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Discuss the relationship between liver cirrhosis and haemochromatosis
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Polina Lobacheva20029235
Blood Science 6H5Z1003_2122_9Z6
Discuss the relationship between liver cirrhosis and haemochromatosis.
Liver disease is a condition where liver functions, such as clotting factors, other proteins, detoxification
of harmful products of metabolism, and excretion of bile, deteriorate (Sharma and Bari, 2015). This
illness is a continuous process of inflammation, destruction, and regeneration of liver parenchyma,
which leads to fibrosis and cirrhosis. Cirrhosis is the end stage of chronic liver disease where the
structure of the liver is damaged by the formation of widespread nodules and presence of vascular
reorganisation (Sharma and Bari, 2015). Due to liver disease the individual is likely to develop a
haemostatic disorder, as the liver plays an essential role in regulating haemostasis. These haemostatic
abnormalities may include decreased production of clotting factors, thrombocytopenia, platelet
dysfunction and increased circulating fibrinolytic activity (Denninger, 1999). Therefore, it is vital that
liver disease is studied in more depth to discover more efficient treatments that will aid in preventing
the illness from progressing quickly.
Being one of the largest organs in the human body the liver plays an essential role in converting
nutrients from the foods we consume into substances the body can utilise, in addition to storing them
for later use (IQWiG, 2006). With the help of hepatocytes, the main parenchymal cells of the liver, it
helps to control and maintain biochemical and metabolic processes that help the liver breakdown,
digest and absorb fat, proteins and carbohydrates (Alves ‐Bezerra and Cohen, 2017). Fats are broken
down through fat emulsification which is a process where bile breaks down fatty acids by increasing the
surface area of fats and grouping them into small clusters. These clusters can then be used for
immediate energy or stored for later use like ADP, metabolic processes, digestion and respiration
(PASQUIER et al., 1996).
In the process of metabolising carbohydrates, the liver ensures the level of blood glucose is maintained.
If the blood glucose increases, e.g. after a meal, the liver will remove the excess through the portal vein
and store in the the form of glycogen. Vice versa, in case of low blood glucose levels, the liver will break
down the stored glycogen and release glucose into the blood (IQWiG, 2006). The liver converts amino
acids for more energy or to make carbohydrates or fats, however a harmful by-product of this process is
ammonia. Through the urea cycle, the liver is able to convert ammonia to urea and excrete it through
urine (IQWiG, 2006). A buildup of urea can disrupt nitrogen balance, urine concentration, and acid-base
homeostasis, therefore it is essential the liver functions well to excrete ammonia (Weiner, 2014).
In addition to being able to break down old and damaged blood cells, vitamin K allows the liver to
produce proteins that are essential in blood clotting. Vitamin K serves as an essential cofactor for a
carboxylase that catalyses carboxylation of glutamic acid residues on vitamin K-dependent proteins
(Vermeer, 2012). These proteins include coagulation factors (FII (prothrombin), VII, IX and X) and
coagulation inhibitors (proteins C, S and Z) (Vermeer, 2012).
Liver disease is responsible for nearly 2 million deaths per year worldwide, where liver cirrhosis
contributes to 1 million of those (Asrani, 2019). Cirrhosis is the development of a collagenous scar on an
injured liver tissue resulting in the continuation of connective tissue production and deposition -
fibrogenesis (Schuppan, 2008). Cirrhosis develops a distorted hepatic vasculature, which leads to portal
hypertension and damage to the blood supply exchange between hepatic sinusoids (Figure 1) and the
adjacent liver parenchyma (i.e. hepatocytes) (Schuppan, 2008).
, Polina Lobacheva
20029235
Blood Science 6H5Z1003_2122_9Z6
One of the most common causes of liver disease is alcohol abuse, as the substance inhibits the enzymes
that break down and remove scar tissue, leading to a reduction in healthy cells and a buildup of scar
tissue (Singh, 2017). Consumed alcohol is metabolised in the liver by enzyme alcohol dehydrogenase
(ADH), which converts alcohol to acetaldehyde by the oxidation process (Maher, 1997). Acetaldehyde is
a harmful substance to the body, however when the liver is functioning correctly, the enzyme aldehyde
dehydrogenase (ALDH) is able to rapidly oxidise acetaldehyde to acetate. Acetaldehyde has a tendency
to bind to proteins like enzymes, microsomal proteins, and microtubule and form adducts with
dopamine, a neurotransmitter, which can result in alcohol dependence (Zakhari, 2006). Formation of
protein adducts in hepatocytes damages protein secretion which is associated with liver enlargement,
hepatomegaly (Zakhari, 2006). Another cause of liver dysfunction includes obesity, which results in a
buildup of fatty acids leading to chronic inflammation and formation of scar tissue due to the
enlargement of the liver (Fabbrini, 2009). The main cause of liver cirrhosis is prior liver disease left
untreated.
Altered liver function has a significant impact on the haemostasis of the body, further shown in Figure 2.
Haemostatic imbalances that are a consequence of liver disease include thrombocytopenia, reduced
levels of coagulation factors and inhibitors, platelet dysfunction, reduced number of fibrinolytic proteins
and increased plasma levels of coagulation factor VIII and VWF (Lisman, 2010). In patients with liver
disease, elevated levels of platelet activation, thrombin and fibrin generation, and fibrinolysis are
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