Download Advanced Pharmacology Study Guide Exam and more Exams Pharmacology in PDF only on Docsity!
Advanced Pharmacology Study Guide Exam
- Explain Pharmacokinetics: The study of how drugs are moved through the body and are encompassed in mechanisms of: Absorptio n Distributi on Metabolis m 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 patholog- ical 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 med- ication between the amount that gives an effect (effective dose) and the amount that gives more adverse effects than desired effects
weakness, fatigue More severe: hypersensitivity, mental depression, hypotension, paradoxical stimula- tion, 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 15-20 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 ²2-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/dro- mo/chronotropic effects anti-arrhythmics: may enhance their effects leading to unwated
tion 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 transmem- brane calcium channels Non specific effects in blood coagulation by inhibiting platelet aggregation in the clotting cascade
- CCB indications: Hypertension, angina, dysrhythmias
- CCB Adverse effects: Peripheral edema, flushing, palpitations, headache Pulmonary edema, rebound tachycardia, bradycardia, skin rash
- CCB drug interactions: BB and other antiarrhythmics can potentiate their effects increased concentrations of theophyliine and digoxin may occur
- Non-depolarizing Neuromuscular Blocker MOA: 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: 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: Hy- pokalemia can enhance effects Hyperkalemia can reduce effects
- Activated Charcoal w sorbitol: Dose: 30-100 g in 250 ml water (5- times the estimated weight of the drug/chemical) PO/NG/OG peds: 1-12 yo: 1 gm/kg
- Activated Charcoal w sorbitol: Contraindications: Pt who has ingested cor- rosive agent or petroleum distillate violent pt with ALOC Altered pt and not intubated with no NG/OG in place
- Activated Charcoal w sorbitol: Caution: Not effective for cyanide, mineral acids, caustic alkaloids, organic solvents, iron, ethanol, methanol, lithium Can cause vomiting and can cause severe ALI if aspirated 38. Adenosine (adenocard) antiarrhythmic (naturally occurring nucleoside): MOA: 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 39. Adenosine (adenocard) antiarrhythmic (naturally occurring nucleoside): Indications: Stable/unstable Narrow complex regular tachycardias 40. 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 41. 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) 42. 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
longs 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 44. 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) 45. 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 ( 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 46. Amiodarone HCL (codarone) class III vw anti-arrhythmic: Contraindications: 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
47. Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen) Salicylate, antiplatelet, antipyretic, anti-inflammatory: MOA: Anti-platelet: at low
-MFI with Ketamine: decreasing bronchial secretions due to the cholinergic effects of ketamine
54. 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. 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)*** 55. Atropine Anticholinergic: contraindications: HSN Glaucoma Tachycardia 56. Atropine Anticholinergic: Notes: Do not delay external pacing in pt with signs of poor perfusion S/S of atropine (anti-cholinergic) overdose: midriasi s agitatio n 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 57. CaCl (calcium chloride) Electolyte: MOA: Needed for maintenance of nervous, muscular, skeletal
Is used as a membrane stabilizing measure in the presence of life threatening hyperkalemia
- CaCl (calcium chloride) Electolyte: Indications: Hyperkalemia CCB overdose/BB overdose Hypocalcemia Hypermagnesemia 59. CaCl (calcium chloride) Electolyte: Dose: 500 - 1000 mg of 10% solution VERY SIVP (no more than 100 mg/min) prn Peds: 20 mg/kg over 10 min prn 60. CaCl (calcium chloride) Electolyte: Contraindications: Hypercalcemia digitalis toxicity renal calculi VF (accept in the setting of suspected hyperkalemia) 61. CaCl (calcium chloride) Electolyte: Cautions/notes: 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 62. 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 63. Clopidogrel (Plavix) Platelet aggregation inhibitor: Indications: STEMI CVA 64. Clopidogrel (Plavix) Platelet aggregation inhibitor: Dose: 75 mg PO once daily 65. 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
