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IHO Week 2 > Anemia > Flashcards

Anemia Flashcards

1
Q

In warm autoimmune hemolytic anemia, what antibody coats the RBCs?

A

IgG

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2
Q

What happens to the IgG-coated RBCs?

A

they get either get competely eaten by the macrophages in the spleen or they’re nibbled at in such a way that the cells become spherocytes

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3
Q

What is the main diagnostic factor for warm autoimmune hemolytic anemia?

A

DAT

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4
Q

What are the treatment options for warm autoimmune hemolytic anemia?

A

steroids and splenectomy if necessary

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5
Q

What antibody coats the RBCs in cold autoimmune hemolytic anemia?

A

IgM (plus complement)

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6
Q

How is cold autoimmune hemolytic anemia temperature dependent?

A

IgM falls off the cells in warm body parts - so it affects the periphery

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7
Q

What does the IgM coat cause the RBCs to do? WHat does the complement coat cause?

A

they form bridges with each other, causing agglutination

the complement causes the intravascular hemolysis

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8
Q

What will a presentation of cold autoimmune hemolytic anemia look like?

A

general pallor, but cyanosis in cold body parts - aggragated by cold temperatures

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9
Q

What is the most important hemoglobinopathy (qualitative Hb abnormality)?

A

sickle cell anemia

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10
Q

What’s the best lab test to look for hemoglobinopathies?

A

hemoglobin electrophoresis (HbS won’t travel as far as HbA - normal)

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11
Q

What’s the mutation for sickle cell anemia?

A

it’s a point mutation in the beta chain gene (valine for glutamate) yielding HbS

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12
Q

What does HbS do upon deoxygenation?

A

It aggregates and polymerizes in the RBC, causing it to form a sickle shape - very fragile
this clogs up vessels

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13
Q

Which ethicity has sickle cell anemia most often?

A

african americans

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14
Q

What is the treatment for sickle cell anemia?

A

you prevent the trigger (like infection, fever, dehydration, etc)

blood transfusions

bone marrow transplantation

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15
Q

While sickle cell was a qualitative Hb abnormality, what is a general example of quantitative Hb abnormalities?

A

thalassemias

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16
Q

Are thalassemias normochromic or hypochromic. normocytic, microcytic or macrocytic?

A

hypochromic microcytic

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17
Q

Do you have a increased or decreased RBC count in thalassemia? What other anemia does this differentiate thalassemia from?

A

increased! - this is how you can differentiate thalassemia from IDA

18
Q

What are the two general types of thalasemias?

A

beta thalassemia and alpha thalassemia

19
Q

What are the genotypes/phenotypes in beta thalassemias? Is it a defect or an absence of the gene?

A

A defect in the gene!
B gene = norma, B+ = make some beta chains, B- = make no beta chains

B thalassemia minor: B0/B or B+/B

B thalassemia intermedia: B0/B or B+/B+

B thalassemia major: B0/B0 or B0/B+

20
Q

WHat are the genotypes/phenotypes in alpha thalassemias? Defect or absence of the gene?

A 
An absence of the gene!
-a/aa = silent
--/aa or -a/-a = a-thal trait
aa/-a = HbH disease
--/-- = hydrops faetalis
21
Q

Part of the issue in alpha thalassemias is that you have excess unpaired Hb chains. What do you see regarding this in newborns vs. adults?

A

newborns: gamma tetramers of Hb (Hb barts)

adults; beta tetramers of Hb

22
Q

What morphology will you see on smear in a thalassemia?

A

hypochromatic, microcytic anemia
varying anisocytosis and poikilocytosis
target cells
basophilic stippling

23
Q

Which ethnic groups typically have alpha thalassemia? beta thalassemia?

A 
alpha = asians and blacks
beta = mediterraneans, blacks, asians
24
Q

Why do G6PD deficient red cells die?

A

they can’t reduce ROS, so the ROS attacks the Hb
The heme breaks away from the globin and the globin denatures, sticking to the red cell membrane to form Heinz bodies. THe spleen then bites out the Heinz bodies (bite cells) or just destroys them period

25
Q

What happens to RBC in a microangiopathic hemolytic anemia? in general…

A

It’s a physical trauma to red cells - you need to figure out why!

26
Q

What are some things that can cause physical trauma to RBCs?

A

artificial heart valves, anthing causing disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, or hemolytic uremic syndrome

27
Q

How do prekeratocytes (blister cells) form in microangiopathic hemolytic anemia?

A

the RBCs get draped over fibrin transiently, this causes damage to the cell membrane, the damaged membrane fuses and produces a clear area lacking any hemoglobin

28
Q

How do fragmented cells form in microangiopathic hemolytic anemia?

A

Similar to the prekeratocytes…the RBC gets draped over the fibrin, but it ends up ripping the cell into pieces (forms helmet cells and triangulocytes/schistocytes)

29
Q

How do keratocytes (horn cells) form?

A

the prekarotocyte’s fused membrane ruptures in the cirulation, which open up and form two “horns” - a “horn cell”

30
Q

For anemia of acute blood loss, what will Hb do?

A

It will be normal at first! But watch it!

31
Q

After 2-3 days of an anemia of blood loss, what cell will you see more of on smear?

A

reticulocytes

32
Q

What are general medical conditions that cause anemia of chronic disease?

A

infections, malignant conditions, and inflammatory conditions

33
Q 
What will you see on the following labs in anemia of chronic disease?
serum iron
transferrin
ferritin
marrow storage iron
A

decreased serum iron, decreased transferring (remember it’s all stuck in the cell)
increased ferritin
increased marrow storage iron

34
Q

How are labs in iron deficiency anemia different from labs in ACD?

A

you have increased transferrin, decreased ferritin and decreased bone marrow storage )it’s basically all about the binding capacity)

35
Q

What is the cause of the anemia you see in end-stage renal failure?

A

you don’t have erythropoietin

36
Q

What types of mishappen RBCs do you see in anemia of renal failure?

A

echinocytes

37
Q

Anemia is frequent in liver disease as well. What misshapen RBCs might you see?

A

acanthocytes, target cells

38
Q

What are the “uncomplicated” causes of anemia in liver disease?

A

decreased RBC survival and impaired marrow response - folate deficiency and iron deficiency complicate

39
Q

What characterizes aplastic anemia?

A

It’s pancytopenia with empty bone marrow - most are idiopathic

40
Q

What are some of the causes of aplastic anemia?

A

mot are idiopathic, but drugs, viruses, pregnancy, and fanconi anemia

41
Q

What are the clinical findings of aplastic anemia?

A

pallor, dizziness, fatigue, recurrent infection, bleeding and bruising

42
Q

What is the treatment for aplastic anemia?

A

give blood products

drugs: G-CSF, prednisone, ATG

bone marrow transplant is last reort

IHO Week 2 (13 decks)

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