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Tis redistribution is Mismatch acts as a restriction to fow: It raises the not as useful afer prolonged anesthesia (fat partial pressure in front of the restriction purchase kemadrin 4 medications list, lowers the pres- pressures of anesthetic will have come “closer” to sure beyond the restriction discount kemadrin online medications reactions, and reduces the fow arterial partial pressures at the time the anesthetic through the restriction buy kemadrin 5mg overnight delivery medications by class. The overall efect is an was removed from fresh gas)—thus, the speed of increase in the alveolar partial pressure (particularly recovery also depends on the length of time the anes- for highly soluble agents) and a decrease in the arte- thetic has been administered. Tus, a bronchial intubation or a right-to- lef intracardiac shunt will slow the rate of induction Pharmacodynamics of with nitrous oxide more than with halothane. The multitude of substances capable of usually accounts for a minimal increase in the rate producing general anesthesia is remarkable: inert of decline of alveolar partial pressure. Its greatest elements (xenon), simple inorganic compounds impact is on the elimination of soluble anesthetics (nitrous oxide), halogenated hydrocarbons (halo- that undergo extensive metabolism (eg, methoxyfu- thane), ethers (isofurane, sevofurane, desfurane), rane). The greater biotransformation of halothane and complex organic structures (propofol). A unify- compared with isofurane accounts for halothane’s ing theory explaining anesthetic action would have faster elimination, even though it is more soluble. Difusion of anesthetic through agents interact with numerous ion channels present the skin is insignifcant. Nitrous The most important route for elimination of oxide and xenon are believed to inhibit N -methyl- inhalation anesthetics is the alveolus. Additionally, some studies suggest that inha- Anesthetic binding to these sites could expand the lational agents continue to act in a nonspecifc man- bilayer beyond a critical amount, altering membrane ner, thereby afecting the membrane bilayer. Although this possible that inhalational anesthetics act on multiple theory is almost certainly an oversimplifcation, it protein receptors that block excitatory channels and explains an interesting phenomenon: the reversal of promote the activity of inhibitory channels afect- anesthesia by increased pressure. Laboratory animals ing neuronal activity, as well as by some nonspecifc exposed to elevated hydrostatic pressure develop membrane efects. Perhaps the pres- T ere does not seem to be a single macroscopic sure is displacing a number of molecules from the site of action that is shared by all inhalation agents. Anesthetics have might afect neuronal transmission and away from also been shown to depress excitatory transmission the critical volume hypothesis. Difering aspects of anesthesia may be lular systems, including voltage-gated ion channels, related to diferent sites of anesthetic action. For ligand-gated ion channels, second messenger func- example, unconsciousness and amnesia are probably tions, or neurotransmitter receptors. Tere seems to be removal of the cerebral cortex did not alter the a strong correlation between anesthetic potency potency of the anesthetic! Tis hypothesis proposes that all tion is enhanced by inhalation anesthetics, is another inhalation agents share a common mechanism of potential anesthetic site of action. Tis was previously The tertiary and quaternary structure of amino supported by the observation that the anesthetic acids within an anesthetic-binding pocket could potency of inhalation agents correlates directly with be modifed by inhalation agents, perturbing the their lipid solubility (Meyer–Overton rule). The receptor itself, or indirectly producing an efecThat a implication is that anesthesia results from molecules distant site. It molecular targets for the one(s) that provide opti- has been suggested that early exposure to anesthet- mum efects with minimal adverse actions will be ics can promote cognitive impairment in later life. Xenon has an anti-apoptotic efect former population is likewise having surgery and that may be secondary to its inhibition of calcium ion receiving the attention of the medical community. Other inhalational agents, Consequently, children receiving anesthetics may be such as sevofurane, have been shown to reduce more likely to be diagnosed with learning difculties markers of myocardial cell injury (eg, troponin T), in the frst place. As of this writing, there is insufcient in response to a standardized stimulus (eg, surgical and conficting evidence to warrant changes in anes- incision). Ischemic preconditioning implies that a brief ment in response to surgical incision will be sup- ischemic episode protects a cell from future, more pressed as 1. High altitude requires a higher inspired concentration of anesthetic to achieve the same partial pressure. Nitrous oxide is a relatively inex- Inert (probably nontoxic with no metabolism) pensive anesthetic; however, concerns regarding its Minimal cardiovascular effects safety have led to continued interest in alternatives Low blood solubility such as xenon ( Table 8–5). Does not trigger malignant hyperthermia Environmentally friendly Nonexplosive E ﬀ ects on Organ Systems A. Myocardial depression may be Hypoxic drive, the ventilatory response to arterial unmasked in patients with coronary artery disease hypoxia that is mediated by peripheral chemorecep- or severe hypovolemia. Constriction of pulmonary tors in the carotid bodies, is markedly depressed by vascular smooth muscle increases pulmonary vas- even small amounts of nitrous oxide. Tis is a con- cular resistance, which results in a generally modest cern in the recovery room. Because of possible teratogenic efects, dental surgery, labor, traumatic injury, and minor nitrous oxide is ofen avoided in pregnant patients surgical procedures. Neuromuscular tion by afecting chemotaxis and motility of poly- In contrast to other inhalation agents, nitrous oxide morphonuclear leukocytes. In fact, at high concentrations in hyperbaric cham- Contraindications bers, nitrous oxide causes skeletal muscle rigidity. Although nitrous oxide is insoluble in comparison Nitrous oxide is not a triggering agent of malignant with other inhalation agents, it is 35 times more hyperthermia. Renal difuse into air-containing cavities more rapidly than nitrogen is absorbed by the bloodstream. For Nitrous oxide seems to decrease renal blood fow instance, if a patient with a 100-mL pneumothorax by increasing renal vascular resistance. Tis leads inhales 50% nitrous oxide, the gas content of the to a drop in glomerular fltration rate and urinary pneumothorax will tend to approach that of the output. Hepatic into the cavity more rapidly than the air (princi- Hepatic blood fow probably falls during nitrous pally nitrogen) difuses out, the pneumothorax oxide anesthesia, but to a lesser extent than with the expands until it contains 100 mL of air and 100 volatile agents. Gastrointestinal Examples of conditions in which nitrous oxide Use of nitrous oxide in adults increases the risk of might be hazardous include venous or arterial postoperative nausea and vomiting, presumably as air embolism, pneumothorax, acute intestinal a result of activation of the chemoreceptor trigger obstruction with bowel distention, intracranial zone and the vomiting center in the medulla. A small amount difuses tracheal tube cufs, increasing the pressure against out through the skin. Tese enzymes include use as a complete general anesthetic, it is frequently methionine synthetase, which is necessary for myelin used in combination with the more potent volatile formation, and thymidylate synthetase, which is agents. Although nitrous oxide loblastic anemia) and even neurological defciencies should not be considered a benign carrier gas, (peripheral neuropathies). However, administration it does attenuate the circulatory and respiratory of nitrous oxide for bone marrow harvest does not efects of volatile anesthetics in adults. Although organ blood oxide fowing through a vaporizer can infuence the fow is redistributed, systemic vascular resistance is concentration of volatile anesthetic delivered. Respiratory (ie, increasing oxygen concentration) increases the Halothane typically causes rapid, shallow breath- concentration of volatile agent despite a constant ing. Tis disparity is due to the relative to counter the decreased tidal volume, so alveolar solubilities of nitrous oxide and oxygen in liquid vol- ventilation drops, and resting Paco2 is elevated. The second gas efect was discussed Apneic threshold, the highest Paco2 at which a earlier.
The patient was given a diagnosis of atypical ketosis-prone type 2 diabetes (T2D) and rapidly uptitrated on multiple daily injections with glargine and aspart insulin plus metformin cheap kemadrin 5 mg without prescription treatment xdr tb guidelines. Given his blurry vision purchase 5mg kemadrin fast delivery treatment regimen, the patient was given insulin pens to rely on the clicking mechanism to assist with dosing discount kemadrin 5mg mastercard medicine used to stop contractions. Over several weeks, he was titrated up to 40 units of glargine at night, 12 units of asparThat each meal with a correctional factor, plus 1 g of metformin twice a day. On this regimen, his glucose values decreased dramatically to near euglycemia with values rarely exceeding 150 mg/dL (8. Patients are typically obese with a family history of T2D and presentation most commonly is seen in African Americans, Hispanics, and Asians. Initial treatment requires aggressive insulin therapy to relieve glucose toxicity and to allow for endogenous β-cell function to recover. Inpatient management is frequently required for aggressive hydration, intravenous insulin therapy, and intensive diabetic education on insulin injections and blood glucose monitoring. After normalization of blood glucose values, the majority of patients are able to come off insulin therapy entirely with frequent normalization of blood glucose levels that occurs in weeks to months. However, in one cohort of patients that was followed for 10 years, although the majority came off of insulin initially, 60% of patients ultimately required insulin at the end of the follow-up 2 period. In this way, acute remission is frequently followed by repeated “exacerbations” or recurrence over time. The patient followed a classic course for atypical T2D in that his glucose profile rapidly normalized, but he was not able to come off insulin therapy entirely. Additionally, without specific lipid therapy, his cholesterol profile essentially normalized. As seen in this patient, this can result in rapid normalization or near-normalization of the lipid panel. Studies have shown that the dysfunction appears to be temporary with rapid improvement in insulin secretion after only 10 weeks of 4 follow-up (as shown in Fig. In this regard, the patient’s lipid panel becomes even more interesting in that the lipid derangements may not only represent a result of the β-cell failure, but also may contribute to or compound the underlying cause as well. This particular class of agents has shown some effect in helping β-cells reduce apoptosis in the 5 setting of multiple insults, including lipotoxicity. Ketosis-prone type 2 diabetes in patients of sub-Saharan African origin: clinical pathophysiology and natural history of beta-cell dysfunction and insulin resistance. Professor of Clinical Medicine in the Department of Endocrinology and Diabetes at University of Southern California, Professor of Clinical Medicine in the Department of Obstetrics and Gynecology at University of Southern California. Per the family, the patient was experiencing general lack of coordination, difficulty walking, difficulty speaking, and worsening confusion. It was noted that the patient had not taken her insulin for a few days before this presentation. The patient’s exam showed the following: Blood pressure 221/96 mmHg Heart rate 82 bpm Oxygen saturation 97% on room air Sodium 115 mEq/L Potassium 5. On exam, the patient was alert and oriented but noted to have intermittent nonrhythmic movement of the left side of the face, more on the lower part of the face, as well as of the left arm. This hyperglycemia and hyperviscocity can cause perfusion changes in the contralateral striatum, which then can result in excessive inhibition of the subthalamic 1 nucleus. Damage to the subthalamic nucleus thus results in an increase of the thalamic excitation of the motor and 2 premotor cortex resulting in involuntary movements. Magnetic resonance angiogram of the head showed normal flow of bilateral high cervical, petrous, cavernous, and supraclinoid internal carotid arteries with no evidence of significant stenosis. Clinical and radiological signs usually resolve within 6 months following correction of hyperglycemia, but some case reports have documented resolution of hemiballistic movements as soon as 24–48 h after the correction of 4 hyperglycemia. Hemiballistic movements initially improved but then worsened, interfering with eating. The hospital stopped clonazepam and started diazepam 5 mg every 8 h and divalproex 250 mg q. Two weeks later she presented to our clinic still complaining of worsening movements. Divalproex was increased to 500 mg every 8 h and diazepam was continued at 5 mg every 8 h. Two weeks later, the patient was seen in the neurology clinic still having constant large and small amplitude involuntary movements of the left upper and lower extremities. Neurology believed the patient’s hemiballistic movements could have been caused by a small lacunar stroke in the right basal ganglia, given her sudden onset of dramatic hemichorea, which was exacerbated by her poorly controlled blood glucose. They recommended tapering and discontinuing diazepam and giving quetiapine 50 mg at night. Hyperglycemia-induced hemiballismus hemichorea: a case report and brief review of literature. He had a history of longstanding poor glycemic control but recent improvement with intensive insulin therapy in the inpatient setting. Three days before transfer, he was ambulating with a new orthotic device under supervision when he noted sudden onset of right thigh pain. The pain worsened over the next few days requiring addition of narcotics but with minimal effect. He was afebrile with normal heart and respiratory rate and mild hypertension at 142/76 mmHg. His pain was 5/10 at rest and 10/10 pain with active or passive movement of right hip. There was no tenderness of the right lower leg, foot, or ankle; however, flexion of the right knee was limited by pain, and substantial tenderness to palpation was noted in the right lateral thigh. Skin examination showed an area of tenderness, erythema, and warmth over the anterior lateral right thigh. Site of left below-the-knee amputation showed good granulation tissue without infection. Laboratory values were remarkable for the following: Blood urea nitrogen 52 mg/dL Creatinine 6. Diabetic myonecrosis was first described by Angervall and Stener in 1 1965 and is a rare end-organ complication of diabetes. It is often seen in patients with poorly controlled, longstanding diabetes >15 years with end-organ damage, including retinopathy (71%), nephropathy (57%), and 2 neuropathy (55%). Although the exact pathophysiology has yet to be clarified, it is hypothesized to result from atherosclerotic and diabetic microangiopathy leading to muscle infarction. The most common presentation is the abrupt onset of nontraumatic pain and swelling of the affected muscle, sometimes accompanied by a palpable mass and fever. Areas most commonly affected are the quadriceps (60–65%), hip adductors (13%), hamstrings 3 (8%), and hip flexors (2%). Less commonly reported are cases involving the upper limb or both upper and lower limb muscle groups.
Subsequent to the discovery of the speciﬁc mutation involved cheap kemadrin 5 mg free shipping medicine 319 pill, this dis- ease was shown to have a large spectrum of phenotypes buy kemadrin 5mg without a prescription medicine used to induce labor, with juvenile and adolescent forms kemadrin 5mg generic symptoms pink eye, and survival into Fig. Diﬀuse cerebral white matter involvement predominates, with progres- volume loss also occurs with time. Huntington disease presents clinically in the fourth and later decades, In this category of disease, there is a deﬁciency of lysosomal with choreoathetosis and progressive dementia. Excretion in the urine of incompletely degraded mucopolysaccha- rides is characteristic. The imaging presentation is one of Diseases Aﬀecting Both White and Gray Matter dilated perivascular spaces (an identifying feature), atro- phy with varying degrees of hydrocephalus, together with Canavan Disease white matter changes that are initially more focal in na- This autosomal recessive disease presents in the ﬁrst few ture (Fig. These lesions progress with time to resem- weeks of life due to marked hypotonia, with early devel- ble a nonspeciﬁc metabolic disorder, but if treated early by opment of macrocephaly and seizures. Stenosis at the patients, imaging studies demonstrate a nonspeciﬁc, sym- craniovertebral junction is a known additional associated metric diﬀuse abnormality of the cerebral white mat- ﬁnding. The subcortical white matter is involved early in the common), Hunter (next most common), Sanﬁlippo, and disease process, a possible diﬀerentiating ﬁnding. Late in the disease process, most of the leukodystro- phies cannot be diﬀerentiated, and feature generalized cerebral atrophy (reﬂected by ventricular enlargement in this pediatric patient) together with patchy to diﬀuse abnormal high signal intensity white mat- ter on T2-weighted scans. However, on the T1-weighted scan illustrated, there is a ﬁnding that is characteristic for the muco- polysaccharidoses, speciﬁcally Hunter and Hurler diseases, and that is the numerous strikingly enlarged dilated perivascular spaces (arrows). The parietal and occipital speciﬁc for this diagnosis, with identiﬁcation and clini- cortex and subcortical white matter are most frequently cal follow-up critical for treatment. A suspicion on imaging of not follow speciﬁc arterial distributions, a diﬀerentiating this diagnosis should prompt laboratory evaluation, with feature from thrombotic or embolic infarction. The thalami and white matter are involved early, with cerebral and cerebellar atrophy a late ﬁnding. The image presented is from poral lobes (with these two areas communicating) are characteristic an 11-month-old patient with cessation of normal development for glutaric acidemia type 1, as shown. Myelination would be appropriate in the axial more diﬃcult to recognize due to the age of this patient (6 months), image presented for a newborn, with high signal intensity in the include increased signal intensity on T2-weighted images in the peri- posterior limb of the internal capsule, but is markedly delayed for a ventricular white matter as well as the globus pallidus and putamen child near 1 year of age. Early recognition of this entity is important, as it is T1-weighted images should appear near complete, with high signal readily treated and otherwise leads to permanent sequelae. There may be accompanying involvement of shown) and post-contrast with abnormal enhancement (illustrated, arrows), is the most characteristic ﬁnding in this disease from an the basal ganglia. Wernicke Encephalopathy This entity is caused by thiamine deﬁciency, and is hyperintensity can be noted in the mamillary bodies, seen in severe malnutrition, in particular with alcohol around the third ventricle, and in the medial thalami, tec- abuse. The mamil- lary bodies can also have abnormal contrast enhancement, as can occur in the other involved areas. The signal intensity char- acteristics are thought to reﬂect manganese deposition. With time, this is replaced by gliosis and cystic en- cephalomalacia, with the chronic appearance being one of symmetric atrophy of the nuclei (Fig. Subtle abnormal high signal intensity (arrow, ﬁrst image) is present bilaterally in the globus pallidus on a T1-weighted scan in this patient, consistent with manganese deposition. Presumably dependent on the amount of abnormal metal accumulation, the ﬁndings range in patients from some- what subtle to striking hyperintensity. Also noted in this case is bilateral abnormal hy- perintensity in the thalami (arrow, second image), which can also be seen in hepatic encephalopathy (involving any of the basal ganglia), but is less common. On the heavily T2-weighted fast is small (atrophic) bilaterally, with symmetric lesions therein dem- spin echo scan, the very high signal intensity ﬂuid centrally within onstrating peripheral gliosis and central cavitation (ﬂuid). Note that the lateral and more posterior portions of the pons are spared, together with the more anterior (ventral) pons and the corticospinal tracts. On pathology, there is atrophy of the hip- pocampus and adjacent structures, with disease bilateral This disease, previously referred to by the term central in up to 20%. Mesial temporal sclerosis is a common cause pontine myelinolysis, occurs due to too rapid correction of of complex partial seizures. In its classic presentation, there is ipsilateral fornix, with resultant mild enlargement of the abnormal symmetric involvement of the central pons, spar- adjacent temporal horn (Fig. Extrapontine myelinolysis is most com- monly seen in conjunction with central pontine myelin- olysis (the term osmotic demyelination encompasses both entities), with symmetric involvement of the basal ganglia ■ Hemorrhage and cerebral white matter, and less commonly other areas. Note the preservation of architecture and distinct layers of gray and white mat- ter in the normal left hippocampus (white arrow). In part 2, thin section (1 mm) contigu- ous coronal T1-weighted scans conﬁrm the atrophy of the right hippocampus and widening of the adjacent anterior temporal horn (asterisk). These sections also demonstrate that the right hippocampus is small, when compared to the left, throughout its extent from anterior to posterior (black arrows). On ini- temporal evolution has occurred to extracellular methemoglobin, tial presentation, this posterior temporal hematoma (white arrow) with high signal intensity on the T2-weighted scan. Five months fol- demonstrates low signal intensity on the T2-weighted scan, in- lowing presentation, there has been resorption of most of the ﬂuid, dicative of deoxyhemoglobin. Also present is surrounding vaso- together with resolution of the edema, leaving a low signal intensity genic edema, with abnormal high signal intensity. Within hours, how- subarachnoid hemorrhage is commonly due to rupture of ever, deoxyhemoglobin (acute hemorrhage) is evident an intracranial aneurysm. Typical locations for hyperten- with distinctive low signal intensity on T2-weighted scans. Methemoglobin (subacute hemorrhage) has tions of the appearance of hemorrhage in the literature are distinctive high signal intensity on T1-weighted scans, predominantly for parenchymal bleeds. To some extent, the and bleeds can be further subdivided temporally into appearance of subarachnoid hemorrhage is similar. By 1 to 4 weeks, a hematoma will be isodense cellular in location, with distinctive high signal intensity to brain, and in the chronic phase may appear hypodense. Magnetic susceptibility orrhage thus exhibiting pronounced low signal intensity eﬀects, which cause decreased signal intensity depending on T2-weighted scans again due to susceptibility eﬀects. If not resorbed, there will be a central ﬂuid collection Oxyhemoglobin (hyperacute) progresses to deoxyhemo- with high signal intensity on both T1- and T2-weighted globin (acute), to intracellular methemoglobin (early sub- scans, surrounded by a hemosiderin rim. With the passage acute), then extracellular methemoglobin (late subacute), of years, the ﬂuid collection may change in appearance and eventually to hemosiderin (chronic). There has also been extravasation of blood into the ven- tricular system, with hemorrhage seen in the frontal horns, third ventricle, and atria of the lateral ventricles. A small amount of hemorrhage is also seen in the fourth ventricle posteriorly, which is com- pressed due to mass eﬀect. The pons and cere- bellum, considered together, are the third most common site for hypertensive hemorrhage, after the putamen/external capsule (ﬁrst) and the thalamus (second). Initially, but for a very short time, a parenchy- sociated vasogenic edema and mass eﬀect in the acute stage. The mal hemorrhage contains oxygenated hemoglobin and is seen as a third patient illustrates a subacute, extracellular methemoglobin ﬂuid collection, with slight hyperintensity on a T2-weighted scan. There is a small amount of associated vaso- rim, with low signal intensity, already present on the T2-weighted genic edema and marked mass eﬀect upon the right lateral ventricle. This large, acute, left external capsule hema- case emphasizes the importance of looking for the cause of a hem- toma evolves from a ﬂuid collection containing deoxyhemoglobin orrhage, as the post-contrast scan reveals the associated enhancing (white asterisk, with low signal intensity on T2-weighted scans), to metastasis (black arrows). One arachnoid hemorrhage due either to a time delay (a few key to the recognition of parenchymal hemorrhage, not days) between the hemorrhage and imaging or the small discussed in detail, is the presence of edema surrounding quantity of blood present.
This enzyme has should be prescribed along with an appropriate gastro- a number of isoforms buy generic kemadrin online medicine quinine, the most studied being cyclo- protective agent (see p purchase kemadrin us in treatment 1. Among other functions kemadrin 5 mg visa symptoms questions, the prostaglandins result of hypertension secondary to fluid retention). Cur- produced by cyclo-oxygenase act to protect the gastric mu- rent guidelines suggest that all cyclo-oxygenase-inhibiting cosa,maintainnormalbloodflowinthekidneyandpreserve drugs should be used with caution in patients with known normal platelet function. It can be used on its own, or synergistically ate analgesics for use in acute inflammatory pain. Its major drawback is the liver tox- a careful risk–benefit assessment should be made prior to icity seen in acute overdose due to the accumulation in the use in view of the side-effects associated with long-term use. Modern medical practice still benefits from the use of its alkaloids, employ- Mor- Phenylperi- Diphenylpro- Esters phinans dines phylamines ing them as analgesics, tranquillisers, antitussives and in the treatment of diarrhoea. Morphine Meriperidine Methadone, Remifentanil The principal active ingredient in crude opium was iso- Codeine Fentanyl Dextropropo- lated in 1806 by Friedrich Sertu¨rner, who tested pure mor- xyphene phine on himself and three young men. Opium contains many alkaloids, but the only important Pure Partial Mixed Antagonists opiates (drugs derived from opium) are morphine (10%) agonists agonists action andcodeine. As described later, the properties of opioids Opioids produce their effects by activating specific G pro- may be predicted on the basis of activity on opioid and tein-coupled receptors in the brain, spinal cord and per- other receptor systems. Although studies suggest the existence of Opioids act to reduce the intensity and unpleasantness of subtypes of all three major opioid receptor classes, the ev- pain. The common side-effects are due to their action on idence is controversial and the sub-classification is of little different opioid receptors. They include sedation, eupho- practical value except, perhaps, to explain the change in ria, dysphoria, respiratory depression, constipation, pruri- side-effect profile sometimes seen during opioid rotation tis, and nausea and vomiting. Constipation sium channels and prevent the opening of voltage-gated and dry mouth (leading to increased risk of dental caries) calcium channels. This reduces neuronal excitability and are more resistant to the development of tolerance and re- inhibits the release of pain neurotransmitters. Impairment of hypo- thalamic function also occurs with long-term opioid use and may result in loss of libido, impotence and infertility. Classification of opioid drugs Adverse effects associated with the use of opioids in acute Opioids have been traditionally classified as strong, interme- pain (and occasionally in chronic non-malignant pain) can diate and weak, according to their perceived analgesic prop- often be managed simply by reducing the opioid dose or erties and propensity for addiction. In palliative medicine, misleading, as it implies that weak opioids such as codeine unwanted effects related to long-term opioid use are often are less effective but safe. Codeine may be less potent than treated proactively, laxatives for constipation, excessive morphine but can cause respiratory depression if given in sedation by methylphenidate or dextroamphetamine. Codeine-like drugs are also frequently Rotating to another opioid, or using more frequent but abused. Opioids may also be classified according to their smaller doses of opioids may also help. Patients taking opioid analgesics often report less distress, Opioids cause a tonic increase of smooth muscle tone even when they can still perceive pain. Reduced peristalsis and frequently, particularly in the early stages of treatment, delayed gastric emptying results in constipation, greater but often resolves although it can remain a problem, espe- absorption of water and increased viscosity of faeces, cially at higher doses, and is a common cause of drug and exacerbation of the constipation (but the effect is use- discontinuation in the chronic pain population. Opioid-induced constipation in pallia- The sensitivity of the respiratory centre to hypercarbia tive care can be managed by increasing the fibre content of and hypoxaemia is reduced by opioids. Hypoventilation, the diet to >10 g/day (unless bowel obstruction exists) due to a reduction in respiratory rate and tidal volume, and prescribing a stool softener (e. Prolonged 100 mg twice or three times daily), usually with a stimu- apnoea and respiratory obstruction can occur during sleep. Stimulant laxatives These effects are more pronounced when the respiratory should be started at a low dose (e. Senna 15 mg daily) drive is impaired by disease, for example in chronic ob- and increased as necessary. Persistent constipation can structive pulmonary disease, obstructive sleep apnoea be managed with an osmotic laxative (e. Respiratory depression sphincter of Oddi is increased after opioid administration in use relates to high blood opioid concentrations, for and gives rise to colicky pain with morphine which can be example with an inappropriately large dose that fails to both diagnosed and relieved by a small dose of the opioid account for differences in patient physiology (e. Pethidine (meperidine) is held to hypovolaemic trauma or the elderly), or because the produce less spasm in the sphincter of Oddi than other opi- patient is unable to excrete the drug efficiently (as a con- oids due to its atropine-like effects and is preferred for bil- sequence of renal impairment). At higher equi-analgesic unusual in patients established on long-term opioids due doses, the effect of pethidine on the sphincter is similar to the development of tolerance. Increased tone in the detrusor muscle and contraction of Nausea and vomiting commonly accompany opioids the external sphincter, together with inhibition of the void- used for acute pain. Opioid administration is often associated with cutaneous Miosis occurs due to an excitatory effect on the parasym- vasodilatation that results in the flushing of the face, neck pathetic nerve innervating the pupil. Cardiovascular system Pharmacokinetics Opioids cause peripheral vasodilatation and impair sympa- thetic vascular reflexes. Postural hypotension may occur, Bio-availability varies between opioids after oral adminis- but this is seldom troublesome in the reasonably fit patient tration but is generally poor. Intrave- exceeding total body water) and most have an elimination nous morphine titrated carefully may benefit patients with half-life in the range (3–10 h). Notable exceptions are acute myocardial infarct and left ventricular failure as mor- alfentanil (t½1. The dorsal horn of the spinal cord is rich in opioid receptors, and equivalent analgesia can be Hydromorphone 20 provided using a lower dose of opioid, resulting in fewer Morphine 30 systemic side-effects. The use of intraventricular morphine appears to Codeine 60 be beneficial in treating recalcitrant pain due to head and neck malignancies and tumours (e. Morphine Duration of analgesia usually correlates with half-life un- less the parent drug has active metabolites (morphine) or if Morphine remains the most widely used opioid analgesic the drug has a high affinity for opioid receptors (buprenor- for the treatment of severe pain. Opioid sensitivity is increased in the neonate and in against which other opioids are compared. Variation inresponse and the narrow therapeutic given intramuscularly, intravenously, or orally, it can also index ofopioids makeitessential totitrate effects for individ- be administered per rectum and into the epidural space or ual patients. Unlike most opioids, it is relatively wa- frequent monitoring of pain relief, sedation, respiratory rate ter soluble. Metabolism is by hepatic conjugation and and blood pressure is necessary to guide dosage adjustment. The duration of useful analgesia providedbymorphineisabout3–6 h,butvariesgreatlywith Route of administration different drug preparations and routes of administrations. Morphine 6-glucuronide (M6G), one of its major metabo- The oral route is preferred as it is simple, non-invasive and lites,isanagonistatthemreceptorandalsoatthedistinctM6G relatively affordable. With slower onset of action renders this route less convenient repeated use ofmorphine,morphine 6-glucuronide is respon- for use in acute pain. The oral route is also unsuitable when sible for a significant amount of pharmacological activity.
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