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The radionuclide liver-spleen scan can be a useful imaging modality when searching for an accessory spleen cholesterol medication side effects buy 10 mg zetia fast delivery. Hereditary elliptocytosis comprises a family of inherited hemolytic anemias caused primarily by defects in one or more of the proteins that make up the two-dimensional membrane skeletal network cholesterol levels hdl vs ldl order zetia without a prescription. The four clinical phenotypes of hereditary elliptocytosis appear to be caused by different 871 sets of molecular defects cholesterol lowering foods fish zetia 10 mg with mastercard. Mild hereditary elliptocytosis and hereditary pyropoikilocytosis arise most often from alpha- and/or beta-spectrin chain defects that affect the ability of spectrin heterodimers to self-associate cholesterol medication causing dementia zetia 10mg line, and from protein 4. Spherocytic hereditary elliptocytosis can be caused by defects in the beta-chain of spectrin that may affect spectrin-ankyrin binding as well as spectrin self-association; other mutations are the subject of current investigation. In general, mild hereditary elliptocytosis and spherocytic hereditary elliptocytosis are inherited as autosomal dominant traits, and hereditary pyropoikilocytosis is inherited in an autosomal recessive pattern. The incidence of mild hereditary elliptocytosis is about 1 in 2500 among northern Europeans and as common as 1 in 150 in some areas of Africa, although the disease can occur in any population. Hereditary pyropoikilocytosis and spherocytic hereditary elliptocytosis are considerably more rare. In mild hereditary elliptocytosis, a molecular defect near the "head" region of the spectrin heterodimer. In both cases, red cells are released from the bone marrow with a normal discocytic shape, but the membrane skeletons (and consequently, the red cells themselves) undergo plastic deformation to a permanent elliptocytic shape as the cells traverse the microcirculation. Because the "vertical" interactions that couple the membrane skeleton to the overlying lipid bilayer remain intact in these cells, membrane loss does not occur, and the cells may have a relatively normal lifetime in the circulation. Hereditary pyropoikilocytosis, in contrast, results from either a homozygous or a compound heterozygous defect in spectrin (typically, alpha-spectrin) or protein 4. When paired in trans with an alpha-spectrin coding region mutation, however, the polymorphism causes the majority of spectrin heterodimers at the membrane to carry the hereditary elliptocytosis defect, which leads to the much more severe hereditary pyropoikilocytosis phenotype. In spherocytic hereditary elliptocytosis, the molecular defect in the spectrin beta-chain appears to affect both "horizontal" interactions at the spectrin self-association site and "vertical" interactions at the spectrin-ankyrin binding site. This combined defect results in features of both hereditary elliptocytosis (because of the "horizontal" interaction defect) and hereditary spherocytosis (because of the "vertical" interaction defect). The great majority of individuals with mild hereditary elliptocytosis are heterozygous carriers of a dominantly inherited molecular and cellular defect that is clinically insignificant. These individuals have no anemia, little or no hemolysis (reticulocyte count, 1 to 3%), and no splenomegaly. Diagnosis is based on the presence of prominent elliptocytosis (often greater than 40%) on the blood smear, a normal osmotic fragility test, and a positive family pedigree. Mild hereditary elliptocytosis can be associated with significant hemolysis in patients in whom splenic enlargement develops from, for example, viral infection or portal hypertension. Neonates with mild hereditary elliptocytosis often exhibit a syndrome, called transient infantile poikilocytosis, characterized by a moderately severe hemolytic anemia for the initial 6 to 12 months of life. Elevated levels of this normal metabolite weaken the ternary spectrin-actin-protein 4. Hereditary pyropoikilocytosis is a recessively inherited disorder that is clinically manifested by a severe (sometimes life-threatening) hemolytic anemia in which the blood smear contains bizarre poikilocytes and red cell fragments. The mean cell volume is markedly decreased (45 to 75 fL), and because spectrin deficiency and spherocytosis are often secondary consequences of the combined molecular defects, osmotic fragility is increased. The name is derived from the property of hereditary pyropoikilocytosis red cells to fragment at 45 to 46°C rather than the normal 49°C; this abnormal heat sensitivity is most often due to a lowering of the temperature at which the mutant spectrin chains denature. As implied by the name, spherocytic hereditary elliptocytosis has clinical and diagnostic features of both hereditary spherocytosis and mild hereditary elliptocytosis. Patients manifest mild to moderate hemolytic anemia with splenomegaly and intermittent jaundice, the blood smear contains rounded elliptocytes and sometimes spherocytes, and osmotic fragility is increased. Spherocytic hereditary elliptocytosis should be treated like hereditary spherocytosis, with the considerations for and against splenectomy as noted above. Virtually all patients with hereditary pyropoikilocytosis require splenectomy, which ameliorates but does not completely cure the hemolytic anemia. As in treating patients with moderate to severe hereditary spherocytosis, it is important to defer splenectomy until 3 to 5 years of age if possible, especially because of the possibility that a severe poikilocytic anemia in the neonatal and infant period could represent transient infantile poikilocytosis rather than true hereditary pyropoikilocytosis. The hallmark of this rare autosomal dominant disorder is an alteration in red cell membrane cation permeability that leads to a net loss of intracellular cations and water and to cell dehydration. The differential diagnosis of dehydrated red cells also includes the much more common sickle cell syndromes, hereditary spherocytosis, and hemoglobin C disease. This rare autosomal dominant 872 disorder appears to be due to an inherited defect in Na+ permeability that leads to a net influx of Na+ and water and to cell swelling.
Obliteration 826 Figure 157-5 Cholangiographic appearance of cholestatic disorders lower cholesterol in free range eggs discount 10mg zetia overnight delivery. The tumor is obstructing the common bile duct and the pancreatic duct worst high cholesterol foods purchase zetia canada, producing proximal dilatation of both (double duct sign) reduce cholesterol by food buy generic zetia 10mg on-line. A cannula extending from the endoscope has been passed through the area of obstruction and its tip lies in the proximal common hepatic duct cholesterol journal articles order zetia 10 mg with amex. A large cholesterol gallstone in the common bile duct appears as a radiolucent shadow outlined by radiodense contrast material. Multiple strictures are present in both the intrahepatic and extrahepatic biliary tree. Beadlike areas of dilatation can be noted between areas of stricture, but the fibrotic process in the liver prevents generalized dilatation of the proximal biliary ducts. Cholestasis of metabolic origin may be seen commonly in severely ill patients and is associated with trauma, surgery, sepsis, and parenteral hyperalimentation. Numerous drugs and estrogen also can produce cholestasis either as a direct effect or as an idiosyncratic reaction (see Chapter 148). Cholestasis of pregnancy appears to reflect sensitivity to the direct cholestatic effects of estrogen. In sarcoidosis (see Chapter 81), an idiopathic disease characterized by non-caseating granulomas in lung and other tissues, liver involvement is common. Usually these patients are symptom free with mild abnormalities of liver function tests. Granulomas in the portal tracts may produce fibrotic obliteration of small bile ducts. Rarely, bile duct obliteration may be sufficiently 827 severe to produce biliary cirrhosis. Although some experts consider hepatic involvement in sarcoidosis to be an indication for glucocorticoid therapy, glucocorticoids have not been proven to alter the natural history of sarcoidosis involving the liver. Primary biliary cirrhosis (see Chapter 153) is a progressive cholestatic disorder characterized by autoimmune destruction of small interlobular bile ducts. Injury is thought to occur as a result of cytotoxic T cell-mediated immune attack directed against bile ductular epithelial cells. Progressive familial intrahepatic cholestasis typically presents as mild to moderate cholestasis in infancy or childhood. Liver biopsy specimens appear generally unremarkable except that bile ductules can be identified in fewer than 50% of portal tracts. Severity and prognosis are variable: some patients develop biliary cirrhosis requiring transplantation in childhood, whereas others have an indolent course. A variety of genetic defects in pathways of bile acid synthesis or biliary lipid secretion have been implicated in the pathogenesis of this disorder. Chronic graft-versus-host disease occurs when T cells from an allogenic source are infused into an immunodeficient patient, most typically at the time of bone marrow transplantation (see Chapter 182). After hepatic transplantation (see Chapter 155), chronic hepatic allograft rejection is associated with immunologic injury to biliary ductules and hepatic arterioles. Arterial intimal injury leading to intimal hyperplasia may compromise hepatic circulation and accelerate the progression of liver injury. A benign intrahepatic cholestasis of metabolic origin is seen commonly in severely ill patients. Predisposing factors include major trauma or surgery, severe infection, and parenteral hyperalimentation. Serum bilirubin often is markedly elevated, whereas elevations of the alkaline phosphatase typically are modest, and aminotransferase levels usually are near normal. With elimination of the precipitating factors, cholestasis typically resolves over a few weeks. Intrahepatic cholestasis of pregnancy is a relatively common disorder that usually appears late during the third trimester of pregnancy, disappears after delivery, and can occur in subsequent pregnancy. In its usual form, the only manifestation is generalized itching (pruritus gravidarum), but more severe cases it may be accompanied by jaundice.
Platelets adhere to the subendothelial matrix in the injured vessel cholesterol in large shrimp order zetia 10 mg online, and platelet aggregation and thrombus formation begin simultaneously (see Chapter 183) cholesterol video order zetia american express. A variety of drugs can interfere with different aspects of hemostasis (Table 184-1) cholesterol content foods list order zetia 10 mg with mastercard, and therefore a medication history is particularly important what cholesterol medication has the least side effects buy zetia online. Thrombus formation is similar to normal hemostasis except that abnormalities in activation, inhibition, or fibrinolysis result in pathologic clots. Anatomic and/or biochemical alterations of the vascular intima are by far the most frequent causes of pathologic thrombosis. A variety of pathologic alterations of the vessel wall modify endothelial function in a prothrombotic fashion. At one extreme, the endothelial lining may be physically disrupted with exposure of circulating blood to extracellular matrix and tissue factor. It is not difficult to imagine how rupture of an atherosclerotic plaque results in pathologic initiation of clotting that terminates in vascular occlusion. Thrombosis is an important event in atherosclerotic vascular disease: (1) platelet thrombi are found in the coronary circulation in fatal myocardial infarction, and (2) fibrinolytic therapy can restore blood flow early in coronary occlusion. Platelets are disk-shaped cells 2 to 4 mm in diameter normally found in the peripheral blood (150,000 to 300,000 per microliter). In Wright-stained blood smears, they are identified by their blue-gray cytoplasm and red (lysosomal) granules and by lack of a nucleus. Platelets are formed in the bone marrow from giant polyploid cells called megakaryocytes. Megakaryocytes mature by a series of nuclear replications within a common cytoplasm (endomitosis) that lead to four- to six-lobed nuclei, as well as by elaboration of specific granules in the cytoplasm. Following maturation, the megakaryocyte cytoplasm becomes demarcated into platelet subunits, and the platelets are released into the circulation through the marrow sinusoids. A hematopoietic growth factor specific for megakaryocytes, thrombopoietin, has been identified. Various forms of the recombinant protein are currently being tested in clinical trials. The expectation is that it will be approved for the treatment of patients with thrombocytopenia caused by inadequate production of platelets. Normally, 3 to 10 megakaryocytes are seen in bone marrow smears under low-power magnification, but none appear in peripheral blood. Approximately one third reside in a splenic pool, which exchanges freely with the circulating pool. In diseases associated with platelet antibodies, the spleen is frequently the site of destruction. In addition, in disorders causing secondary splenic enlargement, thrombocytopenia may result from splenic sequestration (see Chapter 178). An estimate of platelet number in the peripheral blood film (normal, increased, decreased) is useful in detecting patients with abnormally low platelet counts. Normally, 3 to 10 platelets per high-power (oil immersion) field appear on peripheral smears. Platelets contain three types of secretory granules: lysosomes, alpha-granules, and dense bodies (electron-dense organelles) (Fig. In addition to release of potent vasoconstrictors from intracellular 997 Figure 184-1 Electron micrograph of an unstimulated platelet. Activated platelets expose specific receptors that bind Factor Xa and Va and in this way increase their local concentration, thus accelerating prothrombin activation. Platelets contain a membrane phospholipase C that, upon stimulation by activating agents, hydrolyzes endogenous phosphatidylinositol to form a diglyceride. The diglyceride, in turn, is converted to arachidonic acid by a diglyceride lipase. Arachidonic acid is a substrate for prostaglandin synthetase (cyclooxygenase), a reaction inhibited by aspirin and non-steroidal anti-inflammatory drugs, and is subsequently converted to prostaglandins. Von Willebrand disease prolongs the bleeding time not as a result of a platelet defect but rather because of the lack of a plasma factor important for normal platelet function. Although imperfect, the bleeding time is the only test of platelet function that correlates with susceptibility to bleeding.
Although most often patients have no gastric symptoms after abdominal vagotomy cholesterol in an eggs order 10mg zetia otc, 5 to 10% have delayed gastric emptying cholesterol levels british heart foundation cheap zetia 10mg with mastercard. This complication is more likely to occur if the patient had gastric outlet obstruction caused by a primary disease cholesterol reduced eggs buy zetia 10mg free shipping. Metoclopramide improves symptoms in many patients with delayed gastric emptying after a vagotomy cholesterol ratio 2.7 good discount zetia online. The usual dose of metoclopramide (10 mg orally, four times a day) can cause anxiety, fatigue, or sedation or dyskinesia in about 15% of patients. Domperidone, also a dopamine antagonist, does not cross the blood-brain barrier and has fewer central nervous system side effects but is investigational in the United States. Cisapride, which releases acetylcholine from the enteric neurons, may be useful in gastroparesis. Erythromycin, a macrolide antibiotic, initiates phase 3 in the stomach, improving gastroparesis symptoms. Roux-en-Y anastomoses after gastric resection occasionally cause poor gastric emptying, especially of solids. The migrating motor complex and the postprandial motor response are abnormal in the roux limb. Delayed gastric emptying of solids is the major functional disturbance; liquid gastric emptying may be normal. Patients with severe vomiting can be treated with subcutaneous bethanechol, further gastric resection, or elimination of the roux loop. Leuprolide may reduce symptoms, and some patients may benefit from a near-total gastrectomy. Chronic delayed gastric emptying, associated with long-standing insulin-dependent diabetes mellitus, is a greater clinical problem. Such patients have frequent episodes of nausea and vomiting, which affect food intake and complicate insulin requirements. Retinopathy, nephropathy, peripheral neuropathy, and other complications are commonly present. Absence of the gastric migrating motor complex, necessary for emptying of non-digestible material more than 1 mm, predisposes the diabetic patient to bezoars, causing abdominal discomfort, early satiety, and vomiting. Vagal neuropathy is thought to be the pathogenesis of gastric stasis in diabetes mellitus, although a demonstrable autonomic neuropathy is not always present. Metoclopramide improves the symptoms of gastric stasis in patients with diabetes mellitus both by increasing gastric emptying and decreasing the central nervous system recognition of nausea and distention. Bethanechol also stimulates an increase in gastric motility and improves symptoms in patients with diabetic gastric stasis. Erythromycin improves symptoms of gastroparesis by increasing antral contractions and fundal tone. The gastric emptying of solids, but not of liquids, is slowed in patients with anorexia nervosa (see Chapter 227), but not in patients with bulimia. The delayed gastric emptying is associated with antral dysrhythmia, fundal hypotonia, decreased postprandial plasma concentrations of norepinephrine and neurotensin, and impaired autonomic function (decreased resting diastolic blood pressure and skin conductance). Patients with equal weight loss but without the psychiatric disorder do not have delayed gastric emptying. Reversal of the underlying psychiatric disturbance appears necessary for complete resolution of symptoms. Delayed gastric emptying in progessive systemic sclerosis may exacerbate problems with esophageal reflux. The decreased gastric emptying associated with an acute viral infection usually resolves quickly. Up to 25% of patients with reflux esophagitis, associated with an incompetent lower esophageal sphincter, have delayed gastric emptying, which must be corrected to treat the reflux esophagitis adequately. Lesions such as tumors, infarction, or viral encephalitis that affect the vagal complex in the medulla can delay gastric emptying. There is no evidence that infection with Helicobacter pylori affects gastric emptying. Rapid Gastric Emptying Rapid gastric emptying occurs in some patients with duodenal ulcer disease and Zollinger-Ellison syndrome as a result of duodenal insensitivity to an acid load (Chapter 130). Rapid liquid emptying occurs in patients with pancreatic insufficiency (Chapter 141) and possibly with celiac sprue because of poor feedback inhibition of gastric motility by fat due to a maldigestion or malabsorption.
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