Vice Chair, University of Vermont College of Medicine
Two of the subunits have chains and two of the subunits have chains; thus spasms trailer purchase 250mg mefenamic amex, normal adult hemoglobin is called 22 spasms 7 weeks pregnant order 500mg mefenamic with visa. Fetal hemoglobin [hemoglobin F (HbF)] In fetal hemoglobin quetiapine muscle relaxer 500mg mefenamic sale, the a chains are replaced by f chains; thus muscle relaxant over the counter discount mefenamic online, fetal hemoglobin is called 22. O2-binding capacity of blood is the maximum amount of O2 that can be bound to hemoglobin in blood. O2 content of blood is the total amount of O2 carried in blood, including bound and dissolved O2. Fifty percent saturation means that, on average, two of the four heme groups of each hemoglobin molecule have O2 bound. The sigmoid shape of the curve is the result of a change in the affinity of hemoglobin as each successive O2 molecule binds to a heme site (called positive cooperativity). Binding of the first O2 molecule increases the affinity for the second O2 molecule, and so forth. This change in affinity facilitates the loading of O2 in the lungs (flat portion of the curve) and the unloading of O2 at the tissues (steep portion of the curve). By tightly binding O2, the free O2 concentration and O2 partial pressure are kept low, thus maintaining the partial pressure gradient (that drives the diffusion of O2). The lower affinity of hemoglobin for O2 in this steep portion of the curve facilitates the unloading of O2 to the tissues. The P50 is increased, and unloading of O2 from arterial blood to the tissues is facilitated. The shift to the right decreases the affinity of hemoglobin for O2 and facilitates the delivery of O2 to the tissues during this period of high demand. The P50 is decreased, and unloading of O2 from arterial blood into the tissues is more difficult. Causes of a shift to the left are the mirror image of those that cause a shift to the right. Because deoxyhemoglobin is a better buffer for H+ than is oxyhemoglobin, it is advantageous that hemoglobin has been deoxygenated by the time blood reaches the venous end of the capillaries. Pressures are much lower in the pulmonary circulation than in the systemic circulation. For example, pulmonary arterial pressure is 15 mm Hg (compared with aortic pressure of 100 mm Hg). Resistance is also much lower in the pulmonary circulation than in the systemic circulation. Distribution of pulmonary blood flow When a person is supine, blood flow is nearly uniform throughout the lung. When a person is standing, blood flow is unevenly distributed because of the effect of gravity. Blood flow is lowest at the apex of the lung (zone 1) and highest at the base of the lung (zone 3). The high alveolar pressure may compress the capillaries and reduce blood flow in zone. This situation can occur if arterial blood pressure is decreased as a result of hemorrhage or if alveolar pressure is increased because of positive pressure ventilation. Moving down the lung, arterial pressure progressively increases because of gravitational effects on hydrostatic pressure. Arterial pressure is greater than alveolar pressure in zone 2, and blood flow is driven by the difference between arterial pressure and alveolar pressure. Moving down toward the base of the lung, arterial pressure is highest because of gravitational effects, and venous pressure finally increases to the point where it exceeds alveolar pressure. In zone 3, blood flow is driven by the difference between arterial and venous pressures, as in most vascular beds. Regulation of pulmonary blood flow-hypoxic vasoconstriction In the lungs, hypoxia causes vasoconstriction. This response is the opposite of that in other organs, where hypoxia causes vasodilation.
Most patients are cyanotic from birth or develop cyanosis by the end of the first year of life spasms throat generic mefenamic 250 mg with visa, since even mild obstruction of right ventricular outflow is progressive infantile spasms 7 month old buy line mefenamic. The tetralogy of Fallot is the most common cause of cyanosis after 1 year of age and causes 10% of all forms of congenital heart disease muscle relaxant japan generic mefenamic 250 mg otc. Hypoxic attacks and syncope are serious complications spasms kidney stones generic mefenamic 500 mg overnight delivery, forming the most common mode of death from this disease during infancy and childhood. Other complications include infectious endocarditis, paradoxical embolism, polycythemia, and cerebral infarction or abscess. Examples of defects that initially involve a left-to-right shunt, from the higher-pressure left side to the lower-pressure right side, include ventricular septal defects (the most common of all heart defects), atrial septal defects, patent ductus arteriosus, and persistent truncus arteriosus. These defects initially do not produce cyanosis, but cyanosis may develop later (tardive cyanosis). A defect that initially involves a right-to-left shunt is the tetralogy of Fallot. This is the most common cyanotic congenital heart disease of older children and adults. Cyanosis does not occur until later, when the shunt reverses, becoming right-to-left. This occurs because with time the pulmonary vessels become hyperplastic and irreversible pulmonary hypertension develops because of the volume overload to the lungs. The fusion of the spiral ridges results in division of the truncus into the pulmonary and aortic arteries. Occasionally the spiral is reversed, resulting in the aorta arising from the right ventricle and the pulmonary artery from the left. This is a complete transposition of the great vessels and produces two completely separate blood systems. This situation obviously is incompatible with life unless some type of mixing of blood can occur between these separate systems. In utero, mixing of blood occurs across the atrial septum and in connections with the placental circulation. Cases that survive to corrective surgery must have a persistent atrial septal defect or patent ductus arteriosus to allow mixing of blood. Usually, at birth, breathing decreases pulmonary resistance and this then reverses flow through the ductus arteriosus. This oxygenated blood (flowing from the aorta into the ductus) inhibits prostaglandin production, which in turn closes the ductus arteriosus. Markedly decreased blood levels of which one of the listed substances are most characteristic of intravascular hemolysis Alkaline phosphatase Bilirubin Haptoglobin Lactate dehydrogenase Methemoglobin 211 Copyright 2002 the McGraw-Hill Companies. Glucose-6-phosphate dehydrogenase deficiency Thalassemia Hereditary spherocytosis Drug-induced hemolytic anemia Normal response 186. Two days after receiving the antimalarial drug primaquine, a 27-yearold black man develops sudden intravascular hemolysis resulting in a decreased hematocrit, hemoglobinemia, and hemoglobinuria. Examination of the peripheral blood reveals erythrocytes with a membrane defect forming "bite" cells; when crystal violet stain is applied, many Heinz bodies are seen. Hereditary spherocytosis Glucose-6-phosphate dehydrogenase deficiency Paroxysmal nocturnal hemoglobinuria Autoimmune hemolytic anemia Microangiopathic hemolytic anemia Hematology 213 187. A single nucleotide change in a codon on chromosome 11 that causes valine to replace glutamic acid at the sixth position of the chain of hemoglobin is associated with a. What laboratory method or test can be used to detect the presence of hemoglobin S Hemoglobin A Increased Increased Increased Decreased Decreased Hemoglobin A2 Increased Increased Decreased Increased Decreased Hemoglobin F Increased Decreased Increased Increased Decreased 214 Pathology 191. A 49-year-old female presents with signs of anemia and states that every morning her urine is dark. Warm autoimmune hemolytic anemia Paroxysmal nocturnal hemoglobinuria Paroxysmal cold hemoglobinuria Isoimmune hemolytic anemia Cold-agglutinin autoimmune hemolytic anemia 192. Which one of the listed types of antibodies is the best example of a cold agglutinin that is associated with cold autoimmune hemolytic anemia The neutrophil in the photomicrograph shown below was obtained from peripheral blood and is most likely to be found in association with a.
Small (microscopic) laminated calcifications within tumors are called psammoma bodies and are due to single-cell necrosis back spasms 20 weeks pregnant purchase mefenamic 500 mg free shipping. Psammoma bodies are characteristically found in papillary tumors spasms or twitches order mefenamic 500mg without prescription, such as papillary carcinomas of the thyroid and papillary tumors of the ovary (especially papillary serous cystadenocarcinomas) muscle relaxant herbal supplement buy mefenamic paypal, but they can also be found in meningiomas or mesotheliomas spasms prednisone buy mefenamic 250 mg mastercard. For example, calcification of a tumor of the cortex in an adult is suggestive of an oligodendroglioma, while calcification of a hypothalamus tumor is suggestive of a craniopharyngioma. With dystrophic calcification the serum calcium levels are normal, while with metastatic calcification the serum calcium levels are elevated (hypercalcemia). Apoptosis as originally defined is a purely morphologic process that differs from necrosis in several respects. Apoptosis involves single cells, not large groups of cells, and with apoptosis the cells shrink and there is increased eosinophilia of cytoplasm. The shrunken apoptotic cells form apoptotic bodies, which may be engulfed by adjacent cells or macrophages. With apoptosis there is no inflammatory response, the cell membranes do not rupture, and there is no release of macromolecules. One mechanism of apoptosis involves cytochrome c being released into the cytoplasm from mitochondria via bax channels, which are upregulated by p53. Cytochrome c then binds to and activates apoptosis activating factor 1 (Apaf-1), which then stimulates a caspase cascade. The product of bcl-2 is normally located on the outer mitochondrial membrane, endoplasmic reticulum, and nuclear envelope. This product inhibits apoptosis by blocking bax channels and by binding to and sequestering Apaf-1. Cytotoxic T lymphocytes stimulate apoptosis by expressing FasL or secreting substances like perforin (which forms pores) or granzyme B. Apoptosis is the type of cell death seen with embryonic development, death of immune cells, hormone-induced atrophy, and some bacterial toxins or viral infections. Examples of apoptosis of immune cells include the involution of the thymus with aging and the destruction of proliferating B cells in germinal centers of lymph nodes. Examples of apoptosis resulting from hormone-induced atrophy exclude the death of endometrial cells during menses, ovarian follicular atresia after menopause, and regression of the lactating breast after weaning. An example of a viral infection causing apoptosis is the formation of Councilman bodies in the livers of patients with viral hepatitis. Coagulative necrosis, characterized by loss of the cell nucleus, acidophilic change 98 Pathology of the cytoplasm, and preservation of the outline of the cell, is seen in sudden, severe ischemia of many organs. Myocardial infarction resulting from the sudden occlusion of the coronary artery is a classic example of coagulative necrosis. In contrast, with liquefactive necrosis the dead cells are completely dissolved by hydrolytic enzymes. This type of necrosis can be seen in ischemic necrosis of the brain, but classically it is associated with acute bacterial infections. Fat necrosis, seen with acute pancreatic necrosis, is fat cell death caused by lipases. Fibrinoid necrosis is an abnormality seen sometimes in injured blood vessels where plasma proteins abnormally accumulate within the vessel walls. Caseous necrosis is a combination of coagulative and liquefactive necrosis, but the necrotic cells are not totally dissolved and remain as amorphic, coarsely granular, eosinophilic debris. Gangrenous necrosis of extremities is also a combination of coagulative and liquefactive necrosis. In dry gangrene the coagulative pattern is predominate, while in wet gangrene the liquefactive pattern is predominate. Primary lysosomes are cytoplasmic vacuoles that contain numerous acid hydrolases produced by the Golgi. These vacuoles combine either with vacuoles containing cellular components (autosomes) or with clathrin-coated endocytic vesicles that contain extracellular material (phagosomes). This fusion forms the secondary lysosome (multivesicular body, or phagolysosome) in which the macromolecules are degraded. The products of the normal lysosomal function are usually reutilized by the cell, but if the material is not digestible.
Other painful phenomena include flexor spasms due to spasticity spasms pancreas cheap mefenamic uk, contractures muscle relaxant prescription drugs 250 mg mefenamic with mastercard, and dysuria due to urinary tract infection muscle relaxant gaba buy discount mefenamic 500mg line. The impairment begins as blurred or clouded vision and progresses to cause reading impairment and visual field defects (central scotoma or diffuse defects) muscle relaxants quizlet buy generic mefenamic 500 mg. Involvement is often asymmetrical and mainly in the legs, especially in the early stage of the disease. Spasticity makes its first appearance in the form of extensor spasms; flexor spasms develop later. Central Nervous System 215 Test for visual field defects (confrontation test) Multiple Sclerosis Incoordination. Intention tremor, dysarthria, truncal ataxia, and oculomotor dysfunction are common. Gait unsteadiness due to motor incoordination is often experienced by the patient as dizziness or lightheadedness. Psychological factors such as depression, insecurity, and marital conflict often play a role as well. Mental changes (depression, marital conflict, anxiety) and cognitive deficits of variable severity can occur both as a reaction to and as a result of the disease. Spinocerebellar ataxias, adrenoleukodystrophy, endocrine diseases, mitochondrial encephalomyelopathy, vitamin B12 deficiency (funicular myelosis). The disease takes a malignant course, with major disability within 5 years, in fewer than 5 % of patients. Complaints of pain, paresthesiae, abnormal fatigability, or episodic disturbances are often, by their nature, difficult to objectify. Clinical examination may reveal no abnormality because of the episodic nature of the disease itself. Low amplitude of evoked potentials, on the other hand, often indicates a pathological process of another type. Circulating antibodies to various components of myelin can also be detected (for abbreviations, see below1). Lesions develop in myelin sheaths (which are extensions of oligodendroglial cell membranes) and in axons when the inflammatory process outstrips the capacity of repair mechanisms. Axonal damage seems to be the main cause of permanent neurological deficits, as dystrophic axons apparently cannot be remyelinated. Medications, physical, occupational, and speech therapy, social, psychological, and dietary counseling, and mechanical aids. The possible benefits of oligodendrocyte precursor cell transplantation for remyelination, and of growth factors and immunoglobulins for the promotion of endogenous remyelination, are currently under investigation in both experimental and clinical studies. A focus of bacterial infection of the brain is called a brain abscess, or cerebritis in the early stage before a frank abscess is formed. Pus located between the dura mater and the arachnoid membrane is called a subdural empyema, while pus outside the dura is called an epidural abscess. The epidemiological pattern of infection may be sporadic, endemic or epidemic, depending on the pathogen. Clinical Manifestations Meningitis and encephalitis rarely occur as entirely distinct syndromes; they usually present in mixed form (meningoencephalitis, encephalomyelitis).
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