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Anemia Pt. 2 Electric Boogaloo > It's Hemo-Lit-ic Fam > Flashcards

It's Hemo-Lit-ic Fam Flashcards

1
Q

Which of these are not indicators of hemolysis?

a. Increased bilirubin
b. Decreased hemosiderin in macrophages
c. Decreased reticulocytes
d. Decreased haptoglobin
e. Increased isoenzymes 1 & 2

A

B & C are both false, they both show increased levels during hemolysis

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2
Q

Why can RBC indices sometimes not reflect the presence of anemia during acute blood loss?

A
  • Both plasma and rbcs are lost simultaneously, so RBC indices are decreased relative to each other.
  • Body has not had time to fully compensate with fluid retention
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3
Q

How can Hydremia affect RBC indices?

A

Increase in plasma volume, which can lead to decreased H&H and “appearing” as anemic on paper

Hydro- (water related) & -emia (involving blood)

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4
Q

What can cause Hydremia?

A
  • Hyperproteinemia (which can also cause a false Pos SickleDex tube test)
  • Pregnancy
  • Massive IV or FFP infusion
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5
Q

What are the 4 main groups of RBC membrane defects?

A

HS
HE (includes Pyropoik- and SE Asian Ovalocytosis)
Hereditary Stomatocytosis
Hereditary Xerocytosis

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6
Q

Which 2 groups of membrane defects are caused by horizontal spectrin-ankyrin defects?

A

HE and Pyropoikilocytosis

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7
Q

Which membrane defect group is caused by vertical spectrin-ankyrin defects?

A

HS

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8
Q

Classical Presentations of HS include:

A
  • Jaundice
  • Splenomegaly
  • Anemia (mild to severe)
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9
Q

What result do you expect to see in an osmotic fragility test with HS?

A

Increased osmotic fragility

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10
Q

True or False
EDTA tubes can be used to collect samples for an osmotic fragility test?

A

False
Heparin Tubes are used

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11
Q

What is the expected result of an osmotic fragility of a normal RBC?

A

Normal RBCs will begin to lyse at .45% saline and fully lyse at .35% saline.

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12
Q

Which types of cells are associated with a decreased osmotic fragility?

A

Target Cells

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13
Q

What other lab findings (including RBC indices) are seen with HS?

A
  • DAT negative
  • Folic Acid Decreased
  • MCV Decreased to Norm
  • MCHC Increased, often >36
  • Retics Increased (polychromasia)
  • RDW Increased
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14
Q

What’s the range of severity for HE?

A

Silent carrier to severe

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15
Q

Classical Presentations of HS include:

A
  • Jaundice
  • Splenomegaly
  • Anemia (mild to severe)
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16
Q

What other lab findings (including RBC indices) are seen with HE?

A
  • Elliptocytes
  • MCV Normal to Increased
  • MCHC Normal
  • Osmotic Fragility Normal
  • Some may have mildly heat sensitive RBCs
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17
Q

What’s the treatment for all HE cases?

A

Splenectomy

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18
Q

What hallmark is seen in Southeast Asian Ovalocytosis?

A

Spoon shaped ovalocytes with a transverse bar across central pallor space (think double stomatocyte)

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19
Q

What two defect types are associated with Hereditary Pyropoikillocytosis?

A
  • Alpha or Beta horizontal spectrin mutation
  • Decreased synthesis of alpha spectrin
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20
Q

True or False
Splenectomy fully resolves hemolysis in Pyropoik

A

False
Some hemolysis remains and some cells may fragment at body temp

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21
Q

What population is most affected by HPP and what symptoms are generally seen?

A
  • Black populations are mostly affected
  • Symptoms seen include Facial bone deformities, Gallbladder Disease, and stunted growth
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22
Q

What Lab Findings are seen when observing HPP sample results (CBC/Diff)?

A
  • MCV Very Decreased
  • MCHC Usually Increased
  • Bizarre Micro Poik (RBC Budding & Fragments, other bizarre shaped rbcs)
  • Elliptocytes
  • Spherocytes
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23
Q

What deficiency do most patients with Hereditary Stomatocytosis show and what is its theorized function?

A

Deficiency of Stomatin
Theorized to regulate an unidentified ion channel

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24
Q

What causes Hereditary Stomatocytosis?

A

Failure of Na/K pumps leading to increased H2O influx to cells and swelling.

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25
What's the treatment for Hereditary Stomatocytosis?
Splenectomy
26
What's the range of hemolysis for Stomatocytosis?
Mild to Severe
27
What Lab Findings are seen with Hereditary Stomatocytosis (CBC/Diff & others)?
* MCV Increased * MCHC Decreased bc of H2O dilution * Abundant stomatocytes * Osmotic Fragility Increased * Decreased 2,3-BPG (leads to increased O2 affinity in Hgb and decreased O2 delivery)
28
What are some of the causes of Acquired Stomatocytosis?
* Acute Alcoholism * Drug therapy * Liver disease * Cardiovascular disease * Occasionally in marathon runners after races
29
What defect causes Xerocytosis and what happens to the RBCs?
Unknown defect causes K loss bc of RBC permeability defect Cells dehydrate and become raisins (not really lol)
30
True or False Splenectomy can partially resolve Xeroctosis hemolysis
False It doesn't correct the hemolysis bc they aren't sequestered in the spleen
31
What are the Lab Findings for Xerocytosis?
* MCV Increased due to macrocytes * MCHC Increased * Stomatocytes * Target Cells * "Puddle Cells" (think the "Signet Rings of RBCs") * Decreased 2,3-BPG * Decreased Osmotic Fragility
32
Which type of Hereditary Group abnormality is caused by abnormal membrane lipids?
Acanthocytosis
33
In what population of cells is acanthocytosis shape defect not seen in?
Shape defect is not present in young RBCs
34
What is the cause associated with hereditary acanthocytosis?
Abetalipoproteinemia
35
What are the non-hereditary causes (or the ones we didn't focus on) for Acanthocytosis?
* Liver disease * Malnutrition * Certain Blood groups (McCloud, related to Kel and Lutheran) * Vit E deficiency
36
What's the general appearance of RBCs in Liver Disease Associated Anemia?
Target Cells, Round Macrocytes, Acanthocytes
37
What's the most common enzyme deficiency associated with the E-M Pathway?
P-K Deficiency
38
What inclusions are seen with oxidative denaturation of hemoglobin?
Heinz Bodies
39
How is the rate of reticulocytosis associated with hemolysis in G-6-PD deficiencies?
Inversely proportional, older cells with less enzyme are hemolyzed and the younger cells survive and reign supreme.
40
What's the most common hereditary enzyme deficiency that causes anemia?
G-6-PD Deficiency (x-linked)
41
What is Favism?
Fava beans causing oxidative damage and incurring a hemolytic crisis in G-6-PD deficient pts
42
What CBC/Diff results do you expect to see in G-6-PD deficiency?
* Reticulocytes Greatly Increased * Heinz Bodies on a Supravital Stain * Generally normo/normo * Morphology changes based on amount of hemolysis
43
What does a positive G-6-PD deficiency result look like under UV testing?
Positive result for deficiency will show NO fluorescence
44
In a PK Deficiency, what are the expected Lab Findings?
* Anemia (fully compensated to severe range) * Increased 2,3-BPG (increased O2 delivery) * Increased Reticulocytes * Generally normal rbc morphology
45
How does splenectomy affect PK-deficient hemolysis?
It doesn't correct hemolysis, but does usually increase Hgb by 1-3 grams
46
What does a positive PK deficiency result look like under UV testing?
Positive PK deficiency result will show fluorescence under UV light
47
What causes hemolysis in PNH?
Complement fixation to RBCs due to a membrane defect of decreased GPI anchor protein (especially in low pH and reduced ionic strength environments, ie nighttime)
48
What Lab Findings are seen with PNH?
* Possible development of IDA or Aplastic Anemia (if the latter wasn't there already) * Thrombosis * Thrombocytopenia * Neutropenia * Dual population of RBCs (malignant and normal) * Hemoglobinemia (with possible hemoglobinurea) * Hemosiderinurea
49
How can PNH be tested for?
Flow cytometry for surface expression of GPI-anchoring proteins on RBCs and Granulocytes
50
What's the difference between DIC and MAHA?
MAHA is a chronic condition, while DIC is usually considered to be acute.
51
What two disorders are associated with MAHA?
TTP and HUS
52
What RBC characteristics are seen with pts post-splenectomy?
HJ Bodies, Target Cells, Siderocytes
53
Name the pentad of findings associated with TTP
* Hemolytic anemia with schistocytes * Thrombocytopenia (hemorrhage) * Fluctuating Neurological Signs * Fever * Progressive Renal Disease
54
What is the surmised cause of small platelet agrgregates and subsequent occlusions in organ capillaries with TTP?
Unusually large VonWillebrand Factor present on epithelial cells that would normally be cleaved by circulating ADAMSTS13
55
Acquired TTP is defined by an:
Auto-antibody to ADAMSTS13 -or- a rare inherited variant of TTP caused by ADAMSTS13 deficiency
56
What is the Triad of findings present in HUS?
* MAHA * Thrombocytopenia * Acute Renal Failure
57
How is TTP differentiated from HUS?
HUS has an acute renal failure aspect while TTP is a chronic renal failure HUS lacks neurological symptoms
58
What is the general principle of HUS?
Follows enteric infections Toxins target renal capillary endothelium May set off DIC/local fibrinolysis doesn't occur May cause plt activation
59
How do an aortic valve replacement and March Hemoglobinuria cause hemolytic anemia?
* Non-flexible implant leads to mechanical damage to RBCs * Continued stress to RBCs and vasculature due to nonstop marching (I assume?) - no schistocytes usually seen
60
What microorganisms can cause hemolytic anemia?
* Malaria * Babesia * Bartonella * Clostridia * Strep
61

Anemia Pt. 2 Electric Boogaloo (3 decks)

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