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(CK, Troponins, LDH, Cardiac Disease Markers)
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Enzyme of muscle energy metabolism.
Converts:
Creatine + ATP ⇄ Creatine phosphate + ADP
| Isoenzyme | Location | Clinical Use |
|---|---|---|
| CK-BB (CK1) | Brain, lung | CNS injury |
| CK-MB (CK2) | Heart | MI marker |
| CK-MM (CK3) | Skeletal muscle | Muscle injury, rhabdomyolysis |
Rises: 3–6 hours
Peak: 18–24 hours
Returns to normal: 2–3 days
Useful for detecting reinfarction because it falls early.
MI (CK-MB)
Myocarditis
Duchenne muscular dystrophy
Rhabdomyolysis
Polymyositis
Hypothyroidism
Seizures, trauma
(Most sensitive & specific markers of myocardial injury)
Troponin C: Calcium binding
Troponin I: Inhibitory subunit
Troponin T: Tropomyosin-binding
Cardiac forms are unique, so highly specific.
Rises: 3–4 hours
Peak: 24–48 hours
Stay elevated: 7–14 days (very long)
Most specific marker for MI
Detected early
Useful even in small non-STEMI
Remains elevated long after CK-MB normalizes
MI
Myocarditis
Takotsubo cardiomyopathy
Sepsis
Renal failure
Severe pulmonary embolism
Heart failure (acute)
Converts:
Lactate ⇄ Pyruvate
| Isoenzyme | Organ | Note |
|---|---|---|
| LDH1 | Heart, RBCs | Flipped pattern in MI |
| LDH2 | Heart, RBCs | Normally > LDH1 |
| LDH3 | Lung | Pneumonia, pulmonary infarct |
| LDH4 | Kidney, pancreas | Renal diseases |
| LDH5 | Liver, muscle | Liver injury, rhabdomyolysis |
LDH1 > LDH2 (flipped pattern) = classic sign of MI
Rises: 12–24 hours
Peaks: 2–3 days
Duration: 7–10 days
Useful when patient presents late.
MI
Hemolysis
Megaloblastic anemia
Liver disease
Cancer
Muscle injury
Kidney disease
Troponin I & T → gold standard
CK-MB → reinfarction detection
Myoglobin → earliest marker but nonspecific
| Marker | Rise | Peak | Normalization |
|---|---|---|---|
| Myoglobin | 1–2 h | 6–9 h | 24 h |
| CK-MB | 3–6 h | 18–24 h | 2–3 d |
| Troponin I/T | 3–4 h | 24–48 h | 7–14 d |
| LDH | 12–24 h | 2–3 d | 7–10 d |
From ventricles during stretch → marker of heart failure.
Marker of inflammation
Predictor of atherosclerosis and CV risk.
Mildly elevated in MI but nonspecific.
Released early after MI; used with troponin as dual marker.
Troponin = best, most specific MI marker.
CK-MB = best for reinfarction detection.
LDH1/LDH2 flip = late MI marker.
Myoglobin = earliest rising but poorest specificity.
BNP = heart failure marker.
High troponins may occur without MI in renal failure and sepsis.
Catalyzes:
Aspartate + α-ketoglutarate ⇄ Oxaloacetate + Glutamate
Requires pyridoxal phosphate (Vitamin B6).
Highly concentrated in:
Heart
Liver
Skeletal muscle
Kidneys
RBCs
Marker of hepatocellular injury
Also elevated in muscle injury, cardiac injury, hemolysis
AST : ALT > 2 → Alcoholic liver disease (very high-yield)
AST > ALT → Cirrhosis, muscle disease
ALT > AST → Viral hepatitis (usually)
Acute viral hepatitis
Alcoholic hepatitis
Myocardial infarction
Muscle trauma, rhabdomyolysis
Hemolysis
Catalyzes:
Alanine + α-ketoglutarate ⇄ Pyruvate + Glutamate
Requires Vitamin B6.
Most specific enzyme for liver injury
Highest concentration in hepatocytes.
Best marker for hepatocellular damage.
ALT rises higher and stays elevated longer than AST in acute viral hepatitis.
ALT > AST in:
Viral hepatitis
Toxic hepatitis
Non-alcoholic fatty liver disease (NAFLD)
Drug-induced liver injury (DILI)
Seen in:
Acute viral hepatitis
Acetaminophen toxicity
Ischemic hepatitis
Hydrolyzes phosphate esters at alkaline pH (optimal pH ~9–10).
Liver (bile canaliculi)
Bone (osteoblasts)
Intestine
Placenta
Kidney
Elevated in cholestasis (bile obstruction).
Increased in:
Extrahepatic obstruction (stones, tumors)
Intrahepatic cholestasis
Primary biliary cholangitis
Primary sclerosing cholangitis
Elevated when bone turnover is high:
Rickets
Osteomalacia
Paget disease
Bone metastasis
Hyperparathyroidism
Healing fractures
GGT (Gamma-glutamyl transferase):
↑ ALP + ↑ GGT → Hepatobiliary origin
↑ ALP + normal GGT → Bone origin
Pregnancy (placental ALP)
Adolescence (bone growth)
Third trimester
AST → Heart + Liver + Muscle (Alcohol > Viral)
ALT → Most specific for liver (Viral > Alcohol)
ALP → Cholestasis & Bone turnover marker
AST:ALT > 2 → Alcoholic hepatitis
ALP ↑ + GGT ↑ → Obstructive liver disease
ALP ↑ + GGT normal → Bone disorder
Hydrolyzes 5′-nucleotides → nucleosides + phosphate.
Works at alkaline pH, similar to ALP.
Liver (bile canalicular membranes)
Also present in:
Kidney
Intestine
Pancreas
Brain
Very sensitive marker of cholestasis.
Especially useful when ALP is elevated but the source is unclear (bone vs liver).
| Marker | High in Liver Disease? | High in Bone Disease? |
|---|---|---|
| ALP | Yes | Yes |
| GGT | Yes | No |
| 5’-Nucleotidase | Yes | No |
📌 Therefore:
↑ ALP + ↑ 5′-Nucleotidase = Liver source
↑ ALP + normal 5′-Nucleotidase = Bone source
Cholestasis (intra & extrahepatic)
Primary biliary cholangitis
Primary sclerosing cholangitis
Drug-induced cholestasis
Metastatic liver disease
Transfers γ-glutamyl groups in glutathione metabolism.
Helps amino acid transport.
Liver (highest)
Kidney
Pancreas
Intestine
Prostate
Highly sensitive marker of cholestasis & hepatobiliary disease.
Often elevated earlier than ALP.
GGT ↑ + ALP ↑ → hepatobiliary cause.
GGT normal + ALP ↑ → bone disease.
Alcohol intake
Drugs such as phenytoin, phenobarbital → microsomal enzyme induction
Alcoholic liver disease
Fatty liver
Biliary obstruction
Chronic cholangitis
Pancreatic disease
Hepatotoxic drugs
Organize liver biomarkers by type of liver injury:
Most specific marker of liver cell injury.
Higher than AST in viral, toxic, ischemic hepatitis.
Elevated in liver, muscle, and heart injury.
AST:ALT > 2 → alcoholic hepatitis.
Mild elevation in hepatitis.
High LDH with normal ALT suggests ischemic hepatitis.
From bile canalicular cells.
Markedly elevated in obstructive jaundice.
Elevated in liver obstruction & alcohol intake.
Helps differentiate liver ALP from bone ALP.
Highly specific for cholestasis.
Not increased in bone diseases.
Decreased in chronic liver disease.
Prolonged in acute liver failure (short half-life factor VII).
Often decreased in advanced liver disease.
Unconjugated ↑: hemolysis, Gilbert, Crigler–Najjar
Conjugated ↑: cholestasis, Dubin–Johnson, Rotor, hepatocellular injury
Elevated in hepatic encephalopathy.
GGT ↑↑ (enzyme induction)
AST:ALT > 2:1
Macrocytosis (MCV ↑)
High triglycerides
Low magnesium
↓ Albumin
↑ INR
↑ Bilirubin
↓ Platelets (splenic sequestration)
↑ GGT and ALP (if cholestatic component)
AFP (Alpha-fetoprotein) → hepatocellular carcinoma
ALP & GGT ↑ → metastatic liver disease
ALT = Most specific for liver injury
AST:ALT > 2 = Alcoholic hepatitis
ALP ↑ + GGT ↑ = Cholestasis
ALP ↑ + GGT normal = Bone disease
5′-Nucleotidase = Specific for cholestasis
GGT = Alcohol, drugs, liver
Albumin & INR = Liver synthetic function
PT prolongation = Acute liver failure
AFP = HCC marker
Hydrolyzes phosphate esters at acidic pH (~5).
Present in lysosomes.
Prostate (highest concentration)
RBCs
Platelets
Liver
Spleen
Bone (osteoclasts)
Marker of prostate carcinoma (especially metastatic).
Historically used → now replaced by PSA, but still asked in exams.
Increased in:
Hairy cell leukemia (very high-yield)
Osteoclast activity (Paget disease)
Elevated in Gaucher disease and Niemann–Pick disease.
Osteolytic lesions
Paget disease
Hyperparathyroidism
Two types:
Found in RBCs, nerves, neuromuscular junctions.
Rapidly hydrolyzes acetylcholine.
Synthesized in liver.
Found in plasma, liver, pancreas.
Important for drug metabolism.
Indicates impaired hepatic synthesis or inhibition.
Seen in:
Liver failure
Organophosphate poisoning (irreversible inhibition)
Malnutrition
Pregnancy (normal physiological decrease)
Genetic variants (atypical pseudocholinesterase)
Certain drugs:
Succinylcholine
Echothiophate
Neostigmine
Patients show prolonged apnea after succinylcholine because they cannot break it down.
Detected using dibucaine number.
Normal: > 80% inhibition
Heterozygous atypical: 40–70%
Homozygous atypical: < 20%
First enzyme of the HMP (pentose phosphate) pathway.
Produces NADPH, which keeps glutathione (GSH) in reduced form.
GSH protects RBCs from oxidative damage.
RBCs lack mitochondria → NADPH only from HMP shunt.
Without NADPH → oxidative stress → hemolysis.
X-linked recessive disorder.
Most common enzyme defect in humans.
RBCs are vulnerable to oxidative stress.
Drugs:
Antimalarials (primaquine)
Sulfonamides
Nitrofurantoin
Dapsone
Infections
Fava beans (favism)
Naphthalene (mothballs)
Oxidative stress → RBC membrane damage → Hb precipitates into Heinz bodies → removed by spleen → bite cells → hemolytic anemia.
↑ Reticulocyte count
↑ Indirect bilirubin
↓ Haptoglobin
Heinz bodies (crystal violet stain)
Bite cells on peripheral smear
G6PD assay (after hemolysis resolves to avoid false normal result)
Fluorescent spot test
Acute hemolytic crisis after drug/fava beans
Neonatal jaundice
Chronic nonspherocytic hemolytic anemia (rare variant)
ACP: prostate cancer marker; TRAP ↑ in hairy cell leukemia.
Cholinesterase: ↓ in liver failure & organophosphate poisoning; dibucaine number confirms atypical variant.
G6PD: NADPH producer; deficiency → Heinz bodies + bite cells after oxidative stress.
Hydrolyzes starch → maltose & dextrins.
Works at neutral pH.
Pancreatic amylase (P-type)
Salivary amylase (S-type)
Pancreas
Salivary glands
Fallopian tubes
Small intestine
Acute pancreatitis (most important)
Pancreatic trauma
Gallstone obstruction
Mumps (salivary gland inflammation)
Renal failure (reduced clearance)
Macroamylasemia (bound to Ig; benign)
Rises: 3–6 hours
Peaks: 24–30 hours
Returns to normal: 2–4 days
Stays elevated longer than serum.
Useful when serum values normalize early.
Hydrolyzes triglycerides → fatty acids + glycerol.
Produced in pancreatic acinar cells.
Most specific marker for acute pancreatitis (more specific than amylase).
Rises: 4–8 hours
Peaks: 24 hours
Remains elevated: 8–14 days
More specific to pancreas.
Remains elevated longer.
Not affected by salivary gland disease.
Pancreatic cancer
Perforated peptic ulcer
Intestinal obstruction
Renal failure
Cholecystitis
Enzyme of glycolysis:
Fructose-1,6-bisphosphate → DHAP + G3P
Skeletal muscle
Heart muscle
Liver
Brain
Historically used for muscle diseases, but now partly replaced by CK.
Duchenne muscular dystrophy
Inflammatory myopathies:
Polymyositis
Dermatomyositis
Hepatitis
Myocardial infarction
Aldolase rises in muscle disease when CK is normal (e.g., some myopathies).
Glycolytic enzyme:
2-phosphoglycerate → phosphoenolpyruvate (PEP)
Neuron-specific enolase (NSE) → brain
Muscle enolase
Non-specific enolase
Tumor marker for:
Small cell lung carcinoma (SCLC)
Neuroblastoma
Pancreatic endocrine tumors
Stroke
Brain injury
Subarachnoid hemorrhage
Amylase ↑ → acute pancreatitis, mumps, renal failure.
Lipase ↑ → most specific for acute pancreatitis (stays elevated longer).
Aldolase ↑ → muscle diseases like DMD, polymyositis.
NSE ↑ → small cell lung carcinoma, neuroblastoma.
Enzymes used as drugs for treatment of various conditions.
Used to dissolve blood clots.
Streptokinase
From Streptococcus.
Activates plasminogen → plasmin.
Used in MI, DVT, pulmonary embolism.
Urokinase
Direct plasminogen activator.
Used in pulmonary embolism.
tPA (Tissue Plasminogen Activator) / Alteplase
Recombinant human enzyme → very specific.
Used in acute MI, ischemic stroke.
Pancreatin / Pancrelipase
Lipase, amylase, proteases.
Used in chronic pancreatitis, CF.
Lactase
Used in lactose intolerance.
Serratiopeptidase (proteolytic enzyme)
Reduces swelling, inflammation.
Chymotrypsin / Trypsin
Used in wound debridement.
Used in genetic enzyme deficiencies.
Imiglucerase for Gaucher disease
Laronidase for Hurler syndrome
Idursulfase for Hunter syndrome
Agalsidase for Fabry disease
Asparaginase (L-Asparaginase)
Used in ALL (acute lymphoblastic leukemia).
Depletes asparagine → kills leukemic cells.
Dornase alfa (DNase I)
Used in cystic fibrosis to reduce sputum viscosity.
Depolymerizes hyaluronic acid.
Used to increase drug absorption, reduce edema, and in ophthalmic surgery.
Enzymes measured in blood or tissues to diagnose diseases.
CK-MB → myocardial infarction
Troponins (T, I) → most specific for MI
LDH1 > LDH2 flip → late MI
ALT, AST → hepatocellular injury
ALP, GGT, 5′-nucleotidase → cholestasis
LDH5 → liver damage
Amylase, Lipase → acute pancreatitis
Lipase is more specific.
Bone ALP → rickets, Paget disease, bone metastasis
ACP (osteoclast) → bone turnover
CK-MM → skeletal muscle injury
Aldolase → myopathies (DMD, polymyositis)
Acid phosphatase (ACP) → historically used in prostate cancer
Now replaced by PSA, but still asked in exams.
Neuron-specific enolase (NSE) → small cell lung carcinoma, neuroblastoma
Placental ALP → seminoma
G6PD assay → G6PD deficiency
Galactose-1-phosphate uridyl transferase → galactosemia
Enzymes fixed onto a solid support so they can be reused, stabilized, or continuously used.
Reuse of expensive enzymes
Increased stability (temperature/pH)
Easy separation from products
Continuous operation in bioreactors
Increased shelf-life
Physical binding on carriers (charcoal, resins).
Simple, but enzyme may leach out.
Strong binding to support (agarose, silica).
More stable but may reduce activity.
Trapped in polymer matrix (alginate, polyacrylamide).
Substrate must diffuse in and out.
Enzymes enclosed in semipermeable membranes.
Enzymes linked with bifunctional reagents (glutaraldehyde).
Forms large, stable aggregates (CLEAs).
Glucose isomerase → HFCS manufacture
Lactase → lactose-free milk
Lipases → biodiesel production
Proteases → detergent industry
Urease electrodes → biosensors
Glucose oxidase → glucose biosensors (glucometers)
Immobilized DNases and RNases
Immobilized proteases for digestion in mass spectrometry
Streptokinase, alteplase → thrombolytics.
Asparaginase → ALL treatment.
Pancrelipase → chronic pancreatitis.
ALT/AST → liver injury; ALP/GGT → cholestasis.
CK-MB, troponins → MI diagnosis.
NSE → small cell carcinoma.
Immobilized enzymes → glucose oxidase for glucometers; glucose isomerase for HFCS.
These are crisp, high-value facts that students reliably get asked in theory, MCQs, and viva.
Enzymes leak into blood when cells are damaged.
Tissue specificity of an enzyme determines its diagnostic value.
Isoenzymes help localize disease (e.g., CK-MB for heart, LDH isoenzymes for organs).
Half-life of enzymes determines usefulness in early or late diagnosis.
Most specific & sensitive markers of MI.
Rise: 3–4 h, Peak: 24–48 h, Stay high: 7–14 days.
Useful for late presentation.
Rises early and falls early → best to detect reinfarction.
Rise: 3–6 h, Normal: 48–72 h.
CK-MB > 5% of total CK strongly suggests MI.
LDH1 > LDH2 (flip) = classic sign of late MI.
Remains elevated for 7–10 days.
Earliest marker (1–2 h) but not specific.
Most specific marker of hepatocellular injury.
Higher in viral hepatitis.
Found in heart, muscle, liver → less specific.
AST:ALT > 2 → alcoholic hepatitis (very high yield).
Elevated mainly in cholestasis.
Also high in bone disorders.
Elevated in cholestasis + alcohol use.
Helps differentiate liver ALP from bone ALP.
Highly specific for cholestasis.
Normal in bone disease.
Rises rapidly, normalizes in 2–4 days.
Not specific — also ↑ in mumps, renal failure.
More specific for acute pancreatitis.
Stays elevated for up to 2 weeks.
Elevated in skeletal muscle injury, rhabdomyolysis.
Higher in Duchenne muscular dystrophy.
Elevated in muscle diseases, sometimes when CK is normal.
Historically used for prostate cancer.
Now replaced by PSA.
TRAP (tartrate-resistant ACP) high in hairy cell leukemia.
Key enzyme for NADPH.
Deficiency causes oxidative hemolysis → Heinz bodies, bite cells.
Assay should be done after crisis resolves to avoid false normal.
Marker for small cell lung carcinoma and neuroblastoma.
Elevated in seminoma.
Streptokinase, Urokinase, Alteplase (tPA) → thrombolysis in MI, stroke.
Asparaginase → treatment of ALL.
Pancrelipase → chronic pancreatitis.
Dornase alfa (DNase I) → cystic fibrosis.
Hyaluronidase → increases drug diffusion.
Used in glucometers (glucose oxidase).
Used industrially → glucose isomerase for HFCS.
Immobilization improves stability, reuse, and continuous operation.
Troponin = best MI marker.
CK-MB = best for reinfarction.
Lipase > Amylase for pancreatitis.
GGT + ALP ↑ = cholestasis; ALP ↑ + GGT normal = bone disease.
TRAP ↑ = hairy cell leukemia.
ALT > AST = viral hepatitis.
AST > ALT = alcoholic hepatitis.
G6PD deficiency → oxidative hemolysis with Heinz bodies.
NSE ↑ = small cell carcinoma.
A. CK-MB
B. LDH1
C. Troponin I
D. AST
Answer: C. Troponin I
Most sensitive and specific.
A. Troponin T
B. LDH
C. Myoglobin
D. CK-MB
Answer: C. Myoglobin
A. Troponin I
B. CK-MB
C. LDH
D. BNP
Answer: B. CK-MB
Falls early → useful for recurrence.
A. Hepatitis
B. Acute MI
C. Rhabdomyolysis
D. Renal failure
Answer: B. Acute MI
A. ALP
B. AST
C. ALT
D. GGT
Answer: C. ALT
A. Viral hepatitis
B. Alcoholic hepatitis
C. Biliary obstruction
D. Cirrhosis
Answer: B. Alcoholic hepatitis
A. ALP
B. ALT
C. LDH
D. Creatine kinase
Answer: A. ALP
A. Obstructive jaundice
B. Paget disease
C. Rickets
D. Hemolytic anemia
Answer: D. Hemolytic anemia
A. Bone metastasis
B. Alcohol intake
C. Hypothyroidism
D. Viral fever
Answer: B. Alcohol intake
A. LDH
B. CK-MB
C. GGT
D. AST
Answer: C. GGT
A. AST
B. ALT
C. γ-GT
D. 5′-Nucleotidase
Answer: D. 5′-Nucleotidase
A. Amylase
B. Lipase
C. LDH
D. AST
Answer: B. Lipase
A. Acute pancreatitis
B. Mumps
C. Renal failure
D. Malaria
Answer: D. Malaria
A. Diabetes
B. Polymyositis
C. Hypothyroidism
D. Viral fever
Answer: B. Polymyositis
A. CML
B. Hairy cell leukemia
C. Hodgkin lymphoma
D. Cirrhosis
Answer: B. Hairy cell leukemia
A. ALT
B. ACP
C. ALP
D. CK
Answer: B. ACP (prostatic acid phosphatase)
A. ATP depletion
B. Increased 2,3-BPG
C. Failure to regenerate NADPH
D. Vitamin K deficiency
Answer: C. Failure to regenerate NADPH
A. Spherocytes
B. Bite cells
C. Auer rods
D. Target cells
Answer: B. Bite cells
A. CEA
B. AFP
C. NSE
D. CA-125
Answer: C. NSE (Neuron Specific Enolase)
A. Pancreatitis
B. Lactose intolerance
C. Celiac disease
D. Crohn disease
Answer: B. Lactose intolerance
A. Streptokinase
B. Asparaginase
C. Urokinase
D. Lipase
Answer: B. Asparaginase
A. Diagnostic enzyme
B. Therapeutic enzyme
C. Immobilized enzyme (industrial)
D. Fibrinolytic enzyme
Answer: C. Immobilized enzyme
A. Liver function tests
B. Glucometers
C. Lipid profile
D. Tumor markers
Answer: B. Glucometers
A. True cholinesterase
B. Pseudocholinesterase
C. LDH
D. Lipase
Answer: B. Pseudocholinesterase
A. G6PD deficiency
B. Atypical cholinesterase
C. Hemophilia
D. Wilson disease
Answer: B. Atypical cholinesterase
Answer: Early acute MI
(Troponin & CK-MB rise early; LDH is still normal.)
Answer: CK-MB
(Falls within 48–72 hours → useful for detecting new infarction.)
Answer: LDH (LDH1 > LDH2)
(Remain elevated for 7–10 days.)
Answer: Cholestatic liver disease
(All cholestasis markers high.)
Answer: Bone origin
(GGT normal → not hepatobiliary.)
Answer: Alcoholic liver disease
Answer: Acute pancreatitis
(Lipase stays elevated longer.)
Answer: Pancrelipase / Pancreatin
Answer: G6PD deficiency
Answer: G6PD deficiency (neonatal form)
Answer: Pseudocholinesterase
(Diagnosed using dibucaine number.)
Answer: Mumps (parotitis)
Answer: Macroamylasemia
(Amylase binds Ig → cannot pass into urine.)
Answer: Polymyositis / Dermatomyositis
(Aldolase sometimes rises when CK is normal.)
Answer: Gaucher disease
(RBC ACP elevated.)
Answer: Paget disease of bone
(Osteoclast activity → ACP ↑; bone turnover → ALP ↑.)
Answer: PSA (prostate-specific antigen)
Answer: ALP ↑ + GGT ↑
(Best cholestasis combination.)
Answer: Small cell lung carcinoma
Answer: LDH1 > LDH2
(Also seen in MI, but clinical context suggests hemolysis.)
Answer: Skeletal muscle injury or hepatic injury
(AST alone is non-specific.
Answer: Dornase alfa (recombinant DNase)
Answer: Converts plasminogen → plasmin → fibrinolysis
Answer: Liver disease
(Plasma cholinesterase synthesized in liver.)
Answer: ALT ↑↑, AST ↑↑, Cholesterol ↓, PT ↑ (synthetic failure)
A measurable enzyme in blood used to assess organ damage.
High tissue specificity, rapid release after injury, and measurable half-life.
Troponin I / Troponin T.
Myoglobin.
CK-MB.
LDH1 > LDH2 (“flip pattern”).
CK-BB, CK-MB, CK-MM.
CK-MB.
Skeletal muscle injury or rhabdomyolysis.
Lipase.
It has a longer half-life and slower clearance.
Mumps (parotitis).
Serum amylase (urine amylase is low).
ALT (SGPT).
Alcoholic liver disease.
Cholestasis or bone disease.
Check GGT or 5′-nucleotidase.
Elevated = liver source; normal = bone source.
5′-nucleotidase.
Alcohol induces microsomal enzymes, increasing GGT.
Tartrate-resistant acid phosphatase — high in hairy cell leukemia.
Acid phosphatase (ACP).
Neuron-specific enolase (NSE).
Glucose-6-phosphate dehydrogenase.
Generates NADPH for maintaining reduced glutathione.
RBCs cannot handle oxidative stress → Heinz bodies → hemolysis.
Denatured hemoglobin precipitates inside RBCs.
RBCs with portions removed by splenic macrophages removing Heinz bodies.
Primaquine and fava beans.
Pseudocholinesterase deficiency.
To detect atypical pseudocholinesterase.
L-asparaginase.
Streptokinase / Alteplase (tPA).
Pancrelipase.
Glucose isomerase (for HFCS production).
Glucose oxidase.
Reusable, more stable, easy to separate from products.
Liver disease or skeletal muscle injury.
Pulmonary conditions like pneumonia or pulmonary infarction.
Higher specificity and remains elevated longer.
Bone ALP.
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