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2 Path Unit > 11/4 and 11/5 Anemia 1 AND 2 > Flashcards

11/4 and 11/5 Anemia 1 AND 2 Flashcards

1
Q

List the steps of maturation into a red cell

A
  • Pronormoblast
  • Basophilic Normoblast
  • Polychromatophilic Normoblast
  • Orthochromatic Normoblast
  • Reticulocyte (Polychromatic Erythrocyte)
  • Erythrocyte
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2
Q

Normal Hgb value?

A

12-15

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3
Q

Normal Heatocrit value?

A

40-50%

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4
Q

Normal RBC/uL?

A

5 million

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5
Q

MCV, MCHC, MCH, RDW stand for?

A
  • mean cell vol
  • mean cell Hb conc.
  • Mean cell Hb
  • red cell distribution width
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6
Q

How long after acute blood loss till reticuloctyes show in blood?

A

1 wk (polychromatophilic cells- slightly bluer cytoplasm)

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7
Q

T/F blood smear will show anemia after acute loss of 2,000 mL of blood?

A

F. (takes time for blood dilution to occur)

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8
Q

Labs of hemolytic anemia? (3)

A
  • Up indirect bilirubin
  • Up LDH
  • Down haptoglobin
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9
Q

Chronic hemolytic anemia blood smear features?(2) Marrow features?(1)

A
  • Reticulocytosis (polychromasia)
  • Anisocytosis (variations in size, since young RBC are bigger)
  • More erythroid precursors in marrow
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10
Q

intracorpuscular defect is?

A

problem in the RBC [so extracorpuscular would be any other problem]

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11
Q

intravascular hemolysis is?

A

destroyed inside vessel (only 2 examples are fragmentation anemia & complement-mediated hemolysis) [Thus extravascular would be anything else, including when spleen destroys RBC’s]

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12
Q

Labs of intravascular hemolysis? (4)

A
  • Up: plasma Hb
  • Down: haptoglobin
  • Urine pos. for: Hb, Hemosiderin [these 2 always absent in extravascular!]
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13
Q

hereditary spherocytosis is in what population? incidence? molecular defect?

A
  • N. Europeans
  • 1 in 5000
  • spectrin, ankyrin, band 3 (ankyrin most common)
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14
Q

What causes the hemolysis in hereditary spherocytosis?

A

spleen. [removal is curative!]

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15
Q

G6PD deficiency: how diagnosed? Inheritance?

A
  • quantitate levels of G6PD in blood

- X-linked

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16
Q

Which RBC’s are most affected by G6PD deficiency? How would we treat this?

A
  • older cells [young unaffected cuz have more enzyme]

- avoid oxidants

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17
Q

I have blister cells. What disease do I have?

A

G6PD likely. Heinz bodies will also be present.

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18
Q

I have target cells. What disease do I have?

A

hemoglobinopathies (S, SC, C)

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19
Q

I have shistocytes. What disease do I have?

A

-Fragmentation hemolytic anemia (basically anything that causes shearing of RBC’s, like DIC, TTP, prosthetic heart valve)

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20
Q

I have spherocytes. What disease do I have? (2 possible)

A

-Immune hemolytic anemia (because a key protein is bitten off by spleen)
OR
-Hereditary spherocytosis

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21
Q

I have Howell-Jolly bodies. What disease do I have?

A

Your spleen is gone. Either: 1) Removed (hereditary spherocytosis treatment) or 2) Destructed (by Sickle Cell)

[Howell-Jollies are retained nuclear material]

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22
Q

I have a valine at 6 position of Beta globin chain. what do I have?

A

Sickle trait.

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23
Q

I have a lysine at 6 position of beta globin chain. What do I have?

A

Hemoglobin C trait.

24
Q

When do sickle cells crystalize? What removes these?

A
  • homozygous trait with low oxygen tension

- macrophages

25
Q

What organs are most affected by painful infarcts in sickle cell?

A
  • Spleen, bones

- Also strokes, retinopathy, kidney, lungs

26
Q

Why do you not want your spleen removed?

A

Increases chance for infection

27
Q

T/F sickle cells are seen in a heterozygote for sickle? (S/A)
T/F sickle cells are seen in a heterozygote for S/C?

A

F. (asymptomatic, no blood abnormalities!!)

T. (sickle crises occur but are less severe)

28
Q

T/F people with sickle cell disease have a complete lack of Hb A on electrophoresis?

A

T! (a key lab finding, along with presence of Hb S)

29
Q

T/F Hb C crystals are present in C trait (CA)?

How about in SC disease?

A

F. (also asymptomatic!)

T.

30
Q

What are the symptoms of Hb CC disease?

A

MILD anemia WITHOUT painful crisis

31
Q

3 types of fully assembled hemoglobin are each composed of what globin chains? HbA, HbA2, HbF

A

HbA=alpha, beta
HbA2=alpha, delta
HbF=alpha, gamma

32
Q

I have a disease class with BOTH ineffective erythropoiesis and hemolysis. What class of disease do I have? What does this give me protection against?

A
  • Thalassemia

- Plasmodium falciparum malaria

33
Q

Alpha thalassemias: what type of mutation? What happens when 2 genes are affected? 3? 4?

A
  • deletion

- 2 is mild anemia (3 is moderate anemia w/ Hemoglobin H, 4=hydrops fetalis)

34
Q

Beta thalassemia: What type of mutation?

A

-point, splicing

35
Q

My RBC’s have membrane damage due to a precipitate, I have no or mild anemia with microcytosis, and elevated Hb A2. What disease do I have?

A

Beta thalassemia minor (alpha chains precipitate).

36
Q

I have a furry skull X-ray, skeletal deformities, systemic iron overload, and excess alpha chains. What disease do I have?

A

Beta thalassemia major (iron overload due to chronic transfusions)

37
Q

I have a positive direct antiglobulin test (Coombs) and spherocytes. What disease?

A

Immune hemolytic anemia (Antibodies against red cell membrane)

38
Q

2 types of microangiopathic hemolytic anemia are?

A
  • TTP (thrombotic thrombocytopenic purpura)

- DIC

39
Q

I have anemia, low reticulocytes count, oval macrocytes, hypersegmented neutrophils, hypercellular bone marrow, and ineffective erythropoiesis. What disease?

A

Megaloblastic anemia.

40
Q

I have megaloblastic anemia, but I started taking a supplement for it and it went away. Now I’m starting to go insane. What do I have?

A

B12 deficiency (the anemia can be corrected by folate supplementation, neural defects can’t)

41
Q

Most common cause of B12 deficiency?

A
  • Pernicious Anemia (autoimmune to intrinsic factor)

- Others: vegans, tapeworms, etc

42
Q

I’ve got anemia with high homocysteine & methylmalonic acid labs. What anemia?

A

B12 deficient

43
Q

I’ve got anemia with high homocysteine & normal methylmalonic acid labs. What anemia?

A

Folate deficient.

44
Q

Folate stores: where? how long do they last?

A
  • liver

- 2-4 months

45
Q

B12 is absorbed where? how long do stores last?

A
  • terminal ileum

- several years

46
Q

Where does iron get absorbed in GI? Where is it stored in the body?

A
  • duodenum

- RBC’s

47
Q

Fe deficiency due to chronic blood loss is most commonly due to what?

A

GI bleed, or menses in reproductive age women

48
Q

I have microcytic, hypochromic anemia with high TIBC. What will my serum ferritin levels be?

A

low (I have Fe deficient anemia)

49
Q

I have hypochromic anemia with low TIBC and high ferritin. What will my serum iron be?

A

-low (I have anemia of chronic inflammation)

50
Q

What is the most common cause of anemia? 2nd?

A
  • Fe deficiency

- Anemia of chronic inflammation

51
Q

I have anemia of chronic inflammation. What cytokines are increased? What is the end effect of these cytokines?

A
  • IL-6, BMP-2

- Liver makes hepcidin, which causes iron storage in marrow macrophages

52
Q

Aplastic anemia is usually caused by? Peripheral blood finding is?

A
  • idiopathic (fatty replacement of marrow, MAYBE activated T cells release cytokines which suppress stem cells)
  • pancytopenia
53
Q

My marrow has been replaced, and now I have anemia. What’s my anemia called?

A

myelophthisic anemia

54
Q

I’ve got low erythropoietin. What’s my anemia?

A

Anemia of renal failure or uremia

55
Q

I’ve got myelodysplastic syndrome. What is that, anyway?

A

neoplastic marrow stem cell clones

56
Q

Polycythemia vera is caused by? what’s treatment?

A
  • neoplastic marrow stem cell proliferation due to JAK2 V617F gain of function mutation
  • phlebotomy
57
Q

A 50-year old tells you he itches like crazy when he gets out of the tub, and occasionally has thrombosis, and sometimes bleeding. What does he have?

A

polycythemia vera

2 Path Unit (14 decks)

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