An ulcer is caused due to damage the lining of the gut and exposed the underlying tissue. If we could see inside our gut, an ulcer seems like a small, red crater on the inside lining of the gut. stomach ulcer: Stomach ulcer is the type of peptic ulcer. A stomach ulcer is also often called a gastric ulcer. causes of stomach ulcer:
There is also strong acid released by the glands in the lining of the stomach which helps break down food into a more useable form and also aids in the destruction of most ingested bacteria. After the contents have successfully been broken down they are released into the small intestine. The small intestine is a 22 foot long tube that helps to break down the food with enzymes released from the pancreas and bile released form the liver. In this organ the process of Peristalsis is at work, pushing the food further and further through the small intestine towards the colon. These movements are stimulated by the presence of chyme.
This is important because before potentially harmful products are tested on humans, they should be tested on the worms. First, a pre-test hypothesis (Pau D’Arco is a stimulant) is made about what a certain extract (Pau D 'Arco) will do to the worms heart rate. A worm was chosen and put into a cup of conditioned (unchlorinated) water to sit for ninety seconds. The worm was very squirmy and active during the ninety seconds. It was put on a slide, and three separate tests were taken to determine the control group heart rate.
Stridor and respiratory distress are also noted due to the airway being obstructed. Epiglottitis can cause complete obstruction of the airway and death, so emergent treatment is essential. This diagnosis was ruled out because the patient’s symptoms are not consistent with this condition. The patient exhibits no signs of respiratory distress, drooling, or airway
To get oxygen into its body it defuses into the worm; almost like the oxygen is being pulled into it. From there blood vessels grab the oxygen gas while being circulated by the pumping of its hearts. Soon after, the oxygen is used up and becomes carbon dioxide gas. The gas then defuses, or gets pushed, out of the worm; making room for more
The frequency of this action make the sphincter weak, and the stomach acids begin repeatedly splashing up into the esophagus. Acid reflux can lead to bleeding and scarring of the esophagus. Lastly, many electrolytes such as sodium, chloride, and potassium deplete from the body, causing cardiac arrest, general weakness, and death in the most severe
The parasite infection can include domesticated animals such as dogs and cats, as well as wild animals. These are all capable of acting as reservoirs of the pathogen. Acute, intermediate, and chronic are the three phases of Chagas disease. Depending on the immunocompetence status of the patients these phases can show no symptoms of disease or can become life-threatening. At the entry wound swelling of the side of the face and eyelids may occur near the initial bite wound.
Kidney failure can also be caused by autoimmune disorders, such as lupus erythematosus. Of the many types of disease-causing, most causes of diabetes mellitus. According to Budiman, 45 percent of sufferers of kidney failure caused by diabetes mellitus, 28 percent by high blood pressure, glomerulonephritis by 9 percent, and 18 percent of other
Pylori infection is on a steep decline in most of the western countries mainly due to the success of combination therapies and improve personal hygiene and community sanitation to prevent re-infection. The situation is not improving in many of the developing countries due to failure of treatment regimes and emergence of durg resistance. The infection in some cases leads to chronic superficial gastritis, chronic active gastritis, peptic ulcer disease and gastric adenocarcinoma. Humans are the only important reservoir of H.Pylori. Children may acquire the organism from their parents (more often from the mother) or from other children.
Before haem iron can be absorbed, it must be hydrolysed from the globin part of haemoglobin or myoglobin; this is carried out by proteases in the stomach or small intestine. Once the haem is released from the globin, it is absorbed across the mucosal cells of the small intestine by haem carrier protein 1 (HPC1). Once absorbed, the haem molecule is hydrolysed into inorganic ferrous iron and protoporphyrin by haem oxygenase, and can be used by the intestinal cell, excreted or used by other tissues. Non haem iron must be released from food components in order to be absorbed, this process is aided by gastric secretions such as hydrochloric acid and proteases in the stomach and. Following its release from food, the non-haem iron is present in its ferric form in the stomach.
Necrotizing Fasciitis also known as flesh eating bacterial infection is a rapidly progressing fleshing eating disease which destroy muscle, fat and skin tissue. Flesh eating bacteria release toxin and destroy the surrounded tissue. This infection occurs in people with compromised immune system. The bacterias that caused this infection are Streptococcus pyogenes, Staphylococcus aureus, Vibrio vulnificus, Clostridium perfringens, Bacteroides fragilis, Aeromonas hydrophila. The infection usually begins locally by a trauma that allows the bacteria to enter the body.
This includes increased concentrations of heavy metals such as Mercury (Hg) and Lead (Pb) found in the liver tissue and/or chemical toxins such as man-made Polychlorinated biphenyls (PCBs) and dichlorodiphenyltrichloroethane (e.g. DDTs) and these are found in the blubber tissue of cetaceans.(Pierce et al. 2008; Jepson et al. 1999): To investigate the high proportion of Harbour porpoises dying from infectious disease, chemical sampling was undertaken in the liver/blubber tissue of the strandings to research the effects of PCBs earlier mentioned as well as heavy metals like Mercury (Hb). The amounts of these chemicals were examined in those individuals killed by infectious disease and those that were healthy and died from physical trauma.
Broad spectrum antibiotics tend to kill the bodies normal flora, which then allows bacterium’s like C. difficile to spread and grow rapidly in its vegetative state. Toxin A (enterotoxin) is then produced causing diarrhea, followed by toxin B (cytotoxin) which causes damage to the mucosal cells. Toxin A and B also induce the secretion of cytokines into host cells, which often cause an acute neutrophilic inflammatory infiltrate. Together, these toxins enable the interruption of tight junctions in the intestine and cause inflammation of the colon leading to an extensive amount of fluid secretion (diarrhea). A third toxin has recently been discovered in newer strains of this bacterium called the binary toxin.
After a great deal of research, it was revealed that in individuals that were infected with Helicobacter Pylori, antibodies were found in the bloodstream. Helicobacter Pylori are able to attach to cells as they go through the mucous layer of the stomach. When the bacterium enters the stomach, an enzyme called urease converts the stomach cells chemical urea into ammonia and carbon dioxide. The enzyme urease tends to trigger inflammation.