PHARMACOLOGY EXAM 1: STUDY GUIDE, EXAM PREPARATIONS, and QUESTIONS AND ANSWERS, Exams of Pharmacology

Download PHARMACOLOGY EXAM 1: STUDY GUIDE, EXAM PREPARATIONS, and QUESTIONS AND ANSWERS and more Exams Pharmacology in PDF only on Docsity! 1 PHARMACOLOGY EXAM 1: STUDY GUIDE, EXAM PREPARATIONS, and QUESTIONS AND ANSWERS What you should master to move forward from pharmacology: 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? Start studying from day one with this document, your drug templates, and my PowerPoint’s. Use the textbook to add anything that is s>ll not clear. 2 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? 5 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 substancesfrom 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 6 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. 7 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 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) d. Excretion: 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? 10 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 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”? c. Patient teaching 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? 11 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. 12 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. 15 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- 16 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 17 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 –propran olol 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 (angiotensin converting enzyme inhibitors) (See the Blackboard animation) pril- tells me its an ACE inhibitor. i . Hyperkalemia i i . Contraindicated in pregnancy / breast feeding iii. Angioedema iv. Dry cough – change to ARB (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) a. Calcium channel blockers b. Dihydropyridines versus D= Dilate Prototype: nifedipine (Procardia)- treats HTN ii. Nondihydropyidines N=Nodes f. Ace inhibitors Prototype lisinopril (Zestril) ARBs Prototype losartan (Cozaar) 20 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 21 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 22 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 25 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 Withdrawal- prevention and treatment in the hospital- Prototype: lorazepam Ativan 1. 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 18.Anemia 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 add a benzodiazepine like 26 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 27 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 30 4. Prototype: Aspirin and Plavix 01:40:50 a. Antiplatelet uses (low dose) prevention. 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 (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 b. Prototype: acetyl-salisylic acid Aspirin. g. Prototype: clopidogrel Plavix 31 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 )- 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. 2 . c a r b a m a z e p i n e (Tegretol 4.Benzodiazepin es P r o t o t y p e : l o r a z e p a m (A>van) 32 - FOR GRANMAL SEIZURES i. Role in status ii. Side effects IV versus PO Should chronic benzodiazepines be abruptly stopped? Weaned, never stopped abruptly iv. 23. Antipsychotics A. Conventionals Prototypes: Thorazine and haloperidol (Haldol) a. More EPS i. Acute dystonia ii. Tardive dyskinesia B. Atypicals- Prototypes: olanzapine (Zyprexa) respiradone (Resperdal) clozapine (Clozaril) a. Fewer Extrapyramidal System side effects (EPS) i. (Clozaril) clozapine – bone marrow suppression -agranulocytosis ii. (Zyprexa) olanzapine and iii. ( Risperdal) risperidone -weight gain and hyperglycemia b. 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) W h a t ' s t h e a n P d o t e ? fl u m a z e n i l (Romazicon 35 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 36 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 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) 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 infecPon- not as effecPve as vancomycin b. Do not drink alcohol enPre Pme taking and for 48 -72 hours a^er 37 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) 40 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 patientmaximum 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 41 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 42 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 hrs.peaks 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? 45 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 rhinitis medicamentosa? (rebound congestion) -Limit use to 3 days -pseudoephedrine Limited availability-( ? anybody watch Breaking Bad? What did 46 Jesse and Walter make?) -Common combination ingredient 2. Nighttime cough and cold meds i. Contain 1st generation antihistamine- diphenhydramine Benadryl ii. Antitussives A. Dextromethorphan -OTC i. Safe in therapeutic doses ii. Abuse by adolescents B. Opioid-containing cough medication (pheregan and codeine) i. CNS depression if overdose ii. Lower schedule than pain medications(V) C. guaifenisin (Mucinex) –OTC i. Drink lots of water to break up mucus ii. Common active ingredient iii. Often mixed with dextromethorphan in OTC cough and cold medications That’s all folks. If you can master this content you will ACE Junior I and Junior II