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MHD V: Renal > 11.5: Anemia I > Flashcards

11.5: Anemia I Flashcards

1
Q

What is a pluripotent stem cell?

A

Precursor of all blood cell lines: RBC, WBC, platelet

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2
Q

What is hematopoiesis?

A
  • Series of events in which pluripotent stem cells mature into functional blood cells
  • Occurs in marrow
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3
Q

RBC characteristics?

A
  • Anucleate
  • Bi concave
  • Make up majority of blood cells
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4
Q

What is blood smear?

A
  • Allows visualization of formed blood elements

- Drop of blood on glass then stained

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5
Q

How do you see if there is issue with hematopoiesis?

A

Bone marrow aspirate and biopsy

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6
Q

What is a reticulocyte?

A
  • First stage or RBC released from marrow into periphary

- Cytoplasm may be blueish bind from residual RNA

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7
Q

Life span of RBC?

A

120 Days

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8
Q

What is the structure of RBC membrane? How is it different from other cells?

A
  • **Membrane skeleton controlling bi concave shape and cell malleability: Allows for microcirculation transit
  • Otherwise is phospholipid bilayer with membrane proteins, glycolipids and cholesterol just like other cells
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9
Q

What is hemoglobin?

A
  • Functional protein in RBC allowing for O2 transport
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10
Q

2 Biosynthetic pathways involved in hemoglobin synthesis?

A
  1. Synthesis of HEME

2. Synthesis of globin chains

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11
Q

What is heme?

A
  • 4 pyrrole groups joined in a ring

- Ferrous iron is incorporated in center

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12
Q

What are globin chains?

A
  • 150 aa protein with heme binding site
  • 2 Globin dimers form hemoglobin
  • Hemoglobin A comprises 95% of globin in adults
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13
Q

What is hemoglobin A?

A
  • Makes of 95% of adult hemoglobin

- Composed of 2 alpha and 2 beta chains

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14
Q

How are aging RBCs removed?

A
  • Mononuclear phagocytes in spleen responsible for removal of aged RBCs
  • Heme is divided into iron which is recycled, and porphyrin rings: removed as bilirubin
  • Globin is dismantled into amino acids
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15
Q

What are porphyrin rings?

A
  • Byproduct of heme degradation

- Eliminated as bilirubin

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16
Q

Term for accelerated RBC destruction?

A

Hemolysis

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17
Q

What is anemia?

A
  • Reduced oxygen carrying capacity of the blood

- Reduction in red cell mass

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18
Q

3 Classes of anemia?

A
  1. Blood loss
  2. Hemolytic: increased rate of destruction
  3. Diminished production
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19
Q

Intrinsic factors leading to increased hemolysis?

A
  1. Spherocytosis
  2. G6PD deficiency
  3. Sickle Cell anemia
  4. Thalassemia
  5. PNH (Acquired)
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20
Q

3 types of disturbances in differentiation?

A
  1. Iron deficiency anemia
  2. Megaloblastic anemia: B12/folate
  3. Anemia of chronic disease
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21
Q

What is MCV?

A

“Mean cell volume”

- Reading from CBC

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22
Q

What is MCH?

A

“Mean cell Hemoglobin”

- Reading from CBC

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23
Q

What is MCHC?

A

“Mean cell Hemoglobin concentration”

- Reading from CBC

24
Q

What is RDW?

A

“Red cell distribution width”

  • Measures anisocytosis
  • Variation in RBC volume
25
Q

What is anisocytosis?

A

Variation in RBC size

26
Q

Examples of MICROcytic anemia?

A
  1. Iron deficiency
  2. Thalassemias
  3. Anemia of chronic disease
27
Q

Examples of MACROcytic anemia?

A
  1. Megaloblastic anemia: B12 / Folate deficiency
28
Q

Characteristics of hemolytic anemias?

A
  1. Shortened RBC lifespan
  2. Accumulation of products of RBC metabolism
  3. Increase in erythropoiesis from bone marrow
29
Q

Where does extravascular hemolysis occur?

A

Spleen

30
Q

Where does intravascular anemia occur and what does in cause?

A

Occurs in vascular compartment causing:

  1. Hemoglobinemia
  2. Hemoglobinuria
  3. Hemosiderinuria: byproduct of iron metabolism
31
Q

What happens to free hemoglobin in the blood?

A
  • Binds to haptoglobin and is removed by liver

- Low haptoglobin means hemolytic anemia

32
Q

What does low haptoglobin mean?

A
  • Hemolytic anemia

- It is binding the hemoglobin to remove it from serum

33
Q

What is extravascular hemolysis?

A
  • Accelerated destruction of RBCs in spleen by macs
  • More common than intravascular
  • Don’t see same products in serum
  • Hyperactive reticular system leads to splenomegaly
34
Q

What is hereditary spherocytosis?

A
  • Intrinsic deficiency in RBC spectrin or ankyrin
  • Spheroid RBCs, less malleable
  • More vulnerable to splenic destruction/sequestration
  • Autosomal dominant
35
Q

What is spectrin?

A
  • Main protein in membrane skeleton of RBC

- Deficiency leads to spherocytosis

36
Q

What is ankyrin?

A
  • Protein that anchors spektrin to membrane proteins
  • Deficient in autosomal dominant Spherocytosis
  • Recessive is spectrin deficiency
37
Q

Pathophysiology of spherocytosis?

A
  • Decreased interaction w/ skeleton and lipids layer
  • Reduced membrane stability and loss of fragments
  • Decreased surface are to volume ratio causing spherical shape
38
Q

What does biconcave shape of RBC allow for?

A
  • Deformation allowing it to squeeze through tight spaces in spleen and other areas
  • If you are spherical, takes longer to get through spleen and macs eat you
39
Q

What can improve spherocytosis?

A
  • Splenectomy
  • Prevents destruction of RBCs in spleen
  • Still have disease by symptoms are better
40
Q

What are RBCs w/o central pallor in smear indicative of?

A

Spherocytosis

41
Q

Clinical findings in spherocytosis?

A
  1. Jaundice
  2. Anemia
  3. Splenomegaly
  4. Increased osmotic fragility
  5. Increased MCHC
42
Q

What are anemia, jaundice, and splenomegaly consistent with?

A

Spherocytosis

43
Q

What is Aplastic crisis?

A
  • Occurs in hemolytic anemia
  • Bone marrow ramps up and is maxed out
  • If infection occurs, marrow cannot respond with WBCs
44
Q

What is increased MCHC characteristic of?

A

Spherocytosis

45
Q

How is G6PD deficiency inherited?

A
  • X linked

- Higher incidence in males than females

46
Q

When does G6PD deficiency manifest?

A
  • Usually there are no symptoms

- When there is oxidative stress on RBC from stress or infection

47
Q

What is the glutathione system?

A
  • Manner in which RBCs deal with oxidative stress
  • Glutathione is oxidized by stress to protect RBC
  • NADPH reduces Glutathione so it can be used again becoming NADP in process
  • G6PD responsible for converting back into NADPH
48
Q

How does oxidative stress damage RBC?

A
  • H2O2 oxidizes sulfhydryl groups of globin chains
  • Hemoglobin denatures and precipitates forming Heinz bodies
  • Heinz bodies attach to RBC membrane decreasing maleability
49
Q

What are Heinz bodies?

A
  • Denatured hemoglobin from oxidative stress
  • Bind to RBC decreasing maleability
  • Causes intravascular hemolysis
  • Macs also bit off Heinz bodies leading to spherocytes
50
Q

Clinical course of G6PD deficiency?

A
  • Intravascular hemolysis
  • Hemoglobinemia
  • Hemoglobinuria
  • Decreased hematocrit
  • Bone marrow produces more RBCs to compensate
51
Q

What is Sickle Cell disease?

A
  • Structurally abnormal hemoglobin synthesis
  • Most common form of familial hemolytic anemia
  • Defective HbS
  • You must be homozygous to show symptoms
52
Q

What is the most common form of hemolytic anemia?

A

Sickle cell Disease

53
Q

What is HbS?

A
  • Responsible for sickle cell trait
54
Q

Pathophys of sickle cell?

A
  • Point mutation of valine for glutamic acid in B globin
  • Forms HbS molecules that aggregate and polymerize
  • Red cell distorts into sickle shape
55
Q

3 things sickling of cells dependant on?

A
  1. Fall in PH
  2. Amount of HbS
  3. High MCHC
56
Q

Clinical consequences of sickling?

A
  1. Hemolytic anemia
  2. Occlusion of small vessels
  3. Splenomegaly in kids
  4. Hypoxic damage to spleen leading to fibrosis
  5. Vaso Occlusive / painful crises
  6. Aplastic crises
  7. Increased susceptibility to infection
  8. Ischemic damage from occlusion
57
Q

What happens in sickle cell trait?

A
  • Usually not clinical appearance

MHD V: Renal (28 decks)

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