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78 Cards in this Set
- Front
- Back
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Alpha 1 action |
Peripheral vasoconstriction. Mild bronchoconstriction. |
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Alpha 2 action |
Inhibit the release of norepinephrine. (Antagonistic to alpha 1. Over time, peripheral vasodilation.) |
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Beta 1 action |
Increase in cardiac rate, cardiac force and cardiac automaticity and conduction. |
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Beta 2 action |
Vasodilation. Bronchodilation. |
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Beta 3 action |
Stimulate lipolysis and thermogenesis in skeletal muscle. |
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Dopaminergic receptor action |
Dilation of renal, coronary and cerebral arteries. |
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Positive chronotropic effect |
Increase in heart rate |
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Positive inotropic effect |
Increase in cardiac force |
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Positive dromotropic effect |
Increase in rate of cardiac impulse conduction through the AV node |
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What medication can be used in management of beta-blocker OD? Why? |
Glucagon It activates adenyl cyclase which has chronotropic and inotropic effects. It bypasses the beta receptors in the activation of the cAMP pathway. |
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T/F Patients with bronchospastic disease (asthma, COPD) should receive beta-blockers if needed. |
FALSE! Patients with bronchospastic disease should not receive beta-blockers unless OLMC deems that the benefits outweigh the risks. |
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5 classes of antiarrhythmics in the Vaughan-Williams system |
Class I: Sodium channel blockers Class II: Beta-blockers Class III: Potassium channel blockers Class IV: Calcium channel blockers Class V: Miscellaneous |
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Class IA antiarrhythmics |
Sodium Channel Blockers Quinidine Procainamide Disopyramide |
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Class IB antiarrhythmics |
Sodium channel Blockers Lidocaine Phenytoin Mexiletine |
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Class IC antiarrhythmics |
Sodium channel Blockers Flecainide Propafenone Moricizine |
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Class II antiarrhythmics |
Beta-blockers Propranolol Acebutolol Esmolol Metoprolol |
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Class III antiarrhythmics |
Potassium channel blockers Bretylium Amiodarone |
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Class IV antiarrhythmics |
Calcium channel blockers Verapamil diltiazem |
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Class V antiarrhythmics |
Miscellaneous Adenosine Digoxin |
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Class IA ECG effects |
Widened QRS, prolonged QT |
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Class IB ECG effects |
Widened QRS, prolonged QT |
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Class IC ECG effects |
Prolonged PR, widened QRS |
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Class II ECG effects |
Prolonged PR, bradycardias |
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Class III ECG effects |
Prolonged QT |
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Class IV ECG effects |
Prolonged PR, bradycardias |
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Class V ECG effects |
Prolonged PR, bradycardias |
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Location and effects of H1 receptor |
Histamine 1. Located in smooth muscle and endothelial cells. Major effect is acute allergic reactions. |
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Location and effects of H2 receptor |
Histamine 2. Located in gastric parietal cells. Major effect is increase in secretion of gastric acid. |
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Location and effects of H3 receptor |
Histamine 3. Located in CNS. Major effect is modulation of neurotransmission. |
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Location and effects of H4 receptor. |
Histamine 4. Located in mast cells, eosinophils and T cells. Major effect is regulating immune response. |
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Pancreatic alpha cells release.... which does what? |
glucagon which causes stored carbohydrates, especially glycogen, to be broken down into glucose. |
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Pancreatic beta cells release.... which does what? |
insulin which is required for the passage of glucose into the cells |
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Pancreatic delta cells release.... which does what? |
somatostatin which inhibits the secretion of insulin, glucagon and growth hormone. |
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What 9 classes of drugs have narrow-angle glaucoma as a contraindication? |
Topical anticholinergic Sympathomimetic dilating drops Tricyclic antidepressants Monoamine oxidase inhibitors Antihistamines Antiparkinsonians Antipsychotics Antispasmolytics Sulfa containing medications |
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narcotic/opiate toxidrome |
classic triad: decreased LOC, resp depression, constricted pupils (Note: Demerol and Talwin or pentazocine, may not cause pupil constriction) |
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anticholinergic toxidrome |
Note: commonly seen with antihistamine and TCA overdoses hot as Hell, blind as a bat, dry as a bone, red as a beet, mad as a Hatter pupils will likely be fixed and dilated |
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cholinergic toxidrome |
Note: seen with organophosphate pesticide poisoning SLUDGEM - salivation, lacrimation, urination, defecation, gastrointestinal upset, emesis, miosis (constricted pupils) |
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sympathomimetic syndrome d/t alpha-adrenergic agents |
(e.g. phenylephrine, methoxamine, phenylpropanolamine) hypertension and reflex bradycardia secondary to vasoconstriction of resistance vessels
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sympathomimetic syndrome d/t beta-adrenergic agents |
(theophylline, cafffeine, metaproteronol) tachycardia with or without hypotension (secondary to excessive stimulation of sinus node or vascular smooth muscle dilation) |
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serotonin syndrome |
(SSRI's - Prozac, Zoloft, Celexa citalopram, Lexapro, Paxil, SNRI's - Cymbalta, Effexor, Triptan class of migraine meds - Imitrex, Maxalt) Agitation or restlessness, diarrhea, tachycardia, diaphoresis, hallucinations, confusion, hyperthermia, ataxia, N/V, hyperreflexia, hyper or hypotension. |
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Neuroleptic mailgnant syndrome |
antipsychotic agents (haloperidol), antiemetic medications (prochlorperazine), antiparkinsonian medications. Hyperthermia, muscle rigidity, mental status change, tachycardia, hypertension or hypotension, diaphoresis, tremor, incontinence, tachypnea, metabolic acidosis. |
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Acetaminophen overdose route of exposure |
oral
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Acetaminophen overdose mechanism of toxicity |
90% of acetaminophen is metabolized into nontoxic compounds that are excreted in urine. However this process forms a toxic by-product which normally binds to hepatic glutathione and is excreted in urine. In a massive overdose, the liver's stores of glutathione are depleted and hepatotoxicity occurs. |
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Acetaminophen toxic dose |
7.5 g or 140 mg/kg chronic alcoholics are at a higher risk |
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Acetaminophen OD S/S |
Anorexia, N/V, malaise, pallor, diaphoresis |
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Acetaminophen OD management |
supportive care. Airway support. Determine time of ingestion as accurately as possible. |
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common anticholinergic ODs |
TCA's, dimenhydrinate, diphenhydramine, shrooms |
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anticholinergic OD mechanism of toxicity |
cholinergic blockade occurs both centrally and peripherally and involves muscarinic and nicotinic receptors. Different agents have different degrees of effect on the 2 types of receptors |
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anticholinergic OD management |
Supportive care. Monitor airway, breathing and circulation supplemented with IV access and cardiac monitoring. Treat seizures and arrhythmias as usual except avoid using Class 1a antiarrhythmics. |
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common neuroleptic OD's |
antipsychotics and some tranquilizers. Haloperidol, droperidol |
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neuroleptic OD mechanism of toxicity |
act by blocking neurotransmission involving dopaminergic, adrenergic, muscarinic, and histaminic receptors. Effects vary from agent to agent depending on the degree of blockage of each type of receptor |
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neuroleptic OD S/S |
Dystonic reaction: involuntary muscle spasm. Tx is dyphenhydramine or benztropine Akathisia: restlessness, insomnia. Tx is benztropine, amantadine, propranolol Psudoparkinsonsim: resting tremor, rigidity, masked face. Tx is benztropine, diphenydramine, amantadine. Tardive dyskinesia: lip smacking, tongue protrusion, grimacing and chewing motion Neuroleptic malignant hyperthermia: hyperthermia, rigidity, ALOC, autonomic instability Various: CNS depression, resp depression, pinpoint pupils, anticholinergic symptoms, arrhythmias, PR and QT prolongation. |
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neuroleptic OD management |
ABCs, cardiac monitoring, naloxone, BGL if ALOC. N/S bolus if hypotensive. Treat seizures and arrhythmias per protocol. |
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Beta-blocker OD mechanism of toxicity |
BB cause blockage of B1 and B2 receptors which affects several organ systems but most notably the cardiovascular and repiratory systems. |
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Beta blocker OD S/S |
Bradycardia, AV block, hypotension. ALOC (confusion, seizure, coma). Bronchospasm, CHF. Can mask the signs of hypoglycemia and impair recovery from it. |
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Beta blocker OD management |
Airway management, atropine or catecholamines, glucagon. Glucagon augments HR, AV conduction and myocardial contractility. TCP, fluids, treat seizures and bronchospasm as per protocol. |
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Calcium channel blocker OD Mechanism of toxicity |
any cell that uses calcium can be affected but especially, myocardium, SA and AV nodes and AV nodal conduction pathway. |
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CCB OD S/S |
Hypotension, bradycardia, AV conduction blocks, lethargy, slurred speech, N/V, coma and resp depression |
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Carbon monoxide poisoning Mechanism of toxicity |
CO binds hemoglobin which reduces the availability of hemoglobin to oxygen inducing hypoxemia. It also binds to cardiac and skeletal myoglobin which decreases contractility. In the CNS, CO induces cerebral edema and necrosis of white matter.
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Carbon monoxide poisoning S/S |
<10%: asymptomatic 10-20%: headache and dyspnea 20-30%: headache, fatigue, visual disturbances 40-50%: tachycardia, ALOC, may precipitate angina >60%: coma, seizures and cherry red skin |
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Carbon monoxide poisoning management |
O2 via NRB @ 100% |
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Cyanide poisoning mechanism of toxicity |
cyanide binds a key cellular enzyme causing cellular asphyxia thus affecting all organ systems. |
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cyanide poisoning S/S |
unconscious, noncyanosed patients with hypotension and bradycardia - death occurs in seconds to minutes. less severe - headache, dyspnea, confusion or seizures with hypotension. Pt may have bitter almond odour about them |
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Affinity |
The attraction between a drug and a receptor |
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Allosteric site |
A binding site for substrates not active in initiating a response; a substrate that binds to an allosteric site may induce a conformational change in the structure of the active site, rendering it more or less susceptible to response from substrate. |
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Bioavailability |
The fraction or percentage of a drug that reaches the systemic circulation |
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Biotransformation |
Metabolism or degradation of a drug from an active form to an inactive form |
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Chirality |
Special configuration or shape of a drug; most drugs exist in 2 shapes |
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Clearance |
Removal of a drug from the body |
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Downregulation |
Decreased availability of drug receptors |
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First-pass effect |
The phenomenon by which a drug first passes through the liver for degradation before distribution to the tissues |
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Half-life |
The time required for half of a total drug amount to be eliminated from the body |
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Pharmacodynamics |
Processes through which drugs affect the body |
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Pharmacokinetics |
Processes through which the body affects drugs |
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Receptor |
The site of drug action |
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Second messenger |
A chemical produced intracellularly in response to a receptor signal; this second messenger initiates a change in the intracellular response |
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Therapeutic window |
The range of drug concentration in the blood between a minimally effective level and a toxic level. |
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Threshold |
The level below which a drug exerts little to no therapeutic effect and above which a drug produces a therapeutic effect at the site of action |
