In: Nursing
A 56-year-old male patient is brought in by ambulance after vomiting bright red blood for the last 30 minutes. On examination the patient has a swollen abdomen and gynaecomastia. His partner, when questioned, mentions that the patient has been a chronic drinker for the last 15 years. a. What is the likely cause of the patient vomiting blood? b. What is the underlining cause of all the symptoms the patient has presented with? c. Explain the pathophysiology of each of the symptoms the patient has presented with in relation to the diagnosis in (b).
Answer:- a)This patients symptoms adresses he has liver cirrhosis. Cirrhosis is the result of chronic liver disease that causes scarring of the liver and liver dysfunction. This often has many complications, including accumulation of fluid in the abdomen (ascites), bleeding disorders (coagulopathy), increased pressure in the blood vessels of the liver (portal hypertension), and confusion or a change in the level of consciousness.
B)Cirrhosis is caused by chronic liver disease, infection and long-term alcohol abuse (Alcoholic liver disease). Other causes of cirrhosis include hepatitis B, medications, autoimmune inflammation of the liver, disorders of the drainage system of the liver.
Symptoms
Additional symptoms that may be associated with this disease:
Symptoms may develop gradually, or there may be no symptoms.
C)Cirrhosis slows the normal flow of blood through the liver, thus increasing pressure in the vein that brings blood to the liver from the intestines and spleen. Swelling in the legs and abdomen. The increased pressure in the portal vein can cause fluid to accumulate in the legs (edema) and in the abdomen (ascites).
The liver plays a vital role in synthesis of proteins (for example, albumin, clotting factors and complement), detoxification, and storage (for example, vitamin A). In addition, it participates in the metabolism of lipids and carbohydrates.Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are fully reversible.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal parenchyma. This scar tissue blocks the portal flow of blood through the organ, raising the blood pressure and disturbing normal function. Recent research shows the pivotal role of the stellate cell, a cell type that normally stores vitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma (due to inflammation) leads to activation of stellate cells, which increases fibrosis (through production of myofibroblasts) and obstructs hepatic blood flow.In addition, stellate cells secrete TGF-β1, which leads to a fibrotic response and proliferation of connective tissue. Furthermore, it secretes TIMP 1 and 2, naturally occurring inhibitors of matrix metalloproteinases, which prevents them from breaking down the fibrotic material in the extracellular matrix.
As this cascade of processes continues, fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout. The spleenbecomes congested, which leads to hypersplenism and the spleen's retention of platelets, which are needed for normal blood clotting. Portal hypertension is responsible for the most severe complications of cirrhosis.