Cervical cancer
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"cervical cancer"[MeSH Terms] AND ("screening" OR "treatment" OR "prevention")
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cervical cancer 2025 2026 guidelines screening treatment updates
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Cervical cancer in detail point wise manner
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"cervical cancer"[MeSH Terms] AND ("immunotherapy" OR "pembrolizumab" OR "bevacizumab")
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cervical cancer FIGO 2018 staging treatment guidelines 2025
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This is a fully detailed, point-wise breakdown of cervical cancer covering all major domains. Here is a quick navigation summary:
| Section | Key Highlights |
|---|---|
| Epidemiology | 3rd most common gynecologic cancer; >99% HPV-associated; median age 48 |
| Etiology & Risk | HPV 16/18 = 70% of cases; smoking, HIV, OCP use, multiparity |
| Pathobiology | E6 degrades p53; E7 degrades pRB; persistent infection required for malignancy |
| Precursor Lesions | CIN I/II/III (LSIL/HSIL); HSIL 30% regress, 10% → invasive carcinoma |
| Histology | SCC 80%, adenocarcinoma 15%, neuroendocrine <5% |
| Spread | Local → vagina/parametria/bladder; lymphatic → pelvic/para-aortic nodes |
| Symptoms | Postcoital bleeding, discharge, pelvic pain (early stages often silent) |
| FIGO 2018 Staging | IA1 → IVB; now includes lymph node metastasis in Stage IIIC |
| Treatment | Early: radical hysterectomy (open); advanced: cisplatin + EBRT + brachytherapy; metastatic: chemo + bevacizumab ± pembrolizumab |
| 5-yr Survival | Stage I ~90%, Stage IV <20% |
| Screening (2025-26) | Self-collected hrHPV now endorsed; primary HPV testing q5 years preferred for ages 30-65 |
| Prevention | 9-valent HPV vaccine (ages 9-26); WHO 90-70-90 elimination strategy |
Generate an quiz for me MCQ based for my neet Pg exam
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cd /home/daytona/workspace/attachments/c05626e9-b22a-43f0-a12f-f49c236744b6/ && python3 -c " import pdfplumber with pdfplumber.open('cell injury part 1.pdf') as pdf: print(f'Total pages: {len(pdf.pages)}') for i, page in enumerate(pdf.pages[:5]): print(f'\n--- PAGE {i+1} ---') print(page.extract_text()) "
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cd /home/daytona/workspace/attachments/c05626e9-b22a-43f0-a12f-f49c236744b6/ && python3 -c " from pypdf import PdfReader reader = PdfReader('cell injury part 1.pdf') print(f'Pages: {len(reader.pages)}') for i, page in enumerate(reader.pages): text = page.extract_text() print(f'--- PAGE {i+1} --- chars: {len(text) if text else 0}') if text: print(text[:500]) "
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cd /home/daytona/workspace/attachments/c05626e9-b22a-43f0-a12f-f49c236744b6/ && python3 -c " import subprocess result = subprocess.run(['pdftoppm', '-r', '200', 'cell injury part 1.pdf', '/tmp/cell_injury_page'], capture_output=True, text=True) print('stdout:', result.stdout) print('stderr:', result.stderr) print('returncode:', result.returncode) import os files = [f for f in os.listdir('/tmp') if f.startswith('cell_injury_page')] print('files:', sorted(files)) "
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python3 -c " import pytesseract from PIL import Image import os all_text = '' for i in range(1, 6): img_path = f'/tmp/cell_injury_page-{i}.ppm' img = Image.open(img_path) text = pytesseract.image_to_string(img, lang='eng') all_text += f'\n\n=== PAGE {i} ===\n' + text print(f'Page {i}: {len(text)} chars extracted') with open('/tmp/cell_injury_ocr.txt', 'w') as f: f.write(all_text) print('Done. Total chars:', len(all_text)) "
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I now have all the content needed from both the uploaded PDF and Robbins Pathology. Here is your comprehensive NEET PG MCQ quiz:
🧬 NEET PG MCQ Quiz — Cell Injury (Part 1)
Based on your uploaded notes + Robbins Pathology
SECTION A: BASICS OF CELL INJURY
Q1. The most common cause of cell injury is:
- A) Radiation
- B) Chemical toxins
- C) Hypoxia ✅
- D) Immunologic injury
Explanation: Hypoxia (oxygen deficiency) is the most common and clinically important cause of cell injury. It impairs oxidative phosphorylation, leading to ATP depletion.
Q2. The most common cause of hypoxia is:
- A) Anemia
- B) Carbon monoxide poisoning
- C) Respiratory failure
- D) Ischemia ✅
Explanation: Ischemia (interrupted blood supply) is the most common cause of hypoxia. It not only reduces oxygen delivery but also stops removal of metabolic waste products, making it more damaging than hypoxia alone.
Q3. The most sensitive cell to hypoxia is:
- A) Fibroblast
- B) Hepatocyte
- C) Neuron (Brain cells) ✅
- D) Cardiomyocyte
Explanation: Neurons are the most sensitive to hypoxia - they begin to die within 3-5 minutes of ischemia. They have high metabolic demands and cannot undergo anaerobic glycolysis effectively.
Q4. The most resistant cell to hypoxia is:
- A) Neuron
- B) Cardiomyocyte
- C) Renal tubular cell
- D) Fibroblast ✅
Explanation: Fibroblasts are the most resistant cells to hypoxia. They have low metabolic demands and can survive prolonged oxygen deprivation.
Q5. The correct sequence of events following cell injury adaptation failure is:
- A) Irreversible injury → Reversible injury → Cell death
- B) Reversible injury → Cell death → Irreversible injury
- C) Adaptation fails → Reversible injury → Irreversible injury → Cell death ✅
- D) Adaptation fails → Cell death → Reversible injury
Explanation: The progression is: Normal cell → Stress/Injury → Adaptation (if adequate) → OR if adaptation fails → Reversible injury → (if injury continues) → Irreversible injury → Cell death.
SECTION B: REVERSIBLE CELL INJURY
Q6. The FIRST change that occurs in cell injury at the cellular level is:
- A) Nuclear pyknosis
- B) Plasma membrane rupture
- C) Formation of myelin figures
- D) Mitochondrial dysfunction with decreased ATP production ✅
Explanation: The very first change is mitochondrial dysfunction leading to decreased ATP production. This initiates a cascade including Na-K ATPase pump failure and cellular swelling.
Q7. The FIRST morphological (microscopic) change seen in cell injury is:
- A) Nuclear fragmentation
- B) Myelin figure formation
- C) Cellular swelling / Hydropic change ✅
- D) Fatty change
Explanation: Cellular swelling (hydropic change) is the first morphological change visible on microscopy. It results from Na-K ATPase pump failure causing Na⁺ and water influx.
Q8. Failure of the Na-K ATPase pump in cell injury leads to all of the following EXCEPT:
- A) Cellular swelling
- B) Water influx into the cell
- C) ER swelling
- D) Increased protein synthesis ✅
Explanation: Na-K ATPase failure causes: Na⁺ influx → water influx → cellular swelling, ER swelling, flattening of microvilli, and cytoplasmic bleb formation. Protein synthesis is actually DECREASED (due to ribosome detachment from ER).
Q9. Which of the following is NOT a feature of reversible cell injury?
- A) Cellular swelling
- B) ER swelling
- C) Cytoplasmic bleb formation
- D) Plasma membrane rupture ✅
Explanation: Plasma membrane rupture is a feature of IRREVERSIBLE cell injury. In reversible injury the membrane is intact (though blebs form). Key features of reversible injury: cellular swelling, ER dilation, microvilli loss, bleb formation, myelin figures, fatty change.
Q10. Ribosome detachment from the ER in cell injury leads to:
- A) Increased mitochondrial activity
- B) Nuclear fragmentation
- C) Decreased protein synthesis → Fatty change ✅
- D) Increased glycolysis
Explanation: Ribosome detachment (during ATP depletion) causes decreased protein synthesis. Decreased apoprotein synthesis impairs fat export from hepatocytes → fatty change (steatosis).
Q11. Myelin figures (Concentric Lamellation) in cell injury:
- A) Are seen only in irreversible injury
- B) Are composed mainly of proteins
- C) Are derived from the nucleus
- D) Are seen in both reversible and irreversible injury, more in irreversible ✅
Explanation: Myelin figures are derived from cell membranes and are composed primarily of phospholipids (+ Ca²⁺). They are seen in both reversible and irreversible injury but are more prominent in irreversible injury.
Q12. The composition of myelin figures is:
- A) Proteins and cholesterol
- B) Nucleic acids and lipids
- C) Phospholipids (primarily) and Ca²⁺ ✅
- D) Glycoproteins
Explanation: Myelin figures (concentric lamellation) are derived from damaged cell membranes and are composed primarily of phospholipids with some calcium.
SECTION C: IRREVERSIBLE CELL INJURY
Q13. The two defining/point-of-no-return features of irreversible cell injury are:
- A) Cellular swelling and nuclear pyknosis
- B) Fatty change and myelin figures
- C) Severe mitochondrial damage + Massive Ca²⁺ influx into the cell ✅
- D) Ribosome detachment and ER dilation
Explanation: The two hallmarks of irreversible cell injury are: (1) Severe mitochondrial vacuolization/damage (loss of oxidative phosphorylation) and (2) Massive Ca²⁺ influx, which activates destructive enzymes.
Q14. Massive influx of Ca²⁺ in irreversible cell injury activates which set of enzymes?
- A) Kinases, Ligases, Isomerases
- B) Oxidases, Reductases, Transferases
- C) Phospholipase, Protease, Nuclease ✅
- D) ATPases, Lipases, Synthases
Explanation: Ca²⁺ activates three key destructive enzymes:
- Phospholipase → membrane damage
- Protease → cytoskeletal/structural protein breakdown
- Nuclease → DNA fragmentation
Q15. Nuclear changes in cell injury occur in the following order:
- A) Karyorrhexis → Pyknosis → Karyolysis
- B) Karyolysis → Karyorrhexis → Pyknosis
- C) Pyknosis → Karyorrhexis → Karyolysis ✅
- D) Karyolysis → Pyknosis → Karyorrhexis
Explanation:
- Pyknosis: nuclear shrinkage + chromatin condensation (dark, small nucleus)
- Karyorrhexis: nuclear fragmentation
- Karyolysis: nuclear dissolution (fading/disappearance of nucleus)
Q16. Pyknosis in irreversible cell injury refers to:
- A) Nuclear fragmentation
- B) Nuclear dissolution
- C) Nuclear enlargement with pale staining
- D) Nuclear shrinkage with chromatin condensation (small, dark nucleus) ✅
Explanation: Pyknosis = the nucleus becomes small and dark due to chromatin condensation. It is the first nuclear change in cell death.
Q17. Karyorrhexis refers to:
- A) Chromatin condensation
- B) Nuclear dissolution/fading
- C) Nuclear fragmentation ✅
- D) Nuclear swelling
Explanation: Karyorrhexis means nuclear fragmentation - the condensed nucleus breaks apart into fragments.
Q18. During anaerobic glycolysis in cell injury, the intracellular pH:
- A) Increases (becomes alkaline)
- B) Remains unchanged
- C) Decreases (becomes acidic) ✅
- D) Fluctuates randomly
Explanation: Anaerobic glycolysis produces lactic acid → H⁺ accumulation → acidic pH. This acidic pH causes nuclear chromatin to clump.
SECTION D: NECROSIS
Q19. Necrosis is defined as:
- A) Programmed physiological cell death without inflammation
- B) Cell death due to radiation only
- C) Pathological cell death associated with inflammation ✅
- D) Cell death mediated by caspase activation
Explanation: Necrosis = pathological cell death with inflammation. Cellular membranes are destroyed, enzymes leak out, and local inflammation is triggered to clear the debris. This distinguishes it from apoptosis.
Q20. On microscopy, a necrotic cell appears:
- A) Basophilic (blue)
- B) Pale/clear
- C) Eosinophilic (pink) ✅
- D) Deeply basophilic
Explanation: Necrotic cells appear eosinophilic (pink) on H&E staining due to: (1) decreased cytoplasmic RNA (RNA stains blue), and (2) denatured cytoplasmic proteins (which bind eosin/pink stain more).
Q21. The MOST COMMON type of necrosis overall is:
- A) Caseous necrosis
- B) Liquefactive necrosis
- C) Fat necrosis
- D) Coagulative necrosis ✅
Explanation: Coagulative necrosis is the most commonly occurring type of necrosis. It occurs in solid organs (heart, kidney, liver) following ischemia/infarction.
Q22. The mechanism of coagulative necrosis is:
- A) Enzymatic liquefaction of tissue
- B) Caseation with loss of architecture
- C) Protein denaturation with preservation of tissue architecture ✅
- D) Saponification of fat
Explanation: Coagulative necrosis = denaturation of proteins (structural + enzymatic). The key feature is that the tissue architecture (cell outlines/"tombstones") is PRESERVED even after cell death - the "ghost" cells remain.
Q23. "Tombstone appearance" in coagulative necrosis refers to:
- A) Nuclear fragmentation pattern
- B) Loss of all cellular detail
- C) Preservation of cell outlines without nuclear detail (ghost cells) ✅
- D) Chalky white deposits in tissue
Explanation: In coagulative necrosis, dead cells retain their outlines ("ghost cells" or "tombstone appearance") because proteins are denatured but cell shapes are maintained. This is also seen in Proteus vulgaris infection.
Q24. An infarct in a solid organ typically shows which shape?
- A) Round
- B) Irregular
- C) Rhomboid
- D) Wedge-shaped ✅
Explanation: Infarcts (coagulative necrosis) in solid organs appear wedge-shaped because the vessels supplying them are end-arteries arranged in a cone/fan shape with the apex pointing toward the occluded vessel.
Q25. Liquefactive necrosis most commonly occurs in:
- A) Heart
- B) Kidney
- C) Liver
- D) Brain / CNS ✅
Explanation: The brain undergoes liquefactive necrosis (also called colliquative necrosis) because brain tissue has abundant lipids and little structural protein. Enzymatic digestion dominates over protein denaturation, converting the tissue to liquid.
Q26. Caseous necrosis is characteristically associated with:
- A) Fat necrosis in pancreas
- B) Brain infarction
- C) Tuberculosis (and some fungi like Histoplasma, Coccidioides) ✅
- D) Malignant hypertension
Explanation: Caseous necrosis (cheese-like gross appearance, loss of all architecture microscopically) is the hallmark of tuberculosis. It also occurs in fungal infections like Histoplasmosis and Coccidioidomycosis.
Q27. Fat necrosis produces which characteristic appearance grossly?
- A) Red-brown hemorrhagic areas
- B) Yellow-white caseous material
- C) Chalky white deposits (Ca²⁺ saponification) ✅
- D) Clear fluid-filled cavities
Explanation: Fat necrosis (in pancreas/peripancreatic fat) involves lipase-mediated breakdown of triglycerides → free fatty acids + glycerol. Free fatty acids combine with Ca²⁺ → calcium soaps (saponification) → chalky white deposits.
Q28. Fibrinoid necrosis is characteristically seen in all of the following EXCEPT:
- A) Polyarteritis Nodosa (PAN)
- B) Rheumatic Heart Disease (Aschoff bodies)
- C) Malignant Hypertension
- D) Tuberculosis ✅
Explanation: Fibrinoid necrosis is seen in: PAN, Rheumatic Heart Disease (Aschoff bodies), SLE, Malignant Hypertension. Tuberculosis causes CASEOUS necrosis. Fibrinoid necrosis = immune complex deposition + fibrin deposition in vessel walls, giving a bright pink "fibrin-like" appearance.
Q29. Aschoff bodies are characteristically seen in:
- A) SLE
- B) Polyarteritis Nodosa
- C) Malignant Hypertension
- D) Rheumatic Heart Disease ✅
Explanation: Aschoff bodies are pathognomonic of Rheumatic Heart Disease (RHD). They are foci of fibrinoid necrosis surrounded by Anitschkow cells (caterpillar cells) and Aschoff giant cells.
Q30. Wet gangrene differs from dry gangrene in that it is:
- A) Coagulative necrosis with a line of demarcation
- B) Purely ischemic in origin
- C) Liquefactive necrosis + infection WITHOUT a line of demarcation ✅
- D) Associated with arterial occlusion only
Explanation:
- Dry gangrene = Coagulative necrosis (ischemia) WITH a clear line of demarcation; no infection
- Wet gangrene = Liquefactive necrosis + bacterial infection; NO line of demarcation; more dangerous (systemic spread)
QUICK REVISION TABLE
| Feature | Reversible Injury | Irreversible Injury |
|---|---|---|
| Mitochondria | Swelling (reversible) | Severe vacuolization |
| Plasma membrane | Blebs (intact) | Rupture |
| Nucleus | Normal | Pyknosis → Karyorrhexis → Karyolysis |
| Ca²⁺ influx | Mild | Massive |
| ATP | Decreased | Depleted |
| Myelin figures | Present | More prominent |
| Type of Necrosis | Organ/Disease | Key Feature |
|---|---|---|
| Coagulative | Heart, Kidney, Liver | Architecture preserved; tombstone cells |
| Liquefactive | Brain, Abscess | Enzyme-mediated; colliquative |
| Caseous | TB, fungi | No architecture; cheese-like |
| Fat | Pancreas | Chalky white; saponification |
| Fibrinoid | PAN, RHD, SLE, Malignant HTN | Vessel walls; pink fibrin deposits |
Score yourself:
- 28-30 correct: Excellent - NEET PG ready
- 23-27 correct: Good - revise weak areas
- 18-22 correct: Average - need focused revision
- <18 correct: Revise the full topic
Sources: Your uploaded notes (Cell Injury Part 1) + Robbins & Cotran Pathologic Basis of Disease
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