Microcytic and Normocytic anemias Flashcards Preview

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Flashcards in Microcytic and Normocytic anemias Deck (30)
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1
Q

anemia of chronic disease (ACD) is a result of

A

underlying systemic dx causing:

release of IL-6 and TNF

increased hepcidin that inhibits iron transport into the intestine

stops iron release in macrophages resulting in decreased RBC production in bone marrow from abnormal iron metabolism.

Decreases EPO production and decreased RBC survival

2
Q

bone marrow aspiration of anemia of chronic dx

A

abundant iron in macrophages and no iron in RBC precursors

3
Q

bone marrow aspiration in iron deficency anemia

A

absent iron in macrophages and abscent iron in RBCs

4
Q

TIBC in iron deficiency anemia

A

TIBC - will be high because there’s more spaces for iron to bind to because there’s more “seats” or iron receptors available because there’s low iron

****most specific test to determine if IDA is there****

5
Q

TIBC in anemia of chronic dx

A

normal to low

because there’s no extra transferrin receptors available to bind to iron because of acute phase reactants will cause hepcidin to internalize ferritoportin and transferrin receptors so there’s less receptors available for iron to bind .

6
Q

ferritin represents what in iron metabolism?

A

amount of stored iron but also is an acute phase reactant that can be high in anemia of chronic disease and low in iron deficiency anemia.

<15% ferritin is highly suggestive of IDA

7
Q

test to check for concerns over hemochromatosis

A

check transferrin level because that will be high. It has the most seats full.

8
Q

transferrin saturation levels represent

in Fe deficiency anemia

in anemia of chronic dx

in hemochromatosis

A

the number of seats that are full with iron or receptors bound to iron.

in iron deficiency anemia- there’s low transferrin saturation because low iron.

In anemia of chronic dx, there ls also low to normal because of either less iron available to

In hemochromatosis - there’s high transferrin saturation because there’s a lot of iron bound to these receptors.

9
Q

alpha and beta thalassemia traits have

A

normal to increased total iron and ferritin due to high cell turnover. But total iron binding capacity is normal

10
Q

Thalassemia trait will have a MCV that is ???

A

MCV<70

11
Q

Iron deficiency will have

A

low iron, low ferritin and increased total iron binding capacity and MCV<80 and elevated MCV

12
Q

hemoglobin analysis in alpha thalassemia trait

A

no therapy and normal Hgb analysis

13
Q

chart for thalassemias

A
14
Q

Fe deficiency anemia vs. thalassemia chart

A
15
Q

What does this peripheral smear show?

A

See microcytic, hypochromatic RBCs - microcytic anemia includes Fe deficiency, thalassemia, anemia of chronic dx. Likely Fe because high RDW

16
Q

Chart comparing all the microcytic anemia parameters.

A
17
Q

What causes Fe deficiency?

A

blood loss (Gi or menstral bleeding).

Decreased GI absorption of iron (celiac dx or inflammatory bowel dx, or bariatric surgery)

18
Q

Can give EPO for anemia if

A

undergoing chemotherapy and has Hgb <10 and are asympotmatic.

But use cautiously because increases risk for VTE and cardiovascular complications.

19
Q

Cancer related anemia and management

A

since anemia could be result of Fe deficiency, chemo induced myelosuppression or increased RBC destruction from tumor induced hemolysis (mAHA or autoimmune)

Best to recheck CBC at next visit as long not symptoatmic and Hgb >10

20
Q

Chart of common RBC abnormalities seen on peripheral smear

A
21
Q

Iron deficiency is defined as

What is the goal iron replacement for pts who are on dialysis or ESRD?

A

transferrin saturation<20%, ferritin <100 and (<200 in dialysis pts), and needs to be treated prior to starting EPO

Goal is to reach 20-50% transferrin saturation and 200-500 for ferritin

22
Q

Goal iron replacement for FE defiiciency anemia in CKD and ESRD pt

A

Goal is to reach 20-50% transferrin saturation and 200-500 for ferritin

23
Q

target level for EPO is to increase Hemoglobin to

A

10-11

helps improve physiological parameters and improves quality of life.

>12 adds little benefit and increases mortality and morbidity with stroke, hypertension and vascular access thrombosis.

24
Q

spherocytes can occur in

A

autoimmune hemolytic anemia, clostridial sepsis, snake bites, G6PD dehydrogenase deficiency, MAHA and hereditary spherocytosis

25
Q

if you see spherocytosis, what lab test do you have to order?

A

direct antiglobulin test (DAT)

helps to differentiate between two conditiosn of hereditary spherocytosis and AIHA

26
Q

hereditary spherocytosis is seen with:

A

due to atlered genes for encoding RBC membrane proteins which leads to instability and phagocytosis by spleen.

Autosomal dominant.

See chronic hemolytic anemia, jaundice and splenomegaly and can see increased folate requirement and see bilirubin gallstone formation.

27
Q

hereditary spherocytosis labs:

how is it diagnosed?

A

elevated MCV and increased RDW

can show spherocytosis in varying degrees depending on disease severity

Diagnosis is confirmed by flow cytometery with eosin5 maleimide binding or acidified glycerol lysis test.

28
Q

Treatment of hereditary spherocytosis

A

folic acid supplmentaion

transfusion for symptomatic anemia

splenectomy for severe cases.

29
Q

what is transferrin saturation?

A

iron / TIBC x 100

30
Q

CKD levels of goal iron replacement

A

transferrin saturation level >30%

serum ferritin >500 ng/ml

replace with IV or oral iron

transferrin saturation level is (Fe/TIBC x100)