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Difference Between Lactic Acidosis And Ketoacidosis

Methamphetamine Overdose And Metabolic Acidosis

Methamphetamine Overdose And Metabolic Acidosis

Begin your recovery from addiction today. Change starts with one call. (855) 837-1334 Brought to you by Elements Behavioral Health Methamphetamine Overdose and Metabolic Acidosis Posted in Stimulants by Arny Escobar Metabolic acidosis is a term used to describe the buildup of excessive amounts of acid in the bodys various fluids. In some cases, this buildup stems from excessive acid production inside the body; in other cases, it stems from the kidneys inability to eliminate sufficient amounts of acid from the bloodstream. Whatever the underlying cause, unchecked metabolic acidosis can kill an affected individual. People who use/abuse the illegal street drug methamphetamine can develop metabolic acidosis during the course of a drug overdose. The condition arises as an end result of an unsustainable methamphetamine-related increase in body temperature. Doctors refer to the relative acidity of the human body as the bodys pH level. If this level falls too low, the internal environment becomes too acidic to support good health; if the pH level rises too high, the internal environment becomes too alkaline to support good health. Relative pH is measured on a scale of 0 to 14. A pH level between 0 and 7 falls within the acidic range of this scale, while a pH level between 7 and 14 falls within the alkaline range of the scale. Under normal circumstances, the pH level of human blood falls somewhere between 7.35 and 7.45, which means it has a slightly alkaline quality. Levels that fall below 6.8 or rise above 7.8 can kill a human being. Metabolic acidosis is actually a general term that groups together several specific types of acidosis, including conditions called lactic acidosis, diabetic acidosis and hyperchloremic acidosis. Lactic acidosis occurs when the body contains too mu Continue reading >>

Acid-base Imbalance, Abnormal Blood Ph

Acid-base Imbalance, Abnormal Blood Ph

Metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis, mixed acid-base disorders Derangements in blood pH result from increased intake, altered production or impaired/excessive excretion of acid or base. With time, respiratory and renal adjustments correct the pH towards normal by altering the plasma levels of pCO2 or strong ions (Na+,Cl- ), and result in predictable changes in bicarbonate concentration that can also be used to characterize the disorder (see = [(pCO2 -40)/10] +24= [(pCO2 -40)/3] +24 Acidosis: A physiologic process leading to acidemia Alkalosis: A physiologic process leading to alkalemi. Respiratory: The primary disorder results from an abnormal pCO2 --increased = acidosis; decreased = alkalosis Metabolic: The primary disorder does not result from abnormal pCO2 Mixed (Complex): More than one disorder is present Compensation: Changes in pCO2 or strong ions (Na+,Cl- ) resulting from normal physiologic mechanisms to restore acid-base balance Standard base excess (SBE): Quantity of metabolic acid-base disturbance where a positive value indicates alkalosis and a negative value (also referred to as a base deficit) indicates an acidosis Strong ion difference: The difference in charge between "strong" (completely dissociated) cations (positive) and anions (negative). (See pathophysiology section.) Anion gap: The difference in charge between commonly measured electrolytes (See laboratory findings section.) Acidosis: chloride administration (e.g. saline), aspirin overdose Alkalosis: NaHCO3 administration, antacid abuse, buffered replacement fluid (hemofiltration) Increased acid production: lactic acidosis, diabetic ketoacidosis Hypercapnic respiratory failure, permissive hypercapnia Alkalosis: vomiting, large gastric aspirates, diur Continue reading >>

Types Of Disturbances

Types Of Disturbances

The different types of acid-base disturbances are differentiated based on: Origin: Respiratory or metabolic Primary or secondary (compensatory) Uncomplicated or mixed: A simple or uncomplicated disturbance is a single or primary acid-base disturbance with or without compensation. A mixed disturbance is more than one primary disturbance (not a primary with an expected compensatory response). Acid-base disturbances have profound effects on the body. Acidemia results in arrythmias, decreased cardiac output, depression, and bone demineralization. Alkalemia results in tetany and convulsions, weakness, polydipsia and polyuria. Thus, the body will immediately respond to changes in pH or H+, which must be kept within strict defined limits. As soon as there is a metabolic or respiratory acid-base disturbance, body buffers immediately soak up the proton (in acidosis) or release protons (alkalosis) to offset the changes in H+ (i.e. the body compensates for the changes in H+). This is very effective so minimal changes in pH occur if the body is keeping up or the acid-base abnormality is mild. However, once buffers are overwhelmed, the pH will change and kick in stronger responses. Remember that the goal of the body is to keep hydrogen (which dictates pH) within strict defined limits. The kidney and lungs are the main organs responsible for maintaining normal acid-base balance. The lungs compensate for a primary metabolic condition and will correct for a primary respiratory disturbance if the disease or condition causing the disturbance is resolved. The kidney is responsible for compensating for a primary respiratory disturbance or correcting for a primary metabolic disturbance. Thus, normal renal function is essential for the body to be able to adequately neutralize acid-base abnor Continue reading >>

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 >>

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis). High anion gap acidosis Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis), but it also occurs with chronic alcoholism (see alcoholic ketoacidosis), undernutrition, and, to a lesser degree, fasting. In these conditions, the body converts from glucose to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and beta-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric and methylmalonic acidemia. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Lactate accumulation results from a combination of excess formation and decreased utilization of lactate. Excess lactate production occurs during states of anaerobic metabolism. The most serious form occurs during the various types o Continue reading >>

To Initiate Synjardy Or Synjardy Xr, Determine Appropriate Combination Of The Active Ingredient Of Jardiance And Metformin*

To Initiate Synjardy Or Synjardy Xr, Determine Appropriate Combination Of The Active Ingredient Of Jardiance And Metformin*

Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Symptoms included malaise, myalgias, respiratory distress, somnolence, and abdominal pain. Laboratory abnormalities included elevated blood lactate levels, anion gap acidosis, increased lactate/pyruvate ratio, and metformin plasma levels generally >5 mcg/mL. Risk factors include renal impairment, concomitant use of certain drugs, age ≥65 years old, radiological studies with contrast, surgery and other procedures, hypoxic states, excessive alcohol intake, and hepatic impairment. Steps to reduce the risk of and manage metformin-associated lactic acidosis in these high risk groups are provided in the Full Prescribing Information. If lactic acidosis is suspected, discontinue SYNJARDY or SYNJARDY XR and institute general supportive measures in a hospital setting. Prompt hemodialysis is recommended. JARDIANCE is indicated to reduce the risk of cardiovascular (CV) death in adults with type 2 diabetes mellitus and established CV disease. JARDIANCE, SYNJARDY, AND SYNJARDY XR are indicated as adjuncts to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. SYNJARDY and SYNJARDY XR are indicated when both empagliflozin and metformin hydrochloride are appropriate. Empagliflozin, a component of SYNJARDY AND SYNJARDY XR, is indicated to reduce the risk of CV death in adults with type 2 diabetes mellitus and established CV disease. However, the effectiveness of SYNJARDY AND SYNJARDY XR on reducing the risk of CV death in adults with type 2 diabetes mellitus and CV disease has not been established. JARDIANCE, SYNJARDY, AND SYNJARDY XR are not recommended for patients with type 1 diabetes or for the treatment of Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Increases 0.3-0.7 mEq/l [0.3-0.7 mmol/L] per 0.1 decr pH Difference between measured plasma cation (ie, Na+) and anions (ie, chloride (Cl-), HCO3-) concentrations Lactic acidosis (mild LA may have normal AG) Also called hyperchloremic acidosis (decreased HCO3, increased Cl) Renal tubular acidosis: impairment in renal acidification Type III (term no longer used) Formerly used to define distal RTA with bicarbonate wasting in children Bicarbonaturia resolves with age and is not truly part of a pathologic process Type IV: common in obstructive nephropathy, DM, hyporenin/hypoaldosteronehyper K+, acidosis Intestinal loss of bicarbonate (diarrhea, pancreatic fistula) Carbonic anhydrase inhibitors (e.g. acetazolamide) Dilutional acidosis (due to rapid infusion of bicarbonate-free isotonic saline) Ingestion of exogenous acids (ammonium chloride, methionine, cystine, calcium chloride) Drugs: amiloride, triamterine, Bactrim, chemotherapy, pentamidines As diagnostic aid, is not absolute "Delta gap" = calculated anion gap:nl anion gap In anion gap acidosis, "delta gap" should equal "delta HCO3" If HCO3 higher than predictedsuperimposed metabolic alkalosis If HCO3 lower than predictedsuperimposed non-anion gap metabolic acidosis Allows diagnosisof mixed metabolic disturbance Mixed metabolic disturbance plus respiratory disturbance Check urine pH before initializing therapy NaHCO3 therapy for pH < 7.1 - 7.2 Only used emergently to raise pH to > 7.1 or 7.2 Controversial, depends on disorder and symptoms i.e. NaHCO3 not beneficial in DKA treatment with pH under 7.0) DO NOT give this entire amount 2 ampulesof 8.4% NaHCO3 in 1 Liter of 1/4 NS OR 3-4 ampulesof 8.4% NaHCO3 in 1 Liter D5W Overaggressive NaHCO3"overshoot alkalosis" Bicarbonate level should be corrected only to 15 mEq/L [15 m Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

I. Review of normal lipid metabolism Triglycerides in adipose ==lipolysis==> Long-chain FAs Long-chain FAs==hepatic beta-oxidation==>Acetyl CoA Acetyl CoA==hepatic ketogenesis==>ketone bodies Ketone bodies are Beta-hydroxybutyrate and Acetoacetate Beta-OHB is oxidized to AcAc-; their relative concentrations depend on redox state of cell; Beta-OHB predominates in situation favoring reductive metabolism (e.g. decreased tissue perfusion, met. acidosis, catabolic states--like DKA!) Typical ratio Beta-OHB:AcAc- is 3:1; us. increases in DKA II. Hormonal influences on glucose and lipid metabolism Insulin In liver, increases glu uptake from portal blood; stimulates glycogenesis, inhibits glycogenolysis and gluconeogenesis In skeletal muscle, increases glu uptake from blood, stimulates protein synth, inhibits proteolysis In adipose tissue, required for glu and lipoprotein uptake from blood; stimulates lipogenesis, inhibits lipolysis Tissues which don't require insulin to transport glucose into cells: brain, renal medulla, formed blood elements Counterregulatory hormones: glucagon (major player in DKA), epi/norepi, cortisol, growth hormone (no acute effects, only over days-weeks) Glucagon: increases hepatic beta-oxidation, ketogenesis, gluconeogenesis and glycogenolysis; decreases hepatic FA synth. Epi/Norepi: increase hepatic gluconeogenesis & glycogenolysis; increases adipose lipolysis; decreases peripheral glu utilization Cortisol: major effect is decreased peripheral glu utiliz; little effect on production Growth hormone: increases hepatic gluconeogenesis and glycogenolysis; increases adipose lipolysis In high counterreg. hormone states (see above), require high levels of insulin to avoid progressive hyperglycemia and ketoacidosis--glucagon levels in DKA are 5-6 x nl* III. Pa Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis is a state of insulin deficiency, characterised by rapid onset, extreme metabolic acidosis, a generally intact sensorium, and only mild hyperglycaemia. DKA comes up frequently in the CICM SAQs, but usually as an ABG interpretation exercise. This chapter focuses on the medical side of DKA, including its causes, manifestations, complications, and management strategies. Questions which have required such thinking have included the following: Question 1 from the second paper of 2016 (differences between HONK and DKA) Question 17 from the first paper of 2014 (differences between HONK and DKA) Question 2 from the second paper of 2009 (general approach to management) Question 15 from the second paper of 2000 (whether or not saline is appropriate) Definition of diabetic ketoacidosis How does one discriminate between DKA and HONK even when in about 30% of instances the two disorders coexist? Arbitrary definitions exist, proposed by the American Diabetes Association. In summary: DKA presents with acidosis as the major feature HONK presents with hyperglycaemia as the major feature Discriminating Between HONK and DKA Domain Features suggestive of DKA Features suggestive of HONK Demographic Young Known Type 1 diabetic Elderly Known Type 2 diabetic History Rapid clinical course History of noncompliance with insulin Abdominal pain Shortness of breath Prolonged course History of noncompliance with oral antihyperglycaemic agents and insulin Polydipsia, polyuria, weight loss Neurological symptoms Examination Tachypnoea Normal level of consciousness, or only slightly decreased Coma Seizures Biochemistry Severe acidosis Severe ketosis Mild hyperglycaemia Renal function normalises rapidly Mild acidosis Little ketosis; mainly lactate is raised Severe hyperglycaemia Esta Continue reading >>

High Anion Gap Metabolic Acidosis - Today's Pearl - Statpearls

High Anion Gap Metabolic Acidosis - Today's Pearl - Statpearls

High anion gap metabolic acidosis (HAGMA) is a subcategory of acidosis ofmetabolic (i.e., non-respiratory) etiology. Differentiation of acidosis into a particular subtype, whether high anion gap metabolic acidosisor non-aniongap metabolic acidosis(NAGMA), aids in the determinationof the etiology and hence appropriate treatment. Although there have been many broadly inclusive mnemonic devices for high anion gap metabolic acidosis, the use of "GOLD MARK" has gained popularity for its focus on causes common to the 21st century. Glycols (ethylene glycol, propylene glycol) Oxoproline (pyroglutamic acid, the toxic metabolite of excessive acetaminophen or paracetamol) L-Lactate (standard lactic acid seen in lactic acidosis) D-Lactate (exogenous lactic acid produced by gut bacteria) Methanol (this is inclusive of alcohols in general) Ketones (diabetic, alcoholic and starvation ketosis) Of note, metformin has been omitted from this list due to a lack of evidence for metformin-induced lactic acidosis. In fact, aCochrane review found substantial evidence that metformin was not a cause of lactic acidosis. The same could not be said ofthe older biguanide, phenformin, which does increase the incidence of lactic acidosis by approximately tenfold. Furthermore, the addition of massive rhabdomyolysis would be appropriate given the potentially large amounts of hydrogen ions released by muscle breakdown. High anion gap metabolic acidosis is one of the most common metabolic derangements seen in critical care patients. Exact numbers are not readily available. The most common method of evaluation of metabolic acidosis involves the Henderson-Hasselbalch equation and the Lewis model interpretation of biological acidosis which evaluates the plasma concentration of hydrogen ions. An alternative Continue reading >>

Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

Introduction A 49-year-old man presented to the emergency department complaining of dyspnea for 2 days. He had a history of hypertension, type 2 diabetes mellitus, atrial fibrillation, and a severe dilated cardiomyopathy. He had been hospitalized several times in the previous year for decompensated congestive heart failure (most recently, 1 month earlier). The plasma creatinine concentration was 1.13 mg/dl on discharge. Outpatient medications included insulin, digoxin, warfarin, spironolactone, metoprolol succinate, furosemide (80 mg two times per day; increased from 40 mg daily 1 month earlier), metolazone (2.5 mg daily; added 1 month earlier), and metformin (2500 mg in three divided doses; increased from 1000 mg 1 month earlier). Physical examination revealed an obese man in moderate respiratory distress. The temperature was 36.8°C, BP was 119/83 mmHg, and heart rate was 96 per minute. Peripheral hemoglobin oxygen saturation was 97% on room air, with a respiratory rate of 26 per minute. The heart rhythm was irregularly irregular; there was no S3 or murmur. Jugular venous pressure was about 8 cm. There was 1+ edema at the ankles. A chest radiograph showed cardiomegaly and central venous prominence. The N-terminal pro-B-type natriuretic peptide level was 5137 pg/ml (reference range = 1–138 pg/ml). The peripheral hemoglobin concentration was 12.5 g/dl, the white blood cell count was 12,500/µl (76% granulocytes), and the platelet count was 332,000/µL. Initial plasma chemistries are shown in Table 1. The impression was decompensated congestive heart failure. After administration of furosemide (160 mg intravenously), the urine output increased to 320 ml over the next 1 hour. There was no improvement in the dyspnea. Within 2 hours, the patient’s BP fell to 100/64 mmHg Continue reading >>

Clinical Significance Of The Fractional Excretion Of Anions In Metabolic Acidosis.

Clinical Significance Of The Fractional Excretion Of Anions In Metabolic Acidosis.

Clinical significance of the fractional excretion of anions in metabolic acidosis. Clinical Nephrology [01 Jun 2001, 55(6):448-452] Type: Research Support, Non-U.S. Gov't, Journal Article The fractional excretion of anions has been proposed as a new index for the differential diagnosis of metabolic acidosis, identifying the properties of the conjugate base by examining the renal handling of the anion. Here, we investigated clinical significance of the fractional excretion of anions in pathophysiologic diagnosis of metabolic acidosis by measuring urine ammonium (NH4+) excretion, the ratio of A plasma anion gap/delta plasma HCO3- concentration (deltaAG/deltaHCO3-), and fractional excretion of anions in three different groups of metabolic acidosis: acid overproduction (8 patients with lactic acidosis, 8 with diabetic ketoacidosis, 3 with hippuric acidosis following glue sniffing), acid underexcretion (10 patients with chronic renal failure) and normal controls (10 normal volunteers who underwent 3-day NH4Cl loading). As expected, urine NH4+ excretion was higher in overproduction acidosis than in acid-loaded normal controls (88.1 +/- 12.3 vs. 54.0 +/- 3.7 mmol/day, p < 0.05), and it was lower in chronic renal failure than in acid-loaded normal controls (12.8 +/- 1.7 vs. 54.0 +/- 3.7 mmol/day, p < 0.05). The fractional excretion of anions had no difference between overproduction acidosis and chronic renal failure (41.2 +/- 42.8% vs. 41.0 +/- 8.1%). However, the fractional excretion of anions showed significant differences between the subgroups in acid overproduction (lactic acidosis, 4.7 +/- 0.3%; diabetic ketoacidosis, 45.8 +/- 3.1%; hippuric acidosis, 126.0 +/- 14.4%; p < 0.05). The ratio of plasma deltaAG/deltaHCO3- also exhibited significant differences between the subg 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 >>

Free Physiology Flashcards About Kidney Lect 13

Free Physiology Flashcards About Kidney Lect 13

Acedemia cannot exist without acidosis, but acidosis can exist at any blood pH if more than one disturbance is present; same thing for alkalosis/alkalemia An acidosis or alkalosis resulting from a primary change in the serum bicarbonate concentration What is the difference between acidosis and acidemia? Acidosis: pathophysiological process that tends to decrease blood pH; acidemia: arterial blood pH <7.36 What is the difference between alkalosis and alkalemia? Alkalosis: pathophysiological process that tends to decrease blood pH; alkalemia: arterial blood pH <7.36 An acidosis or alkalosis resulting from a primary change in the P CO2 The physiologic metabolic (renal) and respiratory changes to return the pH toward normal in response to a primary acidosis or alkalosis. Not completely; time course varies: buffering (minutes to 6 hours), respiratory (minutes to 12 hours), metabolic (24-72 hours) A single acid-base process (acidosis or alkalosis) and its expected compensation are present two or more primary acid base disturbances are present. The arterial blood pH will depend on the direction and magnitude of the disturbances What is the primary process and compensation in metabolic acidosis? Primary process: decreased HCO3-; Compensation: decrease PCO2 What is the primary process and compensation in metabolic alkalosis? Primary process: increased HCO3-; Compensation: increase PCO2 What is the primary process and compensation in respiratory acidosis? Primary process: increased PCO2; Compensation: increase [HCO3-] What is the primary process and compensation in respiratory alkalosis? Primary process: decreased PCO2; Compensation: decreased [HCO3-] Metabolic acidoses are categorized on the basis of ... the anion that accumulates replacing the bicarbonate ioninto hyperchloremi Continue reading >>

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