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Glucocorticoids modulate the ex- gens and a long-term increase in the risk of pression of numerous genes; thus 100mg cafergot mastercard shingles pain treatment natural, the pro- neoplasms discount cafergot 100 mg on line joint and pain treatment center thousand oaks. In addition cafergot 100 mg with visa pain management for dog in heat, gluco- rying specific receptors with the appropriate corticoids interfere with inflammatory cyto- antigen-binding site cafergot 100mg low cost pain treatment doctors. B-lymphocytes “recog- kines and signaling molecules at variousoth- nize” antigen surface structures by means of er sites. Glucocorticoids are used in organ membrane receptors that resemble the anti- transplantations, autoimmune diseases, and bodies formed subsequently. Systemic use carries the (and naive B cells) require the antigen to be risk of iatrogenic Cushing syndrome (p. In contrast to glucocorticoids, ter permits recognition of antigenic struc- the plethora of accompanying metabolic ef- tures by means of the T-cell receptor. Theyareusedtosup- lation by cytokines plays an essential part in press transplant rejection reactions. It can be used in inhibits inosine monophosphate dehydro- the treatment ofmultiple sclerosisbesidesβ- genase, which catalyzes purine synthesis in interferon. The culprit antigen Luellmann, Color Atlas of Pharmacology © 2005 Thieme Inhibition of Immune Responses 305 A. Immune reaction and immunosuppressives Antigen Macrophage Virus-infected cell, Glucocorticoids transplanted cell. Risk factors for from animals immunized with human T- cardiovascular diseases may be adversely af- lymphocytes. The antibodies bind to and fected—a critical and important concern in damage T cells and can thus be used to at- long-term prognosis. At the molecular level, peptide composed of 11, in part atypical, however, its “receptor” is not cyclophilin but amino acids. Tacrolimus is ciclosporin is not degraded by gastrointesti- likewise used to prevent allograft rejection. In T-helper cells, it inhibits the Its epithelial penetrability is superior to that production of interleukin-2 by interfering at of ciclosporin, allowing topical application in the level of transcriptional regulation. The latter operates in the sig- The breakthroughs in modern transplanta- naling path leading from the interleukin-2 tion medicine are largely attributable to the receptor to activation of mitosis in lympho- introduction of ciclosporin. Its dosage must be titrated so that blood levels are neither too high (risk of renal injury) nor too low (re- jection reaction). Back-transport of the drug into the gut lumen occurs via the P-glycoprotein ef ux pump, in addition to metabolization by cy- tochrome oxidases of the 3A subfamily. Pro- tracted immunosuppression carries an in- Luellmann, Color Atlas of Pharmacology © 2005 Thieme Inhibition of Immune Responses 307 A. The substance possesses a very high Poisonings iron-binding capacitybutdoes notwithdraw Drugs used to counteract drug overdosage iron from hemoglobin or cytochromes. Oral administration is indicated only if diazepines; antibody (Fab fragments) with enteralabsorptionofironistobecurtailed. It should be noted that bloodletting is the Chelating agents (A) serve as antidotes in most effective means of removing iron from poisoning with heavy metals. They act to the body; however, this method is unsuit- complex and, thus, “inactivate” heavy metal able for treating conditions of iron overload ions. Two their high af nity, chelating agents “attract” additional indications are cystinuria and metal ions present in the organism. In cystinuria, forma- lates are nontoxic, are excreted predomi- tion of cystine stones in the urinary tract is nantly via the kidney, and maintain a tight prevented because the drug can form a di- organometallic bond in the concentrated, sulfide with cysteine that is readily soluble. This antidote cannot penetrate through tion with aldehydes, whereby polymeriza- cell membranes and must be given parent- tion of collagen molecules into fibrils is in- erally. An important step is early emptying of mercaprol forms a liquid, rapidly decompos- thestom achbygastriclavageand,ifneces- ing substance that is given intramuscularly sary, administration of an osmotic laxative. A related compound, both Use of emetics (saturated NaCl solution, ipe- in terms of structure and activity, is dimer- cac syrup, apomorphine s. As a result, the organism is liberated from bitter almonds in the gastro- poisoned with its own transmitter sub- intestinal tract. Time and again, their ensues while erythrocytes remain charged use has led to human poisoning because with O2 (venous blood colored bright red). As a therapeutic measure, so- blockade, and inhibition of neuromuscular dium thiosulfate can be given i. Hydroxyco- poisonswassubsequently“demonstrated”in balamin (= vitamin B12a)isanalternative, smaller local armed conflicts in developing very effective antidote because its central countries. Thus, under- standing the signs of poisoning and the prin- Ferric ferrocyanide (“Berlin blue” [B]) is ciples of treatment are highly important. Brown- which are gastrointestinal disturbances, fol- colored methemoglobin, containing triva- lowedbynerveandbraindamage,aswellas lent instead of divalent iron, is incapable of hair loss. Under normal conditions, ism are secreted into the gut but undergo methemoglobin is produced continuously, reabsorption. The insoluble, nonabsorbable but reduced again with the help of glucose- colloidal Berlin blue binds thallium ions. Substances given orally to prevent absorption of acutely that promote formation of methemoglobin ingested thallium or to promote clearance (B) may cause a lethal deficiency of O2. Tolo- from the organism by intercepting thallium nium chloride is a redox dye that can be that is secreted into the intestines (B). Basi- tion with triamterene or amiloride is often cally, atherosclerosis manifests itself in three advantageous. From the group of antagonists at β-adre- Hypertension is considered to be pre- noceptors, β1-selective blockers are mainly sent when systolic blood pressure exceeds used (e. Owing toblockade of 140 mmHg and the diastolic value lies β2-receptors, β-blockers can impair pulmo- above 90 mmHg. Since cardiovascular risk nary function, particularly in patients with increases over a wide range with increasing chronic obstructive lung disease. If idines with long half-lives are advantageous other risk factors are present, blood pres- because short-acting drugs, which rapidly sure should be brought down to an even lower blood pressure, are prone to elicit re- lower level (in diabetes mellitus below flex tachycardia. Therapeutic objectives com- Fewer that 50% of hypertensive patients prise the prevention of organ damage and are adequately managed by monotherapy. For instance, diuretic-induced loss ethanol/day; inwomen 10–20 g/day), to stop of Na+ and water leads to a compensatory smoking, and to restrict the daily intake of activation of the renin–angiotensin system NaCl (to 6 g/day). Risk factors of atherosclerosis and secondary diseases R i s k f a c o r s Hypertension, hypercholesterolemia, diabetes mellitus, smoking Brain Heart Athero- sclerosis Kidney Coronary heart disease Renal failure Myocardial Stroke: infarction Infarction Congestive Hemorrhage heart failure Diminished life expectancy B. Asarule,the exercise, further dilation of arterioles is oxygen deficit results from inadequate myo- impossible. The underlying causes are agents that act to dilate arterioles would most commonly an atherosclerotic change of thus be inappropriate because at rest they the vascular wall (coronary sclerosis with may divert blood fromunderperfused into exertional angina); very infrequently a spas- healthy vascular regions on account of modic constriction of a morphologically redundant arteriolar dilation. The result- healthy coronary artery (coronary spasm ing “steal effect” could provoke an anginal with angina at rest; variant angina); or more attack.

Babuna Ke Phool (Roman Chamomile). Cafergot.

• How does Roman Chamomile work?
• Are there safety concerns?
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• Dosing considerations for Roman Chamomile.

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The lowest effective dose should be used first and may be repeated in 30 minutes up to a maximum of 10–20 mg purchase cafergot 100 mg without a prescription pain medication for dogs with bite wounds. Sustained- release formulations are effective and may be used but as noted above buy 100 mg cafergot mastercard wrist pain yoga treatment, may be inferior to immediate-release formulations buy generic cafergot 100 mg line elbow pain treatment bursitis. Brattstrom A: Long term effects of St John’s wort (Hypericum perforatum) treatment: A 1 year safety study in mild to moderate depression cheap cafergot 100mg line myofascial pain syndrome treatment guidelines. Butterweck V, Schmidt M: St John’s wort: Role of active compounds for its mechanism of action and efficacy. Sharma M et al: Bactericidal and anti-inflammatory properties of a standardized Echinacea extract (Echinaforce): Dual actions against respiratory bacteria. Shi C et al: Ginkgo biloba extract in Alzheimer’s disease: From action mechanisms to medical practice. Vellas B et al: Long term use of standardized ginkgo biloba extract for the prevention of Alzheimer’s disease (GuidAge): A randomized placebo-controlled trial. Wu D et al: Efficacies of different preparations of glucosamine for the treatment of osteoarthritis: A meta-analysis of randomised, double-blind, placebo-controlled trials. Zeng T et al: A meta-analysis of randomized, double-blind, placebo-controlled trials for the effects of garlic on serum lipid profiles. It has been shown to have a small but significant lowering effect on total cholesterol, but only when dietary controls were not in place. It is advisable to monitor the patient’s blood pressure for 2 weeks after initiating a garlic supplement as he takes prescription medications for hypertension. Several dietary supplements reviewed in this chapter (garlic, ginkgo, and ginseng) have antiplatelet effects that could be additive with aspirin. If this patient were also taking warfarin, additional interactions could occur with coenzyme Q10 (vitamin K-like structure), St. John’s wort (cytochrome P450 1A2, 2C9, 3A4 inducer), and melatonin (in vitro decreased prothrombin time), leading to a decreased warfarin effect, or with glucosamine (increased international normalized ratio), leading to an increased warfarin effect. Medication, surgery, psychiatric treatment, radiation, physical therapy, health education, counseling, further consultation (second opinions), and no therapy are some of the options available. A written prescription is the prescriber’s order to prepare or dispense a specific treatment—usually medication—for a specific patient. When a patient comes for an office visit, the physician or other authorized health professional prescribes medications 67% of the time, and an average of one prescription is written per office visit because more than one prescription may be written at a single visit. The physical form of the prescription, common prescribing errors, and legal requirements that govern various features of the prescribing process are then discussed. Make a specific diagnosis: Prescriptions based merely on a desire to satisfy the patient’s psychological need for some type of therapy are often unsatisfactory and may result in adverse effects. For example, in a patient with a probable diagnosis of rheumatoid arthritis, the diagnosis and the reasoning underlying it should be clear and should be shared with the patient. Consider the pathophysiologic implications of the diagnosis: If the disorder is well understood, the prescriber is in a much better position to offer effective therapy. The patient should be provided with the appropriate level and amount of information about the pathophysiology. Many pharmacies, websites, and disease-oriented public and private agencies (eg, Arthritis Foundation, American Heart Association, American Cancer Society, etc) provide information sheets suitable for patients. Select a specific therapeutic objective: A therapeutic objective should be chosen for each of the pathophysiologic processes defined in the preceding step. In a patient with rheumatoid arthritis, relief of pain by reduction of the inflammatory process is one of the major therapeutic goals that identifies the drug groups that should be considered. Arresting the course of the disease process in rheumatoid arthritis is a different therapeutic goal, which might lead to consideration of other drug groups and prescriptions. Select a drug of choice: One or more drug groups will be suggested by each of the therapeutic goals specified in the preceding step. Selection of a drug of choice from among these groups follows from a consideration of the specific characteristics of the patient and the clinical presentation. For certain drugs, characteristics such as age, other diseases, and other drugs being taken (because of the risk of duplicative therapy or drug-drug interactions) are extremely important in determining the most suitable drug for management of the present complaint. In the example of the patient with probable rheumatoid arthritis, it would be important to know whether the patient has a history of aspirin intolerance or ulcer disease, whether the cost of medication is an especially important factor and the nature of the patient’s insurance coverage, and whether there is a need for once-daily dosing. If the patient does not have ulcer disease but does have a need for low-cost treatment, ibuprofen or naproxen would be a rational choice. Determine the appropriate dosing regimen: The dosing regimen is determined primarily by the pharmacokinetics of the drug in that patient. If the patient is known to have disease of the organs required for elimination of the drug selected, adjustment of the average regimen is needed. For a drug such as ibuprofen, which is eliminated mainly by the kidneys, renal function should be assessed. If renal function is normal, the half-life of ibuprofen (about 2 hours) requires administration three or four times daily. The dose suggested in this book, drug handbooks, and the manufacturer’s literature is 400–800 mg four times daily. Devise a plan for monitoring the drug’s action and determine an end point for therapy: The prescriber should be able to describe to the patient the kinds of drug effects that will be monitored and in what way, including laboratory tests (if necessary) and signs and symptoms that the patient should report. For conditions that call for a limited course of therapy (eg, most infections), the duration of therapy should be made clear so that the patient does not stop taking the drug prematurely and understands why the prescription probably need not be renewed. For the patient with rheumatoid arthritis, the need for prolonged—perhaps indefinite—therapy should be explained, including how to obtain refills. The prescriber should also specify any changes in the patient’s condition that would call for changes in therapy. For example, in the patient with rheumatoid arthritis, development of gastrointestinal bleeding would require an immediate change in drug therapy and a prompt workup of the bleeding. Plan a program of patient education: The prescriber and other members of the health team should be prepared to repeat, extend, and reinforce the information transmitted to the patient as often as necessary. The importance of informing and involving the patient in each of the above steps must be recognized, as shown by experience with teratogenic drugs (see Chapter 59). Many pharmacies routinely provide this type of information with each prescription filled, but the prescriber must not assume that this will occur. The contents of that prescription are specified in the medical staff rules by the hospital’s Pharmacy and Therapeutics Committee. The patient’s name is typed or written on the form; therefore, the orders consist of the name and strength of the medication, the dose, the route and frequency of administration, the date, other pertinent information, and the signature of the prescriber. If the duration of therapy or the number of doses is not specified (which is often the case), the medication is continued until the prescriber discontinues the order or until it is terminated as a matter of policy routine, eg, a stop-order policy. Before dispensing a prescription, the pharmacist must establish the prescriber’s bona fides and should be able to contact the prescriber by telephone if any questions arise.

Patients who are malnourished are regarded as its differential inhibition of enzymes responsible for pros- being at risk at 50% of these plasma concentrations buy cafergot 100mg mastercard pain treatment center brentwood. It is inactivated in the liver buy generic cafergot 100 mg spine and nerve pain treatment center traverse city mi, principally by the smaller generic 100mg cafergot with amex pain treatment algorithm, is thought to have been ingested within the conjugation as glucuronide and sulphate buy cafergot 100 mg on-line pain treatment topics. This substance is normally Specific therapy involves replenishing stores of liver glu- rendered harmless by conjugation with glutathione. Maximal, long- most effective if administered within 8 h of the overdose, term, daily dosing may predispose to chronic renal disease. Her husband said that his wife ‘knew that too much paracetamol was In the 18th century, the Reverend Edmund Stone wrote dangerous but she did not realise there was paracetamol in [the about the value of an extract of bark from the willow tree proprietary preparation]’ which she bought at a supermarket that did not have a dispensary counter where she could have received advice. Aspirin is a common cause of allergic or proved highly successful in the treatment of rheumatic fe- pseudoallergic symptoms and signs. The new preparation proved acceptable aspirin use to the development of the rare Reye’s tohisfatherandpavedthewayfortheproductionofaspirin. Platelets cannotregeneratethe enzyme comfort, tinnitus, deafness, sweating, pyrexia, restlessness, and the resumption of thromboxane A2 production is tachypnoea and hypokalaemia. A large overdose (plasma dependent on the entry of new platelets into the salicylate concentration above 750 mg/L) may result in circulation (platelet lifespan is 7 days). Thus a pulmonary oedema, convulsions and coma, with severe de- continuousantiplateleteffectisachieved withlow doses. Bleeding is unusual, despite the anti- • Respiratory stimulation is a characteristic of aspirin platelet effect of aspirin. In • Although aspirin in high dose reduces renal tubular children under 4 years, severe metabolic acidosis is more reabsorption of uric acid so increasing its elimination, likely than respiratory alkalosis, especially if the drug has other treatments for hyperuricaemia are preferred. Indeed aspirin should be avoided in gout as low doses Serial measurements of plasma salicylate are necessary to inhibit uric acid secretion and on balance its effects on monitor the course of the overdose, for the concentration uric acid elimination are adverse. The main use of aspirin is as an antiplatelet agent to agement of overdose applies, but the following are relevant prevent arterial thrombotic events due to atherosclerosis. Gastric lavage or the use in Kawasaki disease, in combination with intravenous im- of an emetic is no longer recommended. Hydrolysis removes is treated with sodium bicarbonate, which alkalinises the acetyl group, and the resulting salicylate ion is inacti- the urine and accelerates the removal of salicylate in the vated largely by conjugation with glycine. Doses of 75–150 mg/day are used to prevent throm- Colchicine is derived from the autumn crocus (Colchicum botic vascular occlusion; 300 mg as immediate treatment for autumnale). Its anti-inflammatory properties have long myocardial infarction; 300–900 mg every 4–6 h for analgesia. Effects particularly associated with aspi- tion to relieving inflammation in acute gout attacks, it is rin are: used to treat other inflammatory disorders including Beh- • Salicylism (the symptoms of an excessive dose): tinnitus c¸et’s syndrome and the hereditary fever syndrome familial and hearing difficulty, dizziness, headache and Mediterranean fever. The most common adverse effect of colchicine is diar- Most conventional immunomodulatory agents act by rhoea, due to its effects on rapidly proliferating gastrointes- inhibiting activation or reducing proliferation of lympho- tinal epithelial cells. Many have more than one mechanism of action may follow and it is therefore a sign to stop the drug and often the precise way in which they exert their effects and restart at a lower dose. Methotrexate, azathioprine, mycophenolate mofetil and Immunomodulatory drugs are used both to control symp- leflunomide are antimetabolites, interfering with the de toms and to retard or arrest the progression of chronic in- novo synthesis of purines and pyrimidines, on which pro- flammatory diseases. Metho- variety of ways, and reduce the proliferation and activation trexate is thought to have additional anti-inflammatory of lymphocytes. The calcineurin antagonists (ciclosporin and tacro- The terminology surrounding immunomodulatory drugs limus) and sirolimus selectively inhibit T-cell activation has evolved separately in different specialties, although the and proliferation, by inhibiting cytokine expression and underlying management principles are similar. Intravenous immuno- disease progression in illnesses such as rheumatoid or psori- globulin has immunomodulatory effects through interfer- aticarthritis. Treatmentregimensforsystemicvasculitisorse- ence with Fcg receptor signalling, among other vere organ involvement in the connective tissue diseases mechanisms. The precise mechanisms of action of sulfasa- make use of terminology drawn from oncology, with ‘remis- lazine, hydroxychloroquine, thalidomide, dapsone and sion induction’ followed by ‘maintenance’ phases. Many of gold are less clear, but they have been shown to influence thesedrugsaredescribedas‘steroid-sparing’astheirconcom- the expression of a range of pro-inflammatory cytokines. All should only be initiated under specialist hazardous than rash or arthritis and therefore a more supervision and all call for close monitoring, for example of potent but potentially more toxic drug regimen is bone marrow, liver, kidney or other organs, as known tox- justified. Live vaccines in general should not be given to • Adverse-effect profile: both the probability and severity immunosuppressed patients as there is a risk of dissemi- of potential adverse effects need to be considered. Methotrexate was first developed as an anticancer drug • Co-morbidity: drugs causing hypertension or adverse 50 years ago. Many conventional immunomodulatory drugs used in rheumatology practice are anti-metabolites, inhibiting de novo synthesis of purines or pyrimidines; pathways upon which activated lymphocytes are particularly dependent. The mechanisms of action of sulfasalazine, hydroxychloroquine and thalidomide appear to involve inhibition of expression of pro-inflammatory cytokines. Methotrexate is usually prescribed orally, thritis, and in the maintenance phase of therapy for sys- starting at 7. Folic acid is usually prescribed (variably inhibits folate-dependent enzymes involved in purine bio- 5 mg weekly, three times weekly or on all days apart from synthesis, thus reducing lymphocyte proliferation, and this on the methotrexate dosing day), in order to mitigate the was originally thought to be its principal mechanism of ac- adverse effects. This appears to have little effect on the tion (and is likely to be the source of many of its toxic ef- blockade of de novo purine synthesis, unlike folinic acid fects). Increased plasma concentra- Mouth ulcers and nausea occur commonly but may be im- tions of adenosine are thought to mediate many anti- proved by co-prescription of folic acid. Lastly, co-prescription of angiotensin- scribed to patients with moderate to severe renal impair- converting enzyme inhibitors and azathioprine increases ment, liver disease or an active infection. Because of its the risk of myelosuppression; the mechanism is incom- teratogenicity it must not be prescribed for women who pletely understood but has assumed greater importance are or may become pregnant or who are breast feeding. Experience with azathioprine in pregnant women with renal transplants indicates that Azathioprine it is relatively safe, probably because the fetus cannot me- Azathioprine is another antimetabolite which acts by inhi- tabolise 6-mercaptopurine. Although a teratogenic metab- biting purine biosynthesis, thus preferentially acting on olite is present in breast milk, its concentration is low and proliferating lymphocytes. Besides its use to prevent rejec- no evidence for harm exists; nevertheless, breast feeding tion in organ transplant recipients, it has a well established while taking azathioprine is best regarded as unsafe. It is licensed for the prophy- in the presence of glutathione to 6-mercaptopurine and laxis of acute rejection following organ transplantation then to 6-thioguanine. These are similar to azathioprine and in- 25–50 mg and rising over the course of several weeks to clude gastrointestinal disturbances (diarrhoea is particularly a daily dose of 1. The major serious reactions are bone mar- row suppression resulting in leucopenia, anaemia and Leflunomide thrombocytopenia; hepatotoxicity; increased susceptibility to infection; and in the long term an increased risk of neo- The active metabolite of leflunomide (A77 1726) inhibits plasia. As with methotrexate, regular monitoring of full dihydro-orotate dehydrogenase,a mitochondrial enzymere- quired for the synthesis of pyrimidines. Xanthine oxidase, the enzyme inhibited by allopurinol and febuxostat to therapeutic effect in the man- Adverse effects. Diarrhoea is commonest; other gastroin- agement of gout, is involved in the catabolism of azathio- testinal disturbances, hepatitis, leucopenia, alopecia, hyper- prine. In the event of a serious azathioprine may result in profound myelosuppression adverse event, the elimination of leflunomide can be accel- and should be avoided. Oral cyclophosphamide is less frequently used due to the larger cumulative dose and thus increased risk The calcineurin inhibitors ciclosporin and tacrolimus in- of long-term toxicities. Other adverse effects are highly sig- orally to prevent rejection after solid organ transplantation nificant and include bone marrow toxicity and consequent and in chronic inflammatory disorders including cutane- increased risk of opportunistic infection, infertility, teratoge- ous psoriasis, Behc¸et’s syndrome, systemic vasculitis and, nicity, severe nausea and increased incidence of malignancy, occasionally, rheumatoid arthritis.

The tendons of the extensor digiti that occurs within the frst dorsal extensor compartment minimi purchase cafergot 100 mg visa natural treatment for post shingles pain, extensor indicis cheap 100mg cafergot amex wrist pain treatment exercises, and extensor pollicis brevis and involves the extensor pollicis brevis tendon and muscles join these hoods order 100mg cafergot advanced pain treatment center ohio. Patients typically present with signifcant wrist pain preventing appropriate fexion/ • the apex attached to the distal phalanx order cafergot 100mg pain solutions treatment center ga, extension and abduction of the thumb. For example, the syndrome is common in young mothers who are (index, middle, ring, and little fngers) or proximal constantly lifing young children. Tenosynovitis In addition to other attachments, many of the intrinsic Tenosynovitis is inflammation of a tendon and its muscles of the hand insert into the free margin of the hood sheath. By inserting into the extensor hood, these however, it can also be associated with other disorders intrinsic muscles are responsible for complex delicate such as rheumatoid arthritis and connective tissue movements of the digits that could not be accomplished pathologies. This ability to flex the metacarpophalangeal joints, by the deep branch of the ulnar nerve except for the three while at the same time extending the interphalangeal thenar and two lateral lumbrical muscles, which are inner­ joints, is entirely due to the intrinsic muscles of the hand vated by the median nerve. This type of preci­ dominantly innervated by spinal cord segment T1 with a sion movement is used in the upstroke when writing a t contribution from C8. They insert into the proximal phalanx of each digit and into the extensor hood Muscles and are divided into two groups, the dorsal interossei and The intrinsic muscles of the hand are the palmaris brevis the palmar interossei. Unlike the extrinsic muscles that origi­ the complex flexion and extension movements generated nate in the forearm, insert in the hand, and function in by the extensor hoods. Each muscle inserts both into the base of the ments of the fngers through their attachments to the proximal phalanx and into the extensor hood of its related extensor hoods, the dorsal interossei are the major abduc­ digit. Palmar interossei Thenar muscles The three (or four) palmar interossei are anterior to the The threethenarmuscles (the opponens pollicis, flexor pol­ dorsal interossei, and are unipennate muscles originating licis brevis, and abductor pollicis brevis muscles) are associ­ from the metacarpals of the digits with which each is asso­ ated with opposition of the thumb to the fngers and with ciated (Fig. The opponens pollicis muscle is the largest of the thenar The second palmar interosseous muscle originates muscles and lies deep to the other two (Fig. I on the trapezium, so bringing the pad of the thumb into Like the tendons of the dorsal interossei, the tendons of a position facing the pads of the fngers (Table 7. The palmar interossei adduct the thumb, index, ring, The abductor pollicis brevis muscle overlies the oppo­ and little fngers with respect to a long axis through the nens pollicis and is proximal to the flexor pollicis brevis middle fnger. Because the muscles insert into the extensor scaphoid and trapezium and from the adjacent flexor reti­ hoods, they also produce complex flexion and extension naculum, and inserts into the lateral side of the base of the movements of the digits (Table 7. Adductor pollicis The abductor pollicis brevis abducts the thumb, princi­ The adductor pollicis is a large triangular muscle pally at the metacarpophalangeal joint. Its action is most anterior to the plane of the interossei that crosses the palm apparent when the thumb is maximally abducted and the (Fig. It originates as two heads: proximal phalanx is moved out of line with the long axis of the metacarpal bone (Table 7. It originates mainly from the tubercle of the trapezium and adjacent flexor retinaculum, The two heads converge laterally to form a tendon, but it may also have deeper attachments to other carpal which often contains a sesamoid bone, that inserts into bones and associated ligaments. It inserts into the lateral both the medial side of the base of the proximal phalanx side of the base of the proximal phalanx of the thumb. Hypothenar muscles Lumbrical muscles The hypothenar muscles (the opponens digiti minimi, There are four lumbrical (worm-like) muscles, each of abductor digiti minimi, and flexor digiti minimi brevis) which is associated with one of the fngers. The muscles contribute to the swelling (hypothenar eminence) on originate from the tendons of the flexor digitorum profun­ the medial side of the palm at the base of the little fnger dus in the palm: {Fig. The tendons ofthe muscles are anterior tothe deep trans­ The opponens digiti minimi rotates metacarpal V toward verse metacarpal ligaments. Through their insertion metacarpal ligament, which attaches the head of metacar­ into the extensor hoods, they participate in flexing the pal V to that of the ring fnger, the movement is much less metacarpophalangeal joints and extending the interpha­ dramatic than that of the thumb (Table 7. The medial two lumbricals are innervated by the Abductor digiti minimi deep branch of the ulnar nerve; the lateral two lumbricals The abductor digiti minimi muscle overlies the oppo­ are innervated by digital branches of the median nerve nens digiti minimi {Fig. The blood supply to the hand is by the radial and ulnar The abductor digiti minimi is the principal abductor of arteries, which form two interconnected vascular arches the little fnger (Table 7. Vessels to the digits, muscles, and joints originate from the two arches Flexor digiti minimi brevis and the parent arteries: The fexor digiti minimi brevis muscle is lateral to the abductor digiti minimi {Fig. It originates from • The radial artery contributes substantially tothe supply the hook of the hamate bone and the adjacent flexor reti­ of the thumb and the lateral side of the index fnger. The vessel lies between ultimately provide the principal blood supply to the the palmaris brevis and the fexor retinaculum and is lateral side of the little fnger, both sides of the ring and lateral to the ulnar nerve and the pisiform bone. Distally, middle fngers, and the medial side of the index fnger the ulnar artery is medial to the hook of the hamate bone (Fig. Radial artery and deep palmar arch One branch of the ulnar artery in the hand is the deep The radial artery curves around the lateral side of the palmar branch (Figs. It curves medially around the hook of the hamate Itpasses between the two heads of the frst dorsal interos­ to access the deep plane of the palm and to anastomose seous muscle and then between the two heads of the with the deep palmar arch derived from the radial artery. Two vessels, the princeps pollicis artery and the Before penetrating the back of the hand, the radial radialis indicis artery, arise from the radial artery in the artery gives rise to two vessels: plane between the frst dorsal interosseous and adductor pollicis. The princeps pollicis artery is the major blood • a dorsal carpal branch, which passes medially as the supply to the thumb, and the radialis indicisartery supplies dorsal carpal arch, across the wrist and gives rise to the lateral side of the index fnger. Radialis indicis arery metacarpal Palmar arteries metacarpal arteries Dorsal carpal arch Perforating artery Dorsal carpal branch Deep branch of ulnar artery of ulnar artery pollicis muscle Posterior interosseous Deep palmar arch artery Dorsal carpal Dorsa/ view network Fig. If there is little connection between the deep and superfcial palmar arteries, only the thumb and lateral side of the index fnger will fll with blood (become red) when pressure on the radial artery alone is released. The deep veins follow the arteries; the superfcial veins drain into a dorsal venous network on the back of the hand over the metacarpal bones (Fig. Nerves The cephalic vein originates from the lateral side of the The hand is supplied by the ulnar, median, and radial dorsal venous network and passes over the anatomical nerves (Figs. The ulnar The basilic vein originates from the medial side of the nerve innervates all intrinsic muscles of the hand except dorsal venous network and passes into the dorsomedial for the three thenar muscles and the two lateral lumbricals, aspect of the forearm. In the clinic Venipuncture Ulnar nerve In many patients, venous access is necessary for The ulnarnerve enters the hand lateral to the pisiform and obtaining blood for laboratory testing and posteromedially to the ulnar artery (Fig. The ideal ately distal to the pisiform, it divides into a deep branch, sites for venous access are typically in the cubital fossa which is mainly motor, and a superfcial branch, which is and in the cephalic vein adjacent to the anatomical mainly sensory. The veins are simply distended by use of a The deep branch of the ulnar nerve passes with the tourniquet. For and supplies the hypothenar muscles to reach the deep straightforward blood tests the antecubital vein is usually the preferred site, and although it may not aspect of the palm, arches laterally across the palm, deep always be visible, it is easily palpated. The cephalic vein to the long flexors of the digits, and supplies the interossei, is generally the preferred site for a short-term the adductor pollicis, and the two medial lumbricals. Regional anatomy • Hand Area of distribution of supericial branch of ulnar nerve in hand Palmar branch of ulnar nerve from forearm Palmar view Medial two lumbrical muscles Deep branch Superficial branch (of ulnar nerve) (of ulnar nerve) Dorsal branch of ulnar nerve from forearm Dorsal view Fig. Function of the adductor • At the elbow, the nerve lies posterior to the medial pollicis muscle is also lost. In lesions of the ulnar nerve at the elbow, function of • At the wrist, the ulnar nerve passes superfcial to the the flexor carpi ulnaris muscle and fexor digitorum flexor retinaculum and lies lateral to the pisiform profundus to the medial two digits is lost as well. Ulnar nerve lesions at the elbow and wrist result in impaired sensory innervation on the palmar aspect of the medial one and one-half digits. Damage to the ulnar nerve at the wrist or at a site proximal to the wrist can be distinguished by evaluating the status of function of the dorsal branch (cutaneous) of the ulnar nerve, which originates in distal regions of the forearm. Originating from the lateral side The median nerve is the most important sensory nerve in of the median nerve near the distal margin of the flexor the hand because it innervates skin on the thumb, index retinaculum, it curves around the margin of the retinacu­ and middle fngers, and lateral side of the ring fnger lum and passes proximally over the flexor pollicis brevis (Fig. The recurrent branch then passes between the information about the environment fom this area, par­ fexor pollicis brevis and abductor pollicis brevis to end in ticularly from the skin on the thumb and index fnger. They innervate skin on the palmar sur­ The median nerve also innervates the thenar muscles faces of the lateral three and one-half digits and cutaneous that are responsible for opposition of the thumb to the regions over the dorsal aspects of the distal phalanges (nail other digits.

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