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Amyloidosis Fibrinoid and Hyalin PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Amyloidosis, Fibrinoid and Hyalin” by Jaroslava Dušková.

This medical PowerPoint presentation is about amyloidosis, fibrinoid, and hyalin, three different types of pathological deposits that can occur in various tissues and organs of the body.

Amyloidosis refers to the deposition of abnormal protein fragments called amyloid fibrils, which can accumulate in different organs such as the heart, kidneys, liver, and nervous system, leading to dysfunction and damage.

Fibrinoid deposits are typically seen in blood vessels, where they result from the deposition of fibrin and other proteins within the vessel walls. This can occur as a result of inflammation, autoimmune diseases, or other conditions that damage blood vessels.

Hyalin is a type of protein deposit that is usually found in small blood vessels, and it can result from a variety of conditions, including hypertension, diabetes, and certain infections. Hyalin deposits can also be seen in the walls of the kidneys glomeruli, leading to a condition called hyalinosis.

While amyloidosis, fibrinoid, and hyalin deposits are distinct entities, they can sometimes occur together or in association with each other, particularly in diseases that affect multiple organs or tissues. The diagnosis and management of these conditions depend on the specific underlying disease and the affected organs.

Tags : Amyloidosis, Fibrinoid, Hyalin, pathological deposits, Nephrology, Nephrology PowerPoint presentation

Published on : Jun 07, 2023 | Views : 428 | Downloads : 4

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Slide 1-

General Pathology Amyloidosis Fibrinoid, Hyalin Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague http://www1.lf1.cuni.cz/~jdusk/ Jaroslava Dušková
Slide 2-

Amyloidosis DEF.: disorder of protein metabolism accompanied with abnormal extracellular deposition of proteinaceous material - amyloid
Slide 3-

Amyloid = starch like Karl Freiherr von Rokitansky (1804-1878) Rudolf Ludwig Karl Virchow (1821-1902). Amyloid - history
Slide 4-

Karl Freiherr von Rokitansky (1804-1878) Austrian pathologist, born February 19, 1804, Königgrätz, Böhmen, Austrian Empire (now Hradec Králové, East Bohemia, Czech Republic); died July 23, 1878, Wien. Handbuch der pathologischen Anatomie IInd Band, Wien 1842 Amyloid - history 2.
Slide 5-

Amyloidosis – morphology Macroscopy: small amounts – invisible larger deposits – enlarged, firm, waxy organs
Slide 6-

Ultrastructure & Biochemistry of Amyloid 90-95% non branched fibrils diam. 10-12nm 5-10% p-component - glycoprotein + fibronectin, laminin, collagen 4
Slide 7-

Amyloidosis conformational disease (Carrell and Lomas, Lancet, 1997) „…arises when a constituent protein undergoes a change in size or fluctuation in shape with resultant self - association and tissue deposition“ pleated β – sheet structure
Slide 8-

Conformational diseases (Carrell and Lomas, Lancet, 1997) Amyloidosis Prionoses - transmissible spongiform encephalopathies (incl. m. CJD) m. Alzheimeri pleated β – sheet structure
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Amyloidosis Classification: according to the source protein (more than 20 different identified) according to the distribution systemic (generalised) localised
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Systemic Amyloidosis - I. AL - imunocyte dyscrasia associated light chains Ig (mostly ) „primary“ Distribution: tongue, heart, GIT, liver, spleen, kidney Associated diseases: Plasma cell myeloma, B cell lymphoma,
Slide 11-

Systemic Amyloidosis - II. AA - reactive systemic amyloidosis SAA = Serum Amyloid Associated protein „secondary“ Distribution: liver, kidney, spleen, GIT, lymph nodes, bowel, adipose tissue Associated diseases: rheumatoid arthritis, chronic infections (tb, leprosy, bronchiectasiae, osteomyelitis, IBD, neoplasms MLH , RCC
Slide 12-

Systemic Amyloidosis - III. senile systemic SSA 25% people over the age of 80 years (!) normal transthyretin TTR (prealbumin) mostly heart & vessels invilvement
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Systemic Amyloidosis - IV. A2 - hemodialysis associated 2 microglobulin Hereditary AA - Familial Mediterranean Fever ATTR - Famil. polyneuropatia transthyretin (mutated form)
Slide 14-

Systemic Amyloidosis - complications diminished functions of some organs, esp. KIDNEY FAILURE IIIrd stage Amyloid nephrosis
Slide 15-

Localised Amyloidosis - I. Senile cardial ATTR - transthyretin - (structurally normal) Senile cerebral A -  -amyloid protein
Slide 16-

Cardiac Amyloidosis – clinical manifestations Dilated Cardiomyopathy (predominant systolic dysfunction) Restrictive cardiomyopathy (predominant diastolic dysfunction) Congestive heart failure Rhytm abnormalities Coronary insufficiency Valvular dysfunction Pericardial tamponade Enhance sensitivity to digitalis glycosides Atrial thrombosis - embolisation
Slide 17-

Localised Amyloidosis - II. Endocrine ACal - ca medullare gl. thyreoideae AIAPP - islets of Langerhans associated AANF - isolated atrial amyloidosis atrial natriuretic polypeptide Nodular tumoriform amyloid deposits (tongue, lung,larynx, skin, urinary bladder, orbita)
Slide 18-

Clinical Diagnosis of Amyloid Scintigraphy (in vivo) using human serum amyloid component marked with 123J Echocardiography (atrial amyloid)
Slide 19-

Clinical Diagnosis of Amyloid Biochemistry sequening DNA -hered. forms extraction of fibrils (from a biopsy specimen) spectrometry sequening of the amyloid protein
Slide 20-

Amyloidosis – morphology Macroscopy: small amounts – invisible larger deposits – enlarged, firm, waxy organs
Slide 21-

Morphological Diagnosis of Amyloid Macroscopy reaction Virchow I (sol. Lugolli) Virchow II (H2SO4)
Slide 22-

Morphological Diagnosis of Amyloid Microscopy: KONGO red (+POLARISATION!) + KMnO4 thioflavine S,T crystal. violet (metachromasia) IMMUNOHISTOCHEMISTRY (electron microscopy)
Slide 23-

Morphological Diagnosis of Amyloid Materials: GIT (stomach, duodenum rectum, gingiva) biopsy kidney sural nerve & muscle fat aspiration biopsy – needle with an internal diam. 0,7-1,2mm Röcken Ch. Sletten K.: Amyloid in Surgical Pathology Virchows Arch., 2003, 1-26
Slide 24-

CONGO Red synthesized by young chemist at Bayer comp. 1883 as the first of economically lucrative direct (nod needing a mordant) textile dyes patented by AGFA 1885 (Aktiengeselschaft für Anilinfarbenfabrikation) 3 weeks after the conclusion of the West Africa Conference to Europeans in 1885, the word Congo evoked exotic images of far-off central Africa known as The Dark Continent the Congo red stain was named „Congo“ for marketing purposes by a German textile dyestuff company in 1885 Steensma DP: „Congo“ Red. Out of Africa? Arch. Pathol.Lab.Med.,2001, 125, 250-2
Slide 25-

Reversibility of Amyloid The deposits are NOT irreversible. e.g. Hrncic R. et al: Antibody mediated resolution of light chain – associated amyloid deposits. Am.J. Pathol., 2000, 157,12369-46 Progression of generalised amyloidosis can be delayed or stopped by treatment of the underlying disease. Röcken Ch. Shakespeare Ann: Pathology, diagnosis and pathogenesis of AA amyloidosis. Virchws Arch. , 2002, 440, 11-122
Slide 26-

Prevention & Therapy of Amyloid Prevention & treatment of the underlying diseases Vaccination against β am. protein in mice diminished senile plaque formation and improved memory. Nature Medicine, 2001, 7, 18th Jan. A β –based experimental therapies based on degrading enzymes. Zlokovic et al.: Neurovascular Pathways and Alzheimer Amyloid β-peptide. Brain Pathol. , 2005, 15, 78-83
Slide 27-

Fibrinoid & Hyalin disorders of protein metabolism
Slide 28-

Fibrinoid Change of Collagen vessels and connective tissue damage plasmorrhagia (leakage of plasma) deposits of Ag-AB complexes staining characteristics fibrin - like
Slide 29-

Hyaline change Definition (historical, descriptive): intra- or extracellular change of homogenous rose „ glassy“ appearance in the H&E stained histological sections
Slide 30-

Hyaline change Extracellular: corpus albicans, scars, hyalinoses of serous membranes Intracellular: Crooke cells, Mallory´ hyaline, Russell bodies
Slide 31-

Ultrastructure Fibrinoid - collagen fibres surrounded by plasma proteins may be reversible Hyalin – collagen fibres increased in thickness, changed architecture rather stable
Slide 32-

Hyaline change Extracellular: corpus albicans, scars, hyalinoses of serous membranes Intracellular: Crooke cells, Mallory´ hyaline, Russell bodies
Slide 33-

Significance of Fibrinoid Change diminished quality of the collagen ( firmness, permeability) tendency to thrombosis in the vessels, aneurysms formation
Slide 34-

Significance of Hyalin Change diminished quality of the collagen ( elasticity) ischemia in organs with thickened arterial walls intracellular - function, death