Which is better pepto bismol or mylanta

Amoxicillin

The combination of naproxen with amoxicillin has been reported to have caused interstitial nephritis [62,63]. Of course, both of these drugs can have interstitial nephritis, and it is not clear that the combination carries a higher risk.

Antacids

In 14 healthy men who took capsules of naproxen alone or combined with different antacids, sodium bicarbonate increased the Cmax and shortened the tmax of naproxen, while magnesium oxide and aluminium hydroxide reduced the Cmax and prolonged the tmax [64].

However, in 11 healthy volunteers Mylanta (aluminium hydroxide + magnesium hydroxide + simethicone) had no effect on the pharmacokinetics of single oral doses of naproxen 250 mg or multiple oral doses (250 mg bd for 7 days); there were no significant effects on AUC, tmax, Cmax, or half-life [65].

Beta-adrenoceptor antagonists

In a double-blind study in 28 patients with essential hypertension well controlled by atenolol, naproxen significantly increased the systolic blood pressure compared with placebo (mean 4.0 mmHg; 95% CI = 1.1, 7.0) [66].

In contrast, in a placebo-controlled study in 17 patients with hypertension who were taking propranolol, naproxen 500 mg bd had no effect on blood pressure [67], although there have been anecdotal reports of worsening hypertension in such cases [68].

Colestyramine

Colestyramine adsorbs naproxen in vitro to different extents depending on pH, with a maximum of 2.2 mmol/l/g [69]. In eight healthy volunteers the rate of absorption of a single dose of naproxen 250 mg was reduced by colestyramine 4 g, with a delay in tmax and a reduced Cmax; however, absorption was eventually complete.

Ciclosporin

In 11 patients with rheumatoid arthritis who took sulindac or naproxen with or without ciclosporin 5 mg/kg/day there was greater impairment of renal function during administration of the combination, with reductions in glomerular filtration rate and effective renal plasma flow and a blunted response to furosemide [70].

Diuretics

Naproxen reduces the actions of diuretics [68,71,72].

In 6 healthy kidney donors and 6 renal transplant recipients pretreatment with naproxen reduced renal sensitivity to furosemide, shifting the dose- response curve to the right in all the donors and in two of the patients [73]. Resistance to the diuretic effects of furosemide have also been reported in cardiac failure [74].

In 97 patients with mild essential hypertension naproxen and ibuprofen attenuated the antihypertensive effect of hydrochlorothiazide 50 mg/day in a three-phase, multicenter, double-blind, randomized, parallel study, in which the patients served as their own controls [75].

Glucocorticosteroids

In 11 patients with stable rheumatoid disease who were taking prednisolone, naproxen significantly increased the unbound plasma concentration of prednisolone without a change in total prednisolone concentration [76].

Lithium

There were no significant changes in serum lithium concentrations in 12 men taking over-the-counter doses of naproxen (220 mg tds) or paracetamol (650 mg qds) for 5 days [77].

In contrast, in seven patients taking naproxen there were variable increases in steady-state serum lithium concentrations, ranging from no change to a 42% increase, with corresponding reductions in lithium clearance [78]. This may imply differences in individual susceptibility to an interaction.

Methotrexate

Methotrexate alters naproxen kinetics and vice versa, and there have been anecdotal reports of methotrexate toxicity in individuals who took naproxen [79].

In nine children with juvenile rheumatoid arthritis who took their usual doses of methotrexate (0.22–1.02 mg/kg/week) and naproxen (14.6–18.8 mg/kg/day) separately and together, methotrexate caused a 30% or greater change in naproxen kinetics in six and naproxen caused a 30% or greater change in methotrexate kinetics in four [80].

The interaction of methotrexate with tolmetin, indomethacin, naproxen, and aspirin has been studied in seven children with chronic arthritis, of whom six were taking more than one NSAID [81]. The mean methotrexate half-life was prolonged when NSAIDs were co-administered (1.7 versus 1.2 hours). The apparent methotrexate clearance (11 versus 13 l/hour), the AUC (2.1 versus 1.5 hour.μmol/l), and the apparent volume of distribution (23 versus 22 l) were not significantly altered. However, there was wide variation in the effects of NSAIDs on methotrexate clearance, and in six patients the AUC increased by 19–140%, which might be clinically significant in some individuals.

In nine patients with rheumatoid arthritis naproxen reduced the clearance of methotrexate from 10 to 7.9 l/hour, mainly by reducing renal clearance [82].

In contrast, in 12 patients aged 30–78 years with rheumatoid arthritis and normal renal function, who were given oral and intravenous methotrexate 15 mg, methotrexate clearance and plasma protein binding were not altered by oral naproxen 1000 mg/day [83].

Methyldopa

Naproxen reduces the actions of methyldopa [68].

Misoprostol

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A 59 year old man with rheumatoid who was taking naproxen was given misoprostol and within few hours developed ataxia and vomiting [84]. After 5 days he stopped taking the misoprostol and improved rapidly. After another 3 he took one tablet of misoprostol and the ataxia rapidly recurred and lasted several hours. The symptoms recurred when he took another tablet of misoprostol on the next day.

Probenecid

Naproxen inhibits the metabolism and renal excretion of probenecid, prolonging its half-life, and probenecid increases plasma naproxen concentrations [85].

Sulfonylureas

In a double-blind study in 16 patients with type 2 diabetes who were taking tolbutamide, naproxen had no effect on blood glucose concentrations compared with placebo and serum tolbutamide concentrations were not significantly altered [86]. This was subsequently confirmed in 10 patients with type 2 diabetes [87].

Screening Procedures

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Bone mineral density (BMD) screening/assessment is a relatively noninvasive procedure that also can be used to monitor treatment efficacy. BMD measurement is given as a T-score and a Z-score. The T-score is the deviation from the mean bone density of healthy young adults of the same gender and ethnicity, and the Z-score is the deviation from the mean bone density of adults of the same age and gender.

Dual-energy x-ray absorptiometry (DEXA) scans the entire body and measures BMD. From the results, physicians assess the risk for fracture in the hip, spine, and wrist. Radiation exposure is low and time commitment minimal (approximately 5 minutes). DEXA can be used to monitor changes in bone density during treatment.

Quantitative computed tomography (QCT) measures bone density in the hip and spine and produces a three-dimensional image that shows true volume density. The radiation level in QCT is 10 times higher than in DEXA.

Peripheral bone density testing uses ultrasound to identify bone loss in a localized area such as the heel or hand.

X-ray. Unfortunately, osteoporosis does not show up on regular spinal x-rays until there is a 30% loss of bone.

Lifestyle Management

Recognizing and managing the factors that contribute to osteoporosis will help to prevent it or modulate its severity. These include the following:

Get adequate exposure to sunlight.

Consume adequate amounts of calcium in the diet.

Avoid excessive intake of calcium-excreting products such as phosphates in some sodas.

Because bones mineralize fully only when placed under stress, initiate weight-bearing exercise at an early age.

Diet

Include additional calcium along with magnesium in the diet.

Clinical Pearl

Most adults lose the ability to make the enzyme lactase by age 45 (and much younger in some ethnic populations). Most black people lose the ability to make lactase by age 18; therefore milk is not an ideal source of calcium in black adults. Yogurt and buttermilk are suitable sources of calcium for adults because they are fermented products, made with cultures that break down the lactose. Cheese is a protein curd that does not contain lactose and also is appropriate.

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Consume a diet rich in fruits and vegetables, especially green vegetables.

Whole grains, such as brown rice, millet, buckwheat, whole wheat, triticale, quinoa, rye, legumes, and leafy vegetables, are rich in calcium. Whole grains and legumes also are rich in magnesium, which helps bone to incorporate calcium.

Minimize high-protein diets because they can cause larger than normal calcium excretion, thereby increasing the potential for bone loss.

Type of calcium supplementEasily absorbedCalcium content (%)Other benefitsDisadvantagesCalcium AscorbateYes10%Vitamin C is the other componentCalcium AspartateYes20%Calcium CarbonateNot always Should be taken with food for maximum absorption.40%Inexpensive source of calcium. Has antacid effect.Has antacid effect. Can interfere with digestion. May not be well absorbed in people with insufficient output of stomach acid. Can cause gas.Calcium CitrateYes2%Can be absorbed by those with poor digestion. Reduces risk for kidney stones.Larger molecule is bulkier than calcium carbonate, thus requiring more tablets/capsules to achieve the same dosage as calcium carbonate.Calcium LactateYes15%May contain milk and/or yeast byproducts.May contain milk and or yeast byproducts. Larger molecule is bulkier than calcium carbonate, thus requiring more tablets/capsules to achieve the same dosage as calcium carbonate.Calcium amino acid chelateYes10%–20%Lactose intoleranceMay be incorrectly made as a soy blend.Bone MealYes39%Contains many of the minerals needed for bone.May contain lead, arsenic, cadmium, and other unidentified minerals. Some of the organic constituents are destroyed by heat during processing.Microcrystalline Hydroxyapatite Concentrate (MCHC)Yes/No25%Contains collagen and several of the other minerals needed for healthy bone formation, including phosphorous, fluoride, mg, Fe, Zn, cu, ma.More expensive.Calcium phosphate Coral calcium, oyster shell, calcium dolomite, and bone mealNo38%Is essentially calcium carbonate. Better to use purified calcium carbonate products (see above).Least likely to cause constipation.Blocks absorption of iron and other minerals.May contain high levels of lead and other impurities.

Vitamins, Minerals, and Herbs

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Calcium 1000 to 1500 mg/day

Vitamin D (minimum of 400 lU/day)

Herbs for bone health, including oat straw and horsetail

Acupressure

Acupressure points for bone health include kidney 1 between the second and third metatarsals, kidney 3 on the medial side of the foot behind the tibia, and bladder 64 on the little toe.

Spinal Manipulation

Low-force techniques should be used.

Physical Therapy

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Fall risk assessment and prevention

Balance training

Postural reeducation

Spinal extensor strengthening

Core muscle strengthening

Pelvic floor training

Weight-bearing exercises

Hip flexor, erector spinae, and abdominal muscle stretching

Pain management in the presence of fractures

Hydrotherapy when the patient has pain from recent vertebral fracture or postural and balance problems

Transcutaneous electrical nerve stimulation (TENS)

Interferential therapy

Heat therapies

Acupuncture

Aromatherapy

Reflex therapy

Relaxation techniques

Bracing

40 Who is affected by pill-induced esophageal injury?

Anyone of any age who ingests caustic pills is susceptible to pill-induced injury. Reported cases range from 5 to 89 years old. Women outnumber men by a ratio of 1.5:1. It is not uncommon for pills to stick in a normal esophagus during transit. A more sticky gelatin tablet remained in the esophagus for more than 10 minutes in over one-half of normal subjects who ingested the pill in a supine position. Esophageal dysmotility or structural abnormalities, such as rings or strictures, are clearly not required for pill-induced injury.

41 What factors contribute to esophageal retention of pills?

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Impaired esophageal clearance

Supine posture during or immediately after pill ingestion

Structural defects: rings, stricture, extrinsic compression, etc

Swallowing pills without sufficient liquid

Esophageal dysmotility

Pill characteristics: acidic, basic, sticky, large size

Most common history for pill esophagitis: taking the pill with inadequate fluid and lying down immediately afterward are often the only identifiable risk factors.

42 What are the risk factors for pill-induced injury?

Anyone who takes a caustic pill is at risk, but some patients are at particular risk for severe pill-induced esophageal injury, including those with structural abnormalities of the esophagus, both pathologic (stricture, tumor, ring—see Fig. 6-14) and physiologic (hiatal hernia, narrowing of the esophagus secondary to compression from the left atrium, aortic arch, left main stem bronchus). Cardiac disease is a risk factor because of esophageal compression by a dilated left atrium and frequent use of inherently caustic medications (e.g., aspirin, potassium chloride, quinidine).

43 Describe the typical presentation of patients with pill-induced injury

The typical patient has no prior history of esophageal disease and presents with the sudden onset of retrosternal pain, which may have awakened the patient from sleep (particularly if pills were ingested with little liquid just before or while lying down) and may be exacerbated by swallowing. The pain may be mild or so severe that swallowing is impossible. The pain typically increases over the first 3 to 4 days before gradually subsiding. Painless dysphagia is uncommon (20%) and may suggest an alternative diagnosis.

44 How is the diagnosis of pill-induced esophageal injury made?

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Clinical suspicion

Acute onset of odynophagia, dysphagia, and/or chest pain

Exposure to pills commonly associated with esophageal injury

Upper endoscopy preferred over barium swallow, as biopsy is often necessary to exclude infectious causes of esophageal ulcer

45 What does the typical pill-induced lesion look like at time of endoscopy?

The typical lesion of pill-induced esophageal injury is one or more discrete ulcers with normal surrounding mucosa. Ulcers range in size from pinpoint to circumferential lesions that may be several centimeters long. Most ulcers involve only the mucosa, but deeper penetration can occur and localized perforations have been reported. Ulcers may have local surrounding inflammation. Pill fragments have been seen in ulcer craters.

46 How can you remember the many medications that can cause pill-induced esophagitis?

Know your ABCs: N-O-A-A-B-Cs (Table 6-1).

Doxycycline and tetracycline accounted for 293 of 454 reported cases of pill-induced esophageal injury in one recent review.

47 Where are the areas of physiologic narrowing of the esophagus?

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Esophageal sphincters: lower and upper sphincters (LES and UES)

Strictures

Peptic

Webs

Rings

Extrinsic compression

Aortic arch

Left main stem bronchus

Left atrium

Cervical osteophytes

48 What are the options for treating pill-induced esophageal injury?

Most pill-induced injuries heal without active intervention in days to several weeks. Avoid the drug responsible for the injury and other caustic drugs. Administration of medications that buffer or decrease production of stomach acid, or create a barrier coat for the esophagus, is frequently prescribed. The use of topical anesthetics in various combinations (Bemylid—Benadryl, Mylanta, and lidocaine in equal parts) may decrease the immediate symptoms of odynophagia, but their use is limited by potential systemic toxicity.

49 Discuss the epidemiology of caustic ingestion in the United States

Chemical ingestion remains an important problem despite improvements in packaging (e.g., child-proof containers), product labeling, and warnings. Approximately 5000 caustic ingestions occur per year. Adolescents and adults who willfully ingest caustic agents as a suicidal gesture in general consume a larger volume and therefore have more serious injury than do children, who ingest the agent accidentally and often expectorate most of it before swallowing. Children often have minimal esophageal damage, but their oral, pharyngeal, and laryngeal injuries may be more severe. Approximately 80% of caustic ingestions occur accidentally in children younger than 5 years, who most often consume household cleaners. Caustic ingestion is the leading cause of esophageal strictures in children.

50 What are the common caustic agents? Where are they found?

Caustic agents are present in many common household products. The severity of the damage depends largely on the corrosive properties and concentration of the ingested agents. The caustic agents most often responsible for serious injury are strong alkaline cleaning products, such as drain cleaners and lye soaps. Severe alkaline burns also result from the ingestion of disc batteries that contain concentrated sodium or potassium hydroxide. Concentrated acid compounds also cause severe injury but are not common household items; thus, they are encountered less often. The severity of esophageal and gastric injury secondary to caustic ingestion depends not only on the concentration and corrosive properties of the agent but also on the quantity consumed.

51 Describe the pathophysiology of acute alkali esophagitis

When tissue is exposed to strong alkali, the immediate result is liquefactive necrosis, the complete destruction of entire cells and their membranes. Cell membranes are destroyed as their lipids are saponified and cellular proteins are denatured. Thrombosis of the local blood vessels also contributes to tissue damage. Tissue destruction and organ penetration progress rapidly until the alkali is diluted and neutralized by dilution with tissue fluids.

52 The severity of caustic injury to the esophagus can be graded as first, second, or third degree, using the following system

Endoscopy within the first 24 hours may underestimate the severity of esophageal injury (Table 6-2).

53 Describe how an endoscopic grading system guides in management and prognosis of the patient with corrosive injection

Patients with grade 1 or 2A caustic injury have an excellent prognosis without acute morbidity or chronic stricture formation. For these patients, administration of a liquid diet can be started and advanced to a regular diet after 1 to 2 days. Patients with grade 2B to 3A injury develop strictures in 70% to 100% of cases. Grade 3B carries a 65% early mortality rate and a significant need for esophageal resection. Despite this poor prognosis, there is no evidence that medical therapy with antibiotics or steroids are of any benefit. For difficult strictures, barium swallow may be very helpful in defining anatomy and guiding dilation decisions (Fig. 6-15).

54 What is the cancer risk to a patient with stricture after lye ingestion?

The association between esophageal cancer and caustic ingestion is strong. The expected incidence of esophageal carcinoma is higher in patients with caustic ingestion than in the general population. Approximately 1% to 7% of patients with carcinoma of the esophagus have a history of caustic ingestion. The latent period is long, and in one study was an average of 41 years. Vigilance and early endoscopic evaluation of esophageal symptoms are warranted.

55 Describe the emergency department management of a patient with caustic ingestion

The initial steps in the management of a suspected caustic injury are similar to those used on an emergency basis to manage any toxic ingestion. First, airway, breathing, and circulation (ABCs) must be controlled. Patients with caustic ingestion may present with respiratory compromise and require endotracheal intubation to protect the airway and to provide adequate oxygenation. Intubation should be performed only under direct visualization and should not be attempted in a blind manner. Next, hypotension must be addressed with adequate fluid support and resuscitation, as needed. If obvious signs of mediastinitis or peritonitis suggest perforation of a viscus, the patient should be prepared for surgery.

56 What is the role of endoscopic evaluation in patients with caustic ingestion?

Flexible upper endoscopy has a role in the early, emergent and later, subacute management of caustic ingestion. Patients in whom perforation (diagnosed either radiographically or clinically) requires surgical exploration should undergo complete upper endoscopy to identify the extent of disease. For example, in patients with a normal esophagus but injured stomach, surgery may be limited to the abdomen. The risk of upper endoscopy is acceptable once the decision to operate has been made. If surgery is not indicated, endoscopy still should be performed to identify uninjured patients who do not require prolonged hospital observation and to define the severity of burns in injured patients. Timing of endoscopy is based on clinical suspicion of severe injury. If significant esophageal injury is unlikely, esophagogastroduodenoscopy (EGD) should be performed promptly to provide rapid reassurance and to avoid hospital observation. More than 50% of patients with a history of caustic injury are found on endoscopy to have no injury. If internal injury is likely but signs of perforation are absent, a delay of 48 to 72 hours permits development of the inflammatory reaction (little inflammation may be present in the first 24 hours) and easier assessment of the true extent of injury. Although endoscopic evaluation identifies the location of the mucosal injury, it may not accurately predict the depth of invasion.

Is it OK to take Mylanta and Pepto

What works better than Pepto

What is best medicine for stomach upset?

Which is better Pepto