Use pathological processes to guide investigation, management and prevention in O&G.

Pathology in Investigation, Management and Prevention in O&G

Start from the simplest idea this whole chapter rests on: every disease is a sequence of events in tissue, and that sequence can be interrupted. Something injures cells; the cells respond (and may die); the tissue around them responds (inflammation, then repair, scar or adaptation); and if the injury or its driver persists, the tissue may adapt abnormally and, in some sites, drift toward neoplasia. Each arrow in that chain is a place where a clinician can act. A test tries to prove which step the patient is at; treatment tries to interrupt or reverse a step; prevention tries to block the chain before tissue is injured at all.

That single pipeline is the spine of the chapter, so it is worth stating in plain terms before any tables appear:

Injurious agent → cell injury (reversible, then irreversible/death) → inflammation → repair (regeneration or scar) → adaptation (hyperplasia, hypertrophy, atrophy, metaplasia) → dysplasia → invasive neoplasia.

You will recognise this chain from essential basic pathological processes; here we put it to work clinically. Once you can place a patient's problem somewhere on that chain, the rest follows. A patient does not need "bloods" in the abstract; she needs evidence for or against a specific step — anaemia, infection, organ injury, coagulopathy, pregnancy tissue, thrombosis, neoplasia or inflammation. She does not need "treatment" in the abstract; she needs the injurious process reversed, the tissue consequence controlled, and the next avoidable injury prevented.

The central Primary question is therefore:

This chapter deliberately stops at the pathology logic. Applied clinical algorithms are developed in Intermediateacute pelvic pain, Intermediatecervical screening in South Africa, Finalantenatal care and screening and Finalmaternal mortality audit.

The Pathology Chain You Are Always Reasoning About

Before deciding which test to send, locate the patient on the disease chain. The same vocabulary recurs across every O&G problem, so it pays to hold it precisely.

Cell injury comes in two grades. Mild or brief injury — a fall in oxygen delivery, a transient toxin, early ischaemia — produces reversible cell injury: the cell swells, but if the insult is removed it recovers. Beyond a threshold the injury becomes irreversible and the cell dies. There are two distinct death pathways, and telling them apart explains much downstream behaviour:

• Necrosis is uncontrolled death of sheets of cells. Calcium floods in, membranes rupture, intracellular enzymes spill out, and the contents leak into the tissue — which is why necrosis always triggers inflammation and is always pathological. Clinically, necrotic tissue is a problem you must remove: it feeds infection and perpetuates inflammation (necrotising wound infection, infarcted fibroid, devitalised tissue in sepsis).
• Apoptosis is controlled, programmed death of single cells via defined enzyme cascades (caspases), with the dying cell neatly packaged and phagocytosed and no inflammatory spill. Apoptosis is essential to normal life — it sculpts the embryo, removes the corpus luteum, and trims the endometrium each cycle. It becomes pathological only when it is too much or too little.

That distinction matters because the leaked contents of necrotic cells (and the failure to clear them) are exactly what the next link — inflammation — is responding to.

Inflammation is the tissue's stereotyped response to injury, and it comes in two tempos.

• Acute inflammation is fast and neutrophil-led. Its five classical signs — redness, heat, swelling, pain and loss of function — all flow from two events: vasodilatation (more blood flow → redness, heat) and increased vascular permeability (fluid exudes → swelling, and mediators recruit neutrophils → pain, loss of function). Mediators include histamine, prostaglandins, leukotrienes, bradykinins, complement and cytokines such as the interleukin and tumour-necrosis-factor families. On a histology report, "acute inflammation" therefore means neutrophils, and points you toward a recent or ongoing insult — classically infection or necrosis (for example, neutrophils infiltrating the fetal membranes in chorioamnionitis).
• Chronic inflammation is slow, runs alongside attempted healing rather than after it, and is led by mononuclear cells — lymphocytes, plasma cells and macrophages — with fibroblast proliferation. It implies a persistent driver: a smouldering low-grade infection, an autoimmune process, a foreign body, or repeated irritation. A specialised form, granulomatous inflammation, is an organised collection of epithelioid macrophages walling off something the body cannot digest — the pattern of tuberculosis (highly relevant in South African practice), fungal disease, foreign material and sarcoidosis. (Note that granulomatous inflammation and granulation tissue are unrelated despite the similar names.)

Repair closes the loop after injury, by one of two routes. If the tissue can replace lost cells with cells of the same type, it regenerates to near-normal. If it cannot, the defect is filled by granulation tissue and then collagen — a scar. Wounds with apposed edges heal by first intention (a thin scar); gaping or infected wounds heal by secondary intention with more granulation tissue, wound contraction and a larger scar. Healing is degraded by poor blood supply, infection, foreign bodies, movement at the site, and systemic factors such as diabetes — which is why a caesarean or perineal wound in a patient who is anaemic, infected or diabetic is the one that dehisces. Over-exuberant scar (hypertrophic scar, keloid) is the opposite failure mode.

Adaptation is what tissue does when a demand or stimulus is sustained rather than acutely injurious — and it is the bridge from "normal response" to "early disease". Five adaptations recur constantly in O&G, and each is physiological in one setting and pathological in another: