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Alcoholic Ketoacidosis Uptodate

Metformin And Lacticacidosis

Metformin And Lacticacidosis

The major toxic effect of metformin is lactic acidosis. It causes glucose to be converted to lactate in the small intestines, and decreases gluconeogenesis from lactate and pyruvate and alanine- increasing LA and substrates that can get converted to LA. its RARE: Only 5.1 cases per 100,000 patient yrs of lactic acidosis in non-comorbitiy (renal or liver disease) patients. However in patients that do develop LA, there is a mortality of 45%. These deaths were speculated to be related to comorbid conditions, rather than the levels of metformin in their blood. Most accurate predictor was liver function. Lactic acidosis likely to occur in patients with renal insufficiency (Cr above 1.4/1.5), liver or ETOH disease, HF, history of prior LA, hypoxic states, hemodynamic instability. consider bicarb if pH < 7.1, otherwise may cause electrolyte abnormalities. Patients with severe renal insufficiency or are simply very sick require emergent HD. References: Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Salpeter S, Greyber E, Pasternak G, Salpeter E, Cochrane Database Syst Rev. 2006; uptodate.com: metformin poisoning; Metformin. AU Bailey CJ, Turner RC SO, N Engl J Med. 1996;334(9):574. picture Continue reading >>

Malignant Or Benign Leukocytosis

Malignant Or Benign Leukocytosis

1Department of Pathology, Stanford University School of Medicine, Stanford, CA Leukocytosis, or elevated WBC count, is a commonly encountered laboratory finding. Distinguishing malignant from benign leukocytosis is a critical step in the care of a patient, which initiates a vastly different decision tree. Confirmation of the complete blood cell count and the WBC differential is the first step. Examination of the PB smear is essential to confirming the automated blood cell differential or affirming the manual differential performed on the PB smear. Next is separation of the leukocytosis into a myeloid versus a lymphoid process. Distinguishing a reactive lymphoid proliferation from a lymphoproliferative disorder requires examination of lymphocyte morphology for pleomorphic lymphocytes versus a monomorphic population, with the latter favoring a lymphoproliferative neoplasm. Samples suspicious for lymphoproliferative disorders can be confirmed and characterized by flow cytometry, with molecular studies initiated in select cases; precursor lymphoid neoplasms (lymphoblasts) should trigger a BM examination. Myeloid leukocytosis triggers a differential diagnosis of myeloid leukemoid reactions versus myeloid malignancies. The manual differential is key, along with correct enumeration of blasts and blast equivalents, immature granulocytes, basophils, and eosinophils and identifying dysplasia to identify myeloid malignancies. Confirmation and characterization of myeloid malignancies should be performed with a BM examination and the appropriate ancillary studies. Myeloid leukemoid reactions commonly result from infections and show activated neutrophil changes on morphology; these should prompt evaluation for infection. Other causes of reactive myeloid leukocytoses are also discuss Continue reading >>

Apo-gliclazide Mr

Apo-gliclazide Mr

NOTICE: This Consumer Medicine Information (CMI) is intended for persons living in Australia. 30 mg Tablets What is in this leaflet This leaflet answers some common questions about gliclazide. It does not contain all the available information. It does not take the place of talking to your doctor, pharmacist or diabetes educator. The information in this leaflet was last updated on the date listed on the last page. More recent information on this medicine may be available. You can also download the most up to date leaflet from www.apotex.com.au. All medicines have risks and benefits. Your doctor has weighed the risks of you using this medicine against the benefits they expect it will have for you. Pharmaceutical companies cannot give you medical advice or an individual diagnosis. Keep this leaflet with your medicine. You may want to read it again. What this medicine is used for The name of your medicine is APO-Gliclazide MR. It contains the active ingredient gliclazide. The medicine is used to control, blood glucose in patients with Type II diabetes mellitus. This type of diabetes is also known as non-insulin-dependent diabetes mellitus (NIDDM) or maturity onset diabetes. Gliclazide is used when diet and exercise are not enough to control your blood glucose. Gliclazide can be used alone, or together with other medicines for treating diabetes Ask your doctor if you have any questions about why this medicine has been prescribed for you. Your doctor may have prescribed this medicine for another reason. This medicine is available only with a doctor's prescription. How it works Gliclazide lowers high blood glucose by increasing the amount of insulin produced by your pancreas. Glucose is used by the body as fuel, and all people have glucose circulating in their blood. In diabet Continue reading >>

Evaluation Of Delirium

Evaluation Of Delirium

Delirium is an acute, fluctuating change in mental status, with inattention, disorganized thinking, and altered levels of consciousness. [1] Inouye SK, Schlesinger MJ, Lydon TJ. Delirium: a symptom of how hospital care is failing older persons and a window to improve quality of hospital care. Am J Med. 1999;106:565-573. It is a potentially life-threatening disorder characterized by high morbidity and mortality. Guidelines address recognition, risk factors, and treatment for delirium. [2] Barr J, Fraser GL, Puntillo K, et al; American College of Critical Care Medicine. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med. 2013;41:263-306. [3] Neto AS, Nassar AP Jr, Cardoso SO, et al. Delirium screening in critically ill patients: a systematic review and meta-analysis. Crit Care Med. 2012;40:1946-1951. Mortality for those diagnosed with delirium in the hospital is twice that of patients with similar medical conditions without delirium and rises as high as 14% within 1 month of diagnosis. [4] Cole MG, Primeau FJ. Prognosis of delirium in elderly hospital patients. CMAJ. 1993;149:41-46. Delirium occurs in >20% of hospitalizations annually and is the most common hospital-related complication in the US. [5] US Department of Health and Human Services. 2004 CMS Statistics. Washington, DC: Centers for Medicare and Medicaid Services, 2004:34. (CMS Publication No 03445) Delirium is common in the intensive care unit especially among mechanically ventilated patients. In critically ill patients it is associated with an increased length of stay and increased mortality. [6] Cavallazzi R, Saad M, Marik PE. Delirium in the ICU: an overview. Ann Intensive Care. 2012;2:49. Studies have demonstrated a 1 Continue reading >>

Diabetic Ketoacidosis Uptodate - New Videos

Diabetic Ketoacidosis Uptodate - New Videos

Channel: MedCram - Medical Lectures Explained CLEARLY & Total View: 156999 Add Date: January 13, 2013, 2:05 pm & Duration: 00:11:34 Understand the treatment of diabetic ketoacidosis (DKA) with this clear explanation from Dr. Seheult of This is video 2 of 2 on diabetic ketoacidosis (DKA). Board Certified in Internal Medicine, Pulmonary Disease, Critical Care, and Sleep Medicine. MedCram: Medical topics explained clearly including: Asthma, COPD, Acute Renal Failure, Mechanical Ventilation, Oxygen Hemoglobin Dissociation Curve, Hypertension, Shock, Diabetic Ketoacidosis (DKA), Medical Acid Base, VQ Mismatch, Hyponatremia, Liver Function Tests, Pulmonary Function Tests (PFTs), Adrenal Gland, Pneumonia Treatment, any many others. New topics are often added weekly- please subscribe to help support MedCram and become notified when new videos have been uploaded. Subscribe: Recommended Audience: Health care professionals and medical students: including physicians, nurse practitioners, physician assistants, nurses, respiratory therapists, EMT and paramedics, and many others. Review for USMLE, MCAT, PANCE, NCLEX, NAPLEX, NDBE, RN, RT, MD, DO, PA, NP school and board examinations. Channel: Diabetic diet chart & Total View: 15 Add Date: November 21, 2016, 10:58 pm & Duration: 00:03:19 best medicine for diabetes , type 1 diabetes treatments , type 2 diabetes treatments , prediabetes treatments , diabetes treatment at home , diabetes cure found , prevention for diabetes , permanent cure for diabetes , can diabetes be cured without medicine , diabetes cure naturally , is diabetes curable at early stage , can diabetes be cured naturally , new diabetes treatment , is there a cure for diabetes type 2 , is there a cure for diabetes type 1 , diabetes treatment naturally Get here @ - The wo Continue reading >>

Best Case Ever 58 Euglycemic Dka

Best Case Ever 58 Euglycemic Dka

This is EM Cases Best Case Ever 58 – Euglycemic DKA with Walter Himmel, the walking encyclopedia of emergency medicine. It’s not only run of the mill DKA, starvation and alcoholic ketoacidosis that can cause a metabolic acidosis with elevated ketones. Euglycemic DKA can be caused by the newer diabetes medications sodium-glucose co-transporter 2 inhibitors like Canagliflozin; and it’s important to recognize this tricky diagnosis early and initiate treatment for DKA despite a normal serum glucose level, because DKA can lead to serious complications like renal failure, cerebral edema, ARDS, shock, and death. Podcast production, sound design and editing by Anton Helman; Written by Anton Helman, June 2017 Euglycemic DKA can occur in any diabetic and has been reported in the literature since the 1970’s, but there has recently been a rise in incidence of euglycemic DKA associated with sodium-glucose co-transporter 2 inhibitors (SGLT-2 inhibitors, or the “zins”) such as Canagliflozin, Dapagliflozin and Empagliflozin. When to suspect euglycemic DKA Any patient with Type 1 or 2 diabetes taking SGLT-2 inhibitors who presents with nausea, vomiting, SOB or malaise or is found to have a metabolic acidosis should have blood drawn for serum ketones. Triggers of euglycemic DKA are similar to the triggers for any DKA: Alcohol use, infection and reduced oral intake. Distinguishing euglycemic DKA from alcoholic DKA Alcoholic ketoacidosis may also present with nausea, vomiting, malaise, ketones and anion gap metabolic acidosis. The key differentiating factor besides the obvious history of heavy alcohol use vs a diabetic taking an SGLT-2 inhibitor, is that patients with alcoholic ketoacidosis tend to have frankly low glucose. How is treatment of euglycemic DKA different? In addit Continue reading >>

Pyramidal Tetraparesis & Fasting Ketosis: Causes & Diagnoses | Symptoma.com

Pyramidal Tetraparesis & Fasting Ketosis: Causes & Diagnoses | Symptoma.com

Patients typically present after age 40 years with a variable combination of cognitive impairment, pyramidal tetraparesis, peripheral neuropathy, and neurogenic bladder. [humpath.com] tetraparesis, sensory neuropathy in the lowerextremities, neurogenic bladder, and occasionally cognitiveimpairment. [medigoo.com] They presented clinically with late onset pyramidal tetraparesis, micturition difficulties, peripheral neuropathy, and mild cognitive impairment. [eurekamag.com] tetraparesis cognitive impairment white matter abnormalities (MRI) polyglucosan bodies (round intracellular inclusions) found in neuronal and astrocytic processes peripheral [humpath.com] Symptoms: The disorder is characterized bya gradual progression of involvement of both the central andperipheral nervous systems with a variable phenotype that oftenincludes pyramidal [medigoo.com] Glycogen Storage Disease due to Liver Phosphorylase Kinase Deficiency , or lactic acidosis; episodes provoked by fasting, febrile infection, or ingestion of fructose, sorbitol, or glycerol Treatment: Avoidance of fasting and fructose, sorbitol [merckmanuals.com] [] cornstarch, which prevents ketosis. [clinicaladvisor.com] Ketosis after relatively short fasts is a feature. [tp.amegroups.com] Frequency: Rare Onset: Early childhood Clinical features: Benign course with symptoms lessening with aging; growth retardation, hepatomegaly, hypoglycemia, hyperlipidemia, ketosis [merckmanuals.com] Uncooked (raw) cornstarch (1-1.5 grams per kg) administered at bedtime prevents morning hypoglycemia and ketosis. [clinicaladvisor.com] Some medical professionals confuse ketoacidosis , an extremely abnormal form of ketosis, with the normal benign ketosis associated with ketogenic diets and fasting states [ketogenic-diet-resource.com] See als Continue reading >>

Effects Of Chronic Alcohol Exposure On Ischemiareperfusion-induced Acute Kidney Injury In Mice: The Role Of -arrestin 2 And Glycogen Synthase Kinase 3

Effects Of Chronic Alcohol Exposure On Ischemiareperfusion-induced Acute Kidney Injury In Mice: The Role Of -arrestin 2 And Glycogen Synthase Kinase 3

Original Article | Open Effects of chronic alcohol exposure on ischemiareperfusion-induced acute kidney injury in mice: the role of -arrestin 2 and glycogen synthase kinase 3 Experimental & Molecular Medicine volume 49, page e347 (2017) Little is known about the effects of chronic alcohol intake on the outcome of acute kidney injury (AKI). Hence, we examined the effects of chronic alcohol intake on the development of renal fibrosis following AKI in an animal model of bilateral renal ischemiareperfusion (IR) injury. We first found that chronic alcohol exposure exacerbated bilateral IR-induced renal fibrosis and renal function impairment. This phenomenon was associated with increased bilateral IR-induced extracellular matrix deposition and an increased myofibroblast population as well as increased bilateral IR-induced expression of fibrosis-related genes in the kidneys. To explore the mechanisms underlying this phenomenon, we showed that chronic alcohol exposure enhanced -arrestin 2 (Arrb2) expression and Akt and glycogen synthase kinase-3 (GSK3) activation in the kidneys. Importantly, pharmacological GSK3 inhibition alleviated bilateral IR-induced renal fibrosis and renal function impairment. Furthermore, we demonstrated that Arrb2/ mice exhibited resistance to IR-induced renal fibrosis and renal function impairment following chronic alcohol exposure, and these effects were associated with attenuated GSK3 activation in the kidneys. Taken together, our results suggest that chronic alcohol exposure may potentiate AKI via -arrestin 2/Akt/GSK3-mediated signaling in the kidney. Acute kidney injury (AKI) is a major clinical problem that can result in prolonged hospitalization, chronic renal failure and death. 1 , 2 , 3 , 4 , 5 One of the leading causes of AKI is renal ischemi Continue reading >>

Metabolic Acidosis In A Patient With Isopropyl Alcohol Intoxication: A Case Report

Metabolic Acidosis In A Patient With Isopropyl Alcohol Intoxication: A Case Report

Metabolic Acidosis in a Patient With Isopropyl Alcohol Intoxication: A Case Report Xiaomei Meng, MD, PhD; Suman Paul, MBBS, PhD; Douglas J. Federman, MD From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. Author, Article, and Disclosure Information From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. Disclosures: Authors have disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterest Forms.do?msNum=L14-0336 . Background: An elevated plasma osmolal gap is common in all forms of alcohol intoxication. Methyl alcohol and ethylene glycol are metabolized to compounds that produce metabolic acidosis. Isopropyl alcohol, however, is metabolized to acetone, which does not cause metabolic acidosis and cannot be metabolized to compounds that do ( 1 ). Therefore, the presence of metabolic acidosis is used to rule out isopropyl alcohol intoxication. This distinction is important because fomepizole is used to treat methyl alcohol and ethylene glycol intoxication but is contraindicated in isopropyl alcohol intoxication because it reduces the clearance of isopropyl alcohol and thus prolongs its effects ( 2 ). Continue reading >>

Some Thoughts On The Keto Diet

Some Thoughts On The Keto Diet

10 America has a new (old) fad diet. Have you heard of it? The keto diet (short for ketogenic) is a high-fat, adequate-protein, low-carbohydrate diet. It is essentially the Atkins diet of the 2000s, but it dates back to the 1920s, when it was used to treat children with epilepsy. The goal of a keto diet is to get at least 70 percent of your calories from fat, no more than 25 percent of calories from protein and only 5 to 10 percent from carbohydrates. For most people, that means restricting your carbohydrate intake to below 50 grams a day. If you’re a breakfast taco fan like me, two tacos will put you at your daily carbohydrate limit, and don’t even think of putting potatoes in there! Half a cup of roasted potatoes will send you over the 50-gram limit. To further put that number of carbs into perspective, the following contain about 15 grams of carbohydrates: one slice of bread, 1/3 cup of rice, one cup of milk, 15 grapes, half of a large banana and a 12-ounce Bud Light (beers with higher alcohol will most certainly contain much more than 15 grams). The impetus for such a carbohydrate restrictive diet was therapeutic in nature. The diet first started nearly 100 years ago when doctors found that when epileptic children switched to a strict all-fat diet, the brain adapted its fuel source and the children had fewer seizures. The ketogenic diet is used to this day to help treat epilepsy, but over the past year or so, millions of everyday eaters have flocked to it for its purported health weight loss benefits. The goal of this diet is to force the body to burn fat instead of carbohydrates as fuel, which produces ketones. Our body and brain then use these ketones to fuel our cells. The increase in ketones puts the body in ketosis, a natural process the body initiates to h Continue reading >>

Alcoholic Ketoacidosis | Receiving.

Alcoholic Ketoacidosis | Receiving.

Medications: None (the patient does state she is supposed to be on both levothyroxine and coumadin). Social history: Significant for both tobacco and heavy alcohol abuse. No intravenous drug abuse. Vitals: BP 119/84, HR 126, RR 38, T 35.4, SaO2 99% (room air) General: Well developed African American female in respiratory distress. HEENT: Normocephalic, atraumatic. No conjunctival pallor. No scleral icterus. Dry mucous membranes. No pharyngeal erythema. The patients breath has a fruity odor. Cardiovascular: Tachycardic, regular rhythm. No murmurs. No jugular venous distention, no edema. Respiratory: Tachypnic. Lungs clear to auscultation bilaterally, no wheezes or crackles. No accessory muscle use, no retractions. Gastrointestinal: Abdomen soft, slightly tender to palpation in the epigastric area, and non-distended. No rebound tenderness, no guarding. Bowel sounds present. Neurologic: Alert and oriented x 3. Strength equal in all four extremities. Basic metabolic panel: Na 137, K 4, Cl 98, HCO3 5, BUN 13, Cr 1.06, glucose 122 Complete blood count: WBC 15.7, Hb 14.2, Hct 43.5, platelets 338 Coagulation studies: PT 10.9, PTT 29.2, INR 1.03 Arterial blood gas: pH 6.879, pCO2 22.1, pO2 95, HCO3 4 Beta-hydroxybutyrate 77.5 (normal 0.2 2.8) Liver function tests: amylase 97, lipase 888, total bilirubin 0.4, direct bilirubin 0.1, ALT 21, AST 68, alkaline phosphatase 98, albumin 2.9 Urinalysis: 2+ ketones, 2+ protein, specific gravity 1.010, otherwise unremarkable 1. The patients acid base status is best described as which of the following? A) anion gap metabolic acidosis (with complete respiratory compensation) B) non-anion gap metabolic acidosis (with complete respiratory compensation) C) anion gap metabolic acidosis (with incomplete respiratory compensation) D) non-anion gap Continue reading >>

Emedicine - Diabetic Ketoacidosis : Article By Donald W Rucker

Emedicine - Diabetic Ketoacidosis : Article By Donald W Rucker

<scriptlanguage="JavaScript1.2" type="text/javascript" charset="ISO-8859-1"src="<scriptlanguage="JavaScript1.2" type="text/javascript" charset="ISO-8859-1"src="Author:Donald W Rucker, MD, Clinical Assistant Professor of Emergency Medicine, Department of Emergency Medicine, University of Pennsylvania DonaldWRuckeris a member of the following medical societies: American College of Emergency Physicians Editors:Erik D Schraga, MD, Consulting Staff,Permanente Medical Group, Kaiser Permanente, Santa Clara MedicalCenter; Consulting Staff, Department of Emergency Medicine,Mills-Peninsula Emergency Medical Associates; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Howard A Bessen, MD,Professor of Medicine, Department of Emergency Medicine, UCLA School ofMedicine; Program Director, Harbor-UCLA Medical Center; John D Halamka, MD, MS,Associate Professor of Medicine, Harvard Medical School, Beth IsraelDeaconess Medical Center; Chief Information Officer, CareGroupHealthcare System and Harvard Medical School; Attending Physician,Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Barry E Brenner, MD, PhD, FACEP, Program Director, Department of Emergency Medicine, University Hospitals, Case Medical Center Synonyms and related keywords: DKA , diabetes , diabetes mellitus , insulin deficiency , hyperglycemia , low bicarbonate, acidosis , ketonemia , ketonuria , type 1diabetes , type 1 diabetes mellitus , insulin-dependent diabetes , IDD , insulin-dependent diabetes mellitus , IDDM , childhood diabetes ,childhood diabetes mellitus, childhood-onset diabetes, childhood-onsetdiabetes mellitus, diabetes in childhood, diabetes mellitus inchildhood, juvenile-onset diabetes , juvenile-onset diabetes mellitus, ketosis-prone diabetes , autoimmune diabe Continue reading >>

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>

Pulmcrit- Hypertriglyceridemic Pancreatitis: Can We Defuse The Bomb?

Pulmcrit- Hypertriglyceridemic Pancreatitis: Can We Defuse The Bomb?

Medications including propofol, valproic acid, protease inhibitors, thiazides, olanzapine, mirtazapine, estrogen-containing oral contraceptives, tamoxifen, clomiphene, and isotretinoin ( Scherer 2014 ) Identifying the cause of hypertriglyceridemia generally isn't critical for management. However, any potentially causative drugs should be discontinued. Other diagnostic issues in these patients Severe hypertriglyceridemia may cause the serum to appear milky (latescent). Although this may be a useful diagnostic sign, it can also interfere with certain laboratory tests. In particular, measurements of amylase and sodium may be artificially low (pseudohyponatremia; Melnick 2016 ). In extreme cases, the lab may be unable to run multiple tests. General treatment of hypertriglyceridemic pancreatitis The basics of treating hypertriglyceridemic pancreatitis are the same as for treating any patient with pancreatitis. Resuscitation should be performed using a judicious volume of fluid and vasopressors, similar to sepsis resuscitation(rather than blindly drowning patients with massive fluid resuscitation). Intubated patients benefit from early enteral nutrition . Overall, the treatment of pancreatitis largely centers on high-quality supportive care, similar to any other critically ill patient. Patients generally receive lipid lowering medications (e.g. gemfibrozil 600 mg BID). Dietary fat restriction is also sensible. Treatments directed at lowering triglyceride levels When is specific therapy needed to lower triglyceride levels? Triglyceride levels fall naturally over time, without any specific intervention (figure below). This may reflect reduced fat intake and fluid resuscitation. When are additional therapies beneficial to accelerate the fall in triglyceride levels? This questio Continue reading >>

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment Of Alcoholic Ketoacidosis

Exenatide extended-release causes an increased incidence in thyroid C-cell tumors at clinically relevant exposures in rats compared to controls. It is unknown whether BYDUREON BCise causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of exenatide extended-release-induced rodent thyroid C-cell tumors has not been determined BYDUREON BCise is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with the use of BYDUREON BCise and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for detection of MTC in patients treated with BYDUREON BCise Acute Pancreatitis including fatal and non-fatal hemorrhagic or necrotizing pancreatitis has been reported. After initiation, observe patients carefully for symptoms of pancreatitis. If suspected, discontinue promptly and do not restart if confirmed. Consider other antidiabetic therapies in patients with a history of pancreatitis Acute Kidney Injury and Impairment of Renal Function Altered renal function, including increased serum creatinine, renal impairment, worsened chronic renal failure, and acute renal failure, sometimes requiring hemodialysis and kidney transplantation have been reported. Not recommended in patients with severe renal impairment or end-stage renal disease. Use caution in patients with renal transplantation or moderate renal impairment Gastrointestinal Disease Because exenatide is commonly associated with gastrointestinal adverse reactions, not recommended in patients with sev Continue reading >>

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