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These are the slides for discussion in pathology practical give me detailed explanation of these slides

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Here is a detailed, exam-ready explanation for every slide in your practical box.

Pathology Practical Slides - Detailed Explanations


HISTOPATHOLOGY SLIDES


1. Fatty Liver (Hepatic Steatosis)

Stain: H&E
Gross: Enlarged, yellow, greasy liver.
Microscopy - What to say:
  • Hepatocytes show large, clear, sharply defined vacuoles in the cytoplasm that displace the nucleus to the periphery ("signet ring" appearance) - this is macrovesicular steatosis
  • In acute/toxic cases, small droplets surround the nucleus - microvesicular steatosis
  • No significant inflammation or fibrosis in simple steatosis
  • Centrilobular distribution in alcoholic fatty liver; panlobular in obesity/diabetes
Causes: Alcohol (most common), obesity, diabetes mellitus, pregnancy (acute fatty liver of pregnancy - microvesicular), drugs (tetracycline, valproate)
Key point: Fat stains (Oil Red O on frozen section) confirm lipid. On H&E the vacuoles appear empty because fat dissolves during processing.

2. Monckeberg Medial Calcific Sclerosis

Stain: H&E (calcium stains blue-purple; Von Kossa stain confirms)
Gross: "Pipestem" or "eggshell" arteries - hard, calcified, non-compressible vessels.
Microscopy - What to say:
  • Medium-sized muscular arteries (radial, ulnar, femoral, tibial)
  • Calcific deposits in the tunica media, specifically centered on the internal elastic lamina
  • The deposits appear as basophilic (dark blue-purple) irregular plaques in the media
  • Lumen is NOT narrowed - key distinguishing feature from atherosclerosis
  • No intimal plaque, no lipid, no inflammatory cells
  • The media may show "egg-shell" calcification in a ring pattern
Key distinction: Unlike atherosclerosis (intimal), Monckeberg affects the media. Unlike arteriolosclerosis (small vessels), this affects medium vessels. It does NOT cause ischemia directly.
Occurs in: People >50 years, diabetics, chronic kidney disease patients.

3. Acute Appendicitis

Stain: H&E
Gross: Swollen, congested appendix with fibrinous exudate on serosa.
Microscopy - What to say:
  • Transmural neutrophilic infiltration - neutrophils in all layers (mucosa, submucosa, muscularis, serosa)
  • Mucosal ulceration with fibrinopurulent exudate in the lumen
  • Vascular congestion and edema in the submucosa
  • Diagnostic hallmark: neutrophils within the muscularis propria
  • Periappendiceal fat may show edema and acute inflammation
  • In gangrenous appendicitis: areas of necrosis/coagulative necrosis visible
Pathogenesis: Obstruction (fecalith, lymphoid hyperplasia) → bacterial overgrowth → mucosal invasion → transmural spread.
Clinical: RIF pain, fever, raised WBC, positive McBurney's point tenderness.

4. Lobar Pneumonia

Stain: H&E
Gross: Entire lobe affected; appearance depends on stage.
Microscopy - What to say (4 classical stages):
StageDurationGrossMicroscopy
CongestionDay 1-2Red, heavyAlveolar capillary engorgement, proteinaceous fluid, few bacteria, rare neutrophils
Red HepatizationDay 2-4Red, airless, liver-likeAlveoli filled with RBCs, neutrophils, fibrin strands; "hepatized" lung
Grey HepatizationDay 4-8Grey, firmRBCs lysed; alveoli filled with fibrin, neutrophils, macrophages
ResolutionDay 8+Returning to normalEnzymatic digestion of fibrin; macrophage-dominant; alveolar architecture restored
Causative organism: Streptococcus pneumoniae (most common)
Key point: Alveolar architecture is preserved throughout (unlike ARDS). Interalveolar pores of Kohn allow spread to entire lobe.

5. Granulation Tissue

Stain: H&E
Gross: Pink-red, granular, moist tissue at base of healing wound.
Microscopy - What to say (the "3 pillars"):
  1. Proliferating capillaries (angiogenesis): New thin-walled capillaries, often cut in cross-section giving Swiss-cheese appearance; endothelial cells plump and active
  2. Proliferating fibroblasts: Spindle-shaped cells with pale cytoplasm; producing collagen
  3. Inflammatory infiltrate: Predominantly macrophages, lymphocytes, plasma cells; some neutrophils early
  • Edematous, loose connective tissue stroma
  • Myofibroblasts present (contribute to wound contraction)
  • Over time: fibroblasts replace capillaries → scar (fibrosis)
Growth factors: VEGF (angiogenesis), PDGF, TGF-β, FGF (fibroblast proliferation)

6. TB Lymph Node (Tuberculous Lymphadenitis)

Stain: H&E; ZN stain for acid-fast bacilli
Gross: Enlarged, matted lymph node; cut section shows white/yellow caseous material ("cheesy" necrosis).
Microscopy - What to say:
  • Epithelioid granulomas - collections of epithelioid macrophages (large, pale, "shoe sole" nuclei) with abundant pale cytoplasm
  • Langhans giant cells: Large multinucleated cells with nuclei arranged in a horseshoe/peripheral arc pattern at one pole
  • Caseous (cheesy) necrosis at center of granuloma: amorphous, acellular, eosinophilic material ("nuclear dust" - structureless)
  • Peripheral rim of lymphocytes
  • Fibrous capsule around granuloma (older lesions)
ZN stain: Red acid-fast bacilli on blue background (may be sparse - often negative despite active TB)
Caseous necrosis is pathognomonic of TB (though rarely seen in other conditions like histoplasmosis)

7. Actinomycosis

Stain: H&E; Gram stain (Gram-positive filaments)
Gross: Yellow sulfur granules in pus; indurated fibrotic tissue.
Microscopy - What to say:
  • "Sulfur granules" - the pathognomonic finding: basophilic central mass of tangled filaments
  • Peripheral club-shaped, eosinophilic projections ("clubs" or "rosette" pattern around granule) - this is the Splendore-Hoeppli phenomenon
  • Surrounding acute and chronic inflammation (neutrophils, macrophages, giant cells)
  • Dense fibrosis ("wooden" consistency grossly)
  • Draining sinuses may be seen
Organism: Actinomyces israelii - a Gram-positive, filamentous, anaerobic bacterium (part of normal oral flora)
Sites: Cervicofacial (most common - "lumpy jaw"), thoracic, abdominal (after appendiceal rupture), pelvic (IUD-associated)

8. Rhinosporidiosis

Stain: H&E; PAS stain highlights the sporangia
Gross: Polypoid, friable, vascular masses in the nasal cavity; "strawberry-like" or sessile polyps.
Microscopy - What to say:
  • Large sporangia (300-400 μm diameter) - thick-walled, round structures in the submucosa
  • Each sporangium contains thousands of endospores (sporangiospores)
  • Sporangia at various stages: immature (small, pale) to mature (large, packed with spores)
  • Mature sporangia rupture releasing spores into surrounding tissue
  • Surrounding stroma shows edema, vascular congestion, mixed inflammatory infiltrate (lymphocytes, plasma cells, eosinophils, neutrophils)
  • Overlying hyperplastic squamous or respiratory epithelium
Organism: Rhinosporidium seeberi (now classified as a mesomycetozoan, not a true fungus)
Endemic in: India (especially Tamil Nadu, Kerala), Sri Lanka

9. Lipoma

Stain: H&E
Gross: Soft, encapsulated, yellow fatty tumor.
Microscopy - What to say:
  • Composed of mature adipocytes - large cells with single large clear cytoplasmic vacuole pushing nucleus to periphery (signet-ring appearance)
  • Cells are uniform in size and shape - no nuclear atypia, no mitoses
  • Thin fibrous capsule surrounding the tumor
  • Thin fibrovascular septa dividing the lobules
  • Identical to normal fat histologically - diagnosis requires clinical/gross correlation
Distinguish from:
  • Liposarcoma: lipoblasts (cells with multiple small vacuoles indenting the nucleus), nuclear atypia, mitoses
  • Lipoblastoma (children): immature fat cells, myxoid stroma

10. Capillary Hemangioma

Stain: H&E
Gross: Bright red, compressible, lobulated lesion; commonly in skin/subcutis of children.
Microscopy - What to say:
  • Lobular proliferation of small, thin-walled capillary-sized vessels
  • Vessels lined by plump, proliferating endothelial cells - may be so cellular that lumina are nearly absent in early lesions
  • Vessels contain RBCs
  • Thin pericyte layer around vessels
  • Lobules separated by loose fibrous stroma
  • In early (cellular) phase: endothelial cells dominant; in late phase: vessels well-formed, lumina open
  • No nuclear atypia or significant mitotic activity
Types:
  • Strawberry hemangioma (infantile): grows rapidly then involutes
  • Cherry angioma: adults, dermal

11. Schwannoma (Neurilemmoma)

Stain: H&E; S-100 protein positive on IHC
Gross: Encapsulated, firm, whitish nerve sheath tumor; eccentrically placed on nerve.
Microscopy - What to say (the biphasic pattern):
  1. Antoni A areas: Densely cellular; spindle cells with elongated, wavy nuclei arranged in palisading rows ("Verocay bodies") - parallel rows of nuclei with anuclear zones between them
  2. Antoni B areas: Loosely arranged, hypocellular; myxoid/edematous matrix; cells haphazardly arranged; sometimes microcysts and hemorrhage
  • Encapsulated tumor - key feature distinguishing from neurofibroma
  • Thick-walled hyalinized vessels
  • Hemosiderin deposits (due to old hemorrhage)
  • No true nerve fibers within the tumor (nerve displaced to capsule)
S-100 positive throughout (unlike neurofibroma where only some cells stain)

12. Squamous Cell Carcinoma (SCC)

Stain: H&E
Gross: Ulcerated or fungating mass with indurated edges.
Microscopy - What to say:
  • Irregular islands/nests of malignant squamous cells invading the dermis/stroma
  • Keratin pearls (epithelial pearls): Concentric whorls of keratinizing squamous cells with central pink amorphous keratin - pathognomonic of well-differentiated SCC
  • Individual cell keratinization (dyskeratosis) - pink cytoplasm with pyknotic nucleus
  • Intercellular bridges (desmosomes) between cells
  • Nuclear pleomorphism, hyperchromatism, prominent nucleoli
  • Mitotic figures (normal and abnormal)
  • Desmoplastic stromal reaction
  • Surrounding chronic inflammatory infiltrate
Grades: Well-differentiated (many keratin pearls) → Poorly differentiated (few pearls, more anaplasia)

13. Adenocarcinoma Colon

Stain: H&E
Gross: Polypoid or ulcerating mass in colon; "napkin ring" constriction in left colon.
Microscopy - What to say:
  • Malignant glands infiltrating through the bowel wall (muscularis propria, subserosa)
  • Irregular glandular structures lined by columnar cells with nuclear stratification, pleomorphism, hyperchromatism
  • Mucin secretion (intraluminal or intracellular - signet ring cells if mucin displaces nucleus)
  • Loss of normal polarity; nuclei at different levels
  • Mitotic figures, prominent nucleoli
  • Desmoplastic stroma (abundant fibrous reaction around glands)
  • Tumor necrosis ("dirty necrosis") within gland lumina - characteristic of colorectal adenocarcinoma
  • May invade lymphatics, blood vessels, perineural spaces
Grading: Well (>95% gland formation), Moderate (50-95%), Poor (<50%) or undifferentiated

14. Pleomorphic Adenoma (Mixed Tumor of Salivary Gland)

Stain: H&E
Gross: Firm, encapsulated, bosselated (lobulated) tumor; cut section white/translucent with cartilaginous areas.
Microscopy - What to say (the "mix" is the key):
  • Epithelial component: Islands, ducts, nests, and sheets of epithelial cells (duct-forming inner cells + myoepithelial outer cells)
  • Mesenchymal (stromal) component: Myxoid, chondroid (cartilage-like), or even osseous areas - derived from myoepithelial cells
  • Both components mixed intimately within the same tumor
  • Incomplete fibrous capsule (important - can lead to recurrence if not excised completely)
  • Pseudopods/satellite nodules through capsule
"Pleomorphic" = diverse tissue types, NOT nuclear pleomorphism
Malignant transformation: Carcinoma ex pleomorphic adenoma (in ~5% of long-standing cases)

15. Atherosclerosis

Stain: H&E; Masson's trichrome (for collagen); Oil Red O (for lipid in frozen sections)
Gross: Intimal plaques - early (fatty streaks) → fibrous plaques → complicated plaques (calcification, ulceration, thrombosis).
Microscopy - What to say:
  • Fibrous cap: Dense collagen, smooth muscle cells, and scattered foam cells
  • Atheromatous core (necrotic core): Amorphous, acellular debris; cholesterol clefts (needle-shaped spaces left after fat dissolves); extracellular lipid
  • Foam cells: Lipid-laden macrophages with pale, foamy cytoplasm (also smooth muscle cells can form foam cells)
  • Calcification in older plaques (basophilic deposits)
  • Intimal thickening - smooth muscle cell proliferation
  • Vasa vasorum proliferation in adventitia
  • Neovascularization in plaque (intraplaque hemorrhage risk)
  • Disrupted/lost internal elastic lamina (visible on elastic stains)

16. Renal Cell Carcinoma (RCC)

Stain: H&E
Gross: Upper pole mass; yellow (lipid-rich), variegated (hemorrhage, necrosis); pseudocapsule.
Microscopy - What to say (Clear Cell RCC - most common ~75%):
  • Large polygonal cells with abundant clear cytoplasm (glycogen and lipid dissolved in processing)
  • Small, round, centrally placed nucleus
  • Arranged in solid nests, tubules, and acinar patterns
  • Prominent thin-walled sinusoidal vasculature between nests (delicate chicken-wire vascularity)
  • Nuclei may be bland (low-grade) to pleomorphic (high-grade)
  • Hemorrhage and necrosis common
Key associations: 3p deletion, VHL gene mutation (sporadic); VHL syndrome (familial)
Triad: Flank pain + hematuria + palpable mass (late presentation)

17. Benign Prostatic Hyperplasia (BPH)

Stain: H&E
Gross: Enlarged, nodular prostate; encucleated with rubbery nodules; predominant in transition zone.
Microscopy - What to say:
  • Nodular hyperplasia of both glandular and stromal elements
  • Large, irregular glands with papillary infoldings and intraluminal bridging; lined by two cell layers: inner tall columnar secretory cells + outer basal cells
  • Corpora amylacea (amyloid bodies): round, laminated, pink concentric structures within gland lumina - concentric calcified secretions
  • Stromal nodules: proliferating smooth muscle and fibrous tissue
  • No nuclear atypia, no infiltrative growth (benign)
  • May show foci of squamous metaplasia
Mechanism: DHT-mediated (5-alpha reductase converts testosterone to DHT); estrogen increases DHT receptors

18. Leiomyoma (Fibroid)

Stain: H&E; Masson's trichrome (collagen = blue)
Gross: Well-circumscribed, firm, whorled white nodule(s) in uterus; multiple common.
Microscopy - What to say:
  • Interlacing bundles of smooth muscle cells in various directions (whorled pattern)
  • Cells are elongated/fusiform with abundant eosinophilic (pink) cytoplasm
  • Cigar-shaped (blunt-ended) nuclei - no atypia, no mitoses (or rare)
  • Well-demarcated from surrounding myometrium (compressed rim of uterine muscle at periphery)
  • Variable amount of fibrous stroma between muscle bundles
  • Degenerative changes: hyaline degeneration (most common), myxoid, cystic, red/carneous (hemorrhagic infarction in pregnancy), calcification
Estrogen-dependent - grows in reproductive age, regresses after menopause

19. Hydatidiform Mole

Stain: H&E
Gross (Complete mole): Bunch-of-grapes appearance; no fetal parts.
Microscopy - What to say:
Complete Mole:
  • Hydropic (edematous) chorionic villi - large, swollen, fluid-filled villi with central cisterns (acellular spaces)
  • Trophoblastic proliferation (both cytotrophoblast and syncytiotrophoblast) circumferential/diffuse around all villi
  • Absence of blood vessels in villi
  • No fetal/embryonic tissue
Partial Mole:
  • Two populations of villi: some normal, some hydropic (smaller than complete mole)
  • Scalloped/irregular outline of villi ("fjord-like" invaginations of trophoblast)
  • Focal trophoblastic hyperplasia
  • Fetal tissue/RBCs present
Key risk: Complete mole has 2-3% risk of choriocarcinoma. Monitor beta-hCG.

20. Fibroadenoma

Stain: H&E
Gross: Well-encapsulated, rubbery, mobile ("breast mouse"), white/grey tumor.
Microscopy - What to say:
  • Both epithelial and stromal components (benign biphasic tumor)
  • Ducts (epithelial component): Round or compressed slit-like ductal structures lined by two layers (inner epithelial + outer myoepithelial)
  • Fibrous stroma: Hypercellular, myxoid fibrous tissue surrounding the ducts
  • Two architectural patterns:
    • Intracanalicular: Stroma compresses ducts into elongated slits (leaf-like pattern)
    • Pericanalicular: Stroma surrounds open round ducts concentrically
  • No atypia, rare mitoses, encapsulated
Most common breast tumor in young women (<30 years)

21. Multinodular Goitre (MNG)

Stain: H&E
Gross: Markedly enlarged, asymmetric thyroid with multiple nodules; cut section shows colloid-filled nodules, areas of hemorrhage, fibrosis.
Microscopy - What to say:
  • Variably-sized follicles - some markedly distended with colloid, others small and hyperplastic
  • Flattened follicular epithelium in large colloid-filled follicles
  • Foci of follicular hyperplasia: tall columnar epithelium with papillary infoldings
  • Degenerative changes: Hemorrhage (hemosiderin-laden macrophages), fibrosis, calcification, cystic change
  • No significant nuclear atypia (no Orphan Annie nuclei)
  • Colloid appears as homogeneous eosinophilic material; "scalloping" at periphery in active follicles
Iodine deficiency is the most common worldwide cause.

22. Papillary Thyroid Carcinoma (PTC)

Stain: H&E
Gross: Irregular, firm, whitish mass; calcified foci; often multifocal.
Microscopy - What to say:
  • Papillary architecture: Finger-like projections with fibrovascular stalks lined by neoplastic epithelium
  • Nuclear features (most important for diagnosis - even without papillae):
    • "Orphan Annie eye" nuclei: Large, oval, optically clear ("empty-looking") nuclei with pale/powdery chromatin
    • Nuclear grooves: Linear longitudinal infoldings of nuclear membrane
    • Nuclear pseudoinclusions: Cytoplasmic invaginations appearing as pink intranuclear inclusions
  • Psammoma bodies: Concentric calcified laminated structures (50%) - virtually pathognomonic of PTC
  • Follicular variant: follicular architecture but same nuclear features
  • Lymph node metastasis common (lymphotropic)
BRAF V600E mutation in ~60% of cases. Best prognosis among thyroid malignancies.

23. Liver Cirrhosis

Stain: H&E; Masson's trichrome (collagen = blue, best for fibrosis); Reticulin stain
Gross: Small, shrunken, nodular liver with firm fibrotic texture.
Microscopy - What to say:
  • Regenerative nodules: Rounded clusters of hepatocytes separated by fibrous bands; hepatocytes in regenerative nodules show disturbed architecture (thickened plates, pseudoacini)
  • Fibrous septa (bands): Broad bands of fibrous tissue linking portal tracts to central veins ("bridging fibrosis") and portal tract to portal tract
  • Loss of normal lobular architecture
  • Bile duct proliferation at periphery of nodules (ductular reaction)
  • Mixed inflammatory infiltrate in septa
  • Features of underlying etiology may be present: Mallory-Denk bodies (alcohol), steatosis (NASH), bile stasis (PBC)
On Masson's trichrome: Fibrous septa stain bright blue, regenerative nodules appear red/brown.

24. Seminoma Testis

Stain: H&E; PLAP and OCT4 positive on IHC
Gross: Homogeneous, creamy white, lobulated tumor filling the testis.
Microscopy - What to say:
  • Large, uniform polygonal cells arranged in sheets, nests, or lobules divided by delicate fibrovascular septa
  • Cells have: large, centrally placed nuclei with prominent nucleoli; clear cytoplasm (rich in glycogen - PAS positive)
  • Fibrous septa containing lymphocytic infiltrate (T-lymphocytes) - this is characteristic and helps distinguish from embryonal carcinoma
  • Granulomatous reaction (epithelioid granulomas, giant cells) in ~50% of cases
  • No embryoid bodies (unlike embryonal carcinoma)
  • Well-defined cell borders
Tumor marker: Beta-hCG mildly elevated in ~15% (syncytiotrophoblasts); AFP is NOT elevated (elevation suggests non-seminomatous element).
Most common testicular tumor in 30-40 year olds. Exquisitely radiosensitive.

25. Basal Cell Carcinoma (BCC)

Stain: H&E
Gross: Pearly, rolled edges with central ulceration ("rodent ulcer"); sun-exposed skin, especially face/nose.
Microscopy - What to say:
  • Nests and cords of basaloid cells arising from the basal layer of the epidermis
  • Cells: small, scant cytoplasm, oval dark-staining nuclei, no prominent nucleoli, high N:C ratio
  • Peripheral palisading: Cells at the periphery of nests arranged in a neat row with nuclei parallel (like a picket fence)
  • Retraction artifact: Cleft (shrinkage artifact) between tumor nests and surrounding stroma - highly characteristic
  • Desmoplastic stroma (mucinous/myxoid stroma in nests)
  • Mitotic figures present but usually not atypical
  • Connection to overlying epidermis
Most common skin cancer in humans. Local invasion but rarely metastasizes ("basal-cell never goes to lymph nodes" is a teaching point).

26. Chronic Cholecystitis

Stain: H&E
Gross: Thick-walled gallbladder; stones often present; mucosal surface may show green bile staining.
Microscopy - What to say:
  • Rokitansky-Aschoff sinuses: Mucosal herniation/outpouching deep into the muscular layer - pathognomonic
  • Chronic inflammatory infiltrate: Lymphocytes, plasma cells, occasional eosinophils in the lamina propria and submucosa
  • Fibrosis: Thickening of the muscularis and subserosa
  • Mucosal folds may be flattened or atrophic
  • Cholesterol polyps (xanthogranulomatous foci): foamy macrophages laden with lipid
  • Metaplasia: intestinal (goblet cells) or gastric (pyloric) metaplasia of mucosa
Key finding = Rokitansky-Aschoff sinuses + chronic inflammation + fibrosis

27. CVC Lung (Chronic Venous Congestion of Lung)

Stain: H&E; Prussian blue (for hemosiderin)
Gross: "Brown induration" - firm, brown lung due to hemosiderin + fibrosis.
Microscopy - What to say:
  • Hemosiderin-laden macrophages ("heart failure cells") within alveolar spaces - macrophages stuffed with brown granular hemosiderin pigment (from phagocytosed RBCs that leaked from engorged capillaries)
  • Dilated and congested alveolar capillaries and pulmonary veins
  • Interstitial fibrosis: Thickening of alveolar walls and interlobular septa
  • Alveolar spaces may contain pink transudate (edema) and desquamated macrophages
  • Hemosiderin also in interstitium
On Prussian Blue stain: Hemosiderin stains bright blue, confirming nature of pigment.
Cause: Left heart failure (mitral stenosis most classic cause)

28. Caseous Necrosis

Stain: H&E
Gross: Soft, cheesy, white-yellow material (resembles crumbled cheese).
Microscopy - What to say:
  • Amorphous, acellular, eosinophilic (pink) material - all cellular detail is completely lost (unlike coagulative necrosis where ghost outlines remain)
  • No nuclear remnants, no architectural outlines - completely structureless
  • The necrotic material has a "granular, cheesy" appearance at low power
  • Surrounded by epithelioid granuloma: epithelioid macrophages, Langhans giant cells, lymphocytes
  • Central caseous zone + peripheral granulomatous reaction = tuberculous granuloma
Pathognomonic for TB (also seen in other mycobacterial infections, histoplasmosis, sarcoidosis rarely)
Mechanism: Cell-mediated immunity (Type IV hypersensitivity) causes macrophage activation; partially effective killing leads to caseous rather than complete resolution.

29. Mucinous Cystadenoma

Stain: H&E; Mucicarmine/Alcian blue (confirms mucin)
Gross: Large multilocular cyst; ovary (most common); each locule contains thick, viscid mucus.
Microscopy - What to say:
  • Multilocular cysts lined by a single layer of tall columnar mucin-secreting epithelial cells
  • Cells resemble endocervical or intestinal-type epithelium; goblet cells often present
  • Nuclei basally placed, no significant atypia, rare mitoses (benign)
  • Abundant intracellular and intraluminal mucin (pale blue/grey on H&E; bright red on mucicarmine)
  • Thin fibrous stroma between locules
  • No papillary projections or solid areas (if present - borderline or malignant)
Risk: Rupture → pseudomyxoma peritonei (mucinous deposits throughout peritoneum)

30. Cavernous Hemangioma

Stain: H&E
Gross: Bluish-red, sponge-like lesion; common in liver; bleeds profusely when cut.
Microscopy - What to say:
  • Large, dilated, thin-walled vascular spaces (cavernous channels)
  • Channels lined by a single layer of flat (attenuated) endothelial cells - no proliferating or plump cells
  • Channels filled with RBCs or organizing thrombus (phleboliths - organized calcified thrombi)
  • Thin fibrous walls between channels
  • No smooth muscle layer (unlike normal veins)
  • Stroma may show hemosiderin deposits and fibrous scarring
  • Low-power appearance: "Swiss cheese" or sponge-like pattern with large blood-filled spaces
Distinguish from capillary hemangioma: Capillary = small vessels, plump endothelium, lobular; Cavernous = large dilated channels, flat endothelium.

31. Osteoclastoma (Giant Cell Tumor of Bone)

Stain: H&E
Gross: Eccentric, lytic lesion at the epiphysis of long bones; "soap-bubble" appearance on X-ray; may be red-brown and hemorrhagic ("brown tumor" appearance).
Microscopy - What to say:
  • Mononuclear stromal cells (key diagnostic cells): Oval to spindle-shaped cells with round/oval nuclei and moderate cytoplasm; scattered mitoses; nuclei resemble those in osteoclast-like giant cells
  • Multinucleated giant cells (osteoclast-like): Evenly distributed throughout the tumor; enormous cells with 20-100 uniformly distributed nuclei (important: nuclei identical to stromal cell nuclei - same morphology); prominent nucleoli; abundant eosinophilic cytoplasm
  • Hemosiderin deposits (brown pigment)
  • Areas of hemorrhage and necrosis
  • Reactive woven bone at periphery
  • No significant pleomorphism in giant cell nuclei
Location: Epiphysis of long bones (distal femur, proximal tibia, distal radius) in skeletally mature patients (20-40 years)
Behavior: Locally aggressive, 2-5% metastasize to lung despite benign histology.

HEMATOLOGY SLIDES


1. Microcytic Hypochromic Anemia

Stain: Leishman/Giemsa stain (peripheral blood smear)
What to say on PBS:
  • RBCs are smaller than normal (smaller than lymphocyte nucleus - microcytic)
  • Central pallor is enlarged (>1/3 of cell diameter - hypochromic; normally pallor = 1/3 diameter)
  • Cells may appear as "ring forms" with just a thin rim of hemoglobin
  • Anisocytosis: variation in size; Poikilocytosis: variation in shape
  • Target cells (codocytes): Bull's-eye appearance; seen in thalassemia, liver disease, hemoglobin C
  • Pencil/cigar cells: Elongated RBCs - classic for iron deficiency anemia
  • In thalassemia: nucleated RBCs, basophilic stippling, target cells prominent
Causes:
  1. Iron Deficiency Anemia (most common): Low serum iron, low ferritin, high TIBC; pencil cells, koilonychia clinically
  2. Thalassemia: Low/normal iron, low MCV, normal/high RBC count; target cells, basophilic stippling
  3. Sideroblastic anemia, Anemia of chronic disease (usually normocytic but can be microcytic)
Labs: MCV <80 fL; MCH <27 pg; MCHC <32 g/dL

2. Eosinophilia

Stain: Leishman stain
What to say on PBS:
  • Increased eosinophils (>0.5 × 10⁹/L or >5% of differential)
  • Eosinophils identified by: bilobed nucleus + large, coarse, bright orange-red (eosinophilic) granules that fill the cytoplasm
  • Granules are uniform in size; refractile appearance
  • May see toxic granulation or vacuolation in severe cases
Grading:
  • Mild: 0.5-1.5 × 10⁹/L
  • Moderate: 1.5-5 × 10⁹/L
  • Severe (Hypereosinophilia): >5 × 10⁹/L
Causes (NAACP mnemonic):
  • Neoplasms (lymphoma, leukemia, solid tumors)
  • Allergy/Atopy (asthma, eczema, hay fever) - most common in developed world
  • Addison's disease, autoimmune
  • Collagen vascular disease
  • Parasites (helminths - Ascaris, Toxocara, Filaria) - most common worldwide

3. Chronic Myeloid Leukemia (CML)

Stain: Leishman stain
What to say on PBS:
  • Leukocytosis: WBC markedly elevated (often 50,000-200,000/μL)
  • Left shift: Complete spectrum of myeloid maturation visible - myeloblasts, promyelocytes, myelocytes, metamyelocytes, bands, mature neutrophils ("myelocyte bulge" at myelocyte stage)
  • Basophilia - increased basophils (important clue; basophils have dark purple granules, bilobed/irregular nucleus)
  • Eosinophilia also seen
  • Thrombocytosis (platelets increased) in chronic phase
  • Low Leukocyte Alkaline Phosphatase (LAP) score - differentiates from leukemoid reaction (where LAP is high)
  • Myeloblasts <10% in chronic phase; >20% = blast crisis (transformation to AML/ALL)
Key genetic feature: Philadelphia chromosome - t(9;22) translocation → BCR-ABL fusion gene → constitutively active tyrosine kinase → uncontrolled proliferation
Treatment: Imatinib (Gleevec) - BCR-ABL tyrosine kinase inhibitor - transformed prognosis

4. Chronic Lymphoid (Lymphocytic) Leukemia (CLL)

Stain: Leishman stain
What to say on PBS:
  • Lymphocytosis: Marked increase in small, mature-appearing lymphocytes (WBC 20,000-200,000/μL)
  • Lymphocytes: small, scant cytoplasm, round, condensed (clumped) "soccer-ball" chromatin, no visible nucleoli
  • Smudge cells (basket cells): Crushed lymphocytes with smeared nuclear material - pathognomonic of CLL; occur because CLL cells are fragile
  • Occasional "prolymphocytes" (larger cells with prominent nucleolus)
  • Normal or reduced RBCs (anemia if advanced)
  • Thrombocytopenia may be present
Immunophenotype: CD5+ CD19+ CD23+ (co-expression of B-cell marker CD19 with T-cell marker CD5 is characteristic)
Most common leukemia in adults in Western countries. "Disease of the elderly." Indolent course. May develop autoimmune hemolytic anemia (Coombs positive).
Staging (Rai): 0 (lymphocytosis only) to IV (with anemia/thrombocytopenia)

Quick Revision Summary Table

#SlideKey Diagnostic Feature
1Fatty LiverClear cytoplasmic vacuoles displacing nucleus
2Monckeberg SclerosisMedial calcification, lumen preserved
3Acute AppendicitisTransmural neutrophilic infiltration
4Lobar Pneumonia4 stages; alveoli filled with fibrin/cells
5Granulation TissueNew capillaries + fibroblasts + inflammation
6TB Lymph NodeEpithelioid granuloma + Langhans cells + caseous necrosis
7ActinomycosisSulfur granules with clubs (Splendore-Hoeppli)
8RhinosporidiosisLarge sporangia with endospores
9LipomaMature adipocytes, encapsulated, no atypia
10Capillary HemangiomaLobular small vessels, plump endothelium
11SchwannomaAntoni A (Verocay bodies) + Antoni B
12SCCKeratin pearls + intercellular bridges
13Adenocarcinoma ColonMalignant glands + dirty necrosis
14Pleomorphic AdenomaEpithelial + chondromyxoid stroma
15AtherosclerosisIntimal plaque: fibrous cap + necrotic core + foam cells
16RCCClear cells + delicate vascularity
17BPHGlandular hyperplasia + corpora amylacea
18LeiomyomaInterlacing smooth muscle, cigar nuclei
19Hydatidiform MoleHydropic villi + trophoblastic proliferation
20FibroadenomaDucts in fibrous stroma; intracanalicular/pericanalicular
21MNGVariable follicle size, colloid, degenerative changes
22Papillary Thyroid CaOrphan Annie nuclei + psammoma bodies
23Liver CirrhosisRegenerative nodules + fibrous bands
24SeminomaSheets of clear cells + lymphocytic septa
25BCCBasaloid nests + peripheral palisading + retraction
26Chronic CholecystitisRokitansky-Aschoff sinuses + chronic inflammation
27CVC LungHeart failure cells (hemosiderin macrophages)
28Caseous NecrosisAcellular eosinophilic debris + granuloma
29Mucinous CystadenomaMultilocular cysts, mucin-secreting columnar cells
30Cavernous HemangiomaLarge dilated channels, flat endothelium
31OsteoclastomaUniform osteoclast-like giant cells + mononuclear stroma
H1Microcytic HypochromicSmall RBCs, enlarged pallor, pencil cells
H2EosinophiliaIncreased eosinophils with orange granules
H3CMLAll myeloid stages + basophilia + Philadelphia chr.
H4CLLMature lymphocytosis + smudge cells

Exam Tips:
  • Always describe what you see at low power first (overall architecture), then high power (cellular details)
  • Start every slide description with the stain used
  • For practical viva: state the diagnosis, then give 2-3 key histological features that confirm it
  • For carcinomas: mention grade (differentiation) and any invasion you see
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