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Scorpion Sting Scorpion sting is a dramatic 100 mg kamagra polo free shipping erectile dysfunction due to old age, life threatening medical emergency usually encountered in villages of tropical and subtropical countries purchase cheap kamagra polo on line erectile dysfunction treatment houston. Bawaskar from Raigad in Maharashtra has contributed immensely in this field and has helped to reduce mortality purchase generic kamagra polo from india erectile dysfunction guilt in an affair. They are Mesobuthus tamulus (Indian red scorpion) and Palamneus Gravimanus (Indian black scorpion or Ingali). It is found in Maharashtra, Karnataka, Andhra Pradesh, Tamil Nadu, Gujarat and Pondicherry. They are commonly found in underground burrows, crevices in dwellings, under debris and logs of wood, banana, sugarcane and coconut plantations and paddy husks. A scorpion sting does not always mean envenomation because it can control it’s ejaculation of venom. Metabolic effects mediated by alpha receptors stimulation are suppression of insulin secretion, hyperglycemia, hyperkalemia, free fatty acid accumulation and elevation of free radicals (responsible for myocardial damage). Direct toxic effect on neurons: explaining seizures and encephalopathy in few cases. Skin and subcutaneous tissue: Toxin of Indian red scorpion has little or no effect on skin but the black scorpion causes severe skin manifestations. Other manifestations not commonly seen in India are pancreatitis, hepatic necrosis and intravascular hemolysis leading to acute renal failure. Autonomic storm: Cholinergic storm is initial and short lived while adrenergic storm is subsequent and more prolonged. In those patients who have severe local pain, no further systemic manifestations (like autonomic storm, pulmonary edema, etc. The local pain in such patients may reappear during recovery from systemic complications. Sometimes local edema, sweating, pinhead bleed, local fasciculations and spasm of surrounding muscle is seen. Presence of local pain in the beginning and appearance of local pain after treatment, which was absent in the beginning, both are good prognostic indicators. The former indicates nonpoisonous or nonbuthus sting and later indicates recovery from envenomation. Cholinergic storm: Patient initially shows signs and symptoms due to excess acetylcholine outpouring, i. Adrenergic storm – Inotropic phase: Patient manifest with tachycardia, hypertension, cold extremities and arrhythmias. Adrenergic storm–Hypokinetic phase: Hypertensive stress on myocardium, direct myocardial toxicity and catecholamine induced coronary spasm9 contributes to myocardial dysfunction and leads to left ventricular failure causing important clinical feature of scorpion envenomation, i. Tachypnea and intractable cough can be early indicators of developing pulmonary edema. Recovery phase: During recovery phase child’s general condition improves, extremities become warm and pulse volume increases. Sometimes hypotension can be seen during recovery, which is attributed to exhausted catecholamine stores of body, which are yet to be replenished in natural course (and does not need inotrope support). Another feature suggestive of recovery is appearance of local pain, which was absent in the beginning. Local pain relief: Patients with systemic manifestations have mild, tolerable pain and needs no treatment. Fluid therapy: Early cholinergic storm having vomitings and profuse sweating causes fluid loss and can lead to hypotension. Depending on clinical condition of child, either oral or parenteral fluids are administered. Various drugs used are Prazocin, Sodium Nitroprusside, Nitroglycerin or Isosorbide dinitratre. Prazocin: This postsynaptic, competitive, alpha-1 adrenergic receptor antagonist is the first line management of scorpion envenomation. It reverses both inotropic and hypokinetic phases as well as metabolic effects of depressed insulin secretions. First dose phenomenon (leading to hypotension) can be prevented by plenty of oral fluids, not allowing child to sit or stand and monitoring of blood pressure–every 30 minutes for first 3 to 5 hours. Prazocin should be given irrespective of blood pressure in presence of good hydration. Appearance of wide pulse pressure is an early clinical indicator of reduction of preload and afterload. Oral prazocin is cheap, fast acting, free from anaphylaxis, highly effective and easily available. Bottle should be wrapped with opaque paper or cloth and no other drug should be added to infusion. Atropine: It is given for symptomatic relief from clinical effects of cholinergic storm. Corticosteroids: Steroids potentiate the toxic effects of excess catecholamine on myocardium. Lytic cocktail: Potentiates the effects of Scorpion venom, interfere with respiratory reflexes and prolongs hypotension. Severe local pain at the site of sting is unlikely to progress to systemic manifestations. Autonomic storm is the basic pathogenetic mechanism leading to all clinical features and complications of Scorpion sting. Warming up of extremities and appearance of local pain are suggestive of recovery. Oral prazocin is an antidote of Scorpion venom and should be used at the earliest. Avoid using atropine, steroids, lytic cocktail, morphine, nifedipine and captopril. Management of Cardiovascular manifestations of poisoning by the Indian Red Scorpion. Reduced insulin secretion in acute myocarditis produced by Buthus Tamulus venom injected in rabbits. Role of atropine in management of cardiovascular manifestations of scorpion envenoming in humans. Although majority of the exposures require minor or no treatment, there are situations where child may require admission in intensive care set-up. However, a sudden onset of organ dysfunction or clinical deterioration of a previously well child leads to a suspicion of poisoning. At times some toxic substance may cause specific type of symptom owing to their mechanism. This collective symptomatology is known as toxidromes, which may aid in diagnosing a particular class of poisoning. Witnesses and caretakers are asked about medication the child is taking, other medicines at home, empty or open containers of either medication or household products, and the surrounding in which the exposure occurred or child was found.

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Focal cool- systems might also be devised for some patients who have a reliable ing of the perilesional cortical tissue not only prevented the emer- clinical aura of sufcient duration kamagra polo 100 mg amex impotence at 60. A number of challenges remain gence of post-traumatic seizures buy kamagra polo 100mg mastercard erectile dysfunction drugs history, the treatment efect persisted for to be overcome buy cheap kamagra polo 100mg on line erectile dysfunction talk your doctor, however, before any of these systems can be tested up to 10 weeks afer cessation of cooling, with only rare mild sei- in human patients: guaranteeing accuracy of the seizure prediction zures emerging [39]. Tese results are very promising and point in algorithm and protecting against potential confounding factors, an important direction – the prevention of epileptogenesis. Future such as movement artefacts and unnecessary release of drugs, es- studies will be required to address optimal timing and duration of tablishing whether long-term application of drugs leads to toler- cooling for the prevention of post-traumatic seizures, and should be ance [29] and if cessation of treatment leads to withdrawal seizures explored in other models of acute symptomatic seizures. Genetic approaches to treatment As discussed, many of these studies have limitations but, none- theless, they demonstrate a proof of principle that may open new Viral vectors therapeutic avenues for patients with identifed but non-resectable Molecular biology advances mean that now we can not only change epileptic foci, and potentially also for others with poorly localized the genetic make-up of cells in vitro before grafing into the brain onset by targeting known propagation or trigger pathways. Howev- (as will be reviewed in Section Neuronal grafing), but also achieve er, even with the best of slow-release mechanisms or drug delivery modifcations in vivo using recombinant viral vectors to insert systems, in the lifetime of an epilepsy patient, repeated implantation genes into host cells in living brain. This is proving to be a very im- or refll procedures would be needed, with the attendant increasing portant research tool, enabling long-term expression of the inserted risks of complications. In this context, focal treatment approaches gene/relevant protein in a way that is not limited by either poor providing longer-term solutions may be advantageous and are dis- survival of grafed donor cells or the inevitable need to replenish cussed in Sections Focal cooling, Genetic approaches to treatment drug delivery devices during the life of the individual. How- injury to the nervous system: they suppress metabolic activity, de- ever, other vectors, such as herpes simplex virus have also been used crease tissue adenosine triphosphate and oxygen consumption, and both in animal models and in human trials [40]. In addition, the blood–brain barrier becomes less perme- cell-type-specifc promoters and even achieve conditional expres- able, thereby limiting oedema, and infammation is mitigated [31]. The degree of hypothermia used is usually between to suppress gene expression of excitatory neurotransmitters or to 30 and 35°C and is accompanied by potentially life-threatening overexpress genes involved in neuronal inhibition. Shivering has to be controlled with delivered to the piriform cortex or hippocampus alone or in com- neuromuscular blockade. Herpes-based vectors were used ways easy to interpret, given the variation in models, experimental to overexpress the neurotrophic factors fbroblast growth factor-2 detail and variable graf–host integration. In addition, as long as grafs are undertaken before any seizures genic epileptic milieu infuences the transduction efcacy and viral have been provoked, then the seizure threshold is similarly returned tropism for neurons is currently the subject of investigations [53]. Tese studies thus support the poten- Unfortunately, most studies to date involve transfection before the tial of neuronal grafs in terms of neurochemical restoration in epi- epilepsy/seizure-inducing insult in kindling or acute seizure prov- lepsy, but the real question is whether this approach can be utilized ocation models, so are of largely mechanistic rather than clinical in models with spontaneous seizures in the absence of specifc prior interest, although anticonvulsant efects are demonstrable. In addition to this initial acutely provoked (electrical stimulation or chemical, e. The as a treatment for epilepsy, and have been authoritatively reviewed grafs also appear to reverse or prevent other secondary patholog- elsewhere [40,56]. This includes aberrant sprouting of host mossy perimental paradigms in which specifc neurotransmitter inputs to fbres into the dentate supragranular layer, thereby restoring the the hippocampus (noradrenergic, cholinergic or serotonergic) are damaged cytoarchitecture, possibly by providing appropriate target specifcally lesioned using physical or chemical means, increasing neurons. The grafs themselves survive well, diferentiate into ma- susceptibility to subsequent seizure provocations. For good connectivity both the and restoring seizure susceptibility to control (predepletion) levels. In animals receiving untreated fetal hippocampal neurons that established robust projections to the contralateral hip- grafs, in which approximately 30% of grafed cells survived, no pocampus, resembling the projection pattern seen in intact animals. Improvements of similar magnitude were described, when, specifc lesion types and, as the authors point out, in contrast to the using similar experimental paradigms, rats were grafed with stri- kainic acid model, human hippocampal sclerosis involves damage atal precursor cells [71]. When cells were jority of patients with temporal lobe epilepsy do not have a clear grafed 45 days postlesion, and examined 1 month later, cell sur- initial insult and, conversely, many with the commonest insults vival had fallen to 31% [62] in comparison with 69% at 4 days pos- (febrile seizures) do not ever develop epilepsy. It is not known when hippocampal cell loss in epilep- methodological questions (for example relating to cell type, strat- tic patients occurs but it is likely that any grafing would only be egies for enhancing graf survival, timing of grafing, etc. However, survival 1 month afer grafing appeared grafing as a treatment for epilepsy, and in our view it is unlikely this to be a good predictor of long-term (1 year) cell survival [64], and will translate into clinical practice within the next decade. The biggest limitation of these Transplantation of genetically engineered cells studies, however, is that the model did not exhibit spontaneous be- Arguably, a more promising approach is to efectively combine what havioural seizures (personal communication, A. Shetty, 2002), so we know from focal drug studies and epilepsy therapeutics gener- no information on the potential therapeutic benefts of these grafs ally with advances in genetic and stem cell biology, by engineering in terms of seizure outcome is available. It is also recognized that cells for grafing that can efectively serve as a potentially perma- hippocampal cell death is neither necessary nor sufcient for epi- nent drug delivery reservoir. Although grafing had no interneurons are ablated by injections of the neurotoxin saporin efect on subsequent kindling-induced seizures, there was a slight conjugated with substance P. This study is relevant for a number of reasons: frst, the authors Optogenetics is a technique that combines optics and genetics, use a mouse model harbouring a mutation found in a form of hu- and relies on a family of proteins called opsins. Opsins are found in all animal kingdoms, from fag- tical inhibition by increasing inhibitory transmission and reduce ellate algae to higher mammals, where they are crucial to support a seizure severity and duration. An inherent problem of all techniques involving fetal cells is relied on expressing opsin genes from the fy Drosophila in neu- the relative scarcity of fetal tissue. Over the last decade, an array of molecularly Adenosine engineered opsin variants has emerged and continues to expand; Adenosine is an endogenous neuromodulator with established an- it now includes channelrhodopsins with activation wavelengths tiepileptic and neuroprotective actions and, as such, is an attrac- in the infrared spectrum, diferent channel kinetics and from the tive target in epilepsy. However, therapeutic use of adenosine or its species Volvox carteri (reviewed in [83,84]). Initial work in this area used polymer-based Newer inhibitory opsins include an opsin from the fungus Lepto- drug delivery systems but has since moved on, as reviewed in [3], sphaeria maculans (Mac), archaerhodopsin-3 (Arch) [86] and the to bring together technology from drug delivery systems, genetic chloride-conducting channelrhodopsin ChloC [87]. Due to their versatility and their electrophysiological characteristics, the use of New therapeutic approaches for optogenetic tools has revolutionized neuroscience in recent years: focal epilepsy opsins have been used to investigate basic physiological functions The techniques mentioned so far sufer from several limitations. Second, tions to the epileptic network and as potential therapeutic tools the changes efected are likely to be long term and are difcult to (reviewed in [98]). This may increase the risk of unwanted employed cultured hippocampal slices from mice that had been side-efects. Epileptiform discharges were elicited by electrical stimula- neocortex would be an important advance. Yellow light activation of halorhodopsin expressed in pyram- ber of new molecular engineering tools, including optogenetics and idal cells reliably suppressed burst fring, without altering the basic chemical–genetic probes, have emerged as powerful alternative neurophysiological properties of neurons. Since, three independ- ways to suppress seizure activity ‘on demand’ and to silence only ent groups have demonstrated that this approach is feasible also specifc subsets of neurons. The three major classes of opsins used to date are: (lef) excitatory opsins are light-activated cation channels (represented here by channelrhodopsin-2, ChR2), which allow positive charge into the neuron upon illumination and hence depolarize the cell membrane. Targeted expression of opsins in neurons can be achieved by using cell-type-specifc promoters in transgenic animals or using viral vectors. The opsin gene is tagged with a fuorescent protein gene to allow identifcation of the opsin-expressing cells. Illumination with 2-s pulses of 473 nm laser light (two pulses, 1 Hz) drives sustained action potential fring. Yellow light hyperpolarizes the membrane, and inhibits action potential fring during current injection (30 pA, 20 ms pulses). Reproduced with permission from Advances in Clinical Neuroscience and Rehabilitation and John Wiley & Sons. First, optogenetic tools need to lentivirus expressing only green fuorescent protein or fuorescent be optimized; many eforts are already under way with better and beads. Additional- The analysis was complemented with an automated event classi- ly, a better understanding of inducible and cell-subtype-specifc fer, which was trained to detect patterns of epileptiform activi- promoters are required. Tird, caution must be taken in causing ty and separate them from spontaneous behaviour artefacts such expression of potentially immunogenic proteins, although there is as from eating and grooming.

The most common cause Although seizures may be present in a high percentage of these was direct extension from the paranasal sinuses or ear but with [123] purchase kamagra polo 100 mg online erectile dysfunction generics, the number of reported cases is so small that it is likely that more efective antibiotic treatment of sinus infections order 100 mg kamagra polo with visa erectile dysfunction drugs viagra, haematog- these are incidental fndings during epilepsy investigation 100mg kamagra polo visa erectile dysfunction caverject injection. Chronic middle ear infection is the most common cause of direct intracranial spread (acute infection rarely spreads intracranially). Cholesteatoma is an additional risk factor, increasing the incidence Infective lesions of intracranial extension from 23. Brain abscesses relat- In this section, current concepts regarding the diagnosis and surgi- ed to middle ear infection are usually solitary, arising in the infe- cal management of patients with epilepsy associated with infective rior temporal lobe adjacent to the petrous temporal bone. Schistosomiasis, toxocariasis, toxoplasmosis, through existing channels, including the internal auditory meatus, paragonomiasis and gnathostomiasis are not discussed. In contrast to middle ear infections, mastoid infections typically result Pyogenic cerebral abscess in abscess formation in the cerebellum. A brain abscess is a focal suppurative lesion within the brain paren- The majority of abscesses complicating infection in frontal, chyma and 30–50% of patients will have a seizure prior to surgical ethmoidal or maxillary sinuses occur in the frontal lobe and fron- intervention. The primary aim of surgery is not the relief of epilepsy tal lobe abscesses are almost always the result of a complication of but to save the patient’s life by draining the abscess for microbio- underlying sinus infection. Sphenoid sinusitis is the least common logical diagnosis and reduction of mass efect. A brain abscess may of the paranasal infections but must be treated with great caution come to the attention of the epilepsy surgeon afer resolution of the as its complications tend to be more frequent and more severe and abscess with an area of cortical scar causing epilepsy. Intracranial abscesses resulting then similar to other forms of lesional epilepsy. Brain Periodontal infection is implicated in 6–13% of cases of brain ab- abscesses can result in major morbidity and mortality through sup- scess [136]. Organisms spread by either direct extension through puration alone as well as the efects of raised intracranial pressure the skull foraminae or by haematogenous seeding. Recent advanc- molar tooth is more likely to metastasize because it can spread be- es in the diagnosis and management of brain abscesses have led tween the muscles of mastication along fascial planes to the skull to improved survival rates: in the 1950s, the mortality rate asso- base. By togenic cranial abscesses occur following acute rather than chronic the 1980s this had fallen to 25% and the current fgure is 5–10% infections [137]. Cerebral abscess is particularly associat- physiology and management of raised intracranial pressure and the ed with Citrobacter diversus infection and children with this organ- development of new and more efective antibiotics [133]. It occurs one-sixth as frequently ing abscess, bronchiectasis, empyema and cystic fbrosis. Large postmortem series report brain abscess occur- foci include osteomyelitis, wound and skin infections, cholecys- rence rates of 0. In the normal brain the frontal Resective surgery of vascular and infective lesions for epilepsy 865 and parietal lobe receive the majority of cerebral blood fow and brain abscess. Tey are almost invariably associated with pul- bacterial emboli are more likely to be delivered to these areas, lodg- monary infection and are ofen seen in patients with defects in ing at the grey–white junction where cerebral vessels decrease in cell-mediated immunity. Tey are less well encapsulated, multiple in up to 50% of cases (or multiloculated) and have a higher mortality than those Diagnosis that arise from direct spread. The formation of these abscesses The clinical presentation depends on the size, location and number appears to depend on the combination of bacteraemia and the of lesions, the virulence of the organism, the host response and the presence of an appropriate environment, in particular infarcts and amount of cerebral oedema. Parenchymal destruction combined with oedema ofen results in signs of raised intracranial pressure and focal neurological defcit Postoperative abscess but the classical clinical triad of headache, fever and focal neuro- Infection of cranial wounds can lead to formation of a brain abscess. A constant Although it was previously thought that bacterial contamination progressive headache that is refractory to treatment is the most occurred at the time of surgery, a study of paediatric shunt infec- common symptom, occurring in 70–97% of patients [143], which tions suggests that the window of infection extends throughout the may be localized to the side of the abscess but is ofen generalized, postoperative course [138]. Factors infuencing infection include increasing in severity as the abscess expands. Only 50% of adult patients are febrile at the the use of intraoperative chemotherapy (Gliadel® wafers, which re- time of diagnosis and the fever is usually low grade [144]. If the surgeon has opened dren, fever occurs in up to 80% but a high-grade temperature of the paranasal sinuses or mastoid air cells, the operative site may be 38. If the bone fap becomes infected gow Coma Score is seen in up to two-thirds of patients and ranges afer a craniotomy, then removal of the bone fap is almost invaria- from mild confusion and drowsiness, to coma [143]. In most large series, over 60% of Brain abscess complicates approximately 3% of penetrating head patients present with focal neurological defcit [143] and in an anal- injuries, especially gunshot wounds. Metal fragments do not pose ysis of the clinical features of 20 patients with streptococcal brain a signifcant risk of abscess and do not usually require removal; abscess, nine presented with hemiparesis [146]. Whilst the major- however, bone fragments have consistently been recognized as an ity of supratentorial abscesses (especially parietal) tend to result in important factor in brain abscess development and should be re- hemiparesis, those in the temporal lobe cause varying degrees of moved. Several studies of combat-related penetrating head injury dysphasia and visual feld defcit, and cerebellar abscesses lead to reveal a brain abscess incidence of 3–17% [139] with a mortality of ataxia and nystagmus. Post-traumatic abscess development may be signifcant- eratively in larger series, but were a clinical manifestation in only ly delayed: one report describes a brain abscess due to Clostridium one in 20 streptococcal brain abscesses in one series [146]. Occa- bifermentans as a result of a metal fragment from a Vietnam War sionally, brain abscess may mimic stroke: Shintani et al. In another case, a ported a patient in whom sudden-onset homonymous hemianopia brain abscess was formed 10 years following a traumatic head inju- was later found to be caused by a bacterial brain abscess. Adults with a normal immune response frequently show a rapid onset and progression of symptoms but patients with immunode- Microbiology fciency may have an insidious onset of symptoms, and a high in- The species of bacteria responsible for brain abscess depends on the dex of suspicion is necessary to make an early diagnosis. Common organisms are aerobic, under the age of 18 months (prior to fusion of the cranial sutures) anaerobic and microaerophilic streptococci, which are found in present with a bulging fontanelle, enlarging head circumference 60–70% of non-traumatic brain abscesses and many, particularly and suture separation, seizures, irritability, nausea and vomiting. Streptococcus milleri, are part of the normal bacterial fora of the Untreated, brain abscess is usually fulminant, resulting in death in oral cavity, appendix and female genital tract. Enteric bacteria ture of an abscess into the ventricle or subarachnoid space should and Bacteroides are isolated in 20–40% of cases and ofen in mixed be considered. Anaerobic organisms have become increasingly important and despite diagnostic and treatment advances, the mortality asso- and in many instances multiple species are involved. Staphylococcal abscesses account for 10–15% of cases and are usually caused by penetrating Laboratory diagnosis head injury or bacteraemia secondary to endocarditis. Clostridial Routine laboratory studies are of limited value in establishing a di- infections are most ofen post-traumatic. Radiological diagnosis Computed tomography Computed tomography allows early diagnosis, localization and Figure 67. As the early capsule phase is reached, anatomical detail and multiple imaging planes. This ring correlates histologically with the de- mild hypointensity relative to adjacent brain is seen, representing veloping collagen capsule. This surrounds a core of more marked signal duces peripheral enhancement during the cerebritis stage but has hypointensity, which equates to the necrotic centre of the abscess. The characteristic Between these two regions is the capsule, which appears as a dis- features of the capsule help distinguish ring enhancement due to crete rim that is isointense to mildly hyperintense (Figure 67. Other features indicative of On T2-weighted images, the signal intensity of the oedematous brain abscess include multiplicity, multiloculation and location at region increases markedly compared with adjacent brain, while the grey–white junction. Ependymal or leptomeningeal enhance- the centre is isointense to hyperintense compared with grey mat- ment also favours a diagnosis of brain abscess. The capsule has better defnition and is seen as a hypointense penetrating head injury or craniotomy, the fnding of gas within rim at the margin of the abscess.

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Spermiation Spermatozoa order kamagra polo uk medication that causes erectile dysfunction, after they are formed 100mg kamagra polo sale erectile dysfunction pills for high blood pressure, remain in the lumen of the seminiferous tubule sticking to the apical membrane of the Sertoli cells order kamagra polo 100 mg fast delivery food erectile dysfunction causes. The process of detachment of head of spermatozoa and their free release into the luminal fluid is called spermiation. This includes increase in further motility of sperms by which it propels the body of the sperm in forward and preparation for acrosomal reaction. The twisting movement occurs due to the tation is not so much essential for fertilization as fertiliza- interaction between tubulin fibers and dynein side tion can also occur in vitro. The axoneme is surrounded by a fibrous sheath Structure of Spermatozoa that provides strength to the tail. The exact function of this enzyme is not about 65 µm long with average diameter of 2 µm. Head Role of CatSper protein: the principal piece of tail con- Head contains a prominent nucleus at the center, which is tains a protein called CatSper protein, which is a calcium condensed with chromatin. Acrosome is like a lysosome rich in proteolytic enzymes such as hyaluronidase, acrosin, neuraminidase and ester- Duration of Spermatogenesis ases that are activated during acrosomal reaction and In human beings, the process of formation of sperm from help in sperm penetration of the ovum at the time of ferti- the spermatogonium takes 65–74 days. The nucleus decondenses and becomes a pronu- stages of development of sperms are collectively called as cleus at the time of fertilization. Primary spermatocytes to secondary spermatocytes is dria in the form of a spiral sheath surrounding a long axial 23–25 days. Secondary spermatocytes to spermatids is approxi- nine peripheral doublet microtubules surrounding a cen- mately 1 day. The mitochondria provide energy for sperm metabo- Hormones like gonadotropins or androgen influence lism and motility. Normally, new cycles are initi- the tail piece is divided into a principal piece and an end ated in every 2 to 4 weeks before the completion of old cycle. Chapter 67: Male Reproductive System 597 Rate of Production of Sperms (spermatids developing to spermatozoa) is andro- gen dependent. This is roughly same as the the spermatozoa concentrated, which is required for number of sperms in an ejaculate in a normal healthy sperm maturation. Expressed per unit weight of testicular tissue, about that enters rete testis and epididymis unless absorbed 6–7 million sperms are produced per gram per day. The rate of production of sperms falls progressively in the fluid by facilitating fluid reabsorption. The decrease in production in elderly is due to degen- gametogenic functions of testis. Environmental Factors Differences between Spermatogenesis and It is mainly the temperature that influences spermatogen- Oogenesis esis. Lower environmental temperature facilitates sper- There are few basic differences in the process of game- matogenesis. In females, mitotic proliferation of germ cells com- increased temperature inhibits spermatogenesis. There- pletes before birth, whereas in males, spermatogonia fore, in persons taking repeated hot bath or those who grow only at the time of puberty and then continue to regularly use insulated athletic support for the scrotum, proliferate throughout life. In female, the meiotic division of primary oocyte pro- more in comfortable winter and less in intense summer. In female, second meiotic division is completed only upon fertilization, whereas in males second meiotic Semen analysis is one of the important tests for assess- division is completed during spermatogenesis. It is also performed Factors Controlling Spermatogenesis after vasectomy, to check its completeness. Factors controlling spermatogenesis can be broadly divided Analysis of freshly collected sample of semen gives the into two categories: hormonal and environmental. Usually, the sample Hormonal Factors is collected after a period of sexual abstinence for 2 days. In tubule, only the Sertoli (usually, 100 millions/ml is seen normally) cells (not spermatogenic cells), have receptors for Liquefaction : Should liquefy within half-an-hour testosterone. However, it is not clearly Other biochemi- known how testosterone promotes spermato- cal constituents: 1. Fibrinolysin, fibrinogenase In a normal sample, at least 60% of the sperms should exhibit 7. Acid phosphatase forward motility within the first 3 hours of collection of the 8. A Fructose and other biochemical compositions as noted count between 20 to 40 millions/ml indicates borderline above from serial No. The secretion from seminal vesicle Liquefaction constitutes 60% of the semen volume. Secretion from prostate contributes to 20% of the total inflammation of accessory glands or enzyme defects in the semen volume. The abnormalities include abnormal shapes, is 30 kDa serine protease formed and secreted from the prostate and poorly formed head or tail. Volume Fructose Content A low volume might suggest an anatomical or functional the normal fructose content of semen is 2–7 mg/mL. Chapter 67: Male Reproductive System 599 Effects of Vasectomy Vasectomy is the bilateral ligation of vas deferens. However, the incidence is more fol- lowing restoration of patency of the vas deferens in males those who wish to restore their fertility. As such, restoration of patency of the vas (recanaliza- tion) is a difficult procedure. It is the essential hormone for male reproduction and its absence or decreased production leads to sterility. Primarily, it allows the development of male reproductive organs during fetal life, controls spermatogenesis, guides development of Fig. Source enters the target tissues in which it is converted to its Testosterone is synthesized by the Leydig cells of testis. Though, the biosynthetic path- osterone by the enzyme 5α-reductase is essential for the development ways in the endocrine tissue that form steroid hor- of male genitalia during early embryonic life. Therefore, deficiency of mones are similar, minor differences exist among the 5α-reductase in males results in confusing genitalia containing internal enzymes that are involved in the process. Therefore, in testis, pregnenolone is hydroxylated at they are born as female children. At the time of puberty, testosterone secretion increases and they develop male figure with enlargement of 17 position. Pregnenolone is converted to testosterone in two become boys and change their name and sex. The normal plasma concentration the circulating testosterone is converted into 17–ketos- of testosterone is 300–1000 ng/dL in adult males and teroids by the enzyme 17β-dehydrogenase and a small 30–70 ng/dL in females. Ketosteroids are About 98% of testosterone binds with plasma proteins excreted in urine. The free testosterone oid is of adrenal origin and one-third of testicular origin. The production of estrogen increases with advancement of age in males, whereas estrogen produc- tion decreases with age in female.

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