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Obesity 400 mg levitra plus otc, as a complex polygenic trait discount levitra plus 400mg on line, is the result of environmental and genomic effects and there is substantial genetic variation in individual response to this obesogenic pressure to put on weight [3] cheap 400 mg levitra plus. Due to this genetic susceptibility certain ethnic groups have been found to be at even greater risk when they encounter this environment [10] discount levitra plus 400 mg without prescription. However, the emergence of this dramatically increasing rate over the time span of a few generations is too fast for the appearance of new obesity-promoting mutant alleles, therefore cannot be attributed to a pure genetic effect alone. Further, rarer but stronger causal variants have also begun to be found [17,18] and more will be able to be unearthed by whole- genome sequencing studies currently underway. Work, current and on-going in the coming years, will enable the unravelling of the etiological signicance of these genomic loci, with likely therapeutic advances. The ability to detect these epigenetic alterations through genetic means alone though, will range from obligatory to stochastic, depending on their direct association with the underlying genome [23]. These marks can lead to longstanding metabolic 275 changes [25]; consequently epigenetic factors may make up some of the missing heritability in the complex disease of obesity [26e28]. However this obviously can be in only those epigenomic marks that bear some obligatory or facultative relationship with genome sequence or they will not contribute to heritability measures. This maintenance permits lineage-specic epigenomes to be preserved, to allow tissue-specic roles to be performed, in genome-identical somatic cells [23]. This stable mark is also the most well-studied, so will be the major factor discussed herein. Imprinted genes commonly are found in clusters with reciprocally imprinted genes, i. This tissue-specic imprinting is very prevalent in the cells of the placenta and brain [30]. Placental imprinting is key in inuencing this vital interface of resource allocation between the fetus and mother, and this has been proposed as a major driver in its evolution in eutherian (placental) mammals [35]. Genomic imprinting and placentation evolved around a similar time period in mammals [36]. With regards to brain imprinting, the potential complexity of orchestrated imprinting variation amongst the numerous regions of the central nervous system and furthermore throughout the process of brain development has only just begun to be explored [37]. However, intriguing evidence for the intricate interplay of 276 imprinting and imprinting loss for correct neurogenesis in the mouse has recently been published [38]. Obesity is often observed as part of the spectrum of an imprinting abnormality phenotype (see Table 14. Speculation that dysregulation of the imprinted genes in placental resource allocation pathways, or imprinted control of brain development genes involved in the leptinemelanocortin hypothalamic pathway, has been proposed in metabolic disease [39,40]. Understanding why these imprinting mechanisms have evolved may aid in unravelling how they may be causative in obesity. The kinship or gene conict theorem proposes that this evolved to control the allocation of resources from mother to offspring e in terms of the interest of the genes from the two parents. Maternal genes see equal benet in all of their progeny, due to an equal genetic contribution to each, so therefore will hope to provide for all in an equal fashion. However paternal genes are divided between offspring sired by possibly differing fathers [41]. Genetic inuences in higher mammals that help them acquire maternal resources, as well as those within parents that aid this process, have an evolutionary advantage in that they increase the survival and propagation of those genes [36,42]. Imprinted placental genes control nutrition supply and fetal imprinted genes control demand by growth regulation [36]. Deletion of the placenta-specic promoter of this gene leads to decreased permeability, by reducing the exchange barrier and increasing the thickness of the placenta, thereby inuencing nutrient supply with subsequent effects on the growth of the developing fetus in early gestation [45]. This counter- balance is not sufcient to maintain this correction in the late gestation period though. It can be hypothesized that fetal and maternal blood ow and the transportation of nutrients may also be under imprinted genetic regulation [36]. It is possible this conict may also sway maternal postnatal resource allocation via breast milk and the control of suckling. Imprinted genes additionally inuence cognitive and social behavior which may also be used to gain resources [49]. The behavioral and cognitive impairment in these individuals leads to an extreme and uncontrolled appetite, due to a proposed inability to experience the normal satiety response after eating [55]. Therefore a mechanism that disrupts this nely tuned apparatus has been suggested to explain this extreme behavior [55]. This could be interpreted in a reductionist way by the conict theory as indicative of the lack of fetal paternal gene expression, with the later onset of extreme appetite driving the response due Epigenetics in Human Disease to abnormal neurotrophic central pathway formation in the brain during this restricted development. Biallelic, paternally and maternally expressed genes are positioned within this locus. The associated multiple hormone resistance is proposed to be due to these molecules utilizing signaling pathways through G-protein-coupled receptors and the associated obesity is thought similarly to be due to abnormalities of these G-protein receptors centrally [64]. This manipulation of germ cells and embryos that occurs in vitro, especially at such an early crucial point in development, therefore demonstrates the fragility of the epigenome compared to the genome, exemplied by this specic abnormality at an imprinted locus. There is considerable variation in estimates of the actual level of imprinted regions in the mammalian, including the human, genome. Recent evidence has hinted at the possibility of high levels of particular brain tissue-specic imprinting in a mouse model [67]. Soitis plausible that there is still an underestimation of imprinted loci, particularly with the inclu- sion of tissue-specic and developmental-stage-specic variation. Moreover whilst there is as yet no denitive set of human or other eutherian mammalian imprinted genes, there does appear to be signicant dissimilarities between the species. These differences could be reconciled with the paternal conict theory, for instance, as being driven by variation in litter size between mouse and human [73]. This includes the paternally expressed genes Dlk1 (delta-like 1 homolog, Drosophila), Mest (mesoderm specic transcript) (also known as Peg1) and Ndn (Necdin) [74]. Two further paternally expressed genes Mest(Peg1) and Peg3 are involved not only in fetal and postnatal growth, but also can affect maternal nurturing success [77,78]. These imprinted genes are strongly expressed in hypothalamus, preoptic area, and septum, therefore they are excellent candidates for neuronal programming [39]. Metastable epialleles are so termed as these loci of epigenetically variability are established very early in embryogenesis and subsequently remain stable whilst permeating through all ensuing developmental stages and germ layers [79]. In the wild-type mouse the Agouti gene encodes a signaling molecule that produces either black eumelanin (a) or yellow phaeomelanin (A). Transcription is normally initiated from a hair- specic promoter in exon 2, with transient expression of the A allele leading to the mottled brown fur. This overaction results in a lightening of the coat color as ectopic expression of the inverse agonist at melanocortin receptors, agouti, antagonizes the action of melanin [79]. The viable yellow heterozygote vy (A /a) mouse has a shortened live span with yellow fur, obesity, and an increased suscep- tibility to neoplasia [81]. Dietary impact on imprinted genes nevertheless has been documented, in the imprinted Igf2 locus in a mouse model [85]. Instalment of a methyl-donor-decient diet post-weaning led to loss of imprinting at this locus with subsequent modication of expression. The inbred mouse strain C57Bl/6J is documented as being highly susceptible to diet-induced obesity, but furthermore has also been observed to show a wide range of variability in this weight gain when fed a high-calorie diet [86]. Phenotype divergence into those who would become high weight-gainers versus low was even evident in measures before commencing an obesity- 280 promoting diet.

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Genetics and environmental covari- ation between autistic traits and behavioral problems cheap levitra plus 400mg online. Genetic heritability and shared environmental factors among twin pairs with autism order 400mg levitra plus amex. A mouse Mecp2-null mutation causes neurological symp- toms that mimic Rett syndrome order levitra plus 400 mg line. Proportion of the cells with functional X disomy is associated with the severity of mental retardation in mosaic ring X Turner syndrome females order levitra plus 400mg overnight delivery. Methyl CpG-binding protein 2, whose mutation causes Rett syndrome, directly regulates Insulin-like Growth Factor Binding Protein 3 in mouse and human Brains. Folic Acid Supplementation during the Juvenile-Pubertal Period in Rats Modies the Phenotype and Epigenotype Induced by Prenatal Nutrition. Sustained hippocampal chromatin regulation in a mouse model of depression and antidepressant action. Lithium, an anti-psychotic drug, greatly enhances the generation of induced pluripotent stem cells. Pervasive social decits, but normal parturition, in oxytocin receptor-decient mice. Promoting social behavior with oxytocin in high-functioning autism spectrum disorders. Genome-wide analysis of chromatin regulation by cocaine reveals a role for sirtuins. Repeated alcohol administration during adolescence causes changes in the mesolimbic dopaminergic and glutamatergic systems and promotes alcohol intake in the adult rat. Transgenerational in- heritance of epigenetic states at the murine Axin(Fu) allele occurs after maternal and paternal transmission. Inheritable effect of unpredictable maternal separation on behav- ioral responses in mice. Biological memories of past environments: Epigenetic pathways to health disparities. Long-lasting and transgenerational effects of an environmental enrichment on memory formation. Development of type 2 diabetes following intrauterine growth retardation in rats is associated with progressive epigenetic silencing of Pdx1. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Cerebral folate deciency with developmental delay, autism, and response to folinic acid. Transcriptional inhibition of progressive renal disease by gene silencing pyrrole-imidazole polyamide targeting of the transforming growth factor-b1 promoter. Unconventional transcriptional response to environmental enrichment in a mouse model of Rett syndrome. The development of an immune system occurred during the evolution from unicellular to multicellular organisms. Autoim- mune reactions emerged in parallel with the increasing complexity of the immune system to recognize and eliminate pathogenic elements. Epigenetics in Human Disease To achieve specic recognition of harmful agents, it is essential rst to identify their own organic components as something innocuous; in other words, the immune system must be autotolerant. When the ne balance between recognition of self-components and defense against foreign agents is broken the immune system can react against the bodys own components, inducing cell destruction. If the immune system recognizes a particular component located in a specic organ as harmful, and reacts solely against this, it gives rise to a process of organ-specic autoimmunity. Conversely, if the reaction affects various organs and systems it is classied as systemic auto- immunity. This discipline has contributed to our understanding of key aspects of cell biology and the pathogenesis of a variety of diseases, among which cancer is the most widely investigated [1]. Epigenetic mechanisms can also be described as those that register, signal, or perpetuate gene activity states and involve the chemical modication of chromatin. Both groups of modications have direct and/or indirect effects on gene expression and nuclear structure, and ultimately, determine cell identity. Epigenetic modications are implicated in cell differentiation, cell cycle, apoptosis and signaling processes and are able to couple external signals to ne regulation of gene expression. In recent years, some laboratories have begun to elucidate the relevance of epigenetic alterations in autoimmune disorders. Results from these studies highlight the importance of investing further efforts to identify the full range of epigenetic alterations, different cell types involved and to explore the potential of these changes as targets for therapy. This chapter will summarize the most important aspects of our knowledge about the inuence of epigenetic deregulation in human autoimmune disorders (Table 11. Much evidence supports this contribution, including partial concordance between monozygotic twins and the induc- tion of lupus-like syndromes following administration of certain drugs. In both cases, lupus-like 208 symptoms disappear when the treatment is discontinued. With respect to the repetitive elements, a global decrease in the content of 5-methylcytosine suggests hypomethylation in repetitive elements that are the major contributors of CpG dinucleotides to the genome 24. However, to date there is little information on the specic repetitive elements that are affected. The majority of these studies have addressed this issue by using candidate gene analysis. It is likely that this reversion is the result of modication of the histone acety- lation status, although alteration of the acetylation levels of regulatory proteins cannot be discarded. This result not only suggests that histone acetylation might account for this aberrant expression but also that this pharmacological agent may be a candidate for the treatment of this autoimmune disease. In the affected joint, there is an inammatory microenvironment involving many immune cells [37]. These include synovial cells, which are hyperactivated and hyper-reactive due to high concentrations of proinammatory cytokines. They are able to decrease the number of autoreactive Th1 while increasing Treg andTh2, balancing T cells to a more protective status [68e71]. This could explain the increased resistance to apoptosis that this cell type exhibits [49]. Itis a genetically complex disease, but its etiology depends on environmental factors including EpsteineBarr virus infection. It is also thought that epigenetic dysregulation also participates in the onset of the disease driven by environmental factors. In fact, concordance rates of around 25% and 5% in monozygotic and dizygotic twins have been estimated [76].

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Observing standard precautions is critical since people with infectious diseases may have no symptoms and may be unaware that they have a disease levitra plus 400 mg sale. This section discusses engineering controls order levitra plus 400 mg otc, work practice controls cheap 400 mg levitra plus mastercard, and the appropriate use of personal protective equipment purchase 400mg levitra plus with mastercard. Under the Bloodborne Pathogen Standard, employers are required to implement engineering and work practice controls. Dont try to guess whether or not an individual has an infectious disease based on the way he or she looks or acts; you must treat everyone as though he or she were potentially infectious. January 2007 3-3 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Page left blank intentionally. Examples of engineering controls include: Self-sheathing needles Puncture-resistant sharps containers Disposable airway equipment resuscitation bags and mechanical respiratory assist devices (e. Proper handling of needles and sharps and handwashing are also work practice controls. Needles and Sharps Improper handling or disposal of needles and other sharp instruments pose the greatest exposure risk to emergency responders. Your department should have its own standard operating procedure detailing the use and disposal of needles and other sharps. January 2007 3-5 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Page left blank intentionally. Also, remember to flush mucous membranes and/or eyes with water immediately (or as soon as feasible) following contact with blood or other potentially infectious materials or after removing personal protective equipment. Your department must make available an antiseptic hand cleanser or towelette if a handwashing facility is not available. Equipment should be readily available; at a minimum, equipment should be carried in your vehicle. Ideally, your department will provide you with a small cloth pack to wear around your waist to carry equipment. January 2007 3-7 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Page left blank intentionally. Gloves must be used whenever there is a potential for contact with any body fluid. Respirators are used to block the splatter of blood or other potentially infectious materials from entering the mouth, nose, and in some instances, the eyes. Respiratory assistive devices prevent the emergency responder from coming in direct contact with saliva, respiratory secretions, or patient vomitus. Examples of respiratory assistive devices are pocket mouth-to-mouth resuscitation masks, bag-valve masks, and oxygen-demand valve resuscitators. Emergency responders within close proximity of a suspected infectious patient should immediately don a fit-tested respirator. January 2007 3-11 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Page left blank intentionally. Remember to always wear gloves and appropriate protective clothing when handling any contaminated equipment or clothing. Extra plastic bags should be kept in your emergency vehicle for storage of contaminated materials. Your department must provide separate facilities for disinfecting contaminated medical equipment and cleaning personal protective clothing. These facilities must be separate from each other and from the fire station kitchen, living, sleeping or personal hygiene areas. Bleach is harmful to metal surfaces and to structural firefighting gear and equipment. After all visible blood or other body fluid is removed, decontaminate the area with an appropriate germicide. January 2007 3-13 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Page left blank intentionally. January 2007 3-15 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Page left blank intentionally. Situation where sharp or rough Structural firefighting gear including gloves surfaces or a potentially high-heat shall be worn. During cleaning or disinfecting of Cleaning gloves, splash-resistant eyewear clothing or equipment potentially and fluid-resistant clothing shall be worn. Handling sharp objects Following use, all sharp objects shall be placed immediately in sharps containers. January 2007 3-17 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Page left blank intentionally. The amount of protection needed for any given emergency will vary depending on the circumstances of the response. Improper handling of needles poses significant exposure risk to emergency responders. Engineering controls reduce the likelihood of exposure by altering the manner in which a task is performed. You are taking the blood pressure of a patient who appears to be healthy and uninjured. January 2007 3-19 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Objective Determine if you are up-to-date on recommended immunizations and screenings that prevent infectious diseases. Screenings Yes/No Varicella Varicella vaccine is 85 % effective in preventing disease. In addition, first responders who are Hepatitis C positive or have exposure to contaminated water should also consider getting the vaccine. Hepatitis C Baseline antibody tests should be done on all fire fighters to check for previous infection or establish absence of infection. If annual conversion rates are high in a given work group, then testing is recommended every 6 months. A conversion indicates recent exposure to, or infection by, the tubercle bacillus. For certain high risk wounds, a booster shall be given if 5 years have elapsed since last vaccine. However, the test should be offered on a confidential basis as part of post- exposure protocols and as requested by the physician and patient. Measles, Mumps, Measles and mumps vaccines are required for all fire fighters Rubella born in or after 1957. It should be given to all fire fighters if vaccination or disease is not documented. Influenza Influenza viruses change often; therefore influenza vaccine is updated each year. January 2007 3-21 International Association Infectious Diseases of Fire Fighters Unit 3 Prevention Objective For each case study, identify the preventive measures that should have been taken at the scene to reduce or eliminate potential exposure. For each case study, decide which preventive measures should have been taken at the scene to reduce or eliminate potential exposure.

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Plain film of the abdomen can also be diagnostic with findings related to underlying pathology e cheap levitra plus 400mg line. Early diagnosis &referral when indicated Introduction Hepatobiliary structures have significant surgical importance not only in abdominal surgery but also in general outcome of surgical management on any other sites of human body discount 400 mg levitra plus with visa. They are common sites of different surgical diseases due to their big size and very large and double blood supply purchase 400 mg levitra plus with mastercard. The right lobe is the larger buy discount levitra plus 400 mg on line, and gall bladder is attached to its inferior surface. Hepatic artery, portal vein, and the hepatic duct together with lymphatic vessels and nerves enters and leave the liver at the area called porta hepatis,which is found at the interior and posterior aspect of right lobe. Incidence The disease occurs approximately in 3% of patients with intestinal amoebiasis. Hepatic lesion usually occurs in the right lobe and has the following characters: - Is large, single abscess - Contains characteristic liquid material which is reddish brown anchovy paste fluid - Has thin wall with little or no fibrosis Clinical manifestation History: Chief complaints are fever, chills, right upper quadrant pain which may radiate to right shoulder area. There could also be a history of: - Cough, pleuritic chest pain or dyspnea - Painful epigastric swelling if left lobe is involved - History of antecedent diarrhea - Weight loss Physical examination: Physical examination can reveal the following findings: - Tender hepatomegaly : almost constant feature - Tenderness over lower intercostal spaces with /without swelling and skin edema. Rupture: direction of rupture can be into plural cavity, lung, pericardium or peritoneum. The hepatic hydatid cyst is usually superficial and composed of two layers laminated wall. Clinical manifestation - Usually asymptomatic - Symptom of pressure on adjacent organs - Upper abdominal pain and tenderness - Palpable mass or diffuse liver enlargement - weight loss - Jaundice and ascites: uncommon - With secondary infection: fever, chills and tender hepatomegaly - Urticaria and erythema Complications 1. Broncho-pleural and hepato-bronchial fistulas Investigations - U/S of the abdomen :- cyst and daughter cysts - Casoni skin test: if reagents are available. Treatment Expectant: small/dead calcified cyst Medical: Albendazol/mebendazol for 2- 4 weeks for multilocular disease or patients unfit for surgery. Mixed stone (90%): cholesterol is the major component with others like calcium bilirubinate. Pathogenesis: Three important factors implicated in pathogenesis of cholelithiasis are: 1. When bile salt is deficient or when the cholesterol level is in excess in relation to the bile salt, the bile formed is supersaturated or lithogenic 2. Infection: causes increased mucus plug formation and scarring which form a nidus for stone formation. Also many bacteria deconjugate billirubin which will combine with calcium to form insoluble calcium bilirubinate. Clinical Presentation Most (90%) patients with gall stone diseases are asymptomatic. Symptomatic patients present with: History: - Right upper quadrant colicky pain (biliary colicky) - Dyspepsia, fatty food intolerance, flatulence, abnormal post prandial bloating - Symptoms of acute cholecystitis or other complications Physical examination: right upper quadrant tenderness Risk factors can be identified 190 Complications of Gall bladder stone 1. In the gall bladder: chronic cholecystitis acute cholecystitis gangrene perforation empyema mucocele carcinoma 2. The main stay of treatment 2) cholecystostomy for bad risk patients with severe infection (Severe Acute cholecystitis or gall bladder empyema) 191 Acute Cholecystitis Definition Acute cholecystitis is an acute inflammation of gall bladder due to obstruction of neck of gall bladder or cystic duct stone. Another rare form of acute cholecystitis which occurs in absence of stone is called acalculous cholecystitis. Pathogenesis Direct pressure of calculus on the mucosa results in ischemia, necrosis, and ulceration with swelling edema and impairment of venous return. This process increases and extends the extent of inflammation and favors bacterial multiplication. The end result may be:- - Pericholecystic abscess - Fistula formation between gall bladder and bowel - Gall bladder empyema/mucocele - Rarely, perforation of gall bladder and bile peritonitis Commonly involved bacterial species in acute cholecystitis include E. Clinical features History: History of chronic cholecystitis or Cholelithiasis Women more affected than men Moderate to severe right upper quadrant and epigastric pain which may radiate to the back. Differential diagnosis Perforated or penetrated peptic ulcer disease Biliary colic Pneumonia Pancreatitis 192 Hepatitis Pleurisy Appendicitis Myocardial ischemia or infarction. Type of the test Pre hepatic hepatic Post hepatic Serum billirubin:- Total + +++ +++ Direct N ++ +++ Indirect +++ ++ N Serum Alkaline N + +++ phos Liver Enzymes N +++ + Urine : billirubin 0 N +++ urobilinogen +++ N 0 Causes of extra hepatic biliary obstruction Obstruction in the lumen Gall stone(the most common) Parasitic occlusion e. To emphasize the importance of early diagnosis & intervention Introduction Abdominal wall hernias are common surgical problems encountered in all levels of health care facilities. Adequate knowledge to reach to the correct diagnosis and appropriate management plan help the care provider to prevent serious complications which could be fatal. General consideration Definitions Hernia is a protrusion of a viscus through an opening in the wall of the cavity Important terminologies Hernial sac - is an out pouch of the peritoneum. It has four parts: mouth, neck, body and fundus Content- Is a viscus or any other organ inside a sac. It can be: - Small bowel and omentum the commonest - Large bowel appendix - The bladder Reducible hernia- when the protruded viscus can be returned back to the abdomen Irreducible hernia- when the contents cant be returned back Obstructed hernia- the content of the hernia (intestine) is occluded but no impairment of vascular supply Strangulated hernia- when the vascularity of protruded viscus is impaired Richters hernia- when only one side of the wall of the intestine is herniated. Here strangulation of the bowel can occur with out intestinal obstruction Sliding hernia- when an extra peritoneal structure form part of the wall of the sac 198 Risk factors for abdominal wall Hernia development Increased intra abdominal pressure resulting from: - Chronic cough - Straining at urination or defecation - Heavy wt lifting - Abdominal distension Weakened abdominal wall - Advanced age - Malnutrition - Congenital defect ppv - Trauma/surgery Clinical features History - Lump which varies in size - Pain, local aching, discomfort - Factors predisposing to increased intra abdominal pressure - Symptoms of int. Strangulation is a surgical emergency Risk of obstruction and strangulation is very high in femoral hernia, paraumblical hernia and indirect inguinal hernia with narrow neck 199 Principles of management - Spontaneous resolution is unlikely - The risks of irreducibility, obstruction and strangulation increase with time. So surgical intervention is needed in most cases Surgical treatment for abdominal wall hernias 1. Herniotomy - removal of the sac and closure of the neck: Done only in infants and children 2. Obstruction and strangulation This is one of the causes of intestinal obstruction (acute abdomen). Therefore, one shouldnt forget to examine the hernial sites during evaluation of the patient with intestinal obstruction. Treatment options Non operative treatment: Gentle reduction (Taxis) can be indicated in obstructed hernia in infants but not advisable in adults due to the risk of mass reduction. Inguinal hernia - accounts for 80% of all external abdominal wall hernia - commonest is all ages and sexes - 20 x more common is males than women - more common on right side Classification 1. Direct type : Bulges through the post wall of inguinal canal Indirect inguinal hernia - 60% on right, 40% Lt side and 20% bilateral - Due to congenital defect or potential defect which is the remnant of processes vaginalis - 20 times more common in men Direct inguinal hernia - due to wear and tear associated with advanced age and increased intra abdominal pressure 201 Femoral Hernia - acquired downward protrusion of intestinal contents into the femoral canal - 4 times more common in females (middle-aged multiparous) - rare in children Clinical features History - Elderly or middle aged woman with thin body build - lump on anterior and upper thigh - may present with complaints associated with int. Risk factors Female sex Multiple parities Obesity Ascites Complications Obstruction Strangulation Rupture Treatment Expectant: - Spontaneous closure is expected in 80% cases of umbilical hernia in under five children. Surgery: - Beyond five years 202 Incisional Hernia Risk Factors Wound infection Poor surgical technique (improper facial repair) Chronic cough or straining Obesity Clinical features Risk of obstruction and strangulation is very rare. It had been one of the intersecting points for the discipline of internal medicine and surgery. Gastric cancer is one of the top five cancers in frequency, however, it is one of the disease entities with the worst prognosis because of the difficulty to diagnose it early. Therefore one has to have a high index of suspicion to diagnose the disease early for the outcome of treatment heavily depends on the stage of the disease at the time of diagnosis. Peptic ulcer disease Anatomy and physiology of the stomach and duodenum The stomach is an asymmetric dilation of the proximal gastro intestinal tract. Region Mucosa cells Secretion Cardia goblet cell mucus fundus and body parietal cells acid chief cells pepsinogen Antrum and pylorus goblet cells mucus G.

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