2804NRS · Human Pathophysiology And Pharmacology 1
Pathophysiology Foundations
Pathophysiology begins as a failure of homeostasis at the cell. A stressor pushes a cell past what it can cope with, and the body's responses — adaptation, injury, inflammation — produce the signs seen at the bedside. This foundation chapter walks that story end to end: how negative feedback normally holds variables steady, the five reversible cellular adaptations (atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia), the slide from reversible cell injury to necrosis vs apoptosis, the two-phase acute inflammation cascade with its five cardinal signs, the exudate types, and the chain of infection. In 2804NRS these are Modules 1–2 — assessed by the A1 quiz and then the scaffolding under everything that follows: inflammation explains hypersensitivity, cell injury explains cancer, infection explains immunodeficiency.
What this chapter covers
- 011.1 Homeostasis & negative feedback
- 021.2 Cellular adaptation — size, number, type (and dysplasia)
- 031.3 Cell injury & death: necrosis vs apoptosis
- 041.4 Acute inflammation — vascular & cellular phases, 5 cardinal signs
- 051.5 Exudate types — the fluid tells you the cause
- 061.6 Infection basics — the chain of infection
Worked cascade: appendicitis as RF → aetiology → pathophysiology → clinical
- +1Risk factors: low-fibre diet, age 10–30, family history — predispose to luminal obstruction.
- +1Aetiology (trigger): obstruction of the appendiceal lumen (faecolith or lymphoid hyperplasia).
- +1Pathophysiology: obstruction → mucus builds → ↑ intraluminal pressure → wall ischaemia + bacterial overgrowth → acute inflammation (vasodilation, ↑ permeability, neutrophil influx, purulent exudate).
- +1Clinical manifestations: central → right-iliac-fossa pain, fever, nausea, guarding, raised WBC/CRP — the cardinal signs plus systemic markers.
- +1Test + management: raised WBC/CRP with CT/USS confirms; appendicectomy + antibiotics treats.
Key terms
- Negative feedback
- The dominant homeostatic loop: a deviation from the set point is detected and corrected in the OPPOSITE direction, switching off the stimulus once the variable is restored. 'Negative' means stabilising, not bad.
- Hypertrophy vs hyperplasia
- Hypertrophy = increase in cell SIZE (more workload on cells that cannot divide, e.g. left ventricle in hypertension); hyperplasia = increase in cell NUMBER (a mitotic stimulus, e.g. endometrial hyperplasia).
- Necrosis
- Uncontrolled pathological cell death from irreversible injury: the cell swells and ruptures, spills its contents and TRIGGERS inflammation; it needs no ATP and usually kills groups of cells.
- Apoptosis
- Programmed, controlled cell death: the cell shrinks into membrane-bound bodies that are phagocytosed cleanly, so there is NO inflammation; it is ATP-dependent and usually affects single cells.
- Chain of infection
- The six links an infection needs to spread: agent → reservoir → portal of exit → transmission → portal of entry → susceptible host. Breaking any one link interrupts transmission.
Pathophysiology Foundations FAQ
What is the single big idea of this chapter?
Pathophysiology is a failure of homeostasis at the cell. A stressor exceeds what a cell can buffer; its adaptation, injury and inflammatory responses then produce the clinical signs. Every later module is this same story told about a different organ.
What is the difference between necrosis and apoptosis?
Four contrasts: necrosis needs no ATP, apoptosis is ATP-dependent; necrosis swells and lyses, apoptosis shrinks into apoptotic bodies; necrosis kills groups of cells, apoptosis kills single cells; necrosis triggers inflammation, apoptosis does not. The trap is assuming apoptosis is the 'bad' one — it is the normal, programmed one.
What are the five cardinal signs of acute inflammation?
Redness (rubor) and heat (calor) from vasodilation; swelling (tumor) from increased permeability and exudate; pain (dolor) from bradykinin and prostaglandins plus pressure; and loss of function as a consequence of pain and swelling.
Why learn Modules 1–2 if they are not on the final exam?
They are assessed by the A1 quiz, then they become scaffolding: acute inflammation underpins hypersensitivity (Module 3), cell injury and dysplasia open the door to carcinogenesis (Module 4), and the susceptible host underpins immunodeficiency. Learn them once, well.
Exam move
Drill the four high-yield contrasts — negative vs positive feedback, hypertrophy vs hyperplasia, metaplasia vs dysplasia, and necrosis vs apoptosis — because the A1 quiz is built straight from them. Then learn the acute-inflammation cascade as a fluent sequence (vascular changes → increased permeability → leukocyte recruitment → neutrophils first), since it reappears as the pathophysiology band in almost every later disease. Use the appendicitis cascade as your template for writing any condition in the unit.
