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In the new- born with pneumonia cheap viagra professional 50mg free shipping, broad-spectrum antimicrobials (ampicillin with either gen- tamicin or cefotaxime) are customarily prescribed cheap viagra professional 50 mg visa. During the first few months of life, Chlamydia trachomatis is a possibility, particularly in the infant with staccato cough and tachypnea, with or without conjunctivitis or known maternal chlamydia history. These infants also may have eosinophilia, and bilateral infiltrates with hyperinfla- tion on chest radiograph; treatment is erythromycin. Patients with nasal and chest congestion with increased work of breathing, wheezing, and hypoxemia regularly present to the emergency room during the winter months and are admitted for observation, hydration, oxygen, and bronchodilator therapies. A mixed viral and bacterial pneumonia can be present in approximately 20% of patients. Antibacterial coverage should be considered if the clinical scenario, examination, or radiographic findings suggest bacterial infection. Antibiotics in this age group are directed toward Mycoplasma and typical bacteria (pneumococcus). Treatment options include penicillins (amoxicillin, ampicillin), cephalosporins (ceftriaxone, cefuroxime), or macrolides (azithromycin). Vancomycin or clindamycin should be added if commu- nity-acquired methicillin-resistant Staphylococcus aureus is suspected. Pseudomonas and Aspergillus are possibilities in the patient with chronic lung disease (cystic fibrosis). Travel to the southwestern United States may expose patients to Coccidioides immitis, infected sheep or cattle to Coxiella burnetti, and spelunking or working on a farm east of the Rocky Mountains to Histoplasma capsulatum. Mycobacterium tuberculosis has become more problematic over the past decade; multidrug resistance is increasingly seen. Patients may present with symptoms ranging from a traditional cough, bloody sputum, fever, and weight loss to subtle or nonspecific symptoms. This same measurement in an otherwise healthy child without exposures would not be considered positive. Pos- sible sources for acid-fast bacilli for stain and culture (depending on the age of the patient) include sputum samples, first-morning gastric aspirates, cerebrospinal fluid, bronchial washes or biopsy obtained through bronchoscopy, and empyema fluid analysis or pleural biopsy if surgical intervention is required. Standard antitubercu- lous therapy, while awaiting culture and sensitivities, includes isoniazid, rifampin, and pyrazinamide. For possible drug-resistant organisms, ethambutol can be added temporarily as long as visual acuity can be followed. The typical antibiotic course consists of an initial phase of approximately 2 months’ duration on three or four medications, followed by a continuation phase of 4 to 7 months on isoniazid and rifampin. Ultimately, total therapy duration is dependent upon the extent of imaging abnormalities, resistance patterns, and results of follow-up sputum samples in the age-appropriate patient. Group B streptococcal infection (Case 4) and neonatal herpes simplex virus infection (Case 6) are common infections in the newborn period; both can present as pneumonia. The child with tra- cheoesophageal atresia (Case 7) will have recurrent episodes of aspiration resulting in pneumonia. In the first hours of life transient tachypnea of the newborn (Case 8) may result in increased respiratory rate and streakiness on the radiograph; the condition typically self-resolves in the first 2 days of life but occasionally may be confused with neonatal pneumonia. Depending on the cause of the pneumonia (ie, tuberculosis) failure to thrive (Case 10) may result. The child with sickle cell disease (Case 13) is prone to acute chest syndrome, a life-threatening condition of new pulmonary infiltrate on chest radiograph in addition to one of the following: fever, dyspnea, tachypnea, chest pain, or decreased oxygen saturations. His mother relates that he has a 1-week history of nasal congestion and watery eye dis- charge, but no fever or change in appetite. He has nasal congestion, clear rhinorrhea, erythematous conjunctivae bilaterally, and watery, right eye discharge. She has been complaining that her “belly hurts” and has experienced one episode of posttussive emesis, but no diarrhea. Res- pirations are 28 breaths/min, and her examination is remarkable for decreased breath sounds at the left base posteriorly with prominent crackles. Which of the following acute interventions is the next best step in your evaluation? According to your clinic records, his immunizations are current and his weight was at the 25th percen- tile on his examination 6 months ago. He is afebrile, with clear nares and posterior oropharynx, and a normal respiratory effort. Beyond obtaining a chest radiograph, which of the following is the best next step in your evaluation? He recently went on a boy scouts trip to Arizona, where he camped outside for 2 weeks, and excitedly describes how he became trapped in a “haboob” (massive dust storm) for an hour with his troop mates. His mother mentions that one of the other boys in his troop developed an unidentified, painful rash on his shins shortly after returning from the trip. Cough and increased respiratory effort in an afebrile infant with eye dis- charge are consistent with Chlamydia. Approximately 25% of infants born to mothers with Chla- mydia develop conjunctivitis; about half of these develop pneumonia. Most infants present with respiratory infection in the second month of life, but symptoms can be seen as early as the second week. Pulse oximetry should urgently be performed to ascertain whether oxygen is required. Sputum culturing is reasonable for an older patient who can produce sputum, but an adequate and diagnostically useful specimen can only be obtained from a 2-year-old by endotracheal aspirate or bronchoscopy. In this otherwise healthy toddler for whom concerns for atypical pneumonia are high, invasive maneuvers are not indicated. Abdominal pain, as noted in this ques- tion, can be seen as a presenting symptom in pneumonia, probably because of irritation of the diaphragm by pulmonary infection. Neck and perihilar or mediastinal lymphadenopathy and pulmonary or extrapulmonary manifesta- tions can occur, with miliary disease and meningitis more common in infants and younger children. Coccidioides spores often are found in the soil in the southwestern Unites States. Coccidioidomycosis typically results from inhalation of spores dur- ing dust-generating events. Treatment for symptomatic infection is with systemic antifungal (fluconazole, itraconazole). Neo- nates have the greatest risk of group B Streptococcus, toddlers are more likely to have respiratory syncytial virus, and adolescents usually contract Mycoplasma. Tuberculosis at a Glance: A Reference for Practitioners on Basic Tuberculosis Information. He has not had any abdominal pain but for the past week, has sometimes cried with stooling and now cries when she wipes him. She reports he previously had two soft bowel movements per day but over the past month, he has been having only one bowel movement per day. The mother and the child’s father are his only caregivers, and she notes that the change occurred after she started trying to get him to stool in the toilet. Instead, he goes behind the sofa and she will hear him grunt and see his face turn red. He is eating his regular diet of grilled cheese sandwiches with 20 oz of milk and 20 oz of a fruit-flavored beverage each day. On palpation of his abdomen, he has no tenderness, guarding, nor hepatosplenomegaly. On inspection of the rectal area, you find a 7-mm linear split in the posterior midline traversing from the anocutaneous junction to the dentate line. Parents should minimize foods known to be constipating (such as dairy products), increase water intake, and avoid bulking agents (such as fiber). Suppositories should be avoided because they will fur- ther traumatize the fissured skin. Application of petrolatum and gentle wiping should be performed after each stool until the skin no longer bleeds. Considerations Anal fissures are one of the most common causes of rectal bleeding in infants, tod- dlers, children, and adolescents. It is a benign diagnosis that usually results from constipation; large or dried hard stool can cause splitting of the skin. A cycle can then ensue in which the child avoids stooling due to the pain at the fissure site during defecation, which leads to accumulation of bulkier stool. Even though the diagnosis of an anal fissure is made by physical examination, certain details are often found in the child’s history that will suggest the diagnosis.

Presentation of a Case: • There is thickening of the palmar fascia buy discount viagra professional 50 mg on line, more marked along the ulnar side with fexion contracture of 4th and 5th fngers of both hands (may be all the fngers) generic viagra professional 100mg online. Dupuytren contracture Dupuytren contracture Diabetic cheiroarthropathy Q:What is Dupuytren contracture? A: It is characterized by thickening, fbrosis and shortening of superfcial palmar fascia, causing fex- ion contracture of fngers. There is puckering of the skin and palpable nodules, also inability to extend the fngers. It is usually painless, may be bilateral, common after 40 years, but increases in with advancing age. In some patients, it may progress rapidly with severe deformity and functional disability. In this condition, skin of the dorsum of fngers is tight, waxy, shiny and depigmented with joint stiffness and fexion deformities of many fngers. Cause of cheiroarthropathy is unknown, probably there is cross-linking and thickening of colla- gen. It occurs in any type of diabetes mellitus, and is confused with systemic sclerosis. A: As follows: • Bony swelling or enlargement in other parts of the body—Leg (bowing of tibia), spine (kypho- sis), other bony enlargement. A: Paget’s disease is characterized by excessive and disorganized resorption and formation of bone, resulting in deformity and fracture. In Paget’s disease, there is increase in both osteoclastic bone resorption and osteoblastic activity. The disease may involve one bone (monostotic, 10 to 15%) or many bones (polyostotic). A: As follows: • Many cases are asymptomatic (60 to 80%), detected incidentally during X-ray. Appearance of night pain probably indicates development of osteosarcoma in Paget’s disease. A: As follows: • X-ray—Shows enlargement of bone with typical lytic and sclerotic lesion. X-ray skull shows lytic lesion, osteoporosis circumscripta, enlargement and sclerosis, thickening of trabeculae. To prevent further bone break down— • Bisphosphonates—Pamidronate, zoledronate, risedronate are more effective. Presentation of a Case: • There is bluish (or violaceous) discoloration at the tip and ala of the nose. A: It is a multisystem granulomatous disease of unknown aetiology, characterized by non-caseating granuloma in different organs. There is an imbalance between subset of T lymphocyte and disturbance of cell mediated immunity. A: As follows: • Skin lesions—erythema nodosum, plaque, maculopapular rash, hyper or hypopigmentation, subcutaneous nodule. Asymptomatic (incidental fndings are—bilateral hilar lymphadenopathy in X-ray chest or abnormal liver function test). Symptomatic— • Fever, polyarthritis or arthralgia, erythema nodosum, other skin lesions such as lupus pernio, plaque, skin rash. There may be cranial nerve palsy, meningism, seizure, psychosis, diabetes insipidus). Q: What is Heerfordt syndrome (uveoparotid fever or Heerfordt–Waldenström syndrome)? A: In sarcoidosis, presence of fever, bilateral parotid enlargement, anterior uveitis and lower motor neuron facial palsy is called Heerfordt syndrome. May be lung infltrate, pulmonary fbrosis, honeycomb shadow, miliary mottling, eggshell calcifcation). Lung function tests (shows restrictive lung disease, also reduction of gas transfer). Transbronchial or percutaneous (pneumothorax may develop), open biopsy may be required (by thoracotomy). Biopsy is done from the nodule, which shows typical sarcoid lesion (this test is not done now a days). A: Noncaseating granuloma (shows epithelioid cells, macrophages, lymphocytes and multinucleated giant cells). There is progressive ventilatory failure, pulmonary hypertension and cor pulmonale. If the disease is not improved 6 months after the diagnosis—prednisolone should be given, 30 mg for 6 weeks, reduced to alternate day treatment with 15 mg for 6 to 12 months. Other treatment: • Avoid strong sunlight (may precipitate hypercalcaemia and renal impairment). A: As follows: • Severe symptoms such as persistent erythema nodosum, fever, arthritis or arthralgia. Death is due to cardiac involvement, pulmonary fbrosis and cor-pulmonale or renal damage. Look at the patient carefully: • Dyspnoeic or orthopnoeic (may be found in left ventricular failure), cachexia (in severe heart failure). Compare other pulses simultaneously (carotid pulse should not be seen at the same time, may cause syncope due to cerebral ischaemia). Next, measure the height from sternal angle (It indicates mean right atrial pressure. If pulse is absent in one arm or there is radio-radial or radio-femoral delay, then see B. If the thrill coincides with carotid pulse, it is systolic and if it does not coincide (comes after or before), it is diastolic. Apical thrill is best seen by turning the patient to left lateral position with breath hold after expiration. Basal thrill is best seen by palm, the patient sitting and bending forward, breath hold after expiration. Left parasternal heave or lift: Place the fat of right palm in left parasternal area and feel by giving gentle sustained pressure. First heart sound coincides with carotid pulse, second sound does not (comes after). Pathological: • Hyperdynamic circulation (due to fever, anaemia, thyrotoxicosis, arteriovenous fstula, beriberi). It is found in: • Sinus arrhythmia (pulse increases on each inspiration, decreases on each expiration), abolished by exercise. Character of Pulse: • Anacrotic pulse—slow rising, small volume pulse (notch on upstroke). Mechanism of pulsus paradoxus: During inspiration, intrathoracic pressure falls, blood pools in pulmonary vessels and hence left heart flling is reduced with reduction of cardiac output. Causes of pulsus paradoxus: • Pericardial effusion (especially, cardiac tamponade). A:Collapsing pulse is always a high volume pulse, but all the high volume pulses are not collapsing. External jugular vein is not examined as it is tortuous and subject to compression). A: As follows: Venous Arterial 1 It is wavy (two peaks with cardiac cycle) 1 Not wavy 2 It has an upper limit 2 No defnite upper limit 3 Upper limit falls with inspiration 3 Not so 4 Varies with posture 4 Independent of posture 5 It is better seen than palpation 5 It is better felt than seen 6 Upper limit is increased by pressing the abdomen 6 Not so (hepatojugular refux) 7 Just felt or lightly felt 7 Thrusting 8 Obliterated by light pressure at the root of the neck 8 Cannot be obliterated Causes of cannon wave (giant ‘a’ wave): Occurs when atria contracts against closed tricuspid valve. Precordium: Deformity of chest (kyphosis, scoliosis, pectus excavatum and pectus carinatum) may be associated with Marfan’s syndrome, also may cause cor pulmonale. Kyphosis Scoliosis Pectus excavatum Pectus carinatum Apex Beat: It is the lowermost and outermost, defnitely palpable cardiac impulse. Normally, it is 9 cm from midline or 1 cm internal to the mid-clavicular line in left ffth intercostal space. Suprasternal pulse: Usually arterial (due to aneurysm of aorta and atherosclerosis). Pulsation around scapula: Found in coarctation of aorta (due to anastomotic vessels). Also in chronic constrictive pericarditis (this third sound is called pericardial knock). Triple Rhythm: When in addition to frst and second heart sounds, there is another sound either third or fourth, it is called triple rhythm. Gallop rhythm is of 3 types: • Protodiastolic: Extra sound (third heart sound), in early or mid diastole.

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For example purchase viagra professional 100mg otc, if the patient responded to acute therapy with lithium alone cheap viagra professional 50 mg fast delivery, then lithium alone should be tried long term. More recently, antipsychotic agents have been employed for long-term maintenance, either as monotherapy or in combination with a mood stabilizer. Promoting Adherence Poor patient adherence can frustrate attempts to treat a manic episode. Patients may resist treatment because they fail to see anything wrong with their thinking or behavior. P a t i e n t E d u c a t i o n Adherence to Long-Term Therapy After an acute manic episode has been controlled, long-term prophylactic therapy is indicated, making adherence an ongoing issue. Family members can help ensure adherence by overseeing medication use and by urging the patient to visit his or her prescriber or a psychiatric clinic if a pattern of nonadherence develops. Counseling can help patients cope with the sequelae of manic episodes, such as strained relationships, reduced self-confidence, and a sense of shame regarding uncontrolled behavior. Patients should be taught to recognize early symptoms of mood change and encouraged to contact their primary clinician immediately if these develop. Mood-Stabilizing Drugs As noted, mood stabilizers are drugs that can relieve an acute manic or depressive episode and can prevent symptoms from recurring—all without aggravating mania or depression and without accelerating cycling. Beneficial effects were first described in 1949 by John Cade, an Australian psychiatrist. Because of concerns about toxicity, lithium was not approved for use in the United States until 1970. As a result, toxicity can occur at blood levels only slightly greater than therapeutic levels. Chemistry Lithium is a simple inorganic ion that carries a single positive charge. In the periodic table of elements, lithium is in the same group as potassium and sodium. Lithium is found naturally in animal tissues but has no known physiologic function. In manic patients, lithium reduces euphoria, hyperactivity, and other symptoms but does not cause sedation. Antimanic effects begin 5 to 7 days after treatment onset, but full benefits may not develop for 2 to 3 weeks. In the past, lithium was considered the drug of choice for all patients experiencing an acute manic episode, regardless of clinical presentation. Today, however, lithium is reserved primarily for patients with classical (euphoric) mania, and valproate is generally preferred for all other patients (see Table 26. Mechanism of Action Although lithium has been studied extensively, the precise mechanism by which it stabilizes mood is unknown. In the past, research focused on three aspects of brain neurochemistry: (1) altered distribution of certain ions (calcium, sodium, magnesium) that are critical to neuronal function; (2) altered synthesis and release of norepinephrine, serotonin, and dopamine; and (3) effects on second messengers (e. Unfortunately, this research has failed to provide a definitive explanation of how lithium works. Current neurochemical research suggests that lithium may work by (1) altering glutamate uptake and release, (2) blocking the binding of serotonin to its receptors, or (3) inhibiting glycogen synthase kinase-3 beta. There has been growing interest in the neurotrophic and neuroprotective actions of lithium. In animal studies, “therapeutic” doses of lithium doubled the level of neurotrophic Bcl-2 proteins. In addition, lithium has been shown to facilitate regeneration of damaged optic nerves. All of these studies suggest that the benefits of lithium may result at least in part from an ability to protect against neuronal atrophy or promote neuronal growth. Pharmacokinetics Absorption and Distribution Lithium is well absorbed after oral administration. Because of its short half-life (and high toxicity), the drug must be administered in divided daily doses. Large, single daily doses cannot be used, even when a slow-release preparation is prescribed. Because lithium is excreted by the kidneys, it must be employed with great care in patients with renal impairment. Specifically, lithium excretion is reduced when levels of sodium are low because the kidney processes lithium and sodium in the same way. Hence, when the kidney senses that sodium levels are inadequate, it retains lithium in an attempt to compensate. Because of this relationship, in the presence of low sodium, lithium can accumulate to toxic levels. Because diuretics promote sodium loss, these agents must be employed with caution. Also, sodium loss secondary to diarrhea can be sufficient to cause lithium accumulation. Dehydration will cause lithium retention by the kidneys, posing the risk for accumulation to dangerous levels. Monitoring Plasma Lithium Levels Measurement of plasma lithium levels is an essential component of treatment. When the desired therapeutic effect has been achieved, the dosage should be reduced to produce maintenance levels of 0. Blood for lithium determinations should be drawn in the morning, 12 hours after the evening dose. During maintenance therapy, lithium levels should be measured every 3 to 6 months. Adverse Effects The adverse effects of lithium can be divided into two categories: (1) effects that occur at excessive lithium levels and (2) effects that occur at therapeutic lithium levels. In the subsequent discussion, adverse effects produced at excessive lithium levels are considered as a group. Adverse Effects That Occur When Lithium Levels Are Excessive Certain toxicities are closely correlated with the concentration of lithium in blood. Patients should be informed about early signs of toxicity and instructed to interrupt lithium dosing if these appear. In adherent patients, the most common cause of lithium accumulation is sodium depletion. To keep lithium levels within the therapeutic range, plasma drug levels should be monitored routinely. Levels should be measured every 2 to 3 days at the beginning of treatment and every 3 to 6 months during maintenance therapy. Treatment of acute overdose is primarily supportive; there is no specific antidote. Hemodialysis is an effective means of lithium removal and should be considered whenever drug levels exceed 2. B l a c k B o x Wa r n i n g : L i t h i u m To x i c i t y Lithium toxicity is closely related to serum lithium levels and can occur at doses close to therapeutic levels. Facilities for prompt and accurate serum lithium determinations should be available before initiating therapy Adverse Effects That Occur at Therapeutic Levels of Lithium Early Adverse Effects. About 30% of patients experience transient fatigue, muscle weakness, headache, confusion, and memory impairment. Patients may develop a fine hand tremor, especially in the fingers, that can interfere with writing and other motor skills. Lithium-induced tremor can be augmented by stress, fatigue, and certain drugs (antidepressants, antipsychotics, caffeine). To maintain adequate hydration, patients should be instructed to drink 8 to 12 glasses of fluids daily. Polyuria, nocturia, and excessive thirst can discourage patients from adhering to the regimen. Lithium-induced polyuria can be reduced with amiloride [Midamor], a potassium-sparing diuretic. Amiloride appears to help by reducing the entry of lithium into epithelial cells of the renal tubule. However, because thiazides can lower levels of sodium (see Chapter 35), and would thereby increase lithium retention, amiloride is preferred.

Alt er n a- tively buy cheap viagra professional 100mg on-line, shorter-acting agents such as lorazepam can be given as needed viagra professional 50 mg on-line, on ly wh en the patient has symptoms. In either case, the key to successful management is init ially aggressive upward t it rat ion of dosage unt il t he patient is heavily sedated but responsive, followed by rapid downward titration as agit at ion decreases, usually over 48 to 72 hours. Support ive measures are also import ant, such as adequat e hydrat ion, replacement of elect rolyt es such as magne- sium, and supplement at ion wit h thiamine and other B vitamins in malnourished, ch r on ic alcoh olics t o pr event the d evelopment of Wer n icke en ceph alopat h y. W hich of t he following st atement s is most likely other serious diagnoses must be excluded before the patient’s mental status and to be correct? Auditory hallucinations are unique to alcohol withdrawal and cannot be It is important to understand the temporal course of the spectrum of alcohol cau sed by a br ain t u mor. In contrast to other causes of delirium, benzodiazepines are the drugs of choice in B. If the serum blood alcohol level is higher than the legal limits of intoxication, alcohol withdrawal. T h ey can be given on a fixed sch edu le in h igh -r isk pat ient s ( pr e- these symptoms cannot be alcohol withdrawal. If the patient also has hypertension, fever, and tachycardia, he has a 5% of two strategies. Long-acting benzodiazepines such as diazepam or chlordiazepox- to 10% chance of mortality. In either case, the key to successful management is init ially aggressive upward t it rat ion of dosage unt il t he 59. Cocaine and amphet amines bot h act as st imulant s in the brain, import ant, such as adequat e hydrat ion, replacement of elect rolyt es such as magne- increasing levels of dopamine. Remember that delirium is usually acute in onset and fluctuates, whereas dementia (the other answers) is slower and more gradual in onset, and con- sistent in alt erat ion of cognit ion. Auditory hallucinat ions can occur from a num- ber of illicit agents or even brain tumors. The fall in serum blood alcohol level and not the absolute level may induce symptoms of withdrawal. An indi- vid u al wh o ab u ses alcoh ol sh o u ld fir st b e given t h iam in e, b efor e glu cose is administered, t o prevent acut e Wernicke encephalopat hy. Lo w-d o se h a lo p e rid o l ca n b e used to control agitation or psychotic symptoms. Symptom-triggered benzodiazepine therapy for alcoh ol wit h drawal syndrome in the emergency depart ment : a comparison with the standard fixed dose benzodiazepin e regimen. Predictors of severe alcohol withdrawal syndrome: a systematic review and meta-analysis. On e xa m in at io n, h e is sle e p in g o n the st re t ch e r b u t is e a sily a ro u sa b le. He is afebrile with a pulse rate of 115 bpm, blood pressure of 122/72 mm Hg, and respi- ratory rate of 18 b p m. His e yes are b lood - shot but anicteric, his chest is clear to auscultation, and his heart is tachycardic but regular in rhythm, and no murmurs are appreciated. His abdominal examination is sig n ifica n t fo r m ild e p ig a st ric t e n d e rn e ss wit h h yp o a ct ive b o we l so u n d s, b u t n o guarding or tenderness is noted. Urine drug screen is negative, and abdominal x-rays show a normal bowel gas pattern with no signs of obstruction. H is physical examination is significant only for tachycardia and mild epigastric tender- ness. H is laboratory studies are most significant for a low serum bicarbonate level, suggest ive of an acidot ic st at e. T h e Acet est is weakly posit ive for ket ones, but h is serum glucose is not elevated. Understand the two causes of nongap acidosis (bicarbonate losses from the gast r oin t est in al [G I ] t r act an d r en al t u bu lar acid osis). Understand how to distinguish between saline-responsive and saline-resistant metabolic alkalosis. Co n s i d e r a t i o n s This 45 year old man presents with nausea and vomiting after an alcohol binge. The most significant finding in this case is an apparent acidosis with an elevated anion gap. In this patient with a history of alcoholism and an alcohol binge, alcoholic ketoacidosis is most likely, but one must also consider the possibility of other ingestions (methanol, ethylene glycol), either accidental or intentional, that would also present with simi- lar laboratory findings, but may be more serious or even fatal. Sometimes, due to persistent vomiting, there is a coexisting metabolic alkalosis due to volume depletion. An estimation of unmeasured anions in 3 the plasma (phosphate, sulfate, organic acids), with normal being 10 to 12 mmol/ L. If elevated (eg, > 10 mOsm), then suggestive of the presence of signifi- cant ser u m con cent r at ion of an ad dit ion al osm ot ically act ive solut e su ch as m et h a- nol or ethylene glycol. Disturbances in one of these sys- 4 tems cause a compensatory change in the other system. Lactic acidosis most common ly occur s in the set t ing of an acute illness with poor tissue perfusion such as septic shock, heart failure, severe anemia, or poisoning affecting tissue oxygen delivery or cellular respiration (carbon monoxide, cyanide). Acut e bicarbonat e use has been associat ed wit h increased mort alit y, h eart failure, and volume overload. In alcoholic ketoacidosis, decreased car boh ydrat e int ake redu ces in su lin secret ion, and alcohol-induced inhibition of gluconeogenesis leads to stimulation of lipolysis and contributes to increased ketoacid formation, predominantly beta-hydroxybu- tyrate. The nitroprusside reaction test to detect serum ketones (Acetest) can detect acetoacetate, but not beta-hydroxybutyrate, so the nitroprusside reaction may only be weakly positive, and can lead one to underestimate the degree of ketosis. W ith treatment, as the patient improves, the formation of acetoacetate is favored, so the degree of measured ketosis may appear to paradoxically worsen. In alcoholic or fasting ketoacidosis, the primary treatment is administration of dextrose and saline solu- tions; the dextrose will increase insulin secretion and reduce lipolysis, along with saline to replenish fluid deficit s. Elect rolyte deficiencies such as hypophospha- temia, hypokalemia, or hypomagnesemia are also common, and should be cor- rected. M et h an ol an d et h ylen e glycol are fr equ en t ly fou n d in h igh con cen t r at ion in automot ive ant ifreeze and deicing solut ions, windshield wiper fluid, and other solvent s. T hey may be ingested as a substitute for ethanol, by accident, or inten- tionally, for example, in a suicide attempt. If either of these ingestions is suspected, direct laboratory assays of the substances are not usually available, so their presence may be inferred by an elevated osmolal gap. O ther unmeasured solutes, especially low-molecular- weight subst ances such as met h anol will also affect osmolalit y. If the difference between the directly measured serum osmolality and the cal- culated serum osmolality is greater than 10, then the presence of another solute is suspect ed. If et h ylen e glycol is su sp ect ed, on e m ay also exam in e the u r in e for oxalate crystals. In patients with diarrhea and hypokalemia, renal synthesis and secret ion of ammonia are st imulated, causing a buffering of the urine with a pH greater than 5. In pat ient s wit h advan ced ch r on ic kidn ey disease, declin e in fun ct ion al ren al mass also cau ses a propor t ional + reduction in renal N H excret ion. Most pat ient s h ave h ypocit rat ur ia an d h yper- calciur ia, so kidney stones and nephrocalcinosis commonly occur. Treatment usually involves alkalinization and citrate supplement ation with sodium or pot assium cit rat e t o n or malize pH an d prevent st on e for mat ion. Low plasma r en in act ivit y is com mon in diabet ic pat ient s, leading to hyporeninemic hypoaldosteronism. Pat ient s t ypi- cally present wit h hyperkalemia an d a m ild h yp er ch lor em ic met abolic acid osis. T h e hyperkalemia is usually managed with a low potassium diet and use of loop or thiazide diuretics. Re s p i r a t o r y Ac i d o s i s Respiratory acidosis can o ccu r acu t ely or ch r on ically. T h e 2 most common cause of acute respiratory acidosis in hospitalized patients is drug- induced respiratory depression wit h hypovent ilat ion, due to narcot ics, sedat ives, or anesthesia. It can be a respon se t o any disease that causes hypoxia, such as a pulmonary embolism, but is also often seen as a manifest ation of an anxiety disorder with hyperventilation. H ypocapnia causes decreased cerebral blood flow, so symptoms manifest as light-headedness or dizzi- ness.

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