Tomorrow is my viva of pathology neuro + repro module
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Here is your complete viva preparation, pulled directly from Robbins & Kumar Basic Pathology:
PATHOLOGY VIVA PREP: NEURO + REPRODUCTIVE MODULE
Reference: Robbins & Kumar Basic Pathology
PART 1 - NEUROPATHOLOGY
1. Basic CNS Responses to Injury
Q: What are the basic morphologic changes seen in neuronal injury?
Within 12 hours of irreversible hypoxic-ischemic injury, neurons show:
- Shrinkage of cell body
- Pyknosis of nucleus
- Disappearance of nucleolus
- Loss of Nissl substance (rough ER staining)
- Intense eosinophilia of cytoplasm - these are called "red neurons"
Axonal injury causes: cell body enlargement + rounding, peripheral nucleus displacement, prominent nucleolus, peripheral dispersion of Nissl substance = central chromatolysis.
Q: What is gliosis? Who performs it?
Gliosis = the CNS equivalent of scar formation, performed by astrocytes. Injured astrocytes undergo hypertrophy + hyperplasia (gemistocytic astrocytes). Long-standing gliosis produces fibrillary astrocytes with Rosenthal fibers (thick, brightly eosinophilic protein aggregates in astrocytic processes).
Q: What are microglia?
Resident phagocytes of the CNS, derived from the embryonic yolk sac. When activated, they form microglial nodules (common in viral infections).
2. Edema, Herniation, Hydrocephalus
Q: Types of cerebral edema?
| Type | Mechanism | Cause |
|---|---|---|
| Vasogenic | Blood-brain barrier disruption → fluid shifts to extracellular space | Inflammation, tumors |
| Cytotoxic | Intracellular fluid increase due to cell injury | Hypoxia, ischemia, toxins |
In generalized edema: gyri are flattened, sulci narrowed, ventricles compressed.
Q: Define hydrocephalus. Types?
Increase in CSF volume within the ventricular system.
- Communicating hydrocephalus - impaired CSF resorption at arachnoid granulations; ventricular system communicates freely with subarachnoid space
- Noncommunicating (obstructive) - blockage within the ventricular system (e.g., tumor at foramen of Monro)
Q: Types of brain herniation?
- Subfalcine (cingulate) - cingulate gyrus under the falx cerebri
- Transtentorial (uncal) - medial temporal lobe (uncus) over the tentorial edge → compresses CN III (ipsilateral fixed dilated pupil) and cerebral peduncle
- Tonsillar - cerebellar tonsils into foramen magnum → compresses brainstem (fatal)
3. Cerebrovascular Disease
Q: Types of cerebral infarction - red vs. pale?
- Pale (ischemic/anemic) infarct - from thrombotic/embolic occlusion of end arteries in solid tissue
- Red (hemorrhagic) infarct - from reperfusion of infarcted tissue (emboli that lyse, or dual blood supply)
Q: Time sequence of cerebral infarction?
| Time | Changes |
|---|---|
| 12-24 hours | Red neurons, early neutrophil infiltration at edges |
| Day 3-5 | Macrophages (foam cells) appear |
| Day 10 | Reactive gliosis at margins |
| Weeks-months | Cystic cavity with surrounding gliosis |
Q: Causes of intracranial hemorrhage by location?
| Location | Cause |
|---|---|
| Epidural | Rupture of middle meningeal artery (temporal bone fracture) |
| Subdural | Tearing of bridging veins (trauma, elderly, alcoholics) |
| Subarachnoid | Ruptured berry aneurysm (worst headache of life) |
| Intraparenchymal | Hypertension (basal ganglia, thalamus, pons, cerebellum) |
Q: What is cerebral amyloid angiopathy?
Amyloid deposits in vessel walls → "lobar" hemorrhages in subcortical white matter. Associated with Alzheimer disease.
Q: Berry aneurysms - where and why?
Circle of Willis bifurcation points (anterior communicating artery most common). Rupture → subarachnoid hemorrhage with blood in CSF (xanthochromia), sudden onset "thunderclap" headache.
4. CNS Infections
Q: Routes of CNS infection?
- Hematogenous spread (most common)
- Direct implantation (trauma, surgery)
- Local extension (mastoiditis, sinusitis)
- Along peripheral nerves (rabies, HSV)
Q: What is brain abscess? Morphology?
Localized focus of necrotic brain tissue with inflammation.
- Center: liquefactive necrosis
- Surrounding: exuberant granulation tissue with neovascularization
- CSF: high WBC, high protein, normal glucose
- Complications: raised ICP, herniation, rupture → ventriculitis/meningitis
Q: Viral encephalitis - key viruses and features?
- HSV-1 encephalitis - temporal lobe involvement, Cowdry type A inclusions, hemorrhagic necrosis
- CMV - ependymal injury with intranuclear inclusions (owl-eye appearance)
- Rabies - Negri bodies (cytoplasmic inclusions) in hippocampal pyramidal cells and Purkinje cells
- PML (Progressive Multifocal Leukoencephalopathy) - JC virus → intranuclear viral inclusions in oligodendrocytes, demyelination in immunocompromised
Q: Cryptococcal meningitis?
Most common fungal meningitis; seen in immunocompromised. Organisms spread in perivascular spaces ("soap bubble" lesions). Capsule stains with India ink. Diagnosed by CSF cryptococcal antigen.
5. Demyelinating Diseases
Q: Multiple Sclerosis - key features?
- Most common demyelinating disease
- Autoimmune destruction of myelin by CD4+ T cells; oligodendrocytes and axons are relatively spared early
- Lesions = plaques (well-demarcated areas of demyelination)
- Location: periventricular white matter, corpus callosum, brainstem, cerebellar peduncles, optic nerves, spinal cord
- Microscopy: loss of myelin + relative axon preservation, reactive astrocytosis, perivascular lymphocytic infiltrates
- CSF: oligoclonal bands of IgG (hallmark)
- Clinical: relapsing-remitting course, Uhthoff phenomenon (worsening with heat)
6. Neurodegenerative Diseases
Q: Key protein inclusions in neurodegenerative diseases (must memorize table)?
| Disease | Protein/Inclusion | Clinical |
|---|---|---|
| Alzheimer disease | Aβ plaques + Tau (neurofibrillary tangles) | Dementia |
| Parkinson disease | α-synuclein (Lewy bodies) | Hypokinetic movement disorder |
| Huntington disease | Huntingtin (polyglutamine repeats) | Hyperkinetic movement disorder |
| ALS | SOD1, TDP-43 | UMN + LMN weakness |
| Prion disease (CJD) | PrPsc | Dementia + spongiform change |
| FTLD | Tau, TDP-43 | Behavioral changes, language |
Q: Alzheimer Disease - morphology?
- Gross: cortical atrophy (widened sulci, narrowed gyri), predominantly frontal/temporal/parietal
- Microscopy:
- Senile (neuritic) plaques = extracellular Aβ peptide cores with dystrophic neurites
- Neurofibrillary tangles = intracellular hyperphosphorylated tau in neurons
- Amyloid angiopathy in vessel walls
- Loss of neurons with gliosis
Q: Parkinson Disease - morphology?
- Loss of pigmented dopaminergic neurons in the substantia nigra (pale on gross)
- Lewy bodies = round, eosinophilic intracytoplasmic inclusions with pale halo; composed of α-synuclein + ubiquitin
- Clinical triad: resting tremor, rigidity, bradykinesia
Q: Prion disease - mechanism?
PrPc (normal, α-helix rich) → conformational change → PrPsc (abnormal, β-sheet rich, protease resistant). PrPsc induces normal PrPc to adopt abnormal conformation = self-amplifying. Histology: spongiform change (vacuolation of neuronal processes), no inflammatory response.
Q: Huntington Disease?
Autosomal dominant, CAG repeat expansion in huntingtin gene on chromosome 4. Progressive caudate atrophy → enlarged lateral ventricles (classically "box-like" on imaging). Chorea, dementia, psychiatric symptoms.
7. CNS Tumors
Q: Classification of CNS tumors?
Primary CNS tumors arise from glial cells, neurons, meninges, or embryonal cells. Most common primary malignant = glioblastoma. Most common overall intracranial tumor = metastases.
Q: Glioblastoma (GBM) - key features?
- WHO Grade IV astrocytoma
- Most common primary malignant brain tumor in adults
- Butterfly glioma - crosses corpus callosum
- Morphology: necrosis with pseudopalisading (nuclei arranged around areas of necrosis), glomeruloid microvascular proliferation
- IDH-wildtype (most common form)
- Prognosis: median survival ~15 months
Q: Meningioma - features?
- Arise from arachnoid cap cells
- Usually benign (WHO grade I), slow-growing
- Histology: psammoma bodies (concentric calcifications), whorled pattern of cells
- Most common benign intracranial tumor in adults
Q: Medulloblastoma?
- Most common malignant brain tumor in children
- Arises in cerebellum
- Highly cellular, small blue cells (primitive neuroectodermal)
- Spreads via CSF ("drop metastases" to spinal cord)
- Radiosensitive
Q: Primary CNS Lymphoma?
- Usually diffuse large B-cell lymphoma
- Strong association with EBV in immunocompromised (HIV)
- Periventricular location
- Responds to steroids and methotrexate
PART 2 - REPRODUCTIVE PATHOLOGY
8. Vulva
Q: Two types of vulvar squamous cell carcinoma - compare?
| Feature | HPV-related | Non-HPV |
|---|---|---|
| HPV type | High-risk HPV 16 | None |
| Precursor | VIN (vulvar intraepithelial neoplasia) | Lichen sclerosus / dVIN |
| Histology | Basaloid/warty, poorly differentiated | Keratinizing, well differentiated |
| Age | ~60 years | ~75 years |
Q: Paget disease of the vulva?
Intraepidermal proliferation of atypical epithelial cells (large cells with pale cytoplasm = Paget cells). Unlike Paget of the nipple (usually associated with underlying carcinoma), vulvar Paget may or may not have underlying adenocarcinoma. Stains positive with PAS and mucin.
9. Cervix
Q: Pathogenesis of cervical carcinoma?
HPV infection (especially types 16 and 18) → integration of HPV into host genome → E6 protein inactivates p53, E7 protein inactivates Rb → uncontrolled cell proliferation.
Progression: HPV infection → CIN 1 (LSIL) → CIN 2/3 (HSIL) → invasive carcinoma
Q: CIN grading?
| Grade | Full-thickness involvement | Equivalent |
|---|---|---|
| CIN 1 | Lower 1/3 of epithelium | LSIL |
| CIN 2 | Lower 2/3 | HSIL |
| CIN 3 (carcinoma in situ) | Full thickness | HSIL |
Koilocytic atypia (perinuclear halo + wrinkled nucleus) = cytopathic effect of HPV.
Q: Invasive cervical carcinoma types?
- ~80% squamous cell carcinoma
- ~15-20% adenocarcinoma (from endocervical glands)
- Spreads locally → pelvic wall → bladder/rectum → lymphatics
10. Uterus
Q: Endometritis - types?
- Acute - usually ascending infection post-delivery or instrumentation; neutrophils in endometrial glands/stroma
- Chronic - presence of plasma cells in endometrium (plasma cells are the diagnostic hallmark - normally absent from endometrium)
Q: Endometriosis - definition and morphology?
Presence of endometrial glands and stroma outside the uterus.
- Common sites: ovary (most common), posterior cul-de-sac, fallopian tube, peritoneum
- Chocolate cyst (endometrioma) = blood-filled cyst in ovary, dark brown old blood
- Powder burn lesions on peritoneum
- Symptoms: dysmenorrhea, dyspareunia, infertility
Q: Endometrial hyperplasia - types and risk?
| Type | Atypia | Risk of Carcinoma |
|---|---|---|
| Without atypia | No | Low (~2%) |
| With atypia | Yes | ~25-30% |
Cause: unopposed estrogen (obesity, polycystic ovary, estrogen-secreting tumors, hormone therapy without progesterone).
Q: Two types of endometrial carcinoma - compare?
| Feature | Endometrioid (Type I) | Serous (Type II) |
|---|---|---|
| Frequency | ~85% | ~15% |
| Risk factors | Unopposed estrogen, obesity | Not estrogen-related |
| Precursor | Atypical hyperplasia | Serous EIC (SEIC) |
| Mutation | PTEN, DNA mismatch repair | TP53 |
| Grade | Low (Grade 1-2) | High grade by definition |
| Prognosis | Good (90% 5-yr for early stage) | Poor |
| Immunohistochemistry | - | Diffuse strong p53 staining |
Q: Uterine leiomyoma ("fibroid") - key facts?
- Most common uterine tumor; most common tumor in women overall
- Benign smooth muscle tumor
- Estrogen-dependent (regresses after menopause)
- Morphology: well-circumscribed, firm, whorled grey-white cut surface
- Microscopically: interlacing bundles of smooth muscle cells with no mitoses / atypia
- May cause: menorrhagia, pelvic pressure, infertility, recurrent abortions
Q: Leiomyosarcoma vs Leiomyoma?
- Malignant smooth muscle tumor, de novo (does NOT arise from leiomyoma transformation)
- Criteria: >10 mitoses/10 HPF, coagulative necrosis, significant cytologic atypia
- Irregular borders (unlike leiomyoma's sharp borders)
11. Gestational Trophoblastic Disease
Q: Compare complete vs partial hydatidiform mole?
| Feature | Complete Mole | Partial Mole |
|---|---|---|
| Karyotype | 46,XX (or 46,XY) - purely paternal | Triploid (69,XXY) |
| Origin | 2 sperm + enucleated egg (dispermy) or 1 sperm + empty egg then duplication | 2 sperm + normal egg |
| Fetal tissue | Absent | May be present |
| Chorionic villi | All abnormal, hydropic | Some normal, some abnormal |
| hCG | Very high | Less elevated |
| Risk of choriocarcinoma | ~2-3% | <1% |
| Trophoblastic proliferation | Diffuse | Focal |
Q: Choriocarcinoma?
- Malignant trophoblastic tumor
- Composed of cytotrophoblasts + syncytiotrophoblasts; no chorionic villi (distinguishes from mole)
- Very high hCG
- Spreads hematogenously (lungs most common)
- Highly chemosensitive (excellent cure rate with methotrexate/actinomycin D)
- Can arise from: molar pregnancy, normal pregnancy, ectopic pregnancy, abortion
12. Ovary
Q: Classification of ovarian tumors?
| Type | Origin | Examples | Age |
|---|---|---|---|
| Surface epithelial | Coelomic epithelium | Serous, mucinous, endometrioid, clear cell | Adults |
| Germ cell | Oogonia | Teratoma, dysgerminoma, yolk sac tumor | Young women |
| Sex cord-stromal | Granulosa, theca, Sertoli, Leydig | Granulosa cell, thecoma, fibroma | Varies |
Q: Serous tumors of ovary?
| Benign (Cystadenoma) | Borderline | Malignant (Cystadenocarcinoma) |
|---|---|---|
| Single layer of tall columnar ciliated cells | Some atypia, no stromal invasion | Marked atypia + stromal invasion |
| Unilocular, thin wall | - | Often bilateral |
| Most common ovarian tumor | - | Most common ovarian malignancy |
| Psammoma bodies on microscopy | - | Psammoma bodies |
Q: Mucinous tumors - features?
- Multilocular cysts filled with gelatinous mucin
- Lined by tall columnar mucin-secreting cells (resembling endocervical or intestinal epithelium)
- Can be very large
- Pseudomyxoma peritonei = rupture → gelatinous mucin fills peritoneal cavity (most often from appendiceal mucinous tumors)
Q: Granulosa Cell Tumor?
- Low-grade malignancy; most common functional (hormone-secreting) ovarian tumor
- Produces estrogen → endometrial hyperplasia → abnormal uterine bleeding in adults; precocious puberty in children
- Morphology: Call-Exner bodies (small follicle-like spaces lined by granulosa cells with eosinophilic material)
- Coffee bean (grooved) nuclei
Q: Teratoma - types?
- Mature cystic teratoma (dermoid cyst) - most common germ cell tumor; contains hair, teeth, sebaceous gland, thyroid; benign in adults; complications: torsion, malignant transformation (SCC most common)
- Immature teratoma - malignant; contains primitive neuroectodermal tissue
- Struma ovarii - teratoma with predominantly thyroid tissue (can cause hyperthyroidism)
Q: Dysgerminoma?
- Most common malignant germ cell tumor
- Female equivalent of testicular seminoma
- Composed of large cells with clear glycogen-rich cytoplasm + lymphocytic infiltrate
- Radiosensitive and chemosensitive; excellent prognosis
- Elevated LDH and placental alkaline phosphatase
Q: Yolk Sac Tumor (Endodermal Sinus Tumor)?
- Aggressive germ cell tumor, mostly in children/young women
- Produces AFP (alpha-fetoprotein)
- Schiller-Duval bodies (glomeruloid structures resembling endodermal sinuses)
13. Breast
Q: Fibrocystic change - components?
Not a single entity; includes:
- Cyst formation + apocrine metaplasia
- Fibrosis
- Adenosis (increase in acini)
- Epithelial hyperplasia (ductal or lobular)
Risk of carcinoma depends on histologic subtype:
- No increased risk: cysts, fibrosis, mild hyperplasia
- Slightly increased (1.5-2x): moderate hyperplasia, sclerosing adenosis
- Moderately increased (4-5x): atypical ductal or lobular hyperplasia
Q: Fibroadenoma?
- Most common benign breast tumor in women < 35 years
- Estrogen-sensitive (enlarges in pregnancy, regresses after menopause)
- Morphology: well-circumscribed, rubbery, mobile "breast mouse"
- Microscopically: fibrous stroma + compressed elongated ducts (intracanalicular) or surrounding dilated ducts (pericanalicular)
Q: Classification of breast carcinoma?
| Type | Features |
|---|---|
| Ductal carcinoma in situ (DCIS) | Malignant cells within ducts, no basement membrane invasion; comedo type has central necrosis |
| Lobular carcinoma in situ (LCIS) | Malignant cells in lobules; marker of increased bilateral risk |
| Invasive ductal carcinoma (IDC) | Most common invasive type (~75%); hard, fibrous (scirrhous) mass |
| Invasive lobular carcinoma (ILC) | Single-file (Indian file) cells; often bilateral; loss of E-cadherin |
| Medullary carcinoma | Large cells, lymphocytic infiltrate, better prognosis |
| Colloid (mucinous) carcinoma | Mucin-secreting cells floating in mucin; older women; better prognosis |
| Paget disease of nipple | DCIS spreading up ducts to nipple skin; large Paget cells in epidermis; eczema-like rash of nipple |
Q: Molecular subtypes of breast cancer?
| Subtype | ER | PR | HER2 | Prognosis |
|---|---|---|---|---|
| Luminal A | + | + | - | Best |
| Luminal B | + | + | + | Intermediate |
| HER2-enriched | - | - | + | Poor (treatable with trastuzumab) |
| Triple-negative | - | - | - | Worst |
Q: Inflammatory breast carcinoma?
Dermal lymphatic invasion by tumor → lymphatic obstruction → peau d'orange (skin like orange peel), erythema, warmth; clinically mimics infection but is carcinoma. Very aggressive.
Q: Spread of breast carcinoma?
- Medial tumors → internal mammary nodes
- Lateral tumors (most common) → axillary lymph nodes (most important prognostic factor)
- Hematogenous → lungs, liver, bone (osteolytic), brain, adrenals
14. Testis and Prostate (Male Reproductive)
Q: Germ cell tumors of testis - classification?
| Tumor | Features | Marker |
|---|---|---|
| Seminoma | Most common; uniform cells with clear cytoplasm, lymphocytic infiltrate; radiosensitive | LDH, PLAP |
| Embryonal carcinoma | Aggressive; pleomorphic cells in glands/sheets | AFP + βhCG |
| Yolk sac tumor | Most common in infants; Schiller-Duval bodies | AFP |
| Choriocarcinoma | Cytotrophoblasts + syncytiotrophoblasts; hematogenous spread | βhCG |
| Teratoma | Mature (benign in children; malignant in adults) | - |
Q: Benign Prostatic Hyperplasia (BPH)?
- Hyperplasia of transitional zone of prostate (central/periurethral)
- Nodular hyperplasia of glands and stroma
- NOT a premalignant lesion
- Causes: obstructive urinary symptoms (hesitancy, weak stream, incomplete emptying), urinary retention, recurrent UTI
Q: Carcinoma of the Prostate?
- Most common cancer in men; arises in peripheral zone
- Graded by Gleason score (sum of two most predominant patterns, each graded 1-5)
- Gleason score ≥ 7 = clinically significant
- Marker: PSA (Prostate Specific Antigen)
- Extension: local → seminal vesicles, bladder neck; lymphatics → iliac nodes; osteoblastic bone metastases (sclerotic)
HIGH-YIELD VIVA ONE-LINERS
- Red neurons → acute ischemic injury (12-24 hrs)
- Central chromatolysis → axonal injury
- Gliosis = astrocyte response (like fibrosis elsewhere)
- Rosenthal fibers → chronic gliosis + low-grade gliomas
- Cytotoxic edema → cell injury; Vasogenic edema → BBB breach
- Subacute combined degeneration → B12 deficiency; posterior + lateral columns
- MS plaques → periventricular; CSF shows oligoclonal IgG bands
- Berry aneurysm → rupture → worst headache of life (subarachnoid hemorrhage)
- Hypertensive hemorrhage → basal ganglia, thalamus, pons
- GBM hallmark → pseudopalisading necrosis + glomeruloid vascular proliferation
- Medulloblastoma → most common malignant brain tumor in children; cerebellum
- Meningioma → psammoma bodies; benign; arises from arachnoid cap cells
- CNS lymphoma → EBV + HIV; periventricular; large B-cell lymphoma
- CIN → graded by height of epithelial involvement; koilocytes = HPV effect
- Endometrial carcinoma Type I (endometrioid) → PTEN mutation + unopposed estrogen
- Endometrial carcinoma Type II (serous) → TP53 mutation; diffuse p53 IHC staining
- Leiomyoma → whorled, rubbery, estrogen-dependent; most common tumor in women
- Complete mole → 46,XX; no fetus; all villi abnormal; high hCG
- Partial mole → triploid 69,XXY; fetal parts possible
- Choriocarcinoma → no chorionic villi; hematogenous spread; βhCG; chemosensitive
- Granulosa cell tumor → estrogen-secreting; Call-Exner bodies
- Dysgerminoma → LDH; radiosensitive; female seminoma
- Yolk sac tumor → AFP; Schiller-Duval bodies
- Dermoid cyst → most common germ cell tumor; contains ectodermal tissues
- IDC breast → most common; scirrhous (desmoplastic) reaction; axillary node spread
- ILC breast → Indian file cells; loss of E-cadherin; bilateral
- Triple-negative breast cancer → worst prognosis; no targeted therapy
- Paget disease of nipple → DCIS extending to skin; eczema-like rash
- Seminoma → most common testicular tumor; radiosensitive; PLAP + LDH
- Prostate carcinoma → peripheral zone; Gleason score; osteoblastic mets; PSA marker
- BPH → transitional zone; NOT premalignant
All content referenced from Robbins & Kumar Basic Pathology (ISBN 9780323790185). Good luck tomorrow - you've got this!
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