The study of amyloids, calcification, pigmentation and jaundice.

Published March 4, 2013 by niniebulabula3161743

The most basic definition of an amyloid is that its an “abnormal protein”. Amyloid are insoluble fibrous protein aggregates with similar structural traits but are chemically different.
“Amyloids are unlike other fibrous proteins, they do not have a structural, supportive or motility role. Their formation can accompany diseases characterized by a specific protein or peptide that aggregates.” Rambaran ,N 2008, ‘Abnormal protein assembly’, Prion, vol.2(3), Jul-Sep, 112-117. In my understanding of the amyloid process , the proteins are not insoluble from the beginning. The proteins begin as normal soluble proteins which “misfold” into insoluble fibrils made up of the beta-pleated sheets. These insoluble fibrils gather and collocate in tissue initializing the production of amyloidosis. In amyloidosis the the protein fibrils interfere with the normal structure and functioning of the tissue, which results in a state of disease. Amyloidosis is associated with a couple of diseases such as Alzheimer’s, diabetes type2, spongiform encephalopathies. The amyloid fibrils are deposited extracellularly in the the tissue producing a pathogenic effect.
Amyloidosis is classified into amyloid light chain( AL) and associated amyloidosis ( AA). The cause of AL is unknown but it is linked to defective and abnormal antibodies. In AA the deposited protein is serum amyloid A (SAA). The plasma concentration of SAA is highest during inflammation. So AA is associated more with inflammatory diseases.
“Diagnosis of amyloidosis is based upon clinical examination of sample tissue. The examination should depict evidence of characteristic amyloid deposits”. Congo red is the most useful stain in diagnosis of amyloidosis. When combined with polarized light the Congo red stain makes the amyloid deposits appear green.
Calcification is calcium deposits accumulating in soft tissue causing it to get hard. Since the calcium deposition does not occur at a normal site such as bones and teeth, the result of the deposition is bound to be abnormal. A question I ask myself is “ What causes the calcium deposition in the wrong site?”. And another question is “is there a link between a hyper-parathyroid hormone and calcification?”
Firstly according to Harvard Medical School, abnormal calcification does not result from normal consumption of calcium in our diets. Even though high levels of calcium in our blood can lead to abnormal calcification. “The primary cause of hypercalcemia in adults is hyperthyroidism”. Martini, Nath, 2009, Anatomy and physiology, 8th edition,p1022 . This statement makes me consider it to be a possibility for a hyper parathyroid hormone to be linked to calcification .“ calcification can be due to infection, kidney or metabolic disorders, problems with blood vessels or simply ageing” McAdams, M 2011, Calcium deposits and calcification, livestrong.
Calcification can be classified into metastatic and dystrophic calcification. “Dystrophic occurs in damaged tissues either dead or degenerative” . With knowledge of the previous modules, I believe that dystrophic calcification is associated with cell injury. This is a digestive process, whereby macrophages digest necrotic tissue. During this process calcium salts accumulate. “ metastatic calcification may occur in normal tissue whenever there is hypercalcemia” . This statement also contributes to my conclusion that hyperthyroidism is linked to calcification. Metastatic calcification tends to occur where acidic areas excreted ( HCL acid in stomach, uric acid in kidneys, carbonic acid in lungs). This is because calcium precipitates upon alkalization of pH.
Pigmentation means colouring. Skin is given its pigment by skin cells producing melanin( the colour pigment). The darker the hair and skin the individual has, the higher the melanin production. Melanin is not the only pigment associated with the body. There are a couple of other endogenous pigments, like melanin these pigments are produced inside the body. The exogenous pigments are produced externally.
Endogenous pigments such as hemosiderin, hematin, bilirubin and hematoidin are associated with hemoglobin breakdown. Red blood cells are continuously undergoing a hemolysis process, degradation of the red blood cells causes the breakdown of hemoglobin in to globin, iron and heme. The bilirubin arises from the heme, and is eventually excreted in bile and urine. Bilirubin is responsible for the yellow colouring of bruises, and also gives urine its yellow colour. A question that I ponder upon is “ what is bilirubin’s role in the body, and is it needed?”. Wikipedia states that “ bilirubin demonstrates potent antioxidant activity.” This leads to the hypothesis that bilirubin’s main physiological role is as a cellular antioxidant. I would consider this as beneficial, since antioxidants are there to protect our bodies from reactive oxygen species. This could be applicable to adequate levels of bilirubin since high levels can be toxic leading to jaundice. Hematoidin I would consider to have the same action as bilirubin, but in a different area such as tissue instead of bile.
Jaundice results from toxic levels of bilirubin in peripheral tissue, giving the tissue a yellow colour. Hence jaundice is not a diagnosis but a sign of abnormality in the body.
Jaundice can occur in many different diseases. Too much bilirubin being produced and excreted into the blood leads to these diseases. Jaundice can be reflected in the skin pigmentation and eyes.
Common ground between these four processes
A common trait between amyloidosis and calcification is the abnormal accumulation at a foreign site. This leads to defects in function a structure of particular organs or tissue. Pigmentation and jaundice share much more common ground, in the sense that the result of jaundice is caused by a pigment which is bilirubin.
Importance of understanding these processesAmyloidosis,_Node,_Congo_Red



In a clinical situation, a patient may consult me showing particular signs and symptoms associated with any of these processes. With the knowledge of these processes I will have to identify the symptoms and which diseases they are related to. This could lead to diagnosis of a particular disease. For example: a patients exhibits yellow coloured skin, stool check depicts light coloured feaces, urine is dark and brown (this is an abnormal colour). By considering these signs and symptoms of jaundice I would then have a way forward to finding the cause of the jaundice.
1.Rambaran ,N 2008, ‘Abnormal protein assembly’, Prion, vol.2(3), Jul-Sep, 112-117
2.”. Martini, Nath, 2009, Anatomy and physiology, 8th edition,p1022
4.” McAdams, M 2011, Calcium deposits and calcification, livestrong.


One comment on “The study of amyloids, calcification, pigmentation and jaundice.

  • Generally well written. The layout is very poor, no real introduction, not really then addressing the blog requirements, and then not real conclusion. Some integrated aspects at the end, but this appears ‘ad hoc’, is disjointed, and not related to the rest of the structure and writing.

    Referencing too is poor. Where are these numbers in the text? What is ‘wikipaedia’ as a reference? Where is number 5? Why is some facts seemingly referenced specifically, and other facts not referenced at all?

    Imaging is also very poor – just posted randomly – they are meaningless.

    The blog show very little understanding of the work, only a text book version.

    Much improvement required.

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