Question

Activity on Digestive System

Make a concept map that show the parts and function of the digestive system and BRIEFLY discuss your concept map. upload your work here in canvas.

Give at least 3 most common diseases related to Digestive System and give the 4 aspects of disease(Etiology, Pathogenesis, Morphologic Changes, and Clinical Manifestation) to each diseases you give.

REPRODUCTIVE SYSTEM:

Make a concept map that show the parts and function of the reproductive system and BRIEFLY discuss your concept map. upload your work here in canvas.

Give at least 5 most common diseases related to male and female reproductive system and give the 4 aspects of disease(Etiology, Pathogenesis, Morphologic Changes, and Clinical Manifestation) to each diseases you give.

MS Word

Answer 1

GERD: GASTROESOPHAGEAL REFLEX DISEASE

Etiology-

Occasional acid reflux is quite common, often occurring as a result of overeating, lying down after eating, or eating particular foods.

However, recurrent acid reflux, diagnosed as GERD, typically has other causes and risk factors and can have more serious complications.

Gastroesophageal reflux disease occurs in people of all ages, and sometimes for unknown reasons.

In short, GERD occurs when the sphincter at the bottom of the esophagus becomes weak, or opens when it should not.

GERD occurs more commonly in people who are:

• overweight or obese because of increased pressure on the abdomen
• pregnant, due to the same increased pressure
• taking certain medications, including some asthma medications, calcium channel blockers, antihistamines, sedatives, and antidepressants
• smoking, and being exposed to second-hand smoke.

Pathogenesis-

Gastro-oesophageal reflux disease is a condition in which the reflux of gastric contents into the oesophagus provokes symptoms or complications and impairs quality of life. Typical symptoms of gastro-oesophageal reflux disease are heartburn and regurgitation but gastro-oesophageal reflux disease has also been related to extra-oesophageal manifestations, such as asthma, chronic cough and laryngitis. The pathogenesis of gastro-oesophageal reflux disease is multifactorial, involving transient lower oesophageal sphincter relaxations and other lower oesophageal sphincter pressure abnormalities. As a result, reflux of acid, bile, pepsin and pancreatic enzymes occurs, leading to oesophageal mucosal injury. Other factors contributing to the pathophysiology of gastro-oesophageal reflux disease include hiatal hernia, impaired oesophageal clearance, delayed gastric emptying and impaired mucosal defensive factors. Hiatal hernia contributes to gastro-oesophageal reflux disease by promoting lower oesophageal sphincter dysfunction. Impaired oesophageal clearance is responsible for prolonged acid exposure of the mucosa. Delayed gastric emptying, resulting in gastric distension, can significantly increase the rate of transient lower oesophageal sphincter relaxations, contributing to postprandial gastro-oesophageal reflux disease. The mucosal defensive factors play an important role against development of gastro-oesophageal reflux disease, by neutralizing the backdiffusion of hydrogen ion into the oesophageal tissue. While the pathogenesis of oesophageal symptoms is now well known, the mechanisms underlying extra-oesophageal airway manifestations are still poorly understood. Two hypotheses have been proposed: direct contact of gastric acid with the upper airway and a vago-vagal reflex elicited by acidification of the distal oesophagus, leading to bronchospasm. In conclusion, gastro-oesophageal reflux disease can be considered as the result of a complex interplay of factors, all promoting the contact of gastric acidic contents with the oesophageal mucosa, leading to different degrees of oesophageal damage.

Morphological changes: Pathologists are supposed to confirm the presence of morphological changes induced by gastroesophageal reflux. Traditional evaluation of injury, inflammatory and reactive changes of esophageal squamous epithelium lacks both sufficient sensitivity and specificity, and thus the modern diagnostic focuses on chronic metaplastic changes of esophageal mucosa defined as any mucosal type proximal to the upper border of oxyntic mucosa (also called fundic mucosa of the stomach). In the setting of gastroesophageal reflux the esophageal mucosa, under normal conditions lined with squamous epithelium, undergoes columnar metaplasia. According to morphology and immunophenotype of columnar cells, the columnar metaplasia may be further subdivided to oxyntocardiac mucosa, cardiac mucosa, intestinal metaplasia, and an intermediate type of cardiac mucosa expressing intestinal transcription factor CDX2, but devoid of goblet cells. The latter two mucosal types are currently thought to represent the most probable candidates for neoplastic transformation, whereas oxyntocardiac mucosa is believed to represent a stable compensatory change with no risk of further progression. An evaluation of dysplastic changes (intraepithelial neoplasia) in the setting of columnar lined esophagus necessitates correlation with the second opinion of a GI expert to prevent potentially harmful under- or over-treatment of the patient. Regarding invasive adenocarcinoma, the pathologist should avoid overdiagnosis of the infiltration of the space between the two layers of columnar lined esophagus - associated split muscularis mucosae as invasion of submucosa, as it is associated with different prognosis.

Clinical manifestations: Gastroesophageal reflux disease (GERD) is associated with a set of typical (esophageal) symptoms, including heartburn, regurgitation, and dysphagia. ... In addition to these typical symptoms, abnormal reflux can cause atypical (extraesophageal) symptoms, such as coughing, chest pain, and wheezing.

Etiology : The most common causes of peptic ulcers are infection with the bacterium Helicobacter pylori (H. pylori) and long-term use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) (Advil, Aleve, others). Stress and spicy foods do not cause peptic ulcers.

Pathogenesis :

Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer.

In the event of acid and pepsin entering the epithelial cells, additional mechanisms are in place to reduce injury. Within the epithelial cells, ion pumps in the basolateral cell membrane help to regulate intracellular pH by removing excess hydrogen ions. Through the process of restitution, healthy cells migrate to the site of injury. Mucosal blood flow removes acid that diffuses through the injured mucosa and provides bicarbonate to the surface epithelial cells.

• Zollinger-Ellison Syndrome
  • Zollinger-Ellison Syndrome is characterized by enormous increases in stomach acid secretion which overwhelms otherwise normal mucosal defenses.

Morphological changes:

The characteristic histological finding of PUD is full ulceration of the gastric or small intestinal mucosa to the level of the submucosa. Although the term ulceration typically refers to any erosion of the surface epithelium, the term "Peptic Ulcer" is reserved for deeper extents of erosion, into the submucosa. Such a special meaning of "Ulcer" in the gastric and small intestinal context is used as purely epithelial erosions are healed rapidly whereas deeper erosions into the submucosa typically take weeks or months to heal. Classically, peptic ulcers display a smooth base and perpendicular, punched out margins. They must be distinguished from gastric carcinomas of 'excavated' morphology which display an irregular base and heaped-up margins. Nearly all small intestinal ulcers occur in the first part of the duodenum and are five times more common that gastric ulcers.

Clinical menufestaion :

Peptic Ulcers classically present with a gnawing or aching epigastric pain that is relieved with intake of food or antacids; however, vomiting and weight loss can occur. Disease is usually remitting and relapsing over many years. The most feared complications are lower GI bleeding with attendant melena and coffee-ground hematemesis or bowel perforation which can be serious to fatal. Thankfully, neoplastic transformation of the alimentary mucosa due to peptic ulcers does not occur.

IBD (INFLAMMATORY BOWEL DISEASE:

Etiology & Pathophysiology:

IBD is a disease with an unknown cause. Some agent or a combination of agents -- bacteria, viruses, antigens -- triggers the body's immune system to produce an inflammatory reaction in the intestinal tract. Recent studies show some combination of hereditary, genetic, and/or environmental factors may cause the development of IBD. It could also be that the body's own tissue causes an autoimmune response. Whatever causes it, the reaction continues without control and damages the intestinal wall, leading to diarrhea and abdominal pain.

• Genetic susceptibility: As of 2015, 163 IBD-associated gene variants had been discovered. The risk for developing IBD has a positive correlation with gene number; however, gene presence alone accounts for approximately 25% of IBD cases, suggesting that the manifestation of IBD is influenced by the interaction of these genes with each other or with environmental factors.⁷
• Ethnicity: White Northern European and North American populations have the highest IBD prevalence. The lowest prevalence is found in the populations of continental Asia.⁸
• Infection: Gastrointestinal infections confer an increased risk for IBD development, particularly acute gastroenteritis caused by Salmonella, Campylobacter, and Shigella.^9,10 Although the risk is highest in the year following infection, a 2009 cohort study showed that exposed subjects had an elevated risk throughout the 15-year study period.¹⁰
• Environment: A variety of environmental factors have been linked to IBD, particularly those that correspond to a Westernized environment and lifestyle. Of these, smoking, gut microbiota, diet (high-fat, high-sugar), and medications (early and frequent antibiotic exposure in the first years of life) have the strongest supporting evidence for links to IBD.

Morphological changes: Recent ultrastructural investigations revealed early epithelial lesions in Crohn’s disease, while a specific morphological pattern was not identifiable. An increase in plasma cells, lymphocytes, macrophages, mast cells, eosinophilic and neutrophilic granulocytes, as well as focal edema and inflammation of tissue structures was seen in the lamina propria, submucosa and deeper layers. The results are consistent with the frequent discussion about a pathogenetically significant defect of the mucosal ‘barrier function’, which consists of mechanical, cellular, humoral, immunological and nonimmunological mechanisms, including different histotopographically defined lines of defense of the epithelium and lamina propria. An intact epithelial layer plays an important role as the first line of defense. It is evident that components of the epithelial barrier (absorptive cells, goblet cells, Paneth cells, M cells) show ultrastructural signs of alteration or injury, while the primary agent or event remains unknown. Another pathomechanism would be a preexisting defect in intestinal ‘barrier function’. Such a defect would result in an increased uptake of, or an inadequate immune reaction to, ubiquitously occurring antigens/agents (with genetic predisposition). However, no primary defect of epithelial or inflammatory cells has been definitely identified so far. Direct toxic damage of tissue secondarily introducing the inflammatory changes is also possible. Although the morphological alterations in Crohn’s disease are not yet clearly understood and exactly interpreted, transmission electron microscopy has been helpful in defining early lesions and has led to further knowledge about the pathogenesis of this disease.

Clinical menufestaion:

Signs and symptoms that are common to both Crohn's disease and ulcerative colitis include:

• Diarrhea.
• Fever and fatigue.
• Abdominal pain and cramping.
• Blood in your stool.
• Reduced appetite.
• Unintended weight loss.

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