Hematopoietic System
Acute Blood Loss
Identify and manage the specific site of bleeding.
CBC during active bleeding: initial hemoglobin (Hb) and hematocrit (Hct) may be normal if checked immediately; it may take several hours for blood loss to appear in CBC and platelet count.
Reticulocyte count (0.5%–2%) will increase within a few days; reticulocytosis is a normal response in acute blood loss.
Hemodynamic changes by blood loss percentage:
Up to 15\% of blood volume (class I hemorrhage): minimal increase in heart rate; no changes in BP and respiratory rate.
15\%!\text{ to }! 30\% (class II hemorrhage): tachycardia (100\text{--}120\ \text{bpm}), tachypnea (20\text{--}24\ /\text{min}), decrease in pulse pressure.
Significant BP drop usually does not manifest until about 30\%\text{ to }40\% blood loss (severe hemorrhage).
Tachycardia (pulse > 120\,\text{bpm}), weaker pulse, elevated respiratory rate, diminished urine output, and mental status changes; look for signs and symptoms of shock.
Note on hemovigilance and early management: monitor trends, anticipate delayed CBC changes, and treat hypovolemia and ongoing bleeding promptly.
Hemophilia A
Most common type of hemophilia in the United States.
X-linked recessive disease; predominantly affects males with only one X chromosome.
Caused by factor VIII (FVIII) deficiency.
Signs/symptoms: easy/unusual bruising, bleeding into joints (hemarthrosis), delayed bleeding or bleeding for several hours to days (circumcision, dental extractions), severe bleeding with minor trauma, heavy menses, and hematuria.
Medications that increase bleeding (to be avoided): anticoagulants, aspirin, and NSAIDs.
Laboratory pattern: activated partial thromboplastin time (aPTT) often prolonged; prothrombin time (PT), fibrinogen, and platelets typically normal.
Hodgkin’s Lymphoma
Cancer of the beta lymphocytes (B cells).
Classic B symptoms: night sweats, fevers, pain with ingestion of alcoholic drinks (occasionally), generalized pruritus with painless enlarged lymph nodes (neck).
Other symptoms: anorexia and weight loss.
Epidemiology: higher incidence among young adults (20–40 years) or older adults (>60 years); more common in males and White/Black Americans; median age at diagnosis ~39\text{ years} in the United States.
Identified by the presence of Reed–Sternberg cells.
Multiple Myeloma
Cancer of the plasma cells.
Symptoms: fatigue, weakness, bone pain (often in the back or chest).
Associated findings: proteinuria with Bence–Jones proteins, hypercalcemia, normocytic anemia.
Epidemiology: more common in older adults; median age at diagnosis 65\text{ to }74\,\text{years}.
Neutropenia
Definition: absolute neutrophil count (ANC) often < 1{,}500\,/\mu L in adults.
Most common causes: inherited disorders and drug-induced neutropenia.
Medication etiologies: psychotropics, antivirals, antibiotics, NSAIDs, antithyroids, ACE inhibitors (e.g., enalapril, captopril), propranolol.
Initial evaluation:
CBC with differential, blood smear, health history, medications (including OTC meds), and physical examination.
Febrile patients with suspected bacterial infection require urgent evaluation due to high risk for bacteremia/sepsis.
Ethnicity note: African Americans may have slightly lower ANC (benign ethnic neutropenia).
Non-Hodgkin’s Lymphoma
Group of malignant lymphoproliferative disorders derived from B cell progenitors, T cell progenitors, mature B cells, mature T cells, or natural killer cells.
Usually occurs in older adults (>65 years).
Presentation: night sweats, fever, weight loss, painless generalized lymphadenopathy.
Prognosis: generally poorer compared with some other lymphomas; varies by subtype.
Thrombocytopenia
Definition: platelet count < 150{,}000\,/\mu L.
Normal platelet range: 150{,}000\,/\mu L\text{ to }450{,}000\,/\mu L.
Symptoms usually do not appear until platelets < 100{,}000\,/\mu L.
Clinical signs: easy bruising (ecchymosis, petechiae), gum bleeding, spontaneous epistaxis, hematuria.
Vitamin B12 Deficiency
Presentation: gradual onset of symmetric peripheral neuropathy starting in the feet and/or arms; numbness, ataxia (positive Romberg), loss of vibration and position sense, impaired memory, dementia in severe cases.
Peripheral smear: macro-ovalocytes, some megaloblasts, multi-segmented neutrophils (> five or six lobes).
MCV: > 100\ \text{fL} (macrocytosis).
Laboratory Testing and Norms
Hemoglobin (Hb): concentration of Hb in whole blood.
Males: 13.6\text{ to }16.9\ \text{g/dL}
Females: 11.9\text{ to }14.8\ \text{g/dL}
Factors lowering Hb/Hct: vigorous activity, pregnancy, older age.
Factors increasing Hb/Hct: smoking, certain medications, dehydration or hypovolemia, high altitude.
Hematocrit (Hct): proportion of RBCs in 1 mL of blood.
Males: 40\%\text{ to }50\%
Females: 36\%\text{ to }44\%
Mean Corpuscular Volume (MCV): average size of RBCs.
Normal: 82.5\text{ to }98\ \text{fL}
Interpretation:
\text{MCV} < 80\ \text{fL}: microcytic anemia
80\ \leq \text{MCV} \leq 100\ \text{fL}: normocytic anemia
\text{MCV} > 100\ \text{fL}: macrocytic anemia
Mean Corpuscular Hemoglobin Concentration (MCHC): Hb concentration per RBC.
Normal: 32.5\text{ to }35.2\ \text{g/dL}
Decreased in iron-deficiency anemia (IDA) and thalassemia (hypochromic).
Normal in macrocytic and normocytic anemias; very high suggests spherocytosis or RBC agglutination.
Mean Corpuscular Hemoglobin (MCH): average Hb per RBC.
Normal: 25.0\text{ to }35.0\ \text{pg/cell}
Decreased in IDA and thalassemia; normal in macrocytic anemia.
Total Iron-Binding Capacity (TIBC): measure of transferrin availability to bind iron.
Calculation: transferrin concentration × 1.389 ⇒ TIBC.
Elevated in iron deficiency anemia (IDA); normal in thalassemia, vitamin B12 deficiency, folate-deficiency anemia.
Normal value: 300\text{ to }360\ \mu\text{g/dL}
Serum Ferritin: stored form of iron; correlates with iron stores; most sensitive test for IDA.
Also an acute phase reactant (can be elevated with inflammation/infection regardless of iron status).
Serum ferritin decreased in IDA.
With thalassemia trait, ferritin levels are normal to high; may be high if iron supplementation was given due to misdiagnosis.
Normal value: 40\text{ to }200\ \text{ng/mL}
Serum Iron: decreased in IDA; normal to high in thalassemia and macrocytic anemias; value alone is not diagnostic.
Affected by recent transfusions and dietary/pharmacologic iron.
Normal value: 60\text{ to }150\ \mu\text{g/dL}
Red Cell Distribution Width (RDW): variability in RBC size; elevated in IDA, vitamin B12/folate deficiency, and myelodysplastic syndromes.
Reticulocytes: immature RBCs that reflect RBC production; normally released in small amounts.
Reticulocyte count sources: 16\text{ to }130\times 10^3/\mu L (males); 16\text{ to }98\times 10^3/\mu L (females).
Reticulocytosis defined as >2.5\% of total RBC count.
Elevates within a few days with iron/folate/B12 supplementation, during acute bleeding, hemolysis, leukemia, and with erythropoietin (EPO) treatment.
Chronic bleeding does not typically cause reticulocytosis due to compensation.
White Blood Cells (WBC) with differential: percentage of each leukocyte type; sum of differential equals 100%.
Normal WBC: 3.8\text{ to }10.4\times 10^3/\mu L
Neutrophils (segmented): 55\%\text{ to }70\%
Band forms: 0\%\text{ to }5\%
Lymphocytes: 20\%\text{ to }40\%
Monocytes: 2\%\text{ to }8\%
Eosinophils: 1\%\text{ to }4\%
Basophils: 0.5\%\text{ to }1\%
Platelets:
Normal range: 152\text{ to }324\times 10^3/\mu L (males); 153\text{ to }361\times 10^3/\mu L (females).
Platelets form clots to stop/prevent bleeding; thrombocytosis can be reactive or neoplastic; thrombocytopenia can reflect destruction, sequestration, or ineffective thrombopoiesis.
Hemoglobin Electrophoresis: gold-standard to diagnose hemoglobinopathies (sickle cell disease, thalassemias, etc.).
Normal adult Hb: HbA \approx 97\%, HbA2 \approx 2.5\%, HbF < 1\% (fetal Hb).
Tips: RBC Size Descriptions
Common RBC-size descriptors:
\text{MCV} < 80\text{ fL}: microcytic and hypochromic RBCs (small and pale).
\text{MCV} > 100\text{ fL}: macrocytes or macro-ovalocytes (larger RBCs).
When evaluating MCV > 100 fL, order both vitamin B12 and folate levels.
Learn food groups for both folate and vitamin B12.
Anemias (Overview and Lab Comparisons)
Anemia definition: decrease in Hb/Hct or RBC mass below the norm for age/sex due to various causes (blood loss, bone marrow failure, impaired production, or hemolysis).
Table compare common anemias (highlights):
Iron Deficiency Anemia (IDA): ferritin/serum iron decreased; TIBC ↑; RDW ↑; RBCs microcytic (MCV < 80 fL); MCHC ↓; poikilocytosis and anisocytosis.
Thalassemia: Hb analysis/genetic testing; microcytic RBCs; hypochromia; ferritin/iron normal.
Vitamin B12 deficiency (pernicious anemia): B12 ↓; hypersegmented neutrophils (>5–6 lobes); macrocytic RBCs; normal color; MCV > 100 fL.
Folate deficiency: folate ↓; homocysteine ↑; macrocytic/megaloblastic RBCs; normal color.
Anemia of Chronic Disease: MCV 80–100 fL; history of chronic/inflammatory disease; normocytic RBCs.
Sickle Cell Anemia: Hb electrophoresis with HbS/HbF ↑; reticulocytosis; hemolytic features; RBCs normocytic/normochromic; sickle-shaped RBCs with shortened lifespan (10–20 days; norm is 120 days).
Iron Deficiency Anemia (IDA)
Etiology: most common worldwide; major cause is blood loss (overt or occult).
Adults: GI blood loss (peptic ulcer disease, NSAID use, cancer) most likely.
Reproductive-aged females: heavy periods, pregnancy.
Other risk: poor diet, post-gastrectomy, increased physiologic need.
Pediatric considerations: children—low dietary intake; infants—rule out chronic cow’s milk intake causing GI bleeding before 12 months.
Classic case features: many are asymptomatic when mild; moderate/severe may have pallor, fatigue, exertional dyspnea; glossitis; angular cheilitis; pica (cravings for nonfood items).
Severe anemia: possible tachycardia, murmur, or heart failure.
Early labs: Hb/Hct decreased; MCV may still be normal in early IDA or acute blood loss; RBCs may appear normocytic/normochromic in early stages and even CBC normal in high-resource settings.
Peripheral smear: anisocytosis, poikilocytosis.
Treatment:
Identify and correct cause; GI malignancy consideration in older patients.
Ferrous sulfate: 325\ \text{mg} \text{ PO } \text{TID}; take with vitamin C for absorption; can be taken with meals due to GI distress.
Hb/Hct normalization typically in 6\ to\ 8\ \text{weeks}; ferritin normalization may take 3\ to\ 6\ months to replace iron stores.
Severe/symptomatic anemia: RBC transfusion.
Diet/absorption tips: cast-iron cookware can help vegans/vegetarians; increase fiber and fluids; consider fiber supplements for constipation.
Iron-rich foods: red meat, some beans (e.g., black beans), and leafy greens.
Common side effects of iron: constipation, black stools; stomach upset; stool softener (Colace) may be used; avoid taking iron with antacids, dairy, quinolones, or tetracyclines (iron binding reduces effectiveness).
Reticulocytosis after iron supplementation: modest rise in 7\text{ to }10\,\text{days} in moderate/severe anemia; mild anemia may show little to no reticulocytosis.
Lab differentiation tips: IDA vs thalassemia trait/minor
If serum iron and ferritin are low with high TIBC: IDA.
If TIBC and ferritin are normal: thalassemia trait.
Thalassemia
Inherited hemoglobinopathies common in certain regions (sub-Saharan Africa, Asian-Indian subcontinent, Southeast Asia, Mediterranean).
Types: decreased production of alpha or beta chains of hemoglobin (alpha and beta thalassemias) leading to microcytic/hypochromic anemia.
Alpha thalassemia:
More common in southern China, Malaysia, Thailand; mild forms seen in African ancestry.
Beta thalassemia: prevalent in Africa.
Classic case: majority asymptomatic; discovered incidentally via abnormal CBC showing microcytosis/hypochromia; total RBC count may be mildly elevated.
Labs: Hb analysis/genetic testing; alpha-thalassemia shows Hb Bart’s (gamma tetramers) or Hb H (beta tetramers); DNA testing required for alpha-thalassemia minor/minima; beta-thalassemia shows elevated HbA2 and HbF.
RBC changes: microcytosis, increased RBC count, nonimmune hemolysis; blood smear shows poikilocytosis, target cells, teardrop cells, and cell fragments.
Ferritin/iron typically normal (helps distinguish from IDA).
Treatment: individualized; some may need transfusions during stress; thalassemia minor often does not require treatment if anemia is mild.
Genetic counseling and reproductive planning: educate about risk to offspring; consider routine testing for individuals with thalassemia.
Confirmation: Hb analysis and/or genetic testing required for diagnosis.
Ethnic background considerations: thalassemia prevalence varies by ethnicity; questions may not reveal ethnicity.
Anemia of Chronic Disease / Inflammation
Also called anemia of inflammation or hypoferremia of inflammation; second most common worldwide.
Mechanism: autoimmune/inflammatory diseases increase cytokine production and hepcidin, which sequesters iron and reduces RBC production.
Presentation: mild to moderate anemia; normochromic, normocytic RBCs (MCV 80–100 fL).
Inflammatory markers: ESR (sed rate) or CRP often elevated.
Treatment: treat underlying autoimmune/inflammatory disease to reduce inflammation and allow bone marrow recovery.
Anemia of Chronic Kidney Disease (CKD)
Prevalence increases as glomerular filtration rate (GFR) declines.
Definition by Hb: < 13\,\text{g/dL} in adult males and postmenopausal women; < 12\,\text{g/dL} in premenopausal women.
Morphology: hypoproliferative, normocytic, normochromic anemia.
Pathophysiology: decreased renal EPO production reduces reticulocyte/RBC production; possible functional iron deficiency and/or inflammatory conditions.
Initial testing: CBC, ferritin, transferrin saturation, vitamin B12, folate, reticulocyte count.
Treatment plan:
Conventional therapy for anemia.
Erythropoiesis-stimulating agents (ESAs) if Hb < 10\,\text{g/dL} or not improving with standard therapy.
Iron therapy (oral or IV): PO iron for patients not on dialysis; IV iron for hemodialysis patients with severe iron deficiency, severe anemia, ongoing blood loss risk, or intolerance to oral iron.
Pearls on iron therapy:
Best absorbed and cheapest iron form: ferrous sulfate.
Antacid wait time: wait ~4\ \text{hours} before taking iron to reduce binding.
Iron interactions: iron binds with tetracyclines, levothyroxine, and bisphosphonates; take iron 2 hours before/after antibiotic.
Nonresponse to iron therapy despite adherence may indicate ongoing blood loss, misdiagnosis, or malabsorption (e.g., celiac disease).
Safety note: Iron poisoning in children (esp. < 6\ years) can be fatal; store supplements out of reach of children.
Medications that may lower Hb and worsen anemia in chronic diseases: ARBs and ACE inhibitors.
Macrocytic/Megaloblastic Anemias
Vitamin B12–Deficiency Anemia
Cause: deficiency in vitamin B12, essential for neuronal health and DNA production in RBCs; total body supply lasts 3\ to\ 4\ \text{years}.
Common causes: malabsorption (pernicious anemia, gastric disease/infections, medications such as PPIs, H2 blockers, metformin).
Chronic deficiency can cause irreversible neuropathy/brain damage; highest incidence in older women; pernicious anemia is a common cause.
Pernicious anemia (a type of B12 anemia): autoimmune destruction of parietal cells → cessation of intrinsic factor production (intrinsic factor needed for B12 absorption).
Other causes: dietary insufficiency; gastric/bowel/pancreatic disorders; strict vegetarianism; gradual dietary deficiency may take >5 years.
B12 sources: all foods of animal origin (meat, poultry, eggs, milk, cheese).
Classic case: older adult with jaundiced/yellow skin; glossitis; neuropathic symptoms (paresthesias, difficulty walking, fine motor difficulties); possible cognitive effects.
Objective findings: decreased reflexes; possible reduced ankle reflex if legs involved; inflamed tongue glossitis.
Warning: always check both serum B12 and serum folate in macrocytic anemias; dual deficiency possible; folate-enriched diets may mask B12 deficiency.
Labs:
B12 level: normal > 300\,\text{pg/mL}; borderline 200\text{ to }300\,\text{pg/mL}; deficient < 200\,\text{pg/mL}.
CBC: decreased Hb/Hct; macrocytosis (MCV > 100\,\text{fL}); mild leukopenia; thrombocytopenia; low reticulocyte count.
Antibodies: antiparietal antibodies; autoantibodies to intrinsic factor.
Metabolite testing: MMA elevated (not definitive for B12 deficiency); homocysteine elevated.
Schilling test (historic): positive if B12 excretion normal after intrinsic factor; has limited current use.
Peripheral smear: macrocytosis, hypersegmented neutrophils (>5–6 lobes).
Treatment:
Parenteral B12: 1000 mcg (1 mg) IM/SC weekly for 1 month, then monthly.
Oral B12: 1000–2000 mcg daily if adherence is reliable and absorption is adequate.
Tips:
Pernicious anemia is macrocytic, normochromic with risk of neurologic symptoms due to intrinsic factor loss.
B12 level < 200\,\text{pg/mL} is consistent with deficiency.
CBC is a common screening test for anemia; chronic illness/autoimmune disease increases risk for normocytic anemia.
Test reticulocyte count after starting therapy to gauge response (approx. 2 weeks).
Folic Acid (Folate) Deficiency Anemia
Deficiency in folate (vitamin B9) causes DNA damage in RBCs and macrocytosis (MCV > 100\,\text{fL}).
Body’s folate stores last 2\ to\ 3\ months; most common causes: inadequate dietary intake (elderly, infants, alcoholics, overcooking vegetables, low citrus intake).
Other causes: increased physiologic need (pregnancy); malabsorption (e.g., gluten enteropathy, gastric bypass);
Drugs that interfere with folate absorption: Phenytoin, TMP-SMX, metformin, methotrexate, sulfasalazine, zidovudine, and others.
Classic case: older patient or patient with alcoholism; fatigue, pallor or jaundice; glossitis; progressive weakness, ataxia, paresthesias (less common than B12).
Labs: CBC shows macrocytic RBCs; macro-ovalocytes; hypersegmented neutrophils; folate level normal or low depending on intake;
Folate level interpretation: > 4\ ng/mL normal; 2–4 ng/mL borderline; < 2\ ng/mL consistent with deficiency.
MMA typically normal; homocysteine elevated with folate deficiency.
Treatment: folic acid supplementation 1–5 mg/day PO; treat for 1–4 months or until CBC/RBC indices normalize; chronic deficiency may require ongoing therapy.
Women of childbearing age: 400 mcg daily folic acid to prevent neural tube defects; higher doses (4 mg daily) for those with previous neural tube defects.
Aplastic Anemia
Caused by destruction of pluripotent stem cells in the bone marrow; multiple causes (radiation, drug toxicity, viral infections).
Bone marrow production slows/stops; all cell lines affected → pancytopenia (leukopenia, anemia, thrombocytopenia).
Classic case: fatigue, pallor; tachycardia; mucosal bleeding; neutropenia → infections; thrombocytopenia → bruising.
Labs: CBC with differential often shows normocytic/macrocytic RBCs; few mature neutrophils; platelets decreased; low reticulocyte count; bone marrow biopsy required for diagnosis.
Management: refer to hematologist; if septic, ED referral.
Erythrocytosis (Polycythemia)
Definition: abnormal elevation of Hb and/or Hct.
Classification: absolute polycythemia (primary or secondary) vs relative polycythemia (hemoconcentration due to decreased plasma volume).
Absolute polycythemia: mutation-driven (acquired/inherited) increase in RBC mass.
Criteria for polycythemia in adults:
Hct > 48\% in women, > 49\% in men
Hb > 16.0\ \text{g/dL} in women, > 16.5\ \text{g/dL} in men
Hemochromatosis
Hereditary hemochromatosis: genetic iron overload due to increased intestinal iron absorption.
Pathophysiology: gradual iron deposition over decades; iron overload damages liver, heart, joints, and other organs.
Symptoms: fatigue, skin hyperpigmentation (bronze), joint stiffness, swelling (2nd/3rd metacarpophalangeal joints).
Lab findings: elevated AST/ALT, high ferritin (often > 500\ ng/dL), elevated transferrin saturation.
Treatment: therapeutic phlebotomy for symptomatic iron overload.
Hemolytic Anemias
Group of inherited or acquired conditions with shortened RBC lifespan and increased RBC destruction.
Exam focus on two: sickle cell trait and G6PD deficiency.
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency
X-linked recessive; more common in males; often asymptomatic unless hemolysis occurs.
G6PD protects RBCs against oxidative damage; five known variants.
Populations: common in tropical/subtropical regions; Kurdish Jews have higher prevalence.
Triggers of hemolysis: certain drugs (e.g., primaquine, hydroxychloroquine, sulfa drugs, acetazolamide, dapsone), fava beans, infections, stress, fever, etc.
Hemolytic episode timing: typically 2–4 days after triggering exposure; symptoms:
Jaundice, yellow sclerae, pallor, fatigue, tachycardia, dark urine; abrupt Hgb drop by ~3!-\,4\,\text{g/dL}.
Evaluation: CBC and peripheral smear.
Genetics: Pedigree patterns show X-linked inheritance; carrier status in females; affected sons and carrier daughters in typical patterns.
Sickle Cell Disease / Trait
US prevalence: ~100,000 Americans with sickle cell disease; HbSS median survival ~58\ years.
Ethnic risk: higher in African, Mediterranean, Middle Eastern, some Indian populations.
Complications: acute chest syndrome, anemia, AVN, thrombosis, dactylitis, fever/infections, renal/hepatic issues, leg ulcers, pain crises, priapism, pulmonary hypertension, sleep-disordered breathing, splenic sequestration, stroke, vision loss.
Classic case: sickle cell trait usually asymptomatic; disease may present with aplastic crises or frequent vaso-occlusive episodes; sudden severe pain episodes in extremities, back, chest, or abdomen; may have dyspnea, weakness.
Triggers of sickling: hypoxia, infections, high altitude, dehydration, stress, surgery, blood loss, acidosis.
Lab features: CBC shows anemia; peripheral smear shows sickle-shaped RBCs.
Diagnosis: screen with HPLC, isoelectric focusing (IEF), or gel electrophoresis; combined HPLC + IEF provides definitive diagnosis in older children/adults.
Management/Genetics:
Sickle cell is autosomal recessive; genetic counseling recommended if both partners at risk.
Prenatal screening available as early as 8–10 weeks (CVS or amniocentesis).
Individuals with family history or clinical signs should be screened with peripheral smear, Hb solubility test, and hemoglobin electrophoresis.
Management typically involves hematology specialty for acute and chronic complications.
High-altitude stress: lower barometric pressure reduces arterial PO2; CAD/CHF/sickle cell patients at higher risk; advise avoiding elevations > 7,000 ft.
Newborn screening: all US states require newborn screening for sickle cell disease at birth.
Microcytic Anemias Summary
Iron-Deficiency Anemia vs Thalassemia Trait:
Ferritin: low in IDA; normal in thalassemia trait.
Serum Iron: decreased in IDA; normal in thalassemia trait.
TIBC: elevated in IDA; normal in thalassemia trait.
MCHC: decreased in both IDA and thalassemia trait (hypochromia).
Hb electrophoresis: normal in IDA; abnormal (beta-thalassemia) with specific HbA2/HbF patterns in thalassemia.
Ethnic background: IDA most common overall; alpha-thalassemia common in southern China/Malaysia/Thailand and mild forms in African ancestry; beta-thalassemia common in Africa.
Practical/Clinical Pearls & Messages
Serum ferritin is the most sensitive test for IDA but may be affected by inflammation; interpret with context.
Always consider coexisting B12 and folate deficiencies; check both in macrocytic anemia.
Reticulocytosis (> 2.5\%) indicates marrow response; lack of reticulocytosis after acute bleed or supplementation prompts marrow failure workup (aplastic anemia) with bone marrow biopsy.
For IDA, iron therapy is generally effective; monitor response by Hb/Hct and ferritin; if not responding, reassess for ongoing blood loss or malabsorption.
In CKD/CKD-related anemia, ESAs and iron therapy must be balanced; IV iron is preferred in dialysis patients.
In conditions like hemochromatosis, phlebotomy is a mainstay treatment for iron overload.
Genetic conditions require counseling and family planning discussions; testing should be offered to at-risk individuals.
Many medications can affect hematologic parameters; monitor drug side effects on Hb, iron status, and marrow health.
Safety note: certain deficiencies (e.g., B12) can cause irreversible neurologic damage if untreated; early diagnosis and treatment are critical.
Formulas and Key Numbers (summary)
Reticulocyte percentage thresholds:
Normal: 0.5\%\leq \text{retic} \leq 2\%
Reticulocytosis: \text{retic} > 2.5\%
Blood loss classifications (percent of blood volume):
Class I: \%\text{ blood loss} \leq 15\%
Class II: 15\% \leq \% \leq 30\%
Severe: 30\% \leq \% \leq 40\%
Common normal laboratory ranges (selected):
Hb (males): 13.6\text{ to }16.9\ \text{g/dL}
Hb (females): 11.9\text{ to }14.8\ \text{g/dL}
Hct (males): 40\%\text{ to }50\%
Hct (females): 36\%\text{ to }44\%
MCV: 82.5\text{ to }98\ \text{fL}
MCHC: 32.5\text{ to }35.2\ \text{g/dL}
MCH: 25.0\text{ to }35.0\ \text{pg/cell}
TIBC: 300\text{ to }360\ \mu\text{g/dL}
Serum ferritin: 40\text{ to }200\ \text{ng/mL}
Serum iron: 60\text{ to }150\ \mu\text{g/dL}
WBC count: 3.8\text{ to }10.4\times 10^3/\mu L
Platelet count: 152\text{ to }324\times 10^3/\mu L (males); 153\text{ to }361\times 10^3/\mu L (females)
Hemoglobin Electrophoresis (typical adult proportions): HbA \approx 97\%, HbA2 \approx 2.5\%, HbF < 1\%
Vitamin B12 levels: normal > 300\ \text{pg/mL}; borderline 200\text{ to }300\ \text{pg/mL}; deficient < 200\ \text{pg/mL}
Folate levels: normal > 4\ ng/mL; borderline 2\text{ to }4\ ng/mL; deficient < 2\ ng/mL
Notes on Diagnostic Pathways and Counseling
When evaluating anemia, CBC is a screening test; interpret Hb/Hct along with MCV, MCHC, MCH, RDW, ferritin, serum iron, TIBC, and reticulocyte count.
Use Hb electrophoresis and/or genetic testing to confirm thalassemia vs IDA in microcytic anemias when labs are equivocal.
Consider age, sex, ethnicity, and exposure history (diet, alcohol use, medications, infections) to guide testing for B12/folate deficiencies and CKD-related anemia.
Risk communication: discuss genetic risks and family planning with patients when hereditary conditions (thalassemia, sickle cell) are identified.