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Lil Pudgie > Hemolytic Anemia > Flashcards

Hemolytic Anemia Flashcards

1
Q

What are common signs in hemolytic anemia?

A

Jaundice, pallor, Chills, Fever, glossitis, ulcers, aplastic crisis. Kidney Failure can happen bc you can’t clear Hb fast enough and it is toxic to the kidneys.

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2
Q

What is the formula for MCV?

A

(Hematocrit divided by RBC count) X 10fL

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3
Q

What is the formula for MCH?

A

(HGB divided by RBC count) X 10 PG

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4
Q

What is the formula for MCHC?

A

(HGB divided by Hematocrit) X 100%

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5
Q

Steps to evaluate Hemolysis (8)

A

1) Peripheral Smear
2) Retic count
3) Bilirubin
4) LDH
5) Plasma Hemoglobin
6) Urine Hemoglobin
7) Urine Hemosiderin
8) Haptoglobin

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6
Q

What do the presence of microspherocytes indicate?

A

Loss of membrane

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7
Q

What are Schistocytes? How can you get them?

A

Fragmented RBCs

Any disease that leads to fibrous deposition on vessel walls

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8
Q

Alloimmunity is a risk of transfusion in Hemolytic Anemia. What type of cells would be present if this were to happen?

A

Bite cells

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9
Q

Schistocytes can be caused by what?

A

DIC (fibrin strands damage RBCs) and mechanical valves (like the example in class)

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10
Q

What causes TTP? (Thrombotic Thrombocytopenia Purpura)

A

A defect of certain Matrix Metallo-proteinases (MMPs)

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11
Q

True or False

Dark plasma is better than lighter plasma

A

False- the darker the plasma is the worse

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12
Q

What test do you use for Autoimmune Hemolytic Anemias?

A

DAT- Direct Coombs test

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13
Q

Why are some anemias missed on DAT tests?

A

The human body is more sensitive to IgG than the test so about 5% are missed

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14
Q

What do you see in regards to histology of cold acting antibodies?

A

They show massive agglutination

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15
Q

What is March Hemoglobinuria?

A

Breaking of RBCs by extreme exertion on feet, example is foot soldiers. Blood seen in urine.

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16
Q

What do you do when you see a brown recluse spider or a black widow spider?

A

Get a spider cookie and wait til it takes the bait then hit it with your spider smashing shoe. If all else fails, run.

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17
Q

What is a normal RBC lifespan?

A

120 days

18
Q

When RBCs are broken down, what is released?

A

Iron (recirculated via transferrin)
Protoporphyrin (broken down into bilirubin which is converted to other shit)
Globin (broken down into amino acids used for protein synth)

19
Q

What are haptoglobins?

A

Proteins present in normal plasma that bind hemoglobins and then the complex can be removed by the RE system

20
Q

What is an aplastic crisis? Often follows?

A

Abnormal decrease in retic count and sudden increase in anemia

Parvovirus infection

21
Q

In his seasonal hemolysis due to cold agglutinin syndrome slide, What is inversely proportional to environmental temperature?

A

LDH

22
Q

In cold autoimmune hemolytic anemia, what is the Ig type? In warm?

A

IgM

IgG

23
Q

Can you get necrotizing hemolytic anemia from a brown recluse spider bite?

A

You betcha

24
Q

In hemolytic anemia what are haptoglobin levels? Why?

A

Low, bc they are binding up excess Hg (Hg increases as RBC are lysed) and removed by RE system

25
Q

What’s going on in hereditary spherocytosis?

A

Defects in membrane proteins (spectrin, ankyrin, protein 4.2) leads to LOSS of membrane and formation of spherocytes (spherical RBCs) that can’t pass through splenic microcirculation leading to splenomegaly and anemia

26
Q

What’s going on in G6PD deficiency?

A

Can’t produce NADPH so can’t reduce glutathione so can’t protect against oxidative stress–>acute hemolytic anemia

27
Q

What kind of cells do you see in G6PD def?

A

Bite cells due to formation of Heinz bodies and subsequent removal of them by the spleen

28
Q

What is the inheritance pattern of G6PD def?

A

X linked

29
Q

In hemolytic anemia what are haptoglobin levels? Why?

A

Low, bc they are binding up excess Hg (Hg increases as RBC are lysed) and removed by RE system

30
Q

What’s going on in hereditary spherocytosis?

A

Defects in membrane proteins (spectrin, ankyrin, protein 4.2) leads to LOSS of membrane and formation of spherocytes (spherical RBCs) that can’t pass through splenic microcirculation leading to splenomegaly and anemia

31
Q

What’s going on in G6PD deficiency?

A

Can’t produce NADPH so can’t reduce glutathione so can’t protect against oxidative stress–>acute hemolytic anemia

32
Q

What kind of cells do you see in G6PD def?

A

Bite cells due to formation of Heinz bodies and subsequent removal of them by the spleen

33
Q

What is the inheritance pattern of G6PD def?

A

X linked

34
Q

What’s going on in pryruvate kinase deficiency?

A

Decreases ATP formation leads to rigid RBCs and lysis (due to swelling of cell bc no na/k pump)

35
Q

What happens to the oxygen dissociation curve in pryruvate kinase deficiency? Why?

A

Right shift due to increased intracellular 2,3-DPG

36
Q

What are autoimmune hemolytic anemias? What test is used in dx? Two types…?

A

Ab production by body against own RBCs; direct Coombs; warm (Ab reacts at 37 Celsius) and cold (Ab reacts at 4 Celsius)

37
Q

In warm AIHA, what kind of hemolysis do you see? In cold?

A

Extra vascular (phagocytosis by macrophages and removal by RES in spleen) and intravascular (complement lysis)

Intravascular only (complement MAC only)

38
Q

What’s going on in paroxysmal nocturnal hemoglobinuria?

A

Acquired clonal disorder of marrow stem cells (defective pigA gene)–>defective GPI anchor–>lack of DAF and CD59–>complement (intravascular) lysis

39
Q

How do you dx PNH?

A

Flow cytometry

40
Q

What is the tx for PNH? MOA?

A

Ecluzimab

Mab against complement c5

Lil Pudgie (2 decks)

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