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GI disorders pt 2
patho exam 3
| Question | Answer |
|---|---|
| where does chyme enter the small bowel? | via the duodenum |
| What is the primary site of absorption? | bowel |
| What is absorbed in the bowel? | nutrients and vitamins, electrolytes, water |
| What kind of alterations can impaired motility cause? | malabsorption, malnutrition, dehydration |
| inflammatory bowel disease | chronic inflammatory disorder involving the GIT |
| two major IBD disorders | ulcerative colitis (UC), crohn disease (CD) |
| ulcerative colitis | chronic inflammatory condition, limited to mucosal layers of colon |
| what is ulcerative colitis characterized by? | relapsing and remitting episodes of inflammation |
| what does ulcerative colitis develop as? | a continuous lesion |
| crohn disease (CD) | chronic inflammatory condition, may involve any portion of the GI tract, lesions are not always continuous |
| What is crohn disease characterized by? | transmural inflammation of the bowel |
| What does crohn disease most commonly affect? | ileum and proximal colon |
| manifestations of IBD (including UC and CD): active | fever, loss of appetite, weight loss, fatigue and night sweats |
| manifestations of IBD (including UC and CD): remission | symptoms may decrease and even disappear |
| ulcerative colitis etiology | not completely understood, appears to involve environmental factors, microbial imbalance in gut, genetic susceptibility, and inappropriate immune response |
| ulcerative colitis pathogenesis | inflammation of mucosal and submucosal layers of colon, continuous lesions of inflammation may extend into the proximal colon or may affect the whole colon (pancolitis) |
| ulcerative colitis pathogenesis: bowel changes | epithelial damage, inflammation, crypt abscesses, and loss of goblet cells |
| ulcerative colitis manifestations | 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 |
| crohn disease etiology | not completely understood, appears to involve environmental factors, microbial imbalance in the gut, genetic susceptibility, and inappropriate immune response |
| crohn disease pathogenesis | inflammation and destruction of the bowel |
| crohn disease manifestations | nausea, vomiting, and diarrhea with or without blood; abdomical pain and pain with defecation due to anorectal fissures; complications include bowel strictures, obstructions, perforations in the bowel and intra-abdominal abscesses |
| treatment guidelines for IBD | optimize quality of life by treating processes, induce/maintain remission, decrease use of corticosteroids, wholesome nutrition and healthy lifestlye; anti-inflammatory agents, immunosuppressants, anti-tumor necrosis factor agents, antibiotics, probiotics |
| appendicitis etiology | not fully understood, believed to be due to appendiceal obstruction |
| what is obstruction of the appendix thought to lead to? | bacterial overgrowth and luminal distention |
| 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 treatment | gold standard- laparoscopic surgery |
| bowel obstruction etiology, most common | due to adhesions (75% of cases) |
| other causes of bowel obstruction | 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, obstruction may be partial or complete, complications include strangulation and bowel necrosis |
| what can complications of bowel obstruction lead to? | bowel perforation, sepsis, and death |
| bowel obstruction manifestations | abdominal pain, nausea, vomiting, abdominal distention, and inability to satisfactorily pass gas or stool; hyperactive, high pitched bowel sounds often present; bowel sounds will be absent if ileus develops |
| bowel obstruction treatment | 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 |
| adhesions | fibers don't relax and contract |
| intussusception | partial blockage of intestines |
| volvulus | twist in small intestines |
| 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 colonic wall resistance, alterations in colonic motility, low-fiber diets, NSAID use, advanced age, obesity, and lack of exercise |
| diverticular disease manifestations | sudden, constant abdominal pain in left lower quadrant, abdominal distention and nausea; diarrhea, constipation, and decreased appetite; fever, tachycardia, and hypotension |
| diverticular disease treatment: outpatient management | clear liquid diet, oral broad-spectrum antibiotics, and follow up care |
| diverticular disease treatment: inpatient treatment | required if suspected peritonitis or complications present; administration of intravenous fluids and antibiotics, no food or drink by mouth, surgery may be indicated |
| internal and external hemorrhoids | a swollen vein or group of veins in the region of the anus |
| hemorrhoidal disease etiology | straining during bowel movement, risk factors- conditions that increase intraabdominal pressure and/or impede venous return (pregnancy or portal hypertension |
| hemorrhoidal disease pathogenesis | abnormal enlargement of the three vascular mucosal cushions (hemorrhoidal cushions) that assist with anal continence |
| hemorrhoidal disease manifestations | hematochezia, itching, perianal discomfort and soiling; large hemorrhoids may produce sensation of incomplete evacuation |
| hemorrhoidal disease treatment stages I and II | diet modification, topical glucocorticoids, vasoconstrictors, analgesics, and sclerotherapy |
| hemorrhoidal disease treatment stages III and IV | procedural interventions (hemorrhoidal banding and surgical hemorrhoidectomy) |
| adenomas (polyps) of the colon | precursors to most colorectal cancers, 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 15cm from the anal opening |
| pathogenesis of CRC | genetic abnormalities plus environmental factors |
| conventional adenomas and sessile serrated polyps | commonly developmental pathways- chromosomal instability pathway, micro-satellite instability pathway |
| CRC 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 |
| CRC hereditary and medical risk factors | family history of CRC and/or polyps, IBD, type 2 diabetes, aging |
| CRC protective factors | diet rich in whole-grain fiber, use of NSAIDs |
| manifestations of early CRC | typically asymptomatic, potential manifestations: hematochezia and symptoms of anemia, change in bowel habits, weight loss and fatigue, generalized or localized abdominal pain |
| advanced CRC physical assessment | distended abdomen, palpable abdominal mass and lymph nodes, rectal cancer- palpable mass on digital exam |
| manifestations of right-sided cancers (ascending colon) | usually silent, may become 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 |
| manifestations of 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 for CRC | lower GI endoscopy, fecal test for occult blood and DNA testing for mutant genes |
| screening recommendations for CRC | begin screening at age 50, individuals with predisposing genetic factors begin screening earlier than age 50 |
| staging of CRC (national cancer institute classification) | used to determine treatment, usually includes TNM classification (tumor, lymph nodes, and metastases), endoscopy may be used for staging |
| stage 0 crc | in situ |
| stage 1 crc | extension to middle layer |
| stage 2 crc | extension to nearby tissue |
| stage 3 crc | extension beyond the wall |
| stage 4 crc | beyond colon wall to lymph and other organs |
| what does treatment for CRC depend on? | nature and metastasis of CRC |
| treatment for crc: surgery | most often used to treat CRC that has not spread, adenomas may be removed during endoscopy |
| treatment for CRC if cancer extends beyond the bowel wall | chemo with or without radiation, organ or tissue specific therapy |
Created by:
camrynfoster