By Y. Owen. Saint Bonaventure University.
En- the stimulation of endothelin production in the injured dothelial cells of arterioles also release vasodilatory heart may be the damage per se generic 10mg vardenafil. Also buy discount vardenafil 10mg online, increased formation prostaglandins when blood flow and shear stress are in- of angiotensin II and norepinephrine during chronic heart creased cheap vardenafil 10 mg amex. However, 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.
The receiv- though children who are prelingually deaf- er is connected to electrodes in the coch- ened may beneﬁt from early implantation lea that receive impulses and stimulate the to facilitate speech development vardenafil 20 mg amex. Individ- auditory nerve with these digital impuls- uals receiving a cochlear implant should es cheap vardenafil 10 mg on-line, permitting perception of the digitally have realistic expectations for hearing processed information as speech vardenafil 10mg otc. Optimal use Cochlear implants can be life-changing of cochlear implants requires a commit- for many individuals with severe to pro- ment to rehabilitation, training, and dai- found hearing loss. Although the cost of a cochlear speech reading, these individuals may be implant is typically covered by many able to engage in more effective verbal insurances, reimbursement for auditory communication because the implants en- rehabilitation, a key to successful use of able them to distinguish the beginnings implants, may be minimal or nonexistent. Implants can also and have strong ties to the Deaf commu- have a positive impact in work environ- nity may be unprepared for the social ram- ments. In addition to being able to hear iﬁcations of a cochlear implant, since verbal communication, individuals with some individuals in the Deaf culture (dis- cochlear implants are also better able to cussed later in the chapter) are strongly hear and identify warning signals (Saxon, opposed to cochlear implants for cultural Holmes, & Spitznagel, 2001). Consequently, in some instances Although cochlear implants do not re- a cochlear implant can socially isolate store normal hearing and the sound heard individuals from other friends who are is not like an acoustic signal, individuals Deaf (Tucker, 1998). Not all deaf individuals are candidates for Hearing Aids cochlear implants. For adults, the follow- ing criteria should be met before receiving A hearing aid is any mechanical or elec- a cochlear implant: tronic device that improves hearing. Hear- Treatment of Hearing Loss and Deafness 159 ing aids come in different shapes and sizes hearing loss. For instance, individuals with and are prescribed and ﬁtted according to hearing loss at higher frequencies have dif- individual need. Common styles of hear- ﬁculty hearing some higher-pitched tones ing aids are as follows: of speech. Tone control is an attempt to amplify the high frequencies without • Behind-the-ear style, which curves amplifying the lower frequencies. As a result, digital hearing aids can theoretically be programmed for each • a micophone to pick up sound individual hearing loss and provide more • an ampliﬁer that makes sound louder precision and clarity of sound. Many con- • a receiver that conveys sound to the ear tain special “noise-reduction circuits” that • a battery that provides power for the aid in reducing background noise. Digital hearing aid to work hearing aids have become much more Some hearing aids have special features affordable in recent years, with technolo- called telecoil circuitry or tone control. These original ampliﬁcation de- coil of wire that acts as an antenna, pick- vices make all sounds louder with the ex- ing up electromagnetic energy that is then ception of the soft speech sounds so neces- delivered to the receiver of the hearing aid sary for good speech intelligibility. Also available are limited adjustments available, and is a plug called a boot or shoe that is therefore sound quality is often lacking. They may be ﬁtted to one or both device enables individuals to be connect- ears. Monaural refers to one hearing aid, ed to an external sound source, such as a and binaural refers to two. It improves show that binaural ﬁttings are becoming the signal-to-noise ratio, improving sound the norm for a variety of reasons, includ- quality. Telecoil circuitry enables individ- ing improved localization skills, safety, uals to use other assistive listening devices and ease of hearing in noise. Although the hearing aid indus- hearing aid response to the individual’s try has become more regulated, in order 160 CHAPTER 5 HEARING LOSS AND DEAFNESS to prevent potential misuse it is highly the individual. Some individuals may be recommended that individuals seeking resistant to using a hearing aid because amplification consult with a licensed they believe society will view them as less audiologist who specializes in hearing aid capable. As always, a referral from a ous hearing aids have improved accept- friend, family member, or trusted medical ance, negative attitudes are still one factor professional is the best way to ensure that that may prevent many from beneﬁting the individual is working with a skilled from hearing aids. Hearing aids are delicate devices that Although hearing aids may improve need routine care and maintenance to en- hearing and may be beneﬁcial for many sure maximum function.
Compare with Figures 2-16 (page 21) and 2-19 The jugular bulb is a dilated portion of internal jugular vein (IJV) (page 23) buy generic vardenafil 10mg on line. Cerebral Angiogram discount vardenafil 10mg on-line, MRA buy discount vardenafil 20mg on line, and MRV 245 B ACA PCA A SSS MCA SCA TS ICA CS AICA BA VA Anterior cerebral artery (ACA) A2 segment C A1 segment Anterior communicating artery Posterior cerebral artery (PCA) Superior sagittal sinus (SSS) Superior cerebellar artery (SCA) Middle cerebral artery (MCA) M2 segment M1 segment Internal carotid artery (ICA): Cerebral part Sigmoid sinus Cavernous part Petrous part Transverse sinus (TS) Confluence of sinuses (CS) Anterior inferior cerebellar artery (AICA) Basilar artery (BA) Vertebral artery (VA) 8-6 Magnetic resonance angiography (MRA) is a noninvasive terior to posterior. C shows the relative position of the major vessels method for imaging cerebral arteries, veins, and sinuses simultane- and dural sinuses as imaged in A and B. A 3-D phase contrast MRA (A) and an inverted video image seen in A and B, is usually continuous with the right transverse sinus at window (B) of the same view show major vessels and sinuses from an- the conﬂuence of sinuses. Cerebral Angiogram, MRA, and MRV 247 PCA, Cortical branches PCA Thalamoperforating arteries SCA AICA Basilar artery (BA) Vertebral artery (VA) B Posterior cerebral artery, Cortical branches Posterior cerebral arteries (PCA) Thalamoperforating arteries (of the basilar bifurcation) Superior cerebellar artery (SCA) SCA BA AICA Anterior inferior cerebellar artery (AICA) PICA Posterior inferior cerebellar artery (PICA) VA 8-8 A vertebral artery angiogram (anterior–posterior projection, The root of the oculomotor (IIIrd) nerve, after exiting the inferior arterial phase) is shown in A; the same view, but in a different patient, aspect of the midbrain, characteristically passes through the interpe- is shown in B, using digital subtraction methods. Even though the in- duncular cistern and between the superior cerebellar and posterior jection is into the left vertebral, there is bilateral ﬁlling of the vertebral cerebral arteries en route to its exit from the skull through the supe- arteries and of branches of the basilar artery. In this position the IIIrd nerve may be damaged by arteries are important branches of P1 that generally serve rostral por- large aneurysms that impinge on the nerve root. The portion of the ACA arching on the movement of ﬂuid in these structures. These are inverted video around the genu of the corpus callosum is the A3 segment (precallosal) images of 3-D phase contrast MRA images as viewed from the dorsal and the A4 (supracallosal) and A5 (postcallosal) segments are located to ventral (A) and from the lateral aspect (B). Compare these images with anterior cerebral artery (ACA) immediately rostral to the anterior arteries and veins as depicted in Figures 2-18 and 2-19 (page 23), 2-21 communicating artery and inferior to the rostrum of the corpus callo- (page 25), and 2-23 (page 27). Cerebral Angiogram, MRA, and MRV 249 Anterior cerebral artery: Cortical branches A1 segment A Internal carotid artery Branches of middle cerebral artery Middle cerebral artery: Branches on insula (M2) Internal carotid artery M1 segment Posterior communicating artery Cortical branches (M4) Posterior communicating Posterior cerebral artery: artery P2 segment P1 segment Posterior cerebral artery Parieto-occiptal artery Calcarine artery Anterior communicating artery B Orbit Anterior cerebral artery (A1 segment) Ophthalmic artery Middle cerebral artery Cavernosus sinus (branches on insula) (containing internal carotid artery) Petrosal segment of internal carotid artery Middle cerebral artery Superior cerebellar artery (M1 segment) Tumor (vestibular schwannoma) Posterior communicating artery Posterior cerebral artery Basilar artery Calcarine artery Posterior cerebral artery Vertebral arteries 8-10 MRA images of the vessels at the base of the brain forming much of the cerebral arterial circle (of Willis) (A, B). Note the ante- rior, middle, and posterior cerebral arteries as they extend outward from the circle. The upper image is from a normal individual, and the lower image is from a patient with a vestibular schwannoma. Descrip- tions of the segments of the anterior, middle, and posterior cerebral arteries are found on pages 25 and 242. Compare with Figures 2-13 (page 19), 2-16 (page 21), 2- seen in this lateral view (A) and in the anterior-posterior view (B). Blood Supply to the Choroid Plexi 251 A Choroid plexus (CP) in body of lateral ventricle CP in atrium of lateral ventricle CP in roof of third ventricle CP in temporal horn of lateral ventricle Anterior choroidal artery CP in fourth ventricle AICA PICA Posterior communicating artery Lateral posterior choroidal artery BA VA Medial posterior choroidal artery B Medial striate artery Internal carotid artery Middle cerebral artery (M1) A1 P 1 Anterior choroidal artery Anterior choroidal artery Posterior communicating artery Posterior cerebral artery (P2) Lateral posterior choroidal artery Superior cerebellar artery Medial posterior choroidal artery Basilar artery (BA) Anterior inferior cerebellar artery (AICA) AICA branch to choroid plexus at the foramen of Luschka Vertebral artery (VA) Posterior inferior cerebellar artery (PICA) PICA branch to choroid plexus in the fourth ventricle 8-12 Blood supply to the choroid plexus of the lateral, third, and rior lateral choroidal arteries serve the plexuses of the lateral and third fourth ventricles. The choroid plexus in the fourth ventricle and the clump of internal carotid artery and P2 segment of the posterior cerebral artery that choroid plexus protruding out of the foramen of Luschka are served by supply the choroid plexus are accentuated by appearing in a darker red posterior inferior and anterior inferior cerebellar arteries, respectively. In A, a representation of these vessels (origin, course, termination) B, the origins of these branches from their main arterial trunks are shown. Anterior, posterior medial, and poste- See also Figures 2-21 (page 25), 2-24 (page 27), and 2-35 (page 35). The ﬁrst segment (V1) cerebral artery and middle cerebral artery, vertebrobasilar system) as seen is between the VA origin from the subclavian artery and the entrance in an MRA (anterior-posterior view). In approximately 40–45% of indi- of VA into the ﬁrst transverse foramen (usually C6); the second seg- viduals the left vertebral artery is larger, as seen here, and in about 5–10% ment V2 is that part of VA ascending through the transverse foramen of individuals one or the other of the vertebral arteries may be hypoplas- of C6 to C2; the third segment (V3) is between the exit of VA from the tic as seen here on the patient’s right. The MRI in B is a detailed view of transverse foramen of the axis and the dura at the foramen magnum the vertebrobasilar system from the point where the vertebral arteries exit (this includes the loop of the VA that passes through the transverse the transverse foramen to where the basilar artery bifurcates into the pos- foramen of C1/the atlas); the fourth segment (V4) pierces the dura and terior cerebral arteries. CHAPTER 9 Q & A’s: A Sampling of Study and Review Questions, Many in the USMLE Style, All With Explained Answers D. Lancon There are two essential goals of a student studying human neu- cise, some answers may contain additional relevant informa- robiology, or, for that matter, the student of any of the medical tion to extend the educational process. The ﬁrst is to gain the knowledge base and diagnostic In general, the questions are organized by individual chapters, skills to become a competent health care professional. Ref- ing the medical needs of the patient with insight, skill, and com- erence to the page (or pages) containing the correct answer are passion is paramount.
Iodinated tyrosine residues that are close together in the thyroglobulin precursor molecule undergo a coupling reaction buy 20 mg vardenafil overnight delivery, which forms the iodothyronine structure buy vardenafil 10 mg otc. Thy- Follicular Cells Synthesize roid peroxidase vardenafil 10 mg on-line, the same enzyme that initially oxidizes Iodinated Thyroglobulin iodine, is believed to catalyze the coupling reaction The steps involved in the synthesis of iodinated thyroglob- through the oxidation of neighboring iodinated tyrosine ulin are shown in Figure 33. These free radicals synthesis of a thyroglobulin precursor, the uptake of io- undergo addition, as shown in Figure 33. For example, when two The synthesis of the protein precursor for thyroglobulin is neighboring DIT residues couple by this mechanism, T4 is the first step in the formation of T and T. After being iodinated, the thy- 4 3 is a 660-kDa glycoprotein composed of two similar 330- roglobulin molecule is stored as part of the colloid in the kDa subunits held together by disulfide bridges. For example, a typical thyroglobulin mol- vesicles by the Golgi apparatus. These vesicles migrate to ecule contains five to six uncoupled residues of DIT and the apical membrane of the follicular cell and fuse with it. However, T3 is formed in only The thyroglobulin precursor protein is then extruded onto about one of three thyroglobulin molecules. As a result, the the apical surface of the cell, where iodination takes place. The iodide used for iodination of the thy- Thyroid Hormones Are Formed From the roglobulin precursor protein comes from the blood perfus- Hydrolysis of Thyroglobulin ing the thyroid gland. The basal plasma membranes of fol- licular cells, which are near the capillaries that supply the When the thyroid gland is stimulated to secrete thyroid follicle, contain iodide transporters. These transporters hormones, vigorous pinocytosis occurs at the apical mem- move iodide across the basal membrane and into the cy- branes of follicular cells. The iodide transporter is an ac- brane reach into the lumen of the follicle, engulfing bits of tive transport mechanism that requires ATP, is saturable, the colloid (see Fig. Endocytotic vesicles or colloid and can also transport certain other anions, such as bro- droplets formed by this pinocytotic activity migrate to- mide, thiocyanate, and perchlorate. Lysosomes, cell to concentrate iodide many times over the concentra- which are mainly located in the basal region of resting fol- CHAPTER 33 The Thyroid Gland 599 Blood Follicular cell Lumen Tight junction Iodination and - coupling I MIT I- I- H2O2 Tg DIT Iodide T4 Tg transporter T3 Thyroglobulin (Tg) ER precursor Golgi Deiodination Endosomes Micropinocytosis DIT MIT T4 T4 Macropinocytosis Colloid T3 T3 Proteolysis droplet Secretion Lysosomes Pseudopod FIGURE 33. The lysosomes fuse with the colloid droplets with a buffer against drastic changes in circulating thyroid and hydrolyze the thyroglobulin to its constituent amino hormone levels as a result of sudden changes in the rate of acids. As a result, T4 and T3 and the other iodinated amino T4 and T3 secretion. T4 and T3 formed from the roid hormones have long half-lives in the bloodstream. The DIT and MIT Thyroid Hormones Are Metabolized by generated by the hydrolysis of thyroglobulin are deiodi- Peripheral Tissues nated in the follicular cell. The released iodide is then re- utilized by the follicular cell for the iodination of thy- Thyroid hormones are both activated and inactivated by roglobulin (see Fig. The en- zymes that catalyze the various deiodination reactions are Binding of T4 and T3 to Plasma Proteins. Most of the T4 regulated, resulting in different thyroid hormone concen- and T3 molecules that enter the bloodstream become trations in various tissues in different physiological and bound to plasma proteins. Each molecule of TBG has a sin- cretory product of the thyroid gland and is the predominant gle binding site for a thyroid hormone molecule. However, about 40% of the maining T4 and T3 in the blood are bound to transthyretin T4 secreted by the thyroid gland is converted to T3 by enzy- or to albumin. Less than 1% of the T4 and T3 in blood is in matic removal of the iodine atom at position 5 of the thyro- the free form, and it is in equilibrium with the large protein- nine ring structure (Fig. It is this small amount of free thyroid hor- 5 -deiodinase (type 1) located in the liver, kidneys, and thy- mone that interacts with target cells. The T3 formed by this deiodination and that se- The protein-bound form of T4 and T3 represents a creted by the thyroid react with thyroid hormone receptors large reservoir of preformed hormone that can replenish in target cells; therefore, T3is the physiologically active form the small amount of circulating free hormone as it is of the thyroid hormones. A second 5 -deiodinase (type 2) is 600 PART IX ENDOCRINE PHYSIOLOGY NH 2 DIT free Regulation of 5 -Deiodination.
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