Drug Therapy as a Cause and Treatment of Anemia Flashcards
2 groups of anemia based on pathogenesis approach
Increased destruction or loss of RBCs
Reduced production of RBCs
5 symptoms of anemia
Tired Fatigue Pallor Increased HR SOB
3 symptoms of hemolysis
Jaundice
Enlarged spleen
Urine looks dark
Function of the glucose-6-phosphate dehydrogenase enzyme
Reduces NADP to NADPH
NADPH is required for the production of reduced glutathione
Protects Hb and RBC membrane from oxidant stress
What are some things that can cause hemolysis in a G-6PD deficiency (oxidative stress hemolysis)
Medications (antimalarials, analgesics, antibacterial/helminths)
Infections or acute illness
Fava beans
Mothballs
Cardinal features based on history and PE for G-6PD
Typically male (x-linked) Background (west africa, mediterranean, middle eats, SE Asia) Family history Precipitating factor Symptoms of hemolysis
Lab evidence for G-6PD oxidative stress hemolysis
CBC with normocytic anemia
Morphologic evidence of hemolysis on PBS (bite cells, blister cells, polychromasia)
Screening test and/or enzyme assay for G6PD test
In G6PD anemia, is 1. Bilirubin total and unconjugated 2. LDH 3. Haptoglobin 4. Reticulocyte count 5. DAT increased or decreased
- Increased
- Increased
- Decreased
- Increased
- Negative
Microangiopathic hemolytic anemia
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
Is drug induced immune hemolytic anemia intra or extravascular?
Extravascular hemolysis
If you see high retics, what does that tell you about the bone marrow?
Bone marrow is working!
RBC production is ok
Warfarin MOA
Vitamin K antagonist
Vitamin K is an essential cofactor in a liver enzyme
So no vitamin K = decreased vitamin K dependent clotting factors
Vitamin K dependent coagulation factors
Factors 2, 7, 9, 10
Protein C
Protein S
Heparin MOA
Activates antithrombin which then forms complexes with activated coagulation factors
Inactivation of those coag factors inhibits clot formation
Advantages of older anticoags (warfarin and heparin)
Can monitor therapy via lab tests
Long term experience with the drugs
Readily available reversal agents
DOACs can work in what 2 ways
Direct thrombin inhibitors (dabigatran)
Direct factor 10a inhibitors (rivaroxaban, apixaban)
Advantages of the newer anticoags
Ease of administration (oral)
No lab monitoring required
Minimal food and drug interactions compared to warfarin
Same bleeding risk as warfarin
Dabigatran reversal
Idacaruzimab = praxbind
Monoclonal antibody fragment
Binds free and thrombin bound dabigatran and neutralizes its activity
2 indications to reverse warfarin
Exhibiting major bleeding manifestations Requiring urgent (<6 hours) surgical procedures
2 ways to give
1. Iron
2. B12
supplements
- Oral, IV
2. Oral, IM
When should you consider IV iron?
Complete GI intolerance of oral Fe
Very severe Fe deficiency anemia
Hemodialysis patients on erythropoiesis stimulating agents
Pernicious anemia
Common cause of B12 deficiency
Caused by an autoimmune mediated impairment of B12 absorption (attacking the parietal cells that make IF)
What should you also check for before supplementing folate?
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
2 erythropoiesis stimulating agents
Erythropoietin
Darbepoetin
What is the most common/important time to use and erythropoiesis stimulating agent
Chronic kidney disease
