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The humoral immune response is the main protective response against extracellular bacteria heart attack in dogs order altace online. The antibodies act in several ways to pulse pressure variation ppt generic 5mg altace mastercard protect the host from the invading organisms hypertension heart disease discount 5mg altace with amex, including removal of the bacteria and inactivation of bacterial toxins (Figure 17-8). Extracellular bacteria can be pathogenic because they induce a localized inflammatory response or because they produce toxins. The toxins, endotoxin or exotoxin, can be cytotoxic but also may cause pathogenesis in other ways. An excellent example of this is the toxin produced by diphtheria, which exerts a toxic effect on the cell by blocking protein synthesis. Antibody that binds to accessible antigens on the surface of a bacterium can, together with the C3b component of complement, act as an opsonin that increases phagocytosis and thus clearance of the bacterium (see Figure 17-8). In the case of some bacteria-notably, the gram-negative organisms-complement activation can lead directly to lysis of the organism. Antibody-mediated activation of the complement system can also induce localized production of immune effector molecules that help to develop an amplified and more effective inflammatory response. For example, the complement split products C3a, C4a, and C5a act as anaphylatoxins, inducing local mast-cell degranulation and thus vasodilation and the extravasation of lymphocytes and neutrophils from the blood into tissue space (see Figure 17-8). Other complement split products serve as chemotactic factors for neutrophils and macrophages, thereby contributing to the buildup of phagocytic cells at the site of infection. Antibody to a bacteria toxin may bind to the toxin and neutralize it; the antibody-toxin complexes are then cleared by phagocytic cells in the same manner as any other antigenantibody complex. Intracellular bacterial infections tend to induce a cell-mediated immune response, specifically, delayedtype hypersensitivity. Some bacteria have surface structures or molecules that enhance their ability to attach to host cells. A number of gram-negative bacteria, for instance, have pili (long hairlike projections), which enable them to attach to the membrane of the intestinal or genitourinary tract (Figure 17-9). Other bacteria, such as Bordetella pertussis, secrete adhesion molecules that attach to both the bacterium and the ciliated epithelial cells of the upper respiratory tract. Secretory IgA antibodies specific for such bacterial structures can block bacterial attachment to mucosal epithelial cells and are the main host defense against bacterial attachment. Some bacteria evade the IgA response of the host by changing these surface antigens. Variation in the pilin amino acid sequence is generated by gene rearrangements of its coding sequence. Pilin variation is generated by a process of gene conversion, in which one or more minicassettes from the silent genes replace a minicassette of the expression gene. This process generates enormous antigenic variation, which may contribute to the pathogenicity of N. In addition, the continual changes in the pilin sequence allow the organism to evade neutralization by IgA. A classic example is Streptococcus pneumoniae, whose polysaccharide capsule prevents phagocytosis very effectively. This antibody protects against reinfection with the same serotype but will not protect against infection by a different serotype. On other bacteria, such as Streptococcus pyogenes, a surface protein projection called the M protein inhibits phagocytosis. Some pathogenic staphylococci are able to assemble a protective coat from host proteins. These bacteria secrete a coagulase enzyme that precipitates a fibrin coat around them, shielding them from phagocytic cells. Mechanisms for interfering with the complement system help other bacteria survive. In some gram-negative bacteria, for example, long side chains on the lipid A moiety of the cell-wall core polysaccharide help to resist complementmediated lysis. Pseudomonas secretes an enzyme, elastase, that inactivates both the C3a and C5a anaphylatoxins, thereby diminishing the localized inflammatory reaction.

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Tainer and his colleagues analyzed the epitopes on a number of protein antigens (myohemerytherin blood pressure chart dental treatment altace 2.5mg mastercard, insulin arterial ulcer order altace 5 mg visa, cytochrome c pulse pressure limits order 10mg altace amex, myoglobin, and hemoglobin) by comparing the positions of the known B-cell epitopes with the mobility of the same residues. Their analysis revealed that the major antigenic determinants in these proteins generally were located in the most mobile regions. However, because of the loss of entropy due to binding to a flexible site, the binding of antibody to a flexible epitope is generally of lower affinity than the binding of antibody to a rigid epitope. Complex proteins contain multiple overlapping B-cell epitopes, some of which are immunodominant. For many years, it was dogma in immunology that each globular protein had a small number of epitopes, each confined to a highly accessible region and determined by the overall conformation of the protein. However, it has been shown more recently that most of the surface of a globular protein is potentially antigenic. This has been demonstrated by comparing the antigen-binding profiles of different monoclonal antibodies to various globular proteins. The surface of a protein, then, presents a large number of potential antigenic sites. The subset of antigenic sites on a given protein that is recognized by the immune system of an animal is much smaller than the potential antigenic repertoire, and it varies from species to species and even among in- dividual members of a given species. Within an animal, certain epitopes of an antigen are recognized as immunogenic, but others are not. Furthermore, some epitopes, called immunodominant, induce a more pronounced immune response than other epitopes in a particular animal. Gell and Baruj Benacerraf in 1959 suggested that there was a qualitative difference between the Tcell and the B-cell response to protein antigens. Gell and Benacerraf compared the humoral (B-cell) and cell-mediated (T-cell) responses to a series of native and denatured protein antigens (Table 3-5). They found that when primary immunization was with a native protein, only native protein, not denatured protein, could elicit a secondary antibody (humoral) response. In contrast, both native and denatured protein could elicit a secondary cell-mediated response. The finding that a secondary response mediated by T cells was induced by denatured protein, even when the primary immunization had been with native protein, initially puzzled immunologists. For this reason, destruction of the conformation of a protein by denaturation does not affect its T-cell epitopes. As mentioned in Chapter 1, endogenous and exogenous antigens are usually processed by different intracellular pathways (see Figure 1-9). Endogenous antigens are processed into peptides within the cytoplasm, while exogenous antigens are processed by the endocytic pathway. T cells tend to recognize internal peptides that are exposed by processing within antigen-presenting cells or altered self-cells. Rothbard analyzed the tertiary conformation of hen egg-white lysozyme and sperm whale myoglobin to determine which amino acids protruded from the natural molecule. He then mapped the major T-cell epitopes for both proteins and found that, in each case, the T-cell epitopes tended to be on the "inside" of the protein molecule (Figure 3-9). This plot shows the relative protrusion of amino acid residues in the tertiary conformation of hen egg-white lysozyme. Notice that, in general, the amino acid residues that correspond to the T-cell epitopes exhibit less overall protrusion. Landsteiner employed various haptens, small organic molecules that are antigenic but not immunogenic. Chemical coupling of a hapten to a large protein, called a carrier, yields an immunogenic hapten-carrier conjugate. Animals immunized with such a conjugate produce antibodies specific for (1) the hapten determinant, (2) unaltered epitopes on the carrier protein, and (3) new epitopes formed by combined parts of both the hapten and carrier (Figure 3-10). But when multiple molecules of a single hapten are coupled to a carrier protein (or nonimmunogenic homopolymer), the hapten becomes accessible to the immune system and can function as an immunogen. The beauty of the hapten-carrier system is that it provides immunologists with a chemically defined determinant that can be subtly modified by chemical means to determine the effect of various chemical structures on immune specificity. Landsteiner tested whether an antihapten antibody could bind to other haptens having a slightly different chemical structure.

A) Tissue interstitial partial pressure of oxygen (Po2) will increase B) Tissue interstitial partial pressure of carbon dioxide (Pco2) will increase C) Tissue pH will decrease 27 blood pressure medication coreg 10mg altace sale. Blood gas measurements are obtained in a resting patient who is breathing room air blood pressure chart download software cheap altace 5 mg fast delivery. A) An increase in physiological dead space B) Pulmonary edema C) A low Hb concentration D) A low cardiac output 28 arrhythmia recognition course purchase altace with american express. A normal male subject has the following initial conditions (in the steady state): Arterial Po2 = 92 mm Hg Arterial O2 saturation = 97% Venous O2 saturation = 20% Venous Po2 = 30 mm Hg Cardiac output = 5600 ml/min O2 consumption = 256 ml/min Hb concentration = 12 gm/dl If you ignore the contribution of dissolved O2 to the O2 content, what is the venous O2 content? Left Lung Alveolar Pco2 Left Lung Alveolar Po2 Systemic Arterial Po2 A) B) C) D) E) 32. A) Increased Va and unchanged metabolism B) Decreased Va and unchanged metabolism C) Increased metabolism and unchanged Va D) Proportional increase in metabolism and Va 38. The diffusing capacity of a gas is the volume of gas that will diffuse through a membrane each minute for a pressure difference of 1 mm Hg. There is a sympathetic activation resulting in a decrease in blood flow of this muscle to 350 ml/min. Which of the following best describes the effect of decreasing V/Q ratio on the alveolar Po2 and Pco2? A 45-year-old man at sea level has an inspired O2 tension of 149 mm Hg, nitrogen tension of 563 mm Hg, and water vapor pressure of 47 mm Hg. A small tumor pushes against a pulmonary blood vessel, completely blocking the blood flow to a small group of alveoli. A group of alveoli are not ventilated in this student because mucus blocks a local airway. A 67-year-old man has a solid tumor that pushes against an airway, partially obstructing air flow to the distal alveoli. A 55-year-old man has a pulmonary embolism that completely blocks the blood flow to his right lung. The figure above shows a lung with a large shunt in which mixed venous blood bypasses the O2 exchange areas of the lung. What is the O2 tension of the arterial blood (in mm Hg) when the person breathes 100% O2 and the inspired O2 tension is greater than 600 mm Hg? A 32-year-old medical student has a fourfold increase in cardiac output during strenuous exercise. Which curve on the above figure most likely represents the changes in O2 tension that occur as blood flows from the arterial end to the venous end of the pulmonary capillaries in this student? What are the approximate values of Hb saturation (% Hb-O2), Po2, and O2 content for oxygenated blood leaving the lungs and reduced blood returning to the lungs from the tissues? Which diagram best depicts the normal relationship between Po2 (red line) and Pco2 (green line) during resting conditions? Which of the following would be true if the blood lacked red blood cells and just had plasma and the lungs were functioning normally? A) the arterial Po2 would be normal B) the O2 content of arterial blood would be normal C) Both A and B D) Neither A nor B A) B) C) D) E) 100 100 100 90 98 104 104 104 100 140 15 20 20 16 20 80 30 75 60 75 42 20 40 30 40 16 6 15 12 15 49. Which points on the above figure represent arterial blood in a severely anemic person? A stroke that destroys the respiratory area of the medulla would be expected to lead to which of the following? Which of the above O2-Hb dissociation curves corresponds to blood during resting conditions (red line) and blood during exercise (green line)? When the respiratory drive for increased pulmonary ventilation becomes greater than normal, a special set of respiratory neurons that are inactive during normal quiet breathing then becomes active, contributing to the respiratory drive. A) Apneustic center B) Dorsal respiratory group C) Nucleus of the tractus solitarius D) Pneumotaxic center E) Ventral respiratory group 59. A 26-year-old medical student on a normal diet has a respiratory exchange ratio of 0.

During mitral stenosis the ventricle is normal because the atrium produces the extra pressure to hypertension in pregnancy acog buy discount altace 10 mg on-line get blood through the stenotic mitral valve blood pressure zantac purchase altace uk. During diastole blood pressure medication discount 5mg altace with visa, aortic and pulmonary valve regurgitation occur through the insufficient valves causing the heart murmur at this time. Tricuspid and mitral stenosis are diastolic murmurs because blood flows through the restricted valves during the diastolic period. However, tricuspid stenosis and regurgitation, pulmonary valve regurgitation, and pulmonary stenosis are associated with an increase in right atrial pressure and should not affect pressure in the left atrium. In aortic valve stenosis the left side of the heart is enlarged because of the extra tension the left ventricular walls must exert to expel blood out the aorta. In pulmonary valve stenosis, the right side of the heart hypertrophies, and in mitral valve stenosis there is no left ventricular hypertrophy. In tricuspid valve regurgitation, the right side of the heart enlarges, and in tricuspid valve stenosis, no ventricular hypertrophy occurs. C) this patient has a heart murmur heard maximally in the "pulmonary area of cardiac auscultation. The rightward axis shift indicates that the right side of the heart has hypertrophied. The two choices that have a rightward axis shift are pulmonary valve regurgitation and tetralogy of Fallot. In tetralogy of Fallot, the arterial blood oxygen content is low, which is not the case with this patient. A) Right ventricular hypertrophy occurs when the right heart has to pump a higher volume of blood or pump it against a higher pressure. Tetralogy of Fallot is associated with right ventricular hypertrophy because of the increased pulmonary valvular resistance, and this also occurs during pulmonary artery stenosis. Tricuspid insufficiency causes an increased stroke volume by the right heart, which causes hypertrophy. Aortic stenosis, tricuspid valve regurgitation, interventricular septal effect, and patent ductus arteriosis are clearly heard during systole. A) In tetralogy of Fallot, there is an interventricular septal defect as well as stenosis of either the pulmonary artery or the pulmonary valve. Therefore, it is very difficult for blood to pass into the pulmonary artery and into the lungs to be oxygenated. Instead the blood partially shunts to the left side of the heart, thus bypassing the lungs. B) the first heart sound by definition is always associated with the closing of the A-V valves. B) In tetralogy of Fallot, an interventricular septal defect and increased resistance in the pulmonary valve or pulmonary artery cause partial blood shunting toward the left side of the heart without going through the lungs. The interventricular septal defect causes equal systolic pressures in both cardiac ventricles, which causes right ventricular hypertrophy and a wall thickness very similar to that of the left ventricle. C) Mitral regurgitation and aortic stenosis are murmurs heard during the systolic period. A ventricular septal defect murmur is normally heard only during the systolic phase. Tricuspid valve stenosis and patent ductus arteriosus murmurs are heard during diastole. E) the third heart sound is associated with inrushing of blood into the ventricles in the early to middle part of diastole. The next heart sound, the fourth heart sound, is caused by inrushing of blood in the ventricles caused by atrial contraction. The first heart sound is caused by the closing of the A-V valves, and the second heart sound is caused by the closing of the pulmonary and aortic valves. A) A number of things occur in progressive shock, including increased capillary permeability, which allows fluid to leak out of the vasculature, thus decreasing the blood volume. Other deteriorating factors include vasomotor center failure, peripheral circulatory failure, decreased cellular mitochondrial activity, and acidosis throughout the body.

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