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Hematology: Assessment & Patient Care – Comprehensive Exam Notes
Hematology: Assessment & Patient Care – Comprehensive Exam Notes
Hematologic System Assessment (Chapter 33)
Priority Concepts
Ability to transport O
2 and CO
2
Maintenance of coagulation & intravascular volume
Protection against infection
Anatomy & Physiology Review
Bone Marrow – Primary Site of Hematopoiesis
Continuously produces:
\text{RBCs (erythrocytes)}
\text{WBCs (leukocytes)}
\text{Platelets (thrombocytes)}
FUN FACT: Daily marrow release per kg body weight
2.5 \times 10^{9} RBCs
2.5 \times 10^{9} Platelets
1 \times 10^{9} WBCs
Clinical significance: Any marrow failure → pancytopenia, hypoxia, bleeding, infection risk
Blood Components
Plasma proteins
Albumin – maintains oncotic pressure
Globulins – transport & immunity (antibodies)
Fibrinogen – precursor to fibrin in clotting cascade
Cellular elements
RBCs: gas transport
WBCs: immune defense
Platelets: primary hemostasis
Accessory Organs of Blood Formation
Spleen – filters old/defective cells, houses lymphocytes, stores platelets
Liver – produces clotting factors, stores iron, conjugates bilirubin
Hemostasis & Blood-Clotting Sequence
Vessel injury → transient vasoconstriction
Platelet adhesion & aggregation → platelet plug
Activation of coagulation cascade → conversion of fibrinogen to fibrin → stable clot
Anticlotting (Fibrinolytic) Forces
Plasminogen → plasmin → dissolves fibrin
Deficiency of any natural anticoagulant (protein C, protein S, antithrombin) ↑ thrombosis risk
Hematologic Changes Associated with Aging
↓ Total blood volume
Marrow produces fewer cells ⇒ ↓ \text{RBC}, ↓ \text{WBC} counts
Lymphocytes less responsive ⇒ weaker immune responses
Hb falls after middle age (esp. in women post-menopause)
Clinical pearl: fatigue & infection in elders may reflect normal aging OR occult pathology
Comprehensive Patient Assessment
Demographics: age, gender (e.g., menstruation-related iron loss)
Liver function history (clotting factor synthesis)
Medication review: anticoagulants, NSAIDs, chemo, herbals (ginkgo, garlic)
Diet: iron, B₁₂, folate, protein intake
Socio-economic factors: food security, insurance, toxin exposure
Radiation history: past cancer therapy → marrow dysplasia risk
Occupation/hobbies: chemicals, pesticides, solvents, lead, benzene
Home location: altitude (chronic hypoxia), industrial pollutants
Family/genetic disorders: hemophilia, sickle cell, thalassemia
Current symptoms: bleeding, bruising, fatigue, infections, weight loss
Laboratory & Diagnostic Panel (pg 708-712)
Coagulation/bleeding studies
\text{D-dimer} – fibrin degradation; ↑ = active clot breakdown (DVT/PE suspicion)
\text{PT} (Prothrombin Time) – extrinsic pathway; therapeutic target in warfarin therapy
\text{INR} – normalized PT (goal 2.0–3.0 for most indications)
\text{aPTT} – intrinsic pathway; monitors IV heparin (goal 1.5–2.5 × control)
Imaging: ultrasound (DVT), CT (splenomegaly), bone scan
Bone-marrow aspiration/biopsy – definitive for dyscrasias
Care of Patients with Hematologic Problems (Chapter 34)
Priority Concepts
Perfusion → Sickle Cell Disease (SCD)
Immunity → Leukemia
Disorders of Erythrocytes
Sickle Cell Disease – Destruction of RBCs
Genetic mutation → abnormal HbS chains
Deoxygenation, dehydration, acidosis → polymerization → "sickling"
Sickled cells:
Rigid, sticky, obstruct capillaries → ischemia, pain crises
Short lifespan ⇒ chronic hemolytic anemia
Epidemiology: common in African-Americans; protective vs. malaria
Assessment
Severe pain = hallmark (ischemic tissue injury)
Chronic anemia symptoms: fatigue, pallor, jaundice (↑ bilirubin)
Multi-system effects (Fig 34.4):
CVA, acute chest syndrome, splenic sequestration, renal failure, priapism, ulcers
Pain undertreatment common; tolerance necessitates higher opioid doses
Treatment – "HOP to it"
Hydration: isotonic IV fluids (e.g., 0.9\% NS) to ↓ blood viscosity
Oxygenation: prevents further sickling
Pain relief: IV opioids (morphine, hydromorphone)
Drug therapy: hydroxyurea ↑ HbF, L-glutamine, transfusions, crizanlizumab; stem-cell transplant = curative in selected pts
Anemias r/t Decreased Production
Defined by ↓ number of RBCs, ↓ Hb, or ↓ hematocrit
Not a disease itself; indicator of underlying issue (nutritional, marrow, chronic disease)
Polycythemia Vera – Excess RBC Production
Chronic myeloproliferative neoplasm (JAK2 mutation)
↑ RBC mass → hypervolemia + hyperviscosity
Clinical picture:
Ruddy/cyanotic mucosa & facial skin (venous stasis)
Splenomegaly, pruritus, gout, thrombosis risk
End-organ damage (heart, spleen, kidneys)
Tx: phlebotomy (target Hct <45\%), hydration, low-dose aspirin, cytoreductive drugs (hydroxyurea)
Hereditary Hemochromatosis – Excess Iron
Autosomal-recessive (HFE gene) → ↑ intestinal iron absorption
Iron deposition damages liver, pancreas, heart, joints, skin ("bronze diabetes")
Dx: ↑ serum ferritin & transferrin saturation
Tx: serial phlebotomy, deferasirox/deferoxamine if needed, limit iron & vitamin C intake
Disorders of Leukocytes
Leukemia – Uncontrolled Immature WBC Proliferation
Loss of normal cellular regulation → accumulation of "blast" cells in marrow, blood, tissues
Results in:
Anemia (↓ RBC)
Infection (non-functional WBC)
Bleeding (↓ platelets)
Can be acute vs. chronic; myeloid vs. lymphoid
Etiology: multifactorial – oncogene activation, chemo/radiation, viruses, pesticides, smoking, congenital disorders (Down syndrome)
Assessment / Labs
CBC: ↓ Hb & Hct, thrombocytopenia
WBC count may be ↓, normal, or ↑ but with high percentage of blasts
Bone-marrow aspiration/biopsy = diagnostic gold standard
Other: lumbar puncture (CNS involvement), cytogenetics (e.g., Philadelphia chromosome)
Classification (Table 34.25)
AML – \approx 80\% of adult acute cases (>60 yrs)
ALL – \approx 20\% of adult acute cases (>50 yrs)
CML – \approx 20\% chronic adult cases; median 67 yrs; Ph+; phases (chronic ⇒ accelerated ⇒ blast)
CLL – Most common adult leukemia; avg onset 72 yrs; B-cell origin
Treatment & Nursing Interventions
Combination chemotherapy (induction, consolidation, maintenance)
Corticosteroids, targeted therapy (imatinib for CML), radiation (CNS prophylaxis)
Hematopoietic stem-cell transplantation (HSCT) – potential cure
Supportive: infection prophylaxis, transfusions, psychosocial support
Coagulation Disorders
Thrombocytopenia – Platelets <150{,}000/\mu L
Can be acute, severe, prolonged
Bleeding risks: mucosal, cutaneous, intracranial
Immune Thrombocytopenia (ITP)
Autoantibody-mediated platelet destruction & splenic sequestration
Acute in kids; chronic in adults
Tx: corticosteroids, IVIG, splenectomy, rituximab, eltrombopag (TPO agonist)
Heparin-Induced Thrombocytopenia (HIT)
Onset 5–14 days after heparin initiation (sooner if prior exposure)
Pathophysiology: IgG antibodies vs. PF4-heparin complex → platelet activation → paradoxical thrombosis
Up to 5\% of IV heparin pts
Management: stop heparin, start non-heparin anticoagulant (argatroban), avoid platelet transfusion unless life-threatening bleed
Hemophilia – Hereditary Factor Deficiency
X-linked recessive → males affected, females carriers
Types:
Hemophilia A – Factor VIII deficiency ("classic"); 4× more common
Hemophilia B – Factor IX deficiency ("Christmas disease")
Clinical manifestations identical:
Prolonged bleeding, hematomas, hemarthrosis (joint bleeding), GI bleed, intracranial hemorrhage
Any bleeding episode can be fatal
Diagnosis (Table 34.17)
Coagulation studies: prolonged aPTT; normal PT & platelets
Factor assays quantify specific factor activity
Treatment (Table 34.18)
Factor replacement (recombinant VIII or IX) – on demand or prophylactic
Desmopressin (DDAVP) for mild Hemophilia A (releases endogenous factor VIII)
Antifibrinolytics: tranexamic acid for mucosal bleeding
Gene therapy trials emerging
Nursing Care
Prevent trauma: safe environment, protective gear, avoid contact sports
No IM injections or ASA/NSAIDs; use acetaminophen
Educate on bleeding recognition & self-infusion techniques
During bleed: immobilize joint, ice, elevate, give factor, then PT once swelling ↓
Ethical, Philosophical & Practical Considerations
Health disparities: SCD pain bias & under-treatment highlight systemic inequities
Genetic counseling: imperative for hereditary disorders (SCD, hemophilia, hemochromatosis)
Resource allocation: HSCT accessibility, high-cost biologics
Occupational/environmental justice: pesticide exposure & leukemia risk in farmworkers
End-of-life discussions: aggressive leukemias with poor prognosis
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