Study for your ATI Pharmacology exam with these drug card practice questions and answers. This guide covers major drug classes, mechanisms of action, side effects, and nursing implications.
Q: Receptors
Answer: Norepinephrine-Adrenergic (adrenergic comes from the word adrenalin)Alpha 1-all sympathetic target organs except the heart-constrict the blood vessels and dilation of pupilsAlpha 2-Presynaptic adrenergic nerve terminal-inhibits the release of norepinephrineBeta 1-Heart and Kidneys (BETA 1-ONE HEART)-increased heart rate and force of contraction, release of reninBeta 2-All sympathetic target organs-inhibits smooth muscle (BETA 2-TWO LUNGS)
Q: EXAM 1 DRUGS!!!!
Answer: ………..
Q: Beta blockers/olol’s
Answer: Beta-Adrenergic BlockersMetoprolol/Lopressor ENDING OLOLBeta Blockers are use with heart failure, hypertension, angina and with myocardial infarctions.Action = Blocks Beta-Receptors in the heart causing…Decreases = HR, force of contraction, Rate of atrioventricular (AV) conductionSE = Bradycardia, lethargy, GI disturbance, congestive heart failure, decrease BP, depressionThe beta blockers stop sympathetic nervous system stimulation of the heart. Does not allow the heart rate and blood pressure to rise with stress thus lowering the oxygen demand of the heart. It is very heart protective!Will slow the heart rate and lower the blood pressureCan have beta 2 blockage with larger doses-will constrict the bronchioles-watch for clients with known COPD, AsthmaNursing InterventionsCheck pulse-needs to be 60 or aboveCheck blood pressure-if hypotensive do not give (Systolic below 100 is a good rule of thumb I go by)Monitor for sexual dysfunction-impotence for men-a good reason for non-complianceDrowsiness/Fatigue-operating heavy machinery, driving could put client at riskInsomnia-Contraindicated with Heart Blocks, Bradycardia, Worsening Heart FailureIncreases Hypoglycemic effect of Insulin-monitor blood sugars and for hypoglycemia, may need to lower insulin dosageBeta Blockers have to be weaned slowly to prevent rebound hypertension and tachycardia-if a client wants to stop his beta-blocker they need to contract their physician
Q: CCB,/calcium channel blockers
Answer: Nifedipine/Adalat/Procardia/Norvasc-controls blood vesselsDiltiazem/CardizemVerapamil/Calan/Isoptin/Verelan-controls heart rate and blood vesselsAngina/Raynaud’s/Vasospastic Angina/Atrial Arrhythmia’sBlocks calcium channels in the myocardial and vascular smooth muscles, decreases the contraction of smooth muscle-relaxes the arteries-vasodilation. Blocking of calcium channels in the SA and AV node-Slows conduction through the SA and AV node. Decreases the force of contraction slows heart rateGrapefruit juice may increase absorption of nifedipineSide Effects: Relaxes smooth muscle and cardiac muscle-HeadacheDizziness-Take lying, sitting and standing B/P, educate client to sit and stand slowlyPeripheral edema-assess for edema, monitor for worsening (diuretic)FlushingReflex tachycardia-monitor for elevated heart rate (may need a BB)Constipation-increase fibers and fluids (if not restricted) stool softenerFatigue-Due to low heart rate-monitor EKG, pulse rate and rhythmWeakness-Monitor B/P and Heart RateImpotence and sexual dysfunction-Discuss possibility with client-have client to call and not just to stop medicationsHepatotoxicity-ALT, AST, ALK PHOS, BilirubinMI-Monitor for chest pain, dyspnea, increases fatigue, weaknessCHF-Monitor for chest pain, dyspnea, edema, increasing weight, decreasing output, increasing HR and B/PAngioedema-edema in face, throat, trouble swallowing, trouble breathing, thickened tongueGrapefruit juice may increase absorption of nifedipineAcute ToxicityWith an overdose or overmedicatedGastric lavageMonitor EKG-bradycardia-widening QRS, hypotensionNorepinephrine to treat hypotension and decreased cardiac contractilityAtropine or Isoproterenol-Bradycardia and Cardiac BlocksVerapamil (Calan, Covera, Isoptin Verelan)Class IV antidysrhythmicCalcium channel blockerInhibits the flow of calcium ions both into the myocardia cells and the vascular smooth muscle, slow the conductions velocity and stabilizes dysrhythmias. Lowers the blood pressure, reduces cardiac workload and lowers the blood pressure. Dilates the coronary arteries-anti-anginalSide Effects: Headache, constipation, hypotension, edema, bradycardia
Q: Pril/ace inhibitors
Answer: Enalapril/VasotecPRIL-is the ending for ace’sReduces Angiotensin 2 and aldosterone levelsPrevents Angiotensin 1 from converting to Angiotensin 2 in the lungs-leaves the Angiotensin 1 hanging in the lungs-creates irritation-coughVasodilation-mostly arteriole (decreases afterload)Excretion of sodium and water-retention of K (decreases preload)Treats hypertension and heart failureDo not take 2nd and 3rd Trimester of pregnancySE = Angioedema-allergic reaction-swelling of tongue, throat-stop taking and notify mdHyperkalemia-monitor for widening and slowing of pulse/qrs, weakness, fatigue, avoid high K foods, AVOID SALT SUBSTITUTES-usually very high in K, avoid potassium sparing diuretics, sport drinks are high in K alsoOrthostatic Hypotension-teach client to sit and stand slowly, enact fall precautionsNeutropenia/Agranulocytosis-monitor CBC-WBC count, reoccurring infectionsRenal Insufficiency-Monitor weight, edema, I/O, BUN, Cr, and GFRHepatic Insufficiency-Monitor AST, ALT, ALK PHOS, BilirubinCough-Cough lozenges, hard candy, increase fluid intake, sleep with HOB elevated, antihistaminesACE InhibitorsDiscussed these medications with hypertensionArb’s-Angiotensin receptor blockers, sartan’sNo Cough, same effects and side effects as Ace’s-just not as potent
Q: Sartan’s/angiotension blockers/arb’s
Answer: …Arb’s-Angiotensin receptor blockers, sartan’sNo Cough, same effects and side effects as Ace’s-just not as potent
Q: Nitrates
Answer: Nitroglycerin/Nitrostat, Nitro-Bid, Nitro-DurNitrates form nitric acid which is a relaxes smooth muscle and dilates venous and arterial blood vesselsOpen veins-blood pools in the legs-not as much blood returning to the heart-reduces preloadOpen arteries-heart does not have to work as hard to pump blood out of the heart-reduces afterloadOpens the coronary arteries and helps supply blood to the heart tissueCan be given sublingually, orally, topically, IV, buccalCan be for acute or long term useNitroglycerin dilates any artery and vein-including yours if you touch it while administering it-WEAR GLOVESNitroglycerin IV needs a glass bottle and covered from light-some hospitals still use special tubing (nitro is absorbed in the tubing)Short term-nitrostat-sublingually-1 tablet every 5 minutes x 3 for relief of chest pain-still having chest pain call 911/physicianLong-term nitro-dur will last for up to 14 hours in the bodySide Effects:Headache-dilates the cerebral arteries-do not give with head trauma or increased intracranial pressureHypotension and reflex tachycardia-do not give with hypotension, monitor blood pressure and HR when administeringHypotension-correct hypervolemia prior to giving nitroglycerinDO NOT GIVE WITH VIAGRA, LEVITRA, OR CIALIS (nitroglycerin and Viagra increase nitric acid and relaxation of the smooth muscles-can kill a client with hypotension with a combination of these drugs)
Q: Digoxin
Answer: Cardiac GlycosideDigoxin/Digitek, Lanoxin, Lanoxicaps (Dig)Increases the contractility of the heart muscle – Inotropic effect-Increases cardiac outputAlso Suppresses the SA node and slows conduction through the AV nodeHalf-life is 3-4 daysGreat Drug-real side effectsDigoxin SE =DysrhythmiasToxicity 0.5-1.8 normal levelSigns of toxicity-halos around objects, Nausea/Vomiting/Anorexia, blurred vision, fatigueBradycardia-must take an apical pulse for one full minute, must be 60 or above to give digoxinGive with caution with pediatric and geriatric patients due to inadequate renal or hepatic metabolic enzymesHyperkalemia can reduce effects of digoxinDigoxin and Beta Blockers can really lower the pulseGive with caution with renal failure-digoxin excreted via the kidneysDIGIBIND IS THE ANTIDOTE FOR DIGOXIN TOXICITYDigoxinDecreases automaticity of the SA nose and slows conduction through the AV nodeAtrial dysrhythmiasAll the side effects and warnings are still important
Q: Heparin
Answer: Naturally found in the liver and lining of blood vesselsProlong coagulation timeIV immediate onset, Sub Q 1 hourDestroyed by gastric enzymesWeight basedaPTT (PTT also, but in the hospital we use the aPTT)Sub QThrombocytopenia occurs in 30% of clientProtamine Sulfate is the antidote, 1 mg for every100 units of heparin, works for Lovenox also
Q: Coumadin
Answer: Warfarin/CoumadinWarfarin inhibits the action of Vitamin K, and without adequate Vitamin K the synthesis of clotting factors 2, 7, 9, and 10 is diminishedINR/PTWarfarin takes 2-3 days to achieve therapeutic effect-99% of warfarin is bound to plasma proteins and unavailable to produce effectsVitamin K is the antidote-green leafy veggies Aquamephyton-works within 6 hoursNormal INR therapeutic range is 2-3Normal INR for everyone who is not taking an anticoagulant is around 1Category X for pregnancyAvoid alcohol, diuretics, SSRI’s, Antidepressants, Steroids, Antibiotics, Vaccines, Some Vitamins, Amiodarone-all can potentiate warfarinBleeding-
Q: Amiodarone
Answer: Amiodarone (Cordarone/Pacerone)Class III antidysrhythmicPotassium channel blockerVentricular and Atrial Arrhythmias-especially with heart failureIV onset or PO onset looks to be 2-3 days to 1-3 weeksHalf life can be greater than 100 daysCheck K and MG levels prior to starting therapySide Effects: Fibrosis of lungs, destruction of thyroid, Photosensitivity-Smurfs, Liver destruction, N/V, Hypotension, Blindness, very hard on the stomach-GI DistressCan increase serum digoxin levels by 70%, Increase warfarin levels, Increase phenytoion (Dilantin), Stop BB and CCB?
Q: Statins (Lipitor)
Answer: HMG-CoA reductace inhibitor-(liver is where the cholesterol is made, it is where the HMG-CoA work)LDL/Cholesterol is reducedGive with food to reduce GI symptomsLipitor can be taken at anytime, most of the class of this medication needs to be taken at bedtime-cholesterol is made by the liver at nightUp to 30 days to achieve full affectSide Effects:GI-constipation, bloating, gas, nauseaLiver-monitor enzymes-alt, ast, alk phas, bilirubin, jaundice, enlarged liver-ascitesRhabdomyolysis-muscle destruction-CK elevation-muscle pain-MD has to be notified.Renal failure is very common with Rhabdomyolysis-need to make sure urine output is 30 ml or greater an hourNo grapefruit juiceThe statins are hard on the liver-you need to make sure other drugs the client is on is not hard on the liver-Amiodarone and Nizoral are two drugs that come immediately to my mind
Q: furosemide/lasix (-ide)
Answer: …Loop Diuretics-prevents Na/Cl reabsorption, thus Na leaves the body, water follows Na and K follows the waterFurosemide/Lasix, Bumex/Bumetanide, Torsemide/DemadexWork on the entire Loop of Henle-large volumes of water, Na, and K are removedWorks in renal failureHypovolemic and hypokalemia very commonNursing interventionsKnow your potassium level prior to administrationAssess Lung Sounds, Weight, I/O, Edema, SaO2, RR, Blood Pressure, K Level prior to administration, assess all of these post administration, especially K Level and Lung Sounds, Sao2, I/O. If you urine bag is not twice as full 30 minutes post IV Lasix administration, check your IV site. If your client without a Foley has not called to urinate within an hour of giving po Lasix, check your clientWarn your client to get up slowly after taking Lasix, watch for orthostatic hypotensionLasix does have sulfa as a base componentMay not be used with anuria, hepatic comaUse with extreme caution with electrolyte depletionLow K with Digoxin can equal lethal Dysrhythmias, know your potassium level-has a digoxin level been ran
Q: plavix
Answer: Anti-platelet drugsASAPersantineADP Receptor Blockers (Plavix, Ticlid, Effient)Glycoprotein 2b./3a receptor antagonist (Repro, Integrillin, AggrastatADP receptor blockersIrreversibly alter the plasma membrane of platelets, alters the ability of platelets to aggregateTiclid and Plavix are given orallyTiclid can cause Agranulocytosis-only used when someone is allergic to PlavixGlycoprotein is an enzyme necessary for platelet aggregation, IV only, Very expensive used with MI’s Strokes, and PTCA’sClopidogrel (Plavix) Antiplatelet drugADP receptor blockerInhibits ADP binding to its receptor’s-irreversible and will be with the platelet for their lifespan (5-7 days)Used for MI’s, CVA’s, PAD/PVD, Unstable Angina, PTCA’s-first 6 months post ptca’sBleeding is a problem
Q: EXAM 2 DRUGS!!!!!!!!!!!!
Answer: ……….
Q: Vasopressin (pitressin)
Answer: The antidiuretic action of vasopressin is ascribed to increasing reabsorption of water by the renal tubules40u IVAdverse = cardiac ischemia/angina
Q: DDAVP (desmopressin)
Answer: Prevents or controls thirst and frequent urination caused by diabetes insipidus and certain brain injuries.Works on posterior pituitary….Treatment for: diabetes insipidus, bedwetting(nocturia), brain injuries, hemophilia A w/ some factor VIII productionnasally, IV, oral/subling tabup to 20 hours
Q: Synthroid
Answer: Treats hypothyroidism. Also treats an enlarged thyroid gland (goiter) and thyroid cancer.
Q: Cortef
Answer: Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs are primarily used for their potent anti-inflammatory effects in disorders of many organ systems. Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body’s immune responses to diverse stimuli.
Q: Hydrocortisone
Answer: Hydrocortisone belongs to the family of medications known as corticosteroids. It is used to treat many different conditions. It works by reducing swelling, inflammation, and irritation or as a replacement when the body does not make enough cortisol. Hydrocortisone is more commonly used to treat allergic reactions, some skin conditions, severe asthma, lupus, and arthritis.It can also be used to treat steroid deficiency in the body, certain blood disorders, certain types of cancer, multiple sclerosis, and ulcerative colitis.
Q: Cortisol
Answer: When people are under stress, levels of cortisol hormone rise. Chronic stress can result in chronically high levels of cortisol, which can lead to symptoms like weight gain, memory problems, high blood pressure, and other health problems. The stress release of cortisol is designed to enable the flight or fight response with a quick burst of energy, but when people are in a state of constant high stress, levels of the hormone never have a chance to fall back down to normal levels. This is one reason why treatments for chronic stress include exercises and activities that are designed to reduce stress levels, allowing production of this hormone to slow down.
Q: Tapazole
Answer: Treats hyperthyroidism (too much thyroid hormone produced by the thyroid gland).
Q: PTU
Answer: Treats Graves’ disease and hyperthyroidism (too much thyroid hormone from the thyroid gland) in patients who have already been treated with other medicines (such as methimazole) that did not work well.
Q: H2 Blockers (-tidine)
Answer: Ranitidine
Q: PPI’s (-prazole)
Answer: Omeprazole
Q: Antacids
Answer: …
Q: Maalox
Answer: 30mL QID
Q: Mylanta
Answer: This medication is used to treat the symptoms of too much stomach acid such as stomach upset, heartburn, and acid indigestion. Aluminum and magnesium antacids work quickly to lower the acid in the stomach. Liquid antacids usually work faster/better than tablets or capsules.
Q: Mylanta
Answer: This medication works only on existing acid in the stomach. It does not prevent acid production. It may be used alone or with other medications that lower acid production (e.g., H2 blockers such as cimetidine/ranitidine and proton pump inhibitors such as omeprazole).This medication can cause nausea, constipation, diarrhea, or headacheby mouth, usually after meals and at bedtimehis product may react with other medications (e.g., digoxin, iron, tetracycline antibiotics, quinolone antibiotics such as ciprofloxacin), preventing them from being fully absorbed by your body.
Q: Bulk-Producing Laxative
Answer: Metamucildecrease the absorption and effects of Warfarin, Digoxin and Aspirin. Do not give to patients with: GI obstructions, fecal impaction or abdominal pain and N/VMonitor elevated serum glucose
Q: Lomotil
Answer: Antidiarrheal, Anticholinergic
Q: Insulins
Answer: (dec blood sugar)
Q: Insulin
Answer: Is a polypeptide hormone that controls the storage and metabolism of carbohydrates, proteins, and fats. This activity occurs primarily in the liver, in muscle, ind in adipose tissues after binding of the insulin molecules to receptor sites on cellular plasma membranes
Q: Logs –>fast acting
Answer: is a man-made insulin used to control high blood sugar in adults/children with DM.
Q: Reg –>short acting
Answer: Humulin® R U-100 is a polypeptide hormone structurally identical to human insulin synthesized through rDNA technology in a special non-disease-producing laboratory strain of Escherichia coli bacteria
Q: NPH –>intermediate-acting
Answer: Often used in combination with a shorter-acting insulin. NPH insulin is a man-made insulin product is the same as human insulin. It replaces the insulin that your body would normally make. It is an insulin (isophane). It starts to work more slowly but lasts longer than regular insulin. Helps blood sugar (glucose) get into cells so your body can use it for energy.
Q: Lantas –>long-acting insulin
Answer: Treats diabetes mellitus. Insulin is a hormone that helps get sugar from the blood to the muscles, where it is used for energy. This type of insulin usually works longer than regular insulin.
Q: Glucophage (metformin)
Answer: Used with diet and exercise to control blood sugar in patients with type 2 diabetes. May be used alone or with other medicines.starting dose of GLUCOPHAGE (metformin hydrochloride) Tablets is 500 mg twice a day or 850 mg once a day, given with meals. Dosage increases should be made in increments of 500 mg weekly or 850 mg every 2 weeks, up to a total of 2000 mg per day.The purpose of both insulin and metformin is to lower blood glucose levels. Insulin injections replace the insulin your body can no longer make when the cells in the pancreas cease to function. Metformin is an oral hypoglycemic, which lowers blood glucose levels by decreasing the liver’s output of glucose. Metformin also increases insulin sensitivity, and improves not only blood glucose levels but also lipid levels and often results in weight loss.
Q: Diabetics:
Answer: 14% take insulin only57% take oral medications only14% take a combo of both.
Q: Insulin VS Metformin Treatments? Mechanisms
Answer: Oral hypoglycemics are used only in Type 2 diabetes, because Type 1 diabetics make little or no insulin, so reducing the glucose levels produced by the liver won’t reduce blood glucose levels. Without insulin, glucose can’t enter cells and remains in the bloodstream. While all Type 1 diabetics take insulin, some Type 2 diabetics also need insulin in addition or instead of oral hypoglycemics such as metformin. Insulin, which must be injected, comes in several forms and doses, and can have rapid or slow onset.
Q: Insulin VS Metformin Treatments?….Considerations
Answer: For Type 1 diabetics, insulin is the only medication choice. For Type 2 diabetics, medical practitioners generally start with an oral hypoglycemic such as metformin and add insulin only when oral hypoglycemics can’t stabilize blood glucose levels.
Q: Insulin VS Metformin Treatments?….Benefits
Answer: Both metformin and insulin help to normalize blood glucose levels. Keeping blood glucose levels as close to normal levels as possible limits the damage high blood glucose imposes on every blood vessel and organ of the body. High blood glucose levels lead to poor circulation, heart problems, vision problems, nerve damage, susceptibility to infection and kidney damage. While damage occurs earlier in Type 1 diabetics, Type 2 diabetics can also experience complications.
Q: Insulin VS Metformin Treatments?….Side Effects
Answer: Diarrhea, the most common side effect of metformin, improves if metformin is taken with food. Liver failure and increased acidity, acidosis, occur rarely, The Merck Manuals Online Medical Library states. Insulin must be carefully calibrated or blood glucose levels may drop too low, a condition called hypoglycemia. Taking insulin without eating or taking too much insulin for the amount of food eaten can cause hypoglycemia. Symptoms of hypoglycemia include weakness, shakiness, sweating, lightheadedness and confusion; coma and death can result in severe cases.
Q: EXAM 3 DRUGS
Answer: …….
Q: NSAIDS—->Ibuprofen (advil/motrin)
Answer: AntipyreticAnalgesisWork on Cox 1/Cox 2Take with FOODStop production of prostaglandinsCan cause –> kidney toxicityNSAIDS = N/V, gi bleed, platelet aggregation, kidney toxicity possible)
Q: NSAIDS (Ibuprofen)
Answer: Analgesic, anti-inflammatory, antipyretic, antiprostaglandinSodium based = may increase BP/heart failure, causes UlcersSE = N/V, GI bleeding, heartburn, epigastric pain, GI ulcer, renal impairment, bruising, blood in urineCaution = with MI’s and bypass patient’s.No more than 3,200 Mg/day (it can kill the kidneys/especially w/long term use)Nursing interventions = check GFR, platelets, bleeding times, liver enzymes.
Q: Aspirin (ASA)
Answer: Non-opioidnon-steroidalanti-inflammatoryantipyreticBlood thinnerAspirin = binds to Cox 1/Cox 2 (stops platelet aggregation, gi upset, tinnitus, HA, sweating)
Q: Aspirin (ASA)
Answer: Increased risk for GI bleeding (coffee ground emesis, black tarry stool)Increase Prothrombin time (PT/INR) …stop a week before surgery due to platelet life of 7 daysEnteric coated = prevent GI bleed/upsetToxicity = tinnitus, humming, dizzy, bad balance, nauseaCaution = with heparin, lovenox, coumadin, Nsaids
Q: Tylenol (acetaminophen)
Answer: Acetaminophen (Tylenol/APAP)Antipyretic/analgesic-Centrally acting Cox InhibitorActs on hypothalamus—>dilates peripheral blood vesselsNo Anti-inflammatory Property/Enhances opioids for pain reliefHepatotoxic ….NO MORE THAN 4 GRAMS/DAILYSide Effects:Renal/Hepatic failure, N/V, Chills, abd. discomfort, Inhibits warfarin metabolism (can cause it to accumulate)Acetylcystiene/Mucomyst—antidote for Tylenol ODBaby Drops(babies)Liquids (children)
Q: Tylenol
Answer: Anti-pyretic–Analgesis—Centrally acting Cox InhibitorActs on Hypothalamus –> dilates peripheral blood vesselsNo inflammatory property
Q: PCA pumps
Answer: 4 hour dose limitSet machine for how many mg/hour.Encourage = use before activitiesAssess client = LOC, RR, BP, HREducate = it’s very hard to OD on pumpsNursing Intervention = check IV line patency, ask to change PCA to oral med if they’re feeling betterNursing Prejudices = assess their pain, respirations must be 12+Pain 1-4 = PO medsPain 5-10 = IV meds
Q: Narcan (naloxone)
Answer: Opioid antagonistTreats Overdose = competes w/opioid receptorsDon’t give with pregnancy(Rebound resp depression, abstinence syndrome, titrate dosage, rapid infusion)IV, IM, SQ, NOT ORALLY1/2 LIFE = 60-90 MINUTES1/2 LIFE of opioid = 3-4 hoursCan lead to rebound respiratory depressionRespirations = Monitor for 4 hours after giving it
Q: Narcan
Answer: SE = tachycardia, tachypnea, ventricula arrhythmia, pulmonary edemaAbstinence syndrome = cramping, HTN, vomiting (by stopping morphine effect, we can induce withdrawal quickly)Caution = history of heart failure/pulm edema (the HTN/teachycardia can induce heart failure by increasing workload of the heart)Contraindicated = with opioid dependency (immediate withdrawal)Titrate dosage = relieve pain, reverse respiratory depression (if you don’t titrate it can cause sudden onset of pain/withdrawal)Rapid Infusion = HTN, tachycardia, N/V
Q: Morphine (opioid)
Answer: Opioid agonistTX of moderate/severe painInduces pleasureActivates Mu receptors (analgesia, sedation, resp. depression, euphoria)Activates Kappa Receptors (analgesia, sedation, decreased GI motility)Attaches to receptors in CNS & alters perception & response to pain.Complications = respiratory depression, constipation, orthostatic hypotenstion, urinary retention, cough supression (cough hourly), sedation, biliary colic (spasm of sphincter of Oddi–use meperidine), emesisOverdose? Coma, respiratory depression, pinpoint pupilsMonitor –>Breath sounds, vitals, Narcan, mechanical ventilation
Q: Morphine
Answer: PO, SQ, IM, Rectal, IV epi, IntrathecalMust have RR of 12 or higher!!!!Don’t use = premature infants, demerol w/renal failure, with head injuries (LOC is too hard to access)Precautions = asthma, emphasema, older, babies, respiratory depression, pregnancy, labor, obesity, IBD, enlarged prostate, liver/renal disease–prolonged accumulation of drug)Anticholinergic agent–Benadryl, will increase effects of constipation/urinary retentionMAOI = high fever/comaAnti-hypertensive meds = hypotensive effectNursing administration = assess pain, docoument, 1-10 scaleOral = 45 – hr laterIV = 30 mintes laterCancer? give fixed schedule, around the clock, PRNAddicted? Taper off over 3 days!!!
Q: Atrovent (ipratropium) —-> MDInhaler
Answer: Bronchodilator anti-cholinergicBlocks parasympathetic NSTX —> COPD/ASTHMAOnset = 5-15 minutes (2-3 minutes between squirts)**little absorbed, peanut allergy, nasty taste
Q: Atrovent
Answer: Inhaled anticholinergic work well on COPD/brochospasm allergen induced/exercise induced asthmaVery little absorbed from lungs, few systemic effects, dry nasal mucosa, dry mouth, hoarsenessRinse mouth (for nasty taste), peanut allergy (don’t use)Anticholinergic = dry mouth, urine retention (suck on candies/sip liquids)Usually 2 puffs/doseDon’t use with ….GLAUCOMA OR ENLARGED PROSTATE
Q: Afrin (oxymetazoline)
Answer: Nasal decongestant/sympathomimeticShort-term = 3-5 daysStimulates the Alpha adrenergic receptorsArterioles constrict – dries mucous membranes
Q: Afrin
Answer: SE = use for 3-5 days only or could have Rebound congestion (worse than before), insomniaContraindicated = Heart disease, diabetes, HTNNursing Implications = Rebound congestion, taper use one nare @ a time.CNS stimulation (nervous, uneasy, aggitated)Vasoconstriction (avoid with CAD/HTN)Administer = lay on side, lateral, head low on sideEffective? Breathe, sleep, no agitation, no HTN, no chest pain, no nasal congestion**Oral decongestants = work body wide, no rebound congestion, slower (SE = insomnia, anxiety)
Q: Histamines
Answer: Increase capillary permeabilityIncrease BloodIncrease runny noseBrocho-constriction (try to keep out the allergens/dust)
Q: Benadryl (diphenhydramine)
Answer: H1 receptor antagonist (1st Generation)antihistamine/makes you sleepyTreats: N/V, allergic reactionsEffects #1 = dry mouthIM –> Z track, deep injectionAntihistamines = prevent release of histamine by blocking H1 receptor sites on the mast cells in nasal cavity.
Q: Benadryl
Answer: SE = drowsy(excitation in kids)anticholinergic(dry mouth, urinary retention, gi upset)ACUTE toxicity (flushed face, fever, tachy, dry mouth, dilated pupils, mild hypotension)Contraindicated–> BPH, glaucoma, 3rd trimester, breastfeeding, newborn, bowel obstruction, CNS depressants/alcohol INC effectsToxicity = induce vomiting, remove anti-histamine, activated charcoal, tylenol for fever, ice packs, send them to ERMAOI’s = hypertensive crisisEffectiveness? No Rhinitus (runny, itchy nose), no Uticaria (no itching, no allergic reactions)
Q: Beclomethasone (Beconase) –> intranasal
Answer: Intranasal corticosteroidDecrease inflammation of nasal passageFew systemic effects unless swallowed in large amounts
Q: Beconase (nasal)
Answer: SE = Nasal irritation, nosebleed, it masks signs of infectionsLicorice = potentiate effectsAssess = signs of oral fungal infection, alternate nares, hoarseness, changes in voiceInterventions = blow nose before meds!!
Q: Prednisone (ORAL glucocorticoid)
Answer: Anti-inflammatory corticosteroidGlucocorticoids = inhibits making of prostaglandins, suppress histamine, stops some functions of phagocytes/lympocytesShort-term use only/taper them offauto-immune disease = long-term useFever = signs of inflammation/natural defense to neutralize foreign organismsProlonged fever in children = febrile seizuresProlonged fever in adults = breakdown body tissue, delirium/comaObscure causes of fever –> SSRI (serotonin syndrome), Thorazie, Anesthetics (malignant hyperthermia), immunodilators, cytotoxic drugs, chemotherapy, neutropenic agents
Q: Beclomethasone (Beconase) —> inhaled
Answer: Inhaled glucocorticoid/Dilates BronchiAnti-flammatory for Asthma/COPDAllergic RhinitusOnset = 1-4weeks……1/2 life = 15 hours
Q: Beconase (inhaled)
Answer: Supress inflammation, decrease mucous, promote Beta 2 response (dilation of the bronchi)Anti-inflammatory for Asthma, COPD, allergic rhinitis, inhaled corticosteroidSE = hoarse, dry mouth, changes in tasteMUST rinse mouth after/spit the water out –> Can cause Oral CandidiasisOral Candidiasis = fungal yeaste, look for white spots in the mouth.
Q: Corticoidsteroids — glucocorticoids
Answer: Anti-inflammatory drugsMust taper them offInhibits –> Making of prostaglandins, suppress histamines, stops some functions of phagocytes/lympocytes (so, when infection happens they’re aren’t enough WBC to fight off infection)SE = suppress adrenal glands –> Addison’s crisis…hyperglycemia, mood changes, cataracts, PUD, electrolyte inbalance, osteoporosis, mask infections.Long-term = Cushing’s syndromeGlucocorticoids = inhaled, oral, IVEnd in -oneWe give all 3 types for Asthma/COPDSickest = IV, then PO, then inhaled glucocorticoid
Q: ORAL, IV systemic glucocorticoids
Answer: Suppresses the adrenal glandsMust taper them off the dose or…..Can send them into Addison’s CrisisAddison’s = Low BP, no energy, bone loss, increase blood sugar, muscle weakness, PUD (huge issue), take with food/no NSAIDS, sore throat.Sodium Retention = hypokalemia (weak muscle/cramps)Give Ca with Vitamin DWATCH for edema, weight gain, HTNInflammation = Defense brought on by injury, toxic chemicals, heat, microorganisms, cell death, allergen response.Sighs = swell, pain, warmth, rednessAcute = 1-2 weeksChronic = Lupus, RAWho responds to inflammation?Mast cells, Bradykins, leukotrines, histamines, prostaglandins.
Q: Bronchodilators
Answer: Beta 2 adrenergic agonists (Beta 2 – 2 lungs)Activates SNS (relaxes smooth muscle/dilates bronchi)**Relief of bronchospasm, histamine release stopped, increase ciliary motility.
Q: Proventil
Answer: Beta 2 adrenergic agonistBrochodilatorQuick-acting rescue inhaler (5 minutes)Use before exercise to prevent BronchoconstrictionUse beta 2 agonist inhaler before glucocorticoid
Q: Proventil
Answer: SE = HA, irritate throat, tremor, nervousness, tachycardiaCaution = HTN, cardiac, heart failure, seizuresPatients = keep log of attacks/frequency/what triggers themLungs = lotsa blood supply/large surface area, making them a quick onset (we don’t give PO)Use = asthma control, prevent exercise induced asthmaEffective? Clear breath sounds–NO wheezing/rhonchi, respiratory rate @ baseline, SaO2 @ baseline 90%Note = Long-acting are combined w/corticosteroids. Get bronchi open and the corticosteroid can get in there easier when it’s dilated!
Q: Mucomyst
Answer: Antidote for tylenolEffectiveness?? Liver enzymes are normal/no enlargement)
Q: Lovenox….
Answer: Anticoagulant-low molecular weight heparin derivative.
Q: Mechanism of action
Answer: Deactivates thrombin. Also prevents the conversion of fribrinogen and fribrin.
Q: Indications
Answer: Used to inhibit clot formation in ACS including STEMI, NSTEMI, and unstable angina. Also used to prevent pulmonary embolism and DVT in patients predisposed to such problems.
Q: Contraindications
Answer: Known hypersensitivity to the medication, pork products, or heparin.
Q: Adverse reactions
Answer: CNS side effects include confusion and dizziness. Cardiovascular side effects include edema, chest pain, and irregular heartbeat. Irritation, pain, redness or bruising may occur at injection site. Bleeding, angioedema, rash, and hives.
Q: Drug interactions
Answer: Interacts with NSAIDs, warfarin, and anti-platelet agents.
Q: Dose and administration
Answer: *Adult: STEMI: single IV bolus of 30mg plus 1mg/kg SQ dose followed by 1mg/kg SQ every 12 hours (Max 100mg)NSTEMI: 1mg/kg SQ every 12 hours in conjunction with oral aspirin therapy (100-325mg daily)Ped: 1mg/kg SQ
Q: Duration of action
Answer: onset: 3-5 hourspeak: 3-5 hoursduration: varies
Q: Special considerations
Answer: Do not use in patients with active major bleeding or thrombocytopenia. Use with caution in the elderly or any patient with increased risk of bleeding.
Q: Peptic Ulcer
Answer: a break in the lining of the stomach/duodenumcause: IMBALANCE b/w protective/damaging factors2 COMMON factors = H. pylori & NSAIDs
Q: H. pylori
Answer: -gram negative, spiral, found in gastric antrum, orally transmittedcorkscrews through the gastric mucus layer** H. Pylori = inflammation/epithelial cell damageincreased GASTRIN/dec SOMATOSTATIN**its is able to live in such an acidic environment b/c of its production of UREASEUrease = converts urea to ammonia (ammonia buffers the H+ & creates an alkaline cloud around the h.pylori)
Q: Detecting H.pylori
Answer: -C-urea breath test (based on organisms production of urease)*urease converts C-urea to CO2 that is detected in the breath
Q: How do NSAID cause gastric epith cell damage?
Answer: they are weak acids…they become trapped….and cause damage
Q: Zollinger-Ellison syndrome
Answer: Gastrin-secreting TUMOR of the non beta cells of the endocrine pancreas
Q: Cigarette smoking & PUD
Answer: Impairs mucosal blood flow/healing and inhibits pancreatic bicarb production
Q: 4 H2 receptor antagonists -tidine
Answer: -cimetidine – inhibits many cytochrome P450 enzymes and thus can interfere w/ hepatic metabolism; not recommended during pregnancy or nursing. also has antiadrenergic effects –>gynecomastia-ranitidine-famotidine-nizatidine*reversibly and competitively inhibit the binding of HISTAMINE to H2 receptors, resulting in suppression of gastric acid secretion*they also indirectly decrease gastrin and acetylcholine-induced gastric acid secretion-peak plasma levels achieved w/in 1-3 hours**benefits: CHEAPER, with the exception of cimetidine, safe for preg. and adverse effects better studied
Q: PPI’s mechanism -prazole
Answer: -block the parietal cell H+/K+ ATPase (proton pump)-superior to H2 receptor antagonist*OMEPRAZOLE -prototypealso: esomeprazole, rabeprazole, lansoprazole, dexlansoprazole, pantoprazole-all are PRODRUGS that require activation in an acidic env. –> converted to SULFENAMIDE (active form) which reacts with a cysteine residue on the H+/K+ ATPase–>irreversible inhibition of the proton pump-for acid production to resume it takes ~18 hours before new H+/K+ ATPase can be produced**there site of action is in the parietal cell canaliculus (this is why intravenous administration is useful to bypass the acidic stomach and duodenum)
Q: Clinical indication of PPIs
Answer: -to tx H. pylori associated ulcers, hemorrhagic ulcers, AND to allow continued use of NSAIDs in a patient w/ a known peptic ulcer*they also contribute to the eradication of the H. Pylori infection*-clot formation is impaired in acidic environments -so increasing pH allows for clotting of ulcers
Q: Adverse effects of PPIs
Answer: -headache, nausea, disturbed bowel function, abdominal pain-the large increase in gastrin secretion —> can induce ECL cells and parietal cells to hyperplasia –>carcinoid tumors ??? (not observed in humans)-may affect effectiveness of clopidogrel (anti-platelet agent) because CYP2C19 metabolizes PPIs as well as activates clopidogrel: this enzyme has various polymorphisms and is responsible for the variation in clearance rate of PPIs
Q: The most widely used antacids are mixtures of ____ and ____
Answer: -aluminum hydroxide (can cause constipation)-magnesium hydroxide (can cause diarrhea)*so when taken together you can avoid those symptoms-OH combines w/ H+ to form water-metals form salts with bicarbonate
Q: Quadruple therapy for H. pylori
Answer: -tetracycline-metronidazole*both broad spectrum antibiotics-PPI-bismuth (for coating and eradication)
Q: Triple therapy for H. pylori
Answer: -amoxicillin-clarithromycin-PPI
Q: TSH is the best screening test for?
Answer: Primary thyroid dysfunction (usually outpatient)
Q: Hashimoto’s disease
Answer: Autoimmune disease = thyroid gland is attackedSimilar to–>Type 1 Diabetes
Q: Thyroid Replacement….1st step
Answer: Adults1-2 mcg/kgT4 for full replacementChildren generally need more
Q: Thyroid Replacement in Elderly?
Answer: Start SLOWSynthroid25 mcg/day (if 50+/cardio risks)50 mcg/day otherwise
Q: Lab monitoring in stable patients?
Answer: Follow up: 6-12 moNeed for hormone decreases with age
Q: Drug Interactions: Protein binding
Answer: Anticonvulsants, Estrogen, increases Warfarin
Q: Warfarin interaction
Answer: hyperthyroid = decrease warfarinhypothyroid = increase warfarin
Q: Hypothyroid pregnancy?
Answer: increase dose
Q: 1/2 life of T4 is…
Answer: a week
Q: PO dose —> IV?
Answer: cut in 1/2
Q: Myxedema Coma
Answer: SEVERE HypOthyroidism= mental, cold, low HR
Q: Myxedema TX? (mistaken for adrenal dysfunction at times)
Answer: 1. Synthroid by IV2. Glucocorticoids (dec stress on body when metabolism goes up)3. Management/treat causative factors
Q: Toxic diffuse goiter (Graves’ disease)
Answer: Antibodies stimulate TSH receptorsNot TSH but acts like it
Q: Toxic adenoma?
Answer: benign tumors releasing TH
Q: Painful subacute thyroiditis
Answer: Acute = thyroid is destroyed in HashimotosAcute then goes down to hypOthyroidism
Q: Ablation
Answer: • Performed w/radioactive iodine (131)• Initially increase symptoms• Results in chronic hypOthyroidism• Lifelong TH supplement
Q: (PTU) drug for hyperthyroid
Answer: stop TH synthesisagranulocytosis, GI upset, Iiver Damage (especially PTU), Rashes
Q: Hyperthyroidism: During pregnancy?
Answer: PTU preferred in first trimester/Tapazole later in pregnancy
Q: Hyperthyroidism: Monitoring?
Answer: Follow-up 4-12 week intervals initially (3-4 mo when stable)Labs: Symptoms, wt., pulse, Free T4, TSH, CDC Tests
Q: Subclinical disease
Answer: Low TSH = T4 oversupplementation
Q: Thyrotoxicosis –> THYROID STORM!!!!
Answer: Exaggerated signs/symptoms of HYPERTHYROIDISMFever, mental, precipitated by illnessManagement? (Tapazole & PTU)Potassium Iodide, KI = stops release of thyroid hormonePropranolol = treat peripheral effects (lowers BP, angina, irregular Hbeat, migraines, tremors)
Q: types of antacids (MC)
Answer: 1) Ca*2) sodium bicarbonate3) aluminum4) magnesium5) combinations
Q: indications…when to use?
Answer: 1) hyperacidity2) aluminum-hyperhosphatemia3) magnesium-magnesium deficiency, malnutrition
Q: unlabeled uses
Answer: 1) GERD (immediate relief of intermittent heartburn)2) osteoporosis
Q: how do they work
Answer: -weak bases that neutralize HCl acid-raise pH which inactivates pepsin-increase Lower Esophageal Sphincter tone, which decreases reflux-does NOT coat stomach lining
Q: goal of antacid
Answer: 1) symptom relief2) lifestyle modification needed-raise head of bed-limit caffeine-stop smoking-weight loss-diet (increase fiber)
Q: duration of action
Answer: 2 hours
Q: what to use if signs/symptoms >2 hours or occur at bedtime
Answer: H2 blockers
Q: H2 blockers-how long to work?
Answer: 30 min.
Q: H2 use in what severity?
Answer: mild
Q: moderate s/s are…
Answer: s/s several times a week or daily
Q: tx (treatment)?
Answer: H2 blockers BID for 8-12 wks
Q: Treatment (tx) in severe or erosive dz
Answer: PPI q daily
Q: if PPI is uneffective q daily?
Answer: PPI BID for 8-12 wks
Q: what’s common when stop taking meds?
Answer: relapse (80%)
Q: what if that happens
Answer: maintenance tx needed (use lower dose than initial tx)
Q: caffeine effect?
Answer: 1) decrease LES pressure2) increase acidity3) makes GABA less effective
Q: AA w/ highest acid-neutralizing capacity (ex.)
Answer: 1) sodium bicarb (alka-seltzer)2) calcium bicarb (tums & rolaids)
Q: why should you try not to use sodium bicarbonate??
Answer: It increases Na = bad for fluid retention & CHF
Q: Which formulation has highest acid-neutralizing capacity?
Answer: 1) gels2) suspensions
Q: pt. education with tablets?
Answer: chew & take w/ full glass of water
Q: when to take
Answer: 1 hour after meals
Q: when to take to avoid interaction w/ other meds?
Answer: 1 hour before/2 hours after other meds
Q: Calcium & aluminum AA side effects?
Answer: 1) constipation2) precipitate stone (Ca ones)
Q: Magnesium AA Side effect?
Answer: diarrhea
Q: What can help balance the side effects?
Answer: give them together
Q: What AA to give pt. w/ a renal insufficiency?
Answer: magnesium AA
Q: monitor
Answer: check electrolytes periodically
Q: prego cat
Answer: none
Q: What can happen when AA are stopped?
Answer: acid rebound
Q: Chronic Ca carbonate or sodium bicarbonate AA use (can lead to) risk for:
Answer: -milk-alkali syndrome1) alkalosis2) increase Ca3) renal impairment
Q: s/s
Answer: 1) Headache2) nausea3) irritability4) weakness
Q: max. effect occurs?
Answer: taken 1 hour after meals
Q: How soon when taken on empty stomach
Answer: 20-40 min.
Q: tums/rolaid dose
Answer: PRN
Q: amphojel dose
Answer: 600mg po TID or QID
Q: maalox dose
Answer: 30 mL—QID
Q: MOM (milk of mag) dose
Answer: 15-30 mL—QID
Q: what AA have more SE
Answer: Na bicarbonate
Q: H2 blockers uses…(-tidine)
Answer: 1) GERD2) PUD3) hypersecretory conditions (ZE)
Q: PPI uses… (-prazole)
Answer: 1) GERD2) PUD3) hypersecretory conditions4) H. pylori
Q: actions
Answer: decrease amount of acid produced by stomach
Q: which are more powerful (how)
Answer: PPI (decrease acid to greater extent)
Q: nonpharms
Answer: 1) balanced meals at regular intervals2) avoid foods that exacerbate sx3) high fiber diet4) avoid caffeine & alcohol5) stop smoking
Q: goal of tx w/ H2 & PPI
Answer: relieve sx & heal ulcers
Q: 1st line tx in mild-mod dz
Answer: H2 blockers
Q: Treatment (tx) for severe PUD?
Answer: PPI
Q: What if NO improvement in a week with H2 blockers??
Answer: increase dose or change to PPI
Q: length of tx for hypersecretory or erosive conditions
Answer: long-term
Q: Longer treatment with H2 or PPI?
Answer: H2 blockers
Q: tx h. pylori
Answer: H2 or PPI + antibiotics & sometimes Bismuth
Q: SE of bismuth
Answer: dark stool (When Helicobacter pylori is implicated, bismuth acts as an antimicrobial agent, suppressing the organism but not eliminating it. In recent studies, bismuth compounds have been used with conventional antibiotics, producing elimination of the organism, histological improvement)
Q: When are H2 blockers given?
Answer: early evening or after meals
Q: When to take PPI’s?
Answer: 30 min. BEFORE meal
Q: Should you use PPI & H2 together?
Answer: NO
Q: Nursing Interventions?
Answer: 1) check stools/vomit for blood2) LFT (Liver enzyme tests, formerly called liver function tests (LFTs), are a group of blood tests that detect inflammation and damage to the liver. They can also check how well the liver is working. Liver enzyme testing includes ALT, AST, alkaline phosphatase; true liver function tests (LFTs) include PT, INR, albumin, and bilirubin)3) BUN/crea4) don’t crush or chew PPI’s
Q: how long does it take for blood to clear tract
Answer: 72 hours
Q: H2 blocker—Prototype Drug?
Answer: Zantac
Q: why are there less SE w/ axid (H2)
Answer: doesn’t start the P450 system (P450=the major enzymes involved in drug metabolism and bioactivation, accounting for about 75% of the total number of different metabolic reactions.)
Q: Which H2 blocker has lots of SE & drug interactions?
Answer: cimetidine (Tagamet)
Q: PPI ….1/2 life?
Answer: LONG = (72 hours)
Q: MORE side effects: H2 or PPI?
Answer: H2
Q: Drugs that PPI interfere with?
Answer: drugs that need acid environ. for absorption (ex. iron)
Q: cheapest PPI?
Answer: rabeprazole (Aciphex) & pantoprazole (Protonix)
Q: PPI with longer 1/2 life?
Answer: Nexium (esomeprazole)
Q: Zantac (ranitidine) dose?
Answer: Prototype H2 Blocker….150 mg BID/300 mg @ night
Q: pepcid dose
Answer: 20mg BID or 40mg po Q HS
Q: Axid (nizatidine) dose
Answer: 150mg BID or 300 mg Q HS
Q: Prilosec (omeprazole) dose
Answer: PPI –20 mg q daily or 20 mg BID
Q: Prilosec (omeprazole) tx w/ h. pylori
Answer: -40 mg q daily x 2 weeks-then 20 mg w daily x 2 weeks + antibiotic
Q: Prevacid (lansoprazole) dose
Answer: PPI—15 mg q daily x 8 weeks
Q: Prevacid (lansoprazole) in h. pylori?
Answer: 30 mg BID x 2weeks + 2 antibiotics
Q: Aciphex (rabeprazole) dose?
Answer: PPI—-20mg po q daily
Q: Nexium (esomeprazole) dose?
Answer: PPI—20-40mg po q daily
Q: Protonix (pantoprazole) dose
Answer: 40 mg po q daily x 8-16 weeks
Q: Dexilan (dexlansoprazole) dose?
Answer: PPI…….-30 mg q daily-60 mg q daily if more erosive
Q: Nurse can increase gastrin level while on PPI to around what range
Answer: 200-300
Q: How long once PPI’s are stopped to return to normal gastric level??
Answer: 3-5 days
Q: PPI’ s heal 90% gastric ulcers w/in :
Answer: 6 – 8 weeks
Q: PPI’s heal 90% of duodenal ulcers w/in:
Answer: 4 weeks
Q: PPI’s usually taken?
Answer: during the day
Q: Benefits of PPI last:
Answer: 3 – 5 days after therapy is stopped
Q: PPI’s are used for:
Answer: short term control, PUD, GERD
Q: Adverse effects of PPI’s are:
Answer: not common
Q: Most commonly reported adverse effects of PPI’s are:
Answer: – headache- abd pain- diarrhea- N/V
Q: PPI’s are effective at:
Answer: reducing gastric acid secretions
Q: Nexium (esomerprazole):
Answer: PUD, GERD, PO; 20-40mg/day
Q: Prevacid (lansoprazole):
Answer: – PUD- combo w/antibiotics for H. Pylori* PO; 15-60mg/day– Prevacid combines (lansoprazole) w/amoxicillin/clarithromycin
Q: Prilosec (omeprazole):
Answer: – PUD/GERD- often used in combo w/- antibiotics for H. Pylori* 20-60mg 1 -2 daily
Q: Protonix (pantoprazole):
Answer: – mainly for GERD- IV form avail* PO; 40mg/day
Q: AcipHex (rabeprazole):
Answer: _ PUD/GERD* PO; 20mg/day
Q: H1 distribution
Answer: Smooth muscleEndothelium
Q: H2 distribution
Answer: Gastric mucosaCardiac muscleVascular SM
Q: GI Tract
Answer: H2 activation of parietal cells –> gastric acid secretionH1 activation –> contraction of GI Submuc
Q: Role of H2 receptor in acid secretion
Answer: ECL cell stimulation by gastrin or Ach –> histamine release –> H2 receptor activation on parietal cells –> AC activation –> cAMP production –> protein kinase activation –> acid secretion by proton pump (K in; H out)
Q: H2 receptor antag- MOA (mechanism of action)
Answer: Reduce gastric acid secretion
Q: H2 receptor antag – therapeutic use?
Answer: Peptic ulcer disease PUDGastric acid hypersecretionInhibit stimulated acid secretionNocturnal acidity (useful when added to proton pump therapy to control “nocturnal acid breakthrough”)**
Q: H2 receptor antagonists – drug names
Answer: ClimetidineFamotidineNizatidineRanitidineNote: these drugs have different structures and therefore different side effects
Q: H2 receptor antag- pharmacokinetics
Answer: Absorption: well absorbed after oral administrationPeak plasma concentrations reached in 1-2 hoursT1/2: 1-3 hoursSome hepatic biotransformation (cimetidine has the greatest)Mostly excreted unchanged by the kidney
Q: H2 receptor antag that can cause: gynecomastia (male breasts)/galactorrhea (milk leakage)
Answer: CimetidineDue to decreased estrogen metabolism (cyt p450 inhibition)
Q: PPIs – MOA (mech of action)
Answer: Irreversibly inhibit the gastric parietal cell proton pump H/K ATPase (Note: the prolonged duration of action reflects the covalent modification of the pump, rather than prolonged serum half life)**A single daily dose can effectively inhibit 95% of gastric acid secretionProdrugs – activated in an acidic environment
Q: PPIs – Drug of choice (DOC) for…
Answer: Zollinger-Ellison syndrome (g acid secreting tumor)GERD (Gastricesophageal Reflux Disease)
Q: PPIs – use with H2 antagonists?
Answer: Should not be given simultaneously because the H2 antagonist reduces the efficacy of the PPIUsually the PPI is taken during the day and the H2 antagonist is taken at night
Q: PPIs – drug interactions
Answer: Decrease the metabolism and clearance of:–Bendodiazepines–Warfarin–PhenytoinReduce absorption of:–KetoconazoleIncrease the absorption of:–Digoxin
Q: PPIs – drug names
Answer: Omeprazole (children, GERD)Lansoprazole (NSAID ulcers)RabeprazolePantoprazoleEsomeprazole
Q: PPIs- adverse reactions
Answer: Few and generally mildDiarrheaHeadacheDrowsinessMuscle painConstipation
Q: Mucosal protective agents – drug names
Answer: SucralfateColloidal bismuth (Pepto-Bismol)
Q: Sucralfate
Answer: coats stomach ulcer, helping it to heal
Q: H. pylori – risk
Answer: recurrent ulcer (60-85% vs 5-10% if cured)
Q: H. pylori – treatment**
Answer: PPI + 2 of the following antibiotics–Clarithromycin–Metronidazole–AmoxicillinOne week treatment: 90% cure rateTwo weeks of PPI + 1 antibiotic (typically clarithromycin): 10-20% lower cure rateMHD notes:–Tetracycline can be 1 of the 2 antibiotics–Bismuth salts, doxycycline, and metronidazole for 14 days is cheap and effective
Q: Other drugs – Pirezepine
Answer: Blocks binding of Ach to M3 receptors –> decreased acid secretion
Q: Other drugs – Misoprostol
Answer: Blocks binding of prostaglandins to parietal cell receptor –> decreased acid secretion
Q: Insulin (never given PO)
Answer: Available in 1922 (1922-1980’s Insulin from Pork or Beef pancreas)Insulin must be available when glucose is in the bloodControl of Diet-when and what is eatenControl of ExerciseDuring IllnessNever PO-GI Juices destroys the insulinVial in use @ room temp (extra vial in refrigerator)Recombinant DNA (rDNA) now is used almost exclusivelyMost effective, fewer allergies, lower incidence of resistance
Q: LOG’s –Rapid Acting
Answer: Onset 5-15 minutesPeak 1-3 hoursDuration 3-5 hoursThese have to be given with the meal in front of the clientHumalog/Lispro InsulinNovalog/Insulin AspartApidra/Insulin Glulisine
Q: Regular Insulin = Fast Acting
Answer: Humulin R, Novolin R/Insulin RegularOnset 30-60 minutesPeak 2-6 hoursDuration 6-10 hoursTHIS IS THE ONLY Insulin That Can Be Given IV
Q: Intermediate Acting = NPH
Answer: Humulin NNPHOnset 1-2 hoursPeak 6-14 hoursDuration 16-24 hours
Q: Long Acting = Lantus
Answer: Lantus/Insulin GlargineOnset-gradual-1 hourPeak-No PeakDuration-24 hoursOnce/day @ nightCAN’T MIX WITH ANY OTHER INSULIN!!!!
Q: Syringes
Answer: Specially calibrated syringes for insulin.NOTE: NEVER put anything but INSULIN in these syringes
Q: HYPOglycemia
Answer: Blood sugar is low, usually below 70 (70-110 is considered normal range)The brain is not getting sugar, it needs sugar to keep functioningFirst signs are neuro in natureSweatingTremorsIrritabilityBlurred visionDiaphoretic (sweating)HeadacheLightheadednessAnxiousDecreased LOCNauseaPalenessAnd whatever else your patient states is a sign of their hypoglycemia. If your patient states they are hypoglycemic, believe them
Q: Tx for HYPOglycemia (or brain cells will die)
Answer: (HIGH SUGAR SNACK, THEN COMPLEX CARB)High sugar = coke, OJ, candy.Complex carb = peanut butter/crackers. (will stabilize sugar from falling after the high sugar snack)Unconscious? D50, sugar in the buccal area, or glucagon in a tube in buccal areaIn the hospital? get accu check 1st, then get sugar asap!
Q: HYPERglycemia
Answer: 3-P’sPolyuria-frequent urinationPolyphagia-hungerPolydipsia- thirstGlycosuria-high sugar in the urineWeight loss-even though their sugar is high, they aren’t getting nutrients into the cellFatigueKetones- in the urine/breath–gives off ketones (fruity Smell to the breath)No nutrients to the cell, burning fat for energyRapid, Deep Respirations (blowing off the ketones)Dry Skin (Dehydrated from peeing too much)
Q: Tx for HYPERglycemia
Answer: 1. check sugar2. ketones in pee?3. give insulin
Q: Adrenal Glands
Answer: Sit on top of the kidneys.Inner Medulla- Epi/NorepinephrineOuter Cortex – Glucocorticoids (sugars), Mineralocorticoids (salts), gonadocorticoids (sex)
Q: Mineralocorticoids
Answer: Aldosterone-95% of the mineralocorticoids secreted by the adrenalsAldosterone regulates plasma volume: Na REABSORPTION & K EXCRETION by the tubules.1. Plasma volume falls2. Kidney senses this and release renin3. Renin allows angiotensin 1 –>angiotensin 2.4. Angiotensin 2 causes aldosterone secretion5. Allowing sodium reabsorption/potassium depletion (remember, WATER follows salt!)
Q: 2 Ways of increasing FLUID volume?
Answer: ADH/Aldosterone are 2 ways our body maintains homeostasis in fluid volume.ADH-sent by pituitary to make kidneys reabsorb H20 in the collecting ductsAldosterone-sensed by the kidneys-release of renin-converts angiotensin 1 to 2-angiotensin 2 allows aldosterone to act on the kidneys to increase Na reabsorption and K depletion
Q: What are glucocorticoids?
Answer: 1. Hypothalamus senses low glucocorticoid levels in the blood-2. Releases CRF (corticotropin releasing factor) to pituitary gland3. Pituitary releases ACTH (Adrenocorticotropic hormone)4. ACTH travels to adrenal cortex and tells it to release glucocorticoids5. Glucocorticoids support BP, GI functions, Mental Functions, Help control the immune response mechanisms
Q: Use of Glucocorticoids
Answer: Adrenal InsufficiencyAllergiesAsthmaInflammatory Bowel Disease (Crohn’s/Ulcerative ColitisCancer-Hodgkin’s/Leukemia’s/Lymphoma’sTransplant Rejection ProphylaxisRheumatic DisordersShockSkin Disorders
Q: Glucocorticoids (-sone)
Answer: PO, IV, IMPrototype Drug: Hydrocortisone/Cortefw/foodContra Ind: diabetes, osteoporosis, psychoses, liver disease, hypothyroidism
Q: Cortef (hydrocortisone) side effects
Answer: Immune –> susceptible to infection and signs of infection will be maskedPUD-Give w/food, Give prophylactic H2 or PPIdo NOT give with NSAIDSMonitor: abd pain, coffee ground emesis, tarry stools, feverOsteoporosis-Have client take Ca/vit D, walkPsychoses-monitor for irritability, nervousness, mood changes before increasing to hallucinations/suicidal ideation,
Q: Cortef (side effects/monitor?)
Answer: Cataracts/glaucoma (yearly exams, trouble reading?)Na/H2O Retention (BP, wt., I/O, breath sounds, Na/K levels)Metabolic Changes (high sugar, hyperlipidemia, abnormal fat deposits/wt. gain)Myopathy (muscle wasting, hyperkalemia, fatigue/weak, respiratory muscles & eyes)
Q: Interaction w/Cortef (other corticosteroids)
Answer: NSAID’s/alcohol-may increase chance of GI BleedOral Anticoagulants may inc/dec anticoagulationUse with diuretic, increase K depletionMonitor? EKG/K levelsVaccines? May reduce the antibody response to vaccine
Q: Too much cortisol? (Cushing’s syndrome)
Answer: Body is exposed to high levels of the hormone cortisol for a long time. The most common cause of Cushing syndrome, sometimes called hypercortisolism, is the use of oral corticosteroid medication. The condition can also occur when your body makes too much cortisol.Causes? pituitary adenoma, tumor: lungs, pancreas, thyroid or thymus gland.Signs: Adrenal atrophy, osteoporosis, hypertension, increased risk of infections, delayed wound healing, acne, peptic ulcers, general obesity, redistribution of fat around the face-Moon Face-shoulders, and neck-Buffalo Hump.Mood/personality changedHigh mortality rate from the complications such as hypertension from sodium and water retention
Q: Too little cortisol? (Addison’s disease)
Answer: What Causes Addison’s Disease?Result from a problem with the adrenal glands themselves (primary adrenal insufficiency). Autoimmune disease accounts for 70% of Addison’s disease.This occurs when the body’s immune system mistakenly attacks the adrenal glands. This autoimmune assault destroys the outer layer of the glands.When glucocorticoids are in use, especially in higher dose and long term therapy-the adrenal glands shrink/atrophyIf we taper clients off glucocorticoids, then adrenal glands return to normal function.If we suddenly stop the glucocorticoids, we have Addison’s Crisis, the client will start losing there blood pressure, have renal failure, be very tired and lethargic, have nausea and vomiting, asthenia (lack of strength), they will die without getting a dose of glucocorticoids
Q: Corticosteroids
Answer: Corticosteroids produced in the adrenal cortex.Corticosteroids: stress response, immune response, regulation of inflammation, carbohydrate metabolism, protein catabolism, blood electrolyte levels, behavior.Glucocorticoids: Cortisol. Control carbohydrate, fat protein metabolism, anti-inflammatory by preventing phospholipid release, decreasing eosinophil action and a number of other mechanisms.Mineralocorticoids: Aldosterone. Control electrolyte/water levels, mainly by promoting sodium retention in the kidney.
Q: Anti-Diuretic Hormone Drugs
Answer: ADHVassopressin (pitressin) Half-life 2-8 hoursDesmopressin (DDAVP) Half-life 20 hoursPromotes water reabsorption by the kidneys, vasoconstriction, and increased clotting factor VIII-used with hemophilia and von Willebrand’s Disease, off label use-bedwetting in childrenSide Effects: Fluid Overload (reabsorbed too much water)-monitor for edema, hypertension, pounding headache, sleepiness. Myocardial Ischemia from vasoconstrictionmonitor: EKG and blood pressure, chest pain, dyspnea, diaphoresisCategory X for PregnancyDo not use in clients with CAD, Decreased Peripheral Circulation, and Chronic Nephritis
Q: Nursing considerations for ADH meds
Answer: Monitor vital signs, I/O, specific gravity, daily weights, Electrolytes,
Q: Nursing considerations 2
Answer: Monitor for signs of water intoxication-headache, confusion, pounding headache, edema, hypertension, sleepiness
Q: Nursing considerations 3
Answer: Extravasation of IV vasopression can lead to Gangrene
Q: Nursing considerations 4
Answer: Effectiveness-normal urine output, without signs of fluid overload
Q: Diabetes Insipidus (DI)
Answer: No Antidiuretic Hormone = large amt of fluid lost. You will see DI = w/head injuries & lung cancer.
Q: WHAT is ADH?
Answer: ADH = maintain fluid balance, control BP, and cardiac output in your body.Antidiuretic – holds fluidsDiuretics allow fluids to be lost through the kidneysHypothalamus sense if the plasma volume has decreased, if the Nalevel has risen (or the osmolality of the blood) and will send ADH to increase the amount of fluid retained by the kidneys.
Q: Addison’s
Answer: When glucocorticoids are in use, especially in higher dose and long term therapy-the adrenal glands shrink/atrophyIf we taper clients off glucocorticoids, then adrenal glands return to normal function.If we suddenly stop the glucocorticoids, we have Addison’s Crisis, the client will start losing there blood pressure, have renal failure, be very tired and lethargic, have nausea and vomiting, asthenia (lack of strength), they will die without getting a dose of glucocorticoids
Q: Cushing
Answer: Too much glucocorticoids for a long timeSigns Adrenal atrophy, osteoporosis, hypertension, increased risk of infections, delayed wound healing, acne, peptic ulcers, general obesity, redistribution of fat around the face-Moon Face-shoulders, and neck-Buffalo Hump. Mood and personality changedHigh mortality rate from the complications such as hypertension from sodium and water retention
Q: Med interactions w/glucocorticoids
Answer: NSAID’s and Alcohol-may increase chance of GI BleedOral Anticoagulants may increase or decease anticoagulationUse with diuretic, may increase K depletion-monitor EKG and K levelsVaccines-may reduce the antibody response to vaccine
Q: Synthroid (treats hypothyroid ^tsh low t3/t4)
Answer: generic name: levothyroxine
Q: Synthroid–>#1 adverse reaction?
Answer: Nervousness :-/
Q: What will prevent complete absorption of Synthroid?
Answer: Ca, Fe, Mg, Zinc
Q: Why do you need thyroid med?
Answer: to replace/substitute diminished or absent thyroid function
Q: Synthroid is contraindicated with?
Answer: hypersensitivity, recent MI, hypothyroidism (untreated low TSH level but normal T3/T4 levels)
Q: Side effects of Synthroid
Answer: Insomnia, irritable, nervous, arrhythmia, tachycardia, wt loss, cardiovascular collapse.
Q: Monitor blood/urine glucose in what kind of patient’s taking Synthroid?
Answer: Diabetic
Q: When to take Synthroid?
Answer: MORNING/same time every day
Q: Nursing Assessments w/Synthroid?
Answer: Apical pulse, BP, tachyarrthymias, chest pain
Q: LOW
Answer: Initial dose of geriatric/cardiac pt. taking synthroid?
Q: 5-10 mL
Answer: LEVOTHYROXINE SHOULD BE CRUSHED FOR PATIENTS WITH DIFFICULTY SWALLOWING AND PLACE IN HOW MANY ML OF WATER?
Q: Insomnia
Answer: Give synthroid before breakfast to prevent____.
Q: Deficient knowledge R/T medication regimen
Answer: Potential nursing diagnoses for pt. taking Synthroid?
Q: 75-125 mcg/day
Answer: Maintenance dose for levothyroxine?
Q: Monitor: Ht., wt, psychomotor development.
Answer: When a child is taking Synthroid.
Q: HYPERthyroidism?
Answer: Synthroid toxicity/overdose
Q: 100 mcg/over 1 MIN
Answer: IV administration of Synthroid
Q: Take Synthroid with:
Answer: WATER
Q: Test given yearly to pt’s on Synthroid?
Answer: Thyroid Function Test
Q: Thyroid Therapy
Answer: Partial hair loss may be experienced in kids taking __ ___.
Q: Treatment: Synthroid overdose?
Answer: Stop dose for 2-6 days
Q: Treatment: Acute Synthroid overdose
Answer: Stomach pump(puke) + activated Charcoal (treat poisonings)
Q: IV/PO
Answer: Synthroid Routes?
Q: Synthroid metabolic adverse reactions?
Answer: Heat intolerance & weight loss
Q: Synthroid
Answer: Treats hypothryroidism. Know for pharm exam 2.
Q: IV/PO dose
Answer: IV = 200, 500 mcg vialTab = 25-300 mcg
Q: Desmopressin acetate (DDAVP): is
Answer: an antidiuretic hormone, works by limiting the amount of water that is eliminated in the urine.
Q: Desmopressin acetate (DDAVP): duration of action
Answer: up to 20 hours
Q: Desmopressin acetate (DDAVP): available as
Answer: nasally, IV, oral/subling tab
Q: Desmopressin acetate (DDAVP): works on the
Answer: posterior pituitary
Q: Desmopressin (DDAVP): used for
Answer: Treatment for: diabetes insipidus, bedwetting(nocturia), brain injuries, hemophilia A w/ some factor VIII production