Haemoglobin breakdown

Hepatitis could result in symptoms similar to those experienced in this case study, but would be likely to cause jaundice, a yellow skin colouration which is due to the presence of haemoglobin breakdown products in the tissues. 

Haemolysis. The increased haemoglobin breakdown prtxiuces bilirubin which overloads the conjugating mechanism. 

Bilirubin is a product of the breakdown of haemoglobin in red blood cells. Neonatal jaundice occurs when bilirubin builds up faster than a newborn baby s liver is able to break it down. This results in the deposition of water-insoluble bilirubin in the skin (giving the skin a yellow colour) and untreated it can lead to damage of the central nervous system by deposition in brain cells. 

AW s white cell count is raised, probably due to an infection which may well have precipitated this crisis. The low haemoglobin and haematocrit are due to the excessive destruction of red cells that occurs in this haemolytic form of anaemia and the raised bilirubin is due to the rapid breakdown of the cells. Raised reticulocytes are seen in sickle cell anaemia as the body compensates for the increased cell breakdown by increasing production of red cells. Target cells are blood cells which resemble a shooting target and are found in patients with sickle cell anaemia as well as in a number of other conditions. 

Q3 Signs of jaundice jaundice gives a yellowish colour to the skin and mucous membranes, usually easiest to see in the cornea. The yellow colour is due to the presence of breakdown products of haemoglobin such as bilirubin in tissues, which the liver usually removes from the blood. Jaundice is indicative of liver disease, obstruction of the bile ducts or haemolytic disease. Bilirubin stains not only the tissues but also all body fluids, including plasma and urine, and the patient s urine can become really dark. 

Bilirubin a yellow/orange pigment derived from the breakdown of haemoglobin, that is excreted in bile. 

Bilirubin is a potentially toxic compound that is an end-product of the breakdown of the porphyrin moiety of haem-containing compounds such as haemoglobin, myoglobin, cytochromes and catalase. 

Surprising perhaps, carbon monoxide is produced in the body as a result of the normal breakdown of haemoglobin from red blood cells. The enzyme, haem oxygenase, converts the haem group into bilirubin and releases CO into solution. Current research has even suggested that trace amounts of CO may have a physiological role, possibly acting as a neuromodulator. 

The metabolic role of many minerals and vitamins is as prosthetic groups or coenzymes in different enzyme systems. Consequently, mineral and vitamin deficiencies can cause a breakdown of the processing system and precipitate metabolic disease. For example, methylmalonyl-CoA isomerase (see p. 203) is an important vitamin Bi2-dependent enzyme in the gluconeogenic pathway. A deficiency of vitamin B12 (or cobalt) may reduce enzyme activity, decrease the efficiency of glucose synthesis and predispose the animal to ketosis. Similarly, ceruloplasmin is a copper-dependent enzyme responsible for releasing iron from cells into blood plasma. A copper deficiency may reduce ceruloplasmin activity, decrease the efficiency of iron utilisation for haemoglobin synthesis and predispose the animal to anaemia. 

Bilirubin resulting from the breakdown of haemoglobin in the cells of the reticulo-endothelial system passes into the blood plasma where it circulates in combination with the ai-globulin fraction from there it passes into the cells of the hepatic parenchyma which conjugate the bilirubin with glucuronic add and excrete the product in the bile. Furthermore the hepatic parenchyma is the site of considerable protein synthesis, that of the blood plasma proteins. 

Patients who have had a haemolytic crisis will have raised plasma bilirubin levels because the processes within the liver that are responsible for disposing of bilirubin (formed by the breakdown of haemoglobin) have a limited capacity, and when they reach their limit bilirubin levels rise in the blood. It is bilirubin that causes jaundice - the yellow colouring of skin and sclera. A finding of jaundice is characteristic of haemolysis, in which a sudden breakdown of erythrocytes overloads the haemoglobin degradation and disposal mechanism (17b). 

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