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The staging of Hodgkin’s’s disease is accord- ing to the Ann Arbor system cheap 50 mg viagra professional amex erectile dysfunction groups in mi, which is sufﬁxed by B if Chronic myelogenous Leukaemia Bsymptoms are present and A if they are absent (see See Myeloproliferative disorders page 482 discount 100 mg viagra professional with mastercard erectile dysfunction middle age. Microscopy Non-Hodgkin’s lymphoma Classical Reed-Sternberg cells are large cells with a pale cytoplasm and two nuclei with prominent nucleoli said Deﬁnition to resemble owl eyes. Incidence r Mixedcellularity disease which mainly affects older 20 per 100,000 per year. Tumours arise due therapy or a combination depending on the stage of to multiple genetic lesions affecting proto-oncogenes Table12. Clinical features r Indolent: Most patients present with painless slowly Prognosis progressive lymphadenopathy. Lymph nodes may re- Indolent lymphomas have a predicted median survival duce in size spontaneously making it difﬁcult to dis- time of 5–10 years. B symp- ◦ sponsive to chemotherapy but have a predicted median toms (fever >38 C, drenching night sweats, weight survival 2–5 years. On Paraproteinaemias examination there is lymphadenopathy and hep- atosplenomegaly. The cells are trophic to the skin particularly the hands and feet, and result Age in plaques and lumps of associated with generalised Most commonly diagnosed 60–65 years. Gas- trointestinallymphomaisparticularlycommoninthe Pathophysiology MiddleEastandisalsoseeninassociationwithcoeliac There is expansion of a single clone of plasma cells that disease. Cleavage of these immunoglobulins tribution according to the Ann Arbor system, which result in the production of Fab and Fc fragments; the Fab is sufﬁxed by B if B symptoms are present (see fragment is termed the Bence-Jones protein and is found Table 12. Investigations There is also production of osteoclast stimulation fac- Thediagnosisismadebylymphnodebiopsy,cytogenetic tor causing lytic bone lesions, bone pain and hypercal- studies of lymphoma cells may give prognostic informa- caemia. Chapter 12: Paraproteinaemias 491 Clinical features Age r Marrow inﬁltration results in anaemia, thrombocy- Onset most commonly aged 60 years. Spinal cord compression occurs in approx- imately 10–20% of patients at some time during Pathophysiology the course of disease. Hypercalcaemia causes thirst, The abnormal proliferation of lymphoplasmacytoid polyuria, constipation and abdominal pain. Investigations The diagnosis of myeloma is made if there are: Clinical features r Bone marrow aspirate has at least 10–15% plasma Hyperviscosity presents as weakness, tiredness, confu- cells. Patients also often have peripheral lymphadenopa- Other investigations include: thy. Chemotherapy with single alkylating agents improves r Protein electrophoresis shows an IgM parapro- prognosis. Recently, thalidomide has been demonstrated to produce a signiﬁcant response Management in 30% of patients whose disease progressed following Chemotherapy produces a variable response. Supportive care includes blood transfu- pheresis is used for symptomatic hyperviscosity. Unlike multiple myeloma there are preserved levels of 492 Chapter 12: Haematology and clinical immunology normal immunoglobulins, no lytic bone lesions and no Age renal failure. Investigations Sex Electropheresis of serum protein demonstrates a raised X linked; males only affected. Aetiology Mutations on the X chromosome including deletions, Management frame shifts and insertions. One third of cases are new Aproportionofpatients will go on to develop multi- mutations. Clinical features Type 1 and 2 causes mild disease with bleeding following Investigations injury, menorrhagia and epistaxis. Type 3 causes spon- r Activated partial thromboplastin time is raised, but taneous bleeding from early life. Clinical features Investigations Similar to haemophilia A with mild deﬁciency causing r Coagulation studies reveal prolonged clotting times only bleeding post surgery and trauma. Activated partial thromboplastin time is raised, but correctablewith50%normalserum(i.
Clindamycin and anti-toxin therapies for toxic shock syndromes with refractory hypotension (grade 2D) cheap viagra professional 50 mg visa erectile dysfunction doctors huntsville al. Clostridium diffcile colitis should be treated with enteral antibiotics if tolerated discount 100 mg viagra professional free shipping erectile dysfunction and diabetes ppt. In the industrialized world with access to inotropes and mechanical ventilation, initial resuscitation of hypovolemic shock begins with infusion of isotonic crystalloids or albumin with boluses of up to 20 mL/kg crystalloids (or albumin equivalent ) over 5–10 minutes, titrated to reversing hypotension, increasing urine output, and attaining normal capillary refll, peripheral pulses, and level of consciousness without inducing hepatomegaly or rales. If hepatomegaly or rales exist then inotropic support should be implemented, not fuid resuscitation. In non-hypotensive children with severe hemolytic anemia (severe malaria or sickle cell crises) blood transfusion is considered superior to crystalloid or albumin bolusing (grade 2C). Begin peripheral inotropic support until central venous access can be attained in children who are not responsive to fuid resuscitation (grade 2C). Patients with low cardiac output and elevated systemic vascular resistance states with normal blood pressure be given vasodilator therapies in addition to inotropes (grade 2C). Timely hydrocortisone therapy in children with fuid refractory, catecholamine resistant shock and suspected or proven absolute (classic) adrenal insuffciency (grade 1A). Protein C and Activated Protein Concentrate No recommendation as no longer available. During resuscitation of low superior vena cava oxygen saturation shock (< 70%), hemoglobin levels of 10 g/dL are targeted. After stabilization and recovery from shock and hypoxemia then a lower target > 7. Use plasma therapies in children to correct sepsis-induced thrombotic purpura disorders, including progressive disseminated intravascular coagulation, secondary thrombotic microangiopathy, and thrombotic thrombocytopenic purpura (grade 2C). We recommend use of sedation with a sedation goal in critically ill mechanically ventilated patients with sepsis (grade 1D). Monitor drug toxicity labs because drug metabolism is reduced during severe sepsis, putting children at greater risk of adverse drug-related events (grade 1C). Glucose infusion should accompany insulin therapy in newborns and children because some hyperglycemic children make no insulin whereas others are insulin resistant (grade 2C). Enteral nutrition given to children who can be fed enterally, and parenteral feeding in those who cannot (grade 2C). We recommend evaluating for and reversing pneumotho- lead to worsening shock if the patient is not volume loaded. In rax, pericardial tamponade, or endocrine emergencies in those who desaturate despite administration of face mask oxy- patients with refractory shock (grade 1C). Endocrine emergencies include hypoadrenal- can be used to increase functional residual capacity and reduce ism and hypothyroidism. In select patients, intra-abdominal the work of breathing, allowing for establishment of intrave- nous or intraosseous access for fuid resuscitation and periph- hypertension may also need to be considered (513–515). Antibiotics and Source Control is associated with increased mortality in children with menin- 1. We recommend that empiric antimicrobials be adminis- gococcal sepsis because of adrenal suppression effect (504, 505). Because attainment of central access is more diffcult in chil- tered within 1 hr of the identifcation of severe sepsis. Blood dren than adults, reliance on peripheral or intraosseous access cultures should be obtained before administering antibiot- can be substituted until and unless central access is available. We suggest that the initial therapeutic endpoints of resuscita- epidemic and endemic ecologies dictate (eg, H1N1, meth- tion of septic shock be capillary refll of ≤ 2 s, normal blood icillin-resistant S. Thereafter, ScvO2 saturation greater than or equal to 70% and cardiac index Rationale. Antimicrobials can be given intramuscularly or orally (if tolerated) until intravenous line Rationale. We suggest the use of clindamycin and antitoxin therapies ScvO2 and cardiac index, the specifc choice is left to the practi- for toxic shock syndromes with refractory hypotension tioner’s discretion (506–512). Children are more prone to toxic shock than Care Medicine-Pediatric Advanced Life Support guidelines adults because of their lack of circulating antibodies to toxins. The recommended guidelines are summarized toxic shock should be treated with clindamycin to reduce in Figure 2 (510–512).
There ought to be a good physiological reason to exclude her from having the tests based on the results from a study of men 100 mg viagra professional overnight delivery erectile dysfunction medications that cause. However order 100mg viagra professional otc erectile dysfunction drugs rating, each physician must use their best clini- cal judgment to be able to determine whether the results of the study can be used in a given individual patient. Other factors which might affect the characteristics of the test in a single patient, include age and ethnic group. How do the capabilities of the lab or diagnostic center that one is working in compare with the one described in the study? This is a function of the type of equipment used and the operator-dependency of the test. Some very sophisti- cated and complex tests may only be available at referral or research centers and not readily available in the average community hospital setting. The estimated costs of false positive and false negative test results should be addressed, includ- ing the cost of repeat testing or further diagnostic procedures for false positive results and of a missed diagnosis due to false negative results. The cost of the test should be given, as well as the cost of following up on false positive tests and missing some patients with false negative tests. This could include the cost of malpractice insurance and payment of awards in cases of missed disease. This is very complex since the notion of negligence in missing a diagnosis depends more on one’s pretest probability of disease and how one handles the occurrence of a false negative test. This was addressed earlier, and although small deviations from the true pretest probability are not important, large variations are. If the physician estimates that the patient has a 10% probability of disease and the true probability of disease is 90%, this will seriously and adversely decrease the ability to diagnose the prob- lem. Data on pretest probability come from several sources including published studies of symptoms, one’s personal experience, the study itself, if the sample is reasonably representative of the population of patients from which one’s patient comes, and clinical judgment based on the information that is gathered in the history and physical exam process. If none of these gives a reasonable pretest probability, consider getting some help from an expert consultant. Most reasonable and prudent physicians will agree on a ballpark ﬁgure, high, medium, or low, for the pretest probability in most patient presentations of illness. This will happen after a test is studied in one group of patients, usu- ally those with more severe or classical disease and then extended to patients with lower pretest probability of disease. As the test gets marketed and put into widespread clinical use, the type of patient who gets the test tends to be one with a lower and lower pretest probability of disease and eventually, the test is frequently done in patients who have almost zero pretest probability of disease. However, physicians are especially cautious to avoid missing anyone with a dis- ease in the fear of being sued for malpractice. However, they must be equally cautious about over-testing those patients with such low probability of disease in whom almost all positive tests will be false positives. This is probably the most important question to ask about the usefulness of a diagnostic test, and will determine whether the test should or should not be done. Will the resulting post-test probabil- ity move the probability across the testing or treatment threshold? If not, either do not do the test, or be prepared to do a second or even a third test to conﬁrm the diagnosis. Next, is the patient interested in having the test done and are they going to be “part of the team? Give the information to the patient in a manner they can understand and then ask them if they want to go through with the testing. They ought to understand the risks of disease, and of correct and incorrect results of testing, and the ramiﬁcations of a positive and negative test results. The decision making for this problem is very complex and should be done through careful consideration of all of the options and the patients’ situation such as age, general health, and the presence of other medical conditions. Finally, how will a positive or negative result help the patient reach his or her goals for treatment? If the patient has “heartburn” and you no longer sus- pect a cardiac problem, but suspect gastritis or peptic ulcers, will doing a test for Helicobacter pylori infection as a cause of ulcers and treatment with speciﬁc anti-microbial drugs if positive, or symptomatic treatment if negative, satisfy the patient that he or she does not have a gastric carcinoma? If not, then endoscopy, Sources of bias and critical appraisal of studies of diagnostic tests 309 the gold standard in this case, ought to be considered without stopping for the intermediate test.
Patients are at risk of secondary The management of hyperlipidaemia is based on an as- infection cheap viagra professional 50 mg line erectile dysfunction options. Management r General measures include weight loss buy viagra professional 100 mg on-line erectile dysfunction pills from india, lipid-lowering r Prevention of eye disease with adequate diet and diets, reduction of alcohol intake, stopping smoking supplementation in patients with disorders of fat and increasing exercise. In pregnant women, vitamin A but not r Control of hypertension is important preferably β carotene is teratogenic. Corneal transplant may be required 1 Cholesterol-lowering drugs include resins, which for irreversible corneal ulceration. Vitamin B1 (thiamine) deﬁciency Vitamin deﬁciencies See also Wernicke–Korsakoff syndrome in Chapter 7 (Nervous System; page 317) Vitamin A deﬁciency Deﬁnition Deﬁnition Deﬁciency of thiamine (vitamin B1). Deﬁciency of vitamin A, a fat-soluble vitamin, is a major cause of blindness in many areas of the world. Aetiology Insufﬁcient intake of thiamine, which is present in for- Aetiology tiﬁed wheat ﬂour (the natural thiamine is removed by Insufﬁcient intake of carotenoids, especially β-carotene milling, so it is replaced in most countries), fortiﬁed found in carrots and dark green leafy vegetables and breakfast cereals, milk, eggs, yeast extract and fruit. Occasionally it can be seen in disorders of fat malabsorption, such as cystic ﬁbrosis, cholestatic Pathophysiology liver disease and inﬂammatory bowel disease. Thiamine is an essential factor for the maintenance of the peripheral nervous system and the heart. It is also involved in glycolytic pathways, mediating carbohydrate Pathophysiology metabolism. Vitamin A is required for maintenance of mucosal sur- faces, the formation of epithelium and production of Clinical features mucus. Dry beriberi is an endemic form of polyneuritis re- Retinal function is dependent on retinol, a constituent sulting from a diet consisting of polished rice deﬁcient of the retinal pigment rhodopsin. The neuropathy predominantly affects the 512 Chapter 13: Nutritional and metabolic disorders legs with weakness, parasthesia and loss of ankle jerks. Wet beriberi is the high output heart failure caused by thiamine deﬁciency resulting in Management oedema. Supplementation with nicotinic acid and treatment of other coexisting deﬁciencies. Erythrocyte transketolase activity and blood pyruvate Vitamin B6 (pyridoxine) deﬁciency are increased. Deﬁnition Deﬁciency of pyridoxine is rarely a primary disorder, but Management it does occur as a secondary disorder. The cardiac failure usually responds rapidly, but Aetiology neuropathies may only partially resolve if they are long- Important sources of Vitamin B6 are similar to those of standing. Deﬁciency may occur with malabsorp- Niacin deﬁciency (pellagra) tion such as coeliac disease, dietary lack in alcoholism and drug toxicity especially isoniazid. Deﬁnition Niacin (vitamin B3) has two principle forms: nicotinic Pathophysiology acid and nicotinamide. Deﬁciency of niacin causes pel- Pyridoxine is important in the metabolism of amino lagra. In some rare metabolic disorders, pyridoxine deﬁciency is as- Aetiology sociated with infantile convulsions and sideroblastic Niacin is found in plants, meat and ﬁsh. Clinical features Othercausesincludeincreasedtryptophanconsumption Marginal deﬁciency may cause stomatitis, glossitis, dry in the carcinoid syndrome, prolonged use of isoniazid lips, irritability and confusion. Deﬁciency causes men- and Hartnup disease, an autosomal recessive congenital tal confusion, glossitis, dry skin lesions and peripheral disorder with reduced absorption of tryptophan from neuropathy. Management Pathophysiology Oral replacement; however, high doses may cause Nicotinic acid is involved in energy utilisation. Vitamin B12 deﬁciency It is also used in maintaining skin, especially in sun- exposed areas. Vitamin C deﬁciency Clinical features Pellagra is due to lack of nicotinic acid, it often occurs Deﬁnition as part of a more general nutritional deﬁciency. Pellagra Vitamin C deﬁciency causes scurvy, which was ﬁrst de- presents with dermatitis, diarrhoea and dementia. Chapter 13: Metabolic disorders 513 Aetiology/pathophysiology tably in the brain in Alzheimer’s disease. Genetic factors Occurs in the poor, pregnant or those on a peculiar may be involved in predisposing to the development of diet. Vitamin C ﬁbrillogenesis and amyloidosis: (ascorbic acid) is found in citrus fruits, potatoes, green r Geneticmutationsresultinginproteinswithincreased vegetables and fortiﬁed fruit drinks.
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