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In adult females order prevacid with visa, too much vitamin A can increase the risk for hip fracture—apparently by blocking the ability of vitamin D to enhance calcium absorption purchase 30 mg prevacid mastercard. Therapeutic Uses The only indication for vitamin A is prevention or correction of vitamin A deficiency order prevacid with a mastercard. Contrary to earlier hopes buy discount prevacid on-line, it is now clear that vitamin A, in the form of beta-carotene supplements, does not decrease the risk for cancer or cardiovascular disease. In fact, in a study comparing placebo with dietary supplements (beta-carotene plus vitamin A), subjects taking the supplements had a significantly increased risk for lung cancer and overall mortality. Vitamin D Vitamin D plays a critical role in calcium metabolism and maintenance of bone health. The classic effects of deficiency are rickets (in children) and osteomalacia (in adults). Studies suggest that vitamin D may protect against arthritis, diabetes, heart disease, autoimmune disorders, and cancers of the colon, breast, and prostate. However, in a 2011 report—Dietary Reference Intakes for Calcium and Vitamin D—an expert panel concluded that, although such claims might eventually prove true, the current evidence does not prove any benefits beyond bone health. Vitamin E (Alpha-Tocopherol) Vitamin E (alpha-tocopherol) is essential to the health of many animal species but has no clearly established role in human nutrition. Observational studies of the past suggested that vitamin E protected against cardiovascular disease, Alzheimer disease, and cancer. Moreover, there is evidence that high-dose vitamin E may actually increase the risk for heart failure, cancer progression, and all-cause mortality. However, only four stereoisomers are found in our blood, all of them variants of alpha-tocopherol. The vitamin is also found in nuts, wheat germ, whole-grain products, and mustard greens. Accordingly, this limit should be exceeded only when there is a need to manage a specific disorder (e. Symptoms of deficiency include ataxia, sensory neuropathy, areflexia, and muscle hypertrophy. Potential Benefits Vitamin E has a role in protecting red blood cells from hemolysis. The higher dose associated with halting macular degeneration carries substantial risk, as detailed in the discussion that follows. Potential Risks High-dose vitamin E appears to increase the risk for hemorrhagic stroke by inhibiting platelet aggregation. These results are consistent with the theory that high doses of antioxidants may cause cancer or accelerate cancer progression. Studies have also linked high-dose vitamin E therapy with an increased risk for death, especially in older people. Finally, high-dose vitamin E (in combination with vitamin C) can blunt the beneficial effects of exercise on insulin sensitivity. Forms and Sources of Vitamin K Vitamin K occurs in nature in two forms: (1) vitamin K, or phytonadione1 (phylloquinone), and (2) vitamin K. Two other forms2 —vitamin K 4 (menadiol) and vitamin K 3 (menadione)—are produced synthetically. At this time, phytonadione is the only form of vitamin K available for therapeutic use. For most individuals, vitamin K requirements are readily met through dietary sources and through vitamin K synthesized by intestinal bacteria. Because bacterial colonization of the gut is not complete until several days after birth, levels of vitamin K may be low in newborns. Pharmacokinetics Intestinal absorption of the natural forms of vitamin K (phytonadione and vitamin K ) is adequate only in the presence of bile salts. Because the natural forms of vitamin K require bile salts for their uptake, any condition that decreases availability of these salts (e. Malabsorption syndromes (sprue, celiac disease, cystic fibrosis of the pancreas) can also decrease vitamin K uptake. Other potential causes of impaired absorption are ulcerative colitis, regional enteritis, and surgical resection of the intestine. Disruption of intestinal flora may result in deficiency by eliminating vitamin K–synthesizing bacteria. In infants, diarrhea may cause bacterial losses sufficient to result in deficiency. Consequently, to rapidly elevate prothrombin levels and reduce the risk for neonatal hemorrhage, the American Academy of Pediatrics and the Centers for Disease Control and Prevention recommend that all infants receive a single injection of phytonadione (vitamin K ) immediately after delivery. This previously routine prophylactic1 intervention has recently been challenged by parents who believe that the risks outweigh benefits. Subsequent to increases in parents declining prophylaxis, there has been an increase in life-threatening vitamin K deficiency bleeding in recent years. As discussed in Chapter 44, the anticoagulant warfarin acts as an antagonist of vitamin K and thereby decreases synthesis of vitamin K–dependent clotting factors. As a result, warfarin produces a state that is functionally equivalent to vitamin K deficiency. If the dosage of warfarin is excessive, hemorrhage can occur secondary to lack of prothrombin. Hyperbilirubinemia When administered parenterally to newborns, vitamin K derivatives can elevate plasma levels of bilirubin, thereby posing a risk for kernicterus. The incidence of hyperbilirubinemia is greater in premature infants than in full-term infants. Although all forms of vitamin K can raise bilirubin levels, the risk is higher with menadione and menadiol than with phytonadione. Therapeutic Uses and Dosage Vitamin K has two major applications: (1) correction or prevention of hypoprothrombinemia and bleeding caused by vitamin K deficiency and (2) control of hemorrhage caused by warfarin. Vitamin K Replacement As discussed, vitamin K deficiency can result from impaired absorption and from insufficient synthesis of vitamin K by intestinal flora. For children and adults, the usual dosage for correction of vitamin K deficiency ranges between 5 and 15 mg/day. To prevent hemorrhagic disease in neonates, it is recommended that all newborns be given an injection of phytonadione (0. Warfarin Antidote Vitamin K reverses hypoprothrombinemia and bleeding caused by excessive dosing with warfarin, an oral anticoagulant. Preparations and Routes of Administration Phytonadione (vitamin K ) is available in 5-mg tablets, marketed as Mephyton,1 and in parenteral formulations (2 and 10 mg/mL) sold generically. For example, this might be indicated in management of life- threatening bleeding due to vitamin K antagonists (e. Water-Soluble Vitamins The group of water-soluble vitamins consists of vitamin C and members of the vitamin B complex: thiamine, riboflavin, niacin, pyridoxine, pantothenic acid, biotin, folic acid, and cyanocobalamin. They are grouped together because they were first isolated from the same sources (yeast and liver). Vitamin C is not found in the same foods as the B vitamins and hence is classified by itself. Two compounds—pangamic acid and laetrile—have been falsely promoted as B vitamins. Vitamin C (Ascorbic Acid) Actions Vitamin C participates in multiple biochemical reactions. Among these are synthesis of adrenal steroids, conversion of folic acid to folinic acid, and regulation of the respiratory cycle in mitochondria. At the tissue level, vitamin C is required for production of collagen and other compounds that comprise the intercellular matrix that binds cells together. In addition, vitamin C has antioxidant activity and facilitates absorption of dietary iron. Sources The main dietary sources of ascorbic acid are citrus fruits and juices, tomatoes, potatoes, strawberries, melons, spinach, and broccoli. Deficiency Deficiency of vitamin C can lead to scurvy, a disease rarely seen in the United States. Symptoms include faulty bone and tooth development, loosening of the teeth, gingivitis, bleeding gums, poor wound healing, hemorrhage into muscles and joints, and ecchymoses (skin discoloration caused by leakage of blood into subcutaneous tissues). Many of these symptoms result from disruption of the intercellular matrix of capillaries and other tissues. Therapeutic Use The only established indication for vitamin C is prevention and treatment of scurvy.
To reduce the risk for toxicity buy 15 mg prevacid fast delivery, potassium levels should be monitored routinely generic 15mg prevacid overnight delivery, and best 15mg prevacid, when indicated purchase prevacid uk, potassium supplements or a potassium-sparing diuretic should be given. Ototoxic Drugs The risk for furosemide-induced hearing loss is increased by concurrent use of other ototoxic drugs—especially aminoglycoside antibiotics (e. Hence, by lowering sodium levels, furosemide can cause lithium to accumulate to toxic levels. Accordingly, lithium levels should be monitored, and, if they climb too high, lithium dosage should be reduced. Antihypertensive Agents The hypotensive effects of furosemide add with those of other hypotensive drugs. To avoid excessive reduction of blood pressure, patients may need to reduce or eliminate use of other hypotensive medications. Part of the diuretic effect of furosemide results from increasing renal blood flow, which is thought to occur through a prostaglandin-mediated process. Other Loop Diuretics In addition to furosemide, three other loop diuretics are available: ethacrynic acid [Edecrin], torsemide [Demadex], and bumetanide [Burinex, generic only in United States]. They all promote diuresis by inhibiting sodium and chloride reabsorption in the thick ascending limb of the loop of Henle. All are approved for edema caused by heart failure, chronic renal disease, and cirrhosis, but only torsemide, like furosemide, is also approved for hypertension. Thiazides and Related Diuretics The thiazide diuretics have effects similar to those of the loop diuretics. Like the loop diuretics, thiazides increase renal excretion of sodium, chloride, potassium, and water. The principal difference between the thiazides and loop diuretics is that the maximal diuresis produced by the thiazides is considerably lower than the maximal diuresis produced by the loop diuretics. In addition, whereas loop diuretics can be effective even when urine flow is decreased, thiazides cannot. Hydrochlorothiazide Hydrochlorothiazide is the most widely used thiazide diuretic and will serve as our prototype for the group. Because of its use in hypertension, hydrochlorothiazide is one of our most widely used drugs. Mechanism of Action Hydrochlorothiazide promotes urine production by blocking the reabsorption of sodium and chloride in the early segment of the distal convoluted tubule (see Fig. Retention of sodium and chloride in the nephron causes water to be retained as well, thereby producing an increased flow of urine. Because only 10% of filtered sodium and chloride is normally reabsorbed at the site where thiazides act, the maximal urine flow these drugs can produce is lower than with the loop diuretics. The ability of thiazides to promote diuresis is dependent on adequate kidney function. Hence, in contrast to the loop diuretics, thiazides cannot be used to promote fluid loss in patients with severe renal impairment. For many hypertensive patients, blood pressure can be controlled with a thiazide alone, although many other patients require multiple-drug therapy. Edema Thiazides are preferred drugs for mobilizing edema associated with mild to moderate heart failure. Protection Against Postmenopausal Osteoporosis Thiazides promote tubular reabsorption of calcium and may thereby decrease the risk for osteoporosis in postmenopausal women. Before menopause, estrogen from the ovaries acts on renal tubules to promote calcium reabsorption. When menopause occurs, estrogen levels drop, allowing renal excretion of calcium to increase. The resultant decrease in circulating calcium promotes mobilization of calcium from bone and thereby increases the risk for osteoporosis. Because thiazides promote renal calcium retention, they may counteract the calcium loss associated with menopause and may thereby help preserve bone integrity. Adverse Effects The adverse effects of thiazide diuretics are similar to those of the loop diuretics. In fact, with the exception that thiazides are not ototoxic, the adverse effects of the thiazides and loop diuretics are nearly identical. Hyponatremia, Hypochloremia, and Dehydration Loss of sodium, chloride, and water can lead to hyponatremia, hypochloremia, and dehydration. However, because the diuresis produced by thiazides is moderate, these drugs have a smaller effect on sodium, chloride, and water than do the loop diuretics. To evaluate fluid and electrolyte status, electrolyte levels should be determined periodically, and the patient should be weighed on a regular basis. Hypokalemia Like the loop diuretics, the thiazides can cause hypokalemia from excessive potassium excretion. Potassium levels should be measured periodically, and, if serum potassium falls below 3. Hyperglycemia Like the loop diuretics, the thiazides can elevate plasma levels of glucose. Significant hyperglycemia develops only in diabetic patients, who should be especially diligent about monitoring blood glucose. To maintain normal glucose levels, the diabetic patient may require larger doses of insulin or an oral hypoglycemic drug. Hyperuricemia The thiazides, like the loop diuretics, can cause retention of uric acid, thereby elevating plasma uric acid. Although hyperuricemia is usually asymptomatic, it may precipitate gouty arthritis in patients with a history of the disorder. Thiazides increase excretion of magnesium, sometimes causing magnesium deficiency. Drug Interactions The important drug interactions of the thiazides are nearly identical to those of the loop diuretics. By promoting potassium loss, thiazides can increase the risk for toxicity from digoxin. By lowering blood pressure, thiazides can augment the effects of other antihypertensive drugs. By promoting sodium loss, thiazides can reduce renal excretion of lithium, thereby causing the drug to accumulate, possibly to toxic levels. By counterbalancing the potassium-wasting effects of the thiazides, the potassium- sparing diuretics can help prevent excessive potassium loss. In contrast to the loop diuretics, the thiazides can be combined with ototoxic agents without an increased risk for hearing loss. Potassium-Sparing Diuretics The potassium-sparing diuretics can elicit two potentially useful responses. Because their diuretic effects are limited, the potassium-sparing drugs are rarely employed alone to promote diuresis. However, because of their marked ability to decrease potassium excretion, these drugs are often used to counteract potassium loss caused by thiazide and loop diuretics. There are two subcategories of potassium-sparing diuretics: aldosterone antagonists and nonaldosterone antagonists. In the United States only one aldosterone antagonist—spironolactone—is used for diuresis. Spironolactone Mechanism of Action Spironolactone [Aldactone] blocks the actions of aldosterone in the distal nephron. Because aldosterone acts to promote sodium uptake in exchange for potassium secretion (see Fig. The diuresis caused by spironolactone is scanty because most of the filtered sodium load has already been reabsorbed by the time the filtrate reaches the distal nephron. The effects of spironolactone are delayed, taking up to 48 hours to develop (Table 35. Recall that aldosterone acts by stimulating cells of the distal nephron to synthesize the proteins required for sodium and potassium transport. Therefore effects are not visible until the existing proteins complete their normal life cycle—a process that takes 1 or 2 days. Therapeutic Uses Hypertension and Edema Spironolactone is used primarily for hypertension and edema. Although it can be employed alone, the drug is used most commonly in combination with a thiazide or loop diuretic. The purpose of spironolactone in these combinations is to counteract the potassium-wasting effects of the more powerful diuretics. Heart Failure In patients with severe heart failure, spironolactone reduces mortality and hospital admissions.
Preparations Buprenorphine is available in five formulations cheap prevacid 30mg online, four which are discussed here: transdermal patch order 15 mg prevacid amex, buccal film order cheap prevacid line, sublingual tablets cheap 15mg prevacid amex, and a sublingual film. The sublingual products are approved only for opioid addiction—but are used off-label for pain management. The buprenorphine patch, sold as Butrans, is indicated for moderate to severe chronic pain in patients who need continuous analgesia for an extended time. The lowest strength is used for opioid-naïve patients, or for those using an opioid in low dosage (e. Breakthrough pain can be managed with acetaminophen, a nonsteroidal antiinflammatory drug, or a short-acting opioid. Patches are applied to eight sites: upper outer arm, upper front of chest, upper side of chest, and upper back—on the right and left sides of the body. The site should be rotated when a new patch is applied, and no site should be reused within 21 days. The site may be cleaned, but only with water, not with soaps, alcohol, or abrasives. Patches should not be cut or exposed to heat, including heating pads, heated waterbeds, hot baths, saunas, heat lamps, or extended sunshine. If a patch falls off during the 7-day dosing interval, a new patch should be applied, but at a different site. The other two formulations, tablets and films marketed as Suboxone, contain a mixture of buprenorphine/naloxone (2 mg/0. All three sublingual formulations are approved only for managing opioid addiction. To prescribe Suboxone or Subutex, a provider must undergo training and register for appropriate access. A new form of buprenorphine [Belbuca] was approved in 2015 for management of chronic pain. Because it is used for treatment of around-the-clock chronic pain, it has the potential to cause life-threatening respiratory depression. Belbuca should only be prescribed by providers with additional education regarding chronic pain. Prescribing Opioids for Chronic, Noncancer Pain The amount of prescription opioids has risen steeply since 1990. Efforts to improve pain management have led to a 10-fold increase in opioid prescriptions, accompanied by a substantial increase in abuse, serious injuries, and deaths. In 2013, accidental overdose with prescription opioids resulted in 16,235 fatalities. In patients with chronic pain of nonmalignant origin, opioids can reduce discomfort, improve mood, and enhance function. Accordingly, pain experts now recommend that opioids not be withheld from people with chronic pain. Nonetheless, because of concerns about addiction, tolerance, adverse effects, diversion to street use, and regulatory action, physicians, physician assistants, and nurse practitioners are often reluctant to prescribe these drugs. Nonpharmacologic therapy and nonopioid pharmacologic therapy are preferred for chronic pain. Clinicians should consider opioid therapy only if expected benefits for both pain and function are anticipated to outweigh risks to the patient. If opioids are used, they should be combined with nonpharmacologic therapy and nonopioid pharmacologic therapy, as appropriate. Before starting opioid therapy for chronic pain, clinicians should establish treatment goals with all patients, including realistic goals for pain and function, and should consider how therapy will be discontinued if benefits do not outweigh risks. Clinicians should continue opioid therapy only if there is clinically meaningful improvement in pain and function that outweighs risks to patient safety. Before starting and periodically during opioid therapy, clinicians should discuss with patients known risks and realistic benefits of opioid therapy and patient and clinician responsibilities for managing therapy. When opioids are started, clinicians should prescribe the lowest effective dosage. When opioids are used for acute pain, clinicians should prescribe the lowest effective dose of immediate-rdease opioids and should prescribe no greater quantity than needed for the expected duration of pain severe enough to require opioids. Three days or less will often be sufficient; more than seven days will rarely be needed. Clinicians should evaluate benefits and harms with patients within 1 to 4 weeks of starting opioid therapy for chronic pain or of dose escalation. Clinicians should evaluate benefits and harms of continued therapy with patients every 3 months or more frequently. If benefits do not outweigh harms of continued opioid therapy, clinicians should optimize other therapies and work with patients to taper opioids to lower dosages or to taper and discontinue opioids. Before starting and periodically during continuation of opioid therapy, clinicians should evaluate risk factors for opioid-related harms. When prescribing opioids for chronic pain, clinicians should use urine drug testing before starting opioid therapy and consider urine drug testing at least annually to assess for prescribed medications as well as other controlled prescription drugs and illicit drugs. Clinicians should avoid prescribing opioid pain medication and benzodiazepines concurrently whenever possible. Clinicians should offer or arrange evidence-based treatment (usually medication-assisted treatment with buprenorphine or methadone in combination with behavioral therapies) for patients with opioid use disorder. All recommendations are category A (apply to all patients outside of active cancer treatment, palliative care, and end-of-life care) except recommendation 10 (designated category B, with individual decision making required); see full guideline for evidence ratings. Pain and current functional status should be evaluated at every patient appointment. Assessment should include documentation of where the pain is located, what type of pain is present (e. In addition, you should assess for psychological factors that can reduce pain threshold (anxiety, depression, fear, anger). Patient Education It is crucial that the patient understand the risks and benefits of using opioids to treat chronic, noncancer pain. If the risks begin to outweigh the benefits of opioid therapy, a new plan should be developed. Initiating Therapy Nonpharmacologic therapy and nonopioid therapy should be used to treat chronic pain before starting opioid therapy. If these modalities are not successful in improving patient pain and function, opioid therapy can be considered. In addition, use of nonopioid, adjuvant medications should continue to maximize pain control and patient function. Dosage Determination Providers should start with the lowest effective dosage for the patient. For example, if a “standard” 10-mg dose of morphine were employed for all adults, only 70% would receive adequate relief; the other 30% would be undertreated. Not all patients have the same tolerance for pain, and hence some need larger doses than others for the same disorder. Older-adult patients metabolize opioids slowly and therefore require lower doses than younger adults. Because the blood-brain barrier of newborns is poorly developed, these patients are especially sensitive to opioids; therefore they generally require smaller doses (on a milligram-per-kilogram basis) than do older infants and young children. To minimize physical dependence and abuse, opioid analgesics should be administered in the lowest effective dosages for the shortest time needed. Be aware, however, that larger doses are needed for patients who have more intense pain and for those who have developed tolerance. As soon as possible, the patient should be switched to a nonopioid analgesic, such as aspirin or acetaminophen. Avoiding a Withdrawal Reaction When opioids are administered in high doses for 20 days or more, clinically significant physical dependence may develop. Under these conditions, abrupt withdrawal will precipitate an abstinence syndrome. To minimize symptoms of abstinence, opioids should be withdrawn slowly, tapering the dosage over 3 days.
Identification of endocrinopathies should be sought especially in the child with an atypical presen- tation and who is less than 10th percentile in height and/or less than 50th percentile in weight generic prevacid 30 mg on-line. After confirmation by radiographs purchase cheapest prevacid, the patient will require immediate orthopedic surgery evaluation to determine the timeframe for surgical pinning of the femoral head discount prevacid 30 mg without prescription. Reduc- tion increases the risk of vascular compromise and subsequent avascular necrosis of the femoral head generic prevacid 15 mg with amex. Range of motion testing is limited because the patient is guarding and begins crying. Send the patient for an x-ray of his knee and hip joint and ask them to return the same day. Which of the following would be the best diagnostic test for this patient’s condition? Her growth curve shows declining growth velocity from 50th percen- tile several years ago to the 15th percentile currently. Her mother notes that she often is tired and sleeps until noon every day, but attributes it to being a teenager on summer vacation. Upon questioning she reports no trouble falling or staying asleep and goes to bed around 10 pm nightly. On physical examination, he has an antalgic gait, pain on passive range of motion of his right hip, and external rotation during hip flexion. The patient likely has septic arthritis of his right knee and needs immediate hospital admission for intravenous antibiotics. Immediate inpatient or emergency center orthopedic surgery evaluation for the possibility of sur- gical drainage and wash out of his knee joint is appropriate. Moreover, ery- thema and warmth are not typical features of any of these latter conditions. Such patients typically are admitted to the hospital, and a skeletal survey will be done to evaluate for active or heal- ing fractures. Given this adolescent’s findings of fatigue and exces- sive sleeping, hypothyroidism is the most likely cause. An evaluation for depression, rather than simply initiating antidepressant therapy, is appropriate. The patient reports bilateral throbbing frontal pain that is associated with nausea. The headaches do not wake him from sleep, but he does report that bright lights bother him. The headaches have been severe enough to force him to miss school 3 days in the previous week. His past medical history is positive for similar episodes of headaches when he was 5 years old. He denies seeing flashing lights, having vision changes, or weakness prior to or associated with the headache. Perform thorough physical examination, with particular attention to neurologic examination. Identify and understand common signs for serious disease for a patient with headache. Considerations This 10-year-old’s presentation does not identify any concerns for a secondary headache (intracranial lesion, infection, etc). His symptoms, recurrent nature, and presence of positive family history are highly suggestive for the diagnosis of migraine. When a patient presents with complaints of headache, it is important to be able to identify signs or symptoms suggestive of a more serious headache or secondary headache (where the headache is a symptoms of an underlying cause). This requires detailed history taking and a thorough physical and neurologic examination. Areas of concern for secondary headache are as follows: Headache is more severe, frequent or is new/different from previous episodes. Examples include increased intracranial pressure, infection, trauma, bleeding, tumors, and medication overuse. This condition usually has a strong hereditary component, can cause disability, and may be associated with an aura. Usually lasts 5 to 60 min- utes and the headache begins during or within an hour of the aura. The history and physical examina- tion are the most important tools in evaluating a patient with headaches. The goals of the history and physical examination are first to identify whether the patient is experiencing any signs or symptoms for serious, emergent pathology (as described previously) and then to determine whether the headache is primary or secondary. Primary headaches are common, benign, recurrent, and episodic headache dis- orders such as tension headaches and migraines. Secondary headaches may be due to infection (such as meningitis, sinusitis, acute viral illness), trauma, tumors, intra- cranial hemorrhage, increased intracranial pressure, analgesic medication overuse, carbon monoxide poisoning, caffeine or alcohol withdrawal, or lead toxicity. They may be episodic or chronic, and the duration can vary from 1 hour to several days. They typically are not associated with nausea, vomiting, photophobia, phonophobia, or auras. They are not affected by activity and are often associated with muscle pain of the shoulders and neck. Causes of migraines are multifactorial; however, they are associated with a strong genetic predisposi- tion. Migraines can be triggered by stress, illness, fatigue, dehydration, and poor sleep. Unlike adults in whom migraine headaches are usually unilateral, children can present with unilateral or bilateral migraine headaches. Children may also have associated symptoms of nausea and vomiting, abdominal pain, and decrease in activity or appetite. Migraines without aura are the most common form of migraines in adults and children (Table 48–1). Debilitating migraines can cause prolonged absences or poor perfor- mance in school, anxiety, and social withdrawal. The diagnosis of migraine head- aches does not require workup with laboratory testing or imaging. Imaging may be warranted in the presence of signs or symptoms of more serious disease or in the absence of family history of migraine headaches. The goal of abortive or acute therapy is to stop the headache and help the patient to return to their baseline function as quickly as possible. Preventive therapy is recommended for patients who experience frequent (two to three episodes per month) and disabling migraines. Medications used for preventive therapy include topiramate, valproic acid, β-blockers, tricyclic antidepressants, and cyproheptadine. Is not due to another disorder Modifed, with permission, from Headache Classifcation Subcommittee of the International Headache Society. Proper hydration, regular meals, adequate sleep, and caffeine avoidance are important lifestyle factors that may decrease migraine frequency. Failure to thrive (Case 10) and headache may suggest a chronic condition such as brain tumor. Acute onset of headache, especially if associated with acute neurologic symptoms in the patient with sickle cell disease (Case 13) may represent stroke. The younger child with developing neurologic symptoms and headache may be a victim of lead toxicity (Case 25). Bacterial meningitis (Case 27) may present with acute headache along with other symptoms such as fever for organism such as pneu- mococcus or with more chronic headache if associated with organisms such as tuberculosis. A child with head injury (accidental or inflicted) may have a headache associated with subdural hematoma (Case 29). The parents report that for the previous week he has been vomiting, crying, and irritable every morning after awakening from his sleep. They report he holds his head while complaining of pain and that he seems to be bothered by lights and loud sounds. He was seen by his pedia- trician earlier in the week and diagnosed with gastroenteritis.