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Kyphosis

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Normal Spinal Curvatures

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Classification / Types

1. Postural Kyphosis (Round Back)

• Most common type
• No structural vertebral body changes on imaging
• No sharp angulation
• Corrects with backward bending and prone hyperextension - distinguishing feature
• Treatment: hyperextension exercise program
• Miller's Review of Orthopaedics, 9th Ed

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2. Scheuermann's Disease (Structural Kyphosis)

• Increased thoracic kyphosis >45°
• Anterior vertebral wedging of ≥5° at three consecutive vertebrae
• Disc space narrowing and end-plate irregularities
• Schmorl nodes (disc herniation through end-plates)
• Associated spondylolysis in 30-50% of cases
• Associated scoliosis in 33% of cases

• More common in boys
• Affected patients are often overweight
• Kyphosis is not postural - it does NOT fully correct with hyperextension (key distinguishing point from postural kyphosis)
• Neurologic changes are rare; MRI indicated if present
• Aetiology is unknown

• Surgical fusion to the first lordotic disc and the vertebra touched by the posterior sacral vertical line
• Brace treatment improves deformity in ~63% of patients who comply regularly - Bailey & Love's Surgery, 28th Ed

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3. Congenital Kyphosis

• Deformity usually progresses with growth; severity proportional to number of vertebrae involved and growth remaining
• Type I is subdivided further into: posterolateral quadrant vertebrae, posterior hemivertebrae, butterfly vertebrae, and anterolateral wedged vertebrae
• Campbell's Operative Orthopaedics, 15th Ed 2026

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4. Other Causes of Kyphosis

• Miller's Review of Orthopaedics, 9th Ed

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Gibbus Deformity

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Evaluation

• Lateral standing radiograph - measure Cobb angle (T1-T12 or from apex)
• Adams forward bend test - assesses for rotational component; may show rib hump (see scoliosis differentiation)
• MRI - indicated for neurological symptoms, congenital kyphosis (rule out intraspinal anomalies), or atypical features
• Normal thoracic kyphosis: 20-50°; Scheuermann defined as >45° with structural wedging

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Summary

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VMMC Case Charts - Full Answers with Clear Explanations

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SLIDE 2 - Normal OGTT Curve

• Fasting blood glucose: 75 mg/dl
• Peak: 135 mg/dl at 1 hour
• Returns to: 70 mg/dl at 2.5 hours
• Urine sugar & ketone bodies: Nil

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SLIDE 3 - Diabetes Mellitus (OGTT)

• Fasting BG: 180 mg/dl (>126 - high)
• Peak: 300 mg/dl
• Returns to: 170 mg/dl at 2 hours (>200 - high)
• Urine sugar: +++ | Ketone bodies: Nil

• WHO criteria for DM: Fasting plasma glucose >126 mg/dl AND 2-hour glucose >200 mg/dl - both exceeded here
• Glucosuria occurs because blood glucose exceeds the renal threshold (~180 mg/dl) - kidney cannot reabsorb all filtered glucose
• No ketone bodies → insulin is still present enough to prevent lipolysis → Type 2 DM (not ketosis-prone)

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SLIDE 4 - Renal Glycosuria

• Fasting BG: 80 mg/dl (normal)
• Peak: 150 mg/dl (normal)
• Returns to: 105 mg/dl
• Urine sugar: + (positive when BG = 150 mg/dl)

• Blood glucose levels are entirely normal - this rules out diabetes
• Sugar appears in urine at only 150 mg/dl, whereas the normal renal threshold is ~180 mg/dl
• This person's kidneys spill glucose at a lower blood glucose level than normal
• This is a benign condition - the tubular reabsorption capacity for glucose (Tm glucose) is reduced, not a metabolic defect

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SLIDE 5 - Diabetes Mellitus with Symptoms

• Fasting BG: 145 mg/dl (>126)
• 2-hr postprandial BG: 210 mg/dl (>200)
• Urine sugar: 2+ | Albumin: Nil | Ketone bodies: Negative

• Meets WHO diagnostic criteria (FBG >126 and 2-hr BG >200)
• Symptoms: increased appetite (polyphagia - cells starving despite high blood glucose), calf pain (peripheral neuropathy beginning)
• No albumin → kidneys not yet damaged (no nephropathy)
• No ketone bodies → insulin still partially functional → Type 2 DM
• No complications yet detected

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SLIDE 6 - Diabetic Ketoacidosis (DKA)

• pH: 7.2 (acidosis) | HCO₃: 10 mEq/L (low) | Glucose: 450 mg% | Urine sugar: +++ | Urine ketones: +++

• Acetoacetic acid
• Beta-hydroxybutyric acid
• Acetone

1. Acetone
2. Acetoacetic acid (acetoacetate)
3. Beta-hydroxybutyric acid (3-hydroxybutyrate) - the predominant one in DKA

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SLIDE 7 - Respiratory Acidosis (Crush Injury/Hypoventilation)

• pH: 7.2 (acidosis) | HCO₃: 28 mEq/L (normal/slightly raised as compensation) | pCO₂: 70 mmHg (HIGH)

• The primary problem is elevated CO₂ (pCO₂ = 70 vs normal 35-45 mmHg)
• The crowd crush likely caused chest wall compression → impaired breathing → CO₂ retention
• CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ (carbonic anhydrase reaction)
• Excess CO₂ produces excess H⁺, lowering pH
• HCO₃ is slightly elevated (28) = renal compensation (kidneys retaining bicarbonate to buffer the acid)
• Cause: hypoventilation from external compression

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SLIDE 8 - Metabolic Acidosis (Diarrhea)

• pH: 7.23 (acidosis) | HCO₃: 14 mEq/L (LOW) | pCO₂: 38 mmHg (normal)

• Primary problem: LOW bicarbonate (14 vs normal 22-26 mEq/L)
• pCO₂ is normal → the lungs are not the cause
• Diarrheal fluid contains large amounts of bicarbonate (pancreatic secretions, bile are alkaline)
• Severe diarrhea = massive loss of HCO₃⁻ → bicarbonate falls → acidosis
• Low BP and feeble pulse indicate severe dehydration from fluid/electrolyte loss
• Compensation: hyperventilation would lower pCO₂ further (not yet seen here = acute presentation)

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SLIDE 9 - Metabolic Alkalosis (Vomiting + Antacids)

• pH: 7.52 (alkalosis) | HCO₃: 36 mEq/L (HIGH) | pCO₂: 38 mmHg (normal) | Serum Cl⁻: 86 mEq/L (low)

• Primary problem: HIGH bicarbonate
• Vomiting loses HCl (gastric acid) → loss of H⁺ and Cl⁻ → blood becomes relatively alkaline
• Antacids add alkali (NaHCO₃ etc.) directly → further raises HCO₃⁻
• Hypochloremia (86 mEq/L): Cl⁻ lost in vomit; kidneys compensate by retaining HCO₃⁻ in exchange - perpetuating the alkalosis
• pCO₂ normal → respiratory compensation not yet kicking in fully

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SLIDE 10 - Respiratory Acidosis (COPD)

• pH: 7.12 (severe acidosis) | pCO₂: 80 mmHg (very HIGH) | HCO₃: 26 mEq/L (normal)

• Chronic cough + dyspnea → likely COPD/Emphysema/Chronic Bronchitis
• Lungs cannot exhale CO₂ effectively → CO₂ builds up in blood → acidosis
• HCO₃ is normal here (26) = no renal compensation yet → likely an acute exacerbation or compensation incomplete
• The primary driver is pCO₂ elevation

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SLIDE 11 - Respiratory Alkalosis (Hyperventilation)

• pH: 7.6 (alkalosis) | pCO₂: 21 mmHg (LOW) | HCO₃: 28 mEq/L (slightly high)

• Hysteria → hyperventilation → excessive CO₂ blown off → pCO₂ falls to 21
• Less CO₂ means less carbonic acid → fewer H⁺ ions → pH rises (alkalosis)
• HCO₃ slightly elevated = early renal compensation (kidneys starting to excrete HCO₃⁻)
• Treatment: rebreathing into a paper bag raises pCO₂ back

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SLIDE 12 - Starvation Ketoacidosis

• Blood glucose: 55 mg/dl (hypoglycemia) | pH: 7.27 (acidosis) | Benedict's test: Negative | Rothera's test: Positive (ketonuria)

• Blood glucose is LOW (55 mg/dl) → rules out diabetic ketoacidosis (where glucose is very HIGH)
• No glucose in urine (Benedict's negative) → confirms hypoglycemia, not diabetes
• Positive Rothera's test → ketone bodies in urine
• In starvation, glycogen stores are depleted → body breaks down fats → fatty acids → ketone bodies → metabolic acidosis
• The key distinction from DKA: glucose is LOW in starvation ketosis vs HIGH in DKA

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SLIDE 13 - Normal LFT

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SLIDE 14 - Neonatal (Hemolytic/Pre-Hepatic) Jaundice

• Total bilirubin: 25 mg% (HIGH) | Direct: 0.7 | Indirect: 24.3 mg% (very HIGH)
• AST: 60, ALT: 73 (mildly elevated)
• Urine: Urobilinogen +++ | Bile salts -ve | Bile pigments -ve

• Predominantly unconjugated (indirect) bilirubin elevated → hemolysis is occurring (RBC breakdown releases heme → bilirubin before reaching liver)
• In newborns, fetal RBCs are replaced by adult RBCs → massive hemolysis; also the liver's conjugating capacity (glucuronyl transferase) is immature
• Bile salts/pigments absent in urine: unconjugated bilirubin is not water-soluble → cannot be filtered in kidney
• Urobilinogen +++ in urine: more bilirubin enters gut → more urobilinogen formed → absorbed and excreted in urine

• Direct reaction → direct bilirubin (conjugated)
• Indirect reaction (after adding alcohol) → total bilirubin; the difference = indirect/unconjugated bilirubin

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SLIDE 15 - Hepatic (Hepatocellular) Jaundice

• Total bilirubin: 12 mg/dl | Direct: 7.6 | Indirect: 4.4 mg/dl (both elevated)
• AST: 140 IU/L (HIGH) | ALT: 380 IU/L (very HIGH) | ALP: 110 (normal)
• Urine: Bile salts +, Bile pigments +, Urobilinogen +

• Both conjugated AND unconjugated bilirubin elevated = liver cells damaged but not completely blocked
• Damaged hepatocytes release ALT and AST into blood (ALT is most specific for liver damage)
• Bile salts + bile pigments in urine: conjugated bilirubin (water-soluble) leaks from damaged liver cells into blood → filtered by kidneys
• Urobilinogen in urine: some bile still reaches gut normally

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SLIDE 16 - Obstructive (Post-Hepatic) Jaundice

• Total bilirubin: 22.6 | Direct: 18.3 (very HIGH) | Indirect: 4.3
• SGOT: 62, SGPT: 121 (mildly elevated) | ALP: 310 IU/L (very HIGH)
• Total protein: 4.8 g/dl (LOW) | Albumin: 1.6 g/dl (very LOW)
• Prothrombin time: prolonged | Urine: Urobilinogen absent, Bile pigments +++, Bile salts +++

• Predominantly conjugated (direct) bilirubin elevated → bile formed but cannot flow out
• ALP markedly elevated (310) = hallmark of biliary obstruction (produced by bile duct epithelium under pressure)
• Urobilinogen absent in urine: bile cannot reach intestine → no urobilinogen formed in gut → stools are pale/clay-colored
• Bile pigments + salts in urine: conjugated bilirubin backs up → enters blood → excreted in urine (dark urine)
• Itching: bile salts deposited in skin
• Hypoproteinemia/hypoalbuminemia: chronic obstruction leads to liver dysfunction and malnutrition

• Total protein: 4.8 g/dl
• Albumin: 1.6 g/dl
• Globulin: 4.8 - 1.6 = 3.2 g/dl
• A/G ratio: 1.6/3.2 = 0.5:1 (Normal is 1.2-1.5:1)
• This is A/G ratio reversal - seen in liver disease, nephrotic syndrome, malnutrition (albumin falls more than globulin, or globulin rises in infection/inflammation)

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SLIDE 17 - Myocardial Infarction (Enzyme Markers)

• Troponin I and Troponin T (most sensitive and specific cardiac biomarkers)
• CK-MB (Creatine Kinase - MB isoenzyme)
• LDH (Lactate Dehydrogenase)

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SLIDE 18 - Acute Pancreatitis

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SLIDE 19 - Nephrotic Syndrome

• 24-hr urine protein: 4.8 g/day (massive proteinuria - >3.5g/day = nephrotic range)
• Total protein: 4.2 g/dl (low) | Albumin: 1.6 g/dl (low)
• A/G ratio: 0.6:1 (reversed) | Cholesterol: 350 mg/dl (HIGH)

1. Massive proteinuria (>3.5 g/day) - glomerular basement membrane becomes leaky → proteins spill into urine
2. Hypoalbuminemia (1.6 g/dl) - proteins lost faster than liver can synthesize
3. Generalized edema - low albumin → reduced plasma oncotic pressure → fluid leaks into interstitium → swelling of face, ankles, abdomen
4. Hypercholesterolemia (350 mg/dl) - liver compensates for protein loss by upregulating all synthesis including lipoprotein synthesis; also decreased catabolism of lipoproteins

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SLIDE 20 - Night Blindness (Vitamin A Deficiency)

• Vitamin A is required to synthesize rhodopsin (visual purple) in rod cells of the retina
• Rhodopsin = opsin protein + 11-cis retinal (derived from Vitamin A)
• In dim light, rhodopsin undergoes photoisomerization and is broken down → triggers nerve impulse for night vision
• In Vitamin A deficiency, rhodopsin cannot be regenerated → rods fail to function in low light → night blindness

• Animal sources (preformed Vitamin A/retinol): Liver, egg yolk, butter, fish liver oil
• Plant sources (β-carotene/provitamin A): Mango, carrots, papaya, dark green leafy vegetables

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SLIDE 21 - Rickets

• Serum Ca: 6.7 mg/dl (LOW - normal 8.5-9.5) | Serum P: 2.2 mg/dl (LOW - normal 3-4)
• Serum ALP: 575 U/L (markedly elevated - normal 142-335)

• Vitamin D is needed for intestinal absorption of calcium and phosphorus
• Without it → hypocalcemia + hypophosphatemia → inadequate mineralization of growing bone
• Bones remain soft (osteoid tissue without mineral) → deform under body weight → bowed legs, pigeon chest
• ALP is markedly elevated: osteoblasts try to compensate by increasing bone formation → release large amounts of ALP (marker of osteoblast activity)

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SLIDE 22 - Hypothyroidism

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SLIDE 23 - Alkaptonuria

• Normal tyrosine metabolism: Tyrosine → p-hydroxyphenylpyruvate → Homogentisic acid → Maleylacetoacetate (by homogentisate oxidase) → eventually → CO₂ + H₂O
• In alkaptonuria, homogentisate oxidase is absent → homogentisic acid accumulates → excreted in urine
• Homogentisic acid is a reducing substance → positive Benedict's test
• Homogentisic acid undergoes oxidative polymerization in light → dark brown/black pigment (alkapton)
• Long-term: ochronosis (black pigmentation in connective tissues), arthritis

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SLIDE 24 - Wilson's Disease (Painter)

• Serum Ceruloplasmin: 14 mg/dl (LOW - normal 25-50)
• Plasma Copper: 60 µg/dl (LOW - normal 70-150)
• Kayser-Fleischer ring in both eyes

• Caused by mutation in ATP7B gene encoding a copper-transporting ATPase (ATP7B)
• This ATPase normally exports copper from hepatocytes into bile for excretion
• When it is absent → copper cannot be excreted → accumulates in liver, brain (basal ganglia), kidneys, cornea
• Ceruloplasmin is low: normally, ceruloplasmin is synthesized by liver and incorporates copper. In Wilson's disease, the copper-loading of ceruloplasmin is impaired → low serum ceruloplasmin
• Serum copper is low (but total body copper is HIGH): most serum copper is bound to ceruloplasmin; because ceruloplasmin is low, serum copper appears low, but tissue copper is elevated and urinary copper is elevated
• Kayser-Fleischer rings: copper deposits in the corneal periphery (Descemet's membrane) - pathognomonic
• Treatment: Penicillamine (copper chelator), Zinc (competes with copper for intestinal absorption)

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SLIDE 25 - Tetany (Hypocalcemia)

• Serum Ca: 6.5 mg/dl (LOW) | Serum Phosphate: 5.5 mg/dl (HIGH) | Albumin: 4.0 g/dl (normal) | ALP: 120 (normal)
• Symptoms: Muscle cramps, numbness, painful spasm of hands/feet (carpopedal spasm)

• Calcium is required to maintain normal neuronal membrane potential; hypocalcemia increases membrane excitability → spontaneous depolarization → muscle spasms
• Phosphate is elevated (inverse relationship with calcium - regulated by PTH and vitamin D)
• Albumin is normal → the hypocalcemia is real (not pseudohypocalcemia from low albumin)
• ALP is normal → no increased bone turnover/bone disease
• Most likely cause: Hypoparathyroidism (low PTH → low Ca, high Phosphate, normal ALP)
• Distinction from Rickets: in rickets, ALP is markedly elevated and patient is a child with deformities

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SLIDE 26 - Wilson's Disease (School Boy)

• Serum Copper: 40 µg/dl (LOW) | Ceruloplasmin: 5 mg/dl (very LOW) | Urine Copper: 200 µg/dl (very HIGH - normal <25)
• Clinical: hepatomegaly, Kayser-Fleischer ring, behavioral disturbances (liver and brain involvement)

• Urinary copper is HIGH (200 µg/dl): free (non-ceruloplasmin-bound) copper accumulates in tissues and spills into urine - this is the key confirmatory finding
• Behavioral issues = basal ganglia copper deposition (neuropsychiatric Wilson's)
• Hepatomegaly = hepatic copper accumulation → hepatitis/cirrhosis

1. Penicillamine - chelates free copper, forms a complex that is excreted in urine
2. Zinc - induces intestinal metallothionein which binds copper and prevents absorption; used for maintenance therapy

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SLIDE 27 - Gout

• Serum Uric acid: 12 mg/dl (very HIGH) - normal 3.5-7 mg/dl
• Urinary Uric acid: 2.5 mg/dl (LOW) - normal 0.5-0.7 g/day

• Uric acid is the final breakdown product of purine metabolism (adenine, guanine) via xanthine oxidase
• High non-vegetarian diet = high purine intake → increased uric acid production
• Low urinary uric acid = kidneys are not excreting uric acid adequately (underexcretion type - most common in primary gout)
• Uric acid deposits as monosodium urate crystals in joints (particularly first MTP joint → podagra), causing severe inflammatory arthritis
• Treatment: Allopurinol (xanthine oxidase inhibitor to reduce uric acid production); Colchicine (acute attack)

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SLIDE 28 (31A) - Acute Pancreatitis (Amylase + Lipase)

• Pancreatic acinar cell destruction releases both enzymes into blood
• Serum Lipase is more specific for pancreatitis than amylase (lipase not elevated in parotitis)
• Urinary amylase (diastase): amylase is small enough to be filtered by glomerulus → elevated in blood → spills into urine. It remains elevated longer than serum amylase (useful for delayed presentation)
• Normal levels: Serum Amylase 50-120 IU/L | Serum Lipase 50-175 IU/L | Urinary amylase 0-375 IU/L

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SLIDE 29 - Lesch-Nyhan Syndrome

• HGPRTase is needed for the purine salvage pathway - it recycles hypoxanthine and guanine back to nucleotides (IMP and GMP)
• Without HGPRTase, hypoxanthine and guanine cannot be salvaged → they are oxidized to uric acid by xanthine oxidase → massive hyperuricemia
• X-linked recessive disorder → affects males
• Uric acid deposits in joints + kidneys
• Neurological effects: dopamine pathway dysfunction in basal ganglia → self-injurious behavior, choreoathetosis, intellectual disability
• Treatment: Allopurinol (reduces uric acid) but does NOT correct neurological problems

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SLIDE 30 (31B) - Chronic Pancreatitis

• Serum Amylase: 280 IU/L (elevated - normal 50-120)
• Urinary Amylase: 520 IU/L (elevated - normal 0-375)

• Chronic alcohol use is the most common cause of chronic pancreatitis (repeated episodes of inflammation → fibrosis)
• In chronic pancreatitis, serum amylase may be less dramatically elevated than in acute pancreatitis (some residual enzyme due to ongoing low-grade damage)
• Repeated attacks triggered by alcohol or fatty meals
• Eventually leads to exocrine insufficiency (malabsorption, steatorrhea) and endocrine failure (diabetes)

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SLIDE 31 (17A) - Myocardial Infarction (Early Hours)

• Creatine Phosphokinase (CK/CPK) - rises first (within 3-6 hours)
• Also: Troponin I, Troponin T (begin rising around 3-4 hours)

• Males: 15-100 IU/L
• Females: 10-80 IU/L

• CK has 3 isoenzymes: CK-MM (skeletal muscle, 97% of total CK), CK-MB (cardiac muscle), CK-BB (brain)
• CK-MB >6% of total CK is diagnostic of MI
• Troponins are now the preferred gold standard but CK-MB remains important

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SLIDE 32 (17B) - Myocardial Infarction (Multiple Enzyme Elevation)

• All three enzymes originate from cardiac muscle when myocytes die during infarction
• CK (CK-MB fraction): earliest marker
• LDH: late marker, persists for 7-10 days
• AST (SGOT): also released from heart muscle during MI; elevated at 24-48 hours

• LFTs are normal → liver is intact
• AST elevation alone without ALT elevation suggests myocardial (not hepatic) origin (ALT is more liver-specific; AST is found in both heart and liver)
• Obese middle-aged man with dizziness, dyspnea, chest pain = classic MI presentation

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Summary Table: Jaundice Differential (key exam topic from these slides)