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ADVANCED PHARMACOLOGY
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Explain Pharmacokinetics The study of how drugs are moved through the body and are encompassed in mechanisms of: Absorption Distribution Metabolism Excretion Think Kinetic (movement) Pharmacodynamics 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
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?
- 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 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 duration of action of a drug is the length of time that particular drug is effective Explain bioavailability drug's bioavailability can be defined as the proportion of the drug that reaches its site of action 6 rights to medication administration
Anxiety/panic disorders skeletal muscle relaxation seizures sedation for procedures (due to relaxation and amnesic properties) Benzodiazepines adverse effects 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 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 1 5 - 20 min metabolized by the liver and excreted in urine Beta blocker (BB) MOA 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 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 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 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 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
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 To facilitate muscular relaxation for general procedures requiring its purose such as to facilitate ETI, Mechanical ventilation, Surgery Non-depolarizing Neuromuscular Blocker Adverse effects 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 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
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 acts by splitting the bonds of mucoprotein (substance responsible for increased viscosity of mucous secretions in the lungs) Acetylcysteine (mucomyst, pravolex) Mucolytic: Indications Acetaminophen Toxicity Mucolytic action in acute and chronic bronchopulmonary disease; Tracheostomy care Acetylcysteine (mucomyst, pravolex) Mucolytic: Dose Acetaminophen Toxicity: 150 mg/kg IV over 15 min Repeated at 50mg/kg over 4 hours Acetylcysteine (mucomyst, pravolex) Mucolytic: Contraindications HSN to drug Status asthmaticus as it may precipitate bronchospasm Activated Charcoal w sorbitol: MOA
Adenosine (adenocard) antiarrhythmic (naturally occurring nucleoside): Dose (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 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 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 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 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 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
Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen) Salicylate, antiplatelet, antipyretic, anti-inflammatory: Cautions 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 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
- 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 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 HSN Glaucoma Tachycardia Atropine Anticholinergic: Notes 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
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 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 STEMI CVA Clopidogrel (Plavix) Platelet aggregation inhibitor: Dose 75 mg PO once daily Clopidogrel (Plavix) Platelet aggregation inhibitor: Contraindications 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 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 Fever Pain relief mild-moderate Acetaminophen (Tylenol, paracetamol) Analgesic, Anti-pyretic: Dose 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:
Dexamethasone (decadron) Glucocorticoid: Dose 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 Systemic fungal infections live viral vaccines hsn to drug or components Magnesium sulfate (MgSO4) mineral/electrolyte: MOA 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 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 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 Myocardial damaged pts heart blocks coma Pregnant women in actively progressing labor Magnesium sulfate (MgSO4) mineral/electrolyte: Notes
