Finally gastritis diet guidelines discount 20mg aciphex otc, the pain that starts under the rib cage and radiates to liver detoxies (renders less harmful) substances the right shoulder gastritis enteritis order 10mg aciphex fast delivery. If a gallstone blocks the bile such as alcohol and pesticides gastritis diet paleo aciphex 20mg otc, and destroys bac ducts gastritis diet öööþíôòâó÷þêã generic aciphex 20mg free shipping, the gallbladder can rupture and cause teria that have been taken into the blood from peritonitis gastritis diet ÷àò generic aciphex 10 mg without prescription. When the bile is needed to emulsify fats in the digestive tract gastritis neurological symptoms discount aciphex online visa, the Cirrhosis gallbladder contracts and pushes the bile through Cirrhosis is a chronic destruction of liver cells the cystic duct into the common bile duct gastritis recovery diet buy generic aciphex on-line, which accompanied by the formation of brous connec drains into the duodenum gastritis diet x garcinia buy genuine aciphex online. Causes include hepatitis, bile the pancreas is a glandular organ located duct disease, chemical toxins, and malnutrition behind the stomach. These juices enter the duodenum through the Some common symptoms are liver enlargement, pancreatic duct. The enzymes in the juices anemia, indigestion, nausea, edema in the legs include pancreatic amylase or amylopsin (to and feet, hematemesis (vomiting blood), nose break down sugars), trypsin and chymotrypsin bleeds, jaundice (yellow discoloration), and asci (to break down proteins), and lipase or steapsin tes (an accumulation of uid in the abdominal (to act on fats). Insu tion, hallucinations, hepatic coma, and death lin regulates the metabolism, or burning, of occur. Treatment is directed toward preventing carbohydrates to convert glucose (blood sugar) further damage to the liver. The feces or stool becomes hard, dry, and abdominal pain that later localizes at the lower difficult to eliminate. Causes include poor bowel right quadrant, nausea and vomiting, mild fever, habits, chronic laxative use leading to a lazy and elevated white blood cell count. If the appen bowel, a diet low in ber, and certain digestive dis dix ruptures, the infectious material will spill into eases. The condition is usually corrected by a high the peritoneal cavity and cause peritonitis, a seri ber diet, adequate uids, and exercise. Appendicitis is treated by an appen laxatives are sometimes used to stimulate defeca dectomy (surgical removal of the appendix). When gallstones form from crystallized cho Diarrhea is a condition characterized by frequent lesterol, bile salts, and bile pigments, the watery stools. Treatment is directed toward eliminating the taminated by the feces of an infected person. It is cause, providing adequate uid intake, and mod the most benign form of hepatitis and is usually ifying the diet. It is more serious than type A pouches (or sacs) that form in the intestine as the and can lead to chronic hepatitis or to cirrhosis of mucosal lining pushes through the surrounding the liver. When fecal material and bacteria become this B is recommended for all health care workers. Symptoms vary depending on the transmission include sharing needles while amount of inammation but may include abdom injecting drugs, getting stuck with a contami inal pain, irregular bowel movements, atus (gas), nated needle or sharps while on the job, or pass constipation or diarrhea, abdominal distention ing the virus from an infected mother to the infant (swelling), low-grade fever, and nausea and vomit during birth. Treatment methods include antibiotics, stool progress to chronic hepatitis, cirrhosis, or both. Other strains of the ber diet, and in severe cases, surgery to remove hepatitis virus that have been identied include the affected section of colon. Symptoms include fever, anorexia (lack of appetite), nausea, vomiting, fatigue, dark colored urine, clay-colored stool, myalgia (mus Gastroenteritis cle pain), enlarged liver, and jaundice. Treatment methods include rest and a diet high in protein Gastroenteritis is an inammation of the mucous and calories and low in fat. A liver transplant may membrane that lines the stomach and intestinal be necessary if the liver is severely damaged. In severe cases, antibiotics, intravenous uids, and A hernia, or rupture, occurs when an internal medications to slow peristalsis may be used. A hiatal hernia is when the stomach protrudes through the diaphragm Hemorrhoids and into the chest cavity through the opening for Hemorrhoids are painful dilated or varicose veins the esophagus (gure 7-60). They may be caused heartburn, stomach distention, chest pain, and by straining to defecate, constipation, pressure difficult swallowing. Treatment methods include during pregnancy, insufficient uid intake, laxa a bland diet, small frequent meals, staying upright tive abuse, and prolonged sitting or standing. If the hernia cannot be reduced or warm, moist compresses; and in some cases, a (pushed back in place), a herniorrhaphy (surgical hemorrhoidectomy (surgical removal of the hem repair) is performed. Symptoms include burning pain, indiges Stomach tion, hematemesis (bloody vomitus), and melena (dark, tarry stool). Usual treatment methods are antacids, a bland diet, decreased stress, and Pyloric avoidance of irritants such as alcohol, fried foods, sphincter tobacco, and caffeine. Ulcerative colitis is a severe inammation of the colon accompanied by the formation of ulcers and abscesses. The main symptom is diarrhea containing blood, pus, to blood vessels in the pancreas, hemorrhage and and mucus. Pancreatitis may be caused by exces weakness, abdominal pain, anemia, and anorexia. Symptoms include severe inammation, reducing stress with mild seda abdominal pain that radiates to the back, nausea, tion, maintaining proper nutrition, and avoiding vomiting, diaphoresis (excessive perspiration), substances that aggravate the condition. In some and jaundice if swelling blocks the common bile cases, surgical removal of the affected colon and duct. A chole creation of a colostomy (an articial opening in cystectomy, removal of the gall bladder, is per the colon that allows fecal material to be excreted formed if gallstones are the cause. Peritonitis 7:12 Urinary System Peritonitis, an inammation of the abdominal peritoneal cavity, usually occurs when a rupture Objectives in the intestine allows the intestine contents to After completing this section, you should be able enter the peritoneal cavity. Symp toms include abdominal pain and distention, Label a diagram of the urinary system fever, nausea, and vomiting. Each kidney is enclosed in a mass of fatty the urinary system, also known as the excre tissue, called an adipose capsule, and covered tory system, is responsible for removing certain externally by a tough, brous tissue, called the wastes and excess water from the body and for renal fascia, or brous capsule. It is Each kidney is divided into two main sec one of the major body systems that maintains tions: the cortex and the medulla. The cortex is homeostasis, a state of equilibrium or constant the outer section of the kidney. It contains most state of natural balance in the internal environ of the nephrons, which aid in the production of ment of the body. The medulla is the inner section of the are two kidneys, two ureters, one bladder, and kidney. Each kidney has a hilum, a notched shaped organs located on either side of the verte or indented area through which the ureter, nerves, bral column, behind the upper part of the blood vessels, and lymph vessels enter and leave abdominal cavity, and separated from this cavity the kidney. Their location is often Nephrons (gure 7-63) are microscopic l described as retroperitoneal. As these mate capsule, a proximal convoluted tubule, a distal rials pass through the various sections of the convoluted tubule, and a collecting duct (tubule). By Branches of the renal artery pass through the the time the ltered materials pass through the medulla to the cortex, where the blood enters the tubule, most of the water, glucose, vitamins, and rst part of the nephron, the glomerulus, which mineral salts have been reabsorbed. As blood passes through cose and mineral salts, some water, and wastes the glomerulus, water, mineral salts, glucose (including urea, uric acid, and creatinine) remain (sugar), metabolic products, and other sub in the tubule and become known as the concen stances are ltered out of the blood. The ltered collecting ducts, or tubules, located in the blood leaves the glomerulus and eventually medulla. These collecting ducts empty into the makes its way to the renal vein, which carries it renal pelvis (renal basin), a funnel-shaped away from the kidney. It picks up the materials l cle) moves the urine through the ureter from the tered from the blood in the glomerulus and passes kidney to the bladder. In males, the urethra is approximately 20 cm pyramid (8 inches) in length and passes through the pros tate gland and out through the penis. It carries Renal both urine (from the urinary system) and semen papilla (from the reproductive system), although not at Hilum the same time. Waste products dissolved in this liq uid are urea, uric acid, creatinine, mineral salts, Renal and various pigments. Excess useful products, vein such as sugar, can also be found in the urine, but their presence usually indicates disease. It has a mucous mem brane lining arranged in a series of folds, called Incontinence: involuntary urination rugae. The rugae disappear as the bladder Proteinuria: protein in the urine expands to ll with urine. Three layers of visceral Albuminuria: albumin (a blood protein) in the (smooth) muscle form the walls of the bladder, urine which receives the urine from the ureters and stores the urine until it is eliminated from the body. When the bladder is full, Cystitis receptors in the bladder wall send out a reex action, which opens the muscle. Infants cannot Cystitis is an inammation of the bladder, usually control this reex action. It is more common in female individuals because the urethra is the tube that carries the urine of the shortness of the urethra. The external frequent urination, dysuria, a burning sensation opening is called the urinary meatus. The ure during urination, hematuria, lower back pain, thra is different in female individuals and male bladder spasm, and fever. Glomerulonephritis appetite), weight loss, congestive heart failure, pyuria, and nally, renal failure and death occur. Glomerulonephritis, or nephritis, is an inam Treatment is directed at treating the symptoms, mation of the glomerulus of the kidney. Acute and treatment methods include a low-sodium glomerulonephritis usually follows a streptococ diet, antihypertensive drugs, maintenance of u cal infection such as strep throat, scarlet fever, or ids and electrolytes, and hemodialysis (removal rheumatic fever. Symptoms include chills, fever, of the waste products from the blood by a hemo fatigue, edema, oliguria, hematuria, and albu dialysis machine) (gure 7-64). Treatment meth neys are severely damaged, a kidney transplant ods include rest, restriction of salt, maintenance can be performed. With treatment, kidney function is usually Pyelonephritis restored, and the prognosis is good. Chronic Pyelonephritis is an inammation of the kidney glomerulonephritis is a progressive disease that tissue and renal pelvis (upper end of the ureter), causes scarring and sclerosing of the glomeruli. As the disease progresses and fatigue, dysuria, hematuria, and pyuria (pus in additional glomeruli are destroyed, edema, the urine). Treatment methods are antibiotics fatigue, anemia, hypertension, anorexia (loss of and increased uid intake. Anatomy and Physiology 215 Renal Failure Renal failure is when the kidneys stop function ing. Symptoms include oliguria or anuria, headache, an ammonia odor to the breath, edema, cardiac arrhythmia, and uremia. Prompt treatment involving dialysis, restricted uid intake, and correction of the condition caus ing renal failure results in a good prognosis. It can be caused by chronic glomerulonephritis, hypertension, toxins, and endocrine disease such as diabetes mellitus. Symptoms include nausea, vomit ing, diarrhea, weight loss, decreased mental abil ity, convulsions, muscle irritability, an ammonia odor to the breath, uremic frost (deposits of white crystals on the skin), and in later stages, coma prior to death. Treatment methods are dialysis, diet modications and restrictions, careful skin and mouth care, and control of uid intake. Uremia, also called azotemia, is a toxic condition that occurs when the kidneys fail and urinary waste products are present in the bloodstream. It can result from any condition that affects the Renal Calculus proper functioning of the kidneys, such as renal failure, chronic glomerulonephritis, and hypo A renal calculus, or urinary calculus, is a kidney tension. A calculus is formed when salts in the urine nausea, vomiting, an ammonia odor to the breath, precipitate (settle out of solution). Some small oliguria or anuria, mental confusion, convul calculi may be eliminated in the urine, but larger sions, coma, and eventually, death. Treatment stones often become lodged in the renal pelvis or consists of a restricted diet, cardiac medications ureter. Symptoms include sudden, intense pain to increase blood pressure and cardiac output, (renal colic); hematuria; nausea and vomiting; a and dialysis until a kidney transplant can be per frequent urge to void; and in some cases, urinary formed. Initial treatment consists of increasing uids, providing pain medication, and straining all urine through gauze or lter paper to deter Urethritis mine whether stones are being eliminated. Extra corporeal shock-wave lithotripsy is a procedure Urethritis is an inammation of the urethra, usu where high-energy pressure waves are used to ally caused by bacteria (such as gonococcus), crush the stones so that they can be eliminated viruses, or chemicals (such as bubble bath solu through the urine. Treatment methods include sitz baths or warm, Objectives moist compresses; antibiotics; and/or increased uid intake. The endocrine Control various sex processes system consists of the pituitary gland, thyroid gland, parathyroid gland, adrenal glands, pan Table 7-3 lists the main hormones produced creas, ovaries, testes, thymus, pineal body, and by each endocrine gland and the actions they placenta (gure 7-65). Hormones, chemical substances produced and secreted by the endocrine glands, are fre quently called chemical messengers. It is divided into two sections, or lobes: the anterior lobe and the posterior lobe. Diseases and Abnormal Conditions Acromegaly Acromegaly results from an oversecretion of somatotropin (growth hormone) in an adult and is usually caused by a benign (noncancerous) tumor of the pituitary called an adenoma. If a tumor of the Dwarsm results from an undersecretion of pituitary is the cause, surgical removal or radia somatotropin and can be caused by a tumor, tion is the treatment. It is characterized by small body size, short Diabetes Insipidus extremities, and lack of sexual development. Diabetes insipidus is caused by decreased secre Mental development is usually normal. Treatment con sists of either radiation to destroy part of the thy roid or a thyroidectomy (surgical removal of the thyroid). If the thyroid is removed, thyroid hor mones are given for the lifetime of the individual. It is located in front Hypothyroidism of the upper part of the trachea (windpipe) in the Hypothyroidism is an underactivity of the thyroid neck. It has two lobes, one on either side of the gland and a deciency of thyroid hormones. Two larynx (voice box), connected by the isthmus, a main forms exist: cretinism and myxedema. To produce its hormones, tinism develops in infancy or early childhood and the thyroid gland requires iodine, which is results in a lack of mental and physical growth, obtained from certain foods and iodized salt. The leading to mental retardation and an abnormal, hormones secreted by the thyroid gland are dwarfed stature. Symptoms include coarse, dry Diseases and skin; slow mental function; fatigue; weakness; intolerance of cold; weight gain; edema; puffy Abnormal Conditions eyes; and a slow pulse. Treatment consists of Goiter administering oral thyroid hormone to restore A goiter is an enlargement of the thyroid gland. In some countries where Causes can include a hyperactive thyroid, an iodized salt is not available, myxedema may be iodine deciency, an oversecretion of thyroid caused by an iodine deciency. Adding iodine to stimulating hormone on the part of the pituitary the diet corrects this type of myxedema. Symptoms include thyroid enlargement, dysphagia (difficult swallowing), a cough, and a choking sensation. Surgery the parathyroid glands are four small glands may be performed to remove very large goiters. Their hormone, parathormone, regulates the Hyperthyroidism amount of calcium in the blood (see table 7-3). Symptoms include extreme nervousness, sorb calcium, and activates intestinal cells to tremors, irritability, rapid pulse, diarrhea, diapho absorb calcium from digested foods. Anatomy and Physiology 221 calcium circulating in the blood is important for groups: mineralocorticoids, glucocorticoids, and blood clotting, the tone of heart muscle, and gonadocorticoids. The exchange of calcium and phosphate between the adrenal medulla secretes two main hormones: bones and blood, the parathyroid hormone plays epinephrine and norepinephrine. These hor an important function in maintaining the proper mones are sympathomimetic; that is, they mimic level of circulating calcium. This results in hypercalce tion of aldosterone on the part of the adrenal cor mia (increased calcium in the blood), which leads tex. This interferes with the reabsorption of to renal calculi (kidney stones) formation, leth sodium and water and causes an increased level argy, gastrointestinal disturbances, and calcium of potassium in the blood. This condition is often caused by an ade ing to a bronzing (yellow-brown color) of the noma (glandular tumor), and removal of the skin, hypoglycemia (low blood sugar), and edema. Other treatments include surgical removal costeroid hormones, controlled intake of sodium, of the parathyroids followed by administration of and uid regulation to combat dehydration. Symptoms include removal of or injury to the parathyroid and/or hyperglycemia (high blood sugar), hypertension, thyroid glands. Symptoms include tetany (a sus muscle weakness, fatigue, hirsutism (excessive tained muscular contraction), hyperirritability of growth and/or an abnormal distribution of hair), the nervous system, and convulsive twitching. The condition is easily is causing the disease, treatment is removal of the treated with calcium, vitamin D (which increases tumor. If the glands are removed, hormonal ther the absorption of calcium from the digestive apy is required to replace the missing hormones. Each gland has two parts: the outer portion, or cortex, and the inner portion, or the pancreas is a sh-shaped organ located medulla. It is both an exocrine gland roid hormones, which are classied into three and an endocrine gland. Special B, or beta, cells symptoms include hyperglycemia (high blood located throughout the pancreas in patches of sugar), polyuria (excessive urination), polydipsia tissue called islets of Langerhans produce the (excessive thirst), polyphagia (excessive hunger), hormone insulin, which is needed for the cells to glycosuria (sugar in the urine), weight loss, absorb sugar from the blood.
Phenylketonuria gastritis yellow stool order aciphex paypal, forms of lipidosis gastritis yogurt purchase aciphex with visa, tuberous sclerosis gastritis diet íôòâó÷þêã purchase aciphex online from canada, lead encephalopathy gastritis diet juice cheap aciphex online visa, and toxoplasmosis have been specifically mentioned as etiological factors diet of gastritis patient aciphex 20mg amex. In essence gastritis diet àâòîðèà discount aciphex amex, we are dealing with the same dichotomy of idiopathic and symptomatic forms as in infantile spasms-hypsarrhythmia chronic gastritis h pylori cheap 10 mg aciphex visa. Drug Category: Anticonvulsant Prevent seizure recurrence and terminate clinical and electrical seizure activity gastritis ulcer diet buy aciphex 20 mg lowest price. Drug Name Proper attention to concomitant medications, a low starting dose, and a very slow titration can minimize risk of dermatologic idiosyncratic reactions. This is a gloomy picture; the course quite often leads to institutionalization, especially in patients with very early onset. The course of the disease, however, should not be conceived as a linear progression of deterioration. This pattern, too, may gradually vanish and spikes or sharp waves of temporal and especially anterior temporal localization may then become predominant. Interestingly, this change may be associated with the appearance of psychomotor (complex partial) seizures as a new phenomenon or Thus, the patient seems to merge into the mainstream of temporal lobe epilepsy but will remain a deteriorated case with mental deficit or behavioral changes, often fostered by years of institutionalization. Who would have thought that a simple petit mal absence with its rather subtle clinical symptomatology could be the result of massive generalized synchronous epileptic discharges It implies that the clinical and electroencephalographic phenomena of the seizures occurring in this epileptic condition are generalized from the start. This term has superseded older terms such as "centrencephalic epilepsy", "cortico-reticular epilepsy", and "common generalized epilepsy". Its weakness lies in the fact that it seems to burn all bridges for a retreat if a truly focal cortical onset with extremely rapid generalization should ever be convincingly demonstrated in the future. Classical petit mal absences mostly start at age 4 to 6 yr; a special group starts at age 9 to 15 yr. A special manifestation is the petit mal absence status, which may occur in older children, adolescents, adults, and even the elderly. Primary generalized epilepsy is sometimes preceded by a period of febrile convulsions in infancy and early childhood. It is never preceded by severe conditions such as infantile spasms or the Lennox-Gastaut syndrome. The two different forms are 1) simple petit mal absences, starting at age 4 or shortly thereafter, with a large number of absences/day (sometimes exceeding 100/day); and 2) Petit mal absences show a wide variety of mild to moderate motor accompaniment; rhythmical eye blinking in synchrony with the spike waves is the most common motor component. Retropulsion of the head is quite common ("retropulsive petit mal); adversive movements and some rhythmically repetitive oral motions may also occur. Children with petit mal absences often start having grand mal seizures in early adolescence. In most of these cases, the grand mal seizures do not pose a major problem and are readily brought under control. Grand mal attacks in patients with primary generalized epilepsy are very often preceded by sudden bilateral myoclonus. These myoclonic jerks may also occur as isolated events, especially in the morning hours after a night of insufficient sleep. Many patients with this combination of grand mal and myoclonus may never have experienced any petit mal absences earlier in childhood. These bursts are relatively short and dominated by 4/sec or 4-5/sec spike wave complexes which are, contrary to the classical 3/sec or 3-4/sec spike waves, not readily activated by hyperventilation. Many of these patients are flicker-sensitive (photoconvulsive response) and positive family histories are more often obtained in this group. Very prolonged absence-like stages, attacks of petit mal like stupor, or petit mal automatisms have been termed "Petit mal status", whereas the modern terminology recommends the term "absence status. While all of the ictal manifestations of primary generalized epilepsy tend to occur in children and adolescents, the absence status not only occurs in elderlies but may even have its onset in old age. These generalized bursts, with or without clinical absence, are readily triggered by hyperventilation and may materialize after a few deep breaths in untreated patients. Intermittent photic stimulation may occasionally trigger petit mal absences with 3/sec spike waves; more often, it is associated with generalized polyspikes of frontal accentuation, with or without clinical myoclonic jerking, most often at frequencies of 14-18 flashes/sec. As was pointed out above, photosensitivity is more often noted in patients with 4/sec or 4-5/sec spike wave bursts and a history of grand mal and/or myoclonus. The 3 c/s spike/wave discharge with frontal dominance the phenomenon of myoclonus is almost invariably linked with polyspike discharges as far as patients with primary generalized epilepsy are concerned. Polyspikes also contaminate the spike wave sequences in children with massive myoclonus as a variant of petit mal. A remarkable exception is the occurrence of prolonged stretches of rhythmical high voltage 3/sec waves in occipital leads with moderate spread into the vicinity; these bursts occur in a significant number of children with petit mal absences. In some cases, a very small spike component is discernible between the large rhythmical delta waves. The rhythmical posterior activity may be enhanced under treatment with ethosuximide (Zarontin), while the 3/sec spike wave complex disappears. Children with petit mal absences and rhythmical occipital delta trains fall into a special epileptological category. The 3 c/s spike/wave discharge with frontal dominance, notice phase reversal of the spike/wave discharge in the medial frontal regions the sleep records of patients with primary generalized epilepsy show frequent bursts of spikes, polyspikes, and spike waves; with common association between the K complex and the frontal midline maximum of the spike discharges. This maximum over the frontal midline is almost invariably present, not only in sleep but also in the waking state. This indicates that arousal plays an important role in the generation of these discharges. In exceptional cases, the maximum of the 3/sec spike wave bursts lies in the vertex region rather than in frontal midline; these children also show Rolandic spikes. It goes without saying that genetic factors are particularly important in the field of primary generalized epilepsy. Generalized synchronous seizure discharges follow an autosomal dominant pattern of genetic transmission, with variable penetrance regardless of presence or absence of seizures with an unusual characteristic of a very low penetrance at birth which rises to nearly complete penetrance (close to 50%) for age 4. These figures are in excellent agreement with the incidence of generalized synchronous seizure discharges of the 3-4/sec spike-wave type as well as the clinical seizure manifestations of primary generalized epilepsy. This view would shed more light on the demonstration of genetic factors in children with midtemporal spikes. It is a specifically human disorder; for this reason, animal models can provide only partial insight into pathogenetic In the human, the generalized synchronous seizure discharge originates from the interhemispheric frontal portion bilaterally. An increasing number of reports over the past 40 yr gives testimony to growing awareness of this special form of childhood epilepsy. This form of childhood epilepsy is occasionally listed among the primary generalized epilepsies despite its prominent focal features in the ictal and electroencephalographic semiology. There are indeed certain relationships between benign Rolandic epilepsy and primary generalized epilepsies and conversion from one form to the other may occur. There is certainly good reason to separate benign Rolandic epilepsies from the bulk of focal (partial) epileptic seizure disorders which will be presented somewhat later. Disappearance of the seizures during adolescence (or even prior to puberty) is the rule. The seizures may occasionally recur much later in life, probably due to seizure facilitating factors such as severe illness or toxic-metabolic factors. The prevalence is not quite clear and might be somewhere between 5 and 10% in a population of epileptics below age 15 yr. About 80% of the attacks occur in sleep and, of the remaining 20%, about 10% take place shortly after awakening. Preservation of consciousness and hence the ability to describe the experienced seizure was found in 58%; this indicates the predominance of focal seizures. The seizures are hardly ever seen by the physician, even by the epileptologist who sees sizeable numbers of these children. One therefore depends heavily on descriptions by the patient Or his family; nocturnal video tape or biotelemetry recordings are quite helpful. The midtemporal spike localization has been thought to be related to paroxysmal activity in the very closely located lower portion of the motor strip (facio-laryngo-pharyngeal muscles). Hemifacial twitching is definitely more common than clonic motions in the contralateral arm; least common is clonic activity in the leg. In some cases, the entire half of the body participates, but a typical Jacksonian march does not seem to occur. Oropharyngeal involvement is very often reported, with sounds described as "guttural," "gargling," "throaty," "wheezing," or "as if going to vomit. These patients also have focal seizures which are not Rolandic, with blindness, vertigo, and torsion of the body as ictal signs. It is reasonable to presume that 50-70% of these children have seizures and the remaining 50 30% are seizure-free. The spatial distribution of the spike activity requires an appropriate number of electrodes; the International Electrode System is particularly suitable. Otherwise, the Rolandic cortex may lie between a frontal and a parietal electrode and strictly local spiking may escape detection, especially when the midtemporal region is not explored ideally. In my personal experience, a central maximum of spike discharge is slightly more often noted than a midtemporal maximum. The spikes themselves are large and may be either spikes in the strict sense or sharp waves (see chapter on abnormal paroxysmal patterns). Their random character may give way to quasirhythmical or periodical spiking at intervals of less than 1 see; previously unilateral spikes become bilateral synchronous or asynchronous. Bilateral parieto-occipital 4/sec spike wave-like discharges of moderate voltage is occasionally seen in the waking patient. Trains of spikes/sharp waves recorded in a quasirhythmical pattern in a child with benign Rolandic epilepsy. The rest of the tracing is usually normal in these patients and the frequency spectrum corresponds to age. Central mu rhythm is sometimes present and there is reason to presume that central spikes of childhood may be gradually replaced by mu rhythm, at least in some of the patients. There is indubitable evidence that, in a limited number of patients, the central spike activity can be blocked by contralateral fist clenching or, even better, by alternate clenching and opening of the fist. In a small number of cases, the spike activity shows a consistent maximum over the vertex or over the centroparietal midline region, which may be the sole region of spiking, so that omission of midline leads would result in missing the abnormality. Some of these patients show focal motor or sensory ictal activity of leg predominance but, more often, the ictal symptoms do not correspond with the spike localization. Arteriovenous malformation occasionally may be the cause of the discharges and associated seizure. Central, midtemporal, or parietal spikes or spikes over the midline may also occur in children with evidence of cerebral palsy, in mostly diplegic, quadriplegic, or choreoathetoid forms. In these children, Rolandic spikes have a different connotation and do not herald a good prognosis for the seizure disorder. Behavior disorders are very common in children with true Rolandic spikes; they may range from hyperkinetic behavior and signs of minimal cerebral dysfunction to severe anxiety neurosis. The return of a single major convulsion may occasionally occur under the influence of infections, stress, or toxic substances. The presence of central mu rhythm may serve as a hint that the patient has had central spikes in the past, but such conclusions can be made only with reservations. Children with Rolandic spikes and no seizures whatsoever (these children are certainly not epileptics; about 30 to 50% of the children with Rolandic spikes have no overt clinical seizures). Children with Rolandic spikes and a history of antecedent brain damage or cerebral palsy. Children who have typical psychomotor seizures and evidence of temporal lobe epilepsy which may gradually progress in severity; these children may have atypical spike localization (central, midtemporal), while the classical anterior temporal sharp wave focus does not materialize before adolescence. Children with midtemporal spikes, marked tendency to generalization and spike wave formation, clinically with aphasia, probably a temporary inflammatory condition which gradually subsides. Children with frequent focal motor seizures which become progressively worse: "malignant" Rolandic epilepsy of childhood. Children with centroparietal spikes elicited by tactile stimulation of corresponding cutaneous areas of the body (see under benign parietal epilepsy). The differentiation of these conditions rests on a careful combined clinical-electroencephalographic assessment of each case. There is evidence of constant muscle activity, but no authentic cerebral spikes are demonstrable. These children show no neurological or ophthalmological deficit; about 40% of them have clinical seizures, mostly grand mal, with good prognosis. Frontal spike foci in children are associated with epileptogenicity, with about 80% having overt seizures, and a guarded prognosis. Multiple spike foci (two or more areas of independent spiking) are also highly epileptogenic; the prognosis is guarded and probably fairly good if Rolandic spikes predominate. Their etiology is poorly defined; chronic localized encephalitis may be one of the causes (Rasmussen syndrome). Hemispherectomy seems to be the only effective treatment; limited cortical excisions or lobectomics are ineffective. The occurrence of spikes over the parietal region (parasagittal zone) following contralateral tactile stimuli characteristic of this condition. Only 20% of children had clinical seizures; the remaining children were referred because of behavior problems. Cortical biopsy may show inflammatory changes and gliosis with mildly appearance of the meninges over left temporal region. It was mentioned before that generalized synchronous spikes and spike waves in primary generalized epilepsy and focal spikes in benign Rolandic epilepsy can be easily suppressed for a limited period with small doses of iv diazepam, whereas many cases of chronic epileptogenic foci are not touched by such small amounts. Are we dealing with basically normal neurons which fire excessively due to hypersynchronous synaptic input Such an epileptogenic focus would consist of a hyperexcitable "neuronal aggregate". On the other hand, one could view the epileptogenic focus as composed of intrinsically abnormal neurons. There is accumulating evidence that epileptic seizure disorders based upon neuronal hyperexcitability do exist. The key areas of predisposition to epileptic neuronal hyperexcitability may be summarized as follows. Frontal lobe-supplementary motor area in interhemispheric fissure Presumed trigger: arousing stimuli in a state of reduced vigilance. Generalization: very common and very pronounced, exemplified by 3/sec spike waves, with or without petit mal absence (perhaps via cingulate and thalamocortical connections). Generalization: common, exemplified by polyspikes with or without myoclonus, occasionally by spike waves with or without petit mal absence, via occipito-frontocentral connections and/or geniculate thalamocortical fiber systems. Generalization: is not quite as common; seizures, if occurring, are most often of focal motor character. Hyperexcitability of all three key areas may occasionally exist in certain patients with primary generalized epilepsy. The hyperexcitability of the sensory parietal cortex with local spike responses to contralateral tactile stimuli seems to be a related phenomenon. Engel J Jr: Classifications of the International League Against Epilepsy: time for reappraisal. Engel J Jr: International classification: implications for neocortical epilepsies. Sutula T, Cascino G, Cavazos J: Mossy fiber synaptic reorganization in the epileptic human temporal lobe. DeLorenzo and coworkers compared patients with seizures that lasted 10-29 minutes to patients whose seizures lasted 30 minutes or more. Shinnar and co workers identified a subpopulation of children predisposed to prolonged (30 minutes) seizures and concluded that their data supported starting treatment of any seizure that lasts for 5-10 minutes and retaining the 30 minute cutoff in the definition of status epilepticus. Lowenstein, Bleck, and MacDonald argued that basing a definition on the onset of neuronal injury is questionable. A 9-yr-old patient with a history of petit mal absences starting at age 6 yr and grand mal since age 8. There are generalized synchronous spikes of frontal accentuation, often forming double and triple spikes, as well as rudimentary spike wave complexes. High-mortality causes include hypoxia and anoxia, cerebrovascular disease, metabolic disturbances, and tumors. In this early (or compensated) stage, the body changes to meet the demands of the neurons in the brain for increased oxygen and glucose and removal of metabolic waste products. Blood pressure falls, metabolic needs of the cerebral neurons are no longer met by homeostatic mechanisms, and cell death occurs. They conclude that the causes of histopathologic changes can be independent of cerebral physiology. Elaboration of glutamate triggers a sequence of intracellular events that begins with increased intracellular calcium, which then proceeds to dysfunction of multiple intracellular systems, finally resulting in cell death. Disagreement exists regarding the number of stages and the descriptions of individual stages, but enough independent descriptions indicate some sort of progression, at least in experimental animals, to support this proposal. They found that the presence of burst suppression or posttreatment ictal discharges was strongly (statistically) associated with mortality. Well modulated alpha rhythm during or immediately after a spell suggests a psychogenic etiology. Given our current knowledge, having a clear plan of approach is more important than recommending one of the protocols over another. Stabilize coexisting medical problems, treat metabolic abnormalities, and assure airway and oxygenation. In statistical comparison of the pairs, only the difference between lorazepam and phenytoin alone was significant. Fosphenytoin, a water-soluble phenytoin precursor, is an alternative when stability of intravenous access is questionable, since it does not have the tissue toxicity of extravasated phenytoin.
By and large gastritis dogs cheap 20 mg aciphex otc, these systems are based on the risk of agent transmission within the laboratory gastritis with hemorrhage aciphex 20 mg generic, the severity of diseases caused by the agents symptoms of gastritis in cats cheap aciphex 20 mg fast delivery, and the availability of specific prophylactics and anti-infective therapies gastritis diet øàðëîòêà purchase aciphex 20 mg free shipping. A searchable database containing the risk group classification of microorganisms is available at the following web address: my gastritis yellow stool buy discount aciphex. While knowledge of the risk group classification of microorganisms can be important gastritis and gas buy aciphex 20 mg, clinical laboratories should always perform risk assessments for all procedures gastritis vs gastroenteritis order generic aciphex from india. These agents were designated as select biological agents and toxins gastritis diet coke generic 10 mg aciphex otc, commonly referred to as select agents, which consist of a large number of bacteria, viruses, fungi, and toxins. This list is dynamic and undergoes periodic updating as new information is learned about currently-classified agents and as novel agents emerge. An updated list of these agents is available at the following web address. These agents are typically easy to disseminate, cause infection via respiratory exposure, and have a low infective dose. They also carry high rates of morbidity and mortality and specific antibiotic or antiviral therapies may not be available (Table 1). It should be noted that the identification of Tier 1 select agents and toxins require immediate. Bacterial Viral Toxins Bacillus anthracis Ebola virus Botulinum neurotoxins Bacillus cereus biovar anthracis Marburg virus Botulinum neurotoxin Burkholderia mallei Variola major virus (Smallpox) producing Clostridium spp. Burkholderia pseudomallei Variola minor virus (Alastrim) Francisella tularensis Yersinia pestis a Adapted from the Federal Select Agent Program website. In addition, many food testing, veterinary diagnostic, agriculture, 2 and environmental laboratories act as sentinel laboratories. Sentinel laboratories perform in-house testing that includes Gram stains and at least one of the following: lower respiratory tract, wound, or blood cultures. If on-site destruction of the isolate and all testing supplies and clinical specimens linked to the agent(s) cannot be accomplished, all such material should be forwarded to a reference laboratory for proper disposal. These laboratories are also charged with the tasks involved in enacting a timely local response, including initiating epidemiological investigations and providing instructive feedback to sentinel laboratories, to any suspected biothreat incidents. Safety risk assessments are multifaceted, ongoing processes with the ultimate goal of mitigating adverse events such as laboratory-acquired infections or release of potentially infectious agents into the environment. The safety risk assessment process is composed of an initial assessment of risk which considers potential laboratory hazards, existing procedural and engineering controls to mitigate exposure, evidence to support current practices, additional mitigation strategies, and documentation of findings. Risk assessments should be performed when bringing a new assay or test process on board, when a new instrument is placed, when new laboratory staff begin working, or if a new threat or hazard is identified. For example, if a novel influenza virus is identified and is reaching epidemic or pandemic levels, a risk assessment should be performed. A general, standardized approach to each of the specific risk assessment steps is presented in the following sections. However, each laboratory must develop an individualized assessment and mitigation plan appropriate for their specific laboratory needs. It is important to note that risk assessments are a continual process that must be periodically reviewed and evaluated. Risk consists of the biological agent(s), likelihood or incidence of encountering this agent, and laboratory equipment or practices that may be sub-optimal in reducing laboratory or environmental exposure. Importantly, the assessment of risk may change depending on staff changes (such as new hires), facility and test menu changes, recognized outbreaks or biological terrorism events, and the types of samples that may harbor the agent. This in turn can affect standard laboratory practices or result in the implementation of special practices until the heightened risk is alleviated. These events forced laboratories to conduct risk assessments and develop specialized protocols, based on current evidence, to mitigate risk associated with these pathogens. The overarching goal of risk assessments are to guide the implementation of mitigation strategies that are stringent enough to significantly reduce the risk of laboratory acquired infections without overburdening the laboratory and technologists with safety precautions that interfere with routine workflow and are difficult to consistently adhere to . Maintaining this balance is key to the sustainability of a safe laboratory environment. One such proposal for conducting a full risk assessment is shown in Figure 1: 1) identification of hazards, 2) evaluation and prioritization of risks, 3) risk mitigation strategies, 4) implement control measures, and 5) review the risk assessment (1). These classification schemes can be a useful starting point, but may not consider route of transmission or differences in relative risk between specimens, pure cultures, or growth phases of the microorganisms. Therefore, there may not be a direct correlation between a specific risk group and a corresponding biosafety level. Given these limitations, risk group or tier designation should not be the primary focus of risk assessment. Individual laboratories should consider the most likely route(s) of infection as well as the infective form and infective dose of biological agents in their risk assessment. Pure cultures, which have very high concentrations of organisms compared to clinical specimens, of either F. Another consideration in the identification of biological hazards is the frequency of encountering these agents. This can be dependent on the region of endemicity for each agent, risk factors for the population served by the laboratory. Recognized outbreaks or bioterrorism events may also increase the likelihood of encountering specific agents and should be considered when assessing risk. Procedural risks are those risks that are inherent to standard laboratory procedures used in the processing of specimens or cultures and include administrative, procedural, and mechanical features. Administrative features largely refer to the written policies and procedures for the safe manipulation of specimens and cultures in the laboratory. A lack of written policies for the handling of specimens or cultures containing hazardous organisms would constitute an administrative risk. Likewise, outdated policies that do not include current laboratory equipment and safe work practices are administrative hazards. Finally, it is critical that all staff are familiar with the policies and how to quickly access paper or electronic versions when needed. It is important to recognize that many of these tasks are unavoidable; however, recognition of procedures that carry added risk enables the development of specific mitigation strategies to reduce the associated risk to an acceptable level. A regular survey of the laboratory noting practices not in accordance with safety policies can be a good method to identify procedural hazards. Many risks are unique to the instrument itself, therefore each piece of equipment will require an independent assessment of risk. Common risks associated with specific laboratory instrumentation are discussed elsewhere in this guideline (see section 4. A review of routine preventative maintenance specified by the manufacturer and monthly inspection for broken or non-functioning instrumentation can identify these hazards. For equipment essential to safety, daily or weekly function checks using airflow gages, thermometers, or tests of audible alarm systems can help identify unrecognized hazards. A practical approach to identifying procedural risks is to follow a specimen from receipt in the laboratory through final reporting to identify all areas of the laboratory where the specimen or culture will be manipulated, and what instrumentation will be involved. Assessment of personnel is another factor that should be considered while identifying hazards. Less experienced technologists, or those working less than full time may not be able to easily recognize unsafe work practices or faulty equipment. Conversely, even experienced technologists may fail to recognize potential hazards if they are overburdened. Laboratory technologists should be competency assessed for performance and adherence to biosafety practices. Training needs for laboratory personnel can be identified during this part of the risk assessment. Biological factors such as pregnancy or immune compromise may put specific technologists at a higher risk of certain laboratory acquired infections. There is no single model that that will work for every laboratory, however a weighted, multifactorial risk model will often provide the best guidance when evaluating risk. This approach assesses two key factors for each identified hazard: 1) frequency or likelihood of occurrence, and 2) severity of consequences. Each of these two factors is sub-divided into relative risk categories, which together enables assignment of the overall risk or priority for each identified hazard. As an example, likelihood of occurrence could be stratified into rare, unlikely, possible, likely, and highly likely. The specific criteria for each subcategory could be based on the relative occurrence of each hazard using historic data, or could correspond to the expected occurrence over a fixed timeframe such as daily, weekly, monthly, and annually. Likelihood of occurrence example Likelihood Relative occurrence Rare Almost never occurs; will only occur in exceptional circumstances Unlikely Not likely to occur in the foreseeable future Possible May occur within the foreseeable future. Likewise, severity of consequence could be stratified by outcome of infection such as insignificant, minor, moderate, major, and critical. The level of person to person transmission may be considered in this stratification. Some factors that impact consequence include the risk group of the organism, the infectious dose, the concentration of the agent, the environmental setting and process (for example, where the agent manipulated and what was being performed), and the host experience level and immunocompetence. Consequence of exposure example Consequence Outcome Insignificant No treatment required. Major Serious injury requiring specialist medical treatment or hospitalization (infection and recovery). Critical Loss of life, permanent disability, or multiple serious injuries (disease and sequelae). Once assigned a frequency and severity score, the hazard can be plotted on a risk matrix and a determination of risk such as low, medium, high and extreme can be made. A low risk may be determined to require no mitigation steps while medium risk may need mitigation. A high risk will require mitigation before the procedure is followed and an extreme risk will require significant control measures (or an alternate procedure). In general, a laboratory should strive to achieve low risk for all test and safety procedures. Therefore, the hazard of manual transport of a glass bottle from one room to another may be medium risk that at some point may require mitigation (such as a change to plastic bottles, if possible). It is also important to note that, like identification of hazards, the evaluation of risk should be an ongoing process that can be expected to change with staffing, equipment, and changing epidemiology of infectious organisms. Risk matrix example Consequence Matrix Insignificant Minor Moderate Major Critical Rare Low Low Low Medium Medium Unlikely Low Low Medium Medium High Possible Low Medium High High High Likely Low Medium High High Extreme Highly likely Medium Medium High Extreme Extreme 3. Since elimination of a particular hazard may not always be possible, substitution should be considered. For example, substituting glass tubes and blood culture bottles with plastic, if possible, reduces risk. Engineering controls include using safety equipment such as a biosafety cabinet, sharps containers, eyewashes, sealed centrifuge rotors, and use of secondary transport containers that can be used to minimize exposures from accidental drops and spills. Administrative controls are those that affect the way that the laboratory staff works. If there is no feasible mitigation strategy for a risky procedure then it is advisable to not perform the procedure. Another example is the potential hazard of aerosol exposure while pipetting respiratory specimens on the benchtop. In this case it is reasonable to review the laboratory existing policy for handling respiratory specimens, as well as any training and competency records appropriate for that activity. If this activity is not specifically addressed in a lab policy, or the technologist(s) was not trained or competency assessed, the mitigation strategy may be administrative including education, re-education, or modification of a written policy. Installation of clean sinks for handwashing at each entry point to the lab and clearly demarcating clean from dirty areas can reduce the risk of transmission of infectious agents via secondary contact with fomites in an area outside of the lab. This may also reduce the 9 chance of ingestion resulting from storage of food or drink in a dirty area. Distribution of workload among multiple technologists (if possible) or frequent rotation of laboratory duties. Implementation of weekly communications to lab personnel that highlight specific safety topics or short quizzes can identify deficiencies in understanding of safe work practices. Hazards related to specific instrumentation may be mitigated by documentation of acceptable function checks. In many cases the manufacturer or a third party certified to inspect specific laboratory equipment can ensure that instruments are serviced and are functioning properly. Finally, up to date instrument manuals and service contacts should be available in the event of malfunction. The relative infrequency of highly infectious agents is an omnipresent hazard that is difficult to mitigate. In some cases, laboratories have special handling or referral policies for these agents; however, these policies are useless if the agent is unrecognized. Last, part of the mitigation strategy may include developing new training programs. The control plan should be documented and clearly communicated to laboratory staff. Implementation of controls includes ensuring that laboratory workers follow standing operating procedures for all tests that are performed and for all safety procedures, including proper decontamination and disposal of chemicals and biological/medical waste. Remember, risk assessment is a continuous process that must be routinely reviewed, especially after any incidents, accidents, or illnesses that occur among staff. When incidents or accidents 10 occur, identify the causes, make changes, and perform follow-up training with staff. In addition, review the risk assessment when changes to the procedure occur (new equipment or change to the procedure itself), when moving into a new facility or renovating an existing facility, if a new reagent is used in the lab, if a new infectious disease is identified, if a recurring problem is identified, and when new scientific information becomes available. Taken together, a full assessment of risk can aid in determining the relative risk of exposure and can guide the development or modification of standard practices focused to mitigate exposure to the high-risk pathogens most likely to be encountered. Encourage laboratory staff to ask questions and to be involved in the risk assessment process. Ultimately, it is the responsibility of the sentinel laboratory director to ensure that these procedures and protocols are designed and implemented, and that laboratory personnel are thoroughly trained and kept competent. Always keep in mind that a proper safety risk assessment should be performed for all laboratory procedures (see section 3, Laboratory Risk Assessment). All laboratory work surfaces and chairs must be made of non-porous, non absorbent materials that are resistant to chemical and physical agents used during experimentation and for disinfection of those surfaces. Microorganisms in this category (Table 6) are known to consistently cause mild to moderate infectious diseases in healthy adult humans. Also, all laboratory work surfaces, chairs, and floors must be made of or lined with non-porous, non-absorbent materials that are resistant to chemical and physical agents used during experimentation and for disinfection of those surfaces. Ideally, laboratory windows should be sealed; however, if they can be opened to the outside, they must be fitted with screens to prevent the entrance of pests. Type Examples Notes Bacteria Acinetobacter baumannii Aeromonas hydrophila Bordetella parapertussis Bordetella pertussis Campylobacter jejuni Chlamydia trachomatis Clostridium perfringens Corynebacterium diphtheria Erysipelothrix rhusiopathiae Escherichia coli Haemophilus influenzae Helicobacter pylori Klebsiella pneumoniae Legionella pneumophila Mycoplasma pneumoniae Neisseria gonorrhoeae Neisseria meningitidis Isolates causing invasive diseases. Non-tuberculous mycobacteria Pseudomonas aeruginosa Salmonella enterica Enteric fever-causing isolates. Staphylococcus aureus Streptococcus pneumoniae Streptococcus pyogenes Vibrio cholera Yersinia enterocolitica Fungi Aspergillus fumigatus Candida albicans Cryptococcus neoformans 14 Epidermophyton floccosum Fonsecaea pedrosoi Fusarium oxysporum Microsporidia Microsporum canis Sporothrix schenckii Trichophyton mentagrophytes Protozoa Ancylostoma duodenale and Babesia microti Helminths Cryptosporidium spp. Strongyloides stercoralis Toxoplasma gondii Viruses Adenovirus Includes all types of human adenoviruses. Plenums carrying contaminated air must be sealed and must be equipped with dampers to arrest and contain the flow of air in the event of ventilation system failure. This is commonly accomplished by the use of an autoclave, such as a pass-through autoclave, but chemical disinfection or decontamination by other methods may also be appropriate. Work involving select agents requires additional regulatory measures, including strict control and documentation of agents during use, storage, and disposal. Examples of select agent-specific administrative controls include select agent inventory control. Burkholderia mallei Burkholderia pseudomallei Coxiella burnetii Francisella tularensis Mycobacterium tuberculosis complex organisms Orientia tsutsugamushi Rickettsia spp. Yersinia pestis Fungi Blastomyces dermatitidis Sporulating mould-forms of these organisms should be Coccidioides spp. Following completion of work, suits are decontaminated in a chemical shower prior to removal. Personnel must next remove scrubs, socks, and under-gloves and pass through a body shower prior to donning street clothes and exiting the facility. Pass-through autoclaves and chemical disinfectant dunk tanks are used for this purpose. Examples Notes Alkhurma Crimean-Congo hemorrhagic fever virus Ebola viruses Includes Ebola virus, Sudan virus, Bundibugyo virus, Tai Forest virus, and Reston virus. Hendra virus Kyasanur Forest disease virus Lassa virus Lujo virus Machupo virus Marburg virus Nipah virus Omsk hemorrhagic fever virus Sabia virus Tickborne encephalitis virus Variola virus Note: 1Clinical specimens. Conversely, administrative controls are defined as changes in procedural practices that help mitigate workplace hazards to workers. For routine clinical microbiology procedures such as specimen handling and bacterial culture examination, a laboratory coat and disposable gloves are generally sufficient. Instead, surgical masks should be reserved for use in patient care areas to minimize the dispersion of potentially infectious droplets emanating from infected 20 patients. An example of this use is in hospital emergency departments where surgical masks are to be worn by patients who have signs and symptoms of influenza-like illnesses. In most institutions, annual monitoring using an interferon-release assay or tuberculin skin test for detection of M. For specific and up-to-date information, contact local, state, and/or national public health specialists. In addition to exposure monitoring, laboratory personnel should be offered, at no charge to them, vaccinations for vaccine-preventable infectious diseases such as hepatitis B, meningococcal disease, influenza, and others. Disinfection can be defined as the elimination of most or all microorganisms, excluding spores, from, on or within an abiotic surface or matrix.
Parity is expressed as the number of term pregnancies gastritis diet plans order aciphex paypal, preterm pregnancies symptoms of upper gastritis purchase genuine aciphex line, abortions gastritis ginger ale discount 20mg aciphex with mastercard, and live births gastritis and diarrhea purchase aciphex 20 mg mastercard. Assess prior cesarean sections and determine type of C-section (low transverse or classical) gastritis or morning sickness buy discount aciphex on-line, and determine reason it was performed gastritis pictures buy aciphex 20mg with visa. Family history of medical illnesses gastritis symptoms how long do they last generic 10 mg aciphex free shipping, hereditary illness gastritis diet foods list generic aciphex 10 mg online, or multiple gestation is sought. Abdominal pain, constipation, headaches, vaginal bleeding, dysuria or urinary frequency, or hemorrhoids. An extremity and neurologic exam are completed, and the presence of a cesarean section scar is sought. Estimation of gestational age by uterine size (1) the nongravid uterus is 3 x 4 x 7 cm. After 20 weeks, there 238 Prenatal Care is a correlation between the number of weeks of gestation and the number of centimeters from the pubic symphysis to the top of the fundus. Hemoglobin electrophoresis is indicated in risks groups, such as sickle hemoglobin in African patients, B-thalassemia in Mediterranean patients, and alpha-thalassemia in Asian patients. First Doppler heart tones should become detectable at 10-12 weeks, and they should be sought thereafter. Frequency of Prenatal Care Visits in Low-Risk Pregnancies <28 weeks Every month 28-36 weeks Every 2 weeks 36-delivery Every 1 week until delivery D. First-trimester morning sickness may be relieved by eating frequent, small meals, getting out of bed slowly after eating a few crackers, and by avoiding spicy or greasy foods. A high-fiber diet with psyllium (Metamucil), increased fluid intake,andregularexerciseshouldbeadvised. First detection of fetal movement (quickening) should occur at around 17 weeks in a multigravida and at 19 weeks in a primigravida. In women under age 35 years, screening for fetal Down syndrome is accomplished with a triple screen. Maternal serum alpha-fetoprotein is elevated in 20-25% of all cases of Down syndrome, and it is elevated in fetal neural tube deficits. If levels are abnormal, an ultrasound examination is performed and genetic amniocentesis is offered. Low levels of all three serum analytes identifies 60-75% of all cases of fetal trisomy 18. At 15-18 weeks, genetic amniocentesis should be offered to patients $35 years old, and it should be offered if a birth defect has occurred in the mother, father, or in previous offspring. At 24-28 weeks, a one-hour Glucola (blood glucose measurement 1 hour after 50-gm oral glucose) is obtained to screen for gestational diabetes. Those with a particular risk (eg, previous gestational diabetes or fetal macrosomia), require earlier testing. If the 1 hour test result is greater than 140 mg/dL, a 3-hour glucose tolerance test is necessary. Pregnancy induced hypertension symptoms (blurred vision, headache, rapid weight gain, edema) are sought. At 26-30 weeks, repeat hemoglobin and hematocrit are obtained to determine the need for iron supplementation. At 36 weeks, repeat serologic testing for syphilis is recommended for high risk groups. Gonorrhea and chlamydia screening is repeated in the third-trimester in high-risk patients. Lower vaginal and rectal cultures are recommended; cultures should notbecollectedbyspeculumexamination. The patient should call physician when rupture of membranes or contractions have occurred every 5 minutes for one hour. Normal Labor Labor consists of the process by which uterine contractions expel the fetus. The frequency, duration, onset, and intensity of uterine contractions should be determined. Braxton Hicks contractions are often felt by patients during the last weeks of pregnancy. The color of the liquid should be 240 Normal Labor determine, including the presence of blood or meconium. A progressive decrease in fetal movement from baseline, should prompt an assessment of fetal well-being with a nonstress test or biophysical profile. Ultrasound measurement of fetal size before 24 weeks of gestation is an accurate measure of dates. Medical problems during this pregnancy should be reviewed, including urinary tract infections, diabetes, or hypertension. Severe headaches, scotomas, hand and facial edema, or epigastric pain (preeclampsia) should be sought. Past pregnancies, durations and outcomes, preterm deliveries, operative deliveries, prolonged labors, pregnancy-induced hypertension should be assessed. Funduscopy should seek hemorrhages or exudates, which may suggest diabetes or hypertension. Auscultation of the lungs for wheezes and crackles may indicate asthma or heart failure. Until the middle of the third trimester, the distance in centimeters from the pubic symphysis to the uterine fundus should correlatewiththegestationalageinweeks. Towardterm,themeasurement becomes progressively less reliable because of engagement of the presenting part. Thevertexisrounderand harder, feels more globular than the breech, and can be moved separately from the fetal body. The lateral aspects of the uterus are palpated to determine on which side the fetal back or fetal extremities (the small parts) are located. With the fetus presenting by vertex, the cephalic prominence may be palpable on the side of the fetal small parts. The adequacy of the bony pelvis, the integrity of the fetal membranes, the degree of cervical dilatation and effacement, and the station of the presenting part should be determined. The baseline heart rate, variability, accelerations, and decelerations are recorded. Prenatal Care: Date of first exam, number of visits; has size been equal to dates Gynecologic History: Menstrual history (menarche, interval, duration), herpes, gonorrhea, chlamydia, abortions; oral contraceptives. Review of Systems: Severe headaches, scotomas, blurred vision, hand and face edema, epigastric pain, pruritus, dysuria, fever. Cervix: Dilatation, effacement, station, position, status of membranes, presentation. Labor is characterized by uterine contractions of sufficient frequency, intensity, and duration to result in effacement and dilatation of the cervix. The first stage of labor starts with the onset of regular contractions and ends with complete dilatation (10 cm). Thelatentphasestartswiththeonsetofregularuterinecontractionsand is characterized by slow cervical dilatation to 4 cm. The second stage of labor begins with complete dilatation of the cervix and ends with delivery of the infant. The average second stage of labor is one-half hour in a multipara and 1 hour in the primipara. The third stage of labor begins with the delivery of the infant and ends with the delivery of the placenta. Intravenous fluid infused rapidly or given as a bolus should be dextrose-free because maternal hyperglycemia can occur. Narcotics should be avoided if their peak action will not have diminished bythetimeofdelivery. Contraindications include infection in the lumbar area, clotting defect, activeneurologicdisease,sensitivitytotheanesthetic,hypovolemia,and septicemia. Risks include hypotension, respiratory arrest, toxic drug reaction, and rare neurologic complications. Before the epidural is initiated, the patient is hydrated with 500-1000 mL of dextrose-free intravenous fluid. Labor and Delivery Admitting Orders Admit: Labor and Delivery Diagnoses: Intrauterine pregnancy at weeks. Condition: Satisfactory Vitals: q1 hr per routine Activity: May ambulate as tolerated. Asthemultiparouspatientapproachescompletedilatationor as the nulliparous patient begins to crown the fetal scalp, preparations are made for delivery. The mother is usually placed in the dorsal lithotomy position with left lateral tilt. The fetal head is delivered by extension as the flexed head passes through the vaginal introitus. Once the fetal head has been delivered, external rotation to the occiput transverse position occurs. A finger is passed into the vagina along the fetal neck to check for a nuchal cord. If shoulder dystocia is anticipated, the shoulders should be delivered immediately. Episiotomy consists of incision of the perineum, enlarging the vaginal orifice at the time of delivery. If indicated, an episiotomy should be performed when 3-4 cm of fetal scalp is visible. With adequate local or spinal anesthetic in place, a medial episiotomy is completed by incising the perineum toward the anus and into the vagina. Application of pressure at the perineal apex with a towel-covered hand helps to prevent extension of the episiotomy. Delivery of the anterior shoulderisaccomplishedbygentledownward traction on the fetal head. The placenta usually separates spontaneously from the uterine wall within 5 minutes of delivery. Gentle fundal massage and gentle traction on the cord facilitates delivery of the placenta. Time of birth, type of birth (spontaneous vaginal delivery), position (left occiput anterior). Routine Postpartum Orders Transfer: To recovery room, then postpartum ward when stable. A first degree perineal laceration extends only through the vaginal and perineal skin. Repair: Place a single layer of interrupted 3-O chromic or Vicryl sutures about 1 cm apart. A second degree laceration extends deeply into the soft tissues of the perineum, down to , but not including, the external anal sphincter capsule. Reapproximate the superficial layers of the perineal body with a running suture extending to the bottom of the episiotomy. Suture the vaginal mucosa with running, interlocking, 3-O chromic or Vicryl absorbable suture. Identify each severed end of the external anal sphincter capsule, and grasp each end with an Allis clamp. Proximate the capsule of the sphincter with 4 interrupted sutures of 2-O or 3-O Vicryl suture, making sure the sutures do not penetrate the rectal mucosa. The laceration extends through the perineum, anal sphincter, and extends through the rectal mucosa to expose the lumen of the rectum. Place a second layer of running suture to invert the first suture line, and take some tension from the first layer closure. Identify and grasp the torn edges of the external anal sphincter capsule with Allis clamps, and perform a repair as for a third-degree laceration. Fetal heart rate monitoring can significantly reduce the risk of newborn seizures (relative risk 0. The fetus normally tolerates contractions without difficulty, but if the frequency, duration, or strength of contractions becomes excessive, fetal hypoxemia may result. The development of decreased variability in the absence of decelera 246 Fetal Heart Rate Monitoring tions is unlikely to be due to hypoxia. Accelerations are common periodic changes, which are usually associated with fetal movement. These changes are reassuring and almost always confirm that the fetus is not acidotic. Variable decelerations are associated with cord compression, and they usually coincide with the timing of the uterine contractions. Variable decelerations are caused by umbilical cord compression, and theyarethemostcommondecelerationsseeninlabor. Persistent variable decelerations to less than 70 bpm lasting more than 60 seconds are concerning. Variable decelerations with a persistently slow return to baseline are nonreassuring because they reflect persistent hypoxia. Nonreassuring variable decelerations are associated with tachycardia, absence of accelerations, and loss of variability. They are usually shallow (10-30 beats per minute), and they reach their nadir after the peak of the contraction. Late decelerations occur when uterine contractions cause decreased fetal oxygenation. Early decelerations are shallow and symmetrical with a pattern similar to that of late decelerations, but they reach their nadir at the same time as the peak of the contraction. These decelerations occur in the active phase of labor and are benign changes caused by fetal head compression. Thedegreetowhichsuchdecelerationsarenonreassuringdependson their depth and duration, loss of variability, and the frequency and progression of recurrence. Attempt to correct the pattern by correcting the primary problem or by institutingmeasuresaimedatimprovingfetaloxygenationandplacental perfusion. Excessiveuterinecontractions,maternalhypotension, or maternal hypoxemia should be corrected. A pelvic examination is performed to rule out umbilical cord prolapse or rapid descent of the fetal head. If no causes are found, umbilical cord compression is likely to be Fetal Heart Rate Monitoring 247 responsible. Maternal oxygenation may be increased by giving oxygen at a flow rate of 8-10 L/min with a tight-fitting face mask. In the supine position, the vena cava and aortoiliac vessels are compressed by the gravid uterus. This results in decreased return of blood to the maternal heart, leading to a fall in uterine blood flow. Variable decelerations that occur prior to fetal descent at 8-9 cm of dilatationaremostfrequentlycausedbyoligohydramnios. Saline amnioinfusion also decreases newborn respiratory complications from meconium due to the dilutional effect of amnioinfusion. Continuousamnioinfusionbeginswithaloadingdoseof10mL/min for 1 hour, followed by a maintenance dose of 3 mL/min via a double-lumen uterine pressure catheter. Even in the absence of excessive uterine contractions, newborn condition may be improved by tocolytic agents. Persistent late decelerations or severe variable decelerations associatedwithabsenceofvariabilityarenonreassuringandgenerally require prompt intervention unless they spontaneously resolve or can be corrected rapidly with conservative measures (oxygen, hydration, maternal repositioning). In the presence of nonreassuring decelerations, a fetal scalp electrode should be placed. Spontaneous accelerations of greater than 15 bpm, lasting at least 15 seconds indicate the absence of fetal acidosis. Ifthefetus fails to respond to stimulation in the presence of an otherwise nonreassuring pattern, there is a 50% chance of acidosis.
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