Drug Therapy as a Cause and Treatment of Anemia Flashcards

1
Q

2 groups of anemia based on pathogenesis approach

A

Increased destruction or loss of RBCs

Reduced production of RBCs

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2
Q

5 symptoms of anemia

A
Tired
Fatigue
Pallor
Increased HR
SOB
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3
Q

3 symptoms of hemolysis

A

Jaundice
Enlarged spleen
Urine looks dark

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4
Q

Function of the glucose-6-phosphate dehydrogenase enzyme

A

Reduces NADP to NADPH
NADPH is required for the production of reduced glutathione
Protects Hb and RBC membrane from oxidant stress

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5
Q

What are some things that can cause hemolysis in a G-6PD deficiency (oxidative stress hemolysis)

A

Medications (antimalarials, analgesics, antibacterial/helminths)
Infections or acute illness
Fava beans
Mothballs

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6
Q

Cardinal features based on history and PE for G-6PD

A
Typically male (x-linked)
Background (west africa, mediterranean, middle eats, SE Asia)
Family history
Precipitating factor
Symptoms of hemolysis
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7
Q

Lab evidence for G-6PD oxidative stress hemolysis

A

CBC with normocytic anemia
Morphologic evidence of hemolysis on PBS (bite cells, blister cells, polychromasia)
Screening test and/or enzyme assay for G6PD test

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8
Q
In G6PD anemia, is 
1. Bilirubin total and unconjugated
2. LDH
3. Haptoglobin
4. Reticulocyte count
5. DAT
increased or decreased
A
  1. Increased
  2. Increased
  3. Decreased
  4. Increased
  5. Negative
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9
Q

Microangiopathic hemolytic anemia

A

Despite thrombocytopenia, this is a prothrombotic state (drugs can cause it)
Thrombi form in the microvasculature
As blood flows through the microvasculature, the RBCs get sheared and form schistocytes
Causes hemolytic anemia

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10
Q

Is drug induced immune hemolytic anemia intra or extravascular?

A

Extravascular hemolysis

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11
Q

If you see high retics, what does that tell you about the bone marrow?

A

Bone marrow is working!

RBC production is ok

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12
Q

Warfarin MOA

A

Vitamin K antagonist
Vitamin K is an essential cofactor in a liver enzyme
So no vitamin K = decreased vitamin K dependent clotting factors

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13
Q

Vitamin K dependent coagulation factors

A

Factors 2, 7, 9, 10
Protein C
Protein S

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14
Q

Heparin MOA

A

Activates antithrombin which then forms complexes with activated coagulation factors
Inactivation of those coag factors inhibits clot formation

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15
Q

Advantages of older anticoags (warfarin and heparin)

A

Can monitor therapy via lab tests
Long term experience with the drugs
Readily available reversal agents

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16
Q

DOACs can work in what 2 ways

A

Direct thrombin inhibitors (dabigatran)

Direct factor 10a inhibitors (rivaroxaban, apixaban)

17
Q

Advantages of the newer anticoags

A

Ease of administration (oral)
No lab monitoring required
Minimal food and drug interactions compared to warfarin
Same bleeding risk as warfarin

18
Q

Dabigatran reversal

A

Idacaruzimab = praxbind
Monoclonal antibody fragment
Binds free and thrombin bound dabigatran and neutralizes its activity

19
Q

2 indications to reverse warfarin

A
Exhibiting major bleeding manifestations
Requiring urgent (<6 hours) surgical procedures
20
Q

2 ways to give
1. Iron
2. B12
supplements

A
  1. Oral, IV

2. Oral, IM

21
Q

When should you consider IV iron?

A

Complete GI intolerance of oral Fe
Very severe Fe deficiency anemia
Hemodialysis patients on erythropoiesis stimulating agents

22
Q

Pernicious anemia

A

Common cause of B12 deficiency

Caused by an autoimmune mediated impairment of B12 absorption (attacking the parietal cells that make IF)

23
Q

What should you also check for before supplementing folate?

A

Check for and treat coexisting B12 deficiency
Folic acid can improve the anemia and mask B12 deficiency
But the neurologic damage from untreated B12 deficiency can continue

24
Q

2 erythropoiesis stimulating agents

A

Erythropoietin

Darbepoetin

25
Q

What is the most common/important time to use and erythropoiesis stimulating agent

A

Chronic kidney disease