Case and source map

What the supplied questions test

Every case and lecture question that belongs to this chapter, the concept it tests, and the place in the chapter where you practise it. Lecture coverage, case coverage and original practice are labelled separately.

Case map

Source page map

Which lecture pages feed each section. Page numbers are PDF pages of the supplied files.

Sources and notes

Sources

  • L7Lesson 7 Neoplasia.pdf (27 pages)
  • Ch. VII casesCases chap VII.pdf (10 pages)
  • Midterm sim.Cases for simulation of midterm examination on pathology.pdf (16 pages)Mixed midterm simulation, questions numbered as in the file.
  • SyllabusSyllabus 1 (1).pdf — Pathology course syllabus (2 pages)Defines the midterm scope (Chapters 1–7).
  • L1L1 Cell injury.pdf — Cell injury. Cell adaptation. Cell death (59 pages)
  • L3Lesson 3 Immunopathology.pdf (55 pages)
  • L4Lesson 4 Water, electrolyte, acid–base and hemodynamic disorders.pdf (50 pages)
  • L5Lesson 5 Genetic disorder.pdf — Genetic and developmental disorders (38 pages)
  • L6Lesson 6 Environmental pathology and nutritional disorders.pdf (47 pages)
  • Ref.Standard references used to verify mechanismsRobbins & Kumar Basic Pathology; Abbas Cellular and Molecular Immunology; Guyton & Hall Medical Physiology; standard toxicology texts.

Course PDFs are not served by this site. Page numbers refer to the supplied files so you can verify claims. Images labelled “Lecture image” are cropped from those files; “Teaching schematic” marks original drawings.

Source notes: where the sources differ or are ambiguous

  • Metabolism of cancer cells. Source: “Rely on anaerobic glycolysis for energy.” Taught here: The Warburg effect is aerobic glycolysis: tumor cells run glycolysis even when oxygen is available. That is why FDG-PET detects them, and it supplies carbon skeletons for growth rather than maximal ATP. L7 p.3
  • Telomerase. Source: “Upregulation of telomerase activity, which prevents normal apoptosis.” Taught here: Telomerase prevents telomere erosion, replicative senescence and chromosomal crisis, giving limitless replication. Evading apoptosis is a separate hallmark, achieved through BCL2 overexpression or loss of p53. L7 p.4
  • A benign tumor that invades. Source: “Do not invade; except for a dermatofibroma, (invades tissue but does not metastasize).” Taught here: Dermatofibroma has an infiltrative-looking edge because it entraps collagen. The standard example of a tumor that invades locally but almost never metastasizes is basal cell carcinoma, which is malignant. L7 p.4
  • Osteoblastic metastases on imaging. Source: “Serum alkaline phosphatase (ALP) is elevated to produce bone (high radiolucency).” Taught here: New bone absorbs X-rays, so blastic metastases are radiodense (sclerotic). Radiolucency belongs to lytic metastases. L7 p.11
  • UV pyrimidine dimers. Source: “…pyrimidine dimers in DNA, which are normally excised by restriction endonuclease.” Taught here: Pyrimidine dimers are removed by nucleotide excision repair, which is defective in xeroderma pigmentosum. Restriction endonucleases are bacterial enzymes with no role in human DNA repair. L7 p.17
  • TGF-β and familial stomach cancer. Source: Tumor-suppressor table: “TGF-β … Inherited mutation: familial stomach cancer.” Taught here: Hereditary diffuse gastric cancer is caused by germline CDH1 (E-cadherin) mutations. Germline SMAD4, in the TGF-β pathway, causes juvenile polyposis; somatic loss of TGF-β signaling is common in pancreatic and colorectal carcinoma. L7 p.20
  • BRCA and male breast cancer. Source: “BRCA1/BRCA2 … carcinoma of the male breast.” Taught here: Male breast cancer risk among carriers is conferred mainly by BRCA2; BRCA1 chiefly raises female breast and ovarian cancer risk. L7 p.20
  • Anemia of chronic disease. Source: “Anemia of chronic disease (ACD) … (deficiency of iron, folic acid).” Taught here: In anemia of chronic disease iron stores are adequate but sequestered by hepcidin: serum iron is low with a normal or raised ferritin. True iron deficiency in cancer usually means the tumor is bleeding. L7 p.24
  • Cachexia mediators. Source: Lists only proteolysis-inducing factor and lipolysis-mobilizing factor. Taught here: Cytokines are central: TNF (originally cachectin), IL-1 and IL-6 raise metabolic rate, drive proteolysis and lipolysis and suppress appetite, alongside the tumor factors named. L7 p.24
  • Calcitonin and hypocalcemia. Source: Paraneoplastic table: “Hypocalcemia … Medullary carcinoma of the thyroid … Calcitonin.” Taught here: Medullary thyroid carcinoma secretes large amounts of calcitonin, but clinically significant hypocalcemia is rare; calcitonin is used chiefly as a tumor marker and for family screening in MEN 2. L7 p.25
  • CEA-associated sites. Source: “CEA … cancers of lung, stomach, heart.” Taught here: CEA is raised in colorectal, pancreatic, gastric, lung and breast carcinoma. “Heart” appears to be a slip; there is no CEA-producing cardiac carcinoma. L7 p.26
  • Hamartoma as nonneoplastic. Source: “Hamartoma: nonneoplastic overgrowth of disorganized tissue…” Taught here: The developmental definition is kept for exams, but many hamartomas, pulmonary hamartoma among them, carry clonal chromosomal rearrangements and are now regarded as benign neoplasms. L7 p.7
  • Simulation Q6 wording. Source: “Which of the following adaptations to chronic injury best describes these changes…”, with options A, B, C, E. Taught here: Dysplasia is disordered growth and a precursor lesion, not an adaptation. The option list in the source file skips the letter D. Midterm sim. p.2

Brief in the sources, expanded here as supporting context

  • Desmoplasia, teratoma and hepatoma are not named on the slides; they are added in 7.1 because the course checklist asks for them.
  • VEGF, the Warburg effect by name, PD-L1/PD-1 and CTLA-4 are added in 7.2; the lecture mentions growth factors for vessels, anaerobic glycolysis with PET, and MHC class I downregulation.
  • Matrix metalloproteinases and integrins are named in 7.3; the lecture says “collagenase” and “attach to fibronectin”.
  • Sentinel lymph node and the Krukenberg tumor are added in 7.3 as standard extensions of the lecture's lymphatic and seeding routes.
  • Fine-needle aspiration and frozen section are added in 7.6; the lecture states only that biopsy or excision is required for certainty.
  • CD45, HMB-45 and TTF-1 are added to the lecture's immunohistochemistry panel, and β-hCG and calcitonin to its marker list, because questions use them.
  • HPV E6 and E7 targets are named in 7.5; the lecture lists high-risk HPV and its cancers without the mechanism.
  • Aflatoxin and TP53 codon 249, direct- versus indirect-acting carcinogens and P-450 activation expand the lecture's chemical table and its initiation diagram.
  • *Helicobacter pylori* is not in the lecture at all; 7.5 adds gastric adenocarcinoma and MALT lymphoma because the checklist asks for it.
  • TNF in cachexia, RANKL in lytic metastases and the vertebral venous plexus are added as mechanism; the lecture names PIF, LMF, PGE2 and IL-1.
  • Perineural invasion, medulloblastoma and the osteosarcoma of familial retinoblastoma come from the lecture and are kept brief.
  • Chapter 8 vascular tumors are out of scope; angiosarcoma appears only as the signature tumor of vinyl chloride.