(SOLVED) NURSING 3365 Course Map Exam 1&2 | Questions and Answers (100 out of 100) | University of Texas

(SOLVED) NURSING 3365 Course Map Exam 1&2 | Questions and Answers (100 out of 100) What you should master to move forward from pharmacology: Start studying from day one with this document, your drug templates, and my PowerPoint’s. Use the textbook to add anything that is still not clear. This will be the document I will use in our pre-exam concept Reviews 1. FDA process for drug approval (legal) a. Phases I, II, II, clinical trials b. Which Trial does the drug have to pass to be deemed safe and effective? Phase III c. Phase IV (post Marketing) Prescribers to report any issues with medication 2. Patient rights and drug testing (ethics) a. Participation in Clinical Trials b. Informed consent c. Safety of human subjects d. Ethical Principles Define: Autonomy, Beneficence, Non-maleficence, Veracity, Justice e. Regulations: HIPPA (confidentiality of identifiable patient personal information) f. What are the elements of a complete medication order? Drug type, dose, frequency and time, route, patient, and document 3. Scheduled drugs I-V (controlled substances) and nurse’s role – (legal) a. What do the schedules mean in terms of addictive properties? It means how likely a drug is to be misused or addictive 4. Pharmacogenetics and pharmacogenomics a. What are genetic polymorphisms? The gene is the primary organ of hereditary and genetic polymorphism is the one-nucleotide difference in 1% of population that can cause discrepancies in how effective a drug is to the body. b. How do these impact responses to drugs? c. Why is considering a patient’s racial or ethnic heritage important in what medications and doses they are given? SO we don’t overdose them or give them medications that will hurt them. 5. Medication safety and national patient safety goals related to medications Need to have 2 forms of ID: state your name and DOB, check the arm band, check the medication against the order and then against label and the label to the ID band before given a. Medication reconciliation - why is this process important? Crucial for patient safety and established repor with patients and you don’t want to be sending a discontinued medication to the pharmacy. b. What are LASA drugs (look alike sound alike drugs)? (Give an example) Example: Paxil can look like Plavix c. What are High alert drugs? (Give an example) Drugs given and can cause lots of problems- diabetic drugs, anticoags, and antiplatelet drugs d. What are the 9 rights of medication administration? (6 main rights and 3 other rights) Way to prevent medication error. Helps establish repor with patients. You want them to ask questions. Know the 9 rights- focuses on the 6. Rights: drug, patient, dose, route, time, right documentation. e. What are methods of preventing medication errors? Med reconciliation, checking dose 3 times, checking med 3 times before you give it, check right patient, check the 9 rights and speak up and ask questions f. What are factors affecting patient adherence to drug therapy? g. What is polypharmacy? Person taking many medications, herbals, or OTC. Older population experiences this more than any other people h. Who is most likely to experience poly pharmacy? 6. Differences between prescribed, OTC, medications, and dietary supplements OTC and prescribes med are approved by FDA, Dietary supplements and herbal are not. Some vitamins have USP classification, but they are not FDA approved. They can cause drug interactions- let provider know. a. What are the patient teaching issues for each? b. What is the importance of the patient and nurse being aware of the number and type of active ingredients? Know the number of ingredients in medication because it can cause interaction. c. Should medication reconciliation include prescription, OTC, Herbal and nutritional supplements, alcohol, and nicotine use? YES, ALL of those are drugs 7. Difference between generic and trade names SKIP- will use both in exam a. Which is safest to use? Generic b. Can a generic drug have more than one trade name? YES 8. Pharmacokinetics – what body does to the drug How do the following pharmacokinetic processes affect drug therapy? a. Absorption i. Importance of water on absorption-We tell patients to take with full glass of water unless told other wise ii. Effect of food on absorption- Sometimes it will delay absorption, its dependent on bioavailability. iii. How do different formulations of drugs (solution, suspension, capsule, tablet, solid) affect absorption? Solution more rapidly than solid. Suspension, you need to shake if given orally. If suspension injection, reconstitute with saline and role with hands between administered. 1. Factors affecting absorption What are the effects of the following on drug absorption? i. Stomach pH – will affect if the drug is in an ionized or ionized state.- look at the animation in blackboard. Ex: If a patient has to take an antibiotic and if they are on an antacid, they need to take antibiotic and hour before or 2 hours after antacid, so no change in gastric ph. What about if patient is sick and hypotensive? GI blood supply good? No so we will give meds IV route. ii. Ionization versus non-ionization of the drug to be absorbed iii. Other drugs (For example: Think about antacids taken at the same time as an antibiotic) Ex: If a patient has to take an antibiotic and if they are on an antacid, they need to take antibiotic and hour before or 2 hours after antacid, so no change in gastric ph. iv Gastric Blood flow and patient’s health status 2. What are the nursing considerations when administering and educatintion patients about Extended-release and Enteric coated medications? They cannot be crushed or chewed so we need to tell patients that. If a pill has groove means “scored” so it can be cut in half. We also cant out these drug forms down a feeding tube because we would need to crush it and mix with water, suck in syringe and flush with water. Cant block the tube- but regardless don’t use them this way! 3. Bioavailability- Means the extent to which the drug is absorbed (Poor bioavailability (needs taken on empty stomach) like thyroid medication or osteoporosis medication means patient needs to take the drug on an empty stomach) 4. Which routes of administration produce local versus systemic effects? Local effects are by nasal inhalation or topical route Systemic effects by injection or GI route i. Which routes are more likely to cause side effects? ii. Can topical medications ever cause systemic effects? Yes, rectal can and so can topical is high does or heat can cause. iii. Do nasal steroid and inhaled steroid produce local or systemic effects? Inhaled steroids are local effect but inhaled anesthesia is syatemic. b. Distribution To: Blood then tissue Drug needs to bind to albumin (protein). Bound drug- is inert and doesn’t function, no pharm effect. When molecules come off its free drug and we want to see same amount coming in as going out. We reach steady state and equilibrium. Free drug has pharm effect. Look at animations!!!! 1 Protein binding (plasma protein binding = PPB) 2. Low albumin < 3.0 (hypo-albuminemia) and highly PPB drugs- toxicity –why? i. What patient factors contributing to low albumin? Poor diet, genetics ii. What are the effects of bound versus free drug? (See Blackboard animation) iii. What is Equilibrium? How does it relate to steady state? The amount of drugs coming in as are leaving to the cellular site of action. iv. What is competitive protein binding? What may result from this competition? Drug B comes along and if Albumin has a larger specificity and affinity for that Drug B, then it will knock Drug A right off. So we have to be careful so we don’t have toxic level of drug A. Ex: Coumadin binds to Albumin but if you also take aspirin will knock Coumadin off the receptor site and there will be freer Coumadin (and more of it) in the blood leading to toxicity. 3. Protective processes: i. Brain-Blood brain barrier- protects the brain by preventing harmful substances from entering brain tissues and CSF ii. P-glycoprotein – a chemical in cell membranes that pumps toxic substances out back out. For example: P-glycoprotein protects the fetus by pumping drugs back into the maternal circulation from the placenta c. Metabolism What is the purpose of metabolism? Change the drug to water-soluble compound that can be eliminated by kidneys. If by GI route- it will go to GI tract and will be absorbed, by portal vein to the liver- liver will metabolize- blood will go to right side of heart and lungs and left side and circulate again and go back to liver to hepatic artery. All drugs will be metabolized by liver. GI tract- has fist pass effect since its metabolized first i. What is the First pass effect? What route of administration is involved in first pass metabolism? ii. Do drugs that do not go through a first pass effect get metabolized in the liver? Think about the blood supply to the liver. iii. What are CYP450 inducers? Ex: Drug A needs enzymes to metabolize it so it’s considered a substrate drug Drug B (a CYP450 inducer) is introduced and it is telling liver to make more metabolizing enzymes (CYP 450) so Drug A is metabolized faster and more completely so lower therapeutic effect of that drug iv. What are CYP 450 inhibitors? Ex: If we have Drug A and requires enzymes (CYP450) for metabolism and Drug B (CYP450 inhibitor) is introduced, its going to tell liver to make fewer metabolic enzymes, so free level of drug will be accumulating in body and patient will get toxicity. -May not know right away- Some drugs, wont do anything until liver metabolizes them to active metabolite- this is called a pro drug Once metabolism is complete, we have metabolite. These usually are nontoxic and non active- we urinate them off. A pro drug is active metabolite and some are toxic. Tylenol is produced into a toxic metabolite. Some people take excess and can cause liver failure. And is a cause for liver transplant d. Excretion: v. What are the drug interactions, and consequences of drug interactions between CYP450 substrate drugs and an inhibitor or inducer drugs? Remember enzymes work on substrates. (See Blackboard animations) i. What is the main route by which drugs are excreted from the body? Kidney ii. What does serum creatinine tell us about kidney function and drug clearance? Creatine is the byproduct of protein met and serves as marker for telling us how well kidney is functioning and how it can clear (rid of) drug. Serum Creatinin 0.8-1.4. Anything above 1.4 is bad Ex: If patient came in and CREAT 1.4 and next day is 2.4, we would know that something drastic has happened and that the patient is unable to clear drug as well. iii. What is the half-life of a drug? What does that mean? Tine it takes to get half the dose of drug out of the body. Some are short some are long How many half life’s does it take to get a steady state. Ex: If a drug is 24 hour half life, 2 mg- and we agree that 4 half life’s is what it takes to almost reach at steady state. At 5 it is steady state. Between 4 and 5. Look at animation. Ex: 48 hour half-life= so that’s 2 days. 4 half-life’s to reach steady state. 2x4= 8, that would mean 8 days to reach steady state. Ex: 7 days half-life. Taking it everyday. 7x4- 28 days for drug to reach steady state. iv. How many half -lives does it take to reach steady state? 4 v. How does this affect the dosing interval for a drug? vi. Steady state- what is this? (look at the image in Blackboard) vii. How does a loading dose affect steady state? What happens if we have to get to stead state faster? We give a dose that’s higher than the normal daily does given. Also known as loading dose or bolus. 9. Pharmacodynamics- drug on body a. How drugs work- i. Mechanism of action (MOA) (receptors, enzymes, or others)- How a drug works with a receptor or enzyme ii. What is the difference between drug actions versus drug effect? Is it binding or inhibiting enzyme iii. What is the difference between the therapeutic drug effects versus an adverse drug response? TDR- Why you gave the drug in the first place and or the expected outcome. ADE/ADR- Anything that shouldn’t happen. Allergy, side effect. iv. Define Specificity and affinity Look in notes in first lecture v. Define Agonist versus antagonist Agonist- makes something happen Antagonist- prevents something from happening. vi. Define Efficacy versus potency Ex: 10 mg morphine is potent 75 mg of Demerol vii. What is a drug’s therapeutic index (margin of safety)? Why the caution with narrow therapeutic index drugs? Difference between dose of drug that produces effect and a drug that produces toxicity. Narrow margin of safety- we need to draw blood levels. Many drugs with narrow TI viii. Many drugs with narrow therapeutic indices require drug level monitoring ix. Define therapeutic outcome / effect relative to a drugs action b. Adverse drug events: ADRs (Adverse drug reactions) 1. Allergy a. Requires the involvement of the immune system IgE i. May be mild ii. May be severe- anaphylaxis- / angioedema 2. Toxic effects – Often related to the class of drug, high doses, or organ system susceptibility i. Class Effect- toxicity known to all members of a drug class ii. Organ specific – Cardio toxicity; Hepatotoxicity; Nephrotoxicity; Ototoxicity iii. Teratogenic iv. Mutagenic 3. Pharmacogenetics-related reactions (idiosyncratic)-(unpredictable) 4. Side effects are adverse drug reactions (ADRs) but is not usually life threatening (eg. Rash, nausea, diarrhea) i. Bothersome may be mild or severe- predictable ii. Not the same as allergy iii. Nursing - know early signs and symptoms iv. Awareness of drug-drug interactions v. Awareness of synergism (potentiation) 10. The big 3 (Modified Nursing Process) The Pharmacology Equivalent of the Nursing Process (ADPIE) a. Proactivity = Assessment For every drug class, understand (This where your drug templates come in) Proactivity i. What Class of Drug is this? What is the Prototype drug? ii. How does this drug work? Mechanism of action (MOA) iii. From this information, why would we use the drug? (Indication). How would I know if the drug is having the desired effect? iv. What side effects make sense related to the action of the drug? Which ones are most common? Which ones are serious/life-threatening? How will I recognize these side effects? What will I do if they occur? Is there anything I can do to prevent these side effects (check something before I give the drug?) v. Are there any drugs I need to know by name for this drug category? vi. Are there any major drug interactions I need to know about? vii. When would the nurse be concerned enough to hold (not give) the medication? Patient factors Lab values Drug factors viii. What are early signs and symptoms of toxicity of this drug that the proactive nurse can recognize and take immediate action to prevent further harm to the patient? ix. How can the nurse modify the environment to protect the patient from harm? b. Communication (ISBAR= Identification, Situation, Background, Assessment, Recommendation/request for order) i. Example of what you might say to the physician using this form of communication: 1. State the situation and background of the problem A. “Dr. Blank, this is Mr. Murphy, (Identification) I am calling about your patient Mr. John Smith. He is on Tegretol for seizures” (Situation and background) B. State your assessment “He is febrile at 102.6, has chills, a sore throat, and a productive cough of yellow sputum”. C. State your request for the physician’s recommendation and request for an for an order c. Patient teaching i. “I am concerned his WBC may have dropped. I have held the dose this evening – do you want me to check a STAT CBC, and start antibiotics”? When does patient teaching for a ne drug or condition begin? When should discharge teaching begin in the hospital? ii. What do you need to teach your patients to keep them safe when they go home? 1. Name of the drug and what it is for 2. Any diet instructions related to drug 3. Caution about drug-drug interactions (Example: anticoagulants and NSAIDS- risk of GI bleeding) 4. Medical alert identification tags (Example: for patients on chronic steroids, diabetic meds, or anticoagulants) 5. Required lab follow up (Example: Some antibiotics, seizure medications, anticoagulants) 6. Drug administration (Examples: With or without food; Avoidance with other meds/antacids) 7. Side effects and what to report to the health care team 8. Prevention of harm (Example: No alcohol with certain meds; change positions slowly to prevent dizziness and falls, alternate contraception) 9. Self Monitoring- (checking their own blood sugar; Checking their own pulse before taking their beta blocker or digoxin) 10. What do they do when they have side effects? When and who should they call. 11. ANS drugs A. Names that mean the same Muscarinic (cholinergic) versus adrenergic receptors- (Parasympathetic and Sympathetic - Different systems operate under different conditions) B. Cholinergic agonists i. Direct acting- Work on muscarinic receptors to increase acetylcholine- Prototype: bethanechol (Urocholine)- looks at animation and stimulate muscarinic receptors in bladder, detrusor muscle contracts and opens sphincter to cause urination ii. Indirect acting-inhibits acetylcholinesterase’s ability to break down Ach – thereby increasing the acetylcholine available to bind the receptor (also called anti-cholinesterase drugs). BB. So in an indirect way these drugs are cholinergic agonists. Prototype Physostigmine (Antelerium) Donepezil (Aricept) for early Alzheimer’s dementia is also an indirect acting cholinergic agonist C. Key points cholinergic toxicity – excess amount of cholinergic activity i. What could cause cholinergic toxicity? Poisoning from mushrooms, nerve gas, someone is taking excess amount of cholinergic drug activity. ii. Assessment findings Mnemonics: SLUDGE- (Salivation, Lacrimation, Urination, GI upset, Emesis) or DUMBBELLS: (Diaphoresis (sweating) and defecation, Urination, Miosis (constrict), Bradycardia, Bronchoconstriction, Bronchorhea, Emesis, lacrimation, Lethargy, Salivation) (Dumbbells- tells more of the symptoms) Normal situation creates these in normal circumstance but too much like 2013 people in Syria is bad. iii. What is the antidote for cholinergic toxicity? Think- what is the opposite of cholinergic? Physistigmine, it is anticholinergic. What are the nursing assessments needed in cholinergic toxicity? Think about the systems involved. D. Anticholinergic Drugs Drug name you have to know – Prototype: atropine (high affinity and specificity for the muscarinic receptors) generic and trade name and only need small doses due to high affinity and high specificity. Many drugs have effects like Atropine! Eye drops at eye doctor, surgery general anesthetic to prevent wet intubation or juicy peristalsis to dry up secretions. Down below is a list that cause anticholinergic side effects. a. Other drug classes that have anticholinergic side effects: Be thinking about these as we progress through the semester. i. Antihistamines (first generations) diphenhydramine (Benadryl) ii. Antipsychotics (many) iii. Older antidepressants amitriptyline (Elavil) iv. Incontinence medications oxybutinin (Detrol) v. benztaropine (Cogentin) (You will see this again in the Parkinson’s disease chapter) b. Glaucoma- how do anticholinergic drug properties affect glaucoma? They can cause acute narrow angle glaucoma – usually in patients who are unaware they have the condition. Most glaucoma is open angle. (See the textbook for pictures of the eye). c. CNS changes are common in the elderly with anticholinergic medications- many have change in mental status- remember granny case study!! She was taking medicines with anticholinergic effects and she developed anticholinergic toxicity. Shin flushed, dry as a bone, hot as hare, blind as bat (pupils dilated), mad as hatter, full as flask (urine retention). d. Anticholinergic Toxicity (Mnemonic: Red as a beet, = flushed skin tones; dry as a bone= skin and mucus membranes are dry; hot as a hare= skin is warm, blind as a bat= dilated pupils; mad as a hatter= CNS effects –confusion or psychosis; full as a flask= Urinary retention) e. Antidote- physostigmine- an anticholinesterase drug- indirect acting and increases availability of ACH therefore it is an indirectly acting cholinergic agonist (look at the animation in Blackboard). Given if the patient is exhibiting CNS effects of the anticholinergic toxicity. No, bethanechol won’t work, doesn’t cross the BBB. F. Sympathomimetic- Agonists – stimulate sympathetic receptors- Prototype Epinephrine – a. Stimulates Beta 1 receptors, (think heart rate and contractility) Beta 2 receptors (in bronchial smooth muscle think bronchodilation) and Alpha 1 receptors on blood vessels (think vasoconstriction) b. High affinity- low specificity. Uses/ Indications for this drug- Cardiac Arrest and Anaphylaxis c. Administration - IV (Cardiac arrest and anaphylaxis) versus IM/subcutaneous (EPI-Pen) for allergic reactions (buys time to get to ER). d. OTC oral decongestants contain alpha 1 agonists. Oral decongestants Prototype: pseudoephedrine Cause systemic effects anxiety irritability and shakiness. Nasal sprays like /phenylephrine (sympathomimetic) and Afrin exert local effects. e. Beta 2 (SABAs short acting bronchodilators- Beta 2 agonists) Bronchodilation Prototype: albuterol (Proventil) Works as a bronchodilator f. LABAs (long acting bronchodilators) – beta 2 agonists Example: salmeterol often combined with inhaled cortico- steroids g. Isoproteranol- potent non-selective beta adrenergic agonist (beta 1 and 2)-sometimes (rarely) used in critical care h. Dopamine- stimulates dopaminergic receptors- used in critical care in high doses Drugs for HTN- inhibit sympathetic receptors alpha and beta!!! G. Sympatholytics- Antagonists-inhibit (block) sympathetic receptors 1. Beta blocker- key points a. What is the difference between cardio-selective versus non-cardio- selective beta-blockers? Noncardioselective- blocks beta 1 and 2 Cardio selective- only blocks beta 1 Prototype: Propranolol for Noncardioselective b. For what conditions are beta-blockers used? (Hint: There’s more than one) c. How do I know it is safe to administer the beta-blocker? d. Side effects – (hint – look back at selective versus nonselective) e. What is the concern with a non-cardio-selective Beta-blocker and diabetics on insulin? Think about the symptoms a diabetic would experience if hypoglycemic. The body could go into respiratory distress. If you get palpitations f. Beta-blockers and allergic reactions- How well will epinephrine work in anaphylaxis if the patient is on a beta blockers? Not on exam- Beta receptors would be blocked out and wouldn’t work well. g. IV doses versus PO doses of beta-blockers Which is larger and why? IV no pass PO does so it will be larger h. Significant drug interactions (beta 1 blockers, digoxin, and calcium channel blockers)-They all slow the heart rate. 2. Alpha 1 blockers –Powerful Vasodilators- Prototypes doxazosin (Cardura) and tamsulosin (Flomax) a. What happens to BP in vasodilation- goes down so we can use alpha blockers in HTN to bring down BP b. What happens to heart rate when BP drops? When we drop it and someone changes position it can be dangerous and they can fall When we start Alpha blockers dangerous in the first week- body needs to get used to it. Change position carefully/slowly, give it a bed time so they are laying down, limiting orthostatic hypotension, develops tolerance and gets used to it. c. Orthostatic hypotension (Orthostasis is the condition-noun) i. What is important in Patient teaching ii. Given at bedtime to limit orthostatic hypotension iii. Safe care of these patients iv. Used in hypertension (doxazosin (Cardura)and can also be used in BPH- “killing two birds with one stone”) v. Used only for benign prostatic hyperplasia (BPH) tamsulosin (Flomax) Sometimes patients require 3 or 4 BP medications to treat BP to get it down to goal, and NE and EP cause vasoconstriction which increase BP so we don’t want all of that NE circulating in the body. There is a presynaptic receptor in CNS and when stimulated, it vacuums. When NE tries to go to tissue, when that receptor is stimulated by the Clonidine, it vacuums the NE back its to the presynapse. 3. Alpha 2 agonist. Prototype clonidine. Where does this drug work? What does it do? Pre-synaptic receptor – stimulation blocks release of norepinephrine to the tissues. The NE is taken back up into the presynaptic neuron. – helps reduce circulating norepinephrine – therefore helps lower BP. Often added as third or fourth drug in hard to treat hypertension. 4. Antihypertensives a. What are the goals of therapy? To get the BP down and ease work of heart. We use BB and Alpha Blockers but Ace and ARB to open the peripheral resistance and reduce afterload so heart can do work easier. b. What is the relationship of CO to blood pressure? i. Orthostasis with first few doses c. Beta blockers prototype –propranolol i. Non-cardioselective- what does that mean? Doesn’t decide- affects lungs ii. What is the difference between propranolol and atenolol Look back at the sympathetic nervous system d. Alpha 1 Blockers see above e. Alpha 2 agonist see above f. Ace inhibitors Prototype lisinopril (Zestril) (angiotensin converting enzyme inhibitors) (See the Blackboard animation) pril- tells me its an ACE inhibitor. i. Hyperkalemia ii. Contraindicated in pregnancy / breast feeding iii. Angioedema iv. Dry cough – change to ARB g. ARBs Prototype losartan (Cozaar) (angiotensin II receptor blockers)–how do they differ from ACE inhibitors? Prevent to action Can they cause hyperkalemia? Yes and cause angioedema and airway can close airway (anaphylaxis) h. Calcium channel blockers i. Dihydropyridines versus D= Dilate Prototype: nifedipine (Procardia)- treats HTN ii. Nondihydropyidines N=Nodes Prototype: verapamil (Calan) diltiziazem(Cardizem) Slows heart rate and treats HTN iii. What are the major side effects of each? Can get super constipated and need to be told need fluid and stool softener. Can get gingival hyperplasia 12. Diuretics a. What is the danger of diuretics with lithium? Don’t worry about Lithium b. What assessments are required for all diuretics? Well, number 1 allergies, known about weight, 2.2 grams per pound, know the 3 type, if they are pregnant, which is gentle or powerful. A bit if sulfur in all these diuretics and be aware of it ( doesn’t mean if someone has a sulfur allergy but be aware) c. Three different classes 1. Loops- Prototype - furosemide (Lasix) Given by oral if the gut works, patients get IV in hospital since blood supply to GI tract isn’t reliable and we want rapid and complete response. Never given fast and can cause ototoxicity like ringing in the ear. i. What are the indications for Lasix? ii. IV administration- never given fast – causes ototoxicity iii. Recognition of side effects- powerful and waste K and people can be hypokalemia and need for nerve conduction in heart and for muscle contraction so side effects will be: palpitation, skipped beats, feel weak, and muscle weakness. Ex: cardiac – conduction dysrhythmias - related to hypo or hyperkalemia musculoskeletal- hypokalemia –weakness, twitching iv. What’s the effect of diuresis from loop diuretics on serum creatinine? v. ***If you measure daily weight, output and output for accurate dosage and diuresis and fluid. 2. Thiazides- Prototype- hydrochlorothiazide (HCTZ) (gentle and at low can be used alone or with another medicine for HTN affect) (reduction in preload and waste K so hypokalemia) a. Low doses – used for treatment hypertension b. Higher doses – diuretic effect c. Side Effects: Potassium wasting (hypokalemia) i. What’s the effect on serum creatinine? ii. Skin rash – why? Sulfur allergy and can also cause increase in uric acid and can cause gout. iii. Hyperuricemia- what does that cause? iv. Hyperglycemia v. Hypercalcemia 3. Potassium sparing Diuretics a. Two Pototype drugs-spironalactone (Aldactone) triamterene (Dyrenium) b. Potassium-sparing- prevent potassium loss c. What are the side effects common to both? GI upset, and in men is gynocomastia and in woman has abnormal periods and triamterene messes with folic acid. d. What is a specific side effect of spironolactone in men? Gynocomastia e. What is the anemia caused by triamterene? Listed above 4. Hypokalemia a. Replacement- what is preferred route of administration- oral (or through a gastric tube) b. How is it administered intravenously? Slowly over hours not minutes c. What is the risk for patient taking digoxin and diuretics if they develop hypokalemia? Go to BB and look at animation and calcium channel and look at digoxin and the pump and when blood level K low- more digoxin and can bind to gain entry so it does its thing (it allows cell to release calcium which increases force of contraction and slow HR) Hypokalemia=predispose to digoxin toxicity BUT sever toxicity can keep K in blood too much meaning Hyperkalemia 13. Drugs for heart failure and atrial fibrillation: A. Antihypertensives as above B. Digoxin a. Is it used in compensated or uncompensated heart failure? Is it the first drug chosen? Used when nothing else works. The rule is we listen to apical HR 1 minute and then less than 60 hold the dose and call prescriber. c. What is the mechanism of action of digoxin? (see Blackboard animation) 1. How does it affect cardiac muscle contractility? (positive inotrope) 2. What effect does it have on AV node conduction? (negative dromotropic) 3. What effect does it have on heart rate (negative chronotropic) 4. How does hypokalemia predispose to digoxin toxicity (see Blackboard animation). Watch it over and over until you get it. Discussed above 5. How does digoxin toxicity predispose to hyperkalemia? Discussed above d. Narrow therapeutic index drug (0.5-2 mg/ ml) e. Bioavailability issue Capsules vs tablets vs IV- are they all equivalent? Can patients switch between formulations safely? Shouldn’t be switching between formulations because they have different extents that they can be absorbed. Given IV and very slowly- like extremely slow otherwise we change the electron gradient across cell membrane and produce dysrhythmias. f. Long half-life – so how frequently is it given? Long half life- can be given daily but not with food due to binding up and pooping up. NO high fiber FOOD WITH medicine g. IV administration- very slowly due to electron gradient h. Drug interactions- many i. Toxicity i. Recognition- early vs late signs 1. Early signs and symptoms- malaise, GI upset (anorexia, nausea, vomiting) cardiac (abnormal rhythms - pt may complain of palpitations or skipped beats) musculoskeletal (muscle weakness- may be related to hypokalemia) 2. Late signs and symptoms- visual color changes happen late j. How is digoxin toxicity treated? 1. Mild- drug is held. – if its 2.2 (that’s barely above upper level) 2. Severe -Digibind: What is this and when is it used? This is also called Digifab and is super expensive. This is people who have a level of 6 and the K level is similar you would use this. k. Potassium -what’s the big deal with patients on digoxin? Do k+ and digoxin compete for the same binding site on the cell? (Look at the animation in Bbd). l. Suspect toxicity with loop diuretics –why? Watch the labs because diuretics also cause hypokalemia as well. m. Before administering drug check apical heart rate for one minute. When do you hold the drug and call the prescriber? When it is below 60. n. Check Lab results: serum Creatinine and Serum Potassium o. Patient Teaching 1How to take their pulse 2 What to report p. How do you know the drug is working? What symptoms and or signs should improve?**More urine output, less swelling and less preload and can feel pulse in feet and ankle, extremities warmer to touch and more energy and SOB will decrease. 14. Angina drugs:-Prototype nitroglycerine 57:02 A. Acute coronary syndrome versus stable angina. B. What is the goal of anti-anginal therapy? 1. Nitroglycerine a. Mechanism action – Converted to nitric oxide by sulphydrly groups – leads to vasodilation b. Short-acting versus long-acting nitrates i. What are each used for? ii. What drug formulations are short, which are long? iii. Why is a Nitrate-free interval necessary? (those sulfhydryl groups have to be regenerated overnight) We convert and we need sulphhydrol groups to do so and we tell patients to take patch off at night so 8-12 hour interval or if pills, don’t take anything after 5pm. This gives us enough time to generate more. iv. Sexual performance enhancement drugs (Viagra, Cialis) and dangers with Nitrates –especially IV nitroglycerine (they are both powerful vasodilators) c. Treatment of acute chest pain at home with sublingual nitroglycerine- How many? – at what interval? -and when to call 911? They need to put one under tongue and lay or sit down since it causes huge vasodilation and a buzz under the tongue and pain should subside 1 or 2 minutes and if that doesn’t happen, need to call 911. Can take a total of 3 at 5 minutes apart. d. Treatment of acute chest pain in hospital- when is it safe to give the second sublingual nitroglycerin? We go in and take vital signs and give sublingual nitroglycerin and now the systolic is below 90, do you give second dose? NO! They are vasodilator and it is below 90. e. Why wear gloves when applying nitroglycerin ointment? Comes in a tube and there is a grid and you squeeze in line and out it one clean skin and leave on for 12 hours. Take off old patch and rotate site and wear gloves to do so. f. IV nitrates – when and why? Male patient is asked if they have taken erectile dysfunction drugs because they work on different MOA- both can drop BP and that can be dangerous C. Patient teaching- for nitroglycerin tablets (safe drug storage and administration, and side effects). How will the patient know the drug is still good (potent)? Store in dark bottle and no high heat. 15. Lipid-lowering drugs- Look at Key Concepts on this a. Lipids: LDL, HDL, and triglycerides. Which drug classes work best on lowering LDL cholesterol? Statins and the lab test is a Lipid panel and looking at the LDL b. Side effects: i. Myalgias (muscle pain) (rare) ii. Rhabdomyolysis- rare but can be serious (muscle break down, leads to release of myoglobin which blocks renal tubules and leads to renal failure) c. Drug interactions with grapefruit and other CYP inhibitors- what happens to the free drug level and what can that lead to? This can increase the effect of the drug for predispose you to toxicity. d. Therapeutic effects of statins Prototype: atorvastatin (Lipitor ) reduced LDL cholesterol and triglycerides and increased HDL e. Pertinent labs Fasting lipid panel (to assess decrease in LDL cholesterol) j. Fibrates – Gemfibrozil (not recommended) decreases triglycerides (No longer recommended by the FDA). Can cause increased toxicity if given with statins. k. Niacin – mixed hyperlipidemia- not used much any more Used with High cholestol and high triclycerides and can cause flushing and itching so we tell them to take aspirin 30 minutes before to relieve that 1. Side effects: Flushing, burning, and itching (prevented with aspirin 30 minutes before Niacin) l. Bile acid sequestrants 1. Local effect only 2. Many drug-drug interactions 3. Increase fluid intake 4. Don't take other meds at same time 16. Parkinson’s drugs A. Parkinson’s disease is a progressive neurological disorder caused by loss of function of cells of basal ganglia. Reduced dopamine. Imbalance of dopamine and acetylcholine 1. Dopaminergic drugs- Prototype: Levodopa- Carbidopa pro-drug which is converted to dopamine. Why can't dopamine itself be given as a treatment for Parkinson's? a. What is the on and off versus end of dose phenomenon? KNOW THIS b. How do MAOIs help in Parkinson's disease? c. Why are MAO -B inhibitors preferred in Parkinson's? d. What is the "cheese effect"? e. Which antiviral agent was found to have anti-parkinson's effects- amantadine m. Anticholinergic drugs in this disease- Benadryl and Cogentin Used for EPS symptoms. 17. CNS drugs A. Stimulants a. Triptans for Migraine headaches (these drugs will be mentioned briefly) 1. Serotonin syndrome 2. Avoid in patients with heart disease b. ADHD medications- Prototype: methylphenidate (Ritalin) 1. Abuse potential in those without ADHD 2. Monitoring of desired outcomes: stable mood, improved concentration and grades in school and stable appetite and weight. 3. Adverse effects: decreased appetite, weight loss. c. Some stimulants still used in weight loss drugs (phentermine now combined with the antiepileptic drug topiramate to for Qsmia FYI not a prototype). Stimulants by themselves don’t work very long. Patient develops tolerance. d. What is the concern for M.I. with Cocaine abuse? Think about the stimulant sympathomimetic effect on arteries especially the coronary arteries. VERY powerful vasoconstrictor- ask drug history if they have had cociaine B. Depressants 1Alcohol- CNS depressants a. Metabolism chronic alcohol ingestion- CYP 450 inducer- reduces effect of other drugs 18. Anemia 2. Withdrawal- prevention and treatment in the hospital- add a benzodiazepine like Prototype: lorazepam Ativan 3. Alcohol poisoning- can lead to temperature loss, respiratory depression coma and death a. Antabuse is used in hard-core alcoholics who are abstinent. It is considered an aversive agent because of the disulphram type reaction that will occur if they take a drink. They won’t die but they wish they would. This reaction can occur with very small amounts of alcohol. You will see it again with the antibiotic metronidazole(Flagyl). 4. Narcotics: Opioids 5. Marijuana 6. Combining CNS depressant drugs can cause severe respiratory depression and death A. Iron deficiency- focus on this and when to give iron and when not too a. Prevention vs treatment (not all vitamin supplements contain iron- prenatal vitamins do contain iron) b. Patient teaching- we want drug to be absorbed properly 3. Administration of iron PO 4. Improving absorption- take with vitamin C – orange juice 5. Side effects of iron therapy- GI discomfort and black stools (expected outcome) c. Monitoring- CBC (Hemoglobin Hematocrit) and Iron studies we can give PO and occasionally give IV and there are precautions. B. Vitamin B12 deficiency versus folic acid deficiency- need both for making RBC a. Alcoholics - b. Malnutrition c. What is the role of folic acid supplementation in pregnancy- because lack of this can be linked to spina bifita and enechepholy. Shouldn’t be given folic acid until we know the cause of the anemia and folic acid is contraindicated in anemia. V12 given my I Muscular injection but other forms now C. Anemia of chronic renal insufficiency- Kidney produces erythropetin the hormone that stimulates the bone marrow to make RBCs. This is decreased in chronic kidney disease. If you have an insufficiency, you will develop anemia and get shot called Procrit to help bone marrow make RBC. We need to remember that they are procoagulants and can cause with uncontrolled HTN produce MI or stroke. ( if they have high BP or uncontrolled or if noncompliant) SO HTN is contraindication. a. use of ESAs ( erythrocyte stimulating agents) Prototype Erythropoetin alpha (Procrit) or darbopoetin alpha (Aranesp) c. Monitoring: These drugs can increase blood pressure and are procoagulants d. When would you hold these drugs? 19. Thyroid drugs A. Drugs for hypothyroidism a. Most commonly prescribed drug Prototype: levothyroxine (Synthroid) b. Side effects: Insomnia, anxiety, (tachycardia if dose is too high) c. Desired Outcomes Reduced fatigue, increased energy, B. Antithyroid drugs (for Hyperthyroidism) (propylthouricil) a. Side Effects: Agranulocytosis C. Iodides -Potassium iodide used after exposure to ionizing radiation- (think Fukushima) D. Radioactive iodine used to destroy thyroid tissue in hyperthyroid states and thyroid cancer. E. Pregnancy and hyperthyroid treatment a. Propylthiouracil- Pregnancy category D, but its use is necessary in the pregnant patient with hyperthyroidism. First trimester only. b. Methimazole is used for the rest of the pregnancy 20. Women’s health A. Key Concepts FYI only a. Smoking and contraceptives- Increased risk of blood clots -Stroke; MI; DVT/PE (important when considering women and cardiovascular disease) Patient education is important. b. Contraception- alternate form needed when on certain antibiotics c. Contraceptives –alternate form needed when on anti-seizure medications d. Combination estrogen-progestin- are in birth control pills and in post menopausal hormone replacement drugs in women who still have a uterus (ie. they haven’t had a hysterectomy) 21. Coagulation modifiers A. Heparins: Prototypes: Unfractionated heparin and low molecular weight (LMWH) heparin enoxaparin (Lovenox) a. How fast do heparins work? Alpha anticoagulants and works fast b. IV versus subcutaneously uses- we are careful and do test PTT c. How does this relate to dose? i. I.V. Dosed in units/kg ii. Subcutaneous Dosed in mg/kg d. Major and most common side effects a. Bleeding b. HIT-Heparin induced thrombocytopenia Caused by antibodies formed to a complex of heparin and platelet factor 4. The immune system sees this as foreign and mounts a response. One result is: i. Low platelets due to heparin antibody binding to platelet factor 4 (Think of this as an yellow traffic light – telling you -something is not right) ii. Need different kind of anticoagulant –direct thrombin inhibitor (argatroban by continuous IV infusion) iii. Major complication of HIT is paradoxyl clotting 1. Unfractionated Heparin (See the Heparin protocol in Blackboard) a. Weight based Standard or Modified protocol b. Bolus dose and maintenance infusion rate c. PTT monitoring d. When and how often to check PTT? Repeat at 6 hours until 2 consecutive results and then you can change to every 24 hours e. Desired therapeutic range PTT per the protocol? f. What to do if outside of range? Read the protocol. The answer is in front of you. g. What's the heparin antidote? Protamine Sulphate 2. LMWH Prototype enoxaparin (Lovenox) a. How is it administered? Subcutaneuosly b. What is the benefit of LMWH over unfractionated heparin? can be done by yourself, at home and not testing for monitoring 3. Oral anticoagulant : Prototype: warfarin (Coumadin) a. What is the mechanism of action of Coumadin? (What substance does Coumadin inhibit, thereby, preventing the liver from making certain clotting factors? How fast does Coumadin work? Coumadin inhibits clotting factors in the liver that Vit K make -factor 2,7,9,10. So we inhibit the formation of those clotting factors. So the antidote is Vit K. We say be consistent in your intake and read labels for your food or it will be difficult to manage PT/INR b. What is its half-life? How long will it take to reach steady state? Long- 36 hours to get to steady state so half life is 8 days c. Used-prevention and treatment (does it lyse a formed clot?) d. Major and most common side effects i. Bleeding and bruising ii. Skin reactions- very rare e. Prevention of complications Fall and injury prevention Regular drug levels (every month) f. Drug-drug interactions (think highly protein bound drugs and competitive protein binding) g. PT/INR monitoring- every month i. Normal range INR 2.0-3.0 h. What to do if outside of normal range Too low – increased risk clotting – call prescriber- ask if they have evidence of bleeding or blood in urine or abdominal pain Too high- increased risk bleeding DO NOT GIVE IV ANYMORE Assess for bleeding / bruising Hold drug and call prescriber i. What's the antidote for excess Coumadin (over anticoagulation)? Think about what it is inhibiting the formation of. Vit K j. Dietary considerations What advice would you give the patient? k. Patient teaching l. Diet at home and on vacation m. Medication compliance awareness of food and drug labels 4. Prototype: Aspirin and Plavix 01:40:50 a. Antiplatelet uses (low dose) prevention. b. Prototype: acetyl-salisylic acid Aspirin. Hypersensitivity signs and symptoms c. What is the risk of aspirin use in children and teenagers recovering from viral illnesses? d. Major side effect: Bleeding e. Aspirin overdose and acidosis f. Aspirin at higher doses can relieve pain g. Prototype: clopidogrel Plavix (pro-drug must be metabolized to its active metabolite to interact with the receptor on the platelet). Prevents platelet aggregation. Length of therapy after coronary stent placement-1 year of therapy Compliance issues 5. Thrombolytics- Prototype (tissue plasminogen activator tPA) a. Contraindications to therapy- many absolute and relative b. Post therapy monitoring by nursing- monitor for bleeding but also neuro checks every hour for 24 hours. 22. Anti-epileptics Prototypes: phenytoin (Dilantin) (phosphenytoin) Cerebyx (pro-drug- converted to Dilantin so still do Dilantin level but dose is not equivalent). Can be given subcutaneously as well as IV. a. How does it differ from phenytoin? What drug level do we measure? b. Risk of drug error due to doses not being equivalent b. Drug interactions- Many!! c. Pregnancy categories- D f. Which drug/drugs can be used in status epilepticus? g. Lab monitoring - therapeutic range for Dilantin (10-20 mcg/ml) i. Administration- oral or IV j. Enteral feedings- don’t want to give it with tube feedings so we turn off the enteral feeding for one hour before dose is given and for 30 minutes after the dose. k. Acute side effects- fatigue, nystagmus (eyeball moving from left to right ), nausea Toxicity recognition Blurred vision (nystagmus), slurred speech, Unsteady gait (ataxia) (Vision, speak, gait- Dilantin toxicity and you ask for drug toxicity) l. Patient teaching related to these side effect: patient needs to be consistent with dosing 2. carbamazepine (Tegretol)- some take this because they react better a. Major side effects similar to Dilantin b. Does not cause gingival hyperplasia c. Can depress bone marrow production of WBCS, RBCs, Platelets- need to do complete blood count because of this. d. What are similarities and differences between phenytoin (Dilantin), carbamazepine (Tegretol), e. Is it used for the initial treatment of status epilepticus (after Ativan)? 3. Valproic acid a. Can it be used for status? b. Children and Hepatotoxicity / Pancreatitis Other side effects: weight gain and hair loss. 4. Benzodiazepines Prototype: lorazepam (Ativan)- FOR GRANMAL SEIZURES i. Role in status ii. Side effects IV versus PO iii. Should chronic benzodiazepines be abruptly stopped? Weaned, never stopped abruptly iv. What's the antidote? flumazenil (Romazicon 23. Antipsychotics A. Conventionals Prototypes: Thorazine and haloperidol (Haldol) a. More EPS a. Acute dystonia b. Tardive dyskinesia B. Atypicals- Prototypes: olanzapine (Zyprexa) respiradone (Resperdal) clozapine (Clozaril) b. Fewer Extrapyramidal System side effects (EPS) i. (Clozaril) clozapine – bone marrow suppression -agranulocytosis ii. (Zyprexa) olanzapine and iii. ( Risperdal) risperidone -weight gain and hyperglycemia c. Side effects of all antipsychotics i. Orthostatic hypotension ii. Sedation iii. Anticholinergic effects 24. Antidepressants-Older versus newer a. TCA-(Prototype: amitriptyline (Elavil) risk Cardio-toxicity from overdose b. MAO inhibitors (no prototype just be aware of the class) - dietary restriction of tyramine containing foods to prevent hypertensive crisis c. SSRI fluoxetine (Prozac) and SNRIs venlafaxine (Effexor) d. Serotonin syndrome (Shake and Bake) Key assessment features Hyperreflexia and hyperthermia Serotonin withdrawal (FLUSH- flu like symptoms, uneasiness, shakiness, headache d. Uses SSRIs Prozac and SNRIs Effexor e. The SNRI with 4 FDA approvals duloxetine (Cymbalta) approved for depression, diabetic neuropathy, fibromyalgia, chronic musculoskeletal pain (you see this drug could be used to treat all these conditions in a single patient) 25. Anti-mania –Lithium- gold standard anti-mania drug a. Prevention of dehydration and electrolyte (Na) depletion important b. Toxicity - renal failure c. Other drugs used as moods stabilizers: valproic acid, carbamazepine (Tegretol), lamotrigine (Lamictal)- all anti-epileptics used as mood stabilizers 26. Antibiotics A. Narrow spectrum versus broad spectrum a. Which are more likely to promote opportunistic infections? b. Proactivity: Before giving any antibiotic i. Allergy determination ii. Renal function iii. Baseline WBC iv. Site of infection v. Obtain cultures vi. Pregnancy? c. Monitoring- Ongoing antibiotic therapy i. Side effects ii. Opportunistic infections- C diff diarrhea - candidiasis (yeast infection) iii. Side effects specific to drug classes iv. Allergy development d. Renal clearance- monitor creatinine e. Is the patient’s infection improving? i. Signs and symptoms ii. WBC count and differential f. IV site monitoring (thrombophlebitis) B. Beta lactams 1. Penicillins, Cephalosporins and Carbapenems a. allergy potential between pencillin and cephalosporins Prototypes: Penicillin G Injectibles: Benzathine and procaine salts = IM ONLY IV formulations- must be in aqueous form Pen V K – oral formulation b. Resistance issues with penicillins c. Nephrotoxicity d. Seizure with high dose and poor renal clearance 2. Cephalosporins a. 1st generation Prototypes: cephalexin (Keflex) and b. 3rd generation ceftriaxone (Rocephin) – eliminated in bile not renally excreted ( no dose adjustment needed in renal dysfunction) c. Thrombophlebitis with I.V. cephalosporins C. Quinolones Prototype: ciprofloxacin (CIPRO) a. Broad spectrum b. PO and IV- get same blood level c. Cartilage damage/rupture( Black Box warning) d. Contraindications children and pregnancy e. Photosensitivity f. Confusion in elderly g. Bioavailability decreased if given with vitamins, iron, calcium(due to chelation) h. Drug interactions i. Theophylline and seizures (Cipro is a cyp 450 inhibitor can lead to theophylline toxicity) D. Macrolides erythromycin oldest; a. azithromycin (Z-Pak) clarithromycin (Biaxin) relatively new (newer agents -longer half -lives) b. High dose azithromycin IV is bacteriocidal c. Low dose azithromycin PO is bacteriostatic d. Alternative to PCN in allergic patients e. Side effects Cardiac side effects in some patients Thrombophlebitis with erythromycin IV Hepatotoxicity with 1 type of erythromycin base Z-Paks 5 day and TriPak 3 day f. Explain long half-life to patients- (drug still working after last dose taken) E. Clindamycin- a. oral, IV and topical b. Great anaerobic coverage c. Known to cause AAPC F. Vancomycin a. used for gm + organisms MRSA (methicillin resistant staph aureus). IV for severe MRSA ( positive blood cultures). b. Alternative for patients who are allergic to penicillin c. Drug of choice for C difficile diarrhea.. IV versus PO uses (PO only in C difficile diarrhea). IV in C diff if patient NPO. d. IV administration must over be 60-90 minutes or more e. Nephrotoxicity and ototoxicity f. Red man syndrome - not allergy- related to histamine release g. Peak and trough levels to determine adequate dose vs toxicity (FYI only) Zyvox and Synercid Used to treat VRE and limited use due to resistance G. Tetracyclines- Prototype: doxycycline (Vibramycin) a. Mostly used outpatient b. Why can’t we give to children under 8? Think teeth c. Photosensitivity d. Do not give simultaneously with iron, vitamins, or calcium – bioavailability H. Aminoglycosides Prototype: gentamycin (Garamycin) a. Used in severe infections b. IV and topical forms c. Peaks and troughs to determine adequate dose vs toxicity d. Nephrotoxicity and ototoxicity e. Weakness and paralysis especially after anesthesia or weaning from mechanical ventilator f. PCN and aminoglycoside administration IV I. Sulfonamides Prototype: trimethoprim/sufamethoxazole (Bactrim) a. Uses b. Think Skin, skin, skin Major AE Steven's Johnson Syndrome J. Miscellaneous Prototype: metronidazole (Flagyl) a. Used for C. diff diarrhea infection- not as effective as vancomycin b. Do not drink alcohol entire time taking and for 48 -72 hours after c. Disulfuram-like reaction with alcohol intake k. Antifungal Agents: Prototypes: nystatin oral swish and swallow for oral candidiasis fluconazole (Diflucan) Po or IV for systemic candidiasis or vaginal candidiasis. Amphoteracin B for severe systemic fungal infections. Can cause fever and chill if given too fast. Patients get Tylenol before the dose. Can cuse hypokalemia. l. Antiviral Agents: acyclovir (Zovirax) treats herpes simplex I and II and herpes Zoster( shingles) 27. Gastrointestinal medications A. Antacids (No Prototype- just understand as a class) i. How antacids work? Calcium carbonate (TUMS), magnesium containing (MYLANTA), aluminum containing (AMPHOGEL) ii. Can all patients take antacids? Who should not take magnesium or aluminum containing antacids? iii. Are there any complications of therapy? iv. What is the difference between acid reducing drugs and antacids? v. Which are the most effective drugs for PUD and GERD B. H2 blockers- ranitidine (Zantac) famotidine (Pepcid) cimetidine (Tagamet) Prototype i. Uniqueness of Tagamet cimetidine? Strong CYP450 inhibitor ii. Uses heartburn -available OTC iii. We are becoming aware that long-term use is not a good thing. C. Proton Pump Inhibitors (PPIs) Take Powerful inhibitors of Hcl acid production. PO forms 30 minutes before eating for best outcomes Prototype: omeprazole (Prilosec) PO only OTC and prescription ii. esomeprazole (Nexium) PO and IV iii. pantoprazole (Protonix) IV D. Promotility agents: Used for delayed gastric emptying and nausea i. metoclopramide (Reglan) Prototype ii. great for chemotherapy induced nausea iii. Side effects- risk for tardive dyskinesia- suppresses dopamine E. Miscellaneous sucralfate (Carafate) How does this drug work? Is it systemically absorbed? F. Laxatives i. Which ones are most effective for patients with acute constipation? Stimulant laxative- bisacodyl (Dulcolax) PO or Rectal suppository ii. Which ones best to prevent straining? Stool softener – ducosate sodium Colace) iii. Which ones best to promote motility? Stimulant laxatives 1. Abuse potential 2. Suppository versus orally iv. Salines/osmotics 1. (MOM), milk of magnesia, gentle 2. Which ones are used for chronic constipation? Miralax v. Hyperosmolar agents for bowel prep pre-colonoscopy 1. Go Lytely mixed with water to make 4 liters over several hours; drink quickly 8 ounces every 15 minutes 2. SUPREP Two doses about 12 hours apart. smaller volume – (take with apple juice to cover taste) have to drink 32 ounces of water with each dose 3. Compliance critical for good visualization of the entire colon vi. Bulk-forming laxatives: Metamucil or Citrucel Administration- mix completely in 8 oz water vii. Miscellaneous: Lactulose (Enulose) It is a man made sugar. Used to treat constipation Also used to treat hepatic encephalopathy caused by high blood levels of amonia in liver failure. Bacteria in the colon digest lactulose and form chemicals that bind ammonia, thus preventing the ammonia from being absorbed into the bloodstream and reaching the brain. G. Antidiarrheals i. Adsorbents (Questran)-cholestyramine ii. Antacid and Salicylate (PeptoBismol) bismuth subsalicylate and aspirin sensitivity-GI bleeding risk? Stool changes – black stools from the bismuth content iii. Anticholinergics Atropine as a pre-med before surgery or chemotherapy. Why do you think this works? iv. Opiates 1. In OTC anti-diarreals (Imodium) and prescription (Lomotil) 2. Tincture of opium and Paragoric H. Antiemetics i. Which classes are associated with EPS symptoms? - tardive dyskinesia? Think dopamine suppressors (Compazine, Phenergan, Reglan) ii. Which class has few side effects? (5HT3 Serotonin antagonists- ondansetron (Zofran). Can cause headache. Does not cause drowsiness like chlorpromazine (Compazine) and prochlorperazine (Phenergan) iii. How would you administer Phenergan? Preferably orally or by rectal suppository, or a gel applied to the inside of the wrist (nicer than a suppository). If given IV (not preferred- then dilute in at least 10 -15 mls saline and infuse in to a free running IV). iv. Can cause severe tissue injury if infiltrates into tissues- possible amputation of a limb v. Which classes are used for motion sickness prevention? antihistamines diphenhydramine (Benadry), vi. Dramamine and anticholinergics like scopolamine 28. Pain and inflammation i. What is tolerance? ii. Physical dependence- Withdrawal, Is it necessarily a sign of addiction? iii. Addiction- Pyschological dependence- will experience withdrawal if drug of choice not available. 1. NSAIDS- Nonsteroidal anti-inflammatories-ibuprofen (Motrin) and (Advil) naproxen (Aleve) acetylsalicylic acid(Aspirin) i. How do they work?- inhibit prostaglandins - ii. Nonselective NSAIDS -inhibit COX 1(good COX) or COX 1 and 2 versus Celebrex inhibits COX 2 (bad COX) COX 2 is said to be inducible- that means it is only present in the presence of inflammation. iii. Desired outcomes of therapy- reduced fever, pain, inflammation iv. Uses- fever, mild to moderate pain, inflammation v. Side effects PUD – bleeding Renal insufficiency- due to inhibition of the prostaglandins that controls blood flow to the kidney MI and Stroke vi. Nursing care and monitoring-allergies, history, medications vii. What is unique about ketorolac (Toradol)? - powerful NSAID- limited to 5 day course of treatment -why? viii. Hypersensitivity ix. Aspirin toxicity Salicylism - Nausea, vomiting, diaphoresis, and tinnitus, rapid breathing (hyperventilation - body trying to correct a metabolic acidosis) are first signs as a sign of toxicity- later drowsiness -coma x. Why we don’t give aspirin to children and teenagers-Reye’s syndrome- encephalopathy and liver toxicity -avoid in children and teenagers recovering from a viral illness. 2. Tylenol) acetaminophen i. How does it differ from NSAIDS? Does it have anti-inflammatory effects? ii. Toxicity 1. What increases risk for toxicity? 2. What does toxicity look like? Can lead to liver failure- transplant or death. Must be treated within 3 days. Blood level determines level of toxicity 3. How is it treated? N-acetylceistine (Mucomyst) given intravenously after Tylenol blood levels are determined in the toxic range 4. Analgesic of choice if on aspirin or other antiplatelet or anticoagulant drug iii. Patient teaching- Tylenol is in many OTC and some prescription meds. Teach patient maximum safe doses. 3000 mg in 24 hours if healthy, 2000 mg in 24 hours if elderly or alcoholic or lowerin liver disease 3. Opioids Prototype: morphine sulphate i. Full agonists, partial agonists, opioids antagonists ii. What is a PCA pump and why is it used? iii. How fast can you push morphine and other opioids? iv. Morphine first pass effect and PO and IV dosing differences v. Side effects 1CNS- depression- repiratory depresion 2BP- orthostatic hypotension 3GI- constipation due to binding of Mu receptors 4Skin- itching due to histamine release 5Pupils constricted vi. Prevention of complications vii. Drug interactions viii. What is unique about meperidine (Demerol)? ix. Opioid antidote naloxone (Narcan) xi. Opioid withdrawal xii. fentanyl (Duragesic) patch changed every 72 hours. There are IV, nasal inhalation, buccal and lollipop forms of fentanyl May only be used for pain management in patients who are opioid tolerant. IV form used in anesthesia. xiii. hydromorphone (Dilaudid) more potent than morphine lower doses - PO or IV - may be used in a PCA pump xiv. Oral opioids often combined with acetaminophen aspirin or ibuprophen. Why? Oral opioids schedule- Vicodin now schedule II xv. tramadol (Ultram) now schedule IV xvi. Partial agonists- How are they different from full agonists 29. Adrenal agents a. Difference between glucocorticoids Prototypes: prednisone (oral) Solumedrol and Solucortef (IV) and mineralcorticoids b. Pharmacologic dosing versus replacement c. Uses for each dosing category d. Glucocorticoids e. Side effects f. Acute: Hyperglycemia, increased appetite, insomnia, delayed wound healing, immunosuppression, GI bleeding Chronic: Delayed wound healing, immunosuppression, osteoporosis GI bleeding g. Why might patients taking steroids receive H2 blockers or PPIs? h. Acute adrenal insufficiency i. When can it occur? ii. Treatment iii. Prevention i. Mineralcorticoids – Prototype: fludrocortisone flurinef- used for persistent orthostatic hypotension 30. Diabetes A. Insulins i. Short acting/ Rapid acting (used for bolus/mealtime insulin and supplemental insulin) 1. Regular Short acting (The only insulin that can be given I.V.) Onset 30 mins after subcutaneous injection Drawn up first when combined with NPH 2. Rapid acting- lispro-aspart- apidra- onset 15 mins aftersubcutaneous injection 3. Intermediate and Long acting (basal) NPH- onset 1-2 about 4 hours Long acting: glargine (Lantus)- no peak works over 24 hours Cannot be mixed with any other insulin Peak times of insulin (look at the chart in PowerPoint) 4. Combination insulin 70/30, 50/50 only use when specifically ordered. 5. Insulin administration SQ versus IV (which insulin can be given IV?) Syringes, ( only insulin syringes can be used), needles, pens, pump devices Double check order and dose with 2nd RN When do you hold insulin? What’s the normal blood glucose level? At what blood glucose level do we hold insulin? 6. Insulin regimens (Methods of insulin dosing) Basal-bolus (also known as nutritional) Supplemental (also known as sliding scale) Combination of both (basal/bolus and supplemental) Drawing up Regular and NPH insulin together- which one first? 7. Hypoglycemia i. Detection- (Symptoms-Hunger, feeling shaky, dizziness, confusion, headache, tachycardia- patient may describe it as heart pounding or racing) What do you teach the patient on insulin and a beta-blocker to recognize as symptoms of hypoglycemia? ii. Prevention-Eat regularly-carry glucose tablets or candy if on a sulphonyl urea or insulin. iii. Treatment- patient awake alert and can take oral fluids- 4 oz orange juice or milk -if patient NPO or unresponsive- administer 25 mls intravenous D50 (50% dextrose) B. Oral diabetes medications 1. Sulfonylureas glipizide (Glucotrol) i. Use: Type II only ii. Hypoglycemia-stimulates pancreas to secrete insulin iii. PPB- highly plasma protein bound iv. Pt should wear Medic Alert bracelet and carry glucose tablets or candy 2. Biguanide metformin Glucophage i. Uses-Type II only- first drug ordered ii. Side effects diarrhea iii. Risk for lactic acidosis- rare -but severe- avoid -in dehydration -with use of IV iodine contrast - in patient with heart failure due to fluid restriction -elderly(≥ 80)- poor renal function - creatinine greater than 1.5 - alcoholism - metformin and contrast – prevention of complications (Hold 24 hours before and 48 hours after procedure) C. FYI ONLY Glitazones Or Alpha Glucosidase Inhibitors- Oral with first bite of food effects local nt CHO absorption There are newer forms of long acting insulins that are more concentrated than the usual 100 units per milliliter. You will learn about these later. There is also inhaled insulin available but you can learn about that later in your careers. 31. Asthma Allergies/Cold and Cough products A. Asthma 1. Inhaled corticosteroids *USED FOR DAILY PREVENTION OF ATTACKS= Maintenance Therapy* i. LABAs added to inhaled steroids if above does not decrease exacerbations - not used alone for asthma- known to cause asthma deaths used alone - used for long-term prevention Prototype: Advair inhaler ii. SABAs for short term *acute treatment of exacerbation or increased SOB- Rescue inhaler* - albuterol (Proventil) is Protype drug -MDI(hand held) -nebulizer -serial treatments can lead to tremors and increased HR 2. theophylline i. COPD or refractory asthma ii. IV = aminophylline oral (Theodur) iii.Toxicity- low therapeutic index iv. caffeine 3. Systemic steroids IV or high dose PO used for acute moderate to severe exacerbations Some patients may require chronic low dose oral steroids along with their inhaled steroids as maintenance B. COPD i. Anticholinergic ipratropium bromide (Atrovent) - MDI or nebulizer used in COPD Opens medium and small airways Takes longer to work but lasts longer May be combined with albuterol to treat an exacerbation of COPD(Combivent) C. Allergies i. Antihistamines Action: Block histamine 1 receptor, not histamine production Oldest (first generation) diphenhydramine (Benadryl) ii. More side effects-CNS depression when combined with alcohol or other sedating drugs. Strong anticholinergic effects iii. Alternate with less anticholinergic effects chlorpheniramine (Chlor-Trimeton) 2nd generation (Claritin) (Zyrtec) (Allegra) -minimal side effects- Non drowsy -no anticholinergic effects D. Cough/colds 1. Daytime cold and cough meds i. Decongestants pseudoephedrine (sympathomimetics alpha 1 agonists) ii. Nasal or PO - Which one has more side effects? iii. Which one causes