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Clindamycin

By J. Dimitar. Bethune-Cookman College. 2018.

At low oxygen concentrations clindamycin 150 mg with amex bacteria yeast and fungi slides, deoxy HbS polymerizes buy cheap clindamycin 150 mg on line bacteria fermentation, forms fibers, and distorts erythrocytes in to sickle shapes. Sickle Cell Trait The heterozygote individuals (sickle cell trait) (HbA/HbS) is associated with increased resistance to malaria. Sickled erythrocyte exhibits little or less deformity, they no longer move freely through the micorvasculature and often block blood flow. Moreover this cells lose water, become fragile and have a considerably short life span leading to anemia. Sickle Cell Disease Sickle cell disease is caused by an inherited structural abnormality in the β –globin polypeptide. Clinically, an individual with sickle cell disease present with intermittent episode of haemolytic and painful vaso–occlusive crisis. There is also a likely to be impaired growth, increased susceptibility to infections and multiple organ damage. Digestion and Absorption of Proteins Proteins are larger polypeptide molecules coiled by weaker bonds in their tertiary structure the digestion of proteins involves the gradual breakdown of this polypeptide by enzymatic hydrolysis in to amino acid molecules which are absorbed in the blood stream. The protein load received by the gut is derived from two sources 70-100g dietary protein which is required daily and 35 - 200g endogenous protein (secreted enzymes and proteins in the gut or from intestinal epithelia cell turnover) Only 1-2g of nitrogen equivalent to 6-12g of proteins are lost in the feces on a daily basis. Gastric Digestion Entry of a protein in to stomach stimulates the gastric mucosa to secrete a hormone gastrin which in turn stimulates the secretion of Hcl by the parietal cells of the gastric glands and pepsinogen by the chief cells. The acid denatures the protein and the whole protein susceptible to hydrolysis by the action other proteolytic enzymes. This active pepsin cleaves the ingested protein at their amino terminus of aromatic amino acids (Phe, Tyr, and Trp. Pancreatic Digestion Pancreatic zymogens proceed digestion as the acidic stomach contents pass in to the small intestine, A low pH triggers the secretion of a hormone Secretin in the blood. Three of these pro-enzyme are trypsinogen, chymotrypsinogen and procarboxy peptidase, localized in the exocrine cells. Synthesis of these enzymes as inactive precursors protects the exocrine cells from destructive proteolytic attack. By the sequential action of these proteolytic enzymes and peptides ingested proteins are hydrolyzed to yield a mixture of free amino acids which can be transported across the epithelial lining of the small intestine. Intestinal Digestion Since pancreatic juice does not contain appreciable aminopeptidase activity final digestion of di and Oligopeptides depends on the small intestinal enzymes. The lumenal surface of epithelial cells is rich in endopeptidase, and dipptidase aminopeptidase activity The end products of the cell surface digestion are free amino acids and di and tripeptides. From both genetic and transporters studies at least six specific symporter systems have been identified for the uptake of L-amino acids from the intestinal lumen. These transporter systems are also present in the renal tubules and defects in their constituent protein structure can lead to disease called Hartnup disease. Neutral amino Aciduria (Hartnup Disease) Transport functions, like enzymatic functions, are subject to modification by mutations. An example of a genetic lesion in epithelial amino acid transport is hartnup disease; entry resulting from the defect was first recognized. The disease is characterized by the inability of renal and intestinal epithelial cells to absorb neutral amino acids from the lumen. In the kidney, in which plasma amino acids reach the lumen of the proximal tubule through the Ultra filtrate, the inability to reabsorb amino acids manifests itself as excretion of amino acids in the Urine (aminoaciduria). Therefore the clinical symptoms of patients with this are mainly those due to essential amino acid and Nicotinamide deficiencies. The pellagra-like features are explained by a deficiency of Tryptophan, which serves as precursor for nicotinamide. Investigations of patients with Hartnup disease revealed the existence of intestinal transport systems for di - or tripeptides, which are different from the ones for free amino acids. The genetic lesion does not affect transport of peptides, which remains as a pathway for absorption of protein digestion products. Amino Acid Catabolism Transamination The nitrogen component of amino acids, the α - amino groups, must be removed before the carbons can be used in other metabolic pathways.

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The new variants are able to elude human host defences and there is therefore no lasting immunity against the virus cheap clindamycin 150mg fast delivery antibiotic used to treat bv, neither after natural infection nor after vaccination order clindamycin 150mg without prescription antibiotics headache, as is the case with smallpox, yellow fever, polio, and measles. These permanent and usually small changes in the antigenicity of in- fluenza A viruses are termed “antigenic drift” and are the basis for the regular oc- currence of influenza epidemics (Figure 1). In addition, there is now evidence that multiple lineages of the same virus subtype can co-circulate, persist, and reassort in epidemiologically significant ways (Holmes 2005). These major changes in the antigenicity of an influenza virus are called “antigenic shift” (Figure 2). Table 1: Antigenic Shifts and Pandemics* Designation Resulting Pandemic Death Toll 1889 H3N2 Moderate? The new viral strain will eventually reach everywhere, and will infect practically every human being within a period of a few years. Seasonal excess mortality rates due to pneumonia and influenza may remain elevated for many years, as was shown in the A(H3N2)- dominated seasons in the decade after 1968, in persons aged 45–64 years in the United States (Simonsen 2004). Courtesy: National Institute of Allergy and Infectious Disease Global Impact 21 One hallmark of pandemic influenza is a mortality shift towards younger age groups. Half of influenza-related deaths during the 1968 pandemic, and large pro- portions of influenza-related deaths during the 1957 and the 1918 pandemics, oc- curred among persons < 65 years old (Simonson 1998). It was the worst pandemic in history, killing more people than World War I, and it is generally assumed that at least 50 million people died (Johnson 2002). The first wave, which started during the spring of 1918, was highly contagious but not particularly deadly. Symptoms in 1918 were so unusual that, initially, it was misdiagnosed as dengue fever, cholera, or typhoid (Barry 2004). In contrast to subsequent pandemics, most deaths during the 1918 pandemic were among young and healthy persons aged 15 to 35 years old, and 99 % of deaths occurred in people younger than 65 years. According to this investigation, the 1918 virus was not a reassortant virus (like those of the 1957 and 1968 pandemics), but more likely an entirely avian-like virus that adapted to humans. Patients with chronic underlying disease and pregnant women were particularly at risk of developing pulmonary complications (Louria 1957). The mortality impact was not even particularly severe compared to the severe epidemic in 1967–1968 (the last H2N2 epidemic), as well as two severe H3N2 epidemics in 1975–1976, and in 1980–1981 (Simonsen 2004). The death toll has been estimated to have been around 1 million, and in the United States, nearly 50 percent of all influenza-related deaths occurred in the younger population under 65 years of age. Sero-archaeological studies showed that most individuals aged 77 years or older, had H3 antibodies before they were exposed to the new pandemic virus (Dowdle 1999) and that pre-existing anti- H3 antibodies might have protected the elderly (> 77 years old) during the 1968 H3N2 pandemic. Since 1968, there has been only one episode – in 1976 – when the start of a new pandemic was falsely anticipated (Dowdle 1997, Gaydos 2006, Kilbourne 2006). Current Situation Major pandemics have occurred throughout history at an average of every 30 years and there is a general consensus that there will be another influenza pandemic. One possible candidate is the avian H5N1 strain which has become endemic in wild waterfowl and in domestic poultry in many parts of Southeast Asia, and is recently spreading across Asia into Europe and Africa. Recent research has shown that just ten amino acid changes in the polymerase proteins differentiate the 1918 influenza virus sequences from that of avian viruses, and that a number of the same changes Individual Impact 23 have been found in recently circulating, highly pathogenic H5N1 viruses (Taubenberger 2005). Human cases, first documented in 1997 (Yuen 1998), coincided with outbreaks of highly pathogenic H5N1 avian influenza in poultry. Very limited human-to-human transmission of the H5N1 strain was documented in healthcare workers and family members with contact (Katz 1999, Buxton Bridges 2000). Although H5 antibodies were detected in these groups, indi- cating infection with the virus, no cases of severe disease occurred. There are little data to show to what extent asymptomatic infection or mild clinical disease occur following infection with highly pathogenic avian H5N1 strains. The reason for this age distribution (exposure risk, disease reporting bias, intrinsic host issues, etc. Likewise, it is not known whether, and to what extent, genetic composition plays a role in the suscep- tibility and resistance to infection with H5N1 influenza virus (Promed 20060216. However, if we translate the death toll associated with the 1918 influenza virus to the current population, there could be 180 million to 360 million deaths globally (Osterholm 2005). Individual Impact The fate of an individual during an influenza outbreak, be it epidemic or pandemic, is variable. Among the others, clinical presentation varies from afebrile respira- tory symptoms mimicking the common cold, to febrile illnesses ranging in severity from mild to debilitating (Hoffmann 2006a), and may cause disorders affecting the lung, heart, brain, liver, kidneys, and muscles (Nicholson 2003).

Cardiovascular disease becomes as prevalent in women as in men purchase clindamycin 150 mg overnight delivery klebsiella oxytoca antibiotic resistance, possibly because estrogens reduce the amount of cholesterol in the blood vessels generic 150 mg clindamycin visa virus back pain. When estrogen is lacking, many women find that they suddenly have problems with high cholesterol and the cardiovascular issues that accompany it. Osteoporosis is another problem because bone density decreases rapidly in the first years after menopause. In 2002, the Women’s Health Initiative began a study to observe women for the long-term outcomes of hormone replacement therapy over 8. The potential positive effects on cardiovascular disease were also not realized in the estrogen-only patients. The results of other hormone replacement studies over the last 50 years, including a 2012 study that followed over 1,000 menopausal women for 10 years, have shown cardiovascular benefits from estrogen and no increased risk for cancer. Some researchers believe that the age group tested in the 2002 trial may have been too old to benefit from the therapy, thus skewing the results. In the meantime, intense debate and study of the benefits and risks of replacement therapy is ongoing. Reproductive development continues in utero, but there is little change in the reproductive system between infancy and puberty. Development of the Sexual Organs in the Embryo and Fetus Females are considered the “fundamental” sex—that is, without much chemical prompting, all fertilized eggs would develop into females. To become a male, an individual must be exposed to the cascade of factors initiated by a single gene on the male Y chromosome. In both male and female embryos, the same group of cells has the potential to develop into either the male or female gonads; this tissue is considered bipotential. For example, with exposure to testosterone, cells that could become either the glans penis or the glans clitoris form the glans penis. The internal reproductive structures (for example the uterus, uterine tubes, and part of the vagina in females; and the epididymis, ductus deferens, and seminal vesicles in males) form from one of two rudimentary duct systems in the embryo. For proper reproductive function in the adult, one set of these ducts must develop properly, and the other must degrade. In males, secretions from sustentacular cells trigger a degradation of the female duct, called the Müllerian duct. Without such sustentacular cell secretion, the Müllerian duct will develop; without testosterone, the Wolffian duct will degrade. For more information and a figure of differentiation of the gonads, seek additional content on fetal development. Further Sexual Development Occurs at Puberty Puberty is the stage of development at which individuals become sexually mature. Though the outcomes of puberty for boys and girls are very different, the hormonal control of the process is very similar. In addition, though the timing of these events varies between individuals, the sequence of changes that occur is predictable for male and female adolescents. In pre-pubertal children, the sensitivity of the negative feedback system in the hypothalamus and pituitary is very high. In addition to age, multiple factors can affect the age of onset of puberty, including genetics, environment, and psychological stress. One of the more important influences may be nutrition; historical data demonstrate the effect of better and more consistent nutrition on the age of menarche in girls in the United States, which decreased from an average age of approximately 17 years of age in 1860 to the current age of approximately 12. Body fat, corresponding with secretion of the hormone leptin by adipose cells, appears to have a strong role in determining menarche. In girls who are lean and highly active, such as gymnasts, there is often a delay in the onset of puberty. Signs of Puberty Different sex steroid hormone concentrations between the sexes also contribute to the development and function of secondary sexual characteristics. Development of the Secondary Sexual Characteristics Male Female Deposition of fat, predominantly in breasts and Increased larynx size and deepening of the voice hips Increased muscular development Breast development Growth of facial, axillary, and pubic hair, and increased Broadening of the pelvis and growth of axillary growth of body hair and pubic hair Table 27. A growth spurt normally starts at approximately age 9 to 11, and may last two 1312 Chapter 27 | The Reproductive System years or more.

Disease which is limited in extent may be suitable for inter- membrane giving off muscular branches to the extensor compartment ventional procedures such as percutaneous transluminal angioplasty of the leg 150mg clindamycin with visa best antibiotic for sinus infection cephalexin. The arteries of the lower limb 95 43 The veins and lymphatics of the lower limb From lower abdomen Inguinal lymph nodes From perineum and gluteal region Vein linking great and small saphenous veins Great saphenous vein Popliteal lymph nodes Short saphenous vein Fig discount clindamycin 150 mg infection from pedicure. The arrows indicate the direction of lymph flow Superficial epigastric Inguinal ligament Femoral Pubic tubercle artery Edge of saphenous opening Superficial Femoral vein circumflex Deep fascia of thigh iliac Superficial external pudendal Great saphenous vein Fig. Failure of this ‘muscle pump’ to work efficiently, towards becoming varicose and consequently often require surgery. It passes anterior to the medial malleolus, Varicose veins along the anteromedial aspect of the calf (with the saphenous nerve), These are classified as: migrates posteriorly to a handbreadth behind patella at the knee and • Primary: due to inherent valve dysfunction. It pierces the • Secondary: due to impedance of flow within the deep venous circula- cribriform fascia to drain into the femoral vein at the saphenous open- tion. The terminal part of the great saphenous vein usually receives pelvic tumours or previous deep venous thrombosis. They receive lymph from the majority of the superficial tis- below the medial malleolus, in the gaiter area, in the mid-calf region, sues of the lower limb. They in the perforators are directed inwards so that blood flows from receive lymph from the superficial tissues of the: lower trunk below the superficial to deep systems from where it can be pumped upwards level of the umbilicus, the buttock, the external genitalia and the lower assisted by the muscular contractions of the calf muscles. The superficial nodes drain into the deep nodes tem is consequently at higher pressure than the superficial and thus, through the saphenous opening in the deep fascia. In addition they • The small saphenous vein arises from the lateral end of the dorsal also receive lymph from the skin and superficial tissues of the heel and venous network on the foot. The deep nodes over the back of the calf to pierce the deep fascia in an inconstant posi- convey lymph to external iliac and thence to the para-aortic nodes. This can be congenital, due to aberrant lymphatic formation, or acquired The deep veins of the lower limb such as post radiotherapy or following certain infections. In develop- The deep veins of the calf are the venae comitantes of the anterior and ing countries infection with Filaria bancrofti is a significant cause of posterior tibial arteries which go on to become the popliteal and lymphoedema that can progress to massive proportions requiring limb femoral veins. The veins and lymphatics of the lower limb 97 44 The nerves of the lower limb I Anterior superior iliac spine Inguinal ligament Lateral cutaneous External oblique aponeurosis nerve of thigh Femoral nerve Femoral artery Iliacus Femoral vein Femoral canal Psoas tendon Lacunar ligament Pubic tubercle Lateral cutaneous nerve of thigh Pectineus Iliacus Inguinal ligament Femoral nerve Pubic tubercle Nerve to sartorius To pectineus Tensor fasciae latae Pectineus To vastus lateralis Adductor longus Psoas Femoral vein To vastus intermedius Great saphenous vein and rectus femoris Femoral artery Sartorius Saphenous nerve Intermediate To vastus medialis cutaneous nerve Medial cutaneous of thigh nerve of thigh (Skin of front of thigh) (Skin of medial thigh) Rectus femoris Gracilis Obturator externus Pectineus Posterior division Adductor Adductor brevis longus Anterior division Gracilis Deep fascia (Skin of medial leg Branch to and foot) Fig. The latter supply • Course: the majority of the branches of the plexus pass through the sartorius and pectineus. The latter nerve is the only branch to extend • Intra-abdominal branchesathese are described in Chapter 21. Obese patients sometimes describe paraesthesiae over the • Origins: the anterior divisions of the anterior primary rami of lateral thigh. At this point it lies on iliacus, which it supplies, and is situ- • Anterior divisionagives rise to an articular branch to the hip joint ated immediately lateral to the femoral sheath. It branches within the as well as muscular branches to adductor longus, brevis and gra- femoral triangle only a short distance (5 cm) beyond the inguinal liga- cilis. The nerves unite, and are joined by the lumbosacral trunk (L4,5), artery from the lateral to medial side. The nerve • The superior gluteal nerve (L4,5,S1)aarises from the roots of the crosses the posterior tibial artery from medial to lateral in the mid-calf sciatic nerve and passes through the greater sciatic foramen above and, together with the artery, passes behind the medial malleolus and the upper border of piriformis. In the gluteal region it runs below then under the flexor retinaculum where it divides into its terminal the middle gluteal line between gluteus medius and minimis (both branches, the medial and lateral plantar nerves. In the gluteal region it penetrates and supplies gluteus • Sural nerveaarises in the popliteal fossa and is joined by the sural maximus. It pierces the • The posterior cutaneous nerve of the thigh (S1, 2, 3)apasses deep fascia in the calf and descends subcutaneously with the small through the greater sciatic foramen below piriformis. It passes behind the lateral malleolus and under the supply the skin of the scrotum, buttock and back of the thigh up to flexor retinaculum to divide into its cutaneous terminal branches the knee. It sends four motor branches and a cutaneous supply to the region by passing out of the greater sciatic foramen below pirifor- medial 3 /12 digits. It runs forwards in the pudendal plantar artery to the base of the 5th metatarsal where it divides into (Alcock’s) canal and gives off its inferior rectal branch in the superficial and deep branches.

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