By C. Renwik. University of Minnesota-Crookston.
Nurses should recognize that each patient may have different expectations and aspirations c buy eriacta 100mg otc impotence signs. It is important to use quality of life questionnaires before ini- tiating conversations about quality of life 31. The degree of disability is the sole determinant of quality of life in MS b. Recognizing the need to respond to change is more important than the ability to socialize in MS c. Developing and sustaining satisfying relationships is an important factor in MS CHAPTER 22: CERTIFICATION STUDY QUESTIONS 119 32. In general terms, which of the following would be least likely to influence a person’s quality of life in MS? Which of the following statements describes the process termed “molecular mimicry? The foreign target and the self-target of the immune system share molecular features d. An inflammatory process up-regulates adhesion molecules on endothelial cells 35. Analysis of cerebrospinal fluid is helpful when the results of other tests are inconclusive b. If your cerebrospinal fluid is negative, it will confirm that you do not have MS c. Examining your cerebrospinal fluid will help us predict the course of your disease d. A positive result from the cerebrospinal fluid is a definitive test for MS 36. Presence of Lhermitte’s sign 120 NURSING PRACTICE IN MULTIPLE SCLEROSIS: A CORE CURRICULUM 38. In patients who are being treated with steroids, side effects to report include: a. When assessing a patient who complains of cognitive difficul- ties, which of the following would you expect to see? In a woman age 32 who has had MS for 3 years, the risks of pregnancy can be explained as follows: a. Pregnancy has no long-term effect on your disease course but you may have an exacerbation in the postpartum months d. Signs of depression can indicate an acceleration of the disease process c. Depression is an unusual and serious sign in MS CHAPTER 22: CERTIFICATION STUDY QUESTIONS 121 44. When assessing a patient with MS, which of the following is a primary symptom: a. Which intervention would be most effective to decrease the intensity of MS symptoms? Which of the following would indicate that the patient has bladder dysfunction? Which of these instructions would you give to a patient who is experiencing bowel dysfunction? The anticholinergic medication that you are taking will decrease constipation b. When teaching a patient who has cognitive impairment due to MS, all of the following are appropriate except: a. Teaching in a familiar setting 122 NURSING PRACTICE IN MULTIPLE SCLEROSIS: A CORE CURRICULUM Answers to Certification Questions 1.
The whole brain concentration of histamine is relatively low (50±70 ng/g) but there is much evidence for its central action (see Schwartz et al effective eriacta 100 mg impotence icd 9 code. Histidine is a poor substrate for the L-amino- acid decarboxylase responsible for DA and NA synthesis. The synthesis of histamine in the brain can be increased by the administration of histidine, so its decarboxylase is presumably not saturated normally, but it can be inhibited by a fluoromethylhistidine. No high-affinity neuronal uptake has been demonstrated for histamine although after initial metabolism by histamine N-methyl transferase to 3-methylhistamine, it is deaminated by intraneuronal MAOB to 3-methylimidazole acetic acid (Fig. A Ca2-dependent KCl-induced release of histamine has been demonstrated by micro- dialysis in the rat hypothalamus (Russell et al. Histamine receptors were first divided into two subclasses H1 and H2 by Ash and Schild (1966) on the basis that the then known antihistamines did not inhibit histamine- induced gastric acid secretion. The justification for this subdivision was established some years later when Black (see Black et al. A recently developed H2 antagonist zolantidine is the first, however, to show significant brain penetration. It is predominantly an autoreceptor on histamine nerves but is also found on the terminals of aminergic, cholinergic and peptide neurons. All three receptors are G-protein-coupled but little is known of the intracellular pathway linked to the H3 receptor and unlike H1 and H2 receptors it still remains to be cloned. Activation of H1 receptors stimulates IP3 formation while the H2 receptor is linked to activation of adenylate cyclase. Autoradiography and receptor mRNA studies have shown H1 receptors to be located in most of the brain areas innervated by the ascending histaminergic axons, e. Their presence in the cerebellum is not accompanied by appropriate histaminergic innervation. Very few are found in the striatum but this region does show a high density of H2 receptors. H2 receptors are also found with H1 in the cortex, hippocampus and limbic areas, but not in the hypo- thalamus. Although basically presynaptic the H3 receptor is also found postsynaptically in the striatum and cerebral cortex (Pollard et al. Although histamine generally inhibits neuronal firing in the cerebral cortex through H1 receptors it causes a H1-mediated excitation in the hypothalamus. It also appears to potentiate NMDA currents although the receptor type has not been established. In the hippocampus it has been shown to block the long-lasting hyperpolarisation (accommodation) that normally follows neuronal firing and is mediated through a Ca2-activated K conduction. From time to time it has been suggested that histamine has some role in a number of behaviours and motor activity while the established and marked sedative effect of H1 receptor antagonists, mentioned at the start of this section, has consistently been considered to indicate a role for histamine in arousal and the sleep±waking cycle (see Chapter 22). Histamine release in the hypothalamus is higher during the active waking than the quiescent phase of behaviour, whether this is associated with darkness (in rats) or light (rhesus monkey). The firing rate of histamine neurons is also higher during arousal OTHER TRANSMITTERS AND MEDIATORS 271 Figure 13. Current knowledge does not justify presentation of a schematic histaminergic synapse. In the cat the H1 antagonist mepyramine increases the slow-wave sleep pattern while direct injection into the hypothalamus of histamine itself, or an inhibitor of histamine-N-methyltransferase to stop histamine breakdown, produces the opposite effect, but it is still sensitive to mepyramine. Such H1-induced waking effects have not been so clearly established in 272 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION humans. In contrast to these excitatory effects elevating brain histamine levels with metoprine, an inhibitor of histamine-N-methyltransferase protects rodents against maximal electroshock although the specificity of the effect remains to be established. Agonists and antagonists at the H3 autoreceptors, which should decrease and increase histamine release, have been shown to augment and reduce slow-wave sleep in rats and cats. There are in fact numerous demonstra- tions of this using tests which require visual±motor coordination such as vigilance tasks and finger tapping. Since the slowing of such function could result from retarding information processing in the visual cortex it is interesting that the latency of com- ponents of the evoked potential, which follows presentation of a changing (reversing) black and white checkerboard pattern, is prolonged significantly in humans by the H1 antagonist diphenhydramine, which enters the brain, but not by terfenedine which does not (Tharion, McMenemy and Rauch 1994). There is also some evidence that histamine may be involved in food and water intake and thermoregulation (see Hough and Green 1983).
At low lung volumes order eriacta 100mg fast delivery erectile dysfunction treatment costs, pulmonary vascular resistance also increases, as a result of more positive pleural pressure, which compresses the extra-alveolar vessels. Since alveolar and extra-alveolar vessels can be viewed as two groups of resistance vessels connected in series, their resist- ances are additive at any lung volume. Pulmonary vascular resistance is lowest at functional residual capacity (FRC) and increases at both higher and lower lung volumes (Fig. Since smooth muscle plays a key role in determining the caliber of extra-alveolar vessels, drugs can also cause a change in resistance. A, At high lung volumes, alveo- constrictors, particularly at low lung volumes when the ves- lar vessels are compressed but extra-alveolar vessels are actually sel walls are already compressed. Drugs that relax smooth distended because of the lower pleural pressure. However, at low lung volumes, the extra-alveolar vessels are compressed from the muscle in the pulmonary circulation include adenosine, pleural pressure and alveolar vessels are distended. B, Total pul- acetylcholine, prostacyclin (prostaglandin I2), and isopro- monary vascular resistance as a function of lung volumes follows a terenol. The pulmonary circulation is richly innervated U-shaped curve, with resistance lowest at functional residual ca- with sympathetic nerves but, surprisingly, pulmonary vas- pacity (FRC). Hypox- Low Oxygen Tension Increases emia causes vasodilation in systemic vessels but, in pul- monary vessels, hypoxemia or alveolar hypoxia causes Pulmonary Vascular Resistance vasoconstriction of small pulmonary arteries. This unique Although changes in pulmonary vascular resistance are ac- phenomenon of hypoxia-induced pulmonary vasocon- complished mainly by passive mechanisms, resistance can striction is accentuated by high carbon dioxide and low be increased by low oxygen in the alveoli, alveolar hy- blood pH. The exact mechanism is not known, but hypoxia 342 PART V RESPIRATORY PHYSIOLOGY A Regional hypoxia cal changes (hypertrophy and proliferation of smooth mus- cle cells, narrowing of arterial lumens, and a change in con- tractile function). Pulmonary hypertension causes a sub- stantial increase in workload on the right heart, often leading to right heart hypertrophy (see Clinical Focus Box 20. Generalized hypoxia plays an important nonpatho- physiological role before birth. In the fetus, pulmonary vas- cular resistance is extremely high as a result of generalized Hypoxia hypoxia—less than 15% of the cardiac output goes to the lungs, and the remainder is diverted to the left side of the heart via the foramen ovale and to the aorta via the ductus arteriosus. When alveoli are oxygenated on the newborn’s first breath, pulmonary vascular smooth muscle relaxes, the vessels dilate, and vascular resistance falls dramatically. The foramen ovale and ductus arteriosus close and pulmonary B Generalized hypoxia blood flow increases enormously. FLUID EXCHANGE IN PULMONARY CAPILLARIES Starling forces, which govern the exchange of fluid across capillary walls in the systemic circulation (see Chapter 16), Hypoxia Hypoxia also operate in the pulmonary capillaries. Net fluid transfer across the pulmonary capillaries depends on the difference be- tween hydrostatic and colloid osmotic pressures inside and outside the capillaries. In the pulmonary circulation, two ad- ditional forces play a role in fluid transfer—surface tension and alveolar pressure. The force of alveolar surface tension (see Chapter 19) pulls inward, which tends to lower intersti- Effect of alveolar hypoxia on pulmonary ar- tial pressure and draw fluid into the interstitial space. Hypoxia-induced vasoconstriction is trast, alveolar pressure tends to compress the interstitial unique to vessels of the lungs and is the major mechanism regulat- space and interstitial pressure is increased (Fig. A, With regional hypoxia, precapillary constriction diverts blood flow away from poorly ventilated regions; there is little change in pulmonary arterial Low Capillary Pressure Enhances Fluid Removal pressure. B, In generalized hypoxia, which can occur with high altitude or with certain lung diseases, precapillary constriction oc- Mean pulmonary capillary hydrostatic pressure is normally 8 curs throughout the lungs and there is a marked increase in pul- to 10 mm Hg, which is lower than the plasma colloid os- monary arterial pressure. This is functionally important because the low hydrostatic pressure in the pulmonary cap- illaries favors the net absorption of fluid. Alveolar surface can directly act on pulmonary vascular smooth muscle tension tends to offset this advantage and results in a net cells, independent of any agonist or neurotransmitter re- force that still favors a small continuous flux of fluid out of leased by hypoxia. This excess fluid Two types of alveolar hypoxia are encountered in the travels through the interstitium to the perivascular and peri- lungs, with different implications for pulmonary vascular bronchial spaces in the lungs, where it then passes into the resistance. In regional hypoxia, pulmonary vasoconstric- lymphatic channels (see Fig. The lungs have a more tion is localized to a specific region of the lungs and diverts extensive lymphatic system than most organs.
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