CURRENTLY TESTING SOLUTIONS OF Advanced Pharmacology FINAL 2024 EXAM QUESTIONS WITH ACTUA, Exams of Nursing

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CURRENTLY TESTING SOLUTIONS OF Advanced Pharmacology

FINAL 2024 EXAM QUESTIONS WITH ACTUAL CORRECT

DETAILED ANSWERS

Explain Pharmacokinetics - ANSWER-The study of how drugs are moved through the body and are encompassed in mechanisms of: Absorption Distribution Metabolism Excretion Think Kinetic (movement) Pharmacodynamics - ANSWER-study of the biochemical and physiologic effects of drugs on the body Think Dynamic (change) majority of drugs either (a) mimic or inhibit normal physiological/biochemical processes or inhibit pathological processes in animals or (b) inhibit vital processes of endo- or ectoparasites and microbial organisms

Summarize the main drug actions - ANSWER- 1 - stimulating action through direct receptor agonism and downstream effects 2 - depressing action through direct receptor agonism and downstream effects (ex.: inverse agonist) 3 - blocking/antagonizing action (as with silent antagonists), the drug binds the receptor but does not activate it 4 - stabilizing action, the drug seems to act neither as a stimulant or as a depressant 5 - exchanging/replacing substances or accumulating them to form a reserve (ex.: glycogen storage) Desired activity is achieved through what main mechanisms? - ANSWER--Cellular membrane disruption

• Chemical reaction with downstream effects
• Interaction with enzyme proteins
• Interaction with structural proteins
• Interaction with carrier proteins
• Interaction with ion channels
• Ligand binding to receptors: 1)Hormone receptors 2) Neuromodulator receptors 3)Neurotransmitter receptors Explain the therapeutic window - ANSWER-therapeutic window is the amount of a medication between the amount that gives an effect (effective dose) and the amount that gives more adverse effects than desired effects Duration of action - ANSWER-duration of action of a drug is the length of time that particular drug is effective Explain bioavailability - ANSWER-drug's bioavailability can be defined as the proportion of the drug that reaches its site of action 6 rights to medication administration - ANSWER-RIGHT CLIENT RIGHT MEDICATION RIGHT DOSAGE

More severe: hypersensitivity, mental depression, hypotension, paradoxical stimulation, rebound seizures Benzo pharmacokinetics - ANSWER-Widely distributed throughout the body accumulate in lipid rich areas (CNS and adipose tissue) the more lipophilic the agent the faster it is absorbed Onset 30 min- 1 hr lasting 4-6 hours, peak at 1-2 hours IV Admin: onset 1-5 min, peak immediately, last 15-20 min metabolized by the liver and excreted in urine Beta blocker (BB) MOA - ANSWER-Interrupts the nerve impulses across the neurons by antagonizing the receptors with in the cardiac cells resulting in blockade of the beta 1 receptors';

• B1 blockade results in reduction of heart rate (chronotropic), rate of conduction through the AV node (dromotropic), and force of contraction (inotropic) This in turn decreases the oxygen demand on the myocytes, reduction in BP from the reduced HR and inotropic actions Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release of the hormone glucagon, which work together to increase plasma glucose Beta blocker Therapeutic uses - ANSWER-Useful in angina, HTN, cardiac dysrhythmias, MI, HF, Hyperthyroidism, migraines, pheochromocytoma, Glaucoma In angina/MI: reduction of oxygen demand HTN: B1 blockade as well as suppressed renin release via B1 blockade in the kidneys shows a marked decrease in PVR which results in improved stroke volume Beta Blocker Adverse effects - ANSWER-B1 blockade: bradycardia resulting in reduced CO and precipitating HF, AV heart block, Rebound cardiac Excitability B2 effects incl: bronchoconstriction, and Inhibition of glycogenolysis resulting in hypoglycemia

Beta blocker Pharacokinetics - ANSWER-Highly lipid soluble Absorption usually rapid/complete 50% 1st pass metabolism peak concentrations approx. 1.5-2 hours, onset about 4-5 hrs liver metabolized, renal excretion as a metabolite Beta blocker interactions - ANSWER-Calcium channel blockers: Negative Ino/dromo/chronotropic effects anti-arrhythmics: may enhance their effects leading to unwated outcomes Nitrates: may potentiate hypotensive effects MAO inhibitors: may increase reduction of sympathetic activity thus the inability to respond to Fight/flight mechanism resulting in reduced BP/HR overall Digitalis: Can potentiate suppressed AV conduction Calcium Channel Blockers (CCB) MOA - ANSWER-inhibition of calcium movement in smooth and cardiac muscle tissue by selectively antagonizing calcium influx movment across the cellular membrane responsible for smooth/cardiac muscle conduction velocity: produces relaxation of coronary smooth muscles, dilation of coronary arteries; reduced dromotropic effects of the sa/av node and reduced automaticity Effects peripherally result in vasodilation through smooth muscle relaxation Different agents have different effects on different receptors within the transmembrane calcium channels Non specific effects in blood coagulation by inhibiting platelet aggregation in the clotting cascade CCB indications - ANSWER-Hypertension, angina, dysrhythmias CCB Adverse effects - ANSWER-Peripheral edema, flushing, palpitations, headache Pulmonary edema, rebound tachycardia, bradycardia, skin rash CCB drug interactions - ANSWER-BB and other antiarrhythmics can potentiate their effects

Acetylcysteine (mucomyst, pravolex) Mucolytic: MOA - ANSWER-Antidote to Acetaminophen: Exact mechanism is unknown however thought to restore hepatic glutathione and thus inactivating the toxic metabolite of acetaminophen, preventing further hepatic damage Metabolite produced by acetaminophen: N-acetyl-p-benzoquinone imine (NAPQI) accumulates within the body. It is normally conjugated by glutathione, but when taken in excess, the body's glutathione reserves are not sufficient to inactivate the toxic NAPQI. This metabolite is then free to react with key hepatic enzymes, thereby damaging liver cells Acetylcysteine (mucomyst, pravolex) Mucolytic: MOA mucolytic - ANSWER-acts by splitting the bonds of mucoprotein (substance responsible for increased viscosity of mucous secretions in the lungs) Acetylcysteine (mucomyst, pravolex) Mucolytic: Indications - ANSWER-Acetaminophen Toxicity Mucolytic action in acute and chronic bronchopulmonary disease; Tracheostomy care Acetylcysteine (mucomyst, pravolex) Mucolytic: Dose - ANSWER-Acetaminophen Toxicity: 150 mg/kg IV over 15 min Repeated at 50mg/kg over 4 hours Acetylcysteine (mucomyst, pravolex) Mucolytic: Contraindications - ANSWER-HSN to drug Status asthmaticus as it may precipitate bronchospasm Activated Charcoal w sorbitol: MOA - ANSWER-Absorbs ingested toxins by inhibiting their absorption in the GI tract Sorbitol is a sweetener and works as a laxative for the elimination of the poison from the body Activated Charcoal w sorbitol: Dose - ANSWER- 30 - 100 g in 250 ml water (5-10 times the estimated weight of the drug/chemical) PO/NG/OG

peds: 1-12 yo: 1 gm/kg Activated Charcoal w sorbitol: Contraindications - ANSWER-Pt who has ingested corrosive agent or petroleum distillate violent pt with ALOC Altered pt and not intubated with no NG/OG in place Activated Charcoal w sorbitol: Caution - ANSWER-Not effective for cyanide, mineral acids, caustic alkaloids, organic solvents, iron, ethanol, methanol, lithium Can cause vomiting and can cause severe ALI if aspirated Adenosine (adenocard) antiarrhythmic (naturally occurring nucleoside): MOA - ANSWER-In the heart it acts on the AV node to slow conduction and inhibit reentry pathways mediated via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing K+ efflux via inward rectifier K+ channels, subsequently inhibiting Ca2+ current Also produced coronary vasodilation Adenosine (adenocard) antiarrhythmic (naturally occurring nucleoside): Indications - ANSWER-Stable/unstable Narrow complex regular tachycardias Adenosine (adenocard) antiarrhythmic (naturally occurring nucleoside): Dose - ANSWER-(acls) 6 mg RAPID IVP (over 1-2s) followed by a rapid 20 ml NS bolus Repeat x 2 at 12 mg RAPID IVP in 1-2 min (if no conversion) Peds: 0.1 mg/kg Rapid IVP to a max of 6 mg

Hemodynamically stable monomorphic VT Polymorphic VT with a normal QT interval Stable irregular narrow complex tachycardia (AF < 48 hrs) Stable regular Narrow complex tachycardia (unresponsive to adenosine/instances where adenosine is contraindicated) Amiodarone HCL (codarone) class III vw anti-arrhythmic: Dose - ANSWER-Cardiac arrest: 300 mg IVP diluted in 20 ml NS/D5W; repeated at 150 mg in 3-5 min Recurrent life threating ventricular arrhythmias Rapid Infusion: 150 mg/10 min (15 mg/min) q 10 min prn Slow infusion: 360 mg IV over 6 hrs (1 mg/min) Peds: VF/VT pulseless: 5 mg/kg IVP max of 300 mg, repeat twice Ventricular tachyarrhythmias: 5 mg/kg IV over 20-60 min repeated prn max of 15 mg/kg or 2.2 g Amiodarone HCL (codarone) class III vw anti-arrhythmic: Contraindications - ANSWER-Av block, 2/3rd degree without a pacemaker Bradycardia resulting in syncope as it may cause atropine resistant bradycardia Sinus node impairment Cardiogenic shock sensitivity to amiodarone or iodine thyroid disease Other drugs that cause a prolonged QT (procainamide) and stop infusion if QT widens by 50% of baseline or if hypotension results Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen)

Salicylate, antiplatelet, antipyretic, anti-inflammatory: MOA - ANSWER-Anti-platelet: at low doses impedes clotting by inhibiting enzyme CoX-1 and prostaglandin synthesis which prevents formation of platelet aggregating substance Thromboxone A2 (this is irreversible and can prolong bleeding time) All mechanisms are related to inhibition of CoX-1 and prostaglandin acting non specifically on the hypothalamus/platelets/ sites of injury Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen) Salicylate, antiplatelet, antipyretic, anti-inflammatory: Indications - ANSWER-Acute coronary syndromes Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen) Salicylate, antiplatelet, antipyretic, anti-inflammatory: Dose - ANSWER- 160 - 325 mg Po as soon as possible (even if pt states they have taken their own) Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen) Salicylate, antiplatelet, antipyretic, anti-inflammatory: contraindications - ANSWER-HSN to ASA or other NSAIDs Active GI bleeding Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen) Salicylate, antiplatelet, antipyretic, anti-inflammatory: Cautions - ANSWER-Active ulcer disease ashmatics Bleeding disorders Impaired renal/hepatic functions Never given to children/adolescents with viral infections as it may precipitate reye's syndrome Atropine Anticholinergic: MOA - ANSWER-Blocking the effects of acetylcholine (parasympathetic tone) on the SA and AV nodes thereby increasing the SA and AV conduction velocity resulting in increased HR Blocks the actions of parasympathetic nervous system and glands via the Ach receptor blockade producing reduced secretions on bronchial, salivary, and sweat glands

S/S of atropine (anti-cholinergic) overdose: midriasis agitation dry skin fever flushed (blind as a bat, mad as a hatter, dry as a bone, hot as a hare, red as a beet respectively) Tx requires neostigmine CaCl (calcium chloride) Electolyte: MOA - ANSWER-Needed for maintenance of nervous, muscular, skeletal systems and enzyme reactions and normal cardiac contractility as well as blood coagulation Affects secretory activity of the endocrine and exocrine glands Is used as a membrane stabilizing measure in the presence of life threatening hyperkalemia CaCl (calcium chloride) Electolyte: Indications - ANSWER-Hyperkalemia CCB overdose/BB overdose Hypocalcemia Hypermagnesemia CaCl (calcium chloride) Electolyte: Dose - ANSWER- 500 - 1000 mg of 10% solution VERY SIVP (no more than 100 mg/min) prn Peds: 20 mg/kg over 10 min prn

CaCl (calcium chloride) Electolyte: Contraindications - ANSWER-Hypercalcemia digitalis toxicity renal calculi VF (accept in the setting of suspected hyperkalemia) CaCl (calcium chloride) Electolyte: Cautions/notes - ANSWER-Monitor ECG/BP Give slowly and stop if pt c/o discomfort Avoid extravasiation as it can cause necrosis and sloughing of skin (administer in a large bore catheter) Do not administer with NaHCO3 (bicarb) as it will form a precipitate Clopidogrel (Plavix) Platelet aggregation inhibitor: MOA - ANSWER-Inhibits binding of the adenoise Diphosphate (ADP) to its platelet receptor and the subsequent ADP mediated activation of glycoprotein IIb/IIIa complex, thus inhibiting platelet aggregation Clopidogrel (Plavix) Platelet aggregation inhibitor: Indications - ANSWER-STEMI CVA Clopidogrel (Plavix) Platelet aggregation inhibitor: Dose - ANSWER-75 mg PO once daily Clopidogrel (Plavix) Platelet aggregation inhibitor: Contraindications - ANSWER-HSN Active bleeding Significant liver impairment or cholestatic jaundice (due to needing liver activation form is CYP pathway)

hepatitis/hepatic impairment, renal dysfunction/ severe alcoholism history of hereditary angioedema Acetaminophen (Tylenol, paracetamol) Analgesic, Anti-pyretic: Adverse affects - ANSWER-Angioedema disorientation dizziness rash urticarial GI bleeding thrombocytopenia nephrotoxicity hepatotoxicity Dexamethasone (decadron) Glucocorticoid: MOA - ANSWER--Stimulates synthesis of enzymes needed to decrease inflammatory response

• reduces inflammation by suppressing the synthesis of inflammatory mediators, infiltration of phagocytes, release of lysosomal enzymes and proliferation of lymphocytes
• Crosses the placental barrier and promotes fetal lung maturation by increasing the production of surfactant Dexamethasone (decadron) Glucocorticoid: Indications - ANSWER-Anaphylaxis bronchospasm croup Prevention of hyaline membrane disease in premature infants (24-34 wks) Dexamethasone (decadron) Glucocorticoid: Dose - ANSWER-varies

8 - 10 mg IV/IM/PO premature delivery: 5 mg IVP/IMtid 24-48 hrs prior to delivery Peds: 0.6 mg/kg (typically 2-4 mg) IV/IM/PO max of 16 mg/day Dexamethasone (decadron) Glucocorticoid: Contraindications - ANSWER-Systemic fungal infections live viral vaccines hsn to drug or components Magnesium sulfate (MgSO4) mineral/electrolyte: MOA - ANSWER-Replaces magnesium and maintains magnesium levels Interferes with the release of Ach at the myoneural junction Has a tocolytic effect of the vascular smooth muscle system by Suppressing automaticity in depolarized cells having two effects: ◦interferes with calcium uptake in bronchial smooth muscle ◦interferes with acetylcholine release Magnesium sulfate (MgSO4) mineral/electrolyte: Indications - ANSWER-Refractory VF/VT with suspected hypomagnesemia (hx of alcoholism, malnutrition, protracted diarrhea) Life threatening ventricular arrhythmias due to digitalis toxicity Torsades Control of seizures in PIH (eclampsia) Adjunctive therapy in severe bronchospasm Hypomagnesemia

Anti-emetic, antivertigo, antihistamine: MOA - ANSWER-Inhibits nausea and vomiting by centrally depressing sensitivity to the labyrinth apparatus that relays stimuli to the chemoreceptor trigger zone and stimulates the vomiting center of the brain; It also has some mild antagonism of muscarinic acetylcholine receptors in both the central and autonomic nervous system, which inhibits various signal transduction pathways Dimenhydrinate (gravol) Anti-emetic, antivertigo, antihistamine: Indications - ANSWER-Nausea, vomiting, dizziness assoc with motion sickness/vertigo Meniere's disease Dimenhydrinate (gravol) Anti-emetic, antivertigo, antihistamine: Dose - ANSWER-Varies 25 - 50 mg SIVP 50 - 100 mg IM Peds: 1.25 mg/kg IM to a max of 300 mg/day Dimenhydrinate (gravol) Anti-emetic, antivertigo, antihistamine: Contraindications - ANSWER-HSN to drug or benzyl alcohol Any condition made worse by anti-cholinergic effects newborns Diphenhydramine HCl (Benadryl) Anti-histamine, antivertigo, anti-emetic, anti-dyskinetic, sedative): MOA - ANSWER-Antihistamine: competes for H1 receptor sites on smooth muscle of the bronchi, GI tract, uterus, and large vessels; by binding to these cellular receptors, it prevents access of histamine and suppresses histamine induced allergic symptoms (however they do not stop the RELEASE of H1) Centrally acting anti-muscarinic actions of h1 blockade are responsible for the responsible for anti- vertigo/antiemesis

Antidyskinetic: Alleviates extraparmydal symptoms such as akathesia (RLS) as a result of using anti- dompaminergic medications Diphenhydramine HCl (Benadryl) Anti-histamine, antivertigo, anti-emetic, anti-dyskinetic, sedative): Indications - ANSWER-Allergic reaction/anaphylaxis Dyskinesia from anti-psychotic/anti-emetic agents Diphenhydramine HCl (Benadryl) Anti-histamine, antivertigo, anti-emetic, anti-dyskinetic, sedative): Dose - ANSWER- 25 - 50 mg IVP/IM/PO prn peds: 12.5 mg - 25 mg IVP/IM/PO Diphenhydramine HCl (Benadryl) Anti-histamine, antivertigo, anti-emetic, anti-dyskinetic, sedative): Contraindications - ANSWER-HSN Acute asthma attacks breast feeding preterm and neonates as it can induce seizures Dopamine Hcl (inotropin) Adrenergic agonist, vasopressor, sympathomimetic MOA - ANSWER-Immediate precursor to norepi, dopamine stimulates the dopaminergic bet-adrenergic and alpha-adrenergic receptors of the sympathetic nervous system effects are very dose dependent Dopamine Hcl (inotropin)