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By E. Ivan. Life University.

Slide 7 The pattern of visual loss may localize the lesion to the eye order lady era overnight delivery, optic nerve buy cheap lady era 100mg, optic chiasm order lady era with mastercard, optic tract, thalamus, optic radiation, or visual cortices. Slide 8 The pattern of visual loss can be described by visual field testing ranging from simpler confrontation techniques such as finger wiggling or finger counting to computer directed quantitative threshold determination at multiple sites that can be followed with established statistical methods. A scotoma is an area of the visual world where detection of a stimulus is more difficult or impossible. The symmetry and pattern of scotomas reflect the disturbance along the afferent visual pathway and thereby localize the lesion. The effects of retinal and optic nerve lesions can be predicted from known anatomy. The severity of potential causes of impaired vision ranges from sub-clinical signs to no light perception. Slide 10 Any physician caring for children needs to be able to interpret the red pupillary reflex elicited by a direct ophthalmoscope or, as in this photograph, by a camera flash. Also known as the Bruckner reflex, this optical effect gives valuable information about the eye’s optics and the health of the posterior pole. Slide 12 The pathologic signature of this tumor is the Flexner-Wintersteiner rosette, small tubules comprised of neoplastic photoreceptors. In rhegmatogenous retinal detachment a hole in the retina allows fluid to enter and accumulate in the subretinal space. Signs of retinal disease include hemorrhage, infarction, exudation of large proteins from the vascular compartment, and elevation of the transparent retina. The “dry” form causes slow, gradual visual loss and is accompanied by atrophy of the retinal pigment epithelium. The “wet” or exudative form causes visual distortion followed by rapid, marked visual loss and is accompanied by proliferation of abnormally friable neovascular tissue in the subretinal space, exudation, bleeding, scarring, and photoreceptor wipeout. Diabetic retinopathy and hypertensive retinopathy result in damage to the retinal vascular compartment and will be described below. Slide 14 The symptoms of optic nerve disease are blurred vision, either involving central vision or peripheral vision, dimming of vision with secondary decreased pupillary response to light, decreased color perception, and characteristic patterns of visual field loss: centrocoecal and arcuate scotomas, the former usually quite symptomatic and the latter often asymptomatic. Slide 15 Centrocoecal scotoma is a horizontally oval blind spot that includes the visual representations of the fovea (the point of fixation), the optic disc (the physiologic blind spot), and retina beneath the papillomacular bundle (the connecting area of visual field). Slide 16 During direct ophthalmoscopy with a white light, the centrocoecal scotoma is accompanied by pallor of the optic disc most conspicuous along its temporal rim. This pallor represents atrophy of axons with corresponding visible loss of capillary support. There is prominence of the retinal vessels, particularly along the path of the papillomacular bundle and within the macula, giving the retina a crinkly appearance. Slide 17 During direct ophthalmoscopy with a green (red-free) light, visualization of the nerve fiber layer is enhanced and the fundus appearance becomes clarified. As 147 determined after the first month of gestation, axons in the nerve fiber layer of the retina travel anteriorly over the ganglion cell layer, joining to exit the eye as the optic nerve. Loss (atrophy) of bundles of axons creates ruts in the retinal surface parallel to the orientation of these axons. Significant atrophy of nerve fiber layer and ganglion cells causes the internal limiting layer of retina to drape over the remaining retinal vessels onto the underlying inner plexiform layer of retina, giving the retina a crinkly appearance along the papillomacular bundle and within the macula. Optic atrophy is a clinical sign of disease affecting the nerve fiber layer and optic disc accompanied by functional loss. Slide 18 Axons in the papillomacular bundle are very sensitive to metabolic insults, both endogenous and exogenous from and demyelinating disease. Bilateral symmetric, chiefly temporal optic atrophy suggests one of these disorders. Leber’s hereditary optic atrophy is associated with a mitochondrial enzyme mutation and causes sudden visual loss in otherwise healthy young people. Slide 19 Unilateral optic atrophy suggests diseases of ischemic, compressive, and inflammatory origins. Interruption in the vascular supply of the optic nerve creates cranial nerve paresis with sudden painless onset of symptoms. Compressive optic neuropathy is accompanied by slow, often insidious and painless visual loss. Inflammatory conditions are often accompanied by pain exacerbated by eye movement. The optic nerve is surrounded by the origins of the four rectus muscles at the orbital apex. Trigeminal receptors in the inflamed perineural tissues can be stimulated by muscle activity and globe palpation. Slide 20 Anterior ischemic optic neuropathy is accompanied by sudden, painless visual loss due to infarction of the optic disc. Pallid disc swelling evolves into atrophy 4-6 weeks later, a time course typically consistent with ganglion cell soma death following axon damage (Wallerian degeneration). Idiopathic anterior ischemic optic neuropathy is associated with an anatomically crowded optic disc. Slide 21 Giant cell arteritis is an important cause of one of the few ophthalmic emergencies, sudden painless visual loss, because it is treatable, not necessarily to regain the vision in the affected eye but to preserve vision in the other eye. It is a subacute, granulomatous disease affecting the arteries in several organ systems. Visual loss usually occurs from central retinal artery or ophthalmic artery obstruction. Knowledge of the early non-ophthalmic symptoms as well as the emergent nature of sudden painless visual loss is important for any physician who cares for the elderly. Giant cell arteritis is also called temporal arteritis because the temporal artery is often exquisitely tender when involved and is the most common artery biopsied to confirm the presence of this systemic disease. Neuropathologic signs are panarteritis, intimal 148 hyperplasia, and fragmentation of the internal elastic lamina associated with multinucleated giant cells. Slide 22 Compressive optic neuropathy such as due to meningioma is usually accompanied by insidiously slow, painless visual loss with progressive enlargement of scotomas. Slides 23-24 Inflammatory optic neuropathy is usually associated with optic nerve demyelination and pain exacerbated by eye movements. Subacute visual loss can range from subtle symptomatic loss of central vision (acuity) or asymptomatic loss of peripheral vision to no light perception. These people initially have normal appearing optic discs, hence the statement, “Optic neuritis is a disease when the patient sees nothing and the internist sees nothing. Slide 25 Optic atrophy is a common end sign of many diseases purely ocular as well as systemic. As we have seen, sometimes the pattern of atrophy and visual loss can suggest a diagnosis or localize the lesion.

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Dissolved Carbon Dioxide Although carbon dioxide is not considered to be highly soluble in blood buy cheap lady era, a small fraction—about 7 to 10 percent—of the carbon dioxide that diffuses into the blood from the tissues dissolves in plasma order 100mg lady era fast delivery. The dissolved carbon dioxide then travels in the bloodstream and when the blood reaches the pulmonary capillaries buy lady era 100 mg with mastercard, the dissolved carbon dioxide diffuses across the respiratory membrane into the alveoli, where it is then exhaled during pulmonary ventilation. Bicarbonate Buffer A large fraction—about 70 percent—of the carbon dioxide molecules that diffuse into the blood is transported to the lungs as bicarbonate. Most bicarbonate is produced in erythrocytes after carbon dioxide diffuses into the capillaries, and subsequently into red blood cells. As a result, some of the bicarbonate will leave the erythrocytes and move down its – concentration gradient into the plasma in exchange for chloride (Cl ) ions. This phenomenon is referred to as the chloride shift and occurs because by exchanging one negative ion for another negative ion, neither the electrical charge of the erythrocytes nor that of the blood is altered. At the pulmonary capillaries, the chemical reaction that produced bicarbonate (shown above) is reversed, and carbon dioxide and water are the products. Hydrogen ions and bicarbonate ions join to form carbonic acid, which is converted into carbon dioxide and water by carbonic anhydrase. Carbon dioxide diffuses out of the erythrocytes and into the plasma, where it can further diffuse across the respiratory membrane into the alveoli to be exhaled during pulmonary ventilation. Carbaminohemoglobin About 20 percent of carbon dioxide is bound by hemoglobin and is transported to the lungs. Carbon dioxide does not bind to iron as oxygen does; instead, carbon dioxide binds amino acid moieties on the globin portions of hemoglobin to form carbaminohemoglobin, which forms when hemoglobin and carbon dioxide bind. When hemoglobin is not transporting oxygen, it tends to have a bluish-purple tone to it, creating the darker maroon color typical of deoxygenated blood. Because carbon dioxide is released from the lungs, blood that leaves the lungs and reaches body tissues has a lower partial pressure of carbon dioxide than is found in the tissues. As a result, carbon dioxide leaves the tissues because of its higher partial pressure, enters the blood, and then moves into red blood cells, binding to hemoglobin. In contrast, in the pulmonary capillaries, the partial pressure of carbon dioxide is high compared This OpenStax book is available for free at http://cnx. As a result, carbon dioxide dissociates readily from hemoglobin and diffuses across the respiratory membrane into the air. In addition to the partial pressure of carbon dioxide, the oxygen saturation of hemoglobin and the partial pressure of oxygen in the blood also influence the affinity of hemoglobin for carbon dioxide. The Haldane effect is a phenomenon that arises from the relationship between the partial pressure of oxygen and the affinity of hemoglobin for carbon dioxide. However, when oxygen is not bound to heme and the partial pressure of oxygen is low, hemoglobin readily binds to carbon dioxide. However, there are times that the respiratory system must alter the pace of its functions in order to accommodate the oxygen demands of the body. Hyperpnea Hyperpnea is an increased depth and rate of ventilation to meet an increase in oxygen demand as might be seen in exercise or disease, particularly diseases that target the respiratory or digestive tracts. This does not significantly alter blood oxygen or carbon dioxide levels, but merely increases the depth and rate of ventilation to meet the demand of the cells. In contrast, hyperventilation is an increased ventilation rate that is independent of the cellular oxygen needs and leads to abnormally low blood carbon dioxide levels and high (alkaline) blood pH. Muscles that perform work during exercise do increase their demand for oxygen, stimulating an increase in ventilation. However, hyperpnea during exercise appears to occur before a drop in oxygen levels within the muscles can occur. Therefore, hyperpnea must be driven by other mechanisms, either instead of or in addition to a drop in oxygen levels. The exact mechanisms behind exercise hyperpnea are not well understood, and some hypotheses are somewhat controversial. However, in addition to low oxygen, high carbon dioxide, and low pH levels, there appears to be a complex interplay of factors related to the nervous system and the respiratory centers of the brain. First, a conscious decision to partake in exercise, or another form of physical exertion, results in a psychological stimulus that may trigger the respiratory centers of the brain to increase ventilation. In addition, the respiratory centers of the brain may be stimulated through the activation of motor neurons that innervate muscle groups that are involved in the physical activity. Finally, physical exertion stimulates proprioceptors, which are receptors located within the muscles, joints, and 1070 Chapter 22 | The Respiratory System tendons, which sense movement and stretching; proprioceptors thus create a stimulus that may also trigger the respiratory centers of the brain. These neural factors are consistent with the sudden increase in ventilation that is observed immediately as exercise begins. Because the respiratory centers are stimulated by psychological, motor neuron, and proprioceptor inputs throughout exercise, the fact that there is also a sudden decrease in ventilation immediately after the exercise ends when these neural stimuli cease, further supports the idea that they are involved in triggering the changes of ventilation. Although the proportion of oxygen relative to gases in the atmosphere remains at 21 percent, its partial pressure decreases (Table 22. As a result, it is more difficult for a body to achieve the same level of oxygen saturation at high altitude than at low altitude, due to lower atmospheric pressure. In fact, hemoglobin saturation is lower at high altitudes compared to hemoglobin saturation at sea level. For example, hemoglobin saturation is about 67 percent at 19,000 feet above sea level, whereas it reaches about 98 percent at sea level. Partial Pressure of Oxygen at Different Altitudes Example Altitude (feet above Atmospheric Partial pressure of location sea level) pressure (mm Hg) oxygen (mm Hg) New York City, New 0 760 159 York Boulder, Colorado 5000 632 133 Aspen, Colorado 8000 565 118 Pike’s Peak, 14,000 447 94 Colorado Denali (Mt. A lower partial pressure of oxygen means that there is a smaller difference in partial pressures between the alveoli and the blood, so less oxygen crosses the respiratory membrane. Despite this, the tissues of the body still receive a sufficient amount of oxygen during rest at high altitudes. First, the number of oxygen molecules that enter the tissue from the blood is nearly equal between sea level and high altitudes. At sea level, hemoglobin saturation is higher, but only a quarter of the oxygen molecules are actually released into the tissue. Physical exertion, such as skiing or hiking, can lead to altitude sickness due to the low amount of oxygen reserves in the blood at high altitudes. At sea level, there is a large amount of oxygen reserve in venous blood (even though venous blood is thought of as “deoxygenated”) from which the muscles can draw during physical exertion. Because the oxygen saturation is much lower at higher altitudes, this venous reserve is small, resulting in pathological symptoms of low blood oxygen levels. You may have heard that it is important to drink more water when traveling at higher altitudes than you are accustomed to. This is because your body will increase micturition (urination) at high altitudes to counteract the effects of lower oxygen levels. In this way, the overall concentration of erythrocytes in the blood increases, which helps tissues obtain the oxygen they need. Acclimatization is the process of adjustment that the respiratory system makes due to chronic exposure to a high altitude. The low partial pressure of oxygen at high altitudes results in a lower oxygen saturation level of hemoglobin in the blood. Even though there is low saturation of each hemoglobin molecule, there will be more hemoglobin present, and therefore more oxygen in the blood. Until birth, however, the mother provides all of the oxygen to the fetus as well as removes all of the fetal carbon dioxide via the placenta.

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Clot Extravascular coagulation cheap lady era 100 mg fast delivery, whether occurring in vitro or in blood shed into the tissues or body cavities order generic lady era on-line. Retraction of the clot occurs over a period of time and results in the expression of serum and a firm mass of cells and fibrin cheap lady era online. Cold agglutinin disease Condition associated with the presence of cold- reacting autoantibodies (IgM) directed against erythrocyte surface antigens. Colony forming unit A visible aggregation (seen in vitro) of cells that developed from a single stem cell. Colony stimulating factorCytokine that stimulates the growth of immature leukocytes in the bone marrow. The common pathway includes three rate-limiting steps: (1) activation of factor X by the intrinsic and extrinsic pathways, (2) conversion of prothrombin to thrombin by activated factor X, and (3) cleavage of fibrinogen to fibrin. Compensated hemolytic A disorder in which the erythrocyte life span is disease decreased but the bone marrow is able to increase erythropoiesis enough to compensate for the decreased erythrocyte life span; anemia does not develop. Complement Any of the eleven serum proteins that when sequentially activated causes lysis of the cell membrane. Congenital Heinz body Inherited disorder characterized by anemia due hemolytic anemia to decreased erythrocyte lifespan. Erythrocyte hemolysis results from the precipitation of hemoglobin in the form of heinz bodies, which damages the cell membrane and causes cell rigidity. Contact group A group of coagulation factors in the intrinsic pathway that is involved with the initial activation of the coagulation system and requires contact with a negatively charged surface for activity. Continuous flow analysisAn automated method of analyzing blood cells that allows measurement of cellular characteristics as the individual cells flow singly through a laser beam. Contour gating Subclassification of cell populations based on two characteristics such as size (x-axis) and nuclear density (y-axis) and the frequency (z- axis) of that characterized cell type. Coverglass smear Blood smear prepared by placing a drop of blood in the center of one coverglass, then placing a second coverglass on top of the blood at a 45° angle to the first coverglass. Cyanosis Develops as a result of excess deoxygenated hemoglobin in the blood, resulting in a bluish color of the skin and mucous membranes. Cytochemistry Chemical staining procedures used to identify various constituents (enzymes and proteins) within white blood cells. Useful in differentiating blasts in acute leukemia, especially when morphologic differentiation on romanowsky stained smears is impossible. Cytokine Protein produced by many cell types that modulates the function of other cell types; cytokines include interleukins, colony stimulating factors, and interferons. This occurs because the primary hemostatic plug is not adequately stabilized by the formation of fibrin. Döhle bodies An oval aggregate of rough endoplasmic reticulum that stains light gray blue (with Romanowsky stain) found within the cytoplasm of neutophils and eosinophils. It is associated with severe bacterial infection, pregnancy, burns, cancer, aplastic anemia, and toxic states. The antibody reacts with erythrocytes in capillaries at temperatures below 15°C and fixes complement to the cell membrane. Upon warming, the terminal complement components on erythrocytes are activated, causing cell hemolysis. Dysfibrinogenemia A hereditary condition in which there is a structural alteration in the fibrinogen molecule. Dyspoiesis Abnormal development of blood cells frequently characterized by asynchrony in nuclear to cytoplasmic maturation and/or abnormal granule development. Echinocyte A spiculated erythrocyte with short, equally spaced projections over the entire outer surface of the cell. Effector lymphocytes Antigen stimulated lymphocytes that mediate the efferent arm of the immune response. The cell is an oval to elongated ellipsoid with a central area of pallor and hemoglobin at both ends; also known as ovalocyte, pencil cell, or cigar cell. Embolism The blockage of an artery by embolus, usually by a portion of blood clot but can be other foreign matter, resulting in obstruction of blood flow to the tissues. Embolus A piece of blood clot or other foreign matter that circulates in the blood stream and usually becomes lodged in a small vessel obstructing blood flow. Endothelial cells Flat cells that line the cavities of the blood and lymphatic vessels, heart, and other related body cavities. Granules contain acid phosphatase, glycuronidase cathepsins, ribonuclease, arylsulfatase, peroxidase, phospholipids, and basic proteins. Associated with parasitic infection, allergic conditions, hypersensitivity reactions, cancer, and chronic inflammatory states. Erythroblastic island A composite of erythroid cells in the bone marrow that surrounds a central macrophage. These groups of cells are usually disrupted when the bone marrow smears are made but may be found in erythroid hyperplasia. The least mature cells are closest to the center of the island and the more mature cells on the periphery. It is caused by an antigen— antibody reaction in the newborn when maternal antibodies traverse the placenta and attach to antigens on the fetal cells. It contains the respiratory pigment hemoglobin, which readily combines with oxygen to form oxyhemoglobin. The cell develops from the pluripotential stem cell in the bone marrow under the influence of the hematopoietic growth factor, erythropoietin, and is released to the peripheral blood as a reticulocyte. The average life span is about 120 days, after which the cell is removed by cells in the mononuclear-phagocyte system. Erythrocytosis An abnormal increase in the number of circulating erythrocytes as measured by the erythrocyte count, hemoglobin, or hematocrit. Erythrophagocytosis Phagocytosis of an erythrocyte by a histiocyte; the erythrocyte can be seen within the cytoplasm of the histiocyte as a pink globule or, if digested, as a clear vacuole on stained bone marrow or peripheral blood smears. Erythropoiesis Formation and maturation of erythrocytes in the bone marrow; it is under the influence of the hematopoietic growth factor, erythropoietin. Essential A myeloproliferative disorder affecting primarily thrombocythemia the megakaryocytic element in the bone marrow. Evan’s syndrome A condition characterized by a warm autoimmune hemolytic anemia and concurrent severe thrombocytopenia. Extramedullary The formation and development of blood cells at hematopoiesis a site other than the bone marrow. The result falling outside the control limits or violating a Westgard rule is due to the inherent imprecision of the test method. Fibrin monomer The structure resulting when thrombin cleaves the A and B fibrinopeptides from the α and β chains of fibrinogen.

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