Clinical Pathology · MU Sofia

10. Extracellular accumulations: hyalinosis; fibrinoid swelling.

Covers the normal components of the extracellular matrix and how their accumulations are classified, then focuses on hyalinosis: vascular hyaline, benign nephrosclerosis with its kidney arteriole picture, examples such as corpora albicantia and the sugar-coated spleen, and mechanisms of formation. It then explains fibrinoid swelling, its Van Gieson staining, and its three forms with their causes.

Inside: 1 section · 1 labelled picture · 14 flashcards · 3 min

Topic 10 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 514 words (3 min of reading), with 14 flashcards.

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  1. Extracellular accumulations: hyalinosis, fibrinoid swelling

Extracellular accumulations: hyalinosis, fibrinoid swelling

A reminder, that extracellular tissue consists of:

  • Fibrous structural proteins (elastin and collagens)
  • Water hydrated gels (proteoglycans and hyaluronan)
  • Adhesive glycoproteins

Pathologies lead to a change in quantity and/or quality of these normal components.

We classify accumulations in the ECM as follows:

  • Disorders in the metabolism and structure of collagen
  • Disorders in the metabolism and structure of elastin
  • Disorders in the content of the proteoglycans
  • Abnormal accumulations in the ECM
  • Including proteins
  • Fibrinoid
  • Hyalin
  • Amyloid
  • Inorganics
  • Ca²⁺
  • Urates (e.g. Uric acid)

Hyalinosis

Hyaline is a morphological description of a non-structured ‘glassy’ structure, made of a heterogenous mix of proteins, lipids and carbohydrates. Hyalinisation can occur in the ECM of any tissue, below we explore some examples:

  • Vascular hyaline
  • Due to nonenzymatic glycosylation of proteins in the basement membrane of vessels (in diabetes)
  • Is associated with hypertension, usually a secondary product, as high pressure forces proteins into the ECM
  • Can lead to nephrosclerosis
  • Benign nephrosclerosis
  • High pressure in the afferent arteries of the kidneys leads to build up of Hyaline around the glomeruli. (NOTE SLIDE - HYALINOSIS RENIS)

H&E, kidney: hyaline arteriolosclerosis – the arteriole wall (arrows) is replaced by homogeneous, glassy pink hyaline that narrows the lumen; glomerulus on the right.

Image: “Histopathology of renal arteriolar hyalinosis, annotated” by Mikael Häggström , M.D. Author info - Reusing images - Conflicts of interest: None Mikael Häggström , M.D. Consent note , CC0, via Wikimedia Commons.

Examples: hyaline arteriolosclerosis of the renal afferent arterioles in benign hypertension and diabetes (gives benign nephrosclerosis: small, finely granular kidneys); hyalinised old scars and keloids; hyalinised glomeruli in end-stage kidneys; corpora albicantia in the ovary; thickened, glassy capsules over the spleen ('sugar-coated spleen').

We can also divide hyalinosis according to the mechanism of formation:

  • Hyaline as a product of of fibrinoid changes
  • A product of damaged perivascular stroma
  • Hyaline in the finale of plasmatic impregnation
  • A product of buildup in the vascular wall
  • Local hyalinosis as product of inflammation
  • Hyalinosis as a product of necrosis
  • Hyalinosis as a product of sclerosis (hardening of tissue)

Fibrinoid swelling

Fibrinoid swelling, quite simply means swellings that have the characteristics of fibrin. It is the morphological description of non-structured heterogeneous substance predominantly made of plasma proteins. It is stained by Van Gieson (yellow).

There are three main forms of Fibrinoid swelling

  • Fibrinoid in precipitation of immune complexes
  • A product of systemic connective tissue diseases
  • Fibrinoid in accumulation of plasma proteins

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