perception, hallucinations, short-term memory loss, decreased ability to perform multistep tasks, and temporal disintegration. High dose: intense anxiety delusions, paranoia, and state of toxic psychosis. It decreases re-productivity in both men and women. Chronic heavy use: impaired short-term memory, decreased motor coordination, tremors, increased heart rate and respiratory rates, as well as amotivational syndrome, which is characterized by apathy, dullness, and disinterest. Withdrawal symptoms: irritability, restlessness, nervousness, insomnia and tremor. |
| Marijuana: Treatment | The treatment is to relieve symptoms, and the administration of drugs is avoided if possible. There is no antidote or substitution therapy at this time. |
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