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Hematology > 8: Overview of Hematological Pathology > Flashcards

8: Overview of Hematological Pathology Flashcards

0
Q

What are the signs & symptoms of Anemia?

A
  • Tiredness/fatigue/exercise intolerance
  • Fainting
  • Shortness of breath
  • Pallor
  • Trachycardia/Palpitations
  • Worsening of angina
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1
Q

What is Anemia defined as?

A

A reduction in one or more of the major red blood cell (RBC) measurements: hemoglobin concentration, hematocrit, or RBC count

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2
Q

What signs & symptoms of Anemia are more like with persons of Severe Anemia?

A

1) Elderly
2) Sudden drop in HgB concentration
3) Other co-existing pathologies (e.g cardiorespiratory disease)

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3
Q

What signs & symptoms of Mild Anemia are more likely?

A

1) Younger patients
2) Gradual drop in HgB concentration
3) Absence of other diseases

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4
Q

What are Acquired Anemias 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 inflammatory disease such as rheumatoid arthritis, lupus; malignancy; and renal failure)
4) Hemolysis (e.g., AIHA- required autoimmune hemolytic anemia)

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5
Q

What are Iron Deficient Anemias?

A
  • **Most COMMON anemia worldwide!
  • Without iron there is a defective synthesis of hemoglobin, resulting in RBCs that are both:
  • MICROCYTIC* (MCV decreased) & HYPOCHROMIC (MHC & MCHC are decreased)
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6
Q

What can be seen on a blood smear with Iron deficient Anemias? Why?

A

-Occasional “pencil cells” may be seen because of unbalanced surface membrane to cytoplasmic volume due to reduced hemoglobin

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7
Q

What does a reduced rate of hemoglobin synthesis result in?

A
  • More CELL DIVISION & subsequently smaller cells.

- Lower levels of hemoglobin in the RBCs make them appear “pale”.

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8
Q

What are sources of Fe in the stomach?

A

1) Meals
2) Transfusion (RBC–Hemoglobin)
3) Iron pill

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9
Q

Is Iron digested/absorbed in the stomach ?

A

No

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10
Q

Iron is absorbed where?

A

Across the small intestine

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11
Q

What is Transferrin?

A

When Iron binds to proteins to make it soluble.

Controls the level of free iron in biological fluids

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12
Q

Where can the iron be stored? What is iron called when its stored in the liver ?

A

1) Mainly in the LIVER
2) Some in the spleen

***Iron stored in LIVER is called FERRITIN (Hemosiderin)

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13
Q

What does the bone marrow do with the iron when it receives it from the liver?

A

It utilizes it to make Hemoglobin

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14
Q

What are the causes of Iron deficiency ?

A

1) Blood loss
2) Decreased Iron Absorption
3) Dietary
4) Increased Iron Requirements
5) Other

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15
Q

What is the MAJOR cause of iron deficiency? Explain

A

***Blood loss !
-Can be Overt: obvious and easy to recognize
Examples: severe traumatic hemorrhage, hematemesis(vomiting blood), melena (stool), hemoptysis( coughing in sputum), severe menorrhagia (menstruation) and gross hematuria (blood in urine)

-Can be Occult: Difficult to discern

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16
Q

Why would a patient have decreased Iron?

A

A problem w/ the GI tract (e.g., bleeding ulcer, inflammation bowl disease, etc) or an issue w/ a drug impairing iron absorption.

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17
Q

Why would a patient have Dietary Iron deficiency?

A

Most likely vegans and elderly patients

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18
Q

Why would a patient have Increased Iron requirements?

A

Classic examples are pregnancy & growth spurts in children

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19
Q

What does DECREASED vitamin B 12 levels produce?

A
  • RBCs that are MACROCYTIC (MCV elevated)

- “MEGALOBLASTS”–> MEGALOBLASTIC ANEMIA

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20
Q

What do all actively dividing RBCs in the bone marrow require?

A

DNA synthesis in order to undergo mitosis.

-This involves both vitamin B12 & Folate

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21
Q

Is RNA synthesis affected? Explain

A

No; Not being used so protein accumulates and red cells get LARGER.
(Protein synthesis continues )

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22
Q

What are the causes of Vitamin B12 deficiency ?

A

1) Lack of Intrinsic Factor (IF)
2) Dietary
3) Total or Partial Gastrectomy & other stomach procedures

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23
Q

What does LACK of INTRINSIC FACTOR (IF) lead to?

A

DECREASED Vitamin B12 absorption; Vitamin B12 deficiency due to decreased IF produces “PERNICIOUS ANEMIA”

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24
Q

Why would a person LACK INTRINSIC FACTOR (IF) ?

A

1)Due to an autoimmune attack on IF

2) Loss of The PARIETAL CELLS in the STOMACH (This produces chronic atrophic gastritis)
- This is responsible in part for secretion of IF a protein essential for B12 absorption in the ileum.

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25
Q

In regards to DIETARY behavior which persons are more sysceptible to Vitamin B12 deficiency?

A

Strict vegans

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26
Q

What is Vitamin B 12 deficiency common with person that undergo Total/Partial Gastrectomy & Other Stomach procedures?

A

On the rise w/ more people turning to surgical procedures to lose weight

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27
Q

What is the other key player in DNA synthesis ?

A

Folate (more soluble!)

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28
Q

What does a deficiency in folate produce?

A

The same clinical picture as a deficiency in vitamin B 12 (increased MCV)

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29
Q

Does Folate required IF like Vitamin B12 Deficient Anemia?

A

NO does not require IF to be absorbed

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30
Q

What are potential causes of Folate Deficient Anemia?

A

1) Poor nutrition (Seen in poverty, elderly, and alcoholics)
2) Increased requirements (Pregnancy)
3) Malabsorption (inflammatory diseases of the intestine)
4) Drugs (interfering w/ absorption) [e.g., some anti-epileptics, oral contraceptives]

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31
Q

What is Anemia due to acute blood loss? What are the general feature of this?

A

When large volumes of blood are lost from the body in a short space of time.

Features of volume depletion:

1) Increased HR
2) Low blood pressure

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32
Q

Why is the anemia due to acute blood loss described as NORMOCYTIC?

A
  • The hemoglobin concentration will be normal for several hours following the bleed; b/c red cells & plasma are lost together.
  • Anemia only develops once the blood volume has been restored thru the movement of fluid from the extravascular space to the intravascular space.

** The MVC remains normal so its Normocytic

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33
Q

What is Anemia due to Chronic Blood loss due to? Examples?

A

-Often associated w/ iron deficient anemia in the developed world.

Examples: Unrecognized loss from a bleeding gastric ulcer or heavy menstrual flow

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34
Q

What are characteristic of Anemia of Chronic Disease?

A
  • Not clear w/ many chronic diseases that produce anemia as to why they do.
  • Anemia they produce is NORMOCYTIC
  • *Most understood is Renal failure
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35
Q

Why does chronic renal failure cause anemia?

A

Due to the Erythropoietin made in the Kidney being LOW

36
Q

What some characteristics of Acquired Autoimmune Hemolytic Anemia (AIHA)?

A
  • Red cells are destroyed faster than normal (reduced life span)
  • Bone marrow can’t keep up w. the rate of destruction
  • RBCs may live for only 20 days (instead of 120)
  • RBC breakdown is increased as a response to the anemia and so will the production as a response to the anemia.

**IF the bone marrow can increase erythropoiesis sufficiently, the patient may not even become anemic

37
Q

How can Hemolytic anemias be obtained?

A

1) Acquired

2) Inherited

38
Q

What is Acquired Autoimmune Hemolytic Anemia (AIHA)?

A

An autoimmune response directed against the RBCs own antigens

39
Q

What are Inherited Anemias ?

A
  • Hereditary anemias are ALL HEMOLYTIC in nature

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

40
Q

What can the Inherited Anemias be grouped as ?

A

1) Red cell membrane (e.g, hereditary Spherocytosis, hereditary elliptocytosis)
2) Red cell enzymes (e.g., G6PD deficiency)
3) Hemoglobin molecules (e.g sickle cell disease, thalassemias)

41
Q

What is Hereditary Spherocytosis caused by?

A

A variety of molecular defects in the genes that code for spectrin (alpha & beta), ankyrin, band 3 protein, protein 4.2 & other erythrocyte membrane proteins

42
Q

What is the most helpful red cell index for Hereditary Spherocytosis?

A

The mean cell hemoglobin concentration (MCHC)

  • IT is routinely elevated, reflecting membrane loss & red cell dehydration.
  • An elevated red cell distribution width (RDW) also favors the diagnosis of HS.
43
Q

What is Elliptocytosis?

A

A red cell membrane hereditary disorder caused by a variety of molecular defects in the same genes affected by hereditary Spherocytosis.

***The end result is the same–> The defects destabilize the cytoskeletal scaffolding of cells & the cells go poof!

44
Q

What is the Osmotic Fragility Test?

A
  • Used to detect spherocytosis and elliptocytosis (red cell membrane disorders).
  • The degree of red cell lysis caused by incubating red cells in NaCL solutions of carious strengthens is measured
45
Q

What are the curves generated for in the Osmotic Fragility Test?

A

Generated for normal and test samples and the mean corpuscular fragility (MCF) is calculated
-This is the NaCI concentration at which 50% lysis occurs

46
Q

What happens In the Osmotic Fragility Test, normal red cells remain intact until the NaCL concentration reaches 50% ?

A

Lysis increases as the solution becomes more hypotonic

47
Q

What happens if Spherocytes & Elliptocytes, have a lower surface to volume ratio?

A

They lyse more readily

48
Q

What is the red cell enzyme disorder G6PD Deficiency?

A
  • **Most common enzymatic disorder or RBCs in humans
  • Glucose 6-Phosphate dehydrogenase (G6PD) deficiency, an X-linked disorder (so males affected)

(Affects 400 million people) worldwide

49
Q

What is the ONLY source of NADPH in red cells and fully functioning pathway that is essential to keep the red cells intact?

A

G6PD

in the Pentose phosphate pathway

50
Q

What does NADPH do for RBCs?

A

Maintains glutathione in its reduced form

51
Q

What are the particular characteristics seen in G6PD Deficiency?

A

In addition to the hemolytic anemia

1) Heniz bodies
2) Bite cells

52
Q

What are Heinz Bodies?

A

Seen with particular stains where hemoglobin has been rendered unstable due to oxidant damage; the Heinz body is basically a clusteer or denatured hemoglobin

53
Q

What are Bite Cells?

A

thought to result from the processing of cells through the SPLEEN and removal of Heinz bodies.
(Spleen takes a bite :)

54
Q

What is sickle cell disease?

A

A hemoglobin disorder that results from a point mutation in the Beta Globin gene, resulting in a change of amino acid number 6
(Glu–>Val).

55
Q

What is Hemoglobin S (HbS) ?

A

The resultant hemoglobin produced by the faulty gene 6 (Glu–>Val) in sickle cell is HbS

56
Q

What are some characteristic of Sickle Cell?

A

RBCs containing the sickle cell hemoglobin elongate under conditions of reduced oxygenation, and form characteristic sickle cell shaped cells.

57
Q

What does the sickle cell shape cause?

A

Sick cell crises; REDUCED LIFE SPAN = CHRONIC HEMOLYSIS

-Since the RBCs do not flow well thru small vessels and more adherent than normal RBCs to vascular occlusion and lead to the crises.

58
Q

Where is sickle cell mostly seen?

A

Widespread throughout Africa, Middle East, and parts of India and the Mediterranean

59
Q

What is Thalassemias?

A

This groups of disorders arises as a result of diminished or absent production of one or more of the Globin chains.

60
Q

What is the net result of Thalassemias?

A

Unbalanced Globin chain production. Globin chains in excess precipitate w/ Red cells, leading to chronic hemolysis

61
Q

Where do Thalassemias occur?

A

In parts of Africa, the Mediterranean, Middle East, India and Asia

62
Q

What is Thalassemia’s classified as?

A

After the gene affected

-Example: alpha thalassemia, the alpha globin gene is altered in such a way that either alpha globin synthesis is reduced or abolished from RBCs.

63
Q

What is the consequence of impaired production of Globin chains lead to?

A

RBCs being MICROCYTIC and HYPOCHROMIC

64
Q

What are Leukemias?

A

Is caused because the White Blood Cells are in enormous numbers in the peripheral blood of patients w/ leukemia at the time of diagnosis.

65
Q

In Leukemias, cancer occurs with__________?

A

the white blood cell PRECURSORS.

66
Q

Leukeimas are divided into what?

A

ACUTE and CHRONIC FORMS

67
Q

What is Acute Leukemia?

A
  • Tends to present more dramatically

- Must be treated EARLY or DEATH will occur within a short period of time

68
Q

What is Chronic Leukemia?

A
  • More indolent (slow growing)
  • May not require therapy for years
  • Discovered by chance
69
Q

What does Chronic and Acute Lekiemas have in common?

A

1) There is a progressive accumulation of abnormal WBCs in the bone marrow and other organs, which will spill out into the peripheral blood.
2) Progressive bone marrow failure w/ a reduction in other normal cell types
* **Patients tend to also have a REDUCED # of RBCs & Megakaryocytes

70
Q

What are some characteristics of Acute Myeloid Leukemia (Acute Myelogenous Leukemia) AML ?

A

Cancer of the myeloid line of stem cells, characterized by the rapid growth of abnormal WBCs that accumulate in the bone marrow & interfere w/ the production of normal blood cells.

71
Q

What is the most common acute leukemia?

A

Acute Myeloid Leukemia (AML) is the most common acute leukemia affecting adults, and its incidence increases w/ age

72
Q

What are some symptoms of Acute Myeloid Leukemia (AML) ?

A
  • Tiredness, shortness of breath and anemia–> due to reduced RBCs
  • Increased susceptibility to infections–> due to reduced WBCs
  • Bruising & bleeding –>due to reduction in platelets
  • Bone pain–>accumulation of leukemic cells in ling bones
  • Respiratory & neurological symptoms–>due to large number of WBCs in the blood causing hyper-viscosity & “sludging” of blood
73
Q

What are some characteristics of Acute Lymphoblastic Leukemia?(ALL)

A

Cancer of the lymphoid line of stem cells, characterized by the rapid growth of abnormal WBCs that accumulate in the bone marrow & interfere with the production of normal blood cells.

74
Q

What is the most common acute Leukemias in childhood?

A

Acute Lymphoblastic Leukenmia (ALL) most common with a peak incidence at 2-5 years of age

***symptoms similar to AML

75
Q

What is Chronic Myeloid Leukemia (Chronic Myelogenous Leukemia) CML?

A
  • Cancer of the myeloid line of stem cells
  • Presence of the “Philadelphia chromosome”–> The exact chromosomal defect is translocation, in which parts of 2 chromosomes, 9 & 22 swap places.
76
Q

With what persons does CML (Chronic Myeloid Leukemia) most commonly occur ?

A

More common in adults between 40-60 years of age

77
Q

What does the mutation lead to in CML?

A

To transcription of proteins w/ high tyrosine kinase activity

78
Q

What are the 3 main phase of CML?

A

1) Chronic phase
2) Accelerated Phase
3) Blast Crisis

79
Q

What is the Chronic Phase in CML?

A
  • 85% of patients w/ CML are in chronic phase at the time of diagnosis
  • During this phase, patients are usually asymptomatic or have mild symptoms of fatigue, left side pain, joint & hip pain, or abdominal fullness.
  • Duration is variable (average = 5 years) & depends on how early diagnosis is and therapies.
80
Q

What is the Accelerated Phase in CML?

A

Severity of symptoms increase; labs reflect greater shifts in numbers; therapies used in chronic phase become less effective

81
Q

What is the Blast Crisis phase in CML?

A

Resembles an acute leukemia, w/ rapid progression & short survival

82
Q

What is Chronic Lymphoblastic(Lymphocytic) Leukemia? (CLL)

A
  • Cancer of the lymphoid line of stem cells
  • Most COMMON ADULT Leukemia in Western societies w/ a peak incidence in patents between 60-80 & male:female ratio of 2:1
83
Q

What are some characteristics of Chronic Lymphoblastic(Lymphocytic) Leukemia? (CLL) ?

A

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

84
Q

What is the difference between Leukemias & Lymphomas?

A
  • A cancer that occurs in white blood cell precursors & hence, in the bone marrow.
  • The excessively produced WBCs then disseminate int he peripheral blood
  • Lymphomas are SOLID tumor masses and can originate within many different lymphoid tissues, mainly the lymph nodes (MOST COMMON), spleen, liver, GI tract, thymus or bone marrow
85
Q

Who published the first description of lymphomas ?

A

Thomas Hodgkin published it in 1832, specifically of the form names after him Hodgkin’s lymphoma (disease)

-Note: since his time many lymphomas have been characterized

86
Q

What is Hodgkin’s Lymphomas?

A

Cause unknown; annual incidence 2-3 per 100,000

***Reed-Sternberg cells(“POPCORN CELLS”) are characteristically seen when lymph nodes are biopsied; these are B lymphocytes that have lost the ability to produce antibodies

87
Q

What are the symptoms of Hodgkin’s d lymphomas?

A

1) Itchy skin
2) night sweats
3) unexplained weight loss
4) Enlarged lymph nodes
5) Splenomegaly
6) Hepatomegaly

88
Q

What is Non-Hodgkin’s Lymphomas (NHL)

A

Are a group of lymphomas that include everything but Hodgkin’s lymphoma.

  • Cause unknown ; about 66,000 new cases diagnosed per year
  • Similar symptoms to Hodgkin’s Lymphomas

Hematology (8 decks)

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