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By G. Faesul. Valley City State University.

Unilateral hemispheric lesions from stroke can blunt awareness discount cytotec 100 mcg free shipping medicine dosage chart, but do not result in coma unless edema and mass efect cause compression of the other hemisphere discount cytotec 200mcg free shipping medications on airline flights. Global cerebral ischemia, usually resulting from cardiac arrest or ventricular fibrillation, may cause anoxic encepha­ lopathy and coma. Delirium tremens is characterized by hallucinations, disorientation, tachy­ cardia, hypertension, low-grade fever, agitation, and diaphoresis. Most commonly, altered mental status is caused by metabolic derangements, toxin exposure, struc­ tural lesions, vascular insults, seizures, infections, and withdrawal syndromes. The patient should be screened for illicit drugs and possible toxic levels of prescribed medications. The physical examination should address 3 main questions: (1) does the patient have meningitis? The neurological examination should focus on whether there are lateralizing signs suggesting a focal lesion or signs of meningismus and fever that would suggest an infection. The key features to be noted during the physical examination are pupil size and reactivity, ocular motility, motor activity (including posturing), and certain respiratory patterns. Coma without focal signs, fever, or meningismus suggests a dif fuse insult such as hypoxia or a metabolic, drug-induced toxicity, an infectious or postictal state. In the case of coma after cardiac arrest, patients who lack pupillary and corneal reflexes at 24 hours and lack motor responses at 72 hours have a poor chance of meaningful recovery. Patients with focal findings on examination or who exhibit unexplained coma should undergo emergent imaging to exclude hemorrhage or mass lesion. Lumbar puncture is indicated when meningitis or subarachnoid hemorrhage is suspected and when neuroimaging is normal. The possibility of nonconvulsive status epilepticus should be evaluated by emergent electroencephalogram. Delirium may predispose patients to prolonged hospitalization, frequent impairment ofphysical function, and increased rates of institutionalization. This will detect any structural abnormalities and possibly avoid herniation from a lumbar puncture. Diagnosis of Delirium It is critical to diagnose and determine the cause of delirium. To diagnose delirium, a patient must have an acute change in mental status that is fuctuating between altered levels of consciousness. Laboratory testing and physical examination can shed light on the source of the delirium. Does the abnormal behavior fuctuate duringthe day, that is, tend to come and go, or increase or decrease in severity? Inattention Shown by a positive response to the fo llowing: "Did the patient have difculty focusing or concentrating? For example, being easily distracted or havingdifculty keepingtrack ofwhat was being said? Altered level of I Shown by any answer otherthan "alert" to the fo llowing: "Overall, consciousness how wouldyousaywhat the level ofconsciousness ofthe patient is? The more medications the patient is taking, the greater the likelihood that a medication is causing or contributing to the delirium. Patients and caretakers must be aware that medications include any over-the­ counter medications, vitamins, supplements, elixirs, and creams. One should seek for signs of infection, heart failure, myocardial ischemia, dehydration, malnutrition, urinary retention, and fecal impaction. Cerebral imaging, although commonly used, is usually not help­ ful in the diagnosis of delirium unless there is a history of a fall or evidence of focal neurologic impairment. Delirium often results from a combination of underlying vulnerability and acute precipitating fac­ tors (Table 30-2). Amelioration of underlying vulnerability and prevention of acute precipitants will reduce the incidence of delirium. The use of physical restraints is generally avoided because they can increase agitation and the risk for patient injury. Low-dose haloperidol, risperidone, and olanzapine are equally efective in treating agitation associated with delirium. These are associated with little respiratory depressive efect, a feature much desired in the respiratory compro­ mised patient. One should attempt to use the lowest dose of the least toxic agent that successflly controls the agitation. Lorazepam used along with antipsychotics agents is complementary without adding undesirable side efects. A significant part of the treat­ ment of delirium is to institute preventive measures. Vitamin B12 and folic acid should also be administered and patients be hydrated adequately. A quiet, lowly lit environment during the day and an even darker envi­ ronment during the evening and sleeping hours should be maintained. The patient should be advised to avoid reversing the normal rest and sleeping pattern. Medications Neuroleptics should be used with caution to avoid possible undesirable side efects. Low-dose haloperidol causes less sedation and is highly efective in treating delirium, espe­ cially when used in combination with lorazepam. The combination of 5 mg of haloperidol with 1 mg of lorazepam is efective in the treatment of delirium. The use of risperidone has fewer side efects than haloperidol and should be substituted for the latter when possible. Sedatives such as lorazepam are the drugs of choice when treating delirium due to alcohol withdrawal. Respiratory depression can be minimized by carefl monitoring, especially in the elderly. This can lead to rapid withdrawal symptoms including seizures, which now may be untreatable with benzo­ diazepines since flumazenil will block its efect. Naloxone and naltrexone should also be kept in mind with narcotic drug overdose, especially opioid intoxication where they competitively inhibit opioid-binding sites and are therefore usefl in any opioid intoxication. Proper nutrition and removal of precipitating factors are essential in preventing a relapse. Weeks of treatment are needed to recover from delirium and the patient should be monitored continuously. The nurse indicates that the patient recently became disoriented and is not interacting as clearly with her family as she had done previously.

Antibiotics Even if infection is the precipitant for the attack cheap 200mcg cytotec otc symptoms 5 dpo, most will be viral discount 100mcg cytotec mastercard medicine 6469. Many patients with acute asthma will have a cough productive of small amounts of yellow sputum caused by eosinophils rather than neutrophils. Magnesium sulphate Magnesium is a bronchial smooth muscle relaxant and there is some evidence that, in adults, it has a bronchodilating effect. Significant hypotension does occur, particularly in patients with coexisting cardiovascular compromise. Aminophylline is a chronotrope, inotrope, and diuretic with a narrow therapeutic index, and serum levels need to be monitored. A loading dose should be omitted in the presence of major tachycar- dias or if the patient has taken oral theophyllines. Delivery of heliox requires the use of specifically designed or modified breathing circuits and ventilators. Sedation In patients with significant anxiety, benzodiazepines may reduce the respira- tory rate and gas trapping, and occasionally avoid the need for ventilation. This is high-risk practice and should only be done by senior clinicians where there is potential to quickly proceed to intubation, or where there is a known history of previous improvement with such treatment. Mechanical ventilation With asthma the clinical situation may deteriorate markedly after anaes- thesia and institution of mechanical ventilation. Reasons for this include: • Drugs causing histamine release and worsening bronchospasm • Reflex bronchoconstriction due to direct physical stimulation when the trachea is intubated • Positive pressure ventilation may result in dynamic hyperinflation with cardiorespiratory compromise • Positive pressure ventilation may uncover and enlarge a pre-existing pneumothorax • Positive pressure ventilation may cause de novo barotrauma • Cardiovascular instability—positive pressure ventilation, anaesthesia, and hypovolaemia often result in significant hypotension. In addition to adequate intravenous access, if possible an arterial line should be sited prior to intubation. Full resuscitation equipment, including the facility to insert pleural drains, must be immediately to hand. One in 100,000 adrenaline (10mcg/mL) can be used for severe bronchospasm and in the treatment of hypotension. The aim of mechanical ventilation is to keep the patient alive, and to limit iatrogenic damage, until the bronchospasm improves. The first description of permissive hypercapnia was in 1984, in a cohort of asthmatic patients. Because hyperinflation reduces lung compliance, end inspiratory plateau pressure is a good marker of dynamic hyperinflation in asthma. Use slow ventilatory rates, small tidal volumes, and a prolonged expiratory phase. Peak pressure will be significantly higher than plateau pressure, reflecting the high airway resistance. In order to shorten inspiration as much as possible, high inspiratory flows (80–100L/min) should be used. This will further increase the peak airway pressure (but not the plateau pressure). In order to shorten inspiration, the pressure ramp speed should be shortened to 25ms. Whatever strategy is chosen, careful setting of the ventilator and the ventilator alarms is vital. A target sheet for respiratory variables should be left at the bedspace, and significant deviation from these parameters mandates a complete reassessment of the patient, the medical treatment, and the ventilatory strategy. However, there is a concern that if zero end expiratory pressure is set, when the bronchospasm resolves significant atelectrauma may occur. If the blood pressure falls precipitously in an asthmatic patient, consider ventilator disconnection. The effect of small adjust- ments of respiratory parameters should be assessed in terms of the ther- apeutic targets: high pressure and hyperinflation are the dangers to the patient. Once intubated with persisting severe bronchospasm and difficulty in ventilating, inhaled volatile anaesthetic agents (e. Further reading British Thoracic Society/Scottish Intercollegiate Guideline Network. In the developed world cardiogenic pulmonary oedema is predominantly due to coronary artery disease or its complications. Acute heart failure is graded in severity using the Killip scoring system (see box). Cardiogenic shock is officially defined as hypotension and inadequate organ perfusion due to cardiac dysfunction. However, shock states (defined as tissue hypoperfusion) due to myocardial dysfunction may exist in the absence of hypotension. The publication of large registries has given useful epidemiological information about acute heart failure. In-hospital mortality is around 15% but is much higher in the setting of acute myocardial infarction, and higher still in the presence of cardiogenic shock. Indicators of a poor outcome are increasing age, renal dysfunction, and cardiogenic shock. Many patients are asymptomatic until the lesions become large enough to impede coronary flow, at which point they develop exertional angina. Rupture of these atherosclerotic plaques leads to platelet aggregation and thrombus formation, which can cause total, transient, or sub-total arterial occlusion and subsequent myocardial infarction. If occurring shortly after the index infarct, acute mitral regurgitation due to papillary muscle rupture or ventricular septal rupture must be excluded. Decompensation of chronic heart failure The cause of this is commonly unclear, but includes sepsis, anaemia, poor compliance with medication, excess fluid or sodium intake, or the devel- opment of arrhythmias. Non-ischaemic causes of cardiogenic pulmonary oedema Acute • Sepsis-induced myocardial dysfunction. It is thought to be predominantly due to the negative inotropic effects of pro-inflammatory cytokines on the myocardium. Non-cardiogenic causes of pulmonary oedema • Phaeochromocytoma—probably due to the vasoconstricting and direct toxic effects of chronically raised plasma catecholamine levels on the myocardium, which can result in a dilated cardiomyopathy. Thought to be due to reflex hyperactivation of the renin–angiotensin system and subsequent fluid retention due to reduced renal perfusion. Pathophysiology The mechanism underpinning cardiogenic pulmonary oedema is increased intravascular pulmonary pressures with transudation of protein-de- pleted plasma down a pressure gradient into the pulmonary interstitium and alveoli. The pressure required to produce pulmonary oedema is reduced in the presence of capillary leak and hypoalbuminaemia. Diagnosis Clinical presentation The symptoms reflect hypoxia and reflex-increased sympathetic drive. Symptoms include: • Dyspnoea at rest • Orthopnoea • Paroxysmal nocturnal dyspnoea • Cough productive of frothy (occasionally blood stained) sputum.

Clopidogrel Bleeding cheap 200 mcg cytotec fast delivery medicine x boston, diarrhea cheap cytotec 200 mcg medicine wheel teachings, gastrointestinal pain, increased Increases levels of drugs metabolized by liver microsomal cholesterol and triglyceride levels, nausea, and enzymes. Indications embolization and other potentially fatal consequences of Warfarin has been primarily used in the long-term treat- thrombosis. The goals of warfarin therapy are to the sample with that of a standardized control preparation. The most common serious adverse effect of fraction- Treatment of Bleeding ated and unfractionated heparin is bleeding caused by exces- If bleeding occurs, warfarin should be withheld until the sive anticoagulation. Low- molecular-weight fractions have been developed for specifc Indications clinical uses, including enoxaparin, dalteparin, and tinza- Heparin is indicated for the treatment of acute thrombo- parin. Fondaparinux is a synthetic pentasaccharide whose embolic disorders, including peripheral and pulmonary mechanism and effects are similar to those of other heparin- embolism, venous thrombosis, and coagulopathies such as like drugs. It is used prophylac- tically to prevent clotting in arterial and heart surgery, Chemistry and Mechanisms during blood transfusions, and in renal dialysis and blood Heparin is a naturally occurring mixture of sulfated muco- sample collection. Heparin is also used to prevent emboli- polysaccharides found in mast cells, basophils, and the vas- zation of thrombi that might cause a cerebrovascular event cular endothelium. Protamine is administered intravenously for this Several clinical trials have established the effcacy and safety purpose, and the dosage is based on the estimated amount of these drugs in these settings. As with other anticoagulants, the most serious 2 to 4 hours after protamine administration is used to guide adverse effect of hirudin compounds is bleeding. Severe bleeding Argatroban is a synthetic direct thrombin inhibitor given may require the administration of fresh plasma or clotting intravenously for the prophylaxis and treatment of throm- factors. Direct Thrombin Inhibitors The direct thrombin inhibitors include the parenterally Dabigatran administered hirudin derivatives and orally administered Dabigatran is a direct thrombin inhibitor and the frst oral dabigatran. After oral administration, dabigatran Hirudin is a mixture of similar polypeptides produced in the etexilate is converted to its active form, dabigatran, by salivary gland of Hirudo medicinalis, the medicinal leech. Among patients with hip replace- 24 hours if the creatinine clearance falls below 30 mL/min. Dabigatran is not a substrate for cytochrome 12 days (knee replacement) or 35 days (hip replacement). Steady state levels of the drug are reached Bleeding was the most common adverse effect observed in after about 3 days of multiple dose administration. Dabigatran is a potent, com- Apixaban is another oral direct factor Xa inhibitor that petitive, reversible inhibitor of thrombin, a protease enzyme has been evaluated in patients with atrial fbrillation for that converts fbrinogen to fbrin in the fnal step of blood whom warfarin therapy was unsuitable. The adherence of platelets to vascular endothe- taking warfarin are being switched to dabigatran, particu- lium activates the platelets and leads to the synthesis and larly those who are poorly controlled or not well monitored. Aspirin and clopidogrel inhibit the the body, including the gastrointestinal tract. Gastrointestinal complaints such as dyspepsia and gastritis-like symptoms are fairly common with dabigatran. It also inhibits platelet aggregation active metabolite), is a substrate for the P-glycoprotein and is used to prevent and treat arterial thromboembolic (Pgp) transporter (see Chapter 2) in the gut and kidneys, disorders. It is largely metabolized by P450 isozymes, effect on prostacyclin, whereas higher doses inhibit the syn- particularly 3A4, before renal excretion, and dosage adjust- thesis of both prostaglandins. Hence the dosage of aspirin ments should be considered in patients taking strong 3A4 used to inhibit platelet aggregation is usually lower than that inhibitors. His vital signs included a blood pres- Indications sure of 142/92 mm Hg and a heart rate of 88 beats/min. He was placed on metoprolol, lisinopril, and als, and it has been recommended that aspirin be used for clopidogrel and was subsequently transferred to another primary prevention only in men over 45 years of age and hospital for angiography and further treatment. For patients who come to hospitals without facili- ties for percutaneous coronary intervention, fbrinolysis with Adverse Effects and Interactions a drug such as tenecteplase is the most viable option. Aspirin can cause bleeding, especially in the gastrointesti- Studies show that clopidogrel and enoxaparin reduce car- nal tract, where it inhibits the synthesis of prostaglandins diovascular mortality in persons undergoing fbrinolysis or that promote secretion of bicarbonate and mucus. Other adverse effects of aspirin are discussed in In patients who cannot tolerate or are unresponsive to Chapter 30, and interactions are listed in Table 16-3. More recent trials found that perfusion imaging (thallium imaging) to dilate and evalu- prasugrel was superior to clopidogrel in reducing stroke and ate the arteries of patients with coronary artery disease. In addition to its use in stroke and inhibiting platelet adhesion to the vessel wall. This effect leads to inhibition of platelet it can cause severe neutropenia, patients who are treated aggregation and vasodilation. The drug is indicated for the with ticlopidine must have a complete blood count every 2 treatment of intermittent claudication, a symptom complex weeks from the second week to the third month of treat- of pain and weakness in a limb that is sometimes caused by ment, and any time they develop an infection. Cilo- prasugrel, and ticagrelor cause signifcantly less neutropenia, stazol improves blood fow and reduces muscle pain while and white blood cell counts are not required in persons increasing walking distance in persons with this condition. After much contro- Adenosine Diphosphate Inhibitors versy about this potential interaction, experts have concluded Pharmacokinetics that clopidogrel and omeprazole may be used concurrently Clopidogrel, prasugrel, ticlopidine, and ticagrelor are well without signifcantly increasing the risk of adverse cardio- absorbed after oral administration. The reversibility of ticagrelor may be advantageous Abciximab is used to prevent platelet aggregation and in some situations, such as in patients about to undergo thrombosis in patients undergoing percutaneous coronary surgery. It has also been used as an adjunct to thromboly- Fibrinolytic Drugs sis with alteplase and similar drugs (see the discussion of The fbrinolytic drugs (or thrombolytic drugs) include fbrinolytic drugs). Other adverse reactions include thrombocytopenia, urokinase, an enzyme obtained from human neonatal hypotension, and bradycardia. In patients with acute ischemic by preventing fbrinogen cross-linking of platelets. Unlike (thrombotic) stroke, these drugs reduce the incidence of abciximab, tirofban and eptifbatide are competitive, neurologic sequelae. Eptifbatide is a cyclic heptapeptide from rattle- coronary blood fow in hospitals without facilities for angio- snake venom, whereas tirofban is a tyrosine derivative. Eptifbatide is used in two ways: (1) to prevent The fbrinolytic drugs are enzymes that convert plasmino- coronary thrombosis in persons with unstable angina or gen to plasmin. This activator Bleeding is the major adverse effect of tirofban and complex is available for clinical use in the drug preparation eptifbatide. Plasminogen Streptokinase activator Alteplase, reteplase, complex or anistreplase or urokinase Aminocaproic acid Fibrin Fibrinogen Plasmin Fibrin Degradation split products products Figure 16-6. Alteplase, reteplase, and tenecteplase catalyze the conversion of plasminogen to plasmin. Streptokinase combines with plasminogen to form an active catalyst (activator complex) that converts inactive plasminogen to plasmin. Plasmin is a protease that breaks down fbrinogen and fbrin to degradation (split) products. The inhibitor indicated for preventing thromboembolism most common adverse effect is hemorrhage. For this reason, it should not be used repeatedly receptors and are used to prevent thrombosis in in the same patient. These drugs are By competitively blocking plasminogen activation, amino- used to lyse clots in patients with myocardial infarc- caproic acid inhibits fbrinolysis.

The drug is employed to treat diarrhea and to reduce the volume of discharge from ileostomies purchase cytotec paypal symptoms 5 days after iui. Benefits derive from suppressing bowel motility and from suppressing fluid secretion into the intestinal lumen purchase cheap cytotec on-line adhd medications 6 year old. The drug is supplied in 2-mg capsules, in 2-mg tablets, and in two liquid formulations (1 mg/5 mL and 1 mg/7. Like diphenoxylate, difenoxin can elicit morphine-like subjective effects at high doses. To discourage excessive dosing, difenoxin, like diphenoxylate, is formulated in combination with atropine. Paregoric Paregoric (camphorated tincture of opium) is a dilute solution of opium, containing morphine (0. The primary use is diarrhea, although paregoric has the same approved uses as morphine. Opium Tincture Opium tincture is an alcohol-based solution that contains 10% opium by weight. In addition, opium tincture (after dilution) may be given to suppress symptoms of withdrawal in opioid-dependent neonates. When administered in antidiarrheal doses, opium tincture does not produce analgesia or euphoria. Other Nonspecific Antidiarrheals Bismuth Subsalicylate Bismuth subsalicylate [Pepto-Bismol, others] is effective for the prevention and treatment of mild diarrhea. Bulk-Forming Agents Paradoxically, methylcellulose, polycarbophil, and other bulk-forming laxatives can help manage diarrhea. Management of Infectious Diarrhea General Considerations Infectious diarrhea may be produced by enteric infection with a variety of bacteria and protozoa. Indiscriminate use of antibiotics is undesirable in that it (1) can promote emergence of antibiotic resistance and (2) can produce an asymptomatic carrier state by killing most of the infectious agents. Conditions that do merit antibiotic treatment include severe infections with Salmonella, Shigella, Campylobacter, or Clostridium species. However, if symptoms are especially severe, treatment with one of the fluoroquinolone antibiotics—ciprofloxacin (500 mg twice daily) or norfloxacin (400 mg twice daily)—is indicated. Azithromycin [Zithromax] is preferred for children (10 mg/kg on day 1 and 5 mg/kg on days 2 and 3) and for pregnant women (1000 mg once or 500 mg once daily for 3 days). Rifaximin [Xifaxan] (200 mg 3 times a day for 3 days) may also be used, provided the patient is not pregnant or febrile and that stools are not bloody. For patients with mild symptoms, relief can be achieved with loperamide, a nonspecific antidiarrheal. However, by slowing peristalsis, loperamide may delay export of the offending organism and may thereby prolong the infection. Two measures —avoiding local drinking water and carefully washing foods—are highly effective. However, because these drugs can cause serious side effects, prophylaxis is not generally recommended. Clostridium difficile–Associated Diarrhea Clostridium difficile is a gram-positive, anaerobic bacillus that infects the bowel. Symptoms range from relatively mild (abdominal discomfort, nausea, fever, diarrhea) to very severe (toxic megacolon, pseudomembranous colitis, colon perforation, sepsis, and death). The direct medical costs are estimated at $8 billion a year; the indirect costs are much higher—about $25 billion a year. Despite extensive research, no underlying pathophysiologic mechanism has been identified. As a result, mild stimuli that would have no effect on most people can trigger an intense response. In addition, we know that symptoms can be triggered by stress, depression, and dietary factors, including caffeine, alcohol, fried foods, high-fat foods, gas-generating vegetables (beans, broccoli, cabbage), and too much sorbitol, a sweetener found in chewing gum and some diet products. Overproduction of gastric acid and excessive bacterial colonization of the small intestine have also been implicated. Because large meals stretch and stimulate the bowel, switching to smaller, more frequent meals may help. Regarding antispasmodic agents, they concluded that the available data are insufficient to make a recommendation for or against use. Studies suggest that, for some patients, symptoms can be relieved with antibiotics or an acid suppressant. Another study evaluated the effects of drugs that suppress production of stomach acid in patients who routinely experienced exacerbation of symptoms after eating. Two kinds of acid suppressants were used: proton pump inhibitors (lansoprazole or omeprazole) and histamine-2 receptor blockers (famotidine or ranitidine). In all cases, patients experienced a significant reduction of postprandial urgency and other symptoms. Benefits developed quickly (within days) and reversed when the drugs were stopped. Although a fourth drug, tegaserod, exists, it is used only in emergency situations owing to a risk for serious cardiovascular events. To reduce risk, prescribers, patients, and pharmacists must adhere to a strict risk management program (see later). As a result, the drug can increase stool firmness and decrease both fecal urgency and frequency. Symptoms decline 13 to 4 weeks after starting the drug and resume 1 week after stopping the drug. Pharmacokinetics Administration is oral, and absorption is rapid but incomplete (50%–60%). Alosetron undergoes extensive metabolism by hepatic cytochrome P450 enzymes, followed by excretion primarily in the urine. Drug Interactions Alosetron does not interact with theophylline, oral contraceptives, cisapride, ibuprofen, alprazolam, amitriptyline, fluoxetine, or hydrocodone combined with acetaminophen. Because alosetron is metabolized by cytochrome P450 enzymes, drugs that interfere with these enzymes (e. Adverse Effects and Contraindications Although alosetron is generally well tolerated, it can cause severe adverse effects. The most common problem is constipation (29%), which can be complicated by impaction, bowel obstruction, and perforation. B l a c k B o x Wa r n i n g : A l o s e t ro n Alosetron can cause ischemic colitis (intestinal damage secondary to reduced blood flow). Ischemic colitis and complications of constipation have led to hospitalization, blood transfusion, surgery, and death. If, after 4 weeks, the dosage is well tolerated but inadequate, it can be increased to 1 mg twice a day.

Neonatal history: Any problems identified in the neonatal period buy cytotec in united states online treatment diabetes type 2, such as severe jaundice cheap cytotec amex harrison internal medicine, infections, feeding difficulties, and prolonged hospitaliza- tion, should be reviewed, especially for the younger pediatric patients in whom residua of these problems may remain. Surgical history: When, where, and for what reason the surgery was per- formed should be explored. Medical history: Whereas minor illnesses (such as occasional upper respi- ratory infections) can be reviewed quickly, more serious illnesses (such as diabetes mellitus) should be investigated fully. The age at diagnosis, treat- ments prescribed, and response to therapies can be reviewed. For instance, a diabetic patient with frequent hospitalizations for ketoacidosis may indicate a lack of education of the family or underlying psychosocial issues complicating therapy. A child with a history of frequent, serious acci- dents should alert the physician of possible child abuse. Developmental history: For preschool children, a few questions about lan- guage and fine motor, gross motor, and psychosocial skills will provide good clues about development. For school-aged children, school performance (grades) and areas of strength and weaknesses are helpful. Allergies: Reactions to medications should be recorded, including severity and temporal relationship to medications. Immunizations: Dates for primary and booster series of immunizations should be recorded, preferably by reviewing the immunization cards or accessing the state’s immunization registry. If the child is in school, a presumption about state laws regarding immunization completion can be made while the immuni- zation card is being retrieved. Medications: List the names of current medications, dosages, routes of admin- istration and frequency, and durations of use. Sexual history of adolescents: Details of an adolescent’s sexual habits, contracep- tive use, pregnancies, and sexually transmitted diseases should be determined. Family history: Because many conditions are inherited, the ages and health of siblings, parents, grandparents, and other family members can provide impor- tant diagnostic clues. For instance, an obese child with a family history of adult-onset diabetes is at high risk for developing diabetes; early intervention is warranted. Social history: Living arrangements, economic situations, type of insurance, and religious affiliations may provide important clues to a puzzling diagnostic case or suggest important information about the acceptability of therapeutic options. Review of systems: A few questions about each of the major body systems allows the practitioner to ensure that no problems are overlooked and to obtain crucial history about related and unrelated medical conditions. General appearance: Well versus poorly nourished; evidence of toxemia, includ- ing lethargy (defined as poor or absent eye contact and refusal to interact with environment), signs of poor perfusion, hypo- or hyperventilation, and cyano- sis; or stigmata of syndromes (such as Down or Turner). Skin: In smaller children, checking the color of the skin for evidence of pallor, plethora, jaundice, or cyanosis is important. Abnormalities such as capillary hemangiomas (eg, “stork bites” in a newborn), café-au-lait spots, pigmented nevi (eg, “Mongolian spots”), erythema toxicum, or pustular melanosis can be identified. In older children, macules, papules, vesicles, pustules, wheals, and petechiae or purpura should be described, and evidence of excoriation, crust formation, desquamation, hyperpigmentation, ulceration, scar formation, or atrophy should be identified. Vital signs: Temperature, blood pressure (generally begin routine measure- ment after 3 years), heart rate, respiratory rate, height, weight, and head cir- cumference (generally measured until age 3 years). Head: For the neonate, the size of fontanelles and presence of overriding sutures, caput succedaneum (superficial edema or hematoma that crosses suture lines, usually located over crown), or cephalohematoma (hematoma that does not cross suture lines) should be noted. For the older child, the size and shape of the head as well as abnormalities such as swellings, depres- sions, or abnormal hair quality or distribution may be identified. Eyes: For infants, abnormalities in the size, shape, and position of the orbits, the color of the sclera (blue sclera, for instance, may indicate osteogenesis imper- fecta), conjunctival hemorrhages, or the presence of iris defects (such as colo- boma) may be found. Ears: For all children, abnormalities in the size, shape, and position of the ears can provide important diagnostic clues. Whereas tympanic membranes are difficult to assess in newborns, their integrity should be assessed in older children. For all children, the quality and character of discharge from the ear canal should be documented. Nose: The size, shape, and position of the nose (in relation to the face and mouth) can provide diagnostic clues for various syndromes, such as a small nose in Down syndrome. Patency of the nostrils, especially in neonates who are obligate nose breathers, is imperative. Abnormalities of the nasal bridge or septum, integrity of the mucosa, and the presence of foreign bod- ies should be noted. Mouth and throat: The size, shape, and position of the mouth and lips in relation to other facial structures should be evaluated. In infants, common findings of the mouth include disruption of the palate (cleft palate syn- drome), Epstein pearls (a tiny white papule in the center of the palate), and short frenulum (“tongue-tied”). For all children, the size, shape, and posi- tion of the tongue and uvula must be considered. The number and quality of teeth for age should be assessed, and the buccal mucosa and pharynx should be examined for color, rashes, exudate, size of tonsils, and symmetry. Nonetheless, the size, shape, and preferred position of the neck can be evalu- ated for all children. An abnormal mass, such as a thyroglossal duct cyst (midline above the level of the thyroid) or brachial cleft cyst (along the sternomastoid muscle), or unusual findings, such as webbing in Turner syndrome, can be identified. Chest: General examination of the chest should include an evaluation of the size and shape of the structures along with identification of obvious abnormal- ities (such as supernumerary nipples) or movement with respirations. Respira- tory rate varies according to age and ranges from 40 to 60 breaths/min in the neonate to 12 to 14 breaths/min in the toddler. The degree of respiratory dis- tress can be stratified, with increasing distress noted when the child moves from subcostal to intercostal to supraclavicular to suprasternal retractions. Palpation of the chest should confirm the integrity of the ribs and clavicles, and any swelling or tenderness in the joints. Percussion in older children may reveal abnormalities, especially if asymmetry is noted. The chest should be auscul- tated for air movement, vocal resonance, rales, rhonchi, wheezes, and rubs. In adolescent girls, symmetry of breast development and presence of masses or nipple discharge should be evaluated. The chest should be palpated for the location and quality of the cardiac impulse, and to determine if a thrill is present. Murmurs, clicks, rubs, and abnormalities in the heart rate (which vary by age) or rhythm should be identified. Abdominal examination: The abdomen should be inspected to determine whether it is flat or protuberant, if masses or lesions such as striae are obvious, or if pulsations are present. In older children, the abdomen usually is flat, but in the neonate a very flat abdomen in conjunction with respiratory distress may indicate diaphragmatic hernia.

When deficits have been present for many months or for years cheap cytotec american express treatment for piles, recovery is slow: Months may pass before any improvement is apparent order 200 mcg cytotec amex medicine descriptions, and complete recovery may never occur. Long-Term Treatment For patients who lack intrinsic factor or who suffer from some other permanent cause of vitamin B12 malabsorption, lifelong treatment is required. However, large daily oral doses can be just as effective, as can weekly intranasal doses. During prolonged therapy, treatment should be periodically assessed: plasma levels of vitamin B12 should be measured every 3 to 6 months, blood samples should be examined for the return of macrocytes, and blood counts should be performed. Potential Hazard of Folic Acid Treatment with folic acid can exacerbate the neurologic consequences of B12 deficiency. Recall that folic acid, by itself, can reverse the hematologic effects of B12 deficiency—but will not alleviate neurologic deficits. So, by correcting the most obvious manifestation of B12 deficiency (anemia), folic acid can mask the fact that deficiency of B12 still exists. As a result, use of folic acid can lead to undertreatment with B itself12 and can thereby permit neurologic damage to progress. Clearly, folic acid is not a substitute for vitamin B12, and vitamin B12 deficiency should never be treated with folic acid alone. Whenever folic acid is employed during treatment of vitamin B12 deficiency, extra care must be taken to ensure that B12 dosage is adequate. Folic Acid Deficiency In one respect, folic acid deficiency is identical to vitamin B12 deficiency: in both states, megaloblastic anemia is the most conspicuous pathology. However, in other important ways, folic acid deficiency and vitamin B12 deficiency are dissimilar (Table 45. Consequently, when a patient presents with megaloblastic anemia, it is essential to determine whether the cause is deficiency of folic acid, vitamin B12, or both. Under normal conditions, activation occurs through a pathway that employs vitamin B12 (see Fig. However, when large amounts of folate are ingested, some can be activated through an alternate pathway—one that does not employ vitamin B12. Fate in the Body Folic acid is absorbed in the early segment of the small intestine and then transported to the liver and other tissues, where it is either used or stored. That is, folate from the liver is excreted into the intestine, after which it is reabsorbed and then returned to the liver through the hepatic-portal circulation. In contrast to vitamin B12, folic acid is not conserved rigidly: every day, significant amounts are excreted. As a result, if intake of folic acid were to cease, signs of deficiency would develop rapidly (within weeks if body stores were already low). Good sources include peas, lentils, oranges, whole-wheat products, asparagus, beets, broccoli, and spinach. Folic Acid Deficiency: Causes, Consequences, and Diagnosis Causes Folic acid deficiency has two principal causes: (1) poor diet (especially in patients who abuse alcohol), and (2) malabsorption secondary to intestinal disease. Alcoholism Alcoholism, either acute or chronic, may be the most common cause of folate deficiency. Deficiency results for two reasons: (1) insufficient folic acid in the diet and (2) derangement of enterohepatic recirculation secondary to alcohol- induced injury to the liver. Fortunately, with improved diet and reduced alcohol consumption, alcohol-related folate deficiency will often reverse. Sprue Sprue is an intestinal malabsorption syndrome that decreases folic acid uptake. Because sprue does not block folate absorption entirely, deficiency can be corrected by giving large doses of folic acid orally. Consequences With the important exception that folic acid deficiency does not injure the nervous system, the effects of folate deficiency are identical to those of vitamin B12 deficiency. As with B12 deficiency, the most prominent consequence of folate deficiency is megaloblastic anemia. Because we already noted that many of the consequences of vitamin B12 deficiency result from depriving cells of active folic acid, the similarities between folate deficiency and vitamin B12 deficiency should be no surprise. The Developing Fetus Folic acid deficiency very early in pregnancy can cause neural tube defects (e. Accordingly, it is imperative that all women of reproductive age ensure adequate folate levels before pregnancy occurs. Preventive Services Task Force now recommends that all women who may become pregnant consume 400 to 800 mcg of supplemental folic acid each day—in addition to the folate they get from food. Other Consequences As discussed in Chapter 65, folic acid deficiency may increase the risk for colorectal cancer and atherosclerosis. One form is inactive as administered (but undergoes activation after being absorbed). Both forms have several generic names: the inactive form is referred to as folacin, folate, pteroylglutamic acid, or folic acid; the active form is referred to as leucovorin calcium, folinic acid, or citrovorum factor. Indications Folic acid has three uses: (1) treatment of megaloblastic anemia resulting from folic acid deficiency; (2) prophylaxis of folate deficiency, especially during pregnancy and lactation; and (3) initial treatment of severe megaloblastic anemia resulting from vitamin B12 deficiency. However, as noted in Chapter 65, even moderately large doses (1000 mcg/day), when taken long term, may increase the risk for some cancers, including colorectal cancer and cancer of the prostate. Dosage For treatment of folate-deficient megaloblastic anemia in adults, the usual oral dosage is 1000 to 2000 mcg/day. For prophylaxis during pregnancy and lactation, doses up to 1000 mcg/day may be used. Leucovorin Calcium (Folinic Acid) Leucovorin calcium is an active form of folic acid used primarily as an adjunct to cancer chemotherapy. Leucovorin is not used routinely to correct folic acid deficiency because folic acid is just as effective and cheaper. Guidelines for Treating Folic Acid Deficiency Choice of Treatment Modality The modality for treating folic acid deficiency should be matched with the cause. If the deficiency is due to poor diet, it should be corrected by dietary measures— not with supplements (except for women who may become pregnant). Ingestion of one serving of a fresh vegetable or one glass of fruit juice a day will often suffice. In contrast, when folate deficiency is the result of malabsorption, diet alone cannot correct the deficiency, so supplemental folate will be needed. Even in the presence of intestinal disease, oral folic acid can be effective, provided the dosage is high enough. Prophylactic Use of Folic Acid Folic acid should be taken prophylactically only when clearly appropriate. The principal candidates for prophylactic folate are women who might become pregnant and women who are pregnant or lactating.

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