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MTAP 2nd Semester > MTAP W3 (Hematology W14: General=Anemia) > Flashcards

MTAP W3 (Hematology W14: General=Anemia) Flashcards

1
Q

derived from the greek word ‘ANAIMIA’= without blood

A

anemia

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2
Q

decrease in number of RBCs or amount of hemoglobin in the RBCs= decreased oxygen delivery and subsequent tissue -

A

hypoxia

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3
Q

anemia is considered to be present if the HGB and HCT is below the lower limit of the -% reference interval

A

95%

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4
Q

RBC parameters: HGB AND HCT are affected by the individual’s -

A
  1. age
  2. gender
  3. geographical location
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5
Q

anemia arises from decrease oxygen carrying capacity of blood

it can arise if there is:
1. INSUFFICIENT hemoglobin
2. hemoglobin is NONFUNCTIONAL

which is the more frequent cause?

A

insufficient hemoglobin

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6
Q

reduction from baseline value in total number of RBCs; hgb and rbc mass/hct

A

anemia

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7
Q

normal or increased total red cell mass may occur with PREGNANCY, MACROGLOBULINEMIA, SPLENOMEGALY

A

dilutional anemia

pag may PMS=delusional

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8
Q

QUANTITATIVE CHANGES IN RBCs

-decreased RBCs
-decreased oxygen carrying capacity of blood

A

anemia

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9
Q

QUANTITATIVE CHANGES IN RBCs

-too many RBC in circulation
-increased PCV
-hypervolemia
-hyperviscosity

A

polycythemia vera/ erythrocytosis

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10
Q

used as a screening test to evaluate if px has HEMOLYTIC ANEMIA

A

reticulocyte count

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11
Q

normal value of hgb in women

A

12-15 g/dL

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12
Q

normal value of hgb in men

A

13.5-18 g/dL

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13
Q

anemia: typical of hypoproliferation

A

normocytic, normochromic

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14
Q

CLASSIFICATION OF ANEMIA

Iron deficiency
Thalassemia
Sideroblastic anemia

A

low MCV, low MCHC
microcytic, hypochromic

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15
Q

CLASSIFICATION OF ANEMIA

Iron deficiency
Thalassemia
Sideroblastic anemia

A

low MCV, low MCHC
microcytic, hypochromic

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16
Q

CLASSIFICATION OF ANEMIA

Iron deficiency
Thalassemia
Sideroblastic anemia

A

low MCV, low MCHC
microcytic, hypochromic

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17
Q

CLASSIFICATION OF ANEMIA

Bone marrow disorder
Anemia of chronic disorders
Autoimmune disease

A

normal MCV, normal MCHC
normocytic, normochromic

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18
Q

CLASSIFICATION OF ANEMIA

Vitamin B12 deficiency
Folate deficiency
Excessive alcohol ingestion
Hypothyroidism

A

high MCV, normal MCHC
macrocytic, normochromic

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19
Q

MECHANISM OF ANEMIA

term used for marrow erythroid proliferative activity

A

erythropoiesis

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20
Q

MECHANISM OF ANEMIA

  • erythropoiesis: DEFECTIVE progenitor cells, DESTROYED in the BM before maturation
A

ineffective erythropoiesis

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21
Q

MECHANISM OF ANEMIA

  • erythropoiesis: DECREASE in number of erythroid precursor cells in the BM, NOT DESTROYED
A

insufficient erythropoiesis

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22
Q

MECHANISM OF ANEMIA

diseases associated:
1. megaloblastic anemia
2. thalassemia
3. sideroblastic anemia

A

ineffective erythropoiesis

‘MTS’- ineffective medtechs?

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23
Q

MECHANISM OF ANEMIA

the peripheral blood HGB is low despite an increase in RBC precursors in the bone marrow

A

ineffective erythropoiesis

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24
Q

MECHANISM OF ANEMIA

diseases associated:
infection/ parvovirus B19
sarcoidosis
acute leukemia

A

insufficient erythropoiesis

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25
Q

CATEGORIES OF ANEMIA

  1. acute
  2. chronic
A

blood loss

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26
Q

CATEGORIES OF ANEMIA

  1. aplastic
  2. iron deficiency
  3. sideroblastic anemia
  4. anemia of chronic disease
  5. megaloblastic
A

impaired production

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27
Q

CATEGORIES OF ANEMIA

  1. inherited defects
  2. acquired disorders
A

hemolytic

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28
Q

CATEGORIES OF ANEMIA

Normal MCV

A

80-100fL

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29
Q

CATEGORIES OF ANEMIA

Normal MCHC

A

31-37g/dL

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30
Q

CATEGORIES OF ANEMIA
MORPHOLOGICAL CLASSIFICATION

high MCV

A

macrocytic

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31
Q

CATEGORIES OF ANEMIA
MORPHOLOGICAL CLASSIFICATION

low MCV

A

microcytic

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32
Q

CATEGORIES OF ANEMIA
MORPHOLOGICAL CLASSIFICATION

high MCHC

A

hyperchromic

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33
Q

CATEGORIES OF ANEMIA
MORPHOLOGICAL CLASSIFICATION

low MCHC

A

hypochromic

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34
Q

CATEGORIES OF ANEMIA
- CLASSIFICATION

caused by pathophysiological mechanism responsible for the RBC deficit
-decreased erythrocyte production
-increased erythrocyte loss

A

etiologic classification

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35
Q

MORPHOLOGICAL CLASSIFICATION

  1. bleeding
  2. hypoproliferation of hematopoietic stem cells
A

normocytic normochromic anemia

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36
Q

MORPHOLOGICAL CLASSIFICATION

1.IDA
2. sideroblastic anemia

A

microcytic hypochromic anemia

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37
Q

MORPHOLOGICAL CLASSIFICATION

  1. megaloblastic anemia
A

macrocytic normochromic anemia

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38
Q

2 approach for classification of anemia

A
  1. reticulocyte count
  2. MCV
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39
Q

signs and symptoms: NOT seen in ANEMIA

A
  1. prone to infection
  2. ruby complexion
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40
Q

the most important indices is the -

A

MCV

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41
Q

the least important indices is the -

A

MCH

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42
Q

tool to assess bone marrow ability to increase RBC production in response to anemia

A

reticulocyte count

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43
Q

laboratory procedures used to diagnose anemia

A
  1. HGB
  2. PLT
  3. WBC
  4. OFT
  5. bilirubin
  6. haptoglobin

‘ha-bi phow’

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44
Q

plasma protein that binds free hemoglobin

A

haptoglobin

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45
Q

plasma protein that decreases in case of hemolytic anemia

A

haptoglobin

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46
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

increased in hemolytic anemia during lysis, found inside the RBC

A

LDH test

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47
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

reflects the body’s tissue major iron stores

A

serum ferritin

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48
Q

serum ferritin in male:

A

12-300ng/mL

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49
Q

serum ferritin in female:

A

12-150ng/mL

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50
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

body’s ability to transport iron, measured to identify how much iron is being carried in the blood

A

TIBC/ total iron binding capacity

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51
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

measures the total excretion of the breakdown products of heme

A

fecal urobilinogen

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52
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

determine the amount of protoporphyrin not used for hgb synthesis

A

FPE/ free erythrocyte protoporphyrin
ZPP/ zinc protoporphyrin

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53
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

measured by direct-fluorescene-hematofluorometer

A

FEP/ free erythrocyte protoporphyrin
ZPP/ zinc protoporphyrin

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54
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

radioactive iron is injected IV

A

plasma iron turnover

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55
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

PLASMA IRON TURNOVER
rate of disappearance from blood is -hrs

A

2-3hrs

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56
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

PLASMA IRON TURNOVER
70-80% of the injected Fe appears within -days

A

10days

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57
Q

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA

uses radioactive chromium
shorter life span= faster disappearance

A

red cell life span

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58
Q

INCREASED RBC CONCENTRATION

HCT: higher than -L/L in male

A

> 0.52 L/L, 52%

normal value: 40-54%

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59
Q

INCREASED RBC CONCENTRATION

HCT: higher than -L/L in female

A

> 0.50 L/L, 50%

normal value: 35-49%

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60
Q

are young RBCs that lack a nucleus but still contain RESIDUAL RNA

A

reticulocytes

2 days in BM
1 day PB

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61
Q

the adult reference range for reticulocyte -

A

0.5-1.5%

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62
Q

the newborn reference range for reticulocyte -

A

1.5-5.8%

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63
Q

PERIPHERAL BLOOD FILM EXAMINATION

variation in shape is called

A

poikilocytosis

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64
Q

PERIPHERAL BLOOD FILM EXAMINATION

variation in size is called

A

anisocytosis

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65
Q

this serves as a quality control to verify results produced by automated analyzers

A

peripheral blood film examination

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66
Q

a process that determine the M:E ratio

A

bone marrow examination

‘slit-v’
sternum, lumbar,iliac,tibia,vertebrae

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67
Q

bone marrow samples can be obtained by - and -

A

aspiration and trephine biopsy

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68
Q

BONE MARROW EXAMINATION

  • yields semi-liquid bone marrow
A

aspirate

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69
Q

BONE MARROW EXAMINATION

Aspirate=semi-liquid bone marrow
examined under a - microscope
and analyzed by (3)

A

light microscope

flow cytometry
chromosome analysis
PCR

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70
Q

BONE MARROW EXAMINATION

frequently obtained which yields a narrow

A

trephine biopsy

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71
Q

BONE MARROW EXAMINATION

trephine biopsy: examined microscopically with the aid of -

A

immunohistochemistry

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72
Q

RED CELL INDICES

-liter=1 fL

A

10-15

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73
Q

RED CELL INDICES

normal value of MCV

A

80-100fL

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74
Q

RED CELL INDICES

MCV formula

A

HCT % x10/RBC

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75
Q

RED CELL INDICES

average volume of the individual red blood cell

A

MCV

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76
Q

RED CELL INDICES

average weight of hgb of the individual red cell

A

MCH

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77
Q

RED CELL INDICES

normal value of MCH

A

27-32pg/ug

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78
Q

RED CELL INDICES

MCH formula

A

HGB x10/RBC

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79
Q

RED CELL INDICES

the percent of hgb in the average red cell

A

MCHC

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80
Q

RED CELL INDICES

MCHC formula

A

RED CELL INDICES

HGB x100/HCT%

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81
Q

MCV and ANEMIA CLASSIFICATION

is characterized by an MCV of less than 80fL with small RBCs (<6um)

A

microcytic anemia

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82
Q

characterized by an MCHC of less tahn 32g/dL and INCREASED central pallor in the RBCs may accompany microcytosis

A

hypochromia

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83
Q

MCV and ANEMIA CLASSIFICATION

is characterized by an MCV greater than 100fL with large RBCs (>8um)

can be megaloblastic or non megaloblastic

A

macrocytic anemia

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84
Q

MCV and ANEMIA CLASSIFICATION

caused by impaired synthesis of DNA such as Vit 12, B9/folate deficiency or myelodysplasia

A

megaloblasic anemia

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85
Q

the next test after reticulocyte count is - in classifying anemia

A

MCV

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86
Q

ARC->MCV

  1. Thalassemia
  2. Anemia of chronic inflammation
  3. Iron deficiency
  4. Lead poisoning
  5. Sideroblastic anemia
  6. CHronic inflammation?
  7. hemoglobin E
A

microcytic/ low MCV

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87
Q

ARC->MCV

  1. Aplastic anemia
  2. Anemia of renal disease
  3. Myelophthisic anemia
  4. Infection: parvovirus B19
  5. Anemia of chronic inflammation
A

normocytic/ normal MCV

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88
Q

ARC->MCV

  1. Myelodyplastic syndrome
  2. Aplastic anemia
  3. some Drugs
  4. Erythroleukemia
  5. Chronic liver disease
  6. Vitamin B12 deficiency
  7. Folate deficiency

MADEplastiC9-12

A

macrocytic/ high MCV

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89
Q

ARC: excessive RBC loss
HEMOLYSIS

-cause
immune hemolytic anemias

A

EXTRINSIC causes

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90
Q

ARC: excessive RBC loss
HEMOLYSIS

-hemolytic
1. TTP
2. HUS
3. DIC

A

MICROangiopathic hemolytic

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91
Q

can help determine the cause of an anemia when used in conjunction with MCV!

A

RDW

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92
Q

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW

MICROCYTIC/LOW MCV
1. Thalassemia
2. Anemia of chronic inflammation
3. Hb E disease

A

RDW normal/microcytic

‘TAE’

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93
Q

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW

MICROCYTIC/LOW MCV
1. Iron deficiency
2. Sickle cell thalassemia

A

RDW high/microcytic

‘IS’

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94
Q

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW

NORMOCYTIC/NORMAL MCV
1. Anemia of chronic inflammation
2. Anemia of renal disease
3. Acute hemorrhage
4. Hereditary spherocytosis

A

RDW normal/normocytic

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95
Q

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW

NORMOCYTIC/NORMAL MCV
1. Iron, folate, Vit b12 deficiency
2. sickle cell anemia
3. Hb SC disease

A

RDW high/normocytic

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96
Q

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW

MACROCYTIC/HIGHMCV
1. Aplastic anemia
2. Chronic liver disease
3. Alcoholism

A

RDW normal/macrocytic

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97
Q

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW

MACROCYTIC/HIGHMCV
1. folate, B12 deficiency
2. myelodyplastic syndrome
3. chemotherapy
4. cold agglutinin
5. chronic liver dx

A

RDW high/macrocytic

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98
Q

due to defective hemoglobin synthesis resulting to cytoplasmic maturation defect

A

microcytic/hypochromic anemia

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99
Q

MICROCYTIC/HYPOCHROMIC ANEMIA type

abnormalities of iron homeostasis (deficiency in metabolism)

A

defective heme synthesis

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100
Q

MICROCYTIC/HYPOCHROMIC ANEMIA
DEFECTIVE HEME SYNTHESIS

  • anemia: commonly known as the IRON DEFICIENCY ANEMIA
A

sideropenic anemia

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101
Q

MICROCYTIC/HYPOCHROMIC ANEMIA
DEFECTIVE HEME SYNTHESIS

-anemia: adequate or excess iron but defective utilization. ANEMIA OF CHRONIC INFLAMMATION

A

sideroachrestic anemia

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102
Q

MICROCYTIC/HYPOCHROMIC ANEMIA
DEFECTIVE HEME SYNTHESIS

-anemia: defective porphyrin metabolism

A

sideroblastic anemia

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103
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

defective - synthesis
1. sideropenic anemia
2. sideroachrestic anemia
3. sideroblastic anemia

A

defective HEME synthesis

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104
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

defective - synthesis
results to thalassemia and hemiglobinopathies

A

defective GLOBIN synthesis

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105
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

defective - synthesis
deletion or mutation of globin synthesis

A

defective GLOBIN synthesis

106
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

most common form of anemia

A

IDA

107
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

prevalent in infants and children, pregnancy, excessive menstrual flow, elderly with poor diets, malabsorption syndromes, chronic blood loss

A

IDA

108
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

clinical signs and symptoms:
1. glossitis
2. angular cheilosis
3. koilonychia
4. pica

A

IDA

109
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: IDA

sore tongue

A

glossitis

110
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: IDA

inflamed cracks at the corners of the mouth

A

angular chielosis

111
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: IDA

spooning of the fingernails, may be seen if the deficiency is long-standing

A

koilonychia

112
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: IDA

cravings for non food items such as dirt, clay, laundry starch

A

pica

113
Q

major iron store in the body

A

ferritin

114
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA

Stage -

storage depletion

A

stage 1

115
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA

Stage -

transport depletion

A

stage 2

116
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA

Stage -

functional depletion

A

stage 3

117
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA

Stage -

HGB: normal
Serum iron: normal
TIBC: normal
ferritin: decreased

A

stage 1

118
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA

Stage -

HGB: normal
Serum iron: decreased
TIBC: increased
ferritin: decreased

A

stage 2

119
Q

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA

Stage -

HGB: decreased
Serum iron: decreased
TIBC: increased
ferritin: decreased

A

stage 3

120
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

parasites associated with IDA (4)

A
  1. hookworms (necator, ancylostoma)
  2. T. trichiura
  3. S. mansoni
  4. S. haematobium
121
Q

major protein that transport iron in the plasma

A

transferrin

122
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

beta globulin responsible for binding iron and its transport in the blood stream

A

transferrin

123
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

transferrin
1 gram can bind - mg of iron

A

1.25mg

124
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

refers to the total amount of iron that transferrin can carry, capacity of transferrin to bind iron

A

TIBC

125
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

an index of iron storage

A

% saturation

126
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

% saturation
calculated value: -

A

100x serum iron/TIBC

127
Q

rough estimate of body iron content

A

ferritin

128
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

second most common type of anemia

A

anemia of chronic inflammation

129
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

Commonly associated with systemic diseases, including chronic
inflammatory conditions

  1. rheumatoid arthritis
  2. tuberculosis
  3. HIV
  4. malignancies
A

anemia of chronic inflammation

130
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

Due to inability to use available iron for hemoglobin production

A

anemia of chronic inflammation

131
Q

MICROCYTIC/HYPOCHROMIC ANEMIA

Impaired release of storage iron associated with increased Acute
phase reactants such as Hepcidin, Ferritin and lactoferrin

A

anemia of chronic inflammation

132
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

anemia of chronic inflammation
impaired release of APR such as: (3)

A
  1. hepcidin
  2. ferritin
  3. lactoferrin
133
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

anemia of chronic inflammation
impaired release of APR such as: (3)

A
  1. hepcidin
  2. ferritin
  3. lactoferrin`
134
Q

decreases release of iron from
stores

acute phase reactant / inflammation

A

hepcidin

135
Q
  • Hepcidin: Decreased Iron (because hepcidin stops iron to go outside)
A

increased

136
Q
  • Hepcidin: Increase Iron ( because iron will release)
A

decreased

137
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

-Anemia

Caused by BLOCKS IN THE PROTOPORPHYRIN PATHWAY resulting in defective hemoglobin synthesis and iron overload

A

sideroblastic anemia

138
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

-Anemia

Excess iron accumulates in the mitochondrial region of
the immature RBC in the BM and encircles the nucleus;
cells are called ringed sideroblasts (iron accumulates).

A

sideroblastic anemia

139
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

Sideroblastic Anemia

EXCESS IRON ACCUMULATES in the mitochondrial region of
the immature RBC in the BM and encircles the nucleus;
cells are called -

A

ringed sideroblasts (iron accumulates)

140
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

Sideroblastic Anemia

Excess iron accumulates in the mitochondrial region of
the mature RBC in circulation ; cells are called RINGED SIDEROCYTES; inclusions are -
(Pappenheimer bodies on Wright’s stained smears)

A

Sideroticgranules

141
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

Sideroblastic Anemia

Siderocytes are best demonstrated using -

A

Perl’s Prussian blue stain

142
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

Sideroblastic Anemia

  • IRREVERSIBLE; causes of block is UNKNOWN OR IDIOPATHIC
A

primary

143
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

Sideroblastic Anemia

  1. Dimorphic
  2. RARS
A

primary

144
Q

MICROCYTIC/ HYPOCHROMIC ANEMIA

Sideroblastic Anemia

  • REVERSIBLE; causes include alcohol, anti-TB drugs (RIFES), chloramphenicol
A

secondary

145
Q

MICROCYTIC/ HYPOCHROMICANEMIA

is most often normocytic and
normochromic; however, with chronic exposure to lead, a microcytic,
hypochromic clinical picture may be seen

A

lead poisoning

146
Q

MICROCYTIC/ HYPOCHROMICANEMIA

Multiple blocks in the protoporphyrin pathway that affect heme synthesis

A

lead poisoning

147
Q

MICROCYTIC/ HYPOCHROMICANEMIA

Presence of many coarse Basophilic Stippling

A

lead poisoning

148
Q

MICROCYTIC/ HYPOCHROMICANEMIA

lead poisoning will lead to acquired sideroblastic anemia and acquired
porphyria

A

lead poisoning

149
Q

MICROCYTIC/ HYPOCHROMICANEMIA

It inhibits ferrochelatase and D-ALA synthase enzyme in
Heme/Protoporphyrin pathway

A

lead poisoning

150
Q

MICROCYTIC/ HYPOCHROMICANEMIA

It inhibits ferrochelatase and D-ALA synthase enzyme in -

A

Heme/Protoporphyrin pathway

151
Q

MICROCYTIC/ HYPOCHROMICANEMIA

ACUTE exposure to lead: -

A

normocytic, normochromic

152
Q

MICROCYTIC/ HYPOCHROMICANEMIA

CHRONIC exposure to lead: -

A

microcytic, hypochromic

153
Q

Serum iron and serum TIBC is -

A

inversely proportional

154
Q

MICROCYTIC/ HYPOCHROMICANEMIA
DIFFERENTIAL DIAGNOSES

all are decreased
increased TIBC, ZPP

TZ

A

IDA

155
Q

MICROCYTIC/ HYPOCHROMICANEMIA
DIFFERENTIAL DIAGNOSES

all are normal
increased iron, ferritin

IF

A

B-thalassemia

156
Q

MICROCYTIC/ HYPOCHROMICANEMIA
DIFFERENTIAL DIAGNOSES

all are decreased
increased TIBC, ferritin
TF

A

anemia of chronic disease

157
Q

MICROCYTIC/ HYPOCHROMICANEMIA
DIFFERENTIAL DIAGNOSES

all are increased except:
decrease TIBC

T

A

sideroblastic anemia

158
Q

MACROCYTIC/ NORMOCHROMICANEMIA

It is characterized by an MCV greater than -fL w/ large RBC (greater
than 8 um diameter). Macrocytic anemias maybe megaloblastic or
non- megaloblastic.

A

100fL

159
Q

MACROCYTIC/ NORMOCHROMICANEMIA

The most common causesof megaloblastic anemia are acquired,
although congenital forms exist. Deficiencies in -,-, or both account for the majority of cases

A

cobalamin (B12)
folate (B9)

160
Q

Red blood cells in megaloblastic anemias have an abnormal nuclear
maturation and imbalance between nuclear and cytoplasmic maturation

A

MACROCYTIC/ NORMOCHROMICANEMIA

161
Q

Refers to the abnormal marrow erythrocyte precursor seen in processes,
such as pernicious anemia, associated with altered DNA synthesis.

A

MACROCYTIC/ NORMOCHROMICANEMIA

162
Q

CLASSIFICATION BASED ON MCV
MACROCYTIC/MCV

-
1. Aplastic anemia
2. Chronic liver disease
3. Alcoholism

A

nonmegaloblastic

163
Q

CLASSIFICATION BASED ON MCV
MACROCYTIC/MCV

-
1. B12 deficiency
2. B9 deficiency
3. Myelodysplasia
4. Erythroleukemia
5. Drugs

A

megaloblastic

164
Q

CLASSIFICATION BASED ON MCV
NORMOCYTIC/MCV

Reticulocytes: INCREASED= hemolytic anemia -

  1. membrane defects
  2. hemoglobinopathies
  3. enzyme deficiencies
A

intrinsic

165
Q

CLASSIFICATION BASED ON MCV
MACROCYTIC/MCV

Reticulocytes: -

  1. aplastic anemia
  2. anemia of renal dx
  3. myelophthisic anemia
  4. infection; parvovirus B19
  5. anemia of chronic inflammation
A

normal or decreased

166
Q

MACROCYTIC/ NORMOCHROMICANEMIA

disruption of cholesterol-to-phospholipid ratio

NO IMPAIRMENT of DNA synthesis
ROUND
NO HYPERSEGMENTED

A

non-megaloblastic anemia

167
Q

MACROCYTIC/ NORMOCHROMICANEMIA

IMPAIRED DNA synthesis
OVAL
HYPERSEGMENTED

A

megaloblastic anemia

168
Q

MACROCYTIC/ NORMOCHROMICANEMIA
- ANEMIA

  1. B12 deficiency
  2. B9 deficiency
  3. acute erythroleukemia
  4. myelodysplasia
  5. congenital dyserythropoietic anemia type 1 and 3
A

megaloblastic anemia

169
Q

MACROCYTIC/ NORMOCHROMICANEMIA

Defective DNA synthesis causes abnormal nuclear maturation;
RNA synthesis is normal, so the cytoplasm is not affected. The
nucleus matures slower than the cytoplasm (Asynchronism)

A

megaloblastic anemia

170
Q

MACROCYTIC/ NORMOCHROMICANEMIA

Laboratory picture of Pancytopenia,Oval macrocyte, Howell-jolly bodies, Hypersegmentedneutrophil

A

megaloblastic anemia

171
Q

MACROCYTIC/ NORMOCHROMICANEMIA

defect in - affects cytoplasm

A

RNA

172
Q

MACROCYTIC/ NORMOCHROMICANEMIA

defect in - affects nucleus

A

DNA

173
Q

SCREENINGTEST USED TO DIAGNOSE MEGALOBLASTIC ANEMIA (5)

A
  1. CBC
  2. Reticulocyte count
  3. WBC differential
  4. bilirubin
  5. LDH
174
Q

SCREENINGTEST USED TO DIAGNOSE MEGALOBLASTIC ANEMIA

macrocytes, pancytopenia

A

CBC

175
Q

SCREENINGTEST USED TO DIAGNOSE MEGALOBLASTIC ANEMIA

Decreased: megaloblastic anemia

A

reticulocyte count

176
Q

MACROCYTIC/ NORMOCHROMICANEMIA
VITAMIN B12 (COBALAMIN)DEFICIENCY

-anemia: –caused by deficiency of INTRINSIC FACTOR, Antibody to intrinsic factor or antibodies to parietal cells, autoimmune
disease.

A

pernicious anemia

177
Q

MACROCYTIC/ NORMOCHROMICANEMIA
VITAMIN B12 (COBALAMIN)DEFICIENCY

parasite that causes cobalamin deficiency

A

D. latum

178
Q

takes 3-6 years to develop because of high body stores

Clinical symptoms: Jaundice, weakness, glossitis,GIbleeding, numbness
and CNSPROBLEMS

A

pernicious anemia

179
Q

Vitamin B12

intrinsic factor is needed for its proper absorption in the -

intrinsic factor is produced in the PARIETAL cells

A

ileum

180
Q

regulates the folate synthesis (DNA)

A

Vitamin B12

181
Q

MACROCYTIC/ NORMOCHROMICANEMIA
FOLIC ACIDDEFICIENCY

Associated with poor diet, pregnancy or chemotherapeutic anti
folic drugs such as -

A

METHOTREXATE

182
Q

MACROCYTIC/ NORMOCHROMICANEMIA

Clinical symptoms: same with vitamin B12deficiency, except
NO CNSinvolvement

A

folic acid deficiency

183
Q

other name of folic acid

A

Pteroylmonoglutamic acid

184
Q

Vitamin B9/folic acid

absorbed in -

A

jejunum

185
Q

MACROCYTIC/ NORMOCHROMICANEMIA

Acts asco-enzyme in the formation of thymidylate synthetase

A

FolicAcid (Pteroylmonoglutamic acid)

186
Q

MACROCYTIC/ NORMOCHROMICANEMIA

Thymidylate synthetase –needed to produce thymidine (one of
the pyrimidine basesofDNA)

A

FolicAcid (Pteroylmonoglutamic acid)

187
Q

MACROCYTIC/ NORMOCHROMICANEMIA

Dietary aspects: B-: meat

A

B12

188
Q

MACROCYTIC/ NORMOCHROMICANEMIA

Dietary aspects: B-: vegetables

A

B9

189
Q

CAUSESOFFOLICACIDDEFICIENCY

  • is acondition that DAMAGES THE LINING OF THE SMALL INTESTINE and prevents it from absorbing parts of food that are important for staying healthy
A

Celiac disease

190
Q

CAUSESOFFOLICACIDDEFICIENCY

  • is a MALABSORPTION disease
    commonly found in the tropical regions, marked with ABNORMAL FLATTENING OF THE VILLI AND INFLAMMATION of the lining of the SMALL INTESTINE
A

tropical sprue

191
Q

MACROCYTIC/ NORMOCHROMICANEMIA

*Include Alcoholism, Liver disease, and conditions causes
accelerated erythropoiesis
* RBC are ROUND not oval

A

NON- MEGALOBLASTICANEMIA

192
Q

MACROCYTIC/ NORMOCHROMICANEMIA

IMPORTANT FINDINGS IN
MEGALOBLASTIC ANEMIA (5)

A
  1. ineffective erythropoiesis and decreased retics,wbc,platelets
  2. hypersegmented neutrophils
  3. macroovalocytes
  4. howell-jolly bodies
193
Q

anemia is characterized by an MCV in the range of 80 to 100 fL.

A

normocytic

194
Q
  • anemia

a DIMORPHIC POPULATION OF MICROCYTES AND MACROCYTES
that can yield a normal MCV

A

Normocytic-Normochromic
Anemia

195
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

Bone marrow failure causes PANCYTOPENIA (decrease of
blood cells).

A

aplastic anemia

196
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

poor prognosis with complications that
include bleeding, infection, and iron overload due to
frequent transfusion needs.

A

aplastic anemia

197
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

15-20% of cases
1.fanconi anemia
2. dyskeratosis congenita
3. shwachmann-bodian-diamond syndrome

A

INHERITED aplastic anemia

198
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

80-85% of cases
1.idiopathic
2. secondary

A

ACQUIRED aplastic anemia

199
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

most common aplastic anemia

A

ACQUIRED aplastic anemia

200
Q

ANORMOCYTIC-NORMOCHROMIC ANEMIA

  • ACQUIRED aplastic anemia

50-70%
DIAMOND BLACKFAN ANEMIA

A

idiopathic/ unknown cause

201
Q

ANORMOCYTIC-NORMOCHROMIC ANEMIA

ACQUIRED aplastic anemia

10-75%
(exposure to drugs such as sulfonamides and
chloramphenicol) , chemicals (benzene), radiation or infection)

A

secondary

202
Q

A NORMOCYTIC-NORMOCHROMIC ANEMIA

problem
-: microcytic

A

heme

203
Q

A NORMOCYTIC-NORMOCHROMIC ANEMIA

problem
-: macrocytic

A

nucleus

204
Q

A NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

Autosomal recessive trait
Dwarfism, renal disease, mental retardation

A
205
Q

A NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

Strong association with malignancy development,
especially ACUTE LYMPHOBLASTIC LEUKEMIA

A

Genetic aplastic anemia
Fanconi anemia

206
Q

Acquired aplastic anemia (secondary)
caused by:
Antibiotics: (2)

A

1.chloramphenicol
2. sulfonamides

207
Q

Acquired aplastic anemia (secondary)
caused by:
Chemicals: (2)

A
  1. benzene
  2. herbicides
208
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

About 30% of acquired aplastic anemias are due to drug exposure.

A

Acquired aplastic anemia (secondary)

209
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

low RBCs, normal WBC and PLT

A

Diamond-Blackfan anemia

210
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

-anemia

Hypoproliferative anemia caused by replacement of
bone marrow hematopoietic cells by malignant cells or
fibrotic tissue

A

myelophthisic (marrow replacement) anemia

211
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

-anemia

Associated with cancers (breast, prostate, lung,
melanoma) with bone metastasis

A

myelophthisic (marrow replacement) anemia

212
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

-anemia

Laboratory: Normocytic/normochromic anemia;
leucoerythroblastic blood picture (high WBC and high
immature RBC)

A

myelophthisic (marrow replacement) anemia

213
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

-anemia

Characterized by a sudden loss of blood resulting
from trauma or other severe forms of injury

A

acute blood loss anemia

214
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

-anemia

Clinical symptoms: Hypovolemia, rapid pulse, low
blood pressure, pallor

A

acute blood loss anemia

215
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

-anemia

Initially normal reticulocyte count hemoglobin/ hematocrit; in a few hours, increase in platelet count
and LEUKOCYTOSIS with a LEFT SHIFT, drop in hemoglobin/
hematocrit and RBC

A

acute blood loss anemia

216
Q

reticulocytosis in - days

A

3-5 days

217
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

shift to the -: immature WBC

A

left

218
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

shift to the -: hypersegmented cells

A

right

219
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

Characterized by a gradual, lLON-TERM loss of blood;
often caused by gastrointestinal bleeding

A
220
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia

Initially normocytic/normochromic anemia that over time causes a DECREASE in hemoglobin/hematocrit;
gradual loss of iron causes microcytic/hypochromic anemia

A
221
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia due to -

All cause a normocytic/normochromic anemia; usually hereditary
with INCREASE reticulocytosis due to accelerated destruction

A

hemolytic anemias due to intrinsic defects

222
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

  • DEFECT
  1. Hereditary spherocytosis
  2. Hereditary elliptocytosis (ovalocytosis)
  3. Hereditary stomatocytosis
  4. Hereditary acanthocytosis (abetalipoproteinemia)
A

membrane defects

223
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

  • DEFECT
  1. G6PD deficiency
  2. PK deficiency
  3. Paroxysmal nocturnal hemoglobinuria/ PNH
A

enzyme defects

224
Q

one altered copy of a gene is enough to cause a disease

A

autosomal dominant= hereditary spherocytosis

225
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

MOST COMMON membrane defect; autosomal dominant

A

hereditary spherocytosis

226
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

characterized by splenomegaly, variable degree of anemia,
spherocytes on the peripheral blood smear

A

hereditary spherocytosis

227
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

Increased permeability of the membrane to sodium

Results in loss of membrane fragments; erythrocytes have
DECREASED

surface area-to-volume ratio; rigid spherocytes culled/removed by
splenic macrophages

A

hereditary spherocytosis

228
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

Laboratory:
1. MCHC may be >37 g/dL, increased
2. osmotic fragility
3. increased serum bilirubin

A

hereditary spherocytosis

229
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

Autosomal dominant; most persons asymptomatic
due to normal erythrocyte life span; >25% ovalocytes
on the peripheral blood smear

A

hereditary ovalocytosis

230
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

Membrane defect is caused by POLARIZATION OF CHOLESTEROL at the ends of the cell rather than around pallor area.

A

hereditary ovalocytosis

231
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

Autosomal dominant; variable degree of anemia; up
to 50% stomatocytes on the blood smear.

A

Hereditary stomatocytosis

232
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

Membrane defect due to abnormal permeability to
both SODIUM AND POTASSIUM; causes erythrocyte
swelling

A

Hereditary stomatocytosis

233
Q

both altered copies of the gene are needed to cause the dx

A

autosomal recessive

234
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

Autosomal recessive; mild anemia associated with
steatorrhea, neurological and retinal abnormalities; 50-
100% of erythrocytes are acanthocytes

A

Hereditary acanthocytosis (abetalipoproteinemia)

235
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

MEMBRANE DEFECT

Increased cholesterol:lecithin ratio in the membrane
due to abnormal plasma lipid concentrations;
absence of serum p-lipoprotein needed for lipid
transport

A

Hereditary acanthocytosis (abetalipoproteinemia)

236
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

ENZYME DEFECT

SEX-linked enzyme defect; most common enzyme deficiency in
the HEXOSE MONOPHOSPHATE SHUNT

A

G6PD (glucose-6-phosphate dehydrogenase) deficiency

237
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

ENZYME DEFECT

Reduced glutathione levels are not maintained because of
decreased NADPH generation.

A

G6PD (glucose-6-phosphate dehydrogenase) deficiency

238
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

ENZYME DEFECT

Results in oxidation of hemoglobin to methemoglobin (Fe3+);
denatures to form HEINZ BODIES

A

G6PD (glucose-6-phosphate dehydrogenase) deficiency

239
Q

pathway that produces glutathione

A

hexose monophosphate shunt

240
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

ENZYME DEFECT

Autosomal recessive; most common enzyme deficiency
in EMBDEN-MEYERHOF PATHWAY

A

Pyruvate kinase (PK) deficiency

241
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

ENZYME DEFECT

Severe hemolytic anemia with reticulocytosis and
echinocytes

A

Pyruvate kinase (PK) deficiency

242
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

ENZYME DEFECT

An acquired membrane defect in which the red cell
membrane has an increased sensitivity for complement
binding as compared to normal erythrocytes

A

Paroxysmal nocturnal hemoglobinuria (PNH)

243
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

ENZYME DEFECT

decrease of cd55 and cd59

All cells are abnormally sensitive to lysis by complement

A

Paroxysmal nocturnal hemoglobinuria (PNH)

244
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS

ENZYME DEFECT

Characterized by pancytopenia
uses Ham’s and sugar water test

A

Paroxysmal nocturnal hemoglobinuria (PNH)

245
Q

Hams and sugar water test have been tradiotionally used in diagnosis of PNH the standard now used is - to detect CD 55, CD 59

A

flowcytometry

246
Q

decreased CD59 means

A

MRL/ membrane inhibitor of reactive lysis

247
Q

decreased CD55 means

A

DAF/ decay accelerating factor

248
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

  • anemia due to -

All cause a normocytic/normochromic anemia due to defects
extrinsic to the RBC. All are acquired disorders that cause
accelerated destruction with reticulocytosis.

A

Hemolytic Anemias Due to Extrinsic/Immune Defects

249
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO - DEFECTS

  1. Warm autoimmune hemolytic anemia (WAIHA)
  2. Cold autoimmune hemolytic anemia (CAIHA or cold
    hemagglutinin disease)
    3.Paroxysmal cold hemoglobinuria (PCH) (extrinsic)
    4.Hemolytic transfusion reaction
  3. Hemolytic disease of the newborn (HDN)
A

hemolytic anemia due to extrinsic/immune defects

250
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO - DEFECTS

Paroxysmal cold hemoglobinuria/PCH

A

extrinsic

251
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS

  • anemia

RBCs are coated with IgG and/or complement.
Macrophages may phagocytize these RBCs, or they may
remove the antibody or complement from the RBC’s
surface, causing membrane loss and spherocytes.

A

Warm autoimmune hemolytic anemia (WAIHA)

252
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS

  • anemia

60% of cases are IDIOPATHIC; other cases are secondary to
diseases that alter the immune response (e.g., chronic
lymphocytic leukemia, lymphoma); can also be drug
induced.

A

Warm autoimmune hemolytic anemia (WAIHA)

253
Q

IgG and complement react to -c
WITH LYSIS

A

37c/BT

254
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS

  • anemia

Laboratory Findings
1. Spherocytes
2. MCHC may be >37 g/dL
3. Increased osmotic fragility, bilirubin, reticulocyte count
4. Occasional nRBCs present
5. Positive direct antiglobulin test (DAT) helpful in
differentiating from hereditary spherocytosis

A

Warm autoimmune hemolytic anemia (WAIHA)

255
Q

DAT (direct antihuman globulin test)

(+)

A

WAIHA

256
Q

DAT (direct antihuman globulin test)

(-)

A

HS

257
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS

  • anemia

RBCs are coated with IgM and complement at
temperatures below 37°C. RBCs are lysed by complement
or phagocytized by macrophages. Antibody is usually
anti-I but can be anti-i.

A

Cold autoimmune hemolytic anemia (CAIHA or cold
hemagglutinin disease)

258
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS

  • anemia

Can be idiopathic, or secondary to Mycoplasma
pneumoniae, lymphoma, or infectious mononucleosis

If antibody titer is high enough, sample must be warmed
to 37°C to obtain accurate RBC and indices results.

A

Cold autoimmune hemolytic anemia (CAIHA or cold
hemagglutinin disease)

259
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS

  • anemia

Laboratory Findings:
Seasonal symptoms
RBC clumping can be seen both macroscopically
and microscopically
MCHC >37 g/dL
Increased bilirubin and reticulocyte count

Positive DAT detects complement-coated RBCs

A

CAIHA

260
Q

IgM and complement reacts at -c
NO LYSIS

A

4c/ ref temp

261
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS

  • anemia

An IgG biphasic Donath-Landsteiner antibody with
P specificity fixes complement to RBCs in the cold
(less than 20°C); the complement-coated RBCs lyse
when warmed to 37°C.

A

Paroxysmal cold hemoglobinuria (PCH)

262
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA

HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS

  • anemia

Laboratory Findings:
Variable anemia following hemolytic process
Increased bilirubin and plasma hemoglobin
Decreased haptoglobin
DAT may be positive
Donath-Landsteiner test positive

A

Paroxysmal cold hemoglobinuria (PCH)

MTAP 2nd Semester (9 decks)

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