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Nonspecific monitoring of systemic disease the inflammatory response to tissue injury includes changes in plasma concentrations of proteins known as acute phase proteins antiviral ganciclovir purchase medex 1 mg on line. The rise in these liver derived proteins is part of a wider response, which includes fever, leucocytosis and increased immune reactivity. Quantitative measurements of acute phase proteins are valuable indicators of the presence and extent of inflammation and of its response to treatment. These tests are influenced by plasma proteins, which are either slowly responding acute phase reactants. This commonly used but nonspecific test measures the speed of sedimentation of red cells in plasma over a period of 1 hour. It is useful for diagnosing and monitoring temporal arteritis and polymyalgia rheumatica and for monitoring patients with Hodgkin lymphoma. High values (>100 mm/hour) have a 90% predictive value for serious disease, including infections, collagen vascular disease or malignancy (particularly myeloma). Lower than expected readings occur in polycythaemia vera because of the high red cell concentration. Higher than expected values may occur in severe anaemia because of the low red cell concentration. Plasma viscosity Plasma viscosity is affected by the concentration of plasma proteins of large molecular size, especially those with pronounced axial asymmetry: fibrinogen and some immunoglobulins. Lower levels are found in neonates because of lower levels of proteins, particularly fibrinogen. Subsequent binding of C3b on the surface of microorganisms opsonizes them for phagocytosis. These include neutrophil leucocytosis, especially in bacterial infections, leucoerythroblastic or leukaemoid reactions, and, in viral and connective tissue diseases, neutropenia. Platelets may be increased or low in malignant, infectious and other systemic diseases. Disseminated intravascular coagulation is a major cause of thrombocytopenia and fall in coagulation factors. Creactive protein can be used for nonspecific monitoring of systemic disease in the short term (hours or days) and erythrocyte sedimentation rate (or plasma viscosity) over weeks or months. These antibodies are commonly IgG, although some IgM antibodies may also develop, usually in the early phase of an immune response. Only IgG antibodies are capable of transplacental passage from mother to fetus and the most important immune antibody is the Rh antibody, antiD. The A and B alleles catalyse addition of different carbohydrate residues (Nacetyl galactosamine for group A and dgalactose for group B) to a basic antigenic glycoprotein or glycolipid Blood donor In most countries blood donors contribute on a voluntary basis and this is generally preferable in terms of product safety. Red cell antigens and blood group antibodies the clinical significance of blood groups in blood transfusion is that individuals who lack a particular blood group antigen may produce antibodies reacting with that antigen which may lead to a transfusion reaction. Cryosupernatant is used for plasma exchange in thrombotic thrombocytopenic purpura. At the current time there is no reliable test for detecting prions in blood products. The A, B and H antigens are present on most body cells including white cells and platelets. In the 80% of the population who possess secretor genes, these antigens are also found in soluble form in secretions and body fluids. Naturally occurring antibodies to A and/or B antigen (usually IgM but occasionally IgG) are found in the plasma of subjects whose red cells lack the corresponding antigen (Table 30.

Hemoglobin is liberated from the lysed red blood cells in quantities that may be toxic for kidney cells hiv infection chances unprotected purchase cheap medex on line, causing acute renal tubular cell necrosis and kidney failure. High fever, shock, and disseminated intravascular coagulation may also develop, suggestive of release of massive amounts of cytokines. The disseminated intravascular coagulation consumes clot ting factors faster than they can be synthesized, and the patient may paradoxically die of bleeding in the presence of widespread clotting. More delayed hemolytic reactions may result from incompatibilities of minor blood group antigens. These result in progressive loss of the transfused red blood cells, leading to anemia and jaundice, the latter a consequence of overloading the liver with hemoglobin derived pigments. A, Blood group antigens are carbohydrate structures added onto cell surface proteins or lipids by the action of glycosyltransferases (see text). B, Different blood group antigens are produced by the addition of different sugars by different inherited glycosyltransferases. Individuals who express a particular blood group antigen are tolerant to that antigen but produce natural antibodies that react with other blood group antigens. All normal individuals produce a common core glycan, which is attached mainly to plasma membrane proteins. Most individuals possess a fucosyl transferase that adds a fucose moiety to a nonterminal sugar residue of the core glycan, and the fucosylated glycan is called the H antigen. A single gene on chromo some 9 encodes a glycosyltransferase enzyme that may further modify the H antigen. Individuals who are homozy gous for the O allele cannot attach terminal sugars to the H antigen and express only the H antigen. Individuals who express a particular A or B blood group antigen are tolerant to that antigen, but individuals who do not express that antigen produce natural antibodies that recognize the antigen. Almost all indi viduals express the H antigen, and therefore, they are tolerant to this antigen and do not produce antiH anti bodies. Individuals who express A or B antigens are toler ant to these molecules and do not produce antiA or antiB antibodies, respectively. However, blood group O and A individuals produce antiB IgM antibodies, and blood group O and B individuals produce antiA IgM antibodies. Rare individuals who are unable to produce the core H antigens make antibodies against H, A, and B antigens. Predictably, the presence of any blood group antigen induces tolerance to that antigen. In clinical transfusion, the choice of blood donors for a particular recipient is based on the expression of blood group antigens and the antibody responses to them. If a patient receives a transfusion of red blood cells from a donor who expresses the antigen not expressed on self red blood cells, a transfusion reaction may result (described earlier). In general, differences in minor blood groups lead to red blood cell lysis only after repeated transfusions trigger a secondary antibody response. A and B blood group antigens are expressed on many other cell types in addition to blood cells, including endothelial cells. The major clinical significance of anti-Rh antibodies is related to hemolytic reactions in developing fetuses that are similar to transfusion reactions. Rhnegative mothers carrying an Rhpositive fetus can be sensitized by fetal red blood cells that enter the maternal circulation, usually during childbirth. Subsequent pregnancies in which the fetus is Rh positive are at risk because the maternal antiRh IgG antibodies can cross the placenta and mediate the destruction of the fetal red blood cells. This causes erythroblastosis fetalis (hemolytic disease of the newborn) and can be lethal for the fetus. This disease can be prevented by administration of antiRhD antibodies to the mother within 72 hours of birth of the first Rhpositive baby. Other Blood Group Antigens Lewis Antigen the same glycoproteins that carry the A and B blood group determinants can be modified by other glycosyl transferases to generate minor blood group antigens. For example, addition of fucose moieties at other non terminal positions can be catalyzed by different fucosyl transferases and create epitopes of the Lewis antigen system. Lewis antigens have received much attention from immunologists because these carbohydrate groups serve as ligands for Eselectin and Pselectin and thus play a role in leukocyte migration (see Chapter 3).

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Two important components Primary (Congenital) Immunodeficiencies 461 of innate immunity are phagocytes and complement hiv infection by age group cheapest medex, both of which also participate in the effector phase of adaptive immunity. Therefore, congenital disorders of phagocytes and the complement system result in recurrent infections. Phagocyte defects generally result in infections of the skin and respiratory tract with bacteria or fungi, the latter predominantly involving Aspergillus and Candida species. It is a rare disease, estimated to affect approximately 1 in 200,000 individuals in the United States. Approximately two-thirds of cases show an X-linked recessive pattern of inheritance, and the remainder are autosomal recessive. In the X-linked form of the disease, there is a mutation in the gene encoding the 91-kD subunit of cytochrome b558, an integral membrane protein also known as phox-91. This mutation results in defective production of superoxide anion, one of several reactive oxygen species that constitute a major microbicidal mechanism of phagocytes, especially neutrophils (see Chapter 4). Defective production of reactive oxygen species results in a failure to kill phagocytosed microbes. The disease was often fatal in the past, even with aggressive antibiotic therapy, but the prognosis has improved significantly now because of earlier recognition and better control of infections. After neutrophil superoxide production is restored to approximately 10% of normal levels, resistance to infection is greatly improved. Leukocyte Adhesion Deficiencies the leukocyte adhesion deficiencies are a group of autosomal recessive disorders caused by defects in leukocyte and endothelial adhesion molecules. These diseases are characterized by a failure of leukocyte, particularly neutrophil, recruitment to sites of infection, resulting in severe periodontitis and other recurrent infections starting early in life, and an inability to make pus. Different types of leukocyte adhesion deficiencies are caused by mutations in different genes. The absence of sialyl Lewis X results in defective attachment of leukocytes to endothelium, the absence of leukocyte rolling, and therefore the defective recruitment of leukocytes to sites of infection. This deficiency is caused by a defect in the inside-out signaling pathway that mediates chemokine-induced integrin activation that is required for leukocytes to bind firmly to endothelium (see Chapter 3) and for platelets to aggregate. Patients present with severe infections with viruses mainly of the herpesvirus and papillomavirus families. The neutrophils, monocytes, and lymphocytes of these patients contain giant lysosomes. The mutations result in defective phagosomelysosome fusion in neutrophils and macrophages (causing reduced resistance to infection), defective melanosome formation in melanocytes (causing albinism), and lysosomal abnormalities in cells of the nervous system (causing nerve defects) and platelets (leading to bleeding disorders). Giant lysosomes form in neutrophils during the maturation of these cells from myeloid precursors. Some of these neutrophil precursors die prematurely, resulting in moderate leukopenia. Surviving neutrophils may contain reduced levels of the lysosomal enzymes that normally function in microbial killing. These cells are also defective in chemotaxis and phagocytosis, further contributing to their deficient microbicidal activity. In this disorder, differentiation of ectodermderived structures is abnormal, and immune function is impaired in a number of ways. These patients suffer from infections with encapsulated pyogenic bacteria as well as with intracellular bacterial pathogens including mycobacteria, viruses, and fungi such as Pneumocystis jiroveci (see also discussion later in the section on hyper-IgM syndromes). Defects in Splenic Development Splenic development may fail due to an autosomal dominant (and sometimes sporadic) condition called isolated congenital asplenia. Asplenia may also be caused by mutations in genes controlling left-right laterality, which also affects other organs. Congenitally asplenic patients have severe infections with encapsulated bacteria, especially Streptococcus pneumoniae. When there is no block in B cell development, the defect in humoral immunity is due to the absence of T cell help.

Older patients may develop degenerative changes within this tunnel hiv infection mayo clinic medex 5 mg sale, which compresses the ulnar nerve when the elbow joint is exed. The repeated action of exion and extension of the elbow joint may cause local nerve damage, resulting in impaired function of the ulnar nerve. Localized neuritis in this region secondary to direct trauma may also produce ulnar nerve damage. It is located anterior to the elbow joint and is a triangular depression formed between two forearm muscles. The base of the triangle is an imaginary horizontal line between the medial and lateral epicondyles. The bicipital aponeurosis separates the median cubital vein from the brachial artery and median nerve. Other structures within the roof are cutaneous nerves-the medial cutaneous and lateral cutaneous nerves of the forearm. Blood therefore has to be taken from patients into the ltering device and then returned to them. This process of dialysis occurs over many hours and requires ow rates of 250 to 500 mL/min. To enable such large volumes of blood to be removed from and returned to the body, the blood is taken from vessels that have a high ow. As no veins in the peripheral limbs have such high ow, a surgical procedure is necessary to create such a system. In most patients, the brachial artery is anastomosed (joined) to the cephalic vein at the elbow, or the radial artery is anastomosed to the cephalic vein at the wrist. After 6 weeks, the veins increase in size in response to their arterial blood ow and are amenable to direct cannulation or dialysis. Supe rfic ial branc h Pos terior interos s eous artery Interos s eous membrane Anterior view. When taking a blood pressure reading from a patient, the clinician places the stethoscope over the brachial artery in the cubital fossa. The median nerve lies immediately medial to the brachial artery and leaves the fossa by passing between the ulnar and humeral heads of the pronator teres muscle. The brachial artery and the median nerve are covered and protected anteriorly in the distal part of the cubital fossa by the bicipital aponeurosis. This at connective tissue membrane passes between the medial side of the tendon of the biceps brachii muscle and deep fascia of the forearm. The radial nerve lies just under the lip of the brachioradialis muscle, which forms the lateral margin of the fossa. In this position, the radial nerve divides into super cial and deep branches: the super cial branch continues into the forearm just deep to the brachioradialis muscle. High blood pressure (hypertension) requires treatment to prevent long-term complications such as stroke. Low blood pressure may be caused by extreme blood loss, widespread infection, or poor cardiac output. The sphygmomanometer is a device that in ates a cuff around the midportion of the arm to compress the brachial artery against the humerus. The cuff is in ated so it exceeds the systolic blood pressure (greater than 120 mm Hg). The clinician places a stethoscope over the brachial artery in the cubital fossa and listens (auscultates) for the pulse. As the pressure in the arm cuff of the sphygmomanometer is reduced just below the level of the systolic blood pressure, the pulse becomes audible as a regular thumping sound. As the pressure in the sphygmomanometer continues to drop, the regular thumping sound becomes clearer. When the pressure in the sphygmomanometer is less than that of the diastolic blood pressure, the audible thumping sound becomes inaudible. The normal range is 120/80 mm Hg (systolic blood pressure/diastolic blood pressure). Structures pass between the forearm and the hand through, or anterior to , the carpal tunnel. The major exception is the radial artery, which passes dorsally around the wrist to enter the hand posteriorly.