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This area contains few or no ascending even parallel to the forniceal reference plane as de- veins and is frequently used to access the anterior scribed in Chap order desloratadine now allergy symptoms for pollen. Posteriorly discount desloratadine amex allergy medicine under tongue, since the later- my can be easily and precisely displayed purchase desloratadine visa allergy symptoms of flu, including al occipital vein is directed anteriorly, no large vein the finer morphological details. This approach is enters the superior sagittal sinus for a distance of 4– easily obtainable on nearly all available imaging 5 cm proximal to the torcula. Because the whole extent of the central sulcus is displayed, we think 2 The Mesial Venous Drainage System that this approach might be useful for functional techniques (refer to figures in Sect. Both assume a the reliability of these methods is beyond the scope similar distribution as their lateral counterpart. The reader is referred to selected pa- Those coursing superiorly frequently join the con- pers and reviews on the subject (Berger et al. An indirect approach has relied on skull landmarks and, subsequently, on brain refer- ence coordinates (Horsley 1892; Taylor and Haugh- ton 1900; Rowland and Mettler 1948; Matsui et al. Springer, Berlin Heidelberg New York, J Neuroradiol 23:6–18 pp 2–11 Dusser de Barenne (1924) Experimental researches on sen- Bertrand G (1956) Spinal efferent pathways from the supple- sory localization in the cerebral cortex of the monkey mentary motor area. Smith Elder, Functional activation in motor cortex reflects the direc- London tion and the degree of handedness. Trans St Andrews Bertrand G, Vanier M, Ethier R, Tyler J, de Lotbinière A Med Grad Assoc 3:162–207 (selected writings 1:8–36) (1987) Intégration de l’angiographie numérique, de la Jefferson G (1912) The morphology of the sulcus résonance magnétique, de la tomodensitométrie et de la interparietalis. Neurology 43:2311–2318 Neuroradiol 2:149–155 Rassmussen T (1969) The neurosurgical treatment of focal Matsui T, Kawamoto K, Labarre L, Imai T, Tamotsu O, Hirano epilepsy. In: Niedermeyer E (ed) Epilepsy, recent views on A (1977) Anatomical and pathological study of the brain its therapy, diagnosis and treatment. Anatomical study of the normal brain at (Moderns problems of pharmacopsychiatry, vol 4) various angles. Am J Neuroradiol 17:1699–1706 Einseidel H, Jiddane M, Farnarier P, Habib M, Perot S 138 Chapter 4 (1988) Identification of cortical sulci and gyri using mag- the topography of the convolutions and fissures of the netic resonance imaging: a preliminary study. Appl Szikla G, Bouvier G, Hori T, Petrov V (1977) Angiography of Neurophysiol 50:57–62 the human brain cortex. Springer, Berlin Heidelberg New Waterston D (1907) Complete bilateral interruption of the York fissure of Rolando. Presse Med 28:605–609 during a hand motor task in patients with brain tumor Talairach J, Szikla G, Tournoux P, Prossalentis A, Bordas- and paresis. The cortical regions adjacent to the lateral sulcus The lateral fissure or fissure of Sylvius is the major are the frontal, parietal and temporal opercula, or sulcal landmark on the lateral surface of the brain. During later embryonic stages it assumes a Lying in the depth of the horizontal segment of the horizontal course due to the dramatic expanse of the sylvian fissure is the insular lobe of Reil. It is the frontoparietal and temporal opercula over the insula smallest of the cerebral lobes and has a pyramidal (Cunningham 1892). It is distinguished by a triangular base, with The lateral fissure is divided into three segments: the apex of the triangle anterior and inferior. The the first is the hidden stem segment, extending from boundaries of the insula are the anterior limiting the lateral border of the anterior perforated sub- sulcus rostrally, dorsally the superior limiting sulcus stance and coursing over the limen insulae before and ventrocaudally the inferior limiting sulcus. The second, or the limiting sulci are circular and continuous, they are horizontal segment, is the longest and the deepest together called the circular sulcus. The insula is con- segment, coursing on the lateral surface of the hemi- tinuous anteriorly with the preinsular area and pos- sphere. A The Preinsular Area This last segment is complex, asymmetrical and ap- pears to correlate with hemispheric dominance. The preinsular area corresponds to a cortical ribbon Several branches are distinguished on the hori- made by the confluence of the frontal lateral and the zontal segment. This area surrounds the falci- (2–3 cm) are noted, cutting into the inferior frontal form sulcus of Broca. The corresponding to the stem of the sylvian fissure and terminal segment usually bifurcates at its end, in a lateral aspect which is the base of the apex of the about 80% of the cases (Witelson and Kigar 1992), as insula. The terminal ascending branch is the true B The Insular Lobe continuation of the lateral or sylvian fissure. The short descending branch is inconsistent and shal- The insular lobe is a preeminence with a triangular lower, seen mostly over the right hemisphere and base. The apex of this triangle is directed anteriorly represents a “processus acuminis,” resulting from the and inferiorly and overhangs the falciform sulcus 140 Chapter 5 Fig. Anatomy of the lateral aspect of the cerebral hemisphere showing the lateral fissure and the surrounding opercula. Anatomical cut of the cerebral hemisphere passing through the lateral surface of the insula and showing the branches of the posterior ramus of the lateral fissure. Anatomical cut of the brain passing through the insular lobe and displaying the inferior frontal-parietal and the superior temporal lobes. All of eral ventricle; 6, chiasmal cistern; 7, ambient cistern; 8, mes- these anatomic structures are highly consistent topographi- encephalon; 9, calcarine sulcus; 10, inferior recti muscles cally, validating the accuracy of this reference 1234 142 Chapter 5 Anatomic variations of the insula have been rare- ly reported, with additional sulci found in the anteri- or or the posterior lobe (Kodama 1934). C The Anatomic Relationships of the Insula The insular lobe covers the lentiform nucleus, sepa- rated from it laterally to mesially by the extreme capsule, the claustrum, and the external capsule. The uncinate fasciculus, running in the polar as- pect of the insula, is covered laterally by the orbito- frontal operculum anteriorly, and the frontoparietal Fig. Lateral projections of the lateral fissure and the sur- rounding major parallel sulci of frontotemporal lobes, as lo- calized using the proportional system according to Szikla. The limen insulae, or the “seuil de l’insula,” although used frequently in neuro- surgery textbooks, is not clearly defined. The anterior and inferior limiting sulci of the cir- cular sulcus of the insula are frequently interrupted in the region of the falciform sulcus by a communi- cation (“pli de passage”) between the pole of the in- sula and the inferior frontal gyrus anteriorly and posteriorly with the temporal lobe (Fig. It originates from the superior limiting sulcus and is directed ob- liquely towards the falciform sulcus. The anterior lobe is triangular in shape with a su- perior base and is made of three short gyri, the gyri breves. It is composed of two long gyri oblique- ly oriented and originating from a common stem in- B feriorly. Kodama (1934) showed that the length of of the lateral fissure, involving the rostrum and the splenium the insula on the sagittal plane is about 56. The sulci of the insula bear a relatively constant The relationship of the anterior speech area with relationship with the overlying cortical sulci. The vertical ramus of the central rolandic sulcus appears to be continuous sylvian fissure extends through the operculum to with the central sulcus of the insula, interrupted at reach the superior limiting sulcus. The pre- ramus when present also extends from the opercu- central rolandic gyrus covers part of the anterior lum to the circular sulcus (Fig. Anatomy of the insula and its relationship with the sulci of the infe- rior frontal lobe, as disclosed in the depth of the lateral fissure. The superior part of the (Schlesinger 1953) is an angiographic marker of the anterior sulcus, corresponding to the looping of the insula, oriented in the same fashion with its apex middle cerebral sulcus, branches as it leaves the supe- anterior and inferior. Ainsi voilà huits faits où la lésion a siégé dans le tiers postérieur de la troisième circonvolution frontale.
Second order desloratadine in united states online allergy treatment while nursing, diuretics and uric acid are Abuse of diuretics organic acids and compete for the transport mechanism that pumps such substances from the blood into the Psychological abnormality sometimes takes the form of tubular fluid order desloratadine 5 mg without prescription allergy questions. The subject usually de- vented by allopurinol or probenecid (which also antago- sires to slim to become more attractive cheap desloratadine online master card cat allergy treatment uk, or may have an- nises diuretic efficacy by reducing their transport into the orexia nervosa. Magne- Osmotic diuretics sium deficiency brought about by diuretics is rarely severe enough to induce the classic picture of neuromuscular irrita- Osmotic diuretics are small molecular weight substances bility and tetany but cardiac arrhythmias, mainly of ven- that are filtered by the glomerulus but not reabsorbed by tricular origin, do occur and respond to repletion of the renal tubule, and thus increase the osmolarity of the tu- magnesium (2 g or 8 mmol of Mg2þ is given as 4 mL 50% bular fluid. The result is that urine volume increases Carbohydrate intolerance is caused by those diuretics according to the load of osmotic diuretic. In addition to formation and release of insulin, so glucose intolerance its effect on the kidney, mannitol encourages the move- is probably due to secondary insulin deficiency. Insulin ment of water from inside cells to the extracellular fluid, requirements thus increase in established diabetics and which is thus transiently expanded before diuresis occurs. The These properties define its uses, which are for rapid reduc- effect is generally reversible over several months. Because it the loop diuretics; in the short term this is not a serious dis- increases circulatory volume, mannitol is contraindicated advantage and indeed furosemide may be used in the man- in congestive cardiac failure and pulmonary oedema. In the long term, hypocalcaemia may be harmful, Methylxanthines especially in elderly patients, who tend in any case to be in negative calcium balance. Thiazides, by contrast, decrease The general properties of the methylxanthines (theophyl- renal excretion of calcium and this property may influence line, caffeine) are discussed elsewhere (see p. Their the choice of diuretic in a potentially calcium-deficient or mild diuretic action probably depends in part on smooth osteoporotic individual, as thiazide use is associated with muscle relaxation in the afferent arteriolar bed increasing a reduced risk of hip fracture in the elderly. The hypocalciu- renal blood flow, and in part on a direct inhibitory effect ric effect of the thiazides has also been used effectively in on salt reabsorption in the proximal tubule. Their uses in patients with idiopathic hypercalciuria, the commonest medicine depend on other properties. This process is fundamen- 3 nism may involve inhibition of renal prostaglandin tal to the production of either acid or alkaline secretions, 459 Section | 5 | Cardiorespiratory and renal systems and high concentrations of carbonic anhydrase are present because the urine calcium is in less soluble form, owing in the gastric mucosa, pancreas, eye and kidney. Because to low citrate content of the urine, a consequence of meta- the number of Hþ ions available to exchange with Naþ bolic acidosis. Acetazolamide is the most widely used Cation-exchange resins are used to treat hyperkalaemia by carbonic anhydrase inhibitor. This action is not the context of poor urine output or before dialysis (the due to diuresis (thiazides actually raise intraocular pressure most effective means of treating hyperkalaemia). The formation of aqueous humour is an active consist of aggregations of big insoluble molecules carrying process requiring a supply of bicarbonate ions which de- fixed negative charges, which loosely bind positively pends on carbonic anhydrase. Inhibition of carbonic anhy- charged ions (cations); these readily exchange with cations drase reduces the formation of aqueous humour and in the fluid environment to an extent that depends on their lowers intraocular pressure. In cations preferentially with potassium cations in the intes- patients with acute glaucoma, acetazolamide can be taken tine (about 1 mmol potassium per g resin); the freed cat- either orally or intravenously. Acetazolamide is not recom- ions (calcium or sodium) are absorbed and the resin mended for long-term use because of the risk of hypokalae- plus bound potassium is passed in the faeces. The resin mia and acidosis, but brinzolamide or dorzolamide are does not merely prevent absorption of ingested potassium, effective as eye drops, well tolerated, and thus suitable but it also takes up the potassium normally secreted into for chronic use in glaucoma. In hyperkalaemia, oral administration or retention en- High-altitude (mountain) sickness may affect unaccli- emas of a polystyrene sulphonate resin may be used. A matised people at altitudes over 3000 metres, especially af- sodium-phase resin (Resonium A) should obviously not ter rapid ascent; symptoms range from nausea, lassitude be used in patients with renal or cardiac failure as sodium and headache to pulmonary and cerebral oedema. A calcium-phase resin (Calcium Reso- tiating cause is hypoxia: at high altitude, the normal hyper- nium) may cause hypercalcaemia and should be avoided in ventilatory response to falling oxygen tension is inhibited predisposed patients, e. Acetazolamide induces metastatic carcinoma, hyperparathyroidism and sarcoido- metabolic acidosis, increases respiratory drive, notably at sis. Orally they are very unpalatable, and as enemas patients night when apnoetic attacks may occur, and thus helps rarely manage to retain them for as long as necessary to maintain arterial oxygen tension. The usual dose is (at least 9 h) to exchange potassium at all available sites 125–250 mg twice daily, given orally on the day before on the resin. A summary of the sudden falls in plasma Kþconcentration occur due to its ex- main indications appears below. The sites and pathological types of Acidification of urine: injury are as follows: • is used as a test for renal tubular acidosis Glomerular damage. It should not be given to patients with impaired pairment is best reflected in the creatinine clearance, which renal or hepatic function. Theproximaltubule,through Adverse effects whichmostwaterisreabsorbed,experiencesthegreatestcon- centration and so suffers most drug-induced injury. Proximaltubulartoxicity is manifested by leakage of glucose, phosphate, bicarbonate and amino acids into the urine. Drug-induced renal disease The counter-current multiplier and exchange systems of urine concentration (see p. Substances that cause such ten first evident at this site, partly because of high tissue toxicity include: concentration and partly, it is believed, because of ischae- • heavy metals, e. The distal tubule is the site of amphotericin, cephalosporins lithium-induced nephrotoxicity; damage to the medulla • iodinated radiological contrast media, e. Indirect biochemical effect: Methotrexate, for example, is relatively insoluble at low • cytotoxic drugs and uricosurics may cause urate to pH and can precipitate in the distal nephron when the be precipitated in the tubule urine is acid, typically in high dose for chemotherapy. Sim- • calciferol may cause renal calcification by inducing ilarly the uric acid produced by the metabolism of nucleic hypercalcaemia acids released during rapid tumour cell lysis can cause a fa- • diuretic and laxative abuse can cause tubular tal urate nephropathy. This was a particular problem with damage secondary to potassium and sodium the introduction of chemotherapy for leukaemias until the depletion introduction of allopurinol, which is now routinely given • anticoagulants may cause haemorrhage into the before the start of chemotherapy to block xanthine oxidase kidney. A recent and highly effective wide range of injuries: alternative to allopurinol for high-risk patients is recombi- • drugs include phenytoin, gold, penicillins, nant uric acid oxidase (Rasburicase), which catalyses con- hydralazine, isoniazid, rifampicin, penicillamine, version of uric acid to the more soluble allantoin. Crystal probenecid, sulphonamides nephropathy is also reported with agents as diverse as 461 Section | 5 | Cardiorespiratory and renal systems indinavir, orlistat, ciprofloxacin, aciclovir, sulfadiazine and Table 27. Drugs may thus induce any of the common clinical Atenolol 6 100 syndromes of renal injury, namely: Digoxin 36 90 • Acute renal failure, e. Depending on the circumstances, • alternative drugs must be found or special care exercised when • Functional impairment, i. Drugs may: • exacerbate renal disease (see above) Dose adjustment for patients with • be ineffective, e. There are exceptions to this rule of arise for patients with impaired renal function who must be thumb; for example, the volume of distribution of treated with a drug that is potentially toxic and that is digoxin is contracted in uraemic patients due to altered wholly or largely eliminated by the kidney. A knowledge of, or at least access to, sources of pharma- Adjustment of the maintenance dose involves either • cokinetic data is essential for safe therapy for such patients, reducing each dose given or lengthening the time e. The profound influence of impaired renal function on Special caution is needed when the patient is • the elimination of some drugs is illustrated in Table 27. Careful observation is more water soluble than the parent drug, rely on the kidney required in the early stages of dosing until response to for their elimination, and accumulate in renal failure, e. The majority of drugs fall into an intermediate class and are partly metabolised and partly eliminated unchanged by the kidney. Drugs that are partly eliminated by the kidney and partly metabolised: give a normal initial dose and Some physiology modify the maintenance dose or dose interval in the light of what is known about the patient’s renal The detrusor, whose smooth muscle fibres comprise the function and the drug, its dependence on renal body of the bladder, is innervated mainly by parasympa- elimination and its inherent toxicity. The internal sphincter, a concentration of Recall that the time to reach steady-state blood concentra- smooth muscle at the bladder neck, is well developed only tion (see p. Thus, if t½ is prolonged by renal impairment, so adrenoceptors, activation of which causes contraction.
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The elimination rate e constant can be converted into the half-life using the following equation: t1/2 = 0 purchase 5 mg desloratadine overnight delivery allergy testing routes. The volume of distribution (V) can be computed using the following equation4: −kte ′ k 0 1− e V = −kt′ k [ − ee ] e max predose where k0 is the infusion rate buy genuine desloratadine online allergy treatment plano, ke is the elimination rate constant buy desloratadine 5mg fast delivery allergy testing codes, t′=infusion time, Cmax is the maximum concentration at the end of infusion, and Cpredose is the predose concentra- tion. A large absorption rate constant allows drug to enter the body quickly while a small elimination rate constant permits drug to enter the body more slowly. The solid line shows the concentration/time curve on semilogarithmic axes for an elimination rate con- stant equal to 2 h−1. The dashed and dotted lines depict serum concentration/time plots for elimi- nation rate constants of 0. The absorption rate con- stant describes how quickly drug is absorbed with a large number indicating fast absorp- tion and a small number indicating slow absorption (Figure 2-7). An example of the use of this equation would be a patient that is administered 500 mg of oral procainamide as a capsule. It is known from prior clinic visits that the patient has a half- life equal to 4 hours, an elimination rate constant of 0. The capsule that is administered to the patient has an absorption rate constant equal to 2 h−1, and an oral bioavailability fraction of 0. The procainamide serum concentration 4 hours after a single dose would be equal to: FkaD kt kt C = e e − e a Vka − ke −1 (0 85. Since the absorption rate constant is also hard to measure in patients, it is also desirable to avoid drawing drug serum concentrations during the absorption phase in clinical situa- tions. This approach works very well when the extravascular dose is rapidly absorbed and not a sustained- or extended-release dosage form. From previous clinic visits, it is known that the patient has a volume of distribution of 60 L and an elimination rate constant equal to 0. If two or more postabsorption, postdistribution serum concentrations are obtained after an extravascular dose, the volume of distribution, elimination rate constant, and half-life can be computed (Figure 2-8). After graphing the serum con- centration/time data on semilogarithmic axes, the time it takes for serum concentrations to decrease by one-half can be measured and equals 14 hours. Since this was the first dose of valproic acid, the extrapolated concentration at time = 0 (C0 = 70 mg/L) is used to estimate the hybrid volume of distribution/bioavailability (V/F) parameter: V/F = D/C0 = 750 mg/70 L = 10. Even though the absolute volume of distribution and bioavailability cannot be computed without the administration of intravenous drug, the hybrid constant can be used in extravascular equations in place of V/F. Half-life (t1/2) is determined by measuring the time needed for serum concentrations to decline by 1/. The concentration/ e 1/2 time line can be extrapolated to the concentration axis to derive the concentration at time zero (C0 = 70 mg/L) and used to compute the hybrid constant volume of distribution/bioavailability fraction (V/F = D/C0). The elimination rate constant can be translated into the half- life using the following equation: t = 0. The hybrid 1/2 e constant volume of distribution/bioavailability (V/F) is computed by taking the quo- tient of the dose and the extrapolated serum concentration at time = 0. The extrapolated serum concentration at time = zero (C0) is calculated using a variation of the intra- venous bolus equation: C = C/e−ket, where t and C are a time/concentration pair that 0 occur after administration of the extravascular dose in the postabsorption and postdistrib- ution phases. In this situa- tion, the time/concentration pair at 24 hours will be used (time = 24 hours, concentration = −k t −(0. The hybrid volume of distribution/bioavailability constant (V/F) is then computed: V/F = D/C0 = 750 mg / (70 mg/L) = 10. Multiple-Dose and Steady-State Equations In most cases, medications are administered to patients as multiple doses, and drug serum concentrations for therapeutic drug monitoring are not obtained until steady state is achieved. For these reasons, multiple dose equations that reflect steady-state conditions are usually more useful in clinical settings than single dose equations. Fortunately, it is simple to convert single dose compartment model equations to their multiple dose and steady-state counterparts. At steady state, the number of doses (n) is large, the exponential term in the numerator of the multiple dosing factor (−nkiτ) becomes a large negative number, and the exponent approaches zero. Therefore, the steady-state version of the multiple dosing factor −kiτ , becomes the following: 1/(1 − e ) where ki is the rate constant found in the exponential of the single dose equation and τ is the dosage interval. Whenever the multiple dosing fac- tor is used to change a single dose equation to the multiple dose or steady-state versions, the time variable in the equation resets to zero at the beginning of each dosage interval. As an example of the conversion of a single dose equation to the steady-state variant, the one compartment model intravenous bolus equation is: C = (D/V)e−ket, where C is the concentration at time = t, D is the dose, V is the volume of distribution, ke is the elimina- tion rate constant, and t is time after the dose is administered. Since there is only one exponential in the equation, the multiple dosing factor at steady state is multiplied into the expression at only one place, substituting the elimination rate constant (ke) for the rate constant in the multiple dosing factor: C = (D/V)[e−ket/ (1 − e−keτ)], where C is the steady- state concentration at any postdose time (t) after the dose (D) is given, V is the volume of distribution, ke is the elimination rate constant, and τ is the dosage interval. Table 2-1 lists the one compartment model equations for the different routes of administration under single dose, multiple dose, and steady-state conditions. A patient with tonic-clonic seizures is given phenobarbital 100 mg intravenously daily until steady-state occurs. A patient with gram-negative pneumonia is adminis- tered tobramycin 140 mg every 8 hours until steady state is achieved. The steady-state e concentration immediately after a 1 hour infusion equals: C = [k /(kV)][(1 − e−ket′) / (1 − −1 0 e−1 e−keτ)] = [(140 mg/h) / (0. A patient with an arrhythmia is administered 250 mg of quinidine orally (as 300 mg quinidine sulfate tablets) every six hours until steady state occurs. It is also possible to compute pharmacokinetic parameters under multiple dose and steady-state conditions. Table 2-2 lists the methods to compute pharmacokinetic constants using a one compartment model for different routes of administration under single-dose, multiple-dose, and steady-state conditions. The main difference between single-dose and multiple-dose calculations is in the computation of the volume of distribution. How- ever, when multiple doses are given, the predose concentration is not usually zero, and the volume of distribution equation (V) needs to have the baseline, predose concentration (Cpredose) subtracted from the extrapolated drug concentration at time = 0 (C0) for the intravenous bolus (V = D/[C0 − Cpredose], where D is dose) and extravascular (V/F = D/ [C0 − Cpredose], where F is the bioavailability fraction and D is dose) cases. In the case of intermittent intravenous infusions, the volume of distribution equation already has a parameter for the predose concentration in it4: −kte ′ k 0 1− e V = −kt′ k [ − ee ] e max predose where k0 is the infusion rate, ke is the elimination rate constant, t′=infusion time, Cmax is the maximum concentration at the end of infusion, and Cpredose is the predose concentra- tion. For each route of administration, the elimination rate constant (ke) is computed using the same equation as the single dose situation: ke =−(ln C1 − ln C2)/(t1 − t2), where C1 is the first concentration at time = t1, and C2 is the second concentration at time = t2. The following are examples of multiple dose and steady-state computations of phar- macokinetic parameters using a one compartment model for intravenous, intermittent intravenous infusions, and extravascular routes of administration: Intravenous bolus. A patient receiving theophylline 300 mg intravenously every 6 hours has a predose concentration equal to 2. The patient has an elimi- nation rate constant (ke) equal to: ke =−(ln C1 − ln C2)/(t1 − t2) =−[(ln 9. The volume of distribution (V) of theophylline for T in g le o se ultiple o se n d t dy- t t h a rm o k in ti o n st n t o m put tio n s U tilizin g a n o m pa rtm n t o dl R A I ntravenousbolus k e ln C ln C t t) k e ln C ln C t t) k e ln C ln C t t) t k e t k e t k e V V predose V predose C l k eV l k eV l k eV C ontinuous N / N / l k ss intravenousinfusion I nterm ittent k e ln C ln C t t) k e ln C ln C t t) k e ln C ln C t t) intravenousinfusion t k e t k e t k e V [k e ket ] / {k [C e ket ]} V [k e ket ] / {k [C e ket ]} V [k e ket ] / {k [C e ket ]} 0 e max predose e max predose e max predose C l k eV l k eV l k eV E xtravascular k e ln C ln C t t) k e ln C ln C t t) k e ln C ln C t t) ( postabsorption, t k e t k e t k e postdistribution) V/ V/ predose V/ predose C l/ k e V/ l/ k e V/ l/ k e V/ A verage steadystate N / N / l/ ss concentration ( anyroute of adm inistration) S ym bol k ey isdrug serum concentration attim e t, isdrug serum concentration attim e t, k e isthe elim ination rate constant, t isthe half- life, V isthe volum e ofdistribution, k isthe continuousinfusion rate, tisthe infusion tim e, V/ isthe hybrid constantvolum e ofdistribution/ bioavailabilityfraction, isdose, isthe concentration attim e l isdrug clearance, C l/ isthe hybrid constantclearance/ bioavailabilityfraction, C predoseisthe predose concentration, C ssisthe steadystate concentration, N / isnotapplicable. Since the patient is at steady state, it can be assumed that all predose steady-state concentrations are equal. Because of this the pre- dose steady-state concentration 12 hours after the dose can also be considered equal to 2. The volume of distribution (V) of gentamicin for the patient is: −kte ′ k 0 1− e V = −kt′ k [ − ee ] e max predose where k0 is the infusion rate, ke is the elimination rate constant, t′=infusion time, Cmax is the maximum concentration at the end of infusion, and Cpredose is the predose concentra- tion. Average Steady-State Concentration Equation A very useful and easy equation can be used to compute the average steady-state con- centration (Css) of a drug: Css = [F(D/τ)]/Cl, where F is the bioavailability fraction, D is the dose, τ is the dosage interval, and Cl is the drug clearance. The steady-state concentration computed by this equation is the concentration that would have occurred if the dose, adjusted for bioavailability, was given as a continuous intravenous infusion.
His family (B) Hallucinations is getting ready to leave on another such trip cheap desloratadine 5mg line allergy symptoms relief, so he asks (C) Hyperthermia if there is anything he can take to lessen his nausea buy generic desloratadine pills allergy treatment for babies. The (D) Respiratory depression physician prescribes an antinausea drug with anticho- (E) Restlessness linergic activity order genuine desloratadine line allergy medicine ranking. She is given opioid pain medications to 146 A 45-year-old man who smokes three packs of ciga- treat her pain. Which of the following symp- effects from the chronic use of opioids will the patient toms is likely to be attributed to use of this medication? On physical exam, diffuse wheezing is heard He has several comorbidities that are being managed bilaterally. The physician decides to add cromolyn to his home medications, which includes bimatoprost, sim- regimen. Which of (A) Blocks leukotriene receptors the following should be held (not given to him) dur- (B) Inhibits endothelin-1 receptors ing his hospital stay? Which of the fol- including a nicotine patch, nicotine gum, continued lowing agents will provide him with the most effca- smoking, or hypnotherapy. In which of the He has been vomiting and had diarrhea for the past following steps is excitation of the postsynaptic recep- 36 h. She is given a prescription for penicillin and develops a maculopapular rash on her hands and swelling of her tongue. The most likely explanation for these fndings is (A) Arachidonic acid (B) Macrophages (C) Penicillin (D) Penicilloic acid (E) Xanthine oxidase 268 Chapter 7 3 The answer is E: Loratadine. These symptoms are caused precursor for the eicosanoids such as prostaglandins primarily by histamine acting on H receptors. First, phospholipase A2 cleaves cell Histamine is released from mast cells when they en- membrane phospholipids to release arachidonic acid. Leukotrienes cause bronchoconstriction, are all methods employed to reduce symptoms of mucus production, and increased vessel permeability allergic rhinitis. Montelukast severe acute attack but not the best choice for chronic works by blocking leukotriene binding to its receptor. The H antagonists are divided 1 Ipratropium and albuterol work on autonomic ner- into frst-generation (diphenhydramine, hydroxyzine) vous system receptors rather than on the arachidonic and second-generation (loratadine) drugs. Ipratropium is a parasympathetic ond-generation drugs are more specifc for the H re- 1 antagonist, whereas albuterol is a sympathetic ceptor and do not cross the blood–brain barrier as agonist—both work to relax bronchial smooth muscle readily so they have fewer side effects (such as drows- and decrease secretions. Of the options listed, not prevent a signaling molecule from binding to its loratadine is the best choice. It blocks acetylcholine from binding to would not be effective in treating symptoms of aller- muscarinic receptors but does not block arachidonic gic rhinitis. It does not pre- would help counteract his symptoms but not as well vent a signaling molecule from binding its receptor. Symptoms are caused by itching and vasodilation 4 The answer is B: Drying efect on the oral mucous from histamine binding to H receptors. Atropine blocks the salivary glands, 1 released from mast cells as they degranulate, which is producing a drying effect on the oral mucous mem- caused by antigen linking two IgE molecules attached to branes. This before they can react this way, which occurs when IgE agent is commonly infused intravenously at low made by plasma cells attaches to receptors on mast cell doses. Mast cell stabilizers such as cromolyn the gastrointestinal tract but this is not the reason that sodium prevent the release of histamine. It does not agent induces bradycardia at low doses as would be prevent the release of histamine but is an antagonist for given to this patient. Stimulation tion of urinary tract motility is an effect of atropine causes an increase in acid secretion. H receptors are not but is not the reason that an oral surgeon would use 2 important in allergic reactions. Cyclosporine forms a Second-generation antihistamines have higher specifcity complex with protein called cyclophilin. This com- for H1 receptors (therefore fewer side effects) than frst- plex then binds the calcium-calmodulin-calcineurin generation antihistamines. It is a gluco- corticoid and inhibits many pathways necessary 9 The answer is D: Salicylate uncoupling of oxidative for infammation and immune system function. Above high therapeutic short-term nasal spray decongestant products (applied dose, aspirin directly stimulates the respiratory cen- every 12 h) as well as in ophthalmic drops for the relief ter. Oxymetazoline is absorbed in the systemic circulation regardless of the route of administration and may pro- 10 The answer is D: Ketorolac. Its main use is (A) Nasal blood fow is reduced by administration of as an analgesic and can be used in place of or in addi- oxymetazoline. Drugs that interfere with, or liver glutathione (a natural, endogenous antioxidant) is inhibit, the metabolism of propranolol, such as cimeti- depleted. In this case, the patient is taking rifampin; and it is (D) Neither acetaminophen nor its metabolites pro- affecting the metabolism of propranolol and inducing duce appreciable ischemia. Ischemic damage in the rapid metabolism, which is minimizing its antihyper- liver is rare regardless because of its dual blood supply. These chloroquine is a weak base that acts on lysosomes by drugs should not be used in patients with Parkinson’s raising the pH. To be effective, mesalamine must reach the litis; however, in this patient, there is no reason to colon. Sulfasalazine and abnormal involuntary movements (dyskinesias) is made up of a molecule of mesalamine connected to may occur. Levodopa however, sulfapyridine causes enough side effects that can also cause mood changes, depression, psychosis, sulfasalazine is less favorable than other drugs such as and anxiety. It helps with the symptoms of ulcerative colitis tion that this patient is not taking his medications by decreasing the immune response. There are many molecule that stimulates leukocyte activation, bone ways to get around this problem, including supposi- reabsorption, and cartilage degradation. In rheumatoid arthritis, these effects include It is used in the treatment of myasthenia gravis and bone and cartilage destruction in the joints. Infammation, Immune Pharmacology, and Toxicology 271 (E) Pilocarpine is used in the treatment of glaucoma. This results in the accumu- lation of acetaldehyde in the blood, causing fushing, 22 The answer is A: Blockade of adenosine receptors. Disulfram Several mechanisms have been proposed for the has found some use in the patient seriously desiring actions of methylxanthines, including translocation of to stop alcohol ingestion. A conditioned avoidance extracellular calcium, increase in cyclic adenosine response is induced so that the patient abstains monophosphate and cyclic guanosine monophos- from alcohol to prevent the unpleasant effects of phate caused by inhibition of phosphodiesterase, and disulfram-induced acetaldehyde accumulation. Ototoxicity, which acting opiate antagonist that should be used in con- often presents as tinnitus, is a known side effect of junction with supportive psychotherapy. This is especially is better tolerated than disulfram and does not pro- true when given with other ototoxic drugs (such as duce the aversive reaction that disulfram does. It may aminoglycoside antibiotics), in patients with renal work well in this patient who had diffculty taking disease, when given in high doses, or with rapid intra- aldehyde dehydrogenase. Chelating agents are which normally causes sodium reabsorption in the (usually) organic compounds that can form multiple distal tubule.
