By O. Norris. Shaw University.

A torn posterior cruciale liga- ment appears hypoechoic and diffusely thickened; the an- terior cruciale ligament is evaluated by a comparatively posterior approach to the intercondylar region in a trans- verse plane and appears markedly swollen when torn order avalide 162.5mg online blood pressure bottom number is high. Anechoic fluid in a Baker’s cyst with hyperechoic thickened synovial Nerve-sheath ganglia of the peroneal nerve may arise wall (chronic synovitis) buy generic avalide 162.5 mg on-line pulse pressure table. The cyst lies superficial to the medial gas- either in the nerve sheath or from the proximal tibiofibu- trocnemius muscle and has a rounded inferior border (no rupture) lar joint and appear as spindle-shaped cysts buy discount avalide 162.5 mg on-line pulse pressure 19. A ruptured Baker’s cyst mimics a deep thrombophlebitis, and is char- In tendinosis, a focal or diffuse tendon enlargement and acterized by a pointed (not a rounded) inferior border, ac- a hypoechoic appearance is noted; calcifications are a companied by subcutaneous edema and fluid surrounding sign of chronic disease. Chronic traumatic bursitis ciated with pain, while tendon inhomogeneity is correlat- presents as hyperechoic thickened walls and a variable ed with an unfavorable outcome. Hyperechoic foci embedded in a hy- In tenosynovitis, an abnormal amount of fluid is noted poechoic inflammatory substance is a typical presenta- in the tendon sheath (but: less than 3 mm of fluid can be tion of bursitis in chronic gout at the extensor site of the seen at the dependent portions of the peroneal tendons, knees and elbows. Tendon tears may appear as longitudinal splits (espe- The US examination of the meniscus may reveal cially peroneal tendons), partial transverse tears, or com- meniscal expulsion, cyst formation, amputation, tear (Fig. US signs of FTT of the Achilles tendon 13), central degeneration, or meniscocapsular separation. A hypoechoic cleft The retracted torn end of the Achilles tendon (arrows) produces re- reaches the surface of the meniscus fraction artifacts. A chronic hematoma is seen in the gap (star) Musculoskeletal Sonography 165 Mobilization confirms complete rupture and demon- A partial torn ligament shows a focal hypoechoic strates the presence of opposing torn ends. Bursitis of inflammatory or mechanical origin at the lateral or medial malleolus, sole of the foot, superficial to the Achilles tendon, or in a retrocalcaneal position can be References distinguished from other cyst-like formations, such as 1. Jacobson JA, van Holsbeeck MT (1998) Musculoskeletal ul- arthrosynovial or ganglion cyst (frequently septated at the trasonography. Orth Clin North Am 29:135 ankle and foot), or from tumors, such as lipoma, or 2. J Ultrasound The evaluation of the joint space may reveal effusion, Med May 14(5):357-60 3. Am J Sports Med loose bodies and different degrees of ligamentous injury 24(6 Suppl):S2-8 (Fig. Bianchi S, Zwass A, Abdelwahab IF et al (1994) Diagnosis of Morton neuroma appear as hypoechoic nodules in the tears of the quadriceps tendon of the knee: value of sonogra- intermetatarsal web space (Fig. AJR 162:1137 the major axis of metatarsals and in continuity with the 5. Bianchi S, Martinoli C, Abdelwahab IF et al (1998) Sonographic evaluation of tears of the gastrocnemius medial digital nerve. J Ultrasound Med 17:157 In plantar fasciitis, the fascia is thickened (>4 mm) and 6. Martinoli C, Derchi LE, Pastorino C et al (1993) Analysis of becomes hypoechoic. Radiology 186:839 Fibromatosis of the plantar fascia appears as hypoe- 7. Kalebo P, Allenmark C, Peterson L et al (1992) Diagnostic val- choic fusiform avascular nodules without acoustic en- ue of ultrasonography in partial ruptures of the Achilles ten- don. Khan KM, Bonar F, Desmond PM et al (1996) Patellar tendi- The US signs of degenerative or inflammatory joint dis- nosis (jumpers knee): findings at histopathologic examination, eases of the foot and ankle are similar to those of the hands. Diaz GC, van Holsbeeck M, Jacobson JA (1998) Longitudinal split of the peroneus longus and peroneus brevis tendons with disruption of the superior peroneal retinaculum. Prato N, Derchi LE, Martinoli C (1996) Sonographic diagno- sis of biceps tendon dislocation. Magnano GM, Occhi M, Di Stadio M et al (1998) High-reso- lution US of non-traumatic recurrent dislocation of the per- oneal tendons: a case report. Silvestri E, Martinoli C, Derchi LE et al (1995) Echotexture of peripheral nerves: correlation between US and histologic find- ings and criteria to differentiate tendons. Wiener SN, Seitz WH (1993) Sonography of the shoulder in patients with tears of the rotator cuff: accuracy and value for selecting surgical options.

The water moves from an area of high Equation 3 purchase 162.5mg avalide with visa arteria maxillaris, called the van’t Hoff equation buy 162.5mg avalide with visa blood pressure 120 80, is valid only concentration of water to an area of low concentration generic avalide 162.5 mg free shipping blood pressure upper number. Generally, this is not the case at solutes has a low concentration of water, and vice versa. Interactions between dis- Osmosis can, therefore, be viewed as the movement of wa- solved particles, mainly between ions, cause the solution to ter from a solution of high water concentration (low con- behave as if the concentration of particles is less than the centration of solute) toward a solution with a lower con- theoretical value (nC). A correction coefficient, called the centration of water (high solute concentration). Osmosis is osmotic coefficient ( ) of the solute, needs to be intro- a passive transport mechanism that tends to equalize the to- duced in the equation. Therefore, the osmotic pressure of a tal solute concentrations of the solutions on both sides of solution can be written more accurately as: every membrane. If the cell is transferred to ample, the osmotic coefficient of NaCl is 1. As we will see below, many At any given T, since R is constant, equation 4 shows cells have regulatory mechanisms that keep cell volume that the osmotic pressure of a solution is directly propor- within a certain range. This term is known as the osmolal- throcytes, do not have volume regulatory mechanisms and ity or osmotic concentration of a solution and is expressed large volume changes occur when the solute concentration in osm/kg H2O. Most physiological solutions, such as of the extracellular fluid is changed. The os- plasma membrane is the difference in water concentration molality of a solution containing a complex mixture of between the two sides of the membrane. For historical rea- solutes is usually measured by freezing point depression. The os- lower than that of pure water and depends on the total motic pressure of a solution is defined as the pressure nec- number of solute particles. Compared with pure water, essary to stop the net movement of water across a selec- which freezes at 0 C, a solution with an osmolality of 1 tively permeable membrane that separates the solution osm/kg H2O will freeze at 1. When a membrane separates two solu- osmolality can be measured has led to the wide use of this tions of different osmotic pressure, water will move from parameter for comparing the osmotic pressure of different the solution with low osmotic pressure (high water con- solutions. The osmotic pressures of physiological solutions 32 PART I CELLULAR PHYSIOLOGY are not trivial. Consider blood plasma, for example, which A usually has an osmolality of 0. Many Cells Can Regulate Their Volume Cell volume changes can occur in response to changes in the osmolality of extracellular fluid in both normal and pathophysiological situations. Accumulation of solutes also can produce volume changes by increasing the intracellular osmolality. Volume regulation is particularly important in the brain, for example, where cell swelling can have serious consequences because expansion is strictly limited by the rigid skull. A solution’s osmolality is de- termined by the total concentration of all the solutes pres- B ent. In contrast, the solution’s tonicity is determined by the concentrations of only those solutes that do not enter (“penetrate”) the cell. Tonicity determines cell volume, as illustrated in the following examples. Na behaves as a nonpenetrating solute because it is pumped out of cells by the Na /K -ATPase at the same rate that it enters. The NaCl solu- tion is also hypotonic because cells will accumulate water and swell when placed in this solution. The solution is isotonic, however, because it produces no per- manent change in cell volume. The reason is that cells shrink initially as a result of loss of water but urea is a pen- etrating solute that rapidly enters the cells. Urea entry in- creases the intracellular osmolality so water also enters FIGURE 2. Cell volume changes when a cell is urea concentration is the same inside and outside the placed in either a hypotonic or a hypertonic solution. A, In a hy- potonic solution, the reversal of the initial increase in cell volume cells.

If there is a shift of the curve to either the right or the left buy avalide 162.5mg lowest price 7th hypertension, then the noradrenergic response that would be optimal in normal subjects now produces a suboptimal coping response avalide 162.5mg with amex arteria meningea media. In the case of a shift to the left discount 162.5mg avalide with amex pulse pressure widening causes, a reduction in noradrenergic transmission would be required to restore optimal coping whereas for a shift to the right, an increase would be required. One is that the underlying coding is correct but it is the noradrenergic response evoked by the stimulus that is inappropriate. A second is that the amplitude of the noradrenergic response to arousing stimuli is normal but the underlying coding is not. For instance, an early report suggested that there is a positive correlation between the density of (postsynaptic) b-adrenoceptors in rat cortex and behavioural resistance to a mild environmental stress (novelty and frustration) but a negative correlation between these parameters when the stress is intensified (Stanford and Salmon 1992). Evidence suggests that the relationship between these two parameters is described by a bell-shaped curve and so an optimal phasic response is manifest only at intermediate levels of tonic activity (Rajkowski et al. Obviously, it is extremely unlikely that noradrenergic transmission is the sole factor to determine the behavioural response to even simple environmental stimuli. Indeed, a bell-shaped dose±response curve immediately suggests the intervention of one or more additional factors (neurotransmitters? Such interactions with other neurotransmitters could well define the relationship between noradrenergic transmission and the coding of the coping response. Either a reduction or an increase in noradrenergic transmission produces a functional mismatch and diminishes coping. In these normal subjects, optimal coping is attained when the noradrenergic response to a specific stimulus corresponds to that marked (^). If there is a leftward shift of the curve that describes the neurochemical coding of coping, then the (predetermined) noradrenergic response that would be optimal in normal individuals now produces suboptimal coping (*). One remedy for such a dysfunction is to reduce noradrenergic transmission so as to restore optimal coping. Similarly, in the case of a rightward shift of the coping curve (c), a predetermined noradrenergic response to a specific stimulus, that would be optimal in normal individuals, will again produce suboptimal coping (*). In both (b) and (c) an alternative way to restore optimal coping would be to reverse the shift in the noradrenergic transmission/coping curve. This could explain the changes in mood that occur after chronic administration of drugs that cause long- latency changes in neurochemical factors that influence noradrenergic transmission (see Chapters 19 and 20) SUMMARY Much remains to be learned about the neurochemical regulation of noradrenergic transmission and even more research is required before we can define the role(s) of this neurotransmitter in the brain. Nevertheless, it is evident that these neurons are a crucial component of the network of monoamine influences on the limbic system and that they 184 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION are capable of both short- and long-term adaptive changes that will influence emotion, motivation, cognition and many other aspects of behaviour. Aston-Jones, G, Rajkowski, J, Kubiak, P and Alexinsky, T (1994) Locus coeruleus neurons in monkey are selectively activated by attended cues in a vigilance task. Bonisch, H, Hammermann, R and Bruss, M (1998) Role of protein kinase C and second messengers in regulation of the norepinephrine transporter. Cederbaum, JM and Aghajanian, GK (1976) Noradrenergic neurons of the locus coeruleus: inhibition by epinephrine and activation by the alpha-antagonist piperoxane. Fassio, A, Bonanno, G, Fontana, G, Usai, C, Marchi, M and Raiteri, M (1996) Role of external and internal calcium on heterocarrier-mediated transmitter release. Fillenz, M (1993) Short-term control of transmitter synthesis in central catecholaminergic neurones. Harley, CW (1987) A role for norepinephrine in arousal, emotion and learning: limbic modulation by norepinephrine and the Kety hypothesis. Hieble, JP, Bondinell, WE and Ruffolo, RR (1995) Alpha- and beta-adrenoceptors: from the gene to the clinic. Kumar, SC and Vrana, KE (1996) Intricate regulation of tyrosine hydroxylase activity and gene expression. McCormick, DA, Pape, HC and Williamson, A (1991) Actions of norepinephrine in the cerebral cortex and thalamus: implications for function of the central noradrenergic system. McQuade, R and Stanford, SC (2000) A microdialysis study of the noradrenergic response in rat frontal cortex and hypothalamus to a conditioned cue for aversive, naturalistic environmental stimuli. Neff, NH and Costa, E (1966) The influence of monoamine oxidase inhibition on catecholamine synthesis. Pacholczyk, T, Blakely, RD and Amara, SG (1991) Expression cloning of a cocaine- and antidepressant-sensitive human noradrenaline transporter. Papadopoulos, GC and Parnavelas, JG (1991) Monoamine systems in the cerebral cortex: evidence for anatomical specificity. Povlock, SL and Amara, SG (1997) The structure and function of norepinephrine, dopamine and serotonin transporters.

This balance works until the heart rate is below 20 major factors: beats/min generic 162.5mg avalide visa blood pressure medication problems. At this point purchase avalide 162.5mg without prescription hypertension 2013, additional increases in end-dias- 1) Norepinephrine released from cardiac sympa- tolic fiber length cannot augment stroke volume further be- thetic nerves and order 162.5mg avalide amex arrhythmia only at night, to a much lesser extent, circulating cause the maximum of the ventricular function curve has norepinephrine and epinephrine released from the adre- been reached. At heart rates below 20 beats/min, cardiac nal medulla output falls in proportion to decreases in heart rate. If an electronic pacemaker is attached to the right atrium and the heart rate is increased by electrical stimula- tion, surprisingly little increase in cardiac output results. Sympathetic neural activity This is because as the heart rate increases, the interval be- tween beats shortens and the duration of diastole decreases. The decrease in diastole leaves less time for ventricular fill- β β β β 1 1 1 1 ing, producing a shortened end-diastolic fiber length, which Speed of Rate of rise subsequently reduces both the force of contraction and the Force of Conduction contraction velocity contraction and of pacemaker stroke volume. The increased heart rate is, therefore, offset relaxation potential by the decrease in stroke volume. When the rate increases above 180 beats/min secondary to an abnormal pacemaker, stroke volume begins to fall as a result of poor diastolic fill- Duration of systole Heart (small effect) rate ing. Increase Events in the myocardium compensate to some degree Decrease for the decreased time available for filling. First, increases in Stroke volume heart rate reduce the duration of the action potential and, Decrease Treppe thus, the duration of systole, so the time available for dias- Increase (small effect) tolic filling decreases less than it would otherwise. Second, faster heart rates are accompanied by an increase in the Cardiac force of contraction, which tends to maintain stroke vol- output ume. The increased contractility is sometimes called treppe or the staircase phenomenon. Various effects of norepinephrine on the heart com- pensate for the decreased duration of diastole and hold stroke Effects of Increased Heart Rate as a Result of Changes in volume relatively constant, so that cardiac output increases with Autonomic Nerve Activity. The words “Increase” and “Decrease” in occurs because of decreased parasympathetic and in- small type denote quantitatively less important effects than the creased sympathetic neural activity. CHAPTER 14 The Cardiac Pump 245 3) Disease states, such as coronary artery disease, my- ocarditis (see Chapter 10), bacterial toxemia, and alter- ations in plasma electrolytes and acid-base balance 4) Intrinsic changes in contractility with changes in heart rate and/or afterload Heart rate is influenced primarily by sympathetic and parasympathetic nerves to the heart and, by a lesser extent, by circulating norepinephrine and epinephrine. The effect A of heart rate on cardiac output depends on the extent of concomitant changes ventricular filling and contractility. C Heart failure is a major problem in clinical medicine (see Clinical Focus Box 14. A V = C THE MEASUREMENT OF CARDIAC OUTPUT mg mL = The ability to measure output accurately is essential for per- mg/mL forming physiological studies involving the heart and man- FIGURE 14. Cardiac output is measured either by one of The volume (V) of liquid in the beaker equals the amount (A) of several applications of the Fick principle or by observing dye divided by the concentration (C) of the dye after it has dis- changes in the volume of the heart during the cardiac cycle. Cardiac Output Can Be Measured Using Variations of the Principle of Mass Balance A C V The use of mass balance to measure cardiac output is best Because A is known and C can be measured, V can be understood by considering the measurement of an un- calculated: known volume of liquid in a beaker (Fig. The vol- ume can be determined by dispersing a known quantity of V A/C (6) dye throughout the liquid and then measuring the con- When the principle of mass balance is applied to cardiac centration of dye in a sample of liquid. Because mass is output, the goal is to measure the volume of blood flowing conserved, the quantity of dye (A) in the liquid is equal to through the heart per unit of time. A known amount of dye the concentration of dye in the liquid (C) times the vol- or other indicator is injected and concentration of the dye ume of liquid (V): or indicator is measured over time. One possible consequence of heart failure is that pathologically dilated, hypertrophied, or stiff). The signs and symptoms typically associated with to reduce the venous fluid overload, cardiac glycosides this occurrence constitute congestive heart failure (e. This syndrome can be limited to the left ventricle terload reducing agents (e. Left heart failure Heart transplantation is becoming an increasingly vi- (which increases pulmonary venous pressure) can eventu- able option for severe, intractable, unresponsive CHF. Al- ally cause pulmonary artery pressure to rise and right though tens of thousands of patients worldwide have re- heart failure to occur. Indeed, left heart failure is the most ceived new hearts for end-stage heart failure, the supply of common reason for right heart failure. For this reason, car- The causes of CHF are numerous and include acquired diac-assist devices, artificial hearts, and genetically modi- and congenital conditions, such as valvular disease, my- fied animal hearts are undergoing intensive development ocardial infarction, assorted infiltrative processes (e. In the indicator dilution minute (rather than volume, as in equation 6).

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