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Systemic Pathology + Hematology - Detailed Answers

HEMATOLOGY - RBC Disorders

1. Hemolytic Anemia

Definition: A group of disorders with a common feature of accelerated red cell destruction - RBC life span is shortened from the normal 120 days, often to as few as 20-30 days.

Pathophysiology:

Anemia and low tissue O2 → stimulates erythropoietin from kidneys → marrow erythroid hyperplasia + peripheral reticulocytosis
In severe cases, extramedullary hematopoiesis appears in liver, spleen, and lymph nodes

Classification:

Feature	Extravascular Hemolysis	Intravascular Hemolysis
Site	Spleen/macrophages	Within blood vessels
Cause	Reduced RBC deformability	Mechanical, complement, toxins
Jaundice	Yes (hyperbilirubinemia)	Mild
Splenomegaly	Yes	Absent/mild
Hemoglobinuria	No	Yes
Hemosiderinuria	No	Yes
Haptoglobin	Decreased	Markedly decreased
Cholelithiasis	Pigment stones (long-standing)	No

Common Types:

Hereditary Spherocytosis: Autosomal dominant; mutations destabilize the RBC membrane skeleton → loss of membrane → spherocytes → removed in spleen. Presents with anemia, splenomegaly, and cholelithiasis.
Sickle Cell Anemia: See below.
G6PD Deficiency: X-linked; mutations destabilize G6PD → RBCs susceptible to oxidant damage. Triggers: drugs (primaquine, dapsone), infections, fava beans.
Immunohemolytic Anemia: Antibodies against normal RBC constituents → opsonization and extravascular hemolysis. Coombs test positive.
Microangiopathic Hemolytic Anemia (MAHA): Caused by mechanical trauma to RBCs in abnormal microcirculation (DIC, TTP, HUS). Shows schistocytes and helmet cells on smear.

Lab Findings (general):

Reticulocytosis
Decreased haptoglobin
Increased indirect bilirubin
Peripheral smear: specific to type (spherocytes, sickle cells, schistocytes)

2. Sickle Cell Anemia

Genetics: Autosomal recessive; point mutation in the β-globin gene - glutamic acid → valine at position 6 (HbS)

Pathophysiology:

Deoxygenated HbS polymerizes into long rigid rods → distorts and damages the RBC membrane → sickle shape
Sickled cells are rigid, cannot deform to pass through splenic sinusoids → extravascular hemolysis
Sickled cells also obstruct small vessels → vaso-occlusive crises

Triggers of Sickling: Hypoxia, acidosis, dehydration, infection, cold

Clinical Features:

Moderate to severe chronic hemolytic anemia (Hb typically 6-9 g/dL)
Painful vaso-occlusive crises: bone pain (hand-foot syndrome in children), abdominal pain
Acute chest syndrome (pulmonary infarction/infection) - major cause of death
Stroke (especially in children)
Splenic sequestration (acute) and autosplenectomy (chronic infarction → small fibrotic spleen)
Aplastic crisis precipitated by parvovirus B19
Increased susceptibility to encapsulated bacteria (Streptococcus pneumoniae, H. influenzae) due to functional asplenia

Lab:

Sickle cells on peripheral smear
HbS on electrophoresis (HbS >90% in homozygous)
Decreased Hb, increased reticulocytes, increased bilirubin

Sickle Cell Trait (HbAS): Heterozygous - generally asymptomatic; provides protection against falciparum malaria

3. Thalassemia

Definition: Autosomal codominant disorders caused by mutations in α- or β-globin genes that reduce hemoglobin synthesis → microcytic, hypochromic anemia

β-Thalassemia:

Feature	β-Thal Minor (Trait)	β-Thal Major (Cooley's)
Genotype	β+/β or β0/β	β0/β0 or β0/β+
Severity	Mild, asymptomatic	Severe, transfusion-dependent
Smear	Microcytic, hypochromic, target cells	Severe microcytosis, nucleated RBCs, target cells
Hb	Slightly reduced	Markedly reduced (2-3 g/dL)
HbA2	Elevated	Elevated
HbF	Slightly elevated	Very high

β-Thalassemia Major Pathophysiology:

Absent/markedly reduced β-globin → excess unpaired α-chains precipitate in erythroblasts → membrane damage → ineffective hematopoiesis and premature destruction
Massive marrow expansion → "crew-cut" skull on X-ray (hair on end appearance), chipmunk face, frontal bossing
Extramedullary hematopoiesis → hepatosplenomegaly
Iron overload from repeated transfusions → hemosiderosis → damage to heart, liver, endocrine organs

Treatment: Regular blood transfusions + iron chelation (deferoxamine); curative with bone marrow transplantation

4. Iron Deficiency Anemia (IDA)

Most common anemia worldwide

Causes:

Chronic blood loss (most common in adults): GI bleeding (peptic ulcer, colorectal carcinoma, hookworm), menorrhagia
Inadequate dietary intake (infants, toddlers, elderly, vegetarians)
Increased demand (pregnancy, growth spurts)
Malabsorption (celiac disease, post-gastrectomy)

Pathogenesis: Iron stores depleted → insufficient iron for hemoglobin synthesis → small pale RBCs

Stages:

Pre-latent: Depletion of iron stores (decreased serum ferritin) - no anemia
Latent: Iron depletion + elevated TIBC, decreased serum iron - no anemia yet
Overt IDA: Hypochromic, microcytic anemia

Clinical Features:

Pallor, fatigue, exertional dyspnea
Koilonychia (spoon-shaped nails)
Angular stomatitis and glossitis
Plummer-Vinson syndrome: dysphagia due to esophageal webs (rare)
Pica (craving for clay, ice, starch)

Lab:

Low Hb, MCV, MCH, MCHC
Peripheral smear: hypochromic microcytic RBCs, pencil cells (elliptocytes), target cells
Decreased serum ferritin (most sensitive early marker)
Decreased serum iron
Increased TIBC (Total Iron Binding Capacity)
Decreased transferrin saturation (<15%)

5. Megaloblastic Anemia

Definition: Caused by deficiencies of folate or Vitamin B12 → inadequate thymidine synthesis → defective DNA replication → nuclear maturation lags behind cytoplasmic development

Causes of B12 deficiency:

Pernicious anemia (most common): Autoimmune destruction of gastric parietal cells → absent intrinsic factor → impaired B12 absorption
Strict vegetarian diet
Gastrectomy, terminal ileal disease (Crohn's)
Fish tapeworm (Diphyllobothrium latum)

Causes of Folate deficiency:

Poor dietary intake (alcoholics, elderly)
Increased demand (pregnancy, hemolytic anemia)
Drugs (methotrexate, trimethoprim, phenytoin)
Malabsorption (celiac disease)

Clinical Features:

Gradual onset of pallor, fatigue, weakness
Glossitis (beefy red, smooth tongue)
Mild jaundice (ineffective hematopoiesis → elevated indirect bilirubin)
B12 deficiency ONLY: Subacute combined degeneration of spinal cord - posterior columns + lateral corticospinal tracts → paresthesias, ataxia, spastic paraplegia (does NOT occur with folate deficiency)

Lab:

Elevated MCV (macrocytosis), macroovalocytes
Hypersegmented neutrophils (5+ lobes) - pathognomonic finding
Pancytopenia in severe cases (all lineages affected)
Enlarged abnormal precursors: megaloblasts in bone marrow
Elevated serum LDH and bilirubin (ineffective erythropoiesis)
Specific: Low serum B12 or folate; positive anti-intrinsic factor antibody (pernicious anemia); Schilling test

Pernicious Anemia specifically:

Anti-parietal cell antibodies (90%)
Anti-intrinsic factor antibodies (more specific, 60%)

6. Aplastic Anemia

Definition: Pancytopenia resulting from bone marrow failure (aplasia)

Causes:

Idiopathic (~65-70%): immune-mediated (T cells attack stem cells)
Drugs: chloramphenicol, NSAIDs, sulfonamides, benzene
Radiation
Viral: EBV, hepatitis viruses, CMV, parvovirus B19
Inherited: Fanconi anemia (DNA repair defect), dyskeratosis congenita (telomerase defect)

Lab:

Pancytopenia: anemia + neutropenia + thrombocytopenia
Bone marrow biopsy: hypocellular/acellular marrow replaced by fat cells (hallmark finding)
Normal RBC morphology (normocytic, normochromic)

Clinical Features: Fatigue, infections, bleeding

Treatment: Bone marrow transplantation (curative in young); immunosuppression (anti-thymocyte globulin + cyclosporine) in elderly

HEMATOLOGY - WBC Disorders

7. Chronic Myeloid Leukemia (CML)

Definition: Myeloproliferative neoplasm caused by a t(9;22) translocation (Philadelphia chromosome) creating a BCR-ABL fusion gene encoding a constitutively active BCR-ABL tyrosine kinase

Molecular Basis:

t(9;22)(q34;q11) → Philadelphia (Ph) chromosome (abnormal chromosome 22)
BCR-ABL fusion protein has unregulated tyrosine kinase activity → drives uncontrolled myeloid proliferation

Clinical Features:

Insidious onset, typically in adults 40-60 years
Massive splenomegaly (characteristic - often huge)
Hepatomegaly
Symptoms: fatigue, weight loss, night sweats, dragging sensation in abdomen
Gout (due to hyperuricemia from cell turnover)

Lab:

Markedly elevated WBC (50,000-200,000/µL) with full myeloid spectrum (myeloblasts, promyelocytes, myelocytes, bands, neutrophils)
Thrombocytosis (often elevated platelets)
Basophilia and eosinophilia (characteristic)
Low Leukocyte Alkaline Phosphatase (LAP) score (differentiates from leukemoid reaction)
Ph chromosome positive (95%)
BCR-ABL positive (100%)
Bone marrow: hypercellular, myeloid hyperplasia

Phases:

Chronic phase (stable, responds well to treatment)
Accelerated phase
Blast crisis (transforms to AML or B-ALL) - previously fatal, now manageable

Treatment: Imatinib (Gleevec) - BCR-ABL tyrosine kinase inhibitor; highly effective. Second-line: dasatinib, nilotinib.

8. Leukemia vs Leukemoid Reaction

Feature	Leukemia (CML)	Leukemoid Reaction
Cause	Malignant	Severe infection, hemolysis, carcinoma
WBC Count	Very high (>100,000)	Elevated (50,000-100,000)
LAP Score	LOW (hallmark)	HIGH
Philadelphia Chromosome	Present (CML)	Absent
Toxic Granules/Vacuoles	Absent	Present (neutrophils)
Döhle bodies	Absent	Present
Basophilia	Prominent	Absent
Splenomegaly	Massive	Mild or absent
Thrombocytosis	Common	Variable
Cause resolution	Requires treatment	Resolves with treatment of underlying cause

9. Acute Myeloid Leukemia (AML)

Definition: A neoplasm of immature myeloid lineage cells (blasts); most common in adults over age 60

Key Features:

Bone marrow: >20% blasts required for diagnosis
Presents acutely with symptoms of cytopenias: fatigue (anemia), infections (neutropenia), bleeding (thrombocytopenia)

Important Subtypes:

Acute Promyelocytic Leukemia (APL / M3):
- t(15;17) → PML-RARA fusion protein
- Numerous Auer rods (bundles = "faggot cells")
- Associated with DIC (granule release)
- Highly curable with All-trans retinoic acid (ATRA) + arsenic salts
AML with t(8;21): Good prognosis
AML with inv(16): Eosinophilic component

Lab:

Pancytopenia
Circulating blasts
Auer rods in myeloblasts (pathognomonic of myeloid lineage)
Bone marrow >20% blasts
MPO (myeloperoxidase) positive - distinguishes from ALL

HEMATOLOGY - Platelet Disorders

10. Disseminated Intravascular Coagulation (DIC)

Definition: A clinicopathologic syndrome in which simultaneous activation of the coagulation AND fibrinolysis systems results in formation of thrombin AND plasmin with consumption of coagulation factors and inhibitors.

Causes:

Sepsis (most common) - gram-negative > gram-positive
Obstetric complications: abruptio placentae, amniotic fluid embolism, HELLP syndrome, retained dead fetus
Malignancy (especially APL - promyelocytic leukemia)
Massive tissue injury/trauma/surgery
Mismatched blood transfusion

Pathogenesis:

Activation of coagulation → microthrombi throughout vasculature → organ ischemia
Simultaneously, consumption of clotting factors and platelets → hemorrhage from all sites

Clinical Features:

Paradox: Both bleeding AND thrombosis
Bleeding: from venipuncture sites, surgical wounds, mucous membranes
Thrombosis: Microangiopathic hemolytic anemia (schistocytes, helmet cells on smear)
Organ failure (renal, pulmonary, hepatic)

Lab:

Prolonged PT and APTT
Decreased fibrinogen
Elevated D-dimers (fibrin degradation products) - most sensitive
Thrombocytopenia
Schistocytes on peripheral smear
Decreased factors V, VIII

ISTH Scoring System:

Platelet count (<100k = 1, <50k = 2)
Elevated D-dimer (moderate = 2, strong = 3)
Prolonged PT (>3 sec = 1, >6 sec = 2)
Fibrinogen <100 mg/dL = 1
Score ≥5 = overt DIC

11. Immune Thrombocytopenic Purpura (ITP)

Definition: Autoimmune disorder where antibodies (IgG) are directed against platelet glycoproteins (GPIIb/IIIa most common) → platelet destruction by splenic macrophages

Types:

Acute ITP: Children, follows viral infection, self-limiting (2-6 weeks)
Chronic ITP: Adults, women > men, no clear trigger, persists >6 months

Clinical: Petechiae, purpura, mucosal bleeding (epistaxis, gingival), menorrhagia. No splenomegaly typically.

Lab:

Isolated thrombocytopenia (Hb and WBC normal)
Normal or increased megakaryocytes in bone marrow (platelet production is intact but destruction is increased)
Anti-platelet antibodies (GPIIb/IIIa, GPIb/IX)

Treatment: Corticosteroids; IVIG; Splenectomy (for refractory chronic ITP); anti-D immunoglobulin; TPO agonists (romiplostim, eltrombopag)

12. Hemophilia A

Definition: X-linked recessive disorder caused by deficiency of Factor VIII (most common inherited coagulation disorder)

Genetics: X-linked - affects males; females are carriers

Clinical Features:

Deep tissue/muscle hematomas (pathognomonic)
Hemarthrosis (bleeding into joints - knees, elbows, ankles) → chronic arthropathy
Excessive bleeding after surgery/trauma
Easy bruising
No petechiae or purpura (platelet function is normal)

Lab:

Prolonged aPTT (intrinsic pathway affected)
Normal PT, bleeding time, platelet count
Decreased Factor VIII activity (<1% = severe, 1-5% = moderate, 5-40% = mild)

Treatment: Factor VIII concentrate; recombinant Factor VIII; DDAVP (desmopressin - releases stored Factor VIII, for mild cases)

13. Pancytopenia

Definition: Reduction of all three cell lines - RBCs (anemia), WBCs (leukopenia/neutropenia), and platelets (thrombocytopenia)

Causes:

Aplastic anemia (hypocellular marrow)
Megaloblastic anemia (ineffective hematopoiesis)
Bone marrow infiltration: leukemia, lymphoma, metastatic carcinoma, myelofibrosis
Hypersplenism (sequestration)
Systemic lupus erythematosus
Viral infections (HIV, EBV, CMV)
Radiation/chemotherapy

LYMPH NODE & SPLEEN

14. Splenomegaly

Normal spleen weight: ~150 g; splenomegaly = >400-500 g; massive splenomegaly = >1000 g

Causes:

Infectious: Malaria (most common cause worldwide), EBV (mononucleosis), bacterial endocarditis, TB, typhoid
Congestive: Liver cirrhosis (portal hypertension), right heart failure, splenic/portal vein thrombosis
Hematological: CML (massive), thalassemia major, hereditary spherocytosis, hemolytic anemias
Storage Disorders: Gaucher disease, Niemann-Pick disease
Infiltrative/Neoplastic: Lymphoma, leukemia, metastasis
Inflammatory: SLE, rheumatoid arthritis (Felty syndrome), sarcoidosis

Complications of massive splenomegaly:

Hypersplenism (pancytopenia from sequestration)
Splenic infarction
Splenic rupture

15. Hodgkin Lymphoma (HL)

Definition: B-cell tumors that are often associated with inflammatory symptoms; characterized by Reed-Sternberg (RS) cells in a background of reactive inflammatory cells

Reed-Sternberg (RS) Cell:

Giant, binucleated/bilobed cell with large prominent nucleoli ("owl-eye" appearance)
Stain: CD15+ and CD30+ (key immunophenotype)
CD20 negative (unlike most B-cell lymphomas)
Origin: Germinal center B cells

Classical HL Subtypes (WHO):

Subtype	Frequency	Histology	EBV	Prognosis
Nodular Sclerosis	65-70%	Collagen bands, lacunar cells	+/-	Good
Mixed Cellularity	20-25%	Mixed inflammation, many RS cells	++	Intermediate
Lymphocyte Rich	5%	Many lymphocytes, few RS	+	Best
Lymphocyte Depleted	<1%	Few lymphocytes, many RS/fibrosis	+++	Worst

Nodular Lymphocyte Predominant HL: Separate entity; "popcorn cells" (LP cells), CD20+, CD15-, CD30- ; excellent prognosis

Clinical Features:

Painless cervical lymphadenopathy (most common presentation)
Contiguous (orderly) spread from one node group to adjacent groups (unlike NHL)
Mediastinal involvement common (especially nodular sclerosis)
B symptoms: fever, drenching night sweats, weight loss >10% in 6 months
Alcohol-induced pain in lymph nodes (characteristic but rare)
Pruritus

Staging (Ann Arbor):

Stage I: Single lymph node region
Stage II: Two or more on same side of diaphragm
Stage III: Both sides of diaphragm
Stage IV: Extralymphatic involvement (bone marrow, liver)
A = no B symptoms; B = B symptoms present

Treatment: ABVD chemotherapy (Adriamycin, Bleomycin, Vinblastine, Dacarbazine) ± radiation; highly curable (>90% in early stage)

16. Non-Hodgkin Lymphoma (NHL)

Differences from HL:

Non-contiguous (random) spread
More often involves extranodal sites (GI tract, CNS, skin)
More frequently disseminated at diagnosis
Generally older patients
Wide variety of subtypes (B-cell > T-cell)

Key NHL Types:

Diffuse Large B-Cell Lymphoma (DLBCL): Most common NHL; aggressive; BCL6 mutations; t(14;18) in some; ~50% curable with R-CHOP
Follicular Lymphoma: Most common indolent NHL; t(14;18) → BCL2 overexpression; "watch and wait" approach
Burkitt Lymphoma: Very aggressive; t(8;14) → MYC translocation; "starry sky" pattern on histology; endemic form associated with EBV + jaw mass in children; highly curable with intensive chemotherapy
Mantle Cell Lymphoma: CD5+; t(11;14) → cyclin D1 overexpression; moderately aggressive
Small Lymphocytic Lymphoma (SLL)/CLL: Indolent; same disease as CLL (with/without blood involvement)

17. Plasma Cell Tumors / Multiple Myeloma

Definition: Malignant proliferation of a single clone of plasma cells (antibody-secreting B cells) producing a monoclonal immunoglobulin (M protein)

Pathogenesis:

Malignant plasma cells accumulate in bone marrow → produce M protein (usually IgG or IgA)
Bone destruction by osteoclast activation (RANKL pathway) → lytic lesions
Suppression of normal immunoglobulins → recurrent infections

Clinical Features (CRAB criteria):

Calcium elevated (hypercalcemia): Bone resorption → confusion, constipation, polyuria
Renal failure: Light chain deposition, hypercalcemia, amyloidosis, urate nephropathy
Anemia: Bone marrow replacement by plasma cells
Bone pain/lytic lesions: Punched-out lesions on X-ray; pathological fractures; vertebral compression fractures; skull "rain-drop" lesions

Additional Features:

Bence Jones proteinuria: Free light chains (κ or λ) in urine (overflow proteinuria)
Rouleaux formation on peripheral blood smear (red cells stacked like coins due to M protein)
Recurrent infections (decreased normal immunoglobulins)
Hyperviscosity syndrome (headache, visual disturbance, bleeding)
AL amyloidosis in some

Lab:

Serum protein electrophoresis (SPEP): M spike (monoclonal band)
Elevated ESR
Bone marrow biopsy: >10% plasma cells (>60% = defining)
Urine immunofixation: Bence Jones proteins

Diagnosis (IMWG Criteria): Clonal bone marrow plasma cells ≥10% + evidence of end-organ damage (CRAB) or biomarkers (serum free light chain ratio ≥100, etc.)

Treatment: Proteasome inhibitors (bortezomib), IMiDs (lenalidomide), dexamethasone; autologous stem cell transplantation

SYSTEMIC - CVS

18. Acute Myocardial Infarction (AMI)

Definition: Necrosis of heart muscle resulting from ischemia. Defined as acute myocardial injury detected by abnormal cardiac biomarkers in the setting of acute myocardial ischemia.

Pathogenesis:

Atheromatous plaque erosion/rupture → subendothelial collagen exposed
Platelet adhesion, aggregation, activation → thromboxane A2, ADP, serotonin release → further platelet aggregation + vasospasm
Coagulation activation (tissue factor) → thrombus formation
Complete coronary artery occlusion

Within 20-40 min of occlusion: Irreversible myocyte damage and coagulative necrosis

Morphological Changes Over Time:

Time	Gross Finding	Histological Finding
0-6 hours	Normal (no gross change)	Normal; early wavy fibers
6-24 hours	Pallor	Coagulative necrosis begins; neutrophil infiltration starts
1-3 days	Pale, yellow	Coagulative necrosis; neutrophil infiltration (peak at 1-3 days)
3-7 days	Hyperemic border, central yellow	Macrophage infiltration; removal of necrotic debris begins
1-2 weeks	Yellow-white, soft	Granulation tissue (fibroblasts, new vessels)
2+ weeks	Gray-white, firm scar	Dense fibrous scar

Biomarkers:

Troponin I/T: Most sensitive and specific; rises 3-6 hours, peaks 24-48 hours, remains elevated 7-14 days; gold standard
CK-MB: Rises 4-6 hours, peaks 24 hours, normalizes by 48-72 hours; useful for reinfarction
Myoglobin: Earliest (rises 1-2 hours), not cardiac specific

Complications:

Arrhythmias (most common, 80-90%): ventricular fibrillation is the most common cause of early death
Cardiogenic shock (>40% LV infarction)
Papillary muscle rupture → acute mitral regurgitation (3-5 days)
Ventricular wall rupture → cardiac tamponade (3-7 days)
Ventricular septal defect (3-7 days)
Pericarditis (fibrinous, 1-3 days = early; Dressler syndrome at 2-10 weeks = autoimmune)
Mural thrombus → systemic emboli
Left ventricular aneurysm (late complication)

19. Rheumatic Heart Disease

Definition: Cardiac damage resulting from rheumatic fever, caused by molecular mimicry between Group A Streptococcus antigens and cardiac proteins.

Pathogenesis: Anti-streptococcal antibodies cross-react with cardiac valve proteins (Type II hypersensitivity) → pancarditis

Aschoff Bodies: Pathognomonic lesion - central fibrinoid necrosis surrounded by lymphocytes, macrophages, and Aschoff giant cells. Most commonly found in myocardium.

Acute Rheumatic Fever - Jones Criteria:

Major: Carditis, Polyarthritis, Chorea (Sydenham), Erythema marginatum, Subcutaneous nodules
Minor: Fever, elevated ESR/CRP, prolonged PR interval, arthralgia
Diagnosis: 2 major OR 1 major + 2 minor criteria + evidence of prior streptococcal infection (elevated ASO titer, positive throat culture)

Valvular Involvement in Chronic RHD:

Mitral valve most commonly affected (65-70%)
Mitral stenosis: "fish mouth" or "button hole" deformity; commissural fusion; cusps thickened and calcified
Aortic valve second most common
Combined mitral + aortic most common combination
Tricuspid involvement occurs but pulmonary is rarely affected

20. Infective Endocarditis

Definition: Infection of the heart valves or endocardium, with formation of vegetations

Organisms:

Native valve: S. viridans (subacute); S. aureus (acute, most common overall)
IV drug users: S. aureus; right-sided endocarditis (tricuspid valve)
Prosthetic valve (early <60 days): S. epidermidis; early Gram-negative
Prosthetic valve (late >60 days): S. viridans
Dental procedures: S. viridans
HACEK group: H. influenzae, Aggregatibacter, Cardiobacterium, Eikenella, Kingella

Clinical Features (Duke Criteria):

Major: Positive blood cultures; echocardiographic evidence of endocarditis
Minor: Fever >38°C; vascular phenomena; immunological phenomena; predisposing condition

Peripheral Manifestations:

Osler nodes: Painful, tender nodules on fingertips (immunologic)
Janeway lesions: Painless hemorrhagic lesions on palms/soles (embolic)
Roth spots: Oval hemorrhagic retinal lesions with white center
Splinter hemorrhages: Under fingernails
Petechiae

SYSTEMIC - RESPIRATORY

21. Lobar Pneumonia

Definition: Pneumonia involving an entire lobe of the lung (or most of it), due to filling of alveoli with inflammatory exudate.

Most Common Organism: Streptococcus pneumoniae (pneumococcus) - accounts for >90%

Other Causes: Klebsiella pneumoniae (right upper lobe, causes bulging fissure, abscess formation), rarely Staphylococcus

Stages of Lobar Pneumonia (Classic):

Stage	Time	Gross	Microscopy
Congestion	Day 1-2	Heavy, dark red, boggy	Vascular engorgement; intra-alveolar fluid, bacteria
Red Hepatization	Day 2-4	Firm, liver-like, red	Alveoli filled with RBCs, neutrophils, fibrin; airless
Grey Hepatization	Day 4-8	Grey-brown, firm	RBCs lysed; alveoli filled with fibrin, macrophages, neutrophils
Resolution	Day 8+	Returns to normal	Enzymatic digestion of exudate; macrophages clear debris

Hallmark: Air bronchogram on X-ray (air-filled bronchi visible against consolidated lung)

Clinical Features:

Sudden onset: high fever (39-40°C), shaking chills
Productive cough: rusty/blood-tinged sputum (from RBCs in alveoli)
Pleuritic chest pain (when pleura involved)
Decreased breath sounds, dullness to percussion, bronchial breathing over consolidated area
Increased tactile fremitus

Complications: Pleural effusion (para-pneumonic), empyema, bacteremia, abscess, fibrous organization (carnification)

22. COPD

Definition: Persistent airflow limitation that is progressive, associated with enhanced chronic inflammatory response in airways/lungs to noxious particles or gases (mainly cigarette smoke).

Types:

Chronic Bronchitis: Clinical definition - productive cough for ≥3 months in 2 consecutive years without other cause. Reid Index (gland thickness/wall thickness) >0.4.
Emphysema: Permanent enlargement of airspaces distal to terminal bronchioles, with destruction of alveolar walls without fibrosis.
- Centriacinar/Centrilobular: Upper lobes; associated with smoking
- Panacinar: Lower lobes; associated with α1-antitrypsin deficiency

SYSTEMIC - GIT

23. Crohn's Disease vs Ulcerative Colitis

Feature	Crohn's Disease (CD)	Ulcerative Colitis (UC)
Location	Any part of GI tract (mouth to anus)	Colon only; starts at rectum, extends proximally
Distribution	Skip lesions (discontinuous)	Continuous, diffuse involvement
Rectal involvement	Spared in ~50%	Always involved (99%)
Ileum involvement	Terminal ileum (ileitis) common	Not involved
Depth of inflammation	Transmural (full thickness)	Mucosal + submucosal only
Gross appearance	Cobblestone mucosa; deep fissuring ulcers	Continuous ulceration; pseudopolyps
Bowel wall	Thickened, "garden hose"	Thin, shortened
Fistulae/Sinuses	Common	Rare
Perianal disease	Common	Rare
Granulomas	Present (40-60%) - non-caseating	Absent
Smoking effect	Smoking worsens CD	Smoking protects UC
Cancer risk	Lower (than UC)	Higher (especially in pancolitis >10 yrs)
Serological markers	ASCA positive	pANCA positive
Surgery	Not curative; recurrence	Colectomy is curative

Extraintestinal Manifestations (both): Arthritis, ankylosing spondylitis, uveitis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis (more common in UC), liver disease.

24. Pleomorphic Adenoma of Salivary Gland

Most common salivary gland tumor (70% of all salivary gland tumors)

Site: Parotid gland most commonly (80%); rarely submandibular or minor salivary glands

Histology:

Mixed tumor: combination of epithelial cells AND myoepithelial cells set in a stromal matrix (mucoid, myxoid, chondroid, osseous)
Epithelial cells form ducts and sheets; myoepithelial cells form the stroma
Surrounded by an incomplete fibrous capsule

Clinical Features:

Slow-growing, painless swelling in the parotid region
Firm, mobile, well-demarcated mass
Long history (years to decades)

Key Points:

15-25% risk of malignant transformation if untreated (→ carcinoma ex pleomorphic adenoma)
Recurrence after incomplete excision (pseudopods penetrate the capsule)

Treatment: Superficial parotidectomy (with facial nerve preservation); complete excision with cuff of normal tissue (to prevent recurrence)

25. Peptic Ulcer, Colorectal Carcinoma, Gastric Carcinoma, IBD (Brief Overview)

Peptic Ulcer Disease (PUD):

Causes: H. pylori (most common), NSAIDs, acid hypersecretion (ZES)
Sites: Duodenal (more common) > Gastric
Duodenal ulcer: Anterior wall > posterior (risk of perforation), posterior (risk of bleeding - gastroduodenal artery)
Gastric ulcer: Lesser curvature most common; MUST biopsy to exclude malignancy

Gastric Carcinoma:

H. pylori, chronic atrophic gastritis (intestinal metaplasia → dysplasia → carcinoma)
Intestinal type (well-differentiated glands, associated with H. pylori)
Diffuse type: Signet ring cells; associated with E-cadherin mutations; Leather-bottle stomach (Linitis plastica) - diffuse infiltration makes stomach rigid and non-distensible
Spread: Virchow's node (left supraclavicular LN), Krukenberg tumor (bilateral ovarian metastasis, signet ring cells), Sister Mary Joseph nodule (umbilical)

Colorectal Carcinoma:

Risk factors: FAP, Lynch syndrome (HNPCC), IBD, diet (high fat, low fiber), colorectal polyps
Adenoma-carcinoma sequence: Polyp → adenoma → carcinoma (APC gene mutation is the initiating event)
Right-sided: Exophytic mass; iron deficiency anemia; no obstruction
Left-sided: Napkin ring lesion; obstruction; altered bowel habits
Staging: Duke's staging (A=mucosa, B=muscle, C=lymph nodes, D=metastasis)

Sources: Robbins & Kumar Basic Pathology (Elsevier, 2023) and Robbins, Cotran & Kumar Pathologic Basis of Disease from the medical textbook library. Note that the library does not contain Ramdas Nayak's specific textbook, but the above content is drawn from the same standard pathology references (Robbins) that Ramdas Nayak is based upon.All 25 topics from your notes have been covered above with detailed, exam-ready answers. Here is a quick summary of what's included:

Topics Covered

RBC (Hematology)

Hemolytic Anemia - Classification (intravascular vs extravascular), types, lab findings
Sickle Cell Anemia - Genetics, pathophysiology, crises, complications, lab
Thalassemia - α vs β, major vs minor, comparison table, complications
Iron Deficiency Anemia - Stages, causes, clinical features, lab (ferritin, TIBC, transferrin saturation)
Megaloblastic Anemia - B12 vs folate, pernicious anemia, subacute combined degeneration, lab
Aplastic Anemia - Causes, bone marrow findings, treatment

WBC (Hematology)

Chronic Myeloid Leukemia - Philadelphia chromosome, BCR-ABL, lab, phases, imatinib
Leukemia vs Leukemoid Reaction - Comparison table (LAP score is key differentiator)
Acute Myeloid Leukemia - APL with Auer rods, t(15;17), ATRA treatment

Platelets

DIC - Pathogenesis, causes, ISTH scoring, lab (D-dimers, schistocytes)
ITP - Acute vs chronic, treatment
Hemophilia A - Factor VIII deficiency, prolonged aPTT, treatment
Pancytopenia - Causes overview

Lymph Node & Spleen

Splenomegaly - Causes, complications
Hodgkin Lymphoma - RS cells (owl-eye, CD15/CD30+), subtypes table, Ann Arbor staging, ABVD
Non-Hodgkin Lymphoma - Key types (DLBCL, Follicular, Burkitt, Mantle Cell)
Multiple Myeloma - CRAB criteria, Bence Jones protein, M-spike, Rouleaux formation

CVS

Acute MI - Morphological changes over time (key exam table), biomarkers, complications
Rheumatic Heart Disease - Aschoff bodies, Jones criteria, valve involvement
Infective Endocarditis - Organisms, Duke criteria, Osler/Janeway/Roth spots

Respiratory

Lobar Pneumonia - 4 stages (congestion, red hepatization, grey hepatization, resolution), S. pneumoniae
COPD - Chronic bronchitis vs emphysema, Reid index

GIT

Crohn's vs Ulcerative Colitis - Detailed comparison table
Pleomorphic Adenoma - Most common salivary gland tumor, mixed tumor, malignant transformation risk
Gastric/Colorectal Carcinoma, PUD - Key exam points

Note: The library does not contain Ramdas Nayak's textbook specifically, but all content is from Robbins Pathology - which is the primary reference Ramdas Nayak's book itself is based on, so the content is fully aligned with that syllabus.

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1. HEMOLYTIC ANEMIA

Definition

Hemolytic anemias are a diverse group of disorders sharing a common feature: accelerated red cell destruction - the RBC lifespan is shortened from its normal 120 days, often to as little as 20-30 days.

Compensatory response:

Anemia + low tissue O2 → stimulates erythropoietin from kidneys → marrow erythroid hyperplasia + peripheral reticulocytosis
In severe cases: extramedullary hematopoiesis in liver, spleen, lymph nodes

Classification

By Site of Defect:

Type	Definition	Examples
Intracorpuscular (Intrinsic)	Defect is within the RBC itself	Hereditary spherocytosis, Sickle cell, Thalassemia, G6PD deficiency
Extracorpuscular (Extrinsic)	Defect is outside the RBC	Autoimmune hemolytic anemia, Malaria, Mechanical hemolysis

By Site of Hemolysis (More Clinically Important):

Feature	Extravascular Hemolysis	Intravascular Hemolysis
Site	Spleen (macrophages in splenic cords)	Within blood vessels
Mechanism	Reduced RBC deformability → macrophage phagocytosis	Membrane rupture: mechanical trauma, complement, toxins
Jaundice/Hyperbilirubinemia	Yes (hemoglobin → heme → bilirubin in macrophages)	Mild
Splenomegaly	Yes ("work hyperplasia")	Absent or mild
Cholelithiasis (pigment stones)	Yes (if long-standing)	No
Hemoglobinemia	No	Yes
Hemoglobinuria	No	Yes
Hemosiderinuria	No	Yes (Hb absorbed by tubular cells → hemosiderin lost when cells slough)
Iron deficiency	No (iron recycled efficiently by macrophages)	Yes (if chronic - iron lost in urine)
Haptoglobin	Decreased (macrophages "regurgitate" Hb)	Markedly decreased

Key Point: Decreased serum haptoglobin is a feature of both types because macrophages regurgitate enough hemoglobin even in extravascular hemolysis.

Common Types of Hemolytic Anemia

A. Hereditary Spherocytosis

Genetics: Usually autosomal dominant; rare severe autosomal recessive form
Pathogenesis: Inherited defects in membrane skeleton proteins (spectrin, ankyrin, band 3, band 4.1, band 4.2) → weaken the link between the membrane skeleton and lipid bilayer → RBCs shed membrane vesicles → surface area-to-volume ratio decreases → cells become spherical
Consequence: Spherocytes are rigid and non-deformable → trapped in splenic cords → phagocytosed by macrophages (extravascular hemolysis)
Morphology:
- Peripheral smear: spherocytes - dark red, lack central pallor, small
- Splenomegaly (often 500-1000 g; normal 150-200 g)
- Reticulocytosis, pigment gallstones (40-50% of patients)
Clinical: Anemia, jaundice, splenomegaly
Diagnosis: Osmotic fragility test (spherocytes lyse in hypotonic solution); eosin-5-maleimide (EMA) binding test
Treatment: Splenectomy (corrects anemia; spherocytes persist)

B. G6PD Deficiency

Genetics: X-linked recessive - affects males primarily
Pathogenesis: Mutations destabilize G6PD enzyme → RBCs cannot regenerate NADPH → cannot neutralize oxidative damage → Hb precipitates as Heinz bodies → membrane damage → acute intravascular and extravascular hemolysis
Triggers: Drugs (primaquine, dapsone, nitrofurantoin), infections, fava beans
Smear: Heinz bodies (with supravital stain); bite cells (after Heinz bodies are removed by splenic macrophages)
Course: Self-limited; reticulocytes (which have higher G6PD) replace damaged cells

C. Autoimmune Hemolytic Anemia (AIHA)

IgG (warm-type, 37°C) or IgM (cold-type, <4°C) antibodies against RBC surface antigens
Warm AIHA: Extravascular hemolysis in spleen; associated with SLE, CLL, drugs (methyldopa, penicillin)
Cold AIHA: IgM + complement → intravascular hemolysis; associated with Mycoplasma pneumoniae, EBV
Diagnosis: Direct Coombs (DAT) test positive (antibodies/complement on RBC surface)

D. Microangiopathic Hemolytic Anemia (MAHA)

Mechanical fragmentation of RBCs in abnormal microvasculature (fibrin strands in DIC, TTP, HUS, malignant hypertension)
Smear: Schistocytes (fragmented RBCs), helmet cells
Not immune-mediated; DAT negative

General Lab Findings in Hemolytic Anemia

Decreased Hb
Elevated reticulocyte count
Decreased serum haptoglobin
Elevated indirect (unconjugated) bilirubin
Elevated serum LDH (released from lysed RBCs)
Peripheral smear: specific morphology depending on type
Bone marrow: erythroid hyperplasia

2. SICKLE CELL ANEMIA

Definition & Genetics

Autosomal recessive hemoglobinopathy
Point mutation in β-globin gene: Glutamic acid → Valine at position 6 (codon 6, GAG→GTG)
This creates Sickle Hemoglobin (HbS)

Epidemiology:

Most common familial hemolytic anemia
Prevalent where malaria is/was endemic (equatorial Africa, parts of India, Middle East, southern Europe) - HbS confers protection against falciparum malaria
In the USA: ~8% of African-Americans are heterozygous HbS carriers; ~1 in 600 have sickle cell anemia

Normal vs. Abnormal Hemoglobin

Normal adult: HbA (α2β2) = 96%, HbA2 = 3%, HbF = 1%
Sickle cell disease (homozygous HbSS): HbA completely replaced by HbS
Sickle cell trait (heterozygous HbAS): ~40% HbS, ~60% HbA - minimal sickling in vivo because HbA retards HbS polymerization

Pathogenesis

Step-by-Step:

Deoxygenation of HbS → conformational change in β-globin
Deoxygenated HbS molecules self-associate via the abnormal valine residue → form long rigid polymers
These polymers distort the RBC → elongated crescentic/sickle shape (Fig. 10.3 in Robbins)
Initially reversible on reoxygenation
Repeated sickling → calcium influx, loss of K+ and water, membrane skeleton damage → irreversibly sickled cells → prone to hemolysis

Three Key Factors Determining HbS Polymerization:

Factor	Effect
Intracellular HbS concentration	Higher concentration → more polymerization
Presence of other Hb types	HbA and HbF inhibit polymerization (explain why trait is mild and neonates are protected)
Degree of deoxygenation	More deoxygenation → more sickling (hence hypoxia is a trigger)

Triggers of Sickling: Hypoxia, acidosis, dehydration, infection, cold, stasis

HbF protection: Newborns with sickle cell disease do not manifest disease until HbF falls to adult levels - around 5-6 months of age

Pathologic Consequences

Two major pathological consequences:

1. Chronic Hemolytic Anemia

Mean RBC life span: ~20 days (1/6 of normal 120 days)
Severity correlates with number of irreversibly sickled cells
Hematocrit: 18-30% (normal 38-48%)

2. Vascular Obstruction (Vasoocclusive Crisis)

NOT related to number of irreversibly sickled cells
Triggered by: infection, inflammation, dehydration, acidosis
Sickled cells obstruct microvasculature → ischemia, infarction, pain

Morphology (Gross & Microscopic)

Peripheral smear: Elongated, spindled, boat-shaped irreversibly sickled cells; target cells; reticulocytes
Bone marrow: Erythroid hyperplasia (compensatory)
Skeleton: Bone resorption + secondary new bone formation → "crewcut" skull X-ray, prominent cheekbones (similar to thalassemia)
Spleen:
- Children: Moderate splenomegaly (up to 500 g) - red pulp congestion from trapped sickled cells
- Adults: Autosplenectomy - repeated infarcts → fibrotic, small, useless spleen
Multiple organs: Vascular congestion, thrombosis, infarction affecting bones, liver, kidneys, retina, brain, lung, skin
Priapism (frequent): penile vascular congestion → fibrosis and erectile dysfunction
Pigment gallstones (from chronic hemolysis)

Clinical Features

Chronic manifestations:

Chronic hemolytic anemia
Jaundice, pallor, fatigue
Elevated bilirubin → pigment gallstones

Vasoocclusive Crises:

Hand-foot syndrome (dactylitis): Most common presenting symptom in young children - infarction of small bones of hands and feet → painful swelling
Acute Chest Syndrome: Sickled cells in hypoxemic pulmonary vasculature → creates vicious cycle of worsening hypoxia + more sickling → can be fatal. Also triggered by fat emboli from infarcted bone. Leading cause of death along with stroke.
Stroke: Cerebral vasoocclusion; especially in children
Proliferative Retinopathy: Vasoocclusion in retina → visual loss, blindness
Aplastic Crisis: Parvovirus B19 infects erythroblasts → sudden ↓ in RBC production → severe acute anemia (self-limited)
Splenic Sequestration Crisis: Children - sudden pooling of blood in spleen → rapid fall in Hb, hypovolemic shock

Infections (Major problem):

Functional asplenia (autosplenectomy in adults; congestion-related dysfunction in children) → susceptible to encapsulated bacteria: Streptococcus pneumoniae, H. influenzae
Also: gram-negative bacteria (E. coli), Salmonella osteomyelitis (bone infarction provides seeding site)

Diagnosis

Newborn screening: Mandatory in the USA - hemoglobin gel electrophoresis from heel-stick
Peripheral smear: Sickle cells (in homozygous); sickling induced in vitro by hypoxia (in trait)
Hb electrophoresis: HbS band, absence of HbA (in HbSS)
Sickle solubility test (Sickling test): Positive in both SS and AS
Prenatal diagnosis: Fetal DNA from amniocentesis or chorionic villus biopsy

Treatment

Hydroxyurea (mainstay): Inhibits DNA synthesis; reduces crises by:
1. Increasing HbF levels (HbF inhibits HbS polymerization)
2. Anti-inflammatory effect (inhibits WBC production)
3. Increases RBC size → lowers intracellular Hb concentration
4. Metabolized to NO → vasodilation + inhibits platelet aggregation
Prophylactic penicillin + pneumococcal vaccine (especially in children <5 years)
Blood transfusions (for crises, stroke prevention)
Allogeneic bone marrow transplantation (potentially curative)
Gene therapy (promising, potentially curative)

3. THALASSEMIA

Definition

Inherited disorders caused by mutations in globin genes that decrease the synthesis of α- or β-globin chains. Decreased synthesis of one chain leads to:

Deficiency of Hb → microcytic hypochromic anemia
Excess of the unpaired normal globin chain → precipitates → red cell damage and hemolysis

Epidemiology: Common in Mediterranean (β-thal), Africa (α-thal), and Asian regions where malaria is endemic - thalassemia mutations likely protect against falciparum malaria.

Genetics

Globin	Chromosome	Gene copy number
β-globin	Chromosome 11	1 gene per chromosome (2 total)
α-globin	Chromosome 16	2 genes per chromosome (4 total)

Adult HbA = α2β2 tetramer

β-THALASSEMIA

Molecular Basis

Caused mainly by point mutations (>100 different mutations known)
β0: No β-globin produced (complete absence)
β+: Reduced (but detectable) β-globin production
Mutations disrupt: abnormal RNA splicing (most common), promoter mutations (↓ transcription), coding region mutations (↓ translation)
Gene deletions are rare in β-thalassemia (unlike α-thalassemia)

Clinical Genotype Classification:

Clinical Syndrome	Genotype	Clinical Features
β-Thal Major (Cooley's Anemia)	β0/β0 or β0/β+	Severe anemia; transfusion-dependent from infancy
β-Thal Intermedia	β+/β+ or β0/β+ (milder)	Moderate anemia; usually not transfusion-dependent
β-Thal Minor (Trait)	β+/β or β0/β (heterozygous)	Asymptomatic or mild; normal life expectancy

Pathogenesis of β-Thalassemia Major (Two mechanisms):

Mechanism 1 - Inadequate HbA formation:

↓ β-globin → small, poorly hemoglobinized (microcytic, hypochromic) RBCs

Mechanism 2 - Excess unpaired α-globin chains:

α-chains form toxic precipitates → damage RBC and erythroid precursor membranes → apoptosis of erythroblasts in bone marrow = Ineffective erythropoiesis (large fraction never reach circulation)
The few RBCs that are released have a shortened lifespan

Downstream consequences of ineffective erythropoiesis:

Low hepcidin (due to erythroferrone secreted by expanded erythroblast pool) → ↑ intestinal iron absorption → iron overload (even without transfusions)
Massive erythroid hyperplasia → marrow expansion → bone deformities

Morphology of β-Thalassemia Major

Peripheral blood smear:

Marked microcytosis and hypochromia
Poikilocytosis (variation in shape)
Anisocytosis (variation in size)
Target cells (increased surface area-to-volume ratio)
Nucleated red cells (normoblasts) - reflect erythropoietic drive
Basophilic stippling

Bone marrow:

Striking hyperplasia of erythroid progenitors, shifted toward early forms
Expanded erythropoietic marrow fills intramedullary space → invades cortex → impairs bone growth

Skeletal Changes:

"Crew-cut" skull X-ray (hair-on-end appearance)
Frontal bossing, prominent cheekbones ("chipmunk face")
Maxillary overgrowth with malocclusion

Organomegaly:

Massive hepatosplenomegaly (extramedullary hematopoiesis + hyperplasia of mononuclear phagocytes)
Lymphadenopathy

Iron Overload (Hemosiderosis/Secondary Hemochromatosis):

From repeated transfusions + inappropriate gut iron absorption
Deposition in: Heart (cardiomyopathy - major cause of death), liver (cirrhosis), endocrine glands (diabetes, hypogonadism, hypothyroidism)

Clinical Features of β-Thalassemia Major

Manifests postnatally as HbF synthesis diminishes (after ~3-6 months)
Growth retardation starting in infancy
Severe anemia → pallor, fatigue, failure to thrive
Skeletal deformities (bone expansion)
Massive hepatosplenomegaly
With transfusions alone: survival into 2nd-3rd decade
Without iron chelation: cardiac dysfunction (secondary hemochromatosis) → fatal in 2nd-3rd decade
Treatment of choice: Hematopoietic stem cell transplantation at early age (curative)

Clinical Features of β-Thalassemia Minor (Trait)

Usually asymptomatic
Mild microcytic hypochromic anemia (may be mistaken for IDA)
Normal life expectancy
Diagnosis: HbA2 elevated (>3.5%) on electrophoresis; HbF mildly elevated
Important for genetic counseling: two carriers → 25% chance of thal major in offspring

α-THALASSEMIA

Molecular Basis

Caused mainly by gene deletions (unlike β-thalassemia which is due to point mutations)
Since there are 4 α-globin genes (2 per chromosome 16), severity is proportional to number of genes deleted:

Genes Deleted	Syndrome	Clinical Features
1 gene (−/αα)	Silent carrier	Asymptomatic; normal CBC
2 genes (−/−αα or −α/−α)	α-Thal trait	Mild microcytic hypochromic anemia; resembles β-thal minor
3 genes (−/−−α)	HbH disease	Moderately severe anemia; excess β-globin forms β4 tetramers (HbH) → less membrane damage than free α-chains; splenomegaly; usually not transfusion-dependent
4 genes (−/−−−)	Hb Bart's hydrops fetalis	Lethal in utero; excess γ-globin forms γ4 tetramers (Hb Bart) → extremely high O2 affinity → no O2 delivery → severe fetal hypoxia → hydrops fetalis → stillbirth or death shortly after birth

Key point: In α-thal, excess β/γ chains form relatively stable tetramers (HbH, Hb Bart) that cause less membrane damage than the free α-chains of β-thalassemia. Hence, α-thalassemia is generally less severe.

Diagnosis of Thalassemias

Test	β-Thal Major	β-Thal Minor	α-Thal Trait
Hb	Very low (2-3 g/dL)	Mildly low or normal	Mildly low or normal
MCV	Very low (<60 fL)	Low (<75 fL)	Low
Smear	Nucleated RBCs, marked microcytosis, target cells	Microcytosis, hypochromia, target cells	Microcytosis, hypochromia
HbA2 (electrophoresis)	Elevated	Elevated (>3.5%) - key finding	Normal
HbF	Very high	Mildly elevated	Normal
HbH	Absent	Absent	Absent (present in HbH disease)

Distinguishing IDA from β-thal trait:

Both show microcytic hypochromic anemia
IDA: low ferritin, low serum iron, high TIBC
β-thal trait: normal/elevated ferritin, elevated HbA2 on electrophoresis

Sources: Robbins & Kumar Basic Pathology (Elsevier), retrieved from the medical textbook library - directly from the Hemolytic Anemia, Sickle Cell, and Thalassemia chapters.

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