More handpicked essays just for you.
Advanced pathophisology of celiac disease
Pathophysiology for celiac disease
Pathophysiology for celiac disease
Don’t take our word for it - see why 10 million students trust us with their essay needs.
Recommended: Advanced pathophisology of celiac disease
The pathogenesis of CD relies on a complex interplay between a triad of factors: genes, gluten, and environment – all of which work together to result in the disease’s characteristic injury of the small intestinal mucosa, ultimately resulting in nutrient malabsorption.3 HLA-DQ2 and HLA-DQ8, both of which are HLA class II genes, are the main predisposing genetic factors that are displayed in nearly all patients with CD. 3 Many other non-HLA genes are thought to play a role in the development of CD in distinct patient populations, but their role is not nearly as universal as that of the HLA class II genes. The way in which gluten plays a critical role in CD pathogenesis is the fact that both gliadin and glutenin are rich in proline and glutamine peptides, which effectively renders the gluten proteins resistant to proteolytic degradation by gastric, pancreatic, and intestinal brush border enzymes.5 This inadequate digestion will result in the generation and collection of large peptides high in proline and glutamine content in the small intestine.
Women are more likely to be diagnosed with celiac disease than men. Transition: II. Main Point: In celiac patients, gluten causes intestinal damage that may lead to symptoms such as diarrhea, abdominal pain, and extra-intestinal complications such as weight loss, malnutrition, fatigue and neurological disorders. A.
According to Lewis and associates, DM is a chronic disease that affects multiple body systems. For the purpose of this paper, only DM type 2 will be discussed based on the assumption that a majority of patients aged 60 years or older have this type. The primary defects of this disease consist of insulin resistance, decreased insulin production, inappropriate glucose production by the liver, and alterations in production of adipokines. Insulin resistance is the result of defects in the body’s insulin receptors. This finding predates all cases of DM type 2 and the development of impaired glucose tolerance. In insulin resistance, beta cells in the pancreas are stimulated to increase insulin production to compensate for the lack of response by the insulin receptors. Gradually, the beta cells begin to fail to secrete enough insulin to meet the body’s demands resulting in hyperglycemia. As a result of increased glucose in the liver, the liver begins to malfunction and release glucose at inappropriate times, thereby worsening hyperglycemia. Adding to the problem, glucose and fat metabolism is altered in adipose tissue, which is generally abundant in those with DM type 2. (Lewis et al., 2011)
There is a strong family genetic predisposition for this condition, specifically with the Human Leukocyte Antigen (HLA) genes DR3, DQ2 and DQ8. The Caucasian population and people of European descent experience celiac disease. Moreover, women seem to have a higher prevalence than males for this illness. Incidence within the general population is 1 in 3,000 citizens. People from Mediterranean and African ancestries, Jews, and Asian cultures rarely suffer from this disease. Children can also be affected. Patients who suffer from celiac disease may also experience additional autoimmune diseases like arthritis, systemic lupus, sojourn syndrome, down syndrome, intestinal cancer, lactose intolerance, type I diabetes, intestinal insuffici...
Hepatitis B Virus (HBV) is a virus that attacks the liver. The virus is transmitted through blood and bodily fluids. This can occur through direct blood-to-blood contact, unprotected sex, use of contaminated needles, and from an effected mother to her newborn during the delivery process. The majority of people do not have noticeable symptoms when they are first infected with the HBV. People who do not know they are infected with the HBV, their body can respond in different ways. I learned that some of the common symptoms of Hepatitis B infection include fever, fatigue, muscle or joint pain, loss of appetite, mild nausea, vomiting, and dark-colored urine. Some of the serious symptoms that require immediate medical attention and maybe even hospitalization are: severe nausea and vomiting, yellow eyes and skin (jaundice), bloated or swollen stomach.
The cause of Crohn’s disease is unknown and there is no proof that the disease is caused by an infection. At the same time researchers have found that it is the result of an abnormal reaction by the body’s immune system. They think that in the disease the immune system fights bacteria, foods, and other substances that are actually harmless or beneficial to the body. The white blood cells that are released to fight off these substances multiply in the lining of the intestine and that’s what creates the inflammation. The inflammation in the digestive tract also involves other factors as well, such as: the gene the person has inherited in the person’s immune system and the environment. Research has also found that Crohn’s disease is not contagious.
The Hepatitis A Virus affects many different systems within the body. The first being the digestive system and the gastrointestinal system because Hepatitis A causes an acute liver infection. The liver’s job is to process nutrients, filter the blood and toxin from your body, and fight infections. It produces important blood components, proteins, and bile which helps you digest food. The liver also stores glucose and vitamins. The Hepatitis A Virus causes inflammation that interrupts the liver’s ability to perform these vital functions. Having a healthy liver is crucial to your health because it supports many other body systems. For example, one function of the liver is to produce bile which is needed to break down fats. The body stores bile in the gallbladder and then sends it to the beginning section of the small intestine. Bile is then combined with other digestive
Celiac disease is when the lining of the small intestine is damaged due to ingesting foods that contain gluten (WebMD, 2014). It is an autoimmune disorder which means, that the body attacks healthy cells and tissues by mistake. The body forms antibodies to gluten and this causes the attack on the small intestine. As a result, inflammation occurs and this damages the microvilli hairs within the small intestine (WebMD, 2014). Without villi, nutrients can no longer be absorbed. Gluten is a protein and is found in all grains except for corn and rice (Hoehn & Marieb, 2013, p.898). It is often found in foods such as anything with wheat, cookies, cakes, donuts, pizza, muffins, rye, and sometimes canned soups (Celiac Disease and Gluten sensitivity, 2014). Gluten can also be found in products. Medicines, lip balms, and vitamins are all products that gluten may be found in (NDDIC, 2012). As I explained, the small intestine is damaged as a result of celiac disease. The small intestine plays a big role in absorbing nutrients. Damage to the small intestine results in lack of nutrient absorption. Some of the nutrients included are fats, calcium, and iron (WebMD, 2014). This can become a serious issue and must not be left unattended. It can lead to the onset of other diseases such as neurological disorders, other immune disorders, and cancer (NFCA, 2014). Often times when one family member has celiac disease, other immediate family members have it as well. Celiac disease can affect anyone, no matter their age, race, or gender. About 1 in every 100 people has celiac disease (Hoehn & Marieb, 2013, p.898). This is equivalent to about 1% of the population nationally. There is no particular demographic group that is affected.
Crohn’s Disease and Ulcerative Colitis are both in a category of diseases called Inflammatory Bowel Diseases. This is a classification of disease in which inflammation forms in a part of the digestive tract, known as the gastrointestinal tract or GI tract, of the patient. The immune system then treats this area of inflammation as a foreign pathogen and attacks it. The causes of both of these diseases are currently unknown to the medical world.
Although much is yet unknown about Crohn's, there are several risk factors that are bring presented in current research. With a common occurrence between first degree relatives, there is a suggestion t...
In both the clinical experience and the class settings, we have learned how the process of DKA can be life threatening, the importance of following the recommended medical regimen, and the various food types. Financial constraints sometimes make it difficult for families and individuals with DM1to comply with the medical and dietary recommendations.
Several risk factors can be linked with the incidence of colorectal cancer. Age and hereditary factors are the most important factors on which an individual’s cannot able to manage. The probability of being affected by colorectal cancer is increases after the age of 40. More than 90% of colorectal cancer cases reported among people in the age greater than 50 and older (Fairley TL , 2006). In addition, a large number of environmental and behavioral risk factors can also contribute for the development of colorectal cancer; among these dietary factors are the major one (Fatima AH, 2009).
Hepatitis B, an infectious disease caused by the Hepatitis B virus (HBV, a DNA virus), was formerly called serum hepatitis, inoculation hepatitis and post-transfusion hepatitis. Infection with HBV may result in acute, fulminant or chronic hepatitis, sometimes even resulting in a chronic asymptomatic carrier state, apart from hepatocellular carcinoma and liver cirrhosis (Davis 179). The disease is transmitted when an individual comes in contact with infected blood or objects. It may also be transferred from an infected mother to her infant either during or after birth (Zuckerman et al. 211). Transmission may also occur by accidental inoculation from infected needles and hospital equipment, intravenous drug abuse, body piercing, tattooing, and mouth-mouth kissing (Zuckerman et al. 210). The risk of Hepatitis B is particularly high in individuals with multiple sex partners, and in homosexuals. The HBV virus occurs in morphologically different forms in the serum of infected individuals. HBV infection has an incubation period of about 75 days. Systemic symptoms of the disease include fatigue, fever, dyspepsia, arthralgia, malaise, and rash, while local symptoms include hepatomegaly, jaundice, dark urine, and pale stools (Davis 179; Zuckerman et al. 210).
...e in vertebrates. Glycoproteins in the cell wall of yeasts and fungi are known to bear phosphodiester-linked glycans that are generated by a process involving phosphorylation on the C6 position of mannose (28). It is interesting that -DG, which is well conserved as an epithelial cell-surface protein from mammals to lower vertebrates, is likewise modified by this ancient type of cell surface glycosylation. A recent study has shown that the most severe form of CMD—WWS—is a genetically heterogeneous disease. Moreover, only 40% of WWS cases are explained by mutations in known CMD-causative genes (POMT1, POMT2, POMGNT1, FCMD, FKRP and LARGE) (28). It is quite likely that a defect in the phosphorylation of O-linked mannose results in severe CMD, and thus our findings provide a new target to be used for the discovery of mutations in novel genes responsible for WWS.
This disease is characterized by autoantibodies against intrinsic factor producing cells in the stomach (atrophic gastritis). Intrinsic factor is an important molecule that binds to vitamin B12 in the stomach, allowing the vitamin B12/intrinsic factor complex to become absorbed in the small intestine. Other disorders associated with B12 deficiency include celiac disease and inflammatory bowel disease – this occurs as a result of malabsorption. Individuals that have undergone bowel resection of the stomach or small intestine (e.g., ileum) are also at increased risk.
...apter 362. Glycogen Storage Diseases and Other Inherited Disorders of Carbohydrate Metabolism. In D.L. Longo, A.S. Fauci, D.L. Kasper, S.L. Hauser, J.L. Jameson, J. Loscalzo (Eds), Harrison's Principles of Internal Medicine, 18e. Retrieved January 21, 2012 from http://www.accessmedicine.com/content.aspx?aID=9144477.