Lab 1: Anemia Flashcards

1
Q

ID

A

Iron Deficiency Anemia (IDA)

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2
Q

ID

A

Iron Deficiency Anemia (IDA) - microcytic RBCs (smaller than lymphocytes), increased central palor (hypochromic), Echinocytes (Burr cells - no indicative of IDA)

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3
Q

In Iron Defeciency Anemia what are some main causes of the anemia?

A

chronic blood loss (elderly with risk of colon cancer), and malnutriton

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4
Q

Children <12 months old who drink a lot of cow milk are a group at risk for:

A

Iron Deficiency Anemia (IDA)

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5
Q
A

D

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6
Q

What test results would you expect?

A
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7
Q
A

Anemia of chronic disease

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8
Q

Additional laboratory studies are obtained, would you expect an increase of decrease in these values?

A
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9
Q

What is the role of hepcidin in Anemia of chronic disease

A

Hepcidin increases in the setting of inflammation (like a patient with rheumatoid arthritis). When hepcidin is high, the iron transporter ferroportin is degraded. Ferroportin is found on duodenal epithelial cells and macrophages. This leads to
two major consequences: 1. Iron is not absorbed into the peripheral blood from duodenal epithelial cells and cannot be transported to tissues by transferrin and 2. Iron is not released from its storage site in macrophages. This creates the unusual situation of a patient having large amounts of stored iron (ferritin in macrophages) but low levels of iron available to RBC precursors for making hemoglobin, leading to anemia

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10
Q

A 58-year-old male has become progressively more fatigued at the end of the day. This has
been going on for months. In the past month, he has noticed numbness in his hands
(paresthesia). A CBC and peripheral blood smear demonstrate the findings below.

A

Vitamin B12 deficiency

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11
Q

ID

A

macrocytic anemia (either B12 or folate deficiency) - need clinical vignette to ID

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12
Q
A

lead poisoning

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13
Q

what two enzymes are inhibited by lead?

A

δ-ALA dehydratase and
ferrochelatase

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14
Q

What physical signs and symptoms can you look for in lead poisoning?

A

“lead lines” in bones and gingiva (lines of increased bone density on radiograph, hyperpigmented lines in
gingiva)

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15
Q

ID

A

Spherocytosis - Increased numbers of spherocytes, which are round RBCs without discernable
central pallor. There are also increased RBCs with polychromasia (lavender hue to their
cytoplasm)

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16
Q
A

Spherocytosis- Hemolytic Anemia

17
Q

What other laboratory studies would be helpful to support a diagnosis of hemolytic anemia

A

LDH - increased
Haptoglobin - Decreased (binding to free hemoglobin that was lysed)
Bilirubin - Increased
Reticulocyte count - Increased

18
Q

What is the inheritence pattern for Spherocytosis?

A

Autosomal Dominant (AD)

19
Q
A
20
Q

In sickle cell disease a _______ in oxygen leads to sickling

A

decrease - when altitude changes you see sickle crisis

21
Q

Chloroquine or other anti-malarial drugs can produce an oxidant stress that leads to episodic
hemolysis in patients

A

G6PD Deficiency

22
Q

What surgical treatment might be considered for a patient if their hemolytic anemia is severe enough?
What would the surgical treatment put her at risk for in the future? How would the surgical
treatment affect the appearance of her RBCs on a peripheral smear

A

Splenectomy could be considered for this patient if her anemia was severe. Post-splenectomy,
she is at increased risk of infection and would need to be (re)vaccinated against encapsulated
organisms (such as Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis). Normally the spleen
filters these bacteria and decreases the risk of infection.
After a splenectomy, her RBCs may include Howell-Jolly bodies, which are nuclear remnants
that are typically removed from RBCs by the spleen (but can’t be removed when the spleen is
not there). Her peripheral smear would still include spherocytes, though her hemolytic anemia
would be resolved post-splenectomy.

23
Q

ID

A

Howell-Jolly bodies (nuclear remnants)

24
Q
A

Sickle Cell Disease

25
Q

ID

A

Sickle Cell Disease

26
Q

What are the clinical symptoms of the vaso-occlusive crises that characterize Sickle Cell Disease?

A

Vaso-occlusive crises (pain crises) are due to episodic hypoxic injury and infarction that cause
severe pain in affected tissues. Vaso-occlusive crises may be triggered by factors that favor
RBC sickling (infection, dehydration, acidosis), or may not have a clear precipitating factor

27
Q

Why does alpha thalassemia, in general, show a less severe phenotype than beta thalassemia?
What would you expect to see if a patient had both β gene variants and α gene variants?

A

If patients have both β and α globin variants leading to decreased production of both β and α
chains, the hemolytic anemia and ineffective erythropoiesis is typically less than that seen with
only β or only α gene variants. With defects in both types of globin chains, the imbalance in α
and β chains is lessened, leading to fewer opportunities for insoluble globin precipitate
formation

28
Q
A

normocytic anemia and thrombocytopenia,

29
Q

ID

A

Microangiopathic hemolytic anemia (MAHA) - schistocytes in the setting of anemia and thrombocytope

Schistocytes - general term for any fragmented red blood cell which can take on various shapes
Helmet Cells - larger, crescent-shaped schistocyte with a distinct, flat, amputated area

30
Q

What laboratory tests would be helpful to sort out the differential diagnosis for Microangiopathic hemolytic anemia (MAHA)

A

Laboratory tests to consider include D-dimer, fibrinogen activity, PT, aPTT, ADAMTS13 activity for TTP, and shiga-like toxin for HUS

31
Q

marked
elevation of D-dimer is an important laboratory test to clue to

A

Disseminated Intravascular Coagulation (DIC)

32
Q

The best treatment for DIC is:

A

identify and treat the underlying condition (whether
it’s cancer, sepsis, trauma, obstetric complications, etc.)

33
Q

ID

A

Bite Cell - G6PD Deficiency

34
Q

ID

A

Heinz Bodies (denatured hemoglobin) - removed by macrophages and why we see bite cells

35
Q

ID

A

ringed sideroblasts

36
Q

ID

A

Pseudo-Pelger-Huet Cells (top and bottom field seen in Myeldysplastic Syndrome)

37
Q

ID

A

Essential Thrombocytosis - platelets the size of red cells

38
Q

ID

A

Aplastic Anemia