Respo – Biochem

✅ Sphingosine

🧠 Explanation (Why this is correct):

The main difference between glycerophosphatides (phosphoglycerides) and phosphosphingolipids lies in the backbone molecule:

• Glycerophosphatides have a glycerol backbone.

  • Examples: phosphatidylcholine (lecithin), phosphatidylethanolamine, phosphatidylserine

  • Structure: Glycerol + 2 fatty acids + phosphate + polar head group

• Phosphosphingolipids have a sphingosine backbone instead of glycerol.

  • Examples: sphingomyelin

  • Structure: Sphingosine + 1 fatty acid (amide-linked) + phosphate + polar head group

Thus, the presence of sphingosine in phosphosphingolipids is the defining structural difference from glycerophosphatides.

✅ Therefore, Sphingosine is the correct answer.

❌ Explanation of Incorrect Options:

Phosphatides
❌ Wrong — This is a general term for all phospholipids, including both glycerophosphatides and phosphosphingolipids. It does not distinguish between them.

Plasmalogens
❌ Wrong — Plasmalogens are ether-linked glycerophospholipids, a subtype of glycerophosphatides, not the defining difference with phosphosphingolipids.

Lipositol
❌ Wrong — Likely a misspelling of phosphatidylinositol, which is a glycerophosphatide. It is a head group, not the backbone, so it does not differentiate the two classes.

Lecithin
❌ Wrong — Lecithin is phosphatidylcholine, a type of glycerophosphatide. Again, it is a specific example, not the structural differentiator.

✅ Lipase

🧠 Explanation (Why this is correct):

Lipases are enzymes that hydrolyze lipids (fats) into their basic components — fatty acids and glycerol.

There are different types of lipases depending on the substrate:

• Pancreatic lipase acts on triglycerides in the small intestine.

• Phospholipase acts on phospholipids, breaking them into fatty acids and glycerophosphates.

• Lipoprotein lipase acts on chylomicrons and VLDL to release fatty acids for tissue use.

In general, when a question mentions breakdown of phospholipids (or fats) into fatty acids and glycerol, the key enzyme category is lipase.

✅ Hence, Lipase is the correct answer.

❌ Explanation of Incorrect Options:

Phosphatidyl phosphorylase
❌ Wrong — This enzyme does not exist in standard lipid metabolism. The name suggests a phosphorylase acting on a phosphatidyl compound, which is not a known metabolic reaction.

Phosphatidyl kinase
❌ Wrong — Kinases add phosphate groups (phosphorylation), not remove or break down molecules. This enzyme would be involved in synthesis, not breakdown.

Phosphorylase
❌ Wrong — Phosphorylases cleave compounds by adding phosphate (as in glycogen phosphorylase), producing phosphorylated products — not fatty acids and glycerol.

Amylase
❌ Wrong — Amylase digests starches and glycogen into maltose and glucose, not lipids. It acts on carbohydrates, not fats.

✅ Lecithin/sphingomyelin ratio of less than 2

🧠 Explanation (Why this is correct):

This question describes a preterm neonate with tachypnea, respiratory distress, and cyanosis — classic signs of neonatal respiratory distress syndrome (NRDS), also known as hyaline membrane disease.

Pathophysiology:

• The disease results from surfactant deficiency in immature lungs.

• Surfactant, produced by type II pneumocytes, reduces alveolar surface tension and prevents alveolar collapse.

• It mainly contains lecithin (phosphatidylcholine) and sphingomyelin.

During fetal lung maturation:

• Sphingomyelin remains relatively constant.

• Lecithin levels rise sharply after 32–34 weeks of gestation as surfactant production increases.

• Therefore, the lecithin/sphingomyelin (L/S) ratio in amniotic fluid is a good indicator of fetal lung maturity.

In infants of diabetic mothers, fetal hyperinsulinemia delays surfactant synthesis, so even after 34 weeks, the L/S ratio may remain < 2, predisposing to NRDS.

✅ Therefore, an L/S ratio of less than 2 indicates immature lungs and is consistent with the clinical findings.

❌ Explanation of Incorrect Options:

Lecithin/sphingomyelin ratio of more than 2
❌ Wrong — Indicates lung maturity and low risk of RDS. This patient clearly has respiratory distress due to surfactant deficiency, not mature lungs.

Lecithin/sphingomyelin ratio of more than 5
❌ Wrong — This value is unusually high and not physiologically relevant. L/S ratios rarely exceed 3–4 even in very mature lungs.

Lecithin/sphingomyelin ratio of less than 5
❌ Wrong — Technically true but nonspecific; the critical threshold for immaturity is < 2, not < 5.

Lecithin/sphingomyelin ratio of less than 1
❌ Wrong — Would indicate severely immature lungs, typically seen in very premature infants (<30 weeks). At 34 weeks, with maternal diabetes, the ratio is more likely < 2, not necessarily < 1.

✅ Correct Answer: Dipalmitoyl phosphatidylcholine

Explanation:
The major component of pulmonary surfactant is dipalmitoyl phosphatidylcholine (DPPC), a phospholipid synthesized and secreted by Type II alveolar cells (Type II pneumocytes).

Functions of DPPC (surfactant):

• Reduces alveolar surface tension, preventing alveolar collapse (atelectasis) during expiration.

• Increases lung compliance, making it easier for the lungs to expand during inspiration.

• Helps maintain alveolar stability by keeping small alveoli from collapsing into larger ones (as explained by Laplace’s law).

Surfactant also contains phosphatidylglycerol, apoproteins (SP-A, SP-B, SP-C, SP-D), and small amounts of cholesterol, but DPPC is its primary and most functionally important lipid component.

❌ Phosphatidyl lecithin
An older term that sometimes refers to phosphatidylcholine, but DPPC is the specific surfactant molecule responsible for reducing surface tension.

❌ Cerebrosides
These are glycolipids found in myelin sheaths of neurons, not in alveoli.

❌ Gangliosides
Complex glycolipids in neuronal membranes, also unrelated to surfactant.

❌ None of these
Incorrect, since DPPC is clearly the main surfactant component.

✅ Correct Answer: pH meter

Explanation:
A pH meter is an electronic instrument used to measure the hydrogen ion concentration (pH) of a solution accurately.
It works by using a pH electrode (sensitive to H⁺ ions) and a reference electrode to detect a voltage difference that corresponds to the pH value, which is then displayed on the meter.

The measurement principle is based on the Nernst equation, which relates the electrical potential difference to ion concentration.
This makes pH meters more precise than visual methods such as indicators or litmus paper.

❌ pH electrode
It’s the sensor component of the pH meter, not the complete measuring device.

❌ pH detector
A non-standard term; it does not refer to an actual instrument.

❌ pH scale
A numerical range (0–14) used to express acidity or alkalinity — not a tool for measurement.

❌ pH color
Refers to color changes seen with indicators (like litmus or phenolphthalein), but not a method of precise measurement.

✅ Correct Answer: Henderson–Hasselbalch equation

Explanation:
The Henderson–Hasselbalch equation describes the relationship between the pH of a buffer solution, the acid dissociation constant (pKa), and the ratio of conjugate base to acid concentrations:

pH=pKa+log⁡([A−][HA])\text{pH} = \text{pKa} + \log\left(\frac{[\text{A}^-]}{[\text{HA}]}\right)pH=pKa+log([HA][A−]​)

When the concentrations of the acid (HA) and its conjugate base (A⁻) are equal, the ratio [A−][HA]\frac{[\text{A}^-]}{[\text{HA}]}[HA][A−]​ = 1, and since log⁡(1)=0\log(1) = 0log(1)=0:

pH=pKa\text{pH} = \text{pKa}pH=pKa

This condition represents the most effective buffering point, where the buffer resists changes in pH most efficiently.

❌ Water dissociation equation
Refers to the self-ionization of water (Kw=[H+][OH−])(K_w = [H^+][OH^-])(Kw​=[H+][OH−]), not related to acid–base buffer systems.

❌ Hardy–Weinberg equation
Used in population genetics, not chemistry or acid–base balance.

❌ Torricelli’s theorem
A physics principle about fluid flow velocity — unrelated to pH.

❌ pH log equation
A vague term — pH is defined as −log⁡[H+]-\log[H^+]−log[H+], but this does not relate to buffer equilibrium or pKa relationships.

✅ Correct Answer: Strenuous exercise

Explanation:
A rightward shift of the oxygen–hemoglobin dissociation curve indicates that hemoglobin’s affinity for oxygen decreases, allowing more O₂ to be released to the tissues.
During strenuous exercise, several physiological changes occur that collectively cause this shift:

1. Increased temperature

2. Increased CO₂ (hypercapnia)

3. Decreased pH (acidosis) — due to lactic acid buildup

4. Increased 2,3-DPG (diphosphoglycerate) in red blood cells

These changes enhance oxygen unloading from hemoglobin to meet the higher metabolic demands of active muscles — an effect known as the Bohr effect.

❌ Low concentration of 2,3-DPG
Would shift the curve to the left, increasing hemoglobin’s affinity for oxygen and reducing release to tissues.

❌ Fetal hemoglobin
Has higher O₂ affinity, shifting the curve to the left, which helps the fetus extract oxygen from maternal blood.

❌ Low temperature
Also shifts the curve to the left, favoring oxygen binding rather than release.

❌ High pH
Alkalosis decreases H⁺ concentration, stabilizing oxyhemoglobin and shifting the curve to the left.

✅ Correct Answer: pH meter

Explanation:
A pH meter is the instrument used to determine the pH value of a solution. It measures the hydrogen ion concentration (H⁺) indirectly using a pH electrode (glass electrode) and a reference electrode.

Here’s how it works:

• The glass electrode generates a potential (voltage) that depends on the H⁺ ion activity in the solution.

• This potential difference is compared to the reference electrode.

• The meter then converts the voltage difference into a pH value based on the Nernst equation.

This method provides accurate and quantitative pH readings, unlike pH paper or indicators, which give only approximate results.

❌ pH spectrometer
No such instrument exists; spectrometers measure light absorption, not pH.

❌ pH electrode
It’s a component of a pH meter, not the measuring device itself. It senses the H⁺ concentration but needs the pH meter to display the reading.

❌ pH balancer
A non-scientific term — refers generally to substances or systems that adjust pH, not measure it.

❌ pH detector
A vague term; not a recognized laboratory instrument for precise measurement.

✅ Correct Answer: Carbonic anhydrase

Explanation:
Carbonic anhydrase is the enzyme that catalyzes the reversible reaction between carbon dioxide (CO₂) and water (H₂O) to form carbonic acid (H₂CO₃), which then dissociates into bicarbonate (HCO₃⁻) and hydrogen (H⁺) ions:

CO₂+H₂O↔Carbonic anhydraseH₂CO₃↔H⁺+HCO₃⁻\text{CO₂} + \text{H₂O} \xleftrightarrow{\text{Carbonic anhydrase}} \text{H₂CO₃} \leftrightarrow \text{H⁺} + \text{HCO₃⁻}CO₂+H₂OCarbonic anhydrase​H₂CO₃↔H⁺+HCO₃⁻

This reaction is essential for:

• CO₂ transport in the blood (as bicarbonate),

• Regulation of blood pH through buffering, and

• CO₂ elimination in the lungs.

Carbonic anhydrase is abundant in red blood cells, renal tubular cells, and parietal cells of the stomach.

❌ Acetylcholinesterase
Breaks down acetylcholine into acetate and choline at neuromuscular junctions; unrelated to CO₂ transport.

❌ Alkaline phosphatase
Removes phosphate groups from molecules; found in liver, bone, and placenta, not involved in CO₂ hydration.

❌ Adenylate cyclase
Converts ATP to cyclic AMP (cAMP) — part of intracellular signaling, not acid–base balance.

❌ Protein kinase
Transfers phosphate groups to proteins (phosphorylation), regulating cellular activity; unrelated to bicarbonate formation.

✅ Correct Answer: Arachidonic acid

Explanation:
Prostaglandins are lipid mediators derived from arachidonic acid, a 20-carbon polyunsaturated fatty acid present in membrane phospholipids.
When cells are stimulated (e.g., by inflammation, trauma, or hormones), the enzyme phospholipase A₂ releases arachidonic acid from the membrane.
It is then converted into prostaglandins, thromboxanes, and prostacyclins through the cyclooxygenase (COX-1 and COX-2) pathways.

These molecules play important roles in:

• Inflammation (pain, fever, redness)

• Smooth muscle contraction

• Gastric mucosal protection

• Platelet aggregation regulation

❌ Nitric oxide
A gaseous signaling molecule synthesized from arginine, not a fatty acid. It mediates vasodilation, not prostaglandin formation.

❌ Arginine
An amino acid used for nitric oxide synthesis, urea cycle, and protein formation — not for prostaglandins.

❌ Glucose
A carbohydrate and main energy source; not directly involved in prostaglandin synthesis, which follows a lipid pathway.

❌ Oxygen
Although oxygen atoms are incorporated into prostaglandin molecules during COX-mediated reactions, it is not the substrate for synthesis — arachidonic acid is.

✅ Correct Answer: Acid and conjugate base

A buffer solution resists changes in pH when small amounts of acid or base are added. This property arises from the presence of a weak acid and its conjugate base (or vice versa).

• The weak acid neutralizes added bases, while the conjugate base neutralizes added acids.

• The Henderson–Hasselbalch equation,

  pH=pKa+log⁡([A−][HA])\text{pH} = \text{pKa} + \log\left(\frac{[\text{A}^-]}{[\text{HA}]}\right)pH=pKa+log([HA][A−]​)

  shows that the pH of a buffer depends on the ratio of acid to conjugate base concentrations, not just on one component alone.

❌ Weak and strong acid
A strong acid completely dissociates and destroys the buffering capacity. Buffer systems require partial ionization to maintain equilibrium, which a strong acid cannot provide.

❌ Strong acid
A strong acid has no ability to resist pH change because it dissociates fully, drastically altering [H⁺] concentration even with small additions.

❌ Weak acid
A weak acid alone cannot form a buffer; it needs its conjugate base to neutralize added H⁺ ions effectively.

❌ Weak base
Similarly, a weak base alone cannot form a buffer. A conjugate acid–base pair is necessary to resist both acid and base addition.

✅ Metabolic acidosis — Correct.
In metabolic acidosis, excess H⁺ ions lower blood pH. To compensate, the respiratory center increases ventilation (hyperventilation), reducing arterial PCO₂. This lowers carbonic acid levels and helps restore pH toward normal — a mechanism known as respiratory compensation (as seen in Kussmaul breathing in diabetic ketoacidosis).

❌ Metabolic alkalosis — Would cause hypoventilation to retain CO₂.
❌ Respiratory alkalosis — The problem is excessive ventilation itself, so lungs cannot compensate further.
❌ Respiratory acidosis — Compensation is metabolic (via kidneys), not respiratory.
❌ No compensation — The body always attempts some form of compensation for acid–base imbalance.

✅ Impaired surfactant production — Correct.
A decreased lecithin–sphingomyelin (L/S) ratio indicates insufficient surfactant production by type II pneumocytes, suggesting immature lungs and a high risk of respiratory distress syndrome (RDS/ARDS). Normally, an L/S ratio ≥ 2:1 means adequate surfactant and mature lungs.

❌ Adequate surfactant production — Would show a high (≥2:1) L/S ratio.
❌ Adequate lung maturity — Also corresponds to a high ratio.
❌ Increased risk of cardiogenic pulmonary edema — Not related to surfactant levels.
❌ Pneumonia — An infectious cause of respiratory distress, not tied to the L/S ratio.

✅ Lipoxygenase (LOX) — Correct.
Arachidonic acid can follow two main enzymatic pathways:

• The cyclooxygenase (COX) pathway → forms prostaglandins and thromboxanes.

• The lipoxygenase (LOX) pathway → forms leukotrienes.

Lipoxygenase adds oxygen to arachidonic acid to produce hydroperoxy eicosatetraenoic acid (HPETE), which is then converted into leukotrienes (LTB₄, LTC₄, LTD₄, LTE₄) — key mediators of inflammation and bronchoconstriction.

❌ Cyclooxygenase (COX) — Forms prostaglandins and thromboxanes, not leukotrienes.
❌ Prostaglandin synthase — Works downstream of COX in the prostaglandin pathway.
❌ Phospholipase A₂ — Releases arachidonic acid from membrane phospholipids (upstream step).
❌ Thromboxane synthase — Converts prostaglandin H₂ to thromboxane A₂, not leukotrienes.

✅ 1 : 20 — Correct.
At physiologic pH (7.4), the bicarbonate (HCO₃⁻) to carbonic acid (H₂CO₃) ratio is approximately 20:1.

Using the Henderson–Hasselbalch equation:

pH = pKa + log ([HCO3⁻] / [H2CO3])

7.4 = 6.1 + log (ratio)
log (ratio) = 1.3
ratio ≈ 20:1

✅ Correct Answer: Respiratory acidosis

Explanation:

• Step 1: Analyze the pH
  • pH = 7.1 → acidic (normal = 7.35–7.45).
  • Indicates acidemia.
• Step 2: Look at PCO₂
  • PCO₂ = 56 mmHg → elevated (normal = 35–45 mmHg).
  • High CO₂ causes respiratory acidosis because CO₂ combines with water to form carbonic acid, lowering pH.
• Step 3: Look at HCO₃⁻
  • HCO₃⁻ = 25 mmol/L → near normal (normal = 22–28 mmol/L).
  • Indicates renal compensation has not yet fully occurred (acute respiratory acidosis).
• Step 4: Conclusion
  • Elevated PCO₂ with low pH → primary respiratory acidosis.

Why the other options are incorrect:

• Respiratory alkalosis: ❌
  → Caused by low CO₂, pH would be high. Here, CO₂ is high and pH is low.
• Metabolic alkalosis: ❌
  → HCO₃⁻ would be high, pH high. Here, HCO₃⁻ is normal, pH low.
• Metabolic acidosis: ❌
  → HCO₃⁻ would be low; primary problem is not CO₂. Here, HCO₃⁻ is normal, CO₂ is high.
• Pulmonary edema: ❌
  → Can cause hypoxia, but the ABG changes specifically point to respiratory acidosis, not metabolic disturbance.

✅ Correct answer: Lipase

Explanation:

Lipase is the enzyme that catalyzes the breakdown (hydrolysis) of fats or phospholipids into fatty acids and glycerol. It acts on the ester bonds within lipids, releasing free fatty acids and glycerol molecules — a key step in lipid digestion and metabolism.

❌ Phosphatidyl phosphorylase – involved in phosphorylase-type cleavage, not in breaking lipids into fatty acids and glycerol.

❌ Phosphatidyl kinase – adds phosphate groups (phosphorylation), not hydrolysis of fats.

❌ Phosphorylase – catalyzes the addition of a phosphate group to break down glycogen or starch, not fats.

❌ Amylase – digests carbohydrates (starch to maltose), not lipids.

🔹 Composition of Pulmonary Surfactant:

• ~90% lipids (mostly phospholipids)

• ~10% proteins (surfactant proteins A, B, C, and D)

Among the lipids, the key functional component is Dipalmitoylphosphatidylcholine 

🔹 Dipalmitoylphosphatidylcholine (DPPC):

• Also known as lecithin.

• Structurally, it is a phosphatidylcholine molecule with two palmitic acid (16-carbon saturated fatty acids) esterified to the glycerol backbone.

• Its saturated chains allow tight packing, giving it strong surface tension–lowering properties.

• When the alveoli shrink during expiration, DPPC becomes more concentrated at the air–liquid interface, stabilizing alveoli and preventing collapse.

❌ Why the Other Options Are Incorrect:

• Monopalmitoylphosphatidylethanolamine:

  • Not a major constituent of surfactant.

  • Phosphatidylethanolamine is present in cell membranes but does not significantly reduce alveolar surface tension.

• Triacylglycerol:

  • Main storage form of fat, not a surfactant component.

  • Nonpolar and lacks the amphipathic (hydrophilic-hydrophobic) property needed for air–liquid interface stability.

• Cardiolipin:

  • Found mainly in mitochondrial inner membranes, essential for oxidative phosphorylation.

  • Not involved in alveolar surface tension regulation.

• Ceramide:

  • A sphingolipid component of cell membranes involved in signaling and apoptosis.

  • Not a surfactant molecule and has no role in lowering surface tension.

🩺 Clinical Correlates:

• Neonatal Respiratory Distress Syndrome (NRDS):

Caused by deficiency of surfactant, especially DPPC, in premature infants (before 34 weeks gestation).

Leads to alveolar collapse, hypoxemia, and formation of hyaline membranes.

• Adult Respiratory Distress Syndrome (ARDS):

In adults, surfactant production or function may be impaired due to alveolar damage, sepsis, or inhalation injury, leading to alveolar instability and hypoxia.

The chloride shift (also called the Hamburger phenomenon) is a process that maintains electrical neutrality in red blood cells (RBCs) during gas exchange.

Here’s what happens step by step:

1. CO₂ diffuses from tissues into RBCs.

2. Inside RBCs, carbonic anhydrase catalyzes the reaction:

   CO2​+H2​O↔H2​CO3​↔H++ HCO3−​

3. The HCO₃⁻ (bicarbonate) ions formed diffuse out of the RBC into the plasma.

4. To maintain charge balance, Cl⁻ ions move into the RBC from plasma.
   → This inward movement of chloride is the chloride shift.

❌ Why Other Options Are Incorrect

• Chloride ions: Move into the RBC, not out — that’s the defining feature of the chloride shift.

• Potassium ions: Involved in maintaining osmotic balance but not in this exchange.

• Calcium ions: Play no direct role in CO₂ transport or chloride shift.

• Sodium ions: Remain primarily extracellular and do not participate in the bicarbonate exchange.

Henderson–Hasselbalch Equation
pH = pKa + log([A-] / [HA])

When acid and base are in equal concentrations:

If
[A-] = [HA]

then
[A-] / [HA] = 1

and since
log(1) = 0

→ pH = pKa

This is the buffer’s point of maximum buffering capacity, where the solution resists pH changes most effectively.

Why the Other Options Are Incorrect:

The lipid membrane (cell membrane or plasma membrane) is primarily made up of a phospholipid bilayer, which forms the basic structural framework of all biological membranes.

🧩 Main components of the membrane:

1. Phospholipids → most abundant

   • Amphipathic molecules (hydrophilic head + hydrophobic tail)

   • Arrange as a bilayer, forming a semi-permeable barrier

2. Cholesterol → stabilizes membrane fluidity and integrity

3. Glycolipids and sphingolipids → present in smaller amounts, important for cell recognition and signaling

4. Proteins → embedded within or attached to the lipid bilayer

⚖️ Relative Abundance:

To break down phosphoglycerides, the body uses phospholipases — enzymes that cleave specific bonds in phospholipids.

These enzymes are essential for:

• Membrane remodeling

• Signal transduction (e.g., phospholipase C in IP₃/DAG pathway)

• Arachidonic acid release for prostaglandin synthesis

❌ Why Other Options Are Incorrect

• Sphingomyelinase: Breaks down sphingomyelin (a sphingolipid), not phosphoglycerides.

• Lipofructokinase: No such enzyme exists — possibly a distractor term.

• Transferase: Transfers functional groups but doesn’t hydrolyze phospholipids.

• Phosphatase: Removes phosphate groups, not the glyceride bonds.

Phospholipase A₂ (PLA₂) is a hydrolytic enzyme that specifically acts on phosphoglycerides (phospholipids) — major components of cell membranes.

✳️ Reaction Catalyzed by PLA₂:

It cleaves the ester bond at the C2 position of glycerophospholipids → releasing:

• A free fatty acid (commonly arachidonic acid)

• A lysophospholipid

This released arachidonic acid is the key precursor for eicosanoids (prostaglandins, thromboxanes, leukotrienes), which mediate inflammation and immunity.

❌ Why Other Options Are Incorrect:

• Synthesis of triacylglycerol (TAG):
  → Involves acyltransferases, not phospholipases.

• Breakdown of triacylglycerol (TAG):
  → Done by lipases (e.g., hormone-sensitive lipase, lipoprotein lipase), not PLA₂.

• Breakdown of sphingomyelin:
  → Done by sphingomyelinase, not phospholipase A₂.

• Breakdown of sphingolipid:
  → Involves ceramidase or glycosidases, not PLA₂.

✅ Correct Answer:

Arachidonic acid

Prostaglandins are synthesized from arachidonic acid, a 20-carbon polyunsaturated fatty acid found in cell membrane phospholipids.
When cells are stimulated (e.g., by injury, inflammation, or hormones), phospholipase A₂ releases arachidonic acid from membrane phospholipids.
It is then converted into prostaglandin H₂ (PGH₂) through the cyclooxygenase (COX) pathway — the first step catalyzed by COX-1 and COX-2 enzymes.
PGH₂ serves as the common precursor for various prostaglandins, prostacyclins, and thromboxanes that regulate inflammation, vascular tone, and platelet function.

❌ Incorrect Options:

• Nitric oxide — ❌ A gaseous signaling molecule involved in vasodilation, not in prostaglandin synthesis.

• Arginine — ❌ Precursor for nitric oxide, not prostaglandins.

• Glucose — ❌ Used in energy metabolism, not in eicosanoid formation.

• Oxygen — ❌ Required as a reactant by the COX enzyme, but not the substrate from which prostaglandins are synthesized.

A buffer solution is a solution that maintains a nearly constant pH when small quantities of acid or base are added. It does so by containing a weak acid and its conjugate base (or a weak base and its conjugate acid). These components react with any added hydrogen ions (H⁺) or hydroxide ions (OH⁻), preventing large shifts in pH.

In biological systems, maintaining pH is critical — for example, blood is buffered by the carbonic acid–bicarbonate system (H₂CO₃/HCO₃⁻), keeping its pH around 7.4.

❌ Why Other Options Are Incorrect:

• Super-saturated solution: Contains more solute than normally possible at a given temperature; it relates to solubility, not pH stability.

• Strong acid solution: Completely ionizes and drastically changes pH with even small additions of acid or base.

• Unsaturated solution: Has not reached the limit of solute dissolution; again, unrelated to pH buffering.

• Saturated solution: Contains maximum solute at equilibrium, but it does not resist pH changes.

To measure pH accurately, we use a pH meter, which works by detecting the electrical potential difference between two electrodes — typically a glass electrode (sensitive to H⁺ concentration) and a reference electrode (like a calomel or silver/silver chloride electrode).

When these are placed in a solution, the potential difference correlates with the hydrogen ion concentration. The pH meter translates this voltage difference into a numerical pH value displayed on its screen.

Hence, a pH meter is the correct and precise instrument used for determining pH.

❌ Why Other Options Are Incorrect:

• pH spectrometer:
  Spectrometers measure light absorption, not hydrogen ion concentration. Used in spectrophotometry, not pH measurement.

• pH electrode:
  This is only a component of the pH meter (the sensing part), not a standalone instrument for measuring pH.

• pH balancer:
  Not a scientific instrument — refers to cosmetic or chemical products that maintain a certain pH, not measure it.

• pH detector:
  Nonstandard term; there’s no laboratory instrument officially called this.

Pure water is neutral, meaning it has an equal concentration of hydrogen ions (H⁺) and hydroxide ions (OH⁻).

At 25°C, the concentration of both ions is 1 × 10⁻⁷ mol/L.

Thus, the pH of pure water is 7, which is considered neutral — neither acidic nor basic.

However, note that this value slightly changes with temperature (it decreases slightly as temperature rises), but neutrality always occurs when [H+]=[OH−].

❌ Why the Other Options Are Incorrect:

• pH 11: Indicates a strongly basic (alkaline) solution — much fewer H⁺ ions than in water.

• pH 5: Indicates a slightly acidic solution — more H⁺ ions than OH⁻ ions.

• pH 9: Also alkaline, suggesting an excess of hydroxide ions.

• pH 3: Represents a strongly acidic solution — far higher concentration of H⁺ ions than in neutral water.

The bicarbonate buffer system (H₂CO₃ / HCO₃⁻) is the most important and effective physiological buffer in maintaining blood pH (≈7.4).
It functions through the carbonic acid–bicarbonate equilibrium:

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

• The lungs regulate CO₂ (acid component).

• The kidneys regulate HCO₃⁻ (base component).

This dual control provides a rapid and powerful mechanism for pH maintenance, especially during respiratory or metabolic disturbances.

❌ Why the Other Options Are Incorrect:

• Phosphate buffer: Important intracellularly and in the kidneys, but present in low concentration in plasma.

• Potassium, Calcium, Sodium: These are ions involved in many physiological processes but not buffering agents.

🩺 Clinical Correlation:

In respiratory acidosis (e.g., COPD), CO₂ retention shifts the equilibrium rightward, lowering pH.
In metabolic acidosis (e.g., diabetic ketoacidosis), bicarbonate is consumed buffering excess H⁺ — leading to compensatory hyperventilation (Kussmaul breathing) to expel CO₂ and restore pH balance.

✅ Correct Answer:

Phosphate

In phospholipids, the phosphate group is the simplest hydrophilic (water-attracting) moiety.
Phospholipids have a polar head and nonpolar tails:

• The phosphate group (often linked to other molecules like choline or ethanolamine) forms the hydrophilic head, which interacts with water.

• The fatty acid chains form the hydrophobic tails, which repel water.

This dual nature (amphipathic property) allows phospholipids to form bilayers, the structural basis of cell membranes.

❌ Incorrect Options:

• Hydroxyl — ❌ Present in some lipids, but not the main hydrophilic group in phospholipids.

• Sulfate — ❌ Found in glycolipids and proteoglycans, not in standard phospholipids.

• Glucose — ❌ Found in glycolipids, not phospholipids.

• Carbons — ❌ Form the hydrophobic backbone of fatty acids, not hydrophilic.

✅ Correct Answer:

Respiratory acidosis

The symptoms described — shortness of breath, chest tightness, and difficulty breathing — suggest hypoventilation, which leads to CO₂ retention in the blood.
This increase in CO₂ raises the level of carbonic acid (H₂CO₃), resulting in a decrease in blood pH, a condition known as respiratory acidosis.

Common causes include chronic obstructive pulmonary disease (COPD), emphysema, and respiratory muscle weakness, all of which are more common in elderly patients.

❌ Incorrect Options:

• Compensatory respiratory alkalosis — ❌ The body never compensates acidosis with another respiratory disturbance; compensation here is metabolic (via renal H⁺ excretion).

• Respiratory alkalosis — ❌ Occurs due to hyperventilation (excessive CO₂ loss), seen in anxiety or high altitude — not in this patient.

• Metabolic alkalosis — ❌ Results from excessive loss of acid (e.g., vomiting) or retention of base, not from breathing difficulty.

• Metabolic acidosis — ❌ Caused by increased acid production or loss of bicarbonate (e.g., diabetic ketoacidosis), unrelated to hypoventilation.

✅ Correct Answer:

Sphingomyelinase

Sphingomyelinase is the enzyme responsible for degrading sphingomyelin into ceramide and phosphorylcholine.
This reaction is a key step in sphingolipid metabolism and occurs mainly in lysosomes.

A deficiency of sphingomyelinase leads to the accumulation of sphingomyelin within cells, causing Niemann–Pick disease (types A and B) — a lysosomal storage disorder characterized by hepatosplenomegaly, neurological symptoms, and foam cells in the bone marrow.

❌ Incorrect Options:

• Glucocerebrosidase — ❌ Breaks down glucocerebroside, not sphingomyelin; its deficiency causes Gaucher disease.

• Glucosidase — ❌ Hydrolyzes glycosidic bonds in carbohydrates; unrelated to sphingolipids.

• Phosphatase — ❌ Removes phosphate groups from molecules; not specific for sphingomyelin.

• Ceramidase — ❌ Degrades ceramide into sphingosine and fatty acid, a step that comes after sphingomyelin breakdown.

✅ Correct Answer:

Hydrogen ion concentration

The pH of a solution is defined as the negative logarithm of the hydrogen ion concentration:

pH=−log⁡[H+]\text{pH} = -\log [\text{H}^+]pH=−log[H+]

It expresses the acidity of a solution — the higher the hydrogen ion concentration, the lower the pH.

• pH < 7: Acidic

• pH = 7: Neutral

• pH > 7: Alkaline (basic)

This logarithmic scale makes it easier to represent wide variations in hydrogen ion concentration.

❌ Incorrect Options:

• Hydroxyl ion concentration — ❌ Used in calculating pOH, not pH.

• Strong acid — ❌ Refers to a substance, not a measurable quantity.

• Weak base — ❌ Affects pH indirectly but not what pH mathematically represents.

• Weak acid — ❌ Also influences pH, but pH itself is defined by [H⁺], not the acid type.

✅ Correct Answer:

Acid and conjugate base

The pH of a buffer solution depends on the ratio of a weak acid to its conjugate base (or a weak base to its conjugate acid).
This relationship is expressed by the Henderson–Hasselbalch equation:

pH=pKa+log⁡([A−][HA])\text{pH} = \text{pKa} + \log \left( \frac{[\text{A}^-]}{[\text{HA}]} \right)pH=pKa+log([HA][A−]​)

Where:

• [HA][HA][HA] = concentration of the weak acid

• [A−][A^-][A−] = concentration of the conjugate base

By adjusting this ratio, the buffer resists large changes in pH when small amounts of acid or base are added.

❌ Incorrect Options:

• Weak and strong acid — ❌ This combination doesn’t form a buffer; the strong acid completely dissociates.

• Strong acid — ❌ Alone, it cannot resist pH changes; it drastically alters pH with small additions.

• Weak base — ❌ Alone, it can’t buffer effectively without its conjugate acid.

• Weak acid — ❌ Needs its conjugate base to function as a buffer system.

✅ Correct Answer: Metabolic acidosis

Explanation:

Let’s interpret the arterial blood gas (ABG) values step-by-step:

• pH = 7.1 → Acidemia (since normal pH = 7.35–7.45).
• PCO₂ = 25 mmHg → Low (normal: 35–45 mmHg).
• HCO₃⁻ = 5 mmol/L → Low (normal: 22–26 mmol/L).

The primary abnormality is the low bicarbonate (HCO₃⁻), which causes a metabolic acidosis.

The low PCO₂ indicates compensatory respiratory alkalosis, as the lungs try to blow off CO₂ to raise the pH.

Hence, this is a metabolic acidosis with respiratory compensation.

❌ Respiratory alkalosis:

Would have low PCO₂ but normal or slightly decreased HCO₃⁻ due to renal compensation. Here, HCO₃⁻ is very low, pointing to metabolic origin.

❌ Respiratory acidosis:

Would have high PCO₂ and low pH, not seen here.

❌ Metabolic alkalosis:

Would have high HCO₃⁻ and high pH, opposite to the findings.

❌ Mixed disorder:

While mixed disorders can occur, here compensation fits a single primary disturbance (metabolic acidosis with expected respiratory response), not two independent disorders.

✅ Correct Answer:

Lung disease: causing increased retention of CO₂

Explanation:

Respiratory acidosis occurs when the lungs fail to eliminate carbon dioxide (CO₂) effectively. This retention of CO₂ leads to an increase in carbonic acid (H₂CO₃) formation, which dissociates into hydrogen ions (H⁺) and bicarbonate (HCO₃⁻) — thereby lowering blood pH and producing acidosis.

Common causes include chronic obstructive pulmonary disease (COPD), respiratory depression (e.g., due to sedatives or brainstem injury), and airway obstruction. The kidneys later compensate by retaining bicarbonate, but the primary problem lies in the lungs’ inability to excrete CO₂.

❌ Kidney disease, causing increased retention of bicarbonate

This would increase bicarbonate levels and lead to metabolic alkalosis, not acidosis.

❌ Kidney disease, causing increased excretion of bicarbonate

This results in metabolic acidosis, since the kidneys are losing base, not respiratory acidosis (which is CO₂-related).

❌ Lung disease, causing increased exhalation of CO₂

Increased exhalation of CO₂ leads to loss of acid and therefore respiratory alkalosis, not acidosis.

❌ Increased bicarbonate infusion

This increases blood pH and results in metabolic alkalosis, not acidosis.

When a person is nervous and hyperventilating, they exhale too much CO₂.
Less CO₂ → less carbonic acid (H₂CO₃) → pH rises (blood becomes alkaline) →
→ Respiratory alkalosis

❌ Respiratory acidosis

• Happens when there is hypoventilation (slow or shallow breathing).

• CO₂ builds up in the blood → forms more carbonic acid → lowers pH (acidic).

• Opposite of what happens in rapid breathing.
  ✅ Example: COPD, asthma attack, airway obstruction.

❌ Metabolic alkalosis

• This is caused by non-respiratory (metabolic) factors that increase blood pH,
  such as:

  • Excessive vomiting (loss of stomach acid)

  • Overuse of antacids or diuretics

• Not related to breathing rate.

• So, hyperventilation doesn’t cause metabolic alkalosis.

❌ Metabolic acidosis

• Caused by metabolic buildup of acids or loss of bicarbonate, e.g.:

  • Diabetic ketoacidosis

  • Lactic acidosis

  • Severe diarrhea (loss of bicarbonate)

• Again, not due to respiration — it’s a metabolic issue.

❌ Both respiratory acidosis and alkalosis

• They are opposites and cannot occur simultaneously.

  • One results from CO₂ retention (acidosis).

  • The other from CO₂ loss (alkalosis).

• The body can compensate for one, but not have both at once.

🧩 Summary Table

👉 So, rapid breathing due to nervousness → loss of CO₂ → respiratory alkalosis.

✅ Correct Answer: Carbonic anhydrase

Explanation:

Carbonic anhydrase is the enzyme responsible for catalyzing the reversible reaction between carbon dioxide (CO₂) and water (H₂O) to form carbonic acid (H₂CO₃), which then dissociates into bicarbonate (HCO₃⁻) and hydrogen ions (H⁺). This reaction is crucial for CO₂ transport in the blood and acid–base balance. It occurs rapidly inside red blood cells due to the presence of this enzyme. Without carbonic anhydrase, the reaction would be extremely slow, leading to inefficient CO₂ carriage and pH regulation.

❌ Alkaline phosphatase – Catalyzes the removal of phosphate groups from molecules such as nucleotides or proteins, not involved in CO₂ or bicarbonate metabolism.

❌ Acetylcholinesterase – Breaks down the neurotransmitter acetylcholine into acetate and choline at synapses; it plays no role in bicarbonate formation.

❌ Adenylate cyclase – Converts ATP into cyclic AMP (cAMP), a second messenger in hormonal signaling pathways, unrelated to CO₂ metabolism.

❌ Protein kinase – Enzyme that adds phosphate groups to proteins (phosphorylation), involved in intracellular signaling, not CO₂ hydration.

✅

Correct Answer: Henderson-Hasselbalch equation

Explanation:

The Henderson-Hasselbalch equation provides a relationship between pH, pKa, and the ratio of the concentrations of conjugate base and acid in a buffer system.

When the molar concentrations of the acid ([HA]) and its conjugate base ([A⁻]) are equal,

Thus, at this point, the acid is half dissociated, and this equality reflects the buffering capacity of the system — the pH resists change most effectively here.

❌ Water dissociation constant:

This refers to the ionization of water (Kw = [H⁺][OH⁻] = 1 × 10⁻¹⁴ at 25°C), not the acid–base relationship between conjugate pairs.

❌ Michaelis-Menten equation:

Describes enzyme kinetics, showing the relationship between substrate concentration and reaction velocity — unrelated to acid-base chemistry.

❌ Hardy-Weinberg equation:

A genetic equilibrium equation used in population genetics — not related to acid-base balance.

❌ Haldane equation:

Used in respiratory physiology, describing the relationship between oxygenation of hemoglobin and CO₂ transport — again, not relevant to buffer chemistry.

A buffer solution resists changes in pH when small amounts of acid or base are added.
It consists of a weak acid and its conjugate base (or a weak base and its conjugate acid).

The pH of a buffer is given by the Henderson–Hasselbalch equation:

pH = pKa + log ([A⁻] / [HA])

where:

• [A⁻] = concentration of conjugate base

• [HA] = concentration of weak acid

The ratio of conjugate base to acid determines the buffer’s pH and its ability to neutralize added acids or bases.

❌ Incorrect options:

• Weak and strong acid:
  A strong acid fully dissociates and overwhelms the equilibrium, destroying the buffering capacity.

• Strong acid:
  Fully dissociates and cannot resist pH changes; it has no conjugate base to maintain equilibrium.

• Weak base:
  A weak base alone is not a buffer; it needs its conjugate acid (often from a salt) to function as one.

• Weak acid:
  A weak acid alone cannot maintain pH; it must pair with its conjugate base to act as a buffer.

In the peripheral tissues, carbon dioxide (CO₂) is produced as a metabolic byproduct and diffuses into red blood cells. Inside the RBCs, carbonic anhydrase catalyzes the following reaction:

CO2​+H2​O⇌H2​CO3​⇌H++HCO3−​

Most of the CO₂ is converted to bicarbonate ions (HCO₃⁻), which then diffuse out of the RBCs into the plasma in exchange for chloride ions (a process called the chloride shift).

Thus, the majority of CO₂ in the blood (about 70%) is transported as bicarbonate (HCO₃⁻), not as dissolved CO₂ or bound to hemoglobin.

❌Why the Other Options Are Incorrect:

• In combination with carbonic anhydrase:
  Carbonic anhydrase is an enzyme, not a transport form. It facilitates the conversion of CO₂ to bicarbonate but does not carry CO₂ itself.

• In combination with H₂CO₃:
  Carbonic acid (H₂CO₃) is unstable and quickly dissociates into H⁺ and HCO₃⁻. Only a very small fraction of CO₂ exists in this transient form.

• In combination with Hb:
  About 20–25% of CO₂ is carried as carbaminohemoglobin (HbCO₂), where CO₂ binds to the globin part of hemoglobin. This is significant but not the main form.

• CO in the blood:
  Carbon monoxide (CO) forms carboxyhemoglobin, not involved in normal CO₂ transport. This option is unrelated and pathologic.

 The hydroxyl (–OH) groups on the glycerol are the simplest hydrophilic moieties present in these molecules:

• Hydroxyl groups are small, polar functional groups capable of hydrogen bonding with water — this confers hydrophilicity at a very basic chemical level.

• In glycerophospholipids, the glycerol backbone contributes hydroxyl groups that connect to fatty acids (via ester bonds) and to the phosphate group (via a phosphoester). Even before adding the phosphate-head substituent, those hydroxyls are intrinsic polar sites on the molecule.

• Because they are chemically simple (one oxygen and one hydrogen) yet capable of strong polar interactions, hydroxyls qualify as the simplest hydrophilic moiety within the phospholipid structure.

Note: Phosphate-containing head groups (e.g., phosphatidylcholine) are more strongly polar and are often referred to as the main hydrophilic head of phospholipids — but they are chemically larger and more complex than a single hydroxyl group.

❌ Why the Other Options Are Incorrect:

• Phosphate:
  Very polar and central to the phospholipid head, but chemically larger and more complex than a single hydroxyl group — not the “simplest” moiety.

• Cholesterol:
  A sterol that modulates membrane fluidity; it is largely hydrophobic with only a single small hydroxyl, and is not a hydrophilic moiety of phospholipids.

• Sulphate:
  A strongly charged group found in some specialised lipids (e.g., sulfatides), but not a standard component of common phospholipids and is more complex than a hydroxyl.

• Lipid:
  A broad category; most lipids are hydrophobic and the term isn’t a specific hydrophilic functional group.

✅ Correct Answer:

Two

Glycophospholipids (also known as phosphoglycerides) are major components of cell membranes. They are derived from glycerol-3-phosphate, which provides the backbone for:

• Two fatty acids attached to the first and second carbon atoms (C1 and C2) via ester linkages, forming the hydrophobic “tails.”

• The third carbon (C3) is linked to a phosphate group, which in turn connects to an alcoholic head group (e.g., choline, ethanolamine, serine, or inositol).

Thus, each glycophospholipid molecule contains two fatty acids, which are key for forming the bilayer structure of membranes.

❌ Incorrect Options:

• Three — ❌ Seen in triacylglycerols (triglycerides), which have three fatty acids attached to glycerol and serve as energy storage molecules, not membrane components.

• None — ❌ Incorrect; fatty acids are essential for forming the hydrophobic region of the membrane.

• Four — ❌ No known biological lipid has four fatty acids linked to a single glycerol backbone.

• One — ❌ Found in lysophospholipids, where one fatty acid has been removed (often by phospholipase A₂), not in intact glycophospholipids.

✅ Correct Answer:
Henderson–Hasselbalch equation

The Henderson–Hasselbalch equation relates the pH of a buffer solution to the pKa of the acid and the ratio of the concentrations of conjugate base to acid. It is given by:
pH = pKa + log([A-] / [HA])

When the concentrations of acid ([HA]) and base ([A-]) are equal, their ratio becomes 1, and log(1) = 0, making:
pH = pKa

This means the solution’s pH equals the acid’s pKa when the buffer is balanced — the point of maximum buffering capacity.

❌ Incorrect Options:

• Water dissociation equation: Refers to Kw = [H+][OH-] = 10^-14 at 25°C, which applies to pure water, not buffer systems.

• Hardy-Weinberg equation: Belongs to genetics, describing allele frequencies (p^2 + 2pq + q^2 = 1), not acid–base chemistry.

• pH log equation: This simply defines pH as pH = -log[H+]; it does not describe acid–base equilibrium.

• None of these: Incorrect, because the Henderson–Hasselbalch equation clearly fits the described relationship.

Correct Answer:
✅ Phospholipid

• Explanation: The cell membrane (plasma membrane) is primarily composed of phospholipids, which form a bilayer structure. Each phospholipid molecule has:

  • A hydrophilic (polar) head, and

  • Two hydrophobic (nonpolar) fatty acid tails.
    This amphipathic nature allows the membrane to be selectively permeable, flexible, and fluid. Among phospholipids, phosphoglycerides (like phosphatidylcholine and phosphatidylethanolamine) are the most common subclasses.

Incorrect Options:

❌ Phosphoglycerides

• These are a subclass of phospholipids, not the main group name — the broader category “phospholipid” is correct.

❌ Sphingolipid

• Found in smaller amounts, particularly in myelin sheaths and neuronal membranes, but not the most abundant overall.

❌ Glycolipid

• Present in the outer leaflet of the membrane, important for cell recognition, but they make up a small fraction of total membrane lipids.

❌ None of these

• Incorrect — the correct and most common lipid type is clearly phospholipid.

Correct Answer:
✅ Hydrogen ion concentration

The pH of a solution is defined as the negative logarithm (base 10) of the hydrogen ion concentration:
pH = -log10 [H+]

This means that as the concentration of hydrogen ions increases, the pH decreases (the solution becomes more acidic).
For example, if [H+] = 1 × 10^-7, then pH = 7, which is neutral.

Incorrect Options:

❌ Hydroxyl ion concentration
This determines pOH, not pH.
pOH = -log10 [OH-], and pH + pOH = 14

❌ Strong acid
pH is not defined as the log of an acid itself — it depends on the [H+] produced by the acid in solution.

❌ Weak base
A weak base affects hydrogen ion concentration indirectly, but pH is not defined using base concentration.

❌ Weak acid
Similarly, pH depends on how much H+ the acid releases, not on the total concentration of the acid molecules.

Correct Answer:

✅ Gray hepatization

In the natural course of lobar pneumonia, the lung progresses through four classical stages:

Congestion – lungs are heavy, red, boggy due to vascular engorgement and fluid.

• Red hepatization – alveoli filled with RBCs, neutrophils, and fibrin; the lung looks red, firm, and liver-like.
• Gray hepatization – RBCs break down and fibrinopurulent exudate with neutrophils dominates. The lung appears dry, firm, and grayish-brown.
• Resolution – enzymes digest the exudate, and normal architecture is restored.

Thus, a dry, gray lung corresponds to the gray hepatization phase.

Incorrect Options:

❌ Yellow hepatization

• Not a classical phase of pneumonia. It’s a distractor. Pneumonia has red and gray hepatization, but not yellow.

❌ Red hepatization

• At this stage, the lung is red, heavy, and firm due to exudation of RBCs along with neutrophils. It is not gray or dry.

❌ Resolution

• Here, the fibrinous exudate is broken down and cleared, restoring lung function. The lung becomes soft and normal again, not dry and gray.

❌ Fibrosis

• This is not part of typical lobar pneumonia healing. Fibrosis may occur in chronic lung diseases, but lobar pneumonia usually resolves completely without scarring (unless complicated).

Leukotrienes are synthesized from arachidonic acid via the 5-lipoxygenase pathway. The enzyme 5-lipoxygenase (5-LOX), with the help of FLAP (5-lipoxygenase–activating protein), first converts arachidonic acid into 5-hydroperoxy-eicosatetranoic acid (5-HPETE).

• This compound is the first committed product in the leukotriene pathway.

• From 5-HPETE, subsequent conversions occur, producing leukotriene A4 (LTA4) and then other leukotrienes (LTB4, LTC4, etc.), which are important in inflammation and hypersensitivity reactions.

❌ Why Other Options Are Incorrect:

• 5-hydroxy-eicosatetranoic acid (5-HETE): This is a reduced metabolite of 5-HPETE, not the first product.

• Prostaglandin G2 (PGG2): Belongs to the cyclooxygenase pathway, not leukotriene synthesis.

• Leukotriene A4 (LTA4): Formed later from 5-HPETE, not the first product.

• Leukotriene B4 (LTB4): A downstream leukotriene derived from LTA4; not the initial product.

Sphingomyelin is a type of sphingolipid and a key component of cell membranes, especially in the myelin sheath of neurons. Its backbone is sphingosine, which when combined with a fatty acid forms ceramide. Addition of phosphocholine to ceramide produces sphingomyelin.

• Therefore, ceramide is the direct precursor of sphingomyelin.

❌ Why the other options are incorrect:

• Arachidonic acid: Precursor of eicosanoids (prostaglandins, leukotrienes, thromboxanes), not sphingolipids.

• Acetyl CoA: Starting point for fatty acid and cholesterol synthesis, but not directly for sphingomyelin.

• Glycerol: Backbone of glycerophospholipids and triglycerides, not sphingolipids.

• Glucose: Used in glycolipids (e.g., cerebrosides, gangliosides) but not in sphingomyelin.

Prostaglandins are lipid mediators derived from arachidonic acid, a 20-carbon polyunsaturated fatty acid stored in membrane phospholipids. When cells are stimulated by injury, inflammation, or other signals, phospholipase A2 releases arachidonic acid from membranes.

• Through the cyclooxygenase (COX) pathway, arachidonic acid is converted into prostaglandins, prostacyclin, and thromboxanes.

• Through the lipoxygenase (LOX) pathway, it forms leukotrienes.

Thus, arachidonic acid is the direct substrate for prostaglandin synthesis.

❌ Why the other options are incorrect:

• Nitric oxide: A gaseous signaling molecule from arginine, causes vasodilation, not a prostaglandin precursor.

• Arginine: Amino acid used to synthesize NO and other compounds, not prostaglandins.

• Glucose: Provides energy but not a direct substrate for prostaglandin synthesis.

• Oxygen: Needed as a cofactor in COX reactions but not the primary substrate.

✅ Correct Answer:

7.4

🔎 Explanation

• Normal arterial blood pH is 7.35 – 7.45, with an average of 7.4.
• This tight regulation is crucial because even small changes in pH affect enzyme activity, protein structure, and ion distribution.
• Maintenance of blood pH depends on:
  • Buffer systems (mainly bicarbonate buffer in plasma)
  • Respiratory regulation (CO₂ removal)
  • Renal regulation (H⁺ secretion, HCO₃⁻ reabsorption).

❌ Why the others are wrong

• 7.2 ❌ → Too low; indicates acidosis.
• 7.5 ❌ → Too high; indicates alkalosis.
• 7.3 ❌ → Lower than normal; mild acidosis.
• 7.7 ❌ → Severe alkalosis, incompatible with life if persistent.

✅ Correct Answer:

Bicarbonate

🔎 Explanation

• The bicarbonate buffer system (HCO₃⁻ / H₂CO₃) is the most important plasma buffer.
• It works in conjunction with the respiratory system (controls CO₂, hence carbonic acid) and the kidneys (regulate bicarbonate reabsorption and hydrogen ion excretion).
• This system maintains blood pH close to 7.4, making it the primary extracellular buffer. ✅

❌ Why the others are wrong

• Phosphate ❌ → Works mainly as an intracellular buffer and in renal tubular fluid, not the main plasma buffer.
• Albumin ❌ → Acts as a protein buffer, but its contribution is smaller compared to bicarbonate.
• Ammonia ❌ → Important in the renal system for acid excretion, but not a major plasma buffer.
• Water ❌ → Universal solvent, but does not buffer pH.

✅ Correct Answer:

Respiratory acidosis

Why: Extreme drowsiness usually indicates hypoventilation (reduced respiratory drive). Hypoventilation → CO₂ retention → increased H₂CO₃ → ↓ blood pH = respiratory acidosis. Breathlessness can coexist because the patient feels dyspneic despite shallow or ineffective ventilation; rising CO₂ also causes drowsiness, confusion and, if severe, CO₂ narcosis.

❌ Why the other options are wrong

Respiratory alkalosis — occurs with hyperventilation (blowing off CO₂), producing lightheadedness and paresthesias, not extreme drowsiness from CO₂ retention.

Metabolic acidosis — caused by increased acid production or loss of bicarbonate (DKA, renal failure, diarrhea); not the primary consequence of depressed ventilation.

None of these — incorrect because a clear acid–base disturbance (respiratory acidosis) is expected.

✅ Correct Answer: Hydroxyl (-OH) group

• Phospholipids contain a glycerol backbone with hydroxyl (-OH) groups, which are the simplest hydrophilic moieties in the molecule.

• These –OH groups form ester linkages with fatty acids (forming hydrophobic tails) and with the phosphate group (part of the polar head).

• While the phosphate group is also hydrophilic, it’s more complex, consisting of multiple atoms and carrying a formal charge — not the simplest hydrophilic moiety.

• Therefore, when asked for the simplest hydrophilic group in phospholipids, hydroxyl (-OH) is correct.

❌ Why not the others:

• Phosphate: Strongly hydrophilic but more complex; not the simplest.

• Sulfate: Not present in standard phospholipids; seen in other biomolecules.

• Glucose: Found in glycolipids, not phospholipids.

• Carbons: Hydrophobic, form the fatty acid tails.

Correct Answer:
✅ Buffer solution

• Explanation: A buffer solution is a mixture of a weak acid and its conjugate base (or weak base and its conjugate acid) that resists significant changes in pH when small amounts of acid or base are added. Examples include the bicarbonate buffer system in blood and the phosphate buffer system in cells.

Incorrect Options:

❌ Super saturated solution

• Contains more solute than it can normally hold at a given temperature, but does not resist pH changes.

❌ Saturated solution

• Contains maximum solute at equilibrium; no buffering capacity.

❌ Sugar solution

• Just a solute (sugar) in water — does not resist pH changes.

❌ Salt solution

• While some salts may slightly affect pH (acidic/basic salts), they do not function as buffers unless paired with a conjugate acid/base system.

Correct Answer:
✅ Acid and conjugate base

• The pH of a buffer solution is determined by the ratio of a weak acid and its conjugate base (or a weak base and its conjugate acid). This relationship is given by the Henderson–Hasselbalch equation:

pH = pKa + log([A-] / [HA])

Where:
[HA] = concentration of weak acid
[A-] = concentration of conjugate base

The pH depends on the ratio [A-] / [HA].
That’s why buffer solutions resist changes in pH when small amounts of acid or base are added.

Incorrect Options:

❌ Weak and strong acid

• Mixing acids does not create a buffer; it only lowers the pH further.

❌ Strong acid

• Has no buffering capacity since it dissociates completely.

❌ Weak base

• Alone, it cannot act as a buffer unless its conjugate acid is also present.

❌ Weak acid

• By itself, it cannot neutralize added base effectively without its conjugate partner.

Correct Answer:
✅ pH meter

• Explanation: A pH meter is an instrument used to measure the hydrogen ion concentration of a solution, providing an accurate pH value. It uses a pH electrode (glass electrode) as a sensor and a reference electrode to measure the voltage difference, which is then converted into a pH reading.

Incorrect Options:

❌ pH electrode

• This is just the sensor component, not the complete instrument that displays the reading.

❌ pH detector

• Not a standard term in analytical chemistry.

❌ pH scale

• A numerical scale (0–14) to express pH values, not a device for measurement.

❌ pH color

• Refers to color changes with indicators (like litmus), which are crude methods, not precise measurement tools.

✅ Correct Answer: 

Lecithin (Dipalmitoyl phosphatidylcholine)

• The major component of pulmonary surfactant is dipalmitoyl phosphatidylcholine (DPPC), also called lecithin.
• Surfactant reduces surface tension in alveoli, preventing collapse (atelectasis), especially during expiration.
• Clinically, fetal lung maturity is assessed by the Lecithin:Sphingomyelin (L:S) ratio in amniotic fluid (>2 = mature lungs).

❌ Why the Other Options Are Wrong

• Glucocerebroside → a glycolipid; accumulated in Gaucher disease, not part of surfactant.
• Hyaluronic acid → glycosaminoglycan in connective tissue, not alveoli.
• Heparan sulfate → another glycosaminoglycan, present in basement membranes, not surfactant.
• Glycerol → a basic lipid backbone, but not a direct surfactant component.

Correct Answer:
✅ Respiratory acidosis

• Explanation: The patient’s symptoms — chronic cough, chest tightness, and difficulty breathing — suggest an obstructive lung disease such as COPD (common in elderly). In such cases, hypoventilation occurs, leading to CO₂ retention (hypercapnia). Increased CO₂ in blood shifts the equilibrium of carbonic acid:

This results in respiratory acidosis, with elevated PaCO₂ and decreased blood pH.

Incorrect Options:

❌ Metabolic alkalosis

• Caused by vomiting, diuretic use, or excess bicarbonate intake. It presents with weakness or muscle cramps, not cough and chest tightness.

❌ Respiratory alkalosis

• Occurs due to hyperventilation (e.g., anxiety, altitude, pulmonary embolism). It leads to low CO₂, not CO₂ retention.

❌ Metabolic acidosis

• Results from renal failure, diabetic ketoacidosis, or lactic acidosis. Symptoms include Kussmaul breathing, not chronic cough with chest tightness.

❌ Compensatory respiratory alkalosis

• Seen in metabolic acidosis as a compensatory mechanism (e.g., deep, rapid breathing in DKA). That doesn’t fit this clinical scenario.

Correct Answer:
✅ Sphingomyelinase

• Explanation: Sphingomyelinase is the enzyme that specifically hydrolyzes sphingomyelin into ceramide and phosphorylcholine. Deficiency of this enzyme leads to the accumulation of sphingomyelin in cells, which is the basis of Niemann–Pick disease (a lysosomal storage disorder).

Incorrect Options:

❌ Phosphatase

• Removes phosphate groups from molecules, but does not act on sphingomyelin.

❌ Ceramidase

• Hydrolyzes ceramide into sphingosine and free fatty acids. It acts downstream, not directly on sphingomyelin.

❌ Glucocerebrosidase

• Degrades glucocerebroside into ceramide and glucose. Its deficiency causes Gaucher disease, not Niemann–Pick.

❌ Glucosidase

• General enzyme that breaks down glucose-containing polysaccharides or oligosaccharides, unrelated to sphingomyelin metabolism.

Correct Answer:
✅ Hydrogen ion concentration

• Explanation: pH is mathematically defined as the negative logarithm of the hydrogen ion concentration:

pH=−log⁡10[H+]\text{pH} = -\log_{10} [\text{H}^+]pH=−log10​[H+]

This gives a convenient way to express very small concentrations of hydrogen ions in solution. For example, if [H+]=1×10−7 M[H^+] = 1 \times 10^{-7} \, M[H+]=1×10−7M, then pH = 7. A low pH means high hydrogen ion concentration (acidic), while a high pH means low hydrogen ion concentration (basic).

Incorrect Options:

❌ Weak acid

• A weak acid contributes to [H+][H^+][H+], but pH is not the negative log of the acid itself — it is of the hydrogen ion concentration.

❌ Hydroxyl ion concentration

• This is related to pOH, not pH.

pOH=−log⁡10[OH−]\text{pOH} = -\log_{10} [\text{OH}^-]pOH=−log10​[OH−]

pH and pOH are linked through water: pH+pOH=14pH + pOH = 14pH+pOH=14.

❌ Weak base

• A weak base affects the solution’s hydrogen ion concentration indirectly, but pH is not defined in terms of the base itself.

❌ Strong acid

• A strong acid dissociates completely to release [H+][H^+][H+], but pH is still defined as the negative log of hydrogen ion concentration, not the acid.

Correct Answer:
✅ Acid and conjugate base

• Explanation: The pH of a buffer solution is determined by the relative concentrations of a weak acid and its conjugate base (or a weak base and its conjugate acid). This relationship is mathematically expressed by the Henderson–Hasselbalch equation:

pH=pKa+log⁡([A−][HA])\text{pH} = \text{p}K_a + \log \left( \frac{[\text{A}^-]}{[\text{HA}]} \right)pH=pKa​+log([HA][A−]​)

Here, [HA] is the weak acid, and [A⁻] is its conjugate base. It’s the ratio of these two that decides the buffer’s pH, not the absolute amounts.

Incorrect Options:

❌ Weak acid

• A weak acid alone cannot resist pH changes effectively. Without its conjugate base, it cannot neutralize added base.

❌ Weak and strong acid

• Mixing acids does not form a buffer. A strong acid fully dissociates, destroying the delicate balance required for buffering.

❌ Weak base

• A weak base alone is insufficient. It needs its conjugate acid to form a buffer pair.

❌ Strong acid

• Strong acids completely ionize and cannot establish the equilibrium needed for buffering action.