By P. Ben. University of Maryland University College. 2018.
The sympathetic part of the ANS tends to act as an Increase in basal metabolic rate purchase clomid 100 mg menstruation fatigue. It promotes what is called the fight-or-flight response (for near objects) generic clomid 100 mg with amex menopause chills. Effects of the Sympathetic and Parasympathetic Systems on Table 9•4 Selected Organs Effector Sympathetic System Parasympathetic System Pupils of eye Dilation Constriction Sweat glands Stimulation None Digestive glands Inhibition Stimulation Heart Increased rate and strength of beat Decreased rate of beat Bronchi of lungs Dilation Constriction Muscles of digestive system Decreased contraction (peristalsis) Increased contraction Kidneys Decreased activity None Urinary bladder Relaxation Contraction and empty- ing Liver Increased release of glucose None Penis Ejaculation Erection Adrenal medulla Stimulation None Blood vessels to: Skeletal muscles Dilation Constriction Skin Constriction None Respiratory system Dilation Constriction Digestive organs Constriction Dilation 196 CHAPTER NINE Box 9-3 A Closer Look Cell Receptors: Getting the MessageCell Receptors: Getting the Message eurons use neurotransmitters to communicate with other found on effector cells of the parasympathetic nervous sys- Ncells at synapses. ACh can either stimulate or inhibit muscarinic recep- “docking sites,” the receptors on the receiving (postsynaptic) tors depending on the effector organ. A neurotransmitter fits into its receptor like stimulates digestive organs but inhibits the heart. When norepineph- Among the many different classes of identified receptors, rine (or epinephrine) binds to adrenergic receptors, it can ei- two are especially important and well-studied. For example, “beta- Nicotinic receptors (which bind nicotine) are found on blockers” regulate the heart in cardiac disease by preventing skeletal muscle cells and stimulate muscle contraction when 1 receptors from binding epinephrine, the neurotransmitter ACh is present. Saliva, for example, flows more easily and pro- systems not directly involved in the response to stress, fusely, and its quantity and fluidity increase. If you try to eat Most organs of the body receive both sympathetic and while you are angry, you may note that your saliva is thick parasympathetic stimulation, the effects of the two sys- and so small in amount that you can swallow only with dif- tems on a given organ generally being opposite. Under these circumstances, when food does reach 4 shows some of the actions of these two systems. The parasympathetic system brings about con- striction of the pupils, slowing of the heart rate, and con- striction of the bronchial tubes. It also stimulates the for- Checkpoint 9-15 Which division of the ANS stimulates a stress response, and which division reverses the stress response? Learning the meanings of these parts can help you remember words and interpret unfamiliar terms. WORD PART MEANING EXAMPLE The Nervous System as a Whole soma- body The somatic nervous system controls skeletal muscles that move the body. The Spinal Cord myel/o spinal cord Poliomyelitis is an infectious disease that involves the spinal cord and other parts of the CNS. Role of the nervous system (3) Mixed nerve—contains both sensory and motor fibers 9 A. The nervous system at work supplies smooth muscle, cardiac muscle, glands A. Nerve impulse transmitted from presynaptic neuron to (1) Neurilemma—outermost layer of Schwann cell; postsynaptic neuron aids axon repair 2. Receptors—in postsynaptic membrane; pick up neuro- myelinated tissue transmitters B. Sensory (afferent)—carry impulses toward CNS enzyme, return to presynaptic cell (reuptake) 2. Ends between first and second lumbar vertebrae (2) Perineurium—around each fascicle C. White matter around gray matter (1) Sensory (afferent) nerve—contains only fibers that a. Ascending tracts—carry impulses toward brain carry impulses toward the CNS (from a receptor) b. Descending tracts—carry impulses away from brain (2) Motor (efferent) nerve—contains only fibers D. Reflex arc—pathway through the nervous system that carry impulses away from the CNS (to an 1. Receptor—detects stimulus 198 CHAPTER NINE b. Reflex activities—simple reflex is rapid, automatic re- ica, herpes zoster (shingles), Guillain-Barré sponse using few neurons a. Injuries ganglia (celiac, superior mesenteric, inferior mesen- teric) VI. Usually have opposite effects on an organ Questions for Study and Review Building Understanding Fill in the blanks 1. With few exceptions, the sympathetic nervous system cell body by the. Matching Match each numbered item with the most closely related lettered item. The cells involved in most nervous system tu- tic neuron mors are called b.
Agonists of 2-adrenoceptors Histamine mediates a diverse group of processes rang- inhibit antigen-induced histamine release from mast ing from vasodilation to gastric acid secretion order clomid 100 mg on line menstrual irregularities. It pro- cells order clomid 50mg with amex women's health big book of exercises results, whereas muscarinic and -adrenergic agonists en- duces its effects by binding to and activating receptors hance mast cell degranulation. There are at least four recep- Non–Antigen-Mediated Release of Histamine tor populations, H1,H2, H3, and H4. All four receptor Histamine may be released from mast cells by mecha- subtypes have been cloned and belong to the G pro- nisms that do not require prior sensitization of the im- tein–coupled receptor superfamily. Drugs, high-molecular-weight proteins, ceptors can be distinguished on the basis of their venoms, and other substances that damage or disrupt post–receptor signal transduction mechanisms, tissue cell membranes can induce the release of histamine. Cardiovascular System Drugs, particularly organic bases, may release hista- mine from mast cells by physically displacing the amine A slow intravenous injection of histamine produces from its storage sites. Morphine, codeine, d-tubocu- marked vasodilation of the arterioles, capillaries, and rarine, guanethidine, and radiocontrast media can re- venules. Basic polypeptides, such nitude depends on the concentration of histamine in- as bradykinin, neurotensin, substance P, somatostatin, jected, the degree of baroreceptor reﬂex compensation, polymyxin B, and the anaphylatoxins resulting from and the extent of histamine-induced release of adrenal complement activation, also stimulate histamine release. Vasodilation of cutaneous blood vessels Venoms often contain basic polypeptides as well as the reddens the skin of the face, while a throbbing headache histamine-releasing enzyme phospholipase A. Stimulation of H1- Inactivation of Released Histamine receptors produces a rapid and short-lived response, The inactivation of histamine is achieved both by enzy- whereas stimulation of H2-receptors produces a more matic metabolism of the amine and by transport sustained response that is slower in onset. Stimulation processes that reduce the concentration of the com- of H3-receptors on sympathetic nerve terminals inhibits pound in the region of its receptors. Histamine metabo- the release of norepinephrine and its associated vaso- lism occurs primarily through two pathways (Fig. The most important of these involves histamine N- Histamine increases the permeability of capillaries methyltransferase, which catalyzes the transfer of a and postcapillary vessels, resulting in passage of ﬂuid 452 V THERAPEUTIC ASPECTS OF INFLAMMATORY AND SELECTED OTHER CLINICAL DISORDERS TABLE 38. This H1-receptor–mediated process is responsi- secretion by the salivary glands and glands in the small ble for the urticarial effect of histamine on the skin and large intestines. H3-receptors on sympathetic nerve terminals Postsynaptic H1- and H2-receptors are responsible for a in the heart decrease norepinephrine release; however, variety of processes in the CNS. H1-receptors mediate this effect appears to be signiﬁcant only during stress the maintenance of wakeful states, while H1- and H2- states such as ischemia. Presynaptic H3-receptors serve as feedback in- Histamine stimulates bronchiolar smooth muscle con- hibitors of the release of histamine, norepinephrine, and traction through activation of H1-receptors. Asthmatics are generally more the epidermis and dermis mediate itch and pain, respec- sensitive to the bronchoconstrictor actions of histamine tively. Although the magnitude of this effect in humans is nor- mally small, the large amounts of histamine released Lewis Triple Response during anaphylactic reactions can initiate abortion in The Lewis triple response illustrates the effects of hista- pregnant women. Histamine can also stimulate contrac- mine on vascular smooth muscle, vascular endothelium, tion of gastrointestinal smooth muscle, with large doses and sensory nerve endings. Dilation of capillaries in the immediate vicin- Histamine stimulates the secretion of gastric acid and ity of the injection results in a local red or blue pepsin through an effect on the H2-receptors of the pari- region (ﬂush). Dilation of arterioles results in an irregular red complex process that is stimulated by histamine, acetyl- ﬂare over an area that is generally wider than choline, and gastrin and inhibited by somatostatin. The ﬂare ability of H2-receptor antagonists to inhibit the en- probably results from an axon reﬂex in which hanced gastric acid secretion caused by acetylcholine histamine stimulates autonomic nerve endings, and gastrin suggests that histamine release is of primary causing release of vasodilatory mediators. Swelling (wheal) appears in the area of capil- tion sickness, to treat vestibular disturbances, such as lary dilation. Chemistry In addition to the ﬂush, wheal, and ﬂare, transient The H1-receptor antagonists for the most part are sub- stituted ethylamine compounds. In comparison with his- pain and itching result from the effects of histamine on tamine, the H1-antagonists contain no imidazole ring sensory nerve endings. In sensitized individuals, intra- dermal injection of speciﬁc antigens produces a wheal; and have substituents on the side chain amino group. The H1-antagonists are classiﬁed as either ﬁrst- or this reaction is the basis for a skin test to quantify the second-generation compounds.
GALE ENCYCLOPEDIA OF GENETIC DISORDERS 803 Genetic profile and lead to the rapid degradation of neuraminidase inside the lysosome purchase 25mg clomid mastercard menstruation postpartum. Inheritance of neuraminidase deficiency Some mutations in the NEU1 gene lead to a com- Neuraminidase deficiency is an autosomal recessive plete absence of neuraminidase activity purchase clomid 50 mg amex menstruation odors as you get older, with little or no disorder that can be caused by any one of a number of neuraminidase enzyme present in the lysosomes. These different mutations in the NEU1 gene encoding the lyso- mutations usually result in the severe, infantile-onset, somal neuraminidase. Other mutations result in an inactive the NEU1 gene is located on chromosome 6, rather than protein that is present in the lysosome. The disorder is reces- generally result in juvenile-onset, type II sialidosis, with sive because it only develops when both genes encoding symptoms of intermediate severity. Some mutations sig- neuraminidase, one inherited from each parent, are nificantly reduce, but do not obliterate, neuraminidase defective; however, the two defective NEU1 genes do not activity in the lysosome. If the two mutations mutated gene of this type are not completely neu- are identical, the individual is a homozygote. Individuals with one defective NEU1 gene, leading to more severe forms of neu- gene and one normal gene encoding neuraminidase may raminidase deficiency. Demographics All of the offspring of two parents with neu- Neuraminidase deficiency is an extremely rare disor- raminidase deficiency will inherit the disorder. Because of its similarities to many other disorders, it offspring of one parent with neuraminidase deficiency has been difficult to determine its frequency. In the and one parent with a single defective NEU1 gene will United States, it is estimated to occur in one out of every inherit at least one defective NEU1 gene. In Australia, the estimate is one out a 50% chance of inheriting two defective genes and, of 4. Since neuraminidase deficiency is an auto- therefore, developing neuraminidase deficiency. The off- somal rather than a sex-linked disorder, it occurs equally spring of one parent with neuraminidase deficiency and in males and females. The offspring of parents who deficiency requires two copies of the defective gene, one both carry one defective NEU1 gene have a 50% chance inherited from each parent. Thus, neuraminidase defi- of inheriting one defective NEU1 gene and a 25% chance ciency is much more common in the offspring of couples of inheriting two genes and developing neuraminidase who are related to each other (consanguineous mar- deficiency. Finally, the children of one parent with a sin- riages), such as first or second cousins. Type 2 sialidosis seems to occur more frequently defective gene, but will not develop neuraminidase defi- among Japanese. Signs and symptoms Mutations in the NEU1 gene The clinical symptoms of neuraminidase deficiency A number of different mutations that can cause neu- are similar to the symptoms of the mucolipidoses, includ- raminidase deficiency have been identified in the NEU1 ing I-cell disease (mucolipidosis II) and pseudoHurler gene. The type of neuraminidase deficiency, sialidoses polydystrophy (mucolipidosis III). Furthermore, the clin- types I or II, as well as the severity of the symptoms, ical distinctions between sialidoses types I and II may not depends on the specific mutation(s) that are present. Some mutations change one amino acid out of the 415 amino acids that compose a single neuraminidase mole- Sialidosis type I cule. Many of the identified mutations are clustered in The symptoms of sialidosis type I do not appear until one region on the surface of the protein. Infants and children with this result in a sharp reduction in the activity of the enzyme form of neuraminidase deficiency may have a normal 804 GALE ENCYCLOPEDIA OF GENETIC DISORDERS appearance and grow normally until adolescence. At that time, the appearance of red spots in both eyes, known as KEY TERMS cherry-red macules or cherry-red macular spots, may be one of the first symptoms of neuraminidase deficiency. Dysostosis multiplex—A variety of bone and Eventually, color and/or night blindness may develop. Cataracts may occur and vision may deteriorate gradu- Fibroblast—Cells that form connective tissue ally into blindness. Other symptoms of sialidosis type I include Glycoprotein—A protein with at least one carbo- myoclonus. Individuals with this form of neu- raminidase deficiency may have increased deep tendon Homozygote—Having two identical copies of a reflexes and may develop tremors and various other neu- gene or chromosome. There may be a progressive loss of Lipid—Large, complex biomolecule, such as a muscle coordination, called ataxia, and walking and fatty acid, that will not dissolve in water. Lysosome—Membrane-enclosed compartment in The above symptoms also may occur in sialidosis cells, containing many hydrolytic enzymes; where type II.
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