By J. Jaroll. Capella University. 2018.
These effector processes include direct cytotoxicity mediated by cytotoxic T cells; the suppression or activa- The primary structure of an antibody is illustrated in Figure tion of immune mechanisms in other cells—suppressor T 11 discount skelaxin 400 mg otc. Each antibody molecule consists of four polypeptide CHAPTER 11 Blood Components order skelaxin 400mg without prescription, Immunity purchase skelaxin 400mg otc, and Hemostasis 205 be generated by protease digestion and separated by chro- matography skelaxin 400 mg without a prescription. Fc fragments can bind to cells such as neu- trophils, monocytes, and mast cells through their Fc recep- tors. Fc receptor binding amplifies the biological activity of antigen-bound antibody. In addition to the ability to bind antigen, the antibody molecule may have a variety of other important biological functions, depending on its class. IgG is the bonds most prevalent antibody in serum and is responsible for adaptive immunity to bacteria and other microorganisms. Carbohydrate Bound to antigen, IgG can activate serum complement, which releases several inflammatory and bactericidal medi- ators. At the surface of bacteria, exposed Fc portions of IgG Heavy chain molecules facilitate the phagocytosis of bacteria by blood 450 amino acids phagocytes, a process called opsonization. Each heavy chain and light chain pos- of the fundamental Y-shaped antibody unit. In most IgA sesses a constant region (where the amino acid sequence of indi- molecules, two antibody units are held together by a secre- vidual molecules is similar) and a variable region, where tory piece (J chain), a protein synthesized by epithelial alterations in the amino acid sequence convey to the antibody its individual antigen specificity. In this conformation, IgA is actively secreted into saliva, tears, colostrum, and mucus. IgM is the first antibody secreted chains (two heavy chains and two light chains) held together after an initial immune challenge and provides resistance as a Y-shaped molecule by one or more disulfide bridges. Each polypeptide chain possesses both a conserved constant Its size and large number of antigen-binding sites provide region and a variable region, where considerable amino acid the molecule with an excellent capacity for agglutination, sequence heterogeneity is found even within a single anti- the ability to clump particulate antigens, such as bacteria body class. Clumped antigens are efficiently and widely diverse antigen-binding ability of antibody molecules, quickly removed by fixed phagocytic cells of the mono- for it is the variable region that actually combines with the cyte-macrophage system. These The amino terminal portions of the variable regions, the cells are heavily granulated. The granules contain histamine, antigen-binding sites, are known as the Fab regions. Each leukotrienes, and other biologically active agents that in- antibody unit possesses two identical antigen-binding sites, crease vascular permeability, dilate blood vessels (and, one at each end of the “Y. The granules are released when IgE, consisting of Fc and Fab regions of antibody molecules can bound to mast cells at the Fc region, binds its specific anti- TABLE 11. The ensuing allergic responses range from hay fever, openings in blood vessels. The aggregates form a physical hives, and bronchial asthma (induced by local or inhaled al- barrier that begins to limit blood loss soon after the open- lergens) to systemic anaphylaxis, a potentially fatal response ing occurs. Second, phospholipids on the platelet plasma triggered when antigen is given systemically. Platelet activation results in the sequential responses of ad- HEMOSTASIS herence, aggregation, and secretion. Adherence is initiated when one or more substances, released from cells or activated Circulating in a high-pressure, closed system that communi- in plasma at the site of a hemorrhage, bind to receptors in the cates with all tissues and cells in the body, blood exchanges platelet plasma membrane. Receptor binding results, via sec- oxygen, nutrients, and wastes and provides necessary compo- ond messengers, in adherence (to other platelets and the in- nents for host defense. This communication takes place largely ner, endothelial surface of blood vessels) and secretion. Endothelial cells also rapidly de- fragile capillaries may result from minor tissue injury associ- ploy cellular adherence antigens known as integrins on the ated with normal physical activity or from massive tissue outer surface of their plasma membranes during wound trauma as a result of serious injury or infection, and may healing. These adherence antigens are deployed to the cell quickly lead to death.
It contains taste fibers large purchase skelaxin 400mg without prescription, multipolar neurons in the nucleus of for the anterior two-thirds of the tongue (D) the facial nerve (AB2) cheap 400 mg skelaxin free shipping. They arch around and preganglionic fibers for the subman- the abducens nucleus (AB3) (internal genu of dibular and sublingual glands as well as the facial nerve) and emerge on the lateral various lingual glands purchase skelaxin 400mg fast delivery. The cells of the Before it enters the parotid gland best 400mg skelaxin, the facial preganglionic secretory fibers (AB4) form the nerve gives off the posterior auricular nerve superior salivatory nucleus (AB5). The (E17) as well as branches to the posterior taste fibers (AB6) originate from the pseudo- belly of the digastric muscle (CE18) and to unipolar cells in the geniculateganglion (BC7) the stylohyoid muscle (C19). The parotid and terminate in the cranial section of the plexus gives off the temporal branches (E20), solitary nucleus (AB8). The visceroefferent the zygomatic branches (E21), the buccal and taste fibers do not arch around the ab- branches (E22), the marginal mandibular ducens nucleus but join the ascending limb branch (E23), and the cervical branch (E24) of the nerve and emerge as intermediate for the platysma (see vol. The branches nerve (B9) between the facial nerve and the provide innervation to all the muscles of fa- vestibulocochlear nerve. Both parts of the nerve pass through the Ramifications of the cervical branch lying inner auditory canal, the internal acoustic beneath the platysma form the superficial meatus (petrous part of temporal bone, in- cervical ansa by anastomosing with ternal acoustic pore, see vol. The small branches of the nerve in the petrous bone (external departing from the ansa are mixed sen- genu of the facial nerve) lies the geniculate sorimotor nerves. The canal continues above tions of temporal branches, buccal the tympanic cavity (p. The nerve ramifies into terminal branches (parotidplexus) (E11) in the parotid Clinical Note: Injury to the nerve results in atony of all muscles of the affected half of the gland. The mouth region drops, and the eye can no The greater petrosal nerve (BC12), the longer close (F). There is increased sensitivity to stapedius nerve (BC13), and the chorda sound, hyperacusis (p. Seventh Cranial Nerve 123 7 12 25 8 13 3 5 15 6 2 4 14 1 10 18 16 19 A Nuclear region of the facial nerve C Facial nerve, course within 2 3 the petrous bone 7 1 4 6 5 8 12 9 13 10 14 D Tongue area supplied B Exit of the facial nerve by taste fibers 20 21 17 22 11 23 18 24 E Muscles innervated F Paralysis of the by the facial nerve left facial nerve Kahle, Color Atlas of Human Anatomy, Vol. It emerges from the pons with a thick and gingiva (D10); and the mandibular sensory root (greater portion) and a thinner nerve supplies the lower region of the oral motorroot (lesser portion) and then passes to cavity (D11) and the cheeks. The trigeminal ganglion (semilunar ganglion, Ophthalmic Nerve (E) Gasser’s ganglion) lies in a dural pocket, the trigeminal cave, and gives off three main The ophthalmic nerve (E12) gives off a re- branches, namely, the ophthalmic nerve, the current tentorial branch and divides into the maxillary nerve, and the mandibular nerve lacrimal nerve (E13), the frontal nerve (E14), (see p. These branches pass through the superior orbital The sensory fibers (B1) originate from the fissure into the orbit; the nasociliary nerve pseudounipolar cells in the trigeminal gan- enters through the medial section of the fis- glion (semilunar ganglion, Gasser’s gan- sure, the two other branches enter through glion) (BE2); the central processes of these the lateral section. Most of the fibers of the epicritic sen- The lacrimal nerve runs to the lacrimal gland sibility (p. Via a communicating cleus) (AB3), while those of the protopathic branch, it receives postganglionic secretory sensibility (p. The fibers for the outermost semi- junctiva, upper eyelid, and the skin of the circle terminate furthest caudally (onion forehead). The mesencephalic tract (B6) carries The nasociliary nerve runs to the medial proprioceptive impulses from the mastica- corner of the eye, which it supplies with its tory muscles. Thenasociliarynervegivesoffthefol- The mesencephalic nucleus of the trigeminal lowing branches: a communicating branch nerve (AB7) consists of pseudounipolar neu- to the ciliary ganglion (E20), the long ciliary rons, the processes of which run through nerves (E21) to the eyeball, the posterior eth- the trigeminal ganglion without interrup- moidal nerve (E22) to the sphenoidal and tion. These are the only sensory fibers for ethmoidal sinuses, and the anterior eth- which the cells of origin do not lie in a gan- moidal nerve (E23); the latter runs through glion outside the CNS but in a nucleus of the the anterior ethmoidal foramen to the eth- brain stem, so to speak representing a moidal plate and through the plate into the sensory ganglion located inside the brain. Its terminal branch, the exter- nal nasal branch, supplies the skin of the dorsum and the tip of the nose. Fifth Cranial Nerve 125 7 3 7 6 8 8 2 1 A Nuclear region of the trigeminal nerve 3 4 5 B Exit of the trigeminal nerve 9 10 9 4 C Somatotopic organization of the spinal nucleus of the trigeminal nerve (according to Dejerine) 11 16 D Sensory innervation of 18 23 13 14 22 15 mucosa by the three 17 branches of the trigeminal nerve 19 12 2 F Skin innervated by 21 20 the ophthalmic nerve E Ophthalmic nerve (according to Feneis) Kahle, Color Atlas of Human Anatomy, Vol. Motor fibers for the ten- Maxillary Nerve (A, B) sortympanimuscleandforthetensormuscle The maxillary nerve (A1) gives off a menin- of the velum palatinum run to the otic gan- geal branch and then passes through the glion (p. It gives off a communicating geal artery and then unite to form the nerve branch, which contains postganglionic (p.
Treatment of tability buy discount skelaxin 400 mg, sleep disturbance cheap skelaxin 400mg with visa, and generalized nicotine dependence varies widely buy skelaxin 400mg fast delivery, rang- anxiety buy skelaxin 400mg otc. If, however, individuals became ing from the use of nicotine-containing dependent on higher doses, withdrawal gum to hypnosis to behavioral and group can be life-threatening. The success of most programs drawal, especially from barbiturates, can designed to stop tobacco use is directly result in acute psychosis and seizures. Therapeutic withdrawal from a sedative, like the therapeutic withdrawal from Sedatives alcohol, usually involves the administra- tion of a cross-tolerant drug to suppress Sedation implies calmness and tranquil- withdrawal symptoms with gradual taper- ity. The drug being with- pharmacologic action they produce, drawn determines the length of time namely, depression of the central nervous required for tapering. Examples of sedative drugs are 7 to 10 days is sufficient for detoxification. Many symptoms of withdrawal are flulike, Opioids although they may include anxiety, irri- tability, and restlessness. Because opioids (narcotic drugs such as Opiate substitution drugs are sometimes morphine, meperidine [Demerol], pro- used in treatment of opiate addiction and poxyphene [Darvon], oxycodone [Perco- may be used for either detoxification or dan], and codeine) are frequently maintenance. Methadone and another prescribed for pain, addiction can occur opiate-substitute, levomethadyl acetate, through regular prescription use. In oth- may be used to reduce the use of illicit opi- er instances, these medications are ates and the high-risk behaviors associat- obtained illegally. O’Connor, 2000), as well as to provide In addition to producing pain relief, medical assistance with withdrawal of opi- narcotics produce euphoria, sedation, and ates. At first, individu- drug dosage is gradually tapered during als may take illegal narcotics primarily for the withdrawal period. Repeated admin- may be enrolled in a maintenance program istration rapidly produces tolerance and in which they do not undergo detoxifica- intense physical dependence. Eventually, tion but rather receive maintenance dos- as the dosage and/or frequency of drug es of an opiate substitute along with administration increases, individuals need counseling. The goal of such programs is to continue to take the drug regularly to first to help individuals return to a social- avoid symptoms of physical withdrawal. Drugs that are injected increase individuals’ risk of Stimulants contracting HIV infection or hepatitis C if needles are shared. Adding adulterants to Acting directly on the central nervous substances or using nonsterile techniques system, stimulants create an increased state of injection may also produce medical of arousal and concentration and speed up complications. Individuals may (inflammation of tissues), thrombophle- take stimulants for such effects as in- bitis (inflammation of a vein with associ- creased alertness and increased sense of ated clot formation), septicemia (presence well-being, increased confidence, reduc- of toxins in the blood), and bacterial tion of fatigue, or decrease in appetite. They can be taken Withdrawal symptoms vary in severity orally, topically, intravenously, or by inhala- and duration, depending on the particu- tion. In addition to central nervous system 216 CHAPTER 7 CONDITIONS RELATED TO SUBSTANCE USE effects, stimulants have generalized sys- lasts only a matter of minutes, however, temic effects, including an increase in heart and is often followed by irritability, rest- rate, an increase in blood pressure, a rise in lessness, and depression. The aftereffects body temperature, and the constriction of of crack can be so intense that individuals peripheral blood vessels (Sarnyai, Shaham, continue to smoke it, despite obvious & Heinrichs, 2001). It Aside from its psychological, social, and may be taken orally, used intranasally vocational consequences, cocaine use can (snorted), smoked, or injected intraven- have serious medical consequences. The technique of free-basing basing or smoking crack can lead to pul- cocaine, which gained popularity in the monary complications. Chronic use of 1980s, involves heating a flammable sol- intranasal cocaine may cause ulceration or vent such as petroleum or ether, and then perforation of the nasal septum. The process intoxication can produce neurologic effects, “frees” cocaine hydrochloride from its such as confusion, anxiety, hyperexcitabil- salts and adulterants, converting it to a ity, agitation, and violence. The effects are the result of acute cocaine toxi- free-base cocaine can be inhaled or city, which is dose related, in which indi- smoked, usually with a water pipe, for viduals can experience stroke or seizures, direct absorption through the alveoli in severe hyperthermia (increased body the lungs. The technique rapidly delivers temperature), arrhythmia (irregular heart- high concentrations of cocaine to the beat), myocardial infarction (heart brain and results in blood levels as high attack), and, in some instances, sudden as those for self-injection.
These chemical mediators then interact to sensitise nociceptors so that afferent activity to a given stimulus is increased safe skelaxin 400mg. Some of the most important components in inflammation are the products of arachi- donic acid metabolism order skelaxin 400mg online. Arachidonic acid buy skelaxin 400mg with mastercard, a component of cell membranes order 400mg skelaxin with amex, is liberated by phospholipase A2 and subsequently metabolised by two main pathways which are controlled by two different enzymes, cyclo-oxygenase (COX) and lipoxygenase. This metabolism gives rise to a large number of eicosanoids (leukotrienes, thromboxanes, prostacyclins and prostaglandins) (see Chapter 13). These chemicals do not normally activate nociceptors directly but, by contrast, reduce the C-fibre threshold and so sensitise them to other mediators and stimuli. Thus the value of both steroids and the non-steroidal anti-inflammatory (NSAIDs) drugs in pain after tissue damage is based on their ability to block the conversion of arachidonic acid to these mediators. It should be emphasised that these drugs can only prevent further conversion and will not change the effects of eicosanoids that have already been produced. The short half-life of these mediators makes this fact less important than it would be if the mediators had long- lasting effects. The former is a constitutive enzyme, always present so that its inhibition affects not only inflammation but also other actions of the products leading to gastric and renal side-effects. By contrast, COX-2 is induced in the periphery by tissue damage and a new generation of selective COX-2 inhibitors have improved therapeutic profiles over existing non-selective drugs. Several novel agents with actions on this latter enzyme are effective in inflammatory pain. Interestingly, COX-2 is normally present in the brain and spinal cord and so may be responsible for some of the central analgesic effects of NSAIDs. Bradykinin is another chemical with important peripheral actions but, as yet, cannot be manipulated in any direct way by drugs. It is a product of plasma kininogens that find their way to C-fibre endings following plasma extravasation in response to tissue PAIN AND ANALGESIA 457 injury. Bradykinin receptors have been characterised and here again, there are two forms. The B1-receptor is constitutively expressed less than the B2-receptor, but in chronic inflammation, it is upregulated. Pain may arise via the activation of the B2- receptor, which is abundant in most tissues and which can activate C-polymodal receptors. The response to bradykinin can be enhanced by prostaglandins, heat and serotonin, indicating the extent of interactions between these peripheral pain mediators. Hydrogen ions accumulate in tissue damaged by inflammation and ischaemia and so pH is lowered. These protons may activate nociceptors directly via their own family of ion channels as well as sensitising them to mechanical stimulation. Acid-sensing ion channels (ASICS) are a family of sodium channels that are activated by protons Ð of special interest is one type found only in small dorsal root ganglion neurons that possibly are responsible for activation of nociceptors. Although the transduction of mechanical stimuli is poorly understood, ASICs are closely related to channels that respond to stretch. VASCULAR DAMAGE, HEADACHE AND MIGRAINE Serotonin, 5-hydroxytryptamine (5-HT), is released from a number of non-neuronal cells such as platelets and mast cells and can produce an excitation of nociceptive afferents via the activation of its large number of receptors, e. The key role, but not the mechanisms of action, of 5-HT in the pain associated with migraine and other headaches is well established but little is known about the actions of this mediator in other non-cranial pains. The aura of neurological symptoms and/or signs in migraine is thought to be caused by a vascular or a neuronal mechanism, or a combination of the two. One theory suggests that changes in the vasculature are responsible for causing migraine whereas a second theory proposes that the vascular changes only mediate the pain and symptoms of migraine. A third theory suggests the primary abnormality is neuronal and originates within the brain itself. The original hypothesis was that vasoconstriction of intracranial vessels leads to a reduced blood flow, which results in cerebral hypoxia.