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NURS 350 PHARMACOLOGY EXAM 1, Exams of Nursing

NURS 350 PHARMACOLOGY EXAM 1 QUESTIONS AND ANSWERS

Typology: Exams

2024/2025

Available from 11/23/2024

Gabjayz
Gabjayz 🇺🇸

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Download NURS 350 PHARMACOLOGY EXAM 1 and more Exams Nursing in PDF only on Docsity! NURS 350 PHARMACOLOGY EXAM 1 Pharmacokinetics the study of drug movement throughout the body Pharmacokinetics involves absorption, distribution, metabolism, excretion, time course of drug responses For a drug to directly penetrate the membrane it must be lipid soluble polar molecule -molecule with an unequal distribution of charge -no net charge Ions molecule that have a net electrical charge Quaternary ammonium compounds molecules that contain at least one atom of nitrogen and carry a positive charge at all times pH-dependent ionization Acid is a proton donor - tends to ionize in basic (alkaline) media Base is a proton acceptor - tends to ionize in acidic media pH partitioning (Ion trapping) -acidic drugs accumulate on the alkaline side -basic drugs accumulate on the acidic side absorption is Refers to the passage of medication molecules into the blood from site of adminstration the rate of absorption determines how soon effects will begin the amount of absorption determines how intense the effects will be Factors that affect drug absorption -rate of dissolution -surface area -blood flow -lipid solubility -pH partitioning Intravenous route of administration barrier- have to have IV access Advantage- fast disadvantage- dangerous Intramuscular route of administration Toxic concentration therapeutic range plasma drug concentration between the minimum effective concentration and the toxic concentration Pharmacodynamics The study of what the drug does to the body dose-response relationship -minimum amount of drug to be used -maximum response a drug and elicit maximal efficacy the largest effect that a drug can produce relative potency the amount of drug that must be given to elicit an effect receptor functional macromolecule in a cell to which a drug binds to produce its effects important properties of receptors Drugs can only mimic or block the body's own regulatory molecules Drugs cannot give cells new functions Agonist a molecule that activates receptors, makes processes go faster or slower antagonist prevents receptor activation what happens if there is no agonist present Administration of an antagonist will have no observable effect. noncompetitive antagonist -reduce the maximal response of an agonist -impact not permanent competitive antagonist -Drug competes with the agonist for receptor binding. -bind reversibly to receptors Partial agonist -moderate intrinsic activity -maximal effect is less than a full agonist Calcium Channel Blockers agents that inhibit the entry of calcium ions into heart muscle cells Calcium channel blockers end with dipine except for verapamil and dihydropyridines classification dihydropyridines nifedipine Classification Nondihydropyridines verapamil and dilitiazem Dihydropyridines Action arterioles, vascular smooth muscle does not work on the heart Nondihydropyridines action arterioles and on the heart dysrhythmias Verapamil Uses angina, HTN, cardiac dysrhythmias, migraine Verapamil adverse effects constipation, dizziness, facial flushing, headache, edema of ankles and feet, gingival hyperplasia Verapamil interactions digoxin, beta blockers prazosin Drugs that dilate resistance vessels (arterioles) produce a fall in cardiac afterload Drugs that dilate capacitance vessels (veins) Reduce cardiac preload Vasodilators adverse effects postural hypotension, reflex tachycardia, blood volume expansion Hydralazine uses hypertension, hypertensive crisis, heart failure Hydralazine adverse effects Reflex tachycardia Blood volume expansion Systemic lupus erythematosus-like syndrome Headache, dizziness, weakness, and fatigue Hydralazine drug interactions Other antihypertensive agents Given in combination with beta blocker to protect against reflex tachycardia Minoxidil Hypertrichosis drug-drug interactions - whenever two or more drugs taken, there is a potential for interactions drug-drug interaction consequences -increased or decreased in therapeutic effects, adverse effects drug-drug interactions can produce a distinct response basic mechanisms of drug-drug interactions 1. Direct chemical or physical interaction 2. Pharmacokinetic interaction 3. Pharmacodynamic interaction 4. Combined toxicity direct chemical or physical interaction NEVER mix drugs in same container without first establishing compatibility -*Most common in IV solution precipitate: do not administer Pharmacokinetic interactions Changes occurring in absorption, distribution, metabolism, and renal excretion pharmacokinetic interactions altered absorption Increased gastric pH Laxatives Drugs that depress peristalsis Drugs that induce vomiting Adsorbent drugs Drugs that decrease regional blood flow pharmacodynamic interactions at same receptor Almost always inhibitory (antagonist/agonist) a condition that is caused by a medical treatment physical dependence a physiological need for a drug, marked by unpleasant withdrawal symptoms when the drug is discontinued carcinogenic effect drug-induced cancer -takes decades for evidence to appear Hepatoxicity liver toxicity What can QT drugs cause? life threatening dysrhythmias -prolongs QT interval on ECG black box warning A warning that a drug may produce serious or even life-threatening effects in some individuals, in addition to its beneficial effects. Medication errors significant contributor to morbidity and mortality how to reduce medication errors -replace handwritten med orders with computerized -senior clinical pharmacist accompany physicians on rounds -use barcode system -NO error prone abbreviations -perform med reconciliation pharmacodynamic tolerance tolerance due to nervous system sensitivity change metabolic tolerance drug tolerance that results from changes that reduce the amount of the drug getting to its sites of action tachyphylaxis tolerance reduction in drug responsiveness by repeated dose over short term Bioavailability variability able to reach the systematic circulation from site of admin pharmacogenomics study of how genes affect individual drug responses gender variations -Alcohol is metabolized more slowly by women -Certain opioid analgesics are much more effective in women than in men Race variation genetic variations and psychosocial factors Comorbidities increases risk of drug interaction diet -starvation decreases drug protein binding -MAOI hypertensive crisis inability to take medications as ordered -results in problems with manual dexterity, visual acuity, intellectual capability, emotional status, attitude regarding drugs, and ability to pay third trimester drug therapy -renal blood flow is doubled (excretion is quicker) -tone and motility of the bowel are diminished placental transfer of drugs -all drugs are able to cross the placenta adult function at 6-8 months neonates and infants organ function of gastric acidity reaches adult values until 2 neonates and infants absorption -slow -erratic -delayed first days of life from low blood flow neonates and infants IM -more rapid neonates and infants transdermal -more rapid than older children -blood flow greater -increased risk for toxicity neonates and infants Protein binding -albumin binding limited from low amount of albumin in blood neonates and infants protein binding compacity -10 to 12 months to reach adult neonates and infants blood brain barrier -not fully developed -drugs easily access CNS -Dosage should be reduced neonates and infants liver maturation 1 year old Children 1yr and older pharmacokinetics -parameter similar to adults -metabolizes drug faster than adults-until 2 -metabolism declines at puberty promoting adherence -dose size + timing -Route + technique of admin -duration of treatment -drug storage -nature + time course of desired responses and adverse response Older adult patients are more at risk for -drug sensitivity -severity of illness -excessive prescribing -poor adherence Older adult patients should have -individualized treatment -monitored desired and adverse responses -reduced symptoms Older adult patient absorption -Altered GI absorption - Absorption rate declines with age -Delayed stomach emptying and decreased splanchnic blood flow also occurs Older adult patient distribution -Increased percent of body fat -Reduced percent of lean body mass -Reduced total body water (resulting in increased concentration and more profound effects) -Reduced levels of serum albumin resulting in reduced drug protein binding and increased amounts of free drugs Older adult patient metabolism -Hepatic metabolism decreases Reduced hepatic blood flow, reduced liver mass, and decreased activity of some hepatic enzymes occur The half-lives of some drugs may increase, and responses are prolonged Responses to oral drugs may be enhanced first pass effect Older adult patients excretion hydrochlorothiazide adverse effects Hyponatremia, hypochloremia, and dehydration Hypokalemia Use in pregnancy and lactation Hyperglycemia Hyperuricemia Effects on lipids, calcium, and magnesium hydrochlorothiazide interactions -digoxin -augments effects of hypertensive meds -reduce renal excretion of lithium -NSAIDS -can be combined with ototoxic drugs w/o increased risk -NOT OTOTOXIC Spironolactone moa Blocks aldosterone in the distal nephron Retention of potassium Increased excretion of sodium Spironolactone uses hypertension heart failure edematous states primary hyperaldosteronism pms pcos acne in young women Spironolactone adverse effects hyperkalemia benign and malignant tumors endocrine effects. Spironolactone interactions thiazide and loop diauretics agents that raise potassium levels Triamtrene moa disrupts sodium-potassium exchange in distal nephron Triamtrene uses hypertension edema Triamtrene adverse effects hyperkalemia leg cramps nausea vomiting dizziness blood dyscrasias