Pathogenesis and Pathophysiology Analysis

Essay 6
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Essay 6
1 Explain the pathogenesis with common clinical presentation of celiac’s disease
Celiac disease is a chronic disease of the small intestines which occurs when T-cells are triggered by gluten (Sharma, et al., 2020). When susceptible individuals are exposed to gluten, the immune system responds by activating the t-cells, resulting in the inflammation of the intestinal walls. Gluten is gliadins and glutenins which are commonly found in wheat, rye, and barley (Sharma, et al., 2020). For celiac disease to develop, an interaction between the intestinal walls and the gliadins occurs, causing the inter-enterocyte tight junctions to break up (Parzanese et al., 2017). This triggers the release of zonulin which then increases intestinal permeability. Then, t-cells are activated, causing intestinal inflammation.
In the past, celiac disease was thought to be a pediatric disease. However, research has shown that it affects people of all ages (Tye-Din et al., 2018). Various genetic and environmental factors play a role in the development of the disease. Environmental factors include high wheat (gluten) intake and the feeding patterns for infants (Parzanese et al., 2017; Tye-Din et al., 2018). The amount of gluten introduced to children has been considered a contributing environmental factor. Other factors include rotavirus infections in the early years, geographical location (the disease is more common in the northern latitude), and the season of birth (risk of development increases if the child was born during summer) (Tye-Din et al., 2018). Genetic factors include the presence of human leukocyte antigen (HLA) DQ2 and DQ 8 genes, which increase intolerance to gluten (Parzanese et al., 2017; Tye-Din et al., 2018). Other genetic factors include non-HLA genes such as the myosin IXB gene.
Celiac disease can be asymptomatic, latent, typical, or atypical (Parzanese et al., 2017). Among children, it manifests as abnormal intestinal absorption, nausea, and vomiting. It is also characterized by constipation and recurrent abdominal pain. Among adults, it manifests as constipation, bloating, gastrointestinal diarrhea, and abdominal pain.
2 Analyze the pathophysiology of Crohn’s disease and related genetic issues
Crohn’s disease is a chronic inflammatory disease of the intestines (Petagna et al., 2020; Agrawal et al., 2020). The disease can be recurrent and with each relapse, it becomes more severe. Crohn’s disease starts with abscess and trans-mural inflammation of the intestines (Ranasinghe & Hsu, 2020). The inflammation usually occurs in the colon and ileum, but can also occur in the entire gastrointestinal tract. The abscess and inflammation then progress into ulcers which occur in the superficial mucosa first and then develop into the deeper layers. Also, non-caseating granulomas occur in the wall of the bowel, the liver, or in the lymph nodes with continued intestinal inflammation. However, granuloma formation is not always detected or present, although this does not mean that the patient does not have the disease (Ranasinghe & Hsu, 2020). When the inflammation settles, the inflamed sections of the intestinal walls become scarred. Over time, continued inflammation causes irreversible damage to the intestinal tissue (Petagna et al., 2020). The damage manifests as intra-abdominal abscesses or fistulas. The common fistulas associated with the disease include enterovaginal, enterovesical, enterocutaneous, and enteroenteral fistulas (Ranasinghe & Hsu, 2020). Continued scarring and inflammation result in stricture formation and bowel obstruction.
Crohn’s disease has been linked to certain genetic variations. According to Ranasinghe and Hsu, (2020) variations in NOD2 genes increase the risk of developing the disease. The variations in this gene interfere with the immune system and hinder the intestinal cells from responding to bacteria in the gastrointestinal tract. As a result, chronic inflammation occurs. The NOD2 mutation has been associated with more severe ileal disease (Ranasinghe & Hsu, 2020). Thus, some people are more genetically susceptible to the disease than others.
3 Differentiate between hepatitis A, B, C, and viral hepatitis
Hepatitis involves inflammation and damage of the liver tissue (Razavi, 2020). There are different types of hepatitis which include hepatitis A, B, and C, each caused by a different virus. Hepatitis A is an acute infection caused by the hepatitis A virus. Transmission occurs through the consumption of contaminated food and water (Jefferies et al., 2018; Razavi, 2020). It has no serious complications and vaccines against this type of hepatitis are available.
Hepatitis B is caused by the hepatitis B virus and the infection can be acute or chronic. It is transmitted through sexual contact, sharing of injection needles, and mother-to-child (Jefferies et al., 2018; Razavi, 2020). Chronic hepatitis B can lead to liver damage. Effective vaccines against this infection are available.
Hepatitis C is caused by the hepatitis C virus. Like hepatitis B, it can also be acute or chronic (Razavi, 2020). It is also transmitted through sexual contact and sharing of injection needles or anything that involves contact with blood, just like Hepatitis B. However, unlike hepatitis A and B, there are no vaccines currently available for hepatitis C (Razavi, 2020). Also, chronic hepatitis C can lead to liver damage.
However, viral hepatitis is any viral infection that causes inflamm...