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HEMA1 > 2 - HEMA > Flashcards

2 - HEMA Flashcards

1
Q

blood turns red.

A

Addition of 1% Methylene Blue

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2
Q

it will cause cellular damage causing cyanosis

A

> 1.5-3.5% g/dL

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3
Q

will result to a chocolate brown color

A

> 1.5-3.5% g/dL

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4
Q

will convert Hb into hemiglobin causing oxidation of the patients Hb thus once hemiglobin is formed, it can bind to the produced cyanide forming into HiCN.

A

NO2

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5
Q

Reaction in Embden-Meyerhof Pathway that generates NADH.

A

Reduced Diphosphopyridine dinucleotide (DPNH) in the presence of methemoglobin reductase (diaphorase)

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6
Q

deficiency of it will not make it to reduce the ferric into ferrous.

A

NADH

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7
Q

produced in Embden-Meyerhof Pathway in the
Hexose Monophosphate shunt.

A

Reduced Triphosphopyridine nucleotide (TPNH)
in the presence of Glucose-6-PO4 dehydrogenase

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8
Q

With the reduced NADP it can caused the production or reduction of more glutathione which is also a reducing potential. The major reducing capacity of RBC is found in the hexose monophosphate shunt because in this shunt, it can be able to produce

A

1.) NADPH & 2.) GSH

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9
Q

major anti-oxidant since it has a reducing property w/ NADPH

A

Glutathione

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10
Q

important in protecting the Hb from being oxidized

A

Reduced glutathione

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11
Q

can bring back methemoglobin into normal Hb, ferric to ferrous

A

Reduced NAD

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12
Q

Often given to patients suffering from
methemoglobinemia

A

Methylene blue

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13
Q

It will cause the reaction of glucose 6-P to be faster wherein the ____ of NADH will be transferred to the Hb thus reducing Hb however the transfer of _____ is slow wherein methylene blue will enhance this reaction

A

H

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14
Q

a potent reducing agent & also an anti-oxidant

A

Ascorbic acid

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15
Q

commonly attributed to NADH-Methemoglobin reductase deficiency/Diaphorase deficiency which is important in reducing ferric to ferrous

A

Inherited enzyme deficiency

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16
Q

results of various amino acid substitutions in the
globin chain that directly affect the heme group

A

Inherited M

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17
Q

Different structural abnormality but are not protected from being oxidized meaning they are
easily oxidized

A
  1. M-saskatoon
  2. M-boston
  3. M-iwate
  4. M-hydePark
  5. M-milwaekee
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18
Q

Acquired is the effects of chemical or therapeutic agents such as

A

aniline dyes in food, nitrate & nitrite-rich water and foodstuffs ; anti-malarial drugs & sulfonamides

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19
Q

Result of screening test for methemoglobin

A

Red or pink color of blood

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20
Q

Observed in patients taking in oxidant drugs

A

SULFHEMOGLOBIN

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21
Q

Once Hb is converted into sulfhemoglobin it
remains as it is thus it is

A

Irreversible for 120 days

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22
Q

the irreversible formation which prevents it to be measured by drabkins reagent

A

Sulfhemoglobin

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23
Q

Sulfhemoglobin imparts what color?

A

Greenish color

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24
Q

Sulfhemoglobin can be precipitated and can form what inclusion bodies?

A

Heinz bodies

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25
Q

What disease is acquired when there are heinz bodies present?

A

Hemolytic anemia

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26
Q

Abs of sulfhemoglobin

A

600-620 nm

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27
Q

tends to inhibit erythropoietin while androgen
will tend to stimulate more

A

Estrogen

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28
Q

Abs of cyanmethemoglobin

A

540 nm

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29
Q

They migrate fast in electrophoresis

A

Glycosylated hemoglobin

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30
Q

Irreversibly glycosylated at

A

1 or both N-terminal valines (or lysine) of the β-chains

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31
Q

Major fraction which serves as an index of the metabolic control over that last 2-4 months. This is more preferred in monitoring glycemic control.

A

Hb A1c

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32
Q

The present HbA1c levels of the patient reflects on his/her HbA1c levels for the past

A

2-4 months

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33
Q

To which part of the Hgb will the glucose attach?

A

Glucose attaches at 1 or both N-terminal valines (or lysine) or the β- chains.

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34
Q

irreversible meaning the glucose attached to the terminal valine or lysine can no longer be detached.

A

Amadori

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35
Q

a curve that plots the proportion of hemoglobin in its saturated form on the Y axis against the prevailing oxygen tension on the X axis.

A

Oxygen dissociation curve

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36
Q

Deficient ______________ because of enzyme
defect along the synthesis leading to excess iron
& iron will not be utilized in the absence of
_______________. Unused iron will precipitate
into siderotic granules leading to sideroblastic
anemia

A

Protoporphyrin IX,

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37
Q

Deficient Protoporphyrin IX because of enzyme
defect along the synthesis leading to excess iron
& iron will not be utilized in the absence of
protoporphyrin 9. Unused iron will precipitate
into _____________ leading to _____________.

A

Siderotic granules, sideroblastic anemia

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38
Q

problem in the utilization of iron due to deficiency in protoporphyrin 9

A

Sideroblastic anemia

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39
Q

Decreased or non-existent production of one or
more globin chain type

A

Thalassemia

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40
Q

there is a deletion in the gene resulting to incomplete synthesis of A & B chain.

A

Thalassemia (both α & β)

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41
Q

Silent carrier

A

(_A/AA) (AA/_A)

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42
Q

no signs & symptoms of anemia

A

Silent carrier

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43
Q

Thalassemia trait

A

(_ _/AA) (A/A)

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44
Q

w/ mild signs & symptoms

A

Thalassemia trait

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45
Q

Hb H disease

A

(_ _ /A _)

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46
Q

the production of Alpha chain becomes too
insufficient & B chain will be used in excess
resulting to Hb having all B chains

A

Hb H disease

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47
Q

no synthesis of A chain

A

Bart’s Hydrops fetalis

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48
Q

Indication of Deletion: 0 superscript

A

BETA THALASSEMIA

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49
Q

Beta Thalassemia Intermedia

A

B+/B+

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50
Q

present but cannot effect the synthesis of B chain because of partial suppression

A

Beta Thalassemia Intermedia

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51
Q

the patient is devoid of Hb A1 because the patient cannot synthesize B chain & what is elevated is Hb F.

A

Beta Thalassemia Minor/Cooley’s trait

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52
Q

B0/B

A

Cooley’s anemia

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53
Q

Results from the alteration of the DNA genetic
code for the chains

A

HEMOGLOBINOPATHIES

54
Q

Conditions characterized by qualitative
structural abnormalities

A

HEMOGLOBINOPATHIES

55
Q

reason of thalassemia

A

Deletion

56
Q

Example of deletion

A

Hb Gun Hill: (β91 to β 95) → 0

57
Q

caused by cross over during mitosis resulting to fusion

A

Hb Lepore-Baltimore

58
Q

Ex of Hb Lepore baltimore

A

(G(1-50) B(86-146))

59
Q

commonly affects the B chain.

A

Hemoglobinopathies

60
Q

The most well-known hb variant characterized by substitution of glutamic acid by tRNA to valine
on the 6th amino acid position of the β-chain.

A

Hb S

61
Q

Common to black population

A

Hb S

62
Q

The effect of alteration from glutamic acid to
valine is a _________ wherein glutamic is
highly negatively charge compared to valine thus
leading to loss of negative charges & Hb
becomes less negative

A

Negative charge

63
Q

Homozygous (SS)

A

Sickle cell anemia

64
Q

Heterozygous (AS)

A

Sickle cell trait

65
Q

are intracellular species & when present in RBC & when RBC is sickle the parasite inside also dies
does no complication arise

A

Falciparum

66
Q

Blacks who are suffering from this are protected from being infected from developing _____________________.

A

severe falciparum malaria (Resistance)

67
Q

also confer protection in terms of resistance but not immunity meaning these patients may still be infected but may not proceed to chronic stage.

A

Hb C, E, B-Thalassemia & G-6PD deficiency

68
Q

Severe anemia because the patient does not synthesize the normal Hb A

A

SICKLE CELL ANEMIA

69
Q

Causes vasso-obstruction

A

Sickle cell anemia

70
Q

The no. 1 cause of death is infection & in children

A

Sickle cell anemia

71
Q

occurs in bone & joint causing pain

A

Vassoocclusion

72
Q

More severe Hb-S thalassemia

A

Hb S-B

73
Q

Disease with bull’s eye

A

Hb C disease

74
Q

formed when deoxygenated & dehydrated & the crystals are hexagonal or rod-shaped crystals or bar of gold shape & blunt ends & does not deform the cell meaning it retains its shape but becomes rigid

A

Hb CC crystals

75
Q

RBCs – slightly hypochromic

A

Hb C trait

76
Q

Signs & symptoms are milder than SS but more
severe than sickle cell

A

Hemoglobin SC Disease

77
Q

easily crystalize forming a fingerlike
projection w/ more than 1 protrusions where
one is long & protrude away.

A

Hb SC disease

78
Q

Structure of hb SC disease.

A

finger or Washington monument crystal

79
Q

all have different amino acid substitution but the effect is the same & not protected from oxidation

A

Hb Methemoglobin

80
Q

Example of Hb w/ Increase Affinity

A

Hb Chesapeake

81
Q

Example of hb with decrease affinity

A

Hb Kansas

82
Q

Supravital staining is employed (brilliant cresyl
blue & crystal violet)

A

Heinz bodies staining

83
Q

Normal RBC has

A

<7: microcyte ; >8: macrocyte

84
Q

Thickness (MCAT)

A

1.5 – 2.5 um

85
Q

Average volume (MCV)

A

90 fL

86
Q

Average Surface Area

A

160 um2

87
Q

used to measure the effective survival of RBCs in vitro

A

Chromium 51

88
Q

Half survival time range

A

25-32 days

89
Q

<25 days

A

RBC undergoes hemolysis

90
Q

usually utilize for thinner & deformed cells due to acquired condition while ovalocytes are egg shape & not thin, which are often seen in hereditary type.

A

Eliptocytes

91
Q

separates the internal environment to external

A

selective transport membrane

92
Q

crosses phospholipid bilayer

A

Integral protein

93
Q

high amount of sialic acid for imparting negative
charge to maintain zeta potential

A

Integral proteins

94
Q

RBC repel each other due to negative cloud
surrounding them caused by sialic acid.

A

Zeta potential

95
Q

When zeta potential becomes altered this result to

A

rouleau formation

96
Q

Component of zeta potential

A

Glycophorin A & component a (band 3)

97
Q

serves as membrane protein mechanism in order to allow passage of molecules either inward or outward

A

Zeta potential

98
Q

Component (cytoskeleton) of peripheral proteins

A

Spectrin & Actin

99
Q

If excessive cation entered, this will result to ____________ of RBC causing now the entry of water, swelling & __________.

A

hypotonicity, lysis of RBC

100
Q

MEMBRANE ENZYME SYSTEM FOUND OF THE SURFACE OF RBC

A

Na/K ATPase

Ca/Mg ATPase

101
Q

Content of external surface.

A

phosphatidyl choline, glycolipids & sphingomyelin

102
Q

Content of internal surface.

A

Cephalin, phosphatidylinositol & phosphatidylserine

103
Q

Maintains regulation of membrane fluidity &
permeability to electrolytes. It also maintains the
surface area volume of RBC

A

Cholesterol

104
Q

Water content of RBC depends mainly on its
ionic gradient wherein the greater the ionic
gradient, RBC becomes ___________ thus water
enters RBC & too much entry of water causes
__________ of RBC & eventually burst & decrease
surface area volume

A

hypertonic, swelling

105
Q

Cause of the cell to widen.

A

Plasma cholesterol

106
Q

For solubilization

A

Bile acids

107
Q

Ex of red cell antigens

A

ABH antigen
on surface of RBC

108
Q

important in maintaining the shape & size of
RBC & abnormality of these will lead to deformation of cells.

A

A-spectrin, Ankyrin, Band 3, B-Spectrin, Protein 4.2 & 4.1 & Glycoprotein

109
Q

Defective ________ will be spherocytes or pyropoikilocytes

A

Defective A-spectrin

110
Q

for every glucose metabolize, it will produce 2 ATPs for the ______________ & for 2 ATPs for _______________ thus a total of 4 but the net energy utilized is a net of 2

A

glyceraldehyde-3- phosphate, Dihydroxyacetone Phosphate

111
Q

generates NADPH and reduced glutathione (GSH) in the presence of Glucose 6- PO4 dehydrogenase (G6PD). _______ protects the hemoglobin from oxidation by peroxides.

A

Reduced glutathione

112
Q

brings back the ferric form of iron into ferrous.

A

Glutathione

113
Q

RAPOPORT-LUEBERING SHUNT
- Generates ____________ which regulates
the affinity of Hb to O2 by lowering the affinity
promoting release of O2 causing a shift to the
right

A

2,3-DPG

114
Q

Reduction of methemoglobin by NADPH is more
efficient in the presence of _______________ which
serves as an intermediate electron carrier.

A

methemoglobin reductase (cytochrome b5 reductase)

115
Q

prevents oxidation of heme by reducing ferric to
ferrous with the use of NAD.

A

cytochrome b5 reductase

116
Q

an anaerobic & goes as anaerobic glycolytic pathway, mainly for the production of 90-95% of RBC ATPs.

A

EMBDEN MEYERHOF PATHWAY

117
Q

important for the production of NADPH & GSH for the maintenance of Hb iron in the reduced form
because it can reverse the ferric into ferrous.

A

HEXOSE MONOPHOSPHATE SHUNT

118
Q

necessary for production of 2,3 DPG which
maintains affinity of Hb to O2.

A

RAPOPORT-LUEBERING SHUNT

119
Q

serves as reducing property & may also donate its hydrogen to cause reduction of ferric into ferrous.

A

METHEMOGLOBIN REDUCTASE PATHWAY

120
Q

can also detoxify H2O2 converting it into H2O & O2.

A

Reduced glutathione

121
Q

When cells are deformed it will be recognized by splenic macrophages as a damage or senescent RBC wherein spleen filters blood to removed old & damage cells

A

splenicullin

122
Q

destruction of senescent red cells

A

MACROPHAGE-MEDIATED

123
Q

destruction of senescent red cells by who?

A

splenic macrophages

124
Q

Hemoglobin undergoes degradation within the macrophage where iron is stored as _______, amino acids of globin are returned to the metabolic amino acid pool and ________ is converted to ___________ which is released into the plasma and excreted by the liver in bile.

A

ferritin, protoporphyrin, bilirubin

125
Q

synthesize by the liver & released into the plasma

A

Haptoglobin

126
Q

haptoglobin binds w/ free Hb thus forming _______________ & delivered to the ________

A

hemoglobin-haptoglobin, liver

127
Q

Disorder in the a-spectrin gene.

A

HS, HE, HPP, NIHF

128
Q

Disease in the ankyrin gene

A

HS

129
Q

Band 3 gene disease

A

HS, SAO, NIHF

130
Q

B-spectrin gene disorders

A

HS, HE, HPP, NIHF

131
Q

Criteria for pathologic RBC

A

 Size (7-8 um)
 Variation in size (80-100 fL)
 Area of Central Pallor (1/3 & clear)
 Cytoplasm (clear w/out inclusion)

HEMA1 (3 decks)

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