Major Topic


Abbreviation Adrenergic

Major Topic
Cholinergic Corticosteroids

Abbreviation Cholinergic Corticosteroids Cardiovascular

Arti-Anxlety Agents

Anti-Anxiety Agents Cardioysscular

Cancer/ Chemotherapy

H!?oglycemics Miscellareous Narcotic Analgesics Terms/DefinitioDs

Hypoglycemics Misc,

Anti-Histamires Anti-lnfectives
Anti-Psychotics Aspirin/Acetamitrophen/ NSAIDs

Anti-Histamines Anti-Infectives Anti-Psychotics

Narcotic Analgesics Terms/Def



Amphetamines are sympathomimetic amines that cause rapid release of:

. Dopamine in

the brain

. Serotonin in the brain . Norepinephrine in the brain . Acetylcholine in the brain



e 2011':0ll

- Denbl Decks

Amphetamines pass readily into the CNS and cause a rapid release of norepinephrine in the brain. Amphetamines increase systolic and diastolic blood pressures and act as weak bronchodilators and respiratory stimulants. They have a high potential for abuse, resulting in tolerance, psychological dependence, and severe social disability. Abuse causes extreme violence and paranoid psychotic behavior Note: Amphetamines and ephedrine are indirectly acting sympathomimetic (sympathetic-type) drugs. These drugs demonstrate tolerance and are orally active, unlike epinephrine and norepinephrine. Therapeutic uses of amphetamines:

. Attention Deficit Hl?eractivity Disorder (ADHD; hyperkinesis) dextroamphetamine (Dexedrine) and a mix of dextroamphetamine with amphetamine (Adderall); (Adderall XR) sometimes used instead ofmethylphenidate (Ritalin). . Narcolepsy dextroamphetamine (Dexedrine) is used to prevent daltime sleepiness


in these patients.

. Weight loss


phentermine (Ionamin)


structurally similar to dextroamphetamine.

1. Tyrosine hydroxylase catalyzes the rate limiting step in the synthesis of norepinephrine (tr'E) and epinephrine. The enzyme is inhibited by metyrosine.
2. Terrnination oftransrnission by NE takes place primarily by the reuptake

ofNE into prejunctional nerves and secondarily into other cells. Monoamine
oxidase (MAO) and catechol-O-methyl transferase (COMT) then play metabolizing the NE.

role in

. An alpha-adrenergic receptor blocker (alpha-blocker)
. A beta-adrenergic receptor blocker @eta-blocker)

Coplright O

20ll-201? Dmral


. Sympathomimetic

. Sympatholytic
. Sympathetic amine . Adrenergic agent

Coplyighr C 201l-2012 DentalDecks

Examples ofselective alphal-blockers used in medicine: . Doxazosin (Cardura) used to fieat hypertension . Prazosin (Minipress) used to treat hypertension . Terazosin (Hytrin) manage mild/moderate hypertension; treatment ofbenign prostatic hyperylasia frPd) . Tamsulosin (Flomax) used to treat benign prostatic hyperplasia (BPH)


These drugs selectively block tr1-type receptors but not o2-type

Important: Alphay-blockerc cause orthostatic hypotension, also known as postural hypotension. This is a fainting spell which occurs because ofa rapid fall in blood pressure when moving from the supine to the upright position, as in getting rapidly out ofthe dental chair. The symptoms are similar to simple fainting, however the condition is related to positioning. Note: Other adverse effects include tachycardia, nasal congestion and dry mouth. can also result from centrally acting drugs (i.e., clonidine and methyldopa) and direct vasodilators (i.e., hydralazine and diazoxide)
1. Alpha-blockers inhibit the vasoconstrictor response to epinephrine and levonordefrin. 2. Beta-blockers increase the vasoconstrictor response to epinephrine, but reduce the tachycardia resulting from epinephrine. 3. MAO inhibitors (i.e., phenelzine and tranylcypromtue) should not be used with indirectly acting sympathetic drugs (i.e., Tyramine and anphetamines) and with several other drugs such as opioids, especially meperidine. 4. Epinephrine and levonordefrin have exaggerated effects when given with neuron depleting agents like reserpine and quanethidine.

*** Orthostatic hypotention



Four kinds ofadrenergic receptor blockers: fNorc: Thel are allused to trcsl hlpertension)

L Beta-adreDergic blockers:
. Nonselectir€: blocks both betal- and beta2-receptors

. Propmnolol 'Carteolol ' Sotalol . Nadolol . P€nbutolol . Timolol
. Betal-s€lective: . Atenolol . . Metoprolol .


. Betaxolol

Bisoprolol 'Acebutolol

2. Alpha-adrenergic blockers

. \onselective: blocks both alphat- and alpha2- receptors



. Phenoxybenzamine

. .


. Doxazosin
. Tamsulosin


Centrally acting Nlpha2-agonists: Act through stimulation ofceDtral inhibitory alpha'-adrenergic rc-

ceprors.They inhibit sympathetic cardioaccelemtor and vasoconskictor centers. Stimulation ofalpha-adrenergic rcceptors in the brainstem results in rcduccd sympathetic outflow from thc CNS

'Clonidine . Methyldopa

\euronal depleting agents: cncompasses awide variety ofdrugs having different mechanisms ofaction. depletion ofmediator in thc nouron whatever their specific mechanism, the result is usually the same Ierminal or an inability ofth€ medialor to be released from the terminal. . Reserpine - depletes granules containing NE in nerve endings, releases NE . Guanethidine - blocks adrcnergic nerve endings by a series ofactions . Metyrosine - inhibits tytosine hydroxylase; used to treat pheochromocytoma


r-ote; Canedilol and labetalol ar€ nonselective bet|-blockers thai also block alphal-receptors. Tley ate
used for healt failure.

Dental Decks . Alphal -receptors only . Isoproterenol 4 CopFight O 20ll-2012. Epinephrine (Adrena lin) Qr'e o . Both alphal.2 and betar. Ventolin) . D€nral Decks . Albuterol (Proventil. Betal-receptors only .Sy nep . Phenylephine hrin e) .2-receptors .. Both alphal and betat-receptors only CopyiSht O20ll-2012 .

alphal (o. Albuterol: bronchodilation .betal . coronary aneriole. Smooth muscle in blood vessels Stomach. vasoconstriction.beta1. betal (B and beta2 (82). alpha2.alpha. skcletal muscle Deoeased secretion Pancreas Liver Gluconeogenesis . betal. l) Some common adrenergic agonists.' . and beta2 . while beta receptor ieiponses are €\citatory in nature in the heart and inhibitory elsewhere. Clonidine: antihlpertensive . Isoprot€renol: bronchodilation . their main us€s and rec€ptor preference: . uterine smooth muscle.lpha: Beia Betal Most common bcta rcceptor Epifi ephine (No rep i h ep h r i n e ge n e r a I b' combines either weaklJ or not at all) Remember: Alpha reccptor responses are predominantly ercitatory in nature.Note: The adrenergic receptors are divided into the subtypes of: .beta. and betal Adrenergic Receptor Tr"Pe Characterisfics Most common alpha rcccptor Less common alpha receptor Less common beta rcceplor (found on rclls in heafl) Neurotransmitters that Combine With Receptors Norepinephrine or Epinephrine Norepinephrine or Epinephrine Norepinephrine or Epinephrine Alpha -4.1) and alpha2 (a2) . bronchodilation . and alpha. Epinephrine: reverse anaphylaxis. Terbutaline: bronchodilation . \Iethvldopa: antihypertensive .alpha2 . vascular.alphat.alphal.) . and beta2 .alphal. Nor€pinephrine: vasoconstriction -alpha1. alphal. Phenylephrine: nasal vasoconstriction . Dobutamine: cardiac stimulation . intestine Vasoconstriction Decreased motility and tone Increased renin seerction Glucon€ogen€sis Kidney Liver Smooth musclc in blood vessels Increased rate and forcc ofcontraction lncreased renin secretion Vasodilation Bronchial.r . and betal .

Hydroxyamphetamine CopriShr O 201 l-2012' Dsral Decks . Tyramine . Prazosin (Minipress) . Terazosrn (Hytrin) 7 Cop"ighr O 20 | | -2012 . Doxazosin (Cardura) . Epinephrine .D€nral Deks . Propranolol (Indera l) . Methamphetamine . Phentolanine hydrochloride (Regitine) .. Phenoxybenzamine hydrochloride (Dibenzy line) . Amphetamine .

2.-blocker.Two types ofadrenergic agonists: 1. alpha-blockers cause unwanted adve$e rcactions. Indirect-acting: are those that cause the rel€as€ of stored norepinephrine at the postganglionic nerve endings to produce their effects. Terbutaline . *** Aside from hlpotension. Isoproterenol = betal.2 agonist . Aipha-blockers are commonly used to reduce high blood pressure and to treat an enlarged prostate. \on-selective alpha antagonists: block both types of receptors and are generally not used for cardiac conditions because blocking both recepto$ can ca\se tachycardia (rqpid heart beat) and palpitations (pounding he. They are used in the presurgical management of pheochromocytoma. Epinephrine: alphar. . causing them to relax. Phenoxybenzamine and phentolamine both are nonselective alphal and alpha2blockers. which are classified according to the alpha receplor that they block (alphal or alpha).2 and betar. They act on blood vessels. Phenylephine : alphal selective agonist . Among the alphal-blockers it is the prefered agent for hypenension due to a longer duration of action. is a major effect ofalpha-blockade. Some examples of alpha-blockers: .beta2 selective agonist . . Used to treat benign prostatic hypertrophy.2 agonist Remember: Some literature refers to direct and indirect-acting adrenergic agonists as direct and indirect-acting sympathomimetic ag€nts. . Norepinephrine: alphal. - selectiv€ alpha'-blocker lt is rarely used to treat hypertension due to . Direct-acting adrenergic agonists may be receptor selective or receptor non-selective: . They are used in the presurgical management of pheochromocytoma and sometimes in treating Raynaud's phenomenon. which relatively few adverse reactions. Selective alpha antagonists: only block alphal-recepto$ and are more commonly used ro rreat cardiac conditions (h)pertension) and benign prostatic hyperplasia. These terms are almost always slnonl mous. Terazosin selective alphar-blocker. *** Propranolol is a beta-blocker (speclicall. Direct-acting: are those that interact directly with the alpha or beta receptors. Doxazosin .qrt beat). Tyramine and amphetamines cause release of norepinephrine. Prazosin selective alpha.2 and betal agonist . They are agents that bring about tissue responses resembling those produced by stimulation of the sympathetic nervous system.a non-selective beta-blocker) Alpha-blockers are medications that act by competitively inhibiting the action of catecholamines at the alpha receptor site. . There are two types of alpha-blockers. Clonidine : alpha2 selective agonist . Dobutamine = alphat and betal selective agonist . Albuterol : beta2 selective agonist .

l) receptors . Alphar (d. Fat cells .Denral Decks . Neuons in the CNS . Betal (Br) receptors . Alpha2 (02) receptors . Presynaptic newe terminals . (82) receptors 8 Coplrighr @ 2011. All of the above I Coplrighr O 201 l-2012 Dental Deck! . Blood platelets . Beta. Vascular smooth muscle ..2012 .

Postjunctional betar adrenergic receptors are found in the myocardium (heart). and adipose tissue. Postjunctional alpha. Arterioles in skin. of Bela receptors fall inlo t\\o groups: 1. and k jdney Itertrrdrce verre^. arteries.responsible for most ofthe inhibitory effects such as vasodilation and relaxation ofrespiratory smooth muscle. 2. Beta (R) receptors . . the intestinal tract smooth muscle. viscera. -\lpha receptors fall into two groups: 1. l. and veins.. Ane(ioles (on. . Postjunctional beta. mucosa. Alpha (o) receptors responsible for most of the excitatory effects such as vasoconstriction and contraction ofthe uterus and spleen. adrenergic receptors are found in bronchiolar and vascular smooth muscle. \ote: Two fnportant EXCEPIIONS to the above: some alpha receptors mediate relaxatio of gastrointestinal smooth muscle. arterioles. and some beta receptors mediate increases in the torce and rate of contractions ofthe heart. Presynaptic nerve endings Postsynaptic in CNS lnhibil rorepinephrine r€le3s€ Decreased sympathetic tone . Prejunctional alpha. in the GI tract. 2.l arkties in skeletal nuscle) Bronchial and uterine smooth muscl€ lncreased heart mte lncaeased force of contmction There are two main types ofadrenergic receptors: I . adrenergic receptors mediate the inhibition of the release norepinephrine. adrenergic receptors are found in radial smooth muscle of the iris.

Preganglionic sympathetic neurons . Relaxes bronchial smooth muscle (bronchodilation) . Causes . Produces physiological actions opposite to that of histamine 11 Copright O 201l-2012 .Dental Deck . Decrease blood volume in nasal tissues a hypertensive response . Postganglionic sympathetic neurons . Preganglionic parasympathetic neurons . Postganglionic parasympathetic neurons 10 Copyright @ 2011.Denral Decks . Constricts arteriolar blood vessels (vasoconstriction) .2012 ..

Postganglionic neurons ofthc sympathctic branch arc usually adrenergic. with thc structurcs inncrvatcd by the diffcrcnt libcrs and thc chcmical nrcdiators rcsponsible for lransmission at the various loci. f.The autonomic neryous system f. Prcganglionic ncurons ofboth divisions f. is govemed and main- tained by the ANS.._-1 vg Smoolh mmOc Reproduced wilh permission. and throat Common side effects: headaches. To treat bronchospasm associated with hypotension. Note: Adrcnergic blocking agents block thc cffcct of impulses transmittcd by thc adrenergic postganglionic ncurons ofthe sympathetic branch. Mosby. and rectal sphincter tone are regulated by the ANS. Dashed lines indicatc postganglionic autonomic fibcrs. agitation (anxiei)). by decreasing the rate of diffusion and absorption from the injectlon site . Bloodpressure. It is added to local anesthetics as a vasoconstrictor to prolong the activity ofthe local anesthetic solutions. uterus.l Thetureuti. Somatic NeNous System Autonomic N€rvous System Sr_npothctic division Ach Ach G----'------'. sinuses.----------.o|o&\ an. and Yagiela JA. sweating. c}--. and gasEointestinal tract."r. Important: Epinephrine should be used with caution in patients with high blood pressure and hyperthyroidism. eyes. The aulononlic nervous system has cholinergic neurons that secrete acetylcholine and adrenergic neurons that secrctc norepinephrine. from the salivaryglands to thc analsphincter. Agent ofchoice for anaphylactic reactions (given sublingually or subcutaneoush)) . These patients may have an increased sensitivity to epinephrine.ts-lAdrcnal Parasymptlhetic division Fibcrs ofthe somatic and autonomic nervous systcms. To treat hypersensitivity reactions . To relieve congestion ofthe nose. as arc the postganglionic curons ofthc parastmpathetic branch.. Pnamd . and tachycardia. Function ofthe hean. To alleviate symptoms ofan acute asthma attack .t for De.tista. bladder. eli( and paraslnpathetit) are cholinergic.$callf the h'pothalanur. 'meJrlL-E NE n-n * Hcan Arrr G-<Ach-Smoorhmusclc Glands r.\:l rnla/. Thc sympathetic nervous system (fron thoraco-hmbar outJlow) ar. To restore cardiac activity in cardiac arrest . pulse. urinary bladder. as in anaphylaxis .4NS/ controls involtntary (smooth)rnuscle and gland activity.d thc parasympa- thetic nervous system (ton cratlial-socrdl ou|lo\. Therapeutic indications for epinephrine: .'<achr :'"dblhd'*. arc choli ergic = secrcte acelylcholine).om Neidle EA. CNS . . it is composcd of two antagonistic systems.. The ANS is a complcx sct ofncurons that originatc from thc CNS fipe.t). 1989. Onc rXCl'PltON i s thc sympathetic postganglionic ncurons thal inncflate the swcat glands (thei.

Alpha-blocker . The first statement is false. ft has vasopressor activity . . Dental Decks . It causes increased cardiac output . Adrenergic agonist .) 20ll-2012. All ofthe above 13 Coplright (. It has bronchodilator properties . Both e 20lt-2012 Denral Decks "Epinephrine reversal' is a predictable result of the use of epinephrine in a patient rvho has received a/an: . It has a rapid onset ofaction .Epinephrlne is the agent of choice for treating an anaphyhctic reaction because ofits stimulatorv effects on both alpha and beta adrenergic receptors. Both statements are true statements are false 12 Copyrighr . The first statement is true. the second statement is false . Beta-blocker . the second statement is true . All ofthe following are desirable efTects ofepinephrine that make it the agent of choice for treating an anaphylactic reaction.

After the alpha-receptors have been blocked by an alphablocker. Note: Epinephrine is administered either intravenously. . subcutaneously or intramuscularly. receDtors. Alpha receptor stimulation results in a vasopressor response (elevation ofblood pressLtre). As a component of local anesthetic solutions to prolong duration ofanesthesia .Epinephrine is the agent of choice for treating an anaphylactic reaction because of its stimulatory effects on both alpha and beta adrenergic receptors. There is a very rapid onset of action when given by these routes. In this way. sublingually. This is because epinephrine stimulates both alpha and beta-receptors in the cardiovascular system but norepinephrine only stimulates alpha-receptors (norepinephrine lacks beta2effbcts). the pressor effect of norepinephrine is reduced or abolished while epinephrine brings about a fall in blood pressure.In the absence ofblocking agents. Note: A pressor response (produces an increase in blood pressure) is mediated by alphareceptors and a depressor response (produces a decrease in blood pressure) is mediated bv beta.Asthma bronchodilatorproperties Explanation of answer: One of the best known effects of the alpha-receptor trlocking (antiadrenergiy' is their ability to reverse the pressor action of adrenaline fepl^gents nephrine). After blockage ofthe alpha-receptors. only the beta-receptors can be stimulated. epinephrine counteracts the vascular effects of histamine-related anaphylaxis. epinephrine and norepinephrine both cause the blood pressure to rise. To control superficial hemorrhage . Other therapeutic indications for the use ofepinephrine: . Beta receptor stimulation results in air way dilation and increased cardiac output.

Miosrs (contraction ofthe pupil) . Dry mouth 14 Coplrighr O 2011. Neither ofthe above.Dertal Decls r\ '.2012 . Hallucinations .2012 . Drowsiness . \' If norepinephrine or eplnephrine wers to stimul|te or combine with the alpba receptors in the eye. Arthralgia .Denlal Decks . norepinepkine and epinephrine do not stimulate or combine with alpha receptors in the eye t5 Copyright O 2011. which response would you erpect? . Mydriasis (dilation of the pupil) ..

It is used in the treatment ofhypertension.). Metoprolol and Atenolol are both longer-acting and more predictable than Propranolol in producing therapeutic plasma levels. Atenolol (Tenormin) is a competitive. acute angina pectoris and may be helpful after a heart attack. betar-selective adrenergic receptor b\ocker (carlioselectlver. Due to its low lipid solubility. Because they are betar selective adrenergic receptorblockers.eptors) similar to Pindolol. they are also safer to use in patients with a history of asthma or bronchitis.Metoprolol (Lopressor Toprol-XL) is a competitive. betal-selective adrenergic receptor blocker (cardioselective). ctr.. The most common side effects ofbeta-blockers are weakness and drowsiness. thereby having eff'ects on bronchial smooth rnuscle.: Decreases peristalsis (ll Urinary bladder c[l PI Contracts sphincter Contracts trigone and sphincter muscles Relaxes detrusor muscle Excites uterine contactions Inhibits uterine contractions Uterus cLl P2 . lt also has mild intrinsic s) mpathomimetic activ tly (partial agottist actiritl at beta: rc.selective). which is most similar to Atenolol.z ctl Lung Intestine 0. It is used in the treatment ofhypertension and chronic angina pectoris. It has a low lipid solubilin. *** Important points: L \\'ith all "selective" beta-blockers. Propranololl. -\s the dose is increased they also block the beta2 receptors.g. -{cebutolol (Sectral) is a betar-selective adrenergic receptor blocker (cqrdio. Organ/Tissue Heart p1 Receptor Type Response to Adr€nergic Agonists Increases conduction velocity Increases contraction force Increases conhaction mte Increases cardiac output Constricts cerebral arterioles PI p1 0' Anenoles ctl 0: Eve Dilates skeletal muscle arterioles Contracts sphincter muscle. minimally metabolized. $hich reduces its likelihood of producing adverse Crr-S effects. l. selectivity for the betal receptor is lost at high doses. and has a low potential for causing CNS side effects compared to lipid soluble beta-blockers (e. producing mydriasis Relaxes tracheal and bronchial muscles F r. wtth alo]ig plasma halflife (1or1g du'ation ofdction. Atenolol is renally eliminated. lt is used to treat hypertension and to control ventricular arrhythmias.

. Cholinomimetic . Parasympathomimetic . Sympathomimetic 17 Coplrighr O 20ll-2012 Dental Decks . Aminophylline 't6 CoP)right O 20ll-2012 . Antiadrenergic .Denlal Decks Pharmaceutical agents that bring about tissue responses resembling thme produced by stimul*tion of the sympath€tic nervous system are called? l . Histamine . Metaproterenol . Alb]uterol (Proventi I) S almeter ol (S e r e v e n t) (A lup e nt) . Levalbuterol (Xop enex) . .

levalbuterol. In medicine. and viscous mucoid bronchial secrelions. They are used as bronchodilators for asthma attacks and for allergic states including anaphylactic shock. These drugs relax bronchial smooth muscle to improve airway function. wheezing on expiration. sympathomimetics are used as pressor agents to maintain blood pressure in vascular shock. Important: Epinephrine is indicated in medicine to treat bronchospasm and hypersensitivity reactions. norepinephrine. Important: Albuterol is the drug of choice as a "tescue" agent during an acute asthmatic attack. lt is used to restore cardiac activity in cardiac arest. Thus they stimulate the beta recepton in the airway to cause bronchodilation. or emotional stress. coughing. it is used to prolong the duration of local anesthesia. Management and prevention ofan acute asthma attack: . Syrnpathomimetics used in medicine include dopamine. adrenergic receptor agonists. epinephrine. and phenylephrine. Theophylline compounds are administered orally as bronchodilators in reversible airway obstruction due to asthma or COPD (chronic obstructive pulmonary tlisea. albuterol. isoproterenol. As a component of local anesthetic vigorous exercise. Epinephrine is the sympathomimetic agent used in dentistry.Asthma is a respiratory disorder characterized by recurring episodes of paroxysmal dyspnea. It is the vasoconstrictor for anesthetic solulions and the vasoconstrictor component in gingival retraction cords. The terms sympathomimetics. salmeterol and metaproterenol are beta. They are taken via aerosol inhalers and nebulizers. The episodes may be precipitated by inhalation ofallergens or pollutants. . adrenergic agonists and adrenergic agents are almost always synonymous. infection. Note: Arninophylline is an example of a theophylline compound. Epinephrine. It is the agent of choice for reversing anaphylactic reactions. syrnpathomimetic amines.

Treat hypertension .Dental Decks . Bradycardia . All ofthe above 18 Copyrighr e 20ll-2012 . Reverse an anaphylactic reaction . Viosis . Prevent angina pectoris . H)?ertension . Increased salivation Copltighr O 201 I 19 '2012 . Reduce anxiety ..DenblDecks A fear re|ction activates the sympathetic division the autonomic nervous svstem to result in: of .

Sympathetic activation ofthe heart would result in tachycardia. \liosis (pupillaT. Will not reduce arlxiety but will likely increase anxiety since it has central nervous system stimulatory effects Activation ofthe sympathetic portion ofthe autonomic nervous system will cause alpharadrenergic receptor activation to result in arteriolar vasoconstriction with an associated elevation of blood pressure leading to hypertension. Epinephrine is: . Sympathetic activation ofthe salivary glands would result in a thick ropeytype salivary flow.. not increased salivation. constriction). it will increase cardiac output via betar receptor stimulation on the cardiac muscle.--. Sympathetic activation ofthe eye would result in mydri^sis (dilstion) not miosis. . 3. Contraindicated in angina conditions because its cardiostimulatory effects would aggravate this condition . bradycardia. Epinephrine stimulates both beta adrenergic receptors and alpha adrenergic receptors within the sympathetic division ofthe autonomic nervous system. .The prototypical adrenergic agonist agent is epinephrine. and increased salivation are physiological effects all resulting from activation of the parasympathetic division of the aulonomic nen'ous system. \ot!r -. Epinephrine. Anaphylaxis is characterized by rapid. will rapidly reverse the hypotension by causing vasoconstriction via the alphal receptor stimulation. 2. Ineffective in treating hypertension because of its alpha receptor stimulatory actions on the vasculature which could cause an even further elevation ofblood pressure . l. extreme reduction in blood pressure and bronchospasms. it will dilate the bronchial tubes via beta2 receptor stimulation. upon injectable administration. not bradycardia.

Dmtal Decks 21 CoplriShr O 20ll-2012 .. Lungs .Dental D€cks . Liver . Plasma . Kidney 20 Coplright O 201 1-2012 .

They also display cross-allergenicity. The CNS effects include: restlessness. Allergic reactions are more prevalent with the ester-type rather than the amide{ype anesthetics. Hydrolysis ofthe amidc bond L H. can a)so cause allergies . Asthmatic wheezing syndromes have occurred in response to local anesthetic injections . convulsive seizures followed by CNS depression. stimulation. Remember: Esters are metabolized by the plasma enzyme plasma pseudocholinesterase. These reactions are manifested as dermatological reactions and edema at the in- jection site. .5% w. itching. Eridocaine and bupivacaine are highly bound. slowed respiration and even coma .000) \ote: Bupivacainc has the longest duration of action ofany dcntal local anesthetic prescntly available. tremors. Amides are metabolized by three types ofreactions: l. -{dlerse effects caused by local anesthetics L Efltcts resulting from toxicitl are categorized into two major grottps: L E11'ects resulting from allergy Toricities: .000) Articaine 4% Wepinephrine (l : 100./epinephrine (Bupivacaine Wepinephrine | :200. Esters will show greater toxicity in patients with a hereditary deficiency of plasna esterases.ocaine (Xylocairte) . which was used as a perservative. particularly from the amides. Lidocaine and mepivacaine are bound moderately. Lrd. Opioids can increase the systemic toxicity oflocal anesthetics .vdroxylation ofthe aromatic ring The amides vary in protein binding. Ptilocaine (Citane. Note: Bupivacaine is more selective for sensory nerves than etidocaine.Mepivacaine(Carbocoite)'Bup|acarne(Matcaine)'Etidocatnc(Dkranest) Thesc anesthetics are rnetabolized by the hepatic microsomal enzyme system.rt Allergy-': . Hypersensitivities or allergic reactions to local anesthetics.000) Marcaine 0. . are rare. . Lrdocaine 20" w/epinephnne( I: I00. and oral mucosal swelling . Notei The most abundant urinary metabolite of lidocaine is 4-hydroxyxvlidine. which is a plasma esterase.The amide-type local ancsthctics that are used in dentistry and metabolizcd by the liver includc: . A(icain (Ultrucaine) . Too much anesthetic in the bloodstream can cause toxicities to the central nervous system /Cr\t and cardiovascular system . The products formcd do not have anesthetic actions and are excreted p marily in the urine as metabolites. These agents should be used wjth caution ornot at all in patients with compromiscd livcr function. Dealkylation ofthe amino terminus 2. The cardiovascular effects include: bradycardia and reduction ofcardiac . Ester local anesthetic allergic manifestations include: nasolabial swelling. Ilethylparaben.

. Ionized form . Both ionized and nonionized free-base forms 23 CopFight O 20ll-2012. D€ntal Decks . Increases the membrane's permeability to sodium . Decreases sodium uptake through sodium chamels ofthe axon Increases potassium outflow from inside to outside the nerve . Nonionized free-base form .D€nral Decks . Increases the excitability of the nerve axon 22 Cop'right O 201| -2012 . .

r. Sincc axons carry pain scnsations. Key point of all this: The potential action olall local zuresthetics depends on the ability ofthe anesthetic salt to liberate the free-base.24/.u1 onesthctics havc no effects on potassium at thc ncn. Small. Once the local anesthetic is injected the buffering capacity and pH of the tissues /zornallt T.0 or lower.. the pH olthe tissues may be acidic and there is a significant reduction in the concentration of the free-base form. and skclctal musclc tonc /rroto. Local anesthesia can only be obtained if sufficient free-base is ar ailable. ln solution an equilibrium is established between the ionized and the nonionized tbm. t%.Whcn a local ancsthctic solution is injcctcd ncar thc nervc.J% B 0.5%. The proportion ofthe drug in the ionized form depends on rhe pKa of the drug and the pH ofthe solution. follo$cd by touch. arc affcclcd firsr. : :Notc*. D. They are converted to their irater-soluble (hydrophilic.60/0 B t%. 2'/". :. In this situation.25%. 2%.8) into tissue that has a pH of 7. This dccrcascs thc ncrvc cxcitability below a critical lcvcl and nervc impulscs fail to propagalc along lhc axon.3% 30 60 min 64.4 approximately 5-20ulo ofthe local anesthetic is in free-base form which is enough to penetrate and cause anesthesia.5y. Ifinfection or inflammation is present. proprioccption fpler. 05%. thc solutron intcrfcrcs with the uptakc ofsodium from outsidc to insidc thc ncrvc. Note: Ifyou inject lidocaine (pKa = 7. which conducl pain and tcmperaturc scnsations. The lower the pKa ofthe drug and the higher the pH ofthe solution or injected tissues. the local anesthetic may not be effective.34/n i5 min 2-l I'r Local anesthetic free bases are fat-s oluble (lipophilic) ofthe local anesthetic.c axon.1) shifts the equilibrium in favor of free-base formation./.8. l0 min to/r. 4. l. the lidocaine will exist in an equal mixture ofionized and nonionized forms which will be more than enough to Droduce aresthesia. 3% nin Long Actlng 5 min 95.5% 55% c B t%. Thc localanesthctic blocks thc spccific sodium channels thcrcby blocking thc sodium uplakc. This is important because only the nonionized free-base form ofthe drug can readily penerrate tissue membranes. the more free-base will be available. l-5 min 45 90 min 60'120 17. 6-12 min l5 60 nin 5_8% C C t /". At the usual solution pH of 6.2%. nonmyelinated ncrvc Shorr Acdtrg Onret of Bound Ho* Supplied 2-5 min Estc.0.15'/" 5-10 hr Eslcr 91% 75. L Local ancsthctics reversibly block ncrvc impulsc conduction and producc rcvcrsiblc loss ofscnsalion al thcir administcred site. . most local anesthetics are almost completely in the ionized form. | .l hydrochloride salts to allow preparation ofan injectable solution.2%.6% C 0. 1-n.fl/re).. tv/. thcsc scnsalions lvill nol bc carricd and a blockagc ofpain rcsults.. At physiologic pH of 7. 2.

Lungs .2012 . Meperidine 21 Cop)'right O 201 | . Chloral hydrate .. Kidneys 25 Cop)ri8hr O 20ll -2012 . Pentobarbital . Secobarbital .Denial Decks .Denral Decks . Liver . Plasma .

mepivacaine. Ester-type local anesthetics are no longer available as dental anesthetic injectable preparations because of their relatively high incidence of allergy. and articaine. T€trodotoxin: found in a number oftissues ofthe puffer or blowfish . 3. The usual dose for a child is 50 mg/kg up to a maximum of lg. Saxitoxin: is produced by certain stmins ofalgae Remember: Dyclonine hydrochloride is unusual in that it has a ketone linkage between the aromatic moiety and the rcst ofthe anesthetic molecule. When procaine is metabolized by plasma cholinesterase. Chloral hydrate is a prodrug and is metabolized to the active metabolite. tet:acaitrrc. An amide grouping is essentially a bridge or link containing the .CONHCH2-configuration. caustic taste. Chloral hydrate does not relieve pain. Diphenhydramine: H . Procaine (Novocaine) was one of the original est€r-type anesthetics. Amide-tJ*pe local anesthetics all have an amide grouping within their chemical structure. Only the amides are presently available as dental injectable local anesthetic agents.antidepressants. They are also available as medical anesthetic preparations such as propoxyc atne (Ravocaine). An ester grouping is essentially a bridge or link containing the COOCH2-configuration. Many patients developed an allergy to PABA. thus it is poorl). prilocaine. serious toxicity can result if the dose is not controlled. It is used as a topical. Note: PABA can decrease the effectiveness of sulfonamides (antibiotics). 1 antihistamine . )iote: Other chemicals that act like local anesthetics: . l. trichloroethanol. . and dibucaine. Ester-t!'pe local anesthetics all have an ester grouping within their chemical structure. These include lidocaine. and benzodiazepines. Chloral hydrate's metabolite (trichloroethanol) may displace warfarin from "'"ee. chloral hydrate is available as a 500 mg/5 ml solution. Be careful when using Chloral hydrate. It has an unpleasant odor and a bitter. Important: Children will often enter a period ofexcitement and irritability before becoming sedated. For use in children. which can be partially masked in a flavored syrup.1.l its protein binding sites resulting in an increase in the hypoprothrombinemic response to warfarin.Traditionally chloral hydrate has been used orally in the preoperative managem€nt of the anxious pediatric dental patient. Ester-type local anesthetics are mainly available as topical anesthetics and include benzocaine (which does not have an qmi o terminus end therefore cloes not become charged.. Chloral hydrate is rapidly absorbed after oral administration with an onset of 15 to 30 minutes. These additive with other CNS depressants . a highly allergic compound called para aminobenzoic acid lPl BAfor short) is formed. This enzyme splits the ester linkage rvithin the chemical structure rendering the anesthetic ineffective. It affects brain centers that control wakefulness and alertness.'Nnt"q" 2. other CNS depressants include ethanol. soluble in water). . bupivacaine. Ester-type local anesthetics are metabolized by the plasma enzyme plasma cholinesterase. Sedative effects and/or respiratory depression with chloral hydrate may be monitor for increased effect. Its duration ofaction is about 4 hours. Another name for this enzyme is pseudocholinesterase. narcotic analgesics.

Rleumatoid adhritis . Cocaine .] .20l? . Bupivacaine . Biliary tract disease .. Articaine . Dental Dects Which trical anesthetic has no place in the routine practice of dentistry? :'. Hepatic disease Coplright O 201l-2012 . Prilocaine Coplrighr O20ll. Type II diabetes . Lidocaine .Denral Deck .

and it is the only local anesthetic that causes definite vasoconstriction (all other locql anesthetics qre va' sodildtors). In this eutectic mixture. a condition that is characterized by increased levels of methemoglobin in the blood. laryngeal.. It is available as a 4olo solution with or without epinephrine. or epinephrine. Cocaine causes significant euphoria (most likely due to its blockqde of reuptake of dopantine in the bralzl. Cream is a eutectic mixture oflidocaine 2. Prilocaine produces less vasodilation than do equal amounts ofLidocaine fl is somev'hat less potent thqn Lidocaire). used for nerve block. cocaine incresses the pressor activity oJ these $)mP at homim e t ic am i n es ). . It increases the risk of developing cardiac arrhythmias and hypertension (i. but since methemoglobinemia is a possible reaction. Prilocaine is about one-half as toxic as Lidocaine.e.*** Remember: All amides are rnetabolized primarily in the liver. The pharmacology ofcocaine is unique among local anesthetics in that the drug inhibits the uptake ofcatecholamines by adrenergic newe terminals.5% and prilocaine 2. Cocaine is commercially available in a variety of forms and is applied to mucous membranes of the oral. epidural and regional anesthesia. which prolongs the anesihetic effect. It is potent and extremely toxic. Despite being an excellent local anesthetic.5olo topical cream. Note: This methemoglobin is less effective than hemoglobin in catrying oxygen in the blood. It therefore potentiates the ac- tion ol endogenously released and exogenously administered sympathomimetic amines such as dobutamine. and the metabolites are then renally excreted. \ote: EMLA Cocaine is a naturally occurring ester ofbenzoic acid and was the first local anesthetic used in dentistry and medicine. the risk of abuse and the intense local vasoconstriction it produces prevent cocaine from being more widely used clinically. both anesthetics are liquid at room temperature and the penetration and subsequent systemic absorption ofboth prilocaine and lidocaine are enhanced over that which would be seen if each component in cn stalline form was applied separately as a 2. Important: Cocaine has no place in the routine practice of dentistry. It has an intermediate duration ofaction and is longer acting than Lidocaine. Priloc^ite (Citanesrl is a local anesthetic ofthe amide class. and abuse can lead to a physical dependence. a product that can produce m€themoglobinemia. dopamine. and nasal cavities for use as a topical anesthetic. Prilocaine is not used for patients with hypoxic conditions ofany kind. Prilocaine is metabolized to orthotoluidine.5% formulated as an oil in water emulsion.

How much lidocline and epinephrine does the carpule contain? .2012.8 ml of a 27o solution of lidocaine with 1:100. Denbl Decks A dental rnesthetic carpule contains 1. the extracellular fluid dilutes the anesthetic 28 Coplriglt O 2011.0fi) epinephrine. thus inactivating the anesthetic . The pH decreases.6 mg lidocaine and 0.36 mg lidocaine and 0. 3. The pH rises.18 mg epinephrine . thus decreasing available free base .018 mg epinephrine 29 Coplriglt O 20ll-2012.18 mg epinephrine . The pH rises.3. thus decreasing available free base .6 mg lidocaine and 0. Denral Decks . The pH remains the same.018 mg epinephrine . 36 mg lidocaine and 0.. question: I ml ofa 2olo solution oflidocaine with l:100.) alom. approxrmately 10-207o portion ofan infiltrated local anesthetic is in the form of the free base (non-ionized form). When tissues are acidic.4). Therefore. the local anesthetic when infiltrated to the tissue site is not effective at the normal anesthetic doses. That portion which is ionized has difficulty penetrating the nerve and will not be effective. KeJ. .4).000 epinephrine contains 20 mg of lidocaine and 0.s no proton attqched). will chemically exist as a portion which is ionized (has a proton attached) and as a portion which is non-ionized (ha. . Therefore. the more effective it will be. That portion which is non-ionized will penetrate the n€rve to cause anesthesia. a local anesthetic when infiltrated. The more proportion ofthe anesthetic which is in the free base form.8 ml of2% solution oflidocaine with I : 100. Epinephrine (vaso constrictor) is included in local anesthetics for the following reasons: .018 mg epinephrine.At body pH (7. A dental carpule contains 1.8 ml solution. This is enough to penetrate the nerve to cause anesthesia. Note: A proton is nothing more than a hydrogen (H.010 mg of epinephrine. as in the case of tissue infection. It prolongs the duration ofaction It reduces toxicity It reduces the rate ofvascular absorption lt provides a hemostatic effect to reduce bleeding at injection site . When tissue conditions are normal (p11 7. There is not enough free base form to penetrate the nerve to cause anesthesia. That portion which is non-ioniz€d is also known as the free base. less free base portion exists and more ionized portion is present. .000 epinephrine contains 36 mg of lidocaine and 0.

15 milliliters .. ' . Gender 31 Coplright C 20ll-2012 - De alDecks . Height .{ge . $'eight .5 milliliters . l0 milliliters .7. 20 milliliters 30 Coplaigh O 201l-201? Dmtal Decks The maximum reconmended dose ofa local anesthetic that c|n be tdministered to r child < 10 years ofage is determined by: '\ .

3 carpttles (8 cdrpules of 224 Lldocaine can be used) Remember. a dosage of 4. Bolh ofthese agents are known to be hepatic drug metabolizing drug inducers. and this is lhe Drobable mcchanism oftheir druc interaction with lidocaine. :{ote: I kg = 2. Lidocaine clearancc may be accelerated by concomitant use ofphenobarbital or phenytoin. and nadolol are reported to reducc lidocaine clearance due to the decreasg in cardiac output caused by thc beta-blockers. Decreased cardiac output rcsults in reduced liver blood flow which explains the decline in Iidocarne clearance caused by these drugs.8 mL ffu every carpule) = 36 mg / I carpule . Propranolol. Cimetidine also decreases lidocaine clearance. . Because cimetidine does not change liver blood llow.20 ng (in every mL) = 15 mLs . Erample: For Lidocaine (2%) wrth epinephrine.lmportant information to solve qucstions ofthis type: . There arc 20 mg ofLidocaine in every milliliter of2%o Lidocaine 3n0 mg (maximal recommended dose) . it is believed that cimetidine decreases lidocaine clearance by inhibiting hepatic microsomal enz1mes. 300 mg - 36 69 = 3. 20 mg x 1. Lidocaine has serious drug interactions with beta-blockers and cim€tidine that decrease lidocaine clearance 3070 or more. metoprolol. but thc mcchanism ofthe interaction is different.4 mg/kg should not be exceeded (wL\imum is 300 ng).8 mL /l carpule = 36 mg/l calpule .3 lbs 2Yo: 20 mg I mLx 1.

&g 33 Cop]. Large myelinated fibers .Dental Deks . Small unmyelinated fibers Small myelinated fibers .Denbl Decks .rjght O 20: l-2012 . . 100 mg/kg .. Large unmyelinated fibers 32 CopyrSh O 20ll-2012 . I mg&g . 300 mg.

000 (mg) 0.*** These conduct pain and temperature Important: They depress the large myelinated fibers last. The table belo*' shows the following number of dental cartridges containing 1. Touch 4.017 0.7 ml vof ume of solution to provide the indicated amounts of articaine hydrochioride 4% and epi- nenhrine l:100. Remember: Local anesthetics reversibly block nerve impulse conduction and produce the reversible loss of sensation at their administration site.034 0.119 0. Skeletal muscle tone Note: Pain threshold refers to the lowest level ofnain a natient will detect. In a tlpical 70 kg adult male.7 ml) 1 Articaine HCL (4%) (mg) 68 136 Epinephrine l:100.136 340 408 476 544 6 7 8 . the maximum recommended amount of articaine that could be given to a 70 kg adult in one appointment is 490 mgs. Number of Cartridges (1. Temperature 3.051 2 3 204 272 4 5 0. the dose of 7 mghg would equate to a total of490 mgs. Pain 2. They appear to become incorporated within the nerve membrane or to bind to specific membrane sodium ion channels.068 0. restricting sodium pemeability rn response to partial depolarization.000. Thus. Proprioception 5. They do not produce a loss of consciousness.085 0. Clinically the general order of loss of function is as follows: l. The small nerves have the greater surface-volume ratio (this accounts for the rapid onset ofaction).102 0.

Pleasant induction . Oral . Rapid onset ofaction \ .ers pain threshold .IM 34 Cop"ighr O 20ll-2012 . Therapeutic sedative for many medically compromised patients .IV . Produces euphoria . Lou. Inlalation .. Mrtually no adverse effects in absence ofhypoxia .Denral D€cks All of the following are advantages of using nitrous oxide analgesia EXCEPT one. Suitable for all ages 35 Copyrighr O 20ll-2012 D€nral Decks . Which one is the EXCEPTIOM . Rapid and complete recovery . Titratable .

*** The agent used most frequently is nitrous oxide. Mild analgesia is a secondary effect. This results in a temporary increase in either the pressure and/or volume of the cavity depending upon the distensibility ofits walls. . colorless. . This is most noticeabl€ in the bowel . is necessary in . Nitrous oxide delivery machines come pre-equipped with a failsafe m€chanism that patient. to the than 20y" oxygen to be delivered will not allow less . Long term exposure to low doses ofnitrous oxide has been shown to increase the incidence ofspontaneous abortions. Remember: Nitrous oxide has minimal depressant effects on the cardiovascular system and no skeletal muscle relaxant properties. relaxation. Nitrous oxide local anesthetic properties. Oxygen is stored in green tanks.40oh: mild sleepiness. . Above 507o: this is too much nitrous *** Rapid onset: 5 minutes *** Rapid recovery: 5 minutes \ote: Nitrous oxide -nausea. mind dissociation. There is no biotransformation. Nitrous oxide will diffuse into air-containing cavities within the body faster than nitrogen diffirses out. The first symptom ofnitrous oxide onset is tingling of the hands. . Nitrous oxide is a slight sweet smelling. Environmental contamination by nitrous oxide can be kept to a minimum by employing a scayeng€r syst€m. and the gas is rapidly excreted by the lungs when the concentration gradient is reversed. The main therapeutic effect of nitrous oxide is relaxation/sedation (it is used in conscious sedqtion). sweatinq does not provide enough analgesic effect to preclude the use oflocal anesthesia in dental surgery or restorative procedures. Nitrous oxide interacts with vitamin Bt2 synthesis in the human body by interfering with the enzyme methionin€ synthas€. l0o/o . some analgesia. *** \itrous oxide elevat€s pain threshold Important points about nitrous oxide: . the addition oflocal anesthesia procedures in which pain is anticipated. Nitrous oxide is quickly absorbed from the lungs and is physically dissolved in the blood. Dose response for nitrous oxide (always given in mixture with oxygen): . Local anesthetics must be used along rvith nitrous oxide. heightened auditory perception .20%o: tingling ofhands.5 times heavier than air. . When nitrous oxide is used heavily and over an extended period of time. It is 1. depl€ting the body of vitamin -B12. Nitrous oxid€ is stored under pressure (7 50 psi) in sleel cylinderc (in q liquid state) pairltcd has no blue. It is recommended that the patient be maintained on oxygen for 5 to l0 minutes after the sedation period. . It must always be coupled with no less than 207o oxygen. 20o/o . .47) and termrll'attorr. . colorless gas with a slightly sweet odor and tasteless lt is very sta- ble and inert chemically at room temperatures. feet. vitamin 812 depletion will probably become a major problem. as it can cause brain and nerve damage. It is not a respirutory depressant. inert gas. body warmth . lt is a nonirritating. It has a rapid ons et (blood:gas solubility coelrtcient : 0. Therefore.

37 Coplrighl O20ll-2012 . Halothane ..Denral Deck.Dental D€ck! . Desflurane CoplriSh O 201 I -20 12 . Isoflumne . Enflurane . Sevoflurane .

Musclc rclation Hypotheses of General Anesthesia: . thc grcater is thc anesthctic potency. .) . I MAC is the concentration necessary to prcvent responding in ofpopulation .Indicatcd by oil:gas ratio (lipid soluhili\. cnflumne.perception ofpain eliminated . Depression ofspinal motor r€flexes . . Htrpnosis . Lipid Theory: bascd on the fact that anesthetic action is corrclatcd with the oil/gas coefficicnts. 2. Binding theory: anesthetics bind to hydrophobic portion of the ion channel.Incrcased CO = greater induction time at thc brain \lAC hean alveolar concentration). Analgesia . the morc anesthctics will arrivc . Essential Components of Anesthesia: . A measurc ofpotency . Sofubility of gas into blood (blood-g.Thc lower the blood:gas ratio. scvoflumne.unconsciousness .Inhalation ancsthctics arc drugs which are vaporized tiom thc liquid form and inhaled to produce geneml anesthesia. To provide a hernostasis such that local bleeding is conlrolled or reduced. To delay the absorption ofanesthetic into the systemic circulation thus reducing the chance of systemic toxicities. The higher the solubility ofancsthctics is in oil. Phermacokinetics of lnhsled Anesthetics: . Thcse diveisc dnrgs are relatively simplc lipophilic molccules ranging from cthcrs such as halogenated hydrocarbons such as halothane and halogenatcd ethcrs such as isofluranc.5% ancsthctics = 38 mmHg .ts solubiliry coelficient) . Note: Vaporization ofthcsc liquids occus in a vaporizer and dclivery to the patient occurs through an anestbcsia machine via a nasal mask. Partial Pressure of anesthetics . soluble protein. and desflumnc. attempts to cxplain thc GABAA rcceptor is a potcntial targct of ancsthctics acton. . 3. Protein (Receptor) Theoryi based on the fact that ancsthctic potcncy is conelated with thc ability of ancsthctics to inhibit enzynes activity of a pure. 50o% . Also.Avoid cardiovascular depressive concenration ofpotcnt agcnts Epinephrine. Valucs ofMAC are additive: . Cardiac Output . Amount that rarches the brain . a vasoconstrictor' is included in dental local anesthetic preparations for the following three reasons: L It prolongs the duration oflocal anesthesia.

Which stage of general anesthesia begins with unconsciousness?


Stage Stage Stage Stage


. .


CopFighr O


38 l-:012 - Dental Decks

. The first statement

is true; the second statement is false second statement is true

. The first statement is false; the . Both
statements are true

. Both statements are false


Coplrighl O


l-2012 - Dotal Decks

Four stages ofgeneral anesthesia:
Stage I: Amnesia/analg€sia Stage II: Delerium: begins with unconsciousness and ends with loss of€yelid rellex, purposcless movements and h)per-reaction, dilated pupils, reflex vomiting, tachycardia, and hlTe.tension . Stage llli Surgical rnesthesia: four planes with progressive loss ofreflexes and n1uscle control . Stage IV: Medullary paralysis: cessation ofrcspiration, ending with death without proper trearment



Notei These four stages ofanesthesia apply to the inhalaflts and not to the intravenous general anesthetics.
Agents used lbr generrl anesthesia:

. Inhalafion agentsi volatile halogen-containing Iiquids
- Halothane: poses a risk with epinephrine; associated with hepatitis; poor skeletal muscle rclaxant. llowever, it is one ofthe mor€ widely used anesthetics for general surgical anesthesia. - Desrlurane, sevoflurane, isoflurane and enflurane: pose Jess risk with epinephrine; not associated wirh hepatitis; good skeletal muscle relaxants.


Nitrous oxide fN,O) is not considered a gencral ancsthetic since hlpoxic levels are required to producc anesthesia. It is considcred a sedative. It is used alone to produce sedation or in combination with the above agenrs to supplement the anesthetic response. lt is a gas at room temperaturc and pressure.

.Intrar'enous agents: . f ltrashort-acting barbiturates: thiop€ntal (Pentothal) and methohexit^l (Brei[al) . Benzodiazepines: di^zeptm (yaliun), tuidazol^m (Versed.), lor^rcp^m (Ativan) ^nd . \eurolep(ic-opioid combinations which are called neuroroleptanalgesics combine fentanyl loprorrl.) trd d.operidol (a phenothiazine)
. Other agents: . Propolol (Diprivan), a short-acti g hypnotic agent; vasodilator . Ketamine (Ketalar). is considcrcd a dissociative anesthetic. It blocks N-methyl-D-asparate A,VDA) (glutanale) rccpetors. Nofer In some circumstances, ketamine has been known to produce illusions or hallucinations that are enhanced by environmental stinruli {rpon eme.gence liom anesthesia. Diaz€pam is giv€n with ketamine to avoid this. . Etomidate (Anitlate): is a carboxylated imidazole derivative \\.hich acts similar to the ultrashonacting barbituratcs.

Nitrous oxide is unable to produce general anesthesia except ifit is given at concentrations greater rhan 80q'o. At thesc concentrations, thc lack ofoxygen would cause hypoxia in the paticnt. lnhalant aneslhetics such as halothane and isoflurane can produce general anesthcsia al concentrations appro\imating 3-5%. As such they are very useful in anesthesia.
is used to produca sedation and mild analgesia. It is usually used in concentrations of30509'o along rvith pure oxygen. lt is a colorless, nonirritating gas at room tempemture and prcssuc, and is not flammable nor cxplosivc. The onset of sedation is within 5 minutes and the recovery is lu:t as rapid. lt is excreted unchanged by th€ lungs. The most common complaint from patients


taking nitrous oxide is mild nausea.

\ote: -\l*ays give patient

10070 oxygen at thc end

ofthe pfocedure to prcvent diffusion hypoxia.

-\dlerse effects ofnitrous oxide:
Decreased mental performance, audiovisual ability, and manual dexterity

..A.t high doses and/or high exposure: reduced t'ertility, spontaneous abortions, neurological and lrdney disease as well as bone marrow suppression
Nrlrous oxide is contraindicated in patients:

. . . . . . . . .

Head injury

With bowel obstruction
Pneumothorax Middle ear and sinus disease With upper respiratory infections

COPD (emph),sema ol bt'onchitis) In the first trinester ofprcgnancy With whom communication is difficult fi.e., autistic ptttietlts) Having a contagious disease since it is difficult to sterilize entire tubes
hou,'s./ causes bone marrow depression.

Important; Prolonged exposure (e.g., morc than 24

. Water

. Bisulfites . Lidocaine . Epinephrine
(v as oc o nstri c to


Copyrighr O

20ll-2012, Dmral


Of the amide-type local anesthetics, which is the only one that is metabolized in the bloodstrcrm rather than the liver?

. Articaine (Septocaine, Zorcaine) . Vepivacaine
(Ca rbocaine)

. Lidocaine (Xylocaine)
. Prilocaine (Citanest)

. Bupiv

acaine (Marc aine)

41 Copyrighr @


201? - DentalDecks

Patients may exhibit hypersensitivity to sulfites contained in some anesthetic solutions. Sodium metabisullite prevents the oxidation (deterioration) ofthe epinephrine vasoconstrictor in those commercial preparations containing epinephrine. Most ofthe patients reacting to bisulfites have a history of asthma and the airway is hyperactive to the sulfites. Allergic reaction usually results in an asthmatic slardrome ofwheezing and bronchial constriction. Bisulfites are present in only those commercial preparations containing vasoconstrictor. Preparations without vasoconstrictor such as mepivacaine 3olo (Carbocaine
37o) do not contain bisulfites.

Important: All local anesthetics except cocaine are vasodilators, however, mepivacaine has Iess of a vasodilator effect compared to the others and, therefore, is the drug chosen \\'hen a vasoconstrictor is not used with the local anesthetic.

\ote: Hypersensitivity

or allergic reactions to local anesthetics, particularly the amides,

are much more rare than allergic reactions to the bisulfites.

.\nicaine (Septocaine, Zorcaine) isan amide-type local anesthetic. However, it is chemicalll unique in that it has an €ster group attached to its molecule which can be acted upon by plasma cholinesterase to render it ineffective. Therefore, it is the only amide q hich is metabolized in the bloodstream and not the liver. Rapid metabolism ofthis ester
bond gives it a short


as articaine HCL 4% solution with epinephrine l:100,000 ard as articaine HCL 4olo solution with epinephrine l:200,000. It is indicated for local, infiltrative, or conductive anesthesia in both simple and complex dental and periodontal procedures. The onset ofanesthesia following administration ofarticaine has been shown to be I to 6 minutes after injection. Complete anesthesia lasts approximately I hour.

.{nicaine is supplied

Articaine is contraindicated in patients with hypersensitivity to local anesthetics ofthe amide type or to sodium bisulfite.

Denral Decks . Causes vasoconstriction and decreased blood flow in iniection area 43 Coplright O 201 I -20 l2 . Prevents the efflux ofsodium out of the neuron . . Which statement best d€scribes its mechansim ofaction? .Dental Dects Phentolamine mesyhte (OraVerse) is a drug used to reverse coft tissue anesthesia and th€ associat€d functional deficits resulting from a local dental anesthetic containing a yssoconstrictor. Prevents the influx ofsodium into the neuron bv blockins neuronal channels . Causes vasodilation and increased blood flow in iniection area . 10olo decrease 25olo decrease 50olo decrease in the time for normal sensation to retum in the time for normal sensation to retum in the time for normal sensation to rehrrn . . 80oZ decrease in the time for normal sensation to retum 42 Coprighr O 201 l-?012 ..

1mg) of OraYerse if I carhidge of anesthetic was administered .Thus if a local anesthetic such as lidocaine with epinephrine normally takes about 180 minutes to wear off. The local anesthetic is thus carried away at a more rapid rate from the injection site resulting in a more rapid retum to normal nerve sensation. Phentolamine rnesylate (OraVerse) rs an alphat-adrenergic receptor t locker. the anesthetic will wear offin approximately 90 minutes. This represents a 50o% decrease in time for normal sensation to be retored. after phentolamine injection. l/2 a caftridge (0.8mg) of OraVerse if2 cartridges ofanesthetic were administered Note: OraVerse (so lutionJbr injection/dental cartridge) is administered as a submucosal iniection. I cartridge (0. Phentolamine mesylate competitively blocks alpha-adrenergic receptors to produce brief an- tagonism r of circulating epinephrine and norepinephrine and antagonism of the asoconstrictor in the anesthetic preparation. . . 2 cartridges (0. This results in vasodilation of the blood vessels. Note: OraVerse dose is based upon the number of cartridges of local anesthetic with vasoconstrictor administered.2mg) of OraYerse if ll2 cmidge of anaesthetic was administered .

vomiting and diarrhea) . Tiazolam (Halcion) . Flvazepam (Dalmane) . Respiratory depression . Ataxia 45 Coplyighr O 201 l-2012 . Oxazepam (Serai .Dental Deck! . CNS depression (drcwsiness and sedation) . DfrtalDecks . Temazepam (Resortl) . Disorientation . Mrdazolam (Versed) . Clorazepate (Tr anxene) Coplri8h Cr 44 20ll-2012. Chlordiazepoxide (Li brium ) . Confusion . Zolpldem (Anbie ) .All of the following drugs are benzodiazepines EXCEPT one. Whtch one is the EXCEPIIOM . GI disturbances (nausea. Alprazolam (Xanax) . Diazepam (Yalium) .

may bc used to rcverse thc residual effects ofbenzodiazepines in the evcnt ofan overdose. Other useful properties include being an anti-conwlsant and a skeletal musclc relaxant. anticonvulsant and skele- ial muscle relaxanl propcrties. tfthe benzodiazepines are i. thc benzodiazepines have little effect on respiratory systcms in healthy individuals. The benzodiazepines (especially diazepam. barbiturates and narcotic analgesics all produce sedation and have the ability to produce de- pendence. With nomral dosrng. Serious potentiation ofthe sedative eflects ofeach will occur leading to unexpected inebriation and respiratory depresslon. slurred speech. ln general. Important: Zolpidem (Ambien).Those used as hypnotics to overcome insomnia: flurazepam (Dalmane) andtiazolam (Halcion). Adverse effects: . which results in increased neuronal inhibition and CNS depression.-Hydroxylation is a rapid route ofmetabolism that is unique to triazolam. They exert their main effect on central GABA-nergic neurons. 2. Thesc are anti-insomnia agents (called GABA-BZ Agonists). They seem lo be much saler than barbituratcs. midazolaln. \ote: Benzodiazepines should never be taken with any form ofalcohol. drowsiness/sleepiness and conf'usion (do not drive . temazepam and triazolarn are usually prescribed. 3. Midazolam (Ilersed) comes as a liquid for preoperative sedation in children and as injectable for IV conscious sedatron. They may be used as preoperative scdatives and induction agents.azepam (Valirn). The pharmacokinetics ofindividual benzodiazepines difler. Gl effects dry mouth. 1. anticonvulsant.These agents appear to act through the potentiation of GABA on benzodiazepine receptors. The benzodiazepines have clinically useful antianxicty. eszopiclone (Lunesta). . and skeletal muscle rclaxation. Note: They have shown no potential for causins addiction. The term tranquilizer rcfers to a drug that promotes tranquility by calming. soothing. Pharmacological effects of benzodiazepines: antianxiety. especially the omega-1 subunit. Benzodiazepines act by potentiating the action ofGABA. lmportant: Flumazenil (Mazicon). nausea . a bcnzodiazepine antagonist. CNS e{Iects a cqr) - fatigue. an amino acid and an inhibitory neurotansmitter. as \\ cll as supplcrncntal agents for the maintenance ofanesthesia. Following oral administration. This accounts for the vcry mpid metabolism and short sedative actions ofthese drugs. Important Thc benzodiazepines. Tolerance and physical dependence can occur with prolonged high dosage.The benzodiazepines are used as oral preparations to alleviate anxiety and to inducc sleep. Other effects hypotension. and thcrelbre there is a wide range in speed of onset and duration of action anrong these compounds. eszopiclone (L nesta). zolpidem (Ambien). Antipsychotic agcnts arc considered to be major tranquilizers and antianxigty agents fuenzodiazepites) are considercd to be minor tranquilizers. di. quieting orpacifying without sodating or depressant e{lccts. amnesia.effective in helping with insomn ia. muscle relaxation Benzodiazepines used orally as tmnquilizen: chlordiazepoxide (Libtittm). most ofthe benzodiazepines are rapidly absorbed and highly bound to plasma protein. alprazolam (Xonax) and lorazepam (Ativan). lorazepam and midazolan) arc important adjuncts in rhe practice of ancsthesiology. and alprazolam. most of the metabolitcs are conjugated with glucuronic acid and excreted in the urine and f-eces Note: cl. For the treatment of insomnia due to anxiety the benzodiazepines llurazepam. scdative-hypnotic. and intravenously to cause conscious-scdation for outpatient surgery. 4. sedation. Drazepam (Valium) ar'd Clonazepam tKlonopin ) can be used as anticonvulsants. and zaleplon (Sonata) are anti-insomnia age s (cdlled GABA-BZ Agonisls). or zaleplon (Sonata) are ot\en weful.

GABA (gamma-aminobutyric acid) receptor . Dopamine receptor .Dental Dects ..Dental Decks . throat ulcers . Norepinephrine r€ceptor . Vouth. itch . Rash. Difiiculty with urination 17 CopltiShr O 20ll-2012 . fatigue . Serotonin receptor 46 Copyrighr O 2011. Drowsiness.2012 .

and zaleplon (Sonata). Buspirone also differs from other antianxiety agents in that it does not possess anticonvulsant or muscle relaxant properties. eszopiclone (Lunesta). thus preserving deep sleep. muscle spasm. These agents appear to act through the potentiation ofGABA on benzodiazepine r€ceptors. produces some degtee ofannesia. They appear to have minimal disruptive action on the normal sleep cycle.Buspirone (BuSpar) is an orally administered antianxiety agent with a short halfJife (24 hours). They have exhibited some anxioll4ic action but they have little effect on skeletal muscle or seizure thresholds. It has a high therapeutic index. The exact mechanism ofaction olbuspirone is unknown. Diazepam affects the limbic system olthe brain lcontrols emo/iori. Note: They have shown no potential for causing addiction. and can be locally irritating to tissue and may produce local thrombophlebitis when given intravenously. . Diazepam is prescribed in the treaftnent ofanxiety. They are used primarily for insomlia. Remember: GABA-BZ agonists have a chemical struchrre that is dissimilar frorn those ofthe benzodiazepines and on the sedative hypnotics. It is not chemically related to the benzodiazepines. It is used intravenously as the agent ofchoice to reverse status epilepticus induced by a local anesthetic overdose. Contraindication to use: Acute narrow angle glaucoma. it has a higher affinity for serotonin receptors in the CNS and a lesser aflinity for the benzodiazepineGABA receptors. -fhese drugs have short halfliv€s f1 /o 2 how s). However. nervous tension. which is in the ry mixture. does not impair psychomotor function and does not cause sedation (lacks CNS depressant activiry) or physical dependence. Important: The antianxiety effect is achieved via a partial agonist effect on CNS serotonin 5 -HTla receptors that occurs without affecting the benzodiazepine receptors or causing CNS depression. and as an anticon!'ulsant. is the main cause ofthrombophlebitis. \ote: Propylene glycol. or any other anxiolyic agent. Examples include Zolpidem (l mbien). especially the omega-l subunit.

High .Dental Decks . Ulhashort-acting . Short-acting . Lorv lipid solubility. Rapid degree ofbinding to plasma proteins rate ofredistribution from the brain to peripheral tissues . Long-acting 48 Coplright O 201 I -20 l2 . resulting in a minimal concentration in the brain . Intermediate-acting . Rapid rate ofmetabolism in the liver ..Denral Decks The brief duration of general anesthetic rction of an ultra-short-acting barbitumte is due to what factor? . Slow rate ofexcretion by the kidneys 49 Coplright @ 201t-2012 .

These agents will maintain anesthesia only while in the brain. They do not possess significant analgesic propefiies. .tal/. thus the patient wakes up within a few minutes of administration. Examples include phenobarbital phobarbital (Mebarul ) and pi'n]id. (Z bfiabat uminal). This suppresses the :pread of seizlrre activity but does not abolish abnormal discharge from a focus. The most important therapeutic measure to be taken in a case ofbarbifurate poisoning is to assure adequate respiration. Long-acting: for treating certain types ofseizures. Examples include amobarbital (An.The length ofaction can be related to the lipid solubility with the ulhashort being the most lipid solubJe and the long acting having thc least lipid solubility. Short-actingi for (Nenbutal). These drugs possess serious drug dependence potential. phenobatbital)t Ba'rbrrurates rvork by inhibiting the depoladzation ofneurons by binding to the GABAreceptors. Examples include thiopental (Pentothal) and methohexital fBr"evildl. . The cause ofdeath from acute barbiturate poisoning or overdosage is respiratory failure. Contraindications to the use of ultra-short-acting barbiturates for general anesthesia: . Emphysema . Thcy are mctabolized in the liver. treating insomnia. Because of their high lipid solubility.vtal) bital lButisol). Porphyria . Intermediate-acting: 3 to 6 hours .B/?l.e. They also increase the threshold for electrical stimulation ofthe motor conex. and habituation. Eramples of ultra-short-acting barbiturates include thiopental (Pentothal) and methohe\ital (. Ultrashort-acting: 5 to 20 minutes . Intermediate-acting: for treating insomnia. Examples include secobarbital (Seconal) and pentobarbital and . Remember: Benzodiazepines work similarly to barbin-rates. \ote: Remember.are metabolized in the liver) ..rg-acting barbittrates (i. Ultrashort-acting: for . these agents will rapidly leave the brain for other tissues. Important concept for anticonvulsant effect of lo. Other ad\erse reactions include CNS (Mysoli ne). Long-acting: 6 to l0 hours Agents: . Lir er dysfunction (thet. induction of general Remember: Barbiturates do not possess analgcsic properties. Previous addiction to sedative hypnotic drugs Remember: These drugs have the ability to produce dependence. These agents are administered by intravenous injection. euphoria. but they also increase the number of chloride channels whilc facilitating the transmission of chloride ions. Short-acting: I to 3 hours . which enhances the iransmission ofchloride ions. The length ofh)?notic action ofthe four different classes after a single dose are as follows: .

Barbiturates may precipitate acute porphyria in susceptible patients 50 CoplrightO 20ll-2012 .D€nral Decks All the following are classified as antiepileptics fiXCEPI one. tionship . . Which one is the. C arbamazeplne (Tegretol) .Dental Decks . Ethosuximide (Zaron t in) . reducing glutamate-induced depolarizations and potentiating the inhibitory effects of GABA the barbiturates exhibit a steeper dose-response rela- . Gabapenth lN euro h t i n) . Yalproic acid. Primidone (Mysoline) 51 Copright O 20ll-2012 . Compared with benzodiazepines. Phen-\1oin (Di lantin) . Phenobarbttal (Lutn Dlazepam (l/alium) . (Depakene) . Barbiturates may increase the half-lives of drugs metabolized by the liver . Barbiturates depress neuronal activily by increasing membrane ion conductance (primarily chloride).All of tle following statements concerning barbiturates are true .EXdEPIlON? . p Tsp1fsisns (Ryt hn o l) i n a I) .

r. The short-acting agents can be used orally for their hypnotic.1. ttonic and tonic-clonic scizurcs (ulso culled grand nal).: xrr.arc (Topumar) . and lomzcpam /. work similarly to barbituratcs.rnti@t1fllsant) dr$gs.!o/ir?i is mctabolizcd lo phcnobarbital and phcnylcthylmalonanide /PtM.s.! pdit md1).ltprolongsthc .ti... . Barbiturates are metabolized in the liver. Generalized seizuresi seizures that sccm to in\rclve all ofthc brain. Examplcs includc diazepam (lhlium). The long-acting barbiturates are used primarily for daytime sedation and the treatment ofepilepsy. but thcy also incrcasc thc numbcr ofchloridc channcls whilc facilitating thc transmission ofchloridc ions. At sedative doses barbiturates do not effect or have spinal cord (CNS linle effect on the cardiovascular and respiratory systems. 5. 3. L GABA analogs: The cxacl mcchanism ofaction ofvalproic acid /Dcpdkdn. absence tnlso Lalle. The chronic use ofthe barbiturates causes an increase in liver microsomal enz)me activity that appears to be the result ofincreased synthesis ofenzyme. It is also uscd to treat tonicclonic scizurcs /grdrd nd. /Rr1/rnol. Not€: Di^zeprm (Ilalium) is uscd for status cpilcpticus and in cmcrgcncy trcatmcnt ofseizures. antiepifeptic /.and. Barbituratesi Phenob^rbital (Lut inal.\seizureisanakcrationinbchavior. F!. *** Propsfenone ular tschlcardias./ is an antianhlthmic agcnt uscd to trcat both vcnlricuiar arrhythmias and supmvcntric- . Phcnytoin-induccd gingival hyperplasis is common and ma] pa. and ropiftr.n lLlrirc ) . This leads to an increased clearance ofthe affected drugs and possibly leads to a decrease in the drugs effectiveness. These agents can be given preoperatively.nes that metabolize drugs. they are used to induce stage III surgical anesthesia. Succinimides: Ethosu\imlde (Zaro tifi)t \tscd in thc trcatmcnt of abscncc scizures.r!1:!'prlc drugs /. t. *** The uses ofthe barbiturates are determined by their duration ofaction: 1. For extensive procedures. The intermediate-acting agents can also be prescribed to relieve anxiety before a dental appointment. thc cxact mechanism for rcducing scizDrc activity is not clcarly un- Jrrsii\id.a$abirc lcabitril) .4/. 2.{fDrl can bc groupcd into thc following classes: lHldantoinsfPhen]toin/D//drrnrlisuscdinthctrcatmcntoftonicclonic(grandnal)sciz\\rcs. 3. lamotriginc (Lan ida l) . in inhibilory ncurotransmittcr Thcy may inhibit thc voltagc-dcpcndent sodium channcl.i and thc ncwcr GABA analogs is not clcarly undcrs@od. which havc anticonvulsant activity. dnd ata\id. to allay anxiety. and trigcminal ncuralgia.functio./orconsciousncssthatrcsultstiomanabnormalclcctricaldischargc ol ncurons rn thc brain. which cnhanccs lhc transmission ofchloridc ions. For very brief procedures. Misceffaneous: oxcarbazcpi^c (hilepttrl). These drugs possess serious drug dependence potential. . Primidone (t|r. Thc ratc ofdcvclopncnl oflhis condition can bc diminishcd by proper oral hygicnc. Epilepsy. Al1 ofthcm incrcasc thc actions ofGABA. [xamplcs oflhc ncwcr GABA analogs include: gabapcntin (Neuro tin). Barbiturates induce the formation ofthe liver microsomal enz). bascd on horv thc abnormal brain activity bcgins. although their effects will last longer than those of the shoft-acting agents. Generally the primary pharmacological effects ofthe barbiturates involve the brain and depression ofl. clo azcpam (Klonopnt). Fourrypcs ofgcncraiizcd seizurcs cxist. before a dental appointment. .lcvctiftccl^m (Kepptu). The ultrashort-acting agents are used intravenously for the induction of general anesthesia.C^rbamazepine is uscd as prophylaxis for partial scizurcs ilh complcx symptomatology including psychomotor and tcmporal lobc scizurcs. and c rbgm zepine (hegreol).)wo*s by inhibiting dcpolarization ofncurons by bindinglo the GABA rcccptors. calming effect.lrl|rl. dr7lincss. is uscd to dcscribc chronic unprovokcd rccurrcnt srizur. thcrcby stabilizjng thc ncuronal membranes. Serzurcs as classiflcd as eilher panial or generalized. or th€ tcrm scizurc disordcr. fclbamzlc (Felbaror. divalprocx sodium fDryakote). They do not possess significant analgesic - DroDerties. prc9abal.This is falsel barbiturates may decrease the halflives of drugs metabolized by the liver. It rarcly causcs aplastic ancmia. 4. All incrcasc thc threshold ofthc CNS to convulsivc stimuli or inhibit thc sprcad ofscizurc activiry Thc :nri. May cdusc drcwsrncss. . These agents are used for daytime sedation and for the treatment of insomnia (they suppress REM sleep).tially or totally obscurc thc crcwns oftccth. they may be used alone. myoclonic. 6.cri\c rcfBctory pcriod by blocking ncuronal sodium channcls. Partial seizures: when scizurcs appcar 1() rcsult from abnormal activit] in just onc pan ofthe brain.

Phenobarbital . Imipramine Qof'anil) . Doxeprn (Sinequan) 52 Coptrighr O 201 l'2012 . N ortiptyline (P am e I o r) . Irnipramine . Amitr ipty line (E I ai l) . Dental D€cks . Desipramine (Norpramin) . Lithium ..DeDtal Decks Which drug is the current drug ofcholce for the treatment ofthe manic phase ofbipolar disorder (or manic4epressive syndrome)? \ . Haloperidol 53 Coplrighl O 201l-2012.

SR1s) have revolutionized the treatment ofdepression. Drowsiness is the most frequent CNS adverse reaction.. polyuria. The most common side effects of lithium. The selective serotonin reuptake inhibitors (S. Lithium salts Antidepressants are often administered with lithium to manage the depressive phase ofthe illness if lithium alone is not sufficient. Lithium can prevent the occurrence ofboth the depressive as well as the manic episodes in some but not all the patients. . and convul- sions. Bipolar disorder for manic-clepressive syndrome) is characterized by cyclical changes in affectir e state between the manic and depressive phases ofbehavior Bipolar patients cycle ber$ een rhe trvo aflbcted states. unconsciousness. These substances serve as second messengers within the CNS and may have widespread influence on neuronal function. Paroxetine (Paxil). constipation. Important: Amitriptyline displays the greatest anticholinergics effects (especially xerostomia). Neurofeptic agents (also referrecl to as anti-psychotic agents or msjor trqnquilizersl are used in the acute manic episodes. sleepiness. Anticholinergic adverse side effects include: dry mouth. 4. This results in the potentiation oftheir neurotransmitter actions at postsynaptic receptors. are effective in quelling the exheme mania and psychotic behavior i\ote*. are by far the most important drugs for suppressing mania in patients with affective disorders. Diuretics and some NSAIDs reduce lithium excretion and mav cause lithium toxicity. . Sertraline (Zololi) and Fluvoxamine (Luvox) have shorter half-lives and can be given once daily. blurred vision and tachycardia. . and Haloperidol. Approximately 2570 of patients who suffer from mania do not respond to lithium. which is a phenothiazine. Sodium restriction leads to greater retention oflithium in the kidney. Severe intoxication results in vomiting. diarrhea. These drugs are also effective for treating panic attacks. thint. The most important clinical distinction ofthe SSRIs from all other antidepressants is their very high specificity for blocking the reuptake of serotonin. It is not useful for the acute manic episodes. Chlorpromazine. fine hand ftsm61 muscular weakness. anxiety. Carbamazepine (qtl anticonvulsant) andvalproic teid (also an a ticonwlsant) may be effective in some relractory cases. are often associated with initial therapy and usually fade within I to 2 weeks.. These drugs inhitlit the neuronal re-uptake of norepinephrine and s€rotonin (5-HT) in the brain.The tricyclic antidepressants are generally considered to be the drugs of first choice for the treatment ofunipolar disorder (depresslor). 3. and a sluggish feeling. Note: Lithium works inside the cell to prevent the formation of inositol triphosphate and diacylglycerol. agitation. including Gl irritation. Note: Carbamazepine blocks sodium channels and valproic acid blocks both sodium and calcium channels. 2. *'hich is not a phenothiazine but acts in a similar fashion. headaches. Side effects include nausea. Fluoxetine (Prozac:)is the prototlpe and has the longest half-life.-1 1. Citalopram (Celexa) and escilalopram (Lexapro) are used for generalized anxiety disorders. desipramine the least. and sexual dysfunction. insomnia.

.e. Whlch Tiro drugs below are MAO inhlbitors? .. Phenelzine (Nerdil) 54 Coplright O 20ll-201? Denral Decks The vasoconstrietor epinephrins in local anesthetic injections must be used cautiously in patients taking all ofthe following antidepressant drugs EXCEPT one in qrder to avoid transient and signilicant increases in blood pressure. lmipr arnine (P arnate) (Tofr an i I) . Doxepin (Sinequan) . Selective serotonin reuptake inhibitors (i.Monoamine Oxid nse (IWAO) iahibltors are often us€d as third-line Ngents in cases of refractory and atypical depression.. Which one is the . Elavil) . Effexor and Cynbalta) Cop)rightO 20ll-2012 . Tranylcypromine . .e. Prozac and Paxil) Serotonin and norepinephrine reuptake inhibitors (i.e.D€nbl Decks . Tncyclic antidepressants (i.EXCEPTIOM \ .

ln rhe presence of a vasoconstrictor administered via a local anesthetic injection. sponsible for the degradation of the naturally occurring monoamines level of norepinephrine. dopamine. nausea. Early symptoms include occipital headache. \ote: . palpitations. Mirtazapine (Remeron): alphaz -noradrenergic antagonnist . l. including hypertensive crisis. A hypertensive crisis can occur within several hours after ingestion of a substance that contains tyramine. possible serotonin reuptake in- These trvo categories (tt'iclclic qntidepressants snd serotonin and norepinephrine teuprake inhihitors) of antidepressant drugs significantly increas€ norepinephrine levels in tissues. Miscelianeous antidepressants include: \ot€ . thereby raising blood pressure. Tyramine releases norepinephrine and other sympathonrimetic amines. The selective serotonin reuptake inhibitors fi. Prozac and Paxil) have no such effect on norepinephrine in tissues and interaction with a vasoconstrictor like epinephrine is not an issue.e. epinephrine and ephedrine. and sweating. Note: Local anesthetics containing epinephrine are genemlly contraindicated in patients who are taking MAO inhibiton. It is theorized that the increased monoamines in the brain is responsible for the antidepressant effect ofthe MAO inhibitors.SZ/: norepinephrine / dopamine rer.rptake inhibitor . Among the drugs that interact with \1AO inhibitors are meperidine (Demerol). rvhich can be fatal. stiff neck. Trazodone (Desl. The major limitation for the widespread use of the MAO inhibitom for the treatment of depression has been the potential for serious adverse side effects.MAO inhibitors are used are often used as third-line agents in cases ofrefractory and atypical depression.. and serotonin. the patient could experience significant elevation of blood pressure due to the vasopressor actions of the combination. vomiting. MAO inhibitors antagonize the action of monoamine oxidase (MAO) reepinephrine.rel): mechanism not clear. Bupropion (Wellbrr'tu hibitor .

Monoamine oxidase inhibitors (i. Effexor and Cymbalta) . Sertraline (Zoloft) ....e.. Duloxetine (Cym b a I t a) 57 Cop)righl O 201| -2012 .D€ntal Decks . Tricyclic antidepressants (i. N orntpryLine (P am e lor) ..Denhl Decks . Selective serotonin reuptake inhibitors (i. Desrpramne (N o rprami n) . Yenlafaxine (Effexot) . Desvenlafaxine (Prrsfiq) .e. Elavil) . Prozac and Paxil) .e.e. Nardil) 56 Coplright @ 201l-2012 . Serotonin and norepinephrine reuptake inhibitors (i.

These two categories ofantidepressant drugs induce significant dry mouth in:up to 75yo ofpatienls taking these medications. Amitriptyline (E/avll) . Paxil) and monoamine oxidase inhibitors have no secondary anticholinergic effects and therefore do not cause any significant dry mouth. .e.ine (Elfexor) . Serotonin and norepinephrine reuptake inhibitors: . Citaloqam (Celexa) . Tranylcypromine (P arn at e) . (Wel I butrin) Trazodone (Desyrel) Nefazodone (Serzone) Mirtazrpine (Remero n) . Prozac. Paroxerine (Paxil) . Second generation miscellaneous: ..l. The seldctive serotonin reuptake inhibitors (i. Isocarboxazide (Marylan) . S€lective serotonin reuptake inhibitors: . Five major categories of antidepressant drugs: . Phenelzine Q'{ardil) . . These effects are due to the secondary anticholinergic nature ofthese agents. Desvenlafaxine (Pristiq) . Yenlafa:. Bupropror. Sertraline (Zoloft) . Imipramine (Tof'anil) . Monoamine oxidase inhibitors: . Nortriptyline (Pamelor) . Doxeprn (Sinequan) . Escitalopram (Lexapro) . Note: Drug-induced dry mouth must be treated palliatively with artificial salivary substitutes. Fluoxetine (Prozac) . . Desipramine (Norpramin) . Duloxetine (Cymbalta) . Tricvclic antidepr€ssants: .

2012 . GERD (heartburn) . Renal failure 59 CoplrighrO20ll-2012 . Chlorpheniramine . Desloratadine (C lari n ex) 58 Coplrighr C2011. Loratadine (Clantin) . Toxic-shock slndrome ..Dental Decks . Cimetidine (Tagamet) .Debial Decks . Diphenhydramin e HCL (Benadryl) maleate (Chlor-Trimeton) . Prostatitis .

The antihistamines are divided into H. Ioss oJ libido. Antihistamines are antagonizing agents that compete for receptor sites with natuml histamine. Common side effects include drowsiness. which play an extremely important role in allergic reactions and H2-receptors. fexofenadine HCL (Allegra).-receptors. however.retidine (Iaga met). ln general. There are two t)?es of histamine receptors.and H2-receptor blockers depending on the histamine receptor they compete for. Histamine produces ofphysiologic actions in many tissues. which is stored preformed in cyoplasmic granules of tissue mast cells and blood basophils. ose and thrcat). and gtnomastia). antibradykinin and s€dative propefiies. These drugs are also used to treat Zollinger-Ellison syndrome (a hypersecretory disease) and gastroesophageal reflux cialll duodenal ulcers disease /GERDJ. urticaria and angioneurotic edema.It also inhibits liver metabolism which can lead to an increase in activity ofother drugs such as warfarin and carbamazepine. While H2-receptors are located in the GI tract and in vascular and bronchial smooth muscle.-receptor blocke$ do not preYent H2-receptor antagonists compete with histamine at the H2-receptor.lorctadine (Claritin) and deslo- ratadne (Clarinex) *"* Most ofthese agents. ranrtrdrne (Zantac). Inhibition of histamine at the parietal cell interteres u ith one of several mediators for signaling the parietal cell to secrete acid. H1-receptors. . anticholinergic effects /dry moutlt. which are important in gastric acid secretion. They can both stimulate and depress the CNS. the binding is competitive. First-generation (classical) agetts: . These agents are used to treat acid-peptic disease. CetiiztneHCL Qfrlec). because oftheir poor CNS penetratjon (do not ctoss the bloodhrain barrier). espeand occasionally gastric peptic ulcers. Note: Histamine also plays an important role in the control ofacid secxetior] (HCL) in the stomach.These agents are all rev€rsible competitive antagonists ofthe actions of histamine on H. It is released in response to lgB-mediated (immediate) allergic reactions and plays an important role in hay fever. lmportant points: All ofthe H. Second-generation agents: l. cause less sedation and drowsiness than the first-generation agents. Diphenhydramine HCL (Benadryl) and chlorpheniramine maleate (Chlor-Trimetron) *** These agents have a broad spectrurn of action which includes antihistaminic. Note: Cimetidine has an antiandrogen effect (can lead to impotence. and nausea. some second-generation agents bind non-competitively at higher doses. . a s ide variety H'-bfockers incfude: cin. H2-receptor antagonists compete * ith histamine only in the GI tract. famotidlne (Pepcitl) and ntzatidire (Axicl). the release of histamine but rather compete with free histamine for binding at Hl-receptor sites. antiserotonergic.*** Cimetidine is an antihistamine H2-receptor blocker. anticholinergic. dizziness. H1 receptor blockers include: 1.

H2-receptor site 60 Copyright O 20ll-2012. Denial Decks .. Hl-receptor site . Cephradine . Cephalexin . Dertal Dech . Amoxicillin . Tetracycline 6l Coplrighr O 201 l -20 1? .

Cefazofin (Ancefl 1 gor ampicillin 2 g intramuscularly or intravenously t hour prior to the dental Drocedure .134:895-898 cephalexin. Examples ofthese drugs include: cimetidine (Tagamet). Amoxicillin is a mernber of the penicillin family.Reduces motion sickress: first-generation only (i. 128(7):1004-8 and J Amer Dent Assoc 2003. Examples include Cetirizine HCL (Zyrtec). they block the constriction ofthe bronchi and they block capillary permeability which histamine ordinarily causes. or cephradine or amoxicillin can be -either used as the drugs ofchoice lor standard prophylaxis medication in the patient with a total joint replacement. Cephradine (Velose. dose is 2 grams . fexofenadine HCL (AIIegra).e. particularly in mast cells and blood basophils. They block secretion of stomach acid and are used in the treatment ofduodenal ulcers. Diphenhydramine HCL anrl c h I orpheniramine maleate) . H2-r€ceptor antagonists: competitively block H2-receptors. blocking the effects of histamine at these receptors. n \ote: Histamine is found in all tissues. and have a higher risk of cardiac arrhythmias (long QT ellbct). \ote: For patients not allergic to penicillin and unable to take oral medications the f4 lst generation cephalosporin) or ampicillin (member of the penicillin family). prophylaxis dose is 2 grams orally t hour prior to the dental procedure. The two types of histamine antagonists are: H1-receptor antagonists: competitively block H1-receptors blocking the effects of histamine at these receptors.. From the "Advisory Statement. .Promotes sleep: first-generation only Remember: The second generation Ht-receptor antagonists have the following characteristics: Longer halfJives than first generation (l2-24 hours as opposed to 3-6 hours for first generation). vasodilation and bronchoconstriction due to histamine . :. tidine (Zontac). The regimen is as follows: suggested medications are cefazolin . They block the vasodilation. The blockade ofthese effects of histamine overcomes the svmDtoms of seasonal allergies. .Antihistamines are antagonizing agents that compete for receptor sites with natural histamine.loratadine (Cla tin) and desloraradine (Clarinex). . Antibiotic Prophylaxis for Dental Patients with Total Joint Replace)nent" published by the American Dental Association and the American Academy' ofOnhopedic Surgeons. prophylaxis dose is 2 grams orally t hour prior to the dental procedure. It is released in allergic and inflammatory reactions. is a lst generation cephalosporin. Actions of Hl antihistamines: . l. prophylaxis orally I hour prior to the dental procedure. in the J Amer Dent Assoc 1997.Blocks pain and itch. Cephalexin (Keflex) is a lst generation cephalosporin. famottdine (Pepckl) and nrzatrdine (Axrd). they do not cross the blood-brain barrieq they produce little or no sedation.

Chlamydia 63 Cop)righl O 20ll -2012 .. .. Affects cell wall . Hepatitis . Affects cell membrane .Dental Deks . AIDS .Denral Decks Mefloquine fzanlum) belongs to a chss of drugs which is useful in treating which ofthe following conditions? . Valaria . Interferes with normal biosynthetic pathways 62 CopyrSh O 201 I -20 12 . Cancer . Interferes with protein synthesis .

P falciparum is the most deadly species and the subject of most malaria-related research and literature.Clindamycin .Lincomycin .Ch loramphenicol .floxacin. and the South Pacific. \'falaria is a devastating parasitic disease transmitted through the bite ofinfected Anopheles mosquitoes. Ievo.Trimethoprim . and vivax). r ir ax causes up to 65% of malaria in India and is becoming increasingly resistant to malaria drugs. the Middle East. \fefloquine (Lariam) four malaria species. Plasmodium vivax is the most common of four human malaria species (P falciparum.Erythromycin .Lnipenem Cephalosporins . ovale.Azithromycin .e.Cycloserine . Combination ofatovaquone .Fluoroquinolones (i. moxiJloxac'in. P. ciproJloxacin.Mechanisms of action ofantibiotics on the bacteria cell: . norJloxacin.Clarithromycin . By contrast. has been shown to be effective in treating malaria caused by all Other antimalarial drugs are: .Sulfonamides . Conrbination of sulfadoxine and pyrirnethamine (Fansidar) . and gentilloxacin) \ote: * The most corruron clinical cause of bacterial resistanc€ is the use of antibiotics hen they are not indicated.Aztreonam . Agents affecting cell wall: - Penicillins Bacitracin - Vancomycin .Tetracycline . North Africa. North and South America. Agents interfering with normal biosynthetic pathways: .. Halofantrine and proguanil (Malarone) . Chloroquin (Aralen) . Quinine . Endemic to tropical and subtropical areas ofAsia. malariae.Aminoglycosides . Agents interfering with protein synthesis: .

\{ycoplasma pneumonia .2012 . Cefaclor (Ceclor) . Chlamydia infections . Penicillin \fK .. Rickettsial infections . Staphylococcal infections 55 Coplright O 201 I 2012.Dental Decks Tetracyclines ore the drugs of lirst choice in the treatment ofall of the lollowing EXCEPT one. Penicillin G . Which one is the EXCEPTIOM \ . Dental Decks . Erythromycin 64 Coplrighl C 201 1.

cefoperazoqe (Cefobid). cefazoin (AnceJ). Salmonella. Effective against Pseudomas aeruginosa. and Rickensia infections. cefadroxrl (Duncefl. influenzae. and the two newer groups of Popular Tetracyclines include: . Cephalosporins act against a wide range ofgram-positive and gram-negative bacteda. coli and H. and a decreased maximum acti\ ity against gram-positive organisms. and Shigella. Dox) clclin€ (Vibramycin)| used to treat infections caused by Rickettsia. \Iinocycline (Minocin): used to treat acne. coli. transpeptidase) that build/maintain the cell wall. The antibiotic binds to the enzymes fi. aureus. ceftriaxone (Rocephir. . Tetracycline: used to treat acne. Enteroh:rcrer. exacerbations of chronic bronchitis. . . resulting in death ofthe cell. cefprozrl (Cefzil). gonorrhea and syphilis in patients allergic to penicillin. cefoxrtin (Mefoxn). \ote: Approximately 107o of individuals expressing allergy to the penicillin family antibiotics will have cross allergenicity to the cephalosporins. Fourth: cefeprme (Maxipime).Cefaclor is a member ofthe cephalosporin family ofantibiotics.. Have the broadest spectrum ofactivity ofall cephalosporins and are extremely effective against gram- negati\e organisms. . the carbaDenems and the monobactams. cephalospodns. and Pneumococcus. of Remember: Antibiotics containing this betalactam ring are referred to collectively as betalactam antibiotics and include the penicillins. Third: cefixime (Suprax). They are more active against E. The cephalosporins are penicillin-like in action against bacteria. Bacteda eventually lyse. Chlamydia and \{ycoplasma. Cunently there are four generations of cephalosporins. altemative to mefloquine for malaria prophylaxis and treatment of slphilis. Each newer generation has significantly greater gram-negative antimicrobial properties than the preceding one. Mycoplasma infections and Chlamydia infections. This makes the cell wall osmotically unstable. Still have eJficacy against gnm-postivie organisms but also possess good activity against E. . Second: cefaclor (Ceclor). cefuroxime (Ceftin). Klebsiella pneumoniae. cephradine (Velosqf. They are bactericidal antibiotics and act like the penicillins and interfere with cell wall synihesis through inhibition of the synthesis of the peptidoglycan in the cell wall. Group A Beta-hemolytic streptococci. aeents. Important c€phalosporins within each generation: . Most active against S. e. . First: cephalexin (Keflex). anthrax and meningococcal prophylaxis. cefpodoxime /Zartlr).

Quinolone class ofantibiotics . Macrolide class ofartibiotics .201 2 . Renal effects Copyrighr o 201 1. Hematologic effects . GI effects ..Dertat Decks . CNS effects . Glycopeptide class of antibiotics 66 CopriShr C 20ll-2012 . Cephalosporin class of antibiotics .Dental Deck .

) Since they are destroyed by stomach acid. Erylhomycin stearate (E4tthrocin) . about 107o ofpatients receiving clarithromycin. Remember: Intrinsic activity is it-v.lhromycin is metabolized in the liveq excretion is mainly via the bile . oral bioavailability of erythromycin is poor. Zithromax) and clarithrornycin (Biaxin) are members of the macrolide class ofantibiotics in which erythromycin is the prototype agent. a measure ofthe ability ofa drug once bound to the re- ceptor to generate an effect activating stimulus and producing a change in cellular activ- Adverse Gl effects are reported for approximately 2lo% ofpatients receiving er)thromycin. Erylhromycin ethylsuccinate ft. . They are also active against syphilis.t S. In general. causing liver toxicity andjaundice and so should not be given to people who have an underlying liver problem such as an infection with hepatitis C. These two macrolides concentrate within macrophages. The significant tissue penetration ofboth agents and the prolonged elimination half-life of azithromycin (l l -14 hours) allows for once-daily dosing for azithromycin and twicedaily dosing for clarithromycin. The macrolides can have a toxic effect on the liver. This causes the Rr\A to dissociate from the ribosome and prevents protein synthesis. Lyme disease and leprosy and tuberculosis. making them useful against organisms that are taken up by macrophages such as Mycobacterium avium intracellulare. This is a term designating a special coating applied to tablets or capsules which prevents their release and absorption oftheir contents until they reach the intestines **" \ot€: Er. and several salts have been developed to overcome this drawback. \facrolides are bacteriostatic. The mechanism of action involves inhibition of protein s! nthesis that results from binding specifically to the 50s ribosomal subunit.. influenzae and Helicobacter pylori. and less than 504 for azithromycin.Azithromycin (Z-Pak. Note: Macrolide antibiotics are generally used to treat infections caused by streptococcal bacteria and respiratory infections generally. The bacterial spectrums ofactivity ofLzithromycin and clarithromycin are similar to that of erythromycin but possess greater intrinsic activity against H. erythromycins are usually entedc coated. It is readily inactivated by stomach acid.

Erytfuomycins .. Dentat Deck! . Neomycin . Tobramycin . Penicillins . Acetylsalicyclic acid (Aspirin) . Para-aminobenzoic acid (PABA) Copright @ 69 201l-2012 . Streptomycin . Gentamicin 68 Copyright O 201 I -20 12 .Dental Deckj .

Aminoglycosides are used in the treatmcnt of severe infections of the abdomen and urinary tract.. Single daily dosing of aminoglycosides is possible because of their rapid concentration-dependent killing and post-antibiotic effect and has the potcntial for decreased toxicity.g. Sulfonamides are not used for treatment of dental infections because ofa low degree of effectiveness against oral pathogens. It is considered the drug of choice for many urinary tract infections.:. They are also used for prophylaxis. and Serratia. including E. folc acid is not synthesized within the bacteria. coli.:: 2 Sulfonamides are used in medicine primarily for the treatment of urinary tract infections. Two wcll-known adve$e effects are ototoxicity and nephrotoxicity.:r.Aminoglycosides are potent bactericidal antibiotics that act by creating iissures in the outcr membrane of the bacterial cell. The sullbnamides are structurally similar to PABA and this similarity is the basis for their antibacterial actions. gram-negative bacteria and act synergistically against certain gram-positive organisms. Gentamicin is the most commonly used aminoglycoside. PABA is needed by bacteria for the synthesis of folic acid.Note*:. Sulfadoxine. Proteus. as well as bacteremia and endocarditis. Aminoglycosides may aggravate muscle rvcakness in patients with muscular disorders such as myasthenia gravis. or parkinsonism. Enterobacter. Haemophilus influenzae and Salmonella species 4. infant botulism. Although blood dyscrasias are relatively rare. Coli. subse- quently inhibiting protein synthesis. With PABA inhibited.1::. Pneumocystis carinii. but amikacin may be particularly effective against resistant organisms. Suliamethizole. \eom]cin (Myi/iadn. Sulfonamides are predominantly bacteriostatic agents. and"tobramycin (Nebci ). . Gentamicin (Garamycit). These are effective against serious infections caused by aerobic gram-negative bacteria. and Sulfisoxazole. Pseuodomonas aeruginosa.. the sulfonamides compete with PABA and are able to inhibit the actions of PABA. Klebsiella. Klebsiella pneumoniae.. lblic acid is needed for the synthesis of cellular components within the bacteria to allow for cell growth. Because of structural similarities between sulfonamides and PABA. they can be fatal. Aminoglycosidcs bind incvcrsibly to thc 30s ribosomal subunit of bacteria. Amikacin (Aniken). 2. especially against endocarditis. Sulfasalazine. In tum. Sulfadiazine. The trimethoprim component is an antimicrobial and the sulfamethoxazole is one ofthe sulfonamides. and Kanamycin (Ka trer)i Due to its toxic potential ncomycin is used only topically or locally /e. Bactrim is the brand name for the combination of trimethoprim and sulfamethoxazole. Sulfamethoxazole. Aminoglycosides may cause severe neuromuscular weakness lasling hours to days oftheir potential curarelike effect. 3. .. Bacteria susceptible to Bactrim include E. . Avoiding prolonged use. 1. volume depletion and concomitant administration of other potentially ncphrotoxic agents decrcases the risk of toxicity. . Sulfonamides are often referred to as "sulfa drugs" because their molecules contain sulfur atoms. They have a different antibacterial mechanism from that ofthe antibiotics. Kanamycin is rarely used bccause of its marked lendency to cause ototoxicity. Resistance is rare but increasing in frequency. 3. \ot6 - because shown to be effcctive in the treatment oftuberculosis. Streptomycin: The first aminoglycosidc and q. in the GI tract). Aminoglycosides: . '. Examples of sulfonamides: Sulfacetamide. and bacterial cellular growth is inhibited. They are particularly active against aerobic. Hypersensitivity reactions ate common. ls seldon used today. 5. Sulfanilamide.

Dmral Decks . Cephalexin (Keflex) Clindamy cin ( C I e o c i n) . Tetracycline . Penicillin VK . . Erythromycin . Doxycycline 71 Copyn8hi O 201 I -20 12 - Dental Deck. Vancomycin 70 Coplright O 20ll'2012 . Penicillin . .. Chloramphenicol .

antl pyogenes as v'ell qs Staph). probably by facilitated diffusion. and Brucellosis. neck. \ote: \bncomycin is given IV and is used most often in serious or life-threatening staph)lococcal or streptoccocal infections. upper chest. viridans. Note: Fatal chloramphenicol toxicity may develop in neonates. and exEemlnes. It is used as a second or third line drug in medicine to treat serious infections due to organisms resistant to other less toxic antibiotics. The illness. and effectively treatable with other antimicrobial agents. leukopenia. . to a lesser extent. When an. Chlorarnphenicol is a broad-spectrum antibiotic effective against gram-positive and eram-neqative bacteria and against anaerobes. The most important adverse effect of chloramphenicol is on the bone marow Chloramphenicol affects the hematopoietic system in two ways: response manifested by aplastic anemia. in eukaryoric cells. the gray baby syndrome. Clindamycin is bacteriostatic and is active against most gram-positive (i. it emphasizes that the drug should never be employed in undefined situations or in diseases readily. Adverse effects include ototoxicity which may be pemanent and the "red man" syndrome which is characterized by a sudden and profound fall in blood pressure with or without a maculopapular rash over the face. Streplococcus pneumonioe.roxicillin cannot be used for the standard regimen for prevention of bacterial endocarditis in patients undergoing dental procedures . however. These side effects are caused bv the oversrowth of the bacterium known as Clostridium difficile. For example it can be used to treat the following: Typhoid Fever. Bacterial Meningitis. The drug readily penetrates bacterial cells. For prophylaxis for dental patients with totaljoint replacement Important: Clindamycin can be given to patients allergic to penicillins since there is no cross all€rgenicity between penicillins and clindamycin.e.lococcus aureus) and many anaerobic organisms. It remains the drug ofchoice for severe cases ofClostridium difficile. Anaerobic Infections. For treatment ofcommon oral-facial infections caused by aerobic gram-positive cocci and susceptible anaerobes . usually begins 2 to 9 days after treatment is started. In dentistry. leading in many cases to fatal pancytopenia . safely. Chlorarnphenicol inhibits protein synthesis in bacteria and. blocking bacterial protein synthesis. especially premature babies" when they are exposed to excessive doses of the drug.nphenicol acts primarily by binding reversibly to the 50s ribosomal subunit. by a dose-related toxic effect that presents as anemia. including the anaerobic gram-negative bacteria Bacteroides frag- ilis.Clindamycin binds to the 50s ribosomal subunit. or thrombocytopenla . by an non-dose-related idiosyncratic Important: The risk of aplastic anemia does not contraindicate the use of chloramphenicol in situations in which it is necessary. Rickettsial Diseases.. Its use is restricted by its side effects such as severe diarrhea and pseudomembranous colitis. Chlorar. clindamycin is an alternate antibiotic in the following situations: .

Streptomycin . Dianhea caused by Giardia lamblia 72 CoplriShr O 20ll-2012 Dental Decls . Dianhea caused by Clostridium diflicile .Nitazoxanide fllirro.Isoniazid . Pyrazinamide 73 cop)'righr e 201 l-2012 . fufampin .Dental Decks . Malaria . AIDS . Ethambutol .) is an oral antiprotozosl ag€nt us€d to treat which of th€ following conditions? . Leprosy .

It should is not used in pregnancy because of potential adverse effects on the fetus. . Because the \llcobacterium organism tends to develop resistance to any single antitubercular drug. vomiting. . which causes trichomoniasis. and headache. lsoniazid: often given in a four drug regimen along with rifampin. causing cessation of cell multiplication and cell death. *** Antiprotozoal Agents: . It interferes with lipid and nucleic acid biosynthesis in growing organisms. Its mechanism is to interfere with the electron transfer reaction wilhin the protozoa essential to anaerobic metabolism. Ethambutol: usually given in combination with olher agents . DNA-dependent RNA-polymerase activity. This drug is also indicated to be used as a cream to reduce unwanted hair from face and ad- jacent areas under the chin. Atol. Eflornithine (Vaniqa): has orphan drug status for the treatment of meningoencephalitic stage ofTr)?anosoma brucei gambiense tnfection (sleeping srcinesy'. It may be bacteriostatic or bactericidal against M. combination drug therapy is standard in the treatment oftuberculosis. depending on the concentration. Streptomycin: is a bactericidal antibiotic. Pyrazinamide: the mechanism ofaction is unknown. and is the most common protozoan infection in the United States. Rifampin: inhibits . flushing. carinii . . Pl razinamide: popular in combination with rifampin ]Iechanism of action: . . thereby supressing RNA synthesis. . . Clostridium difficile.ntitubercular drugs: .a'quone (Mepror): is an antiprotozoal agent used to treat Pneumocystitis pnetmonia (PCP) in patients who are intolerant to co-trimoxazole. It can be bacteriostatic or bactericidal and is most active against bacteria undergoing cell division. Ethambutol: impairs cellular metabolism. cramps. Furazolidone Tuberculosis is a bacterial infection caused by Mycobacterium tuberculosis. . Streptomycin: often given in combination with isoniazid . Bacteroides species and Fusobacterium species. Note: Alcohol should be avoided because metronidazole and alcohol together can cause severe nausea. The antitubercular drugs either inhibit the growth ofthe bacteria or kill the bacteria. (Furoxone)'. it is one ofthe most effective drugs available against anaerobic bacterial infections. Rifampin: usually given in combination with other agents . Isoniazid: is bacteriostatic for resting organisms and bactericidal for dividing organisms.This type of diarrhea is an intestinal infection also known as Giardiasis. It is bactericidal and is active only against Mycobacterium. Nitazoxanide (Alinia): is an antiprotozoal agent which is used in the treatment of Giardia. pyrazinamide and ethambutol . These include infections caused by Helicobacter pylori. tuberculosis.A. and those protozoal infections caused by Cryptosporidium parvr. In addition. .rm. is a antiprotozoal agent used to treat dianhea caused by susceptible Giardias lamblia and Vibrio cholerae. It acts by interfering with normal protein s)rlthesis. Jletronidazole (Flab-l): is a synthetic antibacterial and antiprotozoal agent that is eflective against Trichomonas vaginalis.

. Herpes simplex type . Papilloma virus (HSv-|) 71 Copyrighl O 20ll-2012 . Didanosine .Dental Decks . Genital herpes 1 . Ritonavir .Denhl Deck . Indinavir . Herpes zoster . Zidowdine . Delavirdine Coplrishr O 2011-2012 .

Docosanol cream (lbreva) . This condition is caused by the herpes simplex type 1 virus. Valacyclovir caplets (Valtrex) AIDS has been recognized since l98l as a unique clinical syndrome brought on by in- fection with the human immunodeficiency virus | (HIr/-l) or virus 2 (HIV-2). Lysine tablets . which are eventually passed on to other host cells such as the immune system macrophages. The integrated DNA segment can produce nerv RNA in the cytoplasm of the host cell. The new RNA in tum synthesizes viral proteins. Ultimately enough ofthe human immune cells are compromised such that has as its R\A immune function is lost. * hich becomes susceptible to opportunistic infections. Penciclovir (Denavir) inhibits viral action by selectively inhibiting herpes viral DNA synthesis and therefore resulting in the inhibition ofviral replication. This DNA segment is then permanently incorporated into the host cell's DNA within the nucleus. This results in a compromised immune system. name Wdex). The HIV drugs such as didanosine @ rand . Other agents indicated for use in treating the condition ofherpes labialis are: . Penciclovir is not available for systemic dosing. HIV is a type ofretrovirus that is responsible for the fatal illness flom AIDS. ritonrvir (brand name Norvry'. and indinavir @rand name Crixivan) work by inhibiting certain steps in the HIV inlection process within the target cells to halt the destruction of the immune system by the HIV retrovirus.Penciclovir (Denavi is a cream formulation indicated for the treatment of recurrent herpes labialis (cold sores) in adults. zidovtldine (brand name Retrovil).The major cellular defect caused by infection with HIV is a depletion ofT cells. A retrovirus nucleic acid and uses the enzyme reverse transcriptase to copy lts genome into the DNA olthe host's cells chtomosomes. primarily the subqpe T-helper cells kaown as CD4 cells. Acyclovir tablets . Acyclovir cream .

Polymyxin-B . Amphotericin-B .Dental Decks .D€ntal Decks . Bacitracin . Nystatin . Erythromycin . Chloramphenicol n CoP)right @ 201l-2012 . Neomycin 76 CoplaiSht @ 201l-2012 .. Penicillin .

g. which causes an inflammatory. Antibiotics in general do not have antifungal properties.lri. "statin" = HMG-CoA reductase inhibitor (e. naclolol ) . the indigenous bacteria ofthese areas. usually competitive peripheral acting skeletal muscle relaxers (e. "dipine" = dihydropyridine calcium channel blockers (e. Note: The suffixes ofthe following generic drug narnes are indicative ofthe conespsonding drug classes: . Nystatin (Mycostatin) is taken as an oral suspension to be sn ished around thc mouth and swallowed. terazosin) .g.. polymyxinB and neomycin are not antifungal agents. Remember: Nystatin and clotrimazole are the two antifungals that are used as "swish and swal- fo\r'' to treat oral candida infections.. Note: Angular cheilitis Oilateral ulcers at the comer of rhe ntoutht has been linked to C.g. "pril" . "ilol" or "alol" = beta-adrenergic receptor blocker that also blocks alphal-adrenergic receptors (e. Candidiasis is an infection.9. enalapril) . usually C.4lDSpalie s). "osin" = alphar-adrenergic reccptor blockers (e. canedilol or labetalol) quatemary ammonium compounds. increasing permeability and permitting the leakage ofintraccllular componcnts. white discharge. especially in patients who have a deficiency in T-ly..azolc (M))celer. is taken as a troche (lozenge) \\hich is slorvly dissolved in the mouth and swallowed.Thisyeast-like fungi is a normal inhabitant of the oral cavity and vaginal tract. pancuronium) . They work by binding to sterols in the fungal cell rnembrane.g.rnphocytes. clotrimazole) .9. Bacitracin.. "coxib" = COX-2 inhibitors fe&.. Clotrj. and in immunosupressed individuals /. nicardipine) . albicaDs. "olol" = beta-adrenergic receptor blockers (e. "onium" or "urium" . usually ofthe oral cavity or vagina. with a candida species. or who are receiving chemotherapy. These are antibiotics effective against susceptible bacteria. "azole" = azole-type antifungal drugs (e. albicans. This leads to the death ofthe atTected fungal cell. "sartan": angiotensin II receptor blockerc (e.. olmesartan) . atoflastatin) : . It is common.g. pruritic infection characterized by a thick..This is an antifungal agent given intravenously or orally for the treatment ofsevere systemic fungal infections caused by fungi such as Candida species. celecoxib) .9.. however it is normally held in check b.9.ACE inhibitors (e..

Penicillin V . Penicillin G . Penicillin G . Penicillin VK . Ampicillin .D€ntal Decks . Amoxicillin . Amoxicillin 7a Coptrighr O 20ll-2012.. Ampicillin 79 Coplrighr O 201 l -2012 . D€nial Decks .

It is used for the treatment of syphilis and prevention ofrheumatic fever Remember: L Penicillins are bactericidal. Acid stable penicilhns (may be used orally) include: . and the two newer goups ofagents. Penicillin VK . This basic structure is synthesized by the penicillium mold from two amino acids. Dicloxacillin . Penicillin G parentzl (Pfzeryen) . Piperacillin . or are penicillinase resistant. Nafcillin . Probenecid increases blood levels of natural penicillins and may be given concurrently for this purpose. Oxacillin .preferred for treating oral infections because it is more acid stable (more reliable oral absorption) . Oxacillin . they inhibit cell wall synthesis. Cloxacillin . Penicillln G (benzylpenicillin) is the prototype for comparison. 2. Ticarcillin *** These two penicillins have the widest spectrum ofall the penicillins Penicillinase-resistant penicillins include: . cephalosporins. Cloxacillin . By side chain substitutions (speciJically. the carbapenems and the monobactams. The betalactam ring is essential for its antitracterial activity. Penicillin VK (Pen Vee K.All penicillins are derivatives of 6-aminopenicillanic acid and contain a beta-lactam ring structurejoined to a thiazolidine ring. the semi-synthetic penicillins are produced which are more acid stable. L-cysteine and L-valine. Ampicillin . Amoxicillin . Penicillin G benz hine (Bicillin C-R) always given by IM route. have a broader spectrum. V-cillin K) . Dicloxacillin Extended spectrum penicillins include: . Nafcillin . this means substituting other groups at the R position ofthe penicillin mol' ecule) of thebasic 6-aminopenicillanic acid molecule. Other naturally occrming penicillins include: . The aminopenicillins - Ampicillin and Amoxicillin Broad spectrum penicillins include: .always given by IM route . Antibiotics containing this betalactam ring are refered to collectively as beta-lactam antibiotics and include the penicillins.

. Ampicillin .Dental Decks . Amoxicillin 80 Copltighr C 201 l-2012 . Penicillin VK 81 Cop)'right O 20ll-2012 .Denral Decks . Tetracycline . Erythromycin . Penicillin \{K . Cefaclor (Celcor) . Tetracycline . Clindamycin .

have patient consult their physician as to need.Children: 50 mglkg (not to exceed adult dose) orally 30-60 minutes prior to appointment Allergy to Amoxicillin: Note: Only ifallergy is not ofanaphylactic type.{zithromycin -Adults: 500 mg orally 30-60 minutes prior to appointment -Children: l5 mg/kg orally 30-60 minutes pdor to appointment .0 g orally 30-b0 minutes prior to appointment -Children: 50 mg/kg orally 30-60 minutes pdor to appointment . Any one ofthe following . particularly with oral dosing. penicillins at normal therapeutic doses have virtually no side effects what so ever Penicillins are bactericidal' that is. Ampicillin has a broader spectrum of action than penicillin VK and cefaclor is a broad spectrum cephalosporin. Penicillin VK has these properries. they actually cause death of the invading bacteria.Premedication requirements for patients with valvular heart disease or congenital cardiac defects. CurrentAmerican Heart Association Guidelines: Published page 142. Clindamycin -Adults: 600 mg orally 30-60 minutes prior to appointment -Children: 20 mg. This incidence probably holds for any ofthe specific penicillins since there is cross allergy from one to the other Skin rash (a delayed reaction) is the most prevalent allergic manifestation. 'Cephalexin -. Tetracycline and clindamycin are bacteriostatic antibiotics and not bacteriocidal.0 g orally 30-60 minutes prior to appointment .\dult. Life threatening anaphylaxis can occur.Adults: 2. If in doubt. Note: The major disadvantage of the penicillins is their rather high incidence ofallergic reactions. Clarithromycin -Adults: 500 mg orally 30-60 minutes prior to apporntment -Children: l5 mg/kg 30-60 minutes pdor to appointment It is prudent to use an antibiotic with narrow spectrum ofaction and one that is bactericidal in order to minimize the development ofbacterial resistance.&g orally 30-60 minutes prior to appointment can be used..: 2. Amoxicillin . Standard Regimen . but is very rare. JADA Volume 138. Approximately l0olo ofthe general population is allergic to penicillins. . June 2007. In non-allergic individuals.

Calcitrol .Dental Decks . \4ethotrexate . Amoxicillin . Dicloxacillin . Penicillin VK . Piperacillin a2 CoDriglt @ 201 I 2012.. Tiazolarn (Hzlcion) . Denral Dects \- Which ofthe following has a clinicrly sign icant drug interaction with Amoxicillin? . Candesartan 83 Coplright O 201 I -20 12 .

and Bacteroides These antibiotics are recommended for the treatment of urinary tract inf€ctions and other infections caused by susceptible gram-negative Pseudomonas species and Proteus specles. higher serum levels. staphylococci. Ampicilf in (Pol1. sinusitis. these agents are active against Pseudomonas. and is less likely to cause adverse GI ef- lects (diarrhea). Amoxicillin is given orally. Penicillin VK has a relative limited spectrum of action against aerobic gram-positive cocci and anaerobes. ampicillin can be given orally or IV. Onipen) and Amoxicillin ( (penicillinase) of either gram-positive or gram-negative bacteria. )rlote: Ampicillin and amoxicillin are preferred agents in the treatment ofurinary tract infections caused by susceptible enterococci (which are facultatively anaerobic. the aminopenicillins are not stable to beta -llct^ma. prolonged serum levels ofmethotrexate. In addition to being active against gram-positive cocci (streptococci. Dicloxacillin has a similar spectrum producing staphylococcus. bronchitis.influenzae. Compared with ampicillin. *** Amoxicillin in large doses inhibits the renal tubular secretion of methotrexate. Note: Gram-negative bacteria that are susceptible to aminopenicillins include: H.Members ofthe penicillin family having the broadest spectrums ofaction are piperacillin and ticarcillin. Proteus and Salmonella. Proteus. Larotid) are ttsedprimarily to treat infections such as otitis media. fungi. a longer halflife.Coli and Proteus mirabilis. Important: None ofthe penicillins are aclive against viruses. Klebsiella. rickettsiae or other nonbacterial orsanisms. and gram-positive rods (bacillus and otfters).cillin. However.{moxicillin is an aminopenicillin which has an extended spectrum ofaction which includes not only aerobic gram-positive cocci and anaerobes. but some gram-negative bacilli such as Hemophilus. grampositive cocci that grow in short chains under extreme conditions mainllt in the intestine). amoxicillin has a higher oral absorption. as penicillin VK but is active against penicillinase- . pneumococci). Aminopenicillins (enpicillin and amoxicillin) are characterized by the amino substitution ofpenicillin G. . Ampicillin also falls into the category of an aminopenicillin. thereby causing higher. some E. They are able to penetrate gram-negative bacteria more readily than are the natural penicillins or the penicillinase-resistant penicillins. and acute bacterial cystitis caused by susceptible organisms.

Penicillinase . Cloxacillin .. Dicloxacillin 84 Coplright O 2011. Denbl Decks Which of the followlng bacterial enzymes belong to the fanily of beta-lactamases? .2012 . AT?ase .Dental Declc . Amoxicillin and clalulanate potassium (Augmentin) . Ampicillin and sulbactam (Unasyn) . Cephalosporinase . Protein kinase coplnshr O 20ll-2012 .

Beta-lactamases are €nzymes produced and secreted by a wide range of gram-positive and gram-negative bacteria as a defense weapon against cephalosporin and penicillin antibiotics. Penicillinase is an enzyme secreted by bacteria which splits open the betalactam ring. which is a four-membered imbedded ring structure consisting ofthree carbons and one nitrogen atom which is responsible for the antibacterial activity of penicillins.A functional part ofthe chemical molecule of all the penicillins is the so-called betalactam ring. Cloxacillin and dicloxacillin resist the actions ofpenicillinase because they have tected beta-lactam ring which prevents the actions ofthe enzyme. \ote: Probenecid is a drug used to treat gout. Probenecid (Benemid).raintained. Any alteration to the beta-lactam ring will also alter the antibacterial activity. One popular commercial preparation is Augmentin. an inhibitor of renal tubular cell secretion raises the blood ler els ofthe penicillins by diminishing their tubular secretion. This renders the penicillin molecule ineffective against those penicillinase secretors. Augmentin is used orally as pill or liquid form. a pro- Augmentin and Unasyn contain the agents clavulanate potassium and sulbactam respectively which block the actions ofpenicillinase from reaching the betalactam ring. Probenecid is sometimes given simultaneously with penicillin to raise the blood levels for increased activirr. By combining clavulanic acid with a penicillin. which contains arnoxicillin and clavulanate potassium. Those beta-lactamases that work against cephalosporins are called cephalosporinases. The majority ofpenicillins are directly excreted into the urine through renal tubular cell secretion. . the betalactamase enzyme is pennanently inhibited by the acid. These enzymes destroy the beta-lactam nucleus within these antibiotics by splitting open the betalactam ring structure. and the antibacterial activity ofthe penicillin is n. and those that work against penicillins are called penicillinases. Sulbactam is another beta-lactamase inhibitor lt is available for intravenous and intratnusculat use combined with ampicillin under the brand name Unasyn. This action renders the antibiotic ineffectir e.

Imipenem ..\ . severe GI upset)? . Clindamycin .Dertal Decks . Probenecid . Azithromycin (Zithromax: Z-Pak) . Hydrochlorothiazide .D€ntal Decks Whlch antlbiotic is used cautiously du€ to its side effects @seudomembranous colitis.righl O 2011.201? . Penicillin VK . Aztreonam 86 Cop]. Cephalexin (Keflex) a7 Coplrighr o2011.2012 .

llne (Miioc ) itl : Ares tin) lnhibits DNA lnhibits cell wall synthesis Inhibits 50S nbosomes .{moxicillin. especially those that are nosocomial in origin. 2. Drugs affected by probenecid include most cephalosporins and natural penicillins. Kebsiella. cloxacillin and dicloxacillin are lipophilic and are excreted by biliary means. Imipenem Penicillins: Penicillin VK Amoxicillin . Aztreonam is a parenteral synthetic betalactam antibiotic (classified as a monobactum). The spectrum is limited to aerobic gram-negative rods (i. No combination with probenecid or dosage adjustment for renal dy'slunction is necessary for these penicillins. and Serratia)./i".. Note: In some cases. It is curently the drug of choice for infections due to Enterobacter and Pseudomonas aeruginosa' It is usually combined with cilastatin and is used to treat severe or reslsta. is a beta-lactam antibiotic derived from thienamycin and is the first drug to be classified as a carbapenem antibiotic. Probenecid interferes with tubular handling of organic acids within the nephron.nt lnfections. lmportant: Nafcillin. and other betalactam-related antibiotics such as aztreonam and imipenem. *** ofthe antibiotic when high tis- The majority ofpenicillins are handled by the kidneys as organic acids and excreted by tubular excretion. oxacillin.faclor (Ceclor) Clindamycin Inhibits cell wall synthesis Same Inhibits 50S ribosomes Tetracyclines: Tel€cycline D oTyxy clir'e ( Yi brary c in Minocy.r/ C. \ot€ l.Ithas no gram-positive or anaerobic activity. The halflife is prolonged as well.This elevates and prolongs the serum concentrations sue concentrations are necessary. Acid /lugn€rtrr) AmpiciUin Cephrlosporins: (Xher: Cephalexin /Ke.e. lt is synergistic with aminoglycosides.Clav. Pseuclonlonqs. probenecid administration can more than double the serum concentration olthe affected drug.

Which ofthe following categorles does this agent b€long to? . Protease inhibitor .Which antibiotic/antimicrobial is associrted with the highest incidenc€ ofdrug allergy? . Crprofloxacin (Cipro) . Non-nucleoside reverse transcriptase inhibitor 89 Copyrighr O 201 l'2012 . Denlal Decls Stavudine (a/so fz own as d4T. Nucleoside reverse transcriptase inhibitor . Clindamycin . Penicillin VK . Mefi oridazole (F I ag! l) 88 Coplright O 201 I 2012.Dental Decks . or Zerit) is an antiretroviral drug used in the treatment of adults with HIV infection in combination \ with other antiretroviral agents.

The rash may be urticarial. replication. Actte epinephrine).levofloxacin (Levaquin). They are not active against Clostridium difficile. bullous. Other agents in this class include didanosine (Wdex). Some agents in this class include delavirdine (Rescriptor). pruritis). clizziness. Death can result in a short time if treatment is not instituted immediately (parenteral administration of l. Haemophilus influenzae. Drugs in this class include ciprofloxacin (Cipro). or maculopapular.g.. adefovfi (Hepsera) and nevirapine (Wramune). and.Three groups ofallergic reactions to the penicillins: (anaphylactic shock): occurs within 30 minutes. Manifestations range from a mild rash to anaphylaxis. Manifested by skin rashes. GI disturbances. These drugs are rr ell tolerated. E.{. This results in an inhibition ofthe HIV viral RNA from being made into a DNA segment. Hypersensitivity reactions occur in up to l07o ofpatients receiving penicillin.g. mild laryngeal edema. thrombopenic purpura develops. and shock. Approximately 80-90% ofall allergic reactions occurring with penicillin are ofthis t1pe. coli. moxifloxacin (Avelox). R€member: The mechanism ofaction ofthe fluoroquinolones is inhibition of DNA gyrase. nelfinavir (nracept)..g. pruritis. and gemifloxacin (Factive). an enzyme that is essential in the transcription. vomiting. bronchoconstriction. Not life threaten- ing' 3. confusion) and dermalologrc le. ritonavir (Norvir). These agents chemically are nucleosides and work by inhibiting the viral enzyme known as reverse transcriptase. \onnucleoside reverse transcriptase inhibitors inhibit the catalytic reaction of reverse transcriptase that is independent ofnucleotide binding. saquinivir (lnvirase). headache. 2. norfloxacin Qtloroxin). vesicular. Fluoroquinolones are active against many gram-positive organisms and gram-negative aerobes. Accelerated: occus 30 to 48 hours after. ddC) and zidovudine (Ret ovir . Rarely. howevet the most common adverse effects are Gl (e. wheezing. . rash. Manifestations include urticaria. and Mycoplasma pneumoniae.. including Moraxella catarrhalis. zalcitabine (Hivid. diqrrheq. AZT). and local inflammatory reactions. abdominal pain). angioedema. lllote: A rash is the most common sign olan allergy to penicillin. Proteas€ inhibitors suppress viral replication by inhibiting protease' the enzyme responsible for cleaving viral precursor peptides into infective virions. Characterized by urticaria. nausea.CNS (e. chlamydia. and repair ofbacterial D\. Delayed: occurs after 2 to 3 days. Some agents in this class include indinavir (Crixivan). thus the genome ofthe HIV virus is not copied from RNA.

.2012. Amoxrcrlhn (Amoxil) 91 Copyight €r 20ll-2012 . Discoloration ofteeth and enamel hypoplasia in young children 90 Coplright O 2011.{mpicillin (P o l:tc i I I in) . Cloxacillin (Cloxapen) . Bone marrow disturbances . Diarrhea . Photosensitivity .Denhl Decks . Denbl Decks . Nausea .. Penicillin VK .

Note: Parenteral ampicillin is recommended as the drug of choice in patients unable to take oral medications and who are not allergic to penicillin for prophylaxis for bacter- ial . Amoxicillin is given orally. The major difference in the drugs is the higher oral absorption. This is due to the wide spectrum of antibacterial action which alters normal flora. Minocycline (Minocin) . and tetrucyc/ire). and longer half-life for amoxicillin compared with ampicillin. Examples include both vaginal and oral candidiasis. They have been used as alternatives to penicillin in patients with ANUG (acute necrotizing ulcerative gingil lll. some Escherichia coli. Fanconi syndrome can be caused by various things that damage the kidne1s.Another common adverse effect is the occurrence ofopportunistic (superintbction) infections caused by Candida albicans. They are not penicillinase resistant. Tetracycline (Generic) . ampicillin can be given orally and IV Remember: Oral amoxicillin is recommended as the drug ofchoice for standard general prophylaxis for bacterial endocarditis in patients undergoing invasive dental procedures. higher serum levels. including certain medications (azathioprine. These conditions are also known as vaginal and oral yeast infections. Fanconi syndrome is a disorder ofthe kidney tubules in which certain substances normally absorbed into the bloodstream by the kidnevs are released into the urine instead. Members of the tetracycline family ofantibiotics include: Short acting: Intermediateacting: Long acting: . They \\ ork against many gram-positive organisms and some gram-negative bacteria such as Haemophilus influenzae. cidolbvir gentamicin. They are used for upper respiratory infections.Demeclocycline (Declomycin) .r/ u'ho require antibiotics. and Proteus mirabilis. These trro antibiotics are characterized by the amino substitution of penicillin G. Doxycycline (4bramycin) Remember: The usefulness of the tetracyclines in the treatment of odontogenic infections is limited since they can cause "yeast'' infections very easily. \ote: In adults.

Affect bacterial DNA . Interfere with bacterial metabolic pathways 92 coplright @ 201 |-2012 - D€ al Decks . Affect bacterial cell wall . Cause mutations within bacterial DNA 93 Coplrighr O 201l-2012 ..Dental Deck! .Interfere with nucleic acid synthesis . Prevent protein synthesis in the bacterial cell . Affect bacterial protein synthesis . Bacterial cell wall destruction .

ciproJloxacin) . no proteins are formed.Fet!. Absorption of the tetracyclines from the GI tract is inhibited by divalent and trivalent cations such as CA--. mineral supplements containing these irons.Tetracycline family . and Al**..Fluoroquinolone family (i.-. The inhibition of this ribosomal function interferes with the attachment of the growing amino acid chain thus preventing complete formation of peptides from the ribosome. These ions form chelation products with the tetracyclines and thus prevent their absorption.. Fe-.. Mg.Clindamycin .Meronidazole (F lagt l) .Sulfonamides (sulfa drugs) The tetracyclines inhibit protein synthesis by binding to the 30 S subunit ofthe bacterial ribosome. the lack thereof will cause a static state in which the bacterium becomes nrlnerable to phagocltosis by the body's imrnune S-v"SIem. Affect bacterial cell wall: . e. Agents affecting bacterial DNA: . or antacids (contain Mg").Penicillin family . Agents affecting bacterial protein synthesis: . Since no peptides are formed.Basic mechanisms of actions ofantibiotics: . Since proteins are necessary for the bacterial cell to metabolically function. Agents interfering with bacterial metabolic pathways: . iron-containing vitamins (contain . .Cephalosporin family .Erythromycin family .Chloramphenicol . This is why tetracyclines should not be given with milk and dairy products (contain Ca--).

. Penicillin G . 30s 50s . 30s 50s 95 Coplrighr O 201 l-2012 . Bacteriostatic. Penicillin VK 94 Copyighr C 201 l-2012 . Bactericidal. Bacteriostatic. Tetracycline .Dertal Decks . Cephalosporins . . . .Dental Decks Erlthromycin is a antibiotic which binds to the ribosomal subunit of susceptible bacteria. The result is the inhibition of protein rynthesis. Bactericidal. Ampicillin .

The inlibition ofthis ribosomal function interferes with the attachment ofthe growing amino acid chain thus preventing complete formation ofpeptides from the ribosome. Treatment ofacne . Erythromycin-type antibiotics are members of the Macrolide family of antibiotics. Eryc) . Iocalized aggressive periodontitis) Important: Tetracyclines are not the drug of choice for Streptococcus or Staphylococcus. Since proteins are necessary for the bacterial cell to metabolically function./ .The tetracyclines are a goup of broad-spectrum. Infections caused by Mycoplasma. Dental: treatment ofperiodontitis associated with the presence of Actinobacillius actinomycetemcomitans (AA) (i. Since no peptides are formed. Erythomycin ethylsuccinate lE E S. T€tracyclines are useful in treating the following infections: .1. bacteriostatic antibiotics that inhibit protein synthesis in the susceptible organism by binding to the 30S ribosome subunit. L)ryne disease (caused by Bon'elia burgdorferi) .e. Members of the Macrofide family /generic and brand names) are. This causes the RNA to dissociate from the ribosome and prevents protein synthesis.. no proteins are formed. Azithromycin (Zithromax. Protozoa or Rickettsia . AII ofthe erythromycins act through the same mechanism to bind to the 50s ribosomal subunit ofsusceptible bacteria. Erythomycin base (E-mycin. Treatment of gononhea and syphilis in patients allergic to penicillin . Chlamydia . the lack thereof will cause a static state in which the bacterium becomes vulnerable to phagocytosis by the body's immune system. Cl ar ithr omy cin (B i ax in ) . Exacerbations of chronic bronchitis . Z-Pak) . Medical infections caused by susceptible gram-positive and gram-negative bacteria . . \ote: GI Tract upset food. is the most common side effect of the erythromycins (tqke with . Erythromycin stearate (Etythrocin) All of the €rythromycins are very effective against gram-positive bacteria but not so effeclive against gram-negative bacteria. thereby impeding the binding of aminoacyl IRNA to the receptor site on the messenger RNA ribosome complex.

Acyclovir (Zovirax) . fumantadine (Flumadine) .Dental Deck . Oseltamli (Tamillu) . Zanarnivir (Relenza) 97 Coplrighr C 20ll-2012 .. Clindamycin 96 Coplrighi o 201I-20t2 . Metr onidazol e (F l a gy l) . Penicillin VK . Tetracycline .Ddtal Decks . -{mantadine (Symmetrel) .

M2. to decrease the severity of the flu. Metronidazole (Flagyl): dizziness. and nausea Note: Metronidazole is not a true antibiotic since it is not found in natural organisms. Like amantadine. rimantadine initially was used to prevent influenzaA during flu season. to decrease the severity ofthe flu. Clindamycin: diarrhea. it is a synthetic substance produced in the chemical laboratory. which is required for the viral particle to become "uncoated" once taken inside a cell by endocytosis. headache.The photosensitivity reaction caused by the tetracycline family of antibiotics results in the appearance ofred rashes or blotches over the skin in the presence of sunlight. Common adv€rse effects caused by the other agents: . Rimantadine is chemically related to arnantadine. and. Acyclovir (Zovirax) is an antiviral that inhibits DNA synthesis rather than neuraminidase enzymes. and. . if given within 24 to 48 hours after the onset of flu symptoms. Note: Rimantadine appears to exen its inhibitory effect early in the viral replicative cycle. Later amantadine was found to cause improvement in the symptoms ofParkinson's disease. lt was initially used to prevent influenza A during flu season. if given within 24 to 48 hours of the onset of flu symptoms. potentially altering virus particle aggregation and release. Penicillin VK: hypersensitivity resulting in skin rash and rare anaphylaxis . but rimantadine has fewer side effects on the nervous system than amantadine. Amantadine is a synthetic anti-viral drug that can inhibit the replication of viruses in cells. . possibly inhibiting the uncoating ofthe virus (similqr to amantadine s nechanism oJ action). known to cause pseudomembranous colitis Oseltamivir (Iarr iflu) and zanrmivir (Relenza) inhibit influenza virus neuraminidase enz! mes. Tamiflu and Relenza are both used to treat acute illness due to influenza (A or B) infectior'. Rimantadine is a synthetic anti-viral drug that can prevent viruses in cells from multiplying. Not€: The mechanism of amantadine's antiviral activity involves interference with a viral protein. abdominal pain.

Denral Decks . Penicillin VK 98 Coplrighr O 201 1. Doxycycline (Wbramycin) .. Laryngeal edema .Denral Decks . GI disturbances . Tetracycline . Minocycline (Minocin) . Severe hypotension . Ufiicada (welts that itch) .2012 . Bronchoconstrictron (ah'wqy constriction) . Shock 99 Coplright @ 2Ol l-2012 .

and local inflammatory reactions. allergic reactions take longer than two days to develop. Basic skin rashes. wheezing. Delayed - . which are generally mild. 80-90% ofpenicillin reactions are ofthis type. Tetracyclines have the ability to chelate calcium ions and become incorporated in the bony tissues. which are bactericidal against susceptible organisms. In general. 2. The teeth ofchildren who have been given the drug may develop a greenish-brown discoloration. These reactions occur in up to 109/o of patients receiving penicillin. This effect is sometimes seen in the newly erupted teeth of infants whose mothers have received tetracycline during pregnancy. R€member: Penicillins. not lifethreatening. This reaction can be fatal if countermeasures such as the injection ofepinephrine are not taken promptly. Ig-E mediated. and D-alanine caboxykinases and are implicated in the final phases ofbuilding and reshaping ofthe bacterial cell wall while it is growing and dividing. The enzymes to which tbey bind are called penicillin-binding proteins (PBPs). **" This reaction most conmonly occurs with parenteral administration ofpenicillin. pruritis. They consist of transpeptidases.Penicillin VK is not harmful to the fetus when taken by pregnant mothers. 3. Accelerated allergic reactions arise 30 minutes to 48 hours after administration. [t is not incorporated into bony tissue or in the teeth ofchildren like the tetracyclines. The most common manifes- ration is a mild rash. The most common adverse effect ofpenicillin therapy is an allergic reaction. transglycosylases. Note: Tetracycline and all members of the tetracycline family are contraindicated in children up to 8 years old and in pregnant women. Epinephrine prevents the release of substances from mast cells and anlagonizes the actions of histamine and leukotrienes of smooth muscle. Allergic reactions to penicillin are classified into three groups: l. fmmediate onset reactions (araphylaxis) ocatr within 30 minutes. disrupt s) nthesis ofthe bacterial cell wall and compete for and bind to specific enzyme proteins that catalyze transpeptidation and cross-linking. Urticaria.

Trifl uoperazine (St e laz ine) t0'l Coplrlgh O 201 I -20 12 . Thioridazine r De-h--"-i-- . The butyrophenones .2012 . Halopeidol (Haldol) . Chlorpromazine (Thorazine) . which one is the cXcrPZolv? . The thioxanthenes . The benzodiazepines 100 Coptrighr O 2011.. The phenothiaz ines .Dental Dsks All of tbe following are phenothiazi nes EXCEPT oae. Prochlorperazine (C omp azin e) .Denbl Decks .

the thioxanthines ( thiothixene) and the btrytophenor\es (haloperidol). is the key drug among the phenothiazine antipsychotic agents. First generation drugs include the phenothiazines (chlorpromazine.ndrome. Second generation (a\)pical) ag€nts: this group includes clozapine. and thioidazine). "typical" drugs that treat the positive but not the negative symptoms associated with a psychotic state. Perphenazine . and to some extent serotonin receptors- Typicaf antipsychotic drrgs (frst generationJ are more potent antagonists ofD2 dopamine receptors than ofDr receptors. quetiapine. bminstem. olanzapine. and D5 receptors. are used commonly in the treatmcnt of a variety ofpsychotic disorders. quetiapine. T rifrtroperczrne (S t e I azin e) . and they are used to treat both positive and negative symptoms ofschizophrenia. Da. Adyerse effects of antipsychotic drugs: . procltlorperazine.{ntipsychotic agents include: . mesoridazine. Dystonia and akathisia (an unpleasant sensation of motot' restlessness) . Currently. risperidone. th€y are prolactin sparing. i. trifluoperazine. Chlorpromazine (Thorazine) . followed by the butyrophenones and the thioxanthenes. :. ziprasidone. Thioxanthenes: a less potent . D2.Antipsychotics. Long QT-interval syndrome and ultimately increase the risk of fatal arhythmias . (second generallor/ or atypical antipsychotic agents affcct different receptor sites compared generation antipsychotics. These drugs are effective in treating schizophrenia and exhibit reduced ability or an inability to induce EPS. including D1.?othalamus. Antimuscarinic effects . ln addition it has been found to be effective in the heatment ofTourette's s). Second generalion agcnts include clozapine. Con\. By fa. Neuroleptic malignant syndrome . ./ is the first ofa new class of atypical antipsychotic agents called dopamine |. Thioridazine . First generation (lr^pical) agentsl I . and medulla. The first generation includes thc older.ulsions . Orthostatic hypotension . the most widely used group ofantipsychotic agents uscd in medicine are the phenothiazines. Mesoridazine . olanzapine. Fluphenazine L But'"rophenones: . perphena:ine. and aripiprazole. They bind dopamine. Thiothixene is antipsychotic. with selecrilely lor limbic dopaminc rcceptors. Prochlorperazine (Compazine) . The first antipsychotic on thc markct. fluphenazine. Phenothiazines: .ceptors. limbic system. receptors compared $ith D" receptors. Second-generation drugs have far fewer extrapyramidal symptoms fEPt and tardive dyskinesia fDJ. ^ripipr^zole sistem stabilizers or dopamine partial agonists. also known as major tranquilizcrs orneuroleptics. They have increased affinity for serotonin /J-11I.It combines the actions ofD2 and serotonin 5-HT2a recePtor antagonism. and aripiprazole. Haloperidol is a highly effective antipsychotic drug used to treat schizophrenia. The exact mechanism of antipsychotic drug action is unknown. chlorpromazine. basal ganglia. These drugs are thought to work by blocking postsynaptic dopamine receptors in the h. antipsychotics are divided into two gcncrations. Parkinsonism . Note: With the exception ofrispcridone.which explains the low incidence ofEPS andTD. They exhibit reduced ability or an inability to induce EPS. \e\\er * ith first Important: (Abilrj. risperidone. ziprasidone. Clozapine is specific for limbic rec€ptors and not for striated (muscle) r. It is used for the treatment ofschizophrenia. .

Clozapine (Clozaril) . Halopeidol (Haldol) 102 Coplrighr O 2011. Dry mouth . Chlorpromaz ine . Azelastrne (Astelin) . Sedation . Olanzapine (Zyprexa) . Headache . Quetiapine (Seraquel) . Onhostatic hypotension . Risperidone (Risp erdo I) .Dmtal Decks Which statement describ€s the extrapyramidal syndrome (EPS) caused by the phenothiazine'type lntipsychotics? . T hioridazine (Me I I ar i I) ..2012 . Muscle spasms ofthe oral-facial region 103 Coplaight O 20ll-2012 .Denral Decks .

They have increased at'linity for serotonin (5-HT ) receptors compared with D2 receptors. About 20 percent ofpeople taking antipsvchotic/neuroleptic drugs for more then one year will be affected. fluphenazine. legs. D2. Note: Haloperidol is a potent dopamine antagonist. Second generation agents include clozapine. fingers. and aripiprazole. including the body trunk. Newer (secontl generation) or atypic l antipsychotic agents affect different receptor siles compared with first generation antipsychotics. Da. Symptoms involve rurcontrollable movement ofvarious body parts. quetiapine. Ertrapyramidal syndrome lEP. or tongue. Important: Clozapine is specific for limbic receptors and not for stdated (muscle) receptors. perphenazine. Da. D2. with selectively for limbic dopamine receptors. They exhibit reduced ability or an inability to induce EPS. ziprasidone. including D1.*** Azelastine (Astelin) Antipsychotics is an antihistamine nasal spray. with selectively for limbic dopamine receptors. including Dl. spasms ofneck and facial muscles. First generation drugs include the phenothia. and aripipra- zole. are primarily indicated for treatment ofpsychosis associated with schizophrenia. and D5 receptors. and D5 receptors. and manic symptoms of manic-depressive illness Typical antipsychotic drugs (lirst generation) are more potent antagonists of D2 dopamine receptors than ofDl receptors. quetiapine. mesoridazine. paranoia. and thioridazine) . olanzapine. Tardive Dvskinesia (TD) is a serious. They exhibit reduced ability or an inability to induce EPS. tremors. These symptoms include: Parkinsonlike movements (shufiIecl gait. olanzapine. lips. irreversible neurological disorder that can appear at any age. muscle rigidiry. arms. the thioxanthines (/riothixene) and the butyrophenones (haloperidol). They bind dopamine. pill-rolling eJlbct oJ fngers). . which explains the low incidence of EPS and TD. mouth. ziprasidone.l) refers to a variety of signs and symptoms that are a result ofthe blockade ofdopamine receptors in specific brain regions. They bind dopamine. They have increased alfinity for serotonin (5-HT) receptors compared with D2 receptors. risperidone. and loss of muscle movement. Remember: Newer (second generation) or atypical antipsychotic agents affect different receptor sites compared with first generation antipsychotics. risperidone. prochlorperazine. Tardive Dyskinesia is a side effect of taking antipsychotic/neuroleptics drugs. trifluoperazine.zines (chlorpromazine. Second generation agents include clozapine.

Motrin ES . Respiratory alkalosis . Nausea the ears) . Yertigo (dizziness) . Naprosyn 105 Copfight @ 20i |. Vomiring 104 Copyright O 20ll-2012 Dental Decks .2012 . Hallucinations . Tinnitus (ringing in .Denral Drcks . Percodan .. Vicodin .

headache. and anti-inflammatory. confusioq dehydration. aspirin has the ability to inhibit the formation of life-threatening thrombi (6/0011clo/s/. hyperthermia. i. vomiting. For the traditional NSAIDS such as ibuprofen. hypcractivity. Excretion ofsalicylates occurs principally via the kidn€). Aspirin inactivates the enzyme known as cyclooxygenase.]cloon'genase).\dYil contains 200 mg ofibuprofen and may be sold over-the-counter. because they inhibit both COX-1 and COX-2 enzymes. NSAIDs also have analgesic. Sincc cyclooxygenaso synthesizes thc prostaglandins. These doses reduce thromboxane production in platelets to result in the inhibition ofplatelet aggregttion. Ihe three chicf metabolic products ofsalicylic acid are salicyluric acid.By doing this they inhibit the cyclooxygenase step ofthe arachidonic acid cascade and thus reduce local prostaglandin synthesis. the inhibition ofthis enz''rne results in the inhibition ofprostaglandin synthesis. Concomitant use of anticoagulants .{sthma. because it inhibits COX-2 enzyme only' it belongs to the category oICOX-2 sel€ctive inhibitors. nausea. . rhinitis. and antip)'retic actions.fluenzu or chiclerpoxl with or without fever due ro a potcniial association with Reye's syndrome (this s). Pregnancy (especictlly during the thit'd lrinester) ' P€ptic ulcers faipil'i nay cduse bleeding ofthe GI tracl) . \onsteroidal anti-inflarrunatory drugs (NSAID. Contraindications to the use ofaspirin: . Chronic aspirin toxicity presents with the following signs and symptoms: salicylism. although other tissues may also be in\ ol\ ed. hlpokalemia. As a result. dizziness. Aspirin is an irre versible plat€let inhibitor and can reduce blood clotting to prolong bleeding. whereas. salic] luric acid. but are capable ofinducing gastrointestinal ulcers. Initial symptoms include respiratory alkalosis with hypcrpnea and tachypnea. In this way. aspirin is analgesic. Note: Rofecoxib (Woxx) and Valdecoxib (Bextra) are also COX-2 selective inhibitors that u. The lirer appearc to be the principal site for salicylate metabolism. naproxen. tinnitus. the cthcr or phcnolic glucuronide and the ester or acyl glucuronid€. The COX-2 selective inhibitors will reduce pain and inflammation without any significant risk ofcausing gastrointestinal ulcers. in the form offree salicylic acid. Ble€ding disorders (aspirin will increase bleeding tine) ' Do not use in children with viral infections (i. Remember: The traditional NSAIDs such as ibuprofen. antipyretic (ever reducing). and hcmatologic abnormalities. Low doses of aspirin taken regularly can have a cardioprotective effect. . naproxen and aspirin inhibit COX-2 along with COX-I.'ere removed from the market because they were found to have added cardiovascular risks in some Datients.. dlotne is a serious neutulogical defecl) . through a combination ofglomerular filtration and tubular cxcrction. Motrin contains . progressing to coma and respiratory collapse. For celecoxib (Celebrcx). and aspirin. they belong to the category of non-selective COX inhibitors. Note: Aspirin inhibits both COX-l and COX-2.e. nasal polyps .An overdosage of saficyl^tes (aaie aspirin /o-riciry/ is life threatening and requires intensive supportivc trcatment in a hospital. bleeding and GI disnrrbances. CNS effects. have anti-inflammatory effects resulting frorn their ability to inactivate the enzyme prostaglandin endoperoxide synthase f. Thus they are effective in reducing pain and inflarnrnation. as well as phenolic and acyl glucuronidcs.100 mg of ibuprofen or higher and can only be sold with a prescription.

Denral Deckj .Dental Deckt .20l2 . Advil) . Acetaminophen . Acetaminophen (Ty I e n o I) .. Codeine . Hydrocodone . Naproxen sodium (l/eve) 106 Cop)"ightO20ll. Ibuprofen (Motrin. Aspirin . Ibuprofen 107 Coplrighl O 201 1-2012 .

Thus. Inhibition of prostaglandin production reduces the inflammatory respons€ at sites of surgery. lt is unclear exactly Codeine and h1-drocodone are narcotic analgesics that effectively reduce pain but do not reduce inflammation. Large doses ofacetarrinophen can cause liver toxicity. Acetaminophen is not effective enough to reduce severe pain. Narcotics work within the brain to block ascending pain impulses traveling from the periphery into the brain. how acetaminophen uorks to reduce pain. . the inflammatory response is not affected to any great degree. Acetaminophen is a weak inhibitor of prostaglandin format ion. Acetaminophen reduces pain through mechanisms other than inflammatory reduction.Acetaminophen has no effect on platelets nor the coagulation pathways and does not affect bleeding times or prothrombin times even with high doses. Acetaminophen has two major pharmacological actions: an analgesic effect and an antipyretic (ever redticey' effect. but it is effective in reducing mild to moderate pain. Reduction of inflammation results in reduction ofperceived pain. Acetaminophen is a weak inhibitor ofprostaglandin production in peripheral tissues. Affect blood clotting Associated with Reye's s)ryldrome Ibuprofen inhibits the production of prostaglandins in peripheral tissues at sites where pain and inflammation are present. Alcohol can seriously increase the hepatotoxic potential of acetaminophen. There are approximately 100 deaths annually due to liver toxicity produced by ingesting large continuous doses of acetaminophen. Acetaninophen very rarely causes drug sensitivities and can be given to patients having an allersv to asnirin. injury or infection.

Meperidine . Ibuprofen .Dental Decks NSAIDs reduce the production of associated with pain and inflammation. Codeine 108 Coplrigh O 201 I -20 12 . Phenobarbital . Cltokines . Interlerons 109 Coprighr C 201 l'2012 . Leukotrienes . Hydrocodone ..Dental D€cks . . Prostaglandins .

Non-narcotic anal- gesics have no liability for abuse or addiction. They afihritis. Cox-2 inhibitors . Oxicams . Mefenamic acid lPorsle4 . Non-steroidal anti-inflammatory drugs 0y'S. They are all controlled substances requiring a DEA number from the prescriber Important: NSAIDs can inhibit the antihypertensive effect ofACE inhibitors. such as metabolism and nen e transmlsslon. antipyretic. Prostaglandins are a group of hormonc-like substances that mediate a range of physiological functions. Ketorolac (Toradol) . Proprionic acid derivatives: .Ibuprofen is an NSAID and is classified as a non-narcotic analgesic. and diuretics. Hydrocodone (Wcodin). Sullndac (Clinoril) . They are not a controlled substances. Contraindications to ihe use ofNSAlDs are impaired renal function.r/cers) \SAIDs have analgesic. Dicloferac sodirm (Votaren) . Eramples offSAlDs: .{cetic acid derivatives: . and anti-inflammatory properties (similat to aspitin). betablockers.4/Dl. and GI disease 1r. pregnancy. Phenobarbital is a barbiturate used as a sedative and to treat epilepsy. . Ibuprofen (Motrin. \aproxen ' Naproxen sodium (Anaprox. inhibit the cyclooxygenase step ofthe arachidonic acid cascade and thus inhibit thc activity ofprostaglandin synthetase. Aleve) (Naprosvn) 'Fenoprofen (Nalfon) . Ketoqofen (Orudis) . Meloxicam (Mobic) . Advcrsc reactions include GI upset @ossible ulcers).lnsaid) 'Oxaprczin (Daypro) . Flurbiprofen (. Meclofenamatc . Celecoxib (Celebrcx) . and prolongation of bleeding irme (reduction in plqtelel aggregatiotl). and painful menstruation. and are controlled substances requiring a DEA number fiom the prescriber. Piroxicam (Feldene) (M ec lomen ) . Etodolac (Lodine) . Barbiturates all have the potential to cause abuse and addiction. Fenamic acid derivatives: . Alkanoic acid derivatives: . Advil) . are used for pain control. Indomethicin llndocll . Nabumetone (Relqfen) . meperidine (Demerol) and codeine are narcotic analgesics with the potential to cause abuse and addiction.

Naproxen . Amlodipine @y'onasc) . F osamax (Alendronate sodium) 111 Copyrighr @ 2011.. Dental Decks . Prednisone . Acetaminophen . Aspirin . Nabumetone 110 Coprighr O 20ll-2012 Dental Decks . Ibuprofen . Ptroxrcarn (Feldene) . Enalapril (Yasotec) .2012.

Note: N-acetylcysteine (NAC) is the specific antidote for acetaminophen poisoning. carbamazepine. Common side effects ofNSAIDs such .Psychological disturbances . Is taking drugs such as probenecid or methotrexate . which normally is detoxihed by glutathione. Prednisone is a corticosteroid and has anti-inflammatory actions. the inhibition ofthis enzyme results in the inhibition of prostaglandin synthesis. drowsiness. Syrnptoms that appear in the ltrst 24 hours are nausea. Acute overdosage ofacetaminophen can result in hepatotoxicity and is life threatening. Is allergic to aspirin . and anti-inflammatory actions.Muscle weakness . Il is used to manage inflammatory disorders and used for the symptomatic treatment ofacute and chronic rheumatoid arthritis and osteoarthritis.Indigestion such as prednisone include: Arthralgia . R€member: . acelaminophen can cause hepatic necrosis. As a result. When glutathione is depleted. Short-term side effects of corticosteroids . Acetominophen is metabolized to a highly toxic int€rmediate product. It is used for the treatment ofa wide variety of inflammatory diseases including rheumatoid arthritis and os- teoarthritis. causing necrosis. Acetaminophen is preferred over aspirin when an analgesic or antipyretic drug is indicated and also the patient: . Is taking anticoagulants Remember: Aspirin and Nonsteroidal Anti-inflammatory Agens (Ibuprofen.Edema (abdominal distension) . and others) inactiYate the enzyme known as cyclooxyg€nase. Is asthmatic . and ethanol. Long-term side effects of corticosteroids include: - . Cyclooxygenase has an acronym ofCOX' Thus the Nonsteroidal Anti-inflammatory Agerrts (NSAlDs) are also known as COX inhibitors. NSAIDS must be used cauriously in patients with peptic ulcer analgesic for low intensity Acetaminophen inhibits central prostaglandin synthesis -it (asplrlr/ in blocking pepain and antipyretic. \qbumetone.Osteoporosis . the toxic intermediate attacks other cells. lethargy. Naproxen. hydantoins. rifampin. Because it is less effective than salicylates ripheral prostaglandin synthesis.Insomnia . antipyretic.Nausea as piroxicam (Feldene) incl'tde: . Note: In large doses p Z 5 g within 8 hours). Since cyclooxygenase s). vomiting. Piroxicam (Feldene) is a non-steroidal anti-inflammatory drug Qr'SlID) that inlibits prostaglandin synthesis. they ha\e analg€sic. it has no anti-inflammatory activity and does not affect platelet function and therefore will not affect clotting time. Is at added risk for an ulcer .Heart bum . Concurr€nt use with the following drugs may increase the risk of hepatotoxicity: barbitumtes.nthesizes the prostaglandins. malaise.Gastric irritation . sulfi npyrazone.Peptic ulcer . ls experiencing bleeding . and confusion.

Steroidal anti-infl ammatories 112 Copright O 201 l-2012 .. Salicyclates . Dopamine 113 Copyrighr O 2011.2012 .Denral Decks . Opiates . Norepinephrine . Acetylcholine .Denial Decks . Epinephrine . COX-2 selective inhibitors . Non-selective COX inhibitors .

parasympathetic gangliq. They are subdivided as follows: . The term L Preganglionic neurons ofboth divisior's (parasympathetic a . 1. . *** Important: (l sympathetic) are cholinparasympathetic division. also.): . Nicotinic receptors (silesr: - - At the skeletal neuomuscular junction (involving sonatic nerves) At ganglionic sites /*** The same type of nicotinic receptor is present in sympathetic ganglia. Two forms of COX exist: COX-I. The traditional NSAIDs such as ibuprofen. referred \ote3 2. but are capable of inducing gashointestinal ulcers. The COX-2 selective inhibitors: - Are not salicylates because they are not aspirin drugs Are not opiates because they do not work like morphine Are not steroidal antiinflammatories because they are not corticosteroids such as hy- droc ort isone Chofinergic is a term for a nerve ending that releases acetylcholine (ACh) as the prrmary neuotransmitter. and others inhibit the COX-I enzyme thus diminishing the fomation of the protective prostaglandins.. is the enzyme which produces prostaglandins. they belong to the category of non-selective COX inhibitors. Muscarinic receptors fsites. phospholipase C (PLC). The COX-2 selective inhibitors will reduce pain and inflammation without any significant risk ofcausing gastrointestinal ulcers. &tt:' nicotinic response is used to describe the stimulating action ofACh on the ganglia. Muscarinic receptors are usually linked to Go. because they inhibit both COX-l and COX-2 enzymes. For the traditional NSAIDs such as ibuprofen. naproxen and aspirin inhibit COX-2 along with COX-I. The traditional NSAIDs such as ibuprofen. ergic. The COX-2 enzyme produces prostaglandins at the sites of surgery infection and inflammation. Thus they are effective in reducing pain and inflamrnation. and the adrenal medulla) Drugs that resemble ACh in chemical structure and bind to these receptors imitate the effects of parasympathetic postganglionic activity. The COX-I enzyme produces prostaglandins in the GI Tract. naproxen. The prostaglandins formed act as a protective substance against the formation of gastrointestinal ulcers. Gastrointestinal ulcers are therefore a potential adverse effect with these drugs. a synapse in which acetylcholine is the primary neurotansmitter. naproxenJ and aspirin. 3.At neuroeffector sites for all postganglionic cholinergic neurons (this is chqracteristic of a ll parasympathetic postgqnglionic nerves) At neuroellector sites ofpostganglionic sympathetic n€rYes to the sweat glands and a few blood vessels (tl ese postganglionic nerves are also cholinergic) - . as well as its actiol at the neuromuscular junction of skeletal muscle. or COX. When this enzyme is inhibited. and COX-2.Cyclooxygenase. Acetylcholine receptors are called cholinergic recepton. aspirin. because it inhibits COX-z enzyme only' it belongs to the category of COX-2 selective inhibitors. andCa". as are postganglionic neurons ofthe 2. The action of acetylcholine at postganglionic parasympathetic sites is often to as a muscarinic response. For celecoxib (Celebrex). less prostaglandins are produced and there is less pain and inflammation. Postganglionic neurons ofthe sympathetic division are usually adrenergic.

salivary tear and bronchial glands 114 Copltight O 20ll-2012 . Propantheline (Pro -Banthine) 115 Coptright @ 201l-2012 . The stimulation ofsweat. The stimulation ofthe smooth muscles of the bronchi. bile duct.Dental Deck All of the following are antimuscarinlc agents . Slowing ofthe heart . Gl) copynolate (Robinul) . bladder and ureters . GI tract.EXCrPf one. Which one is the IqXCEPTIOM .Denhl Deks . gallbladder. Dilation ofthe pupils .. Scopolamine . Vecamylamine (Inversine) . Atropine .

they simply occupy the receptor site and pre\ ent acetylcholine from occupying the same receptor Accepted therapeutic indications include treating Parkinson's disease. postoperative bladder syndrome and traveler's diarrhea. antispasmodic actions and gastric and salivary secretiorrs (dry moutlr). *** Ilecamylamine The tvpical effects is a nicotinic ganglion-blocking drug. -\ rise in body temperature . Slowing ofthe heart (bradycanlia) . The stimulation ofthe smooth muscles ofthe bronchi.The secretions of all glands in the nose. ofanticholinergic drugs include r. urinotion) .lmportant: These drugs are conreduction in traindicated in patients with glaucoma. cholinergic action constricts the pupils. The heart rate increas€s (tachycardia) . control ofupper airway sccrctions Travclcr's diarrhca and antisecretory To produce mydriasis and cycloplegia To prevent or reduce motion sickness . salivary. Acetylcholine causes an alteration in cell membrane permeability to produce the above actions.. Constriction ofthe pupils 0n rosrt Important: Acetylcholine is the chemical mediator at all autonomic ganglia and parasympathetic postganglionic synapses. It is also the transmitter substance of the neuromuscular junction in skeletal muscle (local anesthetics prcvent or rcduce the liberation of ACh at the NMJ) and sweat glands. pharynx and respiratory tract is inhibited (unpIeasant "dry mouth") .*** This false. . The stimulation ofsweat. Inhibit salivation and excessive secretions prcoperatively. Dilation of the puprls (mydriasis) \ot€: Termination of transmission by ACh takes place primarily by metabolism by acetylcholinesterase located on postsynaptic or postjunctional membranes. gallbladdel bile duct.e.r. These drugs have no intrinsic activity oftheir own. tear and bronchial glands . An inhibitory effect on motility throughout the GI tract fmal cause constipatio and uritla4 retention) .{nticholinergic actions: . motion sickless. mouth.rydriasis. GI tract. bladder and ureters (i. Cholinergic actions: .

Atracuium (Tracrium) Cisatr actiurn (N im b ex) '117 . Dental Decks . Succinylcholine (Anectine) .Dental Decks . Tetraethylammonium . Vecuronium (Norcuron) . Trimethaphan 1t6 Cop)Tight O 201 I 2012. P anntr onium (P av u I o n) .. . Mecamylamine . }liYacuium (Mivacron) . Doxacurium (Nuromax) . Rocuronium (Zemuron) Copyrighr O 201| '2012 . Tubocvraflne (Curare) . Hexamethonium .

Important: Succinylcholine should be used with caution in patients with low Ievels of pseudocholinesterase. *** Succinylcholine may cause muscarinic responses such as bradycardia and incrcased glandular se- cretions. It is used in ophthalmology to relax the extraocular muscles. Depol^rhing (non-(onpelilire): S:'lccinylcholine (Afiecttue) is thc only member ofthis group used rn the Unired Statcs.Hexamethonium. ganglionic-blocking drugs are seldom used because ofthe annoying and sometimes disabling parasympathetic ttlockade. It acts like a nicotinic agonist and depolarizes (dese/tsilizes) theneuromuscular end pla1e. The side effects (caused by parasympathetic blockade) tnc\rde a very pronounced xerostomia. Very important: The major danger ofall ofthese ncuromuscular blocking drugs is too much paralysis (the patient cdnnol hrealhe). Respiratory failure may result.. 1 Dantrolene is an skeletal muscle relaxing agent that acts within the skeletal muscle fiber rather than on the neuromuscularjunction fdoes not block the icolinic receptors). These drugs have only \'ery limited clinical uses. crsatracurium and rocuronium. These agcnts interact with nicolinic receptors at ihe skeletal neuromuscularjunction. vecuronium. doxacurium.block of n eurotransmis sion and muscle paralysis. cerebral palsv. \Iecam. A "bloodless field" surserv \euromuscular blocking drugs are important for producing complete skelctal muscle relaxation and facilitate endotracheal intubation. It binds to the ACh receptor and stimulates depolarization causing initial excitation follo\1ed bt. for clinical use. The prototlTre nondepolarizing agent is tubocurare /Cr- l.S. and tetraethylammonium are no longer available in the U. pancuronium. Remember: two major types of nicotinic receptors: 1. Thesc agents bind to |rrrer Other agents include mivacurium. resulting in muscle paralysis. and for muscle dystonias as well as to remove wrinkles. and muhiple sclercsis) and for the prophylaxis and treatment of malignant hyperthermia. Those at the skeletal neuromuscular junction ofthe somatic system *** Neuromuscular blockers act here 2. Note: Neostigmine or pyridostigmine (which are cholineslerase i4hibitots) can reverse the blockade ofthese agents. and postural hypotension.e. constipation. slroke. . Botulinum toxin A fBolo-rl acts on the motor nervc terminal to prcvent the release of ACh. An emergency hypertensive crisis *** lt cause a rapid and reversible fall in blood pressure that enables it to ilrlnediately reverse an emergency hypenensir e inhibits the depolarization-induced release of Car. *** Nicotinic receptor antagonists (nicotitlic blocking agents) are divided into ganglionblocking drugs and neuromuscular blocking drugs. as an adjunct to surgical anesthesia.from the sarcoplasmic reticulum The principal therapeutic applications ofdanffolene are for the re lief of spasticities associated with upper motor ncuron disorderc (i. . Thcrc are t$o classes ofneuromuscular blockers: These agents competitively compete with acetylcholine at the nicotinic recepnicotinic cholinergic receptors and prevent acetylcholine from stimulating moror nenes. \ondepolarizing: rrrr. trimethaphan.'-lamine (nversile) is used clinically for: . atracunum. which breaks down succinylcholinc. blurred vision. Those at the autonomic ganglionic sites (both sympathetic atxd pqrasympathetic) *** Ganglionic blockers act here Aldrough they are among the most potent agents available. :. The treatment of severe or malignant hypertension . 2.

:ltgs EXCEPT one. Carbachol (Isopto-Carbachol) . Neostigmine 118 Coplright O 201 l-2012 . Which one is the -EXCEPIIOM . \4ethacholine .Denlal Decks .. Pilocarpine hydrochloride 119 Copyright O 20ll-20t2 . Bethanechol (Urecholine) . Dobutamine . Phentolamine . Pyridostigmine .Den6l Decks Alf of the foffowing are cholinergic d . Edrophonium . Acetylcholine . Physostigmine .

malathion and sarin. Examples of cholinesterase inhibitors include: . long duration ofaction. . used as an insecticide .4 Clrl. Edrophonium: reversible.*** Phentolamine (and phenotybenzamine) receptor blockeIS. nicotine and olher ganglionic stintu1drlt. With few exceptions fi. or cholinomimetic. and for an antidote for atropine . Topical application ofthese drugs to the eye causes miosis and a decrease in innaocular pressure. neostignine. Choline esters: The most noticeable effects ofthese drugs are a fall in blood pressure attributable to generalized vasodilation. Pilocarpine is the most useful alkaloid being employed as a miotic and to treat open angle glaucoma Pilocarpine is also used to stimulate salivary flow in patients suffedng ftom xerostomia due to radiation therapy in the treatment ofhead and neck cancer. Cholinesterase inhibitors: These drugs include physostigmine. These drugs act as indirect agonists at both muscarinic and nicotinic sites. very short duration ofaction. the action ofacetycholine will be enhanced and prolonged. used to reverse curare-type drugs and to treat myasthenia gravis . used to Alzheimer's disease . pyridostigmine. extended duration ofaction. agents combine with cholinergic receptors (muscorimic or nicotinic or both). are prototypes ofnon-selective alpha-adrenergic Cholinesterase inhibitors act by blocking the enzyme (qce4. Pyridostigmine: reversible. and an infieased tone and actilit-v of both the CI and urinary tracts. The other cholinergic agonists used as drugs are metabolized slowly or not at all by these enzymes.e. to cause a response in an effector. extended duration ofaction. approved to treat mild to moderate Alzheimer's \ote: The stimulation of the skeletal muscle by excess acetylcholine eventually results in muscle oaralvsis.t prominent muscarinic or parasympathomimetic effects. long duration ofaction.. Malathion: irreversible.lcholi esterase) that degrades acetylcholine in the brain. ACh is metabolized by acetylcholinesterase. They inhibit acetylcholinesterase at both mucarinic and nicotinic sites. used to treat myasthenia gravis . Donepezil (Aricept). Acet:-lcholine chloride: used in ophthalmology to produce miosis . Cholin€rgic alkaloidsi These drugs include muscarine. used as a nerve gas Three cholinesterase inhibitors are commonly prescribed for Alzheimer's disease: . Cholinergic drugs are compounds that mimic the actions of the endogenous neurotransmitter acctyl_ chofine /. and some alkaloids. approved to treat all stages of Alzheimer's disease . a slowing ofthe heart rate. Physostigmine: reversible. This results in more acetylcholine in the s). Direct-acting agents: . used for glaucoma. used to reveffe cumre-type drugs . Bethanechol: used for postoperative abdominal distcnsion and urinary rctention . used to Alzheimer's disease . approved to treat mild to moderate Alzheimer's . these agents exe. flushing ofthe skin. Sarin: ineversible. *** Dobutamine is an adrenergic agonist. Tacrine: reversible. ACh (and many olher esters) are rnetabolized by pseudocholinesterase. Direct-acting. pilocarpine. These drugs are longerlasting than ACh because they are not subject to rapid metabolism like ACh.naptic cleft and enhances cholinergic transmission. Indirect-acting agents: . In the plasma and other sites. Donepezil: reversible. These dmgs include: . edrophonium. extended duration of action. various choline-ester congeners ofACh. located near receptors forACh. Neostigmine: reversible. short duration ofaction. Gafantamine (Razadyne). These drugs include ACh. nicotine and lobeline. Rivastigmine (Exelon). Note: Ifany ofthe cholinergic agents are administered before acetylcholine. They are indirect agonists at both muscarinic and nicotinic sites. extended duration ofaction. Carbachol: used in ophthalmology to produce miosis .

Reduce nausea 120 Cop). injectable cholinesterase inhibitor . It is a rapid-acting.2012 .Dental Decks All of ihe following statements concerning edrophonium EXCEPT one.righr O 2011.. Calm an anxious patient . Produce a dry field for taking impressions . It is the drug of choice for diagnosing myasthenia gravis because of its rapid onset of action and reversibility . l'/hich one ls the EXCEPZOM Nrre true . Treat dry mouth by inducing salivation . It is also useful in differentiating a myasthenic crisis from a cholinergic crisis 121 Coplright O 201l-2012 . short-duration.Denral Decks . It is a direcGacting cholinergic agonist (cholinomimetic) .

Symptoms ofa cholinergic crisis include bradycardia (decreased heart rate). is indicated for treatment ofxerostomia caused by salivary gland hypofunction resulting from radiotherapy for cancer of the head and neck. excessive sweating. vasodilation and muscle weakness. miosis. however edrophonium is used to diagnose myasthenia gravis and not in the treatment ofit due to its Yery short du- ration of action. distinguishing the two conditions may be dif- ficult./heartbum/diarrhea due to the cholinergic nature ofthe drug. It's pharmacologic category is cholinergic agonist. increased GI motility and bradycardia. . flushing. extreme salivation. \ote: These drugs are indirect agonists at both muscarinic and nicotinic sites.Cholinergic drugs used in dentistry are: Pilocarpine (Sa/ indicated for the treatment of symptoms of xerostomia in patients with Sj<igren's syndrome. are qll cholinesterase inhibitors). It's pharmacologic category is cholinergic agonist.lacrimation. *** Pyridostigmine is prescribed in the treatment ofmyasthenia gravis. and neostigmine (thq. . physostigmine. and Cevimeline (Evoxac). Administration ofa short-acting cholinomimetic such as edrophonium will improve ml asrhenic crisis but wors€n a cholinergic crisis. Pifocarpine (Salagen) - . Cevimefine (Evoxac) . a Remember: Typical cholinergic effects caused by stimulation of acetylcholine receptors kholi ergic receptorg include salivation. Because a cholinergic crisis can result in muscle weakness like that ofa myasthenic crisis. Prevalent side effects are increased sweating and nausea/heartburn/diarrhea due to the cholinergic nature ofthe drug. Prevalent side effects are excess sweating and nausea. This is falsei edrophonium is an indirect-acting cholinergic agonist (cholittomimetic) as are pyridostigmine.

Bronchoconstriction . Increased urination . Sweating 123 Coplrighr O 20ll-2012 Dental D€cts . Salivation . Carbachol . Pralidoxime . Nicotine 122 Cop)rigbt O 201l-2012 .r Poisoning with an organophosphrte cholitrssterase inhibitor can be treated with: . Tachycardia . Flushing . Edrophonium . Miosis . Increased GI motility .D€ntal Decks . Increased urination .

Tachycardia . Su eat glands: reduced sectetion (atropilte) . tropicamide. Salivation . It is also used to reverse the effects of an overdosage of anticholinesterase agents used in the treatment ofmyasthenia gratts (i. trihexyphenidyl. echothiophate. static h)?crplasia. tropicamide) . Antimuscarinic drugs produce the following effects: . oxybutynin. Indirecl-acting cholin€rgic drugs (cholikesterase inhibltor. Bradycardia Antimuscarinic drugs block the effect ofacetylcholine and all drugs that stimulate muscarinic rcceptors. cyclopcntolate. and tachycardia. reduced secretion (ipratropium) . . GI tract: reduced peristalsis. neostigmine. trihe$'phenidyl) Noreq.Pralidoxime (Protopam) is a cholinesterase reactivator which is used as an antidote to reverse muscle paralysis resulting from organophoshate anticholinesterase pesticide poisoning. prc- -to treat parkinsonism fbenztrcp[ e.e.lncreased GI motility Miosis Nicotinic: . reduced secrelion (ptupa theli .. Coohaindications for using antimuscarinic drugs include: narrow-angle glaucoma. pyridostiSmine and ambenomium). . Bronchoconstiction . . Increase in BP 'Sweating ' Urination . Effects of anticholinesterases: Muscarinic: . bethanecol and pjlocarpine.r/ includc: physostigmine. carbachol. Examples include: . and rpralroplum. Direct-acting cholidergic drugs include: methacholine. pyridostigmine. SAL-TROPINElatropine sulfate. C\S: antimotion sickness 6copolamine) antitremor activity e. homatropine. . Atropine and scopolamine arc prototlpes. weakness . E1-es: mydriasis /lotuatropine. g6\:opvrrolate) l. Isoflurophat€: used in the treatment ofglaucoma Malathion: a widely used insecticide Parathion: an insecticide Echothiophate: used in the treatment ofglaucoma Tabun: one ofthe most potent and toxic nerve gases Soman: nerve gas Sarin: nerve gas *** Bradlcardia is a muscarinic effect ofcholinergic agonists. clclopentolale. sarin and soman. Bronchi: bronchodilation. . Other antimuscarinic drugs include: glycopltolate. . Muscle twitching .J/t are used to stimulate salivary flow 3. Organophosphates are esters ofphosphoric acid and an organic alcohol that inhibit the enzyme cholinesterase. bronchocostriction. benztropinc. 2. diarrhea and skeletal muscle iasciculations (twitching). Symptoms of organophosphate poisoning include: excessive salivation. Salivary glandsr red\tced secretion (atropine) . Bladder: urinary retcnt\or (oq'but)nin) . . propantheline. USP tablelt is indicatcd to reduce salivation and is endorsed with the ADA Seal ofAcceptance . malathion. edrophonium. Pilocarpine and cevime\ne (both cholinergic dsorTr.

Glycopyrrolate (Robinul) . Dexamethasone . Carbachol . Belladonna derivatives .. Prednisone . Triamcinolone . Propantheline bromide (Pro-banthine) 124 Coplright @ 201l-2012 . Atropine sulfate . Prednisolone 125 CopFgh O 201l-20l2 . Cortisol .D€nhl Deks .Dental Decls .

hlperglycemia. prednisone (Delatasone). They consist oftwo major groups: l. The major natural glucocorticoid is cortisol. . and adrenal ins!fiiciency."d/). Contraindications to their use include: . and betamethasone lces/or?e/. AIDS. predrisolone (Delta-Cortef).ortisone. Mineralocorticoids: regulate sodium and potassium reabsorption in the collecting hrbules ofthe kidney. psychosis and salt retention.*** Carbachol is a direct-acting cholinergic drug. cataracts. firethylyprednisolone fMed. Other mineralocorticoids include deoxycorticosterone and fludrocortisone. triamcinolone (Aristocort). Glucocorticoids: have irnportant effects on metabolism. Mineralcorticoids are used in replacemcnt thcrapy in hypoadrenocorticism or Addison's disease. and a range ofmood and behavioral changes. Glucocorticoids are most often used as anti-jnflammatory and immunosupprcssive agmts. . d€cr€ase gastric. Tle majo ty ofthe anti-inflammatory and immunosuppressive actions ofthe glucocorticoids are probably the result of their action on arachidodic acid metabolism. They induce the synthesis of a protein that inhibits pbospholipase A2. Glaucoma Cardiovascular problems Obstruction of the GI or GU tract Asthma These drugs also reduce spasms of smooth muscle in the bladder. herpes infections drugs themselvcs may cause and patients with peptic ulcer disease (specrfcally. The major natural mineralocorticoid in humans is aldosterone. bronchi. 2. They block postganglionic cholinergic fibers. and salivary secretions. dexamethasone (Decadtuh). osteoporosis. immunc responses and inflammation. myopathy. hypertension. relax the iris sphincter. The synthetic glucocorticoids include hydrocortisone (Cortef). Tte corticosteroids are steroid hormones produced by the rdrenal cortex. bronchial. Contraindicrtions to conicosteroid Toric effects ofthe corticostercids include growth inhibition. use include: latent TB or fungal infection. Adverse effects ofthe short-term administration ofsystemic glucocorticoids include secondary infections. hlperglycemia. . and accelerate impulse conduction through the rryocardium by blocking vagal imoulses. catabolism. The other drugs are all classified as anticholinergics. decrease perspiration. thus decreasing the production of both prostrglandins and leukotrienes. They represent replacement only in Addison's disease. gastric ulcers) -these pephc ulcers. . and intestine. . \ote: Corticosteroids do not cure any disease. Loog-term therapy may cause osteoporosis.

Prednisone . Triamcinolone 127 Coplright O 201l-2012 Dsnlal Decks .. which results in increased plasma amino acid levels use . Cortisol . WbiCh ONE iS thE EXCEPTIOM . Dexamethasone .Inhibit local . Decreased lipolysis edema. Increase hemoglobin concentration cells and platelets copy'igl e zor11!112 - o*orn. migration and activation of white blood cells. Stimulate gluconeogenesis in the liver and inhibit peripheral glucose . Stimulate protein breakdown. .Aldosterone . Reduce the immune response . Impaired wound healing ."r.All of the following are pharmacologic effects of glucocorticoids EXCEPT Orc. and phagocytosis by macrophages and increase the numbers ofcirculating red blood . capillary dilation.

] sol. Aldosterone promotes rerbsorption ofsodium into the blood from the glomerular filtrate. These agents readily penetrate the airFay mucosa but have very short half-lives aft€r they enter the bloo4 so that systemic effects and toricity are greatly reduced. Remember: The pharmacologic effccts of mineralocorticoids include an increase in sodium rctention and an increase in potassium depletion which can lead to edema and hypertension if excessive and may lead to dehydration and hypotension ifinsulficielt. prednisone. there would be extreme Ioss 3. Other effects of glucocorticoids include an anti-inflammatory action. immunosuppression. 1. Potassium is lost in the urine because of the electronegativity that is created by the reabsorption of sodium in the kidney tubules. which converts angiotensinogen to angiotensin I. Addison's disease is caused by the hyposecretion of aldosterone and corti-rNote{. ADH constrict (increases blood Dressure). . 2. Remember: Decreased sodium concentration causes the juxtaglomerular cells of the kidneys to secrete renin. budesonide and flunisolide are special glucocorticoids /used as inhalers) that hale been developed for use in chronic rsthmr and bronchial disease.. ofwater into the urine. ADH (Vasopressin) decreases the production of urine by increasing the re*if' absorption of water by the renal tubules (it increases the permeobiliry of the collecting ducts and distal tubules). -. dexamethasone. and triamcinolone are all glucocorticoids. *** Cortisol. causes arterioles to At high concentrations. Note: These effects occur in target cells following the interaction ofthe steroid with a specific glucocorticoid receptor \ote: Beclomethasore.. which.*** This is false. stimulates the adrenal cortex to release aldosterone. Increased Iipolyisis occurs in areas ofadipose accumulation. Without ADH. The secretion ofaldosterone is regulated by ACTH and by the renin-angiotensin system and is very important in the regulation of blood volume and pressure. . Angiotensin I is converted to angiotensin II. Aldosterone is secreted by cells located in the zona glomerulosa ofthe adrenal cortex. and an anti-allergenic action.. and serum fatty acid concentration increases. Note: Increased blood aldosterone levels will result in high sodium and low potassium levels in the plasma. glucocorticoids affect the mobilization of fats from areas of deposition. in tum.

Triamcinolone . Compazine . Cortisone .Dstal Decls .. Methylpredrisolone (Medro I) 124 Coplaight O 201l-2012 . Hydrocortisone .201 2 . \{ethylprednisolone . Prednisone . Dexamethasone 129 CoplriSh O 201 1.Dental Dects . Fluticasone (Flonase) . Prednisone . Hydrocortisone .

There are two subclasses: (l) Leukotriene receptor antagonists which include montelukast (Singulair) and zafirlukast (Accolate) (2) 5Jipoxygenase inhibitor tleukotriene s!nthesis inhibitor) which includes zileuton (Z. beclomethason€ freconase). lupus erythematosus. Budesonide (Pulmicort) . hyperglycemia. and protein metabolism. fl uticasone (Flonase) and budesonide (Rhinocort).fluticasone (Flovmt) andbudesonide (Palnicott). gastric ulcers. and congestive heart failure. which contributes to *** Prochlorperazin e (Compazine) is an anti-psychotic medication in a group ofdrugs called phenothiazines.reqcting substance of anaphylnris [SRS-A]). albuterol/ipratropir'l'm (Combivent) . primarily through their anti-inflammatory and immunosuppresslve acnons. Inhaled corticost€roids used for asthma do not achieve significant blood levels to cause the advene effects listed above for systemic agents. Localized infections with Candida albicans occur frequently in the mouth and pharyrx with repetitive use of inhalant corticosteroids. viral. Reduction of inflammation enhances the bronchodilating effects ofthe beta2-adrenergic agonists. Popular nasal spray corticosteroid products are triamcinolone fNasocorf . the LTs lalso htoutr as slo$. herpes infections. Combination products used in the treatment ofCOPD and asthma include: . arthritis. T\\'o r-ypes of corticost€roids: L Glucocorticoids affect carbohydrate. l. The following are some ofthe other popular inhaled corticosteroids used in the treatment of asthma: . Adverse reactions include Cushing's syndrome (obesit)' qnd weakening oJ uuscles). Important: Leukotriene modifiers act on inflammatory mediators ofasthma. and are use for their localized effects. These dmgs are used to treai a variety ofconditions which include asthma. Beclomethasone (B eco n. Populal aerosol corticosteroids are triamcinolone (Azmacort). 3.Corticosteroids in the inhaled form. Mineralocorticoids regulate sodium and potassium metabolism. AIDS. 4. Flunisolide (AeroBid) Note: Inhaled steroids very often cause a fungal infection ofthe mouth and throat. or bacte' ndr. Contraindications to their use include latent infections (fingal. Triamcinolone (Azmacort) . budesonide/formoterol (Symbicort) ainr ay obstruction. and an increased risk of infection. 2. 2. osteoporosis. They are used as to treat numerous disorders. aphthous stomatitis. Nasal spray corticosteroids used for seasonal allergies also do not achieve significant blood levels. lipid. and TMJ pain. They represent replacement only in Addison's disease. decrease the inflammation in the airway in asthma.tse ) . Corticosteroids do not cure any disease.tflo). . allergies. fluticasone/salmeterol (Advair Diskus) . peptic ulcers.

Dlltiazem (Cardizem) . Nitroglycerin (Ni tros tat) 130 Cop).Denral D€cks AII ofthe following drugs are used ao prevent or to provide relief of angina pectork EXCEPT one. Captopril . Nitroglycerin r I<nfl. Propranolol (Indera l) .2012 . Hydralazine (Apre s o I ine) . Nifedipine (Procardia) .. Which one ls the TXCEPZOM . lsosorbtde (Isordil) 131 Coplrighr O 201 l-2012 . Diazoxide (Prcglycen) .right O 2011.EXCEPZ one.rnnhqtp Qtt i t ros tat) . (Capoten) Sodium nitroprus side Qtlipride) .Dmral Decks . Which one is the EXCEPTIOM \ .All of the following drugs ar€ direct vasodilrtors .

*** Isoflurophate is an organophosphate cholinesterase inhibitor used in the treatment ofglaucoma Angina pectoris is the pain in the heart and chest which occurs during the occlusion ofcoronary arteries. Vertpamil (Calan SR). The two most common adverse effects caused by nitroglycerin are orthostatic hypotension and headache. headache. Triggers that can cause occlusion are physical exertion. diazoxide. increased blood pressure. Propranolol (lnderal) ts representative ofthe beta-blockers used to prevent angina attacks. Antianginal drugs work by reducing cardiac rate and force. It relaxes blood vessels to provide increased blood flow and oxygenation to the heart muscle.zem (Carulizem) are calcium channel blockers used to prevent angina attacks. . Not€: nitroprusside. Betablockers are used to decrease the work load ofthe heart such that less oxygen is required.*** Captopril is an angiotensin-converting enzyme inhibitor. Calcium channel blockers are also effective vasodilators firclirect) ?J]'dhavebeen applied to the management ofhypertension. Compensatory responses may be marked and include salt retention and tachycardia. Remember: Hydralazine and minoxidil are peripheral vasodilators. or dilating coronary blood vessels. Note: Calcium channel blockers as a class have been associated with causing gingival hyperplasia. and vasoconstriction. and Diltiazem (Cardizen) have been given orally for the treatment of mild to moderate hypertenslon. \ifedipine lProca rdia) and diltia. It is sublingually effective within 2-4 minutes. The nitroglycerin skin patch releases the drug over a 12 hour period to pro\ ide sustained blood levels for prevention ofangina. Atenolol (Tenormin) is another popular beta-blocker used for this purpose. Adverse side effects include GI upset. dizziness and tachycardia. Nifedipine (Procardia). Nitroglycerin is a coronary artery vasodilator. These drugs are used to dilate coronary blood vessels for improred blood flow to heart muscle. Direct vasodilators exert their antih)?ertensive effect by a direct vasodilator action on the smooth muscle of arterioles. reducing peripheral vascular resistance. resulting in a decrease in peripheral resistance and blood pressure. hydralazine and nitroglycerin are parent€ral vasodilators which are used in hypertensive emergencies.

Directly increases the force ofmyocardial contractions . All ofthe above 133 Coplright @ 20ll-2012 . ls antagonized by beta-blockers .Dental Decks . Irreversibly binds cyanide . Oxidizes hemoglobin . Competes with cyanide for binding ofcy4ochromes .Amyl nitrile is used ln ths emergency ir€atment of cyonide poisoning because it: .Deutal Decks . Is dependent upon a normal cardiac rhythm . Inhibits tubular reabsolption ofcyanide 132 Coplyight C 201 l-2012 .

nitrite oxidizes hemoglobin to methemoglobin which binds cyanide tightly, keeping it in the peripheral circulation and preventing its access to tissues.

*** Amyl

Amyl nitrite is a vasodilator and a highly volatile substance administered by inhalation only. It is the most rapidly acting ofthe antianginal drugs, producing effects within l0 seconds. Its duration of action is only 3 to 5 minutes. Because of its extreme potency, there are uncomiortable side effects that invariably occur with rts :use (ainting and a pounding headache). lmportant: This drug is rarely prescribed and is not the first drug ofchoice in treating angina. It is abused to produce euphoria and as a sexual stimulant.
Other anti-anginal drugs include:
This drug is the single most effective agent available for the management ofacute angina episodes. Note: It dilates mostly veins. 2. Non-nitrate vasodilator: Dipyridamole (Persantine) 3. Beta adrenergic blocking drugs: reduce cardiac rate and force . P ropr anolol (l ndera I)


Nitrate: Nitroglycerin

. Nadolol (Corgard)

. Atenolol (Tenormin)

Calcium channel blocking drugs: dialte peripheral and coronary blood vessels . ltrapamil (koptin, Calan) . Diltiazem (Cardizem)
. N rfediorne
(P ro card ia )

This positive inotropic effect is independent ofa normal sinus rhythm and adrcnergic stimulation. Thc cardiac gf]cosides are often called "digitalis" because several come from the digitalis (lbxglove) plant. Digoxin /larroxir) is the most versatile and widely used. \otei The) are used to trcat most supraventricular arrhythmias, cardiogenic shock and chronic heart lailure.
These drugs help the heart beat more


strongly (posilire inotopic effect), more slo\\ly (bradycardia)

more elficientl].


Cardiac gl]cosides inhibit the Na*-K*-AlPase membrane pump by inhibiting the adenosine triphosphate enz)-mes (transport ATPase or Na-K-ATPase). Na*-K*-ATPasc splits adenosinc triphosphatc in the nel\e and muscle cell and thus provides the energy necessary for transporting sodium across the cell membranc. Key point: This inhibition of thc NalK*-AIPase enzyme leads to an increased calcium ion influx u'hich augm€nts the positive inotropic effect ofcardiac glycosides. Adverse side effects include nausea and vomiting, appetite loss, dianhea, ventricular anhyhmias, heart block, and visual and mental disturbances. Contraindications to thci.use include ventricular fibrillation andventricular tachycardia.

Drug interactions: Many drugs aff'ect digoxin levels. However, digoxin docs not affect the levels ofother drugs. ln addition, when beta-blockcn are added to digoxin in patients with AV conduction abnormalities, complete heart block can result. Erythromycin. clarithromycin and tetracycline may increase digitalis absorption and toxicity. Thyroid replacement therapy incrcases dose requirements ofdigoxin. D gs that lower plasma potassium levels ae.&, lhiazide and loop diurelics/ increasc digitalis toxicity Drug treatment of mild to moderate heart failure proceeds in the following order:(l) Diuretics in patients \1ith fluid retention (2) ACEIS orARBS in all paticnts unless contraindicated (3) Beta-blockers in all stable inininalJluitl relention) p^tients unless contraindicatcd and (4) Digoxin. Note: Ifthese medications are not suflicient to control heart failure, the following additional drugs may be given: (1) Spironolactone (a aldosterone antctgorlist) (2) Nitrates and hydralazine and (3) Calcium channel blockers (i.e., amlodipine and felotlipine only) Remember: Most drugs useful in treating cardiac arrhythmias act primarily by increasing the re-

fractory period ofcardiac muscle.

. Captopril (Capoten)
. Hydralazine


. Enalapril (Vasotec)

. Lisinopil (Zestril)
. Fosinopril (Monopri l)

Cop).right O 201 1,201 2 , D€ntal Decks

. Propranolol (Inderal) . Acetbutolol fsectra,

. Metoprolol (Lopressor)
. Yeraparnil (Calan)


Cop)'ight O 20ll-2012 - DentalDecks

Hydralazine is a direct peripheral vasodilator. ACE inhibitors interfere with the conv€rsion ofangiotensin I (d veak rasoconstictol) to angiotensin ll (a highly e.f;[ective constrictor). Thcy do this by being inhibitors of angiotensin-convcrting enzyme
(,1CEl. These drugs are used to treat hypertension and congestive heart failure. Adverse cffects includc cough, hypotension, neuhopcnia, anorexia alrd pol]uria. Note: They can alter the sense oftaste and in a few rare cases, cause angioneurotic edema. Angiotensin II is a potent vasoconstrictor and is a stimulus for aldosterone release from the adrenal glands. Reduction in aldosterone secretion results in less waterabsorption and sodium/potassium exchange in the distal renal tubule, causing a slight increase in serum potassium. ACE inhibitors inhibit the breakdown ofbradykinin, a potent and naturally occurring vasodilator, by blocking thc cnzymc kininase IL This though, is thought to be the causc ofthe cough commonly experienced by patients who take this class ofdrugs.


OtherACE inhibitors f,4Ct1t include: . Benaz,eptll (Lotensir./ . Moexipril fLr?i|ascl 'Quinapril (Accupril) 'Captopril (Capoten) . R^rnipfll (Altdce) . Trandolaprll (Mat ik) ' Lisinopril (Zestil) ' Elan |{il (Uasolec) Angiotensin


reccptor blockerc f,4RBs/ include:

. Losarlan (Coaaar) . \'alsafian (Diotan) . C andesanan (Atacand)

. Eprosaftan (Tevete

. Olmesaftan (Benicar)
. Tebllisafian (Mica rd i s)


.lrbesarlan (Avapro)


ARBs block the effects ofangiotensin II by blocking the binding ofangiotensin II to its rcccptors.

Thc: do not effect bradykinin. Adverse effects jnclude dizziness, diarrhea and myalgia.
Thc antih) pcnensive effects ofARBs have been provcn comparable with those ofthe ACEIs ACEIs and {RBs are ofparticular values for the reatment ofhypettensive patients who have concomitant illnesses iuch as diabetcs, rcnal insufficicncy, left ventricular dysfunction, and CHF

\ote: ACE inhibitors and Angiotensin II receptor blockers indirectly inhibit fluid volume increases \\hen interfering with angiotcnsin II because angiotcnsin II stimulates thc r€lease ofaldosterone, which
promotes sodium and water retention.

Thc \ aughan-williams classification system traditionally has been used to classity antianhythmic drugs. This scheme places the available agents into onc of four classes, usually denoted by Roman numcrals I lV This systcm is loosely based on the channel or receptor involvcd. Class


Sodium channel blockers

. Class I drugs are further classified on the basis oftheir effects on action potential duration:
. lA agcnts include; Qu:Lnidinc (Quinidex), procatnamide (Procan SR/ and disopyramidc py'orpaceJ. These agents prolong thc action potential. . fB agents include: LidocainelX.ylocai e). mexiletine (Mexilil) and tocainide (Tonocard. These agents short€n the action potential. . fC agents include: Flecainide (Tambocor) and propafenone (Rythnol). These agents have no effect on action potential dulalion.

Cfass II: Beta-adrenergic blockers Propranolol (Inderal) is the prototype antianh)'thmic beta-blocker Other drugs in this class include: esmolol (Breibloc) acetbutolol (Secn'al) ar'd metoprolol (Lopressor). These agents increase refractory period, decrease conduction velocity and reduce automaticity. Cfass IfI: Potassium channel blockers - Amiod^rone (Cordarore) is the prototype drug in this class. Sotalol (Betapace), tbutilide (Corvert) and dofetilide (Tiko$n) arc also in this class. These drugs increase refractory period and reduce automaticity. Class Il': Calcium channel blockers Yerapamil (Calan)is the prototype. Diltiazem is also included in this group. These drugs increase refractory period, decrease conduction velocity and reduce automaticity.

Note: Miscellaneous antiarrhythmic drugs include: adenosine (Adenocard) which increases refiactory period and reduces automaticity and digoxin (Lanoxin) which increases the force ofcontraction ofthe heart muscle and decrease conduction velocity.

. The first statement is true; the second statement is false

. The first statement

is false; the second statement is true


Both statements are true

. Both statements are false

136 Cop}fighr O

20ll-2012 DenialDecks

. Anglna



. Suprayentricular tachyarrhy'thmias
. All ofthe above

137 Coplrighr O20ll-2012, Dental D€cks

and ventricular tachycardia.liac rate. awl torsade de pointes .actilitv ofthe heart \-erapamif is the prototypical Class lY (celciu channel blockers) antiarrhythmic agent. calcium. are fast-acting antianginal agents \ote: For angina. Of the calcium channel antagonists available. lmportant. Side effects includc bradycardia and hypotension. quinidine and disopyramide.s an uncontnutn varia t ofvetlti'icul4r |acht-cqrdia) . Generally speaking. parcxysmal atrial tachycardia. Lidocaioei convulsions . 3. .". Peripheral arteriolcs dilate (vasodilato. thereby increasing the rccovery period al1er repolarization. excitability. Note: Adverse effects include pulmonary fibrosis. rvhich are concentrated in the SA and AV nodcs.. thyroid abnormaliti!-s. Reduces blood pressurc ifhypertension is present.i. nitroglycerin and nifedipinc arc usually used before verapamil. Propranolol. a Class I action. hypotension. It is the drug ofchoice for the suppression ofparoxysmal supraventricular tachycardias stemming from the AV node (wlrlclr is characteri:ed by a rcpid cer. Procainamide: nental changes. deafness). Calcium channel blockers: flushing. It is not used as an antihypertensive. Nilrites (amyl nilrite) and nitratcs (nittoglyceri\) that are uscd to relieve acute anginal attacks. and total periphcral rcsistance deoreascs. ringing in lhe ears. gingival hyperplasia and reduced cont. Important: Amiodarone (Cordatone) is generally considered a Class Ill agcnt even though it also blocks sodium channels. This has thrcc cffccts: 1. usually 160-190 per minule).g.s L Cornmon adverse effccts ofsome antiafihythmics: . Note. Quinidine is prirnarily used to treat supmventricular tachyanhythmias. only vcrapamil and diltiazem possess significant antianhythmic activity. lncreases oxygen delivery to the myocardium. and contractility by inhibiting the influx of sodium through "fast" channels oI the myocardial cell membrane. Note: Calcium channel blockers (e. skin discoloration. It blocks sodium. and potassium channels as rvell as beta rcceptors. and peripheral neuropathy. Remember. reducing after-load and reducing myocardial oxygen requirements. It jnhibits the intraccllular entry ofcalciurn through the slow channels ofthe calcium dependent tissues of the myocardium. torsade de pointes (TDP . \ot. They block calcium cntry through the membranous calcium ion channels ofcardiac and vascular smooth musclc. atrial flutter. headache. heart block . It is uniqu€ in that it is the most potent and "broad-spectrurn" antianhythmic compound cunently available. dillazem and nifedipile) are useful as antianginal agents and antihypertensive agents as rvcll. It is a derivative ofthe ester local anesthetic procaine. hypotension. Il has impressive ellicacy in suppressing both supraventricular and \ enlricular arhythmias. 2. Procainamide has properties similar to those ofother Class lA agcnts. These drugs decrease myocardial conduction velocity. Quinidine. verapanril. bronchoonstriction. cinchonism @ eadache.Procainamidc is a Class lA antianhythmic agcnt that is uscd in thc trcatment ofseveral cardiac arrhythmias including atrial fibrillation. the use ofbeta-blockers (Class II agents) as antianhythmics is reserved fbr patients who require only control ofventricular ratc during atrial tachyarrhythnias or who have mildly symptomatic vent cular arrhythmias.

Tinzaparin (Innohep) .Denral Decks . Abciximab (Reopro) Anagrehde (Agrylin) . Dalteparin (Fragmin) . . Tirofiban (Aggrastat) 139 Coplrighr O 201I-2012 . Epttfibatide (I nt e gri lin) . Enoxapadn (Lovenox) . Clopidogel (PIavLx) 138 copynsht O 20ll-2012 ..D€ntal Decks .

Note: The glycoprotein IIb/lIIa inhibitors h3! i a raPid onset ofaction.000 to 30.Platclet aggregation inhibition is revcrsible following ccssation ofthc lV 3cmr:inration ollhc drug minutes after an intruvenous infusion. L Thcsc typc ofanticoagulants agcnts f/olr mols...lJ rhromboc\ ron(nir.000 daltons.At thc first sitc factor Xa is tlcutlalizcd and at ihc sccord silc factor lIa Thcy arc administcrcd subcutancously sincc they arc unablc lo bc absorbcd frorn the Gl tract._ :tyotedr by inhibiting platelet aggregttion in an irreversible manne.000 daltons with a mean of 16. thc antidotc lbr warfarin is vitamin K. Low molecular tleight heparins havc a small eflect on pa(ial thromboplastin timc but strongly in- hihit factor Xa hol lla).000 to 8.4ersrnlin€ Tflrditional Adensosine diphosphate-induced clopidogrel/Plavix platelel-fi brinogen binding inhibitors ticlopidine/Ticlid Plalelet Slycogen IIb/IIIa inhibitors ep!ifi bat. 6. 5. Tleie a{cnts block the plafelet glycoprotein IIb/IIIa receptor. von Willebrand r'3. Class Heparrn group Heparin Subclass Gcneric/tr|d€ Name heparin sodium Low molecular weight heparin €noxaparirlllov€nox dalteparin/Fragmin tinzaparir/Innohep Hepadnoids danaparoid/Orgaran fondaparinutAnXtra Direct thrombin inhibitors bi\ alirudin/Aneiornax a4atrobal'Argatroban lepirudinr?.4Ila inhibitors are reversible antiplatelet agents uscd !o prcvcnt acut€ cardiac ischemic complicfiions and used in paticnts with acute coronarv svndrome.000 daltons. Thc antidote fbr heparin is protamine.rr?rrbr.*:.- : :. Heparin acts at multiplc sites in ihc coagulatior systcm and binds with antithrombin III at two spccitic sites.ular \|eight hepdin.efludan Oral anticoagulanls warfanr/Coumadin anisindione.tt4iradon Glrcoprotein IIb. Low molecular-lieight heparins rangc in molccular wcights from 4- 2. rcsulting in irs anticoagulanl cffcct. in'. Standard heparin consists ofcomponcnts wilh molccolar wcights ranging from 4. Thev are adntinistered imtravcnously.tor. arc uscd to treat acute symp_ tomadc dcep vcin lhrombosis.: -.i.{ntegrelin Plarelet-r€ducing agent Phosphodiesterase III inhibitors anagrelide/Asrylin cilostazolry]€tal Thrombolytic agents stieptokinase/Streptase tenecteplase/TNKase urokinase/Abbokinase . 3. rhe binding site for fibrinogen. l.. Inhibition of binding at this final common receptor reversibly blocks phtel€t aggregation and prevenls thrombosis. .- scry' 2.rl hcn un hrce u. Class Plar€ler aggregation inhibitors Subchss Generic/trad€ Name acetylsalicylic acid/aspirin dipyridamol€.. is ncutralizcd.*** Clopidogrel fPlarrt inhibils blood clolting a . Tlrcy arc uscdlo preventdccpvcin thronlbosis following knce orhip su. Their maximal antiplatelet effect occur within minutes after an intravenous in1-li[]r Important: Thc most serious adverse effects of GPIIb/llla anragonists include major bleeding. and othcr ligands.. . ::h:.

Dznapnord (Orgaran) . Lepirudin (Reflidan) .Denta! Decks . Bivalirudin (Ang io m ax) 1& Copfight O 201 t-2012 - D€ al D€cks . PTT (Partiol Thromboplastin Time) .. PT (Prothrombin Time) . Platelet count 141 Coplaighr O 20ll-2012 .

A prolonged PT therefore indicates deficiency in one ofthe factors. Many patients taking anticoagulants have INR values of2-3 and even uo through 6. Once prothrombin times are determined. vitamin K deficiency. This test is a one-stage t€st for detecting certain plasma coagulation defects owing to a deficiency offactors V VII. as in liver disease. to a sample from a normal control. of Their mechanism ofaction is through the direct inhibition of thrombin within the coagulation pathway. for prophylaxis or treatment thrombosis in adults with heparin-induced thrombocytopenia. The length of time required for clot formation in both samples is observed. normal blood clotting would be present. or X. the greater the anticoagulant effect. An INR value of I means normal prothrombin times ofapproximately l2 seconds. INR stands for International Normalized Ratio and essentially is the ratio ofthe prothrombin time measured in the patient divided by a standard prothrombin time value. International Normalized Ratio (/r'R/. or anticoagulation therapy with the drug coumadin. INR values greater thar 1 indicate that there is an anticoagulant effect. Thromboplastin and calcium are added to a sample of the patient's plasma and simultaneously. thromboplastin.These agents are administered intravenously for prevention ofpost-operative deep vein thrombosis following elective hip replacement surgery. and the essential tissue coagulation factors. they are expressed as an INR value. The higher the INR value. Thrombin is formed from prothrombin in the presence ofadequate calcium. . thus inhibiting fibrin formation. and multiplied by a constant.

tMG-CoA Reductase Inhibitors . Angina Pectoris (Unstable Angina) . HPG-CoB Reductase Inhibitors . Coronary Artery Disease (CAD) . HCG-CoG Reductase Inhibitors . HCG-CoB Reductase Inhibitors 143 Cop)"ighr O 201l-201? DmialDecls . Stroke .. Hypertension 112 Cop)righr O 2011. which one is the EXCEPTI0M . Myocardial Infarction (Heart Attack) .2012 .All oftle following conditions are manrged by using anticoagutants and \ \-t snti-platelet agents l9xcEPI one.Dental Decks .

ccssary in thc kcy stcp to synthcsizc cholcsterol. .s bclicvcd to act on a hormonc-scnsitivc lipasc. Stroke: will help prevent thrombus from forming thus preventing threat ofa cerebral embolism. Combination products: examplcs includc lovast^tinlni^cin (Adicor) ezetimibe/simvastatin (l/ttoritt). and colesevel^m (WelchoU.J. Thc family of "statin drugs" includc atorvasaatin and rostt- r.statin /ar. . flu\sstatin (a€r. cholcsrs nor produccd in thc livcr and blood lcvcls dccrcasc. . lovastatin (Mewcor) pr^v^st^tin (Prarachol) is n. Tlc] do fiis by incrcasing lipoprotein lipasc activity. rhc Ingl!ccridcs.frforl.Anticoagulants such as clopidogrel (Plavix) are nsed in the conditions listed for the warfarin (Coamadin) and anti-platelet agents such as aspirin and following reasons: . otkrck). These drugs do nothing to lower blood pressure. Thc primary lipids ofVLDLS .It is advisable for patients medicatedwith a "statin" druts nor to be gi\en eryhromycin nroducts. rri. Ifthc protein overloads the kidneys. .l) rcdnc- lrrol . six classcs ofantihyperlipidemic drugs arc availablc."/. whercas highcr lcvcls ofVLDL incrcasc the risk ofpancrcalitis. Angina pectoris (anstable angina): will help prevent thrombus from forming within the coronary arteries. Selectivc cholestcrol absorption inhibitors: ezetimibe /Zsltdl is thc firsl agcnt in a ncw class ofdrugs that appcar to act on thc brush border of intcstinal cpi(hclial cclls.. which rcsults in i crcascd catabolism ofVLDL. \\'hich lowerblood cholcstcrol arc cficctivc in Currcnrl]. anticoagulant drugs are not necessary in the treatment and management of hypenension.r E\amplcs include cholestymmine fQuc"stdn). and res lt in crcascd caiabolism ofLDLby the lr\. When thc "statin" drugs inhibit this cnzymc. The ert'thromycin drugs enhance the capabilities ofthc "statins" to cause this effect.rrdio\ascular drscasc. Fibric acid derivatites: thcirprimary lipoprotein effect is to dccrcase trigiyccridc andraisc HDL concentrations. \r'hcrcas thc primary lipids ofLDLS arc cholcstcryl cslcrs. and cach class has its own mcchanism tor lot\'cring l::rd 1c\ cls r-ote: Thctwo major lipoprotcins that arc targctcd arcVLDLSand LDLs. Myocardial infarction (MI): drugs that prevent blood clotting have been shown to prevent the threat of future infarcts. lowcr intraccllular storcs ofcholesterol. Coronary artery disease (ClD): will help prevent threat ofmyocardial infarction in CAD patients. Thc inhibition oflipolysis lcads to reduccd frcc fatly acid rranspon ro thc liver and thcrcforc dccrcascd syrlhcsis ofVLDL.. bilc acid scqucstrants increa-sc thc divcrsion ofcholcstcrol ro bilc acid slnthcsis. lt has been cor.D gs such asthc statins. simr'rstatin (ZoLor).or. . ' H\lG-CoA Reductase inhibitors: thc cnzymc 3-hydroxy-3-mcthylglutaryl cocnzymc A (H]tlc-Co.. .srt. . Other agents: nicotinic acid lrtdcin) . Examplcs in c:udc gem fi brozi I /lop id) and fenofrbr^te (Tricor) .l. Important: The "statin" dnrgs have thc capability to increase the breakdo*'n ofskeletal muscle thereby releasing muscle protein. Ifnot trcatcd.clatcd with the lcvcls ofblood cholcstcrol and triglyccridcs. .r/o. this lcads to inhibition of rcleasc offrcc fatty acids from adiposc tissuc /@ob. renal failure could result. ^nd . CAD can lcad ro mloca. Note: Unless there are other accomparying cardiovascular problems such as those listed above. Coronart artery disease fClD/ is a condition ofnarrol'ing ofthe blood vcsscls oflhc hcarl rcstncting oxygcn flow ro heart musclc. Highcr levcls ofLDL incrcasc thc risk rf. whcrc it sclcctivcly inhibits $c absorption ofcholcs' terol from dictary and biliary sourccs. Bile acid sequestrants: thesedrugs bind tobilc acids.dial infarction (heart mlrrjrizing the threat ofCAD.

H]drocodone . The first statement is true.lbuprofen .ACE Inhibltors inhibit the conversion ofinactive angiotensin I to the angiotensin II. Erythromycin . . Denhl Decks Whlch of the drugs below can prolong th€ QT interval of cardiac electrical conduction and thus can lncrease the risk ofcardiac arrhythmias? . the second statement is true . Penicillin VK . Azrtbromyctn (Z-Pak) 145 Coplaighr O 20ll-2012 DentalDeckr . Both statements are false 144 Coplright @ 2011-2012. The first statement is false. Both statements are true . the second statement is false . a vasoconstrictor.

tirnolol (Betinol). Erlthromycin as Erythromycin.r/ and brmet aide (Bumer). Alpha-adr€nergic receptor blockers: cause dilation ofarterioles and veins and reduce peripheral vacular resistance. Diuretics: irclude thiazide and thiazideJike fNd CIJ inhibitors. another member of the erythromycin family of antibiotics is not associated with prolonging the QT intewal.Two tvpes: L Cardioselective alpha-blockers dut tl).re was first described in the 1950's as a congenital syndrome in\'olving QT interval prolongation and syncope and sudden death. an unusual adverse reaction for an antibiotic. dilti- is one ofthe drugs confirmed to prolong the QT interval and is accepted ha\ ing a risk ofcausing anhythmias. . pellbntolol (Levatol). Angiotensin-converting enzyme inhibitors (ACE Inhibitors). pf^zosin l. metopfolol (Lopressor. They do not effect bradykinin. \on-cardioseleclive (alphal and alpha) alpha-blockcrs: cxamples include phentolamine /R?grt- (Mi and phenoxybenzamine (Dibe zNline. and sot^lol (BetapaL") *** Note: labetalol Ard ndate) and c^rledilol (Col€g) are non-selective beta-blockers that also block alphar receptors. Azithromycin. and nifedipine (Procardia): inhibit calcium entry into vascular smooth muscle causing vasodilation ofcoronary and peripheral blood vessels thus iowering blood pressure. esmolol (Brevibloc) ^ceb\tolol 2.). beta-blockers: examples include nadolol (Corya ).'zosin (Hvtrin). Angiotensin II receptor blockers l f/nBt: examples include losartan (Cozaar). a vasoconstrictor. Calctum channel blockers examples include Verapamil (Calail). This type ofcardiac arrhythmia was originally termed "torsade de pointes" (from the french " t**isting of the points "). These drugs inhibit sodium reabsorption in renal tubular cells within the kidney !o cause excess sodium and u nary excretion resulting in reduced blood volume. Both actions result in reduced blood pressure. Azem /Cardizen).r^fiipril (Altace) and etral^pril (Vdsolec/i inhibit thc convcrsion of inactive angiotensin I to the angiotensin II. This results in peripheral vasodilation and secondarily.. . an antibiotic within the erlthromycin family also causes prolongation ofthe QT interval. anl . a Clarithromycin. . an increase in urinary volumc cxcrction.) such as hydrochlorothiazide (HCTZ) and foop diuretics such as furosemide /Zasi. (Secral). The QT interval is measured as the time and disrance benveen the Q point ofthe QRS complex and the end ofthe T wave in the ECG traclng. is considered as having risk of causing torsade de pointes. then a subsequent sinus beat showing marked QT prolongation and deformity.ter. (alpha sreceptor blockert: examples includ€ doxazosin fcdr"iprcss)^11d. Cardiosefective beta-blockefs (bela rreceptor block in heart muscle/: examples includ€ at€nolol (Tenormin). ir. Toprol XL). \alsartan (Dioand candesaftalr (Atacand). . Non-cardioselective (beta I and beta. . ARBS block the effects of angiotcnsin II by blocking the binding ofangiotensin Il to its receptors. propr^nolol lndera0. -{ long QT syndrorr. Beta-adren€rgic receptor blockers (6era-bloct?/sl: rcduce the volume ofcardiac output irlto the circulation resulting in reduce peripheral pressure. an antibiotic used to tr€at bacterial infections. examples includc lisinoprll (P nivil: Zet ti l). Two types: l.Antihypertensiv€ agents arc classified by mechrnisms otaction: . These congenital long QT svndromes were characterized by a peculiar electrocardiographic appearance of the QRS complex involving a premature atria beat followed by a pause. ^mlodipine lNorvasc).

Aromatase inhibitors . Antimetabolites . Chronic leukemias .16 Cop)righr O 20ll -2012 . AIDS . Myelomas . Antibiotics . Alkylating agents . Lymphomas . Antimicrotubular 1.. Carcinomas ofthe breast and ovary 117 Coplrishr O 201 I -20 12 - Dental D€cks .Denlal Decks .

In breast cancers where growth is estrogen dependent. . multiple myeloma. The alkJ-'lating agents contain a diverse group ofcompounds which all form alkyl bonds to nucleic acids. Nitrogen .CC N U) Lomtstine (CC NU. It is used as first line treat- ment ofhormone receptor positive or metastatic breast cancer in postmenopausal women. leukemias. including brain cancer Nitrosoureas: callnustine (BCN U. The alkylating agents lorm covalent bonds with nucleic acids. including brain cancer Several types ofcancer. Letrozole (Femara) worksby a similar mechanism as above. Cy-clophosphamide 1C1 rorar/ Chl or ambI'cil (L e u ke r a n) l\telphalan (Alkerat) Hodgkin's diseasc and oiher lymphomas Lymphomas. It prevents conversion of androgens to estrogens by tying up the enzyme aromatase. including brain cancer and Hodgkin's disease Seveml types ofcancer. and proreins. Exemestane is used in the treatment ol advanced cancer in post menopausal women whose disease has progressed following tamoxifen therapy. It is also indicated as an extended adjuvant treatment of early breast cancer in postmenopausal women who have received 5 years ofadjuvant tamoxifen therapy. All ofthese agents share a similar mechanism of action and mechanism of resistance. The N-7 position ofguanine is a common binding site. retinoblastoma. this drug will lower circulating estrogens.Exemestane is an irreversible.Vustsrds: Ilechlorethamine (Marlalget. neuroblasloma. and cancers ofthe breast and ovary Chronic lymphocytic leukemia Hodgkin's disease and other lymphomas Several types ofcancer. B iCN U) Cee NU) Sen\usline (Me I hy I . steroidal aromatase inactivator.

DenralDecks . Denral Decks 149 Copldght C 2011. Immune modulators . Colony stimulating factors . Monoclonal antibodies . Immunosuppressants 1. Interferons .18 Cop)'right O 20ll-2012..2012 .

Gonadotropin hormone-releasing antigen . Antiestrogens: tamoxtfen Q''lolvadex). It is used to decrease the incidence of infection by stimulation of granulocyte production in patients with nonmyeloid malignancies. -\ntimicrotubular . is used for myeloid reconstitution after autologous bone Listed below are the eight classes ofdrugs used in chemotherapy: 1. Popular agents include Cisplatin and Cyclophosphamide. Alkylating agents . . Asparaginase deprives tumor cells ofcertain amino acids such that protein production is blocked. Pegfilgrastim Qtleulasta): stimulates the production. The popular agent is Paelitaxel (Taxol).These drugs stimulate the production the hematopoietic process. -{ntiestrogen these agents block the tumors on which estrogen has a stimulatory effect. The popular agent is Leuprolide. Anthracyclines these agents destroy DNA such that the cell cannot replicate. Popular agents include Daunorubicin and Doxorubicin. 8. fulvesttant (Fasloder). \ote: The anticancer drugs Asparaginase and Interferons do not fall within any category but are used in the treatment ofcertain cancers. 6-Mercaptopurine and \Iethotrexate. Sargramostin (Leukine)z marrow transDlantation.these agents interfere which selected biochemical reactions necessary tbr cell growth. Aromatase inhibitors: letrozole /Feuara) and exernestar\e (Aromasi ) . Popular agents are s-Fluorouracil (5-FU). 5. maturation and activation of neutrophils. ? \'inca Alkaloids . 2.affects the microtubular assembly with cells to inhibit cell mitosis. Darbepoetin alpha: induces erythropoiesis by stimulating the division and differentiation of erythroid progenitor cells. andtorcmifene (Fqreston). .these inhibit gonadotropin secretion. Interferons boost the immune system. The agent in this class is Dactinomycin. 6.these are mitotic spindle poisons. 3. -{ntimetabolites .hich is effective in reducing certain carcinomas. It is used to treat anemia associated with chronic renal failure. Examples include Vinblastin€ and \-incristine.{ntibiotics . an action \\. -1. ofneutrophils and erythroid progenitor cells in . Agents used in treating breast canc€r: . The popular agent is Tamoxifen (Nolvadex).these antibiotics are not used for antibacterial therapy but were specifically designed for cancer chemotherapy. . .these agents alkylate DNA such that it cannot replicate.

Hair loss (alopecia) . Changes within the tissues ofthe oral cavity such as mucosititis .. low calcium. Peptic ulcers . Glaucoma 151 Coplriglu O 201 1. Peripheral neuropathy . Renal failure . Low red blood cells (anemia) . Low white blood cells .2012. Blood test abnormahties (low magnesium. low potassium) . Nausea and vomiting . Denlal Decks .2012 _ Denrat D€cks . Alopecia . Xerostomia Copyighr C 201 lso 1.

and degeneration of lymphatic tissue. Most people do not experience all ofthe side effects . \ausea and vomiting Orher lesr common side effects include: ." Remember: Alkylating agents these agents alkylate DNA such that it cannot replicate. During chemotherapy and radiation therapy. methotexate and doxorubicin are commonly associated with the development ofoml mucosihs. Thc mucosal int€grity is broken and is secondarily infected by oral flora. lncreased chance ofbruising. bleeding. Notes about cisplatin side ellects (a d dost chemotherapy drugs): . high doses may produce more severe side effects. mucosal tissues begin to desquamate and deleiop into ulcerations. increased incidence ofinfection (especially Candidias.9. [t is an inflammation ofthc mucous membranes. . The side effects are almost always reversible and will go away after treatment is complete. Xc. In other words. Popular agents include Cisplatin and Cyclophosphamide. Mucosititis . Low WBCS . Anemia . Remember: Most chemotherapy drugs have been shown to be teratogenic in humans and should be avoided by pregnant women. Fatigue . \ot€: Mucosititis Alopecia (hair Ioss) occurs with administration ofmost clremotherapeutic agents one to tlr o weeks after treatment.ostomia . Other common side effects include GI upset. Dn and/or discolored skin . The side effects are often predictable in terms oftheir onset and duration . \ene and muscle problems .Cisplatin is ar\ anti-cancer ("antineoplastic") chemotherapy drug. It is classified as an "alkylating agent. Appetite and weight changes . \ot€: \Iethotrexate mav cause ulceration of the oral tissues. Hair loss . Palliarive treatment is indicated formucositis. The side effects and their severity depend on how much of the drug is given. The most common side effects ofchemotherapy are: . Sexual and fertility issues because ofeffects on reproductive organs is a common reaction to cancer chemotherapy. The antineoplastics such as 5-fluorouracil (JFU). and infection . . Kidney and bladder iritation .

Dsral Decks . Hydrochlorothiaz ide (HCIZ) . G2 phase ofthe cell cycle Coplrjght @ 152 20ll-2012 . Triamterene (Dyrenium) copynsht O 201 I -2012 . ofthe cell cycle .. Furosemide (Zasry' . G0 phase or resting phase S phase ofthe cell cycle .Denbl Decks . Spironolactone (l ldactone) . G. phase ofthe cell cycle .

eth^crynic ^cid cause hr?eruricemia. Diuretics are used to tr€at congestive hcart failure by relieving edema and symptoms ofdyspnea arising liom pulmonary congestion. and degeneration of lymphatic tissue. and in the management ofedema associated $irh heparic or renal disease.pertension. Sodit|m channel blockers: these agents inhibit sodium reabsorption through sodium channels in renal epithelial cells.4! Fixed-dose combination therapy: Dyazide is the brand name for the combination oftriamterene and hldrochlorothiazide filcfz). Tlis product combines the potassium-sparing diuretic with HCTZ for geater eflicacy than eith€r on€ individually. no potassium is lost fiom the body as is the case with other diuretics such as the lhiazides and loops. They are also used to treat h]. Cetegories of widely used diuretics: . This inhibition creates a negative potential in the luminal membranes ofprincipal cells. f. . . Note: Thes€ drugs can cause hypokalemia (ab nornally lot level ofpotarsium in lhe blood) . Aldost€rone antagonists: thes€ drugs competitively inhibit the aldostercne receptor This causes incrcased amounts of sodium and water to be cxcreted. inamrinone. Note| These drugs can include bumetanide (B umer). Thus. located in the distal convolutedtubule and collecting duct.Triamlerene (D)'refiiutfi) and amiloride (Midamor) are examples of this drug group. . increased incidence ofinfection fespecially Candidiasis). sodium and chloride. They attack the cells in the S phase of the reproduction cycle by interfering with the biosynthesis ofthe purine and pyrimidine bases. Other common side effects include GI upset. tinnitus. Proto0pe agent is furosemide (rasir. Loop diuretics: inhibit reabsorption ofsodium and chloride in the ascendiog Loop ofHcnle thus causing increased secretion ofwater. and milrinone These drugs may be given intravenously to stimulate heart conhactions and help keep blood circulating They are only used temporarily because long-term use shortens life. Important: Alopecia (hair loss) occtrs with the administration ofmost chemotherapeutic agents one to two weeks after treahrent. Potassium-sprring diuretics: . nnd torcefiide (Demadat) . Thiazides: inhibit sodium reabsorption in th€ distal portion ofthe renal tubule within the kidney causing increased excretion ofsodium andwater Prototpe agent is hydrochlorothi^zide (HCTZ) Otherexamples include chlorothiazide (Diuril). hearing loss. other examples (E. these include dobutamine. (Lozol). indapamid. hlponatremia and excessive fluid loss. Remember: Most chemotherapy drugs have been shown to be teratogenic in humans and should be avoided by pregnant women. and metolazon (Zarcxolyn).*** The S phase ofthe cell cycle = DNA synthesis Antimetabolites are one ofthe oldest and most important classes ofantineoplastic agents.hponatremia (abnormally loN' level of sodium in the blood)and may increase plasma uric acid. while potassium is retained Spironolactone dactone) and epleJerone (1aplal are examples. dopamine.1ecfin).Conserve potassium while caus ing diuresis. ** Notei Positive itrotropic dlngs (drugs that make muscle contract more forcefullv) canbe used in the acute trerlment of heart failure. Negative potential reduces secretion ofpotas_ sium andhydrogen ions. .

Glyburide (DiaBeta) .Which of the following is a pharmacologie antagonist of aldosterone in the collecting tubule? . Vetformin (Glucophage) .right O 201 l-2012 Dental Decks . Spironolactone (Aldactone) . Urea (Ureaphil) 154 Coplright O 20ll-2012 . Glinepiide (Anaryl) 155 Cop). Glipizide (Glucotrol) .Denral Decks . Mannitol (Osmifuol) . Glycerrn (Glyrol) .

Block the sodium channels in the collecting tubules: . drug interactions that may cause (Glucophage. and urea.Potassium-sparing diuretics result in increased sodium and decreased polassium concentrations at the end ofthe distal convoluted tubules. Amiloride (Midamor) *** The most impodant toxic effect of potassium-sparing diuretics is hyperkalemia.S. .e required for thcsc medications to work. Examples include: mannitol. Note: Functioning beta-cells a. and incrcase the sensitivity oftargeI organs to insulin. . 2.ha\'e a major drawback. glycerin. Once dislodged. Bccausc they bind to proteins in the blood. This enryme inhibition delays glucose absorption. stimulate the beta cells to produce more insulin. tol^z nride (Tolindrel. Elyburide (Micronase) and glimepiride (Amaryl). in 1955. Thiazofidinediones: rosiglitazone (Avandia) and pioglit^zone (Actos) increase senstivify in the musclc and liverby improving control ofglycemic utilization. Second gen€ration sulfonylureas includc glipizide (Glucotol). . close potassium channels in ccll mcmbranes. There are two cat€gories ofpotassium-sparing diuretics: l. Osmotic diuretics are highly filtered by the glomerulus and exert a solute-induced diuresis in the proximal tubule. ofthis.. thcy can be dislodged by other medications that bind to thcse same proteins. *** Metformin is classified as a biquanide Antidiabetic agents or oral hypoglycemic agents are drugs used as adjuncts to dietto treat non-insulin dependent diabetes mellit\rs (tfpe 2 diabetes)that cannot be controlled by diet alone. Meglitinides: repaglinide (Prundin) and oateglinide /Slarllxl lower blood sugar by stimulating the rclease ofinsulin fiom the pancreas in short bursts. Biquanides: metlotfiin . . Remember: Carbonic anhydrase inhibitors fi.set act through inhibition ofpancreatic d-amylase and membrane-bound intestinal cr-glucosidc hydrolase enzymes. These enzymes do not enhance insulin secretion .These drugs have an advantage for those who use other medications since rhey do not bind to carrier proteins in the blood. and chlorprop^mide (Diabinese). It may be useiul in the treatment of heart failure because hyperaldosteronism is comfironly seen in this condition. Bccause lorr blood sugars are less likely. They are used to reduce excess edema associated with neurosurgery or traura to the CNS. These drugs work well in lowering the blood sugat but thel. Note: Acetazolamide is used to prevent and reduce the symptoms of altitude sickness. Triamterene (Dyrenium) . SulfonJ-lureas. Notei Functioning beta-cells are required for these medications to work.) primarily decreases hepatic glucose production. . the first drug group introduced into the U. It also has minor effects on insulin sensitivity in both the liver and peripheral tissues. The original "first g€neration " sulfonylureas include tolbnt^mide (Orittdse). Antagonist of aldosterone in the collecting tubules: . It has no direct effect on lhe pancreas and therefore does not enhance insulin secretion. o-Glucosidase inhibitors: acarbose fPl€coreJ and miglitol /Gf. their activity can increase tapidlr'and lead to low blood sugars. .e.. This in tum reduces circulating insulin levels. Spironolactone (Aldactone) Note: Spironolactone has been found to be effective in the treatment of primary aldosteronism. lcetazolamide) arerelatively weak diuretics because ofthe ability of more distal sites in the loop ofHenle to increase theirreabsorption of sodium.

Decreased gluconeogenesis storage . Intermediate-acting insulin with a duration of l0-16 hours . Increased glycogen synthesis 157 cop]righr O 201l-2012 .Denbl Deks .Dental Decks AII of lhe following are elfects of insulirt EXCEPT one. Which one is the EXCI'PZIO ry . Increased triglyceride . Short-acting insulin with a duration of6-8 hours .. Decreased protein s)'nthesis . Long-acting insulin with a duralion of20-24 hours . Rapid-acling insulin with a duration of3-4 hours 't 56 Coprighr C 201 l-2012 .

which is required for the proper utilization ofglucose in normal metabolism. Rapid-acting Insulin aspart (Vovolog) Insulin glulisine (lpi dra) 5- Onset Peak Duration 3-5 hours 3-4 hours 3-4 hours l5 min t-3 hours 30-90 min 30-90 min 5-15 min lnsdin li spr o (Hum a I o g) Short-acting lnsulin reg ar (Humulin R) 30-60 min Intermediate-acting NPH (Humulin N) 2-4 hours 6-10 hours 10- 24 hours 6-8 hours l6 hours Long-acting lnsulin detemir lnsulln glar gine (L ev em i r ) t hour 2 hours No peak No peak 6-24 hours 20-24 hours (L an tus ) lmportant: Hypoglycemia (low blootl sagay' is the most serious complication ofinsulin thempy. *** This is false. oral hypoglycemics can often be used because the beta cells are able to secrete insulin. confusion. They are used in type 1 diabetes and in type 2 diabetes which cannot be controlled completely by the oral antidiabetic drugs or by diet alone. Insulin injection is by subcutaneous administration. although in a more sluggish manner . In treating type 2 diabetes mellitus. insulin increases protein slrnthesis. Remember: Insulin is required in treating type I diabetes mellitus because the beta cells of the pancreas are devoid of insulin. weakness. Administration ofa concentrated glucose source will relieve mild hypoglycemia.Insulin preparations mimic the activity ofendogenous insulin. Insulin is a pancreatic hormone secreted by the pancreatic beta-cells of the islets ol Langerhans and is essential for the metabolism of glucose and for the homeostasis of blood glucose (it reduces blood glucose by increasing the {onversion to glycogen and -/at. Symptoms include: sweating. slurred speech and blurred vision.

Dent. Slow .. Slow onset. long duration 158 copyrighr O 201l-2012 .l Decks .Dental D€cks . Prothrombin . Plasmin '| 59 Coplaighr O 201 l.?012 . Heparin . Fast onset. short duration Fast onset. long duration . onset. short duration . Fibrin .

The administration ofheparin \'ents the conversion offibrinogen to fibrin. These cells occur tn connective tissue and in extracellular spaces near blood vessels. ?. \ot6 - will result in an increase in bleeding time due ro a potentiation of antithrombin III thereby inactivating thrombin. but also blocks thromboplastin generation. It is used for prophyla-ris and treatment of thromboembolic disorders. Heparin is contained within mast cells and basophils. Note: Using either agent alone would not provide both the fast onset of insulin action along with the long duration. the regular insulin component /30o2) provides a fast onset ofblood sugar control beginning one-half hour after injection and the insulin NPH component (702o) starts acting within a couple ofhours to provide a long duration ofblood sugar control. Mixtures Humulin 70130 Novolin 70130 Novolog 70130 Humulin 50150 HumalogT5/25 Onset 30 min 30 min Peak 2-4 hours 2-12 hours 1-4 hours Duration l4-24 hours Up to 24 hours Up to 24 hours l0-20 min 30 min 15 min 2-5 hours 30 min l8-24 hours 2hours - l6-20 hours Premixed insulins are a combination of specific proportions of intermediate-acting and rapid-acting or short-acting insulin in one bottle or insulin pen (the numbers following the brqnd name indicate the percentage of each 4. Remember: Heparin not only neutralizes tissue thromboplastin. This o.Humulin 70/30 mixture is a popular form ofinsulin that many diabetic patients take. . lts advantage is that after a single injection./ insulin).

right O 20Il-2012. Drugs which lnhibit the actions of CYP 3A4 would affect triazolam in which wav? . Cause oftriazolam . Denral Decks . Etanercept (Enbrel) . Cause an increase in serum levels oftriazolam a decrease in serum levels . Adalimumab (Humira) 160 Copyright O 2011.. Cause no change in serum levels of triazolam 161 Cop'. a pre'operative sedative in dentistry.Dental Decks Tnazolam (Halcion). is metabolized in the liver by the P-450 isoform CYP 3A4 enzyme.2012 . Infliximab (Remicade) .

Infliximab (Remicade) is used to treat Crohn's disease and rheumatoid arthritis. \ote: Triazolam is known to interact with drugs that inhibit its metabolism via the CYP 3A4 enzyme. Drugs that inlibit the metabolic pathway may have a profound effect on the clearance oftriazolam.urd TNF. and Crohn's disease. ifneeded. Adalimumab is effective in RA. ketoconazole. Consequently. .4. Jluconazole.There are currently three tumor necrosis factor alpha (TNF) inhibitors FDA approved for the treatment ofRA (listed in order oftheir approval Jbr k4): . and ankylosing spondyli- tis. Adalimumab (Humira) is a fully human anti-TNF monoclonal antibody with high specificity for TNF. The resultant effects would be an increase in serum concentrations \\ith an associated unexpected increase in the actions of triazolam. Tumor necrosis iaclor alpha (TNF) is a pro-inflammatory cytokine produced by macrophages and lymphocfes. These antifungal agents inhibit the CYP 3A4 isoform responsible for heparic metabolism oftriazolam. triazolam should be avoided in patients receiving very potent inhibitors ofCYP 3.It is a recombinant DNA-derived protein which binds to tumor necrosis factor alpha (l'ly'F). thereby interfering with endogenous TNF activity. voriconazole) can significantly elevate the serum levels of triazolam resulting in toxicity with therapeutic doses. TNF is one ofthe critical cytokines that mediate joint damage and destruction due to its activities on many cells in the joint as well as effects on other organs and bodv svstems. -\ntifungaf agents (itroconazole. Adalimumab binds specifically to TNF and blocks its interaction with the p55 and p75 cell surface TNF receptors. miconazole. Thus the normal metabolism oftriazolam is inhibited. Adalimumab binds to both soluble as well as cell bor.A. . Infliximab is a chimeric monoclonal antibody that binds to tumor necrosis factor alpha (TNF) thereby reducing the inflammatory actions ofthis endogenous compound. It is administered by subcutaneous injection every two weeks but can be increased to weekly. . Psoriatic arthritis. It is lound in large quantities in the rheumatoid joint and is produced locally in the joint by synovial macrophages and lymphocyes infiltrating the joint synovium. Etanercept (Enbrel) is used to reduce the signs and symptoms ofactive rheumatoid arthritis in patients who have had inadequate response to one or rnore disease-modifring anti-rheumatic drtgs (DMARD). Do not administer triazolam to patients taking any ofthese antifungal agents.

Four times a day 162 Copltight @ 201 l'2012 . Twice a day .Dental Decks . Pilocarpine (lsopto-Carpine) .. Three times a day . Betaxolol (Betoptic) . Bimatoprost (L umiga n) 163 Coplright O 2011. Latanoprost (Xa latan) . Every 4 hours .Dental Deck .2012 .

4.i. . Bimatoprost fZ. miganl same action as latanoprosl (Xalatan) .i.rn. b.: every 12 hours .l2. q.l ounce = 30 g or 30 mI Glaucorna is characterized by an increase in intraocular pressure. : : as needed before meals . : twice a day . = Label Note: Always document prescriptions that are given to a patient in the patient's chart. Bet^xolol (Betoptic): abeta-blocker. ' Sig.h. eye drops in the eye reduces intraocular pressure by reducing the production of aqueous humor . along with the date they were written and any specilic instructions for patient use. p. I grain = 65 mg . Latanoprost (Xalatan)z a prostaglandin analog. h. Pilocarpine (1sop to-Carpine)r eye drops in the eyes causes papillary constriction thus allowing for drainage ofthe aqueous humor to reduce pressure . = immediately . t. stat. = qfrar ma. : three times a day . a.h.d. Remember: .d.Other popular and common abbreviations used when writing prescriptions: . q. = every 4 hours .s. It is caused by poor drainage of the aqueoushumor (luid in the eye) and can cause blindness. : at bedtime . h. eye drops in the eye reduces intraocular pressure by increasing the outflow ofthe aqueous humor .

Atropme . the second statement is false . Both stalements are true ..' . Diphenlydramin e (Benadryl) . The first statement is true. The first statement is false.Dental Decks . Both statements are false 16s Cop''right O 201 I -2012 .Denbl Decks .The following drugs are noted for causing what prominent oral slde effect? - . Amrnipqline (Elavil) . DiazepNn (Valiun) '| 64 Coprigh O 201| -2012 . the second statement is true .

large doses are requrf3d. It is a chronic. Diphenhydramine (Bena&yl) is representative olthe sedating-type antihistamines. . the neurotransmitter thal is deficient in this disorder Parkinson's disease i/PD) results from a relative excess ofcholinergic activity and a deficiency ofdopaminergic actilitr in the basal ganglia. another enzlme that metabolizes dopamine. . They probably work through an anticholinergic action. pcrgolide. Note: The D2-recep_ :. . a class ofdrugs that causes significant xerostomia. and ropinitule (Requi . and these are apt to caus€ unwanted side-effects. a class of drugs lhat causes significant xerostomia. Administering carbidopa in combination \r'ilh levodopa fsir?emet. inhibiting the effscts ofacetylcholine. apomoryhtne (Apokrn).T1rese drugs irreversibly inhibir the enzyme MAO-B. and rasallllne (Azilect).r subllTre is lhe p mary modulatorofboth clinical improv€ment and adverse rcactions such asdystonia and *** hrllucinations. . This causes dopamine to accumulate in surviving nerve cells and reduces the symptoms ofPD . Anticholinergic agents (antimuscarinic drugs): benztropine (Cogentin) and ftlhexyphentdyl (Tasmar). when levodopa is grr er alone. rhus prolonging the actron of dopamine. Lerodopa has been thc single most important drug in the treatment ofPD. much ofrhe dose is metabolized befor€ the drug reaches the brain.Xerostomia can be caused by certain drug classes that inhibit the production and secretion of saliva. Drug treatment for PD has cenrered on increasing the availability ofdopaminc in the CNS. Thus. Atropine is a powerful anticholinergic which blocks the production of saliva in the salivary glands. which is responsible for the oxidative deamination ofdopamine in the brain. Other anticholinergics will have a similar action. and entacapone fcotntan) T1\ese drugs are inhibitors ofCOMT. . These drugs supprcss central cholinergic activity and may inhibit reuptakc and storage ofdopamine in the CNS. . Amitriptyline (Elavil) is representative of the tricyclic antidepressants. co-administration ofcarbidopa plus levodoPa in the form ofSinemet al_ lo\\s a significant reduction oflevodopa dosage without rcducing the desired effccts. These d gs are direct dopamine receptor agonists. debilitating disease with no kno$'i cure. llfonoamine oridas€ B (MA)-B) inhibitorsr seleglline (El. Levodopa is used in the treatment of Parkinson's disease to replenish th€ brain's supply ofdopamine.lepy. They probably work through an an- ticholinergic action. Other rntiparkinson agents: . .dopa. Gfutamate antagonist (anliirury amartadine ($'mmetrel) appearc to potentiate dopamineryic responses. and a$cmpring to prevent further cell m€mbmne damage through neuroprotective trials. . Since carbidopa does not cross the blood-brain barrier. This action simultaneously reduces the likelihood ofperipheml side effecls and allows more lev- riopa ro reach the brain. Dopamine agonists: bromocriptine. pramipexole (Mirupex). These drugs have moderate anticholinergic actions to reduce the outflow of saliva. Carbidopa inhibits the pcripheral decarboxylation of lerr. . The xerostornia actions produced by these classes ofdrugs are reversible with nor- mal salivary flow regained after discontinuance ofthe drug.. reduces lhe required dose of levodopa by about 75%. Certain antidepressrnts and antihistamines such as diphenhydramine that have antimuscarinic actions may be given in the early stages ofdisease. Diazepam (Vctlium) \ote: is representative of the benzodiazepine tranquilizers. the levodopa in the brain is conlened rhere to dopamine. Catechol-O-methyl t r^osfer^se (COMT) ilhibitorsi tolcapone i1zQsma. Therefor€.

Lidocaine (Xylocaine) .Denral Decks . Propafenone (Rythno I) .Which artiarrhlthmic agent is €ffectlve only on the ventricle and is often administered IV to trert life.Denhl Decks 167 Copt?ight O 20lt-2012 . Quinidine (Quinidex) . Flecainide (Tambocor) .threatening ventricular arrhythmias? . None of the above 166 Copyight O 20ll-2012 .

Directions to the patient (SigJ Signature of person prescribing medication must appear . Transcription or signa ) . date . Any stare 00000 (000) 5s5- License # Federal Drug Registry # l2l2 Age: Date: Patient's Name: Patient's Ad&ess: Amoxicillin 500 mg. Four (4) tabs Sig: Take 4 tabs f2000 mg) 30-60 minutes prior to dental appointment Signature: Substitution permissible Substitution not permissible Number of refills Notes: . effective in a wide range ofventricular and atrial arrhythmias and tachycardias.When lidocaine is used IV to treat ventricular arrhythmias.e. age. It can effectively reverse a life-theatening situation. Subscription . address. Signature - . Propafenone (Rythnol) is used to treat both ventricular arrhlthmias and supraventricular tachycardias.Directions to the pharrnacist (dosage form and amount to be given Disp . Quinidine is considered as the prototype antianh)'thmic agent and is used primarily to treat atrial fibrillation. 500 mg tablets) . Flecainide (Tambocor) is potent antiarrhythmic agent. tablets Disp. Superscription - Patient's name. Dr I John Doe. DDS I Any Street Any Ciry. It is not effective in treating life-threatening ventricular fibrillahon.. Inscription ' Name of drug and the strength ofthe drug fi. it acts on the fibrillating ventricles to decrease the cardiac excitability and spares the atria.

Lansoprazole (Prevaci d) '| 69 Decft s Coprdght C 201 l'1012 .All of the following drugs are useful for treating whrt common medical condition? .Dental . Cimetidine (Tagamet) . Gold injections . Ranitrdine (Zantac) . Nabrmetone (RelaJbn) . Piroxicam (Feldene) 168 Coprighr O 201 I 201? . Omeprazole (Prilosec) . Methotrexate .Derral Decls Which IIIO gastroint€stinal drugs listed below reduce the formation of stomach acid by inhibiting the proton pump of the stomach parietal cells? . Prednisone . Famottdine (Pepcid) .

\ote: All of Hydrochloric acid (l{Cl) is produced by the parietal cells ofthe stomach through a pump u ithin each cell which pumps protons (H. histamine stimulates the gastric parietal cells to produce hydrochloric acid. cimetidine and famotidine block the effects of histamine by blocking at the H2-receptors. but may affect immune function . indigestion. The pump is called tbe H-/K' ATPase pump. calcium carbonate (Tums) magnesium hydroxide (Maalox) and sodium bicarbonate.Rheumatoid arthritis (RA) is a chronic inflammatory disease ofjoints that results in joint pain. Stomach acid can also be reduced by inhibiting the effects of histamine in the stomach at the histamine type-2 receptors (H2 receptors). and destruction. Antacids include aluminum hydroxide (Amphogel). How these drugs work in treating rheumatoid artkitis: . Remember: Antacids neutralize excess stomach acid by a chemical reaction. Ordinarily. there is the accumulation of prostaglandins. Piroxicam (Feldene): ar NSAID that inlibits prostaglandin synthests the above drugs except gold injections are also useful in the treatment of osteoarthritis (OA). These tkee drugs are classified as H2-receptor blockers. These nvo drugs are classified as proton-pump inhibitors. Methotrexate: unknown. Gold injections: may decrease prostaglandin production . Prednisone: decreases the inflammatory response . leukotrienes and other mediators in the inflammatory changes and tissue destruction in the synovial lining.) into the stomach contents. . swelling. bismuth subsalicylate (Pepto-Bismol). With disease progression. Agents useful in treat ing OA provide an analgesic and anti-inflarnrnatory action to reduce pain within thejoint. OAis characterized by progressive loss of articular cartilage. which lines the joint. This may be the result of excessive loads on the joint or other factors. HCI is used for food digestion but an abundancy can cause heart bum and acid indigestion. Omeprazole and lansoprazole inhibit the pump such that no protons are pumped into the stomach contents and thus no HCI is produced. RA is characterized by chronic inflammation ofthe synovium. Both the proton-pump inhibitors and H2-blockers are used to feat heartbum. sour stomach. Nabumetone fRela/en): an NSAID that inhibits prostaglandin synthesis . active duodenal ulcer disease and gastroesophageal reflrx disease (GERD). Ranitidine.

pamidronate (Aredia). Warfarrn (Coumadin) 170 Copyight O 20ll-2012 . \4ucositis . Oral yeast infection . Cloprdogrel (Plavix) .. Osteonecrosis ofthe jaw bone . Xerostomia 171 Cop)righr O 20ll-2012 . Heparin .Denhl Decks . znlendronic ^cid ibandronate @azira) and alendronxte (Fosamax)? . risedrontte (A ctonel). Vitamin K . Aspirin . Angular cheilitis ..Denlal Decks What serious dental elfect is associrted with the following drugs: (Zo meta).

Clopidogrel /P/avx) inhibits blood clotting by inhibiting platelet aggregation in an irreversible manner. However. IX and X. and prothrombin in the liver.eceptor modulatorsl. coagulopalh!. Vitamin D: helps to ensure that the body absorbs and retains calcium and phosphorus. Zoledronic acid (Zometa).25-dihydroxycholecalciferol is the biologically active form ofvitamin D (Cholecalciferol) . pamidronate (Aredia).Heparin inactivates thombin and prevents the conversion of fibrinogen to f:Jc.. Note: 1. is a naturally occurring hormone that is produced by parafollicular C-cells in the thyroid gland. Bisphoshonate therapy has been associated with osteonecrosis. tir an affinity for hydroxyapatite crystals in bone and act as antitesorpTheir primary mechanism ofaction involves inhibition ofosteoclastic bone resorption. Once-daily adminishation of P'lH (tefiparatide IForleol) stimulates new bone formation via preferential stimulation of osteoblastic activify over osteoclastic activity. SERlls fse/ectil. but also in patients with postmenopausal osteoporosis and other diagnoscs.e. fisedrci^te (Acto el). primarily ofthe jaw. Orher agents that have an effect on bone: . VII. and alendror. Thus the effects on blood clotting are the same as aspirin. It also stimulates the production ofthe active form of vitamin D in the kidney. Inhibition ofplatelet aggregation prevents activation ofthe coagulation pathway. radiotherupy or corticosteroids. and anticogulants (i. renal tubular reabsorprion ofcalcium and phosphate. as a precautionary measure. Important: Bisphosphonates have e agents. . Symptoms included nonhealing cxtraction socket or an a diagnosis e\posed jawbone.ate (Fosamax) are members ofthe bisphosphonate class ofdrugs used to heat and manage Pag€t's diseas€. infection or pre-existing dental disease. abciximab (ReoPro). It is known to block bone resorption through its potent inhibitory elTects on osteoclasts . Physiologic actions include regulation ofbone metabolism. dental exams and preventativ€ dentistry should be perlormed prior to placing patients with risk factors on chronic bisphosphonate therapy.rin (blood clot).e . this has been observed mostly in cancer patients. \ote: Cfopidogrel. Aspirin inhibits blood clotting by inhibiting platelet aggregation in an irreversible manner. heparin) are used to lessen the chance of heart attack in people who need percutaneous coronary in- ten ention fPCl). anemia. osteoporosis and to prevent hypercalcemia ofmalignancy. Discontinuation ofaspirin for 5 to 7 days allows for normal clotting time to reappear due to the svnthesis of new platelets. aspirin. IX and X resulting in the inability ofthe coagulation pathway to form ftbrin (blood clot). discontinuation oftherapy reduces the risk ofde\ eloping osteonecrosis. ib^odtonate (Bohiw).w^rfarin (Coumadin) rnterferes with the hepatic synthesis of vitamin-K dependent coagulation factors lI. Note: PTH also acts on th€ kidneys by reducing renal clearance ofcalcium which increases plasma calcium. Calcitonin: eJtrcgen . Vitamin K is a group of fat soluble vitamins that are essential for the synthesis of coagdation factors II. Hormones: . thus no fibrin (c/ot) is formed. and intestinal calcium absorption. VII. a procedure to open blocked arteries ofthe heart. which are critical for building bone. Aspirin does not affect the coagulation pathway. It is used for heating osteoporosis. Clopidogrel rPlatix) does not cause gastric ulcers like aspirin does and is the antiplatelet agent of choice in patients with history ofulcers. R^lo\ifeie (Evisla) reduces rcsorption ofbone and decreascs overall bone fumover. Risk factoN include ofcancer. Adr erse effects /6esider osteohecftrsis of the jaw bor€) include GI symptoms and esophagcal erosions. Vitamin K will enhance blood clotting rather than inhibit blood clotting. There is no data addressing whethe. with concomitant chemotherapy. Parathyroid hormone: PTH is the primary regulator of calcium and phosphate metabolism in bone and kidney.

Opioid abuse .. Ethanol abuse . Nicotine abuse . NSAID abuse '| 73 Copyriglt O 201 I -2012 - Dsral Decks . Renin . Lysozyme . Heparin 172 Coplriglt O 201 1-201 2 . Plasmin .Dental Deck .

Renin is proteolytic enz)'rne produced by and stored in the juxtaglomerular apparatus
that surrounds each arteriole as it enters a glomerulus. Renin acts on the precursor substance angiotensinogen, which is manufachrred by the liver and is present in the blood. Renin converts angiotensinogen to angiotensin I. In turn, angiotensin I is converted to angiotensin II by a converting enzyme associated with the walls ofcapillaries, particularly in the lungs.

Important: "The converting enzyme that converts angiotensin I to angiotensin II known as angiotensin converting enzyme or ACE."


II is a potent vasopr€ssor. It not only increases total peripheral resistance but, by stimulating aldosterone release, leads to an increase in plasma volume, venous retum, stroke voh.rme, and ultimately an increase in cardiac output.
\ote: Aliskiren (Tehuma)
is a renin inhibitor used to treat hypertension. This is the first ofa new class of drugs and little information is available. It is used alone or in combination with other agents for the treatment ofhypertension.

Disulfiram is not a cure for alcoholism but is a deterrent to ethanol consumption. Disulfiram is an antioxidant that interferes with the hepatic oxidation ofthe acetaldehyde metabolized from alcohol. Specifically it inhibits aldehyde dehydrogenase, a mitochondrial enz]'me found in the liver Even the ingestion of small amounts ofethanol results in high
concentrations ofacetaldehyde in the body. The unpleasant reaction that occurs (called the Disulliranr-Ethanol Reaction or DER) consists ofa throbbing headache, dyspnea, throbbing in the neck, nausea, copious vomiting, thirst, tachycardia and hypotension. \ote: lletronidazole, also inhibits aldehyde dehydrogenase.

Ethanol is

a sedative-hypnotic drug and is the most important alcohol ofpharmacologic

interest. Its abuse is responsible for many socioeconomic problems. Drugs that are synergistic with ethanol include diazepan, meperidine, pentobarbital and chlorpromazine. When combined with alcohol these drugs could cause fatal oversedation.

Remember: Synergism refers to the combined action oftwo or more drugs that is greater

than that achieved with a single drug.

. The first statement is true; the second statement is false

. The first statement

is false; the second statement is true


Both statements are true

. Both statements are false

Coplrighr O 201 I -20 l2 - Denral Decks

. Anaphylaxis . Heart attack

. Syncope . Urticaria

Copraight O 20l l-2012 - Dental Decks

Gastric antacids are drugs that directly neutralize the gastric acrd (HCL) secreted in the stomach. Antacid therapy is directed at decreasing the concentration and total load ofgas-

tric acid.
Some common over-the-counter antacid products:

. Sodium bicarbonate
- Alka-Seltzer


. Calcium carbonate products:
- Amitone

- Tums

. Aluminum hydroxide products: - Altema GEL - Amphojel

. Magnesium hydroxide products: - Milk of magnesia . Bismuth salt products:
- Pepto-Bismol

. \Iagnesium and aluminum products:
- Maalox - \4ylanta

is the most potent of these but has less neutralizing capacity than calcium carbonate or sodium bicarbonate.

*** Aluminum hydroxide

Note: Dyspepsia means an impairment ofthe power or function ofdigestion.

Inlaled ammonia irritates trigeminal nerve sensory endings, with a resulting reflex stimulation of medullary respiratory and vasomotor centers. An aromatic amrnonia vaporole

oforlgen rrrll aid

is crushed betrveen the fingers and held near the patient's nose. Note: The administration in combating tissue anoxia.

The sl mptoms of syncope include beads ofsweat on the upper lip, a weak thready pulse, cold clammy skin, pallor and a dizzy feeling. The loss of normal vasomotor tonus produces pooling of blood peripherally so that the normal blood volume becomes insufficient. Placing the patient in a supine position and elevating th€ feet gives the patient a transf'usion ofwhole blood by utilizing the forces of gravity. Note: The head should not be more than about 10 degrees lower than the rest ofthe body.

Tl pes of syncope:

. Vasor agal ) . \eurogenic Trear uirh high-flowing 1007o oxygen I . C)nhostatic -f . Hyperventilation syndrome Oxygen is not indicated

Note: 100% oxygen is contraindicated for
tive pulmonary disease (COPD).

a person who suffers from chronic obstruc-

. Growth Hormone
. Insulin
. Antidiuretic Hormone (ADH)

. Epinephrine

176 Coplright
@ 201 I

'2012 - Dental Decks

. Dopamine

. Aldosterone . Vasopressin . Somalotropin


coplrighr O 20ll-2012 - D€nhl D@ks

particularly in men. Ethanol (ethyl alcoftoi) inhibits the production ofADH. Note: Human growth hormone is adminislered as subcutaneous injection or intramuscuIar injection. usually tbree times per week. suppressing the activities of excitatory nerve pathways and increasing the activities of inhibitory nerve pathways. Alcohol acts primarily on the nerve cells within the brain. Cerebellum . Increased rate ofprotein synthesis in all cells ofthe body .ADH is a hormone that decreases the production of urine by increasing the reabsorption of water by the renal tubules. Medulla lbrain stem) Grorlth hormone (GI{) is produced by. and secreted from the anterior pituitary gland. Increased mobilization offats and use of fat for energy Human growth hormone is prepared commercially and used as replacement therapy in patients with growth hormone deficiency. wine. Human growth hormone is indicated in children for the treatment of growth failure due to lack ofadequate endogenous growth hormone secretion. Limbic system . Note: Recent evidence has shown that ftequent ingestion of moderate amounts ofalcohol in any form (beer. The commercial preparation is prepared as the purified polypeptide hormone of recombinant DNA origin with the same amino acid sequence as that produced by the pituitary gland. It has been used in adults who have a growth hormone deficiency as a result ofpituitary disease. Remember: Ethyl alcohol dilates blood vessels of the skin. distilled spiits) will reduce the risk of heart disease. Hypothalamus and pituitary gland . there would be extreme loss of water into the urine. Basic Metabolic eff€cts of growth hormone: . The order in which alcohol affects the various brain centers is as follows: . Without ADH. depresses the CNS. . and in blood levels in excess of400 mg o/o usually results in coma and death. Cerebral cortex . Decreased rate ofcarbohydrate utilization thoughout the body . Alcohol interferes with communication between nerve cells and all other cells.

D€nral Decks . Allopurinol 178 Coplriglt O 20ll-2012 .Dental Decks . Probenecid . Norepinephrine . Epinephrine . Sulfinpyrazone . Colchicine . Isoproterenol . Chlolpromazine . Dopamine .. Indomethacin . Dobutamine 179 Copyright O 20ll-2012 .

ob€siry. hean failure lmfirdiaia precursor of NE Dng (Not Catcchol4nine) Amphctsmin€.e. to caus€ To cause vasoconstriclion in h)?otension Comm€nb Stimulat s th€ myocardiun Stirmlatcs thc myocardium Dopamine Dobulamin€ Shock.The therapeutic management of gout involves three different aspects ofthe disease: l. 2. Colchicine should never be given IM or subcutaneously (it causes tissue irritation). 3. long-term therapy may cause bone marrow depression. pr€mature labor To cause nasal decongestion (long Or}. the proxintal convoluted tubules) and inhibit the secretion of other weak acids (i. nelaDrolercnol te6utaline Narcolepsy. norepinephrine and dopamine). It is most effective when initiated 12 to 36 hours after symptoms begin. glaucoma. Some catecholamines are produced naturally by thebody (called endogenous) andftnction as key neurological chemicals (i. Remember: Normally penicillins and cephalosporins have to be given in high and frequent doses due to their high rate of elimination by the kidneys.lnet ?oline. penicillin). and xanthine to uric acid. in addition to inhibiting the reabsorption of uric acid. 2. decongesrion Asthma. These agents act primarily in the kidney (. *** Chlorpromazine is a dopamine antagonist and antipsychotic agent. to cause vasoconstriction. phEnmeirEine Ephedrine Pheryl€phrine Albuterol. head failure Shock. Indomethacin (rzay cause renal damage or bone maruow depressiar) is most commonly used. an enzyme that converts hypoxanthine to Note: Epinephrine.yecifcally. Reducing the inflammation during acute attacks: The drug ofchoice is colchicine. It inhibits xanthine oxidase. rasocon. Notes: l. Catecholamin€s are any one ofa group of sympathomimetic compounds composed of a catechol molecule and the aliphatic portion ofan amine. Colchicine impairs leukocytic migration to inflamed areas and disrupts urate deposition and the subsequent inflammatory response. Their excretion is slowed by giving probenecid. Decreasing uric acid production: Allopurinol (Zyloprin) is the drug ofchoice in the management ofchronic gout. attenrion deficit disorder Urinary inconlinence. Enhancing uric acid clearance: Uricosuric agents include probenecid (Benemid) and sulfinpyrazone (Anturane).. Remember: NSAIDs are also important for the treatmenl ofacute gouty arthritis.. decongestion Tocau\e m)dria. epinephrine. aslhma. \orepinephrine and Isoproterenol are considered to be direct-acting catecholamines.e. Colchicine can severely damag€ the liver and kidney. May cause GI disturbances. xylom€lazoline acting .tricrion. Drug Epitr€pkine \orepinephrine Clinical ApplicatioDs Anapbylaxis.

Carisoprodol (. Slccinylcholine (Anectin e) ..2012 . Halopeidol (Haldol) . Baclofer (Lioresal) . Selegiline (Eldepryl) . Pergolide (Permax) .Dental Decks . Methocarbamol (Ro b axin) .DentatDecks . Bromocriptine (Parlodel) . Levodopa (Dopar) . Cyclobenzaprine (F lexer i l) . Amantadine (Synmetrel) 181 Copyright O 2011.Sozc) 180 Cop)'right O 20ll-2012 .

s disease. multiple sclerosis. painful musculoskeletal conditions and in the management oftetanus. its site ofaction in reducing muscle spasms is the spinal cord. . cerebrovascular accidents) that are associated with painful muscle spasms. 1. Carisoprodol fsoranJ: is used in the treatment ofmuscle spasms and pain associated with acute temporomandibularjoint pain. It stimulates CABABreceptors that are linled to the G protein. or may be given laterwhen levodopa. . and the COMT ir*ibito. They act in the CNS or in the skeletal muscle cell mther than at the neuromuscular end plate. . $ilh lcvodopa in later stages. . \otrs Dental implications ofAnti-parkinson's agents. lt is used in thc early stages for mild diseasc. lt is used to relieve acute. ll may be tr€ated fbr ot cured)with a wide varietv of .e. certaitl . Antichofinergic drtgs (benztropine and ttiheryphenidyl. Schedule appointmcnt times based on when the patient is feeling the bcst. It is given with carbidopa to incrcase effectrvcness and rcduce or pergolide are dopamine agonists which are often given in addition to lev_ odopa earlv in the treatmcnt to enhance levodopa's action.l/t are agents that relieve muscle spasms without paralysis. resulting in an increase in K conductance and a decrease in Ca. agents (mai y levodopa. It is not efllctir e for muscle spasm secondary to cerebral or spinal cord disease. painful musculoskeletal conditions. Gt.uttidepressa hi<tunrines such as diphenhydranine) may be given without levodopa in thc early stages ofdis_ ease. the direct dopamine dgonists and the COMT inhibitors) have been associated wilh orthostatic hypotensior. By reducing the spasms there is a reduction in pain and improved mobility for the patient. Used is the treatment of mriltiple sclerosis and other spinal cord diseases.s iid. *** Haloperidol is used to treat psychotic syndromes.*** Succinylcholine is the prototype depolarizing neuromuscular blocking drug."t can prescnt a chal_ lenge whcn trying to perform dental treatmcnt. \lethocarbamol (RobcLrin): is a centrally acting muscle relaxant that is used to relieve acute. Xerostomia lcarsed by a ticholinetgics antl MAO_B inhibitorst. It has ie\craf distinguishing chamcteristics: tremor (shaking) when at rest.. . lts precise mechanism ofaction is not clear but many effects have been ascribed to its central deDressive action. Bromocriptine ride ellects. Spasmolytic drugs (skeletal muscle relax4. Antiparkinsonian actions are unrelated to thc antiviral cffects. Anti-Parkinson's . \ote: Quinine is widely used for the effective relief of noctumal leg cramps. possibly at the brain stem level. . the direct dopamine agonist. . ln Parkinson. Drugs used for chronic muscle spasm: is a derivative ofGABA. lt is the main treat_ ment 1br Parkinson's discase. sluggish initiation ofmove_ mcnls and musclc rigidity. Le\ odopa /in couhi ation tith carbidopcJ is the precursor of dopanine._ odopa.' conductance. . J* g. Baclofen (Lioresal): Drugs Lrsed for acute muscle spasm: .l anti_ Parkinson's disease is a slowly progressing. It is used as an adjunct to levodopa. eft'ects become more ofa problcm. the enzyme that is rcsponsible for the oxrdatir c deamination ofdopamine in the brain. ' selegiline is a selectivc inhibitor ofMAo rype B. All ofthe other skeletal muscle relaxants do not bind to the GABABrecepto$: Diazepam (Valium) and tizanidine (Za aflex) also act rn the spinal cord and are effective muscle relaxants. ts an. . These drugs are used in certain chronic diseases ofthe CNS (i. dcgenerative disorder of the nervous system. C!clobenzaprine (Flexeril): relieves muscle spasm through a central action. Dyskinesia (abnonnul muscle movenents) caused by some ofthe drugs (nainly let.s. nerve cclls in the basal ganglia degcneratc! re_ sultine in lo* er production ofdopamine. '-\mantadine appears to potentiate dopaminergic responscs. cerebtal palsy.

Doxapram (Dopram) . Phendimetrazine . Stomach complaints . D€nial Decks . Sleep disruption .. Feelings of anxiely and nervousness . Strychine 142 Copyright O 20ll-2012 . Phenobarbital . Diuresis . Methylphenidate . Caffeine .Dental Deks . Coughing . Palpitations and arrhlthmias 183 Cop)right O 2011-2012 . Irritability .

with the cortex being the most and the :oinal cord beine the least excited. nerh.e. Analeptics and respiratory stimulants: doxapram and strychnine. but are occasionally indicated to stimulate respiration when a patient has pulmonary disease or to hasten recovery from a general anesthetic. CNS stimulants are a heterogenous group ofcompounds that produce various degrees of stimulation. It stirnulates the respiratory centers ofthe medulla and is able to cause bronchial dilation in patients $'ith asthma. Theophylline is the only xanthine important in the treatment ofasthma. Sl mpathomimetic amines include the amphetamines and other related agents fi.rlphenidate. tdke l. Note: Their use for respiratory depression caused by an overdose ofCNS depressants is generally not safe or recommended. sulfer side efects li'ctn hating too much calfeine. theophylline and theobromine. These agents have limited use. etc).. Theophylline and theobromine are weaker CNS stimulants than calleine. Analeptic is a term that refers to a CNS stimulant which has the ability to overcome drug-induced respiratory depression and hypnosis. but today they have only limited clinical application. Important: Caft'eine stimulates the CNS unequally. Note: It has a low therapeutic index and its metabolism is affected b1 ser eral other drugs. Caffeinism is a term used for people who are dependent upon catTeine ( is thought to occur ifyou have an intake ofabove 600 to 750 mg ofcafterne per day /rrore than 10 cups of coffeel..*** Phenobarbital is a barbiturate (sedative-hypnotic). They are used ro treat narcolepsy. They are potent CNS stimulants. reduce the urge to sleep and elevate the mood. obesity and attention deficit disorder. Xanthines include caffeine.tryer"amounts and neetl to keep drinking calfeine to function properll). In the past the CNS stimulants were widely used therapeutically. These stimulants improve mental alertness. Caffeine is the only approved OTC stimulant. phendimetrazine. . Drinking more than 1000 mg per day is well into :he to\rc range.

Controlled-delivery methylphenidrte (Metadate CR) . Atemoxetine (Str att eru) .ndrome in children . Attention deficit hyperactivity disorder (ADHD) . Mixed amphetamine salts (Adderal) . lnsomnia in children 184 Copltight O 20ll-1012 ' Dental Decks PIIARMACOLOGY Which of the following drugs is a mernber of the opioid family and reduces GI motility ? . Dexmethylphenidxte (Fo calin) . Loperamide (Imodiun) . Lorazepam (Ativan) .All of the following drugs on the right are used to treat what condition? .Denral Decks . Tourette's sy. Insomnia in adults . Diphenoxylate and atropine (Lonotil) . Extended-release methylphenid|te (Concefta) . Propranolol (hderal) 185 Cop)right aO 201 I 201? . Lisdexamfetamine (Vyanse) .

c sror oil. Serotonin 5-HT3 receptor antagonists: HCL fj$. It does not penetrate the cenffal nervous system like the opioids such as codeiner thus it can b€ sold ov€r the counter. It is approved for use in children and adults. Extended-release methylphenidate (Concerlq): idate.Thc . morphine dnri neperidine). reduction in hyperativity.Drugs used to treat ADHD: . and scopolamine A/arrderTrtScop) . dimenhydrln te (Dramamine). Lisdexamfetamine (Vyvanse): Lisdexamfetamine is a prodrug.Loper L Is an anti-diarrheal which acts on intestinal musclcs to inhibit p€ristrlsis. after adminishation it is converted to dextroamphetamine (Adderall) in the rntestines and/or liver. Atemoxetine (Struttera)t the brand name for atemoxetine. 2. another long acting form ofthe drug. Antiemetics:actonthc'vomitingcenter"inthemedulla-Thiscenterhasfourdifferentsourcesofstimuli. and an improvement in behavior. Antihistamines: meclizine (Antivert). this drug results in an increase in attention span.Diphenoxt-late is an anti-dianh€al and inhibits excessive GI tract motiliry and Gl propulsion. Antisecretory:bismuth st$sahcylate (P epto-B . atropine (Lomatil). ^mide (I m mod iu m) | . granisetron . .rr. is responsible for the effect of lisdexarnfetamine in ADHD. Adsorbents: attapulgile (Kaopectate) is mo I) R€member: Laxatives act in the revene manner ofthe anti-diarrheals and increase the motility of the CI . a long-acting form of methylphen- Antidiarrheals: ' Opiate and opioid derivatives . In children with ADHD. . the first non-stimulant approved for treating ADHD. \letamucil and methylcellulose. Commercial prcparations contain a sub-therapeutic amount ofatropine to discourage abus€. The dextroamphetamine. Diphenoxylat€ and. Anticholinergics: ..4/orl) ond ^t\sgtron HCL (Zotan). Examples include: magnesium hydroxide (Milt ry'Magnesid).hemoreceplor rrigger zone (CTz) is located outside the blood-brain barrier near the vomiting center in the medulla. Antidopaminergic: . dolasetron (Anzemer. . Adderal (dextroamphetamine): the brand name for mixed amphetamine salts which act the same as methylphenidate in treating ADHD. Tle] are used to trcat constipation. rcquires a prescription. . . Dexmethylphenidate (Foc in): a form of methylphenidate called dexmethylphenidate.t/i. J. Benzamidesi metoclopramide /Re8/dnl and fiimcthobenzamide HCL flgdnl . Methylphenidate (Ritalin)z arnrld central nervous system stimulant. unlike loperamide flrrodiu. . an amphetamine and stimulant for the brain. It communicares with th€ vomiting center after input is received from drugs and hormones. Metadate CR: the brand name for a controlled-delivery methylphenidate. . and palonosetron (. Is a member ofthe opioid family. Phenothiazines: prochlorpcrazine (Conqazi ne) a'nd prcmelhazioe (Phenerydn) . IIas no €vidence of drug abus€ or dependence (utllike other opioicls such os codeine. The classes of antiemetics are: .aci.

. Initability

. Xerostomia . Loosened teeth . Gum disorders . Sluned . Tremors

186 Coptright O 20ll,2012 - Dental Decks

Of the amino acid neurotransmitters listed below which one is an excitatory neurotransmitter?

. Glycine . Glutamate


(y -eminobutyric acid)

. None ofthe above

147 Coplright O 20ll'2012 - Dmral Decks


Excessive saliva is a prominent toxic effect ofmercury not xerostomia

of the chronic form, which results from the inhalation of the vapors ofdust ofmercurial compounds or from repeated ingestion ofvery small amounts. The presence of mercury in the body is determined by a urine test. Treatment may include gastric lavage with milk and egg white or sodium bicarbonate, chelation with British antilewisite (BlI), and fluid therapy.
Not€: British Anti-Lewisite (BAL) or Dimerc prol and p€nicillamin€ are two drugs currently marketed for promoting the excretion of mercury, lead, and several other agents. A few additional agents are available for the treatment of poisoning by metals other than mercury

These symptoms are all

k.9., edetote colciunt disodium for lead and deferoxamine for iron). Mercury that is absorbed into the circulatory system may be deposited in any tissue.
Higher-than-average accumulations occur in the brain, livel and kidney. Mercury does not collect irreversibly in human tissues. There is an average half-life of 55 days for transport through the body to the point of excretion. Thus, mercury that came into the bodl years ago is no longer present in the body.

foftr' .., ,._ :,

Children and adults wbo are to be treated for lead poisoning should only be given the Edetate Calcium Disodium (Calcium Disodium Versenate) form of


2. Penicillamine is also a highly effective chelator ofcopper and is ofprimary im-

portance in the management of Wilson's drsease Thepatolenticulqr degeneratiotr). 3. Deferoxamine is a drug that chelates to absorbed iron very well and is eliminated in urine. 4. For carbon monoxide poisoning the fteatment is 100%o oxygen therapy fzvolves breathing oxygen thxtugh a tight-ftting uask). 5. Cyanide poisoning can be treated with rapid oxygen administration and the antidotes sodium nitrite and sodium thiosulfate.

Chemicals that ransmit the signal from one neuron to the next are called neurotransmitlers They are synthesizcd in the ccll body or nen'e terminal of the pr€synaptic neuron. Neuroffansmitters are rcleased from thc s\napse and cross the synaptic cleft. The d€ndrite on the nerve cell body receives the signal. Various receptors on the posts!naptic membrane ofthe dendrite accept only certain neurotransmitte$.


the brain. 30 differcn! neurotrarlsmitters have been classified as amino acids, amines, and neuropeptides.

. Amino acid neutofransmitters: - Glutamate, GABA, and glycine. Glutamate is an excit|tory neurctransmitter. GABA and glycine are inhibitort neurotransmitters. GABA is the major inhibitory neurotransmitter within the CNS. - Include the catecholamin€s

histamine, and acetylcholin€,-dopamine,

norepinephrin€, and epinephrine





. \europeptides are also hormones; these include vasopressin, oxytocin, insulin, somatostatin, trin. substance P, -most endoryhin, and enkephalin. Remember:

Acetltcholin€: effects in CNS generated by interaction with a mixture ofnicotinic and muscarinic



. Dopamine:

catecholamine which acts thrcugh at least two subt?es D7 (activates aden![


(inhibits adenyl cjclase)

. serotonin:

is s-hydroxytryptamine which works through at lcast 14 subreceptor "trtPtominergic" OTe

Biosynthetic pathway


(l) Choline (taken up into nenevia action ofpermease) St€p (2) Choline acetylcholinesterase catalyzes the synthesis of Ach liom acetyl CoA and choline

2.Biosynthesis of NE and


Step (1) Tyrosine to DOPA (enzyme is tvrosine hvdrorylase Step (2) DOPAto Dopamine (enzlme is aromatic L-amino acid decarborylase) Step (3) Dopamine to NE (enz-vme is dopamine bela h)dro\lase) Step (4) fnorlb in the ddrenal nedulla): NE ro E lenzvme is phen ethanolamine N-meth translbrase)

Oral contraceptives block ovulation by inhibiting which ?TrlO ant€rior pituitary hormones below?

. Follicle stimulating hormone
. Growth hormone (GII)


. Th).roid stimulating hormone (TSll)
. Luteinizing hormone (I11)

. Adrenocorticotrophic horrnone (ACTH)

188 Coplrighr o 201 1,201: - Dental Decks

. The first statement is true; the second statement

is false

. The first statement is false; the second statement is true

. Both statements are true . Both statements are false

189 CoplriSht O 20ll-2012 - Dental Decls

In addition to the above effects, oml contraceptives produce altemtions in the genital trac! including changes in cervical mucus, rcndering it unfavomble for sperm penetration even if owlation occurs. Changes in the endometrium may also occur .endering it unfavorable for nidation (lnrp lantotion of the -fertili.ed owm). Esttogens and progesterone-like compounds (p/ogertrrs) are used for oml contraception.

. Estrogens: are a group of chemically similar steroid hornones. In humans, estrogens are made primarily in the female ovaries and in small amounts in the male testes and the adrenal glands, brain, and fat ofboth sexes. Estradiol is the most abundant and potent natural estrogen in humans. Other gstrogens inlcude ethinyl estradiol and mestranol. . Progestins: ar€ a gloup of chemically similar steroid homones as well. In humans, progestins are made primarily in the female ovaries and male testes. Progesterone is the most abundant and potent progestin in humans. Other progestins include levonorgestrel, rorethindrone, medroxyprogesterone,
norgestimate and norgestrel.
Types of oral contrac€ptives:

. Combination: oml

contraceptive agents usually contain both an estrogen agent and a progestin agent. Combination drugs include:

. ethinyf estradiol . ethinyl estradiol
. thinyf

and norethindrone fovcor 50, Brevicon 21, and Modicon 28) and fevonorgestrel fPolria 0.15/30, Alesse 28 and Aviane 21) estradiol and norgestrel (Cryselle, Ovral, and Oryestrel)

. Progestin-onfy: nor€ fiindrone (Micronor) . Emergency contrrception: levonorgestrol (P/dn B) \\'ernings/Prccautions with OIal Contraceptives:
. Tle risk of cardiovascular side effects increases inwomenwho smoke cigarettes, especially those who are
>.15 .veaN


. May increase the risk ofthromboembolism. Women with h)?ertension shouldbe encouraged to use anonhormonal folm of contraception.

\ote: Antibiotics have the potential to diminish the effectiveness oforal contraceptives. Advise patients to use additional method ofbirth control when taking antibiotics and oral contmceptives concunently.

the blood stream by binding to albumin protein, which is abundant in plasma. In this way, drugs can be carried to all the tissues and organs. A dmg which is bound to plasma albumin always has some fraction which is not bound. The unbound portion is free to leave the blood compartment to be taken up by tissues where the drug will elicit its pharmacological ellect. The remaining bound fraction of drug then aontinuously releases more free drug to be taken up by tissues. Eventually all drug in the blood compartment will be taken up by this process.

*** Most drugs travel though

lmportant: Interactions betw€en two or more drugs can occur ifthey compete for binding on the plasma albumin. If drug A is bound to albumin prior to the patient taking drug B, and drug B has a geater binding affinity to albumin than drug A, then when drug B is taken, it will displace drug A from albumin to result in large amounts ofunbound drugAwhich could lead to adverse reactions due to the sudden large amounts gaining access to the tissues.
One ofthe most fundamental aspects of drug action is the relationship between dose administered and the effect obtained (drugs are dose dependent), Dose and response are related and can be represented by a dose-response curve. There are two basic types ofdose-response curves:

. The graded dose-response (Dn, curve plots the degree ofa given response against the concentration ofthe drug. These curves are useful for determining characteristics ofagonists and antagonists. . The quantal dose-elTect curve: In this case, a given quantal eIlect is chosen (e.9., .t certain degree of cough suppression), and the concentntion ofthe drug is plotted against the percentage of a specific population in which the drug produces the effect. The median effective dose (8D50 or the dose at which 50%o of the individuals exhibit the specifed quantal effecr) and the median lethal dose (2D50 or the dose at which death is produced in 50'% oJ the expelimental animals in preclinical sludies) canbe estimated from quantal dose-eIlect curves. With this tlpe of curve, the relative effectiveness ofvarious drugs for producing a desired or undesired effect, as well as the relative safety between various drugs, can be determined.

Location ofpain .t Coplriehr O 201l'201? . andll (prothrombin) and anticoagulant proteins C and S? . Aspirin . Sex ofpatient . Heparin .X.Dental Decks .DentalDecks Z'\ Which of the following competitively blocks vitamin K-binding sites . Patient's weight .What are four criteri| to consider when selecting atr analgesic agent for a patient? . Type ofpain . Age ofpatient . Warfarin (Coumadin) . lX. Anagrelide t 9. Concurrent medication . Pregnancy t 9{) Coplrighr O 20ll 2012 .nd inhibits the synthesis of vitamin Kdependent coagulation factors VII.

Adult ) When calculating dosage. Type ofpain: . Oral anticoagulants do not reverse ischemic damage or lyse an established thrombus but rather prevent extension ofthe existing thrombus and the formation ofnew thrombi by blocking synthesis of clouing factors. Severe . his/her physician should have documentation of INR values to assess anticoagulant effects. especially with the elderly. An INR value of I means normal prothrombin times of approximately 12 seconds. provides the most widely used system to grade the teratogenic effects ofmedications. warfarin decreases liver synthesis of vitamin K-dependent clotting factors by 30o% to 50olo. D. normal blood clotting would be present. use acetaminophen (Tylenol) for pain control. Moderate 2. Corcurrent medications: Consider unwanted interactions. in the treatment ofpulmonary embolism. Elderly: drug response is affected by age-related changes in physiology and pharmokinetics 3. Al- ways check medical history. For this reason.t hr) vs. If patient is on anticoagulants. X category medications: Studies in animals or humans have demonstrated fetal abnormalities or there is positive evidence of fetal risk based on adveme teaction reports from investigational or marketing experience. and the risk ofthe use ofthe drug in a pregnant woman clearly outweighs any possible benefit (/or example. drug use in pregnant patients is a source of special concem (clrcck with patient s OB/GYN). . and in the treatment ofvenous thrombosis. safer tlrugs or otherfotms of therapy are available). and multiplied by a constant. C. At therapeutic levels. l{ote: Enhanced anticoagulant effects are seen when these drugs are combined with aspirin. body surface area and renal hepatic be taken into account . Infant . Ag€ ofthe patient: . INR values greater thar I indicate that there is an anticoagulant effect. Pregnancy: Because virtually any drug a pregnant womar takes can cross th€ placenta and enter the fetal circulation. The FDA assigns a safety category for medications by using a slefter system: A. 4. the govemm€nt agency that ovemees the safety ofdrugs. 3 and even up through 6. with A being considered the most safe. Factor WI has the shortest halfJife {6. The higher the INR value. These clotting factors have different half-lives. the height. the greater the anticoagulant effect.Criteria considered when selecting an analgesic agent: l. or both. INR stands for International Normalized Ratio and essentially is the ratio of the prothrombin time measured in the patient divided by a standard prothombin time value. Child . Mild . FDA Rating System for the T€ratog€nic Eff€cts of Drugs: The FDA.f function must . Many patients taking anticoagulants have INR values of2. Oral anticogulants are used after a myocardial infarction to prevent coronary occlusion. and X. Patients on anticoagulant therapy may have excess bleeding after dental treatment. B. weight. factor lI andx (up to 72 hr).

Dental Deck! . Immune globulins . Breast cancer . Osteoporosis . Mucositis caused by radiation therapy 193 Coprighr O 20ll-2012 .. Interferons 192 Coplrighi O 201 I -20 12 . Keratinoc). Emesis caused by cancer chemotherapy .te growth factor .Denral Decks Grunisetron (Klttil) rnd ondansetron (Zofran) *e selective 5-IIT3 receptor antagonists used to treat what condition? ) . Immunosuppressants .

recurring genital warts (interferon alpha-n3) and treatment of multiple s clerosis (interferon beta. as keratinocle growth factor promote cell proliferation and angio- The 5-HT3 receptor is a serotonin receptor which when activated during chemotherapy for cancer. Growth factors such genesis. Both granisetron and ondansetron are indicated for prophylaxis of chemotherapy-related emesis.a variety ofconditions including: hairy cell leukemia (intederon alpha-2a) chronic hepatitis B (interferon alpha-2b). Other s€rotonin 5-HT3 receptor antagonists include: dolasetron (Anzemet) and palonosetron @/oxr) \ote: 5-HT3 stands for 5-hydroxytryptamine type 3 receptor. prophylaxis of nausea and vomiting associated with radiation therapy. and prophylaxis and treatment ofpostopera- tive nausea and vomiting (PONV). . causes emesis (nausea and vomiting). Immunosuppressants are drugs such as cyclosporin which prevent organ transplant rejection.I a) . Interferons are used for Immune globulins provide passive immunity by increasing antibody titers.

Denlal Decks The following drugs belong to what pharmrceuticsl class of agents: . Interferons . Immunosuppressants . Immune modulators . Colony stimulating factors 151 Copyright O 201 I .. Trastuzumab . Monoclonal antibodies .2012 .Dental Decks . Adrlimumab . Monoclonal antibodies . Alefacept . Interferons . Inflixim|b . Colony stimulating factors t95 CoplriSh O 201l-2012 . Immunosuppressants . Irnmune modulators .

Infliximab (Remicade) is a monoclonal antibody used to treat ankylosing spondylitis.Pimecrolimus (Elidel) is an immunosuppressant agent used for treatment of mild to moderale atopic dermatitis. Sirolimus (Rapamune) is an immunosuppressant agent used for prophylaxis of organ rejection in patients receiving renal transplants. Crohn's disease. It is used to treat active rheumatoid anhritis. Like adalimumab. Adalimumab (Humira) rs arecombinant monoclonal antibody that binds to human tumor necrosis factor alpha (TNF-alpha) receptor sites. infliximab works by binding to TNF-alpha receptor sites. Tacrolimus (Protopic) is an immunosuppressant agent used to treat moderate to severe atopic dermatitis in patients not responsive to conventional therapy. and rheumatoid arthritis. . Trastuzumab (Herceptin) is a monoclonal antibody which binds to the extracellular domain of the human epidermal growth factor receptor 2 protein (HER-2) ' It is used for the treatment of patients with metastatic breast cancer whos€ tumors overexpress the HER-2 protein and who have not received chemotherapy for their metastatic disease. Afefacept (Amevive) is a monoclonal antibody used to treat moderate to severe plaque psoriasis.

Improve walefi ness during daytime sleepiness . Echinacea . Treat mental depression 196 Coplrighi O 201l-2012 . Ginseng t97 Coplriglr () 2011.2012. Manage psychotic disorder . DmialDecks .Dental Decks Which herbal supplement below is known to be somewhrt €ffective in treating rnild forms ofmental depression? . Ginkgo biloba . St Johls Wort . Improve salivary flow in dry mouth disorders . Garlic ..

a natumlly-occurring compound with anticoagulant or bloodrhinning effects. Of all the herbal supplements available to the consumer. This effect is similar to those antidepressants u'ithin the flnoxetine (Plozac) fatrily. Some studies have shown the St Johns Wort can inhibit the re-uptake of serotonin at neurcnal synapses resulting in the elevation of serctonin within the CNS. It should not be combined with warfarin or other anticogulants- S. Ginseng is a herbal supplement used to stimulate the immune system.Modafinil (Provigil) represents a class of central nervous system stimulants used to improve wakefuhess in patients with excessive daytime sleepiness associated with narcolepsy and shift work sleep disorder. The exact mechanism of modafinil is unclear. Ginkgo biloba is a herbal supplement used as a peripheral anery vasodilator Garlic is a herbal supplement used to lower cholesterol and to inhibit platelet aggregation resulting in a decrease in blood clotting. has long been used in Europe to treat an enlarged prcstate or benign prostatic hyperpla- . however part of its action may be do to decreased GABA-mediated neurotransmission. It also has an unlabeled use to treat attention defi cit/hyperactivity disofier (ADHD). and ease spasm and discomfort in the digcstive tract. The active constiuents of chamomile have anti-inflammatory palmetto sia (BPH). Echinacea is a herbal supplement and immune stimulator used to minimize the severity ofthe common cold and seasonal flu. St Johns Wort is associated with use as a mild antidepressant. Chamomile has a long history of use in Europe for digestive ailments. \ote: Chamomile contains coumarin.

Increase the effectiveness ofmedications . Naratriptan (Amerge) .Dental Decks AII ofthe following drugs are serotonin 5-HT1a receptor agonists us€d to trert migraines EXCEPT one. Increase the toxicity ofmedications 198 copyriSlrO 201 | -2012 . Frcyatiptan (Froya) . Zolmrtrrptan (Zomig) 199 Coplrighr O 20ll-2012 . Donepezil (Aricept) .. Aknolnplan (Axert) . . Kzatiptan (Mamlt) . Decrease the effectiveness ofmedications .Whrch ow is the EXCEPTION? . Sumalliptan (Imitre.Dental Decks .

which is added to many migraine combinations. The most common form ofdrug-drug inleraction is one drug affecting the metabolism ofanother drug. Ergotamine derivatives demonstrate partial agonist and/or antagonist activity against dopamine. Ergotamine derivatives have three primary actions. St. helps to promote constrictive properties. which exerts an analgesic effect. Important:The rate ofdrug metabolism can vary greatly. . and ginkgo /gir. Note: Methylsergide (Sansert) blocks 5-HT2 receptors for prophylaxis against migraines." All 5-HTl receptor agonrsts (triptans) have a similar chemical structure and a comparable mechanism of action. Ultimately. The antihypertensive nifedipine Drug-drug interactions can involve prescription or nonprcscription fo). 4. a mild sedative that acts centrally to allay an"riety. Examples include: erotamine tartrate (C aferyo t) and dihydroergotamrne (D H E .4 5) Combination drugs: Midrin is a combination capsule that contains 65 mg of isometheptene mucale (an ergotamine derivative). depending on their site. and reduced transmission in trigeminal pain pathways. 325 mg of acetaminophen. Inhibition ol metabolism: is a process by which one drug either competes for metabolism ofanolher or directly inhibits drug-metabolizing drrJgs. . and with which drugs. Echinac€a has potential interactions with immunosuppressants. More rapid metabolism of a drug equates to less active drug available and less fdec/edre4 effectiveness. I nd uction of metabolism : is a reaction to certain drugs in *. resulting in a reduction in the €flic! ofthe other drug. and enhances absorption. The sedative midazolam .hich the number of liver enzymes increases. *** Donepeztl (Aricep. is a cholinesterase inhibitor used in the treatment ofAlzheimer's disease.. They (1) depress central vasomotor centel (2) constrict peripheral and cranial blood vessels. John's wort is the herbal product most often reported !o be involved in drug-herb interac- l. data indicates probable intcractions betwe€n St Johns Wort and iis effect in decreasing the actions ofihe following drugs: . The antirejection medication cyclosponn . Note: Caffeine. rdditive cardiovascular effects when taken with caf]eine. -\otee: *ith '' g. Dnrgs interact by acting at lhe same receptor or signal transduction paihway. intracranial blood vessels that become di)ated during a migraine attack and on nerve terminals in the trigeminal system. 2. Migraine medications: . depending on the cytochrome p450 isozyme profile the next few years. genetic screening ofthc c)'tochrome p450 system will be able to idenriry $hich patients are likely to develop toxicity or drug-drug interactions. Remember: Chamomile contains coumarin and should not be used in patients taking warfarin for fear ofan additivc affect. or more commonly. which results in cranial ves- sel constriction. a drug may af]'ect the pharmacokinetics ofanother dnrg. Many herbal weight loss and "herbal speed" products rely on the pharmacodynamic interaction and pseubetween ephedra and caffeine. fs erotonin antagotrist) and is used . .(go 6i1o6.St Johns Wort may induce the cytochrome P450 enzyme system to result in a more rapid metabolism ofmany drugs in rhis pathway. Therapeutic activity is caused by activation ofthese receptors. involving eifier induction or inhibition ofmetabolizing enzymes. Two primary alkaloids containcd in ephedra -ephedrine At higher doses. The most commonly used migraine medications are the serotonint f5-11fl receptor agonists. Herbal medicines such as l. 5-HTl s and 5-HTtD receptors located on the extracerebral. metabolic screening based on studies using highly-specific probcs could bclp decide whether or not a drug is ola patient. and (3) reduce extracranial blood florv and decrease hyperfusion ofthe basilar artery area. The HIV-l protease inhibitor indinavir . inhibition of neuropeptide release. commonly known as the "triptans. Over prescribed. . and 100 mg ofdichloralphenazone.rlic. doepbedrine -have the ephedra-caffcine interaction has been cited as a cause ofdcath. and alpha-adrenergic receptors. ginseng. are thought to interact anticoagulant or antiplatelet th€rapy. Specifically. tryptaminergic.

the second statement is false .Dental Decks Nlcotine is rapidly absorbed across the pulrnonary caplllary membrane and is delivered to the brain in high concentration within seconds of inhalstion. Liotbyr onine (Cytome l) . The nasal spray bas the fastest delivery of the NRTs and more closely resembles the ons€t ofthe nicotine effects ofsmoking.righr O 201l-2012 D€ntal Decks . Both statements are true .. The first statement is false.2012 . Methimazole (Tapazo le) 200 Cop)r'ghr O 201 1. Liotrrx (Thyrolar) . . Levothyroxine sodirtm (Synthroid) . the second statement is true . The first statement is true. Both statements are false 201 Cop).

Each cartridgc contains l0 mg nicotinc and dclivers 4 mg. h current usc arc thc nicotinc rcplaccnlcnt thcrapy l\'Rl products. tachycardia. 3. \fan) phannacologic approachcs havc bccn uscd to hclp pcoplc stop smoking. They arc not mcant to belp gct rhrough a long flight or an all-day mccting in a nonsmoking building. 6.thyroid hormone synthesis is nrne (Tj).Thyroid medications: . Thyroid suppressants: used to treat hyperthl. Methimazole (Tapazole) .1. Name Nicorette Formulation Gum Nicorine replacement lherapy Nicotine polacrilex Nicotine Nicodem CQ Habitrol Transdemal Transdemal Transdermal Transdermal Nasal spray Nicohol ProStep Nicotrol NS Nicotrol inhaler Co1nmit Anridepressant N Oral inhaler Tablet Tablct Bupropion Varenicline Zyban. Thc nasal spray has thc fastest delivery ofnicotinc ofthc NRTs. 5. Thc gum dclivcrs nicotinc faster than thc patch and can be uscd for incidcncc ofcraving. \icotine rcplaccmcnt producls are meant to help palients stop smoking. dianhea. Its mcchanism ofaction is unclcar 7. Propylthiouracil (PIUI \ote: These drugs inhibit thyroid peroxidase. \ote: Thyrogen is a recombinant DNA source ofhuman TSH useful in the management and lreatment of thvroid cancer oatients. . Liothyronine (synthetic Tj) ' Liotrix (T4. . Adverse side effects include nervousness. Levothyroxine sodi|dm (synthetic T4) . or triiodothyroulin for the production of the thyroid hormones .roidism . and thoughls ofsuicidc. !arenicline is thc ncwcst dmg in thc smoking ccssation arscnai. scvcrc mood swings. abnormal drcam statcs. tremoq weight loss and heat intolerance. ofNRT' Patchcs arc availablc in l5 and 2. a paticnt Class Generic Name Tr. and its effects are cumulative over several weeks. Wellbutrin icotine rcceptor agonist Chanlix used tvpe \ote_q ). bupropion r'4'han ll/elbutriD zt\d \arcnicline (Cha tn).73= 4 l) Note: These drugs are usually taken orally in a single daily dose. Thc lozenge also comcs in 2 mg and 4 mg doscs and dclivcrs about 25% morc nicotinc than gum. Thc gum is availablc in two strcngths: 2 mg and 4 mg. Through reduced absorption of iodine. nausea. T3 has a more rapid onset ofaction and dissipation ofaction. lt has a relatively slow onset of action. and agranulocytosis.'lhcp^tch (trunsdamdl) is thc most commonly 2l mg strcngths for trcatmcnt inilialion. Adverse effects include rash.The treatment of choice for hypothyroidism is T4. . nausea. Thyroid supplements: used to treat hypothyroidism . preferably before breakfast. It also contains I ng mcnthol. Inhaled nicotine (xslng the nirctine ifihaler) is absorbcd in lhc mouth not in the lungs. Bupropion as a systcmic medication sccms to rcducc thc craving forcigarcttes orlhc urgc !o smokc. Note: Thc FDA has issucd an alcrt to providcrs to monitor patients taking this medication for dcpressior.. which is an enzyme expressed mainly in the thyroid that liberates iodine for addition onto tyrosine residues on thyroglobthyroxine (I4.

. Hydrocodone . Anti-inflammatories . Oxycodone . Morphine . Fentanyl 203 CopFighr O 201l-2012 .Denlal Decks . Antidiarrheals .Dental Decks . Antitussives . Preanesthetic medications 202 Coplright e 20ll-2012 . Analgesics . Codeine . Meperidine .

as: .As the severity ofintoxication increases. They cause constipation and thus are effective antidiarrheal agents.E: lucuron id e). producing alteralions in reaction to painful stimuli. It is the only narcotic agent tbat does not cause miosis lPupillary con5. They suppress the cotgh reflex (tntitussive). ln combination with acetaminophen it is known as P€rcocet or Tylox. i\oq: '. nightmares and insomnia. \ote: Death from acute intoxication by an opioid analgesic is the result ofpmfound. direct respiratory depression. Abuse can and does occur with all the narcotics.. A DEA number is required in order to prescribe narcotics. Opiate rcccptors in each of thcse areas interact with neurotransmittcn ofthe autonomic nervous system. . coma ensucs. They are all controlled drugs falling under DEA Schedule II or DEA Schedule III ofthe schedules of controlled substances. Dro\\'siness . 3. Buprenorphine fsrrrle.rr pol€r. lightheadedness. and limbic system. Orthostatic hypotension @upillan.l50 2D6. thalamus. Remember: L Codeine is weaker f/e. Meperidline (Denero. is an opioid partial agonist uscd to treat opioid dependence. Respiratory depression . This relatively minor structural change pro\ldes codeine with significant oral effectiveness. a narurally occurring opiate tha! is metaboliTed chiefly through glucuronidation by uridine ciphLriphare glucuronosyl transferase fUG4 €nzymes in the liver These enzymes produce an active analgesic meiaboltle ( m o rp h i n e. Euphoria . Depression ofthe cough reflcx . dizziness and nausea. 6. irregular/labored breathing /dyspnea). has a similar potency as morphine. Methadone (Doloprl. is more potent than codeine but less potent than morphine butjust as addictive.. \fentalcloudrng . bminstcm. 3. than morphine and less addictiv€.6 .a : . 11 is converted to morphine by cyrochrome p. 2. Note: It diffcrs from morphine in that a methoxy (-OXIIj) substitution replaces the hi dro\yl (-OH) group on the aromatic ring ofthe molecule./plls/ and depressed respimtion. Respiratory d€pression is dose related and is the cause of death in narcotic drug overdose.. When used as preanesthetic medications. Nausea and vomiting .Opiates are very effective analgesics. In combination with acetaminophen it is known as :. Opioid analgesics are thought to inhibit paintul stimuli in the substantia gelatinosa ofthe spinal cord. Some common side effects ofopiates (narcotics) include: sedation/drowsiness.e) is an opioid agonist used in maintenance for treating opioid addiction. Other less common adverse effects are vomiting. h)?otension. It can happen with any of the narcotics. rcticular activating system. opiates permit a reduction in the amount of general anesthetic required for surgical anesthesia. It has a shorter duration ofaction.. Decreased peristaltic motility . . fhc opioid action ofthc drug manil-e\1. ox]codone vicodin and Lorcet. \Iorphine is Srgri and s]mptoms ofacute opioid intoxication:!he intoxicaled person is stuporous or asleep and has cons-icied pupils /pir-poi t p?. \lrosts constriction) . l. HJ''drocodone has a similar potency as morphine.

Which sdverse effect is associated with opioid anNlgesics and not non-narcotic pain relievers? .DenlalD€cks PIIARMACOLOGY All ofthe folfowing are opium alkaloids.EXCZ'PZ1O1V? . Codeine 205 Cop). Vomiting . EXCEPT oae. Morphine .right O 20ll 2012. DenialDecks . Respiratory depression 20t Coplright C 20ll 2012 . Which one is the. Allergic response . Meperidine . Nausea .

Nalbuphine /?fuDaif . Diphenoxylate (in Lomotil) . Morphine . Oral form can bc vcry effective for cancer pain. \ri!h aspidn or acetaminophen to Can be used instead Le\'olphano! Hr"drocodone Oxr codone Pentazocine lV or IM: 4 hours tsy mouih: 4 hours By moulh: 4-6 hours Bv mouth: 3-4 hours By mouthr up to 4 hours oral form is strong. Alphaprodine (Nisentil) . of Chernical classihcation of opioid analgesics: Opium alkaloids: . When opioids are appropriately used. Meperidine (Demerol) . Sufentanil (&r&rta) . Aboul as strong a codeine. Death secondary to opioid overdose is nearly always due to respiratory depression. Percocet and Tylox) Synthetic narcotics: . )Iorphine group: . Methadone group: . Oxymorphone (l'l umorphan) . Hydrocodone (in Vicodin) . Loperamide (in Imodium) . Methadone (Dolophine) .The most significant and well-known adverse reaction to opioids is respiratory depr€ssion. especially in the elderly. lV or lM: 2-3 hours By rnouth: 3-4 hours Sustaincd relcase: 8-12 hours Codeine By mouth: 3-4 hours Taken \lith aspirin or acetaminophen Less potent than morphine Meperidine Methadone Propoxyphene IV or IM: about 3 hours Can cause seizurcs. tremors. Propoxyphene (Darvott) . Meperidine group: . and muscle spasms By mouth: not very effective Bv mouth:4-h hours. Can cause confirston and arlxiety. Alfentanil (Alfenta) . Codeine Sl nthetic deriYatives: . Hydromorphone (Dilaudid) . Drug Morphine Length ol Effcctivcness Other Information Starts to work quickly. Codeine group: . Fentanyl (Sublimaze) . the risk of severe respiratory depression is generally small as tolerance rapidly develops to this effect. somelimes longcr By mouth: 3-4 hours Also used for treatins heroin withdmwal Gererally taken treat mild pain morphine Usuallv combined wirh acetaminophen Usually combined with aspirin or acetaminophen Can block painkilling action of other opioids. Oxycodone (in Percodan.

Ibuprofen 206 Cop). Enkephalins .Dental Decks .D€ntal Decks . Propranolol . Naloxone .. Morphine .2012 . Dynorphins 207 Coptrigln @ 20i 1. Morphine .righr O 201 I . Beta-endorphins .2012 .

and naltrexone (Rena) Lnclude: . . and supression ofopiale withdrawal. inhibition ofneurotransmitter rcleasc f.. Nalmefene (Revex) and naltrexone (ReWa) are the other two narcotic reversal agents used to reverse the respiratory depressive effects olthe narcotic analgesics. movement. opiate receptors in the CNS mediate analgesic the primrry alferent terminals in the spinal cord and activrtion ofdescending inhibitory controls in the midbrain. influence feeding behavior at the hlpothalamic levcl and function with other cndogenous opioids to regulatc the cardiovascular systcm. The opioid reccplors all have a common general strucfur€. intramuscularly or subcutaneously. Note: The €nkephalins are considered to be the q?ical agonist tbr this rec€ptot L kappa (K) mediate spinal analgesia. allowing i! !o diffxse within the plasmn menbmne. *** Opioid analgesics (i. Opioid receptors: l. \ote: The dynorphins are (!) (6) thought to be the R?ical agonist for this receptor Sites of analgesic action of opioids: The opioid drugs produce analgcsia by actions at several levels ofthe ncwous system. propoxvp. \{eperidine (Demextl) . They are characleristically G protein-linked receptors enrbedded in thc plasma nrembrane ofneurons. Note: Naloxone does not have agonist activity at any opioid receptors. in particular. Beta+ndorpbins bind to opioid receptors in the brain and have potent analgesic activity. respiratory depression. mu mediate morphinelik€ supraspinal analgesia. . nalmefene (Revex). and sedation. The G protein moves within the an cnzyme or an ion channel. Enkephalins bind to opioid reccptors in the brain and are more widely distributed in the brain than lhc bera-endorphins. Fentanyl \ote: Naltrexone (Rel/ia) is also used to treat alcohol dependence. membrane until it rcaches ils larget Opi[)id receplors in lhe centml nervous system are thought to be activated by endogenous chemicals under Fh\ iiologic condirions. and behavior .ftcn€. Morphine . Naloxone is given intravenously. Overdose of narcotics results in respiratory depression and death due to respiratory shut down. physical dependence. della mediate antagonist activity.e. Hydrocodone ' Oxycodone . Codeine . motphine. Opioid agonists occupy the same receptors as en_ dogcnous opioid peptides. respiratory depression. They decrease presyraptic release ofneurotranmitters and incrcasc postslnaptic potential. a portion ofthe G prorein /Gtl is activated. Nolei The protot)?ical opioid agonist for this receptor is morphine. mood. €uphoria.) mimic endogenous opioids at CNS opiate recepiors. Some research supports the theory that they regulate pain at the spinal cord level. Typical narcotic analgesic drugs which are reversed by naloxone (Narcan). mepericline. codeine.. eL. fie body coniains three types ofthese chemicals that produce morphine-like effects -cithcr . Seem !o play a role in pain perception. Once the receptors are bound. raising the pain threshold and increasing pain tolerance.Naloxone (Narcaz) is a narcotic antagonist and is used in medical emergencies to teverse narcotic overdose. Naloxone will reverse the respiratory depressant effects ofthe narcotics thus counteracting the lethal effects of these agents. mitosis. and its analgesic activity is considered to depend on its binding to this reccptor 2. Dlnorphins are the most powerful ofthese cbemicals and are lbund throughout the central and peripheml nen ous syslems. and both alterthe central release ofueurotransmitters ilom afferentrerves sensitive to no\ious stimuli.

Oxycodone (component of Percocet) . Acetaminophen . Fentanyl 204 Coplriglit C 201 I -20 l2 . Aspirin 209 Cop)right @ 201 l'2012 . Ibuprofen (Motrin. Advil) .Denral Decks . Hydrocodone (component of Wcodin) . Hydrocodone with acetaminophen .Dmral Decls . Codeine . Meperidine (Demerol) . Morphine ..

l. 4. Thus. Lorcet. Hydrocodone and the entire drug class ofnarcotic analgesics do not affect blood clotting and will not enlance the anticoagulant effects of warfarin (Coumadin). and lllox. Fentanyl is available as a transmucosal preparation known as Actiq. This action would enhance the anti-coagulant effect of warfain (Coumodin) to increase the risk ofbleeding. hydrocodone products are commonly the drues ofchoice. 8. Morphine is not used in dentistry because ofits high addictive liability. Oxycodone in combination with ibuprofen is known as Combunox. 3. Common brand names for this combination are Vicodin. Ibuprofen and other non-selective NSAIDs (inhibitors of both cyclo-oxygenase I and q clo-orygenase 2 enzymes) snch as naproxen (Anaprox) and flurbiprofen (Ansaid) inhibit platelet aggregation. Codeine in combination with acetaminophen is known as Tllenol #3. . 2. a trarsdermal patch formulation known as Duragesic and as an intravenous prepa- ration known as Sublimaze. as antitussives. It is more potent than codeine. Ilydrocodone in combination with ibuprofen is known as Vicoprofen. Aspirin inhibits platelet aggregation to potentiate the anticoagulant effects of warfarin (Coumadin) and increase the risk ofbleedlng. Narcotics with acetaminophen can be given safely to patients taking warfarin (Coumadin). Acetaminophen is a non-narcotic analgesic that do€s not affect platelet aggregation nor does it affect the coagulation pathway. and as antidiarrheals. Oxycodone in combination with acetaminophen is known as Roxicet Percocet. Acetaminophen can be given safely to patients taking warfarin lCoumadi . it will not affect the anticoagulant nature of warfartn (Coumadin). Meperidine (Demerol) in combination with promethazine is known as Mepergan Fortis. Maxidone. Oxycodone alone is klown as Oxycontin. and Zydone. 9. Note: They are administered with caution to patients with head injury or those with a history ofdrug abuse and dependency. 6. 5.Therapeutic indication for opioids (narcotic analgesics) are the relief of moderate-tosevere pain. 7. Among the opiates available for use in dentistry. Hydrocodone in combination with acetaminophen is known as Vicodin. as analgesic adjuncts during anesthesia. as preanesthetic medications. Hyrocodone with acetaminophen is a combination ofa narcotic analgesic with acetaminophen. Lorcet and Lortab. Lortab.

Insomnia .righl O 201 I .D€ntal Decks Which drug is r synthetic opioid analgesic used as an inkrvenous sedative and is more potent than morpbine? . Peptic ulcers . Propoxyphene (Danon) . Meperidine (Demerol) . Constipation 210 Cop'.2012 . Fentanyl 211 Copldght O 201 l'2012 .Dental D€cks . Pentazocine (Talwin) . Nausea ..

Fentan!-l (Sublimaze)is a potent narcotic analgesic used primarily as an intravenous supplement during conscious sedation procedures or proccdures requiring general anesthesia. is a CNS stimulant. Nor do they cause insomnia. It is not a scheduled drug. The cause of death from overdose ofnarcotics is respiratory depression and shut down ofthe respirarory sysrem.lzine ard tru llcypromine) Pentazocine (Talwin) is chemically related to morphine and has weak analgesic properties. Tramadol (Ultran) is an opioid partial agonist. Darvocct-N 100 has low abuse liability. l\-ote: lt is less potent than codeine and a metabolite. Note: Talwin Nx tablets contain naloxone which is added to deter misuse.g. it is less potent than morphine and much less potent than fentanyl. It is taken orally and not used inlravenously. 1t is mixed agonist-antagonist drug. lmportant. Note: Fcntanyl congeners include Alfentanil.. having agonist activity at some reccptom and antagonist activity at other rcceptors. Meperidine (Demerol) is also wed as an oral medication for pain control aftcr dental surgery. The most serious side effect of the narcotic analgesics is respiratory depression. a Propoxyphene fDanon) in the form ofpropoxyphene napsylate with acetaminophen is known as Darvocet-N 100 and is useful tb. normeperidine. . is a CNS stimulant. phenylzine and tranylcypromine). pain control after dental surgery. Use great caution in combination with MAOIs (e. It is not used intravenously to produce conscious sedation. phen.g. Pentazocine has abuse liability. norpropoxyphene. Sufentanil. However. but rather would cause drowsiness and sedation since narcotics depress the conscious centers of the brain. Meperidine (Denerol) is used as an intravenous supplement during conscious scdation procedures. Contfaindicated with MAO inhibilors (e. and Remifentanil. Narcotic analgesics do not cause peptic ulcers..The most common side effect of the narcotic (opiqte) analgesics is nausea. Fentanyl is also avaifable as a lollipop-type lozenge (brand name Actiq) for transmucosal absorption and as a transdcnnal patch (brand name Duragesic) for dclivcry thrcugh a patch applied to the skin. Fcntanyl is 80100 times more potent than morphine. Note: A mctabo- lite.

The anterior thigh 213 Coplright O 201 I -2012 . Which one is the EXCEPTIOM . The buttocks . Hydrocodone .Dental Deks . Voltaren 212 Cop'.. The biceps muscle . Oxycodone . The deltoid muscle . Meperidine (Demerol) . Morphine .D€ntalDecks AII of the followitrg sites are generally accepted for IM injections EXCEPT one.righr O 20ll 2012 . Codeine .

a Absorption from an intrarnuscular injection is often faster and there is abilit]' than with oral administration. Opiate drugs used in dentistry to provide pain reliefafter dental surgery include: . They are also klown as narcotic analgesics since the actions ofthis family is to cause drowsiness and sleep as a side effect. higher bioavail- Proper depth of needle in muscle: In big muscle (adult) go in one inch. The opiates produce drug dependence leading to addiction. Never go beyond two-thirds ofthe needle length. Psychic dependence is unlikely if an opiate is taken for a short period for pain relief. and tolerance can develop upon repealed administration. in children go in one-quarter of an inch. the anterior thigh is usually the place to give IM injections. . Physical dependence is a condition in which continued administration of the drug is required to prevent unpleasant withdrawal symptoms. Psychic dependence. Oxycodone (Percocet rylox) .*** Voltaren is a NSAID which do not produce drug dependence and addiction. Tolerance occurs when increasingly large doses ofopiate are required in order to produce the same degree ofanalgesia. physical dependence. Codeine . The other analgesics belong to the opiate class of drugs. Hy drocodone O)icodin) . Meperidine (Demerol) *** For young children.

Oral ingestion .Dental Decks .2012 . Pharmacologic agonist . Topical administration .. Subcutaneous inj ection . Intravenous injection 215 Coptrighr O 201|.D€ntal Decks . Pharmacologic antagonist 211 Copright C 201 l-2012 .

Transdermal . painless and economical. . Enteraf administration @y v. Common routes of administration ofdrugs: 1. Competitiv€ antagonism occurs when a response can be achieved by increasing the dose of agonist in the presence ofantagonist.Drugs that bind to physiologic receptors and mimic the regulatory effects ofendogenous signaling compounds will produce a pharmacologic effect as a result of binding to the receptor. the agonist drug cannot reach the receptor site to proWhen artagonist effect. Or^ltum 3. Inhalation 4. Acts very rapidly. a drug which binds to the physiologic receptor but does not trigger an is present. where it is promptly absorbed . Subcutaneous - injection beneath the skin. An antagonist is 1.q) ofthe intestine or GI tract) .diectly into the bloodstream. A partial agonist is a drug which acts on the physiologic receptor but elicits an effect which is only partly as effective as an agonist drug.the drug in solution (enema) or suppository form is inserted into the rec- . Buccal or sublingual a tablet is placed under the tongue or in the cheek (most common route). It is the most convenient for safe drug administration. Intravenous (lV) . the drrrg is swallowed. . Parenteral administration (not by wa!" ofintestine or GI tract) . Noncompetitive antagonism occurs when a response cannot be achieved with increasing doses of agonist in the presence ofantagonist. A drug that elicits a full response through this process is referred to as a phar- macologic agonist. duce an effect. the drug is placed on the skin for a local effect. Intramuscular |1M/ injected into a muscle area. Rectal . Topical - the drug is given as an aerosol into the respiratory tract. It is safe. 2. Absorption may be less rapid.the drug is placed within a "patch" and placed on the skin to be absorbed into the systemic circulation. administration 5. 2. .

Kidneys . Does. intrinsic . Gastrointestinal tract 216 CoplriSht O 201 l-2012 . Does not. Does not.2012 . extrinsic . Lungs . Brain .Dental Decks . intrinsic 217 copyiShr o 201 I .Dertal Decks . extrinsic . Does. Liver ..

First.. \. G protein-coupled receptors: When drug binds to these receptors. cell surface protein kinases): These kinases exert their regulatory effects by phosphorylating proteins within the cell which alters the cellular biochemical activities. Phas€ II reactions: . Conjugations occur in the liver. . . an active parent drug may be converted to a second active compound which is subsequently con- verted to an inactive compound. the parent drug is effectively rendered inactive and transport€d out ofthe body by this process. The most common r€action in drug metabolism is an oxidation reaction in which oxygen in the form ofhydroxyl group is attached to the drug molecule.. Conjugation ofdrugs results in polar. Conjugation reactions involve coupling the drug with an acid present in cells (rrsaalh glucuronic acid). the active parent drug can be converted to the inactive metabolite. Receptors as enzymes 6." . lA2). drug metabolism occurs in three basic pattems. thirdly an inactive parent drug may be . Receptors in c€ll nucleus: . in a drug effect. Thus.Hepatic metabolism of drugs occurs in Phase I reactions catalyzed by a microsomal mixed-function oxidase system (a/so known es the P-450 system) and in Phase II reactions known as conjugation reactions. This results Receptors for steroid hormones are soluble DNA-transcription factors within the nucleus that regulate the transcription of specific genes. drugs can also cause the alteration in biochemical activities resulting in a drug effect. kidney and to a lesser extent in other tissues.e. This alters the cell's membrane potential to result in a drug effect. .Thusrhe enzyme CYP lA2 is a distinct drug metabolizing enzyme that converts a variety of drugs to the oxidized product. Phase I reactions: . water-soluble compounds that are rapidly excreted in urine. second messengers are produced such as cyclic AMP to produce an effect within the cell. Modification ofthe transcriptions ofthese genes results in a drug effect. . There are four major families ofphysiological receptors that drugs can bind to produce effects: .In this system.g. the process is known as glucuronide conjugation with the resulting metabolite refened to as the "glucuronide.. Occur in the liver microsomal enzyme system (mixed-lilnction oxidase system or P450 system). . Ion channels: Drugs can bind to ion channels in cell membranes to cause opening or closing. and transfonned to an active compound.lhen coupled to glucuronic acid. Second. There are at least eight distinct groups of microsomal drug metabolizing enzymes: These enzymes "families" are identified as a cytochrome (CYP preJix) followed by their numerical digestion (e. By binding to these kinases.

Actlve transport .Dental Decks .. Simple diffirsion Copltisht @ 201 219 l'2012 .Dental Decks . Facilitated diffusion .IV . Oral . Filtration . Inhalation 218 Coplrishr O 201 I '2012 . Rectal .

injected there is an open line through which emergency drugs can be One major disadvantage of IV injection is that since it has such a rapid onset ofaction. . Filtration: water-soluble molecules small enough to pass through membrane channels may be carried through the pores by the bulk flow of water. drugs will generally be absorbed best from the duodenum. Note: A major advantage of IV administration ofa drug is it allows for titration ofthe drug. Remember: The physiochemical properties ofdrugs that influence their passage across biologic membranes are: lipid solubility.Howeveq it is also the most unpredictable and least effective route available. and molecular size and shaoe. 3. The majority of drugs penetrate biomembranes by this process this by. Other advantages of IV administration include: . . Specialized transport Note: Osmosis is the movement of a pure solvent. In case of emergency. Moreover.ricrovilli. unpredictable and inegular due to the presence of variable amounts of food in different stages of digestion and to the varying degrees ofacidity and alkalinity ofthe digestive are shuttled across plasma membranes by forming complexes with specific membrane constituents called carriers. as water. These carrier molecules within a cell fumish energy for ransportation ofthe drug to regions ofhigher concentration. The amount of drug dissolving in the membrane at any time is directly proportional to the concentration gradient and its degree of lipid solubility (Note: Only nonionized drugs are soluble in lipid). througl't a semipermeable membrane from a solution that has a lower solute concentration to one that has a higher concentration. . degree of ionization. Facilitated diffusion is the term given to carrier-based transfer when the driving force is simply the concentration difference ofthe drug across the membrane.' through membrane phospholipids. Rapid onset . Absorption may be slow. overdosage may have effects so immediate that it is impossible to reverse them. The mechanism of drug transfer across biological membranes is by: L Passive transfer essential to various processes of metaboltsm -is . Simple diffusion: Iipid-soluble substances move across the lipoprotein membrane process. The duodenum has a large surface area due to the presence of villi and n. The membrane is impermeable to the solute but is permeable to the solvent.000 or less can "filter" through capillary membranes. Drugs ofmolecular u eights of 60. Active transport: lipid-insoluble substances (for example gluco. Note: After oral administration. These considerations make it clear that oral administration is usually unsuitable in emergencies or on other occasions when a rapid effect is needed. blood from the intestinal tract passes first to the liv€r: some drugs are metabolized in the liver and others may be stored there to be released only slowly. Drugs taken by mouth have to be absorbed (as ually fr om the small intestine) before they can be transported to their site ofaction. Drugs that cause irritation when administered subcutaneously can be given IV with no irritation .

Prazosin (Minipress) . Dmial Decks . Indomethacin (Indocin) . l0 milliliters . 5 milliliters . Dopar) .'right C 201l-2012 .Dental Dsks . Morphine 221 Cop. l5 milliliters . 20 milliliters 220 Copfight C 20ll-2012. Levodopa (Larodopa..

-Lntiparkinson drugs: for example levodopa (Larodopo. Many factors have been identi- fied that rnay be responsible for the development of orthostatic hypotension.The incidence increases with age. ulcers and possible stomach perforation. They include the administration and ingestion ofdrugs. . including several which are important to the practice of dentistry. an inadequate postural reflex. Dopur) and carbidopa ler odopa /Slnenet) * Orthostatic h)'potension (also called postural hypotension) is abnormally lorv blood pressure occuning when an individual assumes the standing posture. Phenothiazines: for exanple chlorpromazine and thiondazine (Mellaril) . Addison's disease. physical exhaustion and starvation and chronic orthostatic hypotension (Shy-Drager sludrome). -{ntih} pertensiyes: for example prazosm (Minipress) *** . orthostatic hypotension is the most likely cause of transient unconsciousness in the dental office. Important: Following vasovagal syncope. amitriptyline (E/avll) and imipramine I Tolianil) . pregnancy.lndomethacin (ndoclry' is an NSAID which may cause GI bleeding. various defects in the legs. prolonged recumbency and convalescence. Triclclic antidepressants: for example doxepin (Sinequan). Drugs that may produce orthostatic hypotension: . \arcotics: for example meperidine (Demerol) and rnorphine .

Dental Decks . Schedule II . Phantom pain 222 Coplaighr C2011. Schedule I . Intractable pain .Dental Decks . Schedule V Copltighr O 201 l-2012 .2012 . Schedule IV . Psychogenic pain .Pain that has no organic basis and is fixed upon some portion ofthe anatomy is referred to as: . Schedule III . Refened pain .

Oxycodone.e. heroin.\'lenol #3) and various analgesic combination compounds containing hydrocodone (i.a category ofdrugs considered to have less potential for abuse or addiction than Schedule I or II drugs. Schedule V a category of drugs that have a small potential for abuse or addiction. alprazolam (Xanax). hydrocodone and acetaminophen Schedule IV . LSD. and chloral hydrate. Among the substances so classified by the DEA are Morphine. Note: Schedule II and III must have a written prescription signed by the health professional (aws vary from stqte to state). The prescription must have the address ofthe patient and dentist as well as the DEA number olthe dentist.lorazepam (Ativan). Methadone. Pentobarbital.. Among the substances so classified by the DEA are mescaline. Schedule III .*** For example. Among the substances so classified by the DEA are diazepam (Valiurn). The FDA determines which drugs are to be sold by prescription only. and marijuana.a category of drugs that have less pot€ntial for abuse or addiction than those of Schedules I to III. Psychogenic pain: is pain produced or caused by psychic or mental factors rather than organic factors Remember: Pain threshold refers to the lowest level ofpain a patient will detect. . -l'icodin. although that limb has been am- Other terms to know: . such as pain near the shoulder associated with biliary disease . Schedule I - a Schedule II a category ofdrugs considered to have a strong potential for abuse or addiction. Among the substances so classified by the DEA are many commonly prescribed medications that contain a small amount ofCodeine. triazolam (Halcion). category ofdrugs not considered legitimate for medicinal use.e. Special licensing procedures must be followed to use these or other Schedule I substances. but which have legitimate medical use. Among the substances so classified by the DEA are var- ious analgesic combination compounds containing codeine fi.Intractable pain: is pain that is resistant or refractory to ordinary analgesic agents . Cocaine. Referred pain: is pain felt in an area other than the site of odgin.. the sensation ofpain felt in a limb. and straight Codeine. putated. Lorcet). acetaminophen and codeine .

Low therapeutic index and is. Inhalation . High therapeutic index and is. therefore. very dangerous . High therapeutic index and is. therefore. Low therapeutic index and is. Intramuscular . Oral 225 Coplright O 201 I.Dental Decks . relatively safe .20 l2 . therefore. Sublingual . relatively safe 224 Cop. very dangerous . therefore.righr O 201l-2012 . Denial Decks ..

. Unlike allergy. 1. Intramuscular injection is an injection made into a large muscle. Some drugs have a very nanow therapeutic window. This considera- rion makes it clear that oral administration in usually unsuitable in emergencies or on other occasions when a rapid effect is needed. A quantitative aspect ofacute toxicity testing is the determination of the drug's lethal dose using mice. 3. .. The speed ofabsorption of drugs given by IM injection depends on dre vehicle in which they are dissolved: absorption is rapid from aqueous solutions and slow from oily solutions. not people oftherapeutic window is not the same as therapeutic index. Blood from the intestinal ract passes first to the liver: some drugs are metabolized in the liver ( "lirst-pass elfect") and others n. a quantity which is often known as the therapeutic index (a measure of drug safety). the less lik€ly that fatalities will follow an accidental overdose.g.ray be stored there to be released slowly. 6. making patient monitoring especially important. specific to a particular person.:Noted. unlike a side effect. Side effect: an adverse effect that occurs within the therapeutic dose range ofthe drug. The therapeutic window describes the range between the lowest therapeutic concentration and the beginning of toxicity.. in theory 50% ofpeople will die. Idiosyncratic reaction: a reaction to a medication that is unusual and unpredictable.4 *** Lethal doses are always determined in mice. lt is easy and the patient can take the drug without help from anyone else..Explanation: The purpose ofan acute toxicity test is to determine the nature and extent ofthe untoward reactions which might iollow the administration ofa single dose (or an overdose) of a dntg.' --. LD56 is the lethal dose at which. One ofthe disadvantages of drugs taken by mouth is that they have to be absorbed (trsuulh fiom the small intestine) before they can be transported to their site ofaction. 4. This is usually expressed as the LD59. it can occur on first exposure to the medication. ED5g is the effective dose at which 50o% ofpeople will respond. Standing alone. .The greater a drug's therapeutic index. it conveys less information than does the ratio of the lethal to the effective doses (LD5/ED50). it affects only very few individuals. The advantages of IM injection are that it results in uniform absorption and that it can be used for solutions too iritant for subcutaneous injection. The oral administration of a drug is the one most acceptable to the patient. The concept 5. Toxicity results when the dose ofthe drug is excessive for the particular patient. It is convenient because drugs can be given in the form oftablets or capsules which contain an exact dose... .' 2.

.. Microsomal enzyme inhibition . The movement of The term bioavailability ofa drug r€fers to: a drug into the body tissues over time . Microsomal enzyme induction .: . . The amount ofdrug destroyed by the liverprior to syslemic absorption from the GI tract 226 CoplriSht O 20ll-2012 . The measurement of the rate and amount of therapeutically active drug that reaches the systemic circulation . Genetic factors . All of the above 227 CoD{iglu O 20ll-2012 - D{tal Decks . . The dissolution of a drug in the GI tract .Dental Decks Factors inlluencing hepatic drug metabolism include which ofthe followlng? . Plasma protein binding . The relationship between the physical and chemical properties ofa drug and the systemic absorption ofthe drug . Liver disease .

nd then dilluse across mcmbranes: basic drugs tend to ionize and arc not well absorbed in the stomach 2. Thus many drugs which ordinarily are metabolized by the particular CYP inhibited will not be effectively metabolized and will achieve higher than expected blood levels. and cxcr. The destnrction ofa drug by the liver Phrrmrcokinetics focuscs on the proccsscs concemed with absorption. Liver disease: hepatic impairment and liver disease most often will result in impairment ofthe microsomal drug metabolizing system. Acidic drugs become nonionized in the acidiry ofthe stomach . Drug chxncteristics: . thus resulting in a longer plasma halfJife ofthe drug.ry frctors that must be considered in evaluating drug absorption: l. Routes of edministration: the most common routcs for giving medications include oral. Co[centration of the dru$ the higher the concentration. The dissolution ofa dnrg in thc Gl tract .tlon (elim r'nalior) of drugs. or hydrolysis.The bioavailability of a drug is allected by: . Absorption: thcre are four prim. topical. infamlscular. 3. Involves two major stcps: Phas€ I makcs the drug morc hydrophilic through oxidation. Plasma protein binding: drugs highly bound to plasma proteins will not enter the liver to be metabolized. Dc:crcased circlJl^tion (as see'n fu congestiw heart fail rc) vtill result in dccrcascd drug absorptlon. . Cell membrrne ous tissues in thc body chtractedstics: dtugs cross membranes via passivc diffusion or active tmnsport . Phase lI is called glu' curonidrtion. it involves conjugrtion. intravenously. Microsomal enyzne inhibition: many drugs . tubuhr secretion' rdd par- wo tirl rerbsorDtion. Distribution: is thc trrnsport ofa dnrg in body fluids from thc bloodstesm (at lhe sile ofabsorptiotr) to vai. subcutancous. . Thc proc€sses involved in r€nal elimiDation consist ofglom€rular liltrution. Eliminrtio[: is the proccss by which drugs and their metabolites kidney are are removcd from the body. Blood flowi circulation at the sitc ofadministration is importrant in the drug absorption Foccss. The live. Factors Influencing Hepatic Drug Metabolism: and environmental agents can inhibit many of the CYP isoforms of the P-450 microsomal drug metabolizing system. 4. It occurs primarily in the liver. the more quickly the drug is absorbcd . reduclion. Note: Mos! drugs are given at lower doses in hepati cally impaired individuals. . Lipophilic drug formulrtions are morc rcadily rbsorbsble: nonionized drugs are more lipid soluble and may readily difuse across cell membmn€s . Biotranstormation a/n etabolism)t is the chemical inactivation of a drug lhrough convcrsion to a more waler-soluble compoud that can be excreted from th€ body. . . 8nd the major organs responsible for elimination. Genetic factors: there is individual variance through genetic factors which contribute to differing rates of drug metabolism in the hepatic microsomal enzyme system. Most climination occurs through excrction by thc kidneys. . This most often results in elevated levels of unmetabolized drug. biotransfomation (metabo' lisn). Formulrtion ot the drug . Microsomal enzyme induction: agents which induce higher levels ofthe microsomal drug metabolizing enzymes may cause a more rapid metabolism ofother drugs thus resulting in lower than expected blood levels ofa drug. and rectal. distribution. .

Active hansport tbrough renal tubular cells Coplright C 201l-2012 Dental Decks The average time for ths onset of drug effect after subcutaneous rdministration is: . Microsomal enzyme induction . 5 minutes . 30 minutes 229 CoDright O 20ll-2012 . 15 minutes . Immediate . Renal tubular reabsorption .Detrtal Decls . Glomerular filtration ..

. . Topical: This route includes ointments and creams applied to the skin and mucous membranes. capsules and liquids. Subcutaneous injection: Onset ofaction ofdrugs injected under the skin takes about l5 rninutes. Active transport through renal tubular cells: the rate of renal elimination also depends on whether active transport into or out ofthe tubular fluid occurs. Most drugs can be detected in saliva after administration. Routes of Drug Administration: .. the converse is that highly polar compounds are not effectively reabsorbed and are effectively excreted from the renal tubules. . This is not as prevalent as urinary excretion. . . . Glomerular liltration: all drugs are filtered through the glomerulus to enter the renal tubules. but the salivary glands are not considered a route ofdrug excretion since the drug is re-swallowed along with the saliva. The gastrointestinal tract excretes some drugs through the feces. Oral route allows for use ofmany different dosage forms including tablets. Inhalation: Gases such as nitrous oxide are absorbed rapidly though the lungs and gain access to the general circulation within 5 minutes. Oral route: It takes approximately 30 minutes for onset of drug effect after drug is swallowed. Nitrous oxide and the volatile general anesthetics are excreted by this route. Some drugs are excreted in the sweat' but this route accounts for only a small percentage of drug excreiion. Intramuscular injection: Onset of action of drugs injected into muscle occurs rapidly (approximately 5 minutes) because ofhigh blood flow lhrough the muscles. Lungs excrete volatile compounds that were originally inhaled into the system. Other excretory pathways for drugs: . . Reabsorption favors the highly lipid soluble agents. drugs may be reabsorbed back into the blood stream through the renal tubular cells. . . It is not intended for syslemic drug administration. . Tirbular reabsorption: once they enter the renal tubules. The amount of drug varies according to the degree of plasma protein binding. Patch delivery: Onset ofaction ofdrugs in skin patches is about 15 minutes and similar to subcutaneous injection. and bound drugs are not subjected to filtration. Skin patches release drug into the blood stream over a l2 to 24 hour Deriod. .

. Dental Decks . Subcutaneous injection . Intravenous injection .Denbl Decks . Oral administration . Tolerance . Habituation . Intramuscular injection 231 Cop)righ O 20ll-2012 . Addiction . None ofthe above 230 Coplaight e 20ll'2012.

tobacco or alcohol result from the repeated use of the substance but without the addictive. For example. including the drug receptor sites. The drug is delivered rapidly to all tissues. These drugs ofabuse all have the ability lo change one's mood and sensory perception. before the drug reaches its receptor sites. placed into the systemic circulation. usually through degradation by liver enzymes. with tion. the drug may be lost first-pass effects. l\. a portion ofar orally administered drug is eliminated. With other routes of administraThe entire dose is prior to reaching the systemic circulation.lso. it is placed directly into the systemic circulation.A. and therefore the onset of pharmacological effects is slower. physiological need to increase dosage. Note: Physiological dependence is common to all forms ofdrug dependence and abuse. rvhen a drug is given by Remember: The initial distribution ofa drug into the tissues is determined chiefly by the rate of blood flow to the tissue. . the drug must be systemically absorbed prior to distribution to the drug receptor sites.lote: Gastric emptying time and degree of plasma protein binding also have an effect on drug distribution but are less important than the rate ofblood flow to the tissues. For all other routes of drug adminrstralion (v)ith the exception of intra-arterial inj ection). trrhen a drug is given intravenously. whereas drug affinity for the tissue will determine s hether the drug will concentrate at that site. . Psychological and emotional dependence on a drug. Tolerance is the phenomenon ofdecreased responsiveness to a drug following chronic administration. IV injection there is a complete (100o/') bio^v^ilabilif.Habituation is an acquired tolerance from repeated exposure to a particular stimulus.

Idiosyncrasy 232 Coplrighr O 201 1-2012 .When a drug is administered repeatedly. Degree to which it produces physical dependence . Denbl Deck . Potential for abuse . Synergistic response . All ofthe above 233 Coptrighr @ 2011-2012 . Additive effect . The effect ofthis excessive accumulation is knorvn as: of . Degree to which it produces physiological dependence . Cumulative action .Denial Decks The Controlled Substsnce Act of 1970 uses which criterio for inclusion of a drug into one ofthe five schedules? . a higher coneentntion the drug than is desired may be achieved. Medical usefulness .

L . etc. Animal tcsts arc Dcrformed.gcr scale than phasc I sodics and tlpically involvc scvcml hundrcd patients. oi inportan. Prescriptions lor Schedule II drugs can not bc called into the pharmacy ovcr thc telephone. lt should be avoided if a response to a drug that is unusual or abnormal or one that grossly deviates from the routine reaction. The purposc ofthcsc studics is study in a clin. PorcntiaL for abuse r''.)d/ocodotie *'ith acetaninophe . phasc 1 studies arc uscd to determinc how ellcctivc thc drug is. . A synergistic r€sponse occurs when the combined action of two drugs is greater than the sum oftheir individual actions. A ne\\ prcscription mustbcwritten forrefills. oxycodone elc. narcotics.An additive effect occurs when additive drugs are administered. :.c made availablc only for specific approred research pro.)$n be prescribed but can not be refilled. \tcdicaluscfulness Degfcc to which it produces physiological dcpcndcncc Dclrcc to *hich it produccs physical dcpcndcncc Remember: Schedule I d gs (LSD. Phasc I studics are usually conducted on 20 to E0 subiccts. thc drug company submiis to the Food and Drug Administration 1FD. Thcrc is thc a drug can be approvcd for salc lo thc public there is a set ofclinical tests that must Pre-Clinical Research Stage. Schedule II drxgs fdmphetanines.r/ a Ne\r' Drug Application fND. barbiturates and phenothiazines.. Here the drug is s). Schedule III drugs (. Idiosyncrasy is Tle Controlled 1 Substancc Acl of 1970 uses the following critcria fbr inclusion of a drug into onc ofthc fivc schcd- . Thc prcscribcrcan authorizc rcfills without need ofa new writlcn prcscriplion. .. *** After a succcssful phasc III. *** Thc prcscribcr must hsve a Drug Enforcement Agency ruthorization nnmber (DEA #) in ordcr lo prcscribc schcdulcd drugs. The purpose of phrse 2 clinical trials is to dctcrminc thc cfficacy ofa drug to trcat patients with a spccific discasc or condition.1. Clinical testing ofdrugsr Bcfore be pcrformcd. cotleine. Phasc 3 studics gcrcrally involvc scvcral hundrcd to scvcral thousand pcoplc. 'Phase t: clinical studics in this phase represent thc first time that an investigational ncw drug is tested on hu- mans cithcrhealthy voluntccrs or somctimcs patierts. taking these drugs. Examples of synergism: Alcohol is synergistic with diazepam (Valium). structurc-reactivity rclationships. . noryhirc.jccts. Ifthc rccommcndations are positivc. Phase 3 cLinical trials provide morc information about the effects a d safcty ofthe drug and they allow scicntists to cxtrapolate thc rcsults ofclinical studies to thc gcncral population. and side ellccts ofthe drug in sctting thc metabolism. mcchanism ofaction. hercin. and institutional rcvicw boards asscss thc studies and make recommcndations on how to procccd. thcn an application to the FDA occurs and clinical tesls bcgtn.4/ to markct thc dru8.)@nnot be prescribed and a. cotleine \\'ith arctaninophen. The response is no greater than that which would be expected had the drugs been given one at a time.) may be called in to thc pharmacy over the telephonc. There is no enhancement ofpotential ofthe individual drugs as a result ofbeing used in combination. as well as lcam about common short{crm sidc cffccts or risks. These studics are conducted on a la. etc. lfpossiblc.nthcsizcd and purified.

The relative concentrations of two or more drugs that produce the same drug effect . Cumulative action 235 Copyright O 20l l-2012. An antagonistic effect . Denial Decks .' Which ofthe following refers to the efficacy ofa drug? . A synergistic response . An additive effect . The dose ofa drug that will kill a patient 234 Coplri8ht @ 2011.2012. Denral Decks . The ability ofa drug to produce a desired therapeutic effect regardless ofdosage .

then Drug a greater maximum effect than Drug #2. The response is no greater than the sum ofthe individual actions ofeach drug when given alone. the drug that produces the greatest maximum effect is the one with the highest ellicacy. There is no enhancement ofpotential ofthe individual drugs as a result ofbeing used in combination. the greater the potency of the drug. The following is true: Drug #l is flrve times as potent as Drug #2.*** Efficacy refers to the number of receptors that must be activated to yield a maximal response. narcotics and barbiturates. Alcohol is s). Alcohol should be avoided when takins these medications. A drug with high efficacy needs to stimulate only a small percentage ofreceptors. #l is capable ofproducing When comparing drugs with respect to intensity of response. . Intrinsic activity is a measue ofthe ability ofa drug once bound to the receptor to generate an effect activating stimulus and producing a change in cellular ac- tivity. Factors Goyerning Drug Action: Two factors that determine the effect of a drug on physiologic processes are aflinity and intrinsic activity.e. The effect usually chosen is 50% ofthe maximal effect and the dose causing this effect is called the EC56. etc). Halcion. Exampl€: Drug #l in a dose of l0 mg produces the same magnitude ofresponse as Drug #2 in a dose of 50 mg. Potency is determined mainly by the affinity of the receptor for the drug. Potency is a comparative term (o e drug is more polent than another drug).nergistic with the Valium family ofdrugs fi. A synergistic response occurs when the combined action of two drugs having similar pharmacological effects is greater than th€ sum of the individual actions.. Also: tf Drug #l has a great€r eflicacy than Drug #2. Xanax. Affinity is a measure ofthe tightness that a drug binds to the receptor. An additive effect occurs when additive drugs are administered. Note: The smaller the 8C56. Valium. Potency is the relative concentrations of two or more drugs that produce the same drug effect. whereas a drug with lesser efficacy (but still considered to be a full agonist) has to activate a larger proportion of receptors.

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