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Is Ketoacidosis Metabolic Or Respiratory

Acid/base (alkalosis Vs Acidosis, Metabolic Vs Respiratory)

Acid/base (alkalosis Vs Acidosis, Metabolic Vs Respiratory)

This is the general way to approach an acid-base disturbance. They’re not really as bad as they seem at first. You just need to remember that CO2 is acidic and HCO3- is basic. So an increase in CO2 makes the body acidotic and an increase in HCO3- makes the body alkalotic. It’s also good to remember to calculate the anion gap when doing these calculations. AG = Na – (Cl- + HCO3-) it’s just the cations minus the anions. If this gap between the cations and anions is large, it means that the anions are stacking their team and have an extra anion helping out. The classic mnemonic is MUDPILES Methanol Uremia Diabetic ketoacidosis Paraldehyde Isopropyl alcohol Lactic acidosis Ethylene glycol Salicylates If the anion gap is big, it’s good to look at the ratio between the change in the gap and the change in the HCO3-. Increase in AG < decrease in HCO3- = coexisting non-anion gap metabolic acidosis Increase in AG > decrease in HCO3- = coexisting metabolic alkalosis Continue reading >>

66: Acidosis And Alkalosis

66: Acidosis And Alkalosis

Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory system and the control of plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent derangements of neural respiratory control or are due to compensatory changes in response to a primary alteration in the plasma [HCO3−]. The most common clinical disturbances are simple acid-base disorders; i.e., metabolic acidosis or alkalosis or respiratory acidosis or alkalosis. Primary respiratory disturbances (primary changes in Paco2) invoke compensatory metabolic responses (secondary changes in [HCO3−]), and primary metabolic disturbances elicit predictable compensatory respiratory responses (secondary changes in Paco2). Physiologic compensation can be predicted from the relationships displayed in Table 66-1. In general, with one exception, compensatory responses return the pH toward, but not to Continue reading >>

5.5 Metabolic Acidosis - Compensation

5.5 Metabolic Acidosis - Compensation

Acid-Base Physiology 5.5.1 Hyperventilation Compensation for a metabolic acidosis is hyperventilation to decrease the arterial pCO2. This hyperventilation was first described by Kussmaul in patients with diabetic ketoacidosis in 1874. The metabolic acidosis is detected by both the peripheral and central chemoreceptors and the respiratory center is stimulated. The initial stimulation of the central chemoreceptors is due to small increases in brain ISF [H+]. The subsequent increase in ventilation causes a fall in arterial pCO2 which inhibits the ventilatory response. Maximal compensation takes 12 to 24 hours The chemoreceptor inhibition acts to limit and delay the full ventilatory response until bicarbonate shifts have stabilised across the blood brain barrier. The increase in ventilation usually starts within minutes and is usually well advanced at 2 hours of onset but maximal compensation may take 12 to 24 hours to develop. This is �maximal� compensation rather than �full� compensation as it does not return the extracellular pH to normal. In situations where a metabolic acidosis develops rapidly and is short-lived there is usually little time for much compensatory ventilatory response to occur. An example is the acute and sometimes severe lactic acidosis due to a prolonged generalised convulsion: this corrects due to rapid hepatic uptake and metabolism of the lactate following cessation of convulsive muscular activity, and hyperventilation due to the acidosis does not occur. The expected pCO2 at maximal compensation can be calculated from a simple formula The arterial pCO2 at maximal compensation has been measured in many patients with a metabolic acidosis. A consistent relationship between bicarbonate level and pCO2 has been found. It can be estimated from the Continue reading >>

Metabolic Alkalosis And Metabolic Acidosis Nclex Quiz | Acid-base Imbalances Quiz

Metabolic Alkalosis And Metabolic Acidosis Nclex Quiz | Acid-base Imbalances Quiz

This NCLEX quiz will test your ability to differentiate between metabolic acidosis vs metabolic alkalosis. You will be required to know the causes, signs and symptoms, and how to interpret blood gas values in this quiz. As a nursing student, it is crucial you know the basics about acid-base imbalances. Below are common test questions you may encounter on your nursing lecture exam or NCLEX licensing exam. Also, don’t forget to take our free Arterial Blood Gas (ABGs) Quiz. After you are done taking the quiz and click submit, the page will refresh and you will need to scroll down to see what you got right and wrong. In addition, below this quiz is a layout of the quiz with an answer key (if you wanted to print off the quiz..just copy and paste it). Don’t forget to share this quiz with your friends! Please do not re-post on other websites, however. Metabolic Acidosis and Metabolic Alkalosis Quiz NCLEX Diabetic ketoacidosis, aspirin toxicity, and renal failure are examples of the causes of ___________________. A. High anion gap metabolic acidosis B. Normal anion gap metabolic acidosis C. Low anion gap metabolic acidosis D. Normal anion gap respiratory acidosis A patient has the following arterial blood gases: PaCO2 33, HCO3 15, pH 7.23. Which of the following conditions are presenting? A. Metabolic alkalosis partially compensated B. Metabolic acidosis partially compensated C. Respiratory alkalosis not compensated D. Metabolic acidosis fully compensated A patient is in high anion gap metabolic acidosis due to diabetic ketoacidosis. Which of the following signs and symptoms would you expect to see in this patient? A. Kussmaul’s respirations B. Glucose 110 C. Hypoventilation D. Neuro-excitability A patient reports taking Diamox and has been reporting confusion, fatigue, a 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 (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). 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. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

Introduction Recently there have been numerous publications and discussions about whether VBGs can replace ABGs in DKA. The growing consensus is that VBGs are indeed adequate. Eliminating painful, time-consuming arterial blood draws is a huge step in the right direction. However, the ABG vs. VBG debate overlooks a larger point: neither ABG nor VBG measurements are usually helpful. It is widely recommended to routinely obtain an ABG or VBG, for example by both American and British guidelines. Why? Is it helping our patients, or is it something that we do out of a sense of habit or obligation? Diagnosis of DKA: Blood gas doesn’t help These are the diagnostic criteria for DKA from the America Diabetes Association. They utilize either pH or bicarbonate in a redundant fashion to quantify the severity of acidosis. It is unclear what independent information the pH adds beyond what is provided by the bicarbonate. Practically speaking, the blood gas doesn’t help diagnose DKA. This diagnosis should be based on analysis of the metabolic derangements in the acid-base status (e.g. anion gap, beta-hydroxybutyrate level). The addition of a blood gas to serum chemistries only adds information about the respiratory status, which does not help determine if the patient has ketoacidosis. Management: Does the pH help? It is debatable whether knowing or attempting to directly “treat” the pH is helpful. The pH will often be very low, usually lower than would be expected by looking at the patient. This may induce panic. However, it is actually a useful reminder that acidemia itself doesn't necessarily cause instability (e.g. healthy young rowers may experience lactic acidosis with a pH <7 during athletic exertion; Volianitis 2001). A question often arises regarding whether bicarbonate Continue reading >>

Bicarbonate Therapy In Severe Metabolic Acidosis

Bicarbonate Therapy In Severe Metabolic Acidosis

Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>

Acid Base Statuses

Acid Base Statuses

A B Metabolic Acidosis (1) results from cold stress Respiratory Alkalosis (1) results from excessive CO2 blown off Body decr carbonic acid (1) results in slow respirations so that CO2 is retained Acidosis (1) symptoms (a) CNS depression (b) errors in judgment (c) disorientation (d) drowsiness (e) stupor (f) coma Hydrogen Ions excess (1) results in acidosis as pH falls below 7.35 (2) hydrogen ions are forced into the cells causing K+ to move into the cells Diabetic Ketoacidosis metabolic acidosis Metabolic Acidosis dehydration after an extended bout of diarrhea COPD respiratory acidosis Diarrhea (1) respirtory acidosis Anxiety (1)results in respiratory alkalosis (2) associated w/hyperventilation (2) during hyperventilation CO2 is blown off which lowers the amount of acid in the system Severe Asthma Respiratory Alkalosis Acute Renal Failure (1) metabolic acidosis (2) hypermagnesemia (3) hyperkalemia (4) hypocalcemia Diarrhea (1) metabolic acidosis (2) leads to meta acid because there is an over-elimination of bicarbonate Alkalosis (1) signs (a) tingling fingers, toes & face (b) estreme nervousness (c) twitching of muscles (d) tetany Severe Asthma respiratory acidosis Vomiting (1) metabolic alkalosis (2) leads to metabolic alkalosis as hydrochloric acid is lost from the stomach Aspirin metabolic acidosis Overdose of Morphine respiratory acisosis Vigorous Diuresis metabolic alkalosis End Stage Muscular Distrophy respiratory acidosis Severe Hypokalemia metabolic alkalosis Renal Failure (1) results in metabolic acisosis as fluid build up turns acidic Shock (1) metabolic acidosis (2) meta acid because acid is added to the system (3) anaerobic metabolic pathways result in lactate and hydrogen irons (forming lactic acid) Hyperventilation (1) respiratory alkalosis (2) leads to re Continue reading >>

Acid-base And Electrolyte Disturbances In Patients With Diabetic Ketoacidosis

Acid-base And Electrolyte Disturbances In Patients With Diabetic Ketoacidosis

Abstract We undertook the present study to examine the acid-base and electrolyte disturbances in relation to hydration status in patients with diabetic ketoacidosis (DKA). A total of 40 insulin-dependent diabetes mellitus patients (22 male, 18 female), aged 18–61 years with DKA admitted to our hospital during the last 2 years, were studied. The duration of diabetes averaged 9 ± 2 years. In all cases a detailed investigation of the acid-base status and electrolyte parameters was performed. Twenty-one patients had a pure metabolic acidosis with an increased serum anion gap, seven had DKA combined with hyperchloremic metabolic acidosis, nine had DKA coexisting with metabolic alkalosis, while three had DKA with a concurrent respiratory alkalosis. Hydration status as evidenced by the ratio of urea/creatinine seems to play an important role in the development of mixed acid-base disorders (detected by changes in the ratios Δ anion gap/Δ bicarbonate () and sodium/chloride ()). In fact, hyperchloremic acidosis developed in the patients with the better hydration status. However, contradictorily, the severely dehydrated patients who experienced recurrent episodes of vomiting developed DKA with a concurrent metabolic alkalosis. Finally, patients with pneumonia or gram-negative septicemia exhibited DKA combined with a primary respiratory alkalosis. We conclude that patients with DKA commonly develop mixed acid-base disorders, which are partly dependent on patients' hydration status. Continue reading >>

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base disturbances Poor feeding Failure to thrive Lethargy Altered mental status Seizures Hypotonia Ataxia Developmental delay Optic nerve atrophy Deafness Tachypnea, hyperventilation, Kussmaul breathing Nausea/vomiting - due to increased β-hydroxybutyrate Dehydration Polydipsia Lethargy Polyuria, nocturia Acetone "fruity" breath Weight loss Altered mental status; in severe cases, coma Encephalopathy Vomiting Often present as neonates Elevated urine pH, greater than 5.5 Infantile, recessive form Severe hyperchloremic acidosis, serum bicarbonate may be less than 10 mEq/L Growth retardation Hypokalemia Dehydration Rickets Nephrocalcinosis Hearing loss Adolescent form, dominant Nephrocalcinosis Mild acidosis Mild hypokalemia CNS: disturbances of the respiratory regulation - apneustic respirations (or agonal respirations - deep, gasping breaths with pause at full inspiration), central neurogenic hyperventilation (deep, rapid), Cheyne-Stokes respirations (oscillatory pattern of breathing of deep breathing then apnea followed again by deep breaths) due to tumor, meningitis, encephalitis, psychosis or pain. Hyperammonemia. Anxiety and panic attacks. Fever. Nicotine. Salicylates. Methylxanthines. Progesterone. Hyperthyroidism. Paresthesias. Dizziness. Headache. Slurred speech. Brief loss of consciousness due to the combination of hypocarbia-induced cerebral vascular vasoconstriction and decreased off-loading of oxygen from hemoglobin due to the Bohr effect. Hypokalemia. Hypophosphatemia. Hypocalcemia. Extracorporeal removal of toxic metabolite via hemofiltration or hemodialysis. Avoid catabolism. Specific emergency treatment depends upon the diesease entity. A few are below: Urea cycle defects: Arginine Sodium benzoate Sodium phenylacetate Sodium phenylbutyrate Methylmalon 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 >>

Acidosis

Acidosis

The kidneys and lungs maintain the balance (proper pH level) of chemicals called acids and bases in the body. Acidosis occurs when acid builds up or when bicarbonate (a base) is lost. Acidosis is classified as either respiratory or metabolic acidosis. Respiratory acidosis develops when there is too much carbon dioxide (an acid) in the body. This type of acidosis is usually caused when the body is unable to remove enough carbon dioxide through breathing. Other names for respiratory acidosis are hypercapnic acidosis and carbon dioxide acidosis. Causes of respiratory acidosis include: Chest deformities, such as kyphosis Chest injuries Chest muscle weakness Chronic lung disease Overuse of sedative drugs Metabolic acidosis develops when too much acid is produced in the body. It can also occur when the kidneys cannot remove enough acid from the body. There are several types of metabolic acidosis: Diabetic acidosis (also called diabetic ketoacidosis and DKA) develops when substances called ketone bodies (which are acidic) build up during uncontrolled diabetes. Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Lactic acidosis is a buildup of lactic acid. Lactic acid is mainly produced in muscle cells and red blood cells. It forms when the body breaks down carbohydrates to use for energy when oxygen levels are low. This can be caused by: Cancer Drinking too much alcohol Exercising vigorously for a very long time Liver failure Low blood sugar (hypoglycemia) Medications, such as salicylates MELAS (a very rare genetic mitochondrial disorder that affects energy production) Prolonged lack of oxygen from shock, heart failure, or seve Continue reading >>

Acid Base Balance

Acid Base Balance

Concept- ACID BASE BALANCE Concept Definition The process of regulating the pH, bicarbonate concentration and partial pressure of carbon dioxide of body fluids. Key definitions: Acid – a substance that releases hydrogen ions (H+) Base – a substance that takes up hydrogen ions (H+) Bicarbonate (HCO3) - is the most important “base†in the body pH – is the measurement of acidity, alkalinity in a solution, the negative logarithm of hydrogen ion concentration, inverse relationship exists between hydrogen ion concentration and pH) Exemplars Diabetic Ketoacidosis (DKA) – Metabolic Acidosis Hyperventilation-(birthing mother, panic attack) – Respiratory Alkalosis Gastro-intestinal Losses – (pediatric) – Metabolic Alkalosis Drug Overdose with Hypoventilation – Respiratory Acidosis Objectives 1. Explain the correlation between Diabetic Ketoacidosis (DKA) – Metabolic Acidosis, Hyperventilation-(birthing mother, panic attack) – Respiratory Alkalosis, Gastro-intestinal Losses – (pediatric) – Metabolic Alkalosis, and/or Drug Overdose with Hypoventilation – Respiratory Acidosis to the concept of Acid Base Balance (including compromised antecedents, deficit measurement in attributes, a list of negative consequences, and the interrelated concepts which may be involved). 2. Identify conditions that place an individual at risk for imbalance leading to a compromised concept(s) resulting in Diabetic Ketoacidosis (DKA) – Metabolic Acidosis, Hyperventilation-(birthing mother, panic attack) – Respiratory Alkalosis, Gastro-intestinal Losses – (pediatric) – Metabolic Alkalosis, and/or Drug Overdose with Hypoventilation – Respiratory Acidosis. 3. Apply the nursing Continue reading >>

Causes For Acidosis, Metabolic, Lactic, Respiratory, Renal Acidosis And Diabetic Ketoacidosis Symptoms

Causes For Acidosis, Metabolic, Lactic, Respiratory, Renal Acidosis And Diabetic Ketoacidosis Symptoms

Acidosis simply means your body’s fluids have an unhealthy excess of acid. This either occurs from a buildup of acid or a loss of bicarbonate (base). Your lungs and kidneys are the maintenance organs for a healthy “acid to base” ph balance. Primary categories causing symptoms of acidosis: Metabolic acidosis is excessive acidity of your blood. It can be caused by many conditions or situations, notably: Primary symptom for metabolic acidosis is rapid breathing. Confusion or lethargy may also occur. Severe metabolic acidosis can cause death. Lactic acidosis is a build up of lactic acid in your bloodstream, generally produced when oxygen levels drop. It’s most common cause is intensive or prolonged exercise. Yet, it can also be caused by: cancer alcohol hypoglycemia respiratory failure medications ~ salicylates, metformin Symptoms of lactic acidosis are: Diabetic acidosis, also termed diabetic ketoacidosis, is usually a diabetes complication occurring when glucose (sugar) is unavailable due to insufficient insulin. So instead, fat is used as your energy source, producing a ketone build up. This is rarely a complication of type 2 diabetes. Diabetic ketoacidosis might as well be caused by: Symptoms of diabetic acidosis: mental stupor rapid breathing muscle stiffness, aching Left untreated, it can be fatal. Respiratory acidosis happens when your lungs can’t remove all of your body’s carbon dioxide (an acid) production. It is also referred to as hypercapnic acidosis or carbon dioxide acidosis. Causes of respiratory acidosis include: scoliosis ~ makes lungs less efficient nerve & muscle diseases affecting inflation, deflation of lungs Chronic respiratory acidosis leads to a stabilized ph, because your kidneys adjusts to help restore a healthy balance. But, in the cas Continue reading >>

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