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Here are short answers to all six questions:
a. Serum potassium should not be estimated in haemolysed blood sample
RBCs contain ~20-25x more potassium than plasma. Haemolysis releases intracellular K⁺ into the serum, causing a falsely elevated (pseudohyperkalemia) result. Hence haemolysed samples are unsuitable for serum K⁺ estimation.
b. TCA cycle is amphibolic in nature
The TCA (Krebs) cycle is both catabolic (oxidizes acetyl-CoA to generate ATP, NADH, FADH₂, CO₂) and anabolic (intermediates like α-ketoglutarate, oxaloacetate are used for amino acid and glucose synthesis). A pathway serving both functions is called amphibolic.
d. Mitochondria is the powerhouse of the cell
Mitochondria carry out oxidative phosphorylation via the electron transport chain (ETC), producing ~30-32 ATP per glucose molecule. Since the bulk of cellular ATP is generated here, they are called the powerhouse of the cell.
e. Km value of glucokinase is higher than that of hexokinase
- Hexokinase: low Km (~0.1 mM) - high affinity for glucose, works at fasting glucose levels, found in most tissues.
- Glucokinase: high Km (~10 mM) - low affinity, only active at high postprandial glucose; found in liver and β-cells. This makes glucokinase a glucose sensor.
f. Troponin I is a highly preferable cardiac marker compared to CK-MB, LDH and other cardiac markers
Cardiac Troponin I (cTnI) is:
- Exclusively expressed in cardiac muscle (absolute cardiac specificity)
- Rises within 4-6 hours of MI, peaks at 24 hours, remains elevated for 7-10 days
- More sensitive and specific than CK-MB (found in skeletal muscle too) and LDH (non-specific, found in many tissues)
- Not elevated in skeletal muscle injury, making it the gold standard marker for myocardial infarction
g. Explain anion gap
Anion Gap (AG) = [Na⁺] - ([Cl⁻] + [HCO₃⁻])
Normal value: 8-12 mEq/L (or 12 ±2 with K⁺ included)
It represents unmeasured anions (albumin, phosphate, sulfate, organic acids). An elevated AG indicates presence of excess unmeasured anions (e.g., lactate, ketones, salicylates). Used to classify metabolic acidosis: high AG (e.g., DKA, lactic acidosis) vs. normal AG (e.g., diarrhea, RTA).
h. Benedict test is considered a semi-quantitative test
Benedict's test detects reducing sugars. The color of the precipitate changes progressively with glucose concentration:
- Blue = no sugar (negative)
- Green = trace (~0.5%)
- Yellow = ~1%
- Orange = ~1.5%
- Brick red = >2%
Since it gives a range estimate (not an exact value) based on color, it is semi-quantitative rather than quantitative.
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Give ans in short
Here are short answers to all 7 questions based on the clinical case:
Case Summary: 30-year-old male, malaria patient on Primaquine → developed anemia, jaundice, dark urine → Low Hb (7 g%), elevated bilirubin (mostly indirect), low G6PD activity → Classic G6PD Deficiency + Hemolytic Anemia
1. Most Probable Diagnosis
G6PD (Glucose-6-Phosphate Dehydrogenase) Deficiency triggered by Primaquine (an oxidant drug), causing acute hemolytic anemia.
Evidence: Low Hb, low G6PD activity (3.5 vs normal 8-18 units/g Hb), raised indirect bilirubin, dark urine (hemoglobinuria).
2. Reaction catalyzed by G6PD enzyme
G6PD catalyzes the first step of the HMP shunt (Pentose Phosphate Pathway):
Glucose-6-phosphate + NADP⁺ → 6-Phosphogluconolactone + NADPH + H⁺
NADPH is essential for regenerating Glutathione (GSH), which protects RBCs from oxidative damage.
3. Biochemical basis of G6PD deficiency disorder
- G6PD deficiency → ↓ NADPH → ↓ reduced glutathione (GSH)
- Without GSH, RBCs cannot neutralize oxidative stress (H₂O₂, free radicals)
- Hemoglobin gets oxidized → forms Heinz bodies (denatured Hb precipitates)
- RBCs with Heinz bodies are destroyed by spleen → Hemolytic anemia
- Primaquine (oxidant drug) triggers this oxidative crisis
4. Correlation between malaria and G6PD deficiency
- G6PD deficiency is actually protective against malaria (evolutionary advantage)
- Malarial parasite (Plasmodium) needs NADPH for its own oxidative metabolism inside RBCs
- G6PD-deficient RBCs have lower NADPH → hostile environment for parasite → less severe malaria
- However, treatment with Primaquine (oxidant antimalarial) precipitates hemolysis in G6PD-deficient individuals
5. Triggering factors for G6PD deficiency disorders
| Category | Examples |
|---|---|
| Drugs (oxidants) | Primaquine, Dapsone, Nitrofurantoin, Sulfonamides |
| Infections | Malaria, viral hepatitis, bacterial infections |
| Foods | Fava beans (Favism) |
| Metabolic | Diabetic ketoacidosis |
6. Two important functions of HMP shunt pathway
- Generation of NADPH - used for reductive biosynthesis (fatty acid synthesis, cholesterol synthesis) and protection of RBCs from oxidative damage via glutathione reduction
- Generation of Ribose-5-phosphate - essential for synthesis of nucleotides (DNA, RNA, ATP, coenzymes like NAD, FAD, CoA)
7. Why Hemolytic Jaundice occurs in G6PD deficiency
- Hemolysis → massive RBC destruction → large amounts of Hb released
- Hb → broken down to unconjugated (indirect) bilirubin
- Liver is overwhelmed; cannot conjugate all bilirubin fast enough
- Result: ↑ Indirect bilirubin in blood → jaundice (yellow sclera/skin)
- Also: ↑ urobilinogen in urine, dark urine (hemoglobinuria)
- This is pre-hepatic (hemolytic) jaundice - confirmed by the case findings (indirect bilirubin 3 mg/dl vs direct 1 mg/dl)
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1. Lathyrism
A neurotoxic disease caused by excess consumption of Lathyrus sativus (khesari dal). The toxin BOAA (β-oxalyl aminoalanine) inhibits glutamate receptors, causing irreversible spastic paralysis of lower limbs. It is a form of neurolathyrism seen in famine conditions.
2. ORS is used for treatment of diarrhea
Diarrhea causes loss of Na⁺, K⁺, water, and HCO₃⁻. ORS contains glucose + NaCl + KCl + sodium citrate; glucose enhances Na⁺ absorption via Na⁺-glucose co-transporter (SGLT1) in intestine. This promotes water absorption and corrects dehydration and electrolyte loss.
3. Hyperuricemia is observed in Von Gierke's Disease
Von Gierke's disease (Type I glycogen storage disease) is due to glucose-6-phosphatase deficiency. Excess G6P is shunted into HMP pathway → ↑ ribose-5-phosphate → ↑ purine synthesis → ↑ uric acid. Also, lactic acidosis competes with uric acid for renal excretion, further raising serum urate levels.
4. Ethanol is antidote of methanol poisoning
Methanol is metabolized by alcohol dehydrogenase (ADH) to formaldehyde and formic acid, which cause blindness and acidosis. Ethanol has higher affinity for ADH, competitively inhibits methanol metabolism, and prevents toxic metabolite formation. Methanol is then excreted unchanged.
5. Bile salts help in digestion and absorption of lipids
Bile salts are amphipathic (hydrophilic + hydrophobic parts) and emulsify dietary fats into small micelles, increasing surface area for pancreatic lipase action. They also form mixed micelles with fatty acids and monoglycerides, facilitating their absorption through intestinal epithelium.
6. HDL is a good cholesterol
HDL performs reverse cholesterol transport - picks up excess cholesterol from peripheral tissues and arterial walls and carries it back to the liver for excretion as bile acids. High HDL levels are therefore cardioprotective, reducing the risk of atherosclerosis and coronary artery disease.
7. Temperature affects enzyme activity
Enzymes have an optimum temperature (37°C in humans) at which activity is maximum. Below optimum, activity decreases due to reduced kinetic energy; above optimum, high temperature denatures the enzyme protein (disrupts H-bonds, 3D structure), causing irreversible loss of activity.
8. In obstructive jaundice stool is clay colored and urine is dark colored
In obstructive jaundice, bile duct blockage prevents bilirubin/bile from reaching intestine → no stercobilinogen formed → stools are pale/clay colored. Conjugated (water-soluble) bilirubin regurgitates into blood and is filtered by kidneys → excreted in urine → dark (tea-colored) urine (bilirubinuria).
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