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patho
disorders of the upper and lower GI systems ch 42
| Question | Answer |
|---|---|
| four cardinal signs and symptoms of upper and lower GI disorders | pain altered indigestion altered motility bleeding |
| digestive pathway - mouth | food and liquid enters the mouth mastication (chewing and mechanical breakdown) and salivary enzymes (chemical breakdown) |
| digestive pathway - throat | voluntary transport of food and liquids, positioned at the back of the throat for esophageal entry, pushed back into the esophagus (swallowing) involuntary transit into the stomach (happens automatically without conscious control) |
| dysphagia | difficultly swallowing |
| causes of dysphagia | neurological deficit (mental status), muscular disorder (stroke weakness), mechanical obstruction |
| signs of dysphagia | pain with swallowing, inability to swallow larger pieces of solid food, difficultly swallowing liquids |
| aquired dysphagia | developed later in life, rather than from birth |
| fibrosis dysphagia | loss of smooth muscle due to the formation of excess scar tissue in the throat, esophagus, or surrounding structures, also narrowing the esophagus |
| compression dysphagia | difficulty swallowing due to pressure/compression on the esophagus from something outside the esophagus |
| diverticulum dysphagia | difficulty swallowing that results from the presence of a diverticulum (which is a pouch or sac that forms in the wall of the esophagus of undigested food), associated with bad breath |
| Esophageal atresia - dysphagia | refers to difficulty swallowing caused by a condition called esophageal atresia (EA) — a birth defect where the esophagus does not form correctly. |
| congenital atresia - dysphagia | a part of the digestive tract, usually the esophagus, does not fully develop or remains closed (atresia), results from a birth defect |
| congenital tracheoesophageal fistula - dysphagia | a birth defect where there is an abnormal connection (fistula) between the trachea (windpipe) and the esophagus (food pipe). |
| neurological damage to which CN can cause dysphagia | CN V, VII, IX, X, XII |
| achalasia - dysphagia | the lower esophageal sphincter (LES) — the muscle that normally opens to let food enter the stomach — fails to relax properly, and the muscles of the esophagus lose their normal movement (peristalsis), rare disorder |
| esophageal Webs and rings | thin membranes or folds that narrow the esophagus, can limit amount of food that gets by |
| causes of webs and rings | gastroesophageal reflux, iron deficiency anemia, and autoimmune diseases |
| Tx of webs and rings | dietary restrictions (soft food) endoscopic dilation therapy |
| esophageal cancer | primarily squamous cell carcinoma (most common distal esophagus) causes significant dysphagia in later stages, poor prognosis due to late manifestation |
| esophageal cancer associates with | associated with chronic irritation due to: -chronic esophagitis -achalasia -hiatal hernia -alcohol abuse and smoking |
| hernia | a condition where an organ or tissue protrudes through a weak spot in the muscle or connective tissue that surrounds it |
| hiatal hernia | part of the stomach protrudes into the thoracic cavity |
| hiatal hernia etiology | multifactorial, may involve a genetic link |
| hiatal hernia pathogenesis | herniation of stomach through esophageal hiatus of the diaphragm, lower stomach sphincter permits reflux of gastric contents |
| hiatal hernia CM | may be asymptomatic, symptoms of gastroesophageal reflux, Type IV paraesophageal hernia may cause dyspnea, reduces exercise tolerance, syncope, 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 Tx | meds for symptomatic gastric reflux surgery may be indicated |
| esophagitis different etiology types | eosinophilic esophagitis radiation esophagitis corrosive esophagitis pill esophagitis |
| eosinophilic esophagitis etiology | causes unknown, iatrogenic, many associated factors |
| radiation esophagitis | treatment of thoracic cancers; exacerbated by chemotherapeutic agents |
| corrosive esophagitis | ingestion of strong alkaline or acid substances |
| pill esophagitis | swallowed pill lodges transversely in esophageal lumen and causes inflammation |
| esophagitis pathogenesis | irritation to and inflammation of esophageal tissues lead to esophageal damage |
| esophagitis CM | varied based on etiology |
| esophagitis Tx | varied based on etiology thorough physical exam and history is required |
| esophageal diverticulitis | pockets of food build up in the esophagus |
| esophageal diverticulitis etiology | acquired condition, most common cause: impairs esophageal motility, may be caused by traction on esophagus due to inflammatory disease of mediastinum (ex. TB) |
| esophageal diverticulitis pathogenesis | pressure increases esophageal lumen esophageal mucosa protrudes through weakened esophageal wall and produces pouch |
| esophageal diverticulitis CM | mostly asymptomatic vary based on location of diverticula may produce dysphagia and heartburn |
| esophageal diverticulitis Tx | depends on size and location surgical intervention may be needed for large diverticula |
| disorders of the stomach | disorders of secretion (ex. pepsin) disorders of motility (ex. contraction) |
| associated cardinal GI symptoms | pain altered indigestion altered digestion GI tract bleeding |
| peptic ulcer disease | inflammatory disease that damages the lining, but the body can't replace the area so it causes an ulcer (alc can induce b/c its absorbed in the stomach) |
| peptic ulcer disease etiology | various causes most common: H. Pylori infection and NSAID use contributing factors: smoking, excessive alc use, drug use, emotional stress, and psychosocial components |
| peptic ulcer disease CM | epigastric pain and dyspepsia (upset stomach) bleeding, perforation, obstruction |
| peptic ulcer disease Tx | identify causing factor H. Pylori: triple or quadruple therapy NSAID - induced: H2 receptor antagonist and cease NSAID use |
| gastritis | inflammation of the stomach wall, usually comes with ulcers can be acute or chronic |
| actue gastritis etiology | -infection induces - H. Pylori -drug induced - NSAIDs, steriods, some chemo drugs, alc, iron supplements -ulcerohemorrhagic: physiologic stress and ischemia changes caused by shock, hypotension |
| chronic gastritis etiology | -infection induced: H. pylori -chemical and caustic agents (NSAIDs, excessive alc, radiation exposure) -autoimmune disease (Crohn disease, Wegener granulomatosis and sarcoidosis) |
| blood pressure effect on gastritis | hypotension can induce because blood perfusion decreased in the stomach so cells get hypoxic which causes an inflammatory response |
| acute gastritis pathogenesis | acute imbalance between mucosal injury and repair mechanisms development of mucosal hyperemia and erosive changes with histologic presence of inflammation |
| chronic gastritic pathogenesis | begins with superficial gastritis progressed to atrophic gastritis advances to gastric atrophy gastric glandular structures are lost and/or metaplasia gastric atrophy is precursor to gastric cancer |
| acute and chronic gastritis CM | -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 gastritis CM | -more severe symptoms include nausea, vomiting, GI bleeding, fever, and weight loss |
| acute gastritis Tx | elimination of causative agent or exacerbating factor eradication of H. Pylori infection if indication medications to treat dyspepsia surgical intervention for GI bleeding |
| chronic gastritis Tx | elimination of causative agent or exacerbating factor eradication of H. Pylori infection if indication medications to enhance protection of gastric mucosa acupuncture surgical intervention for GI bleeding |
| pyloric stenosis | pyloric sphincter doesn't open common in newborns throws up all the time |
| 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 pathogensis | mechanical obstruction in pyloric region |
| gastric outlet obstruction CM | abdominal pain, distention or bloating vomiting, dehydration, and weight loss may include early satiety and nausea |
| gastric outlet obstruction Tx for 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 Tx for malignant cases | based on underlying cause; may include stenting, chemotherapy, endoscopic balloon dilation, or surgery advanced cancers: palliative procedures may be preferred |
| stomach cancer risk. factors and etiology | H. Pylori infection, cigarette smoking, high alc ingestion, excessive dietary salt, inadequate fruit and vegetable consumption, and pernicious anemia. high-nitrate diet may also inc risk |
| stomach cancer pathogenesis | tumors or neoplasms in the stomach arise from gastric mucosa (adenocarcinoma is most common ~80%) |
| Stomach cancer CM | CMs are known as alarm features most common: weight loss and abdominal pain may include: dysphagia, nausea, early satiety, occult GI bleeding, and palpable abdominal mass |
| stomach Tx | depends on cancer staging upper endoscopy may be used for palliative procedures may require endoscopic resection, radiation, chemotherapy, and/or surgical resection |
| disorders of the small intestines, large intestines, and rectum | absorption in the lower GI tract chyme enters small bowel via the duodenum bowel is primary site of absorption (nutrients and vitamins, electrolytes, water) |
| impaired motility may cause multiple alterations in Sm. I, Lg I, rectum | malabsorption, malnutrition, dehydration |
| inflammatory bowel disease | chronic inflammatory disorder involving the GIT |
| two major IBD disorders | ulcerative colitis (UC) Crohn disease (CD) |
| ulcerative colitis (UC) | localized on colon chronic inflammatory condition limited to mucosal layers of colon characterized by relapsing and remitting episodes of inflamm. developes continuous lesion |
| Crohn Disease (CD) | whole GI tract chronic inflammation condition may involve any portion of the GI tract characterized by transmural inflammation of the bowel most commonly affects ileum and proximal colon lesions are not always continuous (skip lesions) |
| manifestations of IBD (including UC and CD) | active: fever, loss of appetite, weight loss, fatigue, night sweats remission: symptoms may decrease and even disappear |
| inflammatory bowel disease etiology | not completely understood appears to involve environmental factors, microbial imbalance in the gut, genetic susceptibility, and inappropriate immune response |
| inflammatory bowel disease pathogenesis | -inflam. of the mucosal and submucosal layers of colon -continuous lesion of inflam. may extend into the proximal colon or may affect the whole colon (pancolitis) -bowel changes in epithelial damage, inflam., crypt abscesses, and loss of goblet cells |
| inflammatory bowel disease CMs | -bloody and/or mucoid, diarrhea, dehydration, and anemia -crampy abdominal pain, pain with defecation, and tenesmus -involvement of the rectum may also lead to constipation |
| inflammatory bowel disease etiology | not completely understood appears to involve environmental factors, microbial imbalance in the gut, genetic susceptibility, and inappropriate immune response |
| inflammatory bowel disease pathogenesis | inflammation and destruction of the bowel |
| inflammatory bowel disease CMs | nausea, vomiting, diarrhea with or without blood abdominal pain and pain with defecation due to anorectal fissures complications include bowel structures, obstructions, perforations in the bowel and intra-abdominal abscesses |
| treatment guidelines for IBD | -optimize QOL by treating acute processes -induce and maintain remission -decrease use of corticosteroids -whole nutrition and healthy lifestyle -anti-inflamm. agents, immunosuppressants, anti-tumor necrosis agents, antibiotics, probiotics -surgery |
| appendicitis etiology | not fully understood believed to be due to appendiceal obstruction |
| appendicitis pathogenesis | increased intraluminal pressure and/or excessive inflammation can inhibit blood flow causing vascular compromise to the affected tissue. appendix may become gangrenous and can rupture |
| appendicitis obstruction can lead to | bacterial over growth and luminal distention |
| appendicitis CM | cramping abdominal pain, tenderness with palpation of the RLQ, nausea or vomiting, increased WBC count, and low grade fever |
| appendicitis Tx | gold standard: laparoscopic surgery |
| etiology of bowel obstruction | most often due to adhesions (75% of cases) other: hernia, adhesions neoplasm/tumor, gallstone ileus, intussusception, volvulus |
| bowel obstruction pathogenesis | -intestinal tract blockage develops due to various etiologies -up to 80% are small bowel obstructions (SBOs) -obstruction may be partial or complete -complications include strangulation and bowel necrosis (may lead bowel perforation, sepsis, and death) |
| bowel obstruction CM | -abdominal pain, nausea, vomiting, abdominal distention, and inability to satisfactorily pass gas or stool -hyperactive, high-pitched bowel sounds if present -bowel sounds will be absent if ileus develops |
| bowel obstruction Tx | -medical management includes gastric decompression, intravenous fluids, and serial physical and serum tests -surgery may be indicated if medical management fails -if strangulation and bowel ischemia present - emergent surgery needed |
| types of bowel obstruction | herniation adhesions intussusception volvulus |
| diverticular disease | diverticula: -diverticulosis -diverticulitis |
| diverticula | small outpouchings (herniations) of colonic mucosa protrude through muscle layers of the colon wall |
| diverticulosis | diverticula without evidence of inflammation |
| diverticulitis | inflamed diverticula |
| diverticular disease etiology | associated factors include alterations in the colonic wall resistance, alterations in colonic motility, low-fiber diets, NSAID use, advanced age, obesity, and lack of exercise |
| diverticular disease CMs | sudden constant abdominal pain in the left lower quadrant abdominal distention and nausea diarrhea, constipation, and decreased appetite fever, tachycardia, and hypotension |
| diverticular disease Tx | >outpatient management: clear liquid diet, oral broad spectrum Abx, and follow-up care >inpatient Tx required if suspected peritonitis or complications >inpatient Tx: administration of IV fluids and Abx, no food or drink by mouth >surgery possibly |
| Hemorrhoids | can be internal or external a swollen vein or group of veins in the region of the anus |
| hemorrhoidal disease etiology | straining during BM risk factors: conditions that increase intra-abdominal pressure and/or impede venous return (pregnancy or portal HTN) |
| hemorrhoidal disease pathogenesis | abnormal enlargement of the three vascular mucosal cushions (hemorrhoidal cushions) that assist with anal continence |
| hemorrhoidal disease CM | Hematochezia, itching, perianal discomfort and soiling Large hemorrhoids may produce sensations of incomplete BM |
| hemorrhoidal disease Tx | >stages I and II: diet modifications, topical glucocorticoids, vasoconstrictors, analgesics, and sclerotherapy >stages III and IV:procedural interventions (hemorrhoidal banding and surgical hemorrhoidectomy) |
| adenomas (polyps) of the colon | precursors to most colorectal cancers (CRCs) benign tumors form in glandular structures in intestinal mucosal epithelium |
| colon cancer | malignant growth or tumor results from division of abnormal cells in the colon occurs in ascending, transverse, or descending colon |
| rectal cancer | malignant growth or tumor located up to 15 cm from anal opening |
| pathogenesis of CRCs | genetic abnormalities plus environmental factors |
| conventional adenomas and sessile serrated polyps | commonly developmental pathways chromosomal instability pathway micro-satellite instability pathway |
| CRCs modifiable risk factors | obesity sedentary lifestyle smoking moderate to heavy alcohol ingestion heavy consumption of red and processed meats low consumption of fruits and vegetables |
| CRCs hereditary and medical risk factors | family Hx of CRCs and/or polyps inflammatory bowel disease (UC or CD) type 2 diabetes mellitus aging |
| CRCs protective factors | diet rich in whole grain fiber use of NSAIDs (ex: aspirin) |
| CMs of early CRC | typically asymptomatic Hematochezia and symptoms of anemia change in bowel habits weight loss and fatigue generalized or localized abdominal pain |
| physical assessment of advanced CRC | distended abdomen palpable abdominal mass and lymph nodes rectal cancer - palpable mass on digital exam |
| CM of advanced CRCs: RIGHT sided cancers (ascending colon) | usually silent may be painful may develop palpable mass in RLQ tumors stay to one side of the colon wall unlikely to develop intestinal obstruction dark red blood in stool |
| CM of advanced CRCs: LEFT sided cancers (descending colon) | tumors grow circumferentially around the colon stools may become long and pencil-like can lead to intestinal obstruction bright red blood in stool |
| screening for CRC | early detection is essential screening methods: lower GI endoscopy, fecal tests for occult blood and DNA testing for mutant genes screening recommendations: begin at age 50, but for individuals with predisposing genetic factors begin before age 50 |
| staging of CRC | >used to determine Tx >usually includes TNM classifications: tumor, lymph nodes, and metastases >endoscopy may be used for staging |
| Tx for CRC | depends on nature and metastasis of CRC surgery (most often used for CRC that hasn't spread, adenomas may be removed in endoscopy) if cancer extends beyond bowel wall: more interventions may: chemo w/ or w/o radiation, organ- or tissue- specific therapy |
Created by:
ago24