Advanced Pharmacology Exam with Complete Solutions

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 RIGHT ROUTE RIGHT TIME RIGHT DOCUMENTATION Potency - ANSWER-potency is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity (more morphine is needed to give the same effects as fentanyl) Efficacy - ANSWER-Efficacy is the relationship between receptor occupancy and the ability to initiate a response at the molecular, cellular, tissue or system level. In other words, efficacy refers to how well an action is took after the drug is bound to a receptor Affinity - ANSWER-Affinity is how well a drug can bind to a receptor (Fast/strong binding = higher affinity) Benzodiazepine MOA - ANSWER-Act on GABA which is a major inhibitory NTM in the CNS; Effects are produced by interacting with a protein complex with in the neuronal membrane GABA which has a high 'affinity' for benzo's specifically; Inhibition of polysynaptic afferent pathways resulting in skeletal muscle relaxation; It decreases the spread of seizure activity due to an increased pre-synaptic inhibition of the CNS Benzodiazepine uses/indications - ANSWER-Similar actions however different doses/concentrations/combinations produce different actions thus have different uses Anxiety/panic disorders skeletal muscle relaxation seizures sedation for procedures (due to relaxation and amnesic properties) Benzodiazepines adverse effects - ANSWER-Most derived through CNS actions; Ataxia, dizziness, drowsiness/sedation, blurred vision, hypnosis, weakness, fatigue 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 increased concentrations of theophyliine and digoxin may occur Non-depolarizing Neuromuscular Blocker MOA - ANSWER-Prevent Ach from activating Nicotinic 'm' receptors on skeletal muscle, causing relaxation and flaccidity (does not cause depolarization at the neuromuscular endplate) Competes with Ach for biding with Nm receptors, blocking Ach thus preventing stimulation causing the muscle to no longer be engaged and relax; effect lasts until there is insufficient amount available to overtake the Ach (muscles paralyze at different times: Levator muscles of the eyelids first, than limbs, abdomen, and lastly the glottis diaphragm and intercostal) Non-depolarizing Neuromuscular Blocker indications - ANSWER-To facilitate muscular relaxation for general procedures requiring its purose such as to facilitate ETI, Mechanical ventilation, Surgery Non-depolarizing Neuromuscular Blocker Adverse effects - ANSWER-Hypotension: is due to release of histamine from mast cells and partial blockade of Nn receptors in the ANS by suppressing sympathetic tone to peripheral vasculature Myasthenia gravis: condition characterized by an overall decreased number of Nm receptors thus a Nm blocking agent given in this subset could produce a more profound, rapid, and prolonged effect Non-depolarizing Neuromuscular blocking agent drug interactions - ANSWER-Hypokalemia can enhance effects Hyperkalemia can reduce effects Aminoglycoside antibiotics (gentamycin, vancamyacin), tetracycline, non PCN antibiotics: can intensive the response to Nm blockade Cholinesterase inhibitors: Decrease the effectiveness effectively reversing the Nm blockade due to an increased degredation of Ach @ the neuromuscular junction 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 repeated at 0.2 mg/kg Rapid IVP max of 12 mg Adenosine (adenocard) antiarrhythmic (naturally occurring nucleoside): Contraindications - ANSWER-HSN to drug or any component 2/3rd degree block without a pacemaker Sick sinus syndrome Pre-excitation syndromes (AF/Aflutter/VT with accessory pathway like wpw as this may cause hemodynamically unstable ventricular response) Adenosine (adenocard) antiarrhythmic (naturally occurring nucleoside): Caution - ANSWER-caution in asthmatics as it can cause bronchoconstriction caution in those taking carbamazepine (tegretol) or dipyrimdamole (persantine) as it may increase risk of progressive high heart blocks pts who are on stimulants (caffeine) or theophylline may require larger doses as these drugs counter the effects of adenosine Amiodarone HCL (codarone) class III vw anti-arrhythmic: MOA - ANSWER-Amiodarone slows conduction rate and prolongs the refractory period of the SA and AV nodes - and prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability. It has numerous other effects, however, including actions that are similar to those of antiarrhythmic classes Ia, II, and IV. It also inhibits adrenergic stimulation and decreases peripheral vascular resistance- causing some vasodilation Amiodarone HCL (codarone) class III vw anti-arrhythmic: Indications - ANSWER-VF/Pulseless VT unresponsive to CPR and shock therapy 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 Atropine Anticholinergic: Indications - ANSWER--Temporizing measure while awaiting a TCP for pt with symptomatic bradycardia, conduction block, sinus arrest -reversal of neuromuscular blockade prior to admin of anticholinesterases (neostigmine) to -counter their cholinergic effects -Organophosphate poisoning -MFI with Ketamine: decreasing bronchial secretions due to the cholinergic effects of ketamine Atropine Anticholinergic: Dose - ANSWER-Symptomatic Bradycardia: 0.5 mg q 3-5 min prn max of 3 mg total MFI w/ ketamine: 0.01 mg/kg IVP to 0.5 mg once Organophosphate poisioning: 2 mg IVP q 5 prn Peds: 0.2 mg/kg IV max single dose 0.5 mg max total dose 1.0 mg OP poisoning: 0.05 mg/kg IVP prn q 5 min *** Note: smaller doses may precipitate paradoxical bradycardia (0.5mg adult, 0.1mg ped)*** Atropine Anticholinergic: contraindications - ANSWER-HSN Glaucoma Tachycardia Atropine Anticholinergic: Notes - ANSWER-Do not delay external pacing in pt with signs of poor perfusion 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) History of hepatitis/long term ETOH abuse/jaundiced Thrombotic thrombocytopenia Suspected aortic dissection Acetaminophen (Tylenol, paracetamol) Analgesic, Anti-pyretic: MOA - ANSWER-Acts on the hypothalamus to produce antipyresis may work peripherally to pain impulse generation, via inhibition of prostaglandin synthesis in the CNS Selective cyclooxygenase the enzyme needed to make prostalgandins and related compounds in the CNS (limited effects peripherally) Prostaglandins are powerful locally acting vasodilators and inhibit the aggregation of blood platelets as well as found in almost EVERY tissue in the body. Through their role in vasodilation, prostaglandins are also involved in inflammation. They are synthesized in the walls of blood vessels and serve the physiological function of preventing needless clot formation, as well as regulating the contraction of smooth muscle tissue, nervous system transmission etc. Acetaminophen (Tylenol, paracetamol) Analgesic, Anti-pyretic: Indications - ANSWER-Fever Pain relief mild-moderate Acetaminophen (Tylenol, paracetamol) Analgesic, Anti-pyretic: Dose - ANSWER-Varies typically 325- 1000 mg Po q 4 hr prn Peds: 10-20 mg/kg q 6-8 hrs Toxic dose is more than 150 mg/kg or 12 g of acetaminophen Acetaminophen (Tylenol, paracetamol) Analgesic, Anti-pyretic: - ANSWER-HSN 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 Magnesium sulfate (MgSO4) mineral/electrolyte: Dose - ANSWER-Can vary CA/Torsades/Bronchospasm 2 g in 50 ml over 5-10 min In cardiac arrest 2 g in 10 ml SIVP Eclampsia (seizures in pregnancy) loading dose of 4-5 g in 250 ml over 20 min or if no IV obtainable 10 g IM maintenance infusion of 2 g/hr (2g in 1000 ml over 60 min) Peds: for all 25-50 mg/kg IV over 10-30 min For cardiac arrest 25-50 mg/kg in 10 ml SIVP Magnesium sulfate (MgSO4) mineral/electrolyte: Contraindications - ANSWER-Myocardial damaged pts heart blocks coma Pregnant women in actively progressing labor Magnesium sulfate (MgSO4) mineral/electrolyte: Notes - ANSWER-Can cause flushing/sweating and higher doses can cause hypotension or with rapid administration Use caution if pt has renal failure Dimenhydrinate (gravol) 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) Adrenergic agonist, vasopressor, sympathomimetic Indications - ANSWER-~Hemodynamically significant hypotension that is unresponsive to fluids ~cardiogenic shock ~hypotension assoc with bradycardia (chronotropic drugs infusions are recommended as an alternative to pacing in symptomatic unstable bradycardias) ~Maintain cardiac output during a ROSC period Dopamine Hcl (inotropin) Adrenergic agonist, vasopressor, sympathomimetic Dose - ANSWER-5 mcg/kg/min - 20 mcg/kg/min titrated up by 5 until the desired effect 0.5- 3 mcg/kg/min has vasodilation effects in renal/mesentery/coronary/intracerebral vascular beds 5-10 mcg/kg/min has B1 receptor activation 10-20 mcg/kg/min has increased peripheral vasoconstriction (alpha effects) Dopamine Hcl (inotropin) Adrenergic agonist, vasopressor, sympathomimetic Contraindications - ANSWER-Uncorrected tachydysrhythmias VF/VT Pheochromocytoma (can precipitate htn crisis) Allergies to sulfites MAO inhibitors uncorrected hypovolemia (would essentially be useless if you squeeze the tank with no fluid) do no mix with sodium bicarb Droperidol (inapsine) Tranquilizer MOA - ANSWER-Produced marked sedation by directly blocking subcortical receptors; acts a potent D2 (dopamine receptor) antagonist with some histamine and serotonin antagonist activity also blocks CNS receptors at the CTZ producing an anti-emetic effect Droperidol (inapsine) Tranquilizer Indications - ANSWER-Acute psychotic episodes -post operative nausea (hospital) Droperidol (inapsine) Tranquilizer Dose - ANSWER-2.5 mg IM/SIVP repeated at 1.25 mg enoxaparin sodium (lovenox) Low molecular weight heparin MOA - ANSWER-Anticoagulation action: LMWH that accelerates formation of antithrombin III-thrombin complex and deactivates thrombin preventing conversion of fibrinogen to fibrin. enoxaparin sodium (lovenox) Low molecular weight heparin Use - ANSWER-Prevention of DVT and treatment of acute DVT Acute STEMI enoxaparin sodium (lovenox) Low molecular weight heparin Dose - ANSWER-DVT: 1.5mg/kg/day or 1mg/kg twice/day SQ Acute stemi: Acute STEMI when administered with TNK - 30mg IV bolus; then 1mg/kg SQ, maximum dose of 100mg SQ enoxaparin sodium (lovenox) Low molecular weight heparin Contra-indications - ANSWER-Hypersensitivity to heparin or pork products Active major bleeding Acute or sub-acute bacterial endocarditis Heparin or LMWH induced thrombocytopenia Suspected or known intracranial bleeding or spinal epidural hemorrhage IV administration in patients 75 yrs of age ephedrine adrenergic; vasopressor MOA - ANSWER-Ephedrine is both a direct and indirect acting sympathomimetic that stimulates alpha and beta adrenergic receptors. Release of norepinephrine from its storage sites is one of its indirect effects. In therapeutic doses, ephedrine relaxes bronchial smooth muscles and produces cardiac stimulation with increased systolic and diastolic blood pressure when norepinephrine stores aren't depleted. Ephederine Adrenergic, vasopressor Indications - ANSWER-To correct hypotensive states (i.e. sepsis, spinal trauma, head injury, anaphylaxis) Note: Ephedrine can be given as a "bridge drug" (due to it short half life) until an inotropic / vasopressor infusion is started to maintain an adequate BP. Ephederine Adrenergic, vasopressor Dose - ANSWER-Need to ask: What is the likelihood of Ischemic Heart Disease? Low - 10 mg SIVP Moderate - 7.5 mg SIVP High - 5.0 mg SIVP Give every 3-5 minutes until max dose of 50 mg or the desired effect is accomplished; duration of drug is approximately 15 min