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By A. Muntasir. Ringling School of Art and Design. 2019.

The disease process predisposes to the forma- mucosa of pharynx and retinal haemorrhages may tion of thrombus with the potential for emboli order 100 mg januvia overnight delivery diabete definition. Cytokine be seen (Roths spots are haemorrhages with a pale generation causes fever order januvia us diabetes risk factors. Afever and a new or changing murmur is endocardi- r Full blood count shows an anaemia with neutrophilia. Urine cultures may be required to identify r Acute bacterial endocarditis presents with fever, new aurinary tract infection, and renal ultrasound may be or changed heart murmurs, vasculitis and infective indicated to demonstrate a renal abscess. Severe acute heart failure may occur due to r Chest X-ray may show heart failure or pulmonary in- chordal rupture or acute valve destruction. General signs: r Malaise, pyrexia, anaemia and splenomegaly, which Complications may be tender. Cerebral emboli may cause infarction or my- disturbance due to the valve lesion(s), e. Once cultures are sent, intravenous antibiotics should be commenced based on the most likely pathogens if there is a high suspicion of Hypertension and vascular bacterial endocarditis. The r When the culture results are known endocarditis World Health Organisation latest guidelines dene hy- should be treated with the most appropriate antibi- pertension with three grades of severity that reect the otics. It is best to have a multidisciplinary approach fact that systolic and diastolic hypertension are indepen- with early microbiological and surgical advice. M > F The timing of surgery is a balance between the desire to eradicatebacteriapriortotheprocedureandtheneedfor early surgery due to the compromised haemodynamic Geography state. Aftersurgeryafullcourseofdrugtreatmentshould Rising prevalence of hypertension in the developing be given to eradicate the organisms. Prognosis r Modiable: Obesity, alcohol intake, diet (especially Despite advances in treatment, overall mortality is still high salt intake). Complications Hypertension is a major risk factor for cerebrovascular Pathophysiology disease (strokes), heart disease (coronary artery disease, r Hypertension accelerates the age-related process of left ventricular hypertrophy and heart failure) (see Table arteriosclerosis hardening of the arteries and predis- 2. Arterioscler- include peripheral vascular disease and dissecting aortic osis, through smooth muscle hypertrophy and intimal aneurysms. In r The chronic increased pressure load on the heart re- severehypertension,retinalhaemorrhages,exudatesand sults in left ventricular hypertrophy and over time this papilloedema are features of malignant hypertension. Saltand r Benign hypertension and small arteries: There is hy- water retention occurs, which can itself worsen hyper- pertrophy of the muscular media, thickening of the tension. In cases of doubt, r Routine investigations must include fasting plasma 24-hour blood pressure recordings may be helpful such glucose, serum total cholesterol and lipid prole, as when white coat hypertension is suspected. Management Peripheral arterial disease Treatment is based on the total level of cardiovascular Denition risk and the level of systolic and diastolic blood pressure Peripheralarterialdiseasedescribesaspectrumofpatho- (see Tables 2. Stopping smoking as well as the ac- tions mentioned above will also reduce overall cardio- Age vascular risk. If after 3 months their M > F systolic blood pressure is above 139 or the diastolic above 89, treatment should be started. The remainder Geography of patients and those with low or average risk should More common in the Western world. Atheromatous plaques form especially in larger vessels at areas of haemodynamic stress such as at the bifurcation Prognosis of vessels and origins of branches. It may affect younger Patients with untreated malignant hypertension have a patients, particularly diabetics and smokers. In general the risks from Arteriosclerosis, hardening of the arteries, is an age- hypertension are dependent on: related condition accelerated by hypertension. Arterial Venous This can lead to unfolding of the aorta and aortic Position Tips of toes and Gaiter area regurgitation. With increasing severity of ischaemia the Hypertension may be the underlying cause or may be claudication distance falls. Eventually the patient develops pain at rest arterial tree, therefore associated symptoms and signs and this indicates critical arterial insufciency and is a should be elicited, e. On examination, signs include cool, dry skin with loss of hair, thready or absent pulses in the affected areas Complications and a lack of venous lling. Prognosis Management r Five-year patency rates with femoro-distal bypass vary Risk factors should be modied where possible, stop- between 30 and 50%, aortoiliac reconstruction has a pa- ping smoking in particular may prevent further dete- tency rate of 80%. Care peri-operatively and during long-term follow-up is is- should be taken to avoid trauma. Arterioscle- An aneurysm is dened as an abnormal focal dilation of rosis in older patients is difcult to treat surgically, as an artery (see Table 2. A true aneurysm may be further subdivided stenoses or occlusions in medium-sized arteries into saccular in which there is a focal out-pouching suchastheiliac,femoralandrenalarteries;however, or fusiform where there is dilation of the whole cir- as patients often present late the disease may be too cumference of the vessel. A guide wire is inserted and then a bal- occurs following penetrating trauma when there is a loon fed over the wire and inated within the lesion. They may dissect and cut off blood critical ischaemia or severely limiting intermittent supply to tissue or rupture with resulting haemor- claudication, because failed grafting worsens symp- rhage. In addi- r Altered ow patterns predispose to thrombus forma- tion, most patients have other conditions such as tion, which may embolise to distal arteries or cause ischaemic heart disease, diabetes and cerebrovascu- occlusion at the site of the aneurysm. Abdominal aortic aneurysms may be found incidentally as a central expansile mass on examination or as calci- Sex cation on an X-ray. Patients may present with a dull, aching chronic or intermittent epigastric or back pain due to expansion. Geography Rupture causes a tearing epigastric pain that radiates Becoming more common in the developed world. More than half of aneurysms over 6 cm will rupture Pathophysiology within 2 years thromboembolism. The arterial wall becomes thinned and is replaced with brous tissue and stretches to form a dilated saccular or Investigations fusiform aneurysm. Suprarenal aneurysms have a much poorer prognosis with a high risk of renal impairment. Many patients have Management concomitant ischaemic heart disease or cerebrovascular r Ruptured abdominal aortic aneurysm is a surgical disease, which affects outcome. O negative blood may be required untilbloodiscross-matched,asbloodlosscanbemas- Denition sive. Aortic dissection is dened as splitting through the en- r Surgery at a specialist centre gives the best outcome, dothelium and intima allowing the passage of blood into but patients may not be t for transfer. In all cases there is degeneration of collagen r Asymptomatic small aneurysms should be managed and elastic bres of the media, known as cystic me- conservatively with aggressive management of hyper- dial necrosis. Trauma, including insertion of an arterial tension and other risk factors for atherosclerosis and catheter, is also a cause. Whilst surgical techniques remain There is an intimal tear, then blood forces into the aortic the standard treatment, increasingly endovascular wall, it can then extend the split further along the wall stenting techniques are being used that can be per- of the vessel. The most com- to make the diagnosis, particularly in haemodynami- mon site for these to start is at the point of the ductus cally unstable patients. They may extend as far down as the is required, and importantly hypertension should be iliac arteries. Intravenous Dissection classically presents with excruciating sudden -blockers, glyceryl trinitrate and hydralazine may all onset central chest pain, which may be mistaken for an be needed.

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Refer suspected cases of leishmaniasis to hospitals for investigation & treatment 12 cheap januvia 100mg amex diabetes mellitus type 2 cellular level. Design appropriate methods of prevention andcontrol of leishmaniasis Definition: is an infectious disease caused by the protozoa called Leishmania Classification of leishmaniasis There are three major clinical forms of leishmaniasis: Visceral leishmaniasis Cutaneous leishmaniasis Mucocutaneous leishmaniasis Etiologic Agents The different clinical forms of leishmaniasis (listed above) are caused by different species of leishmanial parasites which are listed under each of these diseases discount januvia 100 mg amex diabetes mellitus type 2 guidelines ada. The parasites are seen in two forms Leishmanial form:- ( amastogote ) this is non flagellate form seen in man and extra human vertebrate reservoir Leptomonad forms (also called promastigotes) are flagellated forms The parasite is transmitted by the bite of vectors of the species phlebotomus, Sand flies 56 Internal Medicine Life Cycle of Leshimaniasis Transmitted by the bite of an infected female phlebotomine Sand fly, the leishmaniases are globally widespread diseases. Sand flies are primarily infected by animal reservoir hosts, but humans are also a reservoir for some forms. Animal Reservoirs: include Rodents - Commonly in East Africa, Ethiopia, the Sudan and Kenya and Canines - Mediterranean and Asia. As the sandfly feeds, promastigote forms of the leishmanial parasite enter the human host via the proboscis. Within the human host, the promastigote forms of the parasite are ingested by macrophage where they metamorphose into amastigote forms and reproduce by binary fission. They increase in number until the cell eventually bursts, then infect other phagocyctic cells and continue the cycle. The parasites are transformed inside the fly and delivered to a new host, and the life-cycle continues Fig 3. It is characterized by chronic irregular fever, profound wasting, debility and hepatosplenomegally. Epidemiology Visceral leishmaniasis affects many countries in Africa, mainly Ethiopia and the Sudan the Middle East, Southern soviet union, India and S. Transmission The commonest way of transmission is by inoculation of promastigotes into humans by the bite of sand flies which breed in termite hills and forests. The source of the aflagellate forms may be either humans or extra human vertebrate reservoirs, and the disease may have life cycles that involve humans and sand flies only, or humans, sand flies and extra human vertebrate reservoirs together. Pathogenesis The common site of entrance is the skin where primary cutaneous lesion appears at the sites of sand fly bite. Here a cellular reaction by lymphocytes and plasma cells develop around the amasitigote-filled histiocytes in the dermis. As immune response develops epitheloid and giant cells appear, to be followed in some by healing. In others usually 4-6 months later amastigotes escape to the blood in macrophages, hematogeneous spread occurs and colonize the cells of reticuloendothelial system, where they multiply further and released after rupture of the cells and transported to new cells. The cells affected include that of spleen, liver, bone marrow and lymphatic glands, where the parasite multiplies and cause overcrowding of cells and as a result these organs are enlarged. The liver with its Kuppfer cells packed with amastigotes is enlarged & progress to cirrhosis. Clinical Features Incubation period usually varies from weeks to months but can be as long as years. Diagnosis Definitive diagnosis is based on demonstration of the Parasite - Giemsa stained smear of peripheral blood (in Indian form) and tissue touch preparation of organ aspirates and examined by light microscopy. Following the bite of sand flies, leishmania multiply in the macrophages of the skin. Single or multiple painless nodules occur on exposed areas (mainly the face) within one week to 3 months of the bite. The nodules may enlarge and ulcerate with erythematous raised border and overlying crust which may spontaneously heal over months to years. Different clinical patterns are described depending on the etiologic agents as follows:- 60 Internal Medicine Table I- 3. Investigation for Diagnosis Giemsa staining of smear from a split skin: This demonstrates leishmania in 80% of cases Culture followed by smear 61 Internal Medicine Leishmanin skin test is positive in over 90% of cases although it is negative in diffuse cutaneous leishmaniasis. However large lesions or those on cosmetically important sites require treatment either 0 Locally - by surgery, curettage, cryotherapy or hyperthermia (40-42 c) or Systemic therapy: with drugs like Pentostam. Treatment is less successful than visceral leishmaniasis as antimonials are poorly concentrated in the skin L. Bolivia, Uruguay and Northern Argentina) In the early stage it affects the skin, but in secondary stage of the disease it involves the upper respiratory mucosa. This leads to nasal obstruction, ulceration, septal perforations and destruction of the nasal cartilage called Espundia. Death usually occurs from secondary bacterial infection 62 Internal Medicine References: th 1. Tuberculosis Learning Objective: At the end of this unit the student will be able to 1. Understand the different treatment categories of Tuberculosis be able to categorize any type of Tuberculosis 11. Refer complicated cases of Tuberculosis diseases to hospitals for better management 14. Design appropriate methods of prevention and control of Tuberculosis Definition: Tuberculosis is a Chronic necrotizing disease caused by Mycobacterium tuberculosis complex. The rate of clinical disease is highest during late adolescence and early adulthood, but the reasons are not clear. Activated alveolar macrophages ingest the bacilli; after which they release chemicals to activate other immune system components and try to control the infection or multiplication of bacilli. These activated cells aggregate around the lesion and the center becomes necrotic, soft cheese like material called caseous necrosis. But if the bacteria inside the macrophage multiply rapidly, they will kill the macrophage and are released but to be taken up 66 Internal Medicine by other macrophages again. Clinical Manifestations Pulmonary Tuberculosis: - This can be classified as primary or post primary (Secondary). Primary disease: Clinical illness directly after infection is called primary tuberculosis; this is common in children <4 years of age. Post primary disease: -If no clinical disease is developed after the primary infection, dormant bacilli may persist for years or decades before being reactivated, when this happens, it is called secondary (or post primary) tuberculosis. Most patients have cough, which may be dry at first, but later becomes productive of whitish sputum; it is frequently blood streaked. Chest x-ray findings are non-specific; infiltrations, consolidation or cavitory lesions may be present. Pleural tuberculosis:- Pleural involvement may be asymptomatic or patients could have fever, pleuritic chest pain and dyspnea. Patients may present with swelling and pain on the back with or without paraparesis or paraplegia due to cord compression. Patients present with progressive joint swelling, usually with pain and limitation of movement. Gastro Intestinal Tuberculosis:- Tuberculosis can affect anywhere from the mouth to the anus. Patients usually present with abdominal swelling and pain, weight loss, fever and night sweating. Milliary tuberculosis:- This is secondary to hematogenous dissemination of the bacilli. Patients who have suggestive symptoms and signs for tuberculosis should undergo further tests. If all 3 sputum smears are negative and the patient has suggestive clinical and chest x-ray findings, first the patient should be treated with broad spectrum antibiotics to rule out other bacterial causes.

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Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity cheap 100 mg januvia mastercard blood glucose 70. Clinical Trial: cyclophosphamide pulse therapya promising therapeutic alternative in refractory celiac disease 100mg januvia visa diabetes 1 prevention. Pathogenesis, epidemiology, and clinical manifestations of celiac disease in adults. Antagonist peptides of the gliadin T-cell stimulatory sequences: a therapeutic strategy for celiac disease. Long-Term follow-up of individuals with celiac disease: an evaluation of current practice guidelines. Deamidation of gliadin peptides in lamina propria: implications for celiac disease. Effect of intravenous immunoglobulin on cerebellar ataxia and neuropathic pain associated with celiac disease. The propensity for deamidation and transamidation of peptides by transglutaminase 2 is dependent on substrate affinity and reaction conditions. Dissecting the T cell response to hordeins in celiac disease can develop barley with reduced immunotoxicity. Review article: minimizing tuberculosis anti-tumour necrosis factor-alpha treatment of inflammatory bowel disease. Defining the optimal response criteria for the Crohns disease activity index for induction studies in patients with mildly to moderately active crohns disease. Risk factors associated with progression to intestinal complications of Crohns disease in a population based cohort. Commercial assays to assess gluten content of gluten-free foods: why they are not created equal. Immunoglobulin A anti-tissue transglutaminase antibody deposits in the small intestinal mucosa of children with no villous atrophy. A modified extraction protocol enables detection and quantification of celiac disease- related gluten proteins from wheat. Journal of Chromatography B, Analytical Technologies in the Biomedical Life Sciences 2009;877(10):975-982 van Dommelen P, et al. Screening rules for growth to detect celiac disease: a case-control simulation study. Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population- based registry in The Netherlands. The presence of small intestinal intraepithelial gamma/delta T-lymphocytes is inversely correlated with lymphoma development in refractory celiac disease. Age-related clinical, serological, and histopathological features of celiac disease. Detection of celiac disease and lymphocytic enteropathy by parallel serology and histopathology in a population based study. Prospective human leukocyte antigen, endomysium immunoglobulin A antibodies, and transglutaminase antibodies testing for celiac disease in children with Down syndrome. The evidence base for interventions used to maintain remissions in Crohns Disease. How long is it advisable to prolong maintenance treatment of patients with ulcerative colitis? Genome-wide association defines more than 30 distinct susceptibility loci for Crohns disease. Inflammatory bowel disease: clinical aspects and established and evolving therapies. Blood-based biomarkers can differentiate ulcerative colitis from crohns disease and noninflammatory diarrhea. Aspirin in the aetiology of Crohns disease and ulcerative colitis: a European prospective cohort study. The Safety Profile of Infliximab in Patients with Crohns Disease: The Mayo Clinic Experience in 500 Patients. Advanced age is an independent risk factor for severe infections and mortality in patients given anti tumor necrosis factor therapy for inflammatory bowel disease. Health care resource use and costs for Crohns disease before and after infliximab therapy. Early Combined immunosuppression or conventional management in patients with newly diagnosed Crohns disease: an open randomized trial. Prospective study of the effects of concomitant medications on thiopurine metabolism in inflammatory bowel disease. Psychosocial features of inflammatory bowel disease in the pediatric age group: acceptance of and adaptation to the disease. Gastrointestinal sensory and motoro disturbances in inflammatory bowel diseaseclinical relevance and pathophysiological mechanisms. Guidelines for screening and surveillance of asymptomatic colorectal cancer in patients with inflammatory bowel disease. Increased Risks of Developing Anxiety and Depression in Young Patients With Crohns Disease. Proceedings of the National Academy of Sciences of the United States of America 2007;104(34):13780-5. Application of the Montreal classification for Crohns disease to a single clinician database of 1015 patients. Application of the Vienna classification for Crohns disease to a single clinician database of 877 patients. Natural history and clinical behaviour of Crohns disease extending beyond two decades. Temporal and geographic evolution of longstanding Crohns disease over more than 50 years. Medical therapy and birth outcomes in women with Crohns disease: what should we tell our patients? Mucosal healing in inflammatory bowel disease: results from a Norwegina-based cohort. What Histologic Features Best Differentiate Crohns Disease from Ulcerative Colitis? Inflammatory bowel disease: Current insights into pathogenesis and new therapeutic options; probiotics, prebiotics and synbiotics. Prevalence and management of anemia in children, adolescents, and adults with inflammatory bowel disease. Molecular pathogenesis of inflammatory bowel disease: genotypes, phenotypes and personalized medicine. A population-based study of fatigue and sleep difficulties in inflammatory bowel disease. Venous thromboembolism during active disease and remission in inflammatory bowel disease: a cohort study.

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