Biochemistry Chart Answers

CASE 1 - 5-year-old girl: Slow growth + bone pain

• Blood Sugar: 88 mg%
• Blood Urea: 25 mg%
• Serum Creatinine: 1.8 mg%
• Serum Calcium: 7.6 mg% (LOW - normal 8.5-10.5)
• Serum Inorganic Phosphorus: 2.0 mg% (LOW - normal 2.5-4.5)
• Serum Alkaline Phosphatase: 96 KA units/dL (HIGH - normal 20-30)

Provisional Diagnosis: Rickets (Vitamin D Deficiency)

• Hypocalcemia (7.6 mg%) + hypophosphatemia (2.0 mg%) + markedly elevated alkaline phosphatase = classic triad of Vitamin D deficiency rickets
• Slow growth and bone pain in a 5-year-old are hallmark clinical features
• Elevated ALP reflects increased osteoblastic activity as bone tries to mineralize poorly
• The slightly elevated creatinine (1.8 mg% in a child) may suggest a component of renal rickets (renal osteodystrophy) - but given the age and clinical picture, nutritional rickets is the primary diagnosis

CASE 2 - Jaundiced patient (Blood & Urine - Case A)

• Serum Bilirubin Total: 16.6 mg%
• Conjugated (Direct): 14.8 mg% (VERY HIGH)
• Unconjugated (Indirect): 1.8 mg% (normal)
• Serum ALP: 100 KA units/dL (MARKEDLY HIGH - normal 3-11.5)
• SGPT: 35 units/L (Normal)
• SGOT: 32 units/L (Normal)

• Bile Salt: ++
• Bile Pigment: ++
• Urobilinogen: NIL

Diagnosis: Obstructive (Post-Hepatic) Jaundice

• Predominantly conjugated (direct) hyperbilirubinemia
• Bile salts and bile pigments present in urine (conjugated bilirubin is water-soluble, passes into urine)
• Urobilinogen absent in urine - because bile cannot reach the intestine (no urobilinogen formed and reabsorbed)
• Markedly elevated ALP (100 KA units) - classic marker of biliary obstruction
• Normal transaminases (SGPT/SGOT) - rules out hepatocellular damage
• Causes: choledocholithiasis, carcinoma head of pancreas, cholangiocarcinoma

CASE 3 - Jaundiced patient (Blood & Urine - Case B)

• Serum Bilirubin Total: 12.6 mg%
• Conjugated: 0.6 mg% (LOW/normal)
• Unconjugated: 12 mg% (VERY HIGH)
• Serum ALP: 9.0 KA units/dL (Normal - reference 3-11.5)
• SGPT: 28 units/L (Normal)
• SGOT: 27 units/L (Normal)

• Bile Salt: NIL
• Bile Pigment: NIL
• Urobilinogen: +++ (HIGH)

Diagnosis: Hemolytic (Pre-Hepatic) Jaundice

• Predominantly unconjugated (indirect) hyperbilirubinemia
• Unconjugated bilirubin is lipid-soluble and bound to albumin - cannot be filtered by kidneys, so NO bile salts/pigments in urine (acholuric jaundice)
• Urobilinogen markedly elevated - massive bilirubin load reaches intestine, producing large amounts of urobilinogen that is reabsorbed and excreted in urine
• Normal ALP and transaminases - liver is not damaged
• Causes: hemolytic anemia (sickle cell, thalassemia, G6PD deficiency, malaria)

CASE 4 - Patient with abnormal blood gases (Case A)

• pH: 7.25 (LOW - acidosis)
• HCO3-: 28 mEq/L (Normal to slightly high)
• H2CO3: 2.8 mEq/L (HIGH - normal 1.2)
• pCO2: 80 mmHg (VERY HIGH - normal 35-45)

• pH: 5.0 (Acidic - kidneys compensating by excreting acid)
• NH4+: ↑↑ (High - increased ammonium excretion)

Cause: Respiratory Acidosis (with renal compensation)

• pH 7.25 = acidosis
• High pCO2 (80 mmHg) = primary respiratory failure causing CO2 retention
• HCO3- slightly elevated = kidneys are compensating (retaining bicarbonate)
• Acidic urine + elevated NH4+ in urine = kidneys excreting H+ to compensate
• Causes: COPD, hypoventilation, neuromuscular disease, airway obstruction

CASE 5 - Patient with abnormal blood gases (Case B)

• pH: 7.25 (LOW - acidosis)
• HCO3-: 17 mEq/L (LOW - normal 22-26)
• H2CO3: 1.0 mEq/L (Normal to low)
• pCO2: 36 mmHg (Normal/slightly low - compensatory)

• pH: 5.6 (Acidic)
• NH4+: ↑ (elevated)

Cause: Metabolic Acidosis (with respiratory compensation)

• pH 7.25 = acidosis
• Primary defect: low HCO3- (17 mEq/L) = loss of bicarbonate or accumulation of acid
• Slightly low pCO2 (36 mmHg) = respiratory compensation (Kussmaul breathing blowing off CO2)
• Acidic urine with elevated NH4+ = kidney excreting excess acid
• Causes: diabetic ketoacidosis, renal tubular acidosis, diarrhea (loss of HCO3-), lactic acidosis

CASE 6 - Patient with abnormal blood gases (Case C)

• pH: 7.55 (HIGH - alkalosis)
• HCO3-: 38 mEq/L (HIGH - normal 22-26)
• H2CO3: 1.35 mEq/L (Normal/low)
• pCO2: 40 mmHg (Normal)

• pH: 8.0 (Alkaline)
• NH4+: ↓ (Low)

Cause: Metabolic Alkalosis

• pH 7.55 = alkalosis
• Primary defect: elevated HCO3- (38 mEq/L) = excess bicarbonate
• pCO2 is inappropriately normal (should rise to compensate) = incomplete/early respiratory compensation
• Alkaline urine (pH 8.0) = kidneys excreting excess HCO3-
• Low NH4+ in urine = no need for renal acid excretion
• Causes: prolonged vomiting (loss of HCl), antacid overdose, diuretics (loop/thiazide), Cushing's syndrome, hyperaldosteronism

CASE 7 - Patient with abnormal blood gases (Case D)

• pH: 7.60 (HIGH - alkalosis)
• HCO3-: 25 mEq/L (Normal)
• H2CO3: 0.7 mEq/L (LOW - normal 1.2)
• pCO2: 21 mmHg (VERY LOW - normal 35-45)

• pH: 7.90 (Alkaline)
• NH4+: ↓ (Low)

Cause: Respiratory Alkalosis

• pH 7.60 = alkalosis
• pCO2 21 mmHg = primary hyperventilation causing excessive CO2 loss
• HCO3- is normal (kidneys have not had time to compensate significantly) = acute respiratory alkalosis
• Low H2CO3 confirms CO2 depletion
• Alkaline urine with low NH4+ = kidneys trying to excrete HCO3- to compensate
• Causes: hyperventilation (anxiety, pain), fever, high altitude, mechanical overventilation, aspirin poisoning (early), hepatic failure, pregnancy

CASE 8 - 60-year-old with chest pain

• SGOT (AST): 50 Karmen units/L (210 U/L) - ELEVATED (normal <40 U/L)
• SGPT (ALT): 10 Karmen units/L (40 U/L) - Normal
• CPK: ↑ (Elevated)
• LDH: Normal

Interpretation: Acute Myocardial Infarction (AMI)

• Classic pattern: SGOT/AST elevated but SGPT/ALT normal - the SGOT:SGPT ratio >2 points to cardiac muscle, not liver disease (liver damage raises SGPT more)
• CPK (Creatine Phosphokinase) elevated - CPK-MB isoenzyme is the cardiac-specific marker that rises 4-6 hours post-MI
• LDH normal at this point (LDH rises later, peaks at 48-72 hours - may still be in early phase)
• 60-year-old with chest pain + this enzyme profile = myocardial infarction until proven otherwise
• Note: Today troponin I/T would be the gold standard, but this is a classic older-style enzyme panel

CASE 9 - Elderly patient admitted with left-sided paralysis

• Blood Sugar: 110 mg% (Normal upper limit)
• Blood Urea: 28 mg% (Normal)
• Serum Cholesterol: 310 mg% (HIGH - normal <200 mg/dL)
• Serum Triglycerides: 270 mg% (HIGH - normal <150 mg/dL)
• Serum HDL Cholesterol: 26 mg% (LOW - normal >40 mg/dL in males, >50 in females)
• Serum LDL Cholesterol: 206 mg% (HIGH - normal <100 mg/dL optimal)

Interpretation: Hyperlipidemia (Mixed Type) with Atherosclerosis - Cause of Ischemic Stroke

• Left-sided paralysis = right-sided cerebrovascular accident (stroke)
• Markedly elevated total cholesterol + LDL + triglycerides = severe mixed hyperlipidemia
• Very low HDL (26 mg%) = reduced reverse cholesterol transport = accelerated atherosclerosis
• This lipid profile is a major risk factor for both coronary artery disease and ischemic stroke
• LDL/HDL ratio: 206/26 = ~7.9 (very high risk; should be <3.5)
• Diagnosis: Ischemic stroke secondary to atherosclerosis driven by Type IIb or Type IV hyperlipidemia

CASE 10 - 10-year-old boy: Fever, facial swelling, abdominal swelling (10 days), BP 110/70

• Total Protein: 4.5 gm/dL (LOW - normal 6.0-8.0)
• Albumin: 2.5 gm/dL (LOW - normal 3.5-5.0)
• Cholesterol: 210 mg/dL (HIGH for a child)
• Urea: 20 mg/dL (Normal)
• Creatinine: 0.5 mg/dL (Normal for a child)

• Albumin: +++ (MASSIVE proteinuria)
• Benzidine test: Negative (no blood in urine)

Provisional Diagnosis: Nephrotic Syndrome (Minimal Change Disease)

• Classic tetrad: massive proteinuria (albumin +++) + hypoalbuminemia (2.5 g/dL) + generalized edema (face + abdomen) + hyperlipidemia (cholesterol 210 mg/dL)
• No hematuria (benzidine negative) - distinguishes from nephritic syndrome
• Normal renal function (urea, creatinine) - kidneys not failing, just leaking protein
• Normal blood pressure (110/70) - again favors nephrotic over nephritic syndrome
• No sore throat history and no hematuria makes post-streptococcal GN less likely
• In a 10-year-old child, the most common cause of nephrotic syndrome is Minimal Change Disease (Nil disease), which responds well to steroids
• The hypoalbuminemia causes reduced oncotic pressure → fluid shifts to interstitium → edema
• Low albumin triggers the liver to compensate by synthesizing more lipoproteins → hyperlipidemia and lipiduria

Summary Table

Diagnosis: Iron Deficiency Anemia (IDA)

Clinical Features (from the case)

Lab Findings Analysis

Pathophysiology

1. Ferritin drops first (iron stores depleted)
2. Serum iron falls → transferrin and TIBC rise (compensatory upregulation)
3. Heme synthesis impaired → RBCs produced are small (low MCV) and pale (hypochromic)
4. Variable RBC sizes → elevated RDW (mix of old normal cells and new small cells)

Why NOT other anemias?

Causes in a 10-year-old Girl

• Dietary deficiency - most common cause in children (poor iron intake, vegetarian diet)
• Rapid growth spurts increasing iron demand
• Intestinal malabsorption (celiac disease)
• Hookworm infestation (chronic blood loss)
• Onset of menstruation (less likely at 10, but possible)

Diagnosis: Iron Deficiency Anemia - Microcytic Hypochromic type