Lecture 9 Flashcards
Guidelines for Grading Abnormal Findings
0 – 5 % abnormalities are considered not reportable and normal
-5 – 10% of abnormal colour, size and most shapes are non-specific and not reportable
-SICKLE CELL OR INCLUSIONS ARE ALL REPORTABLE
10-25% abnormalities are moderate
> 25% abnormalities are Marked
Poikilocytosis
-represents variation in RBC shape
-term ‘Poikilocytosis’ or ‘Poik’ is not reported. You need to report the specific abnormality.
-Report as some or many
-Poik - should be visible in all fields know that some shapes can be artifacts
-Poikilocytes are formed by specific mechanism
-some shapes are considered diagnostics like sickle cell or oval macrocytes
Sickle Cells
● AKA Drepanocytes
● Diagnostic cell of Sickle Cell Anemia
● Mutated Globin chains – produce Hgb S instead of Hgb A
● In reduced oxygen state, Hgb S polymerizes and ‘crystallizes’ into long fiber bundles which grow lengthwise and distort the cell membrane causing vaso-occlusion
● RBCs on PBF are dark red to salmon pink, no central pallor, elongated cell with pointed ends
‒ May be curved
‒ Rigid and inflexible
●occurs due to base pair substitution glu-val
●reversible up to a point but repeated sickling damages the cell permanently
Reporting:
‒Occasional -in a sickle patient who is currently ‘well
‒Some - will be seen during a sickle crisis
‒Many
Oval Macrocytes- Round vs Oval
- Diagnostic cell of Megaloblastic anemia
- DNA synthesis is impaired due to vitamin B12 and/or Folate deficiency
- Cells try to divide but unable to duplicate DNA
‒ All cell lines are affected b/c DNA synthesis is impaired
‒ Nuclear division stalled while cytoplasm continues to develop
‒ Cells are larger & oval reported as a variation in SHAPE not size . can be greatly increased
‒ CBC: MCV > 100fL
look like big eggs
Round Macrocytes - like a big ball
Caused by:
* Increased membrane lipids
‒ Increased size and surface area
* Retain shape but more membrane = larger cell
E.g., Liver disease
* Reported with SIZE
Spherocytes
- In circulation, RBCs lose small portions of
membrane which re-seal - Biconcave shape becomes spheroid, appearing as: LOOK LIKE MINI M&MS
‒ Small with normal volume
‒ Round
‒ Dense or stain darker than surrounding RBCs
‒ Lack central pallor
-lowest surface to area to volume ratio
-HGB concentrated but with less membrane
-MCV is normal to slightly reduced - Do NOT report as Microcytes because microcytes have central pallor
Spherocyte Formation
Four Mechanisms of Membrane Loss:
● membrane loss cane be hereditary or through external forces
- mild to severe anemia as spleen removes altered cells – Extravascular hemolysis
* Increased RBC destruction ∴ Increased BM response
‒ Increased Polychromasia and can also see NRBCs
Four Mechanisms of Membrane Loss:
- Intrinsic abnormalities – inherited
- deficiency of sceptrin, ankyrin or band 3
-lipid bilayer and skeleton uncouple
- HEREDITARY SPHERCYOTSIS
- Immune hemolysis – antibodies on membrane
-AB attach to RBC, FC receptor on splenic marcophage binds to AB, the macrophage pits the AB-AG complex causing fragmentation, the cell reseals -MICROSPHEROCYTE - Fibrin strands: RBC impaled on Fibrin strand, the RBC is torn in two one forms helmet cell- schistocyte and other microspherocyte
- Thermal injury- after being heat damaged the largest fragment reseals forming spherocyte
Target Cells
- AKA Codocytes
- results from increase in the RBC surface membrane
- Loss of biconcave shape due to increased surface area-to-volume ratio as a result of either:
‒Decreased cytoplasmic hemoglobin
‒Excess membrane cholesterol &/or phospholipid - Hgb concentrates in the center of the cell and around the periphery, giving “bull’s-eye” appearance ‒May also appear bell or cup shaped
‒Normal in size to slightly macrocytic
target cells are associated with several conditions:
* With macrocytic cells in Liver disease .Increase in free cholesterol in plasma or decreased rate and extent of membrane lipid loss because sometimes after splenectomy retics dont lose them
- With normocytic cells in some hemoglobin disorders ‒ Sickle Cell anemia, Hgb C and E disease. decreased hemoglobin content in hemoglobinopathies
- With microcytic cells in other hemoglobin disorders ‒ Iron Deficiency Anemia ‒ Thalassemia. Loss of HB leads to increased surface: volume ratio. globin chain imbalance in thalassemia
ARTIFACT Target Cell Formation
slow drying, high humidity, HEM C
-hemoglobin collectes in thicker areas of outer rim and center as water evaporates
-a shiny ring in the middle will be seen
-typically affects one area only so make sure you look at the whole slide to conclude that the target cells are not due to artifact
Ovals & Pencils
OVALOCYTES
* Oval or egg-shaped RBCs
‒ Can be normocytic/normochromic
‒ Can be normocytic/hypochromic
‒ Can be normochromic/macrocytic
ELLIPTOCYTES
Pencil- or cigar-shaped RBCs -Cells have parallel sides and Rounded (or blunt) ends
Formed only after RBCs leave bone marrow and mature- morph develops after being stressed in the peripheral circulation
Associated with:
‒ Hereditary Elliptocytosis or Ovalocytosis
‒ Thalassemia major
‒ Iron Deficiency Anemia
‒ Megaloblastic anemia (macro-ovalocytes)
Formation related to condition:
-Iron-deficient red cells have abnormally stiff plasma membranes, which contribute to the formation of elongated hypochromic red cells
-Cells do not return to biconcave shape as hemoglobin decreases and ‘stiffer’ membrane develops
-Pencils or thin Elliptocytes are seen mostly in severe IDA
Hereditary Elliptocytos
Formation related to condition:
* RBC Membrane defect
‒ Mutations in Spectrin or Protein 4.1
‒ Defective proteins disrupt horizontal linkages in cytoskeleton
‒ HGB function not impaired
* Cells leave BM in normal biconcave shape but elongate as they pass through circulation – not able to return to normal shape – hemolysis and anemia result
* Heterozygotes- asymptomatic
* Homozygotes- moderate to severe anemia
Teardrop Cells
- AKA Dacrocyte - tear/pear shaped
- Cells can be normocytic or microcytic
- Cells can be normochromic or hypochromic
-Formed when there is an intracellular precipitate in the RBC cytoplasm which is removed as the cells passes through the basement membrane which separates splenic cord and sinuses. The stretching permanently distorts the cell and membrane
-Formed when normal RBCs pass through abnormal vasculature in the Splenic pores or Bone Marrow.
-The normal function of the spleen is to remove RBC inclusions and allow cell to re-enter circulation - repitting
-true teardrops should have rounded tips or blunt ends
-artifact tears if the tips are short and pointed . All the tips will point in the same direction - Associated with:
‒ Primary myelofibrosis
‒ Thalassemia
‒ Myelophthisic anemia
-Howell- Jolly bodies
-Heinz body
Acanthocytes
- AKA Spur cells
- Small, dense (or dark) cells with multiple, irregular thorny/spikey
- Somewhat rounded center and lack central pallor
- Projections are
‒ Blunt, rounded, pointed with narrow base, or have drumstick ends
‒ Unevenly distributed vary in size, length
-look like blobs with tentacles
Acanthocyte Formation
-hereditary or acquired membrane defects
Formation related to condition:
* Imbalances in plasma phospholipids (sphingomyelin) or abnormal increases in cholesterol
* Absorbed into outer portion of lipid bilayer
* Membrane folds outward into plasma, forming ‘spicules’ with rigid membrane, irreversible and will be hemolyzed by spleen
‒Remodeling in circulation produces long, rigid projections
‒Severe Liver Disease
‒Splenectomy (spleen removal)
‒Malabsorption, Vitamin E deficiency, Hypothyroidism
‒Abetalipoproteinemia
Burr Cells
● AKA Echinocytes
● RBC spikes all over
‒ Projections are short, blunt or pointed spicules
‒ Equal in length and cover entire surface of cell
● Normal size RBCs with ‘normal’ central pallor
● Plasma component causes membrane change – increase in pH, decreased protein (albumin) content, exposure to chemical substances
● Associated with:
‒ Renal disease (uremia), Pyruvate Kinease deficiency, Microangiopathic hemolytic anemia/MAHAs, neonates (especially premature), Burn patients (dehydration), Severe Liver Disease (Burrs and Spurs)
ARTIFACT Burr cell Formation -excess EDTA or
related to prolonged blood storage
- Due to slow drying of blood film artifact
‒ Called ‘Crenated’ cells
‒ Not present in all fields
Stomatocytes
● Normal size RBC with slit-like area of central pallor (stoma or mouth)
● Inherited or acquired membrane defects that affect membrane permeability and alter cell volume
‒ Increases (hydocytosis) and decreases (xerocytosis) in cell volume
‒ Increase in lipid content of inner bilayer leaflet
● Associated with:
‒ Hereditary Stomatocytosis
‒ Acquired Stomatocytosis (Liver Disease, Acute Alcoholism)
‒ Rh deficiency syndrome
● Can be ARTIFACT of PBF drying
‒ Not present in all fields
