1. Megaloblastic

2. Megaloblastoid

3. Disease

A lack of DNA precursors: B12 or Folate deficiency

-ineffective erythropoesis

-pancytopenia

-hypersegmentation of megakaryocytes or >5 lobes in neurtrophils

-abnormal developmental forms

-changes in RBC morphology

What RBC morphology changes are seen in Megaloblastic anemia?

-oval macrocytes

-high MCV

-Remnants of nucleus: Howell-Jolly Bodies or Cabot'sRings (worst case)

-nRBCs

Peripheral neuropathies, loss of coordination, cognitive defects.

--->reversible in early stages of the disease

meat, milk, eggs

--->bc B12 is recycled by the body really well it would take years of lack to become deficient

Decreased comsumption/absorption (vegan, impaired absorption: Pernicious anemia, or just malabsorption)

 or

Increased need (growth, pregnancy)

or

Tapeworms

1.consume radioactive B12; if secreted in urine it is being absorbed

2. test for Pernicious anemia: comsume B12 with intrinsic factor and look for secretion of B12 in urine

if only the second part is positive it is PERNICIOUS ANEMIA (lose protein by antibody to B12)

Anti-intrinsic factor antibody test: detects autoantibody to Intrinsic factor

immune system always active

-systemic lupus erythmatosis

-rhematoid arthritis

-chronic infection; tb, hiv

-cancer, diabetes

1. Treat underlying condition; immunosuppressive therapy

2. administer EPO and iron together

Error in DNA repair enzymes--->causing shortening of telomeres and early senescence, abnormal cell growth

Autosomal Recessive

IMMUNOSUPPRESSION

antibiotics for infection

BM transplant from identical sibling

Acquired: Transfusions

Inherited: BM transplant

---occurs when BM is infiltrated by abnormal cells (cancer cells) or when BM stem cells migrate to the liver or spleen

--->Dyserythropoesis: tear drop, nucleated rbcs, cabot's rings, giant platelets

1. Serum Iron

2. Ferritin levels

3. % transferrin saturation/TIBC

4. Soluble transferring receptor

Total Iron Binding Capacity

--->Add iron to blood until proteins have bound as much as they can...

-->wash away unbound Iron...

--->acidify protein to release all Iron bound

---> measure iron released

Stage 1: Storage Iron Depletion-cells have less iron internally

Stage 2: Transport Iron Depletion-less iron is transported

Stage 3: Functional Iron Depletion (Iron Deficiency Anemia)-not enough iron to make normal RBCs

-decrease in Hb and Hct-->later

-volume loss--->gives crystaloids/colloids to save the heart

-characterized as : normocytic normochromic anemia

1.Hereditary Hemochromatosis

2.Frequent Transfussions

How does Hereditary Hemochromatosis cause accumulation of iron?

by: 1.Excess absorption

2. Mutations in a protein that lowers the affinity of Transferrin-R

1.Transferrin Saturation; if >60% pt should be screened for Hemochromatosis

2. Check for Organ Damage; high liver enzymes, low albumin

islets are destroyed-diabetes

*1. Hereditary Hemochromatosis: Bloodletting-forces mobilization of stored iron

2. Transfusion Pts: Iron Chelating Drugs

drugs and bm toxins like;

-Anti-TB drugs

-Chloramphenicol

-alcohol

-lead

-chemo agents

1. Peripheral blood smear (Pappenheimer bodies/siderotic granules, basophilic stippling)

2. protoporphyrin accumulation (high FEP/ZPP)

3. whole blood lead