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In contrast arthritis in neck and knee cheap 100mg voltaren otc, there was no difference in either C1 or C2 allelic distribution in an earlier study conducted in Caucasian men (Carr et al arthritis knee leg swelling discount 100mg voltaren amex. Cytokine gene polymorphisms have also been suggested to play a role in the pathogenesis of alcoholic liver disease rheumatoid arthritis flare definition generic voltaren 50 mg on line. The í511 146 Chemical/Physical Agents and Autoimmunity allele 2 was found at a higher frequency in patients with cirrhosis than in heavy drinkers without liver disease arthritis foot massage machine buy 50mg voltaren mastercard. Jarvelainen and colleagues (2001) demonstrated that in Finnish males arthritis medication for humans voltaren 50 mg line, expression of one T allele was associated with both alcoholic hepatitis and cirrho sis arthritis in the feet and legs purchase voltaren online from canada. There is conflicting evidence as to whether variations in the genes encoding for manganese superoxide dismutase represent a risk factor for alcoholic liver disease (Degoul et al. The data on cytokine and metabolic enzyme gene polymorph isms in the human population as well as experimental studies with ethanol-fed rodents are indicative of the importance of inflamma tion, oxidative stress, and endotoxin in the pathogenesis of alcohol induced liver damage. Chronic ethanol exposure has been associ ated with the formation of alcohol-modified proteins, leading to autoantibody formation and immune-mediated damage to the liver. Circulating antibodies recognizing acetaldehyde–malondialdehyde adducts have been found in Wistar rats fed an ethanol-containing liquid diet (Xu et al. Immunization with acetaldehyde adducts in conjunction with ethanol feeding stimulated ex vivo lymphocyte proliferation in B6 mice, but not in several other strains (Shimada et al. The antibodies generated by these alcohol-modified proteins may also respond to unmodified self-proteins, leading to a breaking of tolerance and autoimmune pathology. Obese strain chickens spon taneously develop a disease very similar to Hashimoto thyroiditis. They were the first model that showed that exposure to iodine affects the course of disease. Depletion of iodine after hatching, achieved by injections of potassium chlorite, reduced thyroid infiltration. In contrast, the onset of spontaneous thyroiditis was hastened by adding sodium iodide to the diet. This effect, however, was reduced by administration of antioxidants, suggesting that reactive oxygen intermediates are one mechanism by which iodine contributes to cell injury. The Biobreeding/Worcester rat has been widely used as a model for studying spontaneous diabetes mellitus, but it also develops autoimmune thyroiditis. Administration of excess iodine accelerates the appearance of the lymphocytic infiltration of the thyroid and the production of thyroid-specific autoantibodies. The incidence of diabetes is very low, but many of the animals develop autoimmune thyroiditis. Iodinated thyroglobulin is more antigenic than the same molecule lacking iodine, suggesting another mechanism by which iodine enhances thyroiditis. Several studies have evaluated the effects of excessive iodine intake in humans, and antithyroid antibodies and iodine-induced hypo and hyperthyroidism have been reported following long-term iodine treatment for endemic goitre (Boyages et al. Although a few epidemiological analyses have been published, they are often confounded by the absence of a clear-cut diagnosis. Clinical outcomes can be the result of immunoallergic, pseudoallergic, or autoimmune-like mechanisms. However, a comprehensive review of adverse autoimmune responses and autoimmune diseases associated with therapeutic agents is beyond the scope of this monograph, and only a few examples will be discussed below. Table 13 provides an abbreviated list of therapeutic drugs that have reportedly been associated with autoimmune reactions. When considering drug-induced autoimmunity, it is important to differentiate two situations. On the other hand, one given agent is associated with only one given type of autoimmune disease. In the latter case, the disease can be organ specific and then closely mimic the spontaneous disease, except that cessation of the offending agent leads to the progressive recovery of clinical and then biological manifestations of the disease. The disease can also be systemic and consists of clinical manifestations and biological/immunological changes markedly different from those of spontaneous diseases. Interestingly, drug-induced systemic autoimmune-like reactions often resemble systemic hypersensitivity reactions, and this further illustrates overlapping mechanisms between immunoallergic and autoimmune-like reactions. Hydralazine inhibits the covalent 150 Chemical/Physical Agents and Autoimmunity binding reaction of the complement protein C4, and susceptibility to hydralazine-induced lupus, as in idiopathic systemic lupus erythema tosus, may depend partly upon genetically determined C4 levels (Sim & Law, 1985; Speirs et al. Adoptive transfer of T cells made autoreactive by treatment with either hydralazine or procainamide causes a lupus like disease (Yung et al. The possibility of a lupus-inducing effect of the drug on T cell development in the thymus has been suggested (Quddus et al. Studies of the specificities of B cells that respond to chroma tin-reactive T cells at the initiation of this autoimmune process demonstrated a rapid and robust expansion of anti-chromatin-secret ing B cells, thus indicating the presence of a normal immune reper toire that includes non-tolerant autoreactive B cells that respond to strong T cell drive and are readily manifested if Fas-mediated activation-induced cell death is inhibited (Ayer et al. Because of a high incidence of adverse events and the strong association with several autoimmune-like phenomena, including myasthenia, pemphigus, and Goodpasture disease, the clinical use is limited. The adverse effects of D-penicillamine in animals are similar to those observed in humans. A study on the effects of D-penicillamine in various strains of mice indicated that D-penicillamine facilitates the induction of autoantibodies in animals with an inherent suscep tibility to autoimmunity (Brik et al. Studies using the popliteal lymph node assay demonstrated that D-penicillamine is capable of inducing an antigen. In rats, particularly Brown Norway rats, D-penicillamine induces a disease characterized by dermatitis, vasculitis, production of antinuclear antibodies, formation of circulating immune com plexes, and IgG deposits along the glomerular basement membrane (Donker et al. Interestingly, low 152 Chemical/Physical Agents and Autoimmunity dose pretreatment of D-penicillamine-treated Brown Norway rats was found to induce complete tolerance to a subsequent pathogenic dose of the drug (Donker et al. The syndrome was preceded by influenza-like symp toms, such as fever, headache, muscle and joint pains, and myalgia, which generally started within 6–17 days after starting zimeldine treatment. The British Department of Health and Social Security reported that 400 out of 100 000 patients displayed similar adverse responses to zimeldine. A number of experiments performed thereafter were supportive for the immune-based etiology of zimeldine-induced adverse effects (Kristofferson & Nilsson, 1989. Three individuals occupationally exposed to zimeldine developed allergy to the compound and showed positive patch and skin prick tests and positive response to zimeldine in the lymphocyte transformation test. These findings indicate that zimeldine may be immunogenic; indeed, zimeldine has been shown to be positive in the popliteal lymph node assay, based on cell numbers and including germinal centre formation and production of IgM and IgG antibodies (Thomas et al. The most common adverse effects associated with gold therapy appeared in skin and mucous membranes (about 15% of all patients) and kidneys (about 5–10%), mostly as proteinuria. It is suggestive, moreover, that progressive interstitial lung fibrosis was found in gold therapy (Smith & Ball, 1980), possibly with an autoimmune pathogenesis. Gold therapy occasionally causes autoimmune haemolytic anaemia (Hunziker, 1978), autoimmune thrombocytopenia (Kotsy et al. Early studies showed that injections of gold thiomalate caused renal lesions, immune complex nephropathy, and proteinuria in Wistar rats (Nagi et al. The histology of these lesions can be characterized as either interstitial nephritis or glomerulonephritis, with specific diagnosis dependent on the presence of specific autoantibodies. Recent works using inbred animals have provided additional information on the pathogenesis of gold-induced renal autoimmunity. These findings indicate that gold compounds appear to cause polyclonal B cell activation to induce a variety of autoantibodies, but detailed mechanisms have not been established. The main difference between classical low molecular weight pharmaceuticals and biopharmaceuticals is that biopharmaceuticals are large molecules that can be recognized directly by the immune system, without the need of metabolism or haptenation. Indeed, it has become clear that nearly all biopharmaceuticals induce anti bodies, although many are of human origin and thus immunolog ically tolerated (Schellekens, 2003. The formed antibodies may have no effect at all or are neutralizing, but occasionally adverse reactions may occur. For instance, erythropoietin has been shown to induce autoimmune anaemia in macaques (Chenuaud et al. Treatments with recombinant therapeutic cytokines occasionally induce autoimmune phenomena. Identified risk factors included the female sex, presence of pre-existing autoimmune thyroiditis, the treated disease (e. However, the immune effects described for diethylstilbestrol depend largely on the age of the animals at treatment, exposure to diethylstilbestrol, and sex. Short-term exposure of mice to diethylstilbestrol has been described as inducing differential immunological effects, depending upon the dose of hormone and sex (Calemine et al. Aged mice appear especially sensitive to diethylstilbestrol treatment, as highly significant alterations were seen in the thymus and bone marrow of aged 21-month-old mice exposed subacutely to diethyl stilbestrol. Severe thymic hypocellularity develops in treated mice following five consecutive days of intraperitoneal injection with diethylstilbestrol. In the same study, the levels of serum IgG and IgM antibodies to cardiolipin showed age dependent fluctuations but were similar in controls and diethylstil bestrol-treated females; however, the IgG antibodies in diethylstil bestrol-treated females were qualitatively different from those in controls with respect to sensitivity to bovine serum (a source of ȕ2 glycoprotein I), although these antibodies are not associated with autoimmune disease. In contrast to the situation with females, diethylstilbestrol-treated males had higher levels of these antibodies than controls (Forsberg, 2000. A potential role of diethylstilbestrol in autoimmunity is also demonstrated by enhanced autoantibody production both in vitro and in vivo. Plaque forming cells producing autoantibodies specific for bromelain treated red blood cells were significantly increased in mice implanted with diethylstilbestrol. IgM antibody production by B1 cells in vitro was also enhanced by diethylstilbestrol treatment. The authors suggested that diethylstilbestrol modulates autoantibody production by B1 cells and may be an etiologic factor in the development of autoimmune diseases (Yurino et al. A number of studies have also demon strated that perinatal exposure to diethylstilbestrol in mice produces profound thymus atrophy; although a direct cause–effect relationship has not been established, this has the potential to influence negative selection processes and subsequently influence autoimmune dis eases. In a follow-up study, using two different groups of diethylstilbestrol-exposed women and an appro priate control group for each, no differences in the prevalence or serum titre of antibodies to five common viral diseases and six less common ones were observed. However, an increased prevalence was found in diethylstilbestrol-exposed women of a relatively rare immunological hyperreactivity, rheumatic fever, subsequent to microbial infection (strep throat) (Blair et al. In a further study (Blair, 1992), sera of diethylstilbestrol-exposed and non exposed women were examined for the presence of factors associ ated with autoimmune diseases. The study demonstrated that the incidence of high antibody titres to red blood cell antigen was higher in the diethyl stilbestrol-exposed females than in the controls. Blair (1992) concluded that, in general, humans exposed prenatally to diethylstilbestrol do not exhibit severe defects in basic immune function, but their propensity to develop autoimmune disease and other diseases associated with defects in immune regulation is increased. There are relatively few data pertaining to risk of specific autoimmune diseases in relation to in utero diethylstilbestrol expo sure, although some studies suggest an increased rate of respiratory tract infections, other infectious diseases, or allergies (Noller et al. However, in a follow-up study of the children born as part of a randomized clinical trial that had been conducted in the 1950s, there was little difference in the rates of reported symptoms or specific diagnoses of infectious, allergic, or autoimmune conditions in diethylstilbestrol exposed individuals (253 sons and 296 daughters) compared with the controls (241 sons, 246 daughters) (Baird et al. Even with this sample size, however, the statistical power to assess the risk of specific autoimmune diseases was very limited. However, the immune effects of diethylstilbestrol depend largely on the age of the animals at treat ment, dose of diethylstilbestrol, and sex. Immune effects following in utero exposure can persist for the lifetime of the animal. Recent studies also indicate a potential role of diethylstilbestrol in autoimmunity, as demonstrated in mice, including a study in a murine model for systemic lupus erythematosus. Also, studies in humans indicate that individuals exposed prenatally to diethylstilbestrol do not exhibit severe defects in basic immune function, but their tendency to develop autoimmune disease and other diseases associated with defects in immune regulation is increased. This warrants continuing surveillance of humans exposed in utero to diethylstilbestrol for diseases related to immune dysregulation. The concern was especially focused on systemic adverse effects resulting from the potential immune stimulation and interaction with silicones, resulting in some form of autoresponse eventually leading to the fulmination of autoimmune connective tissue diseases. For silicone-related complaints, several terms were used, including, among others, undifferentiated connec tive tissue disease, human adjuvant disease, silicone poisoning, siliconosis, and (silicone) associated connective tissue disease. Evidence for an association between silicone breast implants and such a syndrome is lacking, however (Noone, 1997; Todhunter & Farrow, 1998. Silicon, silicones, and silica sound very similar, but are different entities (Williams, 1996. The basis for naturally occurring and synthetic silicon-based product is the silicon–oxygen bond, which is referred to as siloxane. Polymers with repeating siloxane units, the silicon–oxygen couplet, are called polysiloxane or silicone. Addition of organic groups gives poly dimethylsiloxane, which is a liquid when it forms linear chains (silicone fluids or silicone oils. Cross-linking results in the forma tion of so-called silicone gels (low level of cross-linking) or silicone elastomers (high level of cross-linking. Silica is the silicon dioxide, which can exist in crystalline (quartz) or amorphous form. Silicone breast implants consist of an elastomeric outer shell blended with amorphous silica for reinforcement and silicone gel as filler. Also, for saline implants or hydrogel implants, the outer shell is a silicone elastomer. Thus, even when an implant has a non silicone filling, there is exposure to the silicone elastomeric shell. However, residues and contaminants may be present in the silicone gel that can migrate from the implant. Such low molecular mass species and small cross-linked molecules as intermediates of the production process can easily migrate through the elastomeric silicone shell, as there is a high similarity in chemical composition between the residues and the silicone shell. This phenomenon of gel bleeding is not uncommon for silicone breast implants and cannot be completely avoided, as these low molecular weight residues are extremely difficult to remove (Williams, 1996. In addition, residues of catalysts, such as platinum, may leak from the implants (Lykissa et al. Also, local adverse effects and trauma resulting in implant rupture leading to massive exposure to the content of the implant (silicone gel) will remain a potential hazard for breast implant recipients.

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Note: Dose of each medication can be increased every 1 2 weeks to the maximum doses indicated arthritis pain early pregnancy buy generic voltaren 100mg on line. The mechanisms of cholestasis can be broadly classified into hepatocellular (Intrahepatic) what does arthritis in your neck feel like buy voltaren with paypal, where an impairment of bile formation occurs arthritis pain swelling relief buy voltaren no prescription, and obstructive (extra hepatic) rheumatoid arthritis definition ppt order online voltaren, where impedance to bile flow occurs after it is formed arthritis in feet and knees purchase 50mg voltaren overnight delivery. Intrahepatic causes of cholestasis include viral hepatitis arthritis diet and nutrition cheap voltaren online visa, alcohol, primary biliary cirrhosis, drug toxicity, Hodgkin?s lymphoma and pregnancy. Extra hepatic causes which may be amenable to surgical correction include choledocholithiasis and carcinoma of the biliary tree. Parasitic infections such as Ascariasis may also cause cholestatic jaundice Diagnosis? The prominent features include jaundice, dark urine, pale stools, and itching/pruritis. Liver functions; for elevated serum levels of total bilirubin, direct bilirubin, alkaline phosphatase, gamma-glutamyl transferase, bile salt concetration? Note Refer patiets cholestatic liver disease to specialized centres, particularly if it is severe or prolonged. Diagnosis Confusion, slurred speech, flapping tremors, change in personality that can include being violent and hard to manage to being sleepy and difficult to arouse (refer to grades of hepatic encephalopathy by West Haven Criteria grade 1-4. V infusion) 3 litres/day with 2g (26mmol) potassium chloride added to every litre bag (if renal function is satisfatory. V) 10mg Plus S: Fresh Frozen Plasma initially Add Platelets if count <20 x 10g/l and patient is still bleeding? Note: Hepatic encephalopathy is a medical emergency and requires referral to specialized and equipped centers for proper evaluation and management. Pneumonia can either be primary (to the causing organism) or secondary to pathological damage in the respiratory system. The common causative organisms for pneumonia are bacterial (for example Streptococcus pneumoniae, Hemophilus influenza, and Staphylococcus aureus, and Mycoplasma pneumoiae, viral or parasitic. C, dry or productive cough, central cyanosis, respiratory distress, chest pain and tachypnea. Classification of pneumonia in children is based on respiratory rate whichis fast breathing and chest in-drawing. Chest indrawing is when the lower part of the chest moves in when the child breaths in. Table 1: Important clinical features of pneumonia in underfives Age Signs Classification Infants less than 2? Severe chest in-drawing Severe pneumonia (all young months Or infants with pneumonia are classified as severe)? M once a day) for 5 days; If child responds well, complete treatment at home or in hospital with A: Amoxicillin (15 mg/kg three times a day) Plus A: Gentamicin 7. If there are no apparent complications, switch to 72 | P a g e B: Chloramphenical (25 mg/kg every 6 hours I. Give the first dose at the clinic and teach the mother how to give the other doses at home. Treatment Bronchodialator in Children 1-5 years If a rapid acting bronchodilator is required drugs of choice: Adrenaline (1:1000) 0. The symptoms are caused by constriction of bronchial smooth muscle (bronchospasm), oedema of bronchial mucous membrane and blockage of the smaller bronchi with plug of mucus. Infants under 18 months, however, may not respond well to bronchodilator Asthma attack/ acute asthma Acute asthma is a substantial worsening of asthma symptoms. If conventional spacer not available, take a 500ml plastic bottle, insert the mouth piece of the inhaler into a hole on the bottom of the bottle (the seal should be as tight as possible. The child breathes from the mouth of the bottle in the same way as he would with a spacer 76 | P a g e Silent chest Salbutamol nebulizer 2. Nocturnal Asthma Patients who get night attacks should be advised to take their medication on going to bed. Chronic Asthma in Adults the assessment of the frequency of daytime and nighttime symptoms and limitation of physical activity determines whether asthma is intermittent or persistent. Acute bronchitis is one of the most common conditions associated with antibiotic misuse. Patients with acute bronchitis present with a cough lasting more than five days (typically one to three weeks), which may be associated with sputum production. Patients may get secondary bacterial infection with development of fever and production of thick smelly sputum. Additionally, a generalized sub classification of exacerbations based on health-care utilization is proposed. Chronic bronchitis a chronic, inflammatory condition of the bronchi characterized by coughing and expectoration (spitting-up) of sputum (mucous coughed-up from the lungs) occurring on most days and lasting 3 months or longer for at least two consecutive years. Surgical treatment options for the treatment of patients with advanced emphysema, which include:? The most common cause is viral infection (particularly parainfluenza viruses) but may also be due to bacterial infection. The symptoms include paroxysmal ?barking? cough, insipiratory stridor, fever, wheezing, hoarseness of voice and tachypnoea? Children between 1-5 years of age are most susceptible although non immune adults are also at risk. Diagnosis Diphtheria is characterized by grayish-white membrane, composed of dead cells, fibrin, leucocytes and red blood cells as a result of inflammation due to multiplying bacteria. Gently examine the child?s throat can cause airway obstruction if not carefully done. After an incubation period of 7 ?10 days, the child develops fever, usually with a cough and nasal discharge which are clinically indistinguishable from a common cough and cold 82 | P a g e? In the second week, there is paroxysmal coughing which can be recognized as pertussis? The child is infectious for a period of 2 weeks up to 3 months after the onset of illness? During paroxysms of coughing, place the child head down and prone, or on the side, to prevent any inhaling of vomitus and to aid expectoration of secretions. Diagnosis the diagnosis is usually established clinically on the basis of chronic daily cough with viscid sputum production, and radiographically by the presence of bronchial wall thickening and luminal dilatation on chest x-rays. Antibiotics are used to treat an acute exacerbation and prevent recurrent infection by suppression or eradication of existing flora. Acute excarcebation Adults A: Ciprofloxacin 500mg every 12 hours for 7-10 days Plus A: Metronidazole 500mg every 8 hours for 7-10 days Children: A: Amoxycillin 40mg/kg (O) in 3 divided doses for 5-7 days Plus A: Metronidazole 7. Diagnosis It is characterized by high fever, breathlessness, cough productive of large amounts of foul smelling sputum and haemoptysis. The infection is usually polymicrobial and necessitates the use of combined drugs. Clinical types are recognized according to findings when the patient is first seen. These include: Threatened abortion, inevitable abortion, incomplete abortion, complete abortion and missed abortion. Viginal bleeding which may be very heavy in incomplete abortion, intermittent pain which ceases when abortion is complete and cervical dilation in inevitable abortion? In missed abortion, dead ovum retained for several weeks while sympoms and signs of pregnancy disappear? When infected (septic abortion) patient presents with fever tachycardia, offensive vaginal discharge, pelvic and abdominal pain. Puerperal/Post abortal Sepsis Pyrexia in women who has delivered or miscarried in the previous 6 weeks may be due to puerperal or abortal sepsis and should be managed actively. The uterus may need evacuation however parenteral antibiotics must be administered before evacuation. V)1gm start Plus A: Metronidazole 500mg Plus A: Gentamycin 80mg stat Patient should continue with the following oral antibiotics after evacuation for 5 to 7days For Mild/moderate A: Amoxycillin (O) 500mg every 8 hours for 10 days Plus A: Metronidozole (O)400 mg every 8 hours for 10 days Plus A: Doxycycline (O)100 mg every12hrs for 10 days Treatment Guidelines for severe cases 0? Marked abdominal tenderness are signs of severe post abortal sepsis Drug of Choice: A: Benzylpenicillin (I. V) 500mg every 6 hours Plus A: Metronidazole 500mg 8hrly for 5 days For urgent Delivery irrespective of gestational age A: Benzylpenicillin (I. Continue with antibiotics after delivery for 3-5 days Note: Use of antibiotics for prophylaxis during surgery, should be evaluated from situation to situation and not generalized 5. Admit in the hospital Give B: Normal saline Plus C: Nifedipine 10-20 mg 12 hrly; Plus C: Hydralazine 10 mg (I. High blood sugar levels in the mother?s body are passed through the placenta to the developing baby. Gestational diabetes usually begins in the second half of pregnancy and goes away after the baby is born. Eat close to bedtime; they should give themselves two to three hours to digest food before they lie down? Elevating upper body will help keep the stomach acids where they belong and will aid food digestion. This involves the injection of an oxytocic after the delivery of the foetus followed by controlled cord traction and uterine massage. The infection can happen as an ascending infection from the vagina, after delivery (puerperal sepsis), after an abortion (septic abortion), postmenstrual or after Dilation and Curettage (D&C) operation. The common causative organisms are Neisseria gonorrhea, Chlamydia trachomatis and Mycoplasma hominis. Diagnosis the main clinical features are lower abdominal pain, backache, vomiting, vaginal discharge, menstrual disturbance, dyspareunia, fever, infertility and tender pelvic masses. It may also be used in treatment of dysfunctional uterine bleeding, dysmenorrhea or endometriosis. The goal of therapy in the use of these products for contraception is to provide optional prevention of pregnancy while minimizing the symptoms and long term risks associated with excess or deficiency of the oestrogen and progestogen components. The eligibility for hormonal contraception can be obtained from nearest family planning clinic or unit. This type is suitable for lactating mothers or women with mild or moderate hypertension. Instruct women always to inform the doctor or nurse that they are on contraceptives while attending clinic or hospital. If a major placental separation has occurred, emergency delivery to minimize the possibility of disseminated? Typically, in primary dysmenorrhoea pain occurs on the first day of menses, usually about the time the flow begins, but it may not be present until the second day. It is classified as primary when there has never been a history of pregnancy or it is secondary when there is previous history of at least one conception. Treatment Treatment in all cases depends upon correction of the underlying disorder(s) suspected of causing infertility whether primary or secondary. Alpha-haemolytic streptococci are the most common causes of native valve endocarditis but Staphylococcus aureus is more likely if the disease is rapidly progressive with high fever, or is related to a prosthetic valve (Staphylococcus epidermidis) Diagnosis: Use Modified Dukes Criteria below and consult microbiologist where possible. One-hour peak concentration should not exceed 10mg/l and trough concentration (2 hour pre dose) should be less than 2mg/l. In these cases replace clindamycin with Vancomycin iv [Specialist-only drug] 1g over at least 100 minutes 1-2 hours before procedure. Pharmacological treatment Treatment of acute attack for eradication of streptococci in throat: Regardless of the presence or absence of pharyngitis at the time of diagnosis. Children > 10years 500mg, 5-10 years 250mg, < 5years 125mg two to three times daily for 10 days orally If allergic to Penicillin A: Erythromycin 500mg or 40mg/kg 4 times per day for 10 days orally Treatment of acute Arthritis and Carditis: A: Aspirin orally 25mg/kg* 4 times a day as required. Then reviewsGradual reduction and discontinuation of prednisolone may be started after 3-4 weeks when there has been a substantial reduction in clinical disease. The optimum duration of prophylaxis is controversial, but should be continued up to at least 21 years of age. Congenital Heart Disease It is a congenital chamber defects or vessel wall anomalies Valvular Heart Disease and Congenital structural Heart Disease may be complicated by:? Advise all patients with a heart murmur with regard to the need for prophylaxis treatment prior to undergoing certain medical and dental procedures? Advise patients to inform health care providers of the presence of the heart murmur when reporting for medical or dental treatment Referral? Recommended an alternative contraceptive method for women using oestrogen 108 | P a g e Containing oral contraceptive? Potassium Sparing Diuretics Spirinolactone 25mg once daily Eplerenone 25mg once daily 04. Central Adrenergic Inhibotor Methylodopa 250mg 12hrly 112 | P a g e Clonidine 50?g 8hrly 05. When patients are young (<30 years) or blood pressure is severe or refractory to treatment. Resistant (Refractory) Hypertension Hypertension that remain >140/90mmHgdespite the use of 3 antihypertensive drugs in a rational combination at full doses and including a diuretic. Important adverse effects are dry cough, hypotension, renal insufficiency, hyperkaelamia, and angioedema. Monitor digoxin level trough blood levels (before the morning dose) should be maintained between 0. Drug Management Adjunctive therapy Control cardiac pain C: Glyceryl trinitrate sub-lingual/ spray 0. But Pain not responsive to this dose may suggest ongoing unresolved ischaemia; appropriate measure should be taken to reverse the ischaemia. Thrombolytic Therapy: Thrombolytic agents have shown significant reduction in mortality and should be used in all eligible patients, most beneficial if given first 6 hours but can be given up to 12 hours after onset of chest pain. Check for contraindications before you administer thrombolytics S: Streptokinase, I. Unstable Angina: Angina that is increasing in frequency and or severity, or occurring at rest. Pharmacological therapy C: Aspirin oral, 75 -150 mg (O) daily Plus A: Atenolol 12. Pharmacological therapy C: Aspirin 150 mg (O) daily Plus C: Simvastatin 10 mg (O) day.

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