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Pathophys II > Hematologic Pathophysiology Anemias > Flashcards

Hematologic Pathophysiology Anemias Flashcards

1
Q

Macrocytic refers to

A

larger than normal size cells

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2
Q

Microcytic refers to

A

smaller than normal size cells

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3
Q

Reticulocytes are

A

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

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4
Q

Hemoglobin is

A

four folded globin chains (2 alpha & 2 beta)

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5
Q

Hemolytic anemia is

A

abnormal hemolysis (breakdown) of RBCs

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6
Q

Primary function of RBC is to

A

transport hemoglobin

-transport O2 to tissue

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7
Q

1 gm of hemoglobin can combine with

A

1.34 mLs of oxygen= 100% saturation

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8
Q

Red blood cells are produced in

A

bone marrow

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9
Q

Any condition that decreases oxygen transport to tissues will

A

stimulate erythropoietin- a glycoprotein formed in the kidneys

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10
Q

Red blood cells contain

A 
carbonic anhydrase- enzyme that catalyzes the reaction between CO2 & H2O to form carbonic acid H2CO3
transport CO2 (in the form of HCO3-) to lungs for removal
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11
Q

RBC production and maturation occurs with

A

pluripotent stem cell–> proerythoblast–> erythroblast–> reticulocyte–> erythrocyte

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12
Q

Causes of anemia include

A

blood loss, decreased production, & increased destruction

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13
Q

Describe polycythemia

A

increase in circulating RBCs- main adverse effect is increased blood viscosity

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14
Q

Anemia is the

A

reduced number of circulating RBCs

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15
Q

The main adverse effect of anemia is

A

decreased oxygen-carrying capcaity

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16
Q

WHO defines anemia as hemoglobin concentration less than

A

12 g/dL for women & less than 13 g/dL for men

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17
Q

Anemia in pregnancy is due to

A

decreased Hct in relation to increase plasma volume

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18
Q

With acute blood loss, the body replaces fluid portion of

A

plasma in 1-3 days- leaving a low concentration of RBCs

the RBC concentration usually returns to normal within 3-6 weeks

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19
Q

Chronic blood loss anemia is when

A

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

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20
Q

Transfusion preoperatively in asymptomatic patients for elective surgery

A

are rare

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21
Q

Describe the 10/30 rule.

A

transfuse if the hemoglobin level is <10 g/dL or the Hct is <30%
- no evidence that hemoglobin levels below this level mandate transfusion

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22
Q

There is clear evidence that hemoglobin levels below

A

6 g/dL benefit from transfusion

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23
Q

When deciding whether to transfuse for a procedure, we must take into account

A

patient’s medical history, ongoing bleeding, and risk of end-organ dysfunction
e.g. active coronary artery disease may require lower transfusion thresholds

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24
Q

RBC transfusions can transmit

A

Hep B, Hep C, HIV

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25
Q

Immunomodulatory effects of transfusion include

A

cancer reoccurrence, bacterial infections, transfusion related acute lung injury, & hemolytic transfusion reactions

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26
Q

Describe estimated blood loss & transfusion thresholds.

A

EBL <15%- rarely requires transfusion
EBL 30% replacement w/ crystalloids/albumins
EBL 30-40%- RBC transfusion
EBL >50% massive transfusion protocol- may need accompanied FFP & platelets (1:1:1 ratio)

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27
Q

Describe types of anemia that are decreased production problems.

A

iron deficiency

autoimmune

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28
Q

Describe types of anemia that are increased destruction (life span <120 days).

A

thalassemia, hemolytic anemia, sickle cell

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29
Q

Describe types of anemia that include blood loss.

A

acute & chronic

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30
Q

Describe types of anemia that fall under the infectious category.

A

malaria parasite destroys RBCs
Babesia (parasite usually spread by ticks) causes RBC hemolysis
parovirus (“fifth disease”) virus inhibits erythropoiesis

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31
Q

Types of anemia based on morphology include:

A

microcytic, normocytic, & macrocytic/megaloblastic

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32
Q

Iron deficiency anemia is the result of

A

nutritional deficiency of iron- common in infants, small children, & developing countries

  • depletion of iron stores (e.g. chronic GI bleeds or mensturation)
  • pregnancy
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33
Q

Iron deficiency anemia results in pregnancy because

A

of the increased RBC mass required during gestation

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34
Q

Mild anemia may require

A

preop iron

Hb 9-12 g/dL

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35
Q

Pica is

A

the drive to consume non foodstuff

because they’re not getting enough iron

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36
Q

Depletion of iron stores are due to

A

unable to absorb sufficient iron from the diet at the same rate as chronic loss

37
Q

_______ is required for hemoglobin synthesis

A

Iron

38
Q

Iron deficiency impairs

A

red cell maturation & diminishes red cell production

-produces a microcytic hypochromic anemia

39
Q

The most important adverse effect of anemia is

A

decreased O2 delivery

40
Q

Treatment of iron deficiency includes:

A

oral iron–> if elective surgery can be postponed for 2-4 weeks to allow correction of the iron deficiency
should be continued for at least 1 year after the
source of blood loss has been corrected
IV iron–> urgent surgery within a few weeks
RBC transfusion

41
Q

Hemolytic anemia is due to

A

accelerated destruction (hemolysis) of RBC’s
- removed too quickly or lysed too early
often seen in immune disorders

42
Q

RBC lifespan is

A

<120 days

43
Q

Blood tests for hemolytic anemia include

A

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

44
Q

Sickle cell anemia is an

A

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

45
Q

The most common sickle cell anemia is

A

familial hemolytic anemia

46
Q

Sickle cell anemia is protective against

A

malaria in heterozygotes

“aka carrier”

47
Q

In sickle cell anemia, the mutation in B-globin leads to

A

polymerization of sickle hemoglobin into long, stiff chains when it is deoxygenated
- cell assumes an elongated sickle shape but it returns to its normal shape when oxygenated

48
Q

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

A

intracellular concentration of other hemoglobins
HbA- normal hemoglobin
HbF- fetal hemoglobin

49
Q

Newborns with sickle cell anemia are asymptomatic until

A

HbF falls at 5-6 months of age

50
Q

Consequences of sickling of RBCs include:

A

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

51
Q

Describe chronic hemolytic anemia as a result of sickling of RBCs

A

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

52
Q

Describe ischemic tissue damage with episodic pain as a result of sickling of RBCs.

A

Localized obstruction in the microvasculature

  • acute chest syndrome
  • joints
  • strokes
  • retinal damage
53
Q

Describe the implications of spleen auto infarction.

A

increases the risk of sepsis with encapsulated bacteria

54
Q

Treatment for sickle cell includes:

A

hydroxyurea

stem cell transplants

55
Q

Describe what hydroxyurea does to treat sickle cell.

A

raises HbF levels
anti-inflammatory
decreases the rate of acute chest syndrome & blood transfusions by 50%

56
Q

Autoimmune anemia is also known as

A

autoimmune hemolytic anemia

57
Q

Autoimmune anemia is due to

A

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

RBCs lifespan is severely decreased

58
Q

Causes of autoimmune anemia include

A

idiopathic
leukemias
infections (i.e. mononucleosis)
drug-induced (i.e. penicillin, quinidine)

59
Q

Treatment for autoimmune anemia is

A

immunosuppression & steroids

60
Q

Hemolytic disease of the newborn is due to

A

incompatibility between the mother & the fetus- erythroblastosis fetalis
fetus inherits red cell antigenic determinants from the father that are foreign to the mother

61
Q

Hemolytic disease of the newborn results when the fetus is

A

RhD-antigen positive and mother is RhD antigen negative

62
Q

Fetal red cells can enter maternal circulation during 3rd semester and childbirth (fetomaternal bleed) which

A

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

63
Q

Rhesus (Rh) factors is a

A

protein found on the surface of RBCs

-its genetically inherited

64
Q

________ antigen is the most immunogenic of all the non-ABO antigens

A

Rh(D)

65
Q

Rh(D) status of an individual is normally described with

A

a positive or negative suffix after the ABO type (e.g. someone who is A positive has the A antigen and the Rh(D) antigen, whereas someone who is A negative lacks the Rh(D) antigen

66
Q

Generally, the first-antigen incompatible pregnancy

A

does not produce disease because the mother does not produce anti-red cell IgG antibodies (the type that cross the placenta) before delivery

67
Q

When an Rho(D) incompatibility is detected, the mother receives an

A

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

68
Q

The vast majority of Rh disease is preventable in modern antenatal care by injections of

A

IgG anti-D antibodies (Rho(D) immune globulin) aka RhoGAM

69
Q

G6PD deficiency is an _______

A

X linked genetic disease

70
Q

G6PD is a

A

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

71
Q

The half life of erythrocytes in G6PD is approximately

A

60 days

72
Q

G6PD can be precipitated by

A

infection, DKA, medications, fava beans

73
Q

In G6PD, ________ occurs due to inability of G6PD deficient RBCs to protect itself from

A

hemolysis; oxidative damage

74
Q

G6PD deficiency peripheral smears appear to have

A

“bite” cells, red cells with severely damaged membranes that have portions “bitten off” by macrophages removing patches of membrane with associated hemoglobin precipitates known as Heinze bodies leading to intravascular hemolysis

75
Q

In G6PD, the hemolysis is often transient, even with persistent infection or drug exposure, because

A

lysis of older cells leaves younger cells with higher levels of G6PD that are resistant to oxidant stress

76
Q

For patients with G6PD, avoiding risk of hemolysis includes

A 
not exposing the patient to oxidative drugs such as:
metoclopramide
penicillin & sulfa
methylene blue
hypothermia
acidosis
hyperglycemia
infection
77
Q

Treatment of G6PD deficiency includes

A

no cure
avoid triggers
treat hemolytic episodes with: hydration & blood transfusions

78
Q

Polycythemia is the result of

A

sustained hypoxia which results in compensatory increase in RBC mass & Hct
increases blood viscosity which slows blood flow & decreases oxygen delivery

79
Q

Polycythemia is significant when

A

Hct >55-60%

  • threatens vital organ perfusion
  • at risk for venous/arterial thromboses
80
Q

Relative polycythemia is also known as ____ and can be a result of

A

concentrated

-dehydration, diuretics, & vomiting

81
Q

Physiologic polycythemia occurs in

A

natives who live at altitudes of 14,000 to 17,000 feet

some evidence of heritable genetic adaptation- Tibet in Asia, Andes of the Americas, Ethiopia in Africa

82
Q

Polycythemia vera is a

A

stem cell (or myeloproliferative) disorder in which Hct may be as high as 60-70% instead of the normal 40-55%

83
Q

Polycythemia vera is due to the mutation of the

A

Jak2 gene which doesn’t stop the production of RBC when there are already too many present
-tyrosine kinase JAK2 is a signaling molecule in pathways downstream of the erythropoietin receptor & other growth factor receptors

84
Q

Most symptoms of polycythemia vera appear in the

A

6th & 7th decade of life & include cyanosis, HA, dizziness, GI symptoms, hematemesis, & melena

85
Q

With polycythemia vera, there are excess erythrocytes and possibly

A

platelets & leukocytes

86
Q

Without treatment for polycythemia vera,

A

death from vascular complications occurs within months

  • minimize risk of thrombus
  • phlebotomy- helps extend survival by 10 years
  • myelosuppressive drugs (e.g. hydroxyurea)
87
Q

Anesthetic considerations for patients with polycythemia vera include

A

at risk for thrombosis- reduce Hct prior to surgery- phlebotomy & hydration
Hydration- NPO status vs. IV fluids
continue hydroxyurea (cytoreductive agent)

88
Q

Effects of polycythemia vera include

A

total blood volume increases–> hepatic, coronary or cerebral thrombosis is common presenting sign
viscous & engorged vessels–> increases viscosity
blood passes sluggishly through skin capillaries & a greater amount becomes deoxygenated resulting in a bluish/ruddy skin appearance
Marrow fibrosis (the marrow is replaced by fibroblasts & collagen)

89
Q

30% of patients with polycythemia vera will die from

A 
cancer-leukemia (30%)
thrombotic complications (30%)

Pathophys II (43 decks)

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