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By K. Basir. Millsaps College.

Simultaneous lengthening of the flexor digi- torum profundus is best avoided in a potentially functional hand because it may cause an excessively weak grasp buy 25mg atarax with amex. However purchase atarax 10 mg on-line, if the flexor digitorum profundus is excessively tight order atarax 10 mg visa, it too may require lengthening. When finger flexor contractures are severe, proper hygiene and cleaning of the hand is difficult. In these severe contractures, both the flexor digitorum superficialis and flexor digitorum profundus have to be lengthened. Fractional lengthening at the musculotendinous junction of the flexor digitorum superficialis in mild to moderate deformity is preferred as it does not disrupt the continuity of the muscle and is less likely to result in over- lengthening. Care has to be taken that not too much lengthening occurs or the muscle tendon junc- tion will become completely disrupted. In more severe cases, we prefer to do Z-lengthening, usually lengthening the index and middle finger as a group and also the ring and little finger as a group. Outcome of Treatment There are very few studies that report the outcome of finger flexor length- ening. These results are more specifically a demonstration that the muscles have severe decreased excursion and unless the active range is perfectly placed, they are likely to be perceived as weak- ness. Over time, there is a tendency for the finger flexion contracture to recur, but seldom to the level it was before surgery. Other Treatment Several other methods of lengthening are possible including flexor prona- tor slide (proximal lengthening), Z-lengthening of individual flexor tendons, selective peripheral motor neurectomy,39 and sublimus to profundus trans- fer. The flexor pronator slide provides little control and excessive weakness for children with any function; for those who are severely involved, the Z- lengthening is an easier and simpler operation. Another option similar to the slide is excision of the proximal muscle fascia with detaching the muscle from the bone. With the limited con- trol present in spastic hands, individual tendon Z-lengthening is more com- plicated and provides little gain. Transfers of flexor digitorum superficialis to flexor digitorum profundus to create a single motor unit for the fingers seem to also provide little benefit over simpler lengthening procedures. Most of the function of a hemiplegic hand is for gross finger grasp and thumb key pinch, both ac- tivities requiring power more than fine control. Complications of Treatment The major complication is overlengthening, leaving the fingers with no power in the range where individuals need power for function. This loss of function usually recovers over several years, but only partially. We have not had any individuals with such severe weakness that they desired an operative attempt to correct the overlengthening. Some individuals want ad- ditional lengthening if there is still too much flexion. Those who want addi- tional lengthening are mainly individuals in whom a decision was initially made that the finger flexors need lengthening but no or very minimal length- ening was performed. The other complication is leaving an imbalance with an excessively strong flexor digitorum profundus and extensor digitorum longus causing the swan neck deformity to develop. This deformity can be extremely dis- abling because it locks the fingers so that they cannot be used. Treatment indicated is described in the next section. Finger Swan Neck Tightening of the finger flexors secondary to the wrist flexion deformity plus spasticity of the intrinsic muscles and the extensor digitorum longus results in hyperextension of the proximal interphalangeal joint and flexion of the distal interphalangeal joint, which causes the swan neck deformity. The volar cap- sule of the proximal interphalangeal joint becomes stretched out secondarily. When the deformity is severe, the fingers may become locked into extension and cannot actively flex (Figure 8. This deformity can be the result of over- lengthening the flexor digitorum superficialis in the face of a spastic and co- contracting flexor digitorum profundus and extensor digitorum longus. Treatment The initial treatment should include the use of the figure-of-eight finger or- thotic, which prevents extension of the proximal interphalangeal joint (Fig- ure 8. This splint can be made from plastic and, if tolerated by the patients, cosmetically appealing metal splints, which look like finger rings, can be ordered. If the hyperextension is forceful, many individuals find the rings uncomfortable because of the small area of skin contact, which causes high local skin pressure.

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These spasms are due to a low inflammation of the thyroid discount atarax 10mg with mastercard. The cause may be infection concentration of blood calcium purchase atarax 25 mg with mastercard, and the condition is or autoimmunity cheap 25 mg atarax, that is, abnormal production of anti- called tetany (TET-ah-ne). This low calcium tetany bodies to the thyroid gland. Hashimoto disease is an au- should not be confused with the infection called tetanus toimmune thyroiditis that may be hereditary and may (lockjaw). The disease results in enlargement of the thyroid (goiter) and hypothyroidism. It is treated with thyroid hormone replacement and, in some cases, surgery. Checkpoint 12-6 What is the effect of thyroid hormones on Thyroid cells? These very sensitive tests are used to detect abnormal thy- roid function and to monitor response to drug therapy. A Esophagus test for the level of thyroid-stimulating hormone (from the pituitary) is frequently done at the same time. Further Trachea testing involves giving a person oral radioactive iodine Figure 12-6 Parathyroid glands (posterior view). The four and measuring the amount and distribution of radiation small parathyroid glands are embedded in the posterior surface that accumulates in the thyroid gland. THE ENDOCRINE SYSTEM: GLANDS AND HORMONES 253 In contrast, if there is excess production of PTH, as ◗ Increase in the heart rate may happen in tumors of the parathyroid glands, calcium ◗ Increase in the metabolic rate of body cells is removed from its normal storage place in the bones and ◗ Dilation of the bronchioles, through relaxation of the released into the bloodstream. The loss of calcium from smooth muscle of their walls the bones leads to fragile bones that fracture easily. Be- cause the kidneys ultimately excrete the calcium, the for- Checkpoint 12-8 The main hormone from the adrenal medulla also functions as a neurotransmitter in the sympathetic nervous mation of kidney stones is common in such cases. Checkpoint 12-7 What mineral is regulated by calcitonin and parathyroid hormone (PTH)? Hormones From the Adrenal Cortex There are three main groups of hormones secreted by the adrenal The Adrenal Glands cortex: The adrenals are two small glands located atop the kid- ◗ Glucocorticoids (glu-ko-KOR-tih-koyds) maintain the neys. Each adrenal gland has two parts that act as sepa- carbohydrate reserve of the body by stimulating the rate glands. The inner area is called the medulla, and the liver to convert amino acids into glucose (sugar) in- outer portion is called the cortex (Fig. The production of these hormones in- creases in times of stress to aid the body in responding Hormones From the Adrenal Medulla The hor- to unfavorable conditions. They raise the level of nutri- mones of the adrenal medulla are released in response to ents in the blood, not only glucose, but also amino stimulation by the sympathetic nervous system. The prin- acids from tissue proteins and fatty acids from fats 12 cipal hormone produced by the medulla is epinephrine, stored in adipose tissue. Glucocorticoids also have the also called adrenaline. Another hormone released from ability to suppress the inflammatory response and are the adrenal medulla, norepinephrine (noradrenalin), is often administered as medication for this purpose. The closely related chemically and is similar in its actions to major hormone of this group is cortisol, which is also epinephrine. These two hormones are referred to as the called hydrocortisone. We have already learned about important in the regulation of electrolyte balance. They these hormones in studying the autonomic nervous sys- control sodium reabsorption and potassium secretion tem. When released from nerve endings instead of being by the kidney tubules. The major hormone of this released directly into the bloodstream, they function as group is aldosterone (al-DOS-ter-one). Some of their effects are as follows: ◗ Sex hormones are secreted in small amounts, having ◗ Stimulation of the involuntary muscle in the walls of little effect on the body.

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Redux acted both as an SSRI but astrocytes have a specific high-affinity uptake system for histamine and may be the also increased the secretion of serotonin 10mg atarax, major site of the inactivation and degradation of this monoamine cheap atarax 25mg mastercard. None of the other drugs that affect serotonin levels have this effect cheap 10 mg atarax otc. The enzyme histamine methyltransferase transfers a methyl group from SAM to a ring nitrogen of histamine to form methylhistamine. The second step is oxidation Histamine elicits a number of by MAO-B, followed by an additional oxidation step. In peripheral tissues, histamine effects on different tissues. Hista- undergoes deamination by diamine oxidase, followed by oxidation to a carboxylic mine is the major mediator of the acid (see Fig. Acetylcholine tissues) leads to vasodilation and an increase in the permeability of blood vessel walls. SYNTHESIS leads to the allergic symptoms of a runny The synthesis of acetylcholine from acetyl CoA and choline is catalyzed by the nose and watering eyes. When histamine is enzyme choline acetyltransferase (ChAT) (Fig. This synthetic step occurs in released in the lungs, the airways constrict in an attempt to reduce the intake of the allergic the presynaptic terminal. The compound is stored in vesicles and later released material. The ultimate result of this, however, through calcium-mediated exocytosis. Choline is taken up by the presynaptic ter- is bronchospasm, which can lead to difficulty minal from the blood via a low-affinity transport system (high Km) and from the in breathing. In the brain, histamine is an synaptic cleft via a high-affinity transport mechanism (low Km). Antihistamines from the hydrolysis of phosphatidylcholine (and possibly sphingomyelin) in mem- block histamine from binding to its receptor. Thus, membrane lipids may form a storage site for choline, and their In the tissues, this will counteract histamine’s hydrolysis, with the subsequent release of choline, is highly regulated. The new generation of to the neurologic symptoms of vitamin B12 deficiency. The methyl groups for “non-drowsy” antihistamines have been choline synthesis are donated by SAM, which is converted to S-adenosylho- modified such that they cannot pass through mocysteine in the reaction. Recall that formation of SAM through recycling of homocys- the blood-brain barrier. Thus, the effects on teine requires both tetrahydrofolate and vitamin B12 (unless extraordinary amounts of the peripheral tissues are retained with no methionine are available to bypass the B12-dependent methionine synthase step). Synthesis and inactivation of histamine; note the different pathways for brain and peripheral tissues. Choline is a common component of the diet but also can be synthesized in the human as part of the pathway for the synthesis of phospholipids (see Chapter 33). The only route for choline synthesis is via the sequential addition of three methyl groups from SAM to the ethanolamine portion of phosphatidylethanolamine to form phosphatidylcholine. Phosphatidylcholine is subsequently hydrolyzed to release choline or phosphocholine. Conversion of phosphatidylethanolamine to phos- CH phatidylcholine occurs in many tissues, including liver and brain. CH3 SCoA + HO 2 CH2 3 The acetyl group used for acetylcholine synthesis is derived principally from CH3 glucose oxidation to pyruvate and decarboxylation of pyruvate to form acetyl CoA choline acetyltransferase The supply of choline in the brain can become rate-limiting for acetylcholine O CH3 synthesis, and supplementation of the diet with lecithin (phosphatidylcholine) + CH3 2 2 3 has been used to increase brain acetylcholine in patients suffering from tardive CH dyskinesia (often persistent involuntary movements of the facial muscles and tongue). High levels of phos- acetylcholinesterase phatidylcholine in the maternal milk and a high activity of a high-affinity transport O system through the blood-brain barrier for choline in the neonate help to maintain brain – + choline concentrations. The fetus also has a high demand for choline, and there is a high- CH3 O + HO 2CH2 N (CH3)3 Acetic acid Choline affinity transport system for choline across the placenta. The choline is derived from maternal stores, maternal diet, and synthesis primarily in the maternal liver. Acetylcholine synthesis and degra- choline synthesis is dependent on folate and vitamin B12, the high fetal demand may dation. CHAPTER 48 / METABOLISM OF THE NERVOUS SYSTEM 895 CoA via the pyruvate dehydrogenase reaction.

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