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Why Does Metabolic Acidosis Cause Abdominal Pain

Chronic Metabolic Acidosis Destroys Pancreas

Chronic Metabolic Acidosis Destroys Pancreas

Peter Melamed and Felix Melamed Biotherapy Clinic of San Francisco, USA *Corresponding Author: Biotherapy Clinic of San Francisco 2215 Post Street, Suite 1, San Francisco, CA 94115, USA Phone 1 415 3776643 Fax 1 415 4093909 [email protected] Visit for more related articles at JOP. Journal of the Pancreas Abstract One primary reason for the current epidemic of digestive disorders might be chronic metabolic acidosis, which is extremely common in the modern population. Chronic metabolic acidosis primarily affects two alkaline digestive glands, the liver, and the pancreas, which produce alkaline bile and pancreatic juice with a large amount of bicarbonate. Even small acidic alterations in the bile and pancreatic juice pH can lead to serious biochemical/biomechanical changes. The pancreatic digestive enzymes require an alkaline milieu for proper function, and lowering the pH disables their activity. It can be the primary cause of indigestion. Acidification of the pancreatic juice decreases its antimicrobial activity, which can lead to intestinal dysbiosis. Lowering the pH of the pancreatic juice can cause premature activation of the proteases inside the pancreas with the potential development of pancreatitis.The acidification of bile causes precipitation of the bile acids, which irritate the entire biliary system and create bile stone formation. Aggressive mixture of the acidic bile and the pancreatic juice can cause erratic contractions of the duodenum’s walls and subsequent bile reflux into the stomach and the esophagus. Normal exocrine pancreatic function is the core of proper digestion. Currently, there is no effective and safe treatment for enhancing the exocrine pancreatic function. Restoring normal acid-base homeostasis can be a useful toolfor pathophysi Continue reading >>

Jaime Moo-young, Md

Jaime Moo-young, Md

Diabetic Ketoacidosis (DKA) Pathogenesis · Insufficient insulin for a given carbohydrate load decreased cellular metabolism of glucose · Increased gluconeogenesis, glycogenolysisHyperglycemia · Increased breakdown of free fatty acids as alternative energy source ketone and ketoacid accumulation · Hyperglycemiaserum hyperosmolality osmotic diuresis dehydration and electrolyte derangements (dehydration is most lethal!) · Seen almost exclusively in Type I diabetes; rarely in Type II Definition: Triad of 1. Hyperglycemia (usually between 500 – 800 mg/dL or 27.8-44.4 mmol/L) 2. Anion Gap Metabolic Acidosis (pH usually <7.30) 3. Ketonemia: -hydroxybutyrate, acetoacetate most significant ** Urine ketones do not make the diagnosis, but they can support it** Triggers (the “I’sâ€): Don’t forget to ask about these! · Insulin deficiency: insulin non-compliance, insufficient insulin dosing, new-onset Type I diabetes · Iatrognic: glucocorticoids, atypical antipsychotics, high-dose thiazide diuretics · Infection: UTI, pneumonia, TB · Inflammation: pancreatitis, cholecystitis · Ischemia/infarction: MI, stroke, gut ischemia · Intoxication: Alcohol, cocaine, other drugs Presentation · Symptoms · Polyuria, polydipsia, weight loss · Nausea, vomiting, abdominal pain · Fatigue, malaise · Associated trigger sx (fever/chills, chest pain, etc) · Signs · Volume depletion: skin turgor, dry axillae, dry mucus membranes, HR, BP · Altered mental status: stupor, coma · Kussmaul respirations: rapid, shallow breathing = hyperventilation to counteract metabolic acidosis · Fruity, acetone odor on breath Lab workup and findings · Hyperglycemia: > 250 mg/dL in serum, + glucose on urinalysis · Acidemia (pH <7. Continue reading >>

Acid-base Imbalances: Metabolic Acidosis And Alkalosis

Acid-base Imbalances: Metabolic Acidosis And Alkalosis

Acid-Base Imbalances: Metabolic Acidosis and Alkalosis; Respiratory Acidosis and Alkalosis The hydrogen ion concentration ([H+]) of the body, described as the pH or negative log of the [H+], is maintained in a narrow range to promote health and homeostasis. The body has many regulatory mechanisms that counteract even a slight deviation from normal pH. An acid-base imbalance can alter many physiological processes and lead to serious problems or, if left untreated, to coma and death. A pH below 7.35 is considered acidosis and above 7.45 is alkalosis. Alterations in hydrogen ion concentration can be metabolic or respiratory in origin or they may have a mixed origin. Metabolic acidosis, a pH below 7.35, results from any nonpulmonary condition that leads to an excess of acids over bases. Renal patients with chronic acidemia may show signs of skeletal problems as calcium and phosphate are released from bone to help with the buffering of acids. Children with chronic acidosis may show signs of impaired growth. Metabolic alkalosis, a pH above 7.45, results from any nonpulmonary condition that leads to an excess of bases over acids. Metabolic alkalosis results from one of two mechanisms: an excess of bases or a loss of acids. Patients with a history of congestive heart failure and hypertension who are on sodium-restricted diets and diuretics are at greatest risk for metabolic alkalosis. Metabolic alkalosis can also be caused by prolonged vomiting, hyperaldosteronism, and diuretic therapy. Respiratory acidosis is a pH imbalance that results from alveolar hypoventilation and an accumulation of carbon dioxide. It can be classified as either acute or chronic. Acute respiratory acidosis is associated with a sudden failure in ventilation. Chronic respiratory acidosis is seen in patient Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

What is alcoholic ketoacidosis? Cells need glucose (sugar) and insulin to function properly. Glucose comes from the food you eat, and insulin is produced by the pancreas. When you drink alcohol, your pancreas may stop producing insulin for a short time. Without insulin, your cells won’t be able to use the glucose you consume for energy. To get the energy you need, your body will start to burn fat. When your body burns fat for energy, byproducts known as ketone bodies are produced. If your body is not producing insulin, ketone bodies will begin to build up in your bloodstream. This buildup of ketones can produce a life-threatening condition known as ketoacidosis. Ketoacidosis, or metabolic acidosis, occurs when you ingest something that is metabolized or turned into an acid. This condition has a number of causes, including: shock kidney disease abnormal metabolism In addition to general ketoacidosis, there are several specific types. These types include: alcoholic ketoacidosis, which is caused by excessive consumption of alcohol diabetic ketoacidosis (DKA), which mostly develops in people with type 1 diabetes starvation ketoacidosis, which occurs most often in women who are pregnant, in their third trimester, and experiencing excessive vomiting Each of these situations increases the amount of acid in the system. They can also reduce the amount of insulin your body produces, leading to the breakdown of fat cells and the production of ketones. Alcoholic ketoacidosis can develop when you drink excessive amounts of alcohol for a long period of time. Excessive alcohol consumption often causes malnourishment (not enough nutrients for the body to function well). People who drink large quantities of alcohol may not eat regularly. They may also vomit as a result of drinking too Continue reading >>

Understanding The Presentation Of Diabetic Ketoacidosis

Understanding The Presentation Of Diabetic Ketoacidosis

Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece Continue reading >>

Diabetic Ketoacidosis Causes, Symptoms, Treatment, And Complications

Diabetic Ketoacidosis Causes, Symptoms, Treatment, And Complications

Diabetic ketoacidosis definition and facts Diabetic ketoacidosis is a life-threatening complication of type 1 diabetes (though rare, it can occur in people with type 2 diabetes) that occurs when the body produces high levels of ketones due to lack of insulin. Diabetic ketoacidosis occurs when the body cannot produce enough insulin. The signs and symptoms of diabetic ketoacidosis include Risk factors for diabetic ketoacidosis are type 1 diabetes, and missing insulin doses frequently, or being exposed to a stressor requiring higher insulin doses (infection, etc). Diabetic ketoacidosis is diagnosed by an elevated blood sugar (glucose) level, elevated blood ketones and acidity of the blood (acidosis). The treatment for diabetic ketoacidosis is insulin, fluids and electrolyte therapy. Diabetic ketoacidosis can be prevented by taking insulin as prescribed and monitoring glucose and ketone levels. The prognosis for a person with diabetic ketoacidosis depends on the severity of the disease and the other underlying medical conditions. Diabetic ketoacidosis (DKA) is a severe and life-threatening complication of diabetes. Diabetic ketoacidosis occurs when the cells in our body do not receive the sugar (glucose) they need for energy. This happens while there is plenty of glucose in the bloodstream, but not enough insulin to help convert glucose for use in the cells. The body recognizes this and starts breaking down muscle and fat for energy. This breakdown produces ketones (also called fatty acids), which cause an imbalance in our electrolyte system leading to the ketoacidosis (a metabolic acidosis). The sugar that cannot be used because of the lack of insulin stays in the bloodstream (rather than going into the cell and provide energy). The kidneys filter some of the glucose (suga Continue reading >>

Systemic Causes Of Abdominal Pain

Systemic Causes Of Abdominal Pain

a Department of Emergency Medicine, Thomas Jefferson University Hospital, 1020 Sansom Street, Thompson Building 239, Philadelphia, PA 19107, USA b Division of Emergency Ultrasonography, Department of Emergency Medicine, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104, USA Abstract A variety of systemic and extra-abdominal diseases can cause symptoms within the abdominal cavity. Systemic and extra-abdominal diseases may include abdominal symptoms caused by several mechanisms. This article discusses the most important and common of these causes, namely the metabolic/endocrine causes, hematologic causes, inflammatory causes, infectious causes, functional causes, and the neurogenic causes. Keywords A variety of systemic and extra-abdominal diseases can cause symptoms within the abdominal cavity (Box 1). This article discusses the most important and common of these diseases. Systemic and extra-abdominal diseases may include abdominal symptoms caused by several mechanisms listed in Table 1. Mechanisms include direct pathologic effects on intra-abdominal organs (eg, gallstone formation in sickle cell disease); conversely, systemic illnesses (eg, congestive heart failure, diabetic ketoacidosis [DKA], or addisonian crisis) may themselves be precipitated by diseases in the abdomen. Some systemic illnesses have a direct (eg, constipation in hypercalcemia) or indirect (eg, nausea and vomiting in diabetic or alcoholic ketoacidosis [AKA]) effect on the functioning of the gastrointestinal (GI) tract. Abdominal symptoms may be caused by disease in contiguous organs outside the abdomen (eg, diaphragmatic irritation from disease of adjacent structures in the lung and mediastinum).1–4 Finally, symptoms may be referred to the abdomen from extra-abdom Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>

Lactic Acidosis And Exercise: What You Need To Know

Lactic Acidosis And Exercise: What You Need To Know

Muscle ache, burning, rapid breathing, nausea, stomach pain: If you've experienced the unpleasant feeling of lactic acidosis, you likely remember it. It's temporary. It happens when too much acid builds up in your bloodstream. The most common reason it happens is intense exercise. Symptoms The symptoms may include a burning feeling in your muscles, cramps, nausea, weakness, and feeling exhausted. It's your body's way to tell you to stop what you're doing The symptoms happen in the moment. The soreness you sometimes feel in your muscles a day or two after an intense workout isn't from lactic acidosis. It's your muscles recovering from the workout you gave them. Intense Exercise. When you exercise, your body uses oxygen to break down glucose for energy. During intense exercise, there may not be enough oxygen available to complete the process, so a substance called lactate is made. Your body can convert this lactate to energy without using oxygen. But this lactate or lactic acid can build up in your bloodstream faster than you can burn it off. The point when lactic acid starts to build up is called the "lactate threshold." Some medical conditions can also bring on lactic acidosis, including: Vitamin B deficiency Shock Some drugs, including metformin, a drug used to treat diabetes, and all nucleoside reverse transcriptase inhibitor (NRTI) drugs used to treat HIV/AIDS can cause lactic acidosis. If you are on any of these medications and have any symptoms of lactic acidosis, get medical help immediately. Preventing Lactic Acidosis Begin any exercise routine gradually. Pace yourself. Don't go from being a couch potato to trying to run a marathon in a week. Start with an aerobic exercise like running or fast walking. You can build up your pace and distance slowly. Increase the Continue reading >>

An Exceptional Case Of Diabetic Ketoacidosis

An Exceptional Case Of Diabetic Ketoacidosis

Copyright © 2017 Celine Van de Vyver et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract We present a case of diabetic ketoacidosis, known as one of the most serious metabolic complications of diabetes. We were confronted with rapid neurological deterioration and unseen glycaemic values, which reached almost 110 mmol/L, subsequently resulting in hyperkalaemia and life-threatening dysrhythmias. This is the first reported live case with such high values of blood glucose and a favourable outcome. 1. Introduction Diabetic ketoacidosis (DKA) is known as one of the most serious complications of diabetes, besides hyperosmolar hyperglycaemic syndrome (HHS), and it is associated with significant morbidity and mortality. The symptoms are often nonspecific and there are many diseases that mimic the presentation. The clinical course usually evolves within a short time frame (<24 h). DKA exists of a triad of uncontrolled hyperglycaemia, metabolic acidosis, and increased total body ketone concentration [1]. These three criteria are needed for diagnosis. The most common precipitating factors of DKA are infections and discontinuation of or inadequate insulin therapy. Mainstays of treatment are correction of hypovolemia and hyperglycaemia, rapid administration of insulin, and electrolyte management. Glycaemic values in DKA normally do not exceed 33 mmol/L. In contrast, blood glucose in HHS is often higher [2, 3]. We present a case of severe diabetic ketoacidosis with glycaemic values of almost 110 mmol/L, leading to neurologic sequelae and requiring more aggressive treatment. A similar case report detailing th Continue reading >>

What Is The Origin/mechanism Of Abdominal Pain In Diabetic Ketoacidosis?

What Is The Origin/mechanism Of Abdominal Pain In Diabetic Ketoacidosis?

Other than all papers I could find citing the depth of the keto-acidosis (and not the height of the blood glucose levels) correlating with abdominal pain, nothing else to explain how these two are linked. Decades ago, I was taught that because of the keto-acidosis causing a shift of intracellular potassium (having been exchanged for H+ protons of which in keto-acidosis there were too many of in the extracellular fluid) to the extracellular, so also the blood compartment, resulting in hyperkalemia, paralyzing the stomach, which could become grossly dilated - that’s why we often put in a nasogastric drainage tube to prevent vomiting and aspiration - and thus cause “stomach pain”. This stomach pain in the majority of cases indeed went away after the keto-acidosis was treated and serum electrolyte levels normalized. In one patient it didn’t, she remained very, very metabolically acidotic, while blood glucose levels normalized, later we found her to have a massive and fatal intestinal infarction as the underlying reason for her keto-acidosis….. Continue reading >>

Case 23-2013 — A 54-year-old Woman With Abdominal Pain, Vomiting, And Confusion

Case 23-2013 — A 54-year-old Woman With Abdominal Pain, Vomiting, And Confusion

The description of this case was presented as a Case Challenge. Readers were invited to review the case description, vote on the diagnosis, and submit comments. The full case discussion and final diagnosis now appear below, along with the poll results. Dr. Sara R. Schoenfeld (Medicine): A 54-year-old woman was admitted to this hospital because of abdominal pain, vomiting, and confusion. The patient was in her usual health until approximately 3 days before admission, when she reportedly began to feel unwell, with weakness, chills, and skin that was abnormally warm to the touch. She self-administered aspirin, without improvement. During the next 2 days, her oral intake decreased. Approximately 22 hours before presentation, vomiting occurred. Nine hours before presentation, she began to travel home to Italy from the eastern United States. During the next 2 hours, increasing abdominal pain occurred, associated with vomiting and shortness of breath, and she took additional aspirin for pain. Approximately 2 hours before presentation, while the patient was in flight, abdominal pain markedly worsened, vomiting increased, and she became confused and unresponsive. The flight was diverted to Boston. On examination by emergency medical services personnel, she was nonverbal and was moaning continuously. The blood pressure was 120/70 mm Hg, the pulse 52 beats per minute, and the respiratory rate 26 breaths per minute. The capillary blood glucose level was 116 mg per deciliter (6.4 mmol per liter). She was brought to the emergency department at this hospital by ambulance. The patient's history was obtained from her husband through an interpreter. She had non–insulin-dependent (type 2) diabetes mellitus, hypertension, nephrolithiasis, and chronic kidney disease. Medications included Continue reading >>

Lactic Acidosis: What You Need To Know

Lactic Acidosis: What You Need To Know

Lactic acidosis is a form of metabolic acidosis that begins in the kidneys. People with lactic acidosis have kidneys that are unable to remove excess acid from their body. If lactic acid builds up in the body more quickly than it can be removed, acidity levels in bodily fluids — such as blood — spike. This buildup of acid causes an imbalance in the body’s pH level, which should always be slightly alkaline instead of acidic. There are a few different types of acidosis. Lactic acid buildup occurs when there’s not enough oxygen in the muscles to break down glucose and glycogen. This is called anaerobic metabolism. There are two types of lactic acid: L-lactate and D-lactate. Most forms of lactic acidosis are caused by too much L-lactate. Lactic acidosis has many causes and can often be treated. But if left untreated, it may be life-threatening. The symptoms of lactic acidosis are typical of many health issues. If you experience any of these symptoms, you should contact your doctor immediately. Your doctor can help determine the root cause. Several symptoms of lactic acidosis represent a medical emergency: fruity-smelling breath (a possible indication of a serious complication of diabetes, called ketoacidosis) confusion jaundice (yellowing of the skin or the whites of the eyes) trouble breathing or shallow, rapid breathing If you know or suspect that you have lactic acidosis and have any of these symptoms, call 911 or go to an emergency room right away. Other lactic acidosis symptoms include: exhaustion or extreme fatigue muscle cramps or pain body weakness overall feelings of physical discomfort abdominal pain or discomfort diarrhea decrease in appetite headache rapid heart rate Lactic acidosis has a wide range of underlying causes, including carbon monoxide poisoni Continue reading >>

Case Of Diabetic Ketoacidosis As An Initial Presentation Of Cushing’s Syndrome

Case Of Diabetic Ketoacidosis As An Initial Presentation Of Cushing’s Syndrome

Background Diabetic ketoacidosis (DKA) is an acute metabolic disorder characterized by markedly increased circulating ketone bodies e.g. beta-hydroxybutyrate, aceto-acetate and acetone in the presence of hyperglycemia. DKA is a serious and potentially life-threatening metabolic complication of diabetes mellitus. Some well-known precipitants of DKA include new-onset T1DM, insulin withdrawal and acute illness. In this report, we present a subject who presented with DKA as an initial manifestation of Cushing’s disease secondary to ACTH-producing pituitary adenoma. Case presentation A 48-year-old Caucasian woman was admitted with fever, cough, left-sided chest pain, shortness of breath and hemoptysis. She reported amenorrhea of one-year duration. She was a chronic smoker for over 20 years. Patient was unable to provide a detailed history at the time of admission due to acuteness of her illness and respiratory distress. On physical examination, patient was alert, oriented and in moderate respiratory distress with Kussmaul breathing, temperature: 102 F; respiratory rate: 20/min; pulse: 110/min and blood pressure: 148/98 mmHg; body weight: 158 lbs as well as round flushed face with acne, hirsutism and dark purple striae of the abdominal wall (Fig. 1). Lung examination revealed bronchial breath sounds with crackles in the lower left field. Heart evaluation showed normal heart sounds with tachycardia without a murmur, and neurological assessment was unremarkable. Investigation Complete blood count was significant for WBC 21.600/mL with segmented neutrophils 69%. Serum chemistries showed sodium: 134 mM/L (normal: 135–146); potassium: 3.5 mM/L (normal: 3.5–5.3); chloride: 78 mM/L (normal: 98–110); HCO3−: <10 mM/L (normal: 20–31); anion gap: 50 mM/L (normal: 8–16); se Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

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