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Why Does Metabolic Acidosis Cause Abdominal Pain

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic crises are discussed together followed by a separate section on lactic acidosis. DIABETIC KETOACIDOSIS (DKA) AND HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS) Definitions DKA has no universally agreed definition. Alberti proposed the working definition of “severe uncontrolled diabetes requiring emergency treatment with insulin and intravenous fluids and with a blood ketone body concentration of >5 mmol/l”.1 Given the limited availability of blood ketone body assays, a more pragmatic definition comprising a metabolic acidosis (pH <7.3), plasma bicarbonate <15 mmol/l, plasma glucose >13.9 mmol/l, and urine ketostix reaction ++ or plasma ketostix ⩾ + may be more workable in clinical practice.2 Classifying the severity of diabetic ketoacidosis is desirable, since it may assist in determining the management and monitoring of the patient. Such a classification is based on the severity of acidosis (table 1). A caveat to this approach is that the presence of an intercurrent illness, that may not necessarily affect the level of acidosis, may markedly affect outcome: a recent study showed that the two most important factors predicting mortality in DKA were severe intercurrent illness and pH <7.0.3 HHS replaces the older terms, “hyperglycaemic hyperosmolar non-ketotic coma” and “hyperglycaemic hyperosmolar non-ketotic state”, because alterations of sensoria may be present without coma, and mild to moderate ketosis is commonly present in this state.4,5 Definitions vary according to the degree of hyperglycaemia and elevation of osmolality required. Table 1 summarises the definition of Kitabchi et al.5 Epidemiology The annual incidence of DKA among subjects with type 1 diabetes is between 1% and 5% in European and American series6–10 and this incidence appear Continue reading >>

Metabolic Acidosis: Causes, Symptoms, And Treatment

Metabolic Acidosis: Causes, Symptoms, And Treatment

The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th Continue reading >>

Chapter 16: Acid-base Imbalances

Chapter 16: Acid-base Imbalances

Sort What is the function of a buffer? a) To excrete weak acids b) To secrete hydrogen ions c) To convert strong acids to weak acids d) To convert ammonia to ammonium ions c) To convert strong acids to weak acids -Buffers convert strong acids to weak acids. Excretion of weak acids, secretion of hydrogen ions into the renal tubule, and conversion of ammonia to ammonium ions takes place in the kidneys. A nurse is caring for a patient three days after abdominal surgery who continues to have poorly controlled abdominal pain with green bilious nasogastric output. The patient's respiratory rate is 32 and heart rate is 128. Which acid-base imbalance does the nurse suspect is occurring? a) Mixed acidosis b) Mixed alkalosis c) Metabolic alkalosis d) Respiratory acidosis b) Mixed alkalosis -Mixed alkalosis can occur in a patient who is losing CO2 via hyperventilation (possibly related to pain) while also losing acid by another method, such as prolonged suctioning with a nasogastric tube. Respiratory acidosis occurs when the primary loss of acid is via a respiratory "blow off" of CO2. Metabolic alkalosis occurs with a systemic loss of acid via a metabolic process such as vomiting or suctioning with a nasogastric tube. Mixed acidosis occurs when acid is retained by both respiratory and metabolic systems, such as in a critically ill patient in shock with hypoperfusion and hypoventilation, and will often cause a more profoundly acidotic pH than either condition could independently create. The nurse is caring for a patient that is in respiratory acidosis. What cardiovascular condition should the nurse closely monitor the patient for? a) Diarrhea b) Confusion c) Abdominal pain d) Ventricular fibrillation d) Ventricular fibrillation -Respiratory acidosis causes compensatory hyperkalemia Continue reading >>

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 >>

Master Metabolic Acidosis Assessment With Picmonic For Nursing Rn

Master Metabolic Acidosis Assessment With Picmonic For Nursing Rn

With Picmonic, facts become pictures. We've taken what the science shows - image mnemonics work - but we've boosted the effectiveness by building and associating memorable characters, interesting audio stories, and built-in quizzing. Picmonic for Nursing (RN) covers information that is relevant to your entire Nursing (RN) education. Whether you’re studying for your classes or getting ready to conquer your NCLEX®-RN, Hesi, ATI, TEAS test, Kaplan exams, we’re here to help. Research shows that students who use Picmonic see a 331% improvement in memory retention and a 50% improvement in test scores. "Bravo Team Picmonic on creating a truly revolutionary approach to learning, and for helping me to pass the NCLEX®. Couldn’t have done it without you!" — Steph B., University of Detroit Mercy, class of 2015 TRY IT FREE Continue reading >>

Blood Gases And Acute Pancreatitis

Blood Gases And Acute Pancreatitis

Summarized from Sharma V, Devi T, Sharma R et al. Arterial pH, bicarbonate levels and base deficit at presentation as markers of predicting mortality in acute pancreatitis: a single-centre prospective study. Gastroenterol Rep (Oxf) 2014; 2(3): 226-31 Acute pancreatitis, i.e. acute inflammation of the pancreas, causes sudden onset of severe upper abdominal pain often radiating to the back. Other symptoms include vomiting, constipation and pyrexia. Two main causes - alcohol abuse and gall stone disease – account for the majority (~80 %) of cases. The condition has a variable course. In many cases inflammation resolves with little or no intervention over a period of a few days to a week, with no long-term consequences, but in others the condition can be severe, progressing rapidly to systemic inflammation, sepsis and multiple organ failure. Severe acute pancreatitis is thus a potentially fatal condition that warrants immediate admission to intensive care. A major problem for initial emergency room management of patients presenting with acute pancreatitis is to distinguish those whose course is likely to be benign from those who are likely to suffer severe disease and therefore require admission to intensive care. There is currently no single reliable prognostic test and clinicians must depend on rather cumbersome clinical scoring systems to predict outcome. The authors of a recently published study sought to examine the value of admission acid-base parameters (pH, bicarbonate and base excess) in predicting outcome among patients with acute pancreatitis. The notion that these might be useful prognostic markers is based partially on the observation that metabolic acidosis (characterized by reduced pH, bicarbonate and base excess) is a frequent complication of severe acute Continue reading >>

Cardiovascular Complications Of Ketoacidosis

Cardiovascular Complications Of Ketoacidosis

US Pharm. 2016;41(2):39-42. ABSTRACT: Ketoacidosis is a serious medical emergency requiring hospitalization. It is most commonly associated with diabetes and alcoholism, but each type is treated differently. Some treatments for ketoacidosis, such as insulin and potassium, are considered high-alert medications, and others could result in electrolyte imbalances. Several cardiovascular complications are associated with ketoacidosis as a result of electrolyte imbalances, including arrhythmias, ECG changes, ventricular tachycardia, and cardiac arrest, which can be prevented with appropriate initial treatment. Acute myocardial infarction can predispose patients with diabetes to ketoacidosis and worsen their cardiovascular outcomes. Cardiopulmonary complications such as pulmonary edema and respiratory failure have also been seen with ketoacidosis. Overall, the mortality rate of ketoacidosis is low with proper and urgent medical treatment. Hospital pharmacists can help ensure standardization and improve the safety of pharmacotherapy for ketoacidosis. In the outpatient setting, pharmacists can educate patients on prevention of ketoacidosis and when to seek medical attention. Metabolic acidosis occurs as a result of increased endogenous acid production, a decrease in bicarbonate, or a buildup of endogenous acids.1 Ketoacidosis is a metabolic disorder in which regulation of ketones is disrupted, leading to excess secretion, accumulation, and ultimately a decrease in the blood pH.2 Acidosis is defined by a serum pH <7.35, while a pH <6.8 is considered incompatible with life.1,3 Ketone formation occurs by breakdown of fatty acids. Insulin inhibits beta-oxidation of fatty acids; thus, low levels of insulin accelerate ketone formation, which can be seen in patients with diabetes. Extr Continue reading >>

The Evaluation Of Acute Abdominal Pain In The Elderly Patient

The Evaluation Of Acute Abdominal Pain In The Elderly Patient

Abstract Obstetrician/Gynecologists frequently encounter older patients complaining of acute abdominal pain. Because of physiologic changes, medication use, and preexisting conditions, the elderly patient often does not manifest overt signs of disease. Also, while appendicitis is the most common cause of abdominal pain in the general population, biliary disease, small bowel obstruction and perforated viscus constitute the leading etiologies in the geriatric population. The older patient's physical findings often do not correlate with the severity of disease; however, mental status changes, hypothermia, bandemia, and metabolic acidosis are helpful indicators of significant derangement. Emergent abdominal pain, defined as hemodynamic instability such as that caused by massive hemorrhage, requires immediate surgery. Otherwise, the most effective work-up includes a detailed history and physical examination, and selective screening laboratory tests. When the diagnosis is still unclear, repeat physical examination, in-patient observation, and consultation should be considered. The decision of whether to perform diagnostic laparoscopy or laparotomy should be individualized after assessing the patient's entire clinical presentation and progress. Acute abdominal pain in the older patient is associated with low diagnostic accuracy, but high mortality. Therefore, as a primary care physician, the obstetrician/gynecologist must be proficient in the evaluation of acute abdominal pain in the elderly patient. 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci 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 >>

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 >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

<< Guidelines For The Ed Management Of Pediatric Diabetic Ketoacidosis (dka)

<< Guidelines For The Ed Management Of Pediatric Diabetic Ketoacidosis (dka)

Epidemiology, Etiology, And Pathophysiology Epidemiology and Etiology "Type 1" and "Type 2" Diabetes in Children Type 1 diabetes is the most common type of diabetes seen in children today. The primary metabolic derangement in type 1 diabetes is an absolute insulin deficiency. These patients will have a life-long dependence on insulin injections. The overall incidence of insulin-dependent diabetes is about 15 cases per 100,000 people per year (about 50,000 are diagnosed with type 1 diabetes each year). An estimated 3 children of every 1000 will develop insulin-dependent diabetes by the age of 20. Type 1 diabetes is primarily a disease of Caucasians. The worldwide incidence is highest in Finland and Sardinia and lowest in the Asian and black populations. Type 1 diabetes is more frequently diagnosed in the winter months (the reason for this is not known.) Interestingly, twins affected by type 1 diabetes are often discordant in the development of the disease.13 About 95% of cases of type 1 diabetes are the result of a genetic defect of the immune system, exacerbated by environmental factors.13 The autoimmune destruction of the beta cells of the pancreas results in the inability to produce insulin. Inheritance of type 1 diabetes is carried in genes of the major histocompatibility complex, the human leukocyte antigen (HLA) system. Eventually, this research may lead to a vaccine using the insulin B chain 8-24 peptides to actually prevent type 1 diabetes.13 It is currently thought that islet cells damaged by a virus produce a membrane antigen that may stimulate a response by T killer cells of the immune system in the genetically susceptible patient. The T killer cells misidentify the beta cell as foreign and destroy it. As the beta cells in the pancreas are destroyed, the remai Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be Continue reading >>

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