Exam 3 Hematologic Slide Set 2 Flashcards
Diagnosis of Autoimmune Hemolytic Anemia (AIHA) (Extrinsic Hemolytic Anemia)
Coomb’s & Indirect Coombs antiglobulin test
- detection of antibodies or complement is required to dx.
Warm Ab AIHA
- Mot common form of AIHA
- 50% idiopathic
- 50% secondary to SLE or neoplastic dz (eg lymphoma)
- IgG* is most common (IgA second)
Cold agglutinin AIHA
- IgM Abs bind to RBCs at low temperatures (0-4 C)
- IgM agglutinates & fixes Complement to the surface of the RBC
- 15-30% of these anemias
- Abs appear acutely during recovery from infections (Mono, HIV, Flu, etc) -> self-limiting & rarely causes clinical manifestations
- Will occur chronically idiopathically or in response to some lymphoid neoplasms
- > Raynaud phenomenon
Hemolytic Anemias (Extrinsic) resulting from Trauma
Causes: cardiac prosthesis, narrowing of microasculature (DIC), SLE, malignant HTN, TTP, HUS, cancer.
- Mechanical injury to RBC
- Peripheral smears show RBC fragments (schistocytes, burr cells, helmet cells
- TTP and HUS are the only conditions that cause major clinical problems associated with hemolysis
Anemias of Diminished Erythropoiesis
- Megaloblastic (deficiency) anemias
- Iron Def Anemia
- Anemia of chronic dz
- anemia of renal failure
- marrow stem cell failure (aplastic anemias)
Megaloblastic (macrocytic) anemias
- B-12/folate deficiency (leads to inadequate thymidine) -> megaloblastic changes in all rapidly dividing cells -> b/c RNA synthesis is unaffected
- Inadequate diet & alcoholism
- Impaired DNA synthesis & distinctive morphological changes in the blood & bone marrow*
- TPN/PPN, Azotemia/Uremia, Bacteremia/Septicemia?
Causes of Folic Acid Deficiency
-Alcoholism
-Phenytoin Sodium (anti-seizure medication)
-Anti-Metabolites (cancer drugs)
-HIV/AIDS drugs
(So… only things we do on purpose)
Morphological presentation in Megaloblastic anemia
- RBC size & MCV increased
- Anisocytosis (increased RDW)
- Eosinophils & Neutrophils have hypersegmented nuclei
- Low reticulocytes, some nucleated RBCs present in severe cases
- Marrow is hyper cellular with increase in all myeloid precursors.
Pernicious anemia (cause, associations, populations affected, dx)
- Lack of Intrinsic Factor leads to inadequate absorption of B-12
- Assoc. w/gastric atrophy & achlorhydria, both often
- Assoc. w/H pylori infection has NOT been proven yet
- Pernicious anemia pts have 2-3x increase incidence of gastric carcinoma
- Coexisting iron deficiency common b/c achlorhydria prevents getting ferric iron from food
- Adult pernicious anemia most common in Celtic (English, Irish, Scottish) or Scandanavian origin
- 10-20 cases/100,000 people/year
- Does it all begin with auto reactive T-cell response that targets gastric mucosa???
- *Gold standard dx = biopsy of gastric mucosa showing depleted parietal cells.
Antibodies found in pernicious anemia
- Type 1 blocks binding of B-12 to IF
- Type 2 blocks binding of IF/B-12 combo to its ileal receptor
- Type 3 binds to proton pump, found in 50% of elderly patients with chronic gastritis
- Anti-parietal cell Abs occur in 90% of pts with pernicious anemia and only 5% of healthy individuals
- *Gold standard dx = biopsy of gastric mucosa showing depleted parietal cells.
Pernicious anemia morphology
- Changes in marrow, alimentary tract, and NS
- Alimentary tract = stomach & tongue: glossitis, intestinization (gastric epithelium replaced by goblet cells ie metaplasia)
General/other sx of B12 deficiency
- NS sx in absence of anemia (more common in its taking folic acid or high-folate diet)
- Older pts may present with dementia/Alzheimers sx: memory loss, irritability, personality changes
- Megaloblastic madness: delusions, hallucinations, outbursts, paranoid schizophrenic ideation (myelin los in nerves of the posterior column)
Diagnostic features of B12 deficiency
-low serum RBC & B12, hgb, hct
-MCV elevated
WBC & platelets decreased
Increased homocysteine & methylmalonic acid (risk factors for atherosclerosis & thrombosis)
-Mild jaundice from ineffective erythropoesis & hemolysis
-**Inability to absorb oral B12 supplementation*
How does one become deficient in folate?
- Poor diet (poor, elderly, those who don’t eat… green leafy vegetables, lemons, bananas, melons, yeast & liver!) or eat too much overcooked food.
- *It’s not stored in the body
- Interfering medications: dilantin, lithium, sulfasalazine, oral contraceptives
- Also: alcoholism, hx of malabsorption, & pregnancy
- US 4/100,000ppl have folate deficiency
Morphological presentation of folate deficiency
- Megalocytes (circulating) & Megaloblasts (BM)
- Hypersegmented neutrophils
- Decreased serum folate or RBCs
- Elevated serum homocysteine