Question 62: A metabolic condition in which the capacity of the body to buffer OH- is diminished, is called: (A) Acidosis (B) Alkalosis (C) Kurtosis (D) Lipidosis

Question 62:

A metabolic condition in which the capacity of the body to buffer OH– is diminished, is called:

(A) Acidosis
(B) Alkalosis
(C) Kurtosis
(D) Lipidosis

The correct answer is (B) Alkalosis.

A metabolic condition where the body loses buffering capacity against OH⁻ (hydroxide/base) leads to alkalosis, characterized by elevated blood pH (>7.45) due to excess bicarbonate or base gain.

Option Breakdown

(A) Acidosis

Acidosis occurs when buffering against H⁺ is overwhelmed (pH <7.35), opposite of diminished OH⁻ buffering.​

(B) Alkalosis

Correct; metabolic alkalosis specifically shows reduced ability to neutralize excess OH⁻/HCO₃⁻ from vomiting, diuretics, or alkali loads, raising pH via renal H⁺ loss maintenance.

(C) Kurtosis

Kurtosis is a statistics term measuring distribution peakedness, unrelated to acid-base metabolism.​

(D) Lipidosis

Lipidosis refers to lipid storage disorders (e.g., Tay-Sachs), not acid-base imbalance.​

Introduction to Buffer OH Diminished Alkalosis

Buffer OH diminished alkalosis describes metabolic alkalosis where bicarbonate buffering fails against base excess, elevating pH >7.45. Critical for GATE Life Sciences acid-base physiology questions.

Mechanism of Metabolic Alkalosis

Generation phase: H⁺ loss (vomiting gastric HCl) or HCO₃⁻ gain (antacids). Maintenance: hypokalemia/volume contraction impairs renal HCO₃⁻ excretion. Symptoms include tetany, confusion from hypocalcemia.
ABG shows pH↑, HCO₃⁻↑, PaCO₂↑ (respiratory compensation).

Conditions Comparison Table

Option Acid-Base Effect pH Change Key Feature ​
Acidosis Excess H⁺ ↓ (<7.35) Lactic, ketoacidosis
Alkalosis OH⁻ buffering fail ↑ (>7.45) Vomiting, diuretics
Kurtosis Statistical measure N/A Distribution shape
Lipidosis Lipid accumulation N/A Storage disorders

Identifies buffer OH diminished alkalosis precisely.​

Exam Relevance for Life Sciences Students

Connects prior enzyme kinetics (Kd substrate binding), lipids (membrane stability affects ion channels), liver failure (lactic acidosis risk); master chloride-responsive vs. resistant alkalosis for PYQs.​

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