Fe deficiency & other disorders of Fe metabolism Flashcards
Differentiate b/w IDA (Fe deficiency anaemia) vs ACD (anaemia of chronic disease)
IDA: dec. CHr + inc sTfR + decreased MCV
ACD: not change CHr + sTfR + MCV
Describe absorption of iron
- Fe3+ converted to Fe2+ by duodenal cytochrome B (reductase) on lumen of enterocyte
- Fe2+ absorbed via divalent metal transporter 1 (DMT1) through brush border memb. in duodenum
- Stored in cell - Fe2+ binds to ferritin
- OR Fe2+ converted to Fe3+ by Hephaestin (oxidase) & then transported out via ferroportin-1 (FNP1) in blood
General overview of Iron metabolism
- Fe3+ absorbed via duodenum
- Converted to Fe2+
- Fe2+ stored in ferritin in macrophages
4.
Describe transport & regulation of iron
- Fe3+ binds to transferrin
- transferrin + Fe3+ -> to liver
- Hi [Fe3+] detected => hepcidin released by hepatocytes
- Inhibits ferroportin-1 ≠ stop release of Fe3+ in blood
3 Situations that regulate hepcidin release
- Hi [Fe3+] released in blood
- Anaemia & hypoxia = dec hepcidin = inc. Fe uptake & metabolism
- Inflammation (IL-6) = Hi lvls of hepcidin = inhibit Fe metabolism = anaemia of chronic disease
Explain iron metabolism in erythtropoeisis
Nurse cell (Fe-containing macrophage) transfers Fe to erythroid cells = Erythroblastic island
Stages to developing IDA
- Iron depletion (ID)
- iron deficient erythropoeisis (IDE)
- Iron deficiency anaemia (IDA)
IDA: Cause, which classification it lies under, Morph
a. Fe deficeint
b. Functional: maturation, cytoplasmic
c. microcytic, hypochromic
Results expected to see in blood film & bone marrow of IDA patient
- B FIlm: microcytes, hypochromasia, poikilocytosis, dec. reticulocyte count
- BM: inc. cellularity (erythroid), decreased M:E ratio; absent of haemosiderin in macrophage (Perl’s Prusian blue stain)
Results expected to see FBC of IDA patient
Decreased: Hb, MCV, MCH, MCHC
increased: RDW (wider dist. of RBC size bc micro&normocytic)
Further tests for IDA
- Transferrin (Tf)/TIBC
- Serum iron (SI)
- % saturation
- Soluble transferrin receptor (sTfR)
ACD: What, Morph, expected lab assess., some eg of aetiology
a. mild-moderate anaemia
b. normocytic & normochromic
c. no inc. in reticulocytes
d. DM, malignancy, inflammatory disorders (IL-6 => inc hepcidin = dec. Fe availability)
sideroblastic anaemia: What’s happening, appearance of cells, expected lab assess., some eg of aetiology
a. build up of Fe in mitochon.
b. Fe (stained by Prussian blue) around nucleus = ringed sideroblast & pappenheimer bodies (purple dot in RBC)
Pathophysiology of ACD
Dysregulation of Fe homeostasis
- IL6 => inc hepcidin production = dec. Fe availability
Erythropoesis inhibited
- IL1, TNF-a inhibit renal EPO production = down regulated EPO receptor = dec response to EPO = dec. # reticulocytes
what does cellular hemoglobin in reticulocytes (CHr) detect?
hypochromic reticulocytes
