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Cyclosporine dosage decreases may be necessary to decrease tremor associ- ated with drug therapy while hirsutism is usually addressed using patient counseling purchase viagra plus in india erectile dysfunction treatment vancouver. Gingival hyperplasia can be minimized through the use of appropriate and regular dental hygiene and care order generic viagra plus on-line erectile dysfunction boyfriend. Patients with severe chronic graft-versus-host disease may have involvement of the skin viagra plus 400mg generic smoking and erectile dysfunction statistics, liver order cheapest viagra plus and viagra plus low cost erectile dysfunction drugs, eyes, mouth, esophagus, or other organs similar to what might be seen with systemic autoimmune diseases. Solid organ transplant patients should be monitored for graft rejection consistent with the transplanted organ. For renal transplant patients, increased serum creatinine, azotemia, hypertension, edema, weight gain secondary to fluid retention, graft tenderness, fever, and malaise may result from an acute rejection episode. For hepatic transplant patients, acute rejection signs and symptoms include fever, lethargy, graft tenderness, increased white blood cell count, change in bile color or amount, hyper- bilirubinemia, and increased liver function tests. For heart transplant patients, acute rejection is accompanied by low-grade fever, malaise, heart fail- ure (presence of S heart sound), or atrial arrhythmia. For all solid organ transplant patients, tissue biopsies may be taken from the transplanted tissue to confirm the diagnosis of organ rejection. Other cyclosporine adverse drug reactions that occur less frequently include gastrointestinal side effects (nausea, vomiting, diarrhea), headache, hepatotoxicity, hyperglycemia, acne, leukopenia, hyperkalemia, and hypomagnesemia. If a patient experiences signs or symptoms of graft-versus-host disease or organ rejection, a cyclosporine concentration should be checked to ensure that levels have not fallen below the therapeutic range. If a patient encounters a possible clinical problem that could be an adverse drug effect of cyclosporine therapy, a cyclosporine concentration should be measured to determine if levels are in the toxic range. During the immediate post-transplantation phase, cyclosporine concentrations are measured daily in most patients even though steady state may not yet have been achieved in order to prevent acute rejection in solid organ transplant patients or acute graft-versus-host disease in hematopoietic stem cell transplantation patients. After discharge from the hospital, cyclosporine concentrations continue to be obtained at most clinic visits. In these cases, cyclosporine doses and concentrations are decreased to the minimum required to prevent graft-versus-host reactions or rejection episodes in order to decrease drug adverse effects. Methods to adjust cyclosporine doses using cyclosporine concentrations are discussed later in this chapter. Although newer data are available that suggest determination of cyclosporine area under the concentration/time curve using multiple concentrations6–10 or 2-hour postdose cyclosporine concentrations11–14 may provide better outcomes for some transplant types, many transplant centers continue to use predose trough cyclosporine concentration determinations to adjust drug doses. Cyclosporine has low water solubility, and its gastroin- testinal absorption can be influenced by many variables. Oral cyclosporine solution is pre- pared with olive oil and alcohol to enhance the solubility of the drug. The solution is mixed in milk, chocolate milk, or orange juice using a glass container immediately before swallowing. When the entire dose has been given, the glass container should be rinsed with the diluting liquid and immediately consumed. If microemulsion cyclosporine solu- tion is administered, it should be mixed in a similar fashion using apple or orange juice. Variation in cyclosporine solution absorption is dependent on how accu- rately the administration technique for each dose is reproduced. After liver transplanta- tion, bile production and flow may not begin immediately, or bile flow may be diverted from the gastrointestinal tract using a T-tube. Diarrhea also impairs cyclosporine absorption,24,25 and hematopoietic stem cell transplantation patients may experience diarrhea as a part of graph-versus-host disease. Cyclosporine binds primarily to erythrocytes and lipoproteins, yielding unbound fractions in the blood that are highly variable (1. Lipoprotein concentrations also vary among patients, and hyperlipidemia is an adverse effect of cyclosporine. Hepatic intrinsic clearance is different among individuals, and there is a large amount of variability in this value within individual liver transplant patients that changes according to the viability of the graft and time after transplantation surgery. Of course, changing the unbound fraction in the blood, hepatic intrinsic clearance, or liver blood flow will also change the hepatic first-pass metabolism of cyclosporine. Taking all of these pos- sible factors into consideration that alter absorption and clearance allows one to gain a bet- ter appreciation of why cyclosporine concentrations change on a day-to-day basis. Cyclosporine capsules and solution are available in regular (25-mg, 50-mg, and 100-mg capsules; 100-mg/mL solution) and microemulsion (25-mg and 100-mg capsules; 100-mg/mL solution) form. Although the oral absorption characteristics are more consis- tent and bioavailability higher for microemulsion forms of cyclosporine, it is recom- mended that patients switched from cyclosporine to microemulsion cyclosporine have doses converted on a 1:1 basis. Before administration, each milliliter of the concentrate should be diluted in 20–100 mL of normal saline or 5% dextrose, and the total dose infused over 2–6 hours. Anaphy- lactic reactions have occurred with this dosage form, possibly because of the castor oil dilu- ent used to enhance dissolution of the drug. According to a survey of transplant centers in the United States, the average initial oral dose (± standard deviation) for renal, liver, and heart transplant patients were 9 ± 3mg/kg/d, 8 ± 4mg/kg/d, and 7 ± 3 mg/kg/d. The overall mean for all transplant groups is a clearance of 6 mL/min/kg, a volume of distribution equal to 5 L/kg, and a half-life of 10 hours for adults. Because of this, half-life measurements were taken from studies that allowed at least 24 hours between doses. These results, as with the other pharmacokinetic parameters discussed in this chapter, are based on a specific high-pressure liquid chromatography assay method conducted using whole blood samples. As discussed in a previous section, nonspecific cyclosporine assays measure metabolite concentrations in addition to parent drug, and concurrently measured plasma or serum concentrations are lower than whole blood concentrations. Because the drug is primarily eliminated by hepatic metabolism, clearance is lower (3 mL/min/kg) and half-life prolonged (20 hours) in patients with liver failure. Additionally, patients with transient liver dysfunc- tion, regardless of transplantation type, will have decreased cyclosporine clearance and increased half-life values. Immediately after transplantation surgery, oral absorption of cyclosporine, especially in liver transplant patients with T-tubes, is highly variable. Drugs in this category of drug interactions include aminoglycoside antibiotics, vancomycin, cotrimoxazole (trimethoprim-sulfamethoxazole), amphotericin B, and antiinflammatory drugs (azapropazone, diclofenac, naproxen, other nonsteroidal antiinflammatory drugs). Drugs that inhibit cyclosporine clearance include the calcium channel blockers (verapamil, diltiazem, nicardipine), azole antifungals (flucona- zole, itraconazole, ketoconazole), macrolide antibiotics (erythromycin, clarithromycin), antivirals (indinavir, nelfinavir, ritonavir, saquinavir), steroids (methylprednisolone, oral contraceptives, androgens), psychotropic agents (fluvoxamine, nefazodone) as well as other agents (amiodarone, chloroquine, allopurinol, bromocriptine, metoclopramide, cime- tidine, grapefruit juice). Inducing agents include other antibiotics (nafcillin, rifampin, rifabutin), anticonvulsants (phenytoin, carbamazepine, phenobarbital, primidone), barbitu- rates, aminoglutethimide, troglitazone, octreotide, and ticlopidine. Because of the large number of interacting agents, and the critical nature of the drugs involved in the treatment of transplant patients, complete avoidance of drug interactions with cyclosporine is not possible. Thus, most drug interactions with cyclosporine are managed using appropriate cyclosporine dosage modification with cyclosporine concentration monitoring as a guide. It allows individualized target serum concentrations to be chosen for a patient, and each pharmacokinetic parameter can be customized to reflect specific disease states and conditions present in the patient. Literature-based recommended dosing is a very commonly used method to prescribe ini- tial doses of cyclosporine. Doses are based on those that commonly produce steady-state concentrations in the lower end of the therapeutic range, although there is a wide varia- tion in the actual concentrations for a specific patient. In order to do this, pharmacokinetic parameters for the patient will be estimated using average parameters measured in other patients with similar dis- ease state and condition profiles.

Despite its prompt passage into the brain order 400 mg viagra plus amex erectile dysfunction protocol book scam, midazolam is considered to have a slower effect-site equilibration time than propofol and thiopental cheap viagra plus american express impotence foods. In this regard purchase viagra plus 400 mg otc erectile dysfunction medicines, intravenous doses of midazolam should be sufficiently spaced to permit the peak clinical effect to be recognized before a repeat dose is considered order 400mg viagra plus with amex erectile dysfunction pump uk. Midazolam has the shortest context-sensitive half-time, which makes it the only one of the three benzodiazepine drugs suitable for continuous infusion (Figure 25–8). Although neuroprotective properties have not been shown for benzodiazepines, these drugs are potent anticonvulsants used in the treatment of status epilepticus, alcohol withdrawal, and local anesthetic- induced seizures. Cardiovascular Effects If used for the induction of anesthesia, midazolam produces a greater decrease in systemic blood pressure than comparable doses of diazepam. These changes are most likely due to peripheral vasodilation inasmuch as cardiac output is not changed. Similar to other intravenous induction agents, midazolam’s effect on systemic blood pressure is exaggerated in hypovolemic patients. Respiratory Effects Benzodiazepines produce minimal depression of ventilation, although transient apnea may follow rapid intravenous administration of midazolam for induction of anesthesia, especially in the presence of opioid premedication. Benzodiazepines decrease the ventilatory response to carbon dioxide, but this effect is not usually significant if they are administered alone. More severe respiratory depression can occur when benzodiazepines are administered together with opioids. Another problem affecting ventilation is airway obstruction induced by the hypnotic effects of benzodiazepines. Other Effects Pain during intravenous and intramuscular injection and subsequent thrombophlebitis are most pronounced with diazepam and reflect the poor water solubility of this benzodiazepine, which requires an organic solvent in the formulation. Despite its better solubility (which eliminates the need for an organic solvent), midazolam may also produce pain on injection. Clinical Uses & Dosage Benzodiazepines are most commonly used for preoperative medication, intravenous sedation, and suppression of seizure activity. The slow onset and prolonged duration of action of lorazepam limit its usefulness for preoperative medication or induction of anesthesia, especially when rapid and sustained awakening at the end of surgery is desirable. The amnestic, anxiolytic, and sedative effects of benzodiazepines make this class of drugs the most popular choice for preoperative medication. Midazolam has a more rapid onset, with greater amnesia and less postoperative sedation, than diazepam. The synergistic effects between benzodiazepines and other drugs, especially opioids and propofol, can be used to achieve better sedation and analgesia but may also greatly enhance their combined respiratory depression and may lead to airway obstruction or apnea. Because benzodiazepine effects are more pronounced with increasing age, dose reduction and careful titration may be necessary in elderly patients. Delayed awakening is a potential disadvantage, limiting the usefulness of benzodiazepines for induction of general anesthesia despite their advantage of less pronounced circulatory effects. Although its pharmacokinetics are favorable, endocrine side effects limit its use for continuous infusions. Etomidate is a carboxylated imidazole derivative that is poorly soluble in water and is therefore supplied as a 2 mg/mL solution in 35% propylene glycol. A Pharmacokinetics An induction dose of etomidate produces rapid onset of anesthesia, and recovery depends on redistribution to inactive tissue sites, comparable to thiopental and propofol. Metabolism is primarily by ester hydrolysis to inactive metabolites, which are then excreted in urine (78%) and bile (22%). Clearance of etomidate is about five times that of thiopental, as reflected by a shorter elimination half-time (Table 25–2). Because of etomidate’s minimal effects on hemodynamics and short context-sensitive half- time, larger doses, repeated boluses, or continuous infusions can safely be administered. Etomidate, like most other intravenous anesthetics, is highly protein bound (77%), primarily to albumin. Cardiovascular Effects A characteristic and desired feature of induction of anesthesia with etomidate is cardiovascular stability after bolus injection. In this regard, decrease in systemic blood pressure is modest or absent and principally reflects a decrease in systemic vascular resistance. Therefore, the systemic blood pressure-lowering effects of etomidate are probably exaggerated in the presence of hypovolemia, and the patient’s intravascular fluid volume status should be optimized before induction of anesthesia. Its depressant effects on myocardial contractility are minimal at concentrations used for induction of anesthesia. Respiratory Effects The depressant effects of etomidate on ventilation are less pronounced than those of barbiturates, although apnea may occasionally follow rapid intravenous injection of the drug. Depression of ventilation may be exaggerated when etomidate is combined with inhaled anesthetics or opioids. Endocrine Effects Etomidate causes adrenocortical suppression by producing a dose-dependent inhibition of 11β-hydroxylase, an enzyme necessary for the conversion of cholesterol to cortisol (see Figure 39–1). Despite concerns regarding this finding, no outcome studies have demonstrated an adverse effect when etomidate is given in a bolus dose. Clinical Uses & Dosage Etomidate is an alternative to propofol and barbiturates for the rapid intravenous induction of anesthesia, especially in patients with compromised myocardial contractility. Similar to propofol, during intravenous injection of etomidate there is a high incidence of pain, which may be followed by venous irritation. Involuntary myoclonic movements are also common but may be masked by the concomitant administration of neuromuscular blocking drugs. Awakening after a single intravenous dose of etomidate is rapid, with little evidence of any residual depressant effects. Etomidate does not produce analgesia, and postoperative nausea and vomiting may be more common than after the administration of thiopental or propofol. The characteristic state observed after an induction dose of ketamine is known as “dissociative anesthesia,” wherein the patient’s eyes remain open with a slow nystagmic gaze (cataleptic state). As with other intravenous induction drugs, the effect of a single bolus injection is terminated by redistribution to inactive tissue sites. Norketamine, the primary active metabolite, is less potent (one third to one fifth the potency of ketamine) and is subsequently hydroxylated and conjugated into water-soluble inactive metabolites that are excreted in urine. Organ System Effects If ketamine is administered as the sole anesthetic, amnesia is not as complete as with the benzodiazepines. Reflexes are often preserved, but it cannot be assumed that patients are able to protect the upper airway. Frequently, lacrimation and salivation are increased, and premedication with an anticholinergic drug may be indicated to limit this effect. Nevertheless, these perceived undesirable effects on cerebral blood flow may be blunted by the maintenance of normocapnia. Despite the potential to produce myoclonic activity, ketamine is considered an anticonvulsant and may be recommended for treatment of status epilepticus when more conventional drugs are ineffective. Such reactions may include vivid colorful dreams, hallucinations, out-of-body experiences, and increased and distorted visual, tactile, and auditory sensitivity. These reactions can be associated with fear and confusion, but a euphoric state may also be induced, which explains the potential for abuse of the drug.

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Erythromycin metabolites inhibit cytochrome P450 enzymes and discount viagra plus 400mg on-line herbal erectile dysfunction pills review, thus order viagra plus canada male erectile dysfunction pills, increase the serum concentrations of numerous drugs viagra plus 400 mg on line erectile dysfunction medicine reviews, including theophylline buy viagra plus 400mg overnight delivery erectile dysfunction quad mix, warfarin, cyclosporine, and methylprednisolone. Clarithromycin and erythromycin are similar with respect to antibacterial activity except that clarithromycin is more active against Mycobacterium avium complex (see Chapter 47). The longer half-life of clarithromycin (6 hours) compared with erythromycin permits twice-daily dosing. The recommended dosage is 250–500 mg twice daily or 1000 mg of the extended-release formulation once daily. Clarithromycin penetrates most tissues well, with concentrations equal to or exceeding serum concentrations. Portions of active drug and this major metabolite are eliminated in the urine, and dosage reduction (eg, a 500 mg loading dose, then 250 mg once or twice daily) is recommended for patients with creatinine clearances less than 30 mL/min. The advantages of clarithromycin compared with erythromycin are lower incidence of gastrointestinal intolerance and less frequent dosing. Its spectrum of activity, mechanism of action, and clinical uses are similar to those of clarithromycin. Azithromycin is slightly less active than erythromycin and clarithromycin against staphylococci and streptococci and slightly more active against H influenzae. However, azithromycin penetrates into most tissues (except cerebrospinal fluid) and phagocytic cells extremely well, with tissue concentrations exceeding serum concentrations by 10- to 100-fold. The drug is slowly released from tissues (tissue half-life of 2–4 days) to produce an elimination half-life approaching 3 days. These unique properties permit once-daily dosing and shortening of the duration of treatment in many cases. For example, a single 1-g dose of azithromycin is as effective as a 7-day course of doxycycline for chlamydial cervicitis and urethritis. Community-acquired pneumonia can be treated with azithromycin given as a 500 mg loading dose, followed by a 250 mg single daily dose for the next 4 days. Aluminum and magnesium antacids do not alter bioavailability but delay absorption and reduce peak serum concentrations. Because it has a 15-member (not 14-member) lactone ring, azithromycin does not inactivate cytochrome P450 enzymes and, therefore, is free of the drug interactions that occur with erythromycin and clarithromycin. Recent studies have suggested that azithromycin may be associated with a small increased risk of cardiac death. It is active in vitro against Streptococcus pyogenes, S pneumoniae, S aureus, H influenzae, Moraxella catarrhalis, Mycoplasma sp, L pneumophila, Chlamydia sp, H pylori, Neisseria gonorrhoeae, B fragilis, T gondii, and certain nontuberculosis mycobacteria. Many macrolide-resistant strains are susceptible to ketolides because the structural modification of these compounds renders them poor substrates for efflux pump-mediated resistance, and they bind to ribosomes of some bacterial species with higher affinity than macrolides. Oral bioavailability of telithromycin is 57%, and tissue and intracellular penetration is generally good. Telithromycin is metabolized in the liver and eliminated by a combination of biliary and urinary routes of excretion. It is administered as a once-daily dose of 800 mg, which results in peak serum concentrations of approximately 2 mcg/mL. Other respiratory tract infections were removed as indications when it was recognized that use of telithromycin can result in hepatitis and liver failure. Telithromycin is also contraindicated in patients with myasthenia gravis because it may exacerbate this condition. Mechanism of Action & Antibacterial Activity Clindamycin, like erythromycin, inhibits protein synthesis by interfering with the formation of initiation complexes and with aminoacyl translocation reactions. The binding site for clindamycin on the 50S subunit of the bacterial ribosome is identical with that for erythromycin. Resistance to clindamycin, which generally confers cross-resistance to macrolides, is due to (1) mutation of the ribosomal receptor site; (2) modification of the receptor by a constitutively expressed methylase (see section on erythromycin resistance, above); and (3) enzymatic inactivation of clindamycin. Gram- negative aerobic species are intrinsically resistant because of poor permeability of the outer membrane. Clindamycin penetrates well into most tissues, with brain and cerebrospinal fluid being important exceptions. Clindamycin is metabolized by the liver, and both active drug and active metabolites are excreted in bile and urine. Clinical Use Clindamycin is indicated for the treatment of skin and soft-tissue infections caused by streptococci and staphylococci. It is often active against community-acquired strains of methicillin-resistant S aureus, an increasingly common cause of skin and soft tissue infections. Clindamycin is also indicated for treatment of infections caused by Bacteroides sp and other anaerobes. Clindamycin, sometimes in combination with an aminoglycoside or cephalosporin, is used to treat penetrating wounds of the abdomen and the gut; infections originating in the female genital tract, eg, septic abortion, pelvic abscesses, or pelvic inflammatory disease; and lung abscesses. Clindamycin is now recommended rather than erythromycin for prophylaxis of endocarditis in patients with specific valvular heart disease who are undergoing certain dental procedures and have significant penicillin allergies. The streptogramins share the same ribosomal binding site as the macrolides and clindamycin and thus inhibit protein synthesis in an identical manner. Quinupristin-dalfopristin is rapidly bactericidal for most susceptible organisms except Enterococcus faecium, which is killed slowly. Quinupristin-dalfopristin is active against gram-positive cocci, including multidrug-resistant strains of streptococci, penicillin-resistant strains of S pneumoniae, methicillin-susceptible and resistant strains of staphylococci, and E faecium (but not Enterococcus faecalis). Patients with hepatic insufficiency may not tolerate the drug at usual doses, however, because of increased area under the concentration curve of both parent drugs and metabolites. Clinical Uses & Adverse Effects Quinupristin-dalfopristin is approved for treatment of infections caused by staphylococci or by vancomycin-resistant strains of E faecium, but not E faecalis, which is intrinsically resistant, probably because of an efflux-type resistance mechanism. The principal toxicities are infusion-related events, such as pain at the infusion site, and an arthralgia-myalgia syndrome. Mechanism of Action & Antimicrobial Activity Chloramphenicol is a potent inhibitor of microbial protein synthesis. It binds reversibly to the 50S subunit of the bacterial ribosome (Figure 44–1) and inhibits peptide bond formation (step 2). Chloramphenicol is a bacteriostatic broad-spectrum antibiotic that is active against both aerobic and anaerobic gram-positive and gram-negative organisms. Most gram-positive bacteria are inhibited at concentrations of 1–10 mcg/mL, and many gram-negative bacteria are inhibited by concentrations of 0. H influenzae, Neisseria meningitidis, and some strains of bacteroides are highly susceptible, and for these organisms, chloramphenicol may be bactericidal. Low-level resistance to chloramphenicol may emerge from large populations of chloramphenicol-susceptible cells by selection of mutants that are less permeable to the drug. Clinically significant resistance is due to production of chloramphenicol acetyltransferase, a plasmid-encoded enzyme that inactivates the drug. Chloramphenicol palmitate is a prodrug that is hydrolyzed in the intestine to yield free chloramphenicol. The parenteral formulation is a prodrug, chloramphenicol succinate, which is hydrolyzed to yield free chloramphenicol, giving blood levels somewhat lower than those achieved with orally administered drug. Chloramphenicol is widely distributed to virtually all tissues and body fluids, including the central nervous system and cerebrospinal fluid, such that the concentration of chloramphenicol in brain tissue may be equal to that in serum.

Acting bilat­ length of the vertebral column but are best developed in erally generic 400mg viagra plus fast delivery erectile dysfunction doctors in ny, they straighten the back purchase viagra plus mastercard erectile dysfunction doctor cape town, returning it to the upright the lumbar region purchase viagra plus amex erectile dysfunction drugs at cvs. They are present throughout flexion by contracting and relaxing in a coordinated the length of the vertebral column but are best devel­ fashion buy viagra plus 400mg free shipping erectile dysfunction journal articles. In addition, unilateral contractions of and medially from transverse processes to spinous pro­ muscles attached to the head turn the head to the actively cesses crossing two vertebrae (long rotators) or attach- contracting side. They have an bilaterally, they extend the vertebral column, an action oblique lateral and downward direction and insert into similar to that of the erector spinae group. However, when the rib below the vertebra of origin in the area of the muscles on only one side contract, they pull the spinous tubercle. Contracting bilaterally, this muscle pulls the adjoining vertebrae during movements of the vertebral head posteriorly, whereas unilateral contraction pulls the column to allow more effective action of the large head posteriorly and turns it, causing the chin to move muscle groups. Suboccipital muscles Segmental muscles A small group of deepmuscles in theupper cervical region The two groups of segmental muscles (Fig. Because of their location they are sometimes referred to as suboc­ • Thefrst group of segmental muscles arethelevatores cipital muscles {Figs. The vascular supply to the muscles in this 98 area is from branches of the vertebral and occipital arteries. Regional anatomy • Spinal Cord The contents of the area outlined by these muscles are the posterior ramus of Cl, the vertebral artery, and associ­ ated veins. A weakness in, or an inability to use, the latissimus ® dorsi, resulting from an injury tothe thoracodorsal nerve, diminishes the capacity to pull the body upward ® while climbing or doing a pull-up. An injury to the dorsal scapular nerve, which { innervates the rhomboids, may result in a lateral shif in the position ofthe scapula on the afected side. A fne flament of connective tissue (the pial part Pial par of theflumterminale) continues inferiorly from the apex @ part of of the conus medullaris. It has two major swellings or enlargements in terminale regions associated with the origin of spinal nerves that of subarachnoid innervate the upper and lower limbs. Regional anatomy • Spinal Cord Anterior radicular arery Segmental spinal arter Posterior radicular artery Posterior spinal arteries Posterior radicular artery Anterior radicular artery Segmental medullar artery Segmental spinal artery Posterior branch of left posterior intercostal artery Left posterior intercostal artery B Fig. The radicular arteries follow, and supply, the anterior two branches that bracket the posterolateral sulcus and and posterior roots. These vessels pass directly to the The anterior and posterior spinal arteries are reinforced longitudinally oriented vessels, reinforcing these. The largest of these is the arteria • One midline channel parallels the anterior median radicularis magna or the artery of Adamkiewicz fssure. This vessel arises in the lower thoracic or upper • One midline channel passes along the posterior median lumbar region, usually on the left side, and reinforces the sulcus. These longitudinal channels drain into an extensive internal vertebral plexus in the extradural (epidural) Veins space of the vertebral canal, which then drains into seg­ Veins that drain the spinal cord form a number of longitu­ mentally arranged vessels that connect with major sys­ dinal channels (Fig. The internal vertebral plexus also communicates with intracra­ • Two pairs ofveins oneach side bracket the connections nial veins. The spinal dura mater is the outermost meningeal mem­ brane and is separated from the bones forming the verte­ Subarachnoid space bral canal by an extradural space {Fig. Large with and become part of the outer covering (epineurium) blood vessels are suspended in the subarachnoid space by of the nerves. Arachnoid mater The subarachnoid space extends further inferiorly than The arachnoid mater is a thin delicate membrane the spinal cord. The spinal cord ends at approximately against, but not adherent to, the deep surface of the dura the disc between vertebrae 11 and 111, whereas the Subarachnoid space Posterior spinal artery Pia mater Recurrent meningeal nerves Denticulate ligament Anterior spinal artery Dura mater Fig. The subarachnoid the vertebral canal space is largest in the region inferior to the terminal end of the spinal cord, where it surrounds the cauda equina. It the median plane the roots of the interspinous liga­ extends into the anterior median fssure and reflects as ments and vertebral spinous processes. As the Between the walls of the vertebral canal and the dural roots exit the space, the sleeve-like coatings reflect onto the sac is an extradural space containing a vertebral plexus of arachnoid mater. On each side of the spinal cord, a longitudinally ori­ The vertebral spinous processes can bepalpatedthrough ented sheet of pia mater (the denticulate ligament) the skin in the midline in thoracic and lumbar regions extends laterally from the cord toward the arachnoid and of the back. In lumbar regions, the adjacent spinous processes and the associated laminae oneither side • Medially, each denticulate ligament is attached to the of the midline do not overlap, resulting in gaps between spinal cord in a plane that lies between the origins of the adjacent vertebral arches. When carrying out a lumbar puncture (spinal tap), the • Laterally, each denticulate ligament forms a series of needle passes between adjacent vertebral spinous pro­ triangular extensions along its free border, with the cesses, through the supraspinous and interspinous liga­ apex of each extension being anchored through the ments, and enters the extradural space. When subarachnoid space because the spinal cord terminates procedures are carried out, the patient must be in the around the level of the disc between vertebrae Ll and Lll erect position and not lying on his or her side or in the in theadult. A needle is placed through in the midline in between the spinous processes into the the skin, supraspinous ligament, interspinous ligament, extradural space. Further advancement punctures the and ligamenta flava into the areolartissue and fat around dura and arachnoid mater to enterthe subarachnoid the dura mater. Most needles push the roots awayfrom the tip difuses around the vertebral canal to anesthetize the without causing the patientany symptoms. Once the exiting nerve roots and difuse into the subarachnoid needle is in the subarachnoid space, fluid can be space. Spinal nerves A spinal segment is the area of the spinal cord that Each spinal nerve is connected to the spinal cord by poste­ gives rise to the posterior and anterior rootlets, which rior and anterior roots {Fig. Laterally, the pos­ terior and anterior roots on each side join to form a spinal • The posterior root contains the processes of sensory nerve. Consequently, posterior and anterior roots forming dura, ligaments, intervertebral discs, and blood vessels. Because the spinal cord is much shorter than the verte­ Below the end of the spinal cord, the posterior and ante­ bral column, the roots of spinal nerves become longer and rior roots of lumbar, sacral, and coccygeal nerves pass infe­ pass more obliquely from the cervical to coccygeal regions riorly to reach their exit points from the vertebral canal. Under certain • eight cervical nerves-C1 to C8, circumstances, thevirus becomes activated and travels along the neuronal bundles to the areas supplied by • twelve thoracic nerves-T1 toT12, that nerve (the dermatome). Importantly, this • fve sacral nerves-S1 to S5, typical dermatomal distribution is characteristic of • one coccygeal nerve-Co. There­ fore cervical nerves C2 to C7 also emerge from the verte­ bral canal above their respective vertebrae. As a consequence, all remaining spinal nerves, beginning with T1, emerge from the vertebral canal below their respective vertebrae. Nerves C2 to C7 emerge superior to pedicles Transition in nomenclature of nerves Nerves T1 to Co emerge inferior to pedicles of their respective vertebrae Fig. Enlarged lymph nodes in the Back pain is an extremely common condition afecting pre- and para-aortic region may produce central posterior almost all individuals at some stage during their life. An enlarging pain relates to the vertebral column and its attachments abdominal aorta (abdominal aortic aneurysm) may cause or relates to other structures. Therefore it is The failure to consider other potential structures that critical to think of this structure as a potential cause of may produce back pain can lead to signifcant mortality back pain, because treatment will be lifesaving.