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Clinical Medicine Lecture: _____ Topic: ____________________________________________________________ Date: ______________

Iron Deficiency Anemia Sideroblastic Anemia Anemia of Chronic Disease


1. Dietary Lack Not pathognomonic of any one disease Reduction in proliferation of erythroid
2. Impaired absorption Results from a lack of heme due to poor iron progenitors AND impaired iron utilization
3. Increased requirement incorporation Persistent systemic inflammation associated
Etiology 4. Chronic blood loss with chronic disease leads to impaired RBC
(Pathophysiology): o Most common cause of iron deficiency in production by triggering release of hepcidin
the Western world from the liver making iron less available and
o Internal bleeding may occur as a result of inflammation also inhibits marrow.
cancer
Most common nutritional disorder on Earth Excessive alcohol consumption
o Most common in toddlers, adolescent girls, Myelodysplastic Syndrome (MDS)
Risk Factors and women of childbearing age Mitochondrial disorders
(Demographics): Other copper deficiency, vitamin B-6
(pyridoxine deficiency), lead poisoning, drugs,
hypothermia
S/S of Anemia: S/S of Anemia: S/S of Anemia:
Pallor Pallor Pallor
Fatigue/reduced exercise capacity Fatigue/reduced exercise capacity Fatigue/reduced exercise capacity
Dyspnea on exertion Dyspnea on exertion Dyspnea on exertion
Clinical
the underlying chronic disease
Manifestations
(Signs and
Advanced Iron Deficiency: Sideroblastic Anemia S/S: Most are so mild they have no symptoms
Cheilosis/cheilitis Polyuria, blindness, deafness, optic atrophy
Symptoms):
Koilonychia (associated with DIDMOAD syndrome
Pica diabetes insipidus, diabetes mellitus, optic
Plummer-Vinson Syndrome atrophy, and deafness)
o Esophageal webs (dys/odynophagia)
1. CBC 1. CBC 1. CBC
o Hgb low o Hgb moderately low (9-10) o RBC count decreased
o Hct low o Hct low o Hgb mild to moderate decrease
o MCH, MCHC low o MCH, MCHC low o Hct mild to moderate decrease
o MCV low o MCV low o MCH, MCHC normochromic
2. Peripheral Smear and Reticulocytes 2. Peripheral Smear and Reticulocytes o MCV normocytic
o RBC Appearance microcytic, o RBC Appearance microcytic, o Neutrophilia, monocytosis, and
hypochromic hypochromic thrombocytosis due to underlying disease
Diagnostic Studies:
In severe anemia (7-8 g/dL) o Siderocytes with Pappenheimer bodies 2. Peripheral Smear and Reticulocytes
codocytosis and poikilocytosis o Basophilic stippling of the RBCs is lead o RBC Appearance normocytic,
o Absolute Reticulocytes (0.5-1.5%) poisoning normochromic (75%)
o Reticulocyte Index (1-3%) o Reticulocytes o Reticulocytes
Too few poor RBC production (not Too few poor RBC production (not Too few poor RBC production (not
enough iron) enough heme) enough heme)
3. Iron Studies 3. Iron Studies 3. Iron Studies and Other
o Ferritin low o Ferritin normal o Ferritin increased (as a non-specific
Most convenient test for estimating o SI normal inflammatory reactant)
iron stores o TIBC normal o SI decrease
o Serum Iron (SI) low o TSAT normal o TIBC increase
o Total Iron Binding Capacity (TIBC) high 4. Hemoglobin electrophoresis (probably) o TSAT decrease
o Transferrin saturation (TSAT) low o Normal o Other If these are found, then you can
4. Other 5. Bone Marrow Analysis suspect that the lever and marrow are
o Serum erythropoietin level increased o Definitive/Gold Standard necessary to affected
o RBC protoporphyrin levels increased ( find the RINGED SIDEROBLASTS C-reactive protein (CRP)
100 g/dL, normal is <30 g/dL) 6. Other Erythrocyte sedimentation rate
5. Bone Marrow Analysis o Serum lead, ethanol, copper, zinc, - (ESR, Sed Rate)
o Definitive/Gold Standard (but not glutamyltransferase, vitamin B-6 Hepcidin level
necessary) differentiation between iron Growth differentiation factor 15
deficiency and sideroblastic anemia 4. Plasma erythropoietin level
Too few sideroblasts NOT o May or may not be decreased (EPO levels
RINGED <500 mU/mL may respond to an EPO-
stimulating agent)
1. Oral iron Considerations: Preferred initial therapy is correction of the
o Indications Asymptomatic (no advanced Removal of toxic agents underlying disorder
anemia sx) patient with known iron Pyridoxine, thiamine, and/or folic acid If EPO level decreased and no malignancy
deficiency Transfusions (along with antidotes/chelation if and Hgb is <10 g/dL, then EPO (30,000 to
o Ferrous sulfate 325 mg PO TID for 6-12 iron overload develops from transfusion) 40,000 SQ once weekly) or darbepoetin (300
months (to achieve marrow iron stores of Bone marrow transplantation mcg Q 3 weeks)
0.5-1 g) o LAST RESORT o If using either, should also give
Results in absorption of 50 mg of Liver transplantation supplemental iron
elemental iron per day, which supports o Response Hgb increases 0.5 g/dL by 2-
a RBC production level of 2-3 x normal 4 weeks
o Reticulocyte count should begin to o Stop when hemoglobin levels reach 12
increase within 4-7 days after initiation of g/dL
therapy and peak at 1-1 weeks PRBC transfusion if there is insufficient time
Treatment (First & 2. Parenteral Iron for the patient to respond to above treatments
Second Line): o Indications AND symptomatic anemia
Inability to tolerate oral iron
Needs are relatively acute
Ongoing iron needs, usually due to
PERSISTENT GI blood loss
o 100 mg of elemental iron weekly x 10
weeks
3. RBC transfusion
o Indications
Symptoms of anemia
Cardiovascular instability
Continued and excessive blood loss
from whatever source and who
require immediate intervention
Referral: PRN Hematology recommended for all Not usually necessary