Anemia Part 1 Flashcards

1
Q

define anemia

A

reduction in amount of circulating Hb, in total number of RBCs , or circulating RBC mass

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2
Q

how does the bone marrow compensate for acute anemia

A

3x increase in RBC production

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3
Q

how does the bone marrow compensate for chronic hemolytic anemia

A

up to o 6x - 8x RBC production

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4
Q

what happens when bone marrow cannot compensate for blood loss

A

anemia

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5
Q

what is a result of anemia

A

tissue hypoxia

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6
Q

what are some clinical symptoms of hypoxia from anemia

A
pallor 
dyspnea
angina 
kiolonychia ( spoon nails) 
esophageal webs
pica ( craving for dirt)
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7
Q

what organ compensates due to blood loss? consequences

A

heart

  • heart murmurs
  • congestive heart failure
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8
Q

what does CBC measure

A

hemablgobin
hematorcrit
RBC indices
WBC

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9
Q

what volumes compose the average adult volume

A

3 liters of plasma

2 liters of blood cells

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10
Q

MCV

A

mean corpuscular volume

size of RBC

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11
Q

What is normal MCV

A

8-100

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12
Q

MCH

A

mean corpuscular hemoglobin

average amount/MASS of Hb in RBC

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13
Q

hematorcirt

A

ratio of volume RBC/ total volume of blood

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14
Q

RDW

A

red cell distribution width

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15
Q

anisocytosis

A

highe RDW

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16
Q

reticulocyte

A

young RBC with residual rRNA

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17
Q

how do reticulocytes stain

A

polychromasia, bluish cytoplasm

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18
Q

how is reticulocytes increased

A

EPO

increase bone funciton

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19
Q

Anemia is a sign for what

A

underlying disease, not a diagnosis itself

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20
Q

hemorrhage

A

depletion of RBC

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21
Q

hemolysis

A

excess destruction of RBC

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22
Q

what is the most common classification of anemia

A

microcytic hypochromic

iron deficiency

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23
Q

Iron Deficiency anemia have what lab results

A

decreased MCV, MCH, MCHC

increase RDW

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24
Q

normocytic , normochromic anemia lab results

A

normal MCV, MCH, MCHC

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25
Q

what deficiencies cause macrocytic anemia

A

vitamin B12 and folate

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26
Q

lab results for marcocytic anemia

A

Increased MCV

variable MCH and MCHC

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27
Q

what are blood smear characteristics for iron deficiency anemia

A

hypochromic, microcytic anisoppoikilocytic ( size and shape variable)

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28
Q

what is the major cause of microcytic anemia

A

iron deficiency anemia

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29
Q

thrombocytosis

A

high platelet levels

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30
Q

what is the mechanism of excretion for iron

A

no natural mechanism

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31
Q

what delivers iron to cells in blood vessels, duodenum

A

transferrin

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32
Q

what binds iron, absorbs iron-laden transferrin at cell surface

A

transferrin receptor

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33
Q

what binds iron for storage

A

ferritin

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34
Q

how many grams of total body iron

A

2-4 grams

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35
Q

how much of our iron diet is absorbed

A

10%

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36
Q

what are 3 main causes of iron deficiency in anemia

A

nutritional deficient
malabsorption
blood loss
states that cause increase iron uptake

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37
Q

older men and post-menopausal women, if they have Fe deficiency anemia, what is their likely cause

A

occult gastrointestinal bleeding,

colon cancers

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38
Q

absorption of iron occurs where

A

duodenum

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39
Q

what lines the villi of the duodenum

A

enterocytes

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40
Q

enterocytes transport iron across cell membrane into blood via

A

ferroprotin

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41
Q

how are infants iron deficient

A

mother’s milk low in iron

42
Q

what form of iron is more readily absorbed

A

Fe2+

43
Q

what parasite can cause iron defiency

A

hookworm
necator americanus
ancylostoma duodenale

44
Q

when does the body demand an increase of iron uptake

A

infancy
adolescence
pregnancy
lactation

45
Q

serum iron

A

measure of iron in blood

46
Q

total iron-binding capacity (TIBC)

A

measure of transferrin in blood

47
Q

serum ferritin

A

reflects iron stores in macrophages and liver

48
Q

serum levels in iron deficiency anemia

A

low

49
Q

TIBC levels in iron deficiency anemia

A

high

50
Q

how is transferrin saturation calculated

A

[Fe]/ [TIBC}

51
Q

what is the treatment for iron deficiency anemia

A

iron supplements

52
Q

what is the most common anemia in hospitalized patients

A

anemia of chronic disease

53
Q

what is the peripheral blood for chronic desease

A

normocytic

monochromic

54
Q

what happens to the half life of RBC for anemia of chronic disease

A

shortened

55
Q

what happens to iron in anemia of chronic disease

A

hepcidin sequesters iron in body/phagocytes

56
Q

what happens to the bon marrow in anemia of chronic disease

A

suppression of bone marrow

57
Q

serum iron in anemia of chronic disease

A

low

58
Q

serum ferritin in anemia of chronic disease

A

high

59
Q

transferrin and transferrin saturtion levels in chronic disease

A

low

60
Q

name chronic diseases associated with anemia

A

renal failure
diabetes mellitus
liver disease
alcoholism

61
Q

what are the 2 most common causes of megaloblastic anemias

A

vitamin B12 and folate deficiency

62
Q

what is the CBC report for megaloblastic anemia

A

pancytpenia ( decrease WBC, RBC, platelet)

63
Q

what does the peripheral smear for megaloblastic anemia

A

hypersegmented neutrophils
mactocytic
anisopoikilocytosis
macro-ovalocytes

64
Q

what are some clinical signs and symptoms for B12 deficiency

A

atrophic glossitis: smooth beefy red toungue
neurological defects: demyelination
gastric gland atrophy

65
Q

pernicious anemia is the common cause of what

A

malabsorption

66
Q

what can cause deficient anemia

A

GI surgery, disease

67
Q

what type of diet puts you at risk for pernicious anemia

A

vegans

68
Q

when does the body demand B12

A

pregnancy
disseminated cancer
hyperthroidism

69
Q

what causes pernicious anemia

A

absent intrinsic factor

70
Q

explain the autoimmunity aspect of pernicious anemia

A

autoantibodies in serum either block binding of B12 to IF (type I) or block binding B12-IF complex ( Type II)

71
Q

what autoimmune diseases are associated with pernicious anemia

A

hashimoto’s thyroiditis
adrenalitis
grave’s diseae

72
Q

what causes a folate deficiency

A

dietary insufficiency

73
Q

what is an important negative finding in folate deficiency

A

negative methylmalonic acid ( no neurological defects)

74
Q

what is the drawback of folate treatment

A

partially corrects vitamin B12 deficiency, but does not affect neurologic deficits

75
Q

what is the vitamin B12 treatment

A

intramuscular injections

76
Q

what happens when only stage I of schilling test is abnomral

A

pernicious anemia, no IF available

77
Q

what happens when stage I and stage II of schilling test are abnormal

A

malabsorption of vitamin B12 and IF in the small intestine

78
Q

what are other causes of macrocytic anemia besides vitamin B12 and folate deficiency

A

alcoholism
hypothyroidism
liver disease

79
Q

aplastic anemia

A

damage to hematopoietic stem cell, underproducing

80
Q

in aplastic anemia what happens to the bone marrow

A

turns into fat

81
Q

what does the peripheral blood smear look like in aplastic anemia

A

pancytopenia
normocytic, normochromic anemia
no reticulocytosis

82
Q

what is the biopsy of the bone marrow for aplastic anemia

A

dry tap

83
Q

what is the clinical presentation for aplastic anemia

A

prone to infections, bleeding

no splenomegaly and lymphadenopathy

84
Q

what are acquired causes of aplastic anemia

A
chemicals, toxins, drugs
Chloramphenicol 
radiation
viral infection
SLE
half are idiopathic
85
Q

what is the hereditary aplastic anemia

A

Fanconi’s anemia

86
Q

what happens in Fanconi’s anemia

A

defect in DNA mechanism = chromosomal instability

87
Q

Clinical presenation for Fanconi’s anemia

A

bilateral thumb hypoplasia

chromosome breakage

88
Q

what is the treatment for Fanconi’s anemia

A

immunosuppression

bone marrow transplantation

89
Q

what is the peripheral blood smear for pure red cell aplasia

A

normocytic

no reticulocytosis

90
Q

pure red cell aplasia is an autoimmune disease mediated by

A

T-lymphs or IgG antibody vs. red cell precruors

91
Q

pure red cell aplasia is associated with other diseases

A

thymomas
CLL
SLE

92
Q

what is the primary form of pure red cell aplasia

A

Diamond-Blackfan syndrome

93
Q

what is Diamond Blackfan syndrome

A

severe anemia during first year of life

94
Q

what is the secondary form of pure red cell aplasia

A

parvovirus B19
rheumatic disease
medications

95
Q

what is the treatment for pure red cell aplasia

A

stop drugs
thymoma resection
high dose IV IG
immunosuppression

96
Q

lead poisoning can cause

A

sideroblasts

97
Q

what happens in siderblastic anemias

A

failure to incorporate heme into protoporphyrin to form hemoglobin
- defective utilization of iron within mitochondria of RBC

98
Q

serum iron, ferritin, transferrin saturation levels in sideroblastic anemia

A

high in all

99
Q

how is the herediatory for of siderblastic anemia gotten

A

X-linked recessive

- amino-levulonic acid synthase (ALA synthase) defect

100
Q

how is acquired siderblastic anemia gotten

A

drugs
LEAD
copper deficient

101
Q

what is the treatment for sideroblastic anemia

A

pyridoxine ( vitamin B6)