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SBL 1 > Pathology of RBC and Bleeding Disorders > Flashcards

Pathology of RBC and Bleeding Disorders Flashcards

1
Q

Hematocrit?

A

Percentage of whole blood voume occupied by RBC’s

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2
Q

MCV equation?

A

MCV= HCT/RBC

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3
Q

MCH?

A

MCH=Hgb/RBC

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4
Q

MCHC?

A

MCHC=Hgb/Hct

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5
Q

Describe the values for acute blood loss.

A
  • Normal MCV and MCH
  • Retic count will be low initially and will slowly rise to compensate for anemia in 6-7 days
  • Annemia will show through low Hgb and Hct after 6 to 12 hrs
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6
Q

What anemias are in the catergory of Hemolytic?

A
  • HS
  • G6PD def
  • SC
  • Thalassemia
  • PNH
  • Immunohemolytic anemia
  • Hemolytic anemia due to trauma
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7
Q

What is HS? How to treat? How does it present?

A
  • unstable membrane skeletal proteins on RBC’s
  • travel through the spleen where they are destroyed due to their lack of flexibility
    • Hypersplenism
  • Remove the spleen to increase the lifespan of the RBC’s
    • Howell Jolly bodies present with spleen removed
  • Anemia, Jaundice, Splenomegaly
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8
Q

Where is G6PD deficiency common?

A
  • Sub sarahan africa
  • Middle east
  • Mediterranean
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9
Q

What happens in G6PD deficiency?

A
  • Episodic hemolysis due to oxidative stress caused by:
    • drugs
    • stress
    • infection
    • fava beans
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10
Q

What are heinz bodies?

A
  • precipitation of denatured Hbg and other stromal proteins due to oxidative damage
  • Cells with heinz bodies can’t go through spleen and either get destroyed or heinz bodies removed leading to Bite Cells
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11
Q

What mutation causes Sickle cell?

A
  • Mutation in B chain of Hbg
    • GAG to GTG (Glu to Val)
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12
Q

What makes polymerization of Sickle Cell more likely?

A
  • Hypoxia
  • Intracell dehydradation
  • Low pH
  • Sluggish blood flow
  • Sickled cells undergo vascular hemolysis
  • Vaso occlusion leads to under perfusion looping back around to hypoxia
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13
Q

In what disease will you see target cells?

A
  • SC disease, a milder disease than Sickle Cell
  • The Hbg C can crystalize but it doesn’t polymerize
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14
Q

What drug is used to treat sickle cell?

A

Hyrdoxyurea, it increases HgbF

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15
Q

B Thal Major?

A
  • Severe anemia
  • Preferential switch to Hgb F
  • Dramatic medullary and extramedullary hematopoiesis
  • See “crew cut” from bonw marrow expansion on x ray
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16
Q

What disease is indicated

A

B Thal Major

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17
Q

B Thal Minor?

A
  • Microcytic anemia
  • Mild and asymptomatic
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18
Q

a-Thalassemia 3 genes?

A
  • HbH disease
  • High oxygen affinity
  • Hemolytic and Microcytic anemia and splenomegaly
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19
Q

a-Thalassemia 4 genes?

A

Hb Barts (Hydrops Fetalis)

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20
Q

Parozysmal Nocturnal Hemoglobinuria?

A
  • PIGA mutations affecting HSC so all derived cells are affected
  • Cells lack CD55 and CD59 to protect them from lysis by complement
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21
Q

What is PNH a risk factor for?

A

MDS/AML

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22
Q

How do you treat PNH?

A
  • Eculizamab, a targeted therapy that blocks C5 and C5a
23
Q

What is a “Warm Ab”?

A
  • IgG
  • Idiopathic: autoimmune hemolytic anemia
  • Secondary:
    • CLL
    • Lymphoma
    • SLE
    • Drug related
24
Q

Cold Ab?

A
  • Idiopathic: Chronic hemagglutinin disease
  • Secondary:
    • Mono
    • Mycoplasma pneumonia
    • Lymphoma
25
Q

What is a direct Coombs test?

A
  • Detects presence of Ab bound to red cell surface
26
Q

What is the indirect Coombs test?

A

Detects Ab in the plasma

27
Q

Warm Hemolytic anemia?

A
  • IgG
  • Opsonized cells are phagocytosed in the spleen or they gradually lose their membranes
  • Autoimmune or drugs
28
Q

Cold hemolytic anemia?

A
  • IgM
  • Strong affinity at lower temp
  • More likely to manifest in the nose and fingertips (raynaud)
  • IgM leads to C3b deposition and the liver spleen and bone marrow remove the cells
29
Q

what is indicated if you have a high retic count? (general)

A
  • Bleeding or destruction of RBC’s
30
Q

What is indicatetd if you have a low retic count?

A
  • RBC production problem
31
Q

What causes megaloblastic anemia?

A
  • Impaired DNA synthesis
  • Anemia occurs as a result of not being able to produce RBC’s and growth factor production increases
    • Marrow hyperplasia occurs but hematopoiesis is ineffective
32
Q

With megaloblastic anemia what is seen in the peripheral blood?

A
  • Hypoproliferative (low retic)
  • Macrocytic (high MCV)
  • Ovalocytes
  • Neutrophil hypersegmentation
33
Q

What is pernicious anemia?

A
  • Megaloblastic anemia caused by autoimmunity typically seen in older adults
  • Abs directed against parietal cells which secrete Intrinsic Factor
    • IF needed for B12 absorption
    • B12 needed for DNA synthesis
  • Chronic atrophic gastritis can lead to megaloblastic anemia
    • which can lead to spinal (and brain/peripiheral nerves) demyelination
34
Q

What byproduct of DNA synthesis is high in Pernicious anemia?

A
  • High levels of homocysteine/ MM Co-A
35
Q
A

Iron Deficiency Anemia

  • hypoproliferative
  • Microcytic
  • Hypochromic
  • Anisocytosis
36
Q

Physical manifestations of Iron deficiency anemia?

A
  • Koilonychia
  • Alopecia
  • Atrophic glossitis
  • [Angular chelitis
37
Q

With IDA what will iron studies show?

A
  • Low serum iron
  • Low serum ferritin
  • Low Hepcidein
  • Increased TIBC
38
Q

What is Anemia of chronic disease?

A
  • Impaired RBC production/iron utilization in chronic illnesses
  • Chronic illness makes the body horde iron instead of utilizing it
  • Looks similar to IDA
39
Q

What will an Iron study show with Anemia of chronic disease?

A
  • Low serum iron
  • Reduced TIBC
  • Increased ferritin
  • Abundant iron in the tissues
40
Q
A

A: normal bone marrow

B: Aplastic Anemia

41
Q

How do you diagnose Aplastic anemia?

A
  • Anemia
  • Thrombocytopenia
  • Leukopenia
  • Bone marrow full of adipose
42
Q

when do you see pure red cell aplasia?

A
  • Very rare, seen with thymomas
  • Parvovirus B19 when there is hemolytic anemia
  • The BM shows decreased erythroid precursors
43
Q

What is Myelophthisic anemia?

A
  • Space occupation in the bone marrow seen in metastatic cancer, fibrosis,inflammation, and necrosis replacing the normal hematopoietic cells
  • Abnormal release of erythroid and granulocyte precursors results in leukoerythroblastosis (pic)
44
Q

Periorbital bruising can be a sign of what cancer?

A

Myeloma with perivasscular amyloid deposition

45
Q

What will a patient with Immune thrombocytopenic purpura present with? How do you treat?

A
  • Petechiae and purpura
  • CBC shows thrombocytopenia, and potentially Ab’s to platelets
  • BM shows increased megakaryocytes due to the lack of platelets
  • Tx by reducing the immune response with corticosteroids, IVIg, and Rituximab (anti-CD20)
46
Q

What is the pentad of Thrombotic thrombocytopenic purpura?

A
  • Fever
  • Thrombocytopenia
  • Microangiopathic hemolytic anemia
  • Neuro defects
  • Renal failure
47
Q

What causes TTP? How to treat?

A
  • ADAMTS13 is defective, this is the metalloproteinase that breaks down the multimers of vWF and without this we get massive sized platelet aggregations
  • Plasma exchange therapy
48
Q

What is the typical presesntation of Hemolytic Uremic Syndrome? and atypical?

A
  • Shiga like toxin elaborated by E. coli O157:H7 (bloody diarrhea)
  • atypical is variable linked to complement dysfunction
  • Tx is supportive
49
Q

What is Bernard Soulier and Glanzmann thrombasthenia?

A
  • BS: no adhesion occurs
  • GT: no aggregation occurs
50
Q

vWF disease type 2 and 2A?

A
  • 2: qualitative defects defined by lack of appropriate interaction with ligands
  • 2A is most common and defined by a lack of multimer assembly
51
Q

Who is the universal red cell donor and recipient?

A
  • Donor is O
  • Recipient is AB
52
Q

Who is the universal Plasma donor and recipient?

A
  • Donor: AB
  • Recipient: O
53
Q

What is a TRALI?

A
  • Acute respiratory failure during or after a transfusion with diffuse bilateral pulmonary infiltrates
  • May have fever or hypotension and can be fatal

SBL 1 (8 decks)

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