Protonix

By X. Milok. Clayton College of Natural Health.

Treatment strategies vary by patient age buy protonix paypal, likely pathogens purchase 40mg protonix mastercard, and local resistance pat- terns order protonix in united states online. In the neonatal period buy protonix visa, ampicillin often is combined with a third-generation cephalosporin or an aminoglycoside to cover infections caused by group B Streptococcus, E coli, and L monocytogenes. Neonates in an intensive care unit may be exposed to nosocomial infections; prevalent pathogens in that nursery must be considered. In some locales, more than half of the pneumococcal isolates are intermediately or highly penicillin resistant; 5% to 10% of the organisms are cephalosporin resis- tant. Thus, in suspected pneumococcal meningitis, a third-generation cephalosporin combined with vancomycin is often recommended. The most common long-term sequela is hearing loss (up to 30% of patients with pneumococcus); patients with bacterial meningitis usually have a hearing evaluation at the conclusion of antibi- otic treatment. Mental retardation, neuropsychiatric and learning problems, epi- lepsy, behavioral problems, vision loss, and hydrocephalus are less commonly seen. The child with sickle cell disease (Case 13) has an immune deficiency due to splenic auto-infarction and a higher incidence of infection due to encapsulated (pneumococcus) organisms. These children also are prone to stroke which may present with acute onset of neurologic symptoms similar to those of meningitis. Meningitis due to chronic condition such as tuberculosis may present with failure to thrive (Case 10). Which of the following is the most appropriate next step in the management of this patient? The irritable, fussy infant has a heart rate of 170 beats/min and respiratory rate of 40 breaths/min. The anterior fon- tanelle is full, but he has no nuchal rigidity; the rest of the examination is unremarkable. On examination, he is alert and oriented, but he has nuchal rigidity and a positive Brudzinski sign. Which of the following is the most likely organism respon- sible for this patient’s clinical presentation? Neisseria meningitidis can present as meningococcemia with purpura and shock; in some cases patients will also have meningitis. A course of oral antibiotics, or a single dose of ceftriaxone, is not sufficient to treat meningitis or septicemia. The child described in this case has a history of sickle cell disease likely causing functional asplenia. Because of his asplenia, he is at increased risk of infection with encapsulated bacteria. Streptococcus pneumoniae is more common in older children; whereas, S agalactiae is more common in neonates. Yesterday, he developed a temperature of 104°F (40°C), cramping abdominal pain, emesis, and frequent watery stools. The mother assumed he had the same gastroenteritis as his aunt and many other children in his day care center. While you are asking about his current hydration status, the mother reports that he is having a seizure. You tell her to call the ambulance and then notify the local hospital’s emergency center of his imminent arrival. He has fever, abdominal pain, and watery diarrhea that progressed to bloody diarrhea with mucus. Salmonella infections are self-limited and generally are not treated with antibiotics except in patients younger than 3 months or in immunocompromised individuals; Shigella infections, although self-limited, are generally treated with antibiotics to shorten the illness and decrease organ- ism excretion. Considerations Bloody stools can be caused by many diseases, not all of which are infectious. The description is most consistent, however, with infectious enteritis typical of Shigella or Salmonella. Of particular concern would be ill appearance, the passage of blood or dehydration. Salmonellae organisms are motile, nonlactose fermenters, facultative anaerobic gram-negative bacilli. Salmonellae cause a number of characteristic clinical infections in humans, more common in warmer months. While there are many types of Salmonella, they can be divided into two broad categories: nontyphoidal disease (gastroenteritis, men- ingitis, osteomyelitis, and bacteremia) and typhoid (or enteric) fever, caused primarily by Salmonella typhi. Outbreaks usually occur sporadically but can be food related and occur in clusters. Exposure to poultry and raw eggs probably is the most common source of human infection. Infection requires the ingestion of many organisms; person-to-person spread is uncommon. Gastroenteritis is the most common nontyphoidal disease presentation of Salmonella. The cardinal features of nausea, vomiting, fever, watery or bloody diarrhea, and cramping usually occur within 8 to 72 hours of ingesting contaminated food or water. Most patients develop a low-grade fever; some have neurologic symptoms (confusion, headache, drowsiness, and seizures). Between 1% and 5% of patients with documented Salmonella gastroenteritis develop bacteremia, with subsequent development of a variety of extraintestinal manifestations such as endocarditis, mycotic aneurysm, and osteomy- elitis. Shigellae organisms can survive transit through the stomach because they are less susceptible to acid than other bacteria; for this reason, as few as 10 to 100 organisms can cause disease. Thus, transmission can eas- ily occur via contaminated food and water and via direct person-to-person spread. Infections most commonly occur in warmer months and in patients in their first 10 years of life (peaking in the second and third years). Four Shigella species cause human disease: Shigella dysenteriae, Shigella boydii, Shigella flexneri, and Shigella sonnei. Uncommon intestinal complications include proctitis or rectal prolapse, toxic megacolon, intestinal obstruction, and colonic perforation. Rarely, Shigella causes a rapidly progressive sepsis-like presentation (lethal toxic encephalopathy or Ekiri syndrome) that quickly results in death. Definitive determination of the infecting organism (Salmonella or Shigella) requires stool culture. Fecal leukocytes usually are positive, but this nonspecific finding only suggests colonic inflammation. In Shigella infection, the peripheral white count usually is normal, but a remarkable left shift often is seen with more bands than polymorphonuclear cells. Shigella is self-limited as well; if left untreated, diarrhea typically lasts 1 to 2 weeks. However, antibiotics shorten the illness course and decrease the duration organisms are shed. In addition to the previously listed organisms, enteroinvasive Escherichia coli, Campylobacter sp, and Yersinia enterocolitica can cause dysentery, with fever, abdom- inal cramps, and bloody diarrhea. Enterohemorrhagic (or Shiga toxin–producing) E coli can cause bloody diarrhea but usually no fever. Infection with Vibrio cholera produces vomiting and profuse, watery, nonbloody diarrhea with little or no fever. Hemolytic-uremic syndrome, the most common cause of acute childhood renal failure, develops in 5% to 8% of children with diarrhea caused by enterohemor- rhagic E coli (O157:H7); it is seen less commonly after Shigella, Salmonella, and Yersinia infections. The under- lying process may be microthrombi, microvascular endothelial cell injury causing microangiopathic hemolytic anemia and consumptive thrombocytopenia. Renal glomerular deposition of an unidentified material leads to capillary wall thickening and subsequent lumen narrowing. The typical presentation occurs 1 to 2 weeks after a diarrheal illness, with acute onset of pallor, irritability, decreased or absent urine output, and even stroke; children may also develop petechiae and edema. Most children recover and regain normal renal function; all are followed after infection for hypertension and chronic renal failure. His parents were not overly concerned because he seemed fine between the pain episodes. Today, how- ever, he has persistent bilious emesis and has had several bloody stools. Examination reveals a lethargic child in mild distress; he is tachycardic and febrile.

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In the past 24 hours he has had more than 10 episodes of diarrhea protonix 20mg fast delivery, with the most recent appearing to consist of only blood with no identifiable stool mixed with it discount protonix master card. Bleeding from an anal fissure is not chronic and the amount of hematoche- zia is small discount protonix on line. A hemoglobin that is low enough to cause pallor of the mucosal membranes is not produced from an anal fissure safe protonix 40 mg. Given her age, the most likely cause of her painless rectal bleeding is Meckel diverticulum. A suppository, increased fiber, and stool withholding will worsen the stool bulk and are likely to cause a fissure. If she no longer has constipation but the fissure recurs, then Crohn disease may be the cause and she should have further evaluation. Isotonic saline should be given until volume is restored and then based on the hemoglobin and clotting studies, he may need red blood cells or plasma. His clinical presentation could represent intussusception and if seen on ultra- sound, surgical consultation is needed. He had been having normal activity and intake until about 48 hours prior when he developed a temperature of 102. She reports that he did not sleep well the previous evening, awakening several times complaining of ear pain, but remains somewhat interested in his toys earlier in the day. Crura of stapes Footplate of stapes Incus in oval window Malleus Semicircular canals Tympanic membrane Facial nerve (eardrum) Vestibular nerve Auricle (pinna) External acoustic Internal acoustic meatus (ear canal) meatus Middle ear Cochlear nerve Round window Cochlea Eustachian tube Parotid gland Internal jugular vein Figure 16–1. This procedure is rarely done in the primary care office, but rather is done by the specialist. Common bacterial pathogens include Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrh- alis. Other organisms, Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa, are seen in neonates and patients with immune defi- ciencies. Should antibiotics be deemed necessary and depending on a community’s bac- terial resistance patterns, amoxicillin at doses up to 80 to 90 mg/kg/d for 7 to 10 days is often the initial treatment. In the child begun on amoxicillin who demonstrates clinical failure after 3 treatment days, a change to amoxicillin-clavulanate, cefuroxime axetil, cefdinir, azithromycin, ceftriaxone, or tympanocentesis is considered. Adjuvant therapies (analgesics or antipyretics) are often indicated, but other measures (antihistamines, decongestants, and corticosteroids) are ineffective. If hearing is normal, middle ear effusion often is treated with observation; some prac- titioners treat with antibiotics. The child has mastoiditis, a clinical diagnosis that can require computed tomography scan confirmation. Surgical drainage of the mastoid air cells may be needed if improvement is not seen in 24 to 48 hours. After failing several antibiotic regimens, tympanocentesis and culture of the middle ear fluid are indicated. If a clinical failure is seen on day 3, a change to amoxicillin-clavulanate, cefuroxime axetil, ceftriaxone, or a tympano- centesis is indicated. The mother is concerned that the baby’s manner of crawling, where he drags his legs rather than using a four-limbed movement, is abnormal. She says that the child only recently began crawling and he does not pull to a stand. You noted at his 6-month visit that he was not yet rolling over or sitting; previous visits were unremarkable as was the mother’s pregnancy and vaginal delivery. On examina- tion today, you note that he positions his legs in a “scissoring” posture (ie, legs extended and crossed) when held by the axillae. A complete developmental and neurologic assessment is crucial for initiating therapies that will help him achieve maximal functional outcome. Knowing the etiology can aid in developing a treatment plan, subsequent family planning (especially if the etiology is inherited), and assuaging parental guilt for this child’s condition. This definition recognizes the central origin of the dysfunction, thus dis- tinguishing it from neuropathies and myopathies. Deafness, visual impairments, swallowing difficulty with concomitant aspiration, limb and sensory impairments, and behavioral disturbances are common comorbidities. Contractures and postural deformities may become more severe with time or may improve with therapy. Also, a child’s changing developmental stages early in life can alter the expression of his or her neurologic deficits. Possible imaging findings include periventricular leukomalacia, atrophy, or focal infarctions. Examples of concerning findings are as follows: š A stepping response after the age of 3 months š A Moro reflex beyond 6 months š An asymmetrical tonic neck reflex beyond 6 months Cerebral palsy can be classified in terms of physiologic, topographic, or func- tional categories. Physiologic descriptors identify the major motor abnormality and are divided into pyramidal (spastic) and extrapyramidal (nonspastic) categories. Extrapyramidal types can be subdivided further into choreoathetoid, ataxic, dys- tonic, or rigid types. Hemiplegia refers to involvement of a single lateral side of the body, with greater impairment of the upper extremities than the lower extremities. Diplegia describes a four-limb involvement, with greater impairment of the lower extremi- ties. Spastic quadriplegia is a four-limb involvement with significant impair- ment of all extremities, although the upper limbs may be less impaired than the lower limbs. The motor quotient is derived by dividing the child’s “motor age” (ie, motor skills devel- opmental age) with the chronologic age. A motor quotient of 75 to 100 represents minimal impairment, 55 to 70 is mild impairment, 40 to 55 is moderate impair- ment, and lesser quotients indicate severe impairment. These categories help clini- cians identify children with less obvious impairments so that early treatment can be provided. The yield of diagnostic findings with brain imaging and metabolic or genetic testing is low but can be helpful in managing the patient, in future family planning, and in reassuring the parents. Treatment goals include maximizing motor function and preventing secondary handicaps. School perfor- mance and peer acceptance become important issues for older children. Physical therapy for motor deficits may be supplemented with pharmacologic and surgi- cal interventions. Occupational therapy improves positioning and allows for better interaction with the environment and eases care as the child grows. He walks with the help of leg braces and a walker, and his speech is slurred and limited to short phrases. On examination, you find that the boy has only minimally increased tone in the upper extremities but good fine motor coordination; he has significantly increased tone and deep tendon reflexes in the lower extremities. You will ask which therapies he receives, who provides them, the frequency and goals. The Apgar score at 1 minute reflects the neonatal environment immediately prior to birth; it does not predict an infant’s neurologic outcome. Assessing a child’s development at each checkup is important for detecting abnormalities. If there is abnormal devel- opment or an abnormal examination finding, then referral to a neurologist may be appropriate. In diplegia all four extremities are affected, with greater impairment of the lower extremities. Because most children walk by the age of 14 months, this child’s motor quotient is 14 months/30 months = 0. Even though the office-based hearing evaluation cannot be done for him because it requires verbal participation, his hearing still needs to be assessed; a hearing test that does not require the patient to give a verbal response should be ordered. Asking about behavior that suggests a seizure is part of the review of systems for all children. Although his development is delayed, it is still important to assess in order to identify the age level that he is at for each area of development. His mother reports that he has been diag- nosed with asthma and has an albuterol inhaler to use for wheezing or cough. Since 6 months of age, he has had several similar episodes of “wet” cough and fever, which were diagnosed as bronchitis or pneumonia, and he would improve when treated with antibiotics and albuterol.

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Older adults Because antihistamines can cause sedation cheap generic protonix uk, smaller doses should be used initially and titrated up if needed cheap protonix 20mg on-line. Therapeutic Uses All of the H antagonists are useful in treating allergic disorders buy protonix from india. In people with seasonal allergic rhinitis order protonix with visa, H blockers can reduce sneezing, rhinorrhea, and itching of the1 eyes, nose, and throat. In patients with acute urticaria, these drugs can reduce redness, itching, and edema. The antihistamines can also reduce symptoms of allergic conjunctivitis and urticaria associated with mild transfusion reactions. In all these conditions, benefits result from H receptor blockade—not from1 preventing allergen-induced release of histamine from mast cells and basophils. Because mild allergic reactions may be mediated by substances in addition to histamine, antihistamines often fail to produce complete relief. Motion Sickness Some antihistamines, such as promethazine [Phenergan] and dimenhydrinate [Dramamine], are labeled for use in motion sickness. Benefits derive from blocking H receptors and muscarinic receptors in the neuronal pathway leading1 from the vestibular apparatus of the inner ear to the vomiting center of the medulla. Insomnia The ability of antihistamines to cause drowsiness has been exploited in the treatment of insomnia. As a rule, these responses1 are more of a nuisance than a source of serious discomfort or danger. Because individual antihistamines differ in their abilities to produce particular side effects (Table 54. In fact, the degree of impairment seen with antihistamines equals that seen when blood levels of alcohol exceed the legal limit. Accordingly, patients should exercise extreme caution when driving or performing other hazardous activities. If a preparation with a long half-life is being used, daytime sedation can be minimized by administering the entire daily dose at night. Second, these drugs have low affinity to the type of H receptor found in the brain. In contrast, the first-generation antihistamines are1 relatively small molecules with high lipid solubility and hence can readily cross the blood-brain barrier. For patients who experience disabling sedation with a first-generation H1 antagonist, therapy with a second-generation (nonsedating) antihistamine is likely to help. In some patients, paradoxical excitation occurs, resulting in insomnia, nervousness, tremors, and even seizures. Responses include nausea, vomiting, loss of appetite, and diarrhea or constipation. These antimuscarinic1 actions can produce drying of mucous membranes in the mouth, nasal passages, and throat. Cholinergic blockade may also result in urinary hesitancy, constipation, and palpitations. If dry mouth becomes distressing, discomfort can be minimized by using hard sugarless candy and by taking frequent sips of liquid. Antihistamines should be used with caution in patients with asthma because thickening of bronchial secretions may impair breathing. Care is also needed in patients with other conditions that can be made worse by muscarinic blockade (e. B l a c k B o x Wa r n i n g : P ro m e t h a z i n e Promethazine [Phenergan, Phenadoz] can cause severe respiratory depression, especially in very young patients. Accordingly, the drug is now contraindicated for use in children younger than 2 years and should be used with caution in children older than 2 years. Severe injury can also occur with inadvertent perivascular or intraarterial administration, or with administration into or near a nerve. Accordingly, when parenteral dosing is needed, the preferred route is intramuscular; subcutaneous promethazine is contraindicated. Use in Pregnancy and Lactation Pregnancy The margin of safety of antihistamines in pregnancy is unknown. There have been reports of fetal malformation, but direct involvement of H antagonists has1 not been proved. Given the uncertainty over the safety of these drugs, it is recommended that antihistamines be used only when clearly necessary and only when the benefits of treatment outweigh the potential risks to the fetus. Antihistamines should be avoided late in the third trimester because newborns are particularly sensitive to the adverse actions of these drugs. Lactation The H antagonists can be excreted in breast milk, thereby posing a risk to the1 nursing infant. Because infants, and especially newborns, are unusually sensitive to antihistamines, these drugs should be avoided by women who are breastfeeding. Acute Toxicity Although the antihistamines have a large margin of safety, acute poisoning is nonetheless common, owing to the widespread availability of these drugs. Symptoms The anticholinergic actions of H blockers produce symptoms resembling those1 of atropine poisoning (dilated pupils, flushed face, hyperpyrexia, tachycardia, dry mouth, urinary retention). In extreme cases, intoxication progresses to coma, cardiovascular collapse, and death. Convulsions can be treated with intravenous benzodiazepines (lorazepam, midazolam). Preparations As noted previously, the H antagonists can be divided into two major groups:1 first-generation H antagonists and second-generation H antagonists. In addition, some can be given parenterally, by nasal spray, or by rectal suppository. First-Generation Histamine-1 Antagonists The first-generation antihistamines can be grouped into five major categories (see Table 54. These groups differ in antihistaminic efficacy and the ability to cause sedation and muscarinic blockade. Given these differences, it may be possible, through judicious drug selection, to produce effective H blockade1 while minimizing undesired effects. For many patients, the alkylamines can provide effective H blockade while causing only a modest1 reduction in alertness. If sedation remains excessive with an alkylamine, a second-generation agent should be tried. As a result, they can cause dry mouth, urinary hesitancy, and other typical anticholinergic side effects. In addition to lacking sedative effects, the second-generation agents are largely devoid of anticholinergic actions. Now, three agents—cetirizine, fexofenadine, and loratadine—are available over the counter. Because all of these drugs are very similar, initial selection can usually be based on price. Descriptions that follow are limited to the five second-generation agents that are used for oral therapy. Two other second-generation agents, azelastine [Astelin, Astepro] and olopatadine [Patanase], both used for local effects in the nose, are discussed in Chapter 60. Fexofenadine [Allegra, Allegra Allergy] is approved for oral therapy of seasonal allergic rhinitis and for chronic idiopathic urticaria. Of the second-generation antihistamines now available, fexofenadine appears to offer the best combination of efficacy and safety. In clinical trials, the incidence of drowsiness and other side effects was nearly the same as with placebo. To ensure fexofenadine absorption, patients should not drink fruit juices within 4 hours before dosing or 1 to 2 hours after dosing. Cetirizine is eliminated by a combination of hepatic metabolism and renal excretion. Although cetirizine is generally well tolerated, it can cause drowsiness, fatigue, and dryness of the mouth, nose, and throat.

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