General pathology · Cell injury, adaptation and death
Intracellular accumulations: cholesterol, proteins, hyaline, glycogen !
- Lesion
Cells can fill up with fat, protein, glycogen or other material when they make too much, cannot process it or cannot get rid of it.
Updated 2026-11-01
What it is
Accumulations reflect an imbalance between production and removal. A normal substance may be made faster than it is used (fatty change), an abnormal one may be unable to fold or be degraded (alpha-1 antitrypsin), an enzyme defect may block breakdown (storage diseases), or an indigestible external material may be retained (carbon). Some are harmless, some injure the cell.
Accumulations to recognise
| Material | Where and why | How it looks |
|---|---|---|
| Cholesterol (foam cells) | Macrophages and smooth muscle cells in atheromas take up oxidized LDL | Foamy cytoplasm; cholesterol clefts |
| Protein reabsorption droplets | Proximal tubule cells reabsorb filtered protein in heavy proteinuria | Pink droplets in the tubular epithelium |
| Russell bodies | Plasma cells full of immunoglobulin in the ER | Round eosinophilic inclusions |
| Mallory-Denk bodies | Damaged keratin intermediate filaments in injured hepatocytes | Ropy eosinophilic clumps |
| Alpha-1 antitrypsin globules | Misfolded Z protein retained in hepatocyte ER | PAS-positive, diastase-resistant globules |
| Hyaline arteriolosclerosis | Plasma proteins leak into arteriole walls (hypertension, diabetes); extracellular | Homogeneous pink thickening |
| Glycogen | Enzyme defects in storage diseases; hyperglycemia in tubules | Clear vacuoles; PAS-positive, diastase-sensitive |
| Complex lipids | Lysosomal enzyme defects (Gaucher, Niemann-Pick, Tay-Sachs) | Distended macrophages or neurons |
Clinical notes
- Familial hypercholesterolemia causes tendon xanthomas and premature atherosclerosis from LDL receptor defects.
- In von Gierke disease, glycogen fills hepatocytes and kidney cells, causing hepatomegaly and fasting hypoglycemia.
In the lab
- PAS stains glycogen, mucins and basement membranes; diastase digestion removes glycogen only.
- Oil Red O on frozen tissue shows neutral lipids; Congo red identifies amyloid, an extracellular deposit.
Test yourself
Think of the answer, then tap the question to see it.
What are Russell bodies?
Eosinophilic inclusions of immunoglobulin accumulated in the ER of plasma cells.
How is glycogen distinguished from other PAS-positive material?
Glycogen disappears after diastase digestion; alpha-1 antitrypsin globules and mucins remain.
What are Mallory-Denk bodies made of and where are they seen?
Aggregated keratin intermediate filaments in injured hepatocytes, typically in alcoholic or metabolic steatohepatitis.
Related
- Fatty change (steatosis)
- Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbon
- Endoplasmic reticulum stress and the unfolded protein response
- Pathologic calcification: dystrophic vs metastatic
- Special stains in diagnosis: Congo red, Prussian blue, PAS, Ziehl–Neelsen, Gram
Related conditions
- Atherosclerosis and dyslipidaemia
- Familial hypercholesterolemia
- Von Gierke disease (glycogen storage disease type I)
- Pompe disease (glycogen storage disease type II)
- Niemann–Pick disease
- Gaucher disease
- Tay–Sachs disease
- α1-antitrypsin deficiency
- Alcoholic liver disease (biochemistry)
- Multiple myeloma
- Nephrotic syndrome
- Hypertensive nephrosclerosis
- Diabetic kidney disease
Elsewhere in DurgiPedia
- Lysosomal storage diseases
- Glycogen metabolism
- LDL receptor
- Cholesterol
- α1-antitrypsin
- Microscopy and stains: H&E, PAS, trichrome, silver, immunohistochemistry
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Glycogen storage disease type I: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2024); Familial hypercholesterolemia: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024); Alpha-1 antitrypsin deficiency: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2024).
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Representative model, for educational purposes only.