IM 1 Flashcards
What are the 2 types of autoimmune hemolytic anemia?
- Warm aggultinin AIHA
2. Cold agglutinin AIHA
Compare the etiologies of warm vs. cold agglutinin AIHA.
Warm - drugs (eg, penicillin), viral infections, AI (eg, SLE), immunodeficiency states, lymphoproliferative diseases (eg, CLL)
Cold - infections (eg, M. pneumoniae, mononucleosis), lymphoproliferative diseases
Compare the clinical presentation of warm vs. cold agglutinin AIHA.
Warm - asymptomatic to life-threatening anemia
Cold - symptoms of anemia, livedo reticularis and acral cyanosis with cold exposure that disappears with warming
Compare the Coombs’ test results in warm vs. cold agglutinin AIHA.
Warm - Direct Coombs’ positive with anti-IgG, anti-C3, or both
Cold - Direct Coombs’ positive with anti-C3 or anti-IgM, but usually NOT IgG
Treatment of warm agglutinin AIHA?
High dose corticosteroids
Splenectomy for refractory disease
Treatment of cold agglutinin AIHA?
Avoidance of cold temperatures
Rituximab +/- fludarabine
Compare the complications of warm vs. cold agglutinin AIHA.
Warm - VTE, lymphoproliferative disorders
Cold - ischemia and peripheral gangrene, lymphoproliferative disorders
Presentation of warm AIHA?
Normocytic anemia
Evidence of hemolysis (jaundice, elevated indirect bilirubin, increased serum LDH, decreased serum haptoglobin)
Splenomegaly (erythrocyte entrapment)
Reticulocytosis (BM response)
Peripheral smear appearance in warm AIHA?
Spherocytes, microspherocytes, elliptocytes, or increased number of polychromatophilic cells
Diagnose warm AIHA?
Direct antiglobulin (Coombs) test showing autoantibodies (usually anti-IgG) or complement components (eg, anti-C3) bound to the surface of the patient’s RBCs
What is the next step in management of progressive pain in a patient with prostate cancer and bony metastases after androgen ablation (orchiectomy)?
Radiation therapy (focal external beam therapy to sites of mets)
MOA - flutamide?
Non-steroidal anti-androgen via competitive binding to dihydrotestosterone receptors
List the 4 major classes of anticoagulants.
- Heparin
- Vitamin K antagonists
- Direct thrombin inhibitors (argatroban, bivalirudin, dabigatran)
- Factor Xa inhibitors (direct - rivaroxaban and apixaban, indirect - fondaparinux)
MOA - heparins?
Inhibit Xa and IIa (thrombin)
MOA - vitamin K antagonists?
Inhibit synthesis of II, VII, IX, X (vitamin K-dependent clotting factors) and proteins C and S (vitamin-K dependent ANTICOAGULANT proteins)
Why is it important to know that warfarin can lead to decreased protein S?
May lead to an incorrect diagnosis of an inherited protein S deficiency (if possible, discontinue warfarin for 2 weeks prior to evaluating protein S levels)
MOA - aspirin?
Antiplatelet agent, inhibits COX-1 -> inhibits thromboxane A2 synthesis
MOA - clopidogrel?
Antiplatelet agent, prevents platelet activation by blocking adenosine diphosphate receptors on the surface of platelets
MOA - heparin?
Activates antithrombin III, which inactivates factor IIa, IXa, and Xa
MOA - simvastatin?
Lipid-lowering agent, inhibits 3-hydroxy-3-methylglutaryl-coenzyme reductase
List the 4 hereditary thrombophilias.
- Factor V Leiden
- Prothrombin mutation
- Antithrombin deficiency
- Protein C or S deficiency
Typical inheritance pattern of hereditary thrombophilias?
AD with variable penetrance
Presentation of PE that began as a DVT?
SOB, leg swelling, sinus tachycardia, elevated D-dimer
In a young patient with no obvious risk factor for a DVT/PE, what should be considered?
Hypercoagulable disorder