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Hematology Exam 3 > 8 - Overview of Hematological Pathology > Flashcards

8 - Overview of Hematological Pathology Flashcards

1
Q

8.4 - What is anemia?

A

A reduction in one or more of the major red blood cell measurements:

  • Hemoglobin concentration
  • Hematocrit
  • RBC count
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2
Q

8.4 What are the signs and symptoms of anemia?

A
  1. Tiredness/fatigue/exercise intolerance
  2. Fainting
  3. Shortness or breath
  4. Pallor
  5. Tachycardia/Palpitations
  6. Worsening of angina
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3
Q

8.4 What groups would more likely have signs and symptoms of anemia?

A
  1. Those with severe anemia
  2. Elderly
  3. Sudden Drop in HgB concentration
  4. Other co-existing pathologies, e.g. cardiorespiratory disease
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4
Q

8.4 What groups are less likely to have signs and symptoms of anemia?

A
  1. Mild anemia
  2. Younger patients
  3. Gradual drop in HgB concentration
  4. Absence of other disease
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5
Q

8.5 Acquired anemias include those that are due to:

A
  1. Specific deficiencies (e.g. iron, vitamin B12, folate)
  2. Blood loss (e.g. acute or chronic)
  3. Chronic disease (e.g. chronic infections such as tuberculosis, osteomyelitis; chronic diseases such as rheumatoid arthritis, lupus; malignancy; and renal failure)
  4. Hemolysis (e.g. AIHA - acquired autoimmune hemolytic anemia)
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6
Q

8.6 What is the most common cause of anemia worldwide?

A

Iron deficiency

Iron is a key component of hemoglobin, and without iron there is a defective synthesis of hemoglobin, resulting in RBCs that are both microcytic (MCV is decreased) and hypochromic (MCH and MCHC decreased).

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7
Q

8.6 What kind of RBC’s result from iron deficient anemia?

A

RBCS are both microcytic (MCV decreased) and hypochromic (MCH & MCHC decreased).

Pencil cells may also be seen (unbalanced surface membrane to cytoplasmic volume).

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8
Q

8.6 How does iron deficient anemia affect cell division?

A

A reduced rate of hemoglobin synthesis results in more cell division and subsequently smaller cells. Lower levels of hemoglobin in the RBCs make them appear “pale”.

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9
Q

8.8 Where in the body is iron stored and in what form?

A

Iron is stored in the liver as ferritin

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10
Q

8.9 What are four of the causes of iron deficient anemia?

A
  1. Blood loss (either overt or occult)
  2. Decreased iron absorption (problem with GI or a drug impairing iron uptake)
  3. Dietary (vegans and elderly patients)
  4. Increased iron requirements (pregnancy and growth spurts in children)
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11
Q
  1. 10 Vitamin B12 deficient anemia
    - What kind of RBCs are produced?
    - What is this type of anemia sometimes called?
A

Macrocytic RBCs are produced (MCV is elevated) - referred to as “megaloblasts”

“Megaloblastic anemia”

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12
Q
  1. 10 Vitamin B12 deficient anemia
    - How is DNA synthesis of RBC’s affected?
    - How is RNA synthesis of proteins affected?
A

All actively dividing RBCs in the bone marrow require DNA synthesis in order to undergo mitosis. The pathways involve both vitamin B12 and folate.

RNA synthesis is not affected and so protein synthesis continues. Unfortunately, the protein will accumulate over time and the red cells get larger - hence “megaloblasts”

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13
Q

8.11 What are three causes of Vitamin B12 deficiency?

A
  1. Lack of Intrinsic factor (IF)
  2. Dietary (vegans)
  3. Total or partial gastretomy and other stomach procedures (on the rise with more surgical procedures to lose weight)
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14
Q
  1. 12 How does a lack of Instrinsic Factor (IF) lead to Vitamin B12 deficient anemia?
    - What is this form of anemia also called?
    - What can cause decreased IF levels?
A

Lack of IF leads to decreased vitamin B12 absorption - IF binds to B12 to aid in absorption at the ileum

Pernicious anemia

Decreased IF due to autoimmune attack on IF or on parietal cells in stomach (which also produces chronic atrophic gastritis)

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15
Q

8.13 What are good food sources of B12?

A

Eggs, meat, poultry, shellfish, milk, and milk products

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16
Q
  1. 14 Folate deficient anemia
    - What kind of RBC’s are produced?
    - Wat is this type of anemia sometimes called?
A

Macrocytic RBCs are produced (MCV is elevated) - referred to as “megaloblasts”

“Megaloblastic anemia”

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17
Q
  1. 14 Folate deficient anemia
    - How is DNA synthesis of RBC’s affected?
    - How is RNA synthesis of proteins affected?
A

All actively dividing RBCs in the bone marrow require DNA synthesis in order to undergo mitosis. The pathways involve both vitamin B12 and folate.

RNA synthesis is not affected and so protein synthesis continues. Unfortunately, the protein will accumulate over time and the red cells get larger - hence “megaloblasts”

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18
Q

8.14 What are four causes of Folate deficient anemia?

A
  1. Poor nutrition (seen in poverty, elderly, alcoholics)
  2. Increased requirements (pregnancy)
  3. Malabsorption (inflammatory diseases of the intestines
  4. Drugs (which interfere with absorption - anti-epileptics, oral contraceptives)
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19
Q

8.14 Is intrinsic factor a cause of folate deficient anemia?

A

No, as folate does not require intrinsic factor to be absorbed

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20
Q

8.14 What are foods that are rich in folate?

A

Beans and legumes, citrus fruits and juices, whole grains, dark green leafy vegetables, poultry, pork, shellfish, and liver

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21
Q

8.15 What are two general features of blood volume depletion?

A

Increased heart rate and low blood pressure

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22
Q
  1. 15 How does acute blood loss result in anemia?
    - How is hemoglobin concentration affected?
    - How is MCV affected?
    - What is this anemia also described as?
A

After blood loss, extravascular fluid will move to the intravascular space (usually from red bone marrow).

However, hemoglobin concentration will still be normal for the first several hour (because both red cells and plasma are lost).

MCV also remains normal and so the anemia is described as normocytic.

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23
Q
  1. 17 Do we know why most chronic disease anemias (ACD) occur?
    - What kind of anemia do they normally produce?
A

It isn’t clear why most chronic diseases produce anemia.

They normally produce normocytic anemia.

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24
Q

8.17 Why does chronic renal failure cause anemia?

What kind of anemia is associated with this?

A

Because erythropoietin levels will go down and reduce the overall RBC level.

Normocytic anemia

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25
Q
  1. 18 What is hemolytic anemia?
    - Why does this occur?
    - How is RBC destruction and production affected?
    - How do erythropoietin levels factor into this form of anemia?
A

Disorders in which the red blood cells are destroyed faster than normal (reduced lifespan).

This occurs because the bone marrow cannot keep pace with the rate of destruction. RBC lifespan could be 20 days vs 120 days.

This leads to increased RBC destruction and increased RBC production. If erythropoietin is increased sufficiently, the patient may not even become anemic.

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26
Q

8.18 What is an example of a hemolytic anemia?

A

Acquired autoimmune hemolytic anemia (AIHA)

- An autoimmune response directed against the RBCs own antigens.

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27
Q
  1. 19 Hereditary anemias are typically what form of anemia?

- What kind of pathological process can they be classified with?

A

Hereditary anemias are virtually all hemolytic in nature.

May be classified by the pathological process causing decreased RBC lifespan.

28
Q

8.19 What three groups can hereditary anemias be divided into?

A
  1. Red cell membrane (hereditary sphereocytsis, hereditary elliptocytosis)
  2. Red cell enzymes (G6PD deficiency)
  3. Hemoglobin molecules (sickle cell disease, thalassemias)
29
Q
  1. 20 Hereditary spherocytosis (a red cell membrane disorder)
    - Cause?
A

Caused by a variety of molecular defects in the genes that code for spectrin (α and β), ankyrin, band 3 protein, protein 4.2, and other erythrocyte membrane proteins.

30
Q
  1. 20 Hereditary spherocytosis (a red cell membrane disorder)
    - What two red cell indexs are most helpful? Typically elevated or depressed?
    - What does this red cell index reflect?
A

The most helpful red cell index is the mean cell hemoglobin concentration (MCHC), which is routinely elevated. An eleveated red cell distribution width (RDW) also favors diagnosis.

Reflects membrane loss and red cell dehydration.

31
Q
  1. 22 Hereditary elliptocytosis (a red cell membrane disorder)
    - Cause?
    - Result?
A

Caused by a variety of molecular defects in the same genes affected by hereditary sphereocytosis

Cytoskeletal scaffolding of cells is destabilized and hemolysis occurs

32
Q

8.24 What is the Osmotic Fragility Test used for?

A

To detect spherocytosis and elliptocytosis

33
Q

8.24 What is the Osmotic fragility test?

A

Red cells are incubated in NaCl solutions of various strengths and the degree of red cell lysis is measured. Curves are generated for normal and test samples and MCF (mean corpuscular fragility) is measured.

34
Q

8.24 What is mean corpuscular fragility (MCF)?

What types of RBC shapes tend to lyse more readily?

A

The NaCL concentration at which 50% RBC lysis occurs. As the concentration increases and the solution becomes more hypotonic, more RBC’s will lyse.

Spherocytes and elliptocytes lyse more readily due to their lower surface area to volume ratio.

35
Q
  1. 25 What is the most common enzymatic disorder of red blood cells in humans?
    - What kind of genetic inheritance?
A

G6PD Deficiency (a red cell enzyme disorder)

X-linked disorder

36
Q
  1. 25 G6PD Deficiency (a red cell enzyme disorder)

- What is G6PD’s metabolic function?

A

It is the only source of NADPH in red cells and if this is ever disrupted, it affects RBCs. NADPH maintains glutathione in its reduced form (preventing oxide damage).

37
Q
  1. 26 G6PD Deficiency (a red cell enzyme disorder)

- In addition to normal hemolytic anemia symptoms, what other characteristics are present in RBC’s?

A
  1. Heinz bodies - hemoglobin have been rendered unstable due to oxidant damage - a cluster of denatured hemoglobin
  2. Bite cells - Thought to result from the processing of cells through the spleen and the removal of heinz bodies (a small chunk of RBC missing)
38
Q

8.28 What hemoglobin disorder results from a point mutation in the β globin gene?

A

Sickle cell disease

39
Q
  1. 28 Sickle Cell Disease (hemoglobin disorder)
    - What is the genetic result the point mutation?
    - What do you call the faulty hemoglobin produced?
    - Where does this typically occur in the world?
A

Amino acid number 6 changes from Glu to Val.

The resultant hemoglobin produced by the faulty gene is called hemoglobin S (HbS).

Widespread in Africa, Middle East, and parts of India and the Mediterrean

40
Q
  1. 28 Sickle Cell Disease (hemoglobin disorder)

- What is the physiological disorder?

A

RBCs containing the sickle hemoglobin elongate under conditions off reduced oxygenation and form characteristic sickle shaped cells. These RBCs do not flow well through small vessels and are more adherent than normal RBCs to vascular endothlium - leads to vascular occlusion and sickle cell crises.

Sickled RBCs have reduced lifespan and result in chronic hemolysis.

41
Q
  1. 30 Thalassemias (Hemoglobin disorder)
    - What does this group of disorders arise as a result of?
    - How does chronic hemolysis occur?
A

A result of diminished or absent production of one or more of the globin chains. The net result is unbalanced globin chain production. Globin chains in excess precipitate with the red cells, leading to chronic hemolysis.

42
Q
  1. 30 Thalassemias (hemoglobin disorder)
    - Occurs where in the world?
    - Disorders are classified after what?
A

Occurs in high frequency in parts of Africa, the Mediterranean, Middle East, India, and Asia.

Thalassemia classified after the gene affected, as in α-thalassemia - the α globin gene is altered so that α globin synthesis is reduced or abolished from RBCs.

43
Q
  1. 30 Thalassemias (hemoglobin disorder)

- How are RBC’s affected?

A

RBCs are microcytic and hypochromic

44
Q
  1. 31 Leukemias

- What is the pathophysiology of the cancer?

A

Cancer occurs with white blood cell precursors
- “White Blood” - enormous numbers of white cells in the peripheral blood of patients with leukemia at the time of diagnosis.

45
Q
  1. 31 Leukemia

- What are the two forms?

A

Acute leukemia - dramatic presentation - must be treated early or death will result

Chronic leukemia - slow growing and may not require therapy - can be discovered by chance

46
Q
  1. 31 Leukemia
    - What is the pathology of both acute and chronic leukemia?
    - In addition to WBC’s, what other cell types are affected?
A

Progressive accumulation of abnormal WBC’s in bone marrow and other organs, which spill out into peripheral blood. Progressive bone marrow failure results - leading to a reduction in other normal cell types.

Typically, reduced RBCs and megakaryocytes also result.

47
Q
  1. 32 Acute Leukemias

- What are two types of acute Leukemia?

A
  1. Acute Myeloid Luekemia (Acute Myelogenous Leukemia) (AML)

2. Acute Lymphoblastic Leukemia (Acute Lymphocytic Leukemia) (ALL)

48
Q
  1. 32 Acute Myeloid Leukemia (Acute Myelogenous Leukemia) (AML)
    - Cancer of which line of stem cells?
A

Cancer of the myeloid line of stem cells,

Characterized by the rapid growth of abnormal WBCs that accumulate in the bone marrow and interfere with the production of normal blood cells
- Drop in RBCs, platelets, and normal WBCs

(Neutrophils, Eosinophils, Basophils)

49
Q

8.32 What is the most common acute leukemia affecting adults?

A

Acute Myeloid Leukemia - incidence increases with age

50
Q
  1. 33 Acute Myeloid Leukemia (AML)

- Symptoms?

A
  1. Tiredness, shortness of breath and anemia (due to reduced RBCs)
  2. Increased susceptibility to infections (due to reduced WBCs)
  3. Bruising and bleeding (due to reduction in platelets)
  4. Bone pain (accumulation of leukemic cells in long bones)
  5. Respiratory and neurological symptoms (due to large numbers of WBCs in the blood causing viscosity and “sludging” of blood
51
Q

8.34 What acute leukemia is most common in childhood, with a peak incidence at 2-5 years of age?

A

Acute Lymphoblastic Leukemia (Acute Lymphocytic Leukemia) (ALL)

52
Q
  1. 34 Acute Lymphoblastic Leukemia (ALL)

- Cancer of which line of stem cells?

A

Cancer of the lymphoid line of stem cells

Characterized by the rapid growth of abnormal WBCs that accumulate in the bone marrow and interfere with the production of normal blood cells

(B cells, T cells, and NK cells)

53
Q
  1. 34 Acute Lymphoblastic Leukemia (ALL)

- Symptoms?

A
  1. Tiredness, shortness of breath and anemia (due to reduced RBCs)
  2. Increased susceptibility to infections (due to reduced WBCs)
  3. Bruising and bleeding (due to reduction in platelets)
  4. Bone pain (accumulation of leukemic cells in long bones)
  5. Respiratory and neurological symptoms (due to large numbers of WBCs in the blood causing viscosity and “sludging” of blood
54
Q

8.35 What are some chronic leukemias?

A

Chronic Myeloid Leukemia (CML)

Chronic Lymphoblastic Leukemia (CLL)

55
Q
  1. 35 Chronic Myeloid Leukemia (CML)
    - Cancer of which line of stem cells?
    - When does it commonly present?
A

Cancer of the myeloid line of stem cells

Presentation is more common in adults between 40-60 years of age

56
Q
  1. 35 Chronic Myeloid Leukemia (CML)
    - Presence of what chromosome?
    - Mutation results in what?
A

Presence of the Philadelphia chromosome - translocation of parts of chromosomes 9 and 22

Mutation leads to transcription of proteins with high tyrosine kinase activity

57
Q
  1. 36 Chronic Myeloid Leukemia (CML)

- What are the three phases?

A
  1. Chronic Phase - patients are asyptomatic or have mild symptoms
  2. Accelerated Phase
  3. Blast Crisis
58
Q
  1. 36 Chronic Myeloid Leukemia (CML)
    - Describe the chronic phase
    • What % of patients present with this stage?
    • Symptoms?
    • Duration of chronic phase?
A

~85% of patients with CML are in the chronic phase at time of diagnosis

Patients are asymptomatic or have old mild symptoms of fatigue, left side pain, joint and/or hip pain, or abdominal fullness.

The duration of chronic phase is variable (average of about 5 years) and depends on how early the disease was diagnosed as well as the therapies used.

59
Q
  1. 36 Chronic Myeloid Leukemia (CML)

- Describe the accelerated and blast crisis

A
  1. Accelerated phase - Severity of symptoms increase; labs reflect greater shifts in numbers; therapies used in chronic phase become less effective
  2. Blast crisis - resembles an acute leukemia, with rapid progression and short survival
60
Q
  1. 37 Chronic Lymphoblastic Leukemia (CLL)
    - Cancer of which line of stem cells?
    - Prevalence?
A

Cancer of the lymphoid line of stem cells

Most common adult leukemia in Western societies with a peak incidence in patients between 60-80 and a male:female ratio of 2:1

61
Q
  1. 37 Chronic Lymphoblastic Leukemia (CLL)

- What characterizes this disease?

A

Slow-growing disorder characterized by progressive accumulation of cancerous cells in the bone marrow, spleen, liver, and lymph nodes

62
Q
  1. 38 What are lymphomas?

- Can originate where?

A

They are solid tumor masses and can originate within many different lymphoid tissues, namely the lymph nodes (which is the most common), spleen, liver, GI tract, thymus, or bone marrow

63
Q

8.39 What are symptoms of Hodgkin’s Lymphoma?

A
  1. Itchy skin
  2. Night sweats
  3. Unexplained weight loss
  4. Enlarged lymph nodes
  5. Splenomegaly
  6. Hepatomegaly
64
Q

8.39 What kind of cells are characteristically seen with Hodgkin’s Lympoma?

A

Reed-Sternberg cells (“popcorn cells” or “owl eyes”) are characteristically seen when lymph nodes are biopsied; these are B lymphocytes that have lost the ability to produce antibodies.

65
Q
  1. 41 What are Non-Hodgkin’s Lymphomas (NHL)?

- Cause?

A

NHLs are a group of lymphomas that include everything but Hodgkin’s lymphoma

Cause unknown; about 66,000 new cases diagnosed per year

66
Q

8.41 Non-Hodgkin’s Lymphomas symptoms?

A

Similar symptoms to Hodgkin’s lympoma

  1. Itchy skin
  2. Night sweats
  3. Unexplained weight loss
  4. Enlarged lymph nodes
  5. Splenomegaly
  6. Hepatomegaly

Hematology Exam 3 (2 decks)

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