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In some described as chronic because the symptoms develop gradually buy 100mg lasix free shipping blood pressure medication plendil, places trusted lasix 40 mg arteria carotis communis, the disease is known by its alternative name bilharzia cheap lasix 40 mg with visa blood pressure chart for infants. Approximately 200 discount 100mg lasix with visa arteria nasi externa,000 people die every year in Africa as a result of the complications caused by these parasites. Rural communities living near water bodies such as rivers, lakes and dams may be highly affected by the disease, because the worms have a complex lifecycle in which they spend part of their development living in freshwater snails. First, as a Health Extension Practitioner, you need to know where the disease is common in Ethiopia. Schistosoma mansoni is widespread in several parts of Ethiopia, usually at an altitude of between 1,200 to 2,000 metres above sea level. In many of these locations, more than 60% of schoolchildren are infected with Schistosoma mansoni. A high burden of the disease in children has severe adverse effects on their growth and performance at school. Washing, swimming or standing in infected water exposes people to the risk of infection with Schistosoma parasites. The major reservoirs of Schistosoma parasites are infected humans (the primary hosts) and freshwater snails (the intermediate hosts). The eggs pass out into the water in either the faeces or urine, to continue the infection cycle. The immune reaction causes an acute inammation around the eggs, which can lead to chronic symptoms (see Box 37. Note that the clinical manifestations of schistosomiasis are mainly related to the immune response against the eggs in the intestine or bladder the symptoms are not due to the worms themselves. The adults can survive in the person s body for up to 20 years, releasing around 300 eggs every day. The main symptoms of Schistosoma mansoni infection of the intestines are abdominal pain and bloody diarrhoea. A blood test usually reveals signs of anaemia and the abdomen may be swollen due to enlargement of the liver. If the infection remains untreated it can lead to permanent liver damage in advanced cases. The main symptoms of Schistosoma haematobium infection of the bladder are pain during urination, frequent need to urinate, and blood in the urine. If the infection remains untreated it can lead to chronic bladder diseases, including cancer, and permanent kidney damage. It may also lead to infertility in men, and pain during sexual intercourse and vaginal bleeding in women. The clinical manifestations (described above) should lead you to suspect cases of schistosomiasis. Asking children if they have seen any blood in their urine is an important way of detecting whether Schistosoma haematobium is common in the area. You have an important role as a Health Extension and control categories again Practitioner to teach community members in affected areas how to apply the when we discuss the other vector-borne diseases later in major prevention and control measures, which can be described in ve general this study session. Rapid case detection and referral to the nearest health centre for effective treatment; the drug used to treat schistosomiasis is called praziquantel, which is administered orally at a dosage of 40 60 mg per kg of body weight, given in two or three doses over a single day. You are not expected to prescribe praziquantel, which must be given at the health centre. Education in the community about the causes and modes of transmission of schistosomiasis. Also they should wear protective clothing when standing in infected water, and seek early diagnosis and treatment for any suspected cases. Visceral is visceral leishmaniasis (also known as kala-azar), which affects the internal pronounced viss-urr-al and organs such as the liver and spleen, and cutaneous leishmaniasis,which cutaneous is pronounced kute- affects the skin. Leishmania aethiopica, Leishmania major and Leishmania tropica,allof which cause cutaneous leishmaniasis. During your work in the community, you should know the common places where leishmaniasis is present. Visceral leishmaniasis affecting the internal abdominal organs such as the liver and spleen is widely distributed in the lowlands of Ethiopia. Important endemic locations include Konso woredas (Lake Abaya and Segen Valleys), the Lower Omo plains, the Metama and Humera plains and Adiss Zemen. Cutaneous leishmaniasis occurs in Meta-Abo, Sebeta, Kutaber in Wello, and in some places in South West Ethiopia such as Jimma Zone. Phlebotomine means blood-sucking and phlebotomine sandytakinga is pronounced eb-otto-meen. There are about 30 species of sandies that blood meal from a person s can transmit Leishmania parasites to humans found throughout the tropical arm. The protozoa develop inside the sandyandarepassedonwhenthesandy takes a blood meal from a healthy person. The enlarged abdomen of the sick person on the left indicates visceral leishmaniasis affecting the internal organs. The disease can produce a large number of ulcers sometimes up to 200 which may result in physical disability (e. The visible ulcers are a source of social stigma, which can leave the patient suffering mental distress and rejection in their community. For this reason, visceral leishmaniasis is said to have a high case-fatality rate. The general principles will already be familiar to you from the earlier discussion of schistosomiasis. Rapid case detection and referral to the nearest health centre or hospital prevents the transmission of the parasite to others. Cases of leishmaniasis will be treated using intravenous or intramuscular drugs such as pentostam or amphotericin B. Investigate and control epidemics in epidemic-prone areas:early identication and management of epidemics of leishmaniasis helps to control the disease from spreading to the wider population. Education in the community about the causes and modes of transmission of leishmaniasis. Onchocerciasis is found in the western part of Ethiopia, where there are many rapidly owing rivers and streams, with vegetation along the banks that provide good habitats for the blackies that transmit the parasite. Unlike mosquitoes and sandies, they bite during the day when people are active in the area. The person s immune system attacks the microlaria, causing inammation and damage in the surrounding tissues. Sight defects and eventually blindness develops when the microlaria are embedded in the 61 person s eye. The microlaria migrate to the skin, lymph nodes and eyes of the infected person, causing inammation and tissue damage. They slowly mature into adult worms, which can live for 15 years in the human body. After mating, the female worm releases around 1,000 microlaria a day into the surrounding tissue. When they die, they cause an inammatory response which leads to the clinical manifestations and complications such as blindness. The itching and disguring nodules and blindness are sources of great distress to patients, who may be stigmatised and rejected by their communities. If you suspect that a patient may be infected, you should make a referral for laboratory conrmation and treatment.

Large Endogenous infection may be from perforated oesoph- pneumothoraces produce breathlessness generic 100 mg lasix with mastercard heart attack movie review, pallor purchase lasix 100mg overnight delivery hypertension clinic, tachy- agus or spread from a subphrenic abscess lasix 40mg with amex blood pressure 9058. Pleural malignancy Cystic brosis Pneumonia Aetiology Sarcoidosis The most common cause of pleurisy is infection buy lasix 40mg online blood pressure for 6 year old, related Traumatic Penetrating chest wounds to an underlying bacterial or viral pneumonia. Pleurisy Rib fractures canalsobeafeatureofpulmonaryembolism,pulmonary Oesophageal rupture Iatrogenic Subclavian cannulation infarction, malignancy and connective tissue diseases Positive pressure ventilation such as rheumatoid arthritis. Pleural aspiration Oesophageal perforation during endoscopy Clinical features Lung biopsy Sharp, well-localised pain, worse on inspiration or coughing,andapleuralrubheardonauscultation. Investigations Chest X-ray shows the visceral pleura as a thin line with Macroscopy absent lung markings beyond. Fibrinous exudate is seen over the pleural surfaces and there is variable exudation of uid. Aimed at identication and treatment of the underlying r If the pneumothorax is >20%, particularly if the pa- cause. Nonsteroidalanti-inammatorydrugsandparac- tient has underlying lung disease or is signicantly etamol are used for analgesia. If after a few days disease and embolism the drain continues to bubble and the pneumothorax persists this indicates a bronchopleural stula, i. Denition r Pleurectomy is indicated in recurrent pneumotho- Respiratory failure is dened as a fall in the arterial oxy- racesorfor bronchopleural stulae that fail to close gen tension below 8 kPa. Aetiology/pathophysiology The opposition of lung to the raw area on the chest r Type I failure, sometimes called acute hypoxaemic wall causes the surfaces to adhere to one another. Other signs include required, preferably before patients are completely ex- the use of accessory muscles of respiration, tachypnoea, hausted (see Table 3. With time the arteries undergo a and <8kPa when stable with polycythaemia, nocturnal proliferative change leading to irreversible pulmonary hypoxaemia, peripheral oedema or pulmonary hyper- circulationchanges. Patients increase in blood viscosity and predisposes to must have stopped smoking (for safety reasons), and an thrombosis. Investigations Prognosis Blood gas monitoring is the most important initial in- Fifty per cent of patients with severe chronic breathless- vestigation to establish the type of failure and will dictate ness die within 5 years, but in all stopping smoking is the the mode of oxygen therapy. Pulmonary embolism Pathophysiology Following a pulmonary embolus there is a reduction in Denition the perfusion of the lung supplied by the blocked vessel. Thrombus within the pulmonary arteries causing lack Ventilation perfusion mismatch occurs, leading to hy- of lung perfusion. Production of surfactant also stops if perfu- or uncommonly from the heart embolises to the lungs. Infarct is rare (only occurring in around Prevalence 10% of cases) as the lung is also supplied by the bronchial Common. Aetiology The causes of thrombosis can be considered according Clinical features to Virkhow s triad: The result of a pulmonary embolism depends on the size r Disruptioninbloodowparticularlystasis:Prolonged and number of the emboli. Pleural inam- 1 In massive pulmonary embolism, there is haemody- mationresultsinapleuralfrictionrubandalow-grade namic compromise which may require resuscitative pyrexia. With large emboli, thrombolysis or surgical Clinical signs of a deep vein thrombosis may also be thrombectomy with cardiac bypass may be life-saving. For small or moderate Blood enters the pulmonary vasculature and thus there emboli subcutaneous low molecular weight heparin is is congestion proximal to the blockage. Therapy is converted to warfarin after 48 hours (for 3 Repair results in the formation of a white scar. Lifelong war- farin may be indicated depending on the underlying Microscopy cause, or in recurrent embolism. Typical features include haemorrhage (due to extravasa- 3 If anti-coagulants are unsuccessful or contraindicated tion of blood), loss of cell architecture, cellular inltra- a lter may be inserted into the inferior vena cava to tion and occasionally necrosis. Atelectasis and areas of hypoperfusion may be seen, and large emboli may cause Pulmonary hypertension an elevated hemidiaphragm and enlarged proximal pul- Denition monary arteries. A ventilation perfusion (V/Q) scan is Aetiology usually diagnostic, but is less helpful if the chest X-ray Pulmonary hypertension may be secondary to a variety is abnormal. This in turn raises r Right ventricular strain pattern T wave inversion the pulmonary capillary and arterial pressures (left in leads V1 V4. A similar syndrome is associated with Management sytemic lupus erythematosus, scleroderma and Ray- Treatment is aimed at the underlying cause. The result is a de- disease may benet from oxygen therapy to reduce crease in the lumen of the vessels and hence an increased the vasoconstrictor effect of hypoxia. Progressive fail- r Long-term intravenous infusion of epoprostenol ure of the right side of the heart occurs which is called (prostacyclin) improves the outcome of patients with cor pulmonale. The administra- tion of bosentan (a nonselective endothelin receptor Clinical features antagonist) may also be benecial in patients with Dyspnoea, syncope and fatigue are common. Symptoms primarypulmonaryhypertensionalthoughlong-term of the underlying cause and of right ventricular failure follow-up data are not yet available. Occupational lung disease Right heart failure leads to peripheral oedema and hep- atomegaly. A pulmonary mid systolic ejection murmur and an Introduction to occupational early diastolic murmur of pulmonary regurgitation may lung disease be heard (Graham Steel murmur). Mostpatientswithoccupationallungdisease are entitled to compensation according to their degree Microscopy of disability. If pulmonary hypertension is long-standing, micro- scopy reveals hypertrophy of the media of the vessels with an increase in the amount of smooth muscle. Investigations Incidence r Achest X-ray may show right ventricular and right The incidence of asbestos related disease increased dra- atrialenlargement. Thecentralpulmonaryarteriesare matically in recent decades but appears to have peaked usually prominent and may be pruned peripherally. Itisdebatablewhethertheyarecarcinogenic, Pattern of disease Causative agents but their use has now been banned in new buildings Pulmonary brosis Mineral dusts such as coal, silicon in the United Kingdom. They persist in the lung for alveolitis allergic response many years and are very brogenic and carcinogenic. Theyaretheresultofmacrophages, rally as a bre, and has been widely used for its insulative which surround and attempt to engulf the bres, but properties. It was used in sheets in buildings, sprayed on fail to clear them leading to broblast proliferation pipes as lagging, in shipbuilding and for boiler insula- and brosis. However, it is easily inhaled and the bres induce r Pleural plaques are well-circumscribed elevated abrogenic reaction in the lung. The risk of developing plaques of white hyaline brous tissue arranged sym- pathology from asbestos is dependent on the duration metrically on the parietal pleura over the ribs and di- and intensity of exposure, and the type of asbestos (see aphragm. Fibres are long (up to 2 cm) and are brotic changes in the interstitium, obliteration of Table3. Pleuritic Pleural effusion and knobbly Median survival 2 years 30 35 years from or dull chest wall pleural thickenings with after diagnosis exposure. Two different syndromes result from inhalation: r Malignant mesothelioma: Thoracoscopic or open r Simple pneumoconiosis in which there is deposition lung biopsy may be needed to make the diagnosis. There are peribronchiolar Macroscopically the lesion is thick, may be encapsu- depositsintheupperpartsofthelung,oftenassociated lated, with interlobar ssures. Local invasion antinuclearfactorandthedamageisthoughttobedue is extensive, 50% metastasise. Patients with carcinoma, which is usually adenocarcinoma or squa- progressive massive brosis suffer from considerable ef- mous cell carcinoma. Management r All patients with known asbestos exposure should be Macroscopy/microscopy advised to stop smoking. Routine surveillance with r Simplepneumoconiosisischaracterisedbyaccumula- repeated sputum cytology and chest X-ray does not tion of dust in macrophages at the centre of the acinus, appear to lead to earlier diagnosis. Pleural plaques and asbestos bodies require no treat- r In progressive massive brosis there are nodules of ment. Radiotherapy is in- material, containing little collagen and abundant effective and chemotherapy regimens are under eval- carbon, which frequently cavitates and liquees. Patients with bilateral diffuse pleural thickening, as- ii Dense collagenous tissue and macrophages heavily bestosis and (in those with an occupational history or pigmented by carbon, seen where there is a high other evidence of asbestos exposure) mesothelioma or silica content in the coal dust.

The American College of Rheumatology 1990 criteria for the classification of vasculitis: introduction trusted 100mg lasix pomegranate juice blood pressure medication. Drug-induced cutaneous reactions: a report from the Boston Collaborative Drug Surveillance Program on 15 order lasix 100mg online arrhythmia statistics,438 consecutive inpatients generic 40mg lasix otc blood pressure chart in uk, 1975 to 1983 buy 100mg lasix free shipping blood pressure ratio. Drug eruptions: causative agents and clinical types: a series of in-patients during a 10-year period. Angio-oedema in relation to treatment with angiotensin converting enzyme inhibitors. Severe angioedema after long term use of an angiotensin-converting-enzyme inhibitor. Prevalence and relevance of allergic reactions in patients patch tested in North America 1984 to 1985. Clinical pattern of cutaneous eruption among children and adolescents in North India. Postcoital fixed drug eruption in a man sensitive to trimethoprim-sulfamethoxazole. The interaction between keratinocytes and T cells-and overview of the role of adhesion molecules and the characterization of epidermal T cells. Topical provocation in 31 cases of fixed drug eruptions: change of causative drugs in 10 years. Cutaneous immunofluorescence study of erythema multiforme: correlation with light microscopic patterns and etiologic agents. Drug-induced, photosensitive, erythema multiforme-like eruption: possible role for cell adhesion molecules in a flare induced by rhus dermatitis. Erythema multiforme: microvascular damage and infiltration of lymphocytes and basophils. Lymphocyte subsets and langerhans cells/indeterminate cells in erythema multiforme. Toxic epidermal necrolysis: rapid differentiation between staphylococcal-induced disease and drug-induced disease. Usefulness of case report literature in determining drugs responsible for toxic epidermal necrolysis. Hypersensitivity to pancreatic extracts in parents of patients with cystic fibrosis. Dyspnea, asthma, and bronchoconstriction in relation to treatment with angiotensin converting enzyme inhibitors. Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy: a review of the literature and pathophysiology. Low-dose amiodarone-induced pneumonitis: evidence of an immunologic pathogenic mechanism. Fatal pulmonary failure complicating high-dose cytosine arabinoside therapy in acute leukemia. A mechanism of cell destruction in individuals sensitized to foreign antigens and its implications in autoimmunity. Heparin-induced thrombocytopenia: studies with a new low molecular weight heparinoid, Org 10172. The liver: its role in drug biotransformation and as a target of immunologic injury. Evidence for expression in human liver of halothane induced neoantigens recognized by antibodies in sera from patients with halothane hepatitis. Enflurane metabolism produces covalently bound liver adducts recognized by antibodies from patients with halothane hepatitis. Acute interstitial nephritis due to drug hypersensitivity: an up-to-date review with a report of 19 cases. Acute interstitial nephritis with glomerulopathy due to nonsteroidal anti-inflammatory agents: a review of its clinical spectrum and effects of steroid therapy. Association of protamine IgE and IgG antibodies with life-threatening reactions to intravenous protamine. Sulfonamide-reactive lymphocytes detected at very low frequency in the peripheral blood of patients with drug-induced eruptions. A decade of penicillin related acute intersititial nephritis: more questions than answers. Cross-reactivity between penicillins and cephalosporins: clinical and immunologic studies. Management of aspirin-sensitive rhinosinusitis-asthma syndrome: what role for aspirin desensitization? The incidence of antimicrobial allergies in hospitalized patients: implications regarding prescribing patterns and emerging bacterial resistance. Nature and extent of penicillin side-reactions with particular reference to fatalities from anaphylactic shock. An analysis of 51 episodes in two Dallas hospitals and 97 episodes reported in the English literature. Selection of treatment of cefaclor-associated urticarial, serum sickness-like reactions and erythema multiforme by emergency pediatricians: lack of a uniform standard of care. Benefits of negative penicillin skin test results persist during subsequent hospital admissions. Cross-reactivity between penicillins and cephalosporins: clinical and immunological studies. Risk of administering cephalosporin antibiotics to patients with histories of penicillin allergy. Three cases of fatal anaphylaxis to antibiotics in patients with prior histories of allergy to the drug. Routine elective penicillin allergy skin testing in children and adolescents: study of sensitization. Desensitization of patients allergic to penicillin using orally administered B-lactam antibiotics. Acute and chronic desensitization of penicillin-allergic patients using oral penicillin. Long-term ticarcillin desensitization by the continuous oral administration of penicillin. Detection of human IgE to sulfamethoxazole by skin testing with sulfamethoxazoyl-poly-L-tyrosine. Cutaneous reactions to trimethoprim-sulfamethoxazole in African patients with acquired immunodeficiency syndrome. Trimethoprim-sulfamethoxazole with pentamidine for treatment of Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome. Pentamidine aerosol versus trimethoprim-sulfamethoxazole for Pneumocystis carinii in acquired immune deficiency syndrome. Desensitization to trimethoprim-sulfamethoxazole in patients with acquired immunodeficiency syndrome and Pneumocystis carinii pneumonia. A 5-day course of oral desensitization to trimethoprim/sulfamethoxazole (T/S) is successful in patients with human immunodeficiency virus type-1 infection who were previously intolerant to T/S but had no sulfamethoxazole-specific IgE. A comparison of the effectiveness of three regimens in the prevention of Pneumocystis carinii pneumonia in human immunodeficiency virus-infected patients. Management of sulfadiazine allergy in patients with acquired immunodeficiency syndrome. Management of adverse reactions to prophylactic trimethoprim-sulfamethoxazole in patients with human immunodeficiency virus infection. Successful oral desensitization to trimethoprim-sulfamethoxazole in acquired immune deficiency syndrome. Successful desensitization of two patients who previously developed Stevens-Johnson syndrome while receiving trimethoprim-sulfamethoxazole. Acute desensitization of a patient with cystic fibrosis allergic to both B-lactam and aminoglycoside antibiotics.

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