Comprehensive Molecular, Biochemical, and
Clinical Insights into Hemoglobin Metabolism,
Heme Catabolism, Iron Homeostasis, Bilirubin
Pathways, and Hemoglobinopathies for High-
Yield Board Examination Mastery Exam
Questions Verified and Provided with A+
Graded Rationales Latest Updated 2026
What is hemoglobin broken down into?
heme (Fe3+ & bilrubin)
globin (amino acids)
What is heme broken down into?
iron (Fe3+)- ferric iron
bilirubin
where does the iron go that was broken down from heme?
to the liver
- meets up with transferrin and is taken into the liver via Tf-receptor where it then gets stored
as ferritin
What are some ways we can get too much iron?
- high iron intake
- HFE protein not working
- repeated transfusions
What does excess iron get converted into?
Hemosiderin - an extremely insoluble compound that consists of crystalline aggregates of
ferritin
- will go to our joints and cause pain (ex. joint pain in the knuckles)
Steps of heme degradation
1) Heme → biliverdin *heme oxygenase*
2) Biliverbin → unconj. bilirubin *biliverdin reductase*
1|Page
, 3) Bilirubin transported to liver on albumin
4) Unconj. bilirubin → bilirubin diglucuronide (conj.) *bilirubin glucuronyl transferase* & UDP
5) Conj. bilirubin transported to intestines
6) Conj. bilirubin → Bilirubin
7) Bilirubin → urobilinogen & stercobilin
8) INTESTINES: Urobilinogen & stercobilin → FECES
8) KIDNEYS: Urobilinogen → urobilin → URINE
What converts heme to biliverdin?
What converts biliverdin to bilirubin?
heme oxygenase
biliverdin reductase
What carries bilirubin to the liver?
albumin
What converts unconjugated bilirubin to conjugated bilirubin?
UDP glucuronyl transferase
What gives stool its brown color?
What gives urine its yellow color?
sterocobilin
urobilinogen → urobilen
Hereditary Hemochromatosis
What is significant about the Fe blood levels (inc./dec.)? TQ
Defective human chromatosis protein (HFE) allows for excess Fe absorption
- HFE normally regulates interaction of TF and TF-receptor
Creates Iron Overload (Hemochormatosis) state
-caused by accumulation of hemosiderin
2|Page
Clinical Insights into Hemoglobin Metabolism,
Heme Catabolism, Iron Homeostasis, Bilirubin
Pathways, and Hemoglobinopathies for High-
Yield Board Examination Mastery Exam
Questions Verified and Provided with A+
Graded Rationales Latest Updated 2026
What is hemoglobin broken down into?
heme (Fe3+ & bilrubin)
globin (amino acids)
What is heme broken down into?
iron (Fe3+)- ferric iron
bilirubin
where does the iron go that was broken down from heme?
to the liver
- meets up with transferrin and is taken into the liver via Tf-receptor where it then gets stored
as ferritin
What are some ways we can get too much iron?
- high iron intake
- HFE protein not working
- repeated transfusions
What does excess iron get converted into?
Hemosiderin - an extremely insoluble compound that consists of crystalline aggregates of
ferritin
- will go to our joints and cause pain (ex. joint pain in the knuckles)
Steps of heme degradation
1) Heme → biliverdin *heme oxygenase*
2) Biliverbin → unconj. bilirubin *biliverdin reductase*
1|Page
, 3) Bilirubin transported to liver on albumin
4) Unconj. bilirubin → bilirubin diglucuronide (conj.) *bilirubin glucuronyl transferase* & UDP
5) Conj. bilirubin transported to intestines
6) Conj. bilirubin → Bilirubin
7) Bilirubin → urobilinogen & stercobilin
8) INTESTINES: Urobilinogen & stercobilin → FECES
8) KIDNEYS: Urobilinogen → urobilin → URINE
What converts heme to biliverdin?
What converts biliverdin to bilirubin?
heme oxygenase
biliverdin reductase
What carries bilirubin to the liver?
albumin
What converts unconjugated bilirubin to conjugated bilirubin?
UDP glucuronyl transferase
What gives stool its brown color?
What gives urine its yellow color?
sterocobilin
urobilinogen → urobilen
Hereditary Hemochromatosis
What is significant about the Fe blood levels (inc./dec.)? TQ
Defective human chromatosis protein (HFE) allows for excess Fe absorption
- HFE normally regulates interaction of TF and TF-receptor
Creates Iron Overload (Hemochormatosis) state
-caused by accumulation of hemosiderin
2|Page
