The 83-year-old patient presented in this scenario is suffering from malabsorption syndrome. The condition that the patient is experiencing, and the lack of food intake contributes to protein malnutrition. The main problem of malabsorption syndrome is the lack of nutritional supply in a body due to decreased absorption within the small intestines (McCance & Huether, 2019). The purpose of this discussion is to discuss the genetics, physiological, and cellular components of the scenario presented.
Malabsorption syndrome can have many different causes. Some such causes can stem from outside influences such as intestine dissection, infections, and damage from radiation treatments. However, malabsorption can also come from genetic diseases such as Cystic fibrosis, congenital short bowel syndrome, Celiac disease, and Chron’s disease (Clark & Johnson, 2018).
The scenario presented only states that the patient has a medical history of malabsorption syndrome but does not specify what the cause was. If the patient’s malabsorption was caused by Celiac disease, the genetic factors that would be important to focus on would be the class II human leukocyte antigen (HLA) genes, DQ2 and DQ8.
Patients with these genes are susceptible to celiac disease, where gluten proteins cause CD4T cells to be activated in the mucosal lining of the small intestines. Such activation damages the mucosal lining over time, thereby interfering with the absorption of necessary nutrients (Clark & Johnson, 2018).
The stimulus presented in this scenario is a state of hypoalbuminemia. This condition developed because of the patient’s history of malabsorption syndrome and low protein intake (McCance & Huether, 2019). To understand the physiological response, it is essential to understand the function of protein within the bloodstream. Albumin is the form of protein within the blood responsible for maintaining oncotic pressure.
The albumin does this by using its force to retain water via sodium within the capillaries. Therefore, if there is a lack of albumin in the bloodstream, a weak force keeps the fluid from escaping. This affects the oncotic pressure and allows fluid to leak into the interstitial space. Over time, an accumulation of fluid in the interstitial space leads to swelling, which is the culprit for the patient’s generalized edema and ascites (Darwish & Lui, 2021).
The way nutrients are absorbed into our bodies is through the digestive process. The digestive process begins from the minute food enters our mouths. However, most absorption takes place in the intestinal lumen of the small intestines. The small intestines are made of four main layers: the mucosa, submucosa, muscularis externa, and adventitia.
The mucosal layer contains the epithelium, where the digestive cells live. The digestive cells include the enterocytes, Paneth cells, goblet cells, and neuroendocrine cells. Enterocytes make up the majority of the intestinal epithelium and are responsible for the primary role of absorption (Kong et al., 2018)
Specifically, protein is absorbed in the body with the help of trypsin and chymotrypsin. These enzymes break proteins into tiny forms of amino acids. These amino acids are then transported via the enterocytes across the epithelium to enter blood circulation (Kong et al., 2018). The major clinical problem taking a toll on this patient’s health is malabsorption syndrome. In this case, there is an interruption of the absorptive process at the small intestines, through chemical interruption or a defected brush border, preventing protein absorption for the patient (McCance & Heuther, 2019). A lack of circulating protein is causing the patient’s symptoms, as stated previously.
Malabsorption syndrome can have many different causes, both extrinsic and intrinsic. Older adults are more likely to experience malabsorption due to prolonged illnesses or exposures to medication and chemicals (Clark & Johnson, 2018). Young children, however, are less likely to experience this condition. Therefore, it is easier to pinpoint the cause of the problem in children. If a very young child would present with similar symptoms, I would sooner lookout for diseases such as Cystic fibrosis and milk protein intolerances and their genetic indicators (Cleveland Clinic, 2022).
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