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N935 Advanced Pathophysiology II > Hematologic Anemias > Flashcards

Hematologic Anemias Flashcards

1
Q

erythrocyte

A
  • red blood cell

- produced in the bone marrow

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2
Q

reticulocyte

A

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

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3
Q

anemia

A

deficient number of RBCs

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4
Q

mean corpuscle volume

A

size of cell

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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 sized cells

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8
Q

hemoglobin

A

four folded globin chains (2 alpha 2 beta)

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9
Q

hemolytic anemia

A

abnormal hemolysis or breakdown of RBCs

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10
Q

RBC function

A
  • primary function is to transport hemoglobin which carries oxygen and transports it to the tissue
  • also contains carbonic anhydrase which catalyzes the CO2 hydration reaction (so helps transport CO2 in the form of HCO3- to the lungs for removal)
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11
Q

erythropoietin (EPO)

A
  • a glycoprotein formed in the kidneys that stimulates the production of red blood cells
  • any condition that decreases oxygen transport to the tissues will stimulate production of EPO
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12
Q

erythropoiesis

A
  • RBC production and maturation
  • starts in the bone marrow –> pluripotent hematopoietic stem cell –> proerythroblast –> erythroblast
  • erythroblast loses its nucleus and some organelles and becomes a reticulocyte
  • reticulocyte spends 3 days in marrow and then is ejected into the blood
  • reticulocyte spends 1 day in the blood
  • loses remaining organelles and then becomes an erythrocyte
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13
Q

what percentage of circulating RBCs are retics?

A

~1%

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14
Q

anemia

A
  • reduced number of circulating RBCs
  • main adverse effect = decreased oxygen carrying capacity
  • WHO definition = Hgb less than 12 g/dL for women and less than 13 g/dL for men
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15
Q

physiologic anemia

A
  • occurs during pregnancy

- due to a decreased Hct in relation to plasma volume

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16
Q

polycythemia

A
  • increase in circulating RBCs

- main adverse effect is increased blood viscosity

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17
Q

causes of anemia

A
  • blood loss
  • decreased production of RBCs
  • increased destruction of RBCs
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18
Q

types of blood loss anemia

A
  • acute blood loss

- chronic blood loss

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19
Q

acute blood loss

A
  • the body replaces fluid portion of plasma in 1-3 days
  • leaves low concentration of RBCs
  • RBC concentration usually returns to normal in 3-6 weeks
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20
Q

chronic blood loss

A
  • cannot absorb enough iron from the gut to make Hgb as rapidly as it is lost
  • RBCs are then produced much smaller and have little Hgb inside
  • microcytic hypochromic anemia
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21
Q

transfusion triggers

A
  • “10/30 rule” = transfuse if the Hb level is <10 g/dL or the Hct is 30%; however no evidence that Hb levels below this mandate transfusion
  • Hb levels below 6g/dL = clear evidence that patients benefit from transfusion
  • must take into account patient’s medical history, ongoing bleeding, and risk of end-organ dysfunction
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22
Q

diseases transmitted by RBC transfusions

A
  • Hep B
  • Hep C
  • HIV
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23
Q

immunomodulatory effects associated with transfusion

A
  • cancer recurrence
  • bacterial infections
  • TRALI or TACO
  • hemolytic transfusion reactions
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24
Q

EBL <15%

A

rarely requires transfusion

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25
Q

EBL 30%

A

replacement with crystalloids or albumins

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26
Q

EBL 30-40%

A

RBC transfusion

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27
Q

EBL >50%

A

MTP

may need accompanied FFP and platelets ratios 1:1:1

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28
Q

decreased production anemias

A
  • iron deficiency

- autoimmune

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29
Q

increased destruction anemias

A
  • thalassemia
  • hemolytic anemia
  • sickle cell
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30
Q

blood loss anemias

A
  • acute

- chronic

31
Q

infectious anemias

A
  • malaria parasite destroys RBCs
  • babesia (parasite spread by ticks) causes RBC hemolysis
  • parvovirus (“fifth disease”) virus inhibits erythropoiesis
32
Q

iron deficiency anemia causes

A
  • nutritional deficiency of iron - common in infants, small children, and developing countries; occurs often in those with pica (urge to consume non-food stuff)
  • depletion of iron stores - chronic GI bleed or menstruation; unable to absorb sufficient iron from diet at same rate as chronic loss
  • pregnancy - develops due to increased plasma compared to RBCs
33
Q

mild anemia Hgb value in US

A

9-12 g/dL

34
Q

iron deficiency anemia pathophysiology

A
  • iron required for hemoglobin synthesis
  • deficiency of iron impairs red cell maturation and diminishes red cell production
  • also produces microcytic hypochromic anemia - i.e. small cells with pale pigment
35
Q

iron deficiency anemia treatment

A
  • oral iron - continue for at least 1 year after source of blood loss has been corrected; delay elective surgery 2-4 months
  • IV iron - urgent surgery within a few weeks
  • RBC transfusion
36
Q

hemolytic anemia

A
  • accelerated destruction or hemolysis of RBCs; removed too quickly or lysed too early
  • often seen in immune disorders
  • RBC lifespan is <120 days
37
Q

hemolytic anemia blood tests

A
  • increased reticulocytes (immature erythrocytes)
  • unconjugated hyperbilirubinemia/jaundice
  • increased lactate dehydrogenase (enzyme released from lysed RBCs)
  • decreased haptoglobin (plasma protein that binds free hemoglobin)
38
Q

sickle cell anemia

A
  • autosomal recessive disorder caused by a single amino acid substitution in the beta globin that creates a sickle hemoglobin
  • most common familial hemolytic anemia
39
Q

sickle cell mutation

A

-glutamic acid replaced with valine

40
Q

heterozygous

A
  • 2 different alleles of a gene
  • “carrier”
  • protective against malaria
  • Africa gene frequency = 30%
41
Q

homozygous

A

-2 copies of the same allele for a gene

42
Q

sickle cell anemia pathophysiology

A
  • mutation in the beta globin that leads to the polymerization of sickle hemoglobin (HbS) into long stiff chains when it is deoxygenated
  • cell assumes elongated sickle shape but it returns to its normal shape when oxygenated
43
Q

most important variable that determines whether HbS- containing red cells undergo sickling?

A
  • intracellular concentration of other hemoglobins
  • HbA = normal hemoglobin
  • HbF = fetal hemoglobin
  • concentration or ratio of HbA to HbS*
44
Q

consequences of sickling RBCs

A
  • chronic hemolytic anemia
  • ischemic tissue damage with episodic pain
  • spleen auto infarction
45
Q

chronic hemolytic anemia

A

repeat sickling damages the red cell membrane, eventually producing irreversible sickled cells that are removed from circulation

46
Q

ischemic tissue damage with episodic pain

A
  • localized obstruction in microvasculature
  • acute chest
  • joints
  • strokes
  • retinal damage
47
Q

spleen autoinfarction

A

increases the risk of sepsis with encapsulated bacteria

48
Q

sickle cell anemia treatment

A
  • hydroxyurea

- stem cell transplants

49
Q

how does hydroxyurea work?

A
  • raises HbF levels (magic lol)
  • causes intermittent cytoxic suppression of erythroid progenitors and cell stress signaling, which then affects erythropoiesis kinetics and physiology and leads to recruitment of erythroid progenitors with increased HbF levels
  • anti-inflammatory
  • first tested in sickle cell disease in 1984 and decreased the rate of acute chest syndrome and blood transfusions by 50%
50
Q

autoimmune anemia

A
  • autimmune hemolytic anemia (AIHA)
  • antibodies IgG and IgM directed against a person’s own RBCs
  • RBCs lifespan is severely decreased
  • treatment = immunosuppression and steroids
51
Q

causes of autoimmune anemia

A
  • idiopathic
  • leukemias
  • infectious
  • drug-induced
52
Q

hemolytic disease of the newborn

A
  • incompatibility between the mother and the fetus
  • erythroblastosis fetalis (happens with second preggo)
  • 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 (fetomaternal bleed)
  • sensitizes mother to paternal RBC antigens and leads to production of IgG and anti-D red cell antibodies that cross the placenta and cause hemolysis of fetal red cells
53
Q

RhD antigen in mom and baby during hemolytic disease

A
  • fetus RhD antigen positive

- mother RhD antigen negative

54
Q

Rhesus (Rh) factor

A
  • protein found on the surface of RBCs
  • genetically inherited
  • factor refers to the Rh (D) antigen only
  • most immunogenic of all the non-ABO antigens
55
Q

RhoGAM

A
  • IgG anti-D antibodies

- treatment for hemolytic disease

56
Q

erythroblastosis fetalis fetal S/S

A
  • CHF
  • hepatosplenomegaly
  • edema
  • hemolytic anemia
  • jaundice
  • kernicterus
57
Q

G6PD Deficiency

A
  • X linked genetic disease
  • half-life of erythrocytes is approximately 60 days
  • hemolysis occurs due to inability of G6PD deficient RBCs to protect itself from oxidative damage
58
Q

G6PD function

A

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

59
Q

G6PD Deficiency precipitators

A
  • infection
  • DKA
  • medications
  • fava beans
60
Q

G6PD Deficiency peripheral smears

A
  • bite cells - red cells with severely damaged membranes that have portions bitten off by macrophages removing patches of membranes
  • also has hemoglobin precipitates known as Heinz bodies
61
Q

oxidative stress

A

hemolysis is often transient even 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

62
Q

oxidative drugs - AVOID

A
  • metoclopramide
  • penicillin & sulfa
  • methylene blue
  • hypothermia
  • acidosis
  • hyperglycemia
  • infection
63
Q

G6PD Deficiency treatment

A
  • no cure
  • avoid triggers
  • treat hemolytic episodes with hydration and blood transfusions
64
Q

polycythemia

A
  • sustained hypoxia results in compensatory increase in RBC mass and Hct
  • increases blood viscosity (slows blood flow and decreases oxygen delivery)
65
Q

Hct when polycythemia is severe

A

55-60%
threat to vital organ perfusion
at risk for venous/arterial thromboses

66
Q

relative polycythemia

A
  • dehydration
  • diuretics
  • vomiting
67
Q

physiologic polycythemia

A
  • occurs in natives who live at altitudes of 14,000-17,000 feet
  • atmospheric oxygen is low
  • RBC count rises to approximately 30% compared to non-extreme altitude
  • some places –> tibet, andes, ethiopia
68
Q

polychythemia vera (PCV)

A
  • stem cell disorder in which Hct may be as high as 60-70% instead of the normal 40-50%
  • mutation of JAK2 gene which doesn’t stop the production of RBC when there are already too many present
  • produces excess erythrocytes and number of plts and leukocytes may also be increased
  • most symptoms appear in 6th and 7th decade of life
69
Q

PCV symptoms

A
  • cyanosis
  • HA
  • dizziness
  • GI symptoms
  • hematemesis
  • melena
70
Q

effects of PCV

A
  • total blood volume increase
  • viscous and engorged vessels
  • blood passes sluggishly through skin capillaries and greater amount becomes deoxygenated resulting in bluish/ruddy skin appearance
  • marrow fibrosis (marrow replaced by fibroblasts and collagen)
71
Q

PCV mortality

A
  • 30% die from thrombitc complications

- 30% succumb to cancer (leukemia)

72
Q

PCV treatment

A
  • death from vascular complications occurs within months
  • minimize risk of thrombosis
  • phlebotomy
  • myelosuppressive drugs (hydroxyurea)
73
Q

anesthesia and PCV

A
  • at risk for thrombosis (reduce Hct prior to surgery with phlebotomy and hydration)
  • hydration (NPO status vs IVF)
  • continue hydroxyurea

N935 Advanced Pathophysiology II (16 decks)

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