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Polymyxins are effective against Gram-negative bacteria, particularly pseudomonas species. The major adverse effects are nephrotoxicity dizziness, alterd sensation and neuromuscular paralysis. Protien synthesis inhibitors are divided into two groups: bacteriostatic and bactericidal. Chloramphenicol, macrolides, clindamycin (Lincosamides), and tetracyclines are bacteriostatic whereas aminoglycosides are bactericidal. Mechanisms of action: Chloramphenicol blocks proper binding of 50S site which, stops protein synthesis. It does inhibit mitochondrial ribosomal protein synthesis because these ribosomes are 70S, the same as those in bacteria. Tetracyclines can inhibit mammalian protein synthesis, but because they are "pumped" out of most mammalian cells do not usually reach concentrations needed to significantly reduce mammalian protein synthesis. These activities occur more or less simultaneously, and the overall effect is irreversible and lethal for the cell. Chloramphenicol Chloramphenicol is a bacteriostatic broad-spectrum antibiotic that is active against both aerobic and anaerobic gram-positive and gram-negative organisms. Clinically significant resistance emerges and may be due to production of chloramphenicol acetyltransferase, an enzyme that inactivates the drug. Excretion of active chloramphenicol and of inactive degradation products occurs by way of the urine. Newborns less than a week old and premature infants clear chloramphenicol inadequately. Clinical Uses: Because of potential toxicity, bacterial resistance, and the availability of other effective drugs, chloramphenicol may be considered mainly for treatment of serious rickettsial infections, bacterial meningitis caused by a markedly penicillin-resistant strain of pneumococcus or meningococcus, and thyphoid fever. Adverse Reactions Gastrointestinal disturbances: Adults occasionally develop nausea, vomiting, and diarrhea. Oral or vaginal candidiasis may occur as a result of alteration of normal microbial flora. Bone marrow disturbances: Chloramphenicol commonly causes a dose-related reversible suppression of red cell production at dosages exceeding 50 mg/kg/d after 1-2 weeks. Aplastic anemia is a rare consequence of chloramphenicol administration by any route. It is an idiosyncratic reaction unrelated to dose, though it occurs more frequently with prolonged use. Toxicity for newborn infants: Newborn infants lack an effective glucuronic acid conjugation mechanism for the degradation and detoxification of chloramphenicol. Consequently, when infants are given dosages above 50 mg/kg/d, the drug may accumulate, resulting in the gray baby syndrome, with vomiting, flaccidity, hypothermia, gray color, shock, and collapse. Interaction with other drugs: Chloramphenicol inhibits hepatic microsomal enzymes that metabolize several drugs. Like other bacteriostatic inhibitors of microbial protein synthesis, chloramphenicol can antagonize bactericidal drugs such as penicillins or aminoglycosides. Tetracyclines the tetracyclines are a large group of drugs with a common basic structure and activity. Tetracyclines are classified as short acting (chlortetracycline, tetracycline, oxytetracycline), intermediate acting (demeclocycline and methacycline), or long-acting (doxycycline and minocycline) based on serum half-lives. They are active against for many gram-positive and gram-negative bacteria, including anaerobes, rickettsiae, chlamydiae, mycoplasmas, and are active against some protozoa. The main mechanisms of resistance to tetracycline is decreased intracellular accumulation due to either impaired influx or increased efflux by an active transport protein pump. Pharmacokinetics: Tetracyclines mainly differ in their absorption after oral administration and their elimination. A portion of an orally administered dose of tetracycline remains in the gut lumen, modifies intestinal flora, and is excreted in the feces. Absorption occurs mainly in the upper small intestine and is impaired by food (except doxycycline and minocycline); by divalent cations (Ca2+, Mg2 +, Fe2+ ) or Al3+; by dairy products and antacids, which contain multivalent cations; and by alkaline pH. They are distributed widely to tissues and body fluids except for cerebrospinal fluid. Minocycline reaches very high concentrations in tears and saliva, which makes it useful for eradication of the meningococcal carrier state. Tetracyclines cross the placenta to reach the fetus and are also excreted in milk. Doxycycline, in contrast to other tetracyclines, is eliminated by nonrenal mechanisms. Clinical uses: A tetracycline is the drug of choice in infections with Mycoplasma pneumoniae, chlamydiae, rickettsiae, and some spirochetes. They are used in combination regimens to treat gastric and duodenal ulcer disease caused by Helicobacter pylori. They may be employed in various gram-positive and gram-negative bacterial infections, including Vibrio infections. A tetracycline in combination with an aminoglycoside is indicated for plague, tularemia, and brucellosis. Adverse reactions Gastrointestinal adverse effects: Nausea, vomiting, and diarrhea are the most common and these effects are attributable to direct local irritation of the intestinal tract. Tetracyclines suppress susceptible coliform organisms and causes overgrowth of Pseudomonas, Proteus, staphylococci, resistant coliforms, clostridia, and Candida. This can result in intestinal functional disturbances, anal pruritus, vaginal or oral candidiasis, or enterocolitis (associated with Clostridium difficile) with shock and death. It causes discoloration, and enamel dysplasia; they can also be deposited in bone, where it may cause deformity or growth inhibition. If the drug is given to children under 8 years of age for long periods, similar changes can result. They are hepato and nephrotoxic drug, the also induce sensitivity to sunlight (demeclocycine) and vestibular reactions (doxycycline, and minocycline). Erythromycin Erythromycin is poorly soluble in water but dissolves readily in organic solvents. Antimicrobial Activity: Erythromycin is effective against gram-positive organisms, especially pneumococci, streptococci, staphylococci, and corynebacteria. Mycoplasma, Legionella, Chlamydia trachomatis, Helicobacter, Listeria, Mycobacterium kansasii, and Mycobacterium scrofulaceum are also susceptible. Gram-negative organisms such as Neisseria species, Bordetella pertussis, Treponema pallidum, and Campylobacter species are susceptible. Pharmacokinetics: Erythromycin base is destroyed by stomach acid and must be administered with enteric coating. Clinical Uses: Erythromycin is the drug of choice in corynebacterial infections (diphtheria, corynebacterial sepsis, erythrasma); in respiratory, neonatal, ocular, or genital chlamydial infections; and in treatment of community-acquired pneumonia because its spectrum of activity includes the pneumococcus, Mycoplasma, and Legionella. Erythromycin is also useful as a penicillin substitute in penicillin-allergic individuals with infections caused by staphylococci, streptococci, or pneumococci. Adverse Reactions Gastrointestinal Effects: Anorexia, nausea, vomiting, and diarrhea. Liver Toxicity: Erythromycins, particularly the estolate, can produce acute cholestatic hepatitis (reversibile). It increases serum concentrations of oral digoxin by increasing its bioavailability. Clarithromycin and erythromycin are virtually identical with respect to antibacterial activity except that clarithromycin has high activity against H. Clarithromycin penetrates most tissues, with concentrations equal to or exceeding serum concentrations. The advantages of clarithromycin compared with erythromycin are lower frequency of gastrointestinal intolerance and less frequent dosing. Azithromycin the spectrum of activity and clinical uses of azithromycin is identical to those of clarithromycin. Clindamycin Clindamycin is active against streptococci, staphylococci, bacteroides species and other anaerobes, both grampositive and gram-negative. Clinical uses: Clindamycin is used for the treatment of severe anaerobic infection caused by Bacteroides. It is used for prophylaxis of endocarditis in patients with valvular heart disease who are undergoing certain dental procedures.
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Airborne sounds set the eardrum in motion, which is conveyed to the cochlea by bones of the middle ear. The otolithic organs (saccule and utricle) are sensitive to linear acceleration in vertical and horizontal planes. The functions of the ossicles and the muscles are considered in more detail below. The bony labyrinth is a series of channels in the petrous portion of the temporal bone. It is filled with a K+-rich fluid called endolymph, and there is no communication between the spaces filled with endolymph and those filled with perilymph. The upper scala vestibuli and the lower scala tympani contain perilymph and communicate with each other at the apex of the cochlea through a small opening called the helicotrema. At the base of the cochlea, the scala vestibuli ends at the oval window, which is closed by the footplate of the stapes. The scala tympani ends at the round window, a foramen on the medial wall of the middle ear that is closed by the flexible secondary tympanic membrane. The scala media, the middle cochlear chamber, is continuous with the membranous labyrinth and does not communicate with the other two scalae. This organ extends from the apex to the base of the cochlea and consequently has a spiral shape. In the cochlea, tight junctions between the hair cells and the adjacent phalangeal cells prevent endolymph from reaching the bases of the cells. However, the basilar membrane is relatively permeable to perilymph in the scala tympani, and consequently, the tunnel of the organ of Corti and the bases of the hair cells are bathed in perilymph. Because of similar tight junctions, the arrangement is similar for the hair cells in other parts of the inner ear; that is, the processes of the hair cells are bathed in endolymph, whereas their bases are bathed in perilymph. A receptor structure, the crista ampullaris, is located in the expanded end (ampulla) of each of the membranous canals. The processes of the hair cells are embedded in the cupula, and the bases of the hair cells are in close contact with the afferent fibers of the vestibular division of the eighth cranial nerve. The otoliths, which are also called otoconia or ear dust, range from 3 to 19 m in length in humans and are more dense than the endolymph. The nerve fibers from the hair cells join those from the cristae in the vestibular division of the eighth cranial nerve. Bottom: Structure of the organ of Corti, as it appears in the basal turn of the cochlea. The hair cells are arranged in four rows: three rows of outer hair cells lateral to the tunnel formed by the rods of Corti, and one row of inner hair cells medial to the tunnel. There are 20,000 outer hair cells and 3500 inner hair cells in each human cochlea. Covering the rows of hair cells is a thin, viscous, but elastic tectorial membrane in which the tips of the hairs of the outer but not the inner hair cells are embedded. The cell bodies of the sensory neurons that arborize around the bases of the hair cells are located in the spiral ganglion within the modiolus, the bony core around which the cochlea is wound. By contrast, most of the efferent fibers in the auditory nerve terminate on the outer rather than inner hair cells. The hair cells in the organ of Corti signal hearing; the hair cells in the utricle signal horizontal acceleration; the hair cells in the saccule signal vertical acceleration; and a patch in each of the three semicircular canals signal rotational acceleration. Each is embedded in an epithelium made up of supporting cells, with the basal end in close contact with afferent neurons. Except in the cochlea, one of these, kinocilium (K), is a true but nonmotile cilium with nine pairs of microtubules around its circumference and a central pair of microtubules. The other processes, stereocilia (S), are found in all hair cells; they have cores of actin filaments coated with isoforms of myosin. However, the other processes, which are called stereocilia, are present in all hair cells. Along an axis toward the kinocilium, the stereocilia increase progressively in height; along the perpendicular axis, all the stereocilia are the same height. Displacing the processes in a direction perpendicular to this axis provides no change in membrane potential, and displacing the processes in directions that are intermediate between these two directions produces depolarization or hyperpolarization that is proportionate to the degree to which the direction is toward or away from the kinocilium. Thus, the hair processes provide a mechanism for generating changes in membrane potential proportional to the direction and distance the hair moves. When a stereocilium is pushed toward a taller stereocilium, the tip line is stretched and opens an ion channel in its taller neighbor. The channel next is presumably moved down the taller stereocilium by a molecular motor, so the tension on the tip link is released. When the hairs return to the resting position, the motor moves back up the stereocilium. K+-the most abundant cation in endolymph-and Ca2+ enter via the channel and produce depolarization. Depolarization of hair cells causes them to release a neurotransmitter, probably glutamate, which initiates depolarization of neighboring afferent neurons. It enters supporting cells and then passes on to other supporting cells by way of tight junctions. In the cochlea, it eventually reaches the stria vascularis and is secreted back into the endolymph, completing the cycle. The processes of the hair cells project into the endolymph whereas the bases are bathed in perilymph. In addition, it appears that a unique electrogenic K+ pump in the stria vascularis accounts for the fact that the scala media is electrically positive by 85 mV relative to the scala vestibuli and scala tympani. The dashed arrow indicates the path by which K+ recycles from the hair cells to the supporting cells to the spiral ligament and is then secreted back into the endolymph by cells in the stria vascularis. Sound is the sensation produced when longitudinal vibrations of the molecules in the external environment-that is, alternate phases of condensation and rarefaction of the molecules-strike the tympanic membrane. Other media in which humans occasionally find themselves also conduct sound waves but at different speeds. It is said that the whistle of the blue whale is as loud as 188 decibels and is audible for 500 miles. Such patterns are perceived as musical sounds, whereas waves like that shown in E, which have no regular pattern, are perceived as noise. Generally speaking, the loudness of a sound is correlated with the amplitude of a sound wave and its pitch with the frequency (number of waves per unit of time). The greater the amplitude, the louder the sound; and the greater the frequency, the higher the pitch. Sound waves that have repeating patterns, even though the individual waves are complex, are perceived as musical sounds; aperiodic nonrepeating vibrations cause a sensation of noise.
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The onset of psychotic symptoms is then often sudden and dramatic, accompanied by marked agitation and behavioural disturbance. The phenomenology is pleomorphic with a mixed picture including paranoid, grandiose and religious delusions, auditory, visual and somatic hallucinations, and prominent variable affective changes. While some have reported intermittent delirium, it is important to emphasise that these are true psychotic disorders with psychotic symptoms occurring mainly in the absence of impaired consciousness. In clinical practice, postictal psychosis must be differentiated from non-convulsive status. Periods of impaired consciousness and intermittent motor signs will help identify patients with ongoing partial seizures. Psychotic symptoms, agitation and behavioural disturbance may feature in both disorders. Impaired consciousness points to a diagnosis of status but subtle degrees of clouded consciousness may be impossible to exclude in a severely agitated psychotic patient. Furthermore, intermittent delirium is said to be a feature in some individuals with postictal psychosis. In most cases of postictal psychosis, careful history-taking from an informant will establish a period of normal functioning between termination of seizure activity and psychosis. Postictal disorders Delirium While epileptic seizures characteristically begin abruptly, recovery of normal function is usually gradual. In a complex partial seizure the transition from a state of unresponsiveness and confusion to one of alertness typically takes place over minutes. To an observer the impression is not unlike that of someone coming slowly to their senses after being awoken from sleep. The patient slowly becomes aware of where he is and gradually interacts more appropriately. The duration of clouding of consciousness and automatisms is characteristically more prolonged in temporal lobe seizures, whereas recovery may be surprisingly abrupt following frontal lobe seizures. Typically, patients are alert and responsive within 15 minutes or so, although they will often complain of headache, drowsiness and mental slowing. On occasions, full recovery of consciousness may take much longer, especially in the elderly or in patients with learning difficulties. In such cases the distinction between prolonged postictal delirium and non-convulsive status may be very difficult (Fagan & Lee 1990). In patients with an established history of epilepsy, any pronounced deviation from their habitual pattern of recovery will obviously raise concerns. However, the degree of agitation and behavioural disturbance may be such that hospital admission and sedation with benzodiazepines are required. Postictal psychoses have a tendency to recur and repeated episodes are often relatively stereotyped (Tarulli et al. Between 14% and 20% of patients with postictal psychosis will eventually develop chronic interictal psychoses, often after several years and recurrent episodes of postictal psychosis (Logsdail & Toone 1988; Tarulli et al. It is often stated that the main focus of treatment should be improved seizure control. Most patients with postictal psychosis have epilepsy that has already proved unresponsive to several antiepileptic drugs. However, postictal psychosis is strongly associated with bilateral temporal lobe pathology (see below), which must be carefully excluded before proceeding to lobectomy. There is a potential role for neuroleptics in preventing recurrent episodes of postictal psychosis and even reducing the risk of progression to chronic psychosis. Unfortunately, there is no evidence on which to base decisions about such treatment. With regard to neurological variables, patients with postictal psychosis tend to have more frequent seizure clustering and secondary generalisation (Devinsky et al. These findings have emerged from case series (Logsdail & Toone 1988; Savard et al. In patients being considered for temporal lobe surgery, a history of postictal psychosis should therefore raise a strong suspicion of bilateral pathology. Postictal psychosis was associated with a relative preservation of anterior hippocampal volume and more frequent temporal lobe dysplasia. Bilateral abnormalities were not noted in this series but all patients were undergoing presurgical work-up and this may have led to a selection bias favouring those with unilateral disease. In summary, postictal psychoses are the most common form of psychosis in patients with epilepsy. The clinical presentation is distinctive, with a sudden onset of mixed psychotic and affective features, most notably agitation, following a brief lucid interval after seizures. Individual episodes resolve within days but they tend to recur and a significant minority of patients will eventually develop chronic interictal psychoses. The pathophysiology of postictal psychosis is not understood but it is distinct, on clinical and electrophysiological grounds, from non-convulsive status. Postictal psychosis presumably reflects some transient physiological disturbance superimposed on a substrate of epileptogenic abnormality. Interictal disorders Depression Depression and anxiety are the most frequently encountered interictal psychiatric disorders in epilepsy (Lambert & Robertson 1999; Harden 2002; Kanner 2003). Estimates of the prevalence and incidence of depression in epilepsy have varied up to tenfold. A familiar list of methodological considerations, especially those relating to sample characteristics and case definition, account for this variability. Further studies have examined patients with epilepsy admitted for presurgical evaluation. Bipolar disorder does not appear to be over-represented in epilepsy: even in presurgical series prevalence rates of below 1% are reported. Relatively few studies have compared the prevalence of depression in epilepsy with other medical disorders. People with epilepsy reported more depressive symptoms than those with other disabilities despite similar ratings of disability. Two studies have reported higher rates of depression in patients attending specialist epilepsy centres compared with controls with insulin-dependent diabetes (Perini et al. A further study found higher rates of depression in epilepsy compared with a mixed group of neurological disorders (Kogeorgos et al. Symptoms of depression were most commonly reported by those with epilepsy, but differences between the epilepsy and asthma groups fell short of statistical significance when demographic variables were taken into account. Using similar survey methods, the same investigators have reported higher rates of bipolar symptoms (as distinct from bipolar disorder) in people with epilepsy compared with various medical control groups (Ettinger et al. Although half of those with bipolar symptoms reported being given a past diagnosis of bipolar disorder, it is possible that these findings reflect atypical forms of depression that some authorities have said are common. The syndrome is said to respond to antidepressant treatment perhaps in combination with low-dose neuroleptics (Blumer et al. Most clinicians will recall patients who seem to fit these descriptions but much work needs to be done to establish the validity of the concept. In particular, phenomenological comparisons with the spectrum of affective presentations in people without epilepsy are required to establish whether the syndrome is truly specific to epilepsy. The atypical nature of these presentations is cited as one reason why depression in epilepsy often goes unrecognised and untreated. Controlled trials demonstrating that such symptoms respond to treatment would help support the assertion that patients with atypical presentations represent a significant unmet need. Clinical presentation of depression in epilepsy the possibility that depression in epilepsy may take atypical forms has attracted considerable interest.
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Finally, observations and information from a relative or other informant are systematically recorded. Administration involves approximately 60 minutes with the patient and a further 20 minutes with the informant. The items of information obtained from these multiple approaches are then assembled to produce diagnostic categories according to operational diagnostic criteria. It incorporates tests of orientation, memory, language, perceptual abilities, praxis, attention and abstract thinking and is scored out of 107, with 80 used as a cut-off for dementia. It can stand alone for certain purposes as a valuable brief means of performing a neuropsychological examination. This is available worldwide in many translations and appears to be useful as a screening test for dementia. Aptitude tests Vineland Social Maturity Scale the Vineland Social Maturity Scale (Doll 1947) has been mainly used for studies in child development and mental retardation, but can also be useful in providing a measure of social functioning in brain-damaged adults. Repeat administration after an interval of time can reveal gains or losses in the social field, usefully supplementing measures of intellectual ability. The scale consists of 117 items that sample various aspects of social ability: capacity for self-care, social independence in personal activities and social responsibility. Precise figures are hard to obtain because it is clear that many patients, even with severe incapacities, do not present themselves for continuing medical attention. What is virtually certain is that the mental sequelae outstrip the physical as a cause of difficulty with rehabilitation, hardship at work and social incapacity generally, and in terms of the strain thrown on the families to whom the head-injured patient returns (Thomsen 1984). Only 5 of 22 patients were free from psychiatric sequelae, and psychiatric disturbance was a prominent cause of incapacity for work. Problems in the home included affective outbursts, chronic irritability, epileptiform and hallucinatory episodes and paranoid developments, in addition to impairment of intellectual processes. Yet only two of the patients had been referred for psychiatric advice during the follow-up period. It appears therefore that the psychiatrist sees only a small proportion of the problem (Deb et al. The acute phases of care following a head injury are primarily the province of the casualty officer, neurologist or neurosurgeon. Rehabilitation teams composed of therapists, with medical input usually from a rehabilitation physician or neurologist, manage the sequelae. However, neuropsychologists and psychiatrists are increasingly taking a central role in the rehabilitation phase, helping to ensure that the important long-term neuropsychiatric sequelae are properly managed. The greater part of this chapter is devoted to the long-term mental sequelae of head injury. Nevertheless, correct evaluation of the mechanisms which underlie the longer-term disturbances needs to be based on a proper understanding of the acute effects of head injury. Head Injury Simon Fleminger Maudsley Hospital, London the size of the problem presented by head injuries to medical services and to the economy generally is immense. About 200 per 100 000 population per year suffer a head injury (Bruns & Hauser 2003). In the majority of these the head injury is classified as mild (Sorenson & Kraus 1991), yet perhaps as many as 100 per 100 000 per year go on to suffer significant disability at 1 year (Thornhill et al. However, in the developed world, head injuries may be declining, probably reflecting better road safety, at least in part. High levels of two-wheeled vehicle use, rapidly increasing car ownership but poorly developed road safety infrastructure, and lack of ambulances mean that disability due to head injury is on the increase (Gururaj 2002). The vast majority of head injuries in civilian life are closed injuries and result from acceleration/deceleration forces. Early mortality has been considerably improved as a result of advances in the management of the early acute stages. However, the chronic sequelae remain as a serious challenge to medical care and communal resources, and this can only be reflected very approximately in statistics. Loss of consciousness is particularly likely to follow acceleration/deceleration injuries where there is a rotational component. This may explain why impacts to the temporoparietal area are most likely to produce concussion (McIntosh et al. Presumably rotational forces are particularly likely to produce the swirling movement of the brain that has been observed in monkeys after acceleration injury (Pudenz & Shelden 1946). Side impacts in car accidents are possibly more likely to be associated with severe head injury, perhaps because of the side-to-side forces as the head hits the pillar between the front and rear doors (Nirula et al. However, a more recent study suggests this is not the case and that, in those presenting to accident and emergency departments, a facial fracture increases the likelihood of brain injury (Keenan et al. Static crush closed head injuries, in which there is no acceleration/deceleration of the brain, are relatively unlikely to produce loss of consciousness (Russell & Schiller 1949). This was confirmed in a series of bitemporal crush injuries (Gonzalez Tortosa et al. In open head injuries the dura is breached and laceration of brain tissue is present at the site of impact but contrecoup is slight or even absent. The extent of the damage in open head injuries depends on the velocity of the object. Penetrating injury from a knife or spike causes localised damage around the track. However, bullet wounds, particularly from modern high-velocity rifles, produce massive shock waves throughout the brain causing widespread damage and usually death. Pathology of head injury the more severe injuries that come to post-mortem examination show a variety of pathological changes. Some are the result of direct physical damage to the brain parenchyma, and some the result of complicating factors such as vascular disturbances, cerebral oedema and anoxia. Contusions Severe contusions comprise a mixture of haemorrhage and necrosis, typically near the surface of the brain, due to severe localised forces. In an individual injury, determining where the head was hit, and the direction of the forces, is often difficult. For example, in a road traffic accident there may be more than one blow to the head in quick succession. Thus the concept of contrecoup injury, with contusions occurring on the side opposite the injury, is often not a reliable predictor of contusion location. What is more telling is that there are certain sites of predilection: the orbital surface of the frontal lobes, particularly medially, and the underside and tips of the temporal lobe. Presumably these are the sites where the brain is most at risk of being traumatised by the hard skull. Diffuse axonal injury As already described, acceleration/deceleration injuries produce swirling movements throughout the brain. The resulting rotational and linear stresses tear and damage nerve fibres throughout the brain. The diffuse interruption and degeneration of nerve fibres, with breakdown and resorption of myelin and the formation of retraction balls, is called diffuse axonal injury. First reported in patients dying after very severe brain injuries, it is likely that similar changes occur in some patients with mild closed injuries as well (Strich 1956, 1969; Teasdale & Mendelow 1984). With more severe injuries small haemorrhages are seen, particularly in the corpus callosum and the parasagittal white matter. In the longer term, severe diffuse axonal injury produces ventriculomegaly with thinning of the corpus callosum, often in the absence of sulcal enlargement. Clinically, it may present with prolonged loss of consciousness in the absence of intracerebral contusions, and later result in neurological sequelae related to damage to white matter tracts in the brainstem, particularly the superior cerebellar peduncle, with for example slurring of speech and ataxia. Diffuse axonal injury is now sometimes used to describe a clinical Head Injury 169. However, the use of what is essentially a neuropathological term to define a clinical syndrome in the absence of histological confirmation needs to be treated with a little circumspection. Other sequelae Vascular lesions Vascular lesions include scattered punctate haemorrhages throughout the brain, along with large and small infarcts.
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The letters in the formula for cholesterol identify the four basic rings, and the numbers identify the positions in the molecule. As shown here, the angular methyl groups (positions 18 and 19) are usually indicated simply by straight lines. All secreted C21 steroids have both mineralocorticoid and glucocorticoid activity; mineralocorticoids are those in which effects on Na+ and K+ excretion predominate and glucocorticoids are those in which effects on glucose and protein metabolism predominate. Thus, the C21 steroids secreted by the adrenal have a 4-3-keto configuration in the A ring. In most naturally occurring adrenal steroids, 17-hydroxy groups are in the configuration, whereas 3-, 11-, and 21-hydroxy groups are in the configuration. Its effect on mineral metabolism is usually negligible, but in diseases in which its secretion is increased, its effect can be appreciable. Most of the estrogens that are not formed in the ovaries are produced in the circulation from adrenal androstenedione. Almost all the dehydroepiandrosterone is secreted conjugated with sulfate, although most if not all of the other steroids are secreted in the free, unconjugated form. The secretion rate for individual steroids can be determined by injecting a very small dose of isotopically labeled steroid and determining the degree to which the radioactive steroid excreted in the urine is diluted by unlabeled secreted hormone. Birds, mice, and rats secrete corticosterone almost exclusively; dogs secrete approximately equal amounts of the two glucocorticoids; and cats, sheep, monkeys, and humans secrete predominantly cortisol. When a particular enzyme is deficient, hormone production is blocked at the points indicated by the shaded bars. A number of synthetic steroids are available that have many times the activity of cortisol. The potency of dexamethasone is due to its high affinity for glucocorticoid receptors and its long half-life. The zona glomerulosa lacks 17-hydroxylase activity, and only the zona glomerulosa can convert corticosterone to aldosterone because it is the only zone that normally contains aldosterone synthase. In the mitochondria, it is converted to pregnenolone in a reaction catalyzed by an enzyme known as cholesterol desmolase or side-chain cleavage enzyme. Values are approximations based on liver glycogen deposition or anti-inflammatory assays for glucocorticoid activity, and effect on urinary Na+/K+ or maintenance of adrena-lectomized animals for mineralocorticoid activity. The last three steroids listed are synthetic compounds that do not occur naturally. Pregnenolone moves to the smooth endoplasmic reticulum, where some of it is dehydrogenated to form progesterone in a reaction catalyzed by 3-hydroxysteroid dehydrogenase. Located in another part of the same enzyme is 17,20-lyase activity that breaks the 17,20 bond, converting 17-pregnenolone and 17-progesterone to the C19 steroids dehydroepiandrosterone and androstenedione. Hydroxylation of progesterone to 11-deoxycorticosterone and of 17-hydroxyprogesterone to 11-deoxycortisol occurs in the smooth endoplasmic reticulum. In the zona glomerulosa there is no 11-hydroxylase but a closely related enzyme called aldosterone synthase is present. This is why the zona glomerulosa makes aldosterone but fails to make cortisol or sex hormones. The zona fasciculata has more 3-hydroxysteroid dehydrogenase activity than the zona reticularis, and the zona reticularis has more of the cofactors required for the expression of the 17,20-lyase activity of 17-hydroxylase. Therefore, the zona fasciculata makes more cortisol and corticosterone, and the zona reticularis makes more androgens. Most of the dehydroepiandrosterone that is formed is converted to dehydroepiandrosterone sulfate by adrenal sulfokinase, and this enzyme is localized in the zona reticularis as well. Congenital defects in the enzymes lead to deficient cortisol secretion and the syndrome of congenital adrenal hyperplasia. Cholesterol desmolase deficiency is fatal in utero because it prevents the placenta from making the progesterone necessary for pregnancy to continue. This protein is essential in the adrenals and gonads but not in the placenta for the normal movement of cholesterol into the mitochondria to reach cholesterol desmolase, which is located on the matrix space side of the internal mitochondrial membrane. Because androgens are not formed, female genitalia develop regardless of genetic sex (see Chapter 25). This steroid is a weak androgen that can cause some masculinization in females with the disease, but it is not adequate to produce full masculinization of the genitalia in genetic males. However, the pathway leading to corticosterone and aldosterone is intact, and elevated levels of 11-deoxycorticosterone and other mineralocorticoids produce hypertension and hypokalemia. Cortisol is deficient, but this is partially compensated by the glucocorticoid activity of corticosterone. Unlike the defects discussed in the preceding paragraph, 21-hydroxylase deficiency is common, accounting for 90% or more of the enzyme deficiency cases. Mutations occur at many different sites in the gene, and the abnormalities that are produced therefore range from mild to severe. The characteristic pattern that develops in females in the absence of treatment is the adrenogenital syndrome. Masculization may not be marked until later in life and mild cases can be detected only by laboratory tests. In 75% of the cases, aldosterone deficiency causes appreciable loss of Na+ (salt-losing form of adrenal hyperplasia). In 11-hydroxylase deficiency, virilization plus excess secretion of 11-deoxycortisol and 11-deoxycorticosterone take place. In addition, relatively little free cortisol and corticosterone are found in the urine because of protein binding. The bound cortisol functions as a circulating reservoir of hormone that keeps a supply of free cortisol available to the tissues. The relationship is similar to that of T4 and its binding protein (see Chapter 20). The value for free cortisol is an approximation; in most studies, it is calculated by subtracting the protein-bound cortisol from the total plasma cortisol. At higher plasma levels, binding to albumin increases, but the main increase is in the unbound fraction. This explains why pregnant women have high total plasma cortisol levels without symptoms of glucocorticoid excess and, conversely, why some patients with nephrosis have low total plasma cortisol without symptoms of glucocorticoid deficiency. The glucuronyl transferase system responsible for this conversion also catalyzes the formation of the glucuronides of bilirubin (see Chapter 29) and a number of hormones and drugs. Competitive inhibition takes place between these substrates for the enzyme system. Type 1 catalyzes the conversion of cortisol to cortisone and the reverse reaction, though it functions primarily as a reductase, forming cortisol from corticosterone. Type 2 catalyzes almost exclusively the one-way conversion of cortisol to cortisone. Cortisone is an active glucocorticoid because it is converted to cortisol, and it is well known because of its extensive use in medicine. Little, if any, of the cortisone formed in the liver enters the circulation, because it is promptly reduced and conjugated to form tetrahydrocortisone glucuronide. The tetrahydroglucuronide derivatives ("conjugates") of cortisol and corticosterone are freely soluble.
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Compared to community norms, physical and mental health was poorer in bariatric patients. Relative to psychiatric patients, physical health was worse in bariatric patients, whereas mental health was better. The combination of eating a large quantity of food while feeling out of control predicted worse mental and physical health. When social support was added, it was highly predictive of mental health outcomes. This information suggests the importance of targeting binge eating in the context of social support group. Sexual dissatisfaction is associated with increased risk of divorce and relationship dissolution (Karney, 1995). According to the Kinsey Institute for Research on Sex, Gender and Reproduction (2010), the average age of first sexual intercourse experience is 16. The Kinsey Institute for Research on Sex, Gender and Reproduction (2010) also reported the frequency of sex. Sex is undeniably a large part of our lives and a motive influencing almost every area of human lives. The afore mentioned statistics are of consenting adults, but sexual assault plays a role in sexual strategies and seems imperative that we, as a society continue to inform and educate ourselves with regard to sexual strategies. About 3 million girls are subjected to the procedure every year (World Health Organization, 2006). With such a high percentage of consenting adults for sexual intercourse it is difficult to understand why sexual assault is so prevalent. While both men and women can experience similar fantasies, women more often fantasize about taking a passive role or being dominated while men more often fantasize about taking a dominant role, doing something sexual to their partner, or having multiple partners. After reviewing the various sex roles and sexual strategies presented in this paper, one may begin to compare this to their own life and how their behavior and choices are influenced. While it is an impossible feat of this paper to include all of the theories regarding this topic, the following were included because, although controversial, they have produced the most empirical evidence to support their theories. These four theories attempt to explain sex roles and set a foundation for where sexual strategies began. Sexual Selection Theory was chosen because this paper is grounded from an evolutionary perspective; therefore Darwin (1971) is essential in setting a foundation. The remaining theories were chosen because they have been recently reexamined and empirically investigated by leading social scientists Gillian R. Methods: In 2010, a 10item questionnaire consisting of openended questions was administered to Mount Sinai psychiatric residents who have participated in the Global Health Residency Track of the Mount Sinai School of Medicine. The aim of the questionnaire was to assess what role global psychiatry has within residency training through comparing and contrasting the global mental health elective with more traditional training sites. None of the participants knew that an international elective existed when they participated in the Match, however this would have been a significant factor in their choice of residency. Most felt the experience did not alter their career paths although there was interest in future international work. There was limited knowledge of global mental health prior to the elective with an evolving understanding afterwards. Participants felt that the elective was a place to consolidate skills already learned during residency and resulted in increased professional confidence. There is need for psychiatrists in resourcelimited settings, and the lack of defined role for psychiatrists in international mental health leaves room for future development. Among suicide attempters women are younger, often students, housewives and retirees, while men are more unemployed. Methods: Sixty patients (N=60) (32 males/28 females) admitted to Special hospital of neuropsychiatric diseases in Belgrade from 20082010, were assessed to gender differences regarding to sociodemographic characteristics, clinical diagnosis and suicide attempt method, duration of illness, compliance to treatment, previous suicide attempts, family history of suicide. There were no gender differences in educational level, employment and residential status, clinical diagnosis (mostly depression and schizophrenia), duration of illness, compliance to treatment, previous suicide attempts and family history of suicide. Conclusion: In order to improve successfulness, interventions addressed to reducing suicidal behavior should account gender differences. In fact, an evolutionary perspective about suicide/attempted suicide hypothesizes that defensive behaviours such as fight or flight are activated but viewed as blocked. Entrapment is associated with strong urges to escape from a current situation or feeling state but being unable to. This put the individual into a high stress state where the execution of a defensive behaviour. Gilbert & Allan (1998) identified two types of entrapment, external and internal. External entrapment is linked to being unable to get away from an abusive relationship, or being unable to leave an unpleasant environment. Internal entrapment is feeling unable to stop or get away from painful thoughts and feelings. In suicide research, escape regularly appears as a motivator for suicidal behaviour, whether this is escape from na aversive situation or from a particular state of mind (Baumeister, 1990). Williams (1997) focussed on the importance of defeat within the experience of feeling trapped with no escape, this was linked to the concept of "no rescue". Suicidal behaviour then became seen as a "cry for help", a "cry of pain" and escape from pain. Studies with groups of people who had attempted suicide reported high levels of defeat, high levels of entrapment and desire for escape and low levels of expectation of rescue. These variables also improved the prediction of suicide intent over and above depression and hopelessness. There is variability in the intent behind attempted suicide; some attempt who clearly intend to die (i. Researchers have found that the selfreported reasons for intentional selfinjury vary across of the spectrum of people who experience suicidal thoughts and feelings. Little is known, however, regarding differences in motivation between nonambiguous and ambiguous suicide attempts in people who overdose on prescription pills, drugs, or poisons. To achieve this aim, we recruited a sample of patients who received emergency services due to a suicide attempt by overdose. The primary purpose of this study was to examine if the reasons why people make nonambiguous suicide attempts by overdose differ from those reported by people who make ambiguous suicide attempts through overdose. Method: Participants (n=93) were identified by review of all emergency department admissions representing all times of day, days of the week, and months of the year. Results: Compared with patients reporting an ambiguous suicide attempt, patients who overdosed with the clear intention of dying were: 1) significantly less likely (p<. Conclusions: the results indicate that the reasons why people who utilize overdose as a means of selfharm differ among individuals who make ambiguous versus nonambiguous suicide attempts. This study suggests that each group is unique and may also have different needs in treatment. The first of these, a sense of thwarted belongingness, involves a sense on the part of the individual that he or she lacks meaningful connections to others and that previously solid relationships have become strained or lost. The second, perceived burdensomeness, involves a sense on a part of the individual that he or she is a burden to the world, someone who not only fails to make meaningful contributions but is also a liability. Taken together, the theory says, these two perceptions produce the desire for suicide. The third variable, acquired capability for suicide, involves the degree to which an individual is able to enact a lethal suicide attempt. Joiner posited that, because a lethal or nearlethal suicide attempt is fearsome and often paininducing, habituation to the fear and pain is a prerequisite for serious suicidal behavior. The acquired capability for suicide is thus a necessary but not sufficient risk factor for suicide completion. Unfortunately, reliance upon clinical lore and case reports of adverse events engenders fearful avoidance and misuse of therapeutic antidotes whose uses are not familiar to most psychiatrists. Methods: the study involves systematic review of cases (both retrospective and prospective) employing the reversal agents physostigmine and flumazenil in emergency psychiatric and inpatient critical care toxicology practice.
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The bone marrow stem cells are also the source of osteoclasts (see Chapter 23), Kupffer cells (see Chapter 29), mast cells, dendritic cells, and Langerhans cells. Adults have a few of these, but they are more readily obtained from the blastocysts of embryos. There is not surprisingly immense interest in stem cell research due to its potential to regenerate diseased tissues, but ethical issues are involved, and debate on these issues will undoubtedly continue. It also contains many platelets and plays a significant role in the immune system. Acting together, these cells provide the body with powerful defenses against tumors and viral, bacterial, and parasitic infections that was discussed in Chapter 3. The red, oxygen-carrying pigment in the red blood cells of vertebrates is hemoglobin, a protein with a molecular weight of 64,450. The polypeptides are referred to collectively as the globin portion of the hemoglobin molecule. In normal adult human hemoglobin (hemoglobin A), the two polypeptides are called chains, each of which contains 141 amino acid residues, and chains, each of which contains 146 amino acid residues. The chains also contain 146 amino acid residues, but 10 individual residues differ from those in the chains. There are small amounts of hemoglobin A derivatives closely associated with hemoglobin A that represent glycated hemoglobins. One of these, hemoglobin A1c (HbA1c), has a glucose attached to the terminal valine in each chain and is of special interest because it increases in the blood of patients with poorly controlled diabetes mellitus (see Chapter 21). There are about 300,000/L of circulating blood, and they normally have a half-life of about 4 d. The megakaryocytes, giant cells in the bone marrow, form platelets by pinching off bits of cytoplasm and extruding them into the circulation. Between 60% and 75% of the platelets that have been extruded from the bone marrow are in the circulating blood, and the remainder are mostly in the spleen. The details of the oxygenation and deoxygenation of hemoglobin and the physiologic role of these reactions in O2 transport are discussed in Chapter 36. When blood is exposed to various drugs and other oxidizing agents in vitro or in vivo, the ferrous iron (Fe2+) that is normally in the molecule is converted to ferric iron (Fe3+), forming methemoglobin. Methemoglobin is dark-colored, and when it is present in large quantities in the circulation, it causes a dusky discoloration of the skin resembling cyanosis (see Chapter 36). In solutions with a lower osmotic pressure they swell, become spherical rather than disk-shaped, and eventually lose their hemoglobin (hemolysis). When osmotic fragility is normal, red cells begin to hemolyze when suspended in 0. In hereditary spherocytosis (congenital hemolytic icterus), the cells are spherocytic in normal plasma and hemolyze more readily than normal cells in hypotonic sodium chloride solutions. Abnormal spherocytes are also trapped and destroyed in the spleen, meaning that hereditary spherocytosis is one of the most common causes of hereditary hemolytic anemia. The spherocytosis is caused by mutations in proteins that make up the membrane skeleton of the erythrocyte, which normally maintain the shape and flexibility of the red cell membrane, including spectrin, the transmembrane protein band 3, and the linker protein, ankyrin. Blood was placed on a polyvinyl chloride surface, fixed, and photographed with a scanning electron microscope. Carbon monoxide reacts with hemoglobin to form carbon monoxyhemoglobin (carboxyhemoglobin). The affinity of hemoglobin for O2 is much lower than its affinity for carbon monoxide, which consequently displaces O2 on hemoglobin, reducing the oxygen-carrying capacity of blood (see Chapter 36). Its structure is similar to that of hemoglobin A except that the chains are replaced by chains; that is, hemoglobin F is 22. The chains also contain 146 amino acid residues but have 37 that differ from those in the chain. Hemoglobin F is critical to facilitate movement of O2 from the maternal to the fetal circulation, particularly at later stages of gestation where oxygen demand increases (see Chapter 34). In young embryos there are, in addition, and chains, forming Gower 1 29 29 = 34 34 = Mean diameter of 500 cells in smear 7. In addition, there are five globin genes in tandem on chromosome 11 that encode, and globin chains and the two chains normally found only during fetal life. Switching from one form of hemoglobin to another during development seems to be regulated largely by oxygen availability, with relative hypoxia favoring the production of hemoglobin F both via direct effects on globin gene expression, as well as up-regulated production of erythropoietin. The abbreviations M, V, and P stand for the groups shown on the molecule on the left. Mutant genes that cause the production of abnormal hemoglobins are widespread, and over 1000 abnormal hemoglobins have been described in humans. When an abnormal gene inherited from one parent dictates formation of an abnormal hemoglobin (ie, when the individual is heterozygous), half the circulating hemoglobin is abnormal and half is normal. When identical abnormal genes are inherited from both parents, the individual is homozygous and all the hemoglobin is abnormal. It is theoretically possible to inherit two different abnormal hemoglobins, one from the father and one from the mother. Studies of the inheritance and geographic distribution of abnormal hemoglobins have made it possible in some cases to decide where the mutant gene originated and approximately how long ago the mutation occurred. In general, harmful mutations tend to die out, but mutant genes that confer traits with survival value persist and spread in the population. Many of the abnormal hemoglobins are harmless; however, some have abnormal O2 equilibriums, while others cause anemia. For example, hemoglobin S polymerizes at low O2 tensions, and this causes the red cells to become sickle-shaped, hemolyze, and form aggregates that block blood vessels. The sickle cell gene is an example of a gene that has persisted and spread in the population due to its beneficial effect when present in heterozygous form. There is a corresponding prevalence of 10% among African Americans in the United States. Hemoglobin F decreases the polymerization of deoxygenated hemoglobin S, and hydroxyurea stimulates production of hemoglobin F in children and adults. It has proved to be a very valuable agent for the treatment of sickle cell disease. In patients with severe sickle cell disease, bone marrow transplantation has also been shown to have some benefit. Iron is essential for hemoglobin synthesis; if blood is lost from the body and the iron deficiency is not corrected, iron deficiency anemia results. The most important and best known of these are the A and B antigens, but there are many more. The A and B antigens are complex oligosaccharides that differ in their terminal sugar.
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Some di- and tripeptides are actively transported into the intestinal cells and hydrolyzed by intracellular peptidases, with the amino acids entering the bloodstream. Thus, the final digestion to amino acids occurs in three locations: the intestinal lumen, the brush border, and the cytoplasm of the mucosal cells. In the enterocytes, amino acids released from the peptides by intracellular hydrolysis plus the amino acids absorbed from the intestinal lumen and brush border are transported out of the enterocytes along their basolateral borders by at least five transport systems. Absorption of amino acids is rapid in the duodenum and jejunum but slow in the ileum. Approximately 50% of the digested protein comes from ingested food, 25% from proteins in digestive juices, and 25% from desquamated mucosal cells. Absorbed peptides are digested by cytosolic proteases, and any amino acids that are surplus to the needs of the epithelial cell are transported into the bloodstream by a series of basolateral transport proteins. Almost all of the protein in the stools is not of dietary origin but comes from bacteria and cellular debris. Evidence suggests that the peptidase activities of the brush border and the mucosal cell cytoplasm are increased by resection of part of the ileum and that they are independently altered in starvation. In humans, a congenital defect in the mechanism that transports neutral amino acids in the intestine and renal tubules causes Hartnup disease. However, most patients do not experience nutritional deficiencies of these amino acids because peptide transport compensates. The protein antibodies in maternal colostrum are largely secretory immunoglobulins (IgAs), the production of which is increased in the breast in late pregnancy. They cross the mammary epithelium by transcytosis and enter the circulation of the infant from the intestine, providing passive immunity against infections. Thus, absorption of proteins from the intestine may explain the occurrence of allergic symptoms after eating certain foods. The activated lymphoblasts enter the circulation, but they later return to the intestinal mucosa and other epithelia, where they secrete IgA in response to subsequent exposures to the same antigen. The nucleosides are then split into their constituent sugars and purine and pyrimidine bases. These cylindrical aggregates, which are discussed in more detail in Chapter 29, take up lipids, and although their lipid concentration varies, they generally contain fatty acids, monoglycerides, and cholesterol in their hydrophobic centers. Micellar formation further solubilizes the lipids and provides a mechanism for their transport to the enterocytes. Thus, the micelles move down their concentration gradient through the unstirred layer to the brush border of the mucosal cells. However, acid inhibits the lipase, and the lack of alkaline secretion from the pancreas also contributes by lowering the pH of the intestine contents. Another cause of steatorrhea is defective reabsorption of bile salts in the distal ileum (see Chapter 29). They are of little quantitative significance for lipid digestion other than in the setting of pancreatic insufficiency, however. Most fat digestion therefore begins in the duodenum, pancreatic lipase being one of the most important enzymes involved. This enzyme hydrolyzes the 1- and 3-bonds of the triglycerides (triacylglycerols) with relative ease but acts on the 2bonds at a very low rate, so the principal products of its action are free fatty acids and 2-monoglycerides (2-monoacylglycerols). Its activity is facilitated when an amphipathic helix that covers the active site like a lid is bent back. This 100,000-kDa cholesterol esterase represents about 4% of the total protein in pancreatic juice. Fats are relatively insoluble, which limits their ability to cross the unstirred layer and reach the surface of the mucosal cells. However, they are finely emulsified in the small intestine by the detergent action of bile salts, lecithin, and monoglycerides. There are also carriers that export certain lipids back into the lumen, thereby limiting their oral availability. Fatty acids containing less than 10 to 12 carbon atoms are water-soluble enough that they pass through the enterocyte unmodified and are actively transported into the portal blood. The fatty acids containing more than 10 to 12 carbon atoms are too insoluble for this. The triglycerides and cholesterol esters are then coated with a layer of protein, cholesterol, and phospholipid to form chylomicrons. In mucosal cells, most of the triglyceride is formed by the acylation of the absorbed 2-monoglycerides, primarily in the smooth endoplasmic reticulum. However, some of the triglyceride is formed from glycerophosphate, which in turn is a product of glucose catabolism. Most vitamins are absorbed in the upper small intestine, but vitamin B12 is absorbed in the ileum. This vitamin binds to intrinsic factor, a protein secreted by the stomach, and the complex is absorbed across the ileal mucosa (see Chapter 26). Vitamin B12 absorption and folate absorption are Na+-independent, but all seven of the remaining water-soluble vitamins-thiamin, riboflavin, niacin, pyridoxine, pantothenate, biotin, and ascorbic acid-are absorbed by carriers that are Na+ cotransporters. Apoproteins synthesized in the rough endoplasmic reticulum are coated around lipid cores, and the resulting chylomicrons are secreted from the basolateral pole of epithelial cells by exocytosis. The acylation of glycerophosphate and the formation of lipoproteins occur in the rough endoplasmic reticulum. Carbohydrate moieties are added to the proteins in the Golgi apparatus, and the finished chylomicrons are extruded by exocytosis from the basal or lateral aspects of the cell. Absorption of long-chain fatty acids is greatest in the upper parts of the small intestine, but appreciable amounts are also absorbed in the ileum. Thus, they are more susceptible to the ill effects of disease processes that reduce fat absorption. The absorptive process and its relation to 1,25-dihydroxycholecalciferol are discussed in Chapter 23. Through this vitamin D derivative, Ca2+ absorption is adjusted to body needs; absorption is increased in the presence of Ca2+ deficiency and decreased in the presence of Ca2+ excess. It is inhibited by phosphates and oxalates because these anions form insoluble salts with Ca2+ in the intestine. They are formed by the action of colonic bacteria on complex carbohydrates, resistant starches, and other components of the dietary fiber, that is, the material that escapes digestion in the upper gastrointestinal tract and enters the colon. The losses are generally unregulated, and total body stores of iron are regulated by changes in the rate at which it is absorbed from the intestine. Women have a variable, larger loss averaging about twice this value because of the additional iron lost during menstruation. The average daily iron intake in the United States and Europe is about 20 mg, but the amount absorbed is equal only to the losses.
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Another finding in infarction of the anterior left ventricle is "failure of progression of the R wave"; that is, the R wave fails to become successively larger in the precordial leads as the electrode is moved from right to left over the left ventricle. If the septum is infarcted, the conduction system may be damaged, causing bundle branch block or other forms of heart block. Myocardial infarctions are often complicated by serious ventricular arrhythmias, with the threat of ventricular fibrillation and death. In experimental animals, and presumably in humans, ventricular arrhythmias occur during three periods. There follows a period relatively free from arrhythmias, but, starting 12 h after infarction, arrhythmias occur as a result of increased automaticity. Arrhythmias occurring 3 d to several weeks after infarction are once again usually due to reentry. It is worth noting in this regard that infarcts that damage the epicardial portions of the myocardium interrupt sympathetic nerve fibers, producing denervation super-sensitivity to catecholamines in the area beyond the infarct. Alternatively, endocardial lesions can selectively interrupt vagal fibers, leaving the actions of sympathetic fibers unopposed. In skilled hands, this form of treatment can be very effective and is associated with few complications. It has also been used with success to ablate foci in the pulmonary veins causing paroxysmal atrial fibrillation. The underlying electrical events and the resulting electrocardiographic changes are complex, and only a brief review can be presented here. The first change-abnormally rapid repolarization after discharge of the infarcted muscle fibers as a result of accelerated opening of K+ channels-develops seconds after occlusion of a coronary artery in experimental animals. It lasts only a few minutes, but before it is over the resting membrane potential of the infarcted fibers declines because of the loss of intracellular K+. Starting about 30 min later, the infarcted fibers also begin to depolarize more slowly than the surrounding normal fibers. Because of the rapid repolarization in the infarct, the membrane potential of the area is greater than it is in the normal area during the latter part of repolarization, making the normal region negative relative to the infarct. Clinically, a fall in the plasma level of Na+ may be associated with low-voltage electrocardiographic complexes, but changes in the plasma K+ level produce severe cardiac abnormalities. Hyperkalemia is a very dangerous and potentially lethal condition because of its effects on the heart. Further elevation of the plasma K+ level may result in ventricular tachycardia and ventricular fibrillation. The resting membrane potential of the muscle fibers decreases as the extracellular K+ concentration increases. Hypokalemia is a serious condition, but it is not as rapidly fatal as hyperkalemia. When large amounts of Ca2+ are infused into experimental animals, the heart relaxes less during diastole and eventually stops in systole (calcium rigor). However, in clinical conditions associated with hypercalcemia, the plasma calcium level is rarely if ever high enough to affect the heart. Most cardiac cells have an action potential that includes a rapid depolarization, an initial rapid repolarization, a plateau, and a slow repolarization process to return to resting potential. These changes are defined by sequential activation and inactivation of Na+, Ca2+, and K+ channels. After repolarization to the resting potential, there is a slow depolarization that occurs due to a channel that can pass both Na+ and K+. As this "funny" current continues to depolarize the cell, Ca2+ channels are activated to rapidly depolarize the cell. The rate of spread is dependent on anatomical features, but also can be altered (to a certain extent) via neural input. Because of the contribution of ionic movement to cardiac muscle contraction, heart tissue is sensitive to ionic composition of the blood. Most serious are increases in [K+] that can produce severe cardiac abnormalities, including paralysis of the atria and ventricular arrhythmias. A) sinoatrial node B) atrial muscle cells C) bundle of His D) Purkinje fibers E) ventricular muscle cells 3. In second-degree heart block A) the ventricular rate is lower than the atrial rate. Currents caused by opening of which of the following channels contribute to the repolarization phase of the action potential of ventricular muscle fibers? In complete heart block A) fainting may occur because the atria are unable to pump blood into the ventricles. D) fainting may occur because of prolonged periods during which the ventricles fail to contract. Understand the pressure, volume, and flow changes that occur during the cardiac cycle. Delineate the ways by which cardiac output can be up-regulated in the setting of specific physiologic demands for increased oxygen supply to the tissues, such as exercise. Describe how the pumping action of the heart can be compromised in the setting of specific disease states. This is accomplished when the orderly depolarization process described in the previous chapter triggers a wave of contraction that spreads through the myocardium. In this chapter, we will consider how these changes in contraction produce sequential changes in pressures and flows in the heart chambers and blood vessels, and thereby propel blood appropriately as needed by whole body demands for oxygen and nutrients. As an aside, it should be noted that the term systolic pressure in the vascular system refers to the peak pressure reached during systole, not the mean pressure; similarly, the diastolic pressure refers to the lowest pressure during diastole. The failure may involve primarily the right ventricle (cor pulmonale), but much more commonly it involves the larger, thicker left ventricle or both ventricles. In systolic failure, stroke volume is reduced because ventricular contraction is weak. This causes an increase in the end-systolic ventricular volume, so that the ejection fraction falls from 65% to as low as 20%. The initial response to failure is activation of the genes that cause cardiac myocytes to hypertrophy, and thickening of the ventricular wall (cardiac remodeling). The incomplete filling of the arterial system leads to increased discharge of the sympathetic nervous system and increased secretion of renin and aldosterone, so Na+ and water are retained. These responses are initially compensatory, but eventually the failure worsens and the ventricles dilate. In diastolic failure, the ejection fraction is initially maintained, but the elasticity of the myocardium is reduced so filling during diastole is reduced. This leads to inadequate stroke volume and the same cardiac remodeling and Na+ and water retention that occur in systolic failure. It should be noted that the inadequate cardiac output in failure may be relative rather than absolute. When a large arterior venous fistula is present, in thyrotoxicosis and in thiamine deficiency, cardiac output may be elevated in absolute terms but still be inadequate to meet the needs of the tissues (high-output failure). Treatment of congestive heart failure is aimed at improving cardiac contractility, treating the symptoms, and decreasing the load on the heart. The effects of aldosterone can be further reduced by administering aldosterone receptor blockers. Reducing venous tone with nitrates or hydralazine increases venous capacity so that the amount of blood returned to the heart is reduced, lowering the preload. Drugs that block -adrenergic receptors have been shown to decrease mortality and morbidity. Digitalis derivatives such as digoxin have classically been used to treat congestive heart failure because of their ability to increase intracellular Ca2+ and hence exert a positive inotropic effect, but they are now used in a secondary role to treat systolic dysfunction and slow the ventricular rate in patients with atrial fibrillation. Contraction of the atrial muscle narrows the orifices of the superior and inferior vena cava and pulmonary veins, and the inertia of the blood moving toward the heart tends to keep blood in it.
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The ventral anterior and ventral lateral nuclei are concerned with motor function. They receive input from the basal ganglia and the cerebellum and project to the motor cortex. The anterior nuclei receive afferents from the mamillary bodies and project to the limbic cortex, which may be involved in memory and emotion. Most of the thalamic nuclei described are excitatory neurons that release glutamate. Rather, they are thalamic interneurons and modulate the responses of other thalamic neurons to input coming from the cortex. The axons of these cells usually give off recurrent collaterals that turn back and synapse on the superficial portions of the dendritic trees. Pyramidal neurons are the only projection neurons of the cortex, and they are excitatory neurons that release glutamate at their terminals. The other cortical cell types are local circuit neurons (interneurons) which have been classified based on their shape, pattern of projection, and neurotransmitter. Golgi stain shows neuronal cell bodies and dendrites, Nissl stain shows cell bodies, and Weigert myelin sheath stain shows myelinated nerve fibers. It also contains many of the areas concerned with regulation of heart rate, blood pressure, and respiration. Some of the descending fibers in it inhibit transmission in sensory and motor pathways in the spinal cord; various reticular areas and the pathways from them are concerned with spasticity and adjustment of stretch reflexes. Collaterals funnel into it not only from the long ascending sensory tracts but also from the trigeminal, auditory, visual, and olfactory systems. The complexity of the neuron net and the degree of convergence in it abolish modality specificity, and most reticular neurons are activated with equal facility by different sensory stimuli. The system is therefore nonspecific, whereas the classic sensory pathways are specific in that the fibers in them are activated by only one type of sensory stimulation. Neocortical pyramidal cell, showing the distribution of neurons that terminate on it. A denotes nonspecific afferents from the reticular formation and the thalamus; B denotes recurrent collaterals of pyramidal cell axons; C denotes commissural fibers from mirror image sites in the contralateral hemisphere; D denotes specific afferents from thalamic sensory relay nuclei. Chandelier cells are a powerful source of inhibition of pyramidal neurons because they have axonal endings that terminate exclusively on the initial segment of the pyramidal cell axon. Their terminal boutons form short vertical rows that resemble candlesticks, thus accounting for their name. Spiny stellate cells are excitatory interneurons that release glutamate as a neurotransmitter. In addition to being organized into layers, the cortex is also organized into columns. Neurons within a column have similar response properties, suggesting they comprise a local processing network (eg, orientation and ocular dominance columns in the visual cortex). A characteristic response is seen in animals under barbiturate anesthesia, which eliminates much of the background electrical activity. If the exploring electrode is over the primary receiving area for a particular sense, a surface-positive wave appears with a latency of 5 to 12 ms. This is followed by a small negative wave, and then a larger, more prolonged positive deflection frequently occurs with a latency of 20 to 80 ms. It is primarily an anatomic area made up of various neural clusters and fibers with discrete functions. The primary evoked potential is highly specific in its location and can be observed only where the pathways from a particular sense organ end. An electrode on the pial surface of the cortex samples activity to a depth of only 0. In unanesthetized animals or humans, the primary evoked potential is largely obscured by the spontaneous activity of the brain, but it can be demonstrated by superimposing multiple traces so that the background activity is averaged out. It is somewhat more diffuse in unanesthetized animals but still well localized compared with the diffuse secondary response. The surface-positive diffuse secondary response, unlike the primary, is not highly localized. It appears at the same time over most of the cortex and is due to activity in projections from the midline and related thalamic nuclei. Current flow to and from active synaptic knobs on the dendrites produces wave activity, while all-or-none action potentials are transmitted along the axon. Bipolar records show fluctuations in the potential difference between two cortical electrodes; unipolar records show the potential difference between a cortical electrode and a theoretically indifferent electrode on some part of the body distant from the cortex. When the sum of the dendritic activity is negative relative to the cell, the cell is depolarized and hyperexcitable; when it is positive, the cell is hyperpolarized and less excitable. When a collection of fluid overlies a portion of the cortex, activity over this area may be damped. This fact may aid in diagnosing and localizing conditions such as subdural hematomas. In addition, recurrent axon collaterals end on dendrites in the superficial layers. They are further subdivided into simple partial seizures (without loss of consciousness) and complex partial seizures (with altered consciousness). An example of a partial seizure is localized jerking movements in one hand progressing to clonic movements of the entire arm. Auras typically precede the onset of a partial seizure and include abnormal sensations. The time after the seizure until normal neurological function returns is called the postictal period. Generalized seizures are associated with widespread electrical activity and involve both hemispheres simultaneously. They are further subdivided into convulsive and nonconvulsive categories depending on whether tonic or clonic movements occur. Absence seizures (formerly called petit mal seizures) are one of the forms of nonconvulsive generalized seizures characterized by a momentary loss of consciousness. Recent research provides insight into a possible role of release of glutamate from astrocytes in the pathophysiology of epilepsy. Also, there is evidence to support the view that reorganization of astrocytes along with dendritic sprouting and new synapse formation form the structural basis for recurrent excitation in the epileptic brain. It can occur at any age, but is most often diagnosed in infancy, childhood, adolescence, and old age. According to the World Health Organization, it is estimated that 50 million people worldwide (8. The prevalence in developing countries (such as Colombia, Ecuador, India, Liberia, Nigeria, Panama, United Republic of Tanzania, and Venezuela) is more than 10 per 1000.