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Pathology > Hematology - RBC > Flashcards

Hematology - RBC Flashcards

1
Q

Hematopoiesis requires

A

Hematopoietic stem cells(HSC)

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2
Q

Hematopoietic stem cells

A

Identified by CD34 marker
Pleuripotent stem cells
Have property of self renewal

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3
Q

Hematopoiesis in fetal life

A

Starts from 3rd week
Takes place in Yolk sac

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4
Q

Hematopoiesis after 3 months

A

Usually takes place in Liver and Spleen

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5
Q

Hematopoiesis after birth

A

Bones (Bone marrow)

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6
Q

Hematopoiesis after birth

A

Bone marrow

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7
Q

HSC leads to formation of

A

Lymphoblast and
Myeloblast

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8
Q

Lymphoblast

A

Lymphoid progenitor cells
15micron in size
Condensed nucleus (No nucleoli)
Cytoplasm without granules
Gives birth TO LYMPHOCYTES

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9
Q

Myeloblast

A

Myeloid progenitor cells
20micron in size
Nucleus not condensed (prominent nucleoli)
Cytoplasm with granules
Gives birth to RBC, WBC (except Lymphocytes), Platelets

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10
Q

Lymphoblast size

A

15 micron

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11
Q

Myeloblast size

A

20 micron

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12
Q

Prominent nucleoli is seen in

A

Myeloblast

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13
Q

Lymphoblasts gives birth to

A

Lymphocytes

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14
Q

Myeloblast gives birth to

A

RBC
WBC Except Lymphocytes
Platelets

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15
Q

Most important hormone for RBC production

A

Erythropoietin

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16
Q

Factor needed for formation of granulocytes

A

Granulocyte colony stimulating factor (g-CSF)

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17
Q

Important cytokine for Platelets formation

A

IL-11

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18
Q

Bone marrow Examination includes

A

BM Aspiration
BM Biopsy

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19
Q

BM Aspiration Shows

A

Cell morphology
Enumeration

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20
Q

BM Biopsy shows

A

Cellularity
Fibrosis
Checks infiltrative disorders

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21
Q

Sites of Bone marrow Examination in Adults

A

M.c - Posterior superior iliac spine
- Also in sternum at level of 2nd IC (Only BM Aspiration)

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22
Q

Site of Bone marrow Examination in obese people’s

A

Anterior superior iliac spine

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23
Q

Site of BM Examination in Child (<2yrs)

A

Tibia

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24
Q

Anticoagulant used for BM Examination

A

EDTA (doesn’t affects cell morphology)

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25
Q

Defeciency of RBC, WBC And platelets together

A

Pancytopenia

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26
Q

Stages of RBC Development

A

Myeloid stem cells - Colony forming unit-Erythroid (CFU-E) - Erythroblast - Normoblast(Early, intermediate and late) - Reticulocyte - RBC

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27
Q

Most erythropoietin sensitive cell

A

CFU-E

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28
Q

Hemoglobin appeared first in which cell with electron microscopy

A

Erythroblast

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29
Q

Hemoglobin 1st detection by routine staining

A

Intermediate Normoblast

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30
Q

Nucleus is absent in

A

Reticulocytes and RBCs

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31
Q

1st non-nucleated cell in RBC Development

A

Reticulocyte

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32
Q

Last nucleated cell in RBC Development

A

Late Normoblast

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33
Q

Normoblast types

A

Early (Basophilic) Normoblast
Intermediate (Polychromatophilic) Normoblast
Late (Orthochromatic) Normoblast

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34
Q

Which hormone decreases Hepcidin levels and increases Iron absorption

A

Erythroferrone

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35
Q

Reticulocytes are stained by

A

Supravital staining - New methylene blue

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36
Q

Normal amount of Reticulocytes

A

1-2% of RBC

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37
Q

Reticulocytes time for maturation

A

1 day

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38
Q

Absolute Reticulocyte count

A

= % Reticulocytes/100 x RBC count

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39
Q

Corrected Reticulocyte count

A

Reticulocytes (%) x Hb(patient) / Hb(Normal)

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40
Q

Reticulocyte production index (RPI)

A

Corrected Reticulocyte count / maturation factor or time correction

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41
Q

RPI < 2.5 Shows

A

Decreased proliferation or Maturation disorders

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42
Q

RPI < 2.5 Shows

A

Decreased proliferation or Maturation disorders

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43
Q

RPI > 2.5 (Increased reticulocytes) shows

A

Hemolytic anemia

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44
Q

RBC Normal shape and size

A

Biconcave shape and 7-8micron in size

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45
Q

Most hemoglobin present in RBC

A

Periphery

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46
Q

Parameters of RBC

A

MCH (Mean cell Hb)
MCV (Mean cell volume)
MCHC
RDW (Red cell distribution width)

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47
Q

MCH indicates

A

Avg Hb in RBC
Normal - 27-33pg

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48
Q

MCV Normal value

A

80-100fl

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49
Q

Microcytosis

A

MCV <80fl

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50
Q

Macrocytosis

A

MCV >100fl

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51
Q

MCV is

A

= Hematocrit x 10 / RBC

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52
Q

MCHC =

A

MCH/MCV

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53
Q

In case of anemia MCHC decreases except

A

Hereditary spherocytosis (increases)

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54
Q

Abnormal shape of RBC known as

A

Poikilocytosis

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55
Q

Variations in RBC shape and size

A

Anisocytosis

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56
Q

Index of Anisocytosis

A

RDW

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57
Q

Normal RDW

A

11.5-14.5

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58
Q

Anemia can be classified on the basis of

A

Decreased production of RBC
Blood loss
Hemolytic anemias (premature destruction)

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59
Q

Anemia classification on the basis of Size

A

Microcytosis (<80fl)
Macrocytosis (>100fl)
Normocytic (80-100fl)

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60
Q

Microcytosis anemia includes

A

Sideroblastic anemia
Iron deficiency anemia
Thalassemia
Anemia of chronic diseases (in late stages)

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61
Q

Macrocytosis anemia includes

A

Liver disease
Hypothyroidism
Myelodysplasia
Cell Maturation disorder
B12 and Folic acid deficiency
Alcohol

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62
Q

Normocytic anemia includes

A

Kidney failure
Anemia of chronic diseases (in early stages)
Myelofibrosis
Metastasis

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63
Q

Most common cause of anemia

A

Iron deficiency anemia

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64
Q

Iron absorption takes place in

A

Duodenum

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65
Q

Iron ferric form (Fe3+) converted into Ferrous form (Fe2+) by which enzyme

A

Cytochrome B reductase

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66
Q

Transmembrane protein that transports iron from inside of a cell to outside of cell

A

Ferroportin

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67
Q

Blood plasma glycoprotein that play central role in iron metabolism and responsible for ferric ion delivery

A

Transferrin

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68
Q

Iron stored in the body in the form of

A

Ferritin and Hemosiderin

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69
Q

Hemosiderin is stained by special stain named

A

Prussian blue stain - Perls reaction

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70
Q

Normal serum iron levels

A

100-200mg/dl

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71
Q

Total iron binding capacity

A

300-360mg/dl

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72
Q

Serum ferritin is inversely proportional to

A

Serum transferrin

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73
Q

Causes of IDA

A

Decreased intake of iron (M.C)
Increased requirement
Blood loss

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74
Q

Stage 1 of IDA

A

Decrease of iron in storage site - Serum ferritin level decreases (Earliest indicator)

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75
Q

Stage 2 of IDA

A

Changes in iron profile (No change in shape of RBC)
Serum iron decreases, % transferrin saturation decreases but Total iron binding capacity (TIBC) increases

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76
Q

Stage 3 of IDA

A

Iron deficiency anemia
Morphological changes
Size of RBC decreases, pale in color

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77
Q

Clinical features of IDA

A

Palpitations, weakness
Decreased work capacity
Koilonychia (soft nails)
PICA (Abnormal eating habits)

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78
Q

Plummer vinson Syndrome

A

Triad of IDA, Esophagus web and Glossitis

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79
Q

Gold standard method of diagnosis of IDA

A

BM Examination

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80
Q

Blood sample results in IDA

A

MCV Decreases
MCh Decreases
MCHC Decreases
Deceased osmotic fragility - in severe IDA
Serum ferritin decreases
Serum iron decreases
% Transferrin saturation decreases
TIBC increases

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81
Q

IDA is which type of anemia

A

Microcytic Hypochromic anemia

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82
Q

RBC Protoporphyrin levels in IDA

A

Increases because due to low iron levels Protoporphyrin will not be able to form Heme So there will be increased level of Free protoporphyrin in RBC

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83
Q

Mentzer index =

A

MCV / RBC Count

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84
Q

Mentzer index in IDA

A

> 13

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85
Q

Mentzer index in Thalessemia trait

A

<13

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86
Q

Treatment of IDA

A

Treat primary cause
Iron supplementation

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87
Q

Serum transferrin receptor ratio / Log(ferritin) in IDA

A

> 1.5

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88
Q

Serum transferrin receptor ratio / Log(ferritin) in Anemia of chronic diseases

A

<1.5

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89
Q

Risk factors of Anemia of chronic diseases (AOCD)

A

Chronic infections (TB)
Chronic inflammations (RA)
Cancers/Malignancy
All these leads to release of Cytokines

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90
Q

Cytokines responsible for AOCD

A

IL-6 (Most common) , IL-1 And TNF-Alpha

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91
Q

Effect of Cytokines on Bone marrow in AOCD

A

Decreases erythroid precursors(low erythropoietin) and that leads to decreases RBC production - Anemia

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92
Q

Type of anemia due to effects of Cytokines on Bone marrow

A

Normocytic Normochromic Anemia (No. Of RBC decreases but no change in morphology)

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93
Q

Effect of Cytokines on Liver in AOCD

A

Increases ferritin, Hepcidin levels and Decrease in transferrin levels

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94
Q

Increased Hepcidin levels

A

Inhibits Ferroportin which inhibits iron utilisation in RBC

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95
Q

Type of anemia due to effect of cytokines on Liver

A

Microcytic Hypochromic Anemia

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96
Q

Iron profile in AOCD

A

Serum ferritin increases
Serum iron decreases
% transferrin saturation decreases
TIBC decreases

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97
Q

Treatment of AOCD

A

Treat primary cause
Cancer patients - Erythropoietin

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98
Q

Anemia due to defect in heme metabolism

A

Sideroblastic anemia

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99
Q

Rate limiting enzyme in Heme metabolism

A

ALA Synthase
Needs cofactor Vit. B6

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100
Q

Congenital cause of Sideroblastic anemia

A

Decrease in enzyme activity

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101
Q

Acquired causes of Sideroblastic anemia

A

Alcohol intake
B6 deficiency
Lead poisoning
Decreased Copper levels

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102
Q

Sideroblastic anemia is type of which anemia

A

Microcytic Hypochromic anemia

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103
Q

Ringed sideroblast is seen in

A

Sideroblastic anemia
Myelodysplastic syndrome
Thalessemia
B12 deficiency
Some hemolytic anemias

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104
Q

Iron profile in Sideroblastic anemia

A

S. Ferritin increases
S. Iron increases
% transferrin saturation increases
TIBC Decreases

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105
Q

RBC morphological changes in Sideroblastic anemia

A

RBC decreases in size
Pale in color

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106
Q

BM Examination in Sideroblastic anemia shows

A

Ringed sideroblast

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107
Q

Treatment of Sideroblastic anemia

A

Treat primary cause

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108
Q

Hereditary spherocytosis mode of inheritance

A

Autosomal dominant inheritance

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109
Q

Normal RBC membrane proteins

A

Spectrin
Ankyrin
BAND 3
BAND 41
Glycophorin

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110
Q

Which RBC Membrane protein contribute most in shape

A

Spectrin

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111
Q

Which RBC Membrane protein is most abundant

A

Glycophorin

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112
Q

What happens with aging of RBC

A

RBC becomes less flexible and become more prone to splenic macrophages (Splenic phagocytosis)

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113
Q

Most common defect seen in which RBC membrane protein in Hereditary spherocytosis

A

Ankyrin

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114
Q

Most severe Hereditary spherocytosis seen in defect of which RBC Membrane protein

A

Spectrin

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115
Q

Decrease in life span of RBC in Hereditary spherocytosis

A

From 120 days to 10-15 days

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116
Q

Clinical features of Hereditary spherocytosis

A

Anemia
Splenomegaly
Jaundice
Positive family history

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117
Q

BM Examination in Hereditary spherocytosis

A

Shows increased activity of BM and increased level of Erythroid precursors

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118
Q

Blood test results in Hereditary spherocytosis

A

MCH Normal
Hb decreases
MCV Decreases
MCHC Increases

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119
Q

Peripheral smear of Hereditary spherocytosis

A

Central pallor absent
Spherical RBCs

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120
Q

Spherical RBCs can be seen in which conditions

A

Autoimmune hemolytic anemia
Hereditary spherocytosis
G6PD deficiency
Infections

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121
Q

Most common cause of Spherical RBCs

A

Autoimmune hemolytic anemia

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122
Q

Osmotic fragility in Hereditary spherocytosis

A

PINK test - INCREASES

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123
Q

Procedure of Autohemolyser

A

Take patient blood sample + 0.9% saline solution and wait for 48 hours

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124
Q

Result of Autohemolyser in case of Hereditary spherocytosis

A

> 15% RBC Destruction

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125
Q

Result of Autohemolyser in case of Normal individuals

A

3-4% of RBC Destruction

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126
Q

Dye used for Flow Cytometry

A

5-EMA (Eosin maleimide) dye

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127
Q

Mean fluorescence in case of Hereditary spherocytosis

A

Decreases

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128
Q

Management of Hereditary spherocytosis

A

Removal of spleen - bczz main site of RBC Destruction

129
Q

Increase in average life span of RBC after Splenectomy in Hereditary spherocytosis

A

Can increase upto 60days

130
Q

Is there Change in shape of RBC after Splenectomy

A

No bczz hereditary

131
Q

High level of Bilirubin due to chronic hemolysis can lead to

A

Pigment gall stones
Bilirubin binds with Calcium and increases risk of gall stone development

132
Q

Most common metabolic disorder which leads to RBC Destruction

A

G6PD deficiency

133
Q

G6PD Deficiency mode of inheritance

A

X linked recessive inheritance

134
Q

G6PD normally helps in

A

Neutralizing Oxidative stress with the help of reduced glutathione

135
Q

G6PD deficiency can leads to

A

Increased susceptibility to oxidative stress

136
Q

G6PD deficient patients are sensitive to

A

Infections
Food - like Fava beans
Drugs - Primaquine, Sulfa drugs, Nitrofurantoin, Nalidixic acid

137
Q

Heinz body

A

Indicative of oxidative injury to the erythrocytes

138
Q

Stain used to see Heinz body

A

Supravital staining - Crystal violet

139
Q

If denatured Hb in case of G6PD deficiency precipitates in RBC

A

Known as Bite cell or DEGMACYTE

140
Q

If denatured Hb directly damages RBC

A

Intravascular hemolysis

141
Q

If Denatured Hb forms abnormal connections with RBC

A

Decreased flexibility and destroyed by splenic phagocytosis
Extravascular hemolysis

142
Q

Clinical features of G6PD deficiency

A

Weakness
Altered color of urine

143
Q

G6PD variants

A

G6PD - B (Most common and stable)
G6PD - A+
G6PD - A-
G6PD M (least stable) - severe hemolysis

144
Q

Blood investigation in G6PD deficiency shows

A

Low Hb levels

145
Q

Peripheral smear in G6PD deficient patients on Supravital staining

A

Heinz body

146
Q

Peripheral smear in G6PD deficient patients on Routine staining

A

Bite cell/DEGMACYTE
Blister cell
Spherocytes

147
Q

G6PD estimation can be done by

A

ASSAY
Electrophoresis
Fluorescent spot test - sensitive and screening test

148
Q

Benefits in G6PD deficient patients

A

Protection against Plasmodium falciperum(Malaria)

149
Q

Management of G6PD deficiency

A

Treat primary cause if present
Observation
If taken drugs - discontinue
Self limiting condition

150
Q

Hypoxemia due to increased RBC Destruction can trigger

A

Release of Erythropoietin from Kidney

151
Q

Hemolytic anemia occurs

A

When There is imbalance between RBC Destruction and compensatory mechanism of bone marrow

152
Q

Due to increased Bone marrow activity in Hemolytic anemia there is

A

Increased cellularity (No. Of cells increases)
Reticulocytes increases

153
Q

Due to RBC Destruction in Hemolytic anemia we can see

A

Anemia
Increased serum LDH levels
Increased levels of unconjugated bilirubin - JAUNDICE

154
Q

Destruction of iron in tubular cells of kidney known as

A

Renal hemosiderosis

155
Q

Types of hemolytic anemias

A

Intravascular hemolytic anemia
Extravascular Hemolytic anemia

156
Q

Site of RBC Destruction in intravascular hemolytic anemia

A

Systemic circulation

157
Q

Site of RBC Destruction in extravascular Hemolytic anemia

A

Liver and spleen

158
Q

Massive increase in size of liver and spleen seen in which hemolytic anemia

A

Extravascular Hemolytic anemia

159
Q

Haptoglobin levels in Hemolytic anemia

A

Decreases in both intravascular (more) and extravascular Hemolytic anemia

160
Q

Causes of Hemolytic anemia can be divided into

A

Intracorpuscular causes
Extracorpuscular causes

161
Q

Examples of intravascular hemolytic anemias

A

Paroxysmal nocturnal Hburia(PNH)
G6PD Deficiency

162
Q

Examples of Extravascular Hemolytic anemia

A

Sickle cell anemia
Thalessemia

163
Q

Inherited intracorpuscular causes of HA includes

A

Hereditary spherocytosis
G6PD Deficiency
Sickle cell anemia
Thalessemia

164
Q

Acquired intracorpuscular causes of HA includes

A

Paroxysmal nocturnal Hburia (PNH)

165
Q

Immune mediated Extracorpuscular causes of HA includes

A

ABO RH incompatibility
Autoimmune HA

166
Q

Non immune mediated Extracorpuscular causes of HA includes

A

Clostridium toxin
Snake venom toxin
Mechanical damage

167
Q

Hemoglobinopathies includes

A

Sickle cell anemia
Thalessemia

168
Q

Sickle cell anemia mode of inheritance

A

Autosomal recessive

169
Q

In sickle cell anemia Glutamic acid is replaced by

A

Valine

170
Q

Which chain of Hb is affected in sickle cell anemia

A

Beta chain (Point mutation)

171
Q

Beta|Beta

A

HbA - Normal

172
Q

Beta | Beta s

A

HbA ; HbS - Sickle cell trait

173
Q

Beta s | Beta s

A

HbS - Sickle cell anemia

174
Q

HbS in sickle cell anemia

A

Decreased RBC flexibility - Splenic phagocytosis
And is Sticky which can leads to vascular occlusion and can cause ischemic damage

175
Q

Sickle cell anemia is which type of HA

A

Extravascular Hemolytic anemia

176
Q

Effects of sickle cell anemia on bones

A

Dactylitis (Bone foot syndrome)
Avascular necrosis (femur)

177
Q

Clinical features of sickle cell anemia

A

Skin - non healing ulcer
Retarded growth in childrens
Lungs - acute chest syndrome

178
Q

Spleen in sickle cell anemia

A

Splenomegaly (Abdominal fullness)
Can leads to Autosplenectomy

179
Q

Bodies seen in sickle cell anemia due to Calcium deposition and congestion in spleen

A

Ganma-gandy bodies

180
Q

Osmotic fragility in SCA

A

Decreases

181
Q

Peripheral smear in SCA

A

Drepanocytes (Sickle like cells)

182
Q

HPLC full form

A

High performance Liquid chromatography

183
Q

Thalessemia is which type of disorder

A

Quantitative

184
Q

Alpha-Thalessemia occurs due to

A

Gene deletion - less frequent

185
Q

Beta- Thalessemia occurs due to

A

Gene mutation - 80-90% more common

186
Q

Beta gene isoforms

A

Beta - full synthesis of chains
Beta ° - No synthesis
Beta + - Partial synthesis of Beta chains

187
Q

Most common mutation in Beta Thalessemia

A

Non sense mutation - immediate stop codon comes and stops synthesis

188
Q

Mutations seen in Beta Thalessemia

A

Splicing mutations - MC cause of Beta + Thalessemia
Promoter mutations - makes fixed quantity of chains

189
Q

Beta | Beta

A

Normal

190
Q

Beta + | Beta
Beta ° | Beta

A

Thalessemia minor or trait
Asymptomatic, mild anemia

191
Q

Beta + | Beta +

A

Thalessemia intermedia
Symptoms seen, moderate anemia
Often Requirement of blood transfusion

192
Q

Beta ° | Beta °
Beta ° | Beta +
Beta + | Beta +

A

Thalessemia Major or Cooley’s anemia

193
Q

Signs of Thalessemia major

A

Hb <7g/dl
Symptoms +++
Severe anemia
Repeated history of blood transfusion

194
Q

Pathophysiology of Beta Thalessemia

A

Excess alpha chains forms tetramers which precipitates in Normoblast and damages their membrane Leads to Ineffective erythropoiesis or if it( alpha tetramers) goes to systemic circulation can lead to Reticuloendothelial destruction

195
Q

Thalessemia is which type of HA

A

Extravascular Hemolytic anemia

196
Q

Effect of Thalessemia on bones

A

Increased BM compensatory activity - Extra medullary hematopoiesis - Chimpanji like facial appearance

197
Q

Clinical features in Thalessemia major

A

Weakness
Splenomegaly
Hepatomegaly
Pallor
Dyspnea
Fatigue

198
Q

Repeated blood transfusion in Thalessemia patient can leads to

A

Iron overload - secondary hemochromatosis

199
Q

Blood results in Thalassemia major

A

Decreased Hb
MCH, MCV and MCHC Decreases

200
Q

Peripheral smear in Thalessemia

A

Aniso-poikilocytosis
Target cells (Codocytes)
Basophilic stippling
Hovell jolly bodies

201
Q

Peripheral smear in Thalessemia

A

Aniso-poikilocytosis
Target cells (Codocytes)
Basophilic stippling
Hovell jolly bodies

202
Q

Osmotic fragility in Thalassemia

A

Decreases

203
Q

Genetic methods used in case of Thalassemia

A

HPLC
Electrophoresis
Globin gene sequencing(molecular testing)

204
Q

Best investigation or definitive diagnosis in case of Thalassemia majo4

A

Molecular testing - not available everywhere

205
Q

Radiology signs in Thalessemia

A

Skull - Crew cut appearance or hair on end appearance

206
Q

Treatment of Thalessemia major

A

Blood transfusion for whole life
Iron chelators to prevent iron overload
Allogenic bone marrow transplantation

207
Q

Thalessemia intermedia

A

Less severe than Thalassemia major
Often history of blood transfusion
Hb - 7-10g/dl

208
Q

Thalessemia trait

A

Mild anemia
Asymptomatic
No history of blood transfusion

209
Q

Screening test for Thalessemia

A

Nestrof test - Checks osmotic fragility

210
Q

Nestrof test in case of Thalessemia

A

RBC doesn’t burst due to Decreased osmotic fragility - BLACK LINE NOT VISIBLE

211
Q

Nestrof test in case of Normal

A

Normal RBC burst so BLACK LINE VISIBLE

212
Q

Mentzer index in Thalessemia trait

A

<13

213
Q

Hb HPLC in Thalessemia trait

A

Decreased HbA and Increased HbA2 (>3.5 g/dl)

214
Q

Alpha Thalessemia

A

Relatively uncommon than Beta thalassemia
Gene deletion

215
Q

Alpha,Alpha | Alpha,Alpha

A

Normal

216
Q

Apha,Alpha | Alpha, -

A

Silent carrier (75%)

217
Q

Alpha, Alpha| - , -
Alpha, - | Alpha, -

A

Mild symptoms
In 50%

218
Q

Alpha, - | - , -

A

Beta 4 tetramer - Hb H disease - High affinity to O2 leads to Hypoxia
Extravascular hemolysis

219
Q

Golf ball appearance is seen in

A

Hb H disease

220
Q
  • , - | - , -
A

Gamma 4 tetramer - Barts hemoglobin
High affinity for O2(Hypoxia), risk of congestive failure

221
Q

Source of vitamin B12

A

Animal food

222
Q

Absorption of Vitamin B12 is done by

A

Stomach - intrinsic factor
Pancreas
Gut bacteria
Ileum

223
Q

Vit. B12 in case of Stomach surgery or in Pernicious anemia

A

Decreased level of intrinsic factor

224
Q

Vit. B12 absorption if pancreas not working properly

A

Decreased absorption

225
Q

Increased gut bacteria effect on Vit B12

A

Can consumes B12 and will not be available for absorption

226
Q

Vitamin B12 absorption in ileum pathologies (IBD, Lymphoma)

A

Decreased absorption

227
Q

Vitamin B12 plays role in

A

BM / Blood cells
GIT
Nervous system

228
Q

Homocysteine converted to Methionine with the help of

A

Vitamin B12 and Folic acid
Methionine - Important for DNA formation

229
Q

Methylmalonyl-CoA converted into Succinyl CoA with the help of

A

Vitamin B12

230
Q

Succinyl CoA is important for

A

Myelin formation

231
Q

Increased homocysteine levels can leads to

A

Endothelial cell injury - promote atherosclerosis

232
Q

In BM Vitamin B12 is important for

A

Conversion of precursor cells into mature cells

233
Q

Ineffective erythropoiesis in case of Vitamin B12 deficiency is due to

A

Increased no. Of cells (Hypercellular)
Pancytopenia
Increased no. Of immature cells

234
Q

WBCs in case of Vitamin B12 deficiency

A

Stab cells (immature neutrophils)
Hypersegmented neutrophils

235
Q

Platelets in case of Vitamin B12 deficiency

A

Abnormal shape
Increased in size

236
Q

Effect of Vit. B12 deficiency on Nervous system

A

PNS - Paresthesias
CNS - Subacute combiner degeneration

237
Q

Effects on GIT in Vit B12 deficiency

A

Megaloblastoid changes in epithelium (Epithelial atrophy)
Beefy tongue

238
Q

Clinical features of Vit B12 deficiency

A

Anemia, fatigue, weakness
Mild Jaundice
Neurological manifestation
Increased skin pigmentation due to increased activity of Tyrosinase - increased melanin secretion

239
Q

Peripheral smear of RBC in B12 deficiency

A

Size increases
Howell jolly body
Cabot ring
Basophilic stippling

240
Q

Peripheral smear of WBC In B12 deficiency

A

Hypersegmented neutrophils

241
Q

Serum homocysteine and Methylmalonyl-CoA levls in B12 deficiency

A

Increases

242
Q

Treatment of vitamin B12 deficiency

A

Vitamin B12 supplementation
Iron/Folic acid

243
Q

Treatment of vitamin B12 deficiency

A

Vitamin B12 supplementation
Iron/Folic acid

244
Q

Pernicious anemia is which type of disorder

A

Autoimmune disorder

245
Q

Autoantibodies formed in Pernicious anemia usually effects

A

Gastric fundus of stomach - lead to atrophic gastritis and High risk of development of cancer
Decreased level of intrinsic factor - Decreases vitamin B12 absorption

246
Q

Diagnosis of Pernicious anemia

A

Autoantibodies
Blood/BM exam
Gastric biopsy
Schilling test

247
Q

Schilling test

A

Radioactive vit B12 is given - excretion of B12 from urine (>8%)

248
Q

Folate deficiency is due to deficiency of

A

Folic acid

249
Q

Folic acid is usually absorbed from

A

Jejunum

250
Q

Folic acid is needed in

A

Conversion of homocysteine to Methionine along with vitamin B12

251
Q

Etiology of Folate deficiency

A

Reduced intake of green leafy vegetables
Increased requirement (Pregnancy, lactation)
Malabsorption syndrome
Malignancy
Drugs - Alcohol, OCPs, Phenytoin, Methotrexate

252
Q

Clinical features of Folate deficiency

A

Anemia
No neurological symptoms

253
Q

Blood test results in folate deficiency

A

S. Homocysteine elevated
S Methylmalonyl-CoA Normal
Serum folate levels decreases

254
Q

Figlu test is useful for identification of

A

Folic acid deficiency

255
Q

Folate deficiency during pregnancy can leads to

A

Neural tube defects in newborn

256
Q

Treatment of folate deficiency

A

Give folate + B12 together

257
Q

Autoimmune hemolytic anemia (AIHA) is type of which anemia

A

Extracorpuscular HA

258
Q

AIHA is divided into

A

Warm AIHA
Cold AIHA

259
Q

In Warm AIHA, Antibodies attaches to RBC at what temperature

A

37°C

260
Q

Antibodies responsible in Warm AIHA

A

IgG&raquo_space;> IgA

261
Q

In Warm AIHA, RBC Destruction usually takes place in

A

Spleen&raquo_space;» Liver
RBC membrane loose - Spherical in size (Spherocytes)

262
Q

According to site of RBC Destruction, Warm AIHA is classified into

A

Extravascular Hemolytic anemia

263
Q

Etiology of Warm AIHA

A

Idiopathic
SLE/RA
Cancers
Drugs - Penicillin/Cephalosporin
Quinidine
Alpha-methyldopa

264
Q

Clinicals features of Warm AIHA

A

Anemia
Jaundice
Splenomegaly

265
Q

Diagnosis of Warm AIHA

A

Increased unconjugated bilirubin
Increased LDH levels

266
Q

Peripheral smear in AIHA

A

Spherocytes (no central pale area)

267
Q

Blood test in Warm AIHA

A

Auto Antibodies test - COOMB’S test direct or indirect

268
Q

In Cold AIHA, antibodies attaches to RBC at what temperature

A

<37°C

269
Q

Antibodies responsible for Cold AIHA

A

IgM&raquo_space;> IgG

270
Q

Cold AIHA can be classified into

A

Cold Agglutinin disease
Cold hemolysin disease

271
Q

Site of RBC Destruction in Cold Agglutinin disease

A

Kupffer cells (LIVER)

272
Q

Antigen against IgM in Cold Agglutinin disease

A

‘I’ antigen

273
Q

Etiology of Cold Agglutinin disease

A

Idiopathic
Malignancy
Mycoplasma infection
Infectious mononucleosis

274
Q

Clinical features of Cold Agglutinin disease

A

Acrocyanosis (Cyanosis in peripheral areas)
Jaundice
Anemia

275
Q

Diagnosis of Cold Agglutinin disease

A

Slide test - RBC Forms clumps at low temperature
Chilled slide test

276
Q

Antibodies responsible for Cold Hemolysin disease

A

IgG

277
Q

Antigen in Cold Hemolysin disease against IgG

A

‘P’ Antigen

278
Q

Antibodies activates at what temperature

A

When exposed to cold temperature (like 4°C)

279
Q

Antibodies shows action at what temperature in Cold Hemolysin disease

A

It activates complement system When temperature comes back to 37°C

280
Q

Activation of complement system in Cold Hemolysin disease leads to

A

Formation of Membrane attack complex(MAC) - RBC Destruction - Intravascular hemolytic anemia

281
Q

Clinical features of Cold Hemolysin disease

A

Altered urine color
Mostly affect pediatric population
Anemia
Jaundice

282
Q

Example of Intracorpuscular Acquired genetic defect

A

Paroxysmal nocturnal Hburia

283
Q

PIG-A Gene produces which molecule

A

GPI-P

284
Q

Proteins attached to GPI-P are

A

CD59
CD55
C8 binding protein

285
Q

Function of proteins attached to GPI-P

A

Protection against complement system

286
Q

In PNH there is defect in

A

PIG-A gene - GPI-P doesn’t works properly - also not 1,2,3 protein - increased chances of damage due to activation of complement system

287
Q

In PNH, there is deficiency of which blood cells

A

Pancytopenia (RBC, WBC And platelets)

288
Q

Effect on RBC in PNH

A

Increased destruction by complementary proteins - Intravascular hemolysis - Hburia

289
Q

Effect on WBC in PNH

A

Defective WBC - Increased risk of infection
LAP Score decreases

290
Q

Effect on platelets in PNH

A

Thrombocytopenia
Dysfunctional platelets can undergo aggregation and leads to clot formation - increased risk of Thrombosis

291
Q

Clinical features of PNH

A

Pancytopenia
Altered urine color (most darkest in early morning)
Anemia
Jaundice
Increased risk of infection

292
Q

HAM’S Test

A

Pt. Blood sample + acidified serum - Change in pH - activates Complement system - RBC destruction
Used as screening test

293
Q

Most important test for diagnosis of PNH

A

Flow cytometry

294
Q

Flow Cytometry in PNH shows

A

Absence or presence of CD molecules

295
Q

Dye used for Flow Cytometry in PNH

A

FLAER (Fluorescent labeled Aerolysin)

296
Q

Biphenotypic cells are seen in

A

PNH

297
Q

In PNH patient, in which quadrants we can see scattered cells

A

In Quadrant 1 and 3

298
Q

PNH can progress into

A

Myelodysplastic syndrome
Acute myeloid leukemia
Aplastic anemia

299
Q

Treatment of PNH

A

Eculizumab - inhibits activity of C5 convertase ( Complement system)
Bone marrow or stem cell transplant

300
Q

Defect in Hematopoietic stem cells leads to which type of anemia

A

Aplastic anemia

301
Q

Abnormal stem cells have

A

Decreased replication rate
Decreased rate of differentiation
New antigens activates T cells which leads to activation of Cytokines IFN delta, TNF alpha

302
Q

Bone marrow activity in aplastic anemia

A

Bone marrow Hypoplasia ( Decreased BM activity)

303
Q

Activation of T cells in aplastic anemia can leads to

A

Activation of Cytokines such as IFN- delta, TNF-alpha

304
Q

Aplastic anemia can progress to

A

Myelodysplastic syndrome
AML
PNH - if T cells activation against GPI-P antigen

305
Q

Inherited causes of Aplastic anemia

A

Telomerase enzyme defect
Fanconi’s anemia

306
Q

Fanconi’s anemia

A

Autosomal recessive
DNA repair genes defet
Decreased kidney or spleen size
Bone defects

307
Q

Acquired causes of Aplastic anemia

A

Immune mediated aplastic anemia
Idiopathic (MC)

308
Q

Chemicals related causes of Aplastic anemia

A

Dose related Aplastic anemia - Alkylating agents, antimetabolite drugs, chloramphenicol
Dose unrelated AA - Gold salts, Chloramphenicol

309
Q

Physical agents that can cause aplastic anemia

A

Radiation exposure
Viruses - CMV, varicella zoster, Epstein Barr

310
Q

Clinical features of Aplastic anemia

A

Pancytopenia
Anemia, weakness
Petechiae, purpura
Splenomegaly never seen in AA

311
Q

Blood test results in Aplastic anemia

A

Pancytopenia
Reticulocytopenia

312
Q

Bone marrow exam in Aplastic anemia

A

BM Aspiration - “DRY TAP”
BM Biopsy - decreases HSC - HYPOCELLULAR BM

313
Q

Treatment of Aplastic anemia

A

Bone marrow transplantation
If no suitable donor - antithymoside globulin
Cyclosporine

314
Q

Chemita classification of Aplastic anemia

A

Non severe AA
Severe AA
Very sever AA

315
Q

Non severe AA

A

When BM cellularity <25%

316
Q

Severe AA

A

When BM cellularity <25% + any 2 out of 3 - ANC <500/mm3, Platelets <20,000/mm3, Reticulocytes <60,000/mm3

317
Q

Very severe AA

A

Same as Severe AA except ANC <200/mm3

318
Q

Very severe AA

A

Same as Severe AA except ANC <200/mm3

Pathology (14 decks)

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