RBC Abnormalities Flashcards
1
Q
Components of whole blood and percentages
A
plasma (54%)
buffy coat (1%)
red blood cells/erythrocytes (45%)
2
Q
plasma is a colorless fluid which is composed of?
A
Water (91-92%) Protein (7-8%) Electrolytes Nutrients Blood gases Hormones
3
Q
the layer contaminated with bacteria if blood is not properly processed
A
buffy coat (white cells + platelets)
4
Q
the plasma without the firbinogen; usual specimen submitted for blood exam for serological tests
A
serum
5
Q
volume of RBCs/unit plasma
A
hematocrit
- males: 40-50
females: 35-40%
6
Q
characteristics and shape of normal rbc
A
circular biconcave with smooth edge and central pale area that gradually fades into reddish cytoplasm
7
Q
diameter of normal rbc
A
7-8 micrometers
8
Q
thickness of normal rbc
A
2-5 micrometers
9
Q
volume of normal rbc
A
90 fl.
10
Q
surface area of normal rbc
A
160 micrometers
11
Q
simplest test to check for structure and form of RBCs since they are diagnostic
A
peripheral blood smear
12
Q
What does PBS examine?
A
Distribution of RBCs Concentration of hemoglobin Size of RBCs Shape of RBCs Inclusion of the RBCs
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
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)
15
Q
Rouleaux formation is seen in
THIMP
A
§ Hyperproteinemia § Infection § Multiple myeloma § Tissue necrosis § Increased fibrinogen § Pregnancy
16
Q
Autoagglutination is seen in:
SHAT
A
§ Hemolytic anemia
§ Staphylococcal infections
§ Atypical pneumonia
§ Trypanosomiasis
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
18
Q
[hemoglobin content]
contains normal amoutn of hb which carries oxygen and gives blood its red color
A
normochromic
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)
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)
21
Q
variation in hb content
A
anisochromia
22
Q
T or F: average size of rbc is correlated with MCHC
A
False, with MCV
23
Q
diameter and MCV of macrocytic RBC
A
8.5-9 micrometers and MCV = 100 fl.
24
Q
macrocytic normochromic (megaloblastic) type of anemia
A
Pernicious anemia
25
Pernicious anemia is associated with?
achloryhdria and absence of gastric intrinsic factors necessary for the binding and absorption of vit.b12
26
an erythrocyte maturing factor which is secondary to megaloblastic anemia and secondary to pernicious anemia
vit b12
27
other findings in pernicious anemia
```
atrophic glossitis (large tongue)
gastrointestinal and nervous disorders
```
28
RBC precursors of megaloblastic anemia appearance
Nuclear-cytoplasmic asynchrony (abnormally large and have nuclei that appear much less mature than would be expected from the development of cytoplasm)
29
drugs which can lead to megaloblastic anemia (MAPLE)
```
methotrexate
AZT-Zidovudine (anti-HIV drug)
Phenytoin (Fenytoin-folate deficiency: anti-seizure drug)
liver disease
ethanol
```
30
where macrocytosis is seen
| LAMBMCHC
```
§ Lymphoma
§ Leukemia
§ Alcoholism w/o liver disease
§ Myeloma
§ B12 deficiency
§ Metastatic carcinoma
§ Chronic hemolytic anemia
§ Hypothyroidism
§ Cancer chemotherapy
```
31
MCV of microcytic RBC
below 80 fl.
32
T or F: microcytic rbcs always have less hemoglobin
false, normal or less hb
33
where is microcytic rbcs usually seen?
- After chronic iron deficiency
- During decreased globin synthesis in β Thalassemia, along with the target cell
- In leptocytes
34
variation in RBC size (combination of macrocytosis and microcytosis)
Anisocytosis
35
RBCs that are thinner than normal with colorless centers and increased surface area not proportional to volume;
leptocytes
*Found in thalassemia, obstruction of bile ducts, cirrhosis and steatorrhea
36
variation in shape of rbc
poikilocytosis
37
probable causes of poikilocytosis
```
® Structural and biochemical changes in the cell membrane
® A metabolic state in the cell
® Hemoglobin molecule abnormalities
® Abnormal microenvironment
® RBC age
```
38
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.
β-thalassemia
39
shape of macrocytes in poikilocytes secondary to developmental macrocytosis
oval
| defect in nuclear maturation = macrocytes; may appear hyperchromic due to increased thickness and increased hb
40
T or F: poikilocytes secondary to developmental macrocytosis can be secondary to Folate deficiency only
False, folate and B12 deficiency
41
Poikilocytes Secondary to Membrane Abnormalities
| SCABEES
```
Spherocytes
Elliptocytes/Ovalocytes
Echinocytes/Crenated cells
Burr cell
Acanthocytes
Stomatocytes
Codocytes
```
42
[Poikilocytes Secondary to Membrane Abnormalities]
| with evenly distributed, uniform-sized blunt spicules or bumps on RBC surface; artifact
Echinocytes or Crenated cells
*seen in film prepared from anticoagulated blood several hours old and stored blood
43
[Poikilocytes Secondary to Membrane Abnormalities] T or F: Echinocytes are normally seen in vivo and in pathologic disease
False, not normal and not usually associated with pathologic disease
44
[Poikilocytes Secondary to Membrane Abnormalities]
| Why are echinocytes seen in stored blood/several hours old anticoag blood film?
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
[Poikilocytes Secondary to Membrane Abnormalities]
| normal diameter and characteristic of SPHEROCYTES
diameter: 6.2-7 micrometers; thickness: 2.2-3.4 micrometers
| RBC is round/globular wo central pallor and smaller volume
46
[Poikilocytes Secondary to Membrane Abnormalities]
| How do spherocytes lose thick membrane?
They lose thick membrane when passing through circulation (damaged due to inflexible shape) which causes decreased survival of RBCs and increased osmolality
47
[Poikilocytes Secondary to Membrane Abnormalities]
| Spherocytes are normally seen in
§ Autoimmune hemolytic anemia
§ Hemolysis due to water dilution
§ Microangiopathic hemolytic anemia
48
[Poikilocytes Secondary to Membrane Abnormalities]
| elongated with slit-like area of pallor may be resulting from high cellular sodium and low potassium content
stomatocytes
*may be retained in spleen due to abnormality and seen in normal PBS (may be artifact); hereditary/acquired;
49
[Poikilocytes Secondary to Membrane Abnormalities] This is observed in alcoholisms, cirrhosis, obstructive liver disease
stomatocytes
50
[Poikilocytes Secondary to Membrane Abnormalities] also has spicules but are irregularly shaped and unevenly spaced, echinocyte twin
burr cell
*seen in true pathologic disease like renal insufficiency. SHOULD BE REPORTED IF SEEN
51
[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
Elliptocytes or Ovalocytes
*less 15 in normal RBC are ovalocytes (hereditary)
52
[Poikilocytes Secondary to Membrane Abnormalities] This can be seen in IDA, megaloblastic anemia, sickle cell anemia and thalassemia
Elliptocytes
53
[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);
Acanthocytes
* hereditary/acquired
* spur cells in cirrhosis and metastatic liver disease
54
[Poikilocytes Secondary to Membrane Abnormalities] cause of acanthocytes
changes in the ratio of plasma lipids (lecithins and sphingomyelins)
55
[Poikilocytes Secondary to Membrane Abnormalities] sources of acquired acanthocytosis
- Alcoholic cirrhosis
- Hepatitis of the newborn
- Hemolytic anemia
- Lipid metabolism disorders
- Post-splenectomy
56
[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
codocytes
57
[Poikilocytes Secondary to Membrane Abnormalities] Why are membrane surfaces increased in codocytes? How about greater osmotic resistance?
increased membrane surfaces: cholesterol and phospholipid loading (hypercholesterolemia)
greater osmotic resistance: increase surface to volume ratio
58
[Poikilocytes Secondary to Membrane Abnormalities] T or F: codocytes are always acquired
true
59
[Poikilocytes Secondary to Membrane Abnormalities] These are seen in thalassemia, hemoglobinopathies, obstructive liver
disease, post-splenectomy, iron deficiency
Codocytes
60
[Poikilocytes Secondary to TRAUMA]
```
Schistocytes
Keratocytes
Dacrocytes
Microspherocytes
Semilunar bodies
```
61
What happens to RBCs under excessive physical trauma in cardiovascular system?
fragment and lyse (decreased survival and is subjected to intravascular hemolysis)
62
[Poikilocytes Secondary to TRAUMA] fragmentation in schistocytes result from:
§ 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
[Poikilocytes Secondary to TRAUMA] Shapes of schistocytes
helmet, triangular, small pieces of RBC
64
[Poikilocytes Secondary to TRAUMA] Schistocytes are usually seen in:
severe burns, renal graft rejection, glomerulonephritis, DIC (MAHA), vasculitis, TTP
65
[Poikilocytes Secondary to TRAUMA] These are half-moon (crescent) shaped large, pale pink staining ghost of RBC
semilunar bodies
* always acquired
* seen in malaria and other hemolytic conditions
* membrane remains after content has been released
66
[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
KERATOCYTES
* when cut rbc fuse, vacuole like area ruptures
* PATHOLOGIC (REPORTED IF FOUND)
67
[Poikilocytes Secondary to TRAUMA] Why do keratocytes not remain long in circulation?
increased fragility
68
[Poikilocytes Secondary to TRAUMA] ® Occur in severe burns as small round cells
® Results from thermal damage in the cell’s membrane
MICROSPHEROCYTES
69
[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
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
[Poikilocytes Secondary to ABNORMAL HB CONTENT] These poikilocytes can be diagnostic for
chronic hereditary hemolytic anemia
71
[Poikilocytes Secondary to ABNORMAL HB CONTENT] Three types characteristics of abnormal Hbs
```
Drepanocytes (sickle cells with abnormal Hb S)
HbCC crystals (Hb C-homozygous C)
HbSC crystals (with both Hb S and Hb C)
```
72
[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
Drepanocytes
*can be curved or straight, or S, V or L-shaped
73
[Poikilocytes Secondary to ABNORMAL HB CONTENT]
§ Milder form of Hb S
§ Intra RBC Hb CC crystals in homozygous C (Hb CC) disease
HbCC crystals (Hb C-homozygous C)
§ Tend to be hexagonal with blunt ends and stain darkly
§ Crystal appears free-cell without Hb
74
[Poikilocytes Secondary to ABNORMAL HB CONTENT]
| § Dark-hued crystals which distort the membrane (“rectangular RBC”)
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
a type of hemoglobinopathy which is also called as hb SS disease wherein there is qualitative problem of synthesis of an incorrectly functioning globin
Sickle-cell disease
76
Sickle-cell disease produces specific mutant form of B-globin. What are the two variants of hemoglobin in the b chain gene?
- 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
T or F: abnormal Hb SS is prone to hemolysis when oxygen tension is low
false, crystallization
* long thin sickle forms clump and decrease blood flow and oxygen tension
* might happen in persons with Hb AS
78
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)
thalassemia
79
Types of thalassemia accdg to which chain of hemoglobin is affected
α thalassemia (Hemoglobin H disease and alpha thalassemia hydrops fetalis)
β thalassemia (β thalassemia minor and β thalassemia major/Cooley's anemia)
80
[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)
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
[Thalassemia] What are found in PBS in Hb H disease?
microcytic hypochromic anemia
with target cells and Heinz bodies (precipitated
HbH)
82
[Thalassemia] four alpha loci affected
| see figure 16
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
[Thalassemia] It is inherited in an autosomal-recessive fashion; severity of disease depends on nature of mutation
β thalassemia
*(βo) if they prevent any formation of β chains
(β+) if they allow some β chain formation to occur
84
[Thalassemia] T or F: there is a relative excess of beta chains in β thalassemia
false, alpha chains but these do not form tetramers but bind to rbc membranes (damage) and at high temps, toxic aggregate formation
85
[Thalassemia] differentiate β thalassemia minor and β thalassemia major/Cooley's anemia
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
Developmental inclusions of RBC
```
Howell-Jolly bodies
Basophilic stippling
Pappenheimer bodies
Polychromatophilic Red Cells
Cabot's Ring
```
87
Inclusions of RBC due to abnormal hb precipitation
heinz bodies (denatured globin; round, refractile; differ from Howell-Jolly because it is attached to and tends to ppt on RBC membrane)
88
T or F: Heinz bodies are visible in Wright-stained films
False
| id with supravital staining with basic dyes: meth blue/brilliant cresyl blue; large when alone small when numerous
89
Where are heinz bodies usually seen?
poisoning with aromatic nitro-compounds, amino compd, hemolytic anemias and sulfonamide intake
90
inclusions seen in malaria
Schuffner's stippling or granules
91
refractive artifacts are caused by what?
water contamination of the methanol or wright stain (others: by particles of fat/detergent on glass itself)
92
[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
Pappenheimer bodies
*spleen removed these granules
93
[Developmental inclusions of RBC] Young RBC, diffusely basophilic (due to RNA); Larger than normal, contain ribosome, mitochondria and other organelles
Polychromatophilic Red Cells
*With methylene blue (supravital stain) called reticulocytes (ribosomes and organelles are precipitated)
94
[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
Howell-Jolly bodies
*seen in sc, hemolytic, megalo anemia
95
[Developmental inclusions of RBC] T or F: Howell-Jolly bodies exhibit a positive fulgean reaction due to RNA
False, due to DNA
96
[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
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
[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
Basophilic Stippling
*Fine or coarse deep blue to purple staining inclusions that appear in RBC on a dried Wright-stained film
