Cellular Pathology: Atrophy and Adaptation
Overview
Cells adapt to stress and injury through a spectrum of reversible morphological changes. These adaptations are positioned between normal physiology and irreversible injury, and understanding them is foundational to pathology and interpreting imaging findings of disease evolution.
Atrophy
Atrophy is a reduction in cell size from loss of structural proteins and organelles. The entire organ or tissue shrinks. Mechanisms vary by cause:
- Disuse atrophy: Reduced functional demand (e.g., immobilised limb muscles — CT shows reduced muscle bulk).
- Denervation atrophy: Loss of neural trophic support (e.g., MRI shows fatty infiltration of denervated muscles on T1W).
- Ischaemic atrophy: Chronic poor blood supply (e.g., small shrunken kidneys in renovascular disease).
- Endocrine/nutritional: Adrenal cortex atrophies with exogenous steroid use (suppression of ACTH).
- Pressure atrophy: Tumour pressing on adjacent tissue (e.g., renal cortex thinning over a cyst).
Molecular Mechanism of Atrophy
Cellular proteins are selectively degraded by the Ubiquitin-Proteasome pathway: target proteins are tagged with ubiquitin chains and fed into the barrel-shaped 26S proteasome for degradation. This is the principal mechanism of controlled protein catabolism in atrophy.
WarningLipofuscin: The 'Wear and Tear' Pigment
Lipofuscin is yellow-brown pigment accumulating in lysosomes of atrophic cells (especially hepatocytes, cardiac myocytes, neurons). It represents undigested oxidized lipid-protein complexes, and is a marker of cellular ageing and long-standing cellular stress.
High Yield Facts
LightbulbFRCR / MD Prep Pearl
Fatty replacement (atrophy + lipid infiltration) of muscles is visible on T1W MRI as areas of high signal replacing normally dark muscle fibres. This is irreversible and indicates chronic denervation or severe myopathy. Contrast with denervation oedema (T2/STIR hyperintensity in the acute-subacute phase), which may be reversible.