Hematology/Immunology Flashcards
Anemia
-Defined as Hgb less than 12
-Causes: Anemia, bleeding, decreased production, frequent phlebotomy, iron or b12 deficiency, chronic illness
-Generally transfuse for Hgb of 7 or less
Iron Deficient Anemia
-From insufficient iron intake or iron malabsorption
-Risk factor: increased milk intake
Signs of IDA
-Fatigue
-Pallor
-SOB
-Tachycardia
Treatment for IDA
- Give ferrous sulfate
- Give iron dextran w/ Z-track method
-Encourage intake of iron rich foods (green veg, meat, raisins)
-Increase vitamin C intake
-Decrease calcium intake
Sickle Cell Anemia
Autoimmune recessive genetic disorder that causes chronic anemia, pain, infection, and organ damage
Abnormal sickled hemoglobin changes shape of RBCs
Leads to occlusion of blood vessels and tissue hypoxia
Signs of Sickle Cell Anemia
-Pain
-Fatigue
-Pallor
-SOB
-Jaundice
Diagnosis of Sickle Cell Anemia
-Sickle turbidity test
-HGB electrophoresis
Treatment of Sickle Cell Anemia
-Pain management: PCA or scheduled opioids
-Antibiotics for infection
-Administer IV fluids to dilute blood
-Educate patient on fluid intake and prevent dehydration
Types of Sickle Cell Crises
- Vaso-Occlusive
-Splenic Sequestration
-Aplastic
-Acute Chest Syndrome
-Hyperhemolytic Syndrome
Vaso-Occlusive Crisis
Type of sickle cell crisis
Symptoms: severe pain, swelling of hands and feet
Splenic Sequestration Crisis
Type of sickle cell crisis
Blood flow is blocked out of spleen
Symptoms: splenomegaly, hypovolemia
Aplastic Crisis
Type of sickle cell crisis
Severe anemia related to viral infection
Acute Chest Syndrome
Type of sickle cell crisis
Blood flow to lungs is impaired
Symptoms: Dyspnea, fever, cough
Hyperhemolytic Crisis
Type of sickle cell crisis
Rapid decrease in Hgb and Hct levels
PRBCs
-Stored at 4°C
-21 day shelf life
-Preservatives in stored blood:
-Citrate: binds to calcium for anticoagulation, monitor serum Ca+
levels, replace C+ every 3-4 PRBCs
-Phosphate: used to increase O2 saturation
-Dextrose: used as fuel for blood cells
Can be leukocyte reduced to decrease likelihood of transfusion reaction or washed to reduce leukocytes and plasma, reducing reactions from plasma proteins
Universal Blood Donor Type
O Negative
Universal Blood Recipient Type
AB +
Hemolytic Reaction
PRBC transfusion reaction
- caused by ABO incompatibility
-usually due to human error
-takes less than 5mL to see reaction
Symptoms: fever, tachycardia or bradycardia, dyspnea, chest pain, lower back pain, hypotension, blood in urine
Types of WBCs
-Neutrophils
-Elevated count indicates infection or inflammation
-Bands can indicate infection
-Monocytes
-Big phagocytes that scavenge for bacteria
-Lymphocytes
-Responsible for adaptive immune response
-Eosinophils
-Elevated counts indicate parasitic infection
Leukopenia
Defined as decreased number of WBCs
-immunocompromised
-seen in infection with rapid consumption of WBCs
-increases risk of infection
Platelets
-Normal: 150,000-400,000
-AKA thrombocytes
-Essential for clotting
-65% are circulated in blood, 35% in the spleen
-Lifespan of platelet is 10 days
Thrombocytopenia
-PLT less than 150,000
-Caused by: sepsis, DIC, dialysis, CRRT
-Signs: petechiae, ecchymosis
Medications that cause platelet dysfunction
-aspirin
-clopidogrel
-penicillin
-cephalosporins
-ATP
-heparin
-calcium channel blockers
-nitroglycerin
-nitroprusside
-ketorolac
Warfarin/Coumadin
-Acts on extrinsic and common coagulation pathways
-monitor PT/INR, will be elevated when on warfarin
-PT: 11-13
-INR: 0.8-1.1
-Antidote: Vitamin K & FFP
-give vitamin K slowly
-INR will decrease in 8-12hrs
Heparin
-Acts on intrinsic and common coagulation pathways
-monitor PTT and Anti-Xa
-normal 25-38 sec
-elevated with heparin
-Antidote: Promatine sulfate
-reactions include: bradycardia, hypotension, n/v, anaphylaxis
w/fish allergy
Low Molecular Weight Heparin
Less incidence of HIT
Longer half life: 4-6 hrs
ITP
Immune Thrombocytopenic Purpura
-autoimmune d/o where spleen disorders platelets
- PLT <20,000
-Primary disorder or secondary due to meds or autoimmune disorders like lupus
-Symptoms: petechiae, purpura, epitaxia, splenomegaly
-Treatment: steroids, IVIG, remove spleen
DIC
Disseminated Intravascular Coagulation
-hypercoagulation secondary to widespread endothelial damage
-use up all clotting factors then you bleed
-microvascular thrombus formation
-Causes: sepsis, trauma, obstetric complications
-Symptoms: bleeding from multiple sites, ecchymosis, purpura lesions, bloody stool, bleeding gums and mucous membranes
-PLT <50,000
-Decreased fibrinogen <100
-Increased D-Dimer
-Increased PTT and PT
Treatment: 80% mortality, all treatment is supportive. Treat bleeding w/PLTs and cryoprecipitate (fibrinogen)
Consumptive Coagulopathy
-Decreased PLT
-Increased fibrinogen markers
-prolonged PTT
-Decreased fibrinogen
HIT
Heparin Induced Thrombocytopenia
Patients have IGG antibodies to heparin, decreased PLT by 50% from baseline within 5-10 days of exposure to heparin
Symptoms: fever, chills, tachypnea, tachycardia, erythematous lesions around SQ injection sites
Types of HIT
1: 1-2 days after exposure to heparin, PLT count normalizes with continuous therapy, non-immune disorder than results from direct effect of heparin on PLT activation
2: Occurs 4-10 days after exposure to heparin, immune-mediated disorder that causes clotting, life and limb-threatening thrombotic complications
Types of Thrombus
- Systemic thrombus
-DVT
-Pulmonary embolism
-Arterial thrombus
-Stroke
Risk after orthopedic or heart surgery
Diagnosis of HIT
-clinical exposure to heparin
-decreased PLT
-heparin assay
Treatment for HIT
-Immediately stop heparin infusions
-Draw heparin antibody panel
-Give alternate anticoagulation medications
-direct thrombin inhibitors:
-argatroban (cleared by liver)
-bivalirudin (cleared by kidneys)
-warfarin
-don’t use during active HIT, give after recover
-never give heparin again
