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GI disorders pt 1
patho exam 3
| Question | Answer |
|---|---|
| Parts of the GI tract | mouth, esophagus, stomach, liver, gallbladder, small intestine, pancreas, large intestine, cecum, ileocecal valve, rectum, anus |
| salivary amylase | digests carbs |
| oral cavity | food gets chemically and mechanically digested |
| esophagus | mucosa contracts and retracts in peristalsis movements |
| stomach | vitamin B12 and alcohol is absorbed, proteins are chemically digested in stomach by pepsin |
| large intestine | where most of vitamins and water are absorbed |
| small bowel/intestine | macronutrients absorbed |
| four cardinal signs and symptoms of upper and lower GI system disorders | pain, altered ingestion, altered mobility, bleeding |
| digestive pathway of esophagus | food and liquids enter the mouth, voluntary transport of food and liquids, involuntary transit to the stomach |
| what happens when food and liquids enter the mouth? | mastication (mechanical) and addition of salivary enzymes (chemical) |
| voluntary transport of food and liquids | positioned at back of throat for esophageal entry, pushed into esophagus |
| common manifestations of esophageal defects | pain, alteration in ingestion, and/or bleeding |
| dysphagia | difficulty of swallowing |
| what do most problems with esophagus result in? | dysphagia |
| causes of dysphagia | neurological deficit, muscular disorder, mechanical obstruction |
| results/presentation of dysphagia | pain with swallowing, inability to swallow larger pieces of solid material, difficulty swallowing liquids |
| Acquired causes of dysphagia | fibrosis, compression, diverticulum |
| fibrosis of esophagus | fibrous tissue replaces smooth muscle |
| compression causing dysphagia | mass or tumor in esophagus |
| diverticulum causing dysphagia | fold in esophagus and food gets accumulated, decreases size of passage in esophagus |
| causes of dysphagia esophageal atresia | congenital atresia, congenital tracheoesophageal fistula, neurologic damage to cranial nerves V, VII, IX, X and XII, achalasia |
| congenital atresia | born with; developmental defect-tube with blind ends |
| congenital tracheoesophageal fistula | developmental defect- connection between esophagus and trachea, food and liquids can move into lungs |
| neurologic damage to cranial nerves V, VII, IX, X and XII | control muscles of mastication and affect ability of digestion |
| achalasia | loss of peristalsis in lower esophagus and food collects |
| esophageal rings | A ring, B ring (Schatzki ring if symptomatic), C ring |
| A ring | transient, smooth muscle ring above the vestibule |
| B ring (Schatzki ring if symptomatic) | thin, mucosal ring, at gastroesophageal junction, associated with hiatal hernia |
| C ring | diaphragm indentation, associated with hiatal hernia |
| webs and rings | thin membranes or folds that narrow the esophagus |
| cause of webs and rings | gastroesophageal reflux, iron-deficiency anemia, and autoimmune diseases |
| treatment of webs and rings | dietary restrictions (soft food), endoscopic dilation therapy |
| What is esophageal cancer primarily? | squamous cell carcinoma |
| Where is esophageal cancer most common? | distal esophagus |
| What occurs in later stages of esophageal cancer? | severe dysphagia |
| What kind of prognosis does esophageal cancer have? | poor prognosis due to late manifestation |
| esophageal cancer is associated with chronic irritation due to? | chronic esophagitis, achalasia, hiatal hernia, alcohol abuse and smoking |
| hiatal hernia | part of stomach protrudes into the thoracic cavity |
| types of hiatal hernia | sliding hiatal hernia, paraesophageal (rolling) hiatal hernia |
| sliding hiatal hernia | part of stomach pushes through diaphragm |
| paraesophageal (rolling) hiatal hernia | top part of the stomach rolls up through the diaphragm into the chest cavity, alongside the esophagus |
| hiatal hernia | part of the stomach protrudes into the thoracic cavity |
| hiatal hernia removal | easy to remove with surgery |
| hiatal hernia etiology | multifactorial, may involve genetic link |
| hiatal hernia pathogenesis | herniation of stomach through esophageal hiatus of the diaphragm, lower esophageal sphincter (LES) permits reflux of gastric contents |
| hiatal hernia manifestations | may be asymptomatic, frequently involves symptoms of gastroesophageal reflux, type IV paraesophageal hernia may produce dyspnea, reduced exercise tolerance, syncope, may cause chronic esophagitis |
| hiatal hernia signs | heartburn or pyrosis, frequent belching, increase discomfort when laying down, substernal pain that may radiate to the shoulder and jaw |
| hiatal hernia treatment | medications for symptomatic gastric reflux, surgery may be indicated |
| types of esophagitis | eosinophilic esophagitis, radiation esophagitis, corrosive esophagitis, pill esophagitis |
| eosinophilic esophagitis etiology | cause unknown; many associated factors |
| radiation esophagitis etiology | treatment of thoracic cancers; exacerbated by chemotherapeutic agents |
| corrosive esophagitis etiology | ingestion of strong alkaline or acid substances |
| pill esophagitis etiology | swallowed pill lodges transversely in esophageal lumen and causes inflammation |
| esophagitis pathogenesis | irritation to and inflammation of esophageal tissues lead to esophageal damage |
| esophagitis manifestations | vary based on etiology |
| esophagitis treatment | varies based on etiology, thorough history and physical exam is required |
| esophageal diverticula | formation of diverticulum that can be due to webs on mucosa of upper esophagus or diseases such as TB |
| what is esophageal diverticula a risk factor for? | esophageal cancer |
| esophageal diverticula etiology | acquired condition, most common cause: impaired esophageal motility, may be caused by traction on esophagus due to inflammatory disease of mediastinum (e.g., tuberculosis) |
| esophageal diverticula pathogenesis | pressure increases- esophageal lumen, esophageal lumen, esophageal mucosa protrudes through weakened esophageal wall and produces outpouching |
| esophageal diverticula manifestations | most often asymptomatic (based on size), manifestations vary based on location of diverticula, may produce dysphagia and heartburn |
| esophageal diverticula treatment | treatment depends on size and location, surgical intervention may be needed for large diverticula |
| activity of the stomach | mechanical activity: contracts and relaxes- has 3 layers of smooth muscle |
| what does the stomach secrete to digest proteins? | pepsin |
| What allows pepsin to work? | HCl |
| main categories of stomach disorders | disorders of secretion, disorders of motility |
| disorders of the stomach associated cardinal GI symptoms | Pain, altered ingestion, altered digestion, gastrointestinal tract bleeding |
| What happens when ulcer damages the walls of the stomach? | fluid of stomach will move to surrounding organs, and damage them because the pH of the fluid is too high |
| peptic ulcer disease etiology most common | H. pylori infection and NSAID use |
| peptic ulcer disease etiology contributing factors | smoking, excessive alcohol use, drug use, emotional stress, and psychosocial components |
| peptic ulcer disease pathogenesis | increased gastric acid secretion or a weakened mucosal barrier leads to mucosal erosion or ulceration of GIT |
| peptic ulcer disease common manifestations | epigastric pain and dyspepsia (upset stomach) |
| peptic ulcer disease common complications | bleeding, perforation, obstruction |
| peptic ulcer disease treatment | identify causative factor (and stop it), H.pylori- triple or quadruple therapy (antibiotics can kill), NSAID induced- H2 receptor antagonist and cease NSAID |
| gastritis | inflammation of stomach wall, can cause ulceration |
| infection induced acute gastritis etiology | H. pylori |
| drug induced acute gastritis etiology | NSAIDs, steroids, some chemotherapeutic drugs, alcohol, and iron supplements |
| ulcerohemorrhagic actue gastritis etiology | physiologic stress and ischemic changes caused by shock, hypotension |
| Why can hypotension cause gastritis? | when blood pressure is low the body diverts blood supply, digestive system is one of the areas that doesn't get blood |
| infection-induced chronic gastritis etiology | H. pylori |
| etiology of chronic gastritis | chemical and causative agents, autoimmune disease |
| chemical and causative agents of chronic gastritis | NSAIDs, excessive alcohol ingestion, radiation exposure |
| autoimmune diseases that can cause chronic gastritis | crohn disease, wegener granulomatosis, sarcoidosis |
| acute gastritis pathogenesis | acute imbalance between mucosal injury and repair mechanisms, development of mucosal hyperemia and erosive changes with histologic presence of inflammation |
| chronic gastritis pathogenesis | begins with superficial gastritis, progresses to atrophic gastritis, advances to gastric atrophy, gastric glandular structures are lost and/or metaplasia, gastric atrophy is precursor to gastric cancer |
| gastritis manifestations | most often asymptomatic or report mild dyspepsia, potential symptoms may include abdominal pain or upset, burning sensation in chest or upper abdomen, feeling of fullness, bloating, belching and reflux |
| more severe symptoms of gastritis | nausea, vomiting, GI bleeding, fever and weight loss |
| acute gastritis treatment | elimination of causative agent or exacerbating factors, eradication of H. pylori infection if indicated, medications to treat dyspepsia, surgical intervention for GI bleeding |
| chronic gastritis treatment | elimination of causative agent or exacerbating factors, eradication of H. pylori infection if indicated, medications to enhance protection of gastric mucosa, acupuncture, surgical intervention for GI bleeding |
| gastric outlet obstruction etiology | includes gastric, duodenal, and/or extraluminal pathology, malignancies of digestive organs, surgical and interventional induced obstructions, metastatic cancer |
| gastric outlet obstruction pathogenesis | mechanical obstruction in the pyloric region |
| gastric outlet obstruction manifestations | abdominal pain, distention or bloating; vomiting, diarrhea, and weight loss; may include early satiety and nausea |
| gastric outlet obstruction treatment benign cases | nasogastric tube suction, medications to suppress gastric acid production, IV fluid and electrolyte replacement, nutritional supplementation, trial liquid diet, endoscopic balloon dilation or surgery |
| gastric outlet obstruction treatment malignant cases | based on underlying case; may include stenting, chemotherapy, endoscopic balloon dilation, or surgery |
| gastric outlet obstruction treatment advanced cancers | palliative procedures may be preferred |
| stomach cancer etiology | risk factors include H. pylori infection, cigarette smoking, high alcohol ingestion, excessive dietary salt, inadequate fruit and vegetable consumption, and pernicious anemia; high nitrate diet may also increase risk |
| stomach cancer pathogenesis | tumors or neoplasms in the stomach arise from gastric mucosa (adenocarcinoma- most common (about 85%) |
| stomach cancer manifestations | most common: weight loss and abdominal pain; may include dysphagia, nausea, early satiety, occult GI bleeding, and palpable abdominal mass |
| what are clinical manifestations of stomach cancer known as? | alarm features |
| what does stomach cancer treatment depend on? | cancer staging |
| stomach cancer treatment | upper endoscopy may be used for palliative procedures; may require endoscopic resection, radiation, chemotherapy, and/or surgical resection |
Created by:
camrynfoster