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Satura- findings suggest that the total body store of K is re- tion of transport occurs when the maximal rate of tu- duced effective 100 mg zenegra. Remember that most of the body’s K is within bular transport is reached discount zenegra 100mg fast delivery. In uncontrolled diabetes mellitus order zenegra 100 mg with amex, the osmotic di- results in afferent arteriolar constriction when fluid de- uresis (increased Na and water delivery to the corti- livery to the macula densa is increased; it contributes to cal collecting ducts) zenegra 100mg low price, increased renal excretion of renal autoregulation discount 100 mg zenegra otc. Nephrogenic diabetes insipidus is evated plasma aldosterone level (secondary to volume characterized by increased output of dilute urine. Plasma osmolality is on the high side of the nor- pokalemia or hyperkalemia. The plasma AVP level will fall because of vol- mellitus because there is no glucose in the urine and ume expansion and cardiovascular stretch receptor in- the urine is very dilute. The plasma aldosterone level produce very dilute urine because Na reabsorption is will be low because of inhibited release of renin and inhibited. Neurogenic diabetes insipidus is unlikely be- less angiotensin II formation. The plasma ANP level cause the plasma AVP level is reduced in this case. A mary polydipsia produces output of a large volume of large part of the infused isotonic saline will be filtered dilute urine, but plasma osmolality and AVP levels are through capillary walls into the interstitial fluid. Na is the major osmotically active creased, but these should promote Na excretion, not solute in the ECF and is the major determinant of the lead to Na retention by the kidneys. A decrease in ef- amount of water in and, hence, volume of this com- fective arterial blood volume is the best explanation for partment. Although the plasma osmolality is ex- traordinarily high, the plasma Na , glucose, and BUN Chapter 25 are normal. This indicates the presence of another solute (it could be ethanol) in the plasma. Using the Henderson-Hasselbalch lated osmolality 2 [Na ] [glucose]/18 equation, 6. Simple dehydration would cause a rise in lated from the formula: [H ] 24 PCO2 /[HCO3 ], plasma [Na ]. The normal BUN the Henderson-Hasselbalch equation could be used, does not support the existence of renal failure. The collecting duct is lined by a tight sion of angiotensin I to angiotensin II, and therefore, epithelium and can lower the urine pH to 4. The proximal convoluted tubule is plasma bradykinin level will rise because the convert- lined by a leaky epithelium and can lower tubule fluid ing enzyme catalyzes the breakdown of this hormone. Other nephron blood pressure stimulates renin release, and (2) an- segments beyond the proximal convoluted tubule do giotensin II directly inhibits renin release by acting on not lower tubular fluid pH as much as the collecting the granular cells of afferent arterioles, so that this in- ducts. In response to an increase in dietary mEq/day of HCO3 and usually reabsorb all but a few K intake, the cortical collecting duct principal cells mEq/day; reabsorption of HCO3 occurs via H se- increase the rate of K secretion, accounting for most cretion and consumes the bulk of secreted H. The quantity of free 724 APPENDICES capillary blood flow; note the abnormally low PO. In the process of excreting titratable acid and ammonia, the kidneys generate and add to the 1. Successive small intestinal structures between the serosa and mucosa are longitudinal mus- blood an equivalent amount of new HCO3. Interstitial cells of Cajal are pace- greater H secretion in the proximal tubule and loop maker cells that generate electrical slow waves. Additionally, increased Na reabsorption in the collecting ducts renders the duct lumen more neg- other cell types do not generate electrical slow waves. The subject has a severe metabolic age to the enteric nervous system, including the in- acidosis. The anion gap (140 105 6 19 mEq/L) hibitory motor neurons, frees the musculature from in- is high. In the absence of inhibition, the muscle duces this type of acid-base disturbance, resulting contracts continuously in a disorganized manner. Acute renal fail- fective propulsion is impossible in the absence of the ure would also produce a high anion gap metabolic aci- ENS. Of the possible choices, only cell Uncontrolled diabetes mellitus also produces a high bodies in the dorsal vagal nucleus have axons ending in anion gap metabolic acidosis, but because the plasma the wall of the stomach. Because of the low ambient baromet- receptors stimulate adenylyl cyclase. Fast EPSPs are ric pressure and oxygen tension at high altitude, hy- not hyperpolarizing potentials.

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EXPLANATION DEVELOPMENT OF THE SKULL Development of Bone The formation of the skull is a complex process that begins dur- Bone formation discount zenegra 100 mg on-line, or ossification buy zenegra 100 mg amex, begins at about the fourth week of ing the fourth week of embryonic development and continues embryonic development discount zenegra 100mg, but ossification centers cannot be read- well beyond the birth of the baby zenegra 100 mg sale. Three aspects of the embry- ily observed until about the tenth week (exhibit I) discount zenegra 100mg otc. Bone tissue onic skull are involved in this process: the chondrocranium, the derives from specialized migratory cells of mesoderm (see neurocranium, and the viscerocranium (exhibit II). The viscerocranium (splanchnocranium) is the through a hyaline cartilage stage and then it is ossified as bone. Skeletal System: © The McGraw−Hill Anatomy, Sixth Edition Introduction and the Axial Companies, 2001 Skeleton (continued) EXHIBIT II The embryonic skull at 12 weeks is composed of bony elements from three developmental sources: the chondrocranium (colored blue-gray), the neurocranium (colored light yellow), and the viscerocranium (colored salmon). As the perichondrium calcifies,it gives rise to Epiphyseal border a thin plate of compact bone called the periosteal bone collar. Reserve zone A periosteal bud, consisting of osteoblasts and blood ves- sels, invades the disintegrating center of the cartilage model from Proliferation the periosteum. Once in the center, the osteoblasts secrete os- zone teoid, and a primary ossification center is established. Ossifica- Chondrocytes tion then expands into the deteriorating cartilage. This process is Hypertrophic zone repeated in both the proximal and distal epiphyses, forming sec- Epiphyseal border ondary ossification centers where spongy bone develops. Resorption Once the secondary ossification centers have been formed, zone bone tissue totally replaces cartilage tissue, except at the articular ends of the bone and at the epiphyseal plates. The reserve zone Ossification (zone of resting cartilage) borders the epiphysis and consists of zone Red bone small chondrocytes irregularly dispersed throughout the intercel- marrow lular matrix. The chondrocytes in this zone anchor the epiphy- seal plate to the bony epiphysis. The proliferation zone (zone of Diaphyseal border proliferating cartilage) consists of larger, regularly arranged chon- FIGURE 6. Skeletal System: © The McGraw−Hill Anatomy, Sixth Edition Introduction and the Axial Companies, 2001 Skeleton Chapter 6 Skeletal System: Introduction and the Axial Skeleton 143 TABLE 6. The plates indicate that the bones are still that are arranged in columns. The resorption zone (zone of dechondrification) is the area where a change in mineral content is occurring. The os- sification zone (zone of calcified cartilage) is a region of transfor- mation from cartilage tissue to bone tissue. The chondrocytes within this zone die because the intercellular matrix surrounding them becomes calcified. Osteoclasts then break down the calci- fied matrix and the area is invaded by osteoblasts and capillaries from the bone tissue of the diaphysis. As the osteoblasts mature, osteoid is secreted and bone tissue is formed. The result of this process is a gradual increase in the length of the bone at the epiphyseal plates. The time at which epiphyseal plates ossify varies greatly from bone to bone, but it usually occurs between the ages of 18 and 20 within the long bones (table 6. Because ossification of the epiphyseal cartilages within each bone occurs at predictable times, Spongy bone radiologists can determine the ages of people who are still growing by examining radiographs of their bones (fig. Large discrepan- cies between bone age and chronological age may indicate a ge- netic or endocrine abnormality. Compact bone Bone is continually being remodeled over the course of a person’s life. Bony prominences develop as stress is applied to the Medullary cavity periosteum, causing the osteoblasts to secrete osteoid and form new bone tissue. The greater trochanter of the femur, for exam- ple, develops in response to forces of stress applied to the perios- teum where the tendons of muscles attach (fig. Even Creek though a person has stopped growing in height, bony processes may continue to enlarge somewhat if he or she remains physi- FIGURE 6. Skeletal System: © The McGraw−Hill Anatomy, Sixth Edition Introduction and the Axial Companies, 2001 Skeleton 144 Unit 4 Support and Movement As new bone layers are deposited on the outside surface of ducts into the nasal cavity.

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Materials cheap zenegra 100mg otc, for example zenegra 100 mg with visa, cement fragments buy 100 mg zenegra mastercard, may very rarely become postopera- It is common to see heterotopic new bone formation 100mg zenegra with amex, as tively interposed generic zenegra 100 mg with amex, sometime after closed reduction of a it occurs in about 15-50% of hip replacements. The risk is greater in patients who had infection, trauma, previous Failure of Union at Trochanteric Osteotomy/Abductor hip surgery, ankylosing spondylitis or paralysis prior to Tendon Re-implantation surgery. The extent of ossification reflects the type of os- teoarthritis (OA) preoperatively, with more occurring in In order to gain access to the hip joint, some surgical ap- patients with hypertrophic OA (15/43) than in those with proaches require reflection of the abductor muscles, with atrophic (9/43) OA. Heterotopic ossification may be or without a part of the greater trochanter. Failure of re- classified by the Brooker score, from minor foci to com- implantation results in poor gait and abductor weakness. Various forms of therapy may be em- Patients with poor muscle tone or general debility are at ployed in patients who exhibit excessive new bone for- greatest risk. MRI may be used to confirm the abnormal mation, including radiotherapy and bone-inhibiting anatomy. More rarely, failure of abduction may be due to an ab- ductor neuropathy. Cement Extrusion Fractures, Non-union and Wear Although relatively common, for example, around the ac- etabular cup, this is usually asymptomatic and thought to The insertion of rigid metallic implants focuses loading be unimportant. Occasionally, cement injected under of the skeleton at specific points, for example, the tip of pressure may travel into veins, such as branches of the the femoral stem, rather than loading a longer area of profunda femoris, but this is not considered dangerous. Hence, stress risers occur at these sites and may be Rarely, cement extrusion causes nerve, vessel, bowel or considered a normal, perhaps ‘usual’, finding. The Radiology of Hip and Knee Joint Prostheses 111 Associated Malignant Tumors? Hartford JM, Kwolek C, Circle B (2002) Popliteal pseudoa- neurysm after total knee arthroplasty: MRI of the vascular anatomy. Orthopedics 25:187-189 Publications have linked the finding of a malignant tumor 13. Cyteval C, Hamm V, Sarrabere MP et al (2002) Painful infec- with a joint replacement. These may be bony or soft-tis- tion at the site of hip prosthesis: CT imaging. Radiology sue tumours, most often malignant fibrous histiocytoma 224:477-483. Berger RA, Rubash HE, Seel MJ, Thompson WH, Crossett LS (1993) Determining the rotational alignment of the femoral described in lymph nodes adjacent to prosthetic joints. Clin Orthop Rel Res 286:40-47 an associated malignancy, local or general, is less than 15. Puri L, Wixson RL, Stern SH,et al (2002) Use of helical com- expected. Schmalzried TP, Callaghan JJ (1999) Wear in total hip and knee References replacements. Saleh KJ, Holtzman J, Gafni A et al (2001) Reliability and in- total hip arthroplasty: MR imaging-initial experience. Wilde AH (1993) Management of infected knee and hip pros- [erratum appears in J Bone Joint Surg Am 2001 Nov; 83- theses. Twair A, Ryan M, O’Connell M et al (2003) MRI of failed to- influence of tibial-patellofemoral location on function of tal hip replacement caused by abductor muscle avulsion. Am J the knee in patients with the posterior stabilized condylar Roentgenol 181:1547-1550 knee prosthesis. Duryea J, Grainger AJ, Hide IG, Genant HK, Campbell RS 1040 (2001) Fully automated software to monitor wear in prosthet- 4. Kaplan PA, Montesi SA, Jardon OM, Gregory PR (1988) ic knees using fluoroscopic images. Eur Radiol 11:2184-2187 Bone-ingrowth hip prostheses in asymptomatic patients: radi- 20. Murray DW, O’Connor JJ (1998) Superolateral wear of the ac- ographic features. Goel A, Sharp DJ Heterotopic bone formation after hip re- (2001) Role of nuclear medicine in diagnosis of the infected placement.

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Systemic hypertension: (E) Decreased central blood volume to an increase in systemic vascular Mechanisms and diagnosis buy zenegra 100mg low price. If a person has an arterial blood resistance) and stroke volume and wald E cheap zenegra 100mg overnight delivery, Zipes DP order 100 mg zenegra free shipping, Libby P buy 100mg zenegra otc, eds discount zenegra 100 mg visa. Heart pressure of 125/75 mm Hg, heart rate remain constant, the pulse Disease. Philadelphia: WB (A) The pulse pressure is 40 mm Hg pressure Saunders, 2001. Hy- (C) Diastolic pressure is 80 mm Hg (C) Does not change pertension Primer. Human Cardiovascular Con- mm Hg central blood volume with standing trol. Venules collect blood from the capillaries and act as reser- is a major determinant of capillary hydrostatic voirs for blood volume. Myogenic arteriolar regulation is a response to increased cules from the interstitial space between cells. By-products of metabolism cause the dilation of adjacent endothelial cells. The concentration difference of solutes across the capillary norepinephrine, which constricts the arterioles and wall is the energy source for capillary exchange. Autoregulation of blood flow allows some organs to main- primary forces for fluid filtration and absorption across tain nearly constant blood flow when arterial blood pres- capillary walls. If all microvessels were to dilate are exchanged between the blood and cells. The microcir- fully because of relaxation of their smooth muscle cells, the culation minimizes diffusion distances, facilitating ex- arterial blood pressure would plummet. Virtually every cell in flow in a standing individual would be inadequate, resulting the body is in close contact with a microvessel. Regulation of vascular resistance in cells are in direct contact with at least one microvessel. The lens and cornea are exceptions be- cular resistance to preserve the arterial pressure and simulta- cause their nutrients are supplied by the fluids in the eye. The compromise is to preserve the regulate vascular resistance and thereby interact with car- mean arterial pressure by increasing arterial resistance at the diac output to maintain the arterial blood pressure (see expense of reduced blood flow to most organs other than the Chapter 12). The organs survive this conflict by increas- 262 CHAPTER 16 The Microcirculation and the Lymphatic System 263 ing their extraction of oxygen and nutrients from blood in the microvessels as the blood flow is decreased. The microvasculature is considered to begin where the smallest arteries enter the organs and to end where the smallest veins, the venules, exit the organs. In between are microscopic arteries, the arterioles, and the capillaries. De- pending on an animal’s size, the largest arterioles have an inner diameter of 100 to 400 m, and the largest venules have a diameter of 200 to 800 m. The arterioles divide into progressively smaller vessels to the extent that each section of the tissue has its own specific microvessels. The branching pattern typical of the microvasculature of differ- ent major organs and how it relates to organ function are discussed in Chapter 17. THE ARTERIAL MICROVASCULATURE Large arteries have a low resistance to blood flow and func- tion primarily as conduits (see Chapter 15). As arteries ap- proach the organ they supply, they divide into many small FIGURE 16. In most or- muscle cells wrapping around arterioles of gans, these small arteries, which are 500 to 1,000 m in di- various sizes. Each cell only partially passes around large-diame- ameter, control about 30 to 40% of the total vascular re- ter (1A) and intermediate-diameter (2A) arterioles, but com- sistance. These smallest of arteries, combined with the pletely encircles the smaller arterioles (3A, 4A). The en- blood vessels; together they regulate about 70 to 80% of larged views of 3A and 4A are at 4-times-greater magnification. Constriction of these vessels maintains the rel- testine during maturation. Constriction re- sults from the release of norepinephrine by the sympathetic larger vessel, but may encircle a smaller vessel almost 2 nervous system, from the myogenic mechanism (to be dis- times (see Fig. Vessel Wall Tension and Intravascular Pressure Arterioles Regulate Resistance by the Contraction Interact to Determine Vessel Diameter of Vascular Smooth Muscle The smallest arteries and all arterioles are primarily respon- The vast majority of arterioles, whether large or small, are sible for regulating vascular resistance and blood flow. Ves- tubes of endothelial cells surrounded by a connective tissue sel radius is determined by the transmural pressure gradient basement membrane, a single or double layer of vascular and wall tension, as expressed by Laplace’s law (see Chap- smooth muscle cells, and a thin outer layer of connective ter 14).

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