Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/39

Click to flip

39 Cards in this Set

  • Front
  • Back
Reticulocytes
- Occurs after extrusion of nucleus from orthochromic normoblast
- Remains in marrow for approx 3 days
- Released into circulation – remodeled (in the liver) with loss of water and membrane
- Normal retics are macrocytic (100-110 fL)
What stain do you used on peripheral blood smear to show Reticulocytes?
Supravital stain will show ribosomal RMA (residual reticulin) as blue
Alcohol and RBCs
Mechanism unknown
Acetaldehyde
- can induce membrane changes
- Interferes with cellular division (At bone marrow level interferes with DNA synthesis)
Liver Disease and RBCs
- Mechanism of macrocytosis unclear
- May be caused by increased lipid (or cholesterol) deposition on red cell membranes
- Target Cells
Thyroid Disease and RBCs
- Mechanism of macrocytosis unknown
- Autoimmune thyroiditis associated with anti-parietal cell antibodies
Spurious Macrocytosis
- Artifacts that can occur to normal sized RBCs
- Clumps of RBCs counted as single cells by automated cell counters
Myelodysplastic Syndromes
- : A group of diseases in which the bone marrow does not make enough healthy blood cells. Also called preleukemia and smoldering leukemia.
- abnormal RBC populationg
Histology in Myelodysplastic Syndromes
- Hypolobulated or hypogranular neutrophils
- Large and/or abnormally granulated platelets
- Monocytosis
- Occasional blast forms
Dx of Myelodysplastic Syndromes
Dx on bone marrow morphology…consider the elderly 60+
Megaloblastic anemia
anemia, often pancytopenia, with macrocytic red blood cells and hypersegmented neutrophils due to an impairment in DNA synthesis
What happens on the cellular level of a megablast?
- Inadequate conversion of deoxyuridylate to thymidylate
- Slows DNA synthesis
- Delayed nuclear maturation
- Nuclear/cytoplasmic dyssynchrony (ie, immature nucleus/mature cytoplasm)
Megaloblastic Anemias
Most common causes
B12 (cobalamin) and folate deficiency
Characterization of Megaloblastic Anemia
defect in DNA synthesis resulting in unbalanced cell growth and impaired division
Sources of B12
- Animal Products (fish, eggs, poultry)
- Fortified foods (breakfast cereals)
Sources of Folate
- Leafy greens
- Fortified foods (cereals)
Causes of Iron Deficiency despite eating iron rich foods
- Insufficiency of pancreatic enzyme
- Abs to parietal cells
- Achloridria
- Gastic reconstruction
- Defects in cubulin or transcobalamin
Can you trust a serum folate level?
No because if a person just ate spinach then the serum folate could be normal. Look at Neutrophils (for hypersegmentation) and look at RBCs.
Folate
Normal Serum Level
2.5-20 ng/ml
- low in Folate Deficiency
- normal in B12 Deficiency
Homocysteine
Normal Serum Level
200-900 pg/ml
- normal in Folate Deficiency
- low in B12 Deficiency
Cobalamin
Normal Serum Level
5-16 uM
- High in B12 Deficiency and in Folate Deficiency
Methylmalonic Acid
Normal Serum Level
70-270 nM
- High in B12 Deficiency
- normal in Folate Deficiency
Karyorrhexis
A stage of cellular necrosis in which the fradments of the nucleus fragments and its chromatin are distributed irregularly throughout the cytoplasm
Does MCV vary with age?
NO. If a patient has a change in MCV there is something pathologic occuring .: you must check for nutritional deficiencies.
Does having 1 hypersegemtned neutriphil indicate that there is a pathologic indication?
No, in order to have the classification of hypersegmented nutriphils you must have:
- 1 six-lobed neutrophil
- 5 five lobed neutriphils/ 100 cells
Why would someone will macrocytic cells have an increased lactate dehydrogenase?
there is high cell turnover because macrocytic cells are fragile
Anisocytosis
RBC descriptor to describe
- size variation
Where do you see megaloblastosis in nutritional deficiencies?
In all proliferating cell lines:
including epithelial cells lining the gastrointestinal tract (buccal mucosa, tongue, small intestine), cervix, vagina, and uterus
- But the megaloblastic changes are most striking in the blood and bone marrow
Clinical Manifestations of Cobalamin and Folate Deficiency
- Glossitis
- Secondary malabsorption caused by megaloblastic gastrointestinal changes
- Weight loss or Growth Failure
- Infertility
- Thrombosis
- Hyperpigmentation
- Immune deficiency
Glossitis
Beefy red tongue

- seen in B12 and folate defiencies
Pernicious Anemia
- anemia (autoimmune loss of gastric intrinsic factor) is the most common cause of megalobastic anemia worldwide, especially in persons of African or European ancestry
- a chronic progressive anemia of older adults due to failure of absorption of vitamin B12, usually associated with decreased intrinsic factor, characterized by numbness and tingling, weakness, and a sore smooth tongue, as well as dyspnea after slight exertion, faintness, pallor of the skin and mucous membranes, anorexia, diarrhea, loss of weight, and fever
Neuropsychiatric Manifestations
B12 deficiency
- Peripheral neuropathies
- Dorsal column involvement (loss of position and vibratory sense, ataxia)
- Subacute combined degeneration of spinal cord
- Psychiatric symptoms (dementia, psychosis)
Treatment of B12 and Folate Deficiency
- 1000 ug B12 weekly by IM injection x 8 weeks then monthly for life
- Consider oral therapy with close monitoring
- Folate 1 mg po per day
Why should you always check for folate and B12 deficiency instead of just fixing one?
Warning: Folate repletion without B12 repletion may normalize MCV and Hgb but allow neurologic manifestions to persist
Schilling Test
Part 1: Give radioactive cobalamin by mouth. After 1 hour, give injection of unlabelled cobalamin by injection (“flushing dose”) to saturate plasma B12 binders so that labeled cobalamin will not bind but be excreted via the kidney
Part 2: Give exogenous intrinsic factor with the radiolabeled cobalamin.
Schilling Test at Part 1
Results for Patients with Pernicious Anemia
An individual with pernicious anemia would absorb little or none of the oral B12 since these patients lack intrinsic factor. The amount of radiolabeled B12 recovered in the urine would be less than normal.
Schilling Test at Part 2
Results for Patients with Pernicious Anemia
In a patient with pernicious anemia, this should correct the absorption and increase the urinary excretion into the normal range.
If still abnormal, then the small intestine can’t absorb the B12-IF complex.
If you do not have macrocytosis can you have a nutritional deficiency?
Yes, you can still have folate or cobalamin deficiency
What is the most senstive indicator for cobalamin deficiency?
methylmalonic acid
Causes of folate deficiency
- diet lacking fruits and veggies
- alcoholism
- sprue, chron's dz...
- increased cellular proliferation
- pregnancy
- skin diseases
- hemolysis
- malignancies
- Drugs (antifolates and anticonvulsants)