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Hemolytic Anemia Flashcards

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1
Q

What is hemolytic anemia?

A

Decreased RBC survival usually defined as <100 d from increased destruction of the cells leading to decrease in Hgb concentration.

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2
Q

What are the classifications of hemolytic anemia?

A
  • Hereditary
  • Acquired
  • Intravascular
  • Extravascular
  • Acute
  • Chronic
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3
Q

What are the common causes of autoimmune hemolytic anemia (AIHA)?

A
  • Warm AIHA
  • Cold AIHA
  • Alloimmune: post-transfusion
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4
Q

What are the manifestations of hemolytic anemia?

A
  • Anemia symptoms
  • Manifestations of the cause of hemolysis
  • Manifestations of hemolysis
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5
Q

What is the role of reticulocytes?

A

Markers of erythrocyte production, indicating active bone marrow.

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6
Q

What is the normal peripheral reticulocyte count?

A

0.5-1.5% of total RBCs.

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7
Q

What indicates reticulocytosis in hemolytic or acute blood loss anemia?

A

Reticulocytosis > 2%.

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8
Q

What are the classical laboratory findings in hemolytic anemia?

A
  • ↓ Hemoglobin
  • ↑ Lactate dehydrogenase
  • ↑ Unconjugated bilirubin
  • ↑ Reticulocytes
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9
Q

What are the main types of hemoglobin abnormalities?

A
  • Quantitative abnormalities
  • Qualitative abnormalities
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10
Q

What is thalassemia?

A

Heterogeneous group of disorders due to an imbalance of alpha and beta globin chain synthesis.

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11
Q

What is the clinical feature of thalassemia major?

A

Symptoms detectable since the first year of life due to severe anemia.

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12
Q

What are the signs of thalassemia major?

A
  • Paleness
  • Growth retardation
  • Hepatosplenomegaly
  • Iron overload signs
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13
Q

What is the management for beta thalassemia major?

A
  • Transfusion (life long)
  • Iron chelation therapy
  • Myeloablative hematopoietic stem cell transplantation
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14
Q

What mutation causes sickle cell anemia (SCA)?

A

Point mutation at codon 6 of β chain globin gene (βs).

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15
Q

What are the types of acute crises in sickle cell disease?

A
  • Aplastic crises
  • Splenic sequestration crises
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16
Q

What does hemoglobin electrophoresis show in sickle cell disease?

A

Presence of Hgb S.

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17
Q

What is the definition of MAHA?

A

Microangiopathic hemolytic anemia.

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18
Q

What are the causes/types of MAHA?

A
  • Thrombotic microangiopathy (TMA)
  • DIC
  • HUS
  • TTP
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19
Q

What are the components required for erythropoiesis?

A
  • Folic acid
  • Iron (Ferrous)
  • Vitamin B12
  • Erythropoietin
  • Amino acids
  • Minerals
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20
Q

What is the significance of reticulocyte count in anemia diagnosis?

A

Indicates bone marrow activity in response to anemia.

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21
Q

True or False: Hemolytic anemia can be caused by mechanical heart valves.

A

True.

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22
Q

What is the implication of increased indirect bilirubin in hemolytic anemia?

A

Indicates increased RBC destruction.

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23
Q

Fill in the blank: Hemoglobin abnormalities can lead to _______ anemia.

A

[hemolytic]

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24
Q

What is a common laboratory finding in patients with thalassemia major?

A

Increased indirect bilirubin.

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25
What is the definition of hereditary hemolytic anemia?
Hemolytic anemia due to hemoglobin disorder, membrane disorder, or enzyme disorder.
26
What are the two types of hereditary hemolytic anemia based on membrane disorder?
* Spherocytosis * Elliptocytosis
27
What is the typical blood smear finding in thalassemia carriers?
Mild microcytic hypochromic anemia.
28
What are the signs of iron overload in patients with thalassemia major?
* Hemochromatosis * Iron-induced organ damage
29
What is the expected reticulocyte count in iron or B12 deficiency anemia?
Reticulocytopenic < 2%.
30
What is the role of haptoglobin in hemolytic anemia?
Decreased haptoglobin indicates intravascular hemolysis.
31
What is sickle cell disease characterized by?
Painful swelling of hands and feet (dactylitis) and hemolysis.
32
What is the typical presentation of beta thalassemia major?
Severe anemia, jaundice, and splenomegaly.
33
What is a key feature of hereditary spherocytosis?
Abnormal RBC membrane leading to increased fragility.
34
What is Congestive heart failure?
A condition where the heart is unable to pump effectively, leading to a buildup of fluid in the lungs and other body parts.
35
What is marrow hyperplasia?
An increase in the number of cells in the bone marrow, often in response to increased demand for blood cells.
36
What are the types of acute crisis in SCD?
* Aplastic crises * Splenic sequestration crises * Vaso-occlusive crises (infarction) * Acute chest syndrome * Acute hemolytic crisis
37
What is the most common cause of hospitalization for SCD patients?
Painful vaso-occlusive crises
38
What can precipitate painful vaso-occlusive crises?
* Infections * Dehydration * Rapid change in temperature * Pregnancy * Menses * Alcohol
39
What are the common clinical features of painful vaso-occlusive crises?
* Severe bone and muscle pain * Fever * Leukocytosis
40
What treatment is used to enhance production of HbF in SCD?
Hydroxyurea
41
What is the role of folic acid in SCD treatment?
To prevent folate deficiency
42
What is the primary aim of vaccinations in childhood for SCD patients?
To prevent infections such as pneumococcus, meningococcus, and H. influenzae type b
43
What is hereditary spherocytosis?
The most common type of hereditary hemolytic anemia, characterized by spherical red blood cells.
44
What is the inheritance pattern of hereditary spherocytosis?
Autosomal dominant
45
What is a common clinical presentation of hereditary spherocytosis?
* Anemia * Fatigability * Jaundice * Splenomegaly
46
What is the osmotic fragility test used for?
To diagnose hereditary spherocytosis by assessing the RBCs' response in a hypotonic solution.
47
What are the possible complications of hereditary spherocytosis?
* Gallstone formation * Aplastic crisis due to viral infection (e.g., parvovirus B19)
48
What is the treatment for severe anemia in hereditary spherocytosis?
Blood transfusion
49
What is G6PD deficiency?
A deficiency in glucose-6-phosphate dehydrogenase leading to RBC sensitivity due to oxidative stress.
50
What are common triggers for hemolysis in G6PD deficiency?
* Oxidative stress * Infection * Certain drugs (e.g., sulfonamides, antimalarials) * Food (e.g., fava beans)
51
What is the main therapeutic approach for G6PD deficiency?
Avoiding oxidative stress
52
What is autoimmune hemolytic anemia?
Anemia resulting from the production of antibodies against RBCs.
53
What are the symptoms of autoimmune hemolytic anemia?
* Weakness * Pallor * Tachycardia * Jaundice * Hemoglobinuria
54
What is the Coombs test used for?
To diagnose autoimmune hemolytic anemia
55
What is Paroxysmal Nocturnal Hemoglobinuria (PNH)?
A clonal stem-cell disorder characterized by RBC membrane defects leading to hemolysis.
56
What are the common clinical presentations of PNH?
* Anemia * Hemoglobinuria * Thrombosis of major venous structures
57
What is the primary treatment for severe hemolysis in autoimmune hemolytic anemia?
Steroids
58
What are schistocytes?
Fragmented red blood cells seen in conditions of hemolysis.
59
What does the presence of low haptoglobin indicate?
Intravascular hemolysis
60
What is Thrombotic Microangiopathy (TMA)?
A condition characterized by occlusive microvascular thrombus formation and hemolysis.
61
What are the pathological features of TMA?
* Vessel wall thickening * Swelling and detachment of endothelial cells * Intraluminal platelet thrombosis
62
What is the significance of increased LDH and bilirubin in hemolysis?
Indicates increased destruction of red blood cells.
63
What is Intravascular hemolysis associated with?
Hemoglobinuria increase (bilirubin, LDH, Retics count) ## Footnote Decreased haptoglobin, Schistocytes by blood film, and thrombocytopenia are also indicators.
64
What test result indicates hemolysis caused by mechanical destruction?
Negative Coomb test ## Footnote This indicates that it is not immune-mediated hemolysis.
65
What coagulation factors are normal in thrombosis not dependent on coagulation factor?
Normal PT and PTT and fibrinogen ## Footnote Thrombocytopenia is observed at the site of microangiopathy.
66
What are the two primary forms of TMA?
1. TTP 2. HUS ## Footnote Secondary TMA causes include malignant hypertension, pregnancy-associated (HELLP), DIC, autoimmune/vasculitis, cancer, and drugs (e.g., ticlopidine).
67
What is the pathogenesis of TTP?
Deficiency of metalloproteinase that breaks down ultra large VWF multimers: ADAMTS-13 ## Footnote This can be congenital (genetic absence of ADAMTS-13) or acquired (drugs, malignancy, transplant, HIV).
68
List the clinical features of TTP.
1. Thrombocytopenia 2. MAHA/TMA 3. Neurological symptoms (headache, confusion, focal defects, seizures) 4. Fever 5. +/- renal failure
69
What laboratory findings are indicative of TTP?
1. Decreased platelets 2. Increased schistocytes 3. Normal PT, PTT, and fibrinogen 4. Increased unconjugated bilirubin 5. Increased LDH 6. Decreased haptoglobin 7. Negative Coombs test/DAT
70
What is the mortality rate of untreated TTP?
~90% ## Footnote This highlights the importance of prompt treatment.
71
What is the first-line treatment for TTP?
Plasma exchange ± steroids ## Footnote Platelet transfusion is avoided unless there is a life-threatening bleed.
72
What is a common cause of HUS?
Shiga toxin (E. coli serotype O157:H7) in 90% of cases ## Footnote Other bacteria and viruses can also be involved.
73
List the clinical features of HUS.
1. Severe thrombocytopenia 2. MAHA/TMA 3. Acute kidney injury 4. Bloody diarrhea 5. GI prodrome
74
What laboratory findings are indicative of HUS?
1. Decreased platelets 2. Increased schistocytes 3. Normal PT, PTT, and fibrinogen 4. Increased unconjugated bilirubin 5. Increased LDH 6. Decreased haptoglobin 7. Negative Coombs test/DAT 8. High creatinine and urea
75
What is the treatment for HUS?
Fluids, RBC transfusion, nutrition, etc. ## Footnote Some evidence for plasma exchange; possible role of eculizumab (C5 Ab blocks complement activation) for neurologic symptoms.
76
What is the predominant demographic for immune TTP?
Adults ## Footnote Congenital form predominantly presents in children.
77
What is the predominant demographic for HUS?
Children and elderly

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