For patients who rebleed after an initial attempt at endoscopic hemostasis order topiramate 100 mg fast delivery medications for gout, repeat endoscopy to reassess the lesion and apply further endoscopic treat- ment as needed is appropriate buy discount topiramate 200 mg online 4d medications. However purchase topiramate 200 mg without prescription medicine 751 m, routine second-look endoscopy in patients with no evidence of recurrent bleeding is not advocated purchase 200 mg topiramate with visa treatment 101. Surgery Between 5% and 10% of patients who present with acute upper gastrointestinal bleeding will require surgery because of continued or recurrent hemorrhage. Although this proportion is gradually declining, it remains substantial as improvements in medical and endoscopic therapies are offset by the increasing age and comorbidity of patients admitted with gastrointestinal bleeding. The decision to perform surgery must be individualized, but consider factors such as patient comorbidity, transfusion requirements, the nature of the bleeding lesion and the anticipated success of further endoscopic therapy. Surgery should be considered early in patients at high risk of complications such as perforation (e. Obesity will be discussed in the chapter on nutrition, but it is useful to consider bariatric surgery here within the contest of the rate of common complications arising from gastric surgery performed for any reason. Bariatric procedures Specific procedures o Gastric bypass (Roux-en-Y) Anastomotic leak with peritonitis Stomal stenosis Marginal ulcers (ischemia) Staple line disruption Internal and incisional hernias Nutrient deficiencies (usually iron, calcium, folic acid, vitamin B12) Dumping syndrome First Principles of Gastroenterology and Hepatology A. Unfortunately, these procedures are associated with multiple complications (Table 31a&b). It is a useful exercise to consider the mechanisms responsible for the nutrient deficiencies which may develop after bariatric surgery, let alone any type of gastric surgery which may be used for example for peptic ulcer disease or for gastric malignancy (Table 32). Conclusions Appropriate management of acute upper gastrointestinal hemorrhage entails early resuscitation and triage, careful clinical assessment, early endoscopy, intravenous proton pump inhibitors infusion (if indicated) and access to a skilled surgical team. Given the high prevalence of upper gastrointestinal bleeding, each acute care hospital and health care system should develop institution-specific protocols for its management. These protocols should address aspects of triage and multidisciplinary care including access to a therapeutic endoscopist skilled in endoscopic hemostasis and trained support to assist with urgent endoscopy. Despite remarkable advances in medical and endoscopic therapy, non-variceal upper gastrointestinal hemorrhage continues to impose a significant disease burden. Introduction The term gastritis has been used variously and incorrectly to describe symptoms referable to the upper gastrointestinal tract, the macroscopic appearances of inflammation or injury in the stomach at endoscopy and the histologic features of inflam- mation or injury to the gastric mucosa at microscopy. Unfortunately, there is a very poor correlation between an individuals symptoms and any abnormalities evident at endoscopy or microscopy. Only the histological features compatible with inflammation may be correctly used with the term gastritis, which will be the subject of the present chapter (Table 1). Indeed, it has been proposed that an endoscopy performed without mucosal biopsies is an incomplete examination. In addition to specific lesions or abnormalities, biopsies should also be taken from the antrum (2 biopsies) and body of the stomach (2 biopsies) and some authors also recommend a fifth biopsy from the gastric angulus or incisura to identify possible H. However, even a chemical gastropathy may be accompanied by inflammation and both entities will, therefore, be addressed. Acute gastritis is characterized by an inflammatory infiltrate that is pre- dominantly neutrophilic and is usually transient in nature. Acute gastritis may cause epigastric pain, nausea and vomiting but it may also be completely asymptomatic. Chronic gastritis is characterized by an infiltrate of lymphocytes, plasma cells, or both, that may also be associated with intestinal metaplasia and atro- phy of the epithelium. In intestinal metaplasia, the normal gastric epithelium is replaced by metaplastic columnar absorptive cells and goblet cells; these are usually small-intestinal in morphology although features of a colonic epithelium may be present. The development of atrophic gastritis and intesti- nal metaplasia is considered to be premalignant although the incidence of gastric cancer in gastric intestinal metaplasia is unknown and surveillance is not widely practised. In the Western world, histologic changes of chronic gas- tritis occur in up to 50% of the population in later life although the incidence of gastric cancer is falling, almost certainly due to the decreasing prevalence of H. Chronic gastritis rarely causes symptoms although it can be associated with nausea, vomiting and upper abdominal discomfort. Shaffer 143 In addition to elements of chronicity, gastritis can also be categorized on the basis of identifiable etiology (e. There are numerous causes of histologically diagnosed gastritis, and the importance of knowing the cause of the gastritis is to treat the underlying condition. It must be stressed that even when the cause of the gastritis is treated, such as in the person withy dyspepsia and a chronic H. The characteristic histo- logical finding is owl-eye, intranuclear inclusions in cells of the mucosal epithelium, vascular endothelium and connective tissue. At endoscopy, the gastric mucosa has a cobblestone appearance due to multiple superficial linear ulcers and small raised ulcerated plaques, while histology shows numerous cells with ground-glass nuclei and eosinophilic, intranuclear inclusion bodies surrounded by halos. Over time, the initial antral-predominant gastritis progresses to a pangastri- tis and then to atrophic gastritis and intestinal metaplasia precursors to the development of gastric cancer (the Correa hypothesis). Phlegmonous (suppurative) gastritis is a rare bacterial infection of the submucosa and muscularis propria and is associated with massive alcohol ingestion, upper respiratory tract infection, and immune compromise; it has a mortality rate in excess of 50%. Emphysematous gastritis, due to Clostridium welchii, may lead to the formation of gas bubbles, along the gastric contour on x-ray. Treatment requires gastric resection or drainage and high-dose systemic antibiotics. Mycobacterium tuberculosis gastritis is rare; ulcers, masses, or gastric outlet obstruction may be seen at endoscopy and biopsies show necrotizing granulomas with acid-fast bacilli. Mycobacterium avium complex gastritis is very rare, even in immunocompromised individuals; gastric mucosal biopsies show foamy histiocytes containing acid-fast bacilli. In actinomycosis, endoscopy may reveal appearances suggestive of a gastric malignancy; biopsies show multiple abscesses containing Actinomyces israelii, a gram-positive filamentous anaerobic bacterium. Parasitic causes of gastri- tis include Cryptosporidia, Strongyloides stercoralis, Anisakis (from raw marine fish), Ascaris lumbricoides and Necator americanus (hookworm). Endoscopic findings are non-specific and histology shows cell necrosis (apoptotic bodies intraepithelial vacuoles containing karyorrhectic debris and fragments of cytoplasm) in the neck region of the gastric mucosa. It is associated with other autoimmune disorders such as Hashimotos thyroiditis and Addisons disease. Mucosal atrophy, with loss of parietal cells, leads to decreased production of acid and intrinsic factor; about 10% of these patients develop low serum vitamin B12 levels and pernicious anemia. Chemical Gastropathy (Reactive Gastropathy) A number of different agents can produce gastric mucosal injury, characterized at endoscopy by hemorrhagic lesions and erosions (necrosis to the level of the muscularis mucosa) or ulcers (necrosis extending deeper than the muscularis mucosa). Portal hyper- tension produces a congestive gastropathy, with vascular ectasia but, again, only a minimal inflammatory infiltrate. Crohn disease of the stomach is uncommon, particularly in the absence of disease elsewhere in the gastrointestinal tract. Endoscopy may show mucosal reddening and nodules with or without overlying erosions and ulcers that may be elongated or serpiginous. Histological features include non-caseating granu- lomata, ulceration, chronic inflammation and submucosal fibrosis. Sarcoidosis of the stomach can be difficult to distinguish endoscopically and histologically from Crohn disease and the diagnosis must be based on the presence of other systemic features. Gastritis with Specific Diagnostic Features Collagenous gastritis has been reported in association with collagenous colitis and lymphocytic colitis; it is very rare. At endoscopy, non-specific findings include mucosal hemorrhages, erosions and nodularity while histology shows a chronic gastritis (plasma cells and intra-epithelial lymphocytes), focal atrophy and focal collagen deposition (2075 m) in the lamina propria. Histology shows an infiltrate of the lamina propria in the antrum or body by plasma cells, lymphocytes and rare neutrophils, and a marked intraepithelial infiltrate with T lymphocytes. Eosinophilic gastritis is associated with peripheral eosinophilia and eosinophilic infiltration of the stomach, involving one or more layers of the gastrointestinal tract (mucosa, muscle or subserosa).
During examination size cheap topiramate 200 mg with visa symptoms 4dp5dt fet, shape buy 100mg topiramate otc treatment kidney stones, symmetry and reaction to light should be noted on both eyes order topiramate 100 mg online medications vitamins. Occulocephalic reflex Oculocephalic reflex is elicited by moving the head from side to side or vertically with eyes held open discount 200mg topiramate medications 512. In comatose patient with intact brainstem o If the eyeballs move to the opposite direction of the head movementintact brainstem function (dolls eyes movement is positive. Caloric (occulovestibular) reflex o This test is performed by irrigating the ear with ice (cold) to stimulate the vestibular apparatus. It is lost if the reflex connections between the fifth (afferent) and the seventh (efferent) cranial nerves within the pons are damaged. Motor function /response Posture of the patient: o Quadriparesis and flaccidity: suggest pontine or medullary damage o Decorticate posturing: flexion of the elbows and the wrists with supination of the arms, and extension of the legs, suggests severe bilateral or unilateral hemispheric or diencephalic lesion (damage above the midbrain. Differential Diagnosis: Psychogenic Coma (hysteric coma): patient often has history of psychiatric illness, and non physiologic response on physical examination. Management Ideally the, care of comatose patient is started together with the initial assessment to identify the etiology. This treatment is given if hypoglycemia is even remote possibility, and thiamine is given with glucose in order to avoid eliciting Wernicke disease in malnourished o Naloxone(0. Seizure and Epilepsy Learning objectives: at the end of this lesson the student will be able to: 1. Definition: Seizure is a paroxysmal event due to abnormal excessive discharge of cerebral neurons. Depending on the distribution of the discharge, the manifestations may be: Motor Sensory Autonomic or Psychiatric manifestation. Epilepsy is a syndrome characterized by recurrent (two or more) unprovoked seizure attacks, due to a chronic, underlying process in the brain. This definition implies that a person with a single seizure, or recurrent seizures due to correctable or avoidable circumstances, does not necessarily have epilepsy. International classification of seizures: Epileptic seizures can be classified in many different ways. Commonly used classification is the one developed by International League against Epilepsy. This classification is useful in understanding underlying etiology, selecting appropriate treatment and understanding the prognosis of seizure type. Analysis of 468 epileptics seen in neurology clinics of Addis Ababa showed highest incidence in males aged 11-20 years. The commonest type of seizure was found to be grand mal seizure accounting for 60% of all cases. Etiology of seizure or risk factors: The causes of epilepsy/seizure are vary greatly in different age groups and across different regions of the world Idiopathic or cryptogenic: in which the cause is unknown, accounts for the majority. Partial Seizures: these are seizures, which arise from localized region of the brain. This seizure activity may spread over one side of the body (Jacksonian march) to involve larger body part. The patient is unable to respond appropriately to visual or verbal commands during the seizure, and has impaired recollection or awareness of ictal phase. These are usually tonic-clonic type and difficult to differentiate from primary generalized tonic-clonic seizure. Generalized seizures There are seizure disorders which arise from both cerebral hemispheres simultaneously, with without any detectable focal onset. After 10 20 seconds the tonic phase evolves to clonic phase characterized by bilateral jerking clonic movement involving the whole body. Patients gradually regain consciousness over minutes to hours, and during this transition there is typically a period of postictal confusion, headache, muscle ache and fatigue that can last for many hours. Complications Status epilepticus Accidents Hypoxic brain damage Mental retardation and impairment of intellectual function Sudden death Psychosocial (Social stigma). Diagnostic approach/Evaluation Patients history and physical examination can aid in the determination of whether or not a seizure or some other transient event was responsible for the patients symptoms History should include: - History of the event Presence of any prodromal symptoms Description of seizure by reliable observer 527 Internal Medicine Post ictal symptoms Urinary incontinence, myalgia and tongue bite or oral lacerations are clues to the proper diagnosis. Differential Diagnosis for Seizure Syncope Psychogenic seizure (hysteric conversion) Transient Ischemic attack Migraine 528 Internal Medicine Management: Goal of therapy: Complete control of seizure Prevent development of complications and socioeconomic consequences. Avoidance of precipitating factor Maintain normal sleep schedule Avoid taking excess alcohol Reduce stresses using, physical Exercise, meditation or counseling 3. General principles: An attempt is usually made to prevent subsequent seizure using a single agent, in order to limit side effects. The addition of a second drug is associated with worsening of adverse effects; hence care should be taken, before one decides to add a second drug to the original regimen. Phenytoin: is the usual prescribed as a second line drug in resource limited settings like ours mainly because of its availability and cost. It is often given for the treatment of partial seizure Dosage: a low initial dosage with gradual increase is advised. Side effects Aplastic anemia Dizziness drowsiness 531 Internal Medicine Skin rash Transient diplopia When to stop antiepileptic drugs? The more severe and long lasting a patients active epilepsy before remission, the greater the risk of relapse. When to refer patients to a neurologist or tertiary level hospital Failure to respond to treatment Recurrence of previously controlled seizure Change in clinical pattern of seizure Appearance of previously absent symptoms/sign Development of side effects of a drug 4. Surgical interventions include Temporal lobe resection Corpus callosum sectioning Status epilepticus A condition characterized by continuous or repetitive discrete seizure with impairment of consciousness during interictal period, which lasts for more than 30 minutes. Patients may have mild clonic movement of only the fingers, or fine, rapid movement of the eyes. Complications of Status epilepticus: Aspiration Hypoxia Metabolic acidosis Hypotension Hyperthermia Rhabdomyolysis and associated myoglobinuria Multiple physical injures including vertebral bone fracture Irreversible neuronal injury Management 1. Parkinsons Diseases and other movement disorders Learning objectives: at the end of this lesson the student will be able to: 1. Parkinsonism: Definition: Parkinsonism is a clinical syndrome characterized by:- Bradykineisa: slowness and paucity of movement Tremor: This occurs at rest Rigidity Snuffling gate and Flexed posture Etiologies: 1. These degenerative changes are believed to be due to accumulation of the presynaptic protein -synuclien. Bradykinesia/akinesia: It is the most disabling feature which interferes with all aspects of daily living. Patients have trouble in walking, rising from seated position, turning over in bed, dressing etc. Brief regular interruption of resistance during passive movement may give rise tocogwheels rigidity. Pharmacotherapy of motor symptoms: Therapy to control motor symptoms should be initiated as soon as the patients symptoms begin to interfere with the quality of life. This drug has minimal effect on symptoms when used as monotherapy or as an adjuvant to Carbidopa/levodopa. Advanced Therapy c) Levodopa/Carbidopa Formulation (Sinemet, Atamet) Levodopa: is converted to dopamine by presynaptic neuron and therefore increase the amount of neurotransmitter available to the post synaptic dopamine receptor. Some of the neuroprotecitve treatment trails arte Non steroidal anti-inflammatory agents Estrogens replacement therapy in post menopausal women Selegilline therapy delays the need for levodopa therapy by 9 -12 months in newly diagnosed patients. Studies demonstrated that patients who remain on Selegilline for 7 yrs experienced slower motor decline. Therapy of non motor symptoms Insomnia due to nocturnal akinesia : treated with night time supplemental dose of Carbidopa /levodopa Depression : Responds to anti depressants like Amitriptyline Psychotic patients: first remove anticholinergics and amantadine if the patient is taking.
Management r Any underlying electrolyte disturbance should be identied and managed purchase topiramate 200 mg on-line symptoms 4 weeks. It is now customary to use these in patients Denition known to have a high risk of sudden cardiac death cheap topiramate 100mg on line medicine zocor. Chaoticelectromechanicalactivityoftheventriclescaus- ing a loss of cardiac output buy 100 mg topiramate free shipping symptoms for diabetes. Conduction disturbances Incidence The most common cause of sudden death and the most Atrioventricular block common primary arrhythmia in cardiac arrest cheap topiramate 200 mg free shipping medications zetia. Atrioventricular or heart block describes an alteration in the normal pattern of transmission of action poten- Aetiology tials between the atria and the ventricles. Pathophysiology r complete failure of transmission (third-degree heart The underlying electrical activity consists of multiple ec- block). First degree atrioventricular block Denition Clinical features Atrioventricular block describes an alteration in the The clinical picture is of cardiac arrest with loss of ar- transmission of action potentials between the atria and terial pulsation, loss of consciousness and cessation of the ventricles. Management r Early debrillation is the most important treatment, as the longer it is delayed the less likely reversion to Clinical features sinus rhythm is possible. Patients are usually asymptomatic; however, an irregular pulse is detected on examination. Most commonly every third or fourth atrial Management beat fails to conduct to the ventricle. Ventricular escape may be required either as a temporary measure or beats may be seen. Patients are at risk of progression to third degree heart block, which may present as cardiac syncope. If patients do not return to sinus rhythm or if not associated with myocardial infarction permanent Incidence pacing is indicated. Third degree heart block is complete electrical dissocia- tion of the atria from the ventricles. It may also occur following Cardiac failure, StokesAdams attacks, asystole, sudden a massive anterior myocardial infarction and is a sign cardiac death. Rare r In acute complete heart block, intravenous isopre- causes include drugs, post-surgery, rheumatic fever naline or a temporary pacing wire may be used. Block of conduction in the left branch of the bundle of r Broad complex disease is due to more distal disease of His, which normally facilitates transmission of impulses the Purkinje system. The pacing thus arises within the to the left ventricle myocardium giving an unreliable 1540 bpm rate. In the elderly causes include brosis of the central bundle branches (Lenegres disease). Clinical features Clinical features r Severity of symptoms is dependent on the rate and re- Most patients are asymptomatic but reversed splitting of liability of the ectopic pacemaker, and whether or not the second heart sound may be observed. Symptoms include those of cardiac block the second heart sound is split on expiration, be- failure, dizziness and StokesAdams attacks (syncopal cause left ventricular conduction delay causes the aortic episodes lasting 530 seconds due to failure of ven- valvetocloseafterthepulmonaryvalve. Acute left bundle branch block may be a caused by ischaemic heart disease, brosis of the bundles sign of acute myocardial infarction (see pages 3739). Acute onset right bundle branch block may be associated with pulmonary embolism or a Complications rightventricular infarct. Clinical features Management Right bundle branch block is asymptomatic and is often Treatment is not necessary. There is widened splitting of the heart sounds with the pulmonary sound occurring later Right bundle branch block than normal. Denition Investigations Block to the right branch of the bundle of His, which The characteristic RsR is seen best in lead V1 and a normally facilitates transmission of impulses to the right late S wave is seen in V6. Aetiology/pathophysiology Right bundle branch block is often due to a congenital abnormality of little signicance, but may be associated Complications withatrialseptaldefects. Management ing in a failure to maintain sufcient cardiac output to Treatment is not necessary. The clinical syndrome of heart failure is characterised by breathlessness, fatigue Prognosis and uid retention. Isolated right bundle branch block, particularly in a young person is generally benign. Concomitant left or Prevalence/incidence severe right axis deviation may indicate block in one of 900,000 cases in the United Kingdom; 14 cases per 1000 the fascicles of the left bundle, which can occur as a pre- population per annum. Cardiac failure Aetiology The most common cause of heart failure in the United Heart failure Kingdom is coronary artery disease (65%). Causes in- Denition clude Heart failure is a complex syndrome that can result from r myocardial dysfunction, e. In myocardial dysfunction there is an inability of the normal compensatory mechanisms to maintain cardiac Left-sided heart failure r Causes include myocardial infarction, systemic hyper- output. These mechanisms include r FrankStarling mechanism in which increased tension, aortic stenosis/regurgitation, mitral regurgi- preloadresultsinanincreaseincontractilityandhence tation, cardiomyopathy. It can be acutely Congestive cardiac failure is the term for a combination symptomatic when lying at (orthopnea) or at night of the above, although it is often arbitrarily used for any (paroxysmal nocturnal dysnoea) due to redistribution symptomatic heart failure. Chronic pul- Clinically it is usual to divide cardiac failure into symp- monary oedema results in dilation of the pulmonary toms and signs of left and right ventricular failure, al- veins particularly those draining the upper lobes (up- though it is rare to see isolated right-sided heart failure perlobe vein diversion), pleural effusions and Kerley except in chronic lung disease. Anticoagulation should be con- r Echocardiography is used to assess ventricular func- sidered in atrial brillation or with left ventricular tion. Echocardiographycanalsoshowany patients with severe left ventricular dysfunction sec- underlying valvular lesions as well as demonstrating ondary to ischaemic heart disease. Patientsshouldbeadvisedtostopsmokingandreduce Acute pulmonary oedema alcohol and salt intake. Patients with evidence of Fluidaccumulationwithintheinterstitiallungtissueand uid overload should restrict their uid intake to 1. These should be used in conjunction with a tion in patients with cardiac failure who have chronic diuretic if there is any evidence of peripheral oedema. There is an acute accumulation of uid inhibitors, -blockers and diuretics in patients who in the alveoli. They should be started at low dose and Patients develop acute severe dysnoea at rest, hypox- increased gradually. There may be wheeze and cough pro- r low-dose spironolactone, which improves progno- ductive of frothy pink sputum. On auscultation crepitations may be itoring of renal function and potassium levels. In acute pul- can aggravate myocardial ischaemia and cause further monary oedema there may be bat wing or ground reductionincardiac output. Aminophylline infusion can be considered if there is r Cardiac inotropes are usually necessary to maintain bronchoconstriction. If patient is hypertensive hydralazine or diazoxide (ar- r Any cardiac arrhythmia should be corrected and terial dilators) can be used to reduce cardiac afterload angioplasty considered in patients with cardiogenic and hence increase stroke volume. Any underlying problem such as arrhythmia should r Intra-aortic balloon pumping may be instituted but it be corrected. Severe circulatory failure resulting from a low cardiac output usually characterised by severe hypotension. Aetiology This is an extreme type of acute cardiac failure the most common cause of which is myocardial infarction. Pathophysiology Cardiogenic shock is severe heart failure despite an ad- equate or elevated central venous pressure, distinguish- Incidence ing it from hypovolaemic or septic shock.
Macroscopy Bilateral adrenocortical hyperplasia twice the size of Pathophysiology normal purchase topiramate 100 mg without prescription medications zoloft side effects, with thickening of zona reticularis and the r The mineralocorticoids (90% activity by aldosterone trusted topiramate 100mg symptoms with twins, zona fasciculata purchase topiramate 100mg on line my medicine. The zona glomerulosa appears normal buy 100 mg topiramate free shipping treatment junctional rhythm, some by cortisol) act on the kidneys to conserve because mineralocorticoid production is controlled pri- + + sodium by increasing Na /K exchange in the dis- marily by the reninangiotensin system. In Addisons dis- ease, gradual loss of these hormones causes increased Microscopy sodium and water loss with a consequent decrease in The pituitary tumour is normally a microadenoma. Irradiationisusedpost-surgery,forpatientswhere cytomegalovirus complete resection was not possible. Drugs which in- Autoimmune hibit adrenal cortisol synthesis are often used as adjunc- Vascular haemorrhage (associated with meningococcal tivetherapy,e. Their disadvantage is that they increase thrombosis Neoplastic secondary carcinoma (e. Failure to exchange Na+ samples over a 24-hour period is used to distinguish for H+ ions can lead to a mild acidosis. Reduced cortisol may lead to symptomatic hy- Chronic adrenal insufciency is treated with glucocor- poglycaemia. Par- pituitary, other hormones are also secreted such as enteral steroids are needed if vomiting occurs. It Examination reveals weight loss, hyperpigmentation may also be caused acutely by bilateral adrenal haemor- especially in mouth, skin creases and pressure areas. Addisonian crisis may also occur on cessation of gluco- corticoid treatment including inhaled glucocorticoids in Complications children. Pathophysiology In adrenal failure, there is no glucocorticoid response to Investigations stress. If exogenous high-dose steroids are not provided r Hyponatremia, hyperkalemia and a hyperchloraemic the condition is fatal. Clinical features r Screening can be performed by measurement of early The patient is ill with anorexia, vomiting and abdominal morning cortisol and 24 hour urinary cortisol. A long Synac- r U&Es (hyponatraemia, hyperkalaemia and hyper- then test using a depot injection and repeated cortisol chloraemia). The r Denitive investigations should not delay treatment, muscle weakness may present with paralysis. Polydipsia steroids will not interfere with test results in the short- and polyuria may be a feature. Macroscopy/microscopy Management Adrenal cortical adenomas are well-circumscribed, yel- Immediate uid resuscitation with 0. Intravenous hy- Adrenal cortical carcinomas are larger, with local inva- drocortisone and broad-spectrum antibiotics are given. In hyperplasia, the glands Any underlying causes need to be identied and appro- are enlarged, with increased number, size and secretory priately managed. Hypokalaemia may lead to a mild metabolic alkalosis (H+/K+ ex- Conns syndrome change in the kidney). However, the use of diuretics Denition to treat hypertension may mimic or mask these fea- Conns syndrome is a condition of primary hyperaldos- + tures. If negative, selective In the remainder, there is diffuse hyperplasia of the zona blood sampling may be required to nd the source of glomerulosa. Raised aldosterone is much more commonly a physiological response to reduced renal perfusion as in Management renal artery stenosis or congestive cardiac failure. Bilateral adrenal hyperplasia is usually treated with spironalactone (inhibits the Na+/K+ pump, i. Ade- Aldosterone is the most important mineralocorticoid nomas and carcinomas should be removed surgically. K+ pump in renal tubular epithelial cells in the collecting tubules, distal tubule and collecting duct increasing the absorption of sodium and hence water with increased Prognosis loss of potassium. The rise in blood volume increases re- 30% have persistent hypertension after treatment, nal perfusion and arterial blood pressure. The paroxysmal secretion of Age the hormones may mean repeated measurements are Peak age 4060 years. M = F Management r Surgical excision where possible is the treatment of Aetiology Associated with the Multiple Endocrine Neoplasia choice. The blood pres- with von Hippel-Lindau syndrome, neurobromatosis, sure must be carefully monitored and any rise coun- tuberose sclerosis and the Sturge-Weber syndrome. Pathophysiology r Adrenergic blockade is necessary to oppose the cate- 10% of cases are malignant, 10% are extra-adrenal and cholamine effects before surgery. The adrenal medulla is functionally (an -receptor antagonist) is used initially, followed related to the sympathetic nervous system, secreting by -blockade with propanolol. There is decreased blood supply to the gut, increased Prognosis sphincter activity and metabolic effects, such as diabetes 10% of phaechromocytomas are malignant these have a and thyrotoxicosis. They are found to be hypertensive Adrenalectomy which may be paroxysmal or continuous. Other signs in- Surgical removal of the adrenal glands may be neces- clude pallor, dilated pupils and tachycardia. Large be a postural hypotension secondary to volume deple- tumours, which may be malignant, are removed via a tion. Phaeochromocytoma may present in pregnancy, or with sudden death following trauma or surgery. Bilateral adrenalectomy Bilateral tumours Nodular hyperplasia (causing Cushings or Complications Conns syndrome) Cushings syndrome if Cardiovascular disease or cerebral haemorrhage. Persis- pituitary treatment fails tent hypertension causes hypertensive retinopathy. Lifelong corticosteroid (both glucocorticoid and mineralocorticoid with hydrocortisone and udocorti- sone) replacement therapy is needed following bilateral Increased blood volume adrenalectomy. Increased glomerular filtration rate Replacementismonitoredbybloodpressuremeasure- ment, serum electrolytes and patient well-being. Stress, infection and surgery may all increase corticosteroid re- Continued water reabsorption leads to quirements, and may precipitate an Addisonian crisis production of highly concentrated urine (see page 441). Patients need to be advised of the signs and symptoms and management of such events. Hyponatraemia, low plasma osmolality Thirst axis Shift of fluid from extracellular space into cells e. It acts on the collecting tubules in the kidney to make them more Aetiology permeable to water molecules. There may be muscle twitching Infective Meningitis, encephalitis with an extensor plantar reex. Metabolic Hypokalaemia, hypercalcaemia If water intoxication is severe, diuretics with hypertonic Drugs Lithium, demeclocycline saline infusion is used. Any underlying cause should be Kidney disease Post-obstructive uropathy Chronic kidney diseases Pyelonephritis, polycystic kidneys, identied and treated. Denition Polyuria, thirst & polydipsia resulting from deciency of Complications or resistance to antidiuretic hormone (vasopressin). If left untreated there is progression Aetiology to severe irreversible brain damage and cerebral vessels Diabetes insipidus results from either a deciency in may tear causing intracranial haemorrhage (see page 3). In the water deprivation test the patient is weighed, crease water reabsorption preventing plasma osmolality plasma and urine osmolality measured, then they are fromrising. Lackofvasopressin,orrenalresistancetova- deprived of uid for 8 hours under constant supervision. Unless the thirst centre is also impaired, ris- by >3%, if plasma osmolality exceeds 300 mmol/kg, ing osmolality stimulates thirst and the person drinks or if the urine:plasma osmolality ratio remains <1. Management Age Any underlying cause should be sought and treated if Increases with age. Sex 24F : 1M Aetiology Disorders of the parathyroids Neoplasia of the parathyroid gland(s). There are thought to be genetic and environmental predisposing factors in- Hyperparathyroidism cludingafamilyhistoryofMultipleEndocrineNeoplasia (see page 450) and neck irradiation.
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