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SBL > RBC eval, Anemias due to blood loss, Hemolytic Anemias > Flashcards

RBC eval, Anemias due to blood loss, Hemolytic Anemias Flashcards

1
Q

Main protein in a RBC, that transports oxygen and carbon dioxide

A

Hemoglobin

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2
Q

What is Hematocrit?

A

% of whole blood volume that is occupied by red cells

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3
Q

How do you calculate Mean Corpuscular Volume (MCV)?

A

Hematocrit/RBC

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4
Q

How do you calculate Mean Corpuscular Hemoglobin (MCH)?

A

Hgb/RBC

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5
Q

How do you calculate Mean Corpuscular Hemoglobin Concentration (MCHC)?

A

Hgb/Hematocrit

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6
Q

Microcytic Anemia has a ___ MCV

A

LOW

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7
Q

Macrocytic Anemia has a ____ MCV

A

HIGH

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8
Q

Hypochromic Anemia has a ____ MCH

A

LOW

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9
Q

Red Cell Distribution Width (RDW) measures?

A

The variability in size of RBCs in circulation

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10
Q

Anisocytosis

A

Increased RDW = Increased variability in size of RBCs

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11
Q

Reticulocytes are immature erythrocytes. What do they contain that RBCs do not?

A

RNA

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12
Q

What stain can show the RNA that remains in Reticulocytes?

A

Supravital stain - RNA appears polychromatic (purple-grey)

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13
Q

With Acute Blood loss, what will the MCV and MCH be?

A

Normal

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14
Q

With Acute Blood loss, there is initially a LOW reticulocyte count. How long will it take for there to be an increase in reticulocytes?

A

6-7 days after blood loss

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15
Q

With Acute Blood loss, the anemia will manifest through LOW ____ 6-12 hours later

A

Hemoglobin and Hematocrit

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16
Q

With Chronic Blood loss, how do you get anemia?

A

If the rate of loss exceeds the rate of replacement

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17
Q

How does Chronic Blood loss present?

A

Iron deficient Anemia

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18
Q

Hemolytic anemias involve?

A

Peripheral destruction of RBCs

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19
Q

What attempts to compensate for Hemolytic anemias?

A

Bone marrow

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20
Q

Hereditary spherocytosis

A

Mutations lead to unstable membrane skeletal proteins of the RBC

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21
Q

Mutations lead to unstable membrane skeletal proteins of the RBC

A

Hereditary Spherocytosis

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22
Q

RBCs with Hereditary Spherocytosis are ____ deformable

A

LESS

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23
Q

When the RBCs with Hereditary Spherocytosis travel through the spleen, what occurs?

A

They are quickly degraded

= splenomegaly/hypersplenism

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24
Q

What is the treatment for Hereditary Spherocytosis and its side effects?

A

Remove the spleen

- Increase in Howell - Jolly bodies

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25
Q

What are Howell-jolly bodies and when are they seen?

A

DNA inclusions in RBCs that are normally removed by the spleen
- They are seen in cases of Hereditary spherocytosis where the spleen has been removed, thus the bodies cannot be removed and they remain

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26
Q

3 symptoms of Hereditary spherocytosis?

A

Anemia
Splenomegaly
Jaundice

27
Q

In conditions that over-rely on erythropoiesis (like hereditary spherocytosis), infection with what can cause an aplastic crisis (shut down of new RBCs)?

A

Parvovirus B19 - destroys erythroid precursors

28
Q

How is G6PD deficiency inherited?

A

X-linked recessive

29
Q

Under oxidative stress, how are normal cells protected?

A
  • G6PD creates NADPH
  • NADPH helps create Reduced Glutathione
  • Reduced Glutathione can peroxidase free radicals and get rid of them
30
Q

Under oxidative stress, those with G6PD will see what symptoms?

A

Episodic hemolysis of RBCs a few days after exposure

31
Q

What are Heinz bodies?

A

Denaturation of proteins in RBCs caused by oxidative damage

32
Q

How are Heinz bodies removed and the remaining bite cells are seen with?

A

The spleen “bites” the heinz bodies to remove them

= bite cells are seen with G6PD deficiency

33
Q

Sickle Cell Anemia involves a mutation in the ____ chain = HgbS

A

beta chain

- glutamic acid –> valine

34
Q

Sickle cell trait

A

Heterozygous for HgbS

35
Q

Sickle cell disease

A

Homozygous for HgbS

36
Q

Populations with increased incidence of HgbS will have more?

A

Variants of Hgb

37
Q

With Sickle cell disease, RBCs polymerize and lengthen. What can cause this?

A

Hypoxia
Sluggish blood flow and low pH
Intracellular dehydration

38
Q

Sickled cells can undergo hemolysis and vaso-occlude blood flow = hypoxia (induce polymerization). Damage to the sickled cell membrane causes?

A

Increased adhesion - vaso-occlusion

39
Q

Treatment for Sickle cell Anemia?

A

Hydroxyurea (increased Hgb Fetal)
Supportive care
CRISPR

40
Q

What is a more mild version than Sickle cell (homozygous for SS Hgb)?

A

SC disease

41
Q

SC Disease involves Hgb C, what can it do?

A

Hgb C can crystallize but NOT polymerize

42
Q

What cells will you see with SC disease?

A

Target cells (poikilocytes) = abnormal shape

43
Q

How many genes are there for beta-globin?

A

2

44
Q

How many genes are there for alpha-globin?

A

4

45
Q

1 mutation in beta-globin

A

Beta-thalassemia trait or minor

46
Q

Symptoms of beta-thalassemia minor

A

Mild, microcytic anemia

47
Q

2 mutations in beta-globin

A

Beta-thalassemia major

48
Q

Symptoms of beta-thalassemia major

A

Severe anemia
Extramedullary hematopoiesis
Marrow expansion = crew cut appearance
Switch to Hgb Fetal

49
Q

Severe anemia, extramedullary hematopoiesis, crew cut marrow expansion could indicate?

A

Beta-thalassemia major

50
Q

3 alpha-globin genes hit

A

Hb H disease

51
Q

Hb H disease has a tetramer of beta-globin. This has a ____ oxygen affinity which means?

A

HIGH affinity = poor oxygenator

52
Q

Symptoms of Hb H disease?

A

Anemia and splenomegaly

53
Q

Paroxysmal Nocturnal Hemoglobinuria involves what mutations?

A

PIGA on the x chromosome - affect Hematopoietic stem cells

54
Q

PIGA mutations with Paroxysmal Nocturnal Hemoglobinuria cause lack of?

A

CD55 and CD59 that bind complement

55
Q

Lack of CD55 and CD59 with Paroxysmal Nocturnal Hemoglobinuria causes?

A

MAC to lyse RBCs at night = blood in urine and thrombosis

56
Q

Symptoms of Paroxysmal Nocturnal Hemoglobinuria?

A

Blood in the urine at night and thrombosis

57
Q

Those with PNH are at risk for?

A

AML/MDS

58
Q

What drug can treat PNH by turning off the complement?

A

Eculizamab (blocks C5 -> C5a)

59
Q

Those being treated for PNH with Eculizamab are at risk for infections with?

A

Neisseria species

60
Q

Warm hemolytic anemia involves what Ig binding and where are the cells phagocytosed?

A

IgG

- phagocytosed in the spleen

61
Q

Cold hemolytic anemia involves what Ig binding and where/why are the cells phagocytosed where they are?

A

IgM

- c3b deposits and cells are phagocytosed in the spleen, bone marrow, liver

62
Q

Symptoms of cold hemolytic anemia?

A

Similar to Raynauds - nose and finger manifestations

63
Q

What is an example of red cell trauma that causes hemolysis?

A

Mechanical shear of the cells by a prosthetic heart valve

SBL (48 decks)

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