Lack of iron during heme formation: 1. Increased requirements (pregnancy, growth) 2. Decreased intake (poor diet, malabsorption) 3. Increased loss (hemorrhage)

Micro & Macro Anemia Flashcards by Tatjana Obias

Type of anemia when MCV<80 fL

Microcytic

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Type of anemia when MCV>100 fL

Macrocytic

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M:E ratio is __ in Microcytic anemia

DECREASED; erythroid hyperplasia due to EPO trying to compensate

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Causes of IDA

Lack of iron during heme formation:

Increased requirements (pregnancy, growth)
Decreased intake (poor diet, malabsorption)
Increased loss (hemorrhage)

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Describe 3 stages of IDA

Stored iron (ferritin) is accessed; normal blood results
Stored and serum iron exhausted; iron studies all decreased, dual pop’n of micro/hypo and normo/normo
IDA; iron studies decreased EXCEPT TIBC increased, low Hgb, MCV<80 fL, micro/hypo

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Lab results for IDA (HGB, HCT, RBC, PBS, BM, Indices, WBC, PLT, RETIC, serum iron, serum ferritin TIBC, transferrin sat.)

HGB/ MCH/ MCHC: decreased
HCT: decreased
MCV: <80 fL
RBC: decreased
PBS: hypo/micro
BM: decreased iron stores (prussian-blue)
WBC: decreased M:E ratio
RETIC: decreased
PLT: normal

serum iron: decreased
serum ferritin: decreased
TIBC: INCREASED
transferrin sat: decreased

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Cause of sideroblastic anemia

Decreased protoporphyrin production OR inability to
incorporate iron into heme:

Enzyme deficiency (ALA synthase)
Lead poisoning
Drugs (chloramphenicol, chemotherapy)

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Why are ringed sideroblasts seen in sideroblastic anemia ?

abnormal deposition of iron in mitochondria due to defective incorporation into heme

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RDW is high or low for sideroblastic anemia; why ?

HIGH RDW; defective incorporation of iron leads to inconsistent RBCs (dimorphic)

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Lab results for Sideroblastic anemia (RDW, HGB, HCT, RBC, PBS, BM, Indices, WBC, PLT, RETIC, serum iron, serum ferritin, TIBC, transferrin sat.)

RDW: HIGH
HGB/ MCH/MCHC: decreased
MCV: <80 fL
HCT: decreased
RBC: decreased
PBS: hypo/micro + normo/normo (DIMORPHIC)
BM: increased iron stores (prussian-blue), ringed sideroblasts
RETIC: decreased

serum iron: INCREASED
serum ferritin: INCREASED
TIBC: decreased
transferrin sat: INCREASED

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Cause of Anemia of Chronic Infection

Underlying infection/ inflammation, autoimmune diseases, malignant neoplasms:

Impaired iron kinetics: sequestered iron from pathogen
Impaired erythropoiesis: inflammatory cytokines hinder action of EPO on HSC
Decreased RBC survival: reticuloendothelial cells increase removal of RBCs with small defects

NOTE: reticuloendothelial cells descend from monocytes = phagocytes

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Lab results for Anemia of Chronic Infection (CRP, HGB, HCT, RBC, PBS, BM, Indices, WBC, PLT, RETIC, serum iron, serum ferritin, TIBC, transferrin sat.)

CRP: INCREASED
HGB/MCH/MCHC: decreased
HCT: decreased
RBC: decreased
PBS: micro/hypo
BM: normal to increased iron stores (prussian-blue)
RETIC: decreased

serum iron: decreased
serum ferritin: increased
TIBC: decreased
transferrin sat: increased

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General cause of megaloblastic anemia

Impaired DNA synthesis
vit B12 and folate deficiency

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Pathophysiology of megaloblastic anemia

lack of vit B12 = folate CANNOT donate a methyl group to uracil = NO thymine production
DNA strand has gaps of where thymine should be = DNA development is delayed

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Causes of vit B & folate deficiency

Diet
Malabsorption (surgical removal, inflammatory bowl, parasites)
Increased requirement (pregnancy)

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Megaloblastic anemia: CBC results (HGB, HCT, RBC, Indices, WBC, PLT, RETIC)

HGB: DECREASED
HCT: increased
RBC: decreased
MCV: increased
MCH: INCREASED
MCHC: NORMAL
WBC: HYPERSEG neuts
PLT: DECREASED
RETIC: DECREASED

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Megaloblastic anemia: BM (M:E, iron stores, morph)

M:E decreased; erythroid hyperplasia
NORMAL iron stores
nuclear-cytoplasm asynchrony
enlarged precursors

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Iron studies (serum iron, serum ferritin, TIBC, transferrin sat.) for both Megalo/Non-megaloblastic anemia

NORMAL iron studies in PBS

NOTE: BM may have increased iron stores

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How is megaloblastic anemia differentiated from pernicious anemia ?

Patients with pernicious anemia will be DAT positive due to autoAb

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Cause of pernicious anemia

autoAb destroy parietal cells that produce Intrinsic Factor
IF is required to absorb vit B12

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2 types of pernicious anemia

Type I= competes for vit B12 binding site on IF

Type II= hinders IF by forming a complex

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Causes of non-megaloblastic anemia

liver disease
chronic alcoholism
bone marrow failure (aplastic anemia or MDS)
post-splenectomy

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Non-Megaloblastic Anemia: CBC results (HGB, HCT, RBC, Indices, WBC, PLT, RETIC)

HGB: DECREASED
HCT: increased
RBC: decreased
MCV: increased
MCH: INCREASED
MCHC: NORMAL
WBC: HYPERSEG neuts
PLT: DECREASED
RETIC: DECREASED

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Non-megaloblastic anemia: BM (M:E, iron stores, morph)

M:E decreased; erythroid hyperplasia
NORMAL iron stores
NO megaloblastic changes

What are hemoglobinopathies ?

- qualitative or quantitative - disorders involving hemoglobin

What are heinz bodies ?

- excess globin chains precipitated into cytoplasm - viewed by supravital stains

Describe normal structure of hemoglobin

4 globin chains

Hgb A chains

2 alpha + 2 beta

Cause of Thalassemias

- gene mutations leads to decreased normal Hgb - categorized based on the genes lost (alpha or beta)

Thalassemia A

- deletion of 1 to 4 alpha genes

A Thal minor

deletion of 2/4 alpha genes

A Thal intermedia

deletion of 3/4 alpha genes

A Thal major. What is this called ?

HEMOGLOBIN BARTS: - deletion of ALL FOUR alpha genes - fetus cannot produce other normal Hgb

Which Thalassemia is associated with Hydrops Fetalis ?

Alpha Thalassemia Major

Why is A Thal major incompatible with life ?

NO ALPHA chains = gamma chains form tetrads

Beta Thalassemia

- deletion of one/ both beta genes

Why may beta thalassemia be diagnosed later than alpha thalassemia ?

Beta chains are not synthesized until after fetal Hgb begins the switch to adult Hgb

B Thal major

- two altered genes - two null genes - one altered AND one null gene

B Thal minor

one normal beta gene AND one altered/ null gene

Why do patients with B Thal have ineffective erythropoiesis ?

- decreased beta globin chain = excess alpha chain - excess alpha is precipitated (HEINZ BODIES) - premature cell death DUE TO INCLUSIONS

Alpha and Beta Thal: CBC results (HGB, HCT, RBC, Indices, WBC, PLT, RETIC) and PBS

HGB decreased HCT decreased WBC normal PLT normal RETIC decreased RBC decreased MCV decreased MCH decreased MCHC decreased

Alpha and Beta Thal PBS:

POIKILOCYTOSIS: - micro/hypo - target - tears - schisto - sphero - basophilic stippling - HEINZ BODIES (supravital)

Alpha and Beta Thal: BM (M:E, iron stores, characteristic morph)

- M:E decreased; erythroid hyperplasia - iron stores INCREASED (cannot use)

Alpha and Beta Thal: iron studies (serum iron, serum ferritin, TIBC, transferrin sat.)

serum iron= normal serum ferritin= INCREASED TIBC= normal transferrin sat= normal

Confirmatory tests to differentiate Thalassemias

- Hgb HPLC and electrophoresis - Molecular genetics

Describe the usual genetic abnormality found in Hemoglobin H Disease vs Beta Thalassemia Major

Hemoglobin H Disease (Hemoglobin α-thal intermedia): - 1/4 α genes only β-thal Major: - Gene mutation β°/β° OR β+/β° OR β+/β+

Red cell morphology (color, size, shape(s), inclusions) seen in Hemoglobin H Disease vs Beta Thalassemia Major

Both are very similar with a junky picture : targets, schisto, micro/hypo, baso stippling

1. What are common peripheral blood findings in DIC? 2. How would you differentiate it from HUS

1. DIC would have classic signs of IVH = low PLT and schistocytes on the PBS 2. PT, PTT and D-dimers = prolonged/ increased in DIC

Oxidative denaturation of hemoglobin results in the formation of small particles that are visualized with supravital staining. What is the term for these particles?

Heinz bodies

What is the mechanism/etiology of the anemia in chronic inflammation (ACI)?

Acute phase reactants impair iron mobilization

The substitution of valine for glutamic acid at position 6 of the β chain of hemoglobin results in hemoglobin that: a. Is unstable and precipitates as heinz bodies b. Polymerizes to form elongated crystals c. Crystallizes in a hexagonal shape d. Contains iron in the ferric state

b. Polymerizes to form elongated crystals

How may the macrocytosis caused by liver disease be differentiated from the macrocytosis caused by a B12 or folate deficiency Select all that apply: a. In liver disease the neutrophils are not hypersegmented b. In liver disease, the bone marrow does not show asynchrony c. In liver disease, the MCV will be much higher than in B12 deficiency d. In liver disease, the macrocytes are round not oval

a. In liver disease the neutrophils are not hypersegmented b. In liver disease, the bone marrow does not show asynchrony d. In liver disease, the macrocytes are round not oval

The hypochromic anemias represent a related group of disorders with: a. A quantitative defect in hemoglobin synthesis b. A qualitative defect in globin protein chains c. Excess hemoglobin synthesis d. Vitamin B12 and folate deficiency

a. A quantitative defect in hemoglobin synthesis

What is the function of vitamin B6 (pyridoxine)? a. Incorporate iron into the protoporphyrin ring b. Activate ALA synthetase to promote iron absorption c. Cleave folate from transporters for absorption d. Increase iron absorption

a. Incorporate iron into the protoporphyrin ring

PBS: Hypochromia BM: RBC with ragged cytoplasm, erythroid hyperplasia

Iron Deficiency anemia

Select all conditions in which the iron stores would be increased in the marrow. Select all that apply: a. Megaloblastic anemia b. Hemolytic anemia c. Lead poisoning d. B thalassemia minor

a. Megaloblastic anemia b. Hemolytic anemia c. Lead poisoning

1. A common molecule is implicated in both HUS and TTP. What is this molecule? 2. How does this molecule contribute to the patient pathology/disease for each disorder? 3. List two tests that can be used to distinguish HUS from TTP

1. Von Willebrand Factor 2. - TTP= an ADAMTS-13 deficiency results in decreased cleaving of VWF multimers. This causes binding of WVF to endothelial cells and activation of thrombi - HUS = The Shiga-toxins released by Shigella or E.coli O:157 cause damage to endothelial cells = vWF is released to cause coagulation 3. - bacterial culture to look for Shigella or E. coli in HUS - HUS involves kidney damage = creatine clearance can be tested - PLT count = TTP is much more decreased in comparison to HUS - Molecular genetics for ADAMTS13