NUR 114 PHARM FINAL STUDY GUIDE {2020} – Parkland College | NUR114 PHARM FINAL STUDY GUIDE | Introduction to Pharmacology Final

NUR 114 PHARM FINAL STUDY GUIDE {2020} – Parkland College Introduction to Pharmacology Final 75 multiple choice questions BRING A CALCULATOR (not a cell phone) How do the elements of pharmacokinetics impact drug administration and utility? Absorption, Distribution, metabolism, and excretion Why are medications given by different routes? What are the potential advantages and disadvantages of these routes? 1. Pharmacokinetics focuses on what the body does to drugs after they are administered a. Stomach—portal vein—liver—circulation—target tissue—target cell 2. Drugs use diffusion and active transport to cross plasma membranes to reach their target cells a. Diffusion: movement of chemical from higher to lower concentration (blood to tissues) 3. Absorption is the process of moving a drug from the site of administration to the bloodstream a. Absorption: the 1st step to reaching target cells; move from administration to blood; determines onset/intensity of drug action and higher absorption rates produce a more effective response b. Enteral route: delivered to GI tract either orally or through naso/gastro tubes; oral mucosa, small intestine, and stomach absorption; intended for general circulation absorption (sublingual/buccal c. Extended release designed to dissolve slowly resulting in a longer duration of action d. First pass effect: drugs absorbed from the stomach and small intestine first travel to the liver where the drug may be inactivated before they ever reach their target organs e. Parenteral route: administration of drugs other than enteral or topical; more invasive; intra-arterial, intraosseous, intrathecal (body cavities), intra-venous, intramuscular, intradermal/subcutaneous, or intracardiac (organs) f. Topical: transdermal patches, ophthalmic=eye, otic=ear, intranasal, vaginal 4. Distribution describes how drugs are transported throughout the body a. Distribution: movement of medications throughout the body after they are absorbed b. Good blood flow to desired site is needed for adequate drug distribution c. Anatomic barriers that affect drug distribution = blood/brain barrier, and fetal/placental barrier 5. Metabolism is a process that changes the activity of a drug and makes it more likely to be excreted a. Metabolism: process to chemically change the drug molecule i. Most metabolism is accomplished by the hepatic microsomal enzyme system b. Pharmacotherapy: i. Oral drug taken by patient ii. Drug absorbed across intestinal mucosa iii. Drug enters portal circulation and travels to the liver iv. First pass effect to liver = metabolized to less active forms v. Drug metabolites leave the liver for distribution to tissues 6. Excretion processes remove drugs from the body a. Excretion: removal from the body i. Renal (urine/kidneys), pulmonary (respiratory system), glandular (saliva/sweat/breast milk), fecal/biliary (feces/bile) 7. The route of administration for a medication varies from patient to patient. Most patients prefer capsules, but they have a slow onset time. IV medications go directly to the bloodstream and are the fastest onset, but they are also the most dangerous. a. Oral i. Advantages: 1. Easy 2. Preferred by patients 3. Extended-release preparations may be available to extend duration of action because they dissolve slowly. They have the advantage of being taken at less frequent intervals than immediate-release formulations of the same drug. 4. Drugs can be formulated in such a way as to protect them from digestive enzymes, acid, etc. (Enteric-coated) ii. Disadvantages: 1. Unsuitable in patients who are uncooperative, are vomiting profusely 2. Tablets and capsules must dissolve before drug is available for absorption which gives them a slow onset time. (Oral liquids absorbed faster) 3. Unpredictable absorption due to degradation by stomach acid and enzymes 4. First-pass effect: Drugs absorbed from the stomach and small intestine travel to liver, where they may be inactivated before reaching target organ(s) What is the difference between therapeutic response and side effects? Toxicity? Allergic response? Sensitivity? Adverse drug effects? Therapeutic response of most drugs depends on their concentration in the plasma a. Therapeutic drug monitoring = every patient will react to the therapeutic ranges of drugs differently b. Minimum effective concentration = amount of drug required to produce a therapeutic effect c. Therapeutic range: drug produces the desired therapeutic action d. Toxic concentration: the level of drug that results in serious adverse effects The drug half-life estimates the duration of action for most medications Repeated dosing allows a plateau drug plasma level to be reached - - - -- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -2. Coumadin (warfarin): Anticoagulant; Pharmacologic: Vitamin K antagonist ● Antidote: Vitamin K ● Half life: 0.5-3 days ● Mechanism of action: ○ Inhibits two enzymes involved in formation of activated vitamin K ○ Inhibits synthesis of new clotting factors ● Precautions: Should not be administered to patients with recent trauma, active internal bleeding, serious bleeding disorders, severe hypertension, intracranial hemorrhage. ● Side effects: hot and cold feeling, pain, swelling, sudden and severe leg or foot pain. ● Serious adverse effects: Abnormal bleeding ● Pregnancy category X ● Nursing responsibilities: ○ Complete health history ○ Monitor PT/INR ○ Monitor urine, stool,emesis, liver function, and CBC ○ Monitor risk groups for nonadherence 3. Dabigatran (Pradaxa): Anticoagulant; Pharmacologic: Direct thrombin inhibitor ● Mechanism of Action: Directly inhibits the action of thrombin without requiring the intermediate step of antithrombin III inhibition. ● It is an oral anticoagulant ● Therapeutic effects and uses: ○ Stroke prophylaxis ○ Treatment of DVT and pulmonary embolus 4. Clopidogrel (Plavix): Antiplatelet drug; Pharmacologic: ADP receptor blocker ● Mechanism of Action: Plavix inhibits ADP receptors on platelets and prolongs bleeding time by irreversibly inhibiting platelet aggregation. 5. Alteplaste (Activase): None; Pharmacologic: Thrombolytic/fibrinolytic ● Mechanism of Action: THe primary action of alteplase is to convert plasminogen to plasmin, which then dissolves fibrin clots. 6. Aminocaprioc Acid (Amicar): Hemostatic/antifibrinolytic; Pharmacologic: None ● Mechanism of Action: Aminocaproic acid occupies binding sites on plasminogen and plasmin. This effectively prevents digestion of the fibrin clot by plasmin. Know the indication for the various “meds of the week”- indication 1. Acetaminophen—analgesic/antipyretic 2. Dilantin –antiseizure 3. Lasix – edema/antihypertensive 4. Lisinopril—ACE inhibitor(treats hypertension) 5. Chantix—smoking cessation 6. Lantus—antidiabetic insulin 7. Heparin—anticoagulant 8. Digoxin—cardiac glycoside (treats CHF and arrhythmias) 9. Lovenox—anticoagulant (low molecular weight heparin) 10. Coumadin—anticoagulant 11. Morphine—opioid analgesic 12. Lipitor—antilipidemic (HMG CoA reducatse inhibitor) 13. Prednisone—corticosteroid (treats inflammation from allergies, asthma, and arthritis) Know effect of enzyme inhibition on circulating drug blood levels 1. Angiotensin converting enzyme inhibitors (ACE inhibitors) are drugs that block the body’s production of angiotensin II. Angiotensin II is a hormone that circulates in the blood and has many effects on the cardiovascular system; its main role is to constrict blood vessels. This constriction can cause high blood pressure and increase the work required for the heart to pump blood into the body’s main arteries. This causes a problem for the heart muscle if it has been weakened by a heart attack or heart failure. Blocking production of angiotensin II with ACE inhibitors prevents constriction of blood vessels, lowers blood pressure, and lessens the energy the heart has to expend from beat to beat 2. This is the drug of choice (formerly was cardiac glycosides) for HF –lisinipril 3. Adverse effects would be hypotension, renal insufficiency, and angioedema Heart failure - know prototype agents, typical frontline tx and know digoxin (precautions, therapeutic effect, s/e’s, half-life, antidote) 1. Therapeutic classification = drug for HF (digoxin is prototype drug and is the ONLY cardiac glycoside in the US!) 2. Pharmacologic classification = cardiac glycoside (alters force of energy in muscular contractions 3. Precautions = AV block, dysrhythmias, renal impairment, MI, and hypothyroidism 4. Side effects = dizziness, anorexia, vomiting, hallucinations, ventricular dysrhythmias, sinus bradycardia 5. Antidote = administer digoxin immune Fab (Digibind) 6. ½ life = 1.5-2 days Know rapid vs short vs intermediate vs long acting insulin, safety issues with dosing 1. From chart on page 1118 in the pharm book, all are subcutaneous injections a. Insulin aspart (NOVOLOG)-rapid action, onset 15 min, peak 1-3 hr, duration 3-5hr (5-10 min before meal, can give with NPH, draw aspart first, give immediately b. Insulin lispro (HUMALOG)- rapid action, onset 5-15 min, peak 30 min-1hr, duration 3-4hr (15 min before meal or immediately after meal, can give with NPH, draw lispro first, give immediately) c. Insulin regular (HUMALIN R /NOVOLIN R)- shoRt acting, onset 30-60 min, peak 2-4hr, duration 5-7hr (30-60 min before meal, can be given by IV, can mix with NPH, sterile water, normal saline, do NOT mix with Glargline) d. Isophane insulin suspension (NPH, HUMULIN N)- iNtermediate, onset1-2 hr, peak 4-12 hr, duration 18-24hr (mix (cloudy), can mix with aspart, lispro, regular do not mix with Glargine) e. Insulin Glargine (LANTUS)- Long acting, onset gradual, begins at 1.1 hours, no peak, duration to 24 h, once daily, same time each day, do NOT mix with any other insulin. Also called the “poor man’s insulin” Terms: carcinogenic, teratogenic, mutagenic, Hale’s categories, FDA schedule categories, FDA pregnancy categories, ½ life, onset, duration, peak, steady state 1. Carcinogenic—having the potential to cause cancer 2. Mutagenic—physical/chemical agent that changes the genetic material (usually DNA) of organism 3. Hale’s categories—L1-L5 (safest-dangerous lactation risk categories) how to determine how safe a drug is for lactation purposes 4. ½ life— 5. Onset—time it takes for drug effects to become prominent 6. Duration—how long the drug will last 7. Peak—maximum concentration that a drug achieves 8. Steady state—overall intake of drug is equal to the elimination of the drug 9. FDA schedule categories—drugs with a potential for abuse are categorized into schedules—classified and regulated according to their potential for abuse a. Drug schedule 1-5 (highest to lowest abuse potential) b. Herorin, LSD, marijuiana to things like cough medicine