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This condition 500mg metformin fast delivery, known as acromegaly purchase metformin 500 mg on line, can also be caused by the chronic administration 10 of excessive amounts of GH to adults discount metformin 500 mg on-line. Although the main physiological action of GH is on body growth discount 500mg metformin overnight delivery, it also has important effects on certain as- 5 pects of fat and carbohydrate metabolism metformin 500mg with visa. Its main action on fat metabolism is to stimulate the mobilization of triglycerides from the fat depots of the body. This process, known as lipolysis, involves the hydrolysis of triglycerides 8 AM Noon 4 PM 8 AM Mid- 4 AM 8 AM to fatty acids and glycerol by the enzyme hormone-sensi- night tive lipase. The fatty acids and glycerol are released from Pulsatile GH secretion in an adolescent boy adipocytes and enter the bloodstream. In the adult, GH levels are re- lipolysis is not understood, but most evidence suggests that duced as a result of smaller pulse width and amplitude rather than it causes adipocytes to be more responsive to other lipoly- a decrease in the number of pulses. CHAPTER 32 The Hypothalamus and the Pituitary Gland 593 CLINICAL FOCUS BOX 32. How- Growth hormone (GH) is species-specific, and humans do ever, a random blood sample may be useful to detect GH not respond to GH derived from animals. In the past, the resistance, a syndrome in which the patient exhibits symp- only human GH available for treating children who were toms of GH deficiency but presents with high GH levels in GH-deficient was a very limited amount made from human the blood. This problem was solved when measure the levels of IGF-I, IGF-II, and the IGF-binding pro- the gene for human GH was cloned in 1979 and then ex- tein 3 (IGFBP3) in the blood. The production of large amounts of re- mitogenic effects of GH on tissues in the body. IGF-I and combinant human GH, with all the activities of the natural IGF-II bind to IGFBP3 in the blood. During the 1980s, careful life of the IGFs, transports them to target cells, and facili- clinical trials established that recombinant human GH was tates their interaction with IGF receptors. In children with GH deficiency, the con- Despite the availability of recombinant GH, the diagno- centration of IGFs and IGFBP3 are low. GH is combinant GH will increase IGF-I, IGF-II, and IGFBP3 in the released in periodic bursts, the greatest of which occur in blood, which will result in increased long bone growth. Between pulses of secretion, the The epiphyseal growth plate in the bone becomes less re- blood concentration of GH is nearly undetectable by most sponsive to GH and IGF-I several years after puberty, and techniques. For these reasons, a random measure of GH in long bone growth stops in adulthood (see Chapter 36). GH is also thought to function as one of the counter- Gonadotropins Regulate Reproduction regulatory hormones that limit the actions of insulin on The testes and ovaries have two essential functions in hu- muscle, adipose tissue, and the liver. The first is to produce sperm cells and hibits glucose use by muscle and adipose tissue and in- ova (egg cells), respectively. These effects are array of steroid and peptide hormones, which influence vir- opposite those of insulin. Also, GH makes muscle and fat tually every aspect of the reproductive process. Thus, GH nor- nadotropic hormones FSH and LH regulate both of these mally has a tonic inhibitory effect on the actions of insulin, functions. The production and secretion of the go- much like the glucocorticoid hormones (see Chapter 34). The regulation of human repro- large amounts of GH for an extended time. They may de- duction by this hypothalamic-pituitary-gonad axis is dis- velop insulin resistance and an elevated insulin level in the blood. They may also have hyperglycemia caused by the underutilization and overproduction of glucose. These dis- turbances are much like those in individuals with non-in- TABLE 32. For this reason, this metabolic response to excess GH is called its diabeto- Growth-promoting Stimulates IGF-I gene expression by target genic action. For example, intravenous injection of GH on cell division, resulting in growth in a person who is GH-deficient produces hypoglycemia.

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The liver order 500 mg metformin overnight delivery, which synthe- Why should the hypertonic saline be administered slowly? The endogenous creatinine (CR) clearance (an estimate of Answers to Case Study Questions for Chapter 24 GFR) equals (UCR V)/PCR (60 1 buy 500mg metformin otc. Note that the permeability of with an impaired ability to dilute the urine (note the inap- the glomerular filtration barrier to macromolecules (plasma propriately high urine osmolality) order metformin 500 mg on line, led to severe hypona- proteins) was abnormally high metformin 500mg low cost, but permeability to fluid tremia and water intoxication buy 500 mg metformin with mastercard. Addition of 1 L of 308 mEq Na /L to 25 L produces an in- may be significant and may lead to a reduced fluid perme- ability and GFR. The edema is a result of altered capillary Starling forces and used in this calculation because when hypertonic NaCl is added to the ECF, it causes the movement of water out of renal retention of salt and water. The decline in plasma the cell compartment, diluting the extracellular Na. Because the brain is enclosed in a nondistensible cranium, ing fluid movement out of the capillaries into the interstitial compartment. The edema is particularly noticeable in the when water moves into brain cells and causes them to swell, intracranial pressure can rise to very high values. The abdomi- nal distension (in the absence of organ enlargement) sug- This can damage nervous tissue directly or indirectly by im- gests ascites (an abnormal accumulation of fluid in the ab- pairing cerebral blood flow. The neurological symptoms seen in this patient (headache, semiconsciousness, grand dominal cavity). The kidneys avidly conserve Na (note the low urine [Na ]) despite an expanded ECF volume. The in- though the exact reasons for renal Na retention are contro- creased blood pressure and cool and pale skin may be a consequence of sympathetic nervous system discharge re- versial, a decrease in the effective arterial blood volume sulting from increased intracranial pressure. This leads to activation of the renin-angiotensin-aldosterone system restoration of a normal plasma [Na ] can produce serious damage to the brain (central pontine myelinolysis). The physicians wanted to exclude the presence of a bron- chogenic tumor, which is the most common cause of ments of the nephron reabsorb more Na than usual be- cause of an intrinsic change in the kidneys. Rapid development of hyponatremic seizures in a 1998;338:1202–1211 psychotic patient. Goldman MB, Luchins DJ, Robertson GL Mechanisms of al- CASE STUDY FOR CHAPTER 24 tered water metabolism in psychotic patients with polydipsia Water Intoxication and hyponatremia. A 60-year-old woman with a long history of mental ill- ness was institutionalized after a violent argument with CASE STUDY FOR CHAPTER 25 her son. She experiences visual and auditory hallucina- tions and, on one occasion, ran naked through the ward Lactic Acidosis and Hemorrhagic Shock screaming. She refuses to eat anything since admission, During a violent argument over money, a 30-year-old but maintains a good fluid intake. The assailant escaped, day, she complains of a slight headache and nausea and but friends were able to rush the victim by car to the has three episodes of vomiting. The patient is unconscious, with a blood found on the floor in a semiconscious state, confused pressure (mm Hg) of 55/35 and heart rate of 165 and disoriented. The sub- Her pulse rate is 70/min and blood pressure is 150/100 ject is pale, with cool, clammy skin. On admission, about CHAPTER 25 Acid-Base Balance 447 an hour after the stabbing, an arterial blood sample is tilation is stimulated by the low blood pH, sensed by the pe- taken, and the following data were reported: ripheral chemoreceptors. The anion gap is [Na ] [Cl ] [HCO ] 140 103 3 Glucose 125 mg/dL 70–110 mg/dL (3. Considering the (fasting values) history and physical findings, the high anion gap is most Na 140 mEq/L 136–145 mEq/L likely caused by inadequate tissue perfusion, with resultant K 4. The lac- Cl 103 mEq/L 95–105 mEq/L tic acid is buffered by HCO3 and lactate accumulates as the HCO 4 mEq/L 22–26 mEq/L 3 unmeasured anion. Note that tissue hypoxia can occur if BUN 23 mg/dL 7–18 mg/dL blood flow is diminished, even when arterial PO2 is normal. The low hematocrit is a result of absorption of interstitial Creatinine 1. In response to the blood loss and low blood pressure, kid- PaCO2 14 35–45 mm Hg ney blood flow and GFR would be drastically reduced. The PaO2 97 mm Hg 75–105 mm Hg sympathetic nervous system, combined with increased Hematocrit 35% 41–53% plasma levels of AVP and angiotensin II, would produce in- Questions tense renal vasoconstriction. What is the most appropriate treatment for the acid-base into the gastrointestinal tract, digestion of blood proteins, disturbance? The subject has a metabolic acidosis, with an abnormally isotonic saline solutions and packed red blood cells) would low arterial blood pH and plasma [HCO ].

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Nerves accomplish continuous increase in Na permeability and more Na entry generic metformin 500 mg. Var- snowballing event order metformin 500mg on line, which occurs in a fraction of a mil- ious hormones are also involved in regulating blood pres- sure metformin 500 mg on-line, but their effects are generally slower and last longer 500mg metformin. Feedforward control is another strategy for regulating systems in the body order 500mg metformin visa, particularly when a change with time Depolarization of nerve or muscle is desired. In this case, a command signal is generated, membrane which specifies the target or goal. The moment-to-moment operation of the controller is “open loop”; that is, the regu- lated variable itself is not sensed. Feedforward control mechanisms often sense a disturbance and can, therefore, take corrective action that anticipates change. For example, heart rate and breathing increase even before a person has begun to exercise. Feedforward control usually acts in combination with negative-feedback systems. One example is picking up a Entry of Increase in Na Na into cell permeability pencil. The movements of the arm, hand, and fingers are di- rected by the cerebral cortex (feedforward controller); the movements are smooth, and forces are appropriate only in part because of the feedback of visual information and sen- sory information from receptors in the joints and muscles. Respiratory and cardiovascular adjustments closely match A positive-feedback cycle involved in the FIGURE 1. CHAPTER 1 Homeostasis and Cellular Signaling 5 lisecond, leads to an actual reversal of membrane poten- at the blood capillary level. Even within cells there is com- tial and an electrical signal (action potential) conducted partmentalization. The interiors of organelles are separated along the nerve or muscle fiber membrane. The process is from the cytosol by membranes, which restrict enzymes and stopped by inactivation (closure) of the Na channels. Equilibrium occurs if sufficient time for exchange has which occurs with each heartbeat. Depolarization of the been allowed and if no physical or chemical driving force cardiac muscle plasma membrane leads to a small influx of would favor net movement in one direction or the other. This leads to For example, in the lung, oxygen in alveolar spaces diffuses an explosive release of calcium from the muscle’s sarcoplas- into pulmonary capillary blood until the same oxygen ten- mic reticulum, which rapidly increases the cytosolic cal- sion is attained in both compartments. Many rium between cells and extracellular fluid is normally pres- other examples are described in this textbook. No energy expenditure is required so weakened by disease that it cannot provide adequate to maintain an equilibrium state. This leads to a Equilibrium and steady state are sometimes confused further reduction in cardiac pumping ability, even less with each other. A steady state is simply a condition that coronary blood flow, and further deterioration of cardiac does not change with time. The physician’s task is sometimes to interrupt or concentration of a substance in a compartment is constant. In a steady state, there is no net gain or net loss of a sub- stance in a compartment. Steady state and equilibrium both suggest stable conditions, but a steady state does not nec- Steady State and Equilibrium Are Separate Ideas essarily indicate an equilibrium condition, and energy ex- Physiology often involves the study of exchanges of matter penditure may be required to maintain a steady state. For or energy between different defined spaces or compart- example, in most body cells, there is a steady state for Na ments, separated by some type of limiting structure or ions; the amounts of Na entering and leaving cells per unit membrane. But intracellular and extracellular Na ion compartments: extracellular fluid and intracellular fluid. Extracellular These two compartments are separated by cell plasma mem- [Na ] is much higher than intracellular [Na ], and Na branes. The extracellular fluid consists of all the body fluids tends to move into cells down concentration and electrical outside of cells and includes the interstitial fluid, lymph, gradients. The cell continuously uses metabolic energy to blood plasma, and specialized fluids, such as cerebrospinal pump Na out of the cell to maintain the cell in a steady fluid.

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The reduction in cAMP also indirectly reduces Ca2‡ influx into the terminal and increases K‡ conductance metformin 500 mg free shipping, thereby reducing neuronal excitability (reviewed by Starke 1987) metformin 500mg line. Whichever of these release- controlling processes predominates is uncertain but it is likely that their relative importance depends on the type (or location) of the neuron cheap 500mg metformin visa. The increase in cAMP production resulting from activation of these receptors is an obvious explanation for how this might occur buy 500mg metformin otc. The precise role of these receptors in regulation of noradrenaline release in vivo is uncertain because noradrenaline has a relatively low affinity for these receptors discount metformin 500mg line. However, one suggestion is that, in the periphery, they are preferentially activated by circulating adrenaline which has a relatively high affinity for these receptors. This activation could enable circulating adrenaline to augment neuronal release of noradrenaline and thereby effect a functional link between these different elements of the sympathoadrenal system. However, the extent to which this actually happens is uncertain as is a physiological role for b-adrenoceptors in regulation of nor- adrenaline release in the brain. Nevertheless, there is some evidence from studies of hippocampal synaptosomes that activation of muscarinic, GABAB or adenosine (A1) receptors depresses noradrenaline release while activation of GABAA receptors increases it. A further possible mechanism, that would enable different types of neurons to modify noradrenaline release, is suggested by recent in vitro studies of brain slices. These have revealed that noradrenaline release is increased when the slices are superfused with a solution containing GABA. This release is prevented by an inhibitor of GABA uptake but unaffected by the presence of GABAA receptor antagonists, such as bicuculline. There is no doubt that this form of release depends on vesicular exocytosis because it is Ca2‡-dependent, sensitive to tetrodotoxin and, like impulse- dependent release, it is attenuated by a2-adrenoceptor agonists (see above). The extent to which this process occurs under normal physiological conditions in vivo remains to be seen. NEURONAL REUPTAKE OF NORADRENALINE In common with other monoamines, the actions of released noradrenaline are terminated by its rapid reuptake from the synaptic cleft. This uptake process relies on membrane-bound noradrenaline transporters which are glycoproteins closely related Figure 8. Binding domains for specific ligands are thought to be within regions indicated by the solid bars. All these transporters have 12 hydrophobic transmembrane domains (TMDs), a large hydrophyllic loop between TM3 and TM4, and intracellular N- and C-termini. The hypothetical structure of the noradrenaline transporter is illustrated in Fig. Because co-transport of both Cl7 and Na‡ is required for the uptake of noradrenaline, this is regarded as one of the family of Na‡/Cl7 transporters. Exactly how this transporter carries noradrenaline across the neuronal membrane is not known but one popular model proposes that it can exist in two interchangeable states. This process enables the translocation of noradrenaline from the extracellular space towards the neuronal cytosol. Point-mutation and splicing studies indicate that different zones of the transporter determine its substrate affinity and selectivity, ionic dependence, Vmax, and the binding site for uptake inhibitors such as desipramine (Povlock and Amara 1997). Because the cloned transporter is a target for the reuptake inhibitor, desipramine, it is thought to reflect the native transporter in the brain and peripheral tissues. These are quite distinct uptake mechanisms because they have different substrate affinities and antagonist sensitivities. As yet, few studies have investigated the possibility that more than one uptake process exists in the brain but since two mRNAs for noradrenaline transporters have been isolated from brain tissue (Pacholczyk, Blakely and Amara 1991) there could be more than one transcription factor. At the very least, intracellular messengers could modify substrate affinity of the transporter, by causing its phosphorylation or glycosylation (Bonisch, Hammermann and Bruss 1998), and so markedly affect its function. Whether or not there are different gene products, splice variants, or posttranslational changes, it has been suggested that abnormal distributions of functionally distinctive noradrena- line transporters could underlie some psychiatric and neurological disorders. METABOLISM After reuptake into the cytosol, some noradrenaline may be taken up into the storage vesicles by the vesicular transporter and stored in the vesicles for subsequent release (see above). However, it is thought that the majority is broken down within the cytosol of the nerve terminal by monoamine oxidase (MAO; EC1. The metabolic pathway for noradrenaline follows a complex sequence of alternatives because the metabolic product of each of these enzymes can act as a substrate for the other (Fig 8. This could enable one of these enzymes to compensate for a deficiency in the other to some extent. MAO is bound to the outer membrane of mitochondria and is responsible for the oxidative deamination of noradrenaline.

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