Hematology/Oncology/Immunology (6%) Flashcards
Normal Hgb and MCV values
Hgb: 12-17
MCV 80-100
Microcytic anemia
- Abnormal hgb synthesis
- MCV < 80 (small)
- Examples: iron deficiency anemia, thalassemias minor (alpha and beta)
Iron deficiency anemia
- Microcytic anemia, MCV < 80
- Cause – slow, chronic blood loss (most common causes include gastritis, PUD, GI cancer)
- Lab findings/symptoms – low iron stores, serum iron, and serum ferritin; elevated total iron binding capacity; fatigue, pica
- Treatment – correct underlying problem, replace iron
Thalassemias minor (alpha and beta)
- Microcytic anemia, MCV < 80
- Cause – genetic variation of Hgb
- Lab findings/symptoms – normal iron, RDW normal, Hgb electrophoresis
- Treatment – genetic counseling, transfuse only as needed (not routinely)
Macrocytic anemia
- Abnormal RBC synthesis
- MCV > 100
- Examples: pernicious anemia and folic acid deficiency anemia
Pernicious anemia
- Macrocytic anemia, MCV > 100
- Cause – impaired vitamin B12 absorption
- Lab findings/symptoms – low B12 (< 100), increased intrinsic factor antibodies, neuro symptoms (paresthesias, difficulty with balance, ataxia)
- Treatment – supplement vitamin B12 1000 mcg oral daily or IM 1000 mcg monthly (if no response to oral)
Folic acid deficiency anemia
- Macrocytic anemia, MCV > 100
- Cause – diet deficiency (ex: etoh) or medication
- Lab findings/symptoms – low serum and RBC folate (<150 ng/ml is diagnostic)
- Treatment – correct underlying problem, tapered folate supplements
Sickle Cell Anemia
Occurs as a result of abnormal hgb synthesis
Sickled RBCs can’t fit through capillaries
Sickle cell crisis is an acute pain syndrome
Treatment centers on prevention of crisis – ex: vaccinations, adequate hydration, etc.
Acute crisis treatment is supportive – oxygen, IV antibiotics, aggressive pain management, hydroxyurea (Hydrea) for extreme cases
Rheumatoid arthritis (RA)
- Characterized by symmetric arthritis of the small joints of hands/feet
- Manifestations – pain/stiffness in the morning that improves throughout the day (opposite of OA), SYMMETRIC polyarthritis beginning in small joints and progressing to larger joints
- Extra-articular manifestations include rheumatoid nodules (found on tendon sheaths on bony prominences), boutonniere and swan-neck deformities
- Diagnosis is clinical but can test for anti-CPP (most specific, highly predictive of RA, diagnostic of choice)
- X-ray – uniform joint space narrowing + juxta-articular erosion
- Management – refer to rheumatology; DMARDs (FIRST LINE) including Methotrexate 75 mg PO weekly to start; ASA and NSAIDs help with inflammation but don’t stop erosion or progression of disease
Systemic Lupus Erythematous (SLE)
- Chronic, multisystem, inflammatory autoimmune disorder
- Diagnostic criteria (need at least 4) – malar (butterfly rash), discoid rash, photosensitivity, oral ulcers, arthritis, kidney disease, neurologic disease, etc.
- Labs – ANA (anti-dsDNA and anti-Smith (confirmatory))
- Management – refer to rheumatology; antimalarial drugs (ex: hydroxychloroquine) are new cornerstone of tx; NSAIDs for joint pain; no live viruses (ex: shingles, intranasal influenza)
Giant Cell Arteritis
- Systemic panarteritis affecting medium and large vessels in patients > 50
- Frequently called temporal arteritis because that is the artery frequently involved
- Manifestations – VERY HIGH FEVER, headache, specific scalp tenderness, jaw claudication, temporal artery may be enlarged and tender
- Labs – very high ESR, normal WBC, temporary artery biopsy (definitive dx)
- Management – do not wait for biopsy results before starting steroids (prednisone max 80 mg/day for 1-2 months before tapering or methylprednisolone)
Disseminated intravascular coagulation (DIC)
o Caused by large amounts of traumatized tissue stimulating clotting factors (i.e., sepsis, trauma, infection, etc.); clotting factors are used up and depleted causing lethal bleeding
o Treatment – treat underlying process, supportive tx while underlying process resolves (FFP if fibrinogen is < 100 and significant bleeding is present; cryo is second-line alternative)
Primary Immune Thrombocytopenia Purpura (TIP)
o Autoimmune process of platelet destruction and decreased production
o Typically a diagnosis of exclusion
o Treatment – CORTICOSTEROIDS are first line (prednisone 0.5-2 mg/kg/day PO tapered over 4 weeks or dexamethasone 40 mg PO daily x4 days
Heparin-Induced Thrombocytopenia (HIT)
o Type 1 reaction – direct effect of heparin (onset = 1-4 days after heparin started)
o Type 2 reaction – immune-mediated response (onset = 4-10 days after heparin started; can be < 24 hours after heparin start if they have a hx of HIT)
o Treatment type 1 – can consider discontinuing heparin and observe
o Treatment type 2 – always stop heparin and use alternative anticoagulation (thrombin inhibitors – argatroban)
Acute myelogenous leukemia (AML) vs. chronic myelogenous leukemia (CML)
- AML – occurs in adults; sympotms of anemia, spontaneous bleeding, petechiae, bruising; presence of Auer rods
- CML – occurs in 20-50 year olds; rare in children; INSIDIOUS ONSET of mild anemia symptoms; leukocytosis < 50,000
