Hematologic Assessment and the Anemias - Cheat Sheet
Your 30-minute exam companion for hematologic nursing. Covers CBC interpretation, blood typing, and anemia classification with high-yield facts, lab values, and nursing priorities.
NORMAL HEMATOLOGIC VALUES (CRITICAL)
Common values
Value
13–18 g/dL
Symbol
Hgb
Quantity
Hemoglobin — Male
Value
12–16 g/dL
Symbol
Hgb
Quantity
Hemoglobin — Female
Value
42–52%
Symbol
Hct
Quantity
Hematocrit — Male
Value
37–47%
Symbol
Hct
Quantity
Hematocrit — Female
Value
150,000–400,000/µL
Symbol
Plt
Quantity
Platelets
Value
5,000–10,000/µL
Symbol
WBC
Quantity
WBC
Value
< 80 fL
Symbol
MCV
Quantity
MCV (Microcytic threshold)
Value
100 fL
Symbol
MCV
Quantity
MCV (Macrocytic threshold)
Value
0.5–2%
Symbol
Retic
Quantity
Reticulocyte count
Important facts
- Hemoglobin (Hgb) — MALE: 13–18 g/dL | FEMALE: 12–16 g/dL
- Hematocrit (Hct) — MALE: 42–52% | FEMALE: 37–47% (approximately 3× hemoglobin value)
- RBC count: 4.2–6.1 million/µL
- WBC count: 5,000–10,000/µL (or 5–10 K/µL)
- Platelets (Thrombocytes): 150,000–400,000/µL (or 150–400 K/µL)
- MCV (Mean Cell Volume): 80–100 fL — classifies anemia by cell size
- Reticulocytes: 0.5–2% — reflects bone marrow response to demand
- Absolute Neutrophil Count (ANC) < 500/µL = SEVERE NEUTROPENIA (high infection risk)
- Indirect bilirubin (elevated in hemolysis): normal 0.1–0.3 mg/dL
- Haptoglobin (low in hemolysis): normal 30–200 mg/dL
Diagrams to know
- CBC parameters and what each tells you
- Hematocrit vs. Hemoglobin relationship
MCV-BASED ANEMIA CLASSIFICATION
Formulas
MCV < 80 fL = MICROCYTIC
Meaning
Red cells are smaller than normal; associated with iron deficiency primarily
Watch out
Do NOT confuse with macrocytic; microcytic is the OPPOSITE — small cells, not large
When to use
Interpreting CBC; patient has low Hgb and low MCV
MCV 80–100 fL = NORMOCYTIC
Meaning
Red cells are normal size; seen in bone marrow failure or acute blood loss
Watch out
Normocytic anemias may be hard to differentiate on CBC alone — need additional testing (bone marrow biopsy for aplasia)
When to use
CBC shows low Hgb but normal-sized RBCs
MCV > 100 fL = MACROCYTIC
Meaning
Red cells are larger than normal; seen in B12 or folate deficiency
Watch out
Macrocytic does NOT mean more hemoglobin — means LARGER cells but often FEWER of them
When to use
CBC shows low Hgb, elevated MCV, and hypersegmented neutrophils
Important facts
- IRON DEFICIENCY = microcytic, hypochromic, low ferritin, high TIBC, low serum iron
- B12 DEFICIENCY (pernicious) = macrocytic, megaloblastic, neurologic signs (paresthesias, ataxia)
- FOLATE DEFICIENCY = macrocytic, megaloblastic, NO neurologic signs (key difference from B12)
- APLASTIC ANEMIA = normocytic, pancytopenia, hypocellular marrow
- HEMOLYTIC ANEMIA = normocytic (or microspherocytic), high reticulocytes, high bilirubin, low haptoglobin, positive direct Coombs
- ACUTE BLOOD LOSS = normocytic (initially), low Hgb, high reticulocytes after marrow response kicks in
Key definitions
Microcytic Anemia
Example
Patient with heavy menstrual bleeding, low ferritin, low serum iron, high TIBC
Low hemoglobin with MCV < 80 fL; cells are too small to carry normal O₂; most commonly iron deficiency.
Macrocytic Anemia
Example
Pernicious anemia patient with paresthesias and positive intrinsic factor antibodies
Low hemoglobin with MCV > 100 fL; large immature RBCs from impaired DNA synthesis (B12 or folate deficiency).
Normocytic Anemia
Example
Aplastic anemia with pancytopenia and hypocellular marrow
Low hemoglobin with normal MCV (80–100 fL); RBC size is normal but count is low; suggests marrow failure or acute loss.
Diagrams to know
- MCV classification tree (microcytic → iron deficiency; macrocytic → B12/folate; normocytic → aplasia/acute loss)
- Reticulocyte response pattern (high = compensating; low = marrow failure)
BLOOD TYPING AND COMPATIBILITY (CRITICAL FOR NLE)
Important facts
- TYPE O-NEGATIVE = UNIVERSAL DONOR (no A, B, or D antigens; safe in emergencies)
- TYPE AB-POSITIVE = UNIVERSAL RECIPIENT (no ABO antibodies; can receive all types)
- TYPE A has ANTI-B antibodies (will attack B or AB blood)
- TYPE B has ANTI-A antibodies (will attack A or AB blood)
- TYPE AB has NO ABO antibodies (safe to receive A, B, AB, or O)
- TYPE O has ANTI-A AND ANTI-B antibodies (will attack A, B, or AB)
- Rh-negative + Rh-positive exposure → anti-D antibodies form → future Rh-positive transfusions or pregnancies at risk
- RhoGAM (Rh immunoglobulin) given within 72 hours of Rh-positive exposure in Rh-negative women prevents sensitization
- Crossmatch confirms ABO/Rh compatibility; Coombs detects antibodies (direct = on cells; indirect = in serum)
- Hemolytic transfusion reaction = incompatible type transfused; immediate fever, flank pain, hemoglobinuria, DIC
Key definitions
Type A Blood
Example
Patient with A antigen; will hemolyze if given B or AB blood
Antigen A on RBC; anti-B antibodies in plasma; can RECEIVE from A and O; can DONATE to A and AB.
Type B Blood
Example
Type B patient; reacts to A or AB antigens
Antigen B on RBC; anti-A antibodies in plasma; can RECEIVE from B and O; can DONATE to B and AB.
Type AB Blood (Universal Recipient)
Example
AB-positive patient in massive transfusion can safely receive any ABO type
Antigens A AND B on RBC; NO ABO antibodies in plasma; can RECEIVE from all types (A, B, AB, O).
Type O Blood (Universal Donor)
Example
O-negative used in trauma/emergency before crossmatch; O-positive for non-emergency O recipients
NO A or B antigens on RBC; anti-A AND anti-B antibodies in plasma; can DONATE to all types; can RECEIVE only O.
Rh Factor
Example
Rh-negative mother carrying Rh-positive fetus risks hemolytic disease of newborn in subsequent pregnancies without RhoGAM
RBC antigen (Rh-positive) or absent (Rh-negative); Rh-negative individuals produce anti-D antibodies ONLY after exposure to Rh-positive blood.
Direct Coombs Test
Example
Positive direct Coombs in warm autoimmune hemolytic anemia
Detects antibodies BOUND to patient's own RBCs; positive in immune hemolytic anemia, hemolytic transfusion reactions.
Indirect Coombs Test
Example
Positive indirect Coombs in Rh-negative pregnant woman exposed to Rh-positive blood
Detects FREE antibodies in patient's plasma/serum; used for compatibility testing and prenatal screening.
Diagrams to know
- ABO compatibility matrix (who can give to whom)
- Rh sensitization timeline (exposure → antibody formation → next pregnancy risk)
IRON-DEFICIENCY ANEMIA
Formulas
Serum Ferritin = BEST marker of iron stores
Meaning
Reflects total body iron; low ferritin = iron deficiency
Watch out
Ferritin is an acute-phase reactant; can be falsely elevated in inflammation, infection, or malignancy
When to use
Confirming iron-deficiency anemia diagnosis
TIBC (Total Iron-Binding Capacity) HIGH in iron deficiency
Meaning
Body upregulates iron-binding proteins when iron is scarce; inverse relationship with serum iron
Watch out
TIBC elevated (not low) in deficiency — opposite of ferritin/serum iron direction
When to use
Iron studies panel interpretation
Common values
Value
325 mg tablet
Symbol
Fe²⁺ salt
Quantity
Ferrous sulfate dose
Value
65 mg
Symbol
Fe elemental
Quantity
Elemental iron in ferrous sulfate 325 mg
Value
30–300 ng/mL (gender and age dependent)
Symbol
Ferritin
Quantity
Normal serum ferritin
Value
60–170 µg/dL
Symbol
Fe serum
Quantity
Normal serum iron
Value
250–425 µg/dL
Symbol
TIBC
Quantity
Normal TIBC
Important facts
- CAUSES: chronic blood loss (GI bleeding, heavy menstruation), inadequate intake, malabsorption, increased demand (pregnancy, infancy)
- LABS: low Hgb/Hct, low MCV (< 80), low serum ferritin, low serum iron, HIGH TIBC, low serum iron/TIBC ratio
- SIGNS: koilonychia (spoon nails), glossitis (sore tongue), angular cheilitis (cracks at mouth corners), pica (craving ice, dirt, starch)
- TREATMENT: ferrous sulfate 325 mg (65 mg elemental iron) 1–3 times daily
- ORAL IRON: give on EMPTY STOMACH for absorption; give with VITAMIN C (orange juice) to enhance absorption
- AVOID WITH IRON: milk, antacids, tea, coffee, dairy — these BLOCK absorption
- SIDE EFFECTS: black/tarry stools (harmless, expected), constipation, GI upset — can give with food if intolerable (reduces absorption slightly)
- LIQUID IRON: give through a STRAW to prevent teeth staining
- PARENTERAL IRON (iron dextran, iron sucrose): for malabsorption or intolerance; give IM by Z-TRACK technique to prevent skin staining; watch for anaphylaxis (test dose for dextran)
- INVESTIGATION: always identify and treat SOURCE of blood loss, especially occult GI bleeding in adults
Key definitions
Iron-Deficiency Anemia
Example
Woman with heavy menstrual bleeding, low Hgb, low MCV, low ferritin, high TIBC, koilonychia
Most common anemia worldwide; microcytic, hypochromic RBCs from insufficient iron for hemoglobin synthesis.
Koilonychia
Example
Chronic iron-deficiency anemia patient presents with nails that curve inward
Spoon-shaped nails (concave, inverted) characteristic of iron deficiency.
Diagrams to know
- Iron absorption factors (vitamin C enhances; tea, coffee, dairy block)
- Hemoglobin synthesis pathway (showing iron requirement)
VITAMIN B12 DEFICIENCY & PERNICIOUS ANEMIA
Formulas
B12 required for DNA synthesis + myelin formation
Meaning
Deficiency → impaired cell division (macrocytic anemia) + neurologic damage (demyelination)
Watch out
Neurologic damage may be IRREVERSIBLE if B12 deficiency goes untreated for months/years
When to use
Understanding why B12 deficiency causes BOTH anemia and neurologic signs
Common values
Value
200–900 pg/mL
Symbol
B12 or cobalamin
Quantity
Normal vitamin B12 level
Important facts
- CAUSES of B12 deficiency: pernicious anemia (autoimmune), gastrectomy (loss of parietal cells), ileal disease (malabsorption), strict vegan diet (no animal sources)
- LABS: low B12 level, macrocytic anemia (MCV > 100), hypersegmented neutrophils (> 5 lobes), megaloblastic marrow
- SYMPTOMS: anemia (fatigue, pallor, dyspnea) PLUS neurologic signs — paresthesias (hands/feet), ataxia, impaired proprioception, confusion, dementia if untreated
- KEY DIFFERENCE FROM FOLATE: B12 deficiency has NEUROLOGIC signs; folate deficiency does NOT
- TREATMENT: LIFELONG IM vitamin B12 (cyanocobalamin) — because pernicious anemia is permanent, oral replacement cannot work (no intrinsic factor)
- IM B12 SCHEDULE: initial loading phase (daily or weekly) then monthly maintenance injections FOREVER
- Neurologic damage is IRREVERSIBLE if delayed — early recognition and treatment critical
- Pernicious anemia associated with increased risk of gastric cancer (monitor with endoscopy)
- Schilling test: normal → pernicious anemia ruled out; abnormal corrected by IF → pernicious anemia; abnormal NOT corrected → ileal malabsorption
Key definitions
Pernicious Anemia
Example
Elderly patient with antibodies to intrinsic factor, low B12, macrocytic anemia, paresthesias, ataxia
Autoimmune destruction of gastric parietal cells → loss of intrinsic factor → B12 malabsorption; macrocytic, megaloblastic anemia with neurologic signs.
Intrinsic Factor
Example
Pernicious anemia = lack of intrinsic factor → oral B12 useless; must give IM (bypasses absorption)
Glycoprotein produced by gastric parietal cells; ESSENTIAL for B12 absorption in terminal ileum.
Schilling Test
Example
Poor excretion corrected by intrinsic factor = pernicious anemia; poor excretion NOT corrected = ileal disease
Historically used to diagnose B12 malabsorption; measures urinary excretion of radiolabeled B12 with/without intrinsic factor; now largely replaced by antibody testing.
Beefy Red Glossitis
Example
Pernicious anemia patient with painful, inflamed tongue
Sore, swollen, bright red tongue characteristic of B12 deficiency; also seen in folate and iron deficiency.
Diagrams to know
- B12 absorption pathway (IF binding in stomach → terminal ileum → absorption)
- Neurologic manifestations timeline (early paresthesias → late ataxia/dementia)
FOLATE DEFICIENCY ANEMIA
Common values
Value
2.7–17 ng/mL
Symbol
Folate
Quantity
Normal serum folate
Value
140–960 ng/mL
Symbol
RBC folate
Quantity
Normal RBC folate
Important facts
- CAUSES: inadequate dietary intake (alcoholics, elderly, poor), malabsorption (celiac, Crohn's), increased demand (pregnancy, hemolysis), drugs (methotrexate, anticonvulsants)
- LABS: low serum folate (< 2.7 ng/mL) or RBC folate, macrocytic anemia, hypersegmented neutrophils, megaloblastic marrow
- SOURCES: leafy greens, legumes, fortified grains, citrus fruits
- TREATMENT: oral folic acid 1–5 mg daily or IM if malabsorption
- CRITICAL DIFFERENCE: NO neurologic signs (unlike B12 deficiency)
- CAUTION: treating folate deficiency does NOT treat concurrent B12 deficiency; must rule out B12 deficiency first
- Pregnant women need folate supplementation (400 µg minimum daily) to prevent neural tube defects
Key definitions
Folate-Deficiency Anemia
Example
Homeless patient with poor diet, alcohol abuse, macrocytic anemia, elevated MCV, no paresthesias
Macrocytic, megaloblastic anemia from insufficient folate; impairs DNA synthesis; does NOT cause neurologic signs (key difference from B12).
Diagrams to know
- Macrocytic anemia differential (B12 vs. folate vs. alcohol vs. hypothyroidism)
APLASTIC ANEMIA
Formulas
PANCYTOPENIA (low RBC + low WBC + low platelets) from bone marrow FAILURE
Meaning
All three cell lines suppressed → anemia + infection risk + bleeding risk
Watch out
Not every pancytopenia is aplastic — must confirm with hypocellular bone marrow biopsy
When to use
CBC shows reduced Hgb, WBC, AND platelets; patient at high infection and bleeding risk
ANC < 500/µL = SEVERE NEUTROPENIA (infection emergency)
Meaning
Absolute neutrophil count calculated from WBC differential; < 500 = very high infection risk
Watch out
ANC < 500 is a medical emergency; fever in this setting requires immediate antibiotics
When to use
Interpreting CBC in aplastic anemia or chemotherapy; guides infection precautions
Common values
Value
< 500/µL
Symbol
ANC
Quantity
ANC indicating severe neutropenia
Value
500–1,000/µL
Symbol
ANC
Quantity
ANC indicating moderate neutropenia
Important facts
- CAUSES: idiopathic (most common ~70%), drugs/chemicals (chloramphenicol, benzene, gold salts, NSAIDs), radiation, viral infection (EBV, HIV, parvovirus), autoimmune processes
- PATHOPHYSIOLOGY: bone marrow stem cell damage/destruction → failure to produce RBCs, WBCs, platelets
- LABS: pancytopenia on CBC (normocytic anemia), reticulocyte count LOW (marrow not responding), hypocellular/acellular marrow biopsy
- CLINICAL PRESENTATION: anemia symptoms (fatigue, pallor, dyspnea) + leukopenia signs (fever, recurrent infections) + thrombocytopenia signs (petechiae, bruising, bleeding gums)
- MANAGEMENT: remove causative agent (stop drug, stop radiation), supportive transfusions (RBC and platelet), immunosuppressive therapy (ATG, cyclosporine), stem cell transplant (curative but requires matched donor)
- NURSING PRIORITIES: strict infection precautions (protective isolation), monitor ANC closely, fever = emergency (start antibiotics immediately), bleeding precautions (soft toothbrush, avoid IM injections)
- Prognosis depends on severity and response to immunosuppression; younger patients with matched donors benefit from transplant
Key definitions
Aplastic Anemia
Example
Patient exposed to benzene, develops fever (from leukopenia), bleeding (from thrombocytopenia), fatigue (from anemia)
Bone marrow failure producing pancytopenia (low RBCs, WBCs, platelets); normocytic, normochromic; marrow biopsy shows hypocellular/acellular marrow.
Pancytopenia
Example
CBC: Hgb 7, WBC 2,000, platelets 40,000 = pancytopenia
Simultaneous reduction of all three major blood cell lines (RBCs, WBCs, platelets) reflecting global bone marrow failure.
Diagrams to know
- Bone marrow failure cascade (stem cell damage → pancytopenia → anemia + infection + bleeding)
- Infection risk stratification by ANC
HEMOLYTIC ANEMIA
Formulas
RBC DESTRUCTION faster than marrow replacement → hemolytic anemia
Meaning
Premature RBC death from inherited or acquired causes; marrow tries to compensate (high reticulocytes)
Watch out
Hemolytic anemia is NORMOCYTIC unless microspherocytes or sickled cells change morphology
When to use
Patient has anemia + jaundice + high bilirubin + high reticulocytes + low haptoglobin
DIRECT COOMBS POSITIVE = immune-mediated hemolysis
Meaning
Antibodies bound to RBC surface; classic in autoimmune hemolytic anemia, transfusion reactions, hemolytic disease of newborn
Watch out
Negative Coombs does NOT rule out hemolysis — think mechanical (schistocytes), inherited (sickle, G6PD), drug-induced
When to use
Confirming immune cause of hemolysis
Common values
Value
30–200 mg/dL
Symbol
Haptoglobin
Quantity
Normal haptoglobin
Value
140–280 IU/L
Symbol
LDH
Quantity
Normal LDH
Value
0.1–0.3 mg/dL
Symbol
Bili indirect
Quantity
Indirect bilirubin (normal)
Important facts
- INHERITED HEMOLYTIC ANEMIAS: sickle cell disease (HbS), thalassemia, G6PD deficiency, hereditary spherocytosis
- ACQUIRED HEMOLYTIC ANEMIAS: autoimmune (warm or cold antibodies), transfusion reactions, drugs (penicillin, quinine), mechanical (prosthetic valve, disseminated intravascular coagulation), microangiopathic (TTP, HUS)
- LABS of hemolysis: low Hgb, normocytic (or microspherocytic), HIGH reticulocyte count (marrow compensating), elevated indirect (unconjugated) bilirubin, elevated LDH, LOW haptoglobin, positive direct Coombs (if immune)
- SIGNS OF HEMOLYSIS: jaundice (from bilirubin), dark urine (hemoglobinuria/myoglobinuria), splenomegaly (RBC destruction), gallstones (pigment stones from chronic bilirubin), pallor
- SICKLE CELL CRISIS TRIGGERS: hypoxia, dehydration, infection, acidosis, cold exposure, physical/emotional stress
- SICKLE CELL CRISIS MANAGEMENT: aggressive hydration (IV fluids, maintain urine output), supplemental oxygen (if hypoxic), PAIN CONTROL (IV opioids, NSAIDs), treat underlying infection, monitor for acute chest syndrome
- HYDROXYUREA: increases fetal hemoglobin (HbF) → reduces sickling → decreases crisis frequency
- GENERAL MANAGEMENT: treat cause, folic acid (high marrow turnover), transfusions (exchange transfusion preferred in acute crisis), consider splenectomy (reduces RBC destruction)
- SPLENECTOMY PRECAUTION: must vaccinate against Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis pre-operatively
Key definitions
Hemolytic Anemia
Example
Sickle cell patient in crisis with jaundice, hemoglobinuria, elevated bilirubin, high reticulocytes, positive direct Coombs
Anemia from accelerated RBC destruction (lifespan < 120 days); compensatory marrow response produces high reticulocyte count; normocytic.
Sickle Cell Disease
Example
Patient with SCD presents with acute chest pain, dyspnea, fever = sickle cell crisis triggered by infection
Inherited hemoglobinopathy (HbS); RBCs sickle under hypoxia/dehydration/infection/acidosis/cold → vaso-occlusive crises, organ infarction, chronic hemolysis.
Vaso-Occlusive Crisis
Example
Sickle cell patient with severe bone pain, fever, elevated WBC, positive blood culture (sepsis trigger)
Acute episode of severe pain from microvascular occlusion by sickled RBCs; can affect bone, lungs, spleen, brain, kidneys.
Haptoglobin
Example
Hemolytic patient: low haptoglobin, high LDH, elevated indirect bilirubin, dark urine
Plasma protein that binds free hemoglobin; LOW in hemolytic anemia (Hb-haptoglobin complexes removed from circulation).
Diagrams to know
- Hemolysis cascade (RBC destruction → bilirubin, LDH, low haptoglobin → jaundice)
- Sickle cell crisis triggers and management algorithm
RETICULOCYTE COUNT INTERPRETATION
Formulas
HIGH reticulocytes (> 2%) = Marrow IS responding
Meaning
Bone marrow compensating for RBC loss or destruction; seen in acute hemorrhage, hemolysis, or recovery from nutritional deficiency
Watch out
In hemolytic anemia, reticulocytes may be falsely low if a reticulocytopenia crisis occurs (parvovirus)
When to use
Differentiating bleeding/hemolysis (reticulocytes up) from marrow failure (reticulocytes down)
LOW reticulocytes (< 0.5%) = Marrow is NOT responding
Meaning
Bone marrow failure (aplasia, leukemia), nutritional deficiency (iron, B12, folate), or chronic kidney disease (low erythropoietin)
Watch out
Low reticulocytes in anemia = bad sign (marrow failure); do NOT expect spontaneous recovery without treatment
When to use
Anemia with LOW reticulocytes suggests marrow problem, not blood loss/hemolysis
Common values
Value
0.5–2%
Symbol
Retic
Quantity
Normal reticulocyte count
Value
5–10% or higher
Symbol
Retic
Quantity
Reticulocyte count in acute hemorrhage
Important facts
- Reticulocyte count = barometer of marrow response to anemia
- HIGH reticulocytes indicate adequate marrow function (good prognosis if cause is treatable)
- LOW reticulocytes in anemia = marrow failure (bad prognosis without intervention)
- In acute blood loss: reticulocytes lag initially (takes 2–5 days to peak) because marrow must first increase erythropoietin
- In hemolysis: reticulocytes chronically elevated (marrow working overtime)
- In iron/B12/folate deficiency: initial reticulocytes low; rise after starting replacement therapy
- Corrected reticulocyte count = reticulocyte % × (patient Hct / normal Hct) — accounts for low Hct falsely elevating percent
Key definitions
Reticulocyte
Example
Acute hemorrhage: reticulocytes spike to 5–10% as marrow ramps up RBC production
Immature RBC; contains ribosomes (visible with supravital stain); reflects marrow's recent RBC production; normal 0.5–2% of RBC count.
Diagrams to know
- Reticulocyte response timeline (acute blood loss, hemolysis, post-treatment)
NURSING ASSESSMENT & PHYSICAL EXAM FINDINGS
Important facts
- HISTORY: fatigue, dyspnea, dizziness, palpitations, bleeding/bruising, recurrent infections, diet (iron, B12, folate sources), medications (anticoagulants, NSAIDs, chemotherapy), family history
- GENERAL APPEARANCE: pallor (conjunctiva, nail beds, palms more reliable in darker skin), jaundice (hemolysis), cyanosis (severe hypoxia)
- CARDIOVASCULAR: tachycardia, tachypnea, systolic flow murmur (anemia → high cardiac output)
- MUCOUS MEMBRANES: glossitis (iron/B12/folate), angular cheilitis (cracks at mouth corners), petechiae, bleeding gums (thrombocytopenia or coagulopathy)
- SKIN: petechiae, purpura, ecchymoses (bleeding disorders), spoon nails (iron deficiency)
- NEUROLOGIC: paresthesias, ataxia, impaired proprioception, confusion (B12 deficiency) — key differentiator from folate or iron deficiency
- PALPATION: lymphadenopathy (malignancy, infection), splenomegaly (hemolysis, malignancy, portal hypertension), hepatomegaly (hemolysis, malignancy)
Key definitions
Pallor
Example
Anemia patient with pale conjunctivae and nail beds
Pale appearance from reduced hemoglobin/oxygen; look at conjunctiva, nail beds, palms, oral mucosa (useful in darker skin).
Glossitis
Example
Pernicious anemia with beefy red glossitis
Inflamed, sore tongue; seen in iron, B12, and folate deficiency.
Koilonychia
Example
Iron-deficiency anemia patient with inverted nail beds
Spoon-shaped, concave nails characteristic of chronic iron deficiency.
Petechiae
Example
Aplastic anemia patient with petechiae on lower extremities
Tiny red/purple pinpoint spots from capillary bleeding; non-blanching; sign of thrombocytopenia.
Purpura
Example
Thrombocytopenia with widespread purpura
Larger red/purple patches (> 3 mm) from bleeding; non-blanching; indicates platelet/coagulation problem.
Diagrams to know
- Anemia assessment flow (history → physical exam → CBC → additional labs based on MCV)
TRANSFUSION MANAGEMENT & PRECAUTIONS
Important facts
- UNIVERSAL DONOR (O-negative): no A, B, or D antigens; safe for all recipients in emergencies
- UNIVERSAL RECIPIENT (AB-positive): no ABO antibodies; can receive all ABO and Rh types
- PRE-TRANSFUSION: obtain type and crossmatch (unless life-threatening emergency → use O-negative)
- VERIFY: two nurses verify patient ID, blood type, unit number before hanging transfusion
- INFUSION: start slowly (50 mL over 15 minutes), monitor vitals every 15 min × 1 hour, then per protocol
- HEMOLYTIC REACTION SIGNS: fever, chills, back/flank pain, chest pain, dyspnea, hemoglobinuria (dark urine), hypotension, DIC (bleeding)
- IF REACTION SUSPECTED: STOP transfusion immediately, keep IV patent, check vitals, verify patient/blood unit ID, return blood to blood bank, send patient urine to lab, send blood for direct Coombs
- MANAGEMENT OF HEMOLYTIC REACTION: IV hydration (maintain urine output > 200 mL/hour), loop diuretics (furosemide) to prevent acute tubular necrosis, alkalinize urine (sodium bicarbonate) to prevent Hgb precipitation in tubules
- DELAYED HEMOLYTIC REACTION: occurs 3–10 days post-transfusion; mild fever, anemia worsening (indirect Coombs positive); supportive care
- ROLE OF RhoGAM (Rh immunoglobulin): given within 72 hours to Rh-negative women after exposure to Rh-positive blood (transfusion accident, pregnancy); prevents anti-D antibody formation
Key definitions
Type and Crossmatch
Example
Type O-negative patient receives type O-negative blood (universal donor) after emergency crossmatch
Pre-transfusion test confirming ABO/Rh compatibility and detecting unexpected antibodies via indirect Coombs.
Hemolytic Transfusion Reaction (Acute)
Example
Patient receiving type A blood despite being type B; develops fever, back pain, dark urine within minutes
Immediate immune reaction to incompatible blood; caused by ABO incompatibility or alloimmunization; presents with fever, flank pain, hemoglobinuria, DIC.
Diagrams to know
- Transfusion protocol (identification → verification → infusion → monitoring)
- Hemolytic reaction emergency response algorithm
PHARMACOLOGY: HEMATOLOGIC AGENTS
Common values
Value
325 mg
Symbol
Fe²⁺
Quantity
Ferrous sulfate tablet strength
Value
65 mg
Symbol
Fe elemental
Quantity
Elemental iron in ferrous sulfate 325 mg
Value
1,000 µg
Symbol
Cyanocobalamin
Quantity
Standard B12 IM injection dose
Important facts
- IRON DOSING: ferrous sulfate 325 mg (65 mg elemental) 1–3 times daily on empty stomach
- IRON ABSORPTION: enhanced by vitamin C (orange juice), blocked by milk/antacids/tea/coffee; take 2+ hours apart from these
- IRON SIDE EFFECTS: black/tarry stools (expected, harmless), constipation (give stool softener), nausea/GI upset (take with food, accept slight reduction in absorption)
- IRON DELIVERY: oral for mild deficiency; parenteral (IV iron sucrose or IM iron dextran) for malabsorption, intolerance, or urgent need
- IRON DEXTRAN IM: give by Z-TRACK technique (displace skin laterally before injection, then release to seal iron in muscle) to prevent skin staining/tattooing; test dose first due to anaphylaxis risk
- B12 REPLACEMENT: cyanocobalamin 1,000 µg IM weekly × 4–8 weeks (loading), then monthly maintenance FOREVER; oral B12 ineffective in pernicious anemia (no intrinsic factor)
- B12 RESPONSE: CBC improves in 1–2 weeks; neurologic improvement may take months/years; irreversible if delayed
- FOLIC ACID: 1–5 mg daily oral; used in pregnancy, hemolysis, malnutrition; does NOT treat B12 deficiency (no neurologic benefit)
- HYDROXYUREA: increases HbF (fetal hemoglobin resistant to sickling); reduces crisis frequency in sickle cell; side effect = myelosuppression (monitor CBC monthly)
- IMMUNOSUPPRESSANTS (ATG, cyclosporine): used in aplastic anemia; allow bone marrow to recover by suppressing autoimmune destruction
Key definitions
Ferrous Sulfate
Example
Iron-deficiency anemia patient prescribed ferrous sulfate 325 mg daily
Oral iron supplement (325 mg tablet = 65 mg elemental iron); standard first-line agent for iron-deficiency anemia.
Cyanocobalamin (Vitamin B12)
Example
Pernicious anemia patient receiving cyanocobalamin 1,000 µg IM monthly
Injectable form of vitamin B12; given IM (not orally) for pernicious anemia since intrinsic factor is absent.
Hydroxyurea
Example
Sickle cell patient on hydroxyurea to reduce vaso-occlusive crisis frequency
Chemotherapy agent that increases fetal hemoglobin (HbF); reduces sickling and crisis frequency in sickle cell disease.
Erythropoietin (EPO)
Example
Dialysis patient on epoetin alfa to treat anemia of chronic kidney disease
Hormone stimulating RBC production; used in chronic kidney disease, cancer chemotherapy anemia, and some hemolytic anemias.
Diagrams to know
- Iron therapy decision tree (oral vs. parenteral)
- B12 replacement timeline and neurologic recovery
Must remember
- Normal Hemoglobin: MALE 13–18 g/dL, FEMALE 12–16 g/dL. Hematocrit is roughly 3× the Hgb value.
- MCV Classification: Microcytic (< 80) = iron deficiency; Macrocytic (> 100) = B12 or folate; Normocytic (80–100) = aplasia or acute loss.
- Type O-negative is the UNIVERSAL DONOR (safe in all emergencies). Type AB-positive is the UNIVERSAL RECIPIENT.
- Iron-deficiency anemia: Give ferrous sulfate 325 mg (65 mg elemental iron) on EMPTY stomach with VITAMIN C; expect BLACK STOOLS; use a STRAW for liquid iron to prevent teeth staining.
- Pernicious anemia (B12 deficiency): LIFELONG IM cyanocobalamin monthly because intrinsic factor is absent (oral B12 cannot be absorbed). Neurologic damage (paresthesias, ataxia) is IRREVERSIBLE if delayed.
- Folate deficiency mimics B12 deficiency EXCEPT it causes NO neurologic signs — this is the KEY differentiator.
- Aplastic anemia = PANCYTOPENIA (low RBC + low WBC + low platelets) from bone marrow failure. ANC < 500/µL = severe neutropenia (infection emergency).
- Hemolytic anemia signs: Jaundice, dark urine, splenomegaly, HIGH bilirubin, HIGH reticulocyte count (marrow compensating), LOW haptoglobin. Positive direct Coombs = immune-mediated.
- Sickle cell crisis management: Hydration, oxygen, IV opioids, treat infection. Hydroxyurea increases HbF and reduces crises.
- HIGH reticulocytes = marrow IS responding (good sign in blood loss/hemolysis). LOW reticulocytes in anemia = marrow failure (bad sign, needs treatment).
Last minute tips
- On the NLE, if you see 'microcytic hypochromic + low ferritin + high TIBC' = IRON DEFICIENCY. If you see 'macrocytic + paresthesias + neurologic signs' = PERNICIOUS ANEMIA. These patterns are highly predictable exam questions.
- Always remember that PERNICIOUS ANEMIA requires LIFELONG IM B12 (not oral pills). Students often incorrectly say 'give oral B12' — this will FAIL in pernicious anemia because there is no intrinsic factor for absorption. The question is testing whether you know the pathophysiology.
- For BLOOD TYPING, the key rule is: Type AB has NO antibodies (universal recipient), Type O has BOTH antibodies (universal donor). Type A has ANTI-B (will attack B/AB blood). Type B has ANTI-A (will attack A/AB blood).
- In HEMOLYTIC ANEMIA, remember the lab pattern: HIGH bilirubin, HIGH LDH, LOW haptoglobin, HIGH reticulocytes. This constellation is pathognomonic for hemolysis. Do not confuse with cholestasis (high bilirubin from blocked ducts), which does NOT have low haptoglobin or high retics.
- For APLASTIC ANEMIA, the clinical picture is INFECTION + BLEEDING + ANEMIA all at once (pancytopenia). Contrast with iron-deficiency anemia (only anemia, no bleeding/infection unless there is another reason).
Comparison tables
ANEMIA CLASSIFICATION BY MCV
| Anemia Type | MCV | Cell Appearance | Primary Cause | Key Labs | Hallmark Sign |
|---|---|---|---|---|---|
| Iron-Deficiency | Microcytic (< 80) | Small, pale | Chronic blood loss, inadequate intake | Low ferritin, low Fe, high TIBC | Koilonychia (spoon nails) |
| Pernicious / B12 Deficiency | Macrocytic (> 100) | Large, immature | Lack of intrinsic factor, gastrectomy, vegan diet | Low B12, hypersegmented neutrophils, positive IF antibodies | Paresthesias, ataxia, beefy red glossitis |
| Folate Deficiency | Macrocytic (> 100) | Large, immature | Poor diet, alcohol, malabsorption, drugs | Low serum folate, RBC folate, hypersegmented neutrophils | NO neurologic signs (unlike B12) |
| Aplastic Anemia | Normocytic (80–100) | Normal size but FEW cells | Marrow failure (idiopathic, drugs, radiation, viral) | Pancytopenia, hypocellular marrow, LOW retics | Infection + bleeding + anemia simultaneously |
| Hemolytic Anemia | Normocytic (80–100) | Normal size (unless sickled) | RBC destruction (inherited, autoimmune, mechanical) | HIGH retics, high bilirubin, low haptoglobin, positive Coombs | Jaundice, dark urine, splenomegaly, high bilirubin |
| Acute Blood Loss | Normocytic (80–100) | Normal size (initially) | Trauma, GI bleeding, surgery | Normal Hct initially; retics rise over 3–5 days | Hypotension, tachycardia, normal Hct early |
ABO BLOOD GROUP COMPATIBILITY
| Blood Type | RBC Antigens | Plasma Antibodies | Can RECEIVE From | Can DONATE To | Special Notes |
|---|---|---|---|---|---|
| Type A | A | anti-B | A, O | A, AB | Most common in Philippines (~30%) |
| Type B | B | anti-A | B, O | B, AB | Less common (~20%) |
| Type AB (Universal Recipient) | A and B | None | A, B, AB, O (ALL) | AB only | Rare (~3–5%), but can receive any blood |
| Type O (Universal Donor) | None | anti-A, anti-B | O only | A, B, AB, O (ALL) | Most common (~60%), safe in emergencies |
B12 vs. FOLATE DEFICIENCY
| Feature | Vitamin B12 Deficiency | Folate Deficiency |
|---|---|---|
| CBC Pattern | Macrocytic, megaloblastic | Macrocytic, megaloblastic |
| Cause (Pernicious) | Lack of intrinsic factor → malabsorption | Poor diet, malabsorption, increased demand |
| Neurologic Signs | YES (paresthesias, ataxia, dementia) — IRREVERSIBLE if delayed | NO neurologic signs |
| Tongue Changes | Beefy red glossitis | Beefy red glossitis |
| Treatment Route | IM ONLY (no intrinsic factor for oral absorption) | Oral or IM |
| Treatment Duration | LIFELONG monthly injections | Until cause corrected (usually 3–6 months) |
| Diagnostic Test | Low B12, Schilling test (or antibody testing for IF/parietal cell) | Low serum folate, RBC folate |
SICKLE CELL DISEASE: CRISIS TYPES & MANAGEMENT
| Crisis Type | Trigger | Presentation | Management | Complications |
|---|---|---|---|---|
| Vaso-Occlusive (Painful) | Hypoxia, dehydration, infection, cold, stress | Severe pain (bone, chest, abdominal), fever, elevated WBC | IV hydration, oxygen (if hypoxic), IV opioids, NSAIDs, treat infection | Organ infarction (bone, spleen, kidney), acute chest syndrome |
| Acute Chest Syndrome | Pulmonary infarction, infection, fat embolism | Chest pain, dyspnea, fever, infiltrates on CXR | Oxygen, IV fluids, antibiotics (cover atypical organisms), analgesia, exchange transfusion if severe | ARDS, death if untreated |
| Aplastic Crisis | Parvovirus B19 infection | Severe anemia, reticulocytopenia, fatigue | Supportive transfusions, monitor CBC, self-limited (usually 7–10 days) | Severe anemia, heart failure |
| Splenic Sequestration | Unknown (infants/young children) | Sudden splenomegaly, severe anemia, shock | Urgent transfusions, fluid resuscitation, watch for recurrence | Hypovolemic shock, death if untreated |
Diagrams
Anemia Workup Algorithm: CBC to Diagnosis
Step-by-step decision tree for diagnosing anemia based on MCV and clinical findings. Guides the clinician from CBC results to specific diagnosis and initial management.
Hematologic Assessment & Anemias — Complete Concept Map
Comprehensive mind map organizing all major hematologic concepts: blood composition, CBC interpretation, blood typing rules, anemia classification, and nursing care priorities. Useful for reviewing the entire chapter quickly.
Blood Typing Compatibility Matrix & Transfusion Decision
Practical transfusion decision flowchart showing which blood types can safely receive from which donors, and what to do if wrong blood is given.
Sickle Cell Crisis Recognition & Emergency Management
Crisis management flowchart for sickle cell disease showing the three main crises (vaso-occlusive, acute chest, splenic sequestration), their triggers, and emergency management protocol.
RBC Lifespan & Hemolysis Events
State diagram showing normal RBC maturation and lifespan (120 days) versus premature destruction in hemolytic anemia, including the cascade of lab abnormalities (bilirubin, low haptoglobin, high LDH) and compensatory marrow response.