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N935 Advanced Pathophysiology > Week 3: Hematologic Pathophysiology Anemias > Flashcards

Week 3: Hematologic Pathophysiology Anemias Flashcards

1
Q

Definition of Erythrocyte

A

a red blood cell

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2
Q

Definition of a Reticulocyte

A

immature erythrocyte (day 1 or 2 in the blood steam)

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3
Q

Definition of Anemia

A

deficient number of RBCs

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4
Q

Definition of Mean Corpuscle Volume

A

size

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5
Q

Definition of Normocytic

A

normal sized cell

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6
Q

Definition of Microcytic

A

smaller than normal size cell

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7
Q

Definition of Macrocytic

A

larger than normal size

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8
Q

Definition of Hemoglobin

A

four folded globin chains (2alpha 2 beta)

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9
Q

Definition of Hemolytic anemia

A

abnormal hemolysis (breakdown) of RBCs

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10
Q

Symptoms of Anemia

A 
fatigue
pallor
hypoxia
exercise intolerance
syncopy
hypovolemia/hypotension
irregular heart rate
SOB
chest pain
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11
Q

Primary Function of an RBC

A

to transport hemoglobin

transport oxygen to tissue

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12
Q

1 gram of Hgb can combine with

A

1.34ml of oxygen= 100% saturdation

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13
Q

What is the enzyme in RBCs and what is its function?

A

carbonic anhydrase

catalyzes reaction between CO2 and H2O to form carbonic acid, H2CO3

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14
Q

How is CO2 transported to lungs?

A

in the form of HCO3- to be removed

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15
Q

How is erythropoietin stimulated?

A

any condition that decreases oxygen transport to tissues

a glycoprotein formed in the kidneys

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16
Q

Why do you have elevated reticulocytes in pathological states?

A

Reticulocytes are immature blood cells, in pathological cases RBCs are needed. Therefore a positive feedback loop occurs releasing reticulocytes from bone marrow

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17
Q

What is the main adverse effect of anemia?

A

decreased oxygen-carrying capacity

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18
Q

WHO definition of anemia

A

Hb concentration less than 12 g/dl for women and less then 13g/dl for men

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19
Q

What causes pregnancy “physiologic anemia”?

A

due to decreased Hct in relation to increased plasma volume

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20
Q

What is polycythemia?

A

increase in circulating RBCs

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21
Q

What is the main adverse effect of polycythemia?

A

increase in blood viscosity

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22
Q

What are the main causes of anemia?

A

blood loss
decreased production
increased destruction

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23
Q

What are the two types of blood loss anemia?

A

acute blood loss and chronic blood loss

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24
Q

What is acute blood loss?

A

the body replaces fluid portion of plasma in 1-3 days

leaving low concentration of RBCs

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25
Q

What is chronic blood loss?

A

cannot absorb enough iron from the gut to make Hgb as rapidly as it is lost
RBCs are produced much smaller and have little Hgb inside- microcytic anemia

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26
Q

What is the 10/30 rule?

A

transfuse if the Hb level is less then 10g/dl or Hct is <30%

no evidence that Hb levels below this level mandate transfusion

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27
Q

What is the transfusion trigger?

A

Hb levels below 6g/dl will benefit from transfusion

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28
Q

Risks associated with Transfusion

A 
infections and immunomodulatory effects
Hep B, Hep C, HIV
cancer re-occurance
bacterial infections
transfusion related acute lung injury (TRALI)
hemolytic transfusion reactions
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29
Q

EBL <15%

A

rarely requires transfusion

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30
Q

EBL 30%

A

replacement with crystalloids/ albumins

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31
Q

EBL 30-40%

A

RBC transfusion

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32
Q

EBL>50%

A

massive transfusion

may need accompanied with FFP and platelets (1:1:1)

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33
Q

What are the four types of anemia based on mechanism?

A

decreased production
increased destruction (life span <120 days)
Blood loss
infectious

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34
Q

What are examples of anemia from decreased production? (2)

A

iron deficiency

autoimmune

35
Q

What are examples of anemia from increased destruction? (3)

A

thalassemia
hemolytic anemia
sickle cell

36
Q

What are examples of anemia from blood loss? (2)

A

acute

chronic

37
Q

What are examples of anemia from infectious processes? (3)

A

malaria parasite destroys RBCs
babesia (parasite usually spread by ticks) causes RBC hemolysis
Parvovirus (fifth disease) virus inhibits erythropoiesis

38
Q

What are three types of anemias based on morphology?

A

microcytic
normocytic
macrocytic/megaloblastic

39
Q

What is microcytic anemia? Causes?

A

mean corpuscular volume <80fL
iron deficiency
thalassemia

40
Q

What is normocytic anemia? Causes?

A

mean corpuscular volume 80-100fL
sickle cell anemia
chronic kidney disease, acute blood loss, aplastic anemia
G6PD deficiency

41
Q

What is macrocytic/ megaloblastic anemia? Causes?

A

defects in nuclear maturation
folic acid and vitamin B12 deficiency
liver disease, alcoholism

42
Q

How do you treat iron deficiency anemia?

A

oral iron: if elective surgery can be postponed for 2-4 months to allow for correction
IV iron- urgent surgery within a few weeks
RBC transfusion

43
Q

How long do you need to continue oral iron supplements?

A

1 year after the source of blood has been corrected

44
Q

What is hemolytic anemia?

A

accelerated destruction of RBCs
removed to quickly or lysed to early
RBC life <120 days

45
Q

What will you find in blood test for hemolytic anemia?

A

increased immature reticulocytes
unconjugated hyperbilirubinemia/jaundice
increased lactate dehydrogenase (an enzyme released from lysed RBCs)
decreased haptoglobin (a plasma protein that binds free hemoglobin)

46
Q

What is sickle cell anemia?

A

autosomal recessive disorder caused by a single amino acid substitution in beta globin that creates sickle hemoglobin

47
Q

What is the most common familial hemolytic anemia?

A

sickle cell anemia

48
Q

What is sickle cell anemia protective against?

A

malaria

49
Q

Pathogenesis of Sickle Cell anemia

A

mutation in beta globin that leads to the polymerization of sickle hemoglobin (HbS) into long, stiff chains when it is deoxygenated

50
Q

What is the most important variable that determines whether HbS-containing red cells undergo sickling is

A

the intracellular concentration of other hemoglobins

51
Q

HbA

A

normal hemoglobin

52
Q

HbF

A

fetal hemoglobin

53
Q

What are consequences of Sickling RBCs?

A

chronic hemolytic anemia
ischemic tissue damage with episodic pain
spleen auto infarction

54
Q

What microvascular is affected in sickling RBCs?

A

acute chest syndrome
joints
strokes
retinal damage

55
Q

Treatments for Sickle Cell

A

hydroxyurea

stem cell transplants

56
Q

How does hydroxyurea help?

A

raises HbF levels

anti-inflammatory

57
Q

What is autoimmune anemia or autoimmune hemolytic anemia?

A

antibodies IgG and IgM are directed against a person’s own RBCs
RBCs lifespan is severely decreased

58
Q

What are causes of autoimmune anemia?

A

idiopathic
leukemias
infectious (mononucleosis)
drug-induced (pencillins, quinidine)

59
Q

What is the treatment to autoimmune anemia?

A

immunosuppressants and steroids

60
Q

Describe hemolytic disease of the newborn

A

incompatibility between mother and the fetus
erythroblastosis fetalis
fetus inherits red cell antigenic determinants from the father that are foreign to the mother
fetal red cells can enter maternal circulation during 3rd trimester and childbirth this sensitizes mother to paternal red cell antigens and leads to productoin of IgG anti-D red cell antibodies that cross the placenta and cause hemolysis of fetal red cells

61
Q

Fetus has what antigen and mother is?

A

fetus is RhD antigen positive and mother is RhD antigen negative

62
Q

Rh Factor

A

a protein found on the surface of red blood cells

63
Q

Glucose 6 phosphate dehydrogenase deficiency

A

X linked genetic disease from the lacking of enzyme, G6PD which is involved in the pentose phosphate pathway

64
Q

What is the 1/2 life of RBCs with G6PD?

A

60 days

65
Q

Why does hemolysis occur with G6PD?

A

the inability of G6PD RBCs to protect itself from oxidative damage

66
Q

What can precipitate G6PD?

A

infection
DKA
medications
fava bean

67
Q

Peripheral smears of G6PD

A

bite cells

68
Q

Oxidative stress is

A

transient hemolysis with persistent infection or drug exposure, because lysis of older cells leaves younger cells with higher levels of G6PD that are resistant to oxidant stress

69
Q

What are drugs can induce oxidative stress?

A 
metoclopramide
penicillin and sulfa
methylene blue
hypothermia
acidosis
hyperglycemia
infection
70
Q

Treatment of G6PD is

A

no cure
avoid triggers
treat hemolytic episodes with hydration and blood transfusions

71
Q

How do you develop polycythemia?

A

sustained hypoxia results in compensatory increase in RBC mass and Hct

72
Q

What is significant polycythemia? why?

A

Hct >55-60%
threatens vital organ perfusion
at risk for DVT/ arterial thrombosis

73
Q

What is relative polycythemia?

A

concentrated Hct

74
Q

what can cause relative polycythemia?

A

dehydration, diuretics and vomitting

75
Q

Where does Physiologic Polycythemia occur?

A

natives who live at altitudes of 14,000-17,000 ft

atmospheric o2 is low

76
Q

What is the RBC count in physiologic polycythemia compared to normals?

A

rises approximately 30% compared to non-extreme altitude

77
Q

What causes secondary polycythemia?

A

due to hypoxia (cardiac disease including congenital heart with R to L shunts and low CO) and pulmonary disease (extreme obesity/ pickwickian syndrome)
due to renal disease
surreptitious use of erythropoietin by high performance athletes

78
Q

What is polycythemia vera?

A

stem cell (or myeloproliferative) disorder in which Hct may be as high as 60-70% instead of normal 40-45%
mutation in JAk2 gene (lacks ability to halt production of RBCs when enough present)
produces excess erythrocytes and number of platelets and leukocytes may also be increased

79
Q

when do most symptoms of polycythemia vera present?

A

6-7th decade of life

80
Q

what are the symptoms of PCV?

A

cyanosis, headache, dizziness, gastrointestinal symptoms, hematemesis, and melena

81
Q

What are the effects of PCV?

A

total blood volume increases
viscous and engorged vessels
blood passes sluggishly through skin capillaries and a greater amount becomes deoxygenated resulting in bluish/ruddy appearance

82
Q

What is seen in 10% of PCV patients?

A

marrow fibrosis

83
Q

Treatment of PCV

A 
death from vascular complications occurs within months
minimize thrombosis risk
avoid dehydration
phlebotomy
myelosuppressive drug
ruxolitinib
84
Q

Anesthesia and PCV

A

at risk for thrombosis (reduce Hct prior to surgery)
hydration NPO status vs IV fluids
continue hydroxyurea

N935 Advanced Pathophysiology (9 decks)

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