Ultimate Pathology Exam Guide

Comprehensive, High-Yield, MCQ-Oriented Review

Lecture 1: Pathology of the Breast I

Normal Histology & Hormonal Control
  • The Lobule: The basic secretory unit. Acini are embedded in loose connective tissue and connected to lactiferous ducts.
  • Epithelium: Ductal and lobular cells are surrounded by Myoepithelial cells (which rest on the basement membrane).
  • Hormonal Control (Cyclic Changes):
    • Estrogen dominates the Proliferative phase → Duct proliferation.
    • Progesterone dominates the Secretory phase → Edema, increased secretion, resulting in Cyclical Pain.
    • Menstruation → Decreased edema.
Clinical Presentations
  • Pain: Most common presenting complain. Can be cyclical (hormonal) or non-cyclical (cyst, trauma, infection). Note: 5-10% of breast carcinomas present with pain.
  • Nipple Discharge:
    • Benign: Usually young age, Bilateral (e.g., Fibrocystic changes, Intraductal papilloma, duct ectasia, drugs, pregnancy).
    • Malignant: Usually Unilateral, bloody or serous. Higher risk in women >50 years (~30% malignant).
  • Mass (Lump): 90% are benign (round to oval, circumscribed borders). Palpable masses have a 50% chance of positive Lymph Nodes (LN) if malignant. Masses usually become palpable when >2cm.
  • Congenital Inversion of the Nipple: Must be differentiated from acquired inversion (which is highly suspicious for Carcinoma).
Inflammatory Lesions (MCQ High-Yield)
  • Acute Mastitis & Breast Abscess: Related to Lactation (fissures allow Staphylococcus aureus or Streptococcus to enter). Presents as red, tender, hot, purulent discharge. Morphology: Sheets of neutrophils.
  • Periductal Mastitis: Strongly associated with Smoking (causes relative Vitamin A deficiency → Squamous metaplasia of lactiferous ducts → keratin blocks duct → inflammation). Presents as Subareolar mass with nipple retraction.
  • Mammary Duct Ectasia: Chronic inflammation causing dilation (ectasia). Presents as Periareolar mass with Green-brown nipple discharge. Biopsy shows Plasma cells.
  • Granulomatous Mastitis: Rare. Secondary to Sarcoidosis, Tuberculosis (TB), Fungal infection, Foreign body. Idiopathic Granulomatous Mastitis shows non-caseating granulomas centered around lobules with microabscesses.
  • Traumatic Fat Necrosis: History of trauma (e.g., seatbelt) in pendulous breasts. Painless hard lump with skin retraction (mimics cancer). Histology: Fat necrosis, foamy histiocytes, multinucleated giant cells, fibrosis, and Calcification (Saponification).
Fibrocystic Changes (FCC) & Benign Epithelial Tumors
  • Fibrocystic Changes (FCC): Most common breast lump (30-60%), prominent in premenopausal women. Vague nodularity, sometimes brownish discharge (Blue Domed Cysts).
    • Non-Proliferative FCC (Simple): Fibrosis, Cysts, and Apocrine Metaplasia (tall eosinophilic cells lining cysts). Important: No increased risk of cancer.
    • Proliferative FCC: Epithelial Hyperplasia (>2 cell layers above basement membrane) and Sclerosing Adenosis (increased acini per lobule with fibrosis, produces hard rubbery lump mimicking Carcinoma). Usually bilateral/multifocal.
    • Atypical Hyperplasia (Atypical Ductal Hyperplasia ADH & Atypical Lobular Hyperplasia ALH): Complex architecture with cellular atypia. Increases risk of carcinoma by 5 times (jumps to 10 times if positive family history).
  • Large Duct Papilloma: Middle-aged women. Benign papillary tumor within a lactiferous duct. Presents with Bloody nipple discharge.
  • Tubular & Lactation Adenomas: Well-circumscribed, packed tubules. Nipple Adenoma may ulcerate nipple (Must differentiate from Paget's disease).

💡 High-Yield Hints - Lecture 1

  • Non-proliferative Fibrocystic Changes (including Apocrine Metaplasia) do NOT increase the risk of breast cancer.
  • Atypical hyperplasia combined with a positive family history shoots the breast cancer risk up by 10 times.
  • Mammary duct ectasia is characterized by green-brown discharge and the presence of plasma cells on biopsy.
  • Periductal Mastitis is strongly linked to Smoking (Vitamin A deficiency) leading to squamous metaplasia.
  • Traumatic fat necrosis perfectly mimics cancer clinically (hard mass, skin retraction) and radiologically (calcification due to Saponification).

Lecture 2: Pathology of the Breast II (Tumors)

Stromal & Mixed Benign Tumors
  • Fibroadenoma (FA): Most common benign breast tumor. Estrogen sensitive (grows during pregnancy, shrinks and calcifies in menopause). Mixed epithelial and stromal proliferation. Circumscribed, mobile, easily shelled out.
  • Phyllodes Tumor: Arises from stroma. Characterized by Leaf-like projections into clefts. Classified as Benign (most common), Intermediate, or Malignant (15%). Malignancy features: Increased stromal cellularity, rapid size increase, invasive border, high mitoses.
Carcinoma In Situ
  • Ductal Carcinoma In Situ (DCIS): Fills ductal lumen but intact basement membrane. Rarely palpable, mostly diagnosed via screening Mammography (microcalcifications).
    • Comedo Carcinoma (High Grade DCIS): Pleomorphic nuclei, prominent Central Necrosis (comedonecrosis), abundant microcalcifications. Larger, may have Lymph Node metastasis at presentation!
    • Non-Comedo DCIS (Low Grade): No necrosis. Patterns: Solid, Cribriform, Papillary.
    • Paget Disease of the Nipple: Extension of DCIS up the lactiferous ducts into the skin of the nipple. Presents as crusty, scaly skin. Histology: Large malignant Paget cells in the epidermis. Does not affect staging.
  • Lobular Carcinoma In Situ (LCIS): Small, uniform, discohesive cells (due to loss of E-cadherin) filling acini. Incidental finding (no mass, rarely calcifies). High rate of being Multifocal (70%) and Bilateral (60%). Risk of invasive cancer is equal in both breasts.
Invasive Breast Carcinomas
  • Invasive Ductal Carcinoma (Not Otherwise Specified - NOS): Most common (80%). Hard, painless, fixed mass. 50% occur in the Outer Upper Quadrant.
  • Medullary Carcinoma: Most common type associated with BRCA1 mutations. Soft, fleshy mass mimicking Fibroadenoma. Histology: Pushing borders, sheets of high-grade pleomorphic cells, prominent Lymphocytic infiltrate. Triple-Negative (Estrogen Receptor-, Progesterone Receptor-, HER2-) but ironically has a Better prognosis than NOS.
  • Mucinous (Colloid) Carcinoma: Older (postmenopausal) women. Soft gelatinous mass. Histology: Clusters of uniform cells floating in Lakes of Mucin. ER/PR positive, excellent prognosis if pure.
  • Tubular Carcinoma: Well-formed tubules in dense desmoplastic stroma. Very good prognosis. ER/PR positive.
  • Invasive Lobular Carcinoma: Frequently bilateral and multicentric. Mutation of E-cadherin causes lack of cohesion. Histology: Single cells infiltrating stroma in an Indian File pattern. Signet ring cells common.
  • Inflammatory Carcinoma: A clinical diagnosis. Dermal lymphatics are blocked by tumor cells causing Peau d'orange (edema, redness, swollen tender breast). Extremely rapid and poor prognosis.
Grading, Staging & Prognostic Factors
  • Histological Grading: Bloom-Richardson Grade is based on 3 criteria: 1) Mitotic count, 2) Nuclear pleomorphism, 3) Tubular architecture. (Grade I=low, Grade III=high).
  • Staging (Most important prognostic factor):
    • Stage I: <2cm, LN negative.
    • Stage II: <5cm, +/- mobile LN.
    • Stage III: Skin infiltration, chest wall fixation.
    • Stage IV: Distant Metastasis (Lungs, liver, bone, brain).
  • Sentinel Lymph Node Biopsy: First node draining the tumor. A negative node highly predicts absence of metastatic cancer in remaining axillary nodes.
  • Biological Markers (Intrinsic Subtypes):
    • Luminal A/B (50-65%): Estrogen/Progesterone Receptor positive. Responds to anti-estrogen therapy (Tamoxifen). Better prognosis.
    • HER2 Overexpression (10-20%): Aggressive but responds to targeted therapy monoclonal antibodies (Trastuzumab / Herceptin).
    • Triple-Negative / Basal-like (10-20%): ER-, PR-, HER2-. Worst prognosis overall (except for Medullary variant).

💡 High-Yield Hints - Lecture 2

  • Medullary Carcinoma is Triple-Negative and associated with BRCA1 mutations, yet it has a better prognosis than standard Invasive Ductal Carcinoma.
  • Lobular Carcinoma In Situ (LCIS) is always an incidental finding (does not form masses or microcalcifications) and strongly predisposes to cancer in both breasts.
  • Inflammatory Carcinoma is diagnosed clinically by the presence of Peau d'orange (caused by dermal lymphatic invasion).
  • Paget Disease of the Nipple indicates underlying Ductal Carcinoma In Situ (DCIS) but does not change the clinical stage.
  • Invasive Lobular Carcinoma cells lack cohesion due to E-cadherin mutation, leading to the classic Indian File histopathological pattern.

Lecture 3: Female Genital Tract I (Vulva, Cervix, Uterus)

Vulvar Pathology
  • Bartholin Cyst: Obstruction of Bartholin gland duct. Lined by transitional/squamous epithelium. Treatment: Excision or Marsupialization (opened permanently).
  • Non-Neoplastic Epithelial Disorders:
    • Squamous Cell Hyperplasia (Lichen Simplex Chronicus): Due to chronic rubbing/scratching. Hyperkeratosis, acanthosis. No atypia, no cancer risk.
    • Lichen Sclerosus: Smooth white plaques (leukoplakia) causing Introitus stenosis. Thin epidermis, loss of rete ridges, dermal fibrosis. Carries a 1-5% risk of Squamous Cell Carcinoma (SCC).
  • Condyloma Acuminatum: Benign genital warts (STD). Associated with Human Papillomavirus (HPV) 6 and 11. Histology pathognomonic feature: Koilocytic atypia (enlarged, hyperchromatic, wrinkled nuclei with perinuclear halos in superficial cells).
  • Vulvar Squamous Cell Carcinoma: 95% of vulvar malignancies. Two pathways: 1) HPV-associated (high-risk HPV 16/18, younger women, preceded by VIN). 2) HPV-independent (older women, preceded by Lichen Sclerosus, highly keratinized).
  • Extramammary Paget’s disease: Intra-epidermal adenocarcinoma. Red, scaly, crusted plaque. Minority associated with underlying carcinoma.
Cervical Pathology
  • Cervical Intraepithelial Neoplasia (CIN): Dysplastic changes usually starting at the squamo-columnar junction. Driven by Human Papillomavirus (HPV). (High risk HPV: 16, 18, 31, 33). Pap smear is an effective screening tool.
  • Grading:
    • CIN I (Low-grade SIL): Dysplasia limited to lower 1/3 of epithelium. (60% regress).
    • CIN II (High-grade SIL): Dysplasia extends to middle 1/3.
    • CIN III (High-grade SIL): Dysplasia extends beyond middle 1/3 but not full thickness.
    • Carcinoma in Situ (CIS): Full thickness dysplasia with intact basement membrane.
Uterus (Endometrium & Myometrium)
  • Endometritis:
    • Acute: Postpartum or post-abortion (bacterial).
    • Chronic: Seen with Pelvic Inflammatory Disease (PID), Retained Product of Conception (RPOC), Intrauterine Contraceptive Device (IUCD), or Tuberculosis (TB). Diagnosis requires finding Plasma Cells in stroma.
  • Endometriosis: Presence of ectopic endometrial glands and stroma outside the uterus (e.g., ovaries = chocolate cysts). Tissue has high aromatase and Prostaglandin E2 (PGE2). Treated with NSAIDs and aromatase inhibitors. Diagnosis requires 2 out of 3: Endometrial glands, Endometrial stroma, Hemosiderin pigment.
  • Adenomyosis: Endometrial glands and stroma deep within the Myometrium. Uterus is globally enlarged. Dysmenorrhea and bleeding.
  • Endometrial Hyperplasia: Caused by Prolonged excess estrogen relative to progesterone (Anovulation, Polycystic Ovarian Disease, Obesity, Estrogen tumors).
    • Without atypia: 5% cancer risk.
    • Atypical Hyperplasia (Endometrial Intraepithelial Neoplasia / EIN): Nuclear atypia, PTEN mutation positive. 30% risk of progression to adenocarcinoma.
  • Endometrial Adenocarcinoma: Most common female genital tract malignancy. Postmenopausal.
    • Endometrioid Type (85%): Resembles normal endometrium, estrogen-driven, PTEN mutation, favorable prognosis.
    • Serous Type (15%): Arises in atrophic endometrium, independent of estrogen. High grade, aggressive. Early mutation in p53. Forms small papillae/tufts.
  • Leiomyoma (Fibroid): Most common benign tumor overall (30-50% of women). Estrogen-driven. Well-circumscribed, whorled cut surface. Histology: uniform smooth muscle bundles, NO atypia/mitosis/necrosis.
  • Leiomyosarcoma: Malignant smooth muscle tumor. Single large mass, hemorrhagic/necrotic. Peak 40-60 yrs. Histology: Spindle cells with nuclear atypia, frequent mitoses, and tumor necrosis.
  • Malignant Mixed Müllerian Tumor (MMMT / Carcinosarcoma): Biphasic highly malignant tumor (carcinoma + sarcoma elements). Genetically similar to endometrial carcinoma. Elderly, poor outcome.

💡 High-Yield Hints - Lecture 3

  • Lichen Sclerosus is a non-neoplastic condition causing introitus stenosis but carries a 1-5% risk of Squamous Cell Carcinoma.
  • The pathognomonic sign of Condyloma Acuminatum (HPV 6/11) is Koilocytic atypia (wrinkled nuclei with perinuclear halos).
  • Endometrial Serous Carcinoma arises from an atrophic endometrium (not estrogen-driven) and is characterized by early p53 mutations.
  • Diagnosis of Chronic Endometritis requires the microscopic identification of Plasma Cells.
  • Leiomyoma (Fibroid) is the most common benign tumor, features a whorled cut surface, and shows strictly NO necrosis or mitoses.

Lecture 4: Female Genital Tract II (Ovary & Tubes)

Ovary: Non-Neoplastic Cysts
  • Polycystic Ovary Syndrome (PCOS): Enzyme dysregulation → excessive androgens. Clinical: anovulation, infertility, hirsutism, obesity. Risk for endometrial hyperplasia/carcinoma. Gross: Enlarged ovaries with thickened capsule (Hyperthecosis), multiple subcortical cysts, Absent corpora lutea.
  • Follicular Cyst: Unruptured Graafian follicle.
  • Corpus Luteal Cyst: Normal corpus luteum is cystic, but occasionally forms a large cyst causing delayed menses or rupture (internal bleeding).
Ovarian Tumors
  • Classification: 1) Surface Epithelial (most common), 2) Germ Cell, 3) Sex Cord-Stromal, 4) Metastatic.
  • Epithelial Tumors: Serous, Mucinous, Endometrioid. Serous tumors are the most common.
    • Benign Serous Tumor: Clear fluid, single layer of columnar/ciliated cells.
    • Malignant Serous Cystadenocarcinoma: Complex papillae, invasion, and Psammoma bodies. Propensity to spread to peritoneal surfaces (omentum).
  • Germ Cell Tumors:
    • Teratoma (Mature Cystic / Dermoid Cyst): >90% benign. Contains somatic tissues from 3 germ layers (skin, hair, teeth, bone). Complications: Torsion, 1% undergo malignant transformation (usually to Squamous Cell Carcinoma). Struma Ovarii is a specialized teratoma composed entirely of functional Thyroid tissue.
    • Dysgerminoma: Female counterpart of testicular Seminoma. Solid gray mass. Histology: sheets of large clear cells separated by Lymphocyte-rich fibrous strands. Excellent prognosis (radiosensitive).
    • Yolk Sac Tumor (Endodermal Sinus Tumor): Malignant, aggressive. Pathognomonic histology: Schiller-Duval bodies (glomerulus-like structures). Secretes Alpha-Fetoprotein (AFP).
Gestational Trophoblastic Diseases (GTD)
  • Complete Hydatidiform Mole:
    • Genetics: Empty ovum fertilized by 1 or 2 sperms (all chromosomes are paternal, typically 46,XX).
    • Morphology: Large mass of grape-like vesicles. No fetal parts. Avascular villi with central edema (cisterns) and circumferential trophoblastic proliferation.
    • Clinical: Uterus large for date, very high hCG, higher risk of progression to Choriocarcinoma (2-3%).
  • Partial Hydatidiform Mole:
    • Genetics: Normal ovum fertilized by 2 sperms (Triploid: 69,XXY).
    • Morphology: Fetal parts present. Only some villi are enlarged. Minimal risk for Choriocarcinoma.
  • Choriocarcinoma: Highly malignant. Can follow a complete mole, normal pregnancy, or abortion. Very high hCG. Extremely hemorrhagic. Histology: Sheets of anaplastic syncytiotrophoblasts and cytotrophoblasts, No chorionic villi. Metastasizes hematogenously early (especially to Lungs).

💡 High-Yield Hints - Lecture 4

  • Complete Hydatidiform Mole is entirely paternal in origin (Diploid) with an empty ovum and completely lacks fetal parts.
  • Choriocarcinoma is extremely aggressive, spreads via blood to the lungs, and histologically shows no chorionic villi.
  • Polycystic Ovary Syndrome (PCOS) is characterized by absent corpora lutea and carries a risk for endometrial hyperplasia due to unopposed estrogen.
  • Malignant transformation in a Mature Cystic Teratoma (<1% of cases) most commonly results in a Squamous Cell Carcinoma.
  • Malignant Serous Cystadenocarcinoma frequently contains Psammoma bodies and spreads widely across peritoneal surfaces.

Lecture 5: Bone, Joints & Soft Tissue

Metabolic & Genetic Bone Diseases
  • Osteogenesis Imperfecta (Brittle Bone Disease): Autosomal Dominant mutation in COL1A1 or COL1A2 genes → impaired Type I collagen synthesis. Clinical triad/tetrad: Extreme skeletal fragility, Blue sclera, Hearing loss, and Dentinogenesis imperfecta (misshapen blue-yellow teeth).
  • Osteoporosis: Reduced bone quantity (normal bone quality but less of it). Thin trabeculae. Measured by DEXA scan.
    • Senile OP: Low-turnover (decreased osteoblast activity).
    • Postmenopausal OP: High-turnover. Estrogen drop increases IL-1/TNF → Increased expression of RANK/RANKL → Overactivation of osteoclasts.
  • Osteomalacia & Rickets: Vitamin D deficiency → Accumulation of un-mineralized matrix (osteoid).
  • Paget Disease of Bone (Osteitis Deformans): Three phases: 1) Osteoclastic hypervascular, 2) Mixed, 3) Osteosclerotic. Histology: Dense woven bone with a Mosaic Pattern. Clinical: Increased hat size, Lion face, hearing loss. Major risk: Transformation to Osteosarcoma (or other sarcomas).
Bone Tumors
  • Osteoid Osteoma: Benign, <2cm, diaphysis. Causes Nocturnal pain relieved by Aspirin (due to PGE2 production). X-ray: radiolucent nidus with sclerotic rim.
  • Osteoblastoma: >2cm, posterior elements of vertebrae. Pain is NOT relieved by aspirin.
  • Osteosarcoma (OS): Malignant, produces osteoid matrix. Most common primary bone malignancy (excluding myeloma). Usually <20 years, metaphysis of distal femur/proximal tibia. X-ray: Codman triangle, sunburst pattern.
  • Osteochondroma: Benign, bony excrescence with a Cartilage cap. Metaphysis of long bones.
  • Chondroma (Enchondroma): Benign hyaline cartilage nodule in the medulla of small bones (hands/feet). Multiple in Ollier’s syndrome and Maffucci’s syndrome (high risk of chondrosarcoma).
  • Chondrosarcoma: Malignant cartilage tumor. Old age (>40 years), central skeleton (pelvis, shoulder, ribs).
  • Giant Cell Tumor: Benign but locally aggressive. Epiphysis of long bones. Histology: numerous osteoclast-like giant cells.
  • Ewing Sarcoma: Malignant Small Blue Round Cell Tumor (SBRCT). Diaphysis, young males. X-ray: Onion-skin periosteal reaction. Immunohistochemistry: CD99 positive, PAS positive (glycogen).
  • Nonossifying Fibroma: Common developmental defect in adolescents. Fibroblasts in a Storiform (straw mat) pattern with foamy macrophages. Resolves spontaneously.
  • Fibrous Dysplasia: Developmental arrest. Mutated GNAS1 gene. Histology: Chinese letters (curvilinear trabeculae of woven bone) lacking osteoblastic rimming.
Joints & Soft Tissue Tumors
  • Nodular Fasciitis: Benign, rapidly enlarging reactive myofibroblastic proliferation. History of trauma. Self-limiting.
  • Fibromatosis (Desmoid Tumor): Locally aggressive, non-metastasizing. Superficial (Palmar Dupuytren's, Penile Peyronie's) or Deep (Abdominal wall). Beta-catenin mutation positive.
  • Lipoma: Most common soft tissue tumor. Mature adipocytes.
  • Liposarcoma: Most common adult soft tissue sarcoma. Contains Lipoblasts (scalloped nucleus with lipid vacuoles). Myxoid variant features a "chicken wire" capillary network.
  • Fibrosarcoma: Malignant spindle cells in a Herringbone pattern.
  • Undifferentiated Pleomorphic Sarcoma (UPS): Diagnosis of exclusion. Bizarre multinucleated giant cells and a storiform pattern.
  • Rhabdomyosarcoma: Malignant skeletal muscle tumor. Most common sarcoma in childhood (Embryonal and Alveolar types). Embryonal includes Sarcoma botryoides.
  • Synovial Sarcoma: Uncertain origin, deep soft tissue near joints (knee, thigh). Biphasic (epithelial + spindle) or monophasic.
  • Schwannoma: Benign nerve sheath tumor. Biphasic histology: Antoni A (cellular, nuclear palisading forming Verocay bodies) and Antoni B (hypocellular, myxoid).
  • Leiomyoma & Leiomyosarcoma (Soft tissue): Benign vs malignant smooth muscle tumors. Malignant features: Atypia, mitosis, necrosis.

💡 High-Yield Hints - Lecture 5

  • Osteosarcoma is defined pathologically by its ability to produce malignant osteoid matrix, often presenting with a Codman Triangle on X-ray.
  • Paget Disease of Bone shows a highly characteristic Mosaic Pattern of woven bone and carries a risk of transforming into Osteosarcoma.
  • Ewing Sarcoma is a Small Blue Round Cell Tumor located in the Diaphysis featuring an Onion-skin reaction and CD99 positivity.
  • Myxoid Liposarcoma is classically identified by the presence of lipoblasts and a prominent "Chicken wire" capillary network.
  • Schwannoma histology uniquely displays cellular Antoni A areas containing Verocay bodies, alongside hypocellular Antoni B areas.

🔥 Core Exam Comparisons

High-yield tables summarizing key pathological differences. Scroll horizontally on small screens.

1. Complete vs. Partial Hydatidiform Mole (Lecture 4)
Feature Complete Hydatidiform Mole Partial Hydatidiform Mole
Karyotype Diploid (Paternal origin, typically 46,XX) Triploid (e.g., 69,XXY)
Fetal Parts Absent (Empty ovum) Present
Villous Edema All villi affected Some villi (Focal)
Trophoblastic Proliferation Circumferential (Around the entire villus) Focal
Atypia Marked Mild/Variable
Serum hCG Levels Highly Elevated Less elevated
Risk of Choriocarcinoma 2 - 3% Rare
2. Endometrial Adenocarcinoma: Endometrioid vs. Serous Type (Lecture 3)
Feature Endometrioid Type (85%) Serous Type (15%)
Pathogenesis / Drive Estrogen-driven Independent of Estrogen
Precursor Lesion Endometrial Hyperplasia (with atypia) Atrophic Endometrium
Patient Age Perimenopausal / Younger postmenopausal Older postmenopausal women
Key Mutations PTEN, Mismatch repair genes p53 (early mutation)
Histology Resembles normal endometrial glands Small tufts and papillae, high-grade atypia
Prognosis Favorable (Usually low grade) Aggressive / Poor outcome
3. Lichen Sclerosus vs. Squamous Cell Hyperplasia (Lecture 3)
Feature Lichen Sclerosus Squamous Cell Hyperplasia (Lichen Simplex Chronicus)
Clinical Appearance Smooth white plaques (Leukoplakia) + Introitus stenosis Leukoplakia (often secondary to rubbing/pruritus)
Histology Thin epidermis, loss of rete ridges, dermal fibrosis Hyperkeratosis, Acanthosis, Hypergranulosis
Cancer Risk 1 - 5% risk of Squamous Cell Carcinoma No increased risk of cancer
4. Leiomyoma vs. Leiomyosarcoma (Lectures 3 & 5)
Feature Leiomyoma (Fibroid) Leiomyosarcoma
Nature & Incidence Benign (Most common female tumor: 30-50%) Malignant (Rare: 1/1000 compared to fibroids)
Gross Appearance Multiple, well-circumscribed, firm, whorled cut surface Usually single, large, fleshy, hemorrhagic mass
Nuclear Atypia Absent Present (Marked pleomorphism)
Mitotic Activity Absent or very rare Frequent / Brisk mitoses
Tumor Necrosis Absent Present (Extensive)
5. High-Grade (Comedo) vs. Low-Grade Ductal Carcinoma In Situ (Lecture 2)
Feature High-Grade DCIS (Comedo Carcinoma) Low-Grade DCIS (Non-Comedo)
Nuclear Grade Pleomorphic nuclei, large/multiple nucleoli Small monomorphic nuclei
Necrosis Prominent Central Necrosis (Comedonecrosis) Absent
Microcalcifications Extensive and abundant Rare or minimal
Metastasis Risk May show Lymph Node metastases at presentation Lymph node metastases are uncommon
6. Comprehensive Comparison: Primary Bone Tumors (Lecture 5)
Tumor Behavior Typical Location Age Group Key Pathological / Radiological Features
Osteoid Osteoma Benign Diaphysis (<2cm) Young (Teens/20s) Radiolucent nidus. Nocturnal pain relieved by Aspirin.
Osteoblastoma Benign Vertebrae (Posterior) Young >2cm. Pain is NOT relieved by Aspirin.
Osteosarcoma Malignant Metaphysis (Knee) Adolescents (<20) Produces Malignant Osteoid. Codman triangle / Sunburst X-ray.
Ewing Sarcoma Malignant Diaphysis Children / Young Males Small Blue Round Cell Tumor. Onion-skin periosteal reaction. CD99 positive.
Giant Cell Tumor Locally Aggressive Epiphysis 20 - 40 years Numerous osteoclast-like multinucleated giant cells.
Chondrosarcoma Malignant Central Skeleton (Pelvis, Shoulder) Old Age (>40) Malignant chondrocytes. Bulky tumor with gelatinous/myxoid areas.
7. Comprehensive Comparison: Soft Tissue Sarcomas (Lecture 5)
Tumor Lineage / Origin Key Histological Feature
Liposarcoma (Myxoid) Adipose Tissue Presence of Lipoblasts in a prominent "Chicken wire" capillary network.
Fibrosarcoma Fibroblastic Malignant spindle cells arranged in a classic Herringbone pattern.
Rhabdomyosarcoma Skeletal Muscle Most common in childhood. Forms include Embryonal (Sarcoma Botryoides) and Alveolar.
Synovial Sarcoma Uncertain origin Often near joints. Biphasic (epithelial + spindle) morphology. Driven by t(X;18) translocation.
Undifferentiated Pleomorphic Sarcoma Unknown Diagnosis of exclusion. Bizarre multinucleated cells with a Storiform pattern.