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As proteins are broken down 30gm v-gel with amex, the CNS during the later stages of fasting buy generic v-gel 30gm line. Two products acids released into the blood by the skeletal muscle are ex- resulting from the breakdown of fatty acids purchase v-gel 30gm with visa, acetyl CoA tracted from the blood at an accelerated rate by the liver and citrate, inhibit glycolysis. The amino acids then undergo metabolic use of glucose from the blood is reduced. The newly synthesized glucose is then delivered tion to fasting is to provide the body with glucose pro- to the bloodstream. From that point on, the in this process by maintaining gene expression and, there- body uses mainly fat for energy metabolism, and it can fore, the intracellular concentrations of many of the en- survive until the fat depots are exhausted. Glucocorticoids zymes needed to carry out gluconeogenesis in the liver and do not trigger the metabolic adaptations to fasting but kidneys. For example, glucocorticoids maintain the only provide the metabolic machinery necessary for the amounts of transaminases, pyruvate carboxylase, phospho- adaptations to occur. When present in excessive amounts, needed to carry out gluconeogenesis at an accelerated rate. Cushing’s disease is the name of amounts of these enzymes in the liver are greatly reduced. Cushing’s disease CHAPTER 34 The Adrenal Gland 619 may be ACTH-dependent or ACTH-independent. One plasma membrane phospholipids by the hydrolytic action type of ACTH-dependent syndrome (actually called Cush- of phospholipase A2. Glucocorticoids stimulate the syn- ing’s disease) is caused by a corticotroph adenoma, which thesis of a family of proteins called lipocortins in their tar- secretes excessive ACTH and stimulates the adrenal cortex get cells. Lipocortins inhibit the activity of phospholipase to produce large amounts of cortisol. ACTH-independent A2, reducing the amount of arachidonic acid available for Cushing’s syndrome is usually due toa result of an adreno- conversion to prostaglandins and leukotrienes. Whatever the cause, prolonged exposure of the body to Effects on the Immune System. Glucocorticoids have large amounts of glucocorticoids causes the breakdown of little influence on the human immune system under normal skeletal muscle protein, increased glucose production by physiological conditions. When administered in large the liver, and mobilization of lipid from the fat depots. De- doses over a prolonged period, however, they can suppress spite the increased mobilization of lipid, there is also an ab- antibody formation and interfere with cell-mediated immu- normal deposition of fat in the abdominal region, between nity. Glucocorticoid therapy, therefore, is used to suppress the shoulders, and in the face. The increased mobilization the rejection of surgically transplanted organs and tissues. The underutilization of glucose concentrations of glucocorticoids, decreasing the number by skeletal muscle, coupled with increased glucose produc- of circulating lymphocytes. The destruction of immature T tion by the liver, results in hyperglycemia, which, in turn, and B cells by glucocorticoids also causes some reduction in stimulates the pancreas to secrete insulin. Glucocorticoids are required for the normal responses of vas- Evidence also indicates that excessive glucocorticoids de- cular smooth muscle to the vasoconstrictor action of norep- crease the affinity of insulin receptors for insulin. NE is much less active on vascular smooth muscle result is that the individual becomes insensitive or resistant in the absence of glucocorticoids and is another example of to the action of insulin and little glucose is removed from the permissive action of glucocorticoids. The persisting hyperglycemia continually stimulates the pan- Glucocorticoids and Stress. The result is a form of “diabetes” ing, but least understood, of all glucocorticoid action is the similar to Type 2 diabetes mellitus (see Chapter 35). All that is really The opposite situation occurs in the glucocorticoid-de- known is that the body cannot cope successfully with even ficient individual. Little lipid mobilization and use occur, so mild stresses in the absence of glucocorticoids. One must there is little restriction on the rate of glucose use by tis- presume that the processes that enable the body to defend sues. The glucocorticoid-deficient individual is sensitive to itself against physical or emotional trauma require gluco- insulin in that a given concentration of blood insulin is corticoids. This, again, emphasizes the permissive role they more effective in clearing the blood of glucose than it is in play in physiological processes.

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He still mows his Chest Pain lawn without much difficulty purchase 30gm v-gel with visa, and can walk 1 to 2 miles on A 27-year-old accountant recently drove cross-country to a flat surface at a moderate pace generic 30 gm v-gel overnight delivery. He denied having had any other sig- move proven 30 gm v-gel, she started to experience chest pains. She drove nificant past medical problems, including heart disease, to the emergency department after experiencing 24 hypertension, edema, childhood asthma, or any allergies. She denied any sputum pro- An initial exam shows that the patient is thin but has duction, hemoptysis, coughing, or wheezing. His tive and walks daily and never has experienced any blood pressure is 130/80 mm Hg; respiratory rate, 28 to swelling in her legs. She has never been treated for any 32 breaths/min; heart rate, 92/minute; and oral tempera- respiratory problems and has never undergone any sur- ture, 37. Oral contraceptives are breath sounds in both lung fields, with expiratory wheez- her only medication. A pulse intravenous drugs and has no other risk factors for HIV oximetry reading reveals his blood hemoglobin oxygen disease. Her family history is negative for asthma and saturation is 91% when breathing room air. Pulmonary function tests reveal severe limitation of Physical examination reveals a mildly obese woman airflow rates, particularly expiratory airflow. Her blood Questions pressure is 140/80 mm Hg, and no jugular vein disten- 1. What are the common spirometry findings associated with sion is observed. What are the mechanisms of airflow limitation in emphy- and her temperature is 38 C. What is the most commonly held theory explaining the de- gases, obtained while she was breathing room air, reveal velopment of emphysema? Her alveolar-arterial (A-a)O2 gradient is Answers to Case Study Questions for Chapter 19 40 mm Hg. The hallmark of emphysema is the limitation of airflow out normal flora. In emphysema, expiratory flow rates (FVC, shadow and clear lung fields, except for a small periph- FEV1, and FEV1/FVC ratio) are significantly decreased. A lung scan reveals ever, some lung volumes (TLC, FRC, and RV) are increased, an embolus in the left lower lobe. What is the cause of a widened alveolar-arterial gradient in include hypersensitivity of airway smooth muscle, mucus patients with pulmonary embolism? What causes the decreased arterial PCO2 and elevated arte- creased dynamic airway compression as a result of in- rial pH? Many of the pathophysiological changes in emphysema are Answers to Case Study Questions for Chapter 20 a result of the loss of lung elastic recoil and destruction of 1. This is thought to be a re- embolus will cause blood flow to be shunted to another re- sult of an imbalance between the proteases and antipro- gion of the lung. Because cardiac output is unchanged, the teases ( 1-antitrypsin) in the lower respiratory tree. Nor- shunting of blood causes overperfusion, which causes an mally, proteolytic enzyme activity is inactivated by abnormally low A/ ratio in another region of the lungs. DLCO decreases with anemia because there is less hemoglo- poxemia (a low arterial PO2). In older ever, ventilation is also stimulated as a compensatory individuals, especially those who live alone, insufficient di- mechanism to hypoxemia, which leads to hyperventilation etary intake of animal protein may be the cause; other with a concomitant increase in alveolar PO2. The A-aO2 gra- causes include loss of gastric mucosa or regional enteritis. Philadelphia: Lea & 2 perventilation as a result of the hypoxic drive (low PO ) that Febiger, 1993.

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While the process is phorylation to control smooth muscle activation buy v-gel 30 gm low price, second- not well understood buy v-gel 30 gm otc, it is possible that caldesmon v-gel 30 gm overnight delivery, under ary regulatory mechanisms are present in some types of the control of calcium, could form crosslinks between actin smooth muscle. One of these provides long-term regula- and myosin filaments and, thus, aid in bearing force during tion of contraction in some tissues after the initial calcium- a long-maintained contraction. It is likely that several such mechanisms exist in var- force of contraction may be maintained for long periods. Even during the latch state, increased Mechanical Activity in Smooth Muscle Is Adapted cytoplasmic calcium appears to be necessary for force to be for Its Specialized Physiological Roles maintained. Not all smooth muscle tissue can enter a latch state, however, and the details of the process are not com- The contraction of smooth muscle is much slower than that pletely understood. The source of these and this ion pumping requires a significant portion of the differences lies largely in the chemistry of the interaction cell’s energy supply. Internal pumping of calcium ions into between actin and myosin of smooth muscle. Recall that the the SR during relaxation also requires energy, and the crossbridges of muscle form an actin-myosin enzyme system processes that result in phosphorylation of the myosin light (actomyosin ATPase) that releases energy from ATP so that chains consume a further portion of the cellular energy, as it may be converted into a mechanical contraction (i. The inherent rate of this ATPase corre- Smooth muscle contains both glycolytic and oxidative lates strongly with the velocity of shortening of the intact metabolic pathways, with the oxidative pathway usually muscle. Most smooth muscles require several seconds (or the most important; under some conditions, a transition even minutes) to develop maximal isometric force. A may temporarily be made from oxidative to glycolytic me- smooth muscle that contracts 100 times more slowly than a tabolism. In terms of the entire body economy, the energy skeletal muscle will have an actomyosin ATPase that is 100 requirements of smooth muscle are small compared with times as slow. The major source of this difference in rates is those of skeletal muscle, but the critical regulatory func- the myosin molecules; the actin found in smooth and skele- tions of smooth muscle require that its energy supply not be tal muscles is rather similar. Smooth muscle contractile activ- degree of myosin light-chain phosphorylation. In some cases, smooth muscle makes rapid to 500 times greater than that in skeletal muscle, is vital to phasic contractions, followed by complete relaxation. Economy, as other cases, smooth muscle can maintain a low level of ac- used here, means the amount of metabolic energy input tive tension for long periods without cyclic contraction and compared to the tension produced. In smooth muscle, relaxation; a long-maintained contraction is called tonus there is a direct relationship between isometric tension and (rather than tetanus) or a tonic contraction. The economy is related to the ba- of smooth muscle activated by hormonal, pharmacological, sic cycling rate of the crossbridges: Early in a contraction or metabolic factors, whereas phasic activity is more closely (while tension is being developed and the crossbridges are associated with stimulation by neural activity. The force-veloc- Compared with skeletal muscle, the crossbridge cycle in ity curve for smooth muscle reflects the differences in smooth muscle is hundreds of times slower, and much more crossbridge functions described previously. Although time is spent with the crossbridges in the attached phase of smooth muscle contains one-third to one-fifth as much the cycle. Because the cells are so small produce as much force per unit of cross-sectional area as and numerous, smooth muscle tissue contains a large cell does skeletal muscle. Maintenance of the proper ionic concen- muscle on the force axis would be similar, while the maxi- trations inside the cells requires the activity of the mem- mum (and intermediate) velocity values are very different brane-based ion pumps for sodium/potassium and calcium, (Fig. A and B, Typical peak forces may be similar, the maximum shortening velocity of length-tension curves from skeletal and smooth muscle. Note smooth muscle is typically 100 times lower than that of skeletal the greater range of operating lengths for smooth muscle and muscle. C, CHAPTER 9 Skeletal Muscle and Smooth Muscle 173 force-velocity curves, each corresponding to a different Elastic material Elastic material level of myosin light-chain phosphorylation. Other mechanical properties of smooth muscle are also 5 related to its physiological roles. While its underlying cel- 4 Viscoelastic Viscoelastic lular basis is uncertain, smooth muscle has a length-tension 3 material material curve somewhat similar to that of skeletal muscle, although 2 there are some significant differences (Fig. At lengths 1 at which the maximal isometric force is developed, many 0 smooth muscles bear a substantial passive force. This is 0 5 10 0 5 mostly a result of the network of connective tissue that sup- Time Time ports the smooth muscle cells and resists overextension; in some cases, it may be partly a result of residual interaction between actin and attached but noncycling myosin cross- 5 Slow stretch Rapid stretch bridges. Compared to skeletal and cardiac muscle, smooth muscle can function over a significantly greater range of lengths. It is not constrained by skeletal attachments, and it makes up several organs that vary greatly in volume during 0 the course of their normal functioning.

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