Anemias Flashcards
Describe IDA (Iron deficiency Anemia)
common?
types of rbcs?
most common world wide 2% of men 5% of women
microcytic/hypochromic rbcs (due to decrease hgb/iron)
Describe causes of IDA
Increased demand (childhood/preg)
Excess loss (Menstruation/chronic bleeding)
Decreased absorption (gastrectomy/malabsorption)
Iron poor diet (milk babies/elderly)
Describe stage 1 of IDA
BM
Serum iron
Pt response
hgb/rdw
Ferritin levels
iron depletion
iron in bm decreased to absent
NO DECREASE IN SERUM IRON
pt is asymptomatic/hgb norm/RDW slightly increased
ferritin decreased
Describe stage 2 of IDA
Hgb
Hct
Serum Iron
ZPP/FEP
iron deficiency EPO
hgb decreases
hgb content of rbcs (CHr) decreased
hct normal
serum iron decreased
FEP/ZPP increased
Describe stage 3 of IDA
classic iron deficiency
serum iron/ferritin/% sat/BM Iron/MCHC/hepcidin decreased
STFR TIBC FEP/ZPP increased
Describe ACI (anemia of chronic inflammation)
what can cause it?
chronic disease, secondary to other disease/inflamm/supressive effect
ex. chronic infect
AI
infectious mono
malignancies
TRAPPED IN MACROPHAGES
What are some proposed mechanisms of ACI ?
overactivates what
Inability of rbc to access iron trapped w/in macrophages (Mediated by HEPCIDIN)
Ineffective EPO
Hemolysis overactivates RES
Briefly describe the mechanism of ACI
invasion of malignancy induces cytokines
stimulation of hepcidin/inactivates ferroportin
iron stuck in macrophages
increase DMT1 damage to rbc membrane
inhibit of EPO/no precursors
How do you distinguish between IDA and ACI?
looks similar to distinguish via TIBC and ferritin levels
Lab findings of ACI
Serum iron
ferritin
BM
TIBC
Hepcidin
%sat
serum iron DECREASED TRAPPED IN MACROS
ferritin increase
BM stores increased
TIBC decreased
HEPCIDIN INCREASED
%sat decreased
Important lab findings of ACI
Increased Hepcidin
Serum Iron Low
BM stores high
IDA Review: causes
increased demand
increased loss
decreased absorption
iron poor diet
MICRO/HYPO
ACI review:
causes
inactivates
mediated by
2nd to disease to inflammation
decreased epo
increased hemolysis
MEDIATED BY HEPCIDIN
Inactivates ferroportin
Describe Sideroblastic anemia
defect in what
Hereditary disorders (2)
defect in heme synthesis/inadequate iron utilization
Hereditary defect (rare)
1.) x linked (ALAS2)
2.) recessive Stem cell dysfunction (decreased heme/pancytopenia)
Describe the Aquired defect diseases in Sideroblastic anemia
(2)
Primary - myelodysplastic syndromes
Secondary (exposures) toxins/ LEAD poisoning etc
Briefly describe lead poisoning and the pathways it interferes with
interferes with 3 paths
5-ALA - prophobiligen
Copro III - Protop III
LEAD INHIBITS FERROCHELATASE
Describe the Lab results of Sideroblastic Anemia
HGB/HCT
RBC population
RBC inclusions
low hgb/hct
RBC: dimorphic/micro/hypo
baso stippling
PAPPENHEIMERS
target cells
What does the BM look like in Sideroblastic anemia
erythroid hyperplasia (ineffective EPO) (mainly rbcs)
RINGED SIDEROBLASTS (nrbcs)
Sideroblastic anemia
Serum Iron
TIBC
Serum ferritin
STfRs
FEP/ZPP
Hepcidin
Serum iron increased (overload)
TIBC norm/low
Serum ferritin Increased
STfRs norm/low
FEP/ZPP high
Hepcidin High