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By: X. Tom, M.B. B.CH., M.B.B.Ch., Ph.D.

Medical Instructor, University of Utah School of Medicine

A second membrane, the septum secundum, then develops to the right of the primum but this is never complete; it has a free lower edge that does, however, extend low enough for this new septum to overlap the foramen secundum in the septum primum and hence to close it medications bad for your liver order on line brahmi. After birth, this foramen usually becomes completely fused, leaving only the fossa ovalis on the septal wall of the right atrium as its memorial medications xerostomia generic brahmi 60caps with amex. In approximately 10% of adult subjects, however, a probe can still be insinuated through an anatomically patent, although functionally sealed, foramen. Division of the ventricle is commenced by the upgrowth of a fleshy septum from the apex of the heart towards the endocardial cushions. This stops short of dividing the ventricle completely and thus it has an upper the mediastinum 41 free border, forming a temporary interventricular foramen. At the same time, the single truncus arteriosus is divided into the aorta and pulmonary trunk by a spiral septum (hence the spiral relations of these two vessels), which grows downwards to the ventricle and fuses accurately with the upper free border of the ventricular septum. This contributes the small pars membranacea septi, which completes the separation of the ventricle in such a way that blood on the left of the septum flows into the aorta and on the right into the pulmonary trunk. The primitive sinus venosus absorbs into the right atrium so that the venae cavae draining into the sinus come to open separately into this atrium. The smooth-walled part of the adult atrium represents the contribution of the sinus venosus; the pectinate part represents the portion derived from the primitive atrium and is termed the auricle or the auricular appendage of the right atrium. The original single pulmonary venous trunk entering the left atrium becomes absorbed into it, and donates the smooth-walled part of this chamber with the pulmonary veins entering as four separate openings; the trabeculated part of the definitive left atrium is the remains of the original atrial wall. These arteries curve dorsally around the pharynx on either side and join to form two longitudinally placed dorsal aortae that fuse distally into the descending aorta. The 4th arch on the right becomes the brachiocephalic and right subclavian artery; on the left, it differentiates into the definitive aortic arch, gives off the left subclavian artery and links up distally with the descending aorta. When the truncus arteriosus splits longitudinally to form the ascending aorta and pulmonary trunk, the 6th arch artery, unlike the others, remains linked with the latter and forms the right and left pulmonary arteries. On the left side this arch retains its connection with the dorsal aorta to form the ductus arteriosus (the ligamentum arteriosum of adult anatomy). This asymmetrical development of the aortic arches accounts for the different course taken by the recurrent laryngeal nerve on each side. In the early fetus the vagus nerve lies lateral to the primitive pharynx, separated from it by the aortic arches. What are to become the recurrent laryngeal nerves pass medially, caudal to the aortic arches, to supply the developing larynx. With elongation of the neck and caudal migration of the heart, the recurrent nerves are caught up and dragged down by the descending aortic arches. On the right side, the 5th arch and distal part of the 6th arch become absorbed, leaving the nerve to hook round the 4th arch. This diagram explains the relationship of the right recurrent laryngeal nerve to the right subclavian artery and the left nerve to the aortic arch and the ligamentum arteriosum (or to a persistent ductus arteriosus). Blood is returned from the placenta by the umbilical vein to the inferior vena cava and thence the right atrium, most of it bypassing the liver in the ductus venosus (see page 101). Relatively little mixing of oxygenated and deoxygenated blood occurs in the right atrium since the valve overlying the orifice of the inferior vena cava serves to direct the flow of oxygenated blood from that vessel through the foramen ovale into the left atrium, while the deoxygenated stream from the superior vena cava is directed through the tricuspid valve into the right ventricle. From the left atrium the oxygenated blood (together with a small amount of deoxygenated blood from the lungs) passes into the left ventricle and hence into the ascending aorta for the supply of the brain and heart via the vertebral, carotid and coronary arteries. As the lungs of the fetus are inactive, most of the deoxygenated blood from the right ventricle is short-circuited by way of the ductus arteriosus from the pulmonary trunk into the descending aorta. This blood supplies the abdominal viscera and the lower limbs and is shunted to the placenta, for oxygenation, along the umbilical arteries arising from the internal iliac arteries. At birth, expansion of the lungs leads to an increased blood flow in the pulmonary arteries; the resulting pressure changes in the two atria bring the overlapping septum primum and septum secundum into apposition, which effectively closes off the foramen ovale. Similarly, ligature of the umbilical cord is followed by thrombosis and obliteration of the umbilical vessels.

These substances can stimulate epidermal cells (1) and immune cells (2) or lead to vasodilatation (3), plasma extravasation (4), and smooth muscle contraction (5) symptoms 9 dpo order brahmi 60 caps amex. As evidence to support this hypothesis, they reported that light stroking of the skin leads to an increase in blood flow in the zone of secondary hyperalgesia, but not in normal skin symptoms zoloft buy brahmi from india. Nociceptive innervation of the skin has been suggested to also play a critical role in wound healing. Sensory denervation by capsaicin injection impairs cutaneous wound healing in rats (Smith and Liu 2002). Skin denervation decreases keratinocyte proliferation and leads to decreased skin thickness (Hsieh and Lin 1999). This is paradoxical in the sense that lesions should, one would think, lead to deficits in function. The ongoing pain in patients is frequently associated with enhanced pain in response to natural stimuli, a phenomenon termed hyperalgesia. In this section we consider the role of altered function of nociceptors in neuropathic pain. In considering inflammatory pain it was noted earlier in this chapter that primary hyperalgesia is explained by sensitization of nociceptors whereas secondary hyperalgesia is due to central sensitization. In the case of secondary hyperalgesia, the input of low-threshold mechanoreceptors, normally concerned only with touch sensibility, leads to pain because the synaptic links with central pain-signaling cells in the dorsal horn are strengthened. A similar mechanism of central sensitization appears to also explain the allodynia seen with 28 Section One Neurobiology of Pain this is done pre-emptively (before the L5 spinal nerve is severed) or after the lesion. Thus, interruption of input from the injured L5 spinal nerve fails to reverse the hyperalgesia in the foot, which indicates that ectopic activity from the injured nerve is not essential for the development of neuropathic pain (Li et al 2000). The spontaneous activity appears to emanate at least in part from the skin (Wu et al 2001). Additional evidence for a contribution of non-axotomized nociceptors comes from clinical studies demonstrating that distal therapies are effective in neuropathic pain states. Capsaicin applied to the skin can alleviate the pain associated with nerve injuries. This clinical effect can be understood only by invoking a role of cutaneous nociceptors that survive the injury. Moreover, since the toxicity of capsaicin appears to be restricted to the skin, it is the cutaneous terminal of the nociceptor that must be generating pain. This was demonstrated in human subjects by selectively blocking the neural activity in large fibers (touch fibers) with an ischemic block. When touch sensation was eliminated and the functions of other nerve fibers were still preserved, the allodynia disappeared (Campbell et al 1988b). The relative role of central and peripheral mechanisms in neuropathic pain is not well understood and probably varies not only with the disease but also with factors such as genetic differences. In many cases, however, the abnormal input of neural activity from nociceptive afferents plays a dynamic and ongoing role in maintenance of the pain state. Understanding of neuropathic pain involves two key concepts: (1) inappropriate activity in nociceptive fibers (injured and uninjured) and (2) central changes in sensory processing that arise from these abnormalities. To consider how these mechanisms generate heightened pain we discuss in some depth the simplest of neuropathic pain models: the sequelae of severing a nerve. Ectopic Sensitivity Develops in Injured Fibers When a nerve is severed, the nociceptors are also severed. The injured (transected) nociceptors could in principle function abnormally at the site of nerve transection (the neuroma). Indeed, abnormal spontaneous activity has been observed in A and C fibers originating from a neuroma (see Chapter 64). Given that a substantial proportion of C-fiber afferents are nociceptors, it is likely that this spontaneous activity is in fact occurring in nociceptive afferents.

The upper is the vestibular fold, containing a small amount of fibrous tissue and forming on each side the false vocal cord symptoms of anemia generic 60caps brahmi with mastercard. The mucosa is firmly adherent to the vocal ligament without there being any intervening submucosa medications when pregnant order 60caps brahmi. This accounts for the pearly white, avascular appearance of the vocal cords as seen on laryngoscopy. Oedema of the 314 the head and neck Epiglottis Lateral thyrohyoid ligament Hyo-epiglottic ligament Hyoid Median thyrohyoid ligament Vestibular fold Sinus of larynx Vocal fold Cricovocal membrane Cricothyroid ligament Arytenoid cartilage Vocal and muscular processes of arytenoid Facet on cricoid for inferior horn of thyroid cartilage Cricotracheal ligament (a) (b). These folds demarcate the larynx into three zones: 1 the supraglottic compartment (vestibule) above the false cords; 2 the glottic compartment between the false and true cords; 3 the subglottic compartment between the true cords and the first ring of the trachea. On either side of the larynx the pharynx forms a recess, the piriform fossa, in which swallowed foreign bodies tend to lodge. The remaining muscles constitute a single encircling sheet whose various attachments are denoted by the names of its separate parts: the thyroarytenoid, posterior and lateral cricoarytenoid, the aryepiglottic, thyroepiglottic and interarytenoid muscles. All these muscles except one have a sphincter action; the exception is the posterior cricoarytenoid on each side which, by rotating the arytenoids outwards, separates the vocal cords. Blood supply the larynx receives a superior and inferior laryngeal artery from the superior and inferior thyroid artery, respectively. Below the cords, drainage is to the lower deep cervical nodes, partially via nodes on the front of the larynx and trachea. The vocal cords themselves act as a complete barrier separating the two lymphatic areas, but posteriorly there is free communication between them; a laryngeal carcinoma may thus seed throughout the lymphatic drainage area of the larynx. Nerve supply the nerve supply of the larynx is of great practical importance and comprises the superior laryngeal nerve and the recurrent laryngeal nerve, both being branches of the vagus nerve (X). The superior laryngeal nerve passes deep to the internal and external carotid arteries where it divides; its internal branch pierces the thyrohyoid membrane together with the superior laryngeal vessels to supply the mucosa of the larynx down to the vocal cords. The external branch passes deep to the superior thyroid artery to supply the cricothyroid muscle. The right arises from the vagus as this crosses the front of the subclavian artery, passes deep to and behind this vessel, then ascends behind the common carotid to lie in the tracheo-oesophageal groove accompanied by the inferior laryngeal vessels. The nerve then passes deep to the inferior constrictor muscle of the pharynx to enter the larynx behind the cricothyroid articulation. The left nerve arises on the arch of the aorta, winds below it, deep to the ligamentum arteriosum, and ascends to the trachea. It then lies in the tracheo-oesophageal groove and is distributed as on the right side. The recurrent nerves supply all the intrinsic laryngeal muscles, apart from the cricothyroid (supplied by the external branch of the superior laryngeal nerve) and the mucosa below the vocal cords. The external branch of the superior laryngeal nerve lies immediately deep to the superior thyroid artery and may be injured in ligating this vessel. The recurrent laryngeal nerve, lying in the tracheo-oesophageal groove, is usually behind the terminal branches of the inferior thyroid artery. Occasionally, however, the nerve lies in front of these vessels or passes between them. Moreover, when a large thyroid is pulled forwards during thyroidectomy, the nerve is dragged forwards with it, and is therefore placed in further jeopardy. For all these reasons, meticulous care is necessary to avoid injury to the recurrent laryngeal nerve in thyroid surgery. The larynx 317 2 Damage to the superior nerve causes some weakness of phonation owing to the loss of the tightening effect of the cricothyroid muscle on the cord. Usually the other cord is able to compensate in a remarkable way and speech is not greatly affected; if both nerves are divided, however, the voice is completely lost and breathing becomes difficult through the only partially opened glottis. In bilateral incomplete paralysis, therefore, the cords come together, stridor is intense and tracheotomy may become essential. The enlarged left atrium in advanced mitral stenosis may produce a recurrent laryngeal palsy by pushing up the left pulmonary artery which compresses the nerve against the aortic arch.

During forced expiration, when intrapleural pressure becomes positive, small airways are compressed (dynamic compression) and may even collapse treatment plan goals discount brahmi. The two main components of the work of breathing are the elastic recoil of the lungs and chest wall and the resistance to airflow medicine grapefruit interaction order brahmi with amex. In a normal healthy adult at the functional residual capacity A) alveolar pressure is greater than atmospheric pressure. C) the inward recoil of the lungs is equal and opposite to the outward recoil of the chest wall. Which of the following would be expected to cause increased static lung compliance. A) a relative lack of functional pulmonary surfactant B) diffuse interstitial alveolar fibrosis C) pulmonary vascular congestion D) emphysema E) diffuse alveolar collapse 3. The compliance of the lungs is A) greater at low lung volumes than it is at high lung volumes. During a forced expiration to the residual volume A) intrapleural pressure becomes more negative. A) doubling the tidal volume at the same breathing frequency B) breathing through the mouth instead of the nose C) doubling the breathing frequency at the same tidal volume D) breathing through a 1-cm diameter, 3-ft long tube E) gaining 100 lb of body weight 6. The resistance to airflow in a normal healthy person would be greatest A) during a eupneic inspiration. During inspiration, alveoli expand passively in response to an increased transmural pressure gradient; during normal quiet expiration, the elastic recoil of the alveoli returns them to their original volume. Alveoli are more compliant (and have less elastic recoil) at low volumes; alveoli are less compliant (and have more elastic recoil) at high volumes. Pulmonary surfactant increases alveolar compliance and helps prevent atelectasis by reducing surface tension in the alveoli. Predict the effects of alterations in lung and chest wall mechanics, due to normal or pathologic processes, on the lung volumes. Define anatomic dead space and relate the anatomic dead space and the tidal volume to alveolar ventilation. Predict the effects of alterations of alveolar ventilation on alveolar carbon dioxide and oxygen levels. Describe and explain the regional differences in alveolar ventilation found in the normal lung. Alveolar ventilation is the exchange of gas between the alveoli and the external environment. It is the process by which oxygen is brought into the lungs from the atmosphere and by which the carbon dioxide carried into the lungs in the mixed venous blood is expelled from the body. Although alveolar ventilation is usually defined as the volume of fresh air entering the alveoli per minute, a similar volume of alveolar air leaving the body per minute is implicit in this definition. The size of the lungs depends the height and weight or body surface area, as well as age and sex. It is determined by the force generated by the muscles of expiration and the inward elastic recoil of the lungs as they oppose the outward elastic recoil of the chest wall. It is determined by the strength of contraction of the inspiratory muscles and the inward elastic recoil of the lungs and the chest wall. This decreases the outward elastic recoil of the chest wall, as noted in Chapter 32. Determination of the lung volumes can be useful diagnostically in differentiating between two major types of pulmonary disorders-the restrictive diseases and the obstructive diseases. Obstructive diseases such as emphysema and chronic bronchitis cause increased resistance to airflow. Airways may become completely obstructed because of mucous plugs and because of the high intrapleural pressures generated to overcome the elevated airway resistance during a forced expiration. This is especially a problem in emphysema, in which destruction of alveolar septa leads to decreased elastic recoil of the alveoli and less radial traction, which normally help hold small airways open. The spirometer can therefore measure only the lung volumes that the subject can exchange with it.