By R. Mufassa. Christendom College. 2018.
Such findings fuel speculation that feedback inhibition of transmitter release might involve a transsynaptic mechanism discount plendil 2.5mg visa arrhythmia types ecg. Nevertheless generic 5 mg plendil fast delivery hypertension reading chart, many different types of neurons appear to have auto- receptors, including those that release acetylcholine (M2), dopamine (D2/D3), GABA (GABAB), 5-HT (5-HT1B or 5-HT1D)and histamine (H3). Electrophysiological studies in the CNS have exposed the presence of an a2-autoreceptor with a different function. These are found on the cell bodies of noradrenergic neurons in the nucleus locus coeruleus of the brainstem. When activated, they depress the firing rate of noradrenergic neurons in the nucleus. This means that changes in the concentration of noradrenaline in the medium bathing these somatodendritic a2-autoreceptors will modify the firing rate of central noradrenergic neurons. Examples are: 5-HT1A receptors on serotonergic neurons in the Raphe nuclei and D2/3-autoreceptors on central dopaminergic neurons in the ventral tegmental area and substantia nigra. Autoreceptor-mediated feedback control of transmitter release will obviously depend on enough transmitter accumulating in the synapse to activate the receptors. If the trains of stimuli are either too short, or their frequency too low, then transmitter release is not augmented by the administration of autoreceptor antagonists, implying that there is no autoreceptor activation (Palij and Stamford 1993). Conversely, at higher frequencies and long trains of stimulation, it becomes harder to inactivate the autoreceptors with antagonist drugs, presumably because of competition with increased concentrations of transmitter in the synapse. These receptors are thought to be located on the terminals of, and to modulate transmitter release from, one type of neuron, but are activated by transmitter released from a different type of neuron (Laduron 1985). For example, noradrenaline has been proposed to modulate release of a wide range of transmitters (e. However, one factor that should be borne in mind is that most of the evidence for heteroceptors comes from studies of NEUROTRANSMITTER RELEASE 99 tissue slices with [3H]preloaded transmitter stores. It is therefore hard to be certain that heteroceptors are actually located on the terminals of the [3H]labelled neuron and to rule out the possibility that they form part of a polysynaptic loop. To avoid this problem, a few studies have used synaptosomes to test the effects of one transmitter on K-evoked release of another. This approach has shown that noradrenaline and histamine, at least, blunt [3H]5-HT release from cortical synaptosomes. Whether the same is true for all the other interactions between noradrenaline and 5-HT release, as well as with other transmitters, remains to be seen. Evidence suggests that co-transmitters in a terminal have their own autoreceptors and, in some cases, activation of their own presynaptic receptor can influence the release of the co-stored, classical transmitter. For instance, activation of P2Y-autoreceptors by ATP is thought to affect the release of noradrenaline from sympathetic neurons. However, in other cases, feedback modulation of release of classical and their asso- ciated co-transmitters seems to have separate control mechanisms. This would suggest that either the two types of transmitter are concentrated in different nerve terminals or that mechanisms for regulating release target different vesicles located in different zones of the terminal (Burnstock 1990). COUPLING RECEPTORS WITH EXOCYTOSIS There are several ways in which activation of auto- or heteroceptors on nerve terminals could modify the amount of transmitter released by exocytosis. The fact that this will depend on the influence of second messengers is beyond doubt. What remains to be resolved is whether one mechanism is more important than the others, or whether this varies from tissue to tissue. Taking a2-adrenoceptors as an example, several possible mechanisms have been suggested (see Starke 1987). The first rests on evidence that these autoreceptors are coupled to a Gi (like)protein so that binding of an a2-adrenoceptor agonist to the receptor inhibits the activity of adenylyl cyclase. This leads to a fall in the synthesis of the second messenger, cAMP, which is known to be a vital factor in many processes involved in exocytosis. In this way, activation of presynaptic a2-adrenoceptors could well affect processes ranging from the docking of vesicles at the active zone to the actual release process itself. One possibility arises from evidence that activation of a -adrenoceptors reduces Ca2 influx; this will have obvious effects on 2 impulse-evoked exocytosis.
Respiratory System © The McGraw−Hill Anatomy order plendil 2.5 mg fast delivery blood pressure elevated, Sixth Edition Body Companies cheap plendil 5mg with mastercard heart attack get me going, 2001 Right principal bronchus Left principal bronchus EXHIBIT II The development of the lower respiratory tract. A cleft palate may be hereditary or a complication of some The respiratory system is particularly vulnerable to infectious dis- disease (e. A cleft lip is a genetically based developmental disor- highly social, and the warm, moistened environment along the der in which the two sides of the upper lip fail to fuse. Injury and trauma palates and cleft lips can be treated very effectively with cos- are also frequent problems. Cystic fibrosis is a genetic disorder that af- fects the respiratory system, as well as other systems of the body, Developmental Problems and accounts for approximately 1 childhood death in 20. The ef- fect of this disease on the respiratory system is usually a persistent of the Respiratory System inflammation and infection of the respiratory tract. Birth defects, inherited disorders, and premature births com- Pulmonary alveoli are not developed sufficiently to sus- monly cause problems in the respiratory system of infants. Thus, extrauterine life cleft palate is a developmental deformity of the hard palate of prior to that time is extremely difficult even with life-support- the mouth. Respiratory System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Chapter 17 Respiratory System 627 (a) FIGURE 17. The right side of the thorax appears uniformly dark because it is filled with air; the spaces between the ribs are also greater than those on the left, be- cause the ribs are released from the elastic tension of the lungs. The left lung appears denser (less dark) because of shunting of blood from the right to the left lung. Choking on a foreign object is a common serious trauma to the respiratory system. More than eight Americans choke to death each day on food lodged in their trachea. A simple proce- dure termed the abdominal thrust (Heimlich) maneuver can save the life of a person who is choking (fig. Stand behind the victim or the victim’s chair and wrap (b) your arms around his or her waist. If the victim is lying down: (nosebleeds) because the prominent nose can be easily bumped 1. With one of your hands on top of the other, place the blood pressure or diseases such as leukemia. Press into the victim’s abdomen with a quick upward pneumothorax can result from an external injury, such as a stab- thrust. A severely diseased lung, as in em- physema, can create a pneumothorax as the wall of the lung de- If you are alone and choking, use whatever is available to teriorates along with the visceral pleura and permits air to enter apply force just below your diaphragm. Respiratory System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 628 Unit 6 Maintenance of the Body nately vaccines are available. Sinusitis can be quite painful if the drainage ducts from the sinuses into the nasal cavity become blocked. Tonsillitis may involve any or all of the tonsils and frequently follows other lingering diseases of the oral or pharyn- geal regions. Laryngitis is inflammation of the larynx, which often produces a hoarse voice and limits the ability to talk. Tracheo- bronchitis and bronchitis are infections of the regions for which they are named. Severe inflammation in these areas can cause smaller respiratory tubules to collapse, blocking the pas- sage of air. Pneumonia is an acute infection and inflammation of lung tissue accompanied by exudation (accumulation of fluid). It is usually caused by bacteria, most commonly by the pneumococcus bacterium. Tuberculosis is an inflammatory disease of the lungs contracted by inhaling air sneezed or coughed by someone who is carrying active tuberculosis bacteria. Asthma is a disease that affects people who are allergic to certain inhaled antigens. It causes a swelling and blocking of lower respiratory tubes, often FIGURE 17.
ACKNOWLEDGMENT This chapter is reprinted with permission from Studdert DM discount 5mg plendil amex blood pressure chart based on height and weight, Mello MM plendil 5mg with mastercard hypertension zinc deficiency, Brennan TA. A measure of malpractice: medical injury, malpractice litigation, and patient com- pensation. Of Swords and Shields: The use of clinical practice guidelines in medical malpractice litigation. Medical practice guidelines in malpractice litigation: an early retrospective. Physicians who have lost their malpractice in- surance: their demographic characteristics and the surplus-line companies that insure them. Obstetricians’ prior malpractice experience and patients’ satisfaction with care. The relationship with malpractice claims among primary care physicians and surgeons. Factors that prompted families to file medical malpractice claims following perinatal injuries. State responses to the malpractice insurance “crisis” of the 1970s: an empirical assessment. Legislation on medical malpractice: further developments and a preliminary report card. Kinney, ED, Malpractice reform in the 1990s: past disappointments, future success? Beyond dead reckoning: Measures of medical injury burden, malpractice litigation, and alternative compensation models from Utah and Colorado. United States General Accounting Office, Medical malpractice insurance: mul- tiple factors have contributed to increased premium rates. Medical malprac- tice: Report of the Secretary’s Commission on Medical Malpractice DHEW Publication No. California Medical Association and California Hospital Associa- tion Report on the Medical Insurance Feasibility Study. Patients, doctors, and lawyers: medical injury, malpractice litigation, and patient compensation in New York. Relation between malpractice claims and adverse events due to negligence. Incidence and risk factors for adverse events and negligent care in Utah and Colorado in 1992. Negli- gent care and malpractice claiming behavior in Utah and Colorado. The influence of standard of care and severity of injury on the resolution of medical malpractice claims. Medical malpractice and the American jury: confronting the myths about jury incompetence, deep pockets, and outrageous damage awards. Variability in medical malpractice payments: is the com- pensation fair? Cheney FW, Posner K, Caplan RA, Ward RJ: Standard of care and anesthesia liability. Relation between negligent adverse events and the outcomes of medical malpractice litigation. Reality in the economic analysis of tort law: does tort law really deter? Entman SS, Glass CA, Hickson GB, Githens PB, Whetten-Goldstein K, Sloan FA. Relationship between malpractice claims history and subsequent obstetric care. Effects of the threat of medical malpractice litigation and other factors on birth outcomes. Deterrence of medical errors: theory and evidence for malpractice reform. The cesarean decision in New York state, 1986: economic and noneconomic aspects. Medical malpractice: implications of rising premi- ums on access to health care.
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