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N935 Advanced Pathophysiology > hematologic - anemias > Flashcards

hematologic - anemias Flashcards

1
Q

erythrocyte definition

A

red blood cell

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2
Q

reticulocyte definition

A

immature erythrocyte (day 1 or 2 in the bloodstream)

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3
Q

anemia definition

A

deficient number of RBCs

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4
Q

mean corpuscle volume

A

size of RBC

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5
Q

normocytic

A

normal sized cells

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6
Q

microcytic

A

smaller than normal size cells

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7
Q

macrocytic

A

larger than normal size cells

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8
Q

hemoglobin

A

four folded globin chains (2 alpha and 2 beta)

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9
Q

hemolytic anemia

A

abnormal hemolysis (breakdown) of RBCs

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10
Q

RBC primary function

A

transport hemoglobin which transports oxygen to the tissue

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11
Q

CO2 + H2O —>(carbonic anhydrase)

A

H2C03 –> HCO3 + H

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12
Q

what enzyme do RBCs contain and what does it do

A

carbonic anhydrase - catalyzes the reaction between CO2 and H2O to form carbonic acid (H2Co3)
and transports CO2 in the form of HCO3 to the lungs for removal

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13
Q

where are RBCs produced

A

in the bone marrow

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14
Q

any condition that decreases oxygen transport to tissues will stimulate

A

erythropoietin (glycoprotein formed in the kidneys)

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15
Q

erythropoiesis definition

A

RBC production and maturation

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16
Q

erythropoiesis process

A

pluripotent hematopoietic stem cell –> proerythroblast –> erythroblast –> reticulocyte –> erythrocyte

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17
Q

what percent of circulating RBCs are reticulocytes?

A

about 1%

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18
Q

anemia definition

A

reduced number of circulating RBCs = decreased oxygen carrying capacity

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19
Q

according to the WHO anemia is defined as Hgb concentration as ___ for women and ___ for men

A

12 g/dL for women

<13 g/dL for men

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20
Q

what does a physiologic anemia mean?

A

decreased Hct in relation to increase in plasma volume in pregnant women

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21
Q

polycythemia definition

A

increase in circulating RBCs

increased blood viscosity

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22
Q

some causes of anemia (broad/general terms)

A

blood loss
decreased production of RBCs
increased destruction of RBCs

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23
Q

symptoms of anemia

A

fatigue, tachycardia, SOB, dizziness, paleness, coldness, muscle weakness, splenomegaly, angina/chest pain, hypotension, yellowing of skin or eyes

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24
Q

in acute blood loss the body replaces the fluid portion of plasma in

A

1-3 days leaving a low concentration of RBCs

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25
Q

in acute blood loss when does the RBC concentration return to normal usually?

A

within 3-6 weeks

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26
Q

in chronic blood loss patients

A

cannot absorb enough iron from the gut to make Hgb as rapidly as it is lost so RBCs are much smaller and have little Hgb inside them (microcytic hypochromic anemia)

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27
Q

“10/30 rule”

A

transfuse if the Hgb level is <10g/dL or the Hct is <30%

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28
Q

clear evidence to Hgb levels below ____ benefit from transfusion

A

6 g/dL

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29
Q

active coronary artery disease may require

A

lower transfusion thresholds

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30
Q

RBC transfusions can transmit

A

hep B, C, HIV

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31
Q

EBL <15%

A

rarely requires transfusions

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32
Q

EBL 30%

A

replacement with crystalloids/albumins

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33
Q

EBL 30-40%

A

RBC transfusion

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34
Q

EBL >50%

A

massive transfusion (will need FFP and plts too)

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35
Q

types of anemia from decreased RBC production

A

iron deficiency, autoimmune

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36
Q

types of anemia from increased destruction of RBCs

A

thalassemia, hemolytic anemia, sickle cell

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37
Q

types of anemia from blood loss

A

acute or chronic

38
Q

types of anemia from infection

A

Malaria (destroys RBCs),
Babesia (in ticks - RBC hemolysis),
Parvovirus (fifth disease) - inhibits erythropoiesis

39
Q

Microcytic anemia

A

MCV <80 fL

iron deficiency, thalassemia

40
Q

Normocytic anemia

A

MCV 80-100 fL

sickle cell, CKD, acute blood loss, aplastic anemia, GSPD deficiency

41
Q

Macrocytic/Megaloblastic anemia

A

defects in nuclear maturation

folic acid and vit B12 deficiency, liver disease, alcoholism

42
Q

iron deficiency anemia definition

A

nutritional deficiency in iron (shocker), depletion of iron stores from chronic GI bleed or menstruation for example

43
Q

iron deficiency impairs

A

red cell maturation and diminishes red cell production

44
Q

iron deficiency produces what kind of anemia

A

microcytic hypochromic anemia

45
Q

treatment of iron deficiency anemia

A

oral iron, IV iron, RBC transfusion

46
Q

Hemolytic anemia definition

A

accelerated destruction (hemolysis) of RBCs (removed too quickly or lysed too early)

47
Q

which type of disorders do you commonly see hemolytic anemia in?

A

immune disorders

48
Q

RBC lifespan

A

<120 days

49
Q

blood tests seen with hemolytic anemia

A

increased immature erythrocytes/reticulocytes
unconjugated hyperbilirubinemia/jaundice
increased lactate dehydrogenase
decreased haptoglobin

50
Q

what is lactate dehydrogenase and where does it come from

A

it is an enzyme that is released from lysed RBCs

51
Q

what is haptoglobin

A

a plasma protein that binds free hemoglobin

52
Q

sickle cell anemia is what kind of disorder

A

an autosomal recessive disorder caused by a single amino acid substituition in B globin that creates sickle hemoglobin

53
Q

what is the most common familial hemolytic anemia?

A

sickle cell anemia

54
Q

what anemia is actually protective against malaria in heterozygotes?

A

sickle cell anemia

55
Q

heterozygous

A

2 different alleles of a gene (carrier)

56
Q

homozygous

A

2 copies of the same allele for a gene

57
Q

sickle cell anemia pathogenesis

A

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

58
Q

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

A

the intracellular concentration of other hemoglobins

59
Q

HbA

A

normal hemoglobin

60
Q

HbF

A

fetal hemoglobin

61
Q

newborns with sickle cell anemia are asymptomatic until HbF

A

falls at 5-6 months of age

62
Q

sickling of RBCs leads to what kind of anemia

A

chronic hemolytic anemia

63
Q

consequences of sickling RBCs

A

ischemic tissue damage with episodic pain, spleen auto infarction

64
Q

treatment for sickle cell

A

hydroxyurea - raises HbF levels, stem cell transplants

65
Q

how does hydroxyurea work

A

causes intermittent cytotoxic suppression of erythroid progenitors and cell stress signaling which affects erythropoiesis kinetics and physiology leading to recruitment of erythroid progenitors with increased HbF level

66
Q

what happens in autoimmune anemia

A

antibodies (IgG and IgM) are directed against a person’s own RBCs

67
Q

causes of autoimmune anemia

A

idiopathic, leukemias, infectious (mononucleosis), drug induced (PCN, quinidine)

68
Q

treatment for autoimmune anemia

A

immunosuppression and steroids

69
Q

Erythroblastosis fetalis

A

fetus inherits red cell antigenic determinants from the father that are foreign to the mother, the fetal red cells enter maternal circulation during the 3rd trimester and childbirth

70
Q

in erythroblastosis fetalis the fetus is ____ and the mother is _____

A

RhD antigen positive; RhD antigen negative

71
Q

once the fetal red cells enter maternal circulation what happens in mom’s second pregnancy

A

the mother is sensitized to the paternal red cell antigens and leads to production of IgG anti D red cell antibodies that cross the placenta and cause hemolysis of fetal red cells

72
Q

what is Rh factor?

A

Rhesus (Rh) factor is a protein found on the surface of RBCs

it is genetically inherited

73
Q

factor in Rh factor refers to

A

the Rh (D) antigen only

74
Q

the Rh (D) antigen is the most

A

immunogenic of all the non ABO antigens

75
Q

when any Rh incompatibility is detected the mother

A

receives Rhogam at 28 weeks gestation and at birth to avoid the development of antibodies towards the fetus

76
Q

what adverse effects can babies develop from erythroblastosis fetalis

A

jaundice, hemolytic anemia, edema, hepatomegaly, CHF, kernicterus

77
Q

G6PD deficiency

A

X linked genetic disease

metabolic enzyme involved in the pentose phosphate pathway which is important in RBC metabolism

78
Q

G6PD deficiency can be precipitated by

A

infection, DKA, medications, fava beans

79
Q

some oxidative drugs include

A

metoclopramide, PCN, sulfa, methylene blue, hypothermia, acidosis, hyperglycemia, infection

80
Q

treatment for G6PD deficiency

A

no cure, avoid triggers, treat hemolytic episdoes with hydration and blood transfusions

81
Q

polycythemia

A

sustained hypoxia results in compensatory increase in RBC mass and Hct
increased blood viscosity

82
Q

significant polycythemia is when the Hct is

A

> 55-60%

threatens vital organ perfusion and put at risk for venous/arterial thromboses

83
Q

physiologic polycythemia

A

people who live at high altitudes of 14k-17k where the atmospheric oxygen is low

84
Q

polycythemia vera

A

stem cell or myeloproliferative disorder in which the HCt may be as high as 60-70%
mutation of the JAK2 gene which doesn’t stop the production of RBC when there are already too many

85
Q

polycythemia vera produces

A

excess erythrocytes and number of platelets and leukocytes may also be increased

86
Q

signs and symptoms of polycythemia vera

A

cyanosis, HA, dizziness, GI symptoms, hematemesis, melena

87
Q

relative polycythemia can be caused from

A

dehydration, diuretics, vomiting

88
Q

effects of PCV

A

total blood volume increases , viscous and engorged vessels, and marrow fibrosis

89
Q

30% of patients with PCV will die from

A

thrombotic complications

90
Q

PCV treatment

A

minimize risk of thrombosis, phlebotomy, myelosuppressive drugs (hydroxyurea)

91
Q

anesthesia and PCV

A

risk for thrombosis so reduce HCt prior to surgery (phlebotomy and hydration)
continue hydroxyurea

N935 Advanced Pathophysiology (15 decks)

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