Note
0.0
(0)
Rate it
Take a practice test
Chat with Kai
Explore Top Notes
Chapter 4: Functional Anatomy of Prokaryotic and Eukaryotic Cells
Note
Studied by 48 people
5.0
(1)
Untitled
Note
Studied by 15 people
5.0
(1)
Current Issues and Future Trends in Health Care in Canada,
Note
Studied by 10 people
5.0
(1)
Ap Government Chapter 2 (Constitution)
Note
Studied by 105 people
5.0
(1)
Chapter 1 - Introduction & Test Strategies
Note
Studied by 45 people
5.0
(2)
Module 2: Understanding the Natural World
Note
Studied by 6 people
5.0
(1)
Home
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
Note
0.0
(0)
Rate it
Take a practice test
Chat with Kai
Explore Top Notes
Chapter 4: Functional Anatomy of Prokaryotic and Eukaryotic Cells
Note
Studied by 48 people
5.0
(1)
Untitled
Note
Studied by 15 people
5.0
(1)
Current Issues and Future Trends in Health Care in Canada,
Note
Studied by 10 people
5.0
(1)
Ap Government Chapter 2 (Constitution)
Note
Studied by 105 people
5.0
(1)
Chapter 1 - Introduction & Test Strategies
Note
Studied by 45 people
5.0
(2)
Module 2: Understanding the Natural World
Note
Studied by 6 people
5.0
(1)