Clinical Chemistry 2 (Prelims) — Liver Function, Jaundice, Bilirubin, Enzymes, Hepatitis, and Endocrine Topics

A comprehensive set of practice flashcards covering jaundice and bilirubin metabolism, liver diseases and enzymes, hepatitis viruses, and key aspects of pituitary and thyroid endocrinology as presented in the notes.

What is jaundice (icterus)?

A yellow discoloration of the skin, eyes, and mucous membranes due to increased bilirubin in serum.

What is the normal bilirubin range?

0.2–1.0 mg/dL.

How is jaundice classified by site?

Prehepatic, hepatic, and posthepatic (based on where the bilirubin metabolism problem occurs).

What causes Gilbert's syndrome?

Most common cause of jaundice; intermittent unconjugated hyperbilirubinemia due to a mutation in the UGT1A1 gene (UDP-glucuronosyltransferase).

What are Crigler-Najjar syndrome types I and II?

Congenital deficiency of UDPGT; Type I = complete absence of conjugation; Type II = partial deficiency; risk of kernicterus.

What characterizes Dubin-Johnson syndrome?

Conjugated hyperbilirubinemia with dark liver pigment due to impaired excretion of conjugated bilirubin into bile.

What is Rotor syndrome?

Conjugated hyperbilirubinemia due to hepatic storage/excretion defect; unlike Dubin-Johnson, the liver pigment is not darkened.

What is physiologic jaundice of the newborn?

Mild unconjugated hyperbilirubinemia due to immature UDPGT in newborns; usually self-limited.

Difference between conjugated and unconjugated bilirubin in terms of solubility?

Conjugated bilirubin is water-soluble and excreted in bile; unconjugated bilirubin is not water-soluble and is albumin-bound.

What is kernicterus?

Deposition of indirect (unconjugated) bilirubin in brain nuclei causing neuronal degeneration and potential death.

What are common signs/symptoms of cirrhosis?

Fatigue, weight loss, nausea, jaundice, edema, ascites, hepatomegaly/splenomegaly, itching.

Cirrhosis causes?

Chronic alcoholism, chronic hepatitis, autoimmune hepatitis, inherited disorders, nonalcoholic fatty liver disease, bile duct obstruction, drugs, toxins, infections.

Three stages of alcohol-induced liver injury?

Alcoholic fatty liver (steatosis) → Alcoholic hepatitis → Alcoholic cirrhosis.

What scoring systems are used for alcoholic hepatitis?

Maddrey's Discriminant Function (MDF), Model for End-Stage Liver Disease (MELD), Glasgow Alcoholic Hepatitis Score (GAHS), Lille score.

What is a key drug associated with severe hepatic injury?

Acetaminophen (paracetamol) in massive dosage.

What is Reye’s syndrome?

Acute noninflammatory encephalopathy with fatty degeneration of the liver, often after aspirin use in children with viral infection; ammonia and AST/ALT elevated.

Difference between primary and metastatic liver tumors?

Primary tumors originate in the liver; metastatic disease (90–95%) spreads from colon, lung, breast, etc.

Name a benign liver tumor in women of childbearing age.

Hepatic adenoma.

What is a hemangioma in the liver?

A benign mass of blood vessels in the liver with no known etiology.

What is hepatocellular carcinoma (HCC)?

The most common malignant tumor of the liver; also called hepatocarcinoma or hepatoma.

What is hepatoblastoma?

A hepatic malignancy of children.

What is the diazo reaction in bilirubin testing?

Bilirubin reacts with a diazotized sulfanilic acid solution to form a colored product (azobilirubin).

What did Malloy-Evelyn contribute to bilirubin measurement?

First clinically useful bilirubin quantitation using the classic diazo reaction with 50% methanol as accelerator.

What is Jendrassik–Grof method?

Diazo reaction using caffeine-benzoate-acetate (accelerator) to solubilize unconjugated bilirubin.

What is delta bilirubin?

Conjugated bilirubin covalently bound to albumin; seen with significant hepatic obstruction.

What is bilirubinometry?

Measurement of bilirubin by reflectance spectroscopy in the neonatal population.

What reagents/accelerators solubilize unconjugated bilirubin in testing?

Caffeine-sodium benzoate or caffeine-benzoate-acetate; methanol as accelerator.

Role of ascorbic acid in bilirubin testing?

Stops the diazo reaction and destroys excess diazo reagent to prevent overestimation.

What is the function of alkaline tartrate in bilirubin testing?

Alkalinizes the solution and shifts the azobilirubin absorbance to a blue color, read at 600 nm.

What is measured in bilirubin testing?

Total bilirubin, conjugated bilirubin, unconjugated bilirubin, and delta bilirubin.

Preanalytical handling for bilirubin tests?

Serum or plasma, fasting preferred, protect from light, avoid hemolyzed or lipemic samples, separate serum/plasma if testing is delayed.

What are common sources of error in bilirubin methods?

Standardization of instruments, hemolysis, lipemia, improper storage.

What is urobilinogen?

End product of bilirubin metabolism; produced in the gut, excreted in feces (stercobilin) or reabsorbed to liver (enterohepatic circulation) or excreted by kidneys.

What is Ehrlich’s reagent used for?

p-Dimethylaminobenzaldehyde; used to detect urobilinogen (red color) in urine testing.

Urine urobilinogen units and reference range?

1 Ehrlich unit ~ 1 mg of urobilinogen; typical range 0.1–1.0 Ehrlich units/2 h or 0.5–4.0 Ehrlich units/day.

Fecal urobilinogen measurement method?

Alkaline ferrous hydroxide redox method; normal 75–275 Ehrlich units/100 g fresh feces (75–400 Ehrlich units/24 h).

Which enzymes are hepatocellular markers?

AST (formerly SGOT) and ALT (formerly SGPT); ALT is more liver-specific.

What does ALP indicate in liver disease?

Alkaline phosphatase; elevated in biliary obstruction and cholestasis; also elevated in bone disease.

What is 5′-nucleotidase (5′-NT) useful for?

Liver-specific marker that helps differentiate ALP elevations due to liver disease from bone disease.

What is GGT and what does it indicate?

Gamma-glutamyl transferase; sensitive marker of cholestasis; elevations with alcohol or drug ingestion; helps confirm hepatic origin of ALP elevations.

What is LDH's role in liver pathology?

Lactate dehydrogenase; a nonspecific marker of cellular injury; can be high in carcinoma.

Why is prothrombin time important in liver disease?

Reflects hepatic synthetic ability for clotting factors; prolonged PT indicates poor prognosis and progression monitoring, not diagnostic by itself.

What happens to albumin and globulins in chronic liver disease?

Albumin decreases; gamma globulins (including IgM) increase (e.g., IgM ↑ in primary biliary cirrhosis; IgA ↑ in alcoholic cirrhosis).

Ammonia and hepatic encephalopathy?

The liver converts ammonia to urea; high ammonia indicates liver failure and risk of hepatic coma; samples must be kept on ice and processed promptly.

What are HAV serology and transmission features?

Hepatitis A virus; fecal-oral transmission; IgM anti-HAV indicates acute infection; IgG anti-HAV indicates past exposure; vaccine available.

HBV serology markers and what they indicate?

HBsAg (first marker; current infection or vaccination), Anti-HBc IgM (acute infection), Anti-HBc IgG (past or chronic), HBeAg (active replication; high infectivity), Anti-HBe (lower infectivity), Anti-HBs (immunity).

HBV vaccination and HBIG use?

HBV vaccine provides active immunization; Hepatitis B immune globulin (HBIG) provides passive anti-HBs for post-exposure prophylaxis.

Chronic HBV phases?

Immune tolerance, immune clearance (HBeAg-positive chronic hepatitis), inactive HBsAg carrier, reactivation.

Which viruses cause chronic hepatitis commonly with risk for cirrhosis and HCC?

HBV and HCV; HDV can accelerate disease in HBV-infected individuals.

What is the role of HDV?

Delta hepatitis; defective RNA virus requiring HBsAg for replication; serology includes anti-HDV and HDV RNA; prevention includes HBV vaccination.

HEV characteristics?

Enterically transmitted hepatitis E virus; fecal-oral transmission; IgM anti-HEV indicates recent infection; can be severe in pregnancy; no widely available vaccine.

HBV perinatal infection risk?

Perinatal transmission has a high risk of chronic infection (about 90% perinatal); risk persists in childhood (20–30%).

Pituitary anatomy overview?

Hypophysis (pituitary) with anterior (adenohypophysis), intermediate, and posterior (neurohypophysis) parts.

Trophic hormones of the anterior pituitary?

LH, FSH, TSH, ACTH (targeting gonads, thyroid, adrenal cortex respectively).

Direct effectors of the pituitary?

Growth hormone (GH) and Prolactin (PRL).

What controls prolactin secretion?

Dopamine (inhibits secretion) and circadian rhythm; pregnancy and nursing increase prolactin; suckling provokes episodic prolactin release.

What are prolactin’s clinical effects in women and men?

Women: luteal abnormalities, oligomenorrhea or amenorrhea; galactorrhea. Men: hypogonadism, decreased libido, impotence.

Prolactin reference range and testing?

Females 1–25 ng/mL; Males 1–20 ng/mL; measured by immunoassay.

What is a prolactinoma?

Prolactin-secreting pituitary adenoma; can occur with acromegaly; diagnosed by elevated prolactin and imaging.

What is IGF-1's role in GH assessment?

Insulin-like growth factor 1; used with stimulation data to assess GH axis; normal levels and stimulation tests help diagnose GH deficiency or excess.

How is growth hormone deficiency evaluated?

GH stimulation tests (e.g., insulin tolerance test) with IGF-1 measurements; OGTT-based suppression tests for acromegaly.

What is ghrelin?

Hunger hormone; stimulates GHRH and GH; increases appetite and affects glucose metabolism; pulsatile secretion with sleep stages.

What is the function of somatostatin?

Inhibits GH and TSH secretion, as well as insulin and several gut hormones.

What is somatotropin (GH) measurement standard for diagnosing GH disorders?

Baseline IGF-1 as screening; confirm with GH stimulation tests (e.g., ITT) and glucose suppression tests for acromegaly.

What is ADH (vasopressin) and its main action?

Antidiuretic hormone; acts on renal collecting ducts via V2 receptors to increase water reabsorption and maintain osmolality and blood pressure.

What is diabetes insipidus (DI) and its two main forms?

Condition characterized by diluted urine due to insufficient ADH action; central (decreased ADH) and nephrogenic (renal resistance to ADH).

What is the water deprivation test used for?

Differentiates central vs nephrogenic DI by assessing ADH response and renal water reabsorption after exogenous ADH.

What is oxytocin (pitocin) and its clinical use?

Posterior pituitary hormone; stimulates uterine contractions and milk ejection; used clinically to induce labor.

What are the functions of oxytocin during labor and lactation?

Stimulates uterine contractions, stimulates milk ejection, facilitates maternal behaviors; release triggered by cervical stretching and nursing cues.

What is thyroid anatomy basics?

Thyroid composed of lobes connected by an isthmus with follicles producing thyroid hormones (T4/T3) and parafollicular C cells producing calcitonin.

What are the major thyroid hormones and their precursors?

T4 (thyroxine) and T3 (triiodothyronine); TBG as binding protein; free fractions (fT4, fT3) are clinically important.

What is the primary test for thyroid function and its typical target?

Thyroid-stimulating hormone (TSH) is the principal test; free T4 and free T3 help interpret thyroid status; goal is usually specific TSH ranges in treatment.

What is thyroglobulin (Tg) used for?

A thyroid follicular cell product; used to monitor for recurrence or persistence of well-differentiated thyroid carcinoma.

What is calcitonin and its clinical use?

Hormone produced by parafollicular C cells; a tumor marker for medullary thyroid carcinoma (MTC).

What are TPO antibodies and Tg antibodies?

Autoantibodies against thyroid peroxidase (TPO) and thyroglobulin (Tg); associated with Hashimoto thyroiditis and autoimmune thyroid dysfunction.

What are TRAb (TSH receptor antibodies)?

Antibodies against the TSH receptor; implicated in Graves disease and can predict disease activity and remission.

What is Graves disease?

Autoimmune hyperthyroidism caused by TSH receptor-stimulating antibodies; often with goiter and ocular features; suppression of TSH with elevated T3/T4.

Why is urinary iodine measurement important?

Iodine is required for thyroid hormone production; urinary iodine excretion estimates dietary iodine intake and helps interpret thyroid function tests.

Why is newborn TSH screening important?

Early detection of congenital hypothyroidism; thresholds guide retesting (e.g., TSH values guiding follow-up).

What is L-thyroxine (L-T4) therapy and its goal?

Replacement therapy for hypothyroidism; goal is achieving a TSH in the reference range (often 0.5–2.0 mIU/L in adults).

What is calcitonin’s role in thyroid cancer management?

Marker for medullary thyroid carcinoma (MTC); monitored after thyroidectomy to assess residual or metastatic disease.

What is neonatal hypothyroidism?

Congenital deficiency of thyroid hormone production or action; screened via newborn screening; requires treatment to prevent developmental delay.

What is Hashimoto thyroiditis?

Autoimmune thyroiditis with anti-TPO and anti-Tg antibodies; typically causes hypothyroidism with elevated TSH.