Blood Components & CBC Basics
Understand what blood is made of before studying what goes wrong.
Blood consists of plasma (55%) and formed elements (45%). The formed elements include red blood cells (RBCs — carry oxygen via hemoglobin), white blood cells (WBCs — fight infection), and platelets (thrombocytes — clotting). The bone marrow produces all blood cells through a process called hematopoiesis.
Key CBC Values to Know
Ranges vary by lab, facility, and textbook — for exams, use the range given in the question. See the full NCLEX-PN lab-value reference & sources →
- RBC
- M: 4.6–6.2; F: 4.2–5.4 million/mcL. Low in anemia; high in polycythemia.
- Hemoglobin (Hgb)
- M: 13–18; F: 12–16 g/dL. Oxygen-carrying capacity. <8 g/dL = risk for heart failure.
- Hematocrit (Hct)
- M: 40–55%; F: 36–48%. Roughly 3× the Hgb. Elevated in dehydration, polycythemia.
- WBC
- 4,500–11,000/mm³. Elevated in infection/inflammation; low in bone marrow failure or chemo.
- Platelets
- 150,000–400,000/mm³. <50,000 = bleeding risk; <20,000 = spontaneous bleeding risk.
- Neutrophils
- 55–70% of WBCs. First responders to bacterial infection. ANC <1,000 = neutropenic.
- Reticulocytes
- 0.5–2.5%. Immature RBCs; elevated = bone marrow is actively producing RBCs.
Hematocrit is roughly 3 times the hemoglobin value. If Hgb is 10, expect Hct around 30%. When Hgb drops below 8 g/dL, the heart compensates by increasing cardiac output — watch for tachycardia, dyspnea, and signs of heart failure.
Every key point in this guide fits on one free printable page. Jump to the free cheatsheet PDF →
Iron Deficiency Anemia
The most common type of anemia worldwide.
Iron deficiency anemia occurs when the body doesn't have enough iron to produce adequate hemoglobin. This results in small, pale RBCs (microcytic, hypochromic). Common causes include chronic blood loss (heavy menstruation, GI bleeding), inadequate dietary intake, pregnancy, and poor absorption.
Signs & Symptoms
- Fatigue, weakness, pallor
- Dyspnea on exertion, tachycardia
- Brittle nails (koilonychia — spoon-shaped nails)
- Pale mucous membranes and conjunctivae
- Pica (craving non-food items like ice, dirt, starch)
- Glossitis (smooth, sore tongue)
Treatment & Teaching
- Oral iron supplements (ferrous sulfate) — take on an empty stomach for best absorption
- Take with Vitamin C (orange juice) to enhance absorption
- Do NOT take with milk, antacids, or calcium — they block iron absorption
- Use a straw for liquid iron — prevents tooth staining
- Expect dark/black stools (normal side effect, not a concern)
- Increase dietary iron: red meat, liver, spinach, beans, fortified cereals
- GI side effects are common (nausea, constipation) — may take with food if needed, though absorption decreases slightly
Iron + OJ = yes (vitamin C boosts absorption). Iron + Milk = no (calcium blocks absorption). Dark stools = expected. Straw = protect teeth.
Pernicious Anemia (Vitamin B12 Deficiency)
Caused by lack of intrinsic factor — leads to large, immature RBCs.
Pernicious anemia occurs when the stomach fails to produce intrinsic factor, which is needed to absorb vitamin B12 from the diet. Without B12, the bone marrow produces abnormally large, immature RBCs (macrocytic, megaloblastic) that cannot carry oxygen effectively. It can also be caused by strict vegan diets, gastric surgery, or Crohn's disease affecting the ileum.
Signs & Symptoms
- Standard anemia symptoms (fatigue, pallor, dyspnea, tachycardia)
- Neurological symptoms (unique to B12 deficiency): numbness and tingling in hands/feet (peripheral neuropathy), difficulty with balance and gait, confusion, memory loss
- Beefy red, sore tongue (glossitis)
Diagnosis & Treatment
- Schilling test (historical) or serum B12 level (low)
- MCV elevated (large RBCs)
- Lifelong vitamin B12 injections (IM) — oral supplements do not work because the patient can't absorb B12 without intrinsic factor
- Dietary sources of B12: meat, fish, eggs, dairy
Iron deficiency = small RBCs (microcytic). Pernicious/B12 = large RBCs (macrocytic). Iron deficiency does NOT cause neurological symptoms. B12 deficiency DOES cause neurological symptoms — and if untreated, the nerve damage can become permanent.
Aplastic Anemia
Complete bone marrow failure — all cell lines are affected.
Aplastic anemia is a rare, life-threatening condition where the bone marrow fails to produce adequate amounts of ALL blood cells, resulting in pancytopenia (low RBCs + low WBCs + low platelets). Causes include certain drugs (chloramphenicol, sulfonamides), toxic chemical or radiation exposure, viral infections, and autoimmune disease. Many cases are idiopathic.
Signs & Symptoms — The Triple Threat
- Low RBCs: Fatigue, pallor, tachycardia, dyspnea (anemia symptoms)
- Low WBCs: Frequent and severe infections, fever
- Low platelets: Bleeding, bruising, petechiae, prolonged bleeding from cuts
Treatment
- Remove the causative agent if known
- Blood and platelet transfusions (supportive)
- Bone marrow transplant (definitive treatment for severe cases)
- Immunosuppressive therapy if autoimmune
- Strict infection precautions (patient is immunocompromised)
Pancytopenia = think aplastic anemia. The patient has problems with ALL three cell lines, so they need protection from infection (low WBCs), monitoring for bleeding (low platelets), AND treatment for anemia symptoms (low RBCs) simultaneously.
Sickle Cell Disease
One of the most heavily tested hematology topics — know the crisis types, triggers, and management.
Sickle cell disease (SCD) is an autosomal recessive genetic disorder where abnormal hemoglobin (Hemoglobin S) causes RBCs to become rigid and sickle-shaped under low-oxygen conditions. These sickled cells clump together, block blood vessels, and die prematurely (lifespan ~20 days vs normal 120 days). Both parents must carry the gene for a child to have the disease.
Crisis Triggers (Must Know!)
- Dehydration (#1 trigger)
- Infection or illness
- Cold temperatures
- High altitudes
- Stress (physical or emotional)
- Strenuous exercise
Four Types of Sickle Cell Crisis
- Vaso-occlusivemost common
- Sickled cells block vessels → severe pain, organ ischemia, dactylitis (hand/foot swelling), priapism, stroke risk.
- Splenic sequestration
- Blood pools in spleen → sudden splenomegaly, severe anemia, hypovolemic shock. Can be fatal within hours. Most common in children ages 8 mo–5 yrs.
- Aplastic crisis
- Bone marrow temporarily stops making RBCs. Often triggered by parvovirus B19. Severe anemia, low reticulocyte count.
- Hyperhemolyticrarest
- Rapid RBC destruction. Jaundice, dark urine, worsening anemia.
Nursing Interventions During Crisis
- Hydration is #1 priority — IV fluids and encourage oral intake as prescribed — avoid both dehydration and overhydration. Keeps blood less viscous and prevents further sickling.
- Pain management — opioids (morphine, hydromorphone) are appropriate and necessary. Do NOT undertreat pain.
- Administer oxygen if SpO₂ is low
- Bed rest during acute crisis
- Blood transfusions as ordered
- Monitor for organ damage (stroke, acute chest syndrome, splenic rupture)
- Do NOT palpate the abdomen deeply if spleen is enlarged (rupture risk)
Key Medications
- Hydroxyurea: Increases fetal hemoglobin (HbF) which does not sickle. Reduces frequency and severity of crises and need for transfusions. Monitor CBC (can suppress bone marrow).
- Folic acid: Supports RBC production (high RBC turnover depletes folate).
- Vaccines: pneumococcal, meningococcal, flu — spleen compromise increases infection risk.
A life-threatening complication of SCD. Signs: chest pain, fever, cough, dyspnea, new pulmonary infiltrate on chest X-ray. It mimics pneumonia but can rapidly progress to respiratory failure. Treat with oxygen, IV fluids, antibiotics, pain management, and possibly exchange transfusion.
Polycythemia Vera
Too many RBCs — the opposite of anemia.
Polycythemia vera is a bone marrow disorder where the body produces too many red blood cells, making the blood abnormally thick (increased viscosity). This increases the risk of blood clots, stroke, and MI.
Signs & Symptoms
- Ruddy (reddish) complexion — flushed face
- Headache, dizziness, tinnitus (ringing in ears)
- Blurred vision
- Hypertension
- Pruritus (itching), especially after warm baths
- Splenomegaly
- Risk for DVT, stroke, MI due to thick blood
Treatment
- Phlebotomy — therapeutic blood removal to reduce hematocrit. Goal: Hct <45%.
- Hydration to reduce blood viscosity
- Low-dose aspirin to prevent clots
- Hydroxyurea may be used to suppress RBC production
- Avoid iron supplements (would stimulate more RBC production)
Polycythemia = Poly (many) + cythemia (blood cells). Too many RBCs → thick blood → ruddy face. Treatment removes blood (phlebotomy). Opposite of anemia in every way.
Thrombocytopenia & ITP
Low platelets = bleeding risk. Know the precautions.
Thrombocytopenia is a low platelet count (<150,000/mm³). Causes include bone marrow suppression (chemo), medications (heparin — HIT), autoimmune disorders, and liver disease. ITP (Immune Thrombocytopenic Purpura) is an autoimmune disorder where the body destroys its own platelets.
Signs & Symptoms
- Petechiae (tiny pinpoint red spots — hallmark sign)
- Purpura (larger purple bruises)
- Ecchymosis (bruising)
- Bleeding gums, nosebleeds (epistaxis)
- Blood in urine or stool
- Heavy menstrual bleeding
- Prolonged bleeding from minor cuts
Bleeding Precautions (Heavily Tested!)
- Use a soft-bristle toothbrush
- Use an electric razor (no straight razors)
- Avoid IM injections and invasive procedures when possible
- Apply prolonged pressure to venipuncture sites
- Avoid aspirin, NSAIDs (inhibit platelet function)
- No straining (stool softeners as needed)
- Avoid vigorous nose blowing — use chapstick to prevent dry/cracked lips
- Fall precautions — avoid contact sports
- Monitor stool and urine for occult blood
Platelet count <50,000 = implement bleeding precautions. <20,000 = risk of spontaneous bleeding. <10,000 = critical — may need platelet transfusion. If a question asks about a patient on heparin with a sudden drop in platelets → think HIT (Heparin-Induced Thrombocytopenia). Stop heparin immediately.
Hemophilia
Genetic bleeding disorders — know A vs B, inheritance, and management.
- Hemophilia AFactor VIII deficiency
- Most common. Factor VIII (8). X-linked recessive — primarily affects males. Females are carriers. ~30% are spontaneous mutations. Lab: Prolonged PTT (aPTT). PT/INR normal. Platelet count normal.
- Hemophilia BFactor IX deficiency
- Also called Christmas disease. Factor IX (9). Same inheritance pattern as A. Same labs: prolonged aPTT, normal PT/INR, normal platelets.
Signs & Symptoms
- Hemarthrosis (bleeding into joints) — most common complication. Leads to joint pain, swelling, progressive damage (especially knees)
- Prolonged bleeding from minor injuries, dental procedures, or circumcision
- Easy bruising, hematomas
- GI bleeding, hematuria
- Intracranial hemorrhage (most dangerous complication)
Nursing Interventions — RICE for Active Bleeding
- Rest — immobilize the affected area
- Ice — apply cold packs (vasoconstriction)
- Compression — apply direct pressure
- Elevation — elevate the affected extremity
- Administer factor replacement therapy as ordered (Factor VIII for Hemophilia A, Factor IX for Hemophilia B)
- Avoid aspirin and NSAIDs (inhibit platelet function)
- Avoid IM injections — use smallest gauge needle possible
- Avoid contact sports — encourage low-impact activities (swimming)
- Teach patient to recognize early signs of bleeding
- Desmopressin (DDAVP) may be used for mild Hemophilia A — stimulates release of stored Factor VIII
If a question mentions a child with hemophilia and joint swelling, the answer is to apply ICE (cold packs), not heat. Heat increases vasodilation and bleeding. Cold causes vasoconstriction and slows bleeding.
Disseminated Intravascular Coagulation (DIC)
Clotting AND bleeding at the same time — a life-threatening emergency.
DIC is a condition where the clotting cascade is triggered throughout the body, consuming all available clotting factors and platelets. Once depleted, the patient hemorrhages uncontrollably. DIC is never a primary disease — it is always triggered by an underlying condition.
Two Stages of DIC
Common Triggers
- Sepsis/severe infection (most common cause)
- Trauma, burns, head injury
- Cancer (especially leukemia)
- Obstetric complications (placental abruption, amniotic fluid embolism, HELLP syndrome, retained dead fetus)
- Shock (any type)
Lab Findings in DIC
- D-dimerELEVATED ↑
- Fibrin degradation products from all the clotting — key diagnostic test.
- PT/INRPROLONGED ↑
- Clotting factors are consumed.
- PTT (aPTT)PROLONGED ↑
- Clotting factors are consumed.
- PlateletsDECREASED ↓
- Platelets used up in clotting phase.
- FibrinogenDECREASED ↓
- Consumed in widespread clotting.
Treatment
- Treat the underlying cause — this is the #1 priority (antibiotics for sepsis, delivery for obstetric causes)
- Supportive transfusions: platelets, fresh frozen plasma (FFP), cryoprecipitate
- Heparin may be used in some cases (controversial — stops the clotting cascade)
- Monitor bleeding from all sites
If a question describes a patient with sepsis who is now bleeding from IV sites and has petechiae → think DIC. The key labs to remember: D-dimer UP, platelets DOWN, PT/PTT prolonged, fibrinogen DOWN. Treatment = treat the underlying cause.
Leukemia & Neutropenic Precautions
Understand the basics and — most importantly — how to protect these patients from infection.
Leukemia is cancer of the blood-forming tissues (bone marrow). The marrow produces large numbers of abnormal, immature WBCs (blast cells) that crowd out normal blood cells. This leads to anemia (low RBCs), infection risk (dysfunctional WBCs), and bleeding (low platelets). Diagnosis is confirmed by bone marrow biopsy.
Key Types (Simplified for LPN Level)
- ALLAcute Lymphocytic
- Most common childhood leukemia. Rapid onset. Good prognosis with treatment.
- AMLAcute Myelogenous
- Most common acute leukemia in adults. Aggressive, rapid onset.
- CLLChronic Lymphocytic
- Most common chronic leukemia. Seen in older adults. Slow progression.
- CMLChronic Myelogenous
- Associated with Philadelphia chromosome. Chronic phase may last years.
Neutropenic Precautions (Heavily Tested!)
When the ANC (Absolute Neutrophil Count) falls below 1,000/mm³, the patient is neutropenic and at extreme risk for infection. Infection is the #1 cause of death in leukemia patients.
- Private room — no roommate with active infection
- Strict hand hygiene (#1 infection prevention measure)
- Limit visitors — no visitors who are ill
- No fresh flowers, fresh fruits, or raw vegetables (harbor bacteria/mold)
- Avoid crowds and anyone with infections
- Monitor temperature frequently — fever may be the ONLY sign of infection (patient may not show typical infection signs due to suppressed immune response)
- Avoid rectal temperatures, suppositories, and enemas (risk of rectal tear → infection portal)
- No intramuscular injections
- Meticulous oral care with soft toothbrush
- Report temperature ≥100.4°F (38°C) immediately
Chemotherapy destroys fast-growing cells — including bone marrow cells. The nadir (lowest point of blood counts) typically occurs 7–14 days after chemo. During this time, patients are most vulnerable to infection, bleeding, and severe anemia. Monitor CBC closely.
Blood Transfusions
Know the protocol, the reactions, and the #1 action if a reaction occurs.
Blood Type Compatibility
- O-Universal DONOR
- Can donate to everyone. Can only receive from O-.
- AB+Universal RECIPIENT
- Can only donate to AB+. Can receive from everyone.
- O+
- Can donate to O+, A+, B+, AB+. Can receive from O+, O-.
- A+
- Can donate to A+, AB+. Can receive from A+, A-, O+, O-.
Transfusion Protocol
- Two nurses must verify the blood product against the patient's ID band (name, DOB, medical record number, blood type, Rh factor, expiration date)
- Take baseline vital signs 15 minutes before starting
- Use an 18-gauge or larger IV
- Only normal saline (0.9% NS) is compatible with blood products — no dextrose, no LR, no medications in the same line
- Stay with the patient for the first 15 minutes — most severe reactions occur early
- Monitor vital signs: before, 15 min after starting, then per facility policy, and at completion
- RBCs must be infused within 4 hours (bacteria growth risk after 4 hrs)
- Platelets and plasma: infuse within 30–60 minutes
Transfusion Reactions
- Hemolyticmost dangerous
- Fever, chills, flank pain, hypotension, hemoglobinuria (dark/red urine), tachycardia. Cause: ABO incompatibility — can be fatal.
- Febrile (non-hemolytic)
- Fever, chills, headache (most common reaction). Cause: Antibodies react to donor WBCs.
- Allergic
- Urticaria (hives), itching, flushing; severe: anaphylaxis. Cause: Allergy to plasma proteins.
- Fluid overload (TACO)
- Dyspnea, crackles, JVD, hypertension, tachycardia. Cause: Too much volume too fast (especially in elderly/HF patients).
1) STOP the transfusion immediately. 2) Keep the IV open with NS (new tubing). 3) Stay with the patient. 4) Take vital signs. 5) Notify the provider. 6) Send the blood bag and tubing to the lab. 7) Collect urine sample. 8) Document everything. The first action is ALWAYS stop the transfusion.
? A patient receiving a blood transfusion develops fever, chills, and flank pain 10 minutes in. What is the first nursing action?
Key Labs & Medications
Quick reference for hematology labs and the drugs you need to know.
- HgbM: 13–18; F: 12–16 g/dL
- Low = anemia. <8 = cardiac risk.
- HctM: 40–55%; F: 36–48%
- ~3× Hgb. High = polycythemia or dehydration.
- Platelets150,000–400,000
- <50K = bleeding precautions. <20K = spontaneous bleeding.
- WBC4,500–11,000
- High = infection. Low = immunosuppressed.
- PT/INRPT: 11–13.5 sec; INR: 0.8–1.1
- Monitors warfarin. Prolonged in DIC, liver disease.
- PTT (aPTT)25–35 sec
- Monitors heparin. Prolonged in hemophilia, DIC.
- D-dimer<0.5 mcg/mL
- Elevated = clot breakdown. Key test for DIC and DVT/PE.
- FerritinM: 12–300; F: 12–150 ng/mL
- Best indicator of iron stores. Low = iron deficiency.
- Reticulocyte count0.5–2.5%
- Elevated = marrow is responding (making new RBCs).
- B12200–900 pg/mL
- Low = pernicious anemia.
Key Medications
- Ferrous sulfateiron deficiency
- Take with vitamin C. Avoid milk/antacids. Dark stools expected. Straw for liquid form.
- Cyanocobalamin (B12)pernicious anemia
- Lifelong IM injections. Cannot be absorbed orally without intrinsic factor.
- Epoetin alfa (Epogen/Procrit)anemia of CKD, chemo-induced
- Stimulates RBC production. Monitor BP (can cause HTN). Do not shake vial. Must take iron supplement concurrently.
- Hydroxyureasickle cell disease
- Increases fetal Hgb. Reduces crisis frequency. Monitor CBC (bone marrow suppression risk).
- Folic acidfolate deficiency, sickle cell
- Supports RBC production. Important in pregnancy (prevents neural tube defects).
- Desmopressin (DDAVP)mild Hemophilia A
- Stimulates release of Factor VIII. Also used for von Willebrand disease.
- Factor VIII / IX concentratesHemophilia A / B
- Replacement therapy for missing clotting factors.
- Heparinanticoagulant
- Monitor aPTT. Watch for HIT. Antidote: protamine sulfate.
- Warfarinanticoagulant
- Monitor INR (2.0–3.0). Antidote: Vitamin K. Many food/drug interactions.
Frequently Asked Questions
Common student questions on this topic.
What are normal CBC values to know?
What is the difference between iron-deficiency anemia and pernicious anemia?
What is sickle cell crisis and how is it managed?
What is DIC (disseminated intravascular coagulation)?
What are the signs of leukemia and what is the priority nursing concern?
How do I administer a blood transfusion safely?
Quick-Reference Cheatsheet
Every key point from this guide on a single printable page.
Hematology Disorders Cheatsheet
One-page PDF — free download.