[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Cell injury, adaptation and death](https://durgical.com/en/general-pathology/#a-injury) › Intracellular accumulations: cholesterol, proteins, hyaline, glycogen

[General pathology](https://durgical.com/en/general-pathology/) · [Cell injury, adaptation and death](https://durgical.com/en/general-pathology/#a-injury)

# 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

## Key points

- Four routes: too much normal substance, abnormal protein, enzyme defect, exogenous indigestible material.
- Cholesterol: foam cells in atherosclerosis, xanthomas and cholesterolosis of the gallbladder.
- Protein: reabsorption droplets in proximal tubules (proteinuria), Russell bodies in plasma cells, Mallory-Denk bodies in alcoholic hepatitis.
- Hyaline is a descriptive term for any glassy pink material, inside cells or outside (hyaline arteriolosclerosis).
- Glycogen: storage diseases and kidney tubules in poorly controlled diabetes; PAS-positive and removed by diastase.

## 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.

## Memory aid

Too much in, can’t fold, can’t break down, can’t digest: four doors through which a cell becomes a storeroom.

## 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.

[Add to my cards (3)](https://durgical.app/estudiar/?add=/en/general-pathology/intracellular-accumulations-cholesterol-proteins-hyaline-glycogen/)

## Related

- [Fatty change (steatosis)](https://durgical.com/en/general-pathology/fatty-change/)
- [Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbon](https://durgical.com/en/general-pathology/pigments-in-tissue-lipofuscin-hemosiderin-melanin-bilirubin-carbon/)
- [Endoplasmic reticulum stress and the unfolded protein response](https://durgical.com/en/general-pathology/endoplasmic-reticulum-stress-and-the-unfolded-protein-response/)
- [Pathologic calcification: dystrophic vs metastatic](https://durgical.com/en/general-pathology/pathologic-calcification-dystrophic-vs-metastatic/)
- [Special stains in diagnosis: Congo red, Prussian blue, PAS, Ziehl–Neelsen, Gram](https://durgical.com/en/general-pathology/special-stains-in-diagnosis-congo-red-prussian-blue-pas-ziehl-neelsen-gram/)

## Related conditions

- [Atherosclerosis and dyslipidaemia](https://durgical.com/en/conditions/atherosclerosis-and-dyslipidaemia/)
- [Familial hypercholesterolemia](https://durgical.com/en/conditions/familial-hypercholesterolemia/)
- [Von Gierke disease (glycogen storage disease type I)](https://durgical.com/en/conditions/von-gierke-disease/)
- [Pompe disease (glycogen storage disease type II)](https://durgical.com/en/conditions/pompe-disease/)
- [Niemann–Pick disease](https://durgical.com/en/conditions/niemann-pick-disease/)
- [Gaucher disease](https://durgical.com/en/conditions/gaucher-disease/)
- [Tay–Sachs disease](https://durgical.com/en/conditions/tay-sachs-disease/)
- [α1-antitrypsin deficiency](https://durgical.com/en/conditions/1-antitrypsin-deficiency/)
- [Alcoholic liver disease (biochemistry)](https://durgical.com/en/conditions/alcoholic-liver-disease/)
- [Multiple myeloma](https://durgical.com/en/conditions/multiple-myeloma/)
- [Nephrotic syndrome](https://durgical.com/en/conditions/nephrotic-syndrome/)
- [Hypertensive nephrosclerosis](https://durgical.com/en/conditions/hypertensive-nephrosclerosis/)
- [Diabetic kidney disease](https://durgical.com/en/conditions/diabetic-kidney-disease/)

## Elsewhere in DurgiPedia

- [Lysosomal storage diseases](https://durgical.com/en/biochemistry/topics/lysosomal-storage-diseases/)
- [Glycogen metabolism](https://durgical.com/en/biochemistry/pathways/glycogen-metabolism/)
- [LDL receptor](https://durgical.com/en/biochemistry/enzymes/ldl-receptor/)
- [Cholesterol](https://durgical.com/en/biochemistry/molecules/cholesterol/)
- [α1-antitrypsin](https://durgical.com/en/biochemistry/enzymes/1-antitrypsin/)
- [Microscopy and stains: H&E, PAS, trichrome, silver, immunohistochemistry](https://durgical.com/en/histology/microscopy-and-stains-h-y-e-pas-trichrome-silver-immunohistochemistry/)

[← All of general pathology](https://durgical.com/en/general-pathology/)

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](https://medlineplus.gov/genetics/condition/glycogen-storage-disease-type-i/) (MedlinePlus, US National Library of Medicine, 2024); [Familial hypercholesterolemia: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000392.htm) (MedlinePlus, US National Library of Medicine, 2024); [Alpha-1 antitrypsin deficiency: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/alpha-1-antitrypsin-deficiency/) (MedlinePlus, US National Library of Medicine, 2024).

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Representative model, for educational purposes only.

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