Posted: February 16th, 2023

Describe the pathophysiology, clinical manifestations, evaluation, and treatment of metabolic acidosis and metabolic alkalosis.

Metabolic acidosis and metabolic alkalosis are two distinct pathophysiologic states in which the pH of the blood is outside of its normal range. Metabolic acidosis occurs when there is too much acid present in the body, leading to a decrease in arterial pH, while metabolic alkalosis occurs when there is an excess of bicarbonate ions and an increase in arterial pH. Both conditions can be caused by either primary or secondary processes that lead to imbalances in the body’s acid-base balance.

Pathophysiology: Metabolic acidosis occurs when acids accumulate faster than they can be eliminated from the body, leading to a decrease in serum bicarbonate levels and an increase in plasma hydrogen ion concentration (H+). This may be due to several primary causes such as renal tubular defects or excessive production of lactic acid through increased exercise or tissue hypoperfusion. Secondary causes include ingestion of toxins like alcohol, antifreeze, ethylene glycol; prolonged diarrhea with loss of bicarbonates; pancreatitis; ketoacidosis associated with diabetes mellitus; and hyperchloremic non-anion gap metabolic acidoses due to mineralocorticoid deficiency or ingestion of diuretics that result in decreased urinary excretion of HCO3-.

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Clinical Manifestations: The clinical manifestations depend on the degree and severity of imbalance present. In mild cases only nonspecific symptoms may manifest such as tachycardia, lethargy/malaise, nausea/vomiting, weakness/fatigue, abdominal pain/cramping etc., whereas more severe cases may cause confusion/disorientation along with other CNS disturbances including seizures and coma. Depending upon underlying etiology one may also experience polyuria and polydipsia suggestive for diabetes mellitus while chronic alcohol ingestion might lead to Korsakoff’s psychosis.

Evaluation: Evaluation should begin with collecting patient history followed by physical exam looking for signs suggestive for underlying cause such as altered mentation suggest CNS pathology or presence of jaundice indicating hepatic dysfunction etc.. Laboratory testing includes measuring various electrolytes (Sodium [Na+],Potassium[K+],Chloride[Cl-] & Bicarbonate [HCO3-]) along with ABG(arterial blood gas) analysis which not only provides information about pH but also helps differentiate between respiratory vs metabolic disorders affecting Acid Base equilibrium.

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Anion gap calculation will help identify if it is high anion gap metabolic acidaemia ie additional unmeasured negatively charged species are accumulating alongside sodium & potassium like lactate ,ketone bodies ,sulphatides etc..While low Anion Gap will indicate presence toxic ingestions causing Non Anion Gap Acidaemia .In addition urine osmolality measurement helps determine whether kidney’s ability to conserve filtered water has been affected thus contributing towards volume depletion resulting into compensatory response & consequent abnormal Acid base status .If drug induced toxicity suspected then acetaminophen level estimation might provide invaluable input regarding prognosis & management strategy .

Describe the pathophysiology, clinical manifestations, evaluation, and treatment of metabolic acidosis and metabolic alkalosis.

Treatment: Treatment modalities depend upon severity & underlying cause responsible for shifting Acid Base equilibrium away from homeostasis .Mild forms require no specific therapy except removal /minimizationof causative factor somewhat ensuring reversal back towards normalcy .More severe forms needs aggressive medical intervention sometimes requiring emergent Hemodialysis , depending upon gravity & type off Advanced Renal Failure present simultaneously besides disease process responsible for triggering disturbance initially .

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Buffer System Response :The first line defense against Acid –Base Imbalance lies within buffer system itself comprising combination off Bases (like Sodium Bicarbonate)& Weak Acids(like Phosphoric Acid )which quickly reacts quantitatively neutralizing any free H+ ions released during degradation off organic compounds supplying energy needs e thereby preventing drastic fall off serum PH levelsAlso known as “Piston Mechanism” because it tends pushing balanced equation back towards neutrality regardless whatever directionhas shifted initially providing temporary compensation until specified agents reached kidneys where final correction happens via renal clearance mechanism having capacity clear out any excesses circulating around intravascular space returning things back towards equilibrium again ..In case off acute Metabolic Alkalemia though two systems mentioned above plays vital role however third component termed Chloride Shift takes part functioning similar way opposite occurring whenever chloride levels drops promoting shift order compensate restoring balance ..

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