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Although a part of the extrathoracic blood volume xeroform antimicrobial best buy for sumycin, the blood in the neck and head is less impor- tant because there is far less blood in these regions virus your current security settings cheap sumycin 500 mg with amex, and the blood volume inside the cranium cannot change much be- cause the skull is rigid antibiotics for uti or bladder infection order sumycin in united states online. Blood in the central and extratho- Blood volumes of various elements of the racic arteries can be ignored because the low compliance of FIGURE 15. The volume of blood in the veins of the abdomen and ex- tremities is about equal to the central blood volume; there- fore, about half of the total blood volume is involved in BLOOD VOLUME shifts in distribution that affect the filling of the heart. The blood volume is distributed among the various por- tions of the circulatory system according to the pattern shown in Figure 15. Total blood volume in a 70-kg adult The Measurement of Central Venous Pressure is 5. Provides Information on Central Blood Volume Central venous pressure can be measured by placing the tip of a catheter in the right atrium. Changes in central ve- Three Fourths of the Blood in the Systemic nous pressures are a good indicator of central blood volume Circulation Is in the Veins because the compliance of the intrathoracic vessels tends to Approximately 80% of the total blood volume is located in be constant. In certain situations, however, the physiologi- the systemic circulation (i. About 60% of the total ample, if the tricuspid valve is incompetent, right ventricu- blood volume (or 75% of the systemic blood volume) is lo- lar pressure is transmitted to the right atrium during cated on the venous side of the circulation. In general, the use of central venous ent in the arteries and capillaries is only about 20% of the pressure to assess changes in central blood volume depends total blood volume. Because most of the systemic blood vol- on the assumption that the right heart is capable of pump- ume is in veins, it is not surprising that changes in systemic ing normally. Also, central venous pressure does not neces- blood volume primarily reflect changes in venous volume. Abnormalities in right or left heart function or in pul- monary vascular resistance can make it difficult to predict Small Changes in Systemic Venous Pressure left atrial pressure from central venous pressure. Can Cause Large Changes in Venous Volume Unfortunately, measurements of the peripheral venous pressure, such as the pressure in an arm or leg vein, are sub- Systemic veins are approximately 20 times more compliant ject to too many influences (e. If 500 mL of blood is infused into the circulation, about 80% (400 mL) locates in the systemic circulation. This in- crease in systemic blood volume raises mean circulatory Cardiac Output Is Sensitive to Changes filling pressure by a few mm Hg. This small rise in filling in Central Blood Volume pressure, distributed throughout the systemic circulation has a much larger effect on the volume of systemic veins Consider what happens if blood is steadily infused into the than systemic arteries. Because of the much higher compli- inferior vena cava of a normal individual. As this occurs, the ance of veins than arteries, 95% of the 400 mL (or 380 mL) volume of blood returning to the chest—venous return—is is found in veins, and only 5% (20 mL) is found in arteries. This difference between the input and output of atmospheric) results in little distention of arteries because blood produces an increase in central blood volume. It will of their low compliance, but results in considerable disten- occur first in the right atrium where the accompanying in- tion of veins because of their high compliance. In fact, ap- crease in pressure enhances right ventricular filling, end-di- proximately 550 mL of blood is needed to fill the stretched astolic fiber length, and stroke volume. Increased flow into veins of the legs and feet when an average person stands up. Left cardiac output will increase according but to a lesser extent, because the increase in transmural to Starling’s law, so that the output of the two ventricles ex- pressure is less. Cardiac output will increase until it equals Blood is redistributed to the legs from the central blood the sum of the previous venous return to the heart plus the volume by the following sequence of events.

It is the uppermost portion of the phar- sphenoidal infection medical definition cheap 250mg sumycin otc, and ethmoidal sinuses (fig antimicrobial mouthwash 500mg sumycin amex. Each sinus com- ynx antibiotics names purchase sumycin canada, positioned directly behind the nasal cavity and above municates via drainage ducts within the nasal cavity on its own the soft palate. These sinuses are responsible ditory (eustachian) tubes connect the nasopharynx with for some sound resonance, but most important, they function to the tympanic cavities. The pharyngeal tonsils, or ade- decrease the weight of the skull while providing structural noids, are situated in the posterior wall of the nasal cavity. During the act of swallowing, the soft palate and uvula You can observe your own paranasal sinuses. Face a mirror are elevated to block the nasal cavity and prevent food from in a darkened room and shine a small flashlight into your entering. The frontal sinuses will be illuminated by directing the light just below the eyebrow. The maxillary sinuses are illuminated by shining the light into the oral cavity and closing your mouth around the flashlight. Respiratory System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 608 Unit 6 Maintenance of the Body FIGURE 17. The larynx has two func- occurs before the uvula effectively blocks the nasopharynx, tions. Its primary function is to prevent food or fluid from entering fluid will be discharged through the nasal cavity. Both Laryngitis is the inflammation of the mucosal epithelium of the swallowed food and fluid and inhaled air pass through it. Laryngitis may result from overuse of the voice, inhalation of an irritating chemical, or oropharynx. Paired palatine tonsils are located on the pos- a bacterial or viral infection. Mild cases are temporary and seldom of terior lateral wall, and the lingual tonsils are found on the major concern. It extends inferiorly from the level large unpaired structures, and six are smaller and paired. The of the hyoid bone to the larynx and opens into the esopha- largest of the unpaired cartilages is the anterior thyroid cartilage. It is at the lower laryngopharynx that the The laryngeal prominence of the thyroid cartilage is commonly respiratory and digestive systems become distinct. Tonsils are lymphoid organs and tend to be- come swollen and inflamed after persistent infections. The removal of the palatine epiglottis is located behind the root of the tongue where it aids tonsils is called a tonsillectomy, whereas the removal of the pharyn- in closing the glottis, or laryngeal opening, during swallowing. The entire larynx elevates during swallowing to close the glot- tis against the epiglottis. This movement can be noted by cup- Larynx ping the fingers lightly over the larynx and then swallowing. In this case, the abdominal thrust ducting division that connects the laryngopharynx with the trachea. Respiratory System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Chapter 17 Respiratory System 609 Posterior Base of tongue Vestibular folds Vocal folds Cuneiform Corniculate cartilage cartilage Anterior (a) Posterior Epiglottis Glottis Inner lining of trachea (c) Anterior (b) FIGURE 17. In (a) the vocal folds are taut; in (b) they are relaxed and the glottis is opened. This third unpaired cartilage connects glottis during swallowing and in speech.

Once this new ATP binds virus detector order sumycin with a visa, the newly recharged myosin head best antibiotic for gbs uti order genuine sumycin line, momentarily not attached to the actin fila- The Switching Action of Calcium hpv virus discount 500mg sumycin with amex. An effective switching ment (step 1), can begin the cycle of attachment, rota- function requires the transition between the “off” and “on” tion, and detachment again. This can go on as long as the states to be rapid and to respond to relatively small changes muscle is activated, a sufficient supply of ATP is avail- in the controlling element. The calcium switch in skeletal able, and the physiological limit to shortening has not muscle satisfies these requirements well (Fig. If cellular energy stores are depleted, as curve describing the relationship between the relative force happens after death, the crossbridges cannot detach be- developed and the calcium concentration in the region of cause of the lack of ATP, and the cycle stops in an at- the myofilaments is very steep. This produces an overall stiffness 8 of 1 10 M, the interaction between actin and myosin of the muscle, which is observed as the rigor mortis that is negligible, while an increase in the calcium concentration sets in shortly after death. The crossbridge cycle obviously must be subject to con- This process is saturable, so that further increases in cal- trol by the body to produce useful and coordinated muscu- cium concentration lead to little increase in force. This control involves several cellular tal muscle, an excess of calcium ions is usually present dur- processes that differ among the various types of muscle. In cardiac and smooth muscle, however, only description of the control process. Calcium ions, via the tro- ponin-tropomyosin complex, control the unblocking of the inter- action between the myosin heads (the crossbridges) and the ac- trical excitation of the surface membrane. The geometry of each tropomyosin tial sweeps rapidly down the length of the fiber. Its propa- molecule allows it to exert control over seven actin monomers. When the action potential encounters the openings one troponin molecule, via its tropomyosin connection, to of T tubules, it propagates down the T tubule membrane. Since the calcium control in This propagation is also regenerative, resulting in numer- striated muscle is exercised through the thin filaments, it is ous action potentials, one in each T tubule, traveling to- termed actin-linked regulation. In the T tubules, the velocity of smooth muscle contraction is also exercised by changes of the action potentials is rather low, but the total distance in calcium concentration, its effect is exerted on the thick to be traveled is quite short. This is termed myosin-linked regula- At some point along the T tubule, the action potential tion and is described in Chapter 9. Here the presence of the ac- tion potential is communicated to the terminal cisternae of Excitation-Contraction Coupling Links the SR. While the precise nature of this communication is not yet fully understood, it appears that the T tubule action Electrical and Mechanical Events potential affects specific protein molecules called dihy- When a nerve impulse arrives at the neuromuscular junc- dropyridine receptors (DHPRs). These molecules, which tion and its signal is transmitted to the muscle cell mem- are embedded in the T tubule membrane in clusters of four, brane, a rapid train of events carries the signal to the inte- serve as voltage sensors that respond to the T tubule action rior of the cell, where the contractile machinery is located. They are located in the region of the triad where The large diameter of skeletal muscle cells places interior the T tubule and SR membranes are the closest together, myofilaments out of range of the immediate influence of and each group of four is located in close proximity to a events at the cell surface, but the T tubules, SR, and their specific channel protein called a ryanodine receptor associated structures act as a specialized internal communi- (RyR), which is embedded in the SR membrane. The RyR cation system that allows the signal to penetrate to interior serves as a controllable channel (termed a calcium-release parts of the cell. The end result of electrical stimulation of channel) through which calcium ions can move readily the cell is the liberation of calcium ions into regions of the when it is in the open state. DHPR and RyR form a func- sarcoplasm near the myofilaments, initiating the cross- tional unit called a junctional complex (Fig. When the muscle is at rest, the RyR is closed; when T The process of excitation-contraction coupling, as out- tubule depolarization reaches the DHPR, some sort of link- lined in Figure 8. This muscle, every other RyR is associated with a DHPR cluster; situation results in a steady source of ATP for contraction the RyRs without this connection open in response to cal- that is maintained despite variations in energy supply and cium ions in a few milliseconds. Creatine phosphate is the most important storage of calcium ions from the terminal cisternae into the intra- form of high-energy phosphate; together with some other cellular space surrounding the myofilaments. The calcium smaller sources, this energy reserve is sometimes called the ions can now bind to the Tn-C molecules on the thin fila- creatine phosphate pool.

Generally antibiotic for bacterial vaginosis buy sumycin 250mg low cost, sus nuclei antibiotic resistance essay order sumycin 250mg line, and those from the lateral cortex terminate in the dentate nu- midline lesions result in bilateral motor deficits affecting axial and cleus infection control nurse certification order sumycin 500mg. Also, cerebellar corticonuclear fibers from the anterior lobe typ- proximal limb musculature. Cerebellar corticovestibu- emboliform, and dentate nuclei results in various combinations of the lar fibers originate primarily from the vermis and flocculonodular lobe, following deficits: dysarthria, dysmetria (hypometria, hypermetria), dysdi- exit the cerebellum via the juxtarestiform body, and end in the ipsilat- adochokinesia, tremor (static, kinetic, intention), rebound phenomenon, un- eral vestibular nuclei. One of the more Nucleocortical processes originate from cerebellar nuclear neurons commonly observed deficits in patients with cerebellar lesions is an in- and pass to the overlying cortex in a pattern that basically reciprocates tention tremor, which is best seen in the finger-nose test. The finger-to-fin- that of the corticonuclear projection; they end as mossy fibers. Some ger test is also used to demonstrate an intention tremor and to assess nucleocortical fibers are collaterals of cerebellar efferent axons. The heel-to-shin test will show dysmetria in the lower cerebellar cortex may influence the activity of lower motor neurons extremity. If the heel-to-shin test is normal in a patient with his/her through, for example, the cerebellovestibular-vestibulospinal route. If this test is repeated in the same Neurotransmitters: Gamma-aminobutyric acid (GABA) ( ) is patient with eyes closed and is abnormal, this would suggest a lesion in found in Purkinje cells and is the principal transmitter substance pres- the posterior column-medial lemniscus system. Cerebellar damage in intermittent and lateral areas (nuclei or cor- However, taurine ( ) and motilin ( ) are also found in some Purk- tex plus nuclei) causes movement disorders on the side of the lesion inje cells. GABA-ergic terminals are numerous in the cerebellar nuclei with ataxia and gait problems on that side; the patient may tend to fall and vestibular complex. This is because the cerebellar nuclei pro- fibers in the cerebellar cortex represent the endings of nucleocortical ject to the contralateral thalamus, which projects to the motor cortex fibers that originate from cells in the cerebellar nuclei. Other circuits (cerebellorubal- cerebellar dysfunction including viral infections (echovirus), hereditary rubospinal) and feedback loops (cerebelloolivary-olivocerebellar) fol- diseases (see Figure 7–18), trauma, tumors (glioma, medulloblastoma), low similar routes. Consequently, the motor expression of unilateral occlusion of cerebellar arteries (cerebellar stroke), arteriovenous malfor- cerebellar damage is toward the lesioned side because of these doubly mation of cerebellar vessels, developmental errors (such as the Dandy- crossed pathways. Walker syndrome or the Arnold-Chiari deformity), or the intake of toxins. Lesions of cerebellar efferent fibers, after they cross the midline in Usually, damage to only the cortex results in little or no dysfunction the decussation of the superior cerebellar peduncle, will give rise to unless the lesion is quite large or causes an increase in intracranial pres- motor deficits on the side of the body (excluding the head) contralat- sure. However, lesions involving both the cortex and nuclei, or only eral to the lesion. This is seen in midbrain lesions such as the Claude syn- the nuclei, will produce obvious cerebellar signs. Abbreviations CorNu Corticonuclear fibers MVesSp Medial vestibulospinal tract CorVes Corticovestibular fibers MVNU Medial vestibular nucleus Flo Flocculus NL, par Lateral cerebellar nucleus, parvocellular IC Intermediate cortex region InfVesNu Inferior (spinal) vestibular nucleus NM, par Medial cerebellar nucleus, JRB Juxtarestiform body parvocellular region LC Lateral cortex NuCor Nucleocortical fibers LVesSp Lateral vestibulospinal tract SVNu Superior vestibular nucleus LVNu Lateral vestibular nucleus VC Vermal cortex MLF Medial longitudinal fasciculus Review of Blood Supply to Cerebellum and Vestibular Nuclei STRUCTURES ARTERIES Cerebellar Cortex branches of posterior and anterior inferior cerebellar and superior cerebellar Cerebellar Nuclei anterior inferior cerebellar and superior cerebellar Vestibular Nuclei posterior inferior cerebellar in medulla, long circumferential branches of basilar in pons Cerebellum and Basal Nuclei (Ganglia) 209 Cerebellar Corticonuclear, Nucleocortical, and Corticovestibular Fibers NuCor IC VC CorNu CorVes 4 NuCor 2 CorNu 3 LC 1 NM, par Nodulus NL, par JRB Flo SVNu LVNu MLF InfVNu MVNu LVesSp MVesSp Cerebellar Nuclei: 1= Medial (Fastigial) 2= Posterior Interposed (Globose) 3= Anterior Interposed (Emboliform) 4= Lateral (Dentate) 210 Synopsis of Functional Components, Tracts, Pathways, and Systems Cerebellar Efferent Fibers 7–20 The origin, course, topography, and general distribution of belloreticular-reticulospinal, 3) cerebellothalamic-thalamocortical- fibers arising in the cerebellar nuclei. In addition, some direct cerebellospinal several thalamic areas (VL and VA), to intralaminar relay nuclei in ad- fibers arise in the fastigial nucleus as well as in the interposed nuclei. Most of the latter nuclei project back to the cere- glutamate ( ), aspartate ( ), or gamma-aminobutyric acid ( ). For example, cerebello-olivary fibers from the den- mic fibers, whereas some GABA-containing cells give rise to cerebel- tate nucleus (DNu) project to the principal olivary nucleus (PO), and lopontine and cerebello-olivary fibers. Some cerebelloreticular neurons of the PO send their axons back to the lateral cerebellar cor- projections may also contain GABA. Clinical Correlations: Lesions of the cerebellar nuclei result in a The cerebellar nuclei can influence motor activity through, as ex- range of motor deficits depending on the location of the injury. Many amples, the following routes: 1) cerebellorubral-rubrospinal, 2) cere- of these are described in Figure 7–19 on page 208. Abbreviations ALS Anterolateral system OcNu Oculomotor nucleus AMV Anterior medullary velum PO Principal olivary nucleus BP Basilar pons PonNu Pontine nuclei CblOl Cerebello-olivary fibers RetForm Reticular formation CblTh Cerebellothalamic fibers RNu Red nucleus CblRu Cerebellorubral fibers RuSp Rubrospinal tract CC Crus cerebri SC Superior colliculus CeGy Central grey (periaqueductal grey) SCP Superior cerebellar peduncle CM Centromedian nucleus of thalamus SCP, Dec Superior cerebellar peduncle, decussation CSp Corticospinal fibers SN Substantia nigra DAO Dorsal accessory olivary nucleus SVNu Superior vestibular nucleus DNu Dentate nucleus (lateral cerebellar nucleus) ThCor Thalamocortical fibers ENu Emboliform nucleus (anterior interposed ThFas Thalamic fasciculus cerebellar nucleus) TriMoNu Trigeminal motor nucleus EWNu Edinger-Westphal nucleus VL Ventral lateral nucleus of thalamus FNu Fastigial nucleus (medial cerebellar nucleus) VPL Ventral posterolateral nucleus of thalamus GNu Globose nucleus (posterior interposed VSCT Ventral spinocerebellar tract cerebellar nucleus) ZI Zona incerta IC Inferior colliculus InfVNu Inferior (spinal) vestibular nucleus Number Key INu Interstitial nucleus 1 Ascending projections to superior LRNu Lateral reticular nucleus colliculus, and possibly ventral lateral and LVNu Lateral vestibular nucleus ventromedial thalamic nuclei MAO Medial accessory olivary nucleus 2 Descending crossed fibers from superior ML Medial lemniscus cerebellar peduncle MLF Medial longitudinal fasciculus 3 Uncinate fasciculus (of Russell) MVNu Medial vestibular nucleus 4 Juxtarestiform body to vestibular nuclei NuDark Nucleus of Darkschewitsch 5 Reticular formation Review of Blood Supply to Cerebellar Nuclei and Their Principal Efferent Pathways STRUCTURES ARTERIES Cerebellar Nuclei anterior inferior cerebellar and superior cerebellar SCP long circumferential branches of basilar and superior cerebellar (see Figure 5–21) Midbrain Tegmemtum paramedian branches of basilar bifurcation, short circumferential (RNu, CblTh, branches of posterior cerebral, branches of superior cerebellar CblRu, OcNu) (see Figure 5–27) VPL, CM, VL, VA thalamogeniculate branches of posterior cerebral, thalamo- perforating branches of the posteromedial group of posterior cerebral (see Figure 5–38) IC lateral striate branches of middle cerebral (see Figure 5–38) Cerebellum and Basal Nuclei (Ganglia) 211 Cerebellar Efferent Fibers CSp VL ThCor CM VPL ThFas Zl Position of SCP, NuDark, INu, OcNu, EWNu CblTh, and CblRu RNu SC CeGy 1 CeGy SCP ML 2 CblTh & RetForm RNu CblRu 4 3 CC SN PonNu DNu IC FNu SVNu MLF 5 ML ENu GNu CblOl SN LVNu 5 SCP, Dec InfVNu LRNu MVNu 5 VSCT DAO AMV 5 SCP PO TriMoNu MAO ALS & RuSp ML BP Cerebellospinal fibers 212 Synopsis of Functional Components, Tracts, Pathways, and Systems 7–21 Blank master drawing for pathways projecting to the cere- bellar cortex, and for efferent projections of cerebellar nuclei.

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