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Clinical Microscopy > RBC Abnormalities > Flashcards

RBC Abnormalities Flashcards

1
Q

Components of whole blood and percentages

A

plasma (54%)
buffy coat (1%)
red blood cells/erythrocytes (45%)

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2
Q

plasma is a colorless fluid which is composed of?

A 
Water (91-92%)
Protein (7-8%)
Electrolytes
Nutrients
Blood gases
Hormones
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3
Q

the layer contaminated with bacteria if blood is not properly processed

A

buffy coat (white cells + platelets)

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4
Q

the plasma without the firbinogen; usual specimen submitted for blood exam for serological tests

A

serum

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5
Q

volume of RBCs/unit plasma

A

hematocrit

  • males: 40-50
    females: 35-40%
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6
Q

characteristics and shape of normal rbc

A

circular biconcave with smooth edge and central pale area that gradually fades into reddish cytoplasm

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7
Q

diameter of normal rbc

A

7-8 micrometers

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8
Q

thickness of normal rbc

A

2-5 micrometers

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9
Q

volume of normal rbc

A

90 fl.

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10
Q

surface area of normal rbc

A

160 micrometers

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11
Q

simplest test to check for structure and form of RBCs since they are diagnostic

A

peripheral blood smear

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12
Q

What does PBS examine?

A 
Distribution of RBCs
Concentration of hemoglobin
Size of RBCs
Shape of RBCs
Inclusion of the RBCs
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13
Q

Describe normal distribution of rbc in PBS

A

there is an even distribution in thin portion (part examined): 1/3 of film
RBC in the area should be barely touching each other and no overlapping is seen

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14
Q

abnormal distribution of RBC in PBS would include

A 
Rouleaux formation (should be separated in thin portion; short and long stacks; not seen in normal)
Autoagglutination (when own rbcs agglutinate in own serum or plasma; seen in normal persons)
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15
Q

Rouleaux formation is seen in

THIMP

A 
§ Hyperproteinemia 
§ Infection
§ Multiple myeloma 
§ Tissue necrosis
§ Increased fibrinogen 
§ Pregnancy
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16
Q

Autoagglutination is seen in:

SHAT

A

§ Hemolytic anemia
§ Staphylococcal infections
§ Atypical pneumonia
§ Trypanosomiasis

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17
Q

It is an autoimmune disease characterized by presence of high concentrations of circulating antibodies, usually IgM, directed against red blood cells. There is clumping at low temperatures below 25C

A

Cold agglutinin

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18
Q

[hemoglobin content]

contains normal amoutn of hb which carries oxygen and gives blood its red color

A

normochromic

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19
Q

[hemoglobin content]

RBC lacks central pallor due to excessive amount of hb

A

hyperchromia

*seen in:
spherocytes (thick membrane), sickle cell anemia, hb concentrated in crystal in the abnormal hb, elevated mchc (true state)

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20
Q

[hemoglobin content]

RBC appears pale because of the lower amount of hb due to impaired hb synthesis

A

hypochromia

*seen in IDA (most common cause), rheumatoid arthritis, chronic infxn, inflammation (defective macrophage release of iron)

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21
Q

variation in hb content

A

anisochromia

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22
Q

T or F: average size of rbc is correlated with MCHC

A

False, with MCV

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23
Q

diameter and MCV of macrocytic RBC

A

8.5-9 micrometers and MCV = 100 fl.

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24
Q

macrocytic normochromic (megaloblastic) type of anemia

A

Pernicious anemia

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25
Q

Pernicious anemia is associated with?

A

achloryhdria and absence of gastric intrinsic factors necessary for the binding and absorption of vit.b12

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26
Q

an erythrocyte maturing factor which is secondary to megaloblastic anemia and secondary to pernicious anemia

A

vit b12

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27
Q

other findings in pernicious anemia

A 
atrophic glossitis (large tongue)
gastrointestinal and nervous disorders
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28
Q

RBC precursors of megaloblastic anemia appearance

A

Nuclear-cytoplasmic asynchrony (abnormally large and have nuclei that appear much less mature than would be expected from the development of cytoplasm)

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29
Q

drugs which can lead to megaloblastic anemia (MAPLE)

A 
methotrexate
AZT-Zidovudine (anti-HIV drug)
Phenytoin (Fenytoin-folate deficiency: anti-seizure drug)
liver disease
ethanol
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30
Q

where macrocytosis is seen

LAMBMCHC

A 
§ Lymphoma
§ Leukemia
§ Alcoholism w/o liver disease
§ Myeloma
§ B12 deficiency 
§ Metastatic carcinoma
§ Chronic hemolytic anemia 
§ Hypothyroidism
§ Cancer chemotherapy
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31
Q

MCV of microcytic RBC

A

below 80 fl.

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32
Q

T or F: microcytic rbcs always have less hemoglobin

A

false, normal or less hb

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33
Q

where is microcytic rbcs usually seen?

A
  • After chronic iron deficiency
  • During decreased globin synthesis in β Thalassemia, along with the target cell
  • In leptocytes
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34
Q

variation in RBC size (combination of macrocytosis and microcytosis)

A

Anisocytosis

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35
Q

RBCs that are thinner than normal with colorless centers and increased surface area not proportional to volume;

A

leptocytes

*Found in thalassemia, obstruction of bile ducts, cirrhosis and steatorrhea

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36
Q

variation in shape of rbc

A

poikilocytosis

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37
Q

probable causes of poikilocytosis

A 
® Structural and biochemical changes in the cell membrane
® A metabolic state in the cell
® Hemoglobin molecule abnormalities
® Abnormal microenvironment
® RBC age
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38
Q

a hereditary disorder of β-globin chain synthesis (in Hb) that leads to ineffective
erythropoiesis and a microcytic anemia. Some of the RBCs resemble jigsaw
puzzle pieces.

A

β-thalassemia

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39
Q

shape of macrocytes in poikilocytes secondary to developmental macrocytosis

A

oval

defect in nuclear maturation = macrocytes; may appear hyperchromic due to increased thickness and increased hb

40
Q

T or F: poikilocytes secondary to developmental macrocytosis can be secondary to Folate deficiency only

A

False, folate and B12 deficiency

41
Q

Poikilocytes Secondary to Membrane Abnormalities

SCABEES

A 
Spherocytes
Elliptocytes/Ovalocytes
Echinocytes/Crenated cells
Burr cell
Acanthocytes
Stomatocytes
Codocytes
42
Q

[Poikilocytes Secondary to Membrane Abnormalities]

with evenly distributed, uniform-sized blunt spicules or bumps on RBC surface; artifact

A

Echinocytes or Crenated cells

*seen in film prepared from anticoagulated blood several hours old and stored blood

43
Q

[Poikilocytes Secondary to Membrane Abnormalities] T or F: Echinocytes are normally seen in vivo and in pathologic disease

A

False, not normal and not usually associated with pathologic disease

44
Q

[Poikilocytes Secondary to Membrane Abnormalities]

Why are echinocytes seen in stored blood/several hours old anticoag blood film?

A

stored blood: Caused by depleted ATP and biochemical abnormalities
in plasma
film: release of subs from glass that changes pH and transforms cells into echinocytes

45
Q

[Poikilocytes Secondary to Membrane Abnormalities]

normal diameter and characteristic of SPHEROCYTES

A

diameter: 6.2-7 micrometers; thickness: 2.2-3.4 micrometers

RBC is round/globular wo central pallor and smaller volume

46
Q

[Poikilocytes Secondary to Membrane Abnormalities]

How do spherocytes lose thick membrane?

A

They lose thick membrane when passing through circulation (damaged due to inflexible shape) which causes decreased survival of RBCs and increased osmolality

47
Q

[Poikilocytes Secondary to Membrane Abnormalities]

Spherocytes are normally seen in

A

§ Autoimmune hemolytic anemia
§ Hemolysis due to water dilution
§ Microangiopathic hemolytic anemia

48
Q

[Poikilocytes Secondary to Membrane Abnormalities]

elongated with slit-like area of pallor may be resulting from high cellular sodium and low potassium content

A

stomatocytes

*may be retained in spleen due to abnormality and seen in normal PBS (may be artifact); hereditary/acquired;

49
Q

[Poikilocytes Secondary to Membrane Abnormalities] This is observed in alcoholisms, cirrhosis, obstructive liver disease

A

stomatocytes

50
Q

[Poikilocytes Secondary to Membrane Abnormalities] also has spicules but are irregularly shaped and unevenly spaced, echinocyte twin

A

burr cell

*seen in true pathologic disease like renal insufficiency. SHOULD BE REPORTED IF SEEN

51
Q

[Poikilocytes Secondary to Membrane Abnormalities] Oval egg-shaped to sausage-shaped to pencil-shaped RBCs where Hb appear to be concentrated at ends of the cell thus it has central pallor

A

Elliptocytes or Ovalocytes

*less 15 in normal RBC are ovalocytes (hereditary)

52
Q

[Poikilocytes Secondary to Membrane Abnormalities] This can be seen in IDA, megaloblastic anemia, sickle cell anemia and thalassemia

A

Elliptocytes

53
Q

[Poikilocytes Secondary to Membrane Abnormalities] also known as spur cells; these are smaller than normal RBCs, densely stained and not disk shaped, also has irregularly-spaced pointed spicules (few);

A

Acanthocytes

  • hereditary/acquired
  • spur cells in cirrhosis and metastatic liver disease
54
Q

[Poikilocytes Secondary to Membrane Abnormalities] cause of acanthocytes

A

changes in the ratio of plasma lipids (lecithins and sphingomyelins)

55
Q

[Poikilocytes Secondary to Membrane Abnormalities] sources of acquired acanthocytosis

A
  • Alcoholic cirrhosis
  • Hepatitis of the newborn
  • Hemolytic anemia
  • Lipid metabolism disorders
  • Post-splenectomy
56
Q

[Poikilocytes Secondary to Membrane Abnormalities] target cells/mexican hat where central area of hemoglobin surrounded by a colorless ring and a peripheral ring of hemoglobin

57
Q

[Poikilocytes Secondary to Membrane Abnormalities] Why are membrane surfaces increased in codocytes? How about greater osmotic resistance?

A

increased membrane surfaces: cholesterol and phospholipid loading (hypercholesterolemia)
greater osmotic resistance: increase surface to volume ratio

58
Q

[Poikilocytes Secondary to Membrane Abnormalities] T or F: codocytes are always acquired

59
Q

[Poikilocytes Secondary to Membrane Abnormalities] These are seen in thalassemia, hemoglobinopathies, obstructive liver
disease, post-splenectomy, iron deficiency

60
Q

[Poikilocytes Secondary to TRAUMA]

A 
Schistocytes
Keratocytes
Dacrocytes
Microspherocytes
Semilunar bodies
61
Q

What happens to RBCs under excessive physical trauma in cardiovascular system?

A

fragment and lyse (decreased survival and is subjected to intravascular hemolysis)

62
Q

[Poikilocytes Secondary to TRAUMA] fragmentation in schistocytes result from:

A

§ RBC passes through fibrin strands
§ Damaged heart valves
§ RBC develops a blister
- RBC goes to the spleen, fragments into two pieces.
- Membrane becomes less deformable, making survival less.

63
Q

[Poikilocytes Secondary to TRAUMA] Shapes of schistocytes

A

helmet, triangular, small pieces of RBC

64
Q

[Poikilocytes Secondary to TRAUMA] Schistocytes are usually seen in:

A

severe burns, renal graft rejection, glomerulonephritis, DIC (MAHA), vasculitis, TTP

65
Q

[Poikilocytes Secondary to TRAUMA] These are half-moon (crescent) shaped large, pale pink staining ghost of RBC

A

semilunar bodies

  • always acquired
  • seen in malaria and other hemolytic conditions
  • membrane remains after content has been released
66
Q

[Poikilocytes Secondary to TRAUMA] schistocyte with one or more hornlike projections with relatively normal volume resulting from RBC being caught in fibrin strand and cuts into two

A

KERATOCYTES

  • when cut rbc fuse, vacuole like area ruptures
  • PATHOLOGIC (REPORTED IF FOUND)
67
Q

[Poikilocytes Secondary to TRAUMA] Why do keratocytes not remain long in circulation?

A

increased fragility

68
Q

[Poikilocytes Secondary to TRAUMA] ® Occur in severe burns as small round cells
® Results from thermal damage in the cell’s membrane

A

MICROSPHEROCYTES

69
Q

[Poikilocytes Secondary to TRAUMA] tear-drop shaped or pear-shaped with blunt pointed projection seen in myelofibrosis with myeloid metaplasia, pernicious anemia, TB, tumor in the marrow

A

Dacrocytes

  • size: normal, small or large
  • forms when RBC has inclusion ie heinz bodies because it makes it hard for RBC to pass through small bv; RBC membrane stretches beyond its ability to regain its original shape
70
Q

[Poikilocytes Secondary to ABNORMAL HB CONTENT] These poikilocytes can be diagnostic for

A

chronic hereditary hemolytic anemia

71
Q

[Poikilocytes Secondary to ABNORMAL HB CONTENT] Three types characteristics of abnormal Hbs

A 
Drepanocytes (sickle cells with abnormal Hb S) 
HbCC crystals (Hb C-homozygous C) 
HbSC crystals (with both Hb S and Hb C)
72
Q

[Poikilocytes Secondary to ABNORMAL HB CONTENT] long rod-shaped polymers formed; permanent membrane damage due to polymerization of HbS; thin and elongated with pointed ends filled with Hb

A

Drepanocytes

*can be curved or straight, or S, V or L-shaped

73
Q

[Poikilocytes Secondary to ABNORMAL HB CONTENT]
§ Milder form of Hb S
§ Intra RBC Hb CC crystals in homozygous C (Hb CC) disease

A

HbCC crystals (Hb C-homozygous C)

§ Tend to be hexagonal with blunt ends and stain darkly
§ Crystal appears free-cell without Hb

74
Q

[Poikilocytes Secondary to ABNORMAL HB CONTENT]

§ Dark-hued crystals which distort the membrane (“rectangular RBC”)

A

HbSC crystals (with both Hb S and Hb C)

*§ With parallel sides and one blunt, pointed, protruding end
(Washington monument shaped)
§ Can be finger-like, projections on all direction

75
Q

a type of hemoglobinopathy which is also called as hb SS disease wherein there is qualitative problem of synthesis of an incorrectly functioning globin

A

Sickle-cell disease

76
Q

Sickle-cell disease produces specific mutant form of B-globin. What are the two variants of hemoglobin in the b chain gene?

A
  • Hb S (α2βS2)
    o Change in the properties of hemoglobin which results in sickling of red blood cells.
  • Hb C (α2βC2)
    o Causes a mild chronic hemolytic anemia
77
Q

T or F: abnormal Hb SS is prone to hemolysis when oxygen tension is low

A

false, crystallization

  • long thin sickle forms clump and decrease blood flow and oxygen tension
  • might happen in persons with Hb AS
78
Q

an inherited autosomal recessive blood disease which results in underprod of normal globin proteins often through mutations in regulatory genes causing formation of abnormal hemoglobin molecules (anemia)

A

thalassemia

79
Q

Types of thalassemia accdg to which chain of hemoglobin is affected

A

α thalassemia (Hemoglobin H disease and alpha thalassemia hydrops fetalis)
β thalassemia (β thalassemia minor and β thalassemia major/Cooley’s anemia)

80
Q

[Thalassemia]
Three alpha loci are affected and presence of two unstable hbs in blood (Hemoglobin barts/tetrameric gamma chains and Hemoglobin H/tetrameric beta chains)

A

Hemoglobin H disease

  • barts + H have higher affinity for oxygen than normal hb, resulting in poor o2 delivery to tissues
  • childhood/early adult life (anemia + splenomegaly noted)
81
Q

[Thalassemia] What are found in PBS in Hb H disease?

A

microcytic hypochromic anemia
with target cells and Heinz bodies (precipitated
HbH)

82
Q

[Thalassemia] four alpha loci affected

see figure 16

A

Alpha Thalassemia Hydrops fetalis
*fetus cannot live once outside uterus and may not survive gestation (edematous and have little circulating hb and all hb present are hb barts)

83
Q

[Thalassemia] It is inherited in an autosomal-recessive fashion; severity of disease depends on nature of mutation

A

β thalassemia

*(βo) if they prevent any formation of β chains
(β+) if they allow some β chain formation to occur

84
Q

[Thalassemia] T or F: there is a relative excess of beta chains in β thalassemia

A

false, alpha chains but these do not form tetramers but bind to rbc membranes (damage) and at high temps, toxic aggregate formation

85
Q

[Thalassemia] differentiate β thalassemia minor and β thalassemia major/Cooley’s anemia

A

β thalassemia minor: one β globin allele bears a mutation; Mild microcytic anemia; Asymptomatic and many affected people areunaware of the disorder
β thalassemia major: both alleles have thalassemia mutations; severe microcytic, hypochromic anemia; If untreated, death <20 y.o.; Treatment: periodic blood transfusion,
splenectomy if splenomegaly is present, and treatment of transfusion-caused iron overload; Cure: possible by bone marrow transplantation.

86
Q

Developmental inclusions of RBC

A 
Howell-Jolly bodies
Basophilic stippling
Pappenheimer bodies
Polychromatophilic Red Cells
Cabot's Ring
87
Q

Inclusions of RBC due to abnormal hb precipitation

A

heinz bodies (denatured globin; round, refractile; differ from Howell-Jolly because it is attached to and tends to ppt on RBC membrane)

88
Q

T or F: Heinz bodies are visible in Wright-stained films

A

False

id with supravital staining with basic dyes: meth blue/brilliant cresyl blue; large when alone small when numerous

89
Q

Where are heinz bodies usually seen?

A

poisoning with aromatic nitro-compounds, amino compd, hemolytic anemias and sulfonamide intake

90
Q

inclusions seen in malaria

A

Schuffner’s stippling or granules

91
Q

refractive artifacts are caused by what?

A

water contamination of the methanol or wright stain (others: by particles of fat/detergent on glass itself)

92
Q

[Developmental inclusions of RBC] Siderotic/iron granules ((+) in Prussian stain); Small, irregular, dark-staining granules which appear at the periphery of cells; Seen in young RBC (sideroblast) and excess in iron overload

A

Pappenheimer bodies

*spleen removed these granules

93
Q

[Developmental inclusions of RBC] Young RBC, diffusely basophilic (due to RNA); Larger than normal, contain ribosome, mitochondria and other organelles

A

Polychromatophilic Red Cells

*With methylene blue (supravital stain) called reticulocytes (ribosomes and organelles are precipitated)

94
Q

[Developmental inclusions of RBC] Small, round fragments from the nucleus from incomplete extrusions of the nucleus or chromosomes that were separated from the
spindle during abnormal mitotic division

A

Howell-Jolly bodies

*seen in sc, hemolytic, megalo anemia

95
Q

[Developmental inclusions of RBC] T or F: Howell-Jolly bodies exhibit a positive fulgean reaction due to RNA

A

False, due to DNA

96
Q

[Developmental inclusions of RBC] Thin ring like structure; stains reddish violet in Wright stain; May be circular or appear at the cell periphery; may form figure of 8

A

Cabot’s Ring

(May represent part of the mitotic spindle, remnants of
microtubules or fragments of nuclear membrane and may appear in RBC in megaloblastic anemia or severe anemia, lead poisoning)

97
Q

[Developmental inclusions of RBC] Smaller than Howell-Jolly bodies and are irregularly shaped; Results in alteration in the biosynthesis of hemoglobin such as
in thalassemia; Appears homogenously over the cell

A

Basophilic Stippling

*Fine or coarse deep blue to purple staining inclusions that appear in RBC on a dried Wright-stained film

Clinical Microscopy (10 decks)

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