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By W. Pedar. Christian Bible College and Seminary. 2018.

En- the stimulation of endothelin production in the injured dothelial cells of arterioles also release vasodilatory heart may be the damage per se discount 300 mg zantac. Also buy zantac 150mg online, increased formation prostaglandins when blood flow and shear stress are in- of angiotensin II and norepinephrine during chronic heart creased buy 150mg zantac mastercard. However buy zantac 150mg with amex, NO appears to be the dominant va- disease stimulates endothelin production, probably at the sodilator molecule for flow-dependent regulation. Endothelin has also been implicated as a contributor Endothelial cells also release one of the most potent vaso- to renal vascular failure, both pulmonary hypertension and constrictor agents, the 21 amino acid peptide endothelin. Endothelin is the most potent biological constrictor of sels exposed to blood after a brain injury or stroke associ- blood vessels yet to be found. Two major types of endothelin receptors Regulates Blood Pressure and Flow have been identified and others may exist. The constrictor by Constricting the Microvessels function of endothelin is mediated by type B endothelin re- ceptors. Type A endothelin receptors cause hyperplasia and Although the microvasculature uses local control mecha- hypertrophy of vascular muscle cells and the release of NO nisms to adjust vascular resistance based on the physical from endothelial cells. The precise function of endothelin in and chemical environment of the tissue and vasculature, the the normal vasculature is not clear; however, it is active dur- dominant regulatory system is the sympathetic nervous sys- ing embryological development. As Chapter 18 explains, the arterial pressure is moni- sence of the endothelin A receptor results in serious cardiac tored moment-to-moment by the baroreceptor system, and defects so newborns are not viable. An absence of the type B the brain adjusts the cardiac output and systemic vascular receptor is associated with an enlarged colon, eventually resistance as needed via the sympathetic and parasympa- leading to death. The kidney glomerular capillaries are also fat tissues and increased glucose release from the liver. The most common cause of diabetes mellitus is obesity, The mechanism of many of these abnormalities ap- which increases the requirement for insulin to the extent pears to stem from the fact that hyperglycemia activates that even the high insulin concentrations provided by the protein kinase C (PKC) in endothelial cells. This overall condition tric oxide synthase, so NO formation is gradually sup- is called insulin resistance. This leads to loss of an important vasodilatory Obesity independent of periods of hyperglycemia does stimulus (NO) and vasoconstriction. However, periods of hy- phospholipase C, leading to increased diacylglycerol and perglycemia over time cause reduced nitric oxide (NO) arachidonic acid formation. The increased availability of production by endothelial cells, increased reactivity of vas- arachidonic acid leads to increased prostaglandin synthe- cular smooth muscle to norepinephrine, accelerated ather- sis and the generation of oxygen radicals that destroy part osclerosis, and a reduced ability of microvessels to partic- of the NO present. The consequences are cells of the microvasculature, and produce long-term prob- cerebrovascular accidents (stroke) and coronary artery dis- lems caused by DNA breakage. Because sympathetic nerves form an extensive mesh- work of axons over the exterior of the microvessels, all vas- cular smooth muscle cells are likely to receive norepineph- rine. Since the diffusion path is a few microns, norepinephrine rapidly reaches the vascular muscle and ac- tivates -adrenergic receptors, and constriction begins within 2 to 5 seconds. Sympathetic nerve activation must occur quickly because rapid changes in body position or sudden exertion require immediate responses to maintain or increase arterial pressure. The sympathetic nervous sys- tem routinely overrides local regulatory mechanisms in most organs—except the heart and skeletal muscle—dur- ing exercise. But even in these, the sympathetic nervous system curtails somewhat the full increase in blood flow during submaximal contractions. Certain Organs Control Their Blood Flow via Autoregulation and Reactive Hyperemia If the arterial blood pressure to an organ is decreased to the extent that blood flow is compromised, the vascular resist- ance decreases and blood flow returns to approximately normal. If arterial pressure is elevated, flow is initially in- creased, but the vascular resistance increases and restores the blood flow toward normal; this is known as autoregu- lation of blood flow. Autoregulation appears to be prima- rily related to metabolic and myogenic control, as well as an increased release of NO if the tissue oxygen availability decreases. The cerebral and cardiac vasculatures, followed closely by the renal vasculature, are most able to autoregu- late blood flow. The safe range for blood flow is about 80 to 125% of nor- mal and usually occurs at arterial pressures of 60 to 160 mm Hg peremia. When blood flow to any organ is stopped or re- due to active adjustments of vascular resistance. At pressures duced by vascular compression for more than a few sec- above about 160 mm Hg, vascular resistance decreases because onds, vascular resistance dramatically decreases.

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However order zantac 150 mg line, nicotinic and muscarinic receptor antagonists do not completely prevent this increase cheap zantac 150mg with amex. The residual activation is attributed to peptides of the secretin±glucagon subgroup cheap zantac 300mg line, including VIP and secretin; both these peptides activate cAMP synthesis buy 150 mg zantac fast delivery. Finally, recent findings suggest that, in humans, four different mRNAs for TH are produced from a single gene. The translation products of these mRNAs differ in their amino-acid sequence in the N-terminal domain, rather than the catalytic C-terminus, and are likely to differ in their kinetics and susceptibility to different protein kinases. Regional differences in the distribution of these enzyme isoforms suggest that they might differ functionally, a possibility that is being explored currently. Long-term The first reports that TH activity could be altered without changes in its kinetics came from studies of the adrenal medulla of rats in which catecholamine release was stimulated by exposure of rats to a cold environment. The increase in enzyme activity was prevented by protein synthesis inhibitors, suggesting that it was due to an increase in TH gene transcription rather than activation of existing enzyme. Since then, physiological and pharmacological stimuli that increase demand on the transmitter store have consistently been shown to trigger such induction of TH enzyme. Increased TH protein has also been detected in noradrenergic cell bodies of sympathetic ganglia and the locus coeruleus. At all these sites, as in the adrenal medulla, the increase is evident after about 24 h. However, changes in the terminals take several days to appear, presumably because of the time required for axoplasmic transport of the enzyme. The signal for increased synthesis of TH protein in the adrenal gland certainly depends on an intact cholinergic innervation. Moreover, in the denervated gland, the increase induced by perfusion with exogenous acetylcholine is prevented by nicotinic antagonists. However, nicotinic antagonists do not completely prevent the increase in glands with an intact cholinergic innervation. These findings suggest that activation of nicotinic receptors by ACh is normally only partly responsible for the increase. Other factors now known to regulate TH gene transcription include glucocorticoids and nerve growth factor (NGF). Although details are far from clear, protein kinases (especially PKA), diacyl glycerol and Ca2‡ are all thought to be crucial intracellular messengers for NORADRENALINE 171 increased gene transcription. It should also be borne in mind that enzyme induction is not limited to TH: the same stimuli also increase DbH synthesis but less is known about factors mediating this process. STORAGE In common with other classical transmitters, noradrenaline is stored in vesicles that accumulate in the terminal varicosities. This was first shown by experiments that combined sucrose density±gradient centrifugation of tissue homogenates (see Fig. These studies confirmed that the noradrenaline-rich layers of the gradient coincided with those layers in which the vesicles were clustered. This suggested that the vesicles were the major storage site for noradrenaline within the nerve terminals. Further studies examined the effects of ligation or cooling the axons of sympathetic neurons for several days. Electron micrographs of the zone around the obstruction showed that the vesicles accumulated on the side nearest the cell body, confirming that they were assembled in the cell body and transported to the terminals by anterograde axoplasmic transport. The life cycle of these vesicles was discussed in more detail in Chapter 4. The concentration of noradrenaline in the vesicles is thought to be in the region of 0. The vesicular compartmentalisation of noradrenaline is made possible by its active uptake on vesicular monoamine transporters (VMATs) and its subsequent binding, in an osmotically inert matrix, within the vesicles. One obvious function of these transporters is thus to protect and conserve the releasable vesicular pool of transmitter. However, it is thought that they also protect neurons from potentially toxic effects of an excess of cytoplasmic noradrenaline and also maintain a concentration gradient favouring noradrenaline reuptake from the synapse (see below).

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Note the characteristic ap- artery (see the apposition of this vessel to the nerve root in C) discount zantac 300 mg with mastercard, multi- pearance of the root of the trigeminal nerve as it traverses the sub- ple sclerosis 150mg zantac for sale, tumors order zantac 150 mg fast delivery, and ephaptic transmission within the nerve or arachnoid space (B and C) zantac 150 mg low price, the origin of the trigeminal nerve, and the ganglion. MRI in the axial plane, B, C, D, (all T2-weighted im- mor have hearing loss, tinnitus and equilibrium problems, or vertigo. Also notice the character- weakness (seventh root), numbness (fifth root), or abnormal corneal istic appearance of the cochlea (B, C) and the semicircular canals (C). Treatment is usually by surgery, radiation In addition to these two cranial nerves, the labyrinthine branch of the therapy, or a combination thereof. The Cranial Nerves 43 A Facial nerve Abducens nerve Vestibulocochlear nerve Glossopharyngeal Olivary eminence nerve Vagus nerve Postolivary sulcus Preolivary sulcus Hypoglossal nerve B Preolivary sulcus Pyramid Retroolivary sulcus (postolivary sulcus) Olive (inferior) Glossopharyngeal Glossopharyngeal nerve nerve Flocculus Restiform body Fourth ventricle Tonsil of cerebellum Cerebellum C Pyramid Olive (inferior) Retroolivary sulcus Vagus nerve Fourth ventricle Tonsil of cerebellum Cerebellum D Pyramid Olivary eminence Vagus nerve Postolivary sulcus Restiform body Vagus nerve Fourth ventricle Tonsil of cerebellum 2-44 The glossopharyngeal (IX) and vagus (X) nerves (A) exit the cle is smaller. The ninth and tenth cranial nerves and the spinal portion lateral aspect of the medulla via the postolivary sulcus; the ninth nerve of the accessory nerve (XI) exit the skull via the jugular foramen. Glossopharyngeal neuralgia is a lancinating pain originating from These nerves are generally in line with the exits of the facial and the territories served by the ninth and tenth nerves at the base of the trigeminal nerves; all of these are mixed nerves. Trigger events may include chewing and swallow- sopharyngeal nerve (A, B) is close to the pons–medulla junction and ing. Lesions of nerves passing through the jugular foramen (IX, X, XI) correlates with the corresponding shape (more rectangular) of the may result in loss of the gag reflex (motor limb via ninth nerve), and medulla. The vagus nerve exits at a slightly more caudal position (A, drooping of the ipsilateral shoulder accompanied by an inability to turn C, D); the shape of the medulla is more square and the fourth ventri- the head to the opposite side against resistance (eleventh nerve). This cranial nerve exits in line its relation to the overall shape of the medulla. This shape is indicative with the abducens nerve found at the pons–medulla junction and in line of a cranial nerve exiting at more mid-to-caudal medullary levels. The note its relationship to the preolivary sulcus and olivary eminence. The twelfth nerve exit is characteristically located laterally adjacent to the hypoglossal exits the base of the skull by traversing the hypoglossal pyramid, which contains corticospinal fibers. A lesion of the hypoglossal nerve results in a deviation of the In axial MRI (B, T2-weighted; C, T1-weighted), note the charac- tongue to the ipsilateral side on attempted protrusion. The Insula 45 Precentral gyrus (PrCGy) Superior frontal Central sulcus (CSul) gyrus Postcentral gyrus (PoCGy) Middle frontal gyrus (MFGy) Gyri longi (GyLon–long gyri of the insula) Gyri breves (GyBr–short gyri of the insula) Central sulcus Transverse temporal of the insula (CSulIn) gyrus (TrTemGy) Limen insulae (LimIn) Temporal lobe (TLob) PrCGy PoCGy CSul MFGy TrTemGy GyBr GyLon CSulIn LimIn TLob CSul PrCGy PoCGy MFGy GyBr CSulIn GyLon TLob 2-46 Lateral view of the left cerebral hemisphere with the cortex overlying the insula removed. Structures characteristic of the insular cortex, and immediately adjacent areas, are clearly seen in the two MRIs in the sagittal plane through lateral portions of the hemisphere (inversion recovery—upper; T1-weighted image—lower). Chronic subdural Bacterial infections of the meninges (bacterial meningitis) are hematomas, usually seen in the elderly, are frequently of unknown ori- commonly called leptomeningitis because the causative organisms are gin; may take days or weeks to become symptomatic; and cause a pro- usually found in the subarachnoid space and involve the pia and arach- gressive change in mental status of the patient. The organism seen in about one-half of adult cases is Streptococcus “long and thin,” compared to an epidural hematoma, follows the sur- pneumoniae, while in neonates and children up to about 1 year it is Es- face of the brain, and may extend for considerable distances (see Fig. Treatment is surgical evacua- neck, stupor), may have generalized or focal signs/symptoms, and, if tion (for larger or acute lesions) or close monitoring for small, asymp- not treated rapidly, will likely die. Patients with viral meningitis may become ill over a period The most common cause of subarachnoid hemorrhage is trauma. Symptomatic bleeding from an arteriove- The most common cause of an epidural (extradural) hematoma nous malformation occurs in approximately 5% of cases. Blood collects is a skull fracture that results in a laceration of a major dural vessel, such in, and percolates through, the subarachnoid space and cisterns (see as the middle meningeal artery. Sometimes, the deficits seen (assuming the pa- ing may come from a venous sinus. The extravasated blood dissects the tient is not in coma) may be a clue as to location, especially if cranial dura mater off the inner table of the skull; there is no preexisting (ex- nerves are nearby. Onset is sudden; the patient complains of an excru- tradural) space for the blood to enter. These lesions are frequently ciating headache and may remain conscious, become lethargic and dis- large, lens (lenticular) shaped, may appear loculated, and are “short oriented, or may be comatose. Treatment of an aneurysm is to surgi- and thick” compared to subdural hematomas (see Fig. The patient may lapse into a coma and, if the lesion is left un- development of vasospasm. In some cases, the patient may initially be arachnoid space and cisterns may be removed. These tumors grow Tearing of bridging veins (veins passing from the brain outward slowly (symptoms may develop almost imperceptibly over years), are through the arachnoid and dura), usually the result of trauma, is a com- histologically benign, may result in hyperostosis of the overlying skull, mon cause of subdural hematoma.

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In addition to the four bursae on the anterior side and the One joint capsule surrounds the articulations of the three two on the posterior side discount zantac 300mg free shipping, there are 7 bursae on the lateral and bones cheap zantac 150 mg overnight delivery, and four ligaments support the ankle joint on the outside medial sides generic zantac 150mg online, for a total of 13 discount 300mg zantac amex. Knee injuries often require surgery, and they heal The malleoli form a cap over the upper surface of the talus with difficulty because of the avascularity of the cartilaginous tissue. Unlike Knowledge of the anatomy of the knee provides insight as to its limita- tions. The three C’s—the anterior cruciate ligament, the collateral liga- the condyloid joint at the wrist, the movements of the ankle are ments, and the cartilage—are the most likely sites of crippling injury. Articulations © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 Chapter 8 Articulations 223 FIGURE 8. Articulations © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 224 Unit 4 Support and Movement Navicular Tibia Medial cuneiform Head of first metatarsal bone Talus Tendon of extensor hallucis longus m. Which joints are reinforced with muscles that span the ion, or ankle extension, is checked by the tension of the extensor joint? The most common cause of ankle sprain is excessive inversion of the foot, resulting in partial tearing of the anterior talofibular liga- ment and the calcaneofibular ligament. Less commonly, the deltoid ligament is injured by excessive eversion of the foot. Torn ligaments are extremely painful and are accompanied by immediate local CLINICAL CONSIDERATIONS swelling. Reducing the swelling and immobilizing the joint are about the only treatments for moderate sprains. Extreme sprains may re- A synovial joint is a remarkable biologic system. Its self-lubricating quire surgery and casting of the joint to facilitate healing. Under normal circumstances and in most people,the many joints of the body perform without prob- Knowledge Check lems throughout life. Joints are not indestructible,however,and are subject to various forms of trauma and disease. Articulations © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 Chapter 8 Articulations 225 TABLE 8. Sprains are usually accompanied Joints are well adapted to withstand compression and tension forces. Torsion or sudden impact to the side of a joint, however, can be Luxation, or joint dislocation, is a derangement of the ar- devastating. Joint dislocation is more In a strained joint, unusual or excessive exertion stretches serious than a sprain and is usually accompanied by sprains. The damage is not shoulder and knee joints are the most vulnerable to dislocation. Strains are frequently caused by not “warming up” the muscles and not “stretching” the joints prior to exercise. Articulations © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 226 Unit 4 Support and Movement Self-healing of a dislocated joint may be incomplete, leaving the person with a “trick knee,” for example, that may unexpectedly give way. Subluxation of the hip joint is a common type of birth defect that can be treated by bracing or casting to promote suitable bone development. Because the bursa is close to the joint, the joint capsule may be affected as well. Bursitis may be caused by exces- sive stress on the bursa from overexertion, or it may be a local or systemic inflammatory process. Tendonitis involves inflamma- tion of a tendon; it usually comes about in the same way as bursitis. Not only do the individual vertebrae articulate one (a) (b) with another, but together they form the portion of the axial skeleton with which the head, ribs, and ossa coxae articulate. It may be congenital, disease-related, or idio- The vertebral column also encloses the spinal cord and provides pathic (of unknown cause).

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