IM Essentials Questions •
Melanoma Clinical features that help distinguish melanomas from other pigmented lesions may be remembered by the o ABCD mnemonic: asymmetry (inability to draw a line down the middle to produce two mirror images), border that is irregular, scalloped, or poorly circumscribed, color (more than one color in the same lesion or very dark, black, occasionally occasionally white, red, or blue) Diameter ! mm (the si"e of a pencil eraser)# o $esions suspicious for melanoma re%uire an e&cisional biopsy# Uncomplicated parapneumonic pleural efusion. o A pleural e'usion in the setting of CA is likely parapneumonic# o A parapneumonic e'usion is a noninfected e'usion occurring in the pleural space ad*acent to the site of bacterial pneumonia# +ost parapneumonic e'usions are small and clinically insignicant, and they resolve without specic therapy# therapy# -owever, appro&imately ./0 become complicated or progress to empyema# 1n the setting of a small, free2owing pleural e'usion, it is appropriate to treat the underlying cause# 3he presence of loculated loculated (nonfree2owing) 2uid predicts predicts a poor response response to treatment with antibiotics alone# 3horacentesis is not necessary necessary in patients who have small small pleural e'usions (4. (4. cm between the lung and o chest wall on lateral chest radiograph) associated with heart failure, pneumonia, or heart surgery# surgery# 5ne&plained e'usions larger than . cm should be aspirated# Manage a patient with a h istory o inective endocarditis beore a dental procedure. o 3here are specic specic indications for infective infective endocarditis prophyla&is prophyla&is for patients before certain dental dental or surgical procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa# unrepaired cyanotic o High-risk cardiac conditions include conditions include the presence of a prosthetic cardiac valve, unrepaired congenital heart disease, congenital heart disease repair with prosthetic material or device within the last ! months, presence of palliative shunts and conduits, cardiac valvulopathy in cardiac transplant recipients, and a history of infective endocarditis, as in this patient# High-risk surgical procedures include procedures include dental procedures involving manipulation of gingival tissue or the o periapical region of teeth or perforation of the oral mucosa as well as respiratory tract procedures that involve perforation of the respiratory mucosa (tonsillectomy, adenoidectomy)# o 3he suggested antibiotic regimen regimen before dental procedures procedures is an agent directed directed against viridans group group streptococci, administered administered as a single dose 6/ to !/ minutes before the procedure# Amo&icillin Amo&icillin and cephalosporins, such as cephale&in, are fre%uently prescribed# Clindamycin, a"ithromycin, or clarithromycin are appropriate alternatives in patients with penicillin allergy Evaluate acute stroke -emorrhagic stroke stroke cannot be reliably distinguished from ischemic stroke on clinical grounds alone# 1n the o acute setting, C3 of the head without contrast is the initial test of choice to conrm or e&clude hemorrhagic stroke, stroke, and should be performed without signicant delay as the results are needed to make treatment decisions, particularly related to thrombolytic therapy which should be administered as soon as possible once a patient is determined to be an appropriate candidate# C3 of the head without contrast will easily rule out intracerebral hemorrhage, the principal initial criterion for e&cluding thrombolysis# 7ubtle signs of early infarction can sometimes be seen on a head C3 scan, but many patients with acute o ischemic stroke have normal results on this imaging study# 3he treatment of blood pressure pressure in the acute setting setting depends on whether the patient will be treated with o intravenous tissue plasminogen activator (rtA)# 1n patients who are candidates for this agent, blood pressure should be less than .89../ mm -g, which can be achieved by the continuous infusion of labetalol or nicardipine# After rtA rtA infusion, blood pressure should be targeted to less than .8/./9 mm -g; labetalol or nicardipine is again appropriate for patients whose blood pressure e&ceeds these limits# Vasculitidies hurg!"trauss syndrome is syndrome is a form of systemic vasculitis that most often occurs in the setting of o antecedent asthma, allergic rhinitis, or sinusitis# atients typically have eosinophilia, eosinophilia, migratory pulmonary inltrates, purpuric skin rash, and mononeuritis multiple&; fever, arthralgia, and myalgia also are common presenting features# 5p to
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#ranulomatosis with polyangiitis (formerly known as >egener granulomatosis) is a necroti"ing vasculitis that typically a'ects the respiratory tract and kidneys# ?adiographs show pulmonary inltrates or nodules that are often cavitary, as well as pulmonary hemorrhage Microscopic polyangiitis is a necroti"ing vasculitis that typically involves the kidneys and lungs# o atients fre%uently present with rapidly progressive glomerulonephritis; 9/0 of patients have pulmonary involvement that usually manifests as pulmonary hemorrhage# @ever, arthralgia, purpura, and mononeuritis multiple& can also occur# $olyarteritis nodosa typically presents with fever, abdominal pain, arthralgia, and weight loss that develop o over days to months# 3wo thirds of these patients have mononeuritis multiple&, and one third have hypertension and cutaneous involvement, including nodules, ulcers, purpura, and livedo reticularis (testicular pain also occurs in about one third of male patients)# -owever, lung involvement is uncommon and A=CA test results typically are negative =oncontract abdominal helical C3 is the gold standard for diagnosing kidney stones# %yspepsia 3he ?ome 111 criteria for dyspepsia are one or more of the following predominant symptoms: o (.) bothersome postprandial fullness () early satiety (6) epigastric pain (<) pigastric burning# 3he symptoms should be consistent for at least 6 months with an initial onset at least ! months before o diagnosis# Alarm features such as unintentional weight loss, anemia, vomiting, or dysphagia might suggest an alternative diagnosis and the need for immediate upper endoscopy# &iliary colic is the most common clinical presentation in patients with symptomatic gallstones# o 3he usual presentation of biliary colic is episodic severe abdominal pain typically in the epigastrium andor right upper %uadrant but occasionally in the right lower or mid abdomen# 3he pain rapidly intensies over a .9minute interval to a steady plateau that lasts as long as 6 hours and resolves slowly# 3he pain is often associated with nausea or vomiting and may r adiate to the interscapular region or right shoulder# #astroesophageal re'u( disease )#E*%+ occurs when the re2u& of stomach contents causes symptoms o or complications that are troublesome for the patient# ?D is diagnosed when the predominant symptom is heartburn or acid re2u&# Additional signs may be belching, a sour taste in the mouth, and symptoms that are worse at night or with recumbency# $eptic ulcer disease is asymptomatic in <0 to /0 of patients and is commonly diagnosed because of o complications such as bleeding# 7ymptoms, when present, consist of discomfort typically in the epigastric region that has a burning or gnawing %uality# 3he character of this patients pain, the duration of symptoms, and a lack of response to antacids, weight gain, and the absence of anemia make peptic ulcer disease less likely in this patient# %iagnose $rerenal ,-otemia $rerenal a-otemia generally occurs in patients with a mean arterial pressure below !/ mm -g but may o occur at higher pressures in patients with chronic kidney disease or in those who take medications, such as nonsteroidal antiin2ammatory drugs (=7A1Ds), which can alter glomerular hemodynamics# o atients with prerenal a"otemia may have a history of decreased 2uid intake accompanied by e&amination ndings consistent with volume depletion# o Although her fractional e&cretion of sodium (@=a) is greater than .0, she is on a diuretic which can increase the /E0a even in patients with prerenal a-otemia# Because the ractional e(cretion o urea is less in2uenced by diuretics, it can be helpful in evaluating patients on diuretic therapy# 1t is calculated similarly to the @ =a using the serum and urine urea levels# 1n euvolemic patients, the fractional e&cretion of urea is usually 690, and in those with prerenal a"otemia, the fractional e&cretion of urea is typically below 690, as in this patient# ,cute interstitial nephritis is most commonly caused by a hypersensitivity reaction to a medication# o 5rinalysis ndings include leukocyte casts and eosinophils, neither of which is present in this patient# ,cute tubular necrosis ),10+ is characteri"ed by damage to the renal tubule due to a physiologic insult to o the kidney, such as hyp o&ia, to&ins, or prolonged hypoperfusion# Eidney failure tends to be rapid, and the urine traditionally contains muddy brown casts# A3= may result from prolonged prerenal a"otemia# 0",I%s can induce acute kidney in2ury ),3I+ by several mechanisms and may also e&acerbate other o causes of AE1# %iagnose ,septic Meningitis o
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,septic meningitis is commonly associated with genital infection caused by herpes simple& virus and is characteri"ed by recurrent episodes of fever, headache, vomiting, and photosensitivity &eh4et disease is associated with recurrent painful oral and genital aphthous ulcerations, skin lesions, and o uveitis, with neurologic manifestations in up to 90 of patients# >hen BehFet disease causes aseptic meningitis, the level of C7@ pleocytosis is usually less than .// cellsG$ (/#./ & ./H$)# 1reat ,!5b with 6ararin $ongterm anticoagulation therapy is indicated for patients with atrial brillation who are at increased risk for o thromboembolism# 1n patients who are able to take warfarin, however, clopidogrel plus aspirin is inferior for preventing ischemic stroke# o 1n patients who are not candidates for warfarin treatment, adding clopidogrel to aspirin can reduce the risk of stroke more than aspirin alone, although the risk of ma*or bleeding events is increased# %irect thrombin inhibitors. o Drugs such as dabigatran, have been shown to be slightly superior to warfarin in preventing ischemic and hemorrhagic stroke, although their anticoagulant efect is not easily reversed and they are substantially more expensive than wararin. 3hese agents may be an alternative to warfarin in patients with nonvalvular atrial brillation# ,trial 5brillation ablation is an option in patients who are symptomatic and have been treated o unsuccessfully with at least one antiarrhythmic agent# 3he procedure entails electrical isolation of the pulmonary veins so that premature atrial contractions, which fre%uently originate in the pulmonary veins, cannot initiate atrial brillation# ,trioventricular node ablation is another option for patients who do not benet f rom medical therapy# o A pacemaker is inserted at the time of ablation, so the ventricular rate is controlled by the device# &eers riteria: +edication that should be avoided in older patients due to being ine'ective or having adverse side e'ects# %iphenhydramine is listed as a drug that poses an unnecessary risk for older patients because it is highly o anticholinergic and increases the risk of confusion, dry mouth, constipation, and urinary retention# Diphenhydramine may be appropriate in selected clinical situations such as severe allergic reactions# 1reat 7besity with 7rlistat 7rlistat, available over the counter, is a lipase inhibitor that leads to fat malabsorption and weight loss# o 7econdary benets include reduced $D$ and B# 1n diabetics, glycemic control is improved# =egative e'ects included liver in*ury, malabsorption of ADE (supplementation is advised) &ariatric surgery is recommended as a treatment option for patients who have been unable to maintain o weight loss with diet and e&ercise with or without drug therapy with class 111 obesity, dened as patients who have a body mass inde& (B+1)
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,cute viral hepatitis is characteri"ed by *aundice and signicant elevations of serum aminotransferase levels (greater than .9 times the upper limit of normal)# Kther causes that can result in aminotransferase levels to greater than .9& 5$= are medication reactions or to&icity, autoimmune liver disease, ischemic hepatitis (sometimes referred to as Lshock liverM), and acute bile duct obstruction /ulminant liver ailure should always be considered in patients with acute hepatitis, although this typically o presents with evidence o liver dysunction in addition to the disturbance o bilirubin metabolism # @indings often include an increase in coagulation time (as measured by the international normali"ed ratio) due to a decrease in liver production of coagulation factors and a low serum albumin level due to decreased liver albumin production# :emochromatosis is a chronic metabolic cause of chronic liver disease and is associated with much lower o elevations of liver in2ammation markers than are present in this patient# $rimary biliary cirrhosis is an immunemediated cause of chronic liver in2ammation# $abs show an o elevated serum alkaline phosphatase and bilirubin levels disproportionately higher than the aminotranserase elevation# %iagnose Multiple Myeloma Urine immuno5(ation is diagnostic or MM# o @eatures of multiple myeloma, including bone pain, pancytopenia, kidney disease, and hypercalcemia# +ultiple myeloma is a malignancy of plasma cells# +ost myelomas produce a monoclonal (+) protein consisting of an intact immunoglobulin composed of a heavy chain (1g, 1gA, or 1gD) and a N or O light chain, but they may secrete free light chains alone (.!0 of cases), or, rarely, no immunoglobulin# "ymptomatic myeloma is diagnosed by the presence o ;<= or more c lonal plasma cells on bone marrow biopsy the presence o an M protein and evidence o myeloma!related end!organ damage# 3he + protein is produced and secreted by the malignant plasma cells and is detected by serum protein electrophoresis andor of urine protein electrophoresis combined with immuno&ation of the serum and urine# 1mmuno&ation conrms the presence of an + protein and determines its type# 3he absence of an + protein in the serum and the nding of hypogammaglobulinemia suggest that the + protein is a light chain, which is ltered by the glomerulus and is readily found by urine immuno&ation but not found in the serum# Although ltered light chains are proteins, most routine urinalysis dipsticks test primarily for albumin and may not detect the presence of the myeloma protein in the urine# 3he peripheral blood smear ndings (?ouleau& formation followed by leukopenia and thrombocytopenia) will o support a diagnosis of multiple myeloma but will not help establish the diagnosis# ,8 ,myloidosis> o %iagnosis can be made via an abdominal at pad aspirate revealing amorphous eosinophilic material that demonstrates applegreen birefringence when stained with Congo red and viewed under polari"ed light Characteristic clinical ndings of A$ amyloidosis, such as proteinuria, restrictive cardiomyopathy, and hepatomegaly, which makes this diagnosis unlikely# Manage #out with Urate!lowering agents Because gout is associated with hyperuricemia, patients with recurrent episodes ( attacks in . year) o usually benet from uratelowering therapy to prevent both future attacks and occult urate deposition# -owever, the addition of uratelowering therapy transiently increases the risk for acute gout attacks for at least 6 to ! months; accordingly, prophyla&is with an antiin2ammatory agent such as colchicine, at least during that period, is indicated concurrent with uratelowering therapy# Along with this treatment regimen, management of risk factors can help to lower serum uric acid o concentrations, including reducing dietary purine and fructose and increasing dairy intake (within the limits of individual tolerance), weight loss if indicated, and reducing alcohol consumption# o Medications that raise serum uric acid levels, including thiazide diuretics and low-dose salicylates, should be discontinued i alternative therapy is appropriate. 5se of either allopurinol or febu&ostat would be appropriate but only in the setting of concurrent prophyla&is# o 3he dose of both febu&ostat and allopurinol should be adusted to achieve a serum uric acid level !".# mg$d% &#.'( mmol$%), rather than a *xed dose. 3he relative e'ectiveness of these two agents is not well established; febu&ostat is more potent and more e&pensive than allopurinol ,cute gout attacks can be treated with nonsteroidal antiin2ammatory drugs, glucocorticoids, and o colchicine# Choice of treatment is based on relative ePcacy and, most importantly, the sidee'ect proles of the agents and the risk of to&icity in the individual patient# if a patient has hypopituitarism, KCs can help prevent the development of osteopenia or osteoporosis induced by hypogonadism o
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Endocrine and Metabolism •
Manage subclinical hypothyroidism 7ubclinical -ypothyroidism is dened as an elevated 37- and a normal @ree 3<# atients typically have mild o or no symptoms of hypothyroidism# 3he causes of subclinical hypothyroidism are generally considered the same as for overt hypothyroidism. o Appropriate management of patients with subclinical hypothyroidism with a serum thyroidstimulating hormone (37-) level less than ./ G5m$ (./ m5$) is repeat testing of thyroid function in ! months without levothyro&ine therapy e&cept in certain clinical situations# 3reatment is recommended when serum 37- levels are greater than ./ G5m$ (./ m5$)# o $evothyro&ine also may be considered for patients who have marked symptoms, have a goiter, are pregnant or are planning to become pregnant, or have positive serum thyroid pero&idase antibody titers# +ost evidence to date has shown no clinical advantage of liothyronine compared with levothyro&ine in o patients re%uiring thyroid replacement therapy# Additionally, liothyronine and other triiodothyronine &+ ' ) preparations have a short hal-lie and have been associated with acute spikes in serum + ' levels, which are o particular concern in older patients or patients with cardiac abnormalities # A radioactive iodine uptake study is not useful in establishing the diagnosis of hypothyroidism and thus is o inappropriate for this patient# Manage :ypothyroidism during $regnancy 3ey $oint: arly in pregnancy, levothyro&ine re%uirements are increased by 6/0 to 9/0 in most patients with hypothyroidism# o regnancy is known to increase levothyro&ine re%uirements in most patients receiving thyroid replacement therapy, and this e&pected increase should be anticipated by increasing the levothyro&ine dose# 3his is typically increased in the rst (and sometimes in the second) trimester of pregnancy, with a possible o total increase of 6/0 to 9/0, and an increase in levothyro&ine dose in this range to maintain the thyroid stimulating hormone (37-) level between appro&imately /#. and #9 G5m$ (/#. #9 m5$) is associated with fewer maternal and f etal complications# 3he fetus is largely dependent on transplacental transfer of maternal thyroid hormones during the rst . weeks of gestation, and the presence of maternal subclinical or overt hypothyroidism may be associated with subse%uent fetal neurocognitive impairment, increased risk of premature birth, low birth weight, increased miscarriage rate, and even an increased risk of fetal death# 1n pregnant women with hypothyroidism, thyroid function testing should be fre%uent, preferably every < o weeks, to protect the health of mother and fetus and to avoid pregnancy complications# 37- levels generally should range from /#. to #9 G5m$ (/#.#9 m5$) in the rst trimester, /# to 6#/ o G5m$ (/#6#/ m5$) in the second trimester, and /#6 to 6#/ G5m$ (/#66#/ m5$) in the third trimester 1reat :ypothyroidism 3ey $oint 3he mainstay of thyroid hormone replacement is oral levothyro&ine (3<) therapy# o hysical e&amination ndings of hypothyroidism may include a reduced basal temperature, diastolic o hypertension, an enlarged thyroid gland, bradycardia, pallor, dry and cold skin, brittle hair, hoarseness, and a delayed recovery phase of deep tendon re2e&es, although not all of these ndings may be present in a specic patient :ashimoto thyroiditis is the most fre%uent cause of hypothyroidism and is associated with a positive o thyroid pero&idase antibody measurement# Kther less common causes of hypothyroidism include iatrogenic hypothyroidism, which can occur after radioactive iodine ablation for raves disease, e&ternalbeam radiation to the thyroid bed, or surgical removal of the thyroid gland# 3he mainstay of thyroid hormone replacement is oral levothyro&ine (3<), which should always be taken on an o empty stomach . hour before or to 6 hours after intake of food or other medications# Available 36 preparations ($iothyronine) have a short halflife and can be associated with acute spikes in serum 3 6 levels, which are of particular concern in elderly patients or patients with cardiac abnormalities 1reat central hypothyroidism. 3ey $oint> 3he serum 3hyroidstimulating hormone levels cannot be used to monitor thyroid hormone replacement in patients with central hypothyroidism 1n patients with central hypothyroidism, the pituitary thyrotropes are absent and so, the 37- is always low o regardless of the level of circulating thyroid hormone# 3he goal of thyroid hormone replacement in these patients is to titrate the levothyro&ine dose to normali"e o the free 3< level (or total 3< concentration and free 3< inde&), not to normali"e the 37- level# %iagnose lymphocytic thyroiditis as a cause o hyperthyroidism 3ey $oint: 1n patients with subacute, silent, or postpartum thyroiditis or e&posure to e&ogenous thyroid hormones, the radioactive iodine uptake will be very low, which indicates very little endogenous thyroid production#
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1hyroiditis involves transient destruction of thyroid tissue, which disrupts follicles and causes the release of preformed thyroid hormone into the circulation# @orms of destructive thyroiditis include subacute (de Quervain), silent, and postpartum thyroiditis# "ubacute thyroiditis most commonly occurs after a viral infection and usually involves severe thyroid and neck pain; fever, fatigue, malaise, anore&ia, and myalgia are common# "ilent thyroiditis is painless# $ostpartum thyroiditis is a subset of painless autoimmune thyroiditis and can occur up to . months after parturition# 1t a'ects 90 to 80 of pregnant women in the 5nited 7tates and can recur with each pregnancy# 3hyroiditis is associated with elevated serum free thyro&ine (3<) and triiodothyronine (36) levels and a low o serum thyroidstimulating hormone (37-) level# 3he disorder usually follows a classic course of appro&imately ! weeks of thyroto&icosis, a shorter period of o euthyroidism, < to ! weeks of hypothyroidism, and then restoration of euthyroidism# 1n patients with subacute, silent, or postpartum thyroiditis or e&posure to e&ogenous thyroid hormones, the o radioactive iodine uptake (?A15) will be very low (490 at < hours), which indicates very little endogenous thyroid production# #raves disease is an autoimmune disorder that can a'ect the thyroid gland, ocular muscles, orbital fat, o and skin# -yperthyroidism is by far the most common manifestation# &amination of the thyroid may reveal the classic smooth, rubbery, rm goiter, often associated with a bruit# to(ic adenoma or to(ic multinodular goiter usually reveals one or more palpable nodule(s) or overall o gland enlargement# 3o&ic multinodular goiter and to&ic adenoma result from an activating somatic mutation in the 1": receptor gene, which leads to autonomy of function and secretion of e&cess 3 < and 36 from the a'ected nodule(s)# atients with raves disease, to&ic adenoma, or to&ic multinodular goiter have an elevated or highnormal o ?A15, which indicates endogenous production of thyroid hormones# A thyroid scan will show di'use uptake of radioactive iodine in patients with raves disease or more focal uptake in those with to&ic multinodular goiter or to&ic adenoma# 1reat #raves %isease 3ey point: Acute therapy of symptomatic hyperthyroidism usually includes Jblockade and treatment with an antithyroid agent# #raves disease can present with either subclinical or overt thyroto&icosis# o hysical e&amination ndings may include tachycardia; an elevated systolic blood pressure with a widened pulse pressure; a palpable goiter, which is classically smooth; a thyroto&ic stare due to lid retraction; proptosis; and, infre%uently, an inltrative dermopathy , &!&locker is indicated to control tachycardia. o Although all Jblockers are effective, atenolol is fre%uently used because of its J. selectivity and long halflife that allows once daily dosing in some patients# moderate hyperthyroidism can be treated with either methima"ole or propylthiouracil# o +ethima"ole, which generally has fewer side e'ects and results in %uicker achievement of the euthyroid state than propylthiouracil, is preferred in most patients# Because of a presumed immunomodulatory e'ect, antithyroidal drugs result in drugfree remission rates of between 6/0 and 9/0 in patients with raves disease who are treated for . year# *adioactive iodine therapy preceded or followed by ad*unctive therapy with an antithyroidal drug is o occasionally used to treat raves disease# An antithyroidal drug is given in an attempt to decrease the risk of a transient worsening of the thyroto&icosis after thyroid ablation# Because antithyroidal drugs render the thyroid radioresistant, they must be stopped for several days before and after giving the radioactive iodine# Although an occasional patient becomes euthyroid after radioactive iodine administration, the e&pected outcome is hypothyroidism, which typically occurs within to 6 months of therapy, at which time thyroid hormone replacement therapy is begun# Evaluate thyroid nodules with 5ne!needle aspiration biopsy 3ey point: A neneedle aspiration biopsy is the most accurate way to determine if a thyroid nodule is benign or malignant# +ost thyroid nodules are benign; only appro&imately 90 to .90 are malignant# @=A biopsy is the most o accurate method to determine whether a nodule is benign or malignant# 1t is also the most sensitive and specic method to help diagnose the cause of a thyroid nodule @=A biopsy is recommended for any nodule greater than . cm in diameter that is solid and hypoechoic on o ultrasonography and for any nodule cm or greater that is mi&ed cysticsolid without worrisome sonographic characteristics# Biopsy may be appropriate for smaller nodules (at least 9 mm in diameter) in patients with o
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risk factors, such as a history of radiation e&posure, a family or personal history of thyroid cancer, cervical lymphadenopathy, or suspicious ultrasound characteristics# @=A biopsy is not routinely recommended for thyroid nodules less than . cm in diameter $rediabetes may be diagnosed in the presence of: o a hemoglobin A.c value of 9#I0 to !#<0 an impaired fasting glucose value (fasting plasma glucose level of .// to .9 mgd$ R9#I to !#H mmol$S), An impaired glucose tolerance test (hour postprandial plasma glucose level of . 1n young patients with probable diabetes mellitus, the distinction between type . and type diabetes should be made as soon as possible by checking for the presence of pancreatic autoantibodies, which indicate type . disease# atients with 3.D+ will re%uire immediate insulin therapy# 1nsulin treatment in patients with type . diabetes o helps preserve endogenous insulin secretion for a longer period of time, which makes it easier to achieve e&cellent glycemic control without development of hypoglycemia# 1f testing does not show pancreatic autoantibodies, this patient has type diabetes and should be treated o with lifestyle modications and, possibly, metformin# 1reat hyperglycemic hyperosmolar syndrome with 'uid resuscitation. 3ey $oint: 1n patients with hype rglycemic hyperosmolar syndrome, the preservation of vascular volume is critical, and /#H0 (normal) saline is the initial intravenous 2uid of choice, even before intravenous insulin is administered# ::" develops primarily in patients with type diabetes mellitus in the setting of a medical stressor, such as o infection# Eey 1n patients with hyperglycemic hyperosmolar syndrome, the preservation of vascular volume is critical, o and /#H0 (normal) saline is the initial intravenous 2uid of choice, even before intravenous insulin is administered# 1n both diabetic ketoacidosis and --7, the primary mechanism of disease is a relative deciency of o circulating insulin to ade%uately counteract hyperglycemia# 3his relative deciency is more severe in patients with diabetic ketoacidosis and leads to ketone production, whereas in patients with --7, insulin secretion is ade%uate to suppress ketosis but not hyperglycemia# 3his may lead to marked blood glucose elevation (plasma levels fre%uently T8// mgd$ R<<#< mmol$S) due to progressive dehydration that further stimulates compensatory hormone secretion (such as catecholamines), leading to even greater hyperglycemia# atients with --7 are typically extremely volume contracted with severe ree water and sodium losses, o presenting as dry mucous membranes, hypotension, and tachycardia# 1ntravenous insulin should be given to normali"e his blood glucose concentration, but the most immediate concern is administration of intravenous 2uids to correct hypotension and severe volume decit, which is best achieved with /#H0 saline# Crystalloid 2uids are distributed across the e&tracellular space# 7ince /#H0 saline is almost isotonic with o plasma, more volume stays within the intravascular space than when hypotonic solutions such as /#<90 saline are used, and volume decit is more rapidly corrected# 3herefore, even though --7 patients are hypernatremic when the serum sodium concentration is corrected for the degree of hyperglycemia, initial hydration with /#H0 saline is indicated# "creen or dyslipidemia in a patient with type ; diabetes mellitus. 3ey $oint: 3he American Diabetes Association recommends that patients with type . diabetes mellitus have a fasting lipid panel performed after puberty or at diagnosis if the diagnosis is established after puberty# 3he ADA recommends screening for nephropathy (such as a urine albumincreatinine ratio) once a patient o with type . diabetes is ./ years of age or older and has been diagnosed with diabetes for 9 or more years# 3he rst dilated funduscopic e&amination should be obtained once the child is ./ years of age or older and o has been diagnosed with type . diabetes for 6 to 9 years# %iagnose type ? diabetes mellitus. 3ey $oint: 1f results of two di'erent diagnostic tests for diabetes mellitus are discordant, the test that is diagnostic of diabetes should be repeated# Manage hypoglycemia in a patient taking a sulonylurea.
3ey $oint> 7ulfonylureas, such as glyburide, should be discontinued in patients with suspected symptomatic hypoglycemia#A An elderly patient with a history of D+ with A.c levels within normal range may re2ect a level of control o in an older patient that may be causing episodes of hypoglycemia, which may be responsible for her recent episodes of confusion and forgetfulness# Because it may take several days after discontinuation for the glyburide to decrease to undetectable o levels, checking her clinical symptoms and reevaluating her plasma glucose level in weeks would also be appropriate# +etformin is not associated with hypoglycemia o $ostassium shits in %3, 3ey $oint> Diabetic ketoacidosis (DEA) is associated with hyperkalemia, and e'ective therapy of DEA results in hypokalemia# A DEA patient at presentation will have acidosis and dehydration that contribute to hyperkalemia# 3his is o compounded by a lack of circulating insulin, which is critical for intracellular potassium movement# 3ogether, these changes fre%uently produce serum potassium values ranging from !#/ to I#/ m%$ (!#/ to I#/ mmol$) at th e time of presentation# Because of the presence of hyperkalemia, cardiac monitoring is re%uired# >ith hydration to correct volume contraction, the administration of insulin, and resolution of metabolic o acidosis, the hyperkalemia will resolve and hypokalemia may dev elop# -ydration and improvement in the glomerular ltration rate facilitate urine potassium e&cretion# 1nsulin therapy will stimulate transfer of potassium from the e&tracellular to the intracellular space# 3ogether, these cause a rapid drop in the serum potassium concentration within to ! hours of initial therapy# @or almost all patients with diabetic ketoacidosis, e'ective therapy re%uires adding potassium to the intravenous 2uid when serum potassium concentrations decline to <#/ to <#9 m%$ (<#/ to <#9 mmol$)# >ithout potassium supplementation, dangerous levels of hypokalemia may occur# Manage hyperglycemia in a patient in the medical intensive care unit. 3ey $oint: 3he optimal glucose management for critically ill hospitali"ed patients is unknown, but an insulin drip with a glycemic target plasma glucose level of .hen delivered by this route, o insulin must move from the subcutaneous space into the intravascular space to be active# 1nsulin
receptors are located in the muscles, liver, and pancreas U all of which re%uire insulin to be circulated from place of entry via the arteriovenous system# 3here are many di'erent types of insulin, and nearly all of them di'er in the means by which they are absorbed from the subcutaneous space into the intravascular space# @or e&le, neutral protamine -agedorn insulin is a pentamer of the insulin molecule covalently bound to protamine, which inhibits free insulin release, leading to a long onset of action and prolonged duration of insulin release# 1n contrast, insulin lispro is a regular insulin molecule chemically modied to remove the disulde bond between the amino acids lysine and proline, thus allowing for very rapid absorption from the subcutaneous space to the intravascular space# $heochromocytoma 3ey $oint> 3he classic symptoms of pheochromocytoma are hypertension, headaches, palpitations, and diaphoresis# $heochromocytomas are tumors that are present in less than .0 of patients with hypertension, are o derived from chromaPn cells, and elaborate norepinephrine, epinephrine, and dopamine# 3umors originating in the adrenal glands are referred to as pheochromocytomas, whereas those originating along the sympathetic paraganglia are referred to as paragangliomas# 3he classic symptoms of pheochromocytoma are hypertension, headaches, palpitations, and diaphoresis# o -ypertension is present in more than H/0 of patients with pheochromocytoma: more than 9/0 of these o patients have sustained elevations in blood pressure; 6/0 to
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Carcinoid syndrome is the term applied to symptoms mediated by humoral factors (for example, serotonin) released by some carcinoid tumors. Episodic flushing is most characteristic of the carcinoid syndrome; flushing begins suddenly and lasts up to 30 minutes. Severe flushes are accompanied by a fall in blood pressure and rise in heart rate. he patient does not have flushing or hypotension, ma!ing carcinoid syndrome an unli!ely diagnosis. primary hyperaldosteronism or hypercortisolism ("ushing syndrome) usually presents #ith decreased serum potassium levels, and neither condition is associated #ith headaches, palpitations, and diaphoresis
:yperaldostromism 3ey $oint> 3he most appropriate screening test for hyperaldosteronism is the determination of the ratio of plasma aldosterone toplasma renin activity -ypertension and hypokalemia are two of the main manifestations of primary hyperaldosteronism# o 1ncreases in other mineralocorticoids occur in patients with unusually e&cessive cortisol secretion (Cushing syndrome), in whom the mineralocorticoid activity of cortisol becomes prominent, and in patients with congenital adrenal hyperplasia due to an en"yme deciency# 3he most appropriate screening test for hyperaldosteronism is the determination of the ratio of plasma o aldosterone to plasma renin activity# 3he e&pected ndings include an elevated plasma aldosterone level and suppressed plasma renin activity# 7creening tests can be performed on random blood samples, even in patients taking antihypertensive medications (e&cept the aldosterone receptor antagonists spironolactone and eplerenone)# Conrmation of the biochemical diagnosis involves showing persistent elevation (poor suppressibility) of plasma aldosterone in response to a high salt load# 7creening 3ests for CushingVs syndrome include a de&amethasone suppression test or <hour o measurement of urine free cortisol e&cretion Manage $ituitary tumor apople(y 1n addition to neurosurgical decompression of the pituitary gland, urgent glucocorticoid administration is often necessary in patients with pituitary tumor apople&y because of acute adrenocorticotropic hormone deciency# ituitary tumor apople&y usually occurs in the setting of a pree&isting pituitary adenoma# o A history of fatigue, weight gain, and erectile dysfunction and the laboratory nding of hyponatremia o suggest panhypopituitarism# An acuteonset headache is consistent with acute bleeding into the pituitary gland 1n the setting of local mass e'ect and severe headache, however, neurosurgical decompression of the o pituitary gland is necessary. ecause the leading cause o death in patients with pituitary tumor apoplexy is adrenal insuciency due to acute adrenocorticotropic hormone de*ciency, urgent glucocorticoid administration is oten reuired a lumbar puncture is not only inappropriate but contraindicated in a patient with pituitary tumor o apople&y# +easurement of the serum prolactin level typically is obtained after a diagnosis of pituitary adenoma is o made to e&clude prolactinoma, and may be done after the apople&y is addressed# %iagnose hypercortisolism )ushing syndrome+ as a secondary cause o diabetes mellitus. Warious secondary causes of diabetes e&ist, most involving other endocrinopathies, e'ects of o medications, pancreatic diseases, or genetic conditions#
-ypercortisolism (Cushing syndrome) is a likely cause of secondary diabetes mellitus in a patient with hypertension, central obesity, and hypokalemia# 3he most common cause of hypercortisolism is glucocorticoid therapy, followed by the secretion of adrenocorticotropic hormone (AC3-) by a pituitary adenoma (Cushing disease) and the hyperfunctioning of an adrenocortical adenoma# +easurement of the <hour e&cretion of urine free cortisol is the most appropriate ne&t test in this patient to determine the cause of her diabetes mellitus Computed tomography of the adrenal glands is appropriate after hypercortisolism is diagnosed, especially when it is nonUAC3- dependent, to identify the type of adrenal condition responsible ancreatic imaging could be considered when signs and symptoms (such as abdominal or back pain, o *aundice, or chronic diarrhea) suggest that an underlying pancreatic disorder is the cause of diabetes# measuring the serum glutamic acid decarbo&ylase antibody titer is useful to conrm the presence of o autoimmune (type .) diabetes when no other evidence e&ists# Manage central adrenal insu@ciency. 3ey $oint: atients with primary adrenal insuPciency, which is associated with both cortisol and aldosterone deciencies, re%uire daily glucocorticoid and mineralocorticoid replacement, whereas patients with central adrenal insuPciency have only cortisol deciency and do not re%uire mineralocorticoid replacement# ,utoimmune :ypophysitis ),ka 8ymphocytic hypophysitis+ is dened as in2ammation of the o pituitary gland due to autoimmunity, resulting in central adrenal insuPciency Correctly replaced cortisol (hydrocortisone)will be evidenced by the lack of signs or symptoms of Cushing o syndrome (Cortisol e&cess) such as weight gain, hyperglycemia, hypertension, striae, and abnormal fat distribution# 3here should also be no evidence of hydrocortisone underreplacement,, such as nausea, vomiting, malaise, hypotension, weight loss, hyponatremia, or hypoglycemia 1n adrenocorticotropic hormone de5ciency, adrenal production o mineralocorticoids and potassium o homeostasis remain intact because production is controlled separately by the renin-angiotensin system , therefore, a mineralocorticoid such as 2udrocortisone, is not needed# 1n patients with central hypothyroidism, thyroidstimulating hormone (37-) deciency leads to reduced o secretion of thyro&ine (3<), and measurement of the serum 3< level is necessary to establish the diagnosis# 3hyroid hormone dosing in patients with central hypothyroidism should be ad*usted on the basis of o clinical symptoms to maintain serum free 3 < levels within the middle of the reference range, unless doing so causes iatrogenic hyperthyroidism or hypothyroidism %iagnose central )secondary+ hypogonadism secondary to a prolactinoma. 3ey $oint: Because prolactinomas in female patients often present with galactorrhea and signs and symptoms of secondary amenorrhea, a serum prolactin measurement is an appropriate initial study# alactorrhea without evidence of an elevated serum human chorionic gonadotropin level is e&tremely o suggestive of a prolactinoma# +issed menstrual periods, vaginal dryness, and decreased libido also suggest hypogonadism, which is o likely due to decreased gonadotropin hormone secretion from the anterior pituitary gland (a fre%uent occurrence with a prolactinoma)# Although prolactinomas may lead to classic bitemporal hemianopia, this nding only occurs if they o enlarge ade%uately to compress the optic chiasm# An elevated serum prolactin level would conrm the clinical suspicion that a prolactinoma is inducing o central secondary hypogonadism in this patient# +agnetic resonance imaging of the pituitary gland would be a conrmatory test if the serum prolactin o level is elevated; however, performing imaging studies before a biochemical diagnosis is established is not indicated 7erum estrogen and progesterone and folliclestimulating hormoneUluteini"ing hormone measurements o would likely be abnormal in this patient but would not e&plain the galactorrhea and would not identify the precise cause of her hypogonadism Evaluate an adrenal incidentaloma. 3ey $oint: =early ./0 of adrenal incidentalomas are functional, and testing is usually necessary to identify functional tumors secreting catecholamines, cortisol, or aldosterone# initial laboratory tests should include: o an overnight de&amethasone suppression test (Cortisol production) <hour urine collection for metanephrines (heos) measurement of plasma renin activity and serum aldosterone level (Aldosterone) 7steoporosis 3ey $oint: Ksteoporosis is diagnosed by the presence of fragility fractures or by a bone mineral density score less than U#9 on dualenergy &ray absorptiometry (DXA) scanning# $ab values are normal# $ow bone mass is dened as a bone mineral density score that is between .#/ and #9 7D below the o young adult mean
7steomalacia is a generali"ed disorder of bone resulting in decreased minerali"ation of newly formed osteoid at sites of bone turnover# Although it may be asymptomatic, osteomalacia may present with di'use bone and *oint pain, muscle weakness, and diPculty walking# 1t most commonly occurs in patients with low levels of vitamin D, hypophosphatemia, hypocalcemia, and increased serum parathyroid hormone and alkaline phosphatase levels $aget disease o bone is a focal disorder of bone metabolism characteri"ed by an accelerated rate of o bone remodeling that results in overgrowth of bone at a single or multiple sites and impaired integrity of a'ected bone# Although aget disease is usually asymptomatic, if symptoms are present they are usually due to overgrowth of the a'ected bone, either in the bone itself or from bony overgrowth due to fracture or nerve impingement# 3he serum alkaline phosphatase level is typically elevated, and radiographs show increased bone density in involved areas 1reat osteoporosis with an intravenous bisphosphonate. 3ey $oint: sophagitis is a risk of oral bisphosphonate agents, such as alendronate, and intravenous bisphosphonate therapy (Yoledronic acid) is therefore preferred for patients with esophageal disorders# Bisphosphonates bind to the bone matri& and decrease osteoclast activity, thereby slowing bone o resorption while new bone formation and minerali"ation continue# 1ntravenous bisphosphonates, such as "oledronic acid, are preferred for women with postmenopausal osteoporosis who are unable to take oral bisphosphonates (such as this patient with gastroesophageal re2u& disease) or who desire the convenience of less fre%uent dosing# 3he benecial e'ects of calcitonin are much less pronounced than those of other antiresorptive agents# o Calcitonin in*ections and nasal spray are approved for the treatment of established osteoporosis but not for its prevention# Calcitonin has been shown to prevent primarily vertebral fractures and is generally safe and well tolerated# 3eriparatide (recombinant human parathyroid hormone R.6omens -ealth 1nitiative indicating that estrogen increases the risk of cardiovascular disease and breast cancer# 1reat a woman with low bone mass. 3ey $oint: Antiosteoporotic therapy should be considered in a patient with low bone mass whose @racture ?isk Assessment 3ool (@?AX) risk of ma*or osteoporotic fracture over the ne&t ./ years is /0 or greater or whose risk of hip fracture over the ne&t ./ years is 60 or greater# Alendronate is approved for both osteoporosis prevention and treatment o o
Estrogen is effective in maintaining bone mass in postmenopausal #omen, and in the past #as routinely prescribed for this purpose. $o#ever, it is no longer used for prevention or treatment of osteoporosis because of the potential negative effects in these #omen (thrombosis, breast and endometrial cancer) and the availability of other effective medications. %aloxifene, a selective estrogen receptor modulator, is also approved for osteoporosis prevention by the &'. $o#ever, vasomotor o symptoms are highly associated #ith its use, and it may n ot be #ell tolerated in a patient already experiencing significant hot flushes. Prevent Osteoporosis Key Point Among the modiable risk factors for osteoporosis are ade%uate amounts of both calcium and vitamin o
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D, regular e&ercise, cessation of cigarette smoking, and avoidance of alcohol abuse# 3he 5#7# reventive 7ervices 3ask @orce recommends screening for osteoporosis with DXA in all women o age !9 years or older and also in younger women with an elevated fracture risk# Evaluate or secondary osteoporosis 3ey $oint> A secondary cause for osteoporosis should be suspected in younger patients, in patients without clear risk factors, and in men# 3herefore, screening guided by history and physical e&amination ndings may include testing for o hypogonadism, vitamin D deciency, primary hyperparathyroidism, calcium malabsorption, and multiple myeloma# Calcium malabsorption may occur in patients with celiac disease and may cause secondary osteoporosis, and celiac diseases is a concern, even if 1 symptoms are absent 1nitiation of therapy, such as the bisphosphonate alendronate, can be considered after the evaluation for o secondary causes is completed and his fracture risk is assessed ,d2ust hydrocortisone therapy during a minor illness or a patient with primary adrenal insu@ciency 3ey $oint: Ad*usting (increasing) the dose of hydrocortisone during even minor intercurrent illnesses is crucial to avoid adrenal crisis in patients with adrenal insuPciency# A atients hydrocortisone dose during her intercurrent illness should be increased appro&imately o threefold over her baseline replacement dose, and the increase should be continued for 6 days# 3his step is necessary to minimi"e the possibility of adrenal crisis Manage secondary adrenal insu@ciency due to e(ogenous glucocorticoid administration.
3ey $oint: atients who recently received longterm glucocorticoid therapy and now present with hypotension may have adrenal insuPciency and re%uire prompt treatment with intravenous hydrocortisone# 7econdary adrenal insuPciency produced by decreased adrenocorticotropic hormone (AC3-) release is o often caused by prolonged administration of e&ogenous glucocorticoids that suppress AC3- release and lead to decreased adrenal gland production of cortisol# Decreased cortisol release causes a number of e'ects, most often nausea, vomiting, and abdominal pain# $aboratory studies often show hyponatremia with or without hypokalemia# Kf greatest concern is the presence of hypotension in the setting of infection (such as in this patient with a urinary tract infection) or other physiologic stressors in which cardiovascular collapse may occur if cortisol release is not ade%uate, given its key role in maintaining vascular tone# 3he hypotension is potentially fatal if not treated with hydrocortisone when initially suspected# iven this o patients recent, prolonged stay in an intensive care unit and her persistent hypotension despite administration of broadspectrum antibiotics and intravenous 2uids, adrenal insuPciency should be considered and empirically treated# Because the presentation of adrenal suppression may be diPcult to di'erentiate from sepsis, a low threshold for considering an inade%uate cortisol response to stress should be maintained in patients at risk f or this occurrence#
