Anion gap usmle - anion gap metabolic acidosis normal anion gap metabolic acidosis
Causes Of Metabolic Acidosis
In practically every CICM exam paper, the candidates are presented with an ABG (sometimes several) which expect the diagnosis of a metabolic acidosis of some sort. It is therefore essential to develop some sort of mnemonic aid to recall the differential diagnosis of metabolic acidosis. In spite of its many obvious disadvantages, the anion gap classification of metabolic acid-base disorders is useful tool. Causes of Metabolic Acidosis High anion gap Normal anion gap MUD PILES Methanol and other toxic alcohols Uraemia Diabetic (or other) ketoacidosis Pyroglutamic acidosis Iron overdose Lactic acidosis Ethylene glycol Salicylates PANDA RUSH Pancreatic secretion loss Acetazolamide Normal saline intoxication Diarrhoea Aldosterone antagonists Renal tubular acidosis Type 1 (distal) Ureteric diversion Small bowel fistula Hyperalimentation (TPN) The MUDPILES mnemonic is showing its age. Nowhere is there space for citrate, for instance. This is a problem, as several SAQs (eg. Question 3.3 from the second paper of 2013) present the candidate with a citrate-based acidosis. The "P" in PILES used to be "Paraldehyde", but paraldehyde has fallen out of favour since the 1980s, and so "Pyroglutamic
What is INSULIN SHOCK THERAPY? What does INSULIN SHOCK THERAPY mean? INSULIN SHOCK THERAPY meaning - INSULIN SHOCK THERAPY definition - INSULIN SHOCK THERAPY explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. Insulin shock therapy or insulin coma therapy (ICT) was a form of psychiatric treatment in which patients were repeatedly injected with large doses of insulin in order to produce daily comas over several weeks. It was introduced in 1927 by Austrian-American psychiatrist Manfred Sakel and used extensively in the 1940s and 1950s, mainly for schizophrenia, before falling out of favour and being replaced by neuroleptic drugs in the 1960s. It was one of a number of physical treatments introduced into psychiatry in the first four decades of the twentieth century. These included the convulsive therapies (cardiazol/metrazol therapy and electroconvulsive therapy), deep sleep therapy and psychosurgery. Insulin coma therapy and the convulsive therapies are collectively known as the shock therapies. Insulin coma therapy was a labour-intensive treatment that required trained staff and a special unit. Patients, who were almost invaria
Causes Of Metabolic Acidosis In Canine Hemorrhagic Shock: Role Of Unmeasured Ions
Abstract Metabolic acidosis during hemorrhagic shock is common and conventionally considered to be due to hyperlactatemia. There is increasing awareness, however, that other nonlactate, unmeasured anions contribute to this type of acidosis. Eleven anesthetized dogs were hemorrhaged to a mean arterial pressure of 45 mm Hg and were kept at this level until a metabolic oxygen debt of 120 mLO2/kg body weight had evolved. Blood pH, partial pressure of carbon dioxide, and concentrations of sodium, potassium, magnesium, calcium, chloride, lactate, albumin, and phosphate were measured at baseline, in shock, and during 3 hours post-therapy. Strong ion difference and the amount of weak plasma acid were calculated. To detect the presence of unmeasured anions, anion gap and strong ion gap were determined. Capillary electrophoresis was used to identify potential contributors to unmeasured anions. During induction of shock, pH decreased significantly from 7.41 to 7.19. The transient increase in lactate concentration from 1.5 to 5.5 mEq/L during shock was not sufficient to explain the transient increases in anion gap (+11.0 mEq/L) and strong ion gap (+7.1 mEq/L), suggesting that substantial amoun
Bala Venkatesh (University of Queensland, Australia) busting lactate myths at #SGANZICS on 22 April 2017. Mark your calendar for SGANZICS 17-21 May 2018!
Metabolic Acidosis In The Critically Ill: Part 2. Causes And Treatment
The correct identification of the cause, and ideally the individual acid, responsible for metabolic acidosis in the critically ill ensures rational management. In Part 2 of this review, we examine the elevated (corrected) anion gap acidoses (lactic, ketones, uraemic and toxin ingestion) and contrast them with nonelevated conditions (bicarbonate wasting, renal tubular acidoses and iatrogenic hyperchloraemia) using readily available base excess and anion gap techniques. The potentially erroneous interpretation of elevated lactate signifying cell ischaemia is highlighted. We provide diagnostic and therapeutic guidance when faced with a high anion gap acidosis, for example pyroglutamate, in the common clinical scenario ‘I can’t identify the acid – but I know it's there'. The evidence that metabolic acidosis affects outcomes and thus warrants correction is considered and we provide management guidance including extracorporeal removal and fomepizole therapy. In Part 1 of this review article, we considered the classification and diagnostic approach to metabolic acidosis in the critically ill, including base excess, CO2/HCO–3, and anion gap, and proposed albumin-corrected anion gap
Abstract The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pa ...
Bicarbonate is the major extracellular buffer in the body. It is present in all body fluids and can be generated from CO2 and H2O in the presence of carbonic anhydrase. Bicarbonate on the chemistry panel gives an indication of acid-base status, but does not replace blood gas measurement as it does not supply information about the respiratory component of acid-base status or the pH of the animal. Bicarbonate values on a chemistry panel should alwa ...
There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 6.1, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer. Arterial vs. Venous Gases Venous blood from the dorsum of the hand is moderately arter ...
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 ...
Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarb ...
Watch short & fun videos Start Your Free Trial Today Log in or sign up to add this lesson to a Custom Course. Custom Courses are courses that you create from Study.com lessons. Use them just like other courses to track progress, access quizzes and exams, and share content. Organize and share selected lessons with your class. Make planning easier by creating your own custom course. Create a new course from any lesson page or your dashboard. Click ...