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Hematology-Exam 1 > Hypoproliferative Anemias > Flashcards

Hypoproliferative Anemias Flashcards

1
Q

What retic index or absolute retic count indicates hypoproliferative anemia?

A

Retic index < 2% or ARC <75,000

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2
Q

Group of disorders characterized by a defect in DNA synthesis whose cells have a immature nuclei but a mature cytoplasm

A

megaloblastic anemias

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3
Q

B12 and folate deficiency are the most common causes of which kind of anemia?

A

Megaloblastic anemia

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4
Q

A patient comes in with Anemia,
MCV is elevated, as is RDW
Peripheral smear shows hypersegmented PMNs. What is your differential?

A

Megaloblastic Anemia

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5
Q

What non hematologic features are only seen with B 12 deficiency and not with Folate deficiency?

A

Neuro/psychiatric features

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6
Q

Humans are fully dependent on B12 in diet that are found only in

A

animal products

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7
Q

B12 binds to what protein in the mouth?

A

salivary R protein

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8
Q

Parietal cells secrete what molecule to aid in B12 absorption ?

A

intrinsic factor

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9
Q

What proteins free B12 as it travels from the stomach to the small intestine?

A

pancreatic enzymes

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10
Q

Intrinsic factor binds free B12 and the B12-IF complex taken up by cells in which part of the small intestine?

A

distal ileum

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11
Q

B12 is carried by what protein/enzyme in the blood to the tissues?

A

Transcobalamin II

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12
Q

also known as vitamin B12 deficiency anemia, is a disease caused by destruction of gastric parietal cells (therefore no intrinsic factor)?

A

Perncious anemia

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13
Q

What are the main causes of B12 deficiency?

A
  1. Inadequate consumption (vegan diet)
  2. Inadequate absorption (pernicious anemia, gastric bypass, drugs)
  3. Reduced B12 absorption in the ileum (Chron’s disease, sprue (celiac), metformin)
  4. Competition for B12 (fish tapeworm, bacterial overgrowth)
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14
Q

What are some neurologic changes/signs of B12 deficiency?

A

loss of vibration and position sense in toes due to neurologic changes

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15
Q

Macrocytosis, hypersegmented PMNs, pancytopenia, elevated bili and markedly elevated LDH are lab findings of

A

B12 deficiency

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16
Q

What is pancytopenia

A

low counts of all three blood cell types: platelets, WBC, RBC

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17
Q

What other laboratory testings can be done to confirm B12 deficiency?

A

Homocysteine and methylmalonic acid

18
Q

What are the differences in the absorption of B12 and folate?

A

Folate is absorbed throughout the small intestine without any specific transport protein
B12 is absorbed at the distal end of the ileum and depends on multiple enzymes such as:salivary R, intrinsic factor from parietal cells, and pancreatic enzymes

19
Q

What is our main source of folate?

A

its mainly found in uncooked green leafy vegetables but the government has fortified all of our food with it

20
Q

How does one become folate deficient?

A
  • malnutrition (most common cause)
  • biliary (tube in the bile) drainage causes profound folate deficiency that occurs within hours because folate is concentrated in bile
  • People who need to make lots of DNA can also become folate deficient like pregnant women, people with hemolytic anemias, and anything that can activate cell turnover like psoriasis.
  • drugs can also interfere with metabolism
21
Q

Absolute neutrophil count (ANC) <500/uL
Platelet count <50,000
Absolute reticulocyte count <50,000
Whats on your differential for a patient with this workup?

A

Pancytopenia caused by a severe aplastic anemia

22
Q

What does bone marrow biopsy of pancytopenia due to aplastic anemia show?

A

hypocellularity due to lack of hematopoietic stem cells

23
Q

True or False: Aplastic Anemia is an autoimmune condition

A

True

24
Q

Ionizing radiation, cytotoxic chemotherapy, benzene exposure, EBV, hepatitis, PNH are secondary causes of

A

Aplastic Anemia

25
Q

What is one must testing to do before diagnosing someone with AA?

A

Bone Marrow Biopsy

26
Q

Heavy duty T-cell directed immunosuppression with antithymocyte globulin (ATG) and cyclosporine is used to treat which anemia?

A

Older patients with aplastic anemia

27
Q

Stem cell transplantation is used to treat aplastic anemia in

A

younger patients

28
Q

This form of stem cell transplantation allows us to give cytotoxic therapy in doses that surpass the usual dose limiting toxicity (which is marrow damage), allows for a graft vs tumor effect in some cases, may be a source of un-damaged stem cells (for AA), Can be a source of normal genes (eg thalasssemia major or sickle cell)

A

Allogenic transplant

29
Q

This form of stem cell transplantation allows us to give cytotoxic therapy in doses that surpass the usual dose limiting toxicity (which is marrow damage),

A

Autologous transplant

30
Q

An acquired clonal hematologic disorder that can be the secondary cause of Aplastic Anemia?

The abnormal clone is missing the gene for PIG-A

A

Paroxysmal Nocturnal Hemoglobinuria (PNH)

31
Q

In patients with Paroxysmal Nocturnal Hemoglobinuria (PNH) which two important proteins are missing from the surface of their RBC?

A

CD55 and CD59

32
Q

What is drug of choice for patients with Paroxysmal Nocturnal Hemoglobinuria (PNH)?

A

eculizumab

33
Q

The most common form of inherited aplastic anemia is?

A

Fanconi’s anemia

34
Q

What is the pattern of inheritance of Fanconi’s anemia?

A

AR or x-linked

*common in Jews

35
Q

What is the mechanism of Fanconi’s anemia?

A

DNA repair defect leading to bone marrow failure

36
Q

Which anemia is diagnosed by culturing lymphocytes or fibroblasts with diepoxybutane (DEB) and looking for abnormal (increased) chromosomal breakage?

A

Fanconi’s anemia

37
Q

Progressive pancytopenia with macrocytic anemia, short stature, café-au-lait macules, and hypo plastic thumbs are present in which anemia?

A

Fanconi’s anemia

38
Q

Inherited disorder of telomere shortening involving one of 9 genes. Also an inherited form of AA

A

Dyskeratosis congenita

39
Q

This Classic triad is seen in which disorder?

  1. Mottled hyperpigmentation of skin involving arms, shoulders, neck, torso
  2. Abnormal nails of fingers and toes
  3. Mucosal leukoplakia
A

Dyskeratosis congenita

40
Q

What is the treatment for Dyskeratosis congenita?

A

allogeneic transplant

Hematology-Exam 1 (12 decks)

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