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Clinical Med I > Exam 4 - Anemia Part II > Flashcards

Exam 4 - Anemia Part II Flashcards

1
Q

What can cause a falsely elevated MCV?

A
  • Large number of reticulocytes

- RBC clumping mimicking larger RBC

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2
Q

What deficiencies cause macrocytic anemia?

A

B12 and folate deficiencies

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3
Q

What causes reticulocytosis?

A

Hemorrhage and hemolysis

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4
Q

What is the average daily requirement of folate? What about in pregnancy?

A
  • average is 200-400 micrograms daily

- when pregnant, breast feeding, or trying to conceive recommended about is 400-800

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5
Q

What is the etiology of folate deficiency?

A

Alcoholism, hemodialysis, elderly, anticonvulsant therapy, malabsorption, and hemolytic anemias

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6
Q

What can a deficiency of folic acid in pregnancy lead to?

A

Neural tube defects

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7
Q

What is considered low serum folate?

A

Less than 150 ng/mL

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8
Q

In folic acid deficiency, is homocysteine, serum methylmalmonic acid (MMA), or both elevated?

A

Homocysteine is elevated. MMA is normal

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9
Q

In B12 deficiency, is homocysteine, serum methylmalmonic acid, or both elevated?

A

Both are elevated

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10
Q

What will you see on a peripheral smear in folic acid deficiency?

A

Macro-ovalocytes, hypersegmented neutrophils

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11
Q

What is the treatment for folic acid deficiency?

A
  • Treat underlying cause
  • replacement therapy with 1g PO daily
  • Rule out B12 deficiency
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12
Q

What is the most common cause of B12 deficiency?

A

Inability to absorb

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13
Q

What is the only source of B12 for the body?

A

The diet, present in all animal products

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14
Q

What is the daily B12 requirement?

A

1-2 micrograms

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15
Q

How does B12 get absorbed?

A

It binds to intrinsic factor (IF) in the stomach, released from IF in the ileum where it is absorbed, and then stored in the liver.

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16
Q

What are the common causes of B12 deficiency?

A
  • Pernicious Anemia (most common)
  • Decreased intake (vegan diet)
  • Medications. (Metformin, H2 antagonists, PPIs)
  • Malabsorption (elderly)
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17
Q

What is Pernicious Anemia?

A

An immune disorder that causes the destruction of gastric parietal cells that release intrinsic factor (B12 cannot be absorbed)

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18
Q

What are the common symptoms with B12 Deficiency?

A
  • glossitis, GI symptoms
  • Ataxia
  • Paresthesias
  • Confusion
  • Defective myelin synthesis in the CNS

**these neuro symptoms are reversible IF it is treated within 6 months

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19
Q

What is an MCV of greater than 115 almost always indicative of?

A

Folate or B12 deficiency

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20
Q

What will you see on a peripheral smear with B12 deficiency?

A
  • Hypersegmented neutrophils
  • Anisocytosis
  • Macro-ovalocytes
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21
Q

What is the treatment for B12 deficiency?

A
  • Parenteral B12 (daily IM/SQ injections of 1000micrograms for 1 wee, then weekly for one month, the monthly for life)
  • Treat reversible causes
  • Monitor K+ with treatment
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22
Q

Why is it EXTREMELY important to differentiate between folate and B12 deficiency?

A

-Folate replacement will correct the abnormal labs in a B12 deficiency. But if B12 is not also replaced, the patient may develop serious and irreversible neurological damage called subacute combined degeneration of the spinal cord.

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23
Q

What is the normal lifespan for RBCs?

A

120 days

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24
Q

Bone marrow can compensate for shortened RBC life up until when?

A

20 days

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25
Q

What are the common symptoms with hemolytic anemia?

A
  • Typical anemia symptoms
  • Jaundice if hemolysis is fast enough
  • gallstones
  • dark urine
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26
Q

Anemia with increased reticulocyte count, polychromasia, increased unconjugated bilirubin, and increased serum lactate dehydrogenase is seen in what kind of anemia?

A

Hemolytic anemia

27
Q

What will you seen in a peripheral smear of hemolytic anemia?

A
  • Immature RBCs, nucleated RBCs

- Schistocytes (fragmented RBCs)

28
Q

What are the tests that can help distinguish between hemolytic anemia?

A

Direct antiglobin (Coombs) test and DAT

29
Q

What is extravascular hemolysis?

A

Destruction of the RBCs in the reticuloendothelial system

30
Q

Is serum haptoglobin in intravascular hemolysis increased or decreased? Why?

A

Decreased. It binds to hemoglobin released from lysed RBCs and this decreases the free haptoglobin

31
Q

What is G6PD?

A

An enzyme that is essential for ensuring the normal lifespan of RBCs by protecting against oxidative stress

32
Q

What will you see on peripheral smear in a G6 PD deficiency?

A
  • Bite cells

- Heinz bodies

33
Q

What is the treatment for G6PD deficiency?

A
  • Hemolytic episodes are self limited as red cells are replaced
  • Oxidative drugs should be avoided
34
Q

What are the main causes of oxidative stress is a G6 PD deficient individual?

A
  • Drugs
  • Infections
  • Fava beans
35
Q

What is hereditary spherocystosis?

A

An autosomal dominant disorders with mild hemolytic anemia.

-Caused from an intrinsic defect in the RBC membrane/cytoskeleton

36
Q

What happens to the RBCs in a patient in hereditary spherocytosis?

A
  • RBCs maintain a normal MCV, but a smaller surface area so they have a dense and globular appearance and lack central pallor.
  • They are poorly deformable, get trapped in the splenic sinusoids, and then phagocytized.
37
Q

What are the common symptoms seen in Hereditary spherocytosis?

A
  • Often asymptomatic
  • Mild jaundice or sclera icterus
  • Gallstones
  • splenomegaly
  • Chronic hemolysis creates need for increased folate
38
Q

What is the test for hereditary spherocytosis?

A
  • Osmotic fragility test: RBCs demonstrate increased hemolysis on exposure to hypotonic fluid due to RBC membrane defect
  • Coombs is negative
39
Q

What is the treatment of choice for severe hereditary spherocytosis?

A

Splenectomy

40
Q

What is sickle cell disease?

A

A hereditary disorder of hemoglobin structure transmitted though an autosomal recessive gene.

41
Q

What is the most common feature of sickle cell disease?

A

Pain crisis

42
Q

What are the life threatening features of sickle cell anemia?

A

Hemolytic or aplastic crises

43
Q

What is the best test to confirm diagnosis of sickle cell?

A

Hub electrophoresis reveals Hb S

44
Q

What does a peripheral smear of sickle cell show?

A

A few sickled RBCs, nucleated RBCs, target cells, Howell Jolly bodies and thrombocytosis

45
Q

What is the treatment of sickle cell?

A
  • Avoid precipitating factors
  • Analgestics, fluids, oxygen
  • RBC transfusion if needed
  • Hydroxyurea to decrease incidence of painful crises
  • Bone marrow transplant
46
Q

What causes Autoimmune hemolytic anemia (AIHA)?

A

Autoantibodies that adhere to the surface of RBCs and induce hemolysis by fixing complement and damaging the cell membrane. RBCs with antigen-antibody complex are phagocytized by macrophages and spherocytes are formed which are destroyed by the spleen.

47
Q

What are the two types of antibodies associated with AIHA?

A
  • IgM: “cold” agglutinins, generally more acute

- IgG: “warm agglutinins, attacks RBCs at normal body temp

48
Q

What are patients with AIHA at higher risk for?

A

Venous thromboembolism

49
Q

What are the symptoms associated with AIHA?

A
  • Typical anemia symptoms
  • Fever, fatigue, weakness
  • Lymphadenopathy
  • Hemoglobinurea
  • Acrocyanosis
50
Q

What diagnostic test is positive with AIHA?

A

Positive Coombs test (DAT)

51
Q

How is cold AIHA treated in children?

A

It usually is not treated in children because it is normally viral and self limited

52
Q

How is warm AIHA treated?

A
  • Corticosteroids are first line
  • Rituximab: antibody that targets B cell lymphocytes
  • Splenectomy
  • Immunosuppressants
53
Q

How is cold AIHA treated in adults?

A
  • Avoid cold exposure
  • Rituxumab
  • Plasmapheresis if refractory
54
Q

What is intravascular hemolysis?

A

Destruction of RBCs within the blood stream

55
Q

What is paroxysmal nocturnal hemoglobinurea?

A

-Rare acquired stem cell mutation, complement mediated RBC lysis

56
Q

What are the symptoms of paroxysmal nocturnal hemoglobinurea?

A
  • Hemolytic anemia
  • Dark cola colored urine at night and morning with clearing during the day
  • venous thrombosis of large vessels
  • Pancytopenia
57
Q

How is Paroxysmal nocturnal hemoglobinurea diagnosed?

A
  • Flow cytometry
  • osmotic fragility test
  • Coombs negative
58
Q

How is paroxysmal nocturnal hemoglobinurea treated?

A
  • Monoclonal antibody against complement C5
  • Steroids
  • Stem cell transplant
59
Q

What is the treatment for hemolysis?

A
  • Identify and treat the underlying cause
  • corticosteroids
  • splenectomy
  • Folic acid supplementation
60
Q

What is aplastic anemia?

A

An acquired abnormality of hematopoietic stem cells. May be total, or selective for RBCs, WBCs, or platelets

61
Q

What are the common causes of aplastic anemia?

A
  • Over 50% are idiopathic
  • 20% due to drug or chemical exposure
  • 10% viral illness
62
Q

What is the hallmark feature of aplastic anemia?

A

Pancytopenia

63
Q

What is the treatment of aplastic anemia?

A
  • Identify cause and eliminate it if possible
  • hematology Referral
  • transfusions PRN
  • Bone marrow transplant is the preferred treatment.

Clinical Med I (24 decks)

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