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Pathology > Chapter 14- Red Blood Cell Disorders > Flashcards

Chapter 14- Red Blood Cell Disorders Flashcards

1
Q

What is anemia?

A

Reduced total circulating RBC mass (reduced Hb or Hct)

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2
Q

What are the types of anemias?

A
  1. Blood loss
  2. Increased RBC destruction
  3. Reduced RBC production
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3
Q

What are the two types of anemias of blood loss?

A
  1. Acute- loss of intravascular vol

2. Chronic- rate of loss must exceed marrow regenerative capacity

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4
Q

How is acute blood loss compensated for?

A

Interstitial fluid shifts into blood

Blood is diluted

Low Hct triggers EPO production

Increased retics

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5
Q

What are the two kinds of hemolysis?

A
  1. Extravascular- RBCs are targeted for sequestration and phagocytosis within the spleen
  2. Intravascular- cells are broken up within the vessels via mech injury, complement, parasites
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6
Q

What are the characteristics of hemolytic anemias?

A

Shortened RBC lifespan

Increased EPO

Accumulation of Hb degradation products

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7
Q

What are the types of hemolytic anemias?

A
  1. Heredity spherocytosis
  2. G6PD deficiency
  3. Sickle cell disease
  4. Thalassemias
  5. PNH
  6. Immunohemological
  7. Trauma
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8
Q

What is the defect in hereditary spherocytosis?

A

Cytoskeletal or membrane protein

Mutation in spectrin or ankyrin

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9
Q

What causes cell destruction in hereditary spherocytosis?

A

Spherical cells have diminished deformability and are targeted for extravascular hemolysis

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10
Q

What is the defect in G6PD deficiency?

A

Cells can’t reduce glutathione and are prone to oxidative injury

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11
Q

What is the morphology of G6PD deficiency?

A

Heinz bodies (Hb ppts) cause hemolysis (extravascular and intravascular)

Bite cells

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12
Q

What is the defect in sickle cell disease?

A

Point mutation in beta gloving chain (glu to val) produces HbS

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13
Q

What are the characteristics of HbS?

A

Deoxygenation causes polymerization, deforms RBCs

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14
Q

What affects the degree of sickling?

A

Interaction with other Hb types (HbF interferes with polymerization)

MCHC

Reduced pH (reduced oxygen affinity)

Reduced microvascular transit time

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15
Q

What are sickle cell trait individuals protected against?

A

Falciparum malaria

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16
Q

What are the characteristics of sickle cell disease?

A

Chronic hemolysis

Microvascular occlusion

Tissue damage

Splenomegaly

Fibrosis and autosplenectomy

Schistocytes and fragments

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17
Q

What are the two types of thalassemia?

A
  1. Beta

2. Alpha

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18
Q

What is the defect in thalassemia?

A

Mutations that reduce globin chain synthesis

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19
Q

What type of anemia does beta thalassemia produce?

A

Hypo-micro

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20
Q

What are the two types of beta thalassemia?

A
  1. Major

2. Minor

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21
Q

What is the morphology of beta thalassemia?

A

Inbound alpha chains ppt, cell destruction

Marrow expands (organomegaly)

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22
Q

What is the morphology of alpha thalassemia?

A

Free beta tetramers ppt and have a high oxygen affinity (sequestration and hypoxia)

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23
Q

What is the most severe form of alpha thalassemia and its characteristics?

A

Hydrops fetalis- all four alpha genes absent

Gamma chains form tetramers (Hb Bart’s)

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24
Q

What are the characteristics of paroxysmal nocturnal hemoglobinuria?

A

RBCs are hypersensitive to complement

Thrombosis

Intravascular hemolysis

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25
Q

What can PNH transform to?

A

MDS or AML

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26
Q

How does immunohemolytic anemia exert its effects?

A

Abs attach to RBCs causing their destruction

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27
Q

What are the different types of immunohemolytic anemias?

A

Warm- IgG

Cold- IgM

PCH- cold IgG

Antigenic drugs- form Ab-cell complexes

Tolerance breaking drugs- induce true Ab formation

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28
Q

What is an example of a tolerance breaking drug?

A

Methyldopa

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29
Q

What kind of hemolysis usually occurs with trauma?

A

Intravascular

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30
Q

What cells are seen with hemolytic anemia from trauma?

A

Schistocytes

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31
Q

What can cause trauma to RBCs (and hemolysis)?

A

Turbulent flow and high shear forces

Prosthetic heart valves

Diffuse microvascular narrowing

32
Q

What are possible cause of anemias of diminished erythropoiesis?

A

Impaired RBC production

Deficiency of EPO or viral nutrients

Inherited defects

Neoplasia

SC failure

33
Q

What are the characteristics of megaloblastic anemias?

A

Abnormally large RBCs and erythroblasts

Anisocytosis and macro-ovalocytes and poikilocytosis

PMN nuclear hypersegmentation

Defective nuclear maturation

34
Q

What are the types of megaloblastic anemias?

A
  1. Vit B12 deficiency (pernicious anemia)

2. Folate deficiency

35
Q

What is the most common cause of anemias of vit B12 deficiency?

A

Autoimmune gastritis, loss of IF

Reduced B12 absorption

36
Q

What differentiates anemias of vit B12 deficiency from those of folate deficiency?

A

CNS lesion only in vit B12 deficiency

37
Q

What is the most common worldwide nutritional disorder?

A

Iron deficiency anemia

38
Q

What type of anemia does iron deficiency produce?

A

Hypo-micro (reduced Hb)

39
Q

What are possible causes of iron deficiency?

A

Low intake

Malabsorption

Excessive demand

Chronic blood loss

40
Q

What triad is associated with iron deficiency anemia?

A

Plummer-Vinson

Hypo-micro anemia

Atrophic glossitis

Esophageal webs

41
Q

How does chronic disease result in anemia?

A

Inflammation impairs RBC production

Low EPO

Serum irons low, ferritin high

42
Q

What type of anemia is associated with chronic disease?

A

Micro/hypo-normo

43
Q

What are the characteristics of aplastic anemia?

A

Chronic primary hematopoietic failure

Pancytopenia with hypocellular marrow

44
Q

What are the categories of aplastic anemia?

A
  1. Toxic exposure
  2. Viral infections
  3. Inherited diseases
45
Q

What is pure red cell aplasia?

A

Form of BM failure due to erythroid precursor suppression

46
Q

What can cause pure red cell aplasia?

A

B19 parvovirus

Autoimmune diseases

Neoplasms

47
Q

What are some miscellaneous forms of marrow failure?

A

Myelophthisic anemia (lesions in marrow)

Chronic renal failure

Hepatocellular liver disease

Endocrine disorders (hypothyroidism)

48
Q

What is polycythemia?

A

Abnormally high RBC count

49
Q

What are the two types of polycythemia?

A
  1. Relative (hemoconcentration, reduced plasma volume)

2. Absolute (increase in RBC mass)

50
Q

What are the categories of hemorrhagic diatheses?

A
  1. Increased vessel fragility
  2. Platelet deficiency/dysfunction
  3. Derangement of coagulation
51
Q

What tests are performed to diagnose bleeding disorders?

A

PT (extrinsic)

PTT (intrinsic)

Platelet counts

Platelet function tests

52
Q

What are the possible causes of vessel wall abnormalities?

A

Infections

Drug reactions

Poor vascular support

Henoch-Schonlein purpura (hypersensitivity yo immune complexes)

Hereditary hemorrhagic telangiectasia (dilated, thin walled vessels)

Pervascular amyloidosis

53
Q

What are the characteristics of vessel wall abnormalities?

A

PT, PTT, platelet count and bleeding time normal

Petechiae and purpura

54
Q

What is thrombocytopenia?

A

Reduced platelet number (<100000/uL)

55
Q

At what platelet count is spontaneous bleeding seen?

A

<20000/uL

56
Q

What can cause thrombocytopenia?

A

Reduced production

Reduced survival

Sequestration

Dilution

57
Q

What are the test results for thrombocytopenia?

A

PT, PTT and function tests normal

Low platelet count

58
Q

What are the characteristics of immune thrombocytopenic purpura?

A

Abs against platelets are produced

Extravascular hemolysis

BT, PT and PTT normal

59
Q

What are the types of ITP and their characteristics?

A
  1. Chronic- due to chronic disease (SLE, HIV, B-cell neoplasms)
  2. Acute- often in children after a viral infection
  3. Drug induced- often caused by heparin
60
Q

What are the two types of drug induced ITP?

A
  1. Rapid after onset, heparin causes platelet aggregation

2. Delayed (5-14 days) onset, Abs recognize heparin, platelets are activated, thrombosis, life threatening

61
Q

How can the risk of Type II drip induced ITP be lowered?

A

Low molecular weight heparin

62
Q

How can HIV cause thrombocytopenia?

A

Megakaryocytes express CD4, can be targeted for destruction

63
Q

What are the two forms of thrombotic microangiopathies?

A
  1. Thrombotic thrombocytic purpura (TTP)

2. Hemolytic uremic syndrome (HUS)

64
Q

What are the characteristics of TTP and HUS?

A

Excessive platelet activation and thrombi deposition in small vessels

Widespread hyaline microthrombi (ischemia)

65
Q

What are the functional areas in which platelets can be effective?

A
  1. Adhesion (BSS or vWD)
  2. Aggregation (Glanzmann thrombasthenia)
  3. Platelet secretion
66
Q

What is the characteristic pathology of clotting factor abnormalities?

A

Large ecchymoses/hematomas after trauma

Bleeding into GI, UT and joint spaces

67
Q

What is the difference between acquired and hereditary abnormalities in cloying factors?

A

Acquired- multiple abnormalities

Hereditary- usually involves a single clotting factor

68
Q

What hereditary clotting disorders are there?

A
  1. Factor VIII-vWF complex
  2. vWD- reduced adhesion
  3. Hemophilia A- factor VIII deficiency, prolonged PTT
  4. Hemophilia B- factor IX deficiency/Christmas disease, prolonged PTT
69
Q

What is the most common hereditable bleeding disorder?

A

vWD

70
Q

What are the different types of vWD and their characteristics?

A

Type 1 and 3- reduces levels

Type 2- vWF defects

71
Q

What is DIC?

A

Excessive activation of coagulation

Thrombi formation in microvasculature

72
Q

What is DIC triggered by?

A
  1. Release of TF or thromboplastic substances

2. Widespread endothelial injury

73
Q

In what patients does 50% or DIC occur?

A

Obstetrics

74
Q

What are the clinical manifestations of DIC?

A

Microangiopathic hemolytic anemia (MAHA)

Respiratory symptoms

Convulsions and coma

Oliguria and ARF

Circulatory failure and shock

75
Q

What causes MAHA?

A

RBCs are damaged by fibrin protein meshworks due to increased coagulation (schistocytes)

76
Q

What are the types of transfusion complications?

A

Febrile nonhemolytic

Allergic

Acute hemolytic (IgM- wrong ABO)

Delayed hemolytic (IgG- newly formed)

TRALI- neutrophils activated in lungs

Infectious complications

TACO- physician caused cardiac overload

Pathology (25 decks)

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