By Fatskills Exam Guides Team — the exam nerds behind 28,500+ quizzes and 2.1M practice questions across 500+ global exams.
GENERAL PRINCIPLES Question: What are the two mechanisms of drug metabolism and breakdown? Hepatic and renal. Question: Which enzyme is mostly responsible for drug breakdown in the liver? Cytochrome P-450. Question: What are the three methods of drug excretion from the kidneys? Glomerular filtration, proximal renal secretion, and distal tubule reabsorbtion. AUTONOMIC NERVOUS SYSTEM Question: Which transmitter is released at all preganglionic and postganglionic receptors? Acetylcholine. This interaction of acetylcholine with pre- and postganglionic receptors gives the “flight or fight” responses. Question: What are the two receptors of acetylcholine? Muscarinic and nicotinic. Question: What effect does the sympathetic nervous system have on the cardiovascular system? Increases heart rate and contractility. Parasympathetic system would then reverse this and decrease heart rate. Question: Which organs have both sympathetic and parasympathetic innervation? Heart, eyes, bronchial smooth muscle, and GI and GU smooth muscle. What are some of the main activities of β1-, β2-, and α-receptors? ββα-Contraction and constriction, mostly vasoconstriction Question: What effect does the activation of presynaptic α2-receptors cause? It facilitates the release of norepinephrine. Question: What are some common anticholinergics side effects? Dry eyes, dry mouth, blurred vision, constipation, and urinary retention. Question: What are some uses of muscarinic antagonists? They can be used for problems with urinary frequency, urgency, as well as incontinence. Question: Name the mechanism of action for neuromuscular blockers: They act as competitive blockers at the nicotinic receptors to cause muscle relaxation. Question: What is the mechanism of action for succinylcholine? It is a depolarizing neuromuscular blocker. Question: What is the one potentially fatal side effect of succinylcholine? It can cause malignant hyperthermia. Question: What are the two substances that can activate both α - and β-receptors? Epinephrine and norepinephrine. However, norepinephrine has less of an effect on β2-receptors, making it less effective on actions of bronchospasm like that of epinephrine. Question: What is the main effect of dopamine? It causes renal and coronary vasodilation as well as activates the β1-receptors of the heart at low doses. Question: Name the two major actions that norepinephrine plays on the cardiovascular system: It causes an increase in total peripheral resistance and increases mean arterial pressure. α -agonists have what type of effect on the cardiovascular system? They act by reducing the sympathetic nerve activity, thus lowering blood pressure. Question: What are the major side effects of α-agonists? As you could imagine, postural hypotension and reflex tachycardia. Question: Why should you worry about giving a β-blocker to a diabetic patient? They can stimulate the sympathetic activity of glycogenolysis, gluconeogenesis, as well as lipolysis. What are some other side effects of β-blockers? Bronchoconstriction and decreased heart rate. Question: What is the clinical presentation of anticholinergic poisoning? Mydriasis, tachycardia, hypoactive bowel sounds, urinary retention, dry axilla, hyperthermia, and mental status changes. Remember: Dry as a bone Red as a beet Mad as a hatter Hot as Hades Blind as a bat Question: Name a few substances that have anticholinergic properties: Antihistamines, cyclic antidepressants, phenothiazine, atropine, and, jimson weed. Question: What ECG abnormality is most common in patients who suffer from anticholinergic toxicity? Sinus tachycardia. Other dangerous arrhythmias include conduction problems and V-Tach. Question: What are the common anticholinergic compounds? Atropine, tricyclic antidepressants, antihistamines, phenothiazine, antiparkinsonian drugs, belladonna alkaloids, and some Solanaceae plants (i.e., deadly nightshade and jimson weed). CARDIOVASCULAR SYSTEM Question: What are the three groups of diuretics? Thiazide, loop, and potassium-sparing diuretics. Question: How do the thiazide diuretics function? They limit the sodium and chloride reabsorption in the ascending loop. This in turn increases the urine production. Question: What drug is the treatment of choice in hypertension? Thiazide diuretics. Question: What is a main side effect of thiazide diuretics? Hypokalemia. Question: How does the potassium sparing diuretics function? They act as an antagonist of aldosterone, which will lead to sodium retention. The use of ACE inhibitors functions to lower blood pressure by what mechanism? They convert angiotensin I to angiotensin II, which acts as an aldosterone antagonist, which in turn lowers pressure by retaining sodium. Question: Unlike β-blockers, what advantage does ACE inhibitors have for the treatment of hypertension? They are ideal for diabetics because they do not affect gluconeogenesis. Question: Name some major side effects of ACE inhibitors: Headache, dizziness, abdominal pain, confusion, renal failure, and erectile dysfunction. Question: What is one of the most common side effects of ACE inhibitors? Cough. Question: Do angiotensin II receptor antagonists cause cough? No. Question: What is the main physiological effect by calcium channel blockers? They reduce cardiac afterload by blocking calcium entrance into cells. Question: Name some of the most common side effects of calcium channel blockers: Headaches, dizziness, hypotension. Anything that you can imagine with the action of vasodilation can occur in calcium channel blockers. Question: What action do nitrates have on blood vessels and the cardiac cycle? They vasodilate, which in turn causes a reduction in cardiac preload. At higher concentrations, nitrates will decrease afterload also. Question: What drug is the treatment of choice for relieving coronary vasospasm? Nitroglycerine. Question: What forms of nitrates can be given? Oral, intravenous, sublingual, and transdermal. Question: Which nitrate when metabolized turns into cyanide? Sodium nitroprusside. Question: What are the two main side effects of nitrates? Headache and hypotension. Another possible side effect is postural hypotension. Question: What is the main goal in the treatment of coronary artery disease? Reduction of myocardial oxygen demand. What are the three pharmacologic principles in the treatment of heart failure? Decreasing the cardiac workload, controlling excess fluid, and enhancement of myocardial contractility. Question: What are the main effects of ACE inhibitors with regard to heart failure? They reduce cardiac workload. This will slow the progression of heart failure, which in turn prolongs survival. Question: What class of drugs is used as a mainstay in controlling the excess fluid accumulation in heart failure? Diuretics. Question: How do the cardiac glycosides (digoxin and digitoxin) function to improve myocardial contractility? They inhibit the Na+-K+-ATPase pump, which improves contractility. Question: A 77-year-old male patient with a history of heart failure has been taking both furosemide and digoxin for several months. Over the past 3 weeks, he has noticed having nausea, fatigue, drowsiness, and blurred vision. What could be the possible problem in this patient? Digoxin toxicity. Question: What effect, if any, do diuretics play on the role of digoxin? If a patient on diuretics is not closely monitored for hypokalemia, lower serum potassium levels can have higher than normal therapeutic levels of digoxin, thus leading to possible toxicity. Question: What are some of the common side effects resulting from digoxin toxicity? Arrhythmias, anorexia, nauseam diarrhea, drowsiness, fatigue, and visual disturbances (including a yellow visual appearance). Question: What is the mechanism of dobutamine in the use of heart failure? It increases cardiac output and can be used in cardiac shock. Question: Name three nonpharmacologic treatments for arrhythmias: Pacemakers, implantable defibrillators, and ablation therapy. Figure 18-1 (Cardiac action potential. Note the first action potential shows the class of antiarrhythmics and where they have action. Note the second action potential and what electrolyte plays a major role in that part of the action potential. (Reproduced, with permission, from Stringer JL. Basic Concepts in Pharmacology. 3rd ed. New York, NY: McGraw-Hill; 2006: Fig 13-1.)) What is the role of class I antiarrhythmic drugs? They are sodium channel blockers. Question: Class IA drugs such as procainamide and quinidine are useful in what type of arrhythmias? Both atrial and ventricular arrhythmias. Question: Lidocaine is an IB antiarrhythmic. What type of arrhythmias does this drug work best? Treatment of ventricular arrhythmias such as ventricular tachycardia, ventricular fibrillation, and ventricular ectopy. Question: Are drugs like lidocaine effective in the treatment of supraventricular tachycardia? No, they have almost no effect on this type of arrhythmia. Question: What is the mechanism by the class IC medications? They are used to suppress ventricular arrhythmias. Question: What effects do β-blockers have on the sinoatrial (SA) and atrioventricular (AV) nodes? They slow the conduction at these sites, thus slowing the refractory period. β -blockers are useful in the treatment of which arrhythmias? They are useful in tachyarrhythmias as they can slow transmission. Question: Amiodarone is a potassium channel blocker. Describe how this drug functions as an antiarrhythmic: It acts by slowing the repolarization of the action potential without impairing the resting potential prior to depolarization. Question: Are calcium channel blockers more effective toward atrial or ventricular arrhythmias? Atrial. They slow the conduction at the AV node, which increases the refractory period. Question: What drug is the treatment of choice for paroxysmal supraventricular tachycardia? Adenosine. Question: Does adenosine have a long half-life? No, in fact, it is only seconds long, which is why it is favorable in converting SVT. Question: What are three drugs that will increase heart rate? Atropine, epinephrine, and isoproterenol. Question: What is the first-line pharmacologic treatment of hypercholesterolemia? HMG-CoA reductase inhibitors. These are referred to as the “statins.” What is the effect of statins with respect to cholesterol? It lowers serum LDL and plasma cholesterol. Question: What does niacin do for overall cholesterol levels? It lowers both overall cholesterol as well as triglycerides. Question: What are the two side effects of niacin? Flushing of the skin and liver toxicity. Question: If you have a patient who gets the typical flushing of the skin with the taking of niacin, what can you instruct the patient to do to help reduce this side effect? Usually, taking the medication with an 81 mg aspirin will help as well as instructing the patient to take the medication at night. Question: Gemfibrozil, fenofibrate, and clofibrate, the so-called “fibrates,” act to lower what to lipid values? They can lower triglycerides and HDL. Question: Hemostasis consists of what three phases? Vascular (from tissue injury), platelet, and coagulation phases. Question: What is the main synthesis component, which causes the formation of coagulation? Thromboxane A2. Question: What is the action of nonsteroidal anti-inflammatory drugs? They inhibit prostaglandins, which inhibit platelet aggregation and prolong bleeding time. Question: How do drugs like ticlopidine and clopidogrel work as “blood thinners”? They inactivate the platelet adenosine diphosphate receptors, which in turn inhibit platelet aggregation. Question: Which receptors are critical for the formation of platelet aggregation? Glycoprotein IIb/IIIa receptors. They prevent platelet aggregation by blocking fibrinogen and von Willebrand factors. Question: What is the main side effect of all platelet inhibitors? They all can cause bleeding. That is also the main side effect of anticoagulants. Question: Does heparin interact with the intrinsic or extrinsic coagulation pathway? Actually, both. It binds to antithrombin III and inactivates IIa, IXa, Xa, XIa, XIIa, XIII, and III. Question: What anticoagulant has a longer half-life: heparin or low-molecular-weight heparin (LMWH)? Low-molecular-weight heparin. Which types of patients should avoid the use of LMWH? Those with renal impairment or those with bleeding abnormalities. Question: What is the antidote to heparin? Protamine sulfate. Question: What is the mechanism of action of warfarin? It is an antagonist of vitamin K. Question: If administration of vitamin K is the antidote for warfarin overdose, how long does it take for the anticoagulant properties to take effect? At a minimum, 24 hours. Additional measures such as fresh frozen plasma and platelet transfusions can be given if emergency measures are required. Question: What is the mechanism of action on thrombolytic agents? They act as plasminogen activators to lyse clots that have already formed. The plasminogen will convert to plasmin, which then causes the degradation of fibrin. Question: What is the main side effect of thrombolytic agents? Bleeding, naturally. Question: What can be a serious life-threatening side effect from streptokinase? An allergic-anaphylactic reaction. This is usually because streptokinase is created from a bacterial origin. Question: Which drugs cause methemoglobinemia? Oxidant drugs, such as antimalarials, dapsone, nitrites/nitrates (nitroprusside), and local anesthetics (lidocaine). Methemoglobinemia occurs when the iron moiety of hemoglobin is oxidated from the ferrous to the ferric state. Question: Which common enzyme deficiency predisposes to the development of methemoglobinemia in the presence of the above drugs? G6PD deficiency. Question: What drugs can induce a chronic cough? ACE inhibitors cause chronic cough as a result of the accumulation of prostaglandins, kinins, or substances that excite the cough receptors. (Remember that ACE sitting next to you at the boards!!). β-Blockers evoke bronchoconstriction, and thus coughing, by blocking β-2 receptors. Never give β-blockers to asthmatic patients or other patients with an airway disease. Question: What is the incidence of cough induced by captopril? 1% to 2%. What is the incidence of enalapril-induced cough? 24.7%. Question: True/False: Generally, the cough related to ACE inhibitors resolves within a few days of withdrawal of the drug: False. The resolution of cough may be slow, taking several weeks. Question: How does treatment for a cocaine-induced MI differ from a typical MI? Both are treated the same except that β-blockers are not used for a cocaine-induced MI secondary to potential unopposed α-adrenergic activity. The tachycardia of a cocaine-associated MI is first treated with benzodiazepine sedation. Question: A patient has an arterial pH of 7.5 through alkalization, but her urine pH is still low. What electrolyte is probably responsible? Potassium. When reabsorbing sodium, the renal tubules will preferentially excrete hydrogen ions into the tubular lumen rather than potassium ions. Thus, potassium should be maintained at 4.0 mmol/L. Question: What are the absolute indications for Digibind administration in digoxin poisoning? Ventricular arrhythmias, hemodynamically significant bradyarrhythmias that are unresponsive to standard therapy, and a potassium level greater than 5.0 mEq/L. Question: A patient on Digoxin is bradycardic and hypotensive with significantly peaked T waves. What is the initial line of treatment? Administer 10 vials of Digibind intravenously while simultaneously treating the presumed hyperkalemia with insulin and glucose, sodium bicarbonate, and Kayexalate. After the Digibind is administered, hyperkalemic-induced arrhythmias may safely be treated with calcium chloride. Question: What is the antidote for β-blocker poisoning? Glucagon. Glucagon receptors, located on myocardial cells, are G protein coupled receptors that activate adenylate cyclase, leading to increased levels of intracellular cAMP. Thus, glucagon administration causes the same intracellular effect as β-agonist. Question: What are potential treatment modalities for a calcium channel blocker poisoning? Therapeutic interventions include IV calcium, isoproterenol, glucagon, transvenous pacer, atropine, and vasopressors, such as norepinephrine, epinephrine, or dopamine. Question: What is the mechanism and treatment for clonidine-induced hypotension? Treatment: Includes IV fluid administration and dopamine. Mechanism: Decreased cardiac output secondary to a decreased sympathetic outflow from the CNS. Question: What typical eye response is related to clonidine poisoning? Pinpoint pupils. Clonidine is a centrally acting presynaptic α-2 adrenergic agonist that decreases the central sympathetic outflow. Although its primary use is to treat hypertension, clonidine has additional emergency value in blunting withdrawal symptoms from opiates and ethanol. A clonidine overdose closely resembles an overdose with which other class of drugs? Opiates. Question: Toxicity from clonidine (Catapres) usually occurs within what time period? Within 4 hours. Question: Which agent is a useful “antidote” for clonidine overdose? Naloxone (Narcan) Question: True/False: A patient with acute digitalis OD presents with frequent multifocal PVCs, peaked T waves, and a K+ of 6.2 mEq/L. The correct treatment is to first administer CaCl2, as this is the fastest-acting agent for reducing hyperkalemia: False! Although CaCl2 is the fastest-acting agent for decreasing hyperkalemia, don’t give any more Ca+ to a patient with digitalis-induced cardiac toxicity. β -Adrenergic antagonists have three main effects on the heart. Name these effects: 1. Negative chronotropy 2. Negative inotropy 3. Decrease AV nodal conduction velocity (negative dromotropy) Question: True/False: β-adrenergic antagonists can cause mental status changes and seizures: True. Question: A cocaine addict presents with chest pain but his ECG is normal. What are the odds that he will have abnormal CPK and CPK-MB isoenzymes? 6%–19%. Question: What is the most common arrhythmia induced by chronic, heavy ethanol bingeing ? Atrial fibrillation. Question: What is the antidote for nitrites? Methylene blue 1%, 0.2 mL/kg IV over 5 minutes. Severe methemoglobinemia requires an exchange transfusion. Question: What are the effects of dopamine at various doses? 1–10 mg/kg: Renal, mesenteric, coronary, and cerebral vasodilation 10–20 mg/kg: Both α- and β-adrenergic 20 mg/kg: Primarily α-adrenergic Methylene blue is used to treat: Methemoglobinemia. Question: What are the signs and symptoms of isopropanol poisoning? Sweet breath odor (acetone), hypotension, hemorrhagic gastritis, and CNS depression from isopropanol and from its metabolite, acetone. CENTRAL NERVOUS SYSTEM Question: What is the main pharmacologic goal in the treatment of Alzheimer disease? It is to maintain or elevate the level of acetylcholine by preventing the breakdown of acetylcholine. Question: Define the following terms: Tolerance, cross-tolerance, and dependence: Tolerance is the state by which there is a reduced drug effect with repeated use of the medication. This will necessitate the requirement for more of a medication to produce the same desired result. Cross-tolerance refers to a patient who is tolerant to one drug will also be tolerant to drugs that are in the same class. Dependence is signs and symptoms of withdrawal when drug levels fall. Question: Name the type of medication to use for the following specific seizures: generalized convulsive, partial (simple, complex, secondary), and generalized nonconvulsive: Question: How are all these antiepileptic medications metabolized? Hepatic. Question: What are two major conditions that can be seen with the use of carbamazepine? Granulocyte suppression and apastic anemia. Question: Name some common side effects of phenytoin: Hirsutism, coarse facial features, and gingival hyperplasia. With higher doses, it can cause ataxia and nystagmus. Are antipsychotic and neuroleptic drugs considered to be medications that can cure these diseases? No. They are not curative; they only allow the patient to function in a more normal state. Question: What is the mechanism of neuroleptics? They are α-blockers, muscarinic, and histamine antagonists. Question: What is a common side effect with most antipsychotic drugs? Extrapyramidal side effects (EPS). Question: Name the more common EPSs and give some examples of each: Dystonia—spasms of the face, neck, tongue, and back Parkinsonism—rigidity, shuffling gait, and tremor Akathisia—motor restlessness Tardive dyskinesia—lip smacking, jaw movements, darting of the tongue, and quick involuntary movements Question: What is neuroleptic malignant syndrome? It is a rare syndrome that is potentially fatal as a result of the use of neuroleptic medications. It becomes more common as the doses of medications increase. Question: What are some of the signs of neuroleptic malignant syndrome? These will present with severe forms of parkinsonism, catatonia, autonomic instability, and in some cases stupor. Question: What is the mortality rate for a patient with neuroleptic malignant syndrome? About 10% to 20%. Question: What are the three targets for the pharmacologic treatment of Parkinson disease? Dopamine replacement therapy, dopamine agonist therapy, and anticholinergic therapy. Question: Which dopamine crosses the blood brain barrier (BBB)? Levodopa. Question: Carbidopa does not cross the BBB. How does this drug function? It reduces the peripheral metabolism of l-dopa in the bloodstream, which in turn will increase the amount of dopamine going to the brain. Question: Anticholinergics therapy reduces the effectiveness of uninhibited cholinergic neurons. Describe some of the side effects that these drugs commonly have: They are all the muscarinic side effects that you should be familiar with; dry mouth, confusion, constipation, and urinary retention. The two main anxiolytic and hypnotic drug classes are barbiturates and benzodiazepines. What are the main side effects of these two classes of drugs? Sedation and most induce sleep or hypnosis. At higher doses, they can induce medullary depression and death. Question: What is the mechanism of action of barbiturates? They enhance the function of γ-aminobutyric acid (GABA) in the CNS. Question: What are some potential side effects of barbiturates if not taken appropriately? Sedation, hypnosis, coma, suppression of respiration, and death. Question: A 42-year-old male patient who has been on phenobarbital for the last several years arrives to the emergency department with nausea, vomiting, hypotension, and acute psychosis. By history, you have been told that he has not been taking his phenobarbital that he is normally prescribed. What is the probable diagnosis? Withdrawal symptoms secondary to barbiturate use. Other signs and symptoms include seizures and cardiovascular collapse, which can lead to death. Question: What is the mechanism of action of benzodiazepines? They block a specific site associated with GABAA receptors which increases inhibition. Question: A 23-year-old female patient presents to the emergency department with a suspected benzodiazepine overdose. She has shallow respirations, is hypoxic, and also has confusion, agitation, and restlessness. What is the antidote that could be given in this scenario? Flumazenil. Question: Name one benzodiazepine does not produce dependence: Buspirone. Question: What is the common mechanism of action of antidepressants and lithium? They all act by increasing the concentration of norepinephrine and serotonin. Question: What are some indications for prescribing serotonin-selective reuptake inhibitors (SSRI)? Depression, eating disorders, panic disorders, obsessive–compulsive, and borderline personality disorders. Question: What is the usual onset of improvement of symptoms after starting tricyclic antidepressants? It usually takes 2–3 weeks for patients to have a noticeable difference. Question: How do heterocyclics work as antidepressants? They are potent muscarinic cholinergic antagonists, and have weak α1 and H1 antagonist properties. Question: What is the mechanism of action of monoamine oxidase inhibitors? They increase levels of norepinephrine, serotonin, and dopamine by preventing the degradation of these products. What is the one major complication in taking an MAO inhibitor? They can cause a fatal hypertensive crisis. Question: What are some foods that patients on MAO inhibitors should avoid? Cheeses, beer, and red wines. Any foods that have higher levels of tyramine or other active amines should be avoided. Question: What are the three most common drugs that are used in the treatment of bipolar disease? Lithium, carbamazepine, and valproate. Question: What is the major receptor for the mediation of pain? μ(mu)-Receptors. The other receptors that have less activity are kappa(κ) and delta(δ). Question: What are the three main types of narcotics? Give some examples of each: 1. Agonists—codeine, fentanyl, heroin, morphine, methadone, meperidine 2. Mixed agonist–antagonist—pentazocine, buprenorphine, nalbuphine 3. Antagonists—naloxone, naltrexone, and nalmefene Question: Name some signs and symptoms from narcotic withdraw: Hyperactivity, nausea, vomiting, chills, fever, tearing, runny nose, tremor, abdominal pain, and cramps. Question: What are the main effects of morphine? Analgesia, respiratory depression, spasm of the smooth muscle of the GI and GU tracts, and pinpoint pupils. Question: What is the potency of fentanyl when compared to morphine? It is 80 times more potent but has a much shorter half-life. Question: What is the indication for the use of methadone? It is used for narcotic withdraw and dependence. It acts by reducing the craving for narcotics. Question: What is the drug of choice to reverse a narcotic overdose? Naloxone. Question: What factors influence the elimination of inhaled anesthetics? The rate of ventilation, blood flow, and the solubility of the gas itself. Question: What is the mechanism of action for local anesthetics? They block nerve conduction by the local application of the drug. They do this by blocking the sodium channel of the nerve membrane. Question: Why should not the 600 mg/day of thioridazine (Mellaril) be exceeded? Exceeding this dosage causes retinitis pigmentosa. Thioridazine is a piperidine phenothiazine with low frequency extrapyramidal effects. Why is haloperidol one of the preferred neuroleptics? It can be used IM in emergencies, plus it has few side effects. It does, however, have a high frequency of extrapyramidal effects. Question: What is the only neuroleptic with tardive dyskinesia as a side effect? Clozapine. Unfortunately, patients taking clozapine can develop agranulocytosis and are at a higher risk for seizures than patients on other neuroleptics. Other side effects include hypotension, anticholinergic symptoms, and oversedation. Question: What happens when ethanol is combined with an anxiolytic (benzodiazepine)? Death can occur due to the combined respiratory depressive effects. Question: Name another contraindication to benzodiazepine use: Known hypersensitivity, acute narrow angle glaucoma, and pregnancy, especially in the first trimester. Question: What should be used to treat a hypertensive crisis caused by the combination of MAO inhibitors with a known toxin? An α- and β-adrenergic antagonist, such as labetalol. Also consider nifedipine or nitroglycerin. If unsuccessful, consider IV phentolamine or sodium nitroprusside. Question: Name some drugs contraindicated in a patient on MAO inhibitors: Meperidine (Demerol) and dextromethorphan can cause toxic reactions, such as excitation and hyperpyrexia. The effects of indirect-acting adrenergic drugs are potentiated, including ephedrine, sympathomimetic amines in cold remedies, amphetamines, cocaine, and methylphenidate (Ritalin). Question: Name the three common MAO inhibitors (chemical and brand name): 1. Phenelzine (Nardil) 2. Isocarboxazid (Marplan) 3. Tranylcypromine (Parnate) Question: Name eight drugs that decrease sexual desire: 1. Antidepressants 2. Antihypertensives 3. Anticonvulsants 4. Neuroleptics 5. Cimetidine 6. Digitalis 7. Clofibrate 8. High doses or chronic ingestion of alcohol or street drugs Question: What is the first cardiac finding in a cyclic antidepressant overdose? Sinus tachycardia. How long should a tricyclic antidepressant overdose patient, demonstrating tachycardia and conduction disturbances, be monitored? 24 hours. Question: What major tranquilizer displays the most hypotensive tendency? Thorazine. Question: What is the most significant pathophysiologic mechanism of death from cyclic antidepressants? Myocardial depression, including hypotension and conduction blocks. Question: What antibiotic may either increase or decrease lithium secretion? Tetracycline. Question: How is lithium overdose treated? Lavage, saline diuresis, furosemide, and hemodialysis. Alkalinization may be appropriate. Question: Name seven primary actions of cyclic antidepressant overdose: 1. Inhibition of amine reuptake 2. Sodium channel blockade, which causes negative inotropy 3. Anticholinergic effects, primarily antimuscarinic 4. CNS depression 5. α-Adrenergic antagonism, which contributes further to hypotension 6. GABA antagonism 7. Q-T prolongation Question: What is the appropriate treatment for QRS widening in tricyclic antidepressant (TCA) poisoning? NaHCO3 is administered intravenously for patients with a QRS > 100 ms; 0.5–2.00 mEq/kg are initially administered and repeated until the blood pH is between 7.45 and 7.55. A continuous infusion of NaHCO3, 3 amps in 1 L of D5W, may then be initiated and titrated in over 4–6 hours to maintain an appropriate pH. Potassium levels must be closely monitored as supplementation may be required to prevent hypokalemia. To arrhythmias not responsive to the above, consider lidocaine (1 mg/kg IV). Question: What is the appropriate treatment for TCA-induced seizures? Benzodiazepines (clorazepam or diazepam) and barbiturates (phenobarbital) are the agents of choice. Phenytoin is not generally effective but may be tried for recurrent seizures or those unresponsive to treatment. Bicarbonate and alkalosis are the main stays of treatment. Question: What is the treatment for TCA-induced hypotension? Isotonic saline and peptid alkalinization. If the patient is resistant to fluid resuscitation, a direct-acting α-adrenergic agonist, such as norepinephrine, should be started. Dopamine acts in part by releasing norepinephrine. This agent may already be depleted by the reuptake inhibition of the cyclic antidepressant and by stress. What period of observation is required prior to medically clearing a TCA overdose? 6 hours. Question: What level of lithium is generally considered toxic? 2.0 mEq/L. Question: Will charcoal bind lithium? No. Question: What are the signs and symptoms of lithium toxicity? Neurological signs and symptoms include tremor, hyperreflexia, clonus, fasciculations, seizures, and coma. GI signs and symptoms consist of nausea, vomiting, and diarrhea. Cardiovascular effects include ST-T wave changes, bradycardia, conduction defects, and arrhythmias. Question: What is the treatment for lithium toxicity? Supportive care, normal saline diuresis, hemodialysis for patients with clinical signs of severe poisoning, i.e., seizures and arrhythmias, renal failure, or decreasing urine output. Question: What are the typical CNS findings in mild lithium toxicity? Rigidity, tremor, and hyperreflexia. Question: What are the typical CNS findings in severe lithium toxicity? Seizures, coma, and myoclonic jerking. Question: What are the indications for hemodialysis in lithium toxicity? Serum lithium level above 4.0 mEq/L, renal failure, and severe clinical symptoms (stupor, seizures etc.). Question: True/False: Permanent neurologic sequelae (encephalopathy) can develop from lithium toxicity: True. Question: A 30-year-old man presents to the emergency department 20 minutes after ingesting 30 tablets of amitriptyline. What is the preferred method of gastric emptying? Immediate gastric lavage using a large (34–36 French) orogastric tube. Ipecac should not be used due to the potential for a rapid deterioration in mental status and seizures. Question: What is the initial treatment for hypotension in antidepressant overdose? Intravenous fluids—normal saline or Ringer lactate. Question: What vasopressor should be used to treat hypotension not responsive to IV fluids in antidepressant overdose? Norepinephrine should be used because it is a direct-acting α-adrenergic agonist. The onset of toxicity of monoamine oxidase inhibitors (MAOI) can occur up to what period of time after ingestion? 12 to 24 hours. Question: What over-the-counter cold medications should not be used by people taking MAOIs? Decongestants, antihistamines, and products containing dextromethorphan. Question: A 45-year-old patient presents with a diagnosis of depression, anxiety, and insomnia and is currently taking tramadol, flecainide, and tamoxifen. Can you prescribe an SSRI for her? No. SSRIs are cyp 450 2D6 inhibitors. The drugs she is on utilize the cyp 450 2D6 for their metabolism. Question: Describe the signs, symptoms, and ECG findings associated with lithium toxicity: Tremor, weakness, and flattening of the T waves, respectively. Question: What is the treatment of lithium overdose? Saline diuresis and hemodialysis. Question: What is the difference between low-potency and high-potency neuroleptics and give examples of drugs in each category. Low-potency neuroleptics have greater sedative, postural hypotensive, and anticholinergic effects. High-potency neuroleptics have greater extrapyramidal effects. Low potency: Chlorpromazine (Thorazine) Medium potency: Perphenazine (Trilafon) High potency: Haloperidol, droperidol (Inapsine), thiothixene (Navane), fluphenazine (Prolixin), trifluoperazine (Stelazine) Question: You are considering chemical restraint. List your options: Benzodiazepines: 1. Lorazepam (Ativan), 1–2 mg IV, or 2–6 mg orally every 30 minutes 2. Midazolam (Versed), 2–4 mg IV every 30 minutes 3. Diazepam (Valium), 5 mg IV or orally every 30 minutes Sedative hypnotics: Haloperidol (Haldol), 1–5 mg IM/IV, titrate to clinical response Droperidol (Inapsine), 1–2 mg IV every 30 minutes Benzodiazepines may be given in combination with the sedative hypnotics above to both hasten and potentiate their effect. Titrate to effect and monitor appropriately. Question: Is phenobarbital more quickly metabolized by children or by adults? Adults. Neonates are especially slow at metabolizing phenobarbital. A 32-year-old female patient is prescribed meperidine (Demerol) for an open fracture. The patient is chronically on fluoxetine (Prozac). What is a potential complication? The serotonin syndrome. Question: What signs and symptoms are typical of the serotonin syndrome? Agitation, anxiety, altered mental status, ataxia, diaphoresis, incoordination, sinus tachycardia, hyperthermia, shivering, tremor, hyperreflexia, myoclonus, muscular rigidity, and diarrhea. Question: What are potential pharmacological treatments for the serotonin syndrome? Serotonin antagonists, such as methysergide and cyproheptadine. Benzodiazepines and propranolol have also been successfully employed. Question: A patient ingests a toxic quantity of an MAOI inhibitor and is in a hyperadrenergic state with a blood pressure of 240/160. What is the appropriate treatment? Short-acting antihypertensives, such as phentolamine and nitroprusside, should be employed because the patient may soon develop refractory hypotension. Question: What are the major pharmacological effects of neuroleptics? Blockade of dopamine, α-adrenergic, muscarinic, and histamine receptors. Question: What findings occur with neuroleptic malignant syndrome? Altered mental status, muscular rigidity, autonomic instability, hyperthermia, and rhabdomyolysis. Question: What are the pharmacological effects of barbiturates and benzodiazepines? Both enhance chloride influx through the GABA receptor associated chloride channel. Benzodiazepines increase the frequency of channel opening, whereas barbiturates increase the duration of channel opening. Question: Alkalization of the urine is beneficial in the management of what barbiturates? Long-acting barbiturates such as phenobarbital. Question: What is the pharmacological basis of the anticonvulsant effect of phenytoin? Sodium channel blockade. Phenytoin causes an increasing efflux or a decreasing influx of sodium ions across cell membranes in the motor cortex during generation of a nerve impulse Question: What are the signs and symptoms of phenytoin toxicity? Seizure, heart blocks, bradyarrhythmias, tachyarrhythmias, hypotension, and coma. All dangerous cardiovascular complications of phenytoin OD result from parenteral administration. High levels after PO doses do not cause such signs in a stable patient. Question: What is the treatment for a phenytoin overdose? Systemic support, charcoal, atropine for bradyarrhythmias, and phenobarbital, 20 mg/kg IV, for seizures. What is the treatment for an opiate overdose? Naloxone, 0.4–2.0 mg in an adult and 0.01 mg/kg in a child. Naloxone duration of action is about 1 hour. Higher doses and continuous infusion may be required. Question: What herbal remedies are associated with CNS stimulation? Guarance, ma huang, St. John wart, yohimbe, and ginseng. Question: What four mechanisms induce tricyclic toxicity? 1. Anticholinergic atropine-like effects secondary to competitive antagonism of acetylcholine 2. Reuptake blockage of norepinephrine 3. A quinidine-like action on the myocardium 4. An α-blocking action Question: What is the most common neurologic complication of IV drug abuse? Nontraumatic mononeuritis (i.e., painless weakness 2–3 hours after injection). ANTIBIOTICS Question: Name the four potential adverse effects that can happen with antibiotics: Allergic, toxic, idiosyncratic, and changes to the normal body flora. Question: What is the most common overgrowth of bacteria as a result of antibiotic use? The superinfection of clostridium difficile, which is the causative agent of pseudomembranous colitis. Question: Which laboratory test is the most helpful in determining the proper use of an antibiotic? The culture and sensitivity test. This will give you the mean inhibitory concentration for the bacteria, thus narrowing down your choices of antibiotics. Question: What is the action of antibiotics such as penicillin, cephalosporin, and vancomycin? They all work by inhibiting cell wall synthesis of the bacteria. Question: What is a potentially fatal reaction from penicillin? Hypersensitivity reaction. Question: Name some other common adverse reactions with penicillin use: Urticaria, GI intolerance, and skin rashes (usually 72 hours or later). Question: What are the four syndromes of penicillamine-induced lung toxicity? Chronic pneumonitis, hypersensitivity lung disease, bronchiolitis obliterans, and pulmonary-renal syndrome. Which generation cephalosporin can be used to penetrate the CNS? Third generation. These are typically used for treatment of infections such as meningitis. Question: What is the cross reactivity of cephalosporin’s in relation to penicillin? 7%–18%, depending on the study. Question: A 73-year-old female with a history of atrial fibrillation and on chronic warfarin therapy is diagnosed with a mild cellulitis of her forearm. You would like to prescribe her a first-generation cephalosporin as the first-line treatment. Is this a good choice for this patient? No. Cephalosporins can have an antivitamin K effect. Given that this patient is on chronic warfarin therapy, this may adversely affect her INR and bleeding rate. Your best bet is to choose another antibiotic. Question: Name some adverse effects of using vancomycin: Ototoxicity—tinnitus, hightone deafness, hearing loss, and deafness. Question: Which class of antibiotics acts by gaining entry into the cells and binds to intracellular proteins? Protein synthesis inhibitors, which include aminoglycosides, tetracyclines, macrolides, clindamycin, streptogramins, and chloramphenicol. Question: Name three potential side effects of aminoglycosides: Ototoxicity, nephrotoxicity, and neuromuscular toxicity. Question: When administering tetracycline, how is the medication to be taken to ensure proper absorption? They must be taken on an empty stomach to maximize absorption. Question: A 15-year-old male adolescent has been diagnosed with acne. One of the possible treatment options is the use of tetracycline. Would this be a good choice for this type of patient? No. Tetracycline can cause staining of the teeth, retardation of bone growth, and photosensitivity and should be avoided in children as well as pregnant patients. Question: Mnemonic for erythromycin for the drug of choice in these bacteria: Legionnaires Camp on My Border (legionella, Campylobacter, Mycoplasma, Bordetella). Question: What is the one bacteria that chloramphenicol is not sensitive in eradicating? Pseudomonas aeruginosa. Question: What is gray baby syndrome? It is a fatal syndrome by which infants cannot conjugate chloramphenicol. The antibiotic absorbs into the cerebrospinal fluid. The infants will get abdominal distention, vomiting, cyanosis, hypothermia, decreased respiration, and vasomotor collapse. Which antibiotic has been listed as the most susceptible in contracting Clostridium difficile superinfections? Clindamycin. Question: What is the effect of macrolide antibiotics (erythromycin, clarithromycin) on mucus hypersecretion? Some macrolide antibiotics have the ability to down/regulate mucus secretion by an unknown mechanism. This is thought to be due to an anti-inflammatory activity. Question: Why are quinolones contraindicated in young adults and children? Quinolones are contraindicated because they can suppress the epiphyseal plate and cartilage formation in young adults. In all patients, quinolones can cause tendon rupture, most notably Achilles tendon ruptures. Question: What are the possible side effects? Quinolones are contraindicated because they can suppress the epiphyseal plate and cartilage formation in young adults. In all patients, quinolones can cause tendon rupture, most notably Achilles tendon ruptures. Question: How do quinolones work? They inhibit DNA gyrase synthesis, which is responsible for DNA replication of bacteria. Question: Which bacteria do quinolones effectively kill? They are broad-spectrum killers (gram-negative mostly) and most effective in treating respiratory, bone and joint, urinary tract, and prostatitis. Some are effective in treating Pseudomonas aeruginosa. Question: What is the mechanism of action of isoniazid? It is a simple inhibitor of mycolic acids, which are responsible for the formation of bacterial cell wall envelopes. Question: What two side effects are causes of isoniazid? Hepatotoxicity and peripheral neuropathy. Both can be reversed by stopping the drug. Question: What is the antidote for isoniazid-induced seizures? Pyridoxine. Question: What is a serious side effect of rifampin? Hepatotoxicity. LFTs need to be monitored while patient is on either rifampin or isoniazid. Rifampin will also turn the urine and secretions orange while on the medication. Question: What is the drug of choice for the treatment of leprosy? Dapsone. Question: Fungal infections in general are more difficult to eradicate than bacterial infections. How do drugs like amphotericin B and nystatin function? They act by binding to ergosterol, which is the prinicipal sterol in fungus. How can nystatin be taken? It is limited to topical applications and oral liquids. Systemic nystatin is too toxic and therefore not used. Question: What is the most serious and most common toxicity of amphotericin B? Nephrotoxicity. Question: Why do patients with tinea infections that require griseofulvin need to take such a prolonged course of the medication? These infections must have new skin, hair, and nails that are new—keratin-containing griseofulvin. This usually takes several weeks to accomplish. Question: What is the drug of choice for the treatment of trematodes (flukes)? Praziquantel. Question: Name three drugs that can be used for the treatment of nematodes (roundworms): Albendazole, mebendazole, and pyrantel. Filarial infections must be treated with Ivermectin or diethylcarbamazine. Question: What is the mechanism of action of albendazole and mebendazole? They inhibit tubulin polymerization in worms, which prevents replication. Question: What is the treatment for lymphatic filariasis? Diethylcarbamazine. Question: What are the three mechanisms of controlling viral illnesses? Vaccination, chemotherapy, and stimulation of the hosts natural resistance mechanisms. Question: What is the function of reverse transcriptase inhibitors? All three types (nucleoside, nonnucleoside, and nucleotide) inhibit the formation of viral DNA from RNA by reverse transcriptase. Question: Protease inhibitors are commonly used in the treatment and suppression of HIV. How do these medications work? They interfere with the production of viral proteins, thus preventing replication of new viral particles. Question: What is the most effective treatment for HIV? The triple drug therapy (or cocktail) is the use of two reverse transcriptase inhibitors, and a protease inhibitor. Question: What is the most effective prevention method for influenza? Vaccination. Question: Which type of influenza does amantidine work effectively against? Influenza A. Which class of drugs is effective in reducing the length of both influenza A and B? Neuraminidase inhibitors. They are effective if the medication can be started within 30 hours of onset of symptoms of flu. Question: Which antiviral is effective in the treatment of respiratory syncytial virus (RSV)? Ribavirin. Question: How is ribavirin administered? By aerosol form. Question: What is the treatment of choice for trichomoniasis and giardiasis? Metronidazole. Question: Name some common side effects of metronidazole: Nausea, vomiting, and diarrhea. It will also cause your secretions to turn dark or red-brown in color. Some patients will get a metallic taste. Question: Metronidazole, when mixed with alcohol, will cause a disulfiram like reaction to occur. What are some symptoms that you should look for in this scenario? Abdominal cramping, flushing, vomiting, and headache. Question: What is the one drug that has shown resistance in treating plasmodium falciparum? Chloroquine. Question: Which antiprotozoal drug must be avoided in patients with G6PD deficiency? Primaquine, which can cause hemolytic anemia. Question: Chloroquine is a commonly prescribed drug for the treatment of malaria. What are two ophthalmologic side effects of the drug that need to be monitored? Corneal deposits containing melanin can develop. This can lead to blindness. Question: What is the main goal of most anticancer drugs? They are either cytotoxic drugs, which will block cell replication, or they are drugs, which act on hormonal-sensitive tumors. Question: Patients undergoing chemotherapy are at risk for bleeding and infections. Why? The chemotherapeutic agents’ most serious side effect is bone marrow toxicity. This will cause a drop in the production of all blood products including white cells and platelets. Question: What are the main gastrointestinal side effects of chemotherapy? Nausea and vomiting, which is thought to be a centrally acting effect. Some chemotherapeutic agents can have cardiotoxicity. Name some possible cardiac effects from these drugs: Patients can develop arrhythmias, decreased ventricular function (cardiomyopathy), and focal necrosis of tissue. Question: Why does hair loss occur so frequently in chemotherapy? Most chemotherapeutic agents block the telophase stage of hair production, thus causing a stoppage of hair growth. This will cause hair death. Stopping the chemo will reverse this side effect. Common chemotherapeutic agents and their serious side effects: Question: A 66-year-old female patient is currently under treatment for malignant myeloma. Her calcium is measured at 19 mg/dL and she is showing signs of hypercalcemia on examination. What treatment can be given to help lower the calcium level? Bisphosphonates, creating the volume status of the patient to be euvolemic are the two initial goals. An additional therapy for life-threatening hypercalcemia is plicamycin. Question: How do drugs such as Tamoxifen and toremifene act on breast cancer cells? They are competitive antagonists of estrogen receptors. Question: An acute chest pain syndrome can occur with which chemotherapeutic agents? Methotrexate and bleomycin. Question: What are four distinct presentations of bleomycin lung toxicity? Chronic pulmonary fibrosis, hypersensitivity lung reaction, acute pneumonitis, and acute chest pain syndrome. Question: What are the risk factors for methotrexate (MTX) pulmonary toxicity? Primary biliary cirrhosis, frequency of administration, adrenalectomy, tapering of corticosteroid therapy, and use in multidrug regimens. Question: What drug will produce hilar and mediastinal adenopathy as a toxic reaction? Methotrexate. ENDOCRINE SYSTEM Question: What is the main glucocorticoid and mineralocorticoid produced by the adrenal gland? Glucocorticoid—hydrocortisone (cortisol) Mineralocorticoid—aldosterone Question: What is the function of glucocorticoids? They promote the catabolism of proteins and gluconeogenesis. Question: Why is there an increased risk of infection for those patients on steroids? Glucocorticoids inhibit inflammatory and immunologic responses, which make them more susceptible to infection. Question: What is a potential long-term complication for chronic glucocorticoid use? Osteoporosis. Question: Where does the primary source of estradiol originate? From the ovary. Question: What are the most common side effects of estrogen use? Nausea and vomiting. Question: Which antiestrogen is used to stimulate ovarian function for the purpose of treating infertility? Clomiphene. Question: What are the most common side effects when using progestins? Weight gain, edema, and depression. More serious problems are with the hematologic system. Increased clotting can occur; thrombophlebitis and pulmonary embolus are serious adverse effects of progestins. Question: Progestin alone used in contraceptives can cause what main side effect? Irregular uterine bleeding. Question: The main androgen in the body is testosterone. What are some of the effects that androgens cause in the body? Virilization of women, including deepening of voice, acne, growth of facial hair, and excessive muscle development. Question: What is the treatment of choice for hypothyroidism? Levothyroxine. Question: Name two medications that inhibit thyroid synthesis: Propylthiouracil and methimazole. What is the most common side effect of insulin? Hypoglycemia. Question: What is the treatment for the crystallization of tissue from repetitive use of insulin at the same site of skin? Injections of glucagon to the site will reverse the problem. Question: What is the mechanism of sulfonylureas in the treatment of diabetes? They act to stimulate the β cells of the pancreas. Question: A 65-year-old male patient has a history of diabetes for which he takes metformin. He is having an MI and will be in need of a cardiac catheterization. Is there anything special that this patient needs before the cath? Yes. The metformin needs to be stopped prior to the cath as the dye in combination with the metformin can impair renal function. Question: Describe which histamine receptors act on different systems of the body: H1 receptors act on intestinal and smooth muscle whereas the H2 receptors control gastric secretions. Question: What are H1 antagonists used to treat? They are commonly used to treat allergic rhinitis, motion sickness, and in some cases to help induce sleep. RESPIRATORY SYSTEM Question: What is the main delivery system for β-agonists for respiratory diseases? Inhalation by either aerosol nebulizer or metered dose inhaler. Question: What is the inhaled drug of choice for the treatment of COPD? Ipratropium. Question: Is cromolyn useful in the treatment of acute asthma attacks? No. Question: True/False: β-adrenergic antagonists in massive overdose may cause severe bronchospasm in normal individuals: False. Question: What conditions or commonly used medications result in an increase in serum theophylline concentration? Cimetidine, macrolides, quinolones, verapamil, fever, congestive heart failure, and liver failure. Question: What drugs, activities, and cooking habits are associated with an increased clearance of theophylline (decreasing the theophylline level)? Phenytoin, phenobarbital, cigarette smoking, and charcoal barbecuing. What is the appropriate initial treatment of theophylline-induced seizures? Benzodiazepines and barbiturates. Theophylline-induced seizures warrant hemodialysis or charcoal hemoperfusion. Question: What is the treatment of theophylline-induced hypotension? Fluid administration and β-blockers. Theophylline-induced cardiovascular instability is secondary to β-agonist effects. Therefore, β-blockers can be beneficial in the treatment of arrhythmias and hypotension. GASTROINTESTINAL SYSTEM Question: Of all the H2-blockers used for gastrointestinal complaints, which one has the most potential side effects and why? Cimetidine because it binds to cytochrome P-450. Question: What instructions do you need to give patients that you prescribe sucralfate and why? They must take on an empty stomach because the drug binds to protein. Question: What are the two major types of drugs used to treat constipation? There are bulk-forming agents, which absorb water and soften the stool, and the second is the cathartics and stimulants, which increase water and electrolytes in the stool to increase bowel motility. Two other types are saline salts to draw water into the colon, and docusate, which absorbs into stool to soften. Question: Which drugs are utilized in the treatment of Crohn disease? Sulfasalazine, which is metabolized into 5-ASA and sulfapyridine. MUSCULOSKELETAL SYSTEM Question: What is the main mechanism of non-steroidal anti-inflammatory (NSAIDs)? They act by inhibiting prostaglandin synthesis. Question: What are the most common side effects associated with NSAIDs? GI upset, bleeding, oliguria, fluid retention, renal insufficiency, decreased sodium excretion, and renal failure. They can also prolong bleeding times. Question: What is the only non-reversible COX inhibitor? Aspirin. Question: Why are children not to be given aspirin? Aspirin can cause Reyes syndrome to occur. What are some of the characteristics associated with Reyes syndrome? CNS damage, liver injury, and hypoglycemia. Question: What is the incidence of aspirin-induced bronchospasm in patients with nasal polyps? Up to 75%. Question: True/False: In aspirin-induced bronchospasm, there can be cross-reactivity with nonsteroidal anti-inflammatory drugs: True. Question: What is the major side effect associated with the inhalation of N-acetylcysteine? Cough and bronchospasm, most likely due to irritation from the low pH (2.2) of the aerosol solution. Question: Which acid–base disturbance is typical for salicylate poisoning? Mixed respiratory alkalosis, secondary to central respiratory center stimulation, and metabolic acidosis, secondary to uncoupling of oxidative phosphorylation. Question: What order are the kinetics of elimination for an ASA overdose? Zero-order elimination with hepatic enzymatic clearance saturated and renal clearance becoming important. Question: What is the “magic number” for the dose of a nonenteric coated ASA that must be exceeded to cause toxicity (mg/kg)? 150 mg/kg. Question: What dose of ASA will cause mild to moderate toxicity? 200–300 mg/kg. Greater than 500 mg/kg is potentially lethal. Question: Is hemodialysis used to treat salicylate toxicity? Yes. For severely poisoned patients, i.e., coma, ARDS, cardiac toxicity, serum levels > 100 mg/dL, and for patients who are unresponsive to maximal therapy. Question: What is the treatment for a prolonged prothrombin time in salicylate poisoning? Parenteral vitamin K administration. Salicylates inhibit vitamin K epoxide reductase in poisoning, resulting in an ability for the inactive vitamin K epoxide to be regenerated into the active vitamin K. Question: Can a patient present with salicylate poisoning and a therapeutic level? Yes. Patients with chronic salicylate poisoning have a large Vd (volume of distribution) and thus may present with mental status changes and a therapeutic level. Question: What is the X-ray finding in a patient with salicylate toxicity? Noncardiogenic pulmonary edema. Describe the effects of salicylate poisoning on the central nervous system: Lethargy, confusion, seizures, and respiratory arrest. Question: Salicylate levels should ideally be checked how long after an ingestion? 6 hours. Question: What is the minimum toxic dose of salicylates? 150 mg/kg. Question: What salicylate level, measured 6 hours after ingestion, is associated with toxicity? 45 mg/dL. Question: What acetaminophen level, measured 4 hours after ingestion, is associated with toxicity? 150 μg/mL. Question: What are the signs of salicylate poisoning? Hyperventilation, hyperthermia, mental status change, nausea, vomiting, abdominal pain, dehydration, diaphoresis, ketonuria, metabolic acidosis, and respiratory alkalosis. Question: A child presents with lethargy, seizures, and hypoglycemia. He has had viral syndrome symptoms for several days. Mom states she has only been giving him aspirin. What two disorders should be considered: Reye syndrome and salicylate intoxication. Question: When does acetaminophen become toxic? When there is no glutathione to detoxify its toxic intermediate. Question: Would you like to have four Aces? Of course! So check ACEtaminophen levels 4 hours after ingestion. Question: Which type of acid–base disturbance initially occurs with a salicylate overdose? Respiratory alkalosis. Approximately 12 hours later, an anion gap metabolic acidosis or mixed acid–base picture may occur. Question: Is hyperglycemia or is hypoglycemia expected with a salicylate overdose? Expect either hyperglycemia or hypoglycemia. Question: What are the common signs and symptoms of chronic salicylism? Fever, tachypnea, CNS alterations, acid–base abnormalities, electrolyte abnormalities, chronic pain, ketonuria, and noncardiogenic pulmonary edema. A patient presents with an acute salicylate ingestion. What symptoms are expected with a mild, moderate, and severe overdose? Mild: Lethargy, vomiting, hyperventilation, and hyperthermia Moderate: Severe hyperventilation and compensated metabolic acidosis Severe: Coma, seizures, and uncompensated metabolic acidosis Question: What is the treatment for a salicylate overdose? Decontaminate, lavage and charcoal, replace fluids, supplement with potassium, alkalize the urine with bicarbonate, cool for hyperthermia, administer glucose for hypoglycemia, place on oxygen and PEEP for pulmonary edema, prescribe multiple dose–activated charcoal, and initiate dialysis. Question: What are the four stages of acetaminophen (APAP) poisoning? Stage I: 30 minutes to 24 hours, nausea and vomiting Stage II: 24–48 hours, abdominal pain and elevated LFTs Stage III: 72–96 hours, LFTs peak, nausea, and vomiting Stage IV: 4 days to 2 weeks, resolution or fulminant hepatic failure Question: Which measure of hepatic function is a better prognostic indicator in APAP overdose: liver enzyme levels or bilirubin level and prothrombin time? Bilirubin level and prothrombin time. Question: An acutely intoxicated, nonalcoholic, otherwise healthy patient ingests APAP. Is this patient more or less likely to develop hepatotoxicity? Less likely. An acute ingestion of alcohol will tie up the P-450 system thereby inhibiting the formation of NAPQI. A chronic alcoholic has an induced P-450 system and will suffer greater APAP hepatic toxicity through increased NAPQI formation. Question: What is the minimum dose of APAP that can cause hepatotoxicity in the child? In the adult? Child: 140 mg/kg. Adult: 140mg/kg (or about 7.5 g). Question: What is the antidote for APAP poisoning? Mucomist (NAC) 140 mg/kg followed by 17 doses of 70 mg/kg every 4 hours. Question: According to the Rumack-Matthew nomogram, at what 4-hour APAP level should treatment be initiated? 150 mg/mL. Question: What is the treatment goal in the management of osteoporosis? First is the prevention of further bone loss, and second is the treatment of the osteoporosis already present. Question: What is the mechanism of bisphosphonates? They inhibit osteoclast activity to prevent further bone destruction. TOXICOLOGY AND OVERDOSE Question: What is the most important treatment of all poisoned and toxic patients? Supportive care. Question: What is the difference between methadone and heroin? Methadone causes analgesia, but does not cause euphoria. Habituation occurs with both drugs. The withdrawal symptoms of methadone are less severe, but they last longer. Question: What is the treatment for cocaine toxicity? Acidify the urine and administer neuroleptics and phentolamine Sedate with benzodiazepine Treat unresponsive hypertension with nitroprusside or phentolamine Question: Name some over-the-counter and “street” drugs that may produce delirium or acute psychosis: Salicylates, antihistamines, anticholinergics, alcohols, phencyclidine, LSD, mescaline, cocaine, and amphetamines. Question: Hallucinogens affect what neurotransmitter? Serotonin. Question: What is the treatment for a “bad trip” on LSD? Constantly remind patients that their perceptions are only distortions due to the drug. This is called “talking down.” Chlorpromazine can be used IM for severe or uncontrollable anxiety. Question: PCP most commonly affects what brain system? The vestibulocerebellar system. This has a positive analgesic effect. However, the side effects, including dizziness, muscular incoordination, nystagmus, delirium, anxiety, irritability, and catalepsy, weigh heavily against any positive effect. Question: How is a patient with PCP overdose treated? Acidify the urine with cranberry juice or NH4Cl, give a benzodiazepine, and restrain the patient. Question: Which types of nystagmus are expected with a PCP overdose? Vertical, horizontal, and rotary. Vertical nystagmus is not common with other conditions/ingestions. The most common findings of a PCP overdose are hypertension, tachycardia, and nystagmus. Question: How can the pesticide PCP enter the body? Through inhalation, skin, and ingestion Question: What is the clinical presentation of PCP intoxication? Irritation of skin, eyes, and upper respiratory tract, headache, vomiting, weakness, sweating, hyperthermia, tachycardia, tachypnea, convulsions, coma, pulmonary edema, cardiovascular collapse, and death. Describe the features of the three stages of PCP intoxication: Stage I: agitation or violence, normal vital signs Stage II: tachycardia, hypertension, no response to pain Stage III: unresponsive, depressed respirations, seizures, death Question: Should the urine be acidified in the treatment of PCP intoxication? Although acidification of the urine is theoretically advantageous, clinical experience has not shown this to be efficacious. Let’s call that a “no.” Question: What is a dystonic reaction? A very common side effect of neuroleptics seen in the emergency department. It involves muscle spasms of the tongue, face, neck, and back. Severe laryngospasm and extraocular muscle spasms may also occur. Patients may bite their tongues, leading to an inability to open the mouth, to tongue edema, or to hemorrhage. Question: How do you treat dystonic reactions? Diphenhydramine (Benadryl), 25–50 mg IM or IV, or benztropine (Cogentin), 1–2 mg IV or PO. Remember that dystonias can recur acutely. Question: A patient has ingested a phenothiazine and arrives hypotensive. What intervention(s) may be considered? IV crystalloid boluses usually suffice. Severe cases best managed with norepinephrine (Levophed) or metaraminol (Aramine). These pressors stimulate α-adrenergic receptors preferentially. β-Agonists, such as isoproterenol (Isuprel), are contraindicated because of risks of β-receptor–stimulated vasodilation. Question: What are some common side effects of phenothiazine use? Malaise, hyperthermia, tachycardia, anticholinergic effects, and quinidine-like membrane stabilization. The most dangerous side effect is neuroleptic malignant syndrome. Question: How should stable ventricular tachyarrhythmias associated with phenothiazine overdose be treated? Lidocaine and phenytoin. Question: What factors and substances decrease theophylline metabolism and increase theophylline levels? Factors: Age greater than 50 years, prematurity, liver and renal disease, pulmonary edema, CHF, pneumonia, obesity, and viral illness in children Substances: Drugs that increase theophylline levels include cimetidine, erythromycin, allopurinol, troleandomycin, BCPs, and quinolone antibiotics In smokers, the theophylline half-life is decreased, which causes the levels of serum theophylline to decrease. Phenobarbital, phenytoin, rifampin, carbamazepine, marijuana smoking, exposure to environmental pollutants, and the consumption of charcoal-broiled foods can also decrease serum theophylline levels. Question: Can theophylline be dialyzed? Yes. Why should the use of atropine be considered in a pediatric patient prior to intubation? Many pediatric patients develop bradycardia associated with intubation, which can be prevented by pretreatment with atropine (0.01 mg/kg). Question: What is a “Mickey Finn”? A mixture of alcohol and chloral hydrate. Question: At what rate is alcohol metabolized in an acutely intoxicated person? About 20 mg/dL/h. Question: What is the pharmacological treatment for alcohol withdrawal? Benzodiazepines or barbiturates. Question: What is a normal osmolar gap? <10 mOsm. Question: What is the toxic metabolic end product in methanol poisoning? Formic acid. Question: What cofactor is required to convert formic acid to carbon dioxide and water? Folate. Leucovorin, folinic acid, the active form of folate, is preferentially administered at 1 mg/kg. Folate may be substituted at the same dose if leucovorin is not available. Question: Is sodium bicarbonate (NaHCO3) beneficial in the management of methanol poisoning? Yes. In animal models, maintenance of a normal pH through bicarbonate administration decreased toxicity, including visual impairment. Question: What methanol level mandates dialysis? 50 mg/dL. Other indications include visual impairment, severe metabolic acidosis, and ingestion of greater than 30 cc. Question: What cofactors are administered to a patient with ethylene glycol poisoning? Thiamine and pyridoxine. These cofactors will aid in transforming glyoxylic acid to nontoxic metabolites. Both are administered intravenously in 100 mg increments. Question: Name the three clinical phases of ethylene glycol poisoning: Stage I: Neurological symptomatology (i.e., inebriation) Stage II: Metabolic acidosis and cardiovascular instability Stage III: Renal failure Question: When should dialysis be initiated for an ethylene glycol poisoning case? When the serum level is >25 mg/dL, or when renal insufficiency or severe metabolic acidosis occurs. What is the toxic dose of naloxone? None. Narcan is a safe drug and may be given in large quantities. The usual adult dosage is 2 mg IV; the usual pediatric dose is 0.01 mg/kg. Narcan may precipitate acute withdrawal and may therefore be titrated to effect. Question: What syndrome is associated with Jimson Weed? Anticholinergic poisoning. Question: What are absolute indications for hemodialysis or hemoperfusion in theophylline toxicity? Seizures or arrhythmias that are unresponsive to conventional therapy—a theophylline level >100 μg/mg in an acute overdose or 50 μg/mg in a chronic overdose Question: What are the four stages of iron poisoning? Stage I (0–6 hours): Abdominal pain, nausea, vomiting, and diarrhea secondary to the corrosive effects of iron. In more severe cases, hematemesis, hypotension and altered mental status. Stage II (6–24 hours): Quiescent period during which iron is absorbed (in severe poisoning, a latent period may be absent). Stage III: (12–24 hours): GI hemorrhage, shock, metabolic acidosis, heart failure, CV collapse, coma, seizures, coagulopathy, hepatic, and renal failure. Stage IV: (4–6 weeks postingestion): Gastric outlet or small bowel obstruction secondary to scarring. Question: What dose of iron is expected to produce clinical toxicity? 20 mg/kg of elemental iron. For example, a toddler ingests 10 tablets of 324 mg ferrous sulfate, i.e., 20% elemental iron; this equals 648 mg of elemental iron. The dose would be toxic to a 20 kg child at 32.4 mg/kg. Question: What 4-hour iron level is generally considered toxic? 300–350 μg/dL. Question: What are the indications for deferoxamine therapy? All symptomatic patients exhibiting more than merely transient symptomatology. Patients with lethargy, significant abdominal pain, hypotension, mental status changes, hypovolemia, or metabolic acidosis. Patients with a positive KUB. Any symptomatic patient with a level greater than 300 mg/dL. Question: What oral chelator reduces iron absorption in animal model studies? Magnesium hydroxide or milk of magnesia. Question: What historical disclosure warrants an evaluation after a hydrocarbon ingestion? Coughing. Any patient who coughs after ingesting a hydrocarbon has the potential for developing chemical pneumonitis. Question: At what point can a patient who has ingested a hydrocarbon be safely discharged? After 6 hours, asymptomatic patients, with a normal chest X-ray and pulse oxygen, may be discharged to home. Chronic solvent abusers develop what metabolic complication? Renal tubular acidosis. Question: Methylene chloride is metabolized to which toxin? Carbon monoxide. Question: A 2-year-old child is asymptomatic after ingestion of a button battery. A KUB reveals the foreign body in his stomach. What is the disposition for this patient? Discharge to home. If the battery is lodged in the esophagus, an endoscopy must be performed immediately. Otherwise, reassure the patient’s parents and instruct them to check their son’s stools. Question: What is the potent ingredient in Sarin? An organophosphate. Question: What enzyme is inhibited by organophosphates? Acetylcholinesterase. Question: How do organophosphates enter the body? They can be inhaled, ingested, or absorbed through the skin. Question: What are the signs and symptoms of organophosphate poisoning? 1–2 hours after poisoning patients may have GI upset, bronchospasm, miosis, bradycardia, excessive salivation and sweating, tremor, respiratory muscle paralysis, muscle fasciculations, agitation, seizures, coma and death. Remember: SLUDGE ( Salivation, Lacrimation, Urinary incontinence, Diarrhea, Gastric upset, and Emesis). Question: What antihypertensive agent may induce cyanide poisoning? Nitroprusside. One molecule of sodium nitroprusside contains five molecules of cyanide. To prevent toxicity with long duration infusions, sodium thiosulfate should be infused with sodium nitroprusside at a ratio of 10:1, thiosulfate to nitroprusside. Beware of thiocyanate toxicity! Question: What is corn picker’s pupil? Mydriasis from contact of the eye with Jimson weed. Jimson weed contains atropine, scopolamine, and hyoscyamine. It is a common plant and is available through health food stores. Question: What is the most common cause of chronic heavy metal poisoning? Lead. Question: Organophosphates are found in what kinds of compounds? Pesticides, flame retardants, and plasticizers. Question: What is the rate-limiting step in the metabolism of ethanol? The conversion of ethanol to acetaldehyde by alcohol dehydrogenase. In a nondrinker, what blood ethanol level will cause confusion or stupor? 180–300 mg/dL. The minimum blood alcohol level that can cause coma in a nondrinker is 300 mg/dL. Question: In chronic alcohol users, alcohol withdrawal seizures occur approximately how many hours after cessation of heavy alcohol consumption? 6–48 hours from the time of the last drink. Question: Delirium tremens occurs how long after the cessation of alcohol consumption? On average, 3–5 days. Question: Is there a role for phenytoin in the prevention or treatment of pure alcohol withdrawal seizures? No. Careful titration of benzodiazepines or phenobarbital should be used if necessary. Question: True/False: Status epilepticus is commonly seen in alcohol withdrawal seizures: False. Status epilepticus is rare in alcohol withdrawal seizures and should suggest the need to find other causative pathology. Question: What is the classic triad of Wernicke encephalopathy? Global confusion, oculomotor disturbances, and ataxia. Question: What constellation of findings should prompt consideration of ethylene glycol toxicity? Ethanol-like intoxication (with no odor), large anion gap acidosis, increased osmolal gap, altered mental status leading to coma, and calcium oxalate crystals in the urine. Question: In life-threatening theophylline overdose, what is definitive management? Charcoal hemoperfusion. Question: True/False: Lithium has a narrow therapeutic toxic range: True. Therapeutic lithium levels are between 0.5 amd 1.5 mEq/L and must be monitored closely. Question: How is lithium eliminated after metabolism? By renal excretion. Question: Name five herbal remedies associated with bleeding: Ginger, garlic, ginkgo, ginseng, and feverfew. Question: If a patient has a sulfa or ASA allergy, can they be prescribed a COX II inhibitor? No. Question: Which opiate combination is associated with arrhythmias, pulmonary edema, and hepatic failure? Propoxyphene N 100 plus APAP. Ethylene glycol is the alcohol that is present with hypocalcemia in one-third of the cases. Where does the calcium go? Oxalic acid is one of the metabolites of ethylene glycol. Calcium precipitates with oxalate and forms calcium oxalate crystals. The positive birefringent calcium oxalate dihydrate crystals are pathognomonic of this ingestion. Question: Methanol intoxication causes early death as a result of: Respiratory arrest. The pathophysiology is unknown. Question: Activated charcoal is not an effective treatment for which poisonous substances? Alcohols, ions, acids, and bases. Question: Describe the clinical characteristics of carboxyhemoglobin concentrations, specifically for ranges of 10% to 70%: 10%: Frontal headache 20%: Headache and dyspnea 30%: Nausea, dizziness, visual disturbance, fatigue, and impaired judgment 40%: Syncope and confusion 50%: Coma and seizures 60%: Respiratory failure and hypotension 70%: May be lethal Question: What is the appropriate treatment for cyanide poisoning? Amyl nitrite and sodium nitrite IV, followed by sodium thiosulfate IV. Question: What is the most common cause of chronic heavy metal poisoning? Lead. Arsenic is the most common cause of acute heavy metal poisoning. Question: Cyanide binds to metals and disrupts the function of metal-containing enzymes. Which is the most important of these enzymes? Cytochrome A (also known as cytochrome oxidase) is necessary for aerobic metabolism. Question: Why administer nitrites for cyanide poisoning? Nitrites form methemoglobin and methemoglobin, which strongly bind to cyanide. Question: Why prescribe sodium thiosulfate for cyanide poisoning? Rhodanese, an intrinsic enzyme, transfers cyanide from its attachment to methemoglobin to sulfur, thereby forming thiocyanate. Thiocyanate is excreted. Sodium thiosulfate acts as a sulfur donor for this process. Question: What is the antidote for ethylene glycol? Ethanol and dialysis. What is the antidote for gold? British anti-Lewisite (BAL). Question: What are the potential complications of excess sodium bicarbonate? Cerebral acidosis, hypokalemia, hyperosmolality, and an increased binding of hemoglobin to oxygen. Question: What are common entities in the differential diagnosis of pinpoint pupils? Narcotic overdose, clonidine overdose, and sedative hypnotic overdose, including alcohol, cerebellar pontine angle infarct, and subarachnoid hemorrhage. Question: What mnemonic may assist in recalling the signs of life-threatening cholinergic poisoning? DUELS: Diaphoresis Urination Eye changes (miosis) Lacrimation Salivation Question: Name six common drugs that can cause hyperthermia: SANDS-PCP: 1. Salicylates 2. Anticholinergics 3. Neuroleptics 4. Dinitrophenols 5. Sympathomimetics 6. Phencyclidine (PCP) Question: What drugs cause an acetone odor on the breath? Ethanol, isopropanol, and salicylates. Ketosis is often accompanied by the same odor. Substances or drugs that have an induced odor on breath: What is the mnemonic for remembering drugs that are radiopaque? BAT CHIPS: Barium Antihistamines Tricyclic antidepressants Chloral hydrate, calcium, cocaine Heavy metals Iodine Phenothiazine, potassium Slow-release (enteric-coated) Question: What three toxicologic emergencies require immediate dialysis? Ethylene glycol, methyl alcohol, and Amanita phalloides. Question: What is the antidote for isoniazid? Pyridoxine. Question: What drugs are commonly excreted by using alkaline diuresis? Long-acting barbiturates, INH, tricyclic antidepressants, salicylates, and less commonly, lithium. Question: What are the signs and symptoms of a cyanide overdose? Dryness and burning in the throat, air hunger, and hyperventilation. If the individual is not removed from the toxic environment, loss of consciousness, seizures, bradycardia, and apnea will occur followed by asystole. Question: What drugs can cause methemoglobinemia? Nitrites, local anesthetics, silver nitrate, amyl nitrite and nitrites, benzocaine, commercial marking crayons, aniline dyes, sulfonamides, and phenacetin. Question: For which type of overdoses is atropine used? Organophosphate and carbamate. Question: For which type of an overdose may the drug pralidoxime (2-PAM) be used? Organophosphate. Question: Chronic bromism is treated with what drug? Sodium chloride. Question: Isoniazid and Gyromitra mushroom poisoning is best treated with what drug? Pyridoxine. Question: Name some side effects of alkalization of the urine: Hypernatremia and hyperosmolality. What is the antidote for phosphorus poisoning? Copper sulfate, 1% solution. Remove phosphorus within 30 minutes of exposure. Phosphorus may be identified by the formation of an insoluble black precipitate when swabbing with copper sulfate. Question: What local anesthetics may cause anaphylaxis? The ester derivatives containing para-aminobenzoic acid (PABA) are known to stimulate IgE antibody formation and thereby cause anaphylaxis. Such anesthetics include procaine and tetracaine. Question: What is the best diluent for treating the ingestion of solid lye? Milk. Question: What is the most commonly abused volatile substance? Toluene. Question: A patient presents with hypokalemia of 2.0, hyperchloremia, and acidosis. What is the most likely toxicologic cause? Chronic toluene abuse. Question: A patient has been abusing nitrous oxide for a long time. What symptoms might be expected? Paresthesias and motor weakness may be present in chronic abusers. Such symptoms are often mistaken for symptoms of multiple sclerosis. Question: A patient presents with belladonna alkaloid poisoning resulting in anticholinergic effects. Explain the dangers of treating this patient with physostigmine: Physostigmine acts to increase acetylcholine levels. In doing so, it can precipitate a cholinergic crisis resulting in heart block and asystole. As a result, it is recommended to reserve physostigmine for life-threatening anticholinergic complications. Question: What is the ferric chloride test and what toxic ingestion does it detect? Add a few drops of 10% ferric chloride solution to a few drops of urine. A purple color indicates presence of salicylic acid. Ketones or phenothiazine can lead to falsely positive results. Question: What is the treatment for chloral hydrate overdose? Hemodialysis and/or charcoal hemoperfusion will clear the active metabolite, trichloroethanol. Question: What are the common effects of barbiturate overdose? Hypothermia, hyperventilation, vasodilation with hypotension, and negative inotropic effect on the myocardium. Clear vesicles and bullae may also be seen. Question: What is the pediatric dose of naloxone? 0.01–0.8 mg/kg; may need to repeat. What is the antidote for magnesium sulfate overdose? Calcium gluconate infusion. Question: What are the effects of using ketamine in a pediatric patient? The child’s eyes will be wide open with a glassy stare. He or she will have nystagmus, hyperemic flush, and hypersalivation. There will also be a slight rise in the heart rate. A very rare complication of ketamine use is laryngospasm. Hallucinations are a common side effect in children older than 10 years; as a consequence, ketamine should be restricted to use only in patients younger than 10 years. Note: Ketamine may also cause sympathetic stimulation, which increases intracranial pressure and may cause random movements of the head and extremities. Thus, it is not a good sedative for children going to CT scan. Question: You are having a hard time remembering which anesthetics are amides and which anesthetics are esters. What is a fairly easy way of telling these two classifications apart? With the exception of the suffix -caine, the anesthetics only in the amide classification include the letter I. Amides esters Lidocaine (Xylocaine) Bupivacaine (Marcaine) Mepivacaine (Carbocaine) Procaine (Novocain) Cocaine Tetracaine (Pontocaine) Benzocaine Question: Activated charcoal is not indicated for which types of overdose? Alcohol ingestion, electrolytes, heavy metals, lithium, hydrocarbons, and caustic ingestions. Question: How should barbiturate poisoning be treated? Support, charcoal, alkalinization of the urine, charcoal hemoperfusion, or hemodialysis. Question: A heroin addict presents with pulmonary edema. What is the best treatment? Naloxone, O2, and ventilatory support (not diuretics). Question: What alcohol poisoning is suggested by a plasma bicarbonate level of zero? Methanol. It also produces a large osmolar gap and a large anion gap. Methanol poisoning is treated with IV ethanol and hemodialysis. Question: Positive birefringent calcium oxalate crystals in the urine are pathognomonic for poisoning with what substance? Ethylene glycol. The lethal dose of ethylene glycol is 100 mL. Question: What are the signs and symptoms of ethylene glycol poisoning? Hallucinations, nystagmus, ataxia, papilledema, and a large anion gap. How should ethylene glycol poisoning be treated? This should be treated with gastric lavage, sodium bicarbonate, thiamine and pyridoxine, IV ethanol, and hemodialysis. Question: A patient presents with ataxia, altered mental status, and sixth nerve palsy. What is your diagnosis? Wernicke encephalopathy. Question: Alkalinization of urine will increase the excretion of which drugs? Cyclic antidepressants, salicylates, and long-acting barbiturates. Question: What laboratory test can aid in the evaluation of a possible toxic iron ingestion? Total iron-binding capacity measured 3–5 hours after ingestion. If serum iron level is significantly less than the total iron-binding capacity, a toxic iron ingestion is less likely. Question: What is the antidote for a toxic ingestion of iron? Deferoxamine chelates only free iron. It should be given if the iron level is greater than 350 μg/dL. Question: Which type of hydrocarbons are most toxic? Substances with low viscosities (measured in Saybolt Seconds Universal (SSU)) are more toxic than compounds with high viscosities. Gasoline, kerosene, and paint thinner (all aliphatic hydrocarbons with SSUs < 60) are all more toxic than motor oil, tar, and petroleum jelly, which all have SSUs > 100. Of the compounds with SSUs < 60, the most toxic are those that are not aliphatic, including benzene, toluene, xylene, and tetrachloroethylene. Question: Where is the most reliable site for detecting central cyanosis? The tongue. Question: What are two frequently observed organisms causing septic arthritis in drug addicts? Serratia and Pseudomonas. These are rare causes in nonaddicts. Question: An alcoholic patient presents with complaints of abdominal pain and blurred vision. The patient is very photophobic, and blood gases reveal a metabolic acidosis. Diagnosis? Methanol poisoning. Patients may describe seeing something resembling a snowstorm. Question: What is the lethal dose of methanol? 30 mL. Formate levels in methanol poisoning are greatest in vitreous humor. Question: What is clonidine mechanism of action? Clonidine is a centrally acting α-agonist. It leads to decreased sympathetic outflow and lowers catecholamine levels. What is a common complication of pancuronium? Tachycardia from its vagolytic action. Question: Of the following anesthetics, which has the shortest duration of action—lidocaine, procaine, bupivacaine, or mepivacaine? Procaine. Question: Hepatic failure is commonly associated with what anticonvulsant? Valproic acid. Question: What are the end products of methanol, ethylene glycol, and isopropyl alcohol metabolism? Methanol: Formate Ethylene glycol: Oxalate and formate Isopropyl alcohol: Acetone Question: Which type of alcohol ingestion is associated with hypocalcemia? Ethylene glycol. Question: Which type of alcohol ingestion is associated with hemorrhagic pancreatitis? Methanol. Question: Name some hydrocarbons that are considered to be the most toxic and have SSUs under 60: Aromatic hydrocarbons, halogenated hydrocarbons, mineral seal oil, kerosene, naphtha, turpentine, gasoline, and lighter fluid. Those considered less toxic (with SSUs over 100) include grease, diesel oil, mineral oil, petroleum jelly, paraffin wax, and tar. Question: What drug is absolutely contraindicated when treating hydrocarbon poisoning? Epinephrine, as it sensitizes the myocardium and potentially leads to arrest. Question: What drug is contraindicated in a glue-sniffing patient? Epinephrine. Like solvent abusers, these patients may be scared to death. Question: What is a delayed complication of acid ingestion? Pyloric stricture. Question: What is the difference between carbamates and organophosphates? Carbamates produce similar symptoms as organophosphates; however, the bonds in carbamate toxicity are reversible. A patient presents with miotic pupils, muscle fasciculations, diaphoresis, and diffuse oral and bronchial secretions. The patient has a garlic odor on his breath. What is your diagnosis? Organophosphate poisoning. Question: What ECG changes may be associated with organophosphate poisoning? Prolongation of the QT interval, and ST and T wave abnormalities. Question: What is the key laboratory finding in the diagnosis of organophosphate poisoning? Decreased RBC cholinesterase activity. The serum cholinesterase level (pseudocholinesterase) is more sensitive but less specific. RBC cholinesterase is regenerated slowly and can take months to approach normal levels. Question: What is the treatment for organophosphate poisoning? Decontaminate, charcoal, atropine, and pralidoxime PRN. Question: What signs and symptoms are expected after radiation exposures of 100 REM, 300 REM, 400 REM, and 2000 REM, less than 2 hours after exposure? 100 REM: Nausea and vomiting 300 REM: Erythema 400 REM: Diarrhea 2000 REM: Seizures Question: Psilocybin mushroom is associated with what? Hallucinations. Question: How is pancuronium reversed? Atropine and neostigmine. Question: Of patients who die from CA overdose, what percent are awake and alert at the time of first prehospital contact? 25%. Question: What are the contraindications to TAC? Mucus membranes, burns, and large abrasions. TAC used on the tongue and mucus membranes has led to status epilepticus and patient death. What is the most reliable test for determining the severity of radiation poisoning 48 hours after exposure? Absolute lymphocyte counts. Presence or absence of GI symptoms following near lethal doses is a good indicator of mortality. Lead poisoning (clinical features): Learning disability Encephalopathy Anemia Developmental Poisoning (contraindications for charcoal use): Cyanide Hydrocarbon Acid/alkali Relative small compounds Charged (iron, heavy metals) Organophosphate Alcohol Lithium Question: Match the poison with the antidote:
Question: What percentage of poisons have specific antidotes? 5%. Question: What agent usually causes anaphylactic reactions? Contrast media. Other causative agents include NSAIDs, thiamine, and codeine. Conversely, parenteral penicillin and hymenoptera stings are the most common causes of anaphylactic reactions. Anaphylactic reactions are IgE-mediated reactions in previously sensitized people, while anaphylactoid reactions are due to direct release of mediators, including histamine and leukotriene. Describe the action and side effects of diazoxide: Action begins within 1–2 minutes and lasts up to 12 hours. Side effects may include nausea, vomiting, fluid retention, and hyperglycemia. Diazoxide is a direct arterial vasodilator. It is contraindicated in patients with aortic dissection or angina. REFERENCES Brunton Laurence L, L. J. Goodman and Gilman’s the Pharmacological Basis of Therapeutics. 11th ed. New York, NY: McGraw-Hill; 2006. Fauci AS, Braunwald E, Kasper DL, et al., eds. Harrison’s Principles of Internal Medicine, 17th ed. New York: McGraw-Hill; 2008. McPhee Stephen J, PM. Current Medical Diagnosis and Treatment 2009. New York, NY: McGraw-Hill; 2009. Stringer J. Basic Concepts in Pharmacology—A Students Survival Guide. 3rd ed. New York, NY: McGraw-Hill; 2005.
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