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Clinical Director, Tulane University School of Medicine

The blood-brain barrier is composed anatomically of unique endothelial cells that lack the usual transendothelial channels and that seamlessly abut one another (tight junctions) gastritis diet alcohol order cheap ditropan on-line. This anatomy protects the brain against the fluctuating composition of blood and minimizes the entry of potentially toxic compounds follicular gastritis definition generic ditropan 5mg free shipping. The entry of nutrients and egress of metabolic products cross the blood-brain barrier via simple diffusion gastritis enteritis generic 2.5mg ditropan with mastercard, facilitated transport, or active transport. Lipid-soluble compounds rapidly diffuse across endothelial cell membranes, whereas polar compounds must be transported on special carrier molecules that are driven either by concentration gradients (facilitated transport) or through the expenditure of energy (active transport). Glucose, a highly polar molecule, enters the brain on a special carrier with a Km (7 to 8 mM) just slightly higher than the normal blood glucose concentration. The rate of brain glucose transport is normally two to three times faster than the metabolism of glucose, but since glucose uptake depends so highly on its concentration, a reduction of blood sugar to one third the normal amount, caused by either ischemia or hypoglycemia, may compromise normal metabolism (Table 469-2). The severity of cerebral ischemia, defined as the degree and duration of blood flow loss, largely determines whether the brain suffers only temporary dysfunction, irreversible injury to a few highly vulnerable neurons (selective ischemic necrosis), or damage to extensive areas involving all cell types (cerebral infarction). Cerebral hypoxia-ischemia can be conveniently divided into focal or multifocal ischemia from vascular occlusion, global ischemia from complete 2098 failure of cardiovascular pumping, and diffuse hypoperfusion-hypoxia caused by respiratory disease or reduced perfusion pressure. Focal cerebral ischemia, resulting most frequently from embolic or thrombotic occlusion of extracranial or intracranial blood vessels, variably reduces blood flow within the involved vascular territory. Blood flow to the central zone of the ischemic vascular bed usually is severely reduced but rarely reaches zero because of partial filling from collateral blood vessels. In transition zones between normally perfused tissue and the severely ischemic central core, blood flow is moderately reduced. This rim of moderately ischemic tissue has been called the ischemic penumbra, and although brain cells in this region remain viable longer than do those in the ischemic core, they too will die if left deprived of adequate blood flow. Focal cerebral ischemia sufficient to cause clinical signs or symptoms and lasting only 15 to 30 minutes causes irreversible injury to specific, highly vulnerable neurons. If the ischemia lasts an hour or longer, infarction of part or all of the involved vascular territory is inevitable. Clinical evidence of permanent brain injury from such ischemia may or may not be detectable, depending on the region and the amount of brain tissue involved (see Chapter 470). Global cerebral ischemia, typically caused by cardiac asystole or ventricular fibrillation, reduces blood flow to zero throughout all of the brain. Global ischemia lasting more than 5 to 10 minutes is usually incompatible with recovery of consciousness in normothermic humans. Brain damage from more transient global ischemia, uncomplicated by periods of prolonged hypotension or hyperglycemia, is limited to specific populations of highly vulnerable neurons. While selective ischemic necrosis of neurons typifies transient global ischemia, such injury may also accompany prolonged hypoxemia, carbon monoxide poisoning, and focal cerebral ischemia of brief duration. Cardiac resuscitation complicated by prolonged hypotension or hyperglycemia may cause cerebral infarction, particularly in border zones that lie between the terminal branches of major arterial supplies. Diffuse cerebral hypoxia, uncomplicated by cerebral ischemia, is limited to conditions of mild to moderate hypoxemia, since myocardial contractility and blood pressure fall with severe hypoxemia. As a consequence, pure cerebral hypoxia causes cerebral dysfunction but not irreversible brain injury. Individuals with pure cerebral hypoxia from altitude sickness, pulmonary disease, or severe anemia present with confusion, cognitive impairment, and lethargy. With relatively acute changes in arterial oxygen tension from normal to a Pa O2 of 40 mm Hg (see Table 469-2) or with a fall in the hemoglobin concentration below 7 g dL, compensatory increases of cerebral blood flow become inadequate, and clinical signs and symptoms of cerebral hypoxia develop. Ischemic injury to the brain can be classified on the basis of cytopathologic criteria into four types. Cerebral autolysis, observed most frequently in brain-dead patients preserved on mechanical ventilators for several days, reflects enzymatic autodigestion of the tissue. Cerebral infarction, usually caused by focal vascular occlusion, is characterized histopathologically by necrosis of neurons, glia, and, in some areas, endothelial cells. Cerebral infarcts are frequently described grossly as pale (anemic) or hemorrhagic (showing gross petechial bleeding). Transient arrest of the cerebral circulation (global ischemia) for a few minutes causes selective ischemic necrosis of highly vulnerable neurons (see Table 469-3). The time required for histologic changes to reach their maximum in areas of cerebral infarction differs markedly from the time course of injury encountered in selective ischemic necrosis.

Health can then be viewed as a continual adaptation between the individual and the environment gastritis diet buy genuine ditropan. The frequency of diseases caused by genetic susceptibility to gastritis cystica profunda generic 5 mg ditropan visa the environment varies from rare to gastritis diet for children ditropan 2.5 mg cheap 100%. Scurvy develops in all humans unless ascorbate is provided in the diet because we are all unable to convert glucuronic acid to glucuronolactone and ascorbate. By contrast, humans readily synthesize tetrahydrobiopterin, a cofactor in many hydroxylase reactions, including phenylalanine hydroxylase. In some rare diseases (about 1 in 500,000) of increased blood phenylalanine and severe neurodegeneration, biopterin is not synthesized. Biopterin replacement may treat defects in biosynthesis and exemplifies a group of metabolic disorders known as vitamin dependency disorders. Nutritional management and chemoprevention involve correction of the metabolic imbalance and return of the patient to homeostasis through diet manipulation and drug therapy. Many of the diseases listed in this section are amenable to this approach and use the pathophysiologic mechanisms listed in Table 201-2. For example, in disorders of the urea cycle, protein intake is limited to reduce ammonia accumulation. Arginine is supplemented to provide deficient product of the blocked reaction, and alternative pathways are induced for nitrogen excretion. The latter therapy is made possible by a ubiquitous enzyme, N-glycine-acylase, that forms adducts with benzoic acid and glycine to produce hippuric acid, which is excreted, thus ridding the body of one nitrogen molecule. Orotic aciduria is caused by mutations in the bifunctional enzyme orotate phosphoribosyl transferase-orotidine-5 -monophosphate decarboxylase. The disease process, which includes severe anemia and immune deficiency, is caused by a deficient end product, uridine, and is treated by replacing 100 to 200 mg/kg/day of uridine (orally). Feedback inhibition of pituitary adrenocorticotropic hormone production is important in treating congenital adrenal hypertrophy with replacement doses of hydrocortisone to prevent virilization from testosterone overproduction. Glucose decreases overproduction of the precursors delta-aminolevulinic acid and porphobilinogen in acute intermittent porphyria caused by porphobilinogen deaminase deficiency. Using supraphysiologic amounts of a specific vitamin is important if it is the precursor of a coenzyme required for holoenzyme function. In vitamin B6 -dependent homocystinuria, mutant cystathionine synthase is stabilized to biologic degradation when saturated with pyridoxal phosphate. Others include vitamin B12 -dependent methylmalonic aciduria, thiamine-dependent maple syrup urine disease, and biotin-dependent multiple carboxylase deficiency. Some blocked metabolic reactions can be augmented by inducing transcription of their gene. Trials with estrogen receptor inhibitors in pre-symptomatic, high-risk members of families with breast and ovarian cancer are promising. Similar trials to prevent colorectal cancer by preventing polyps in at-risk offspring of patients are also promising. If the specific protein or enzyme has been purified and engineered to function in its specified organ or subcellular organelle, it can be used to treat an inherited metabolic disease. One good example is glucocerebrosidase, which has been purified in large quantities from placenta and from recombinant mammalian cells. The secreted enzyme is biochemically engineered to contain the mannose recognition site for cellular uptake into lysosomal compartments. Many proteins are now made through recombinant techniques to treat metabolic disease and bypass the risks of acquired immune deficiency syndrome and hepatitis attendant on using human-derived biologicals. Several other engineered proteins used to treat inherited metabolic disease include 1-deamino-8- D-arginine vasopressin to treat X-linked recessive diabetes insipidus and recombinant alpha1 -antitrypsin made stable by inactivating methionine 385 in the treatment of alpha1 -antitrypsin deficiency. Some enzymes such as adenosine deaminase have been modified with polyethylene glycol to reduce immunogenicity and prolong their biologic half-life in blood. For metabolic disorders that are lethal and have no other available therapy, organ transplantation may be life saving. Transplantation with histocompatible organs is clinically available because of 1084 advances in immunology that not only allow for better tissue typing but also enable chronic immunosuppression with such drugs as cyclosporine, azathioprine, and prednisone to prevent rejection. Several principles are required for successful treatment of an inherited metabolic disorder by organ transplantation: (1) the normal enzyme, protein, or function must be provided by the transplanted organ.

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The activity of homogentisic acid oxidase in the normal adult human liver is sufficient to gastritis diet buy 2.5mg ditropan metabolize over 1600 g of homogentisic acid per day gastritis diet jokes order ditropan with amex. In alkaptonuric individuals there is no detectable activity of this enzyme in liver gastritis diet options generic ditropan 2.5mg on-line, kidney, or prostrate where it is normally abundant. Plasma levels of homogentisic acid rise to about 3 mg/dL, and the urinary excretion ranges from 4 to 8 g/day. Mammalian tissue also contains an enzyme 1110 called homogentisic acid polyphenoloxidase that catalyzes the oxidation of homogentisic acid to an ochronotic pigment, but pigment can also be produced non-enzymatically in the presence of oxygen and alkali, as, for example, in urine. The homogentisic acid polymer has a high affinity for cartilage and connective tissue macromolecules. The stained tissue is fragile and eventually may break down, leading to degenerative intervertebral disk or joint disease. Homogentisic acid may also have a direct effect on collagen synthesis through inhibition of lysyl hydroxylase. In the adult alkaptonuric patient, costal, laryngeal, and tracheal cartilages are densely pigmented, sometimes appearing coal-black. Pigmentation is also present throughout the body in fibrous tissue, fibrocartilage, tendons, ligaments, epidermis, endocardium, and intima of larger vessels in various organs including kidney, lung, and prostrate. Urine is colorless when passed but darkens when alkaline or after long exposure to air. Generally, the earliest physical sign is a slight pigmentation of the sclerae or the ears, beginning at age 20 to 30 years. The cartilage of the ears may be slate blue or gray and feel irregular and thickened. Sometimes dusky discolorations of underlying tendons can be seen through the skin over the hands. The arthritis causes limitation of motion of the hips, knee joints, or shoulders; and there may be periods of acute inflammation. In addition, alkaptonuric patients appear to have a high incidence of cardiovascular disease; at least one degenerated pigmented aortic valve has been replaced with a prosthesis. Other complications include ruptured intervertebral disks, prostatitis, and renal stones. Almost pathognomonic, the changes affect vertebral bodies of the lumbar spine, which show degeneration of the intervertebral disks, narrowing of the space, dense calcification of remaining disk material, and variable fusion of vertebral bodies, but little osteophyte formation and minimal calcification of intervertebral ligaments. The degenerative changes of ochronotic arthritis are most severe in the hip, shoulder, and knee; and there may be calcific deposits in the tendons. The sacroiliac joints and smaller joints of the extremities usually show little or no abnormality. The diagnosis is suggested by urine discoloration and presence of non-glucose reducing substance, pigmentation of sclerae or cartilage, arthritic episodes, and typical radiographic changes of the lumbar spine. Homogentisic acid in urine can be identified by chromatographic or enzymatic assays. The ochronotic changes of skin and cartilage, in the past, have been confused with an effect of prolonged use of quinacrine (Atabrine) or of carbolic acid dressings for chronic cutaneous ulcers. The arthritis must be differentiated from rheumatoid arthritis, osteoarthritis, and gout. Dietary restriction of phenylalanine and tyrosine of the degree necessary to reduce homogentisic aciduria is impractical and potentially deleterious. Pharmacologic doses of ascorbic acid, early and continuously, might reduce polymerization and pigmentation because ascorbic acid inhibits the polyphenol oxidase. A detailed discussion of the history, clinical features, and biochemical derangements of alkaptonuria and ochronosis. Phang There are three autosomal recessive genetic disorders in the degradative pathways for proline and hydroxyproline. Although these rare disorders are generally benign, the resulting metabolic abnormalities, at least for one of the disorders, are associated with neurologic manifestations in childhood. The alpha-nitrogen of the imino acids proline and hydroxyproline is incorporated within a pyrrolidine ring. Because of the ring structure, the metabolism of proline, including biosynthesis from glutamate and ornithine and degradation back to glutamate, is catalyzed by a specific set of enzymes. Both synthetic and degradative pathways share Delta1 -pyrroline-5-carboxylate as an intermediate. The cycling of proline may mediate the transfer of reducing-oxidizing potential that may be important under certain conditions.

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Diseases

  • Human monocytic ehrlichiosis
  • Diastrophic dysplasia
  • Burn Goodship syndrome
  • Silver Russell syndrome
  • Mixed connective tissue disease
  • Richieri Costa Colletto Otto syndrome

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