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HEMATOLOGY > RBC DISORDERS AND MORPHOLOGY > Flashcards

RBC DISORDERS AND MORPHOLOGY Flashcards

1
Q

caused by the efflux of fluid from
the blood vessel to the interstitial fluid which causes the
hemoconcentration of the blood within the vasculature

A

RELATIVE POLYCYTHEMIA

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2
Q

influx of fluid from the interstitial tissue or
other source to the blood vessel which causes the hemodilution of the blood

A

RELATIVE ANEMIA

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3
Q

genetic problem which causes the uncontrolled or over production of the blood cells especially the red cell that causes serious health problems if intervention is not applied.
This disorder is known as “Polycythemia vera”

A

Primary absolute polycythemia

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4
Q

gene which leads to spontaneous kinase
production that causes overstimulation of the
hematopoietic cell to multiply unceasingly.

A

JAK2 V617F

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5
Q

High viscosity of blood

A

may cause decreased blood
tissue perfusion and cyanosis

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6
Q

overproduction of the red cells by the bone
marrow.

  • Lab findings on this condition include
    pancytosis (high RBC count, WBC count and
    Platelet count), low ferritin, high LDH, high
    vitamin B12, hypercellular bone marrow and
    the LAP score is high reaching more
    than200.
A

Low EPO

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7
Q

triggered by high EPO stimulation on the bone marrow to promote red cell production which increases the Hgb and Hct value.

A

Secondary polycythemia

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8
Q

driven HPO release
APPROPRIATE 2ndary polycythemia

  • heart and lung problems such as
    COPD, cigarette smoking, living or
    going up on high altitudes
A

Hypoxia

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9
Q

HPO release
INAPPROPRIATE 2ndary polycythemia

  • kidney disorders that accidentally
    release the EPO triggering red cell
    production, and example of these
    are polycystic kidney and kidney
    tumors.
A

NON-hypoxia driven

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10
Q

associated with inadequate intake,
increased need, impaired absorption, errors in
absorption or transport and competition for vitamins.

A

Vtiamin B-12

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11
Q

collected to measure the amount of
excreted radioactive vitamin B12 using a gamma scintillation counter

A

24-hour urine

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12
Q

Normal excretion is _______ of administered
vit-B12 in urine, LESSER = DECREASE OR
LACK OF IF IN STOMACH

A

> 7%

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13
Q

Errors in absorption includes________
syndrome where the intestine lacks the receptor site for IF-Cobalamin complex resulted to inability to absorbed the vitamin B12 from the intestine to the blood.

A

Imerslund-Grasbeck
syndrome

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14
Q

Normal flora of intestine
also compete for Vit B12

A

BLIND LOOP SYNDROME

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15
Q

may occur due to
inadequate intake, increased need, impaired
absorption

A

FOLATE DEFICIENCY

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16
Q

before developing anemia and this starts with low vitamin levels in the blood, followed
by abnormal morphology on WBC

  • > 5 nuclear lobulations
A

HYPER-SEGMENTED NEUTROPHIL

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17
Q

is a psychosis hallucination due to the degeneration of neurons of the central nervous system

A

megaloblastic madness

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18
Q

decreased cell counts

A

Pantocytopenia

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19
Q
  • Several conditions that shows macrocytic red cell in the peripheral blood or with high MCV

macrocytic non-megaloblastic anemias include
reticulocytosis, acquired bone marrow failure, liver diseases and chronic alcoholism

A

MEGALOBLASTOID REACTION

20
Q

abnormal nuclear development of the RBC showing binuclearity or multinuclearity of characterized by ineffective erythropoiesis that resulted to decrease Hct and Hgb

A

CONGENITAL DYSERYTHROPOIETIC ANEMIA

20
Q

Most common type of CDA

A

CDA 2

20
Q

CDA type 1

A

CDAN1

20
Q

CDA type 2

A

SEC23B

20
Q

CDA type 3

A

KIF23

20
Q

CDA type 4

A

KLF1 gene

21
Q

This abnormality deprived the red cells the ability to recoil its membrane after experiencing absolute pressure within the cardiovascular system and also through squeezing to small blood vessels resulted to an elongated shaped red cell called elliptocytes

A

HEREDITARY ELLIPTOCYTOSIS

21
Q

code for a-spectrin

A

Defective SPTA1

21
Q

code for B-spectrin

A

SPTB gene

22
Q

code for protein band 4.1

A

EPB41 gene

23
Q

Can withstand temperature up to 49℃
without causing it to lyse, but the RBC in HE
is easily degraded after exposing it to 41 to
45 ℃

A

HEREDITARY PYROPOIKILOCYTOSIS

24
Q

also affected by the deficiency of
Gerbich membrane protein known as the Leach
phenotype as well as the deficiency of glycophorin C due to defect on GPC gene

A

Protein Band 4.1

25
Q

Quantitative globin synthesis defect

A

THALASSEMIA

26
Q

MCV of less than 80 fL and an MCH of less than 27 pg

A

α-THALASSEMIA TRAIT

27
Q

Hemoglobin concentrations averaging 7 to 10 g/dL and reticulocyte counts of 3% to 10%, although a wide variability in clinical and laboratory findings exists

A

HEMOGLOBIN H DISEASE

28
Q

The fetus can survive until the third trimester because of Hb Portland, but this hemoglobin cannot support the later stages of
fetal growth, and the affected fetus becomes severely anoxic. At delivery there is a severe microcytic, hypochromic anemia (hemoglobin concentration of 3 to 8 g/dL) with high reticulocyte counts and numerous nucleated RBCs in the peripheral blood

A

HEMOGLOBIN BART HYDROPS FETALIS SYNDROME

29
Q

Hemoglobin level can range from approximately 11 to 15 g/dL in affected men and 10 to 13 g/dL in affected women.
The RBCs are microcytic and hypochromic, with a mean cell volume (MCV) less than 75 fL and a mean cell hemoglobin (MCH) less than 26 pg

A

β THALASSEMIA TRAIT/ MINOR

30
Q

Hemoglobin level is below 7 g/dL but can fall as low as 2 to 4 g/dL. The MCV ranges from 50 to 70 fL, and the MCH from 12 to 20
pg.

A

β THALASSEMIA MAJOR

31
Q

The hemoglobin level is between 7 and 10 g/dL.
Shows great heterogeneity

A

β THALASSEMIA INTERMEDIA

32
Q

Peripheral blood smear of individual suffering from sideroblastic anemia shows a combination of microcytic and normocytic red cells.

A

DIMORPHIC BLOOD OR DIMORPHISM

33
Q

observed on patients that underwent bone marrow transplant and blood transfusion

Inclusion bodies such as Pappenheimer bodies and basophilic stippling are commonly observed.

A

ACQUIRED DIMORPHISM

34
Q

genetic defect that promotes the poor development of the red cell’s membrane peripheral proteins which resulted to the impaired interaction of it to the transmembrane or integral membrane proteins

increases the fragility of the red cell that resulted to early red cell destruction which occurs either extravascular or intravascularly

A

HEREDITARY SPHEROCYTOSIS

35
Q

instruct formation of ankyrin

A

ANK1

36
Q

α chain of spectrin

A

SPTA 1 gene

37
Q

β chain of spectrin

A

SPTB 1 gene

38
Q

for protein Band 4.2,

A

EPB42 gene

39
Q

encodes formation of protein
band 3

A

SLC4A1 gene

HEMATOLOGY (5 decks)

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