Pathology — General Pathology, NMC MBBS licence examination syllabus (Nepal Medical Council).
Troponin in the blood is a dead cell's membrane failing. Every test result is a pathological process made visible.
Pathology sits between the basic sciences and the clinic. It explains why a blood test rises, why a lump is fixed rather than mobile, and why one course of illness resolves while another leaves scar.
This chapter covers the general mechanisms — cell injury, inflammation and neoplasia — that the clinical chapters use constantly without stopping to explain.
When a cell is deprived of oxygen, the first failures are energy-dependent: the pumps that maintain the internal environment stop working, so the cell swells. At this stage everything is recoverable — restore the oxygen and the cell returns to normal.
Past a certain point it is not. The cell membrane ruptures, the nucleus breaks down, and no intervention brings the cell back.
That transition is the entire justification for treating vascular emergencies urgently. Reperfusion in myocardial infarction or stroke does not revive dead tissue — it rescues the cells still on the reversible side of the line. Every minute moves more cells across it, which is what "time is muscle" and "time is brain" actually mean.And membrane failure is how we detect it. A cell with a ruptured membrane spills its contents into the blood. Troponin, transaminases, amylase and creatine kinase are all intracellular molecules that appear in serum only when cells have died — which is why they are used as markers of tissue damage, and why the rise takes time to appear.
Necrosis is uncontrolled cell death. The cell swells and bursts, and its contents — which the immune system has never been meant to encounter — spill into the tissue. The immune system reads that as damage, and inflammation follows. Necrosis is always pathological.
Apoptosis is programmed cell death. The cell dismantles itself in an orderly way, packages the fragments in membrane, and neighbouring cells clear them. Nothing leaks, so there is no inflammation.
Apoptosis is not a disease process — it is essential. It sculpts structures during embryological development, removes worn-out cells, and deletes cells whose DNA is damaged beyond repair.
Acute inflammation is the immediate response. Vessels dilate and become leaky, and neutrophils arrive first. The five classical features — redness, heat, swelling, pain and loss of function — are all direct consequences of that vascular change.
Chronic inflammation is what happens when the cause persists or the acute response fails to clear it. The cell population changes to lymphocytes, plasma cells and macrophages, and destruction, attempted repair and fibrosis proceed simultaneously.
The practical consequence for a clinician reading a report: the cell type dates the process. Neutrophils on a slide or in a fluid mean something recent. Lymphocytes and macrophages mean something established. That single fact often distinguishes an acute bacterial process from a chronic one without any further information.A granuloma is a particular pattern of chronic inflammation — macrophages organised into a ball, walling off material the body cannot digest or destroy. It is the characteristic response to tuberculosis, and to some fungi and foreign material. Finding granulomas therefore reframes the differential entirely, which is why the finding is reported specifically.
A neoplasm is new, autonomous tissue growth. The clinical question is always whether it is benign or malignant, and five features separate them.
But benign does not mean harmless, and this is a genuine exam trap. A benign tumour inside the skull kills by occupying space that cannot expand. A benign tumour secreting a hormone kills through its secretion. Benign describes cellular behaviour, not clinical consequence.
Knowing how a tumour spreads tells you where to look for its deposits — which is the practical use of this classification.
So a patient with a gastrointestinal primary has their liver imaged, and a patient with a sarcoma has their chest imaged. The anatomy of drainage predicts the search.
Metaplasia is adaptation, not cancer. When a tissue is chronically irritated it may change to a cell type better able to withstand the insult — respiratory epithelium becoming squamous in a smoker, oesophageal epithelium becoming intestinal in reflux. That change is reversible if the irritant is removed. But persistently irritated metaplastic tissue can progress to dysplasia, which is disordered growth and genuinely premalignant. Chronic irritation is therefore a cancer risk, and the sequence explains why.
Tumour markers are for monitoring, not diagnosis. They are frequently raised in benign disease and normal in some cancers, so a marker cannot confirm or exclude malignancy. Their value is in tracking a known tumour's response to treatment. No marker values are quoted in this chapter, because quoting one invites exactly the misuse this paragraph warns against.
No tumour marker values, staging criteria or laboratory ranges appear here: staging systems differ by site and are revised, and markers differ by assay. Use current local protocols.
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