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The extent of the risk is such that most experts do not recommend periodic endoscopic surveillance purchase 1mg estrace with mastercard. Pill-Induced Esophagitis A large number of oral agents can cause localized esophageal injury order estrace 2 mg fast delivery. The antibiotic doxycycline and the anticholinergic emepronium bromide are two of the most common culprits. Nonsteroidal anti-inflammatory drugs and slow-release forms of potassium chloride are also frequently implicated. Patients with this type of injury typically take their medication with a small amount of water and then immediately lie down to go to bed. They may then wake up several hours later with severe retrosternal chest pain and odynophagia. Capsules and tablets are notorious for being transported through the esophagus quite poorly unless adequate amounts of fluid are ingested at the same time. This is an important point to remember in counselling all patients who take medicines at bedtime. Rarely, the medication becomes lodged and causes a deep esophageal ulcer with perforation. Patients with esophageal motility disorders are particularly prone to this complication. The bisphosphonate alendronate sodium has also been reported to rarely cause esophageal ulceration, but the mechanism of this injury is unclear. Radiation-Induced Esophagitis When included in the field of irradiation, the esophagus becomes inflamed in up to 80% of patients receiving therapeutic radiation for cancer. The patients typically develop chest pain, dysphagia and odynophagia shortly after the initiation of therapy. This can be a serious problem in such patients, who are often already severely malnourished. Disorders of the Oropharyngeal Phase of Deglutition A variety of structural and functional disorders can disrupt the oropharyngeal phase of deglutition and result in oropharyngeal or transfer-type dysphagia (Table 1). In the assessment of these patients it is important to exclude disorders for which specific treatment is available. The most important investigation is a carefully performed video fluoroscopic study of the swallowing mechanism. In addition to the usual barium studies, it is helpful to observe deglutition when the patient swallows barium soaked cookies or bread. Not only will this examination identify and characterize disorders of oropharyngeal coordination, it will also help exclude structural lesions. If an inflammatory, neoplastic or other structural lesion is suspected, direct or indirect laryngoscopy is indicated. Ideally, treatment of oropharyngeal motor disorders should be directed at the underlying disease. Many patients will be able to control their symptoms simply by eating slowly and carefully in a relaxed atmosphere. In patients in whom aspiration develops because of inadequate clearing of the hypopharynx after the initial swallow, it is beneficial to have the patient immediately follow a bolus swallow with a second, First Principles of Gastroenterology and Hepatology A. Correcting denture problems and avoiding foods of certain consistency may also help. Speech-language pathologists have special expertise as swallowing therapists and can be very helpful in the management of these patients. In diffuse esophageal spasm, normal peristaltic waves are interspersed with high-pressure, nonpropulsive (simultaneous) contraction waves and are often repetitive. For patients in whom these simple measures are not helpful and whose symptoms are such that respiratory and nutritional complications are developing, cricopharyngeal myotomy is sometimes performed. This helps patients with true cricopharyngeal achalasia or Zenkers diverticulum (Section 13). More often there is associated weakness of the suprahyoid muscles, which actually open the sphincter, and/or associated problems with pharyngeal peristalsis. Once cricopharyngeal myotomy has been performed, the patient has lost an important defense mechanism against the aspiration of refluxed material. The patient should therefore be instructed to elevate the head of his or her bed on blocks in order to minimize this risk. Classification of disorder causing oropharyngeal dysphagia Central nervous system disease o Cerebrovascular accident (brainstem, pseudobulbar palsy) o Wilsons disease o Amyotrophic lateral sclerosis o Brainstem neoplasm o Tabes dorsalis o Parkinsons disease Peripheral nervous system disease o Bulbar poliomyelitis o Miscellaneous peripheral neuropathies o Head and neck neoplasms o Past-radical neck surgery First Principles of Gastroenterology and Hepatology A. Shaffer 69 Muscle disease o Muscular dystrophy o Polymyositis and dermatomyositis o Metabolic myopathy (e. Motor Disorders of the Esophagus and Lower Esophageal Sphincter Esophageal motor disorders can be classified as either primary or secondary. Primary disorders refer to those that usually affect the esophagus alone and have no known etiology. Secondary disorders are motility derangements caused by some other systemic or local condition.

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Disadvantages Patients will develop Addisons disease and need lifelong Cortisol replacement Nelsons syndrome: in which pituitary adenomas undergo rapid growth discount estrace 1mg with amex, perhaps because it is no longer inhibited by above normal level of cortisol order estrace 2mg online. Hyperaldosteronism Aldosteronism: is a syndrome associated with hypersecretion of the mineralocorticoid, aldosterone. Primary aldosteronism: the cause of excess aldosterone production resides with in the adrenal gland Aldosterone producing adrenal adenoma (Conns syndrome): in most cases, unilateral small adenoma which can occur on either side Adrenal carcinoma: rare cause of aldosteronism Bilateral cortical nodular hyperplasia /idiopathic hyperaldosteronism 2. Secondary aldosteronism: the stimulus for excess aldosterone production is outside the adrenal gland. Signs and symptoms: Moat patients have diastolic hypertension resulting from sodium retention. Patients may complain headache and symptoms of other organ damage Hypokalemia and associated symptoms: muscle weakness and fatigue. While raised aldosteron level with reduced plasma renin activity suggests primary aldosteronism. Surgery: removal of solitary adenoma results cure of hypertension in about 60 % of cases and improvement in another 25 %. Adrenalectomy is done after 4 week treatment with spironolactone (in case of adenoma, hyperplasia) In contrast only 20%-50 % of patients with bilateral hyperplasia are improved with surgery, even if bilateral adrenalectomy is performed. Medical Therapy: Spironolactone inhibits the effects of aldosteron on renal tubule. In idiopathic form: Spironolactone (50-100 mg/d), possibly combined with potassium- sparing diuretics correct the hypokalemia and with anti-hypertensive medication, high blood pressure can be controlled. Anterior pituitary diseases may result from:- i) Insufficient production of pituitary hormones: hypopituitarism ii) Excess production of pituitary hormones: a. Posterior Pituitary diseases I) Hypopituitarism ( Insufficient production of anterior pituitary hormones) Hyposecretion may be generalized (hypopituitarism) or caused by the selective loss of one or more pituitary hormones. Generalized hypopituitarism Definition: Endocrine deficiency syndromes due to partial or complete loss of anterior lobe pituitary function. Infarction of ischemic necrosis of the pituitary Shock, especially post partum ( Sheehans syndrome ) or in Debates mellitus or Sickle cell anemia Vascular thrombosis or aneurysm of the anterior cerebral artery Hemorrhagic infarction : pituitary apoplexy 3. Inflammatory /infectious process : meningitis ( tuberculus ), pituitary abscess 4. Iatrogenic : irradiation or Surgical removal of pituitary tumours or during operation for other bran tumours 480 Internal Medicine Clinical features: The onset is usually insidious and may not be recognized as abnormal by the patient, but occasionally it may be sudden or dramatic. The function of all target glands will decrease when all hormones are deficient (panhypopituitarism). This type of adrenal insufficiency differs from primary adrenal insufficiency in that : There is no hyperpigmentation of skin and mucous membrane Hyponatremia and Hypokalemia are minimal, since aldosteron production, which controls the balance of these electrolytes, mainly depends on the renin-angiotensin system. Symptoms of weakness, hypoglycemia, weight loss, and decreased axillary and pubic hair suggest the diagnosis. There is little bony deformity, soft tissue swelling or enlargement of peripheral nerves. Medical therapy is indicated if surgery and radiotherapy are contraindicated or have failed. Hyperprolactinoma /Galactorrhea Definition: Hyperprolactinoma is a clinical condition resulting from excess secretion of prolactin in men, or in women who are not breastfeeding. Prolactin secreting pituitary adenomas (Prolactinoma), are more common in women than in men, usually appearing during reproductive years. Men tend to have larger tumors (macroadenomas), which usually are suspected because of neurologic impairment and hypogonadism. Damage to the hypothalamus or the pituitary stalk: by tumors, granulomas and other process may prevent the normal regulatory effect of hypothalamic dopamine on lactotrope activity, resulting hypersecretion of prolactin. Drugs: drugs that inhibit dopamine activity, and thus interfere with its regulatory activity on prolactin secretion. Other rare causes : Primary hypothyroidism Chronic liver disease Renal failure Ectopic prolactin production from tumors (paraneoplastic syndromes) 486 Internal Medicine Clinical features: In women: Galactorrhea: is the direct result of prolactin excess. A serum prolactin level greater than 300ng/ml strongly suggests the presence of prolactinoma. Surgical therapy: transsphenoidal surgery: cures most patients with small adenomas. Medical: Bromocriptine is remarkably effective in decreasing prolactin level, usually, to normal. It may be used in conjunction with surgery and bromocriptine to further reduce tumor size and function. Primary/Idiopathic: account for approximately 50 % of the cases of diabetes insipidus. Injury to the hypothalamus pituitary area: may result from head trauma, neurosurgical procedures such as hypophysectomy. Nocturia is almost always present, which may disturb sleep and cause mild day time fatigue or somnolence. A conscious patient with normal thirst mechanism and free access to water will maintain hydration. However rapid and life threatening dehydration and hypovolemia may develop rapidly, if urinary losses are not continuously replaced, which may occur in unconscious patients or infants.

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Only long-acting metoprolol succinate has been shown to perform better than placebo in reducing mortality discount estrace 2mg line. In the short term they can produce decompensation with worsening of heart failure and hypotension purchase estrace 1 mg with mastercard. They should be initiated at low dose and only gradually increased with monitoring up to the target dose. There was a significant 1++ reduction in all-cause and coronary mortality, myocardial infarction, the need for coronary revascularisation and fatal or non-fatal stroke. This significant reduction in cardiovascular events is mainly due to the reduction in the incidence of non-fatal myocardial infarction. Subgroup analysis of the trial showed that benefit from perindopril is mainly in patients with a history of myocardial infarction. There is an increased risk of mortality following both coronary bypass surgery and angioplasty; and there is a substantially increased risk of re-stenosis following angioplasty in diabetic patients, partly ameliorated by the use of coronary stents. Indications for coronary angiography in patients with diabetes with symptomatic coronary disease are similar to those in non-diabetics, recognising the increased risk associated with revascularisation procedures. Patients should be given information to help them recognise the following risk factors: smoking dyslipidaemia hypertension hyperglycaemia central obesity and a plan made to help them reduce those which affect them. The additional factor to be considered is to obtain and maintain good glycaemic control. Microalbuminuria is defined by a rise in urinary albumin loss to between 30 and 300 mg day. This is the earliest sign of diabetic kidney disease and predicts increased total mortality, cardiovascular mortality and morbidity, and end-stage renal failure. Diabetic nephropathy is defined by a raised urinary albumin excretion of >300 mg/day (indicating clinical proteinuria) in a patient with or without a raised serum creatinine level. This represents a more severe and established form of renal disease and is more predictive of total mortality, cardiovascular mortality and morbidity and end-stage renal failure than microalbuminuria. The presence of retinopathy has often been taken as a prerequisite for making a diagnosis of diabetic nephropathy, but nephropathy can occur in the absence of retinopathy. In a Danish study of 93 people with type 2 diabetes, persistent albuminuria and no retinopathy, 69% had diabetic nephropathy, 12% had glomerulonephritis and 18% had normal glomerular structure. In most individuals this diagnosis is made clinically, as biopsy may not alter management. Classic diabetic kidney disease is characterised by specific glomerular pathology. In many individuals, kidney disease will be due to a combination of one or more of these factors, and people with diabetes may develop kidney disease for other reasons not related to diabetes. Patients on dialysis are classified as stage 5D The suffix T indicates patients with a functioning renal transplant (can be stages 1-5). Estimates of prevalence from individual studies must be interpreted in the context of their patient population, such as levels of deprivation and the proportion of individuals from ethnic minorities. The proportions of individuals with microalbuminuria and proteinuria over 15 years of follow up, for participants in the conventional management arm of the study, are shown in Table 6. There are data to 2- suggest that there has been a decrease in the incidence of diabetic nephropathy in people with type 1 diabetes diagnosed more recently, with earlier aggressive blood pressure and glycaemic control. Conventional urine dipstick testing cannot reliably be used to diagnose the presence or absence of microalbuminuria. The literature is confusing in relation to the timing of commencing screening in young people with diabetes. Early microvascular abnormalities may occur before puberty, which then appears to accelerate these abnormalities. Detection of an increase in protein excretion is known 2++ to have both diagnostic and prognostic value in the initial detection and confirmation of renal disease. Annex 3 explains the relationship between urinary protein (and albumin) concentrations expressed as a ratio to creatinine and other common expressions of their concentration. This benefit was at the expense of significantly more severe hypoglycaemic events in the intensive group 2. There are limited data using the surrogate end point of reduction in proteinuria which suggests that thiazolidinediones may have an additive benefit over other hypoglycaemic agents in reducing proteinuria. This may indicate that the maximum benefit of intensive glycaemic control occurs when treatment is initiated at an earlier stage of the disease process. However, in pancreatic transplant recipients with evidence of diabetic kidney disease pre-transplant, histological improvements have been seen after 10 years of euglycaemia. A Reducing proteinuria should be a treatment target regardless of baseline urinary protein excretion. No difference in blood pressure was noted between the treatment groups to explain the reduction in albumin excretion rate.

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