Skip to this module

Exam 2 · Week 3 · BIO 280 Pathophysiology

M3 · Cell Injury & Cancer

How cells adapt before they die, the difference between the two kinds of cell death, and what makes a tumor malignant.

🧩 6 study cards⭐ exam spotlight📊 3 comparison tables🚨 1 never-do rule📱 Foldy-friendly
M3Cell Injury & CancerWeek 3
📚 Outline: Module 3 — Part 1 Cellular Injury · Part 2 Cancer
💡 The one idea

A cell under stress adapts first and dies second. Every adaptation on this page is reversible if the stress is removed — which is exactly why catching it early matters.

Adaptation is survival. Death is what happens when adaptation runs out.

🥚 The five adaptations
ChangeWhat happensExample
AtrophyCells shrink — less work, less blood, less stimulationA limb in a cast; muscle after bed rest
HypertrophyCells get bigger (not more numerous) Cardiac muscle in hypertension; skeletal muscle with training
HyperplasiaMore cells Endometrium under estrogen; BPH
MetaplasiaOne mature cell type replaced by another that tolerates the stress better Airway cells in a smoker; Barrett esophagus in reflux
DysplasiaDisordered growth — abnormal size, shape and organization Cervical dysplasia on a Pap. Pre-cancerous.

Dysplasia is the turning point. The first four are orderly responses. Dysplasia is the cell losing the plot, and it is the step before malignancy.

🚨 Hypoxia is the most common cause of cell injury

No oxygen → no ATP → the sodium–potassium pump stops. Sodium and water flood in, the cell swells, and lysosomes rupture.

Other causes: physical and chemical agents, infection, immune reactions, genetic defects, nutritional imbalance, and free radicals. Reperfusion injury is the cruel one — restoring blood flow floods damaged tissue with oxygen and free radicals and can do more harm than the ischemia did.

☠️ Necrosis vs apoptosis
NecrosisApoptosis
WhyInjury — unplanned Programmed — normal and controlled
CellSwells and burstsShrinks and is packaged up
ContentsSpill outStay contained, cleared by macrophages
InflammationYes — always No
ScaleGroups of cellsSingle cells

Types of necrosis worth knowing: coagulative (most solid organs after ischemia), liquefactive (brain, and abscesses), caseous (TB — cheese-like), fat (pancreatitis), gangrenous (limbs).

⭐ Benign vs malignant
BenignMalignant
GrowthSlowRapid, unpredictable
BorderEncapsulated, well definedInvasive, no capsule
CellsWell differentiated — look like the parent tissue Poorly differentiated (anaplastic)
MetastasisNeverYes — this is the defining feature
RecurrenceRare after removalCommon

Naming: -oma is usually benign (lipoma, adenoma). Carcinoma = epithelial origin. Sarcoma = connective tissue, bone, muscle. Leukemia / lymphoma = blood and lymph. Exceptions that are malignant despite the ending: melanoma, lymphoma, myeloma.

🧬 How cancer starts and how it spreads

Three steps: initiation (a mutation in the DNA), promotion (something makes the mutated cell divide), progression (it invades and metastasises).

  • Oncogenes — the accelerator stuck on.
  • Tumor suppressor genes (p53, BRCA) — the brakes, and they have failed.

Metastasis travels three ways: the bloodstream, the lymphatics, and direct seeding of a body cavity. The commonest destinations are lung, liver, bone and brain — they have the blood supply.

CAUTION — Change in bowel or bladder · A sore that does not heal · Unusual bleeding · Thickening or lump · Indigestion or trouble swallowing · Obvious change in a wart or mole · Nagging cough or hoarseness.

🎯 Module quiz

Questions for this module.

Nothing here yet — drop it in when you have it