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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