Lecture 13 Gastrointestinal System Flashcards
Upper and Lower GI Tracts
- upper: mouth, esophagus, stomach, and duodenum
- lower: small and large intestines
- 70-80% immune cells are in gut
- reduction in normal bacteria may interfere with immune function
Age and GI System
- benign before age of 50
- most common are constipation, incontinence, and diverticular disease
- increased tooth decay, decreased taste buds and sense of smell
- decrease in IF production results in decreased B12 absorption
- atrophic gastritis: chronic inflammation of stomach mucosa, can be result of H. pylori bacteria
Appendicitis
-inflammation of the vermiform appendix
-patho: obstruction of the lumen of the appendix (i.e., fecal mass)-mucus flow is blocked, which distends the organ, affects blood flow and causes severe pain
-bacterial infection
-as intraluminal pressure rises, venous stasis and ischemia ensues
-CM: pain, anorexia, vomiting, low grade fever usually within 12 hours of onset; constant pain may shift to McBurney’s pt which is 2/3 from umbilicus to ASIS
-aggravating factors include anything that increases intrabdominal pressure
-dx: elevated WBC count (>20K/mm3
;leukocytosis); pinch-an-inch test (increased pain when skinfold strikes peritoneum
-tx: appendectomy
-prognosis: good unless delayed diagnosis
SIFTT for Appendicitis
- client may present with symptoms of R thigh, groin pain, pelvic pain or referred pain to the hip
- ask the client to cough: localization of painful symptoms to the site of the appendix is typical
- assess for rebound tenderness
- pinch-an-inch test – over McBurney’s point
- if appendicitis is suspected, medical attention must be immediate
- heat is contraindicated
Botulism
- rare and potentially fatal paralytic illness, less rare in younger kids
- caused by clostridium botulinum
- patho: neurotoxins from bacteria resist gastric digestion and proteolytic enzymes and are readily absorbed into the blood from the proximal small intestine
- circulating toxins reach the cholinergic nerve endings at the myoneural junction and bind to the presynaptic nerve terminals
- flaccid paralysis is caused by inhibition of acetylcholine release from cholinergic terminals at the motor end plate (abolishes transsmision at NMJ)
- GI symptoms: prolonged bloody diarrhea leading to dehydration, weight loss, fever, nausea, and severe abdominal pain
- neurologic involvement: dysphagia, ptosis, difficulty breathing, dysarthria, cranial nerve palsies with visual changes, no sensory changes occur, motor weakness starts in face and neck then progresses to involve diaphragm, accessory muscles of breathing and extremities
- immediate administration of antitoxin prevents further binding of free botulinum toxin to the presynaptic endings
- untreated food botulism can be fatal within 24 hours of toxin ingestion
SIFTT for Botulism
- sudden onset of rapidly progressive symptoms associated with botulism is most likely to be reported to a Dr. rather than to a PT
- presentation of acute symmetric cranial nerve impairment followed by descending weakness or paralysis of the muscles in the extremities or trunk with or without back pain and dyspnea from respiratory muscle paralysis requires immediate medical referral
Crohn’s Disease
- one of the 2 major types of inflammatory bowel disease that may affect any part of the GI tract
- can affect all layers of intestine; diseased areas of intestine with normal intestine between with periods of exacerbation and remission
- lymphatic obstruction, infection, allergies, immune disorders, genetics
- patho: inflammation usually involves all layers of the bowel wall; inflammation is discontinuous so that segments of inflamed areas are separated by normal tissue in a skip pattern (skipping lesions) thick edematous tissue –> ulcerations in those areas; ulcerated granulated areas throughout bowel
- CM: malaise, diarrhea, pain in the right lower quadrant, generalized abdominal pain, and fever
- dx: fecal occult tests (blood in stool), small bowel X-ray, barium enema, sigmoidoscopy and colonoscopy
- tx: drug therapy, lifestyle changes (elimination of various foods), Sx
Diverticular Disease
- presence of outpouchings (diverticula) in the wall of the colon or small intestine (occur most commonly in sigmoid colon)
- mucosa and submucosa herniate through the muscular layers of colon
- multiple diverticula in resected section of colon weak spots in muscle layers of intestinal wall permit mucosa to bulge outward in pelvic cavity
- diverticulosis: diverticula are present, but no symptoms
- diverticulitis: inflamed and infected diverticula d/t trapped food particles or feces
- secondary to low fiber diets
- CM: abdominal pain and rigidity, left lower quadrant pain, fever, chills, hypotension, ribbon like stools, and nausea and vomiting, rectal bleeding, anemias, pelvic pain in females
- dx: CT scan, upper GI series, barium enema, blood studies, colonoscopy
- tx: liquid or bland diet, stool softeners, exercise, antibiotics and other drugs, high fiber diet when inflammation subsides
SIFTT for Diverticular Disease
- must be careful to avoid activities that ↑ intrabdominal pressure
- back pain may occur
- may need to assess for iliopsoas abscess formation-palpation of McBurney’s point
Esophageal Varicies
- dilated tortuous veins in the lower third of the esophagus
- often the first sign of portal HTN
- commonly causes massive vomiting of blood
- occurs when blood flow meets ↑’d resistance
- patho: pressures in the portal vein rises, blood backs up into the spleen and flows through collateral channels to the venous system, bypassing the liver
- CM: hemorrhage, hypotension, cyanosis, hematemesis, dyspnea, and tachycardia
- dx: CT, upper GI series
- tx: drug therapyp
SIFTT Esophageal Varices
-carefully instruct the client in proper lifting techniques and avoid any activities that will ↑ intraabdominal pressure
Gastritis
- inflammation of the lining of the stomach (gastric mucosa), is not a single disease, but represents a group of the most common stomach disorders
- gastric erosions by definition are limited to the mucosa and do not extend beneath the muscularis mucosae
- type A chronic gastritis is associated with pernicious anemia
- type B is caused by H. pylori
- patho: agents known to injure the gastric mucosa (H. pylori, aspirin or other NSAIDS, bile acids, pancreatic enzymes, alcohol); mechanism of mucosal injury is unclear and probably multifactorial; commonly accepted theory for agent-induced mucosal injury is suppression of endogenous PGs that normally stimulate the protective secretion of mucus
- CM: epigastric pain with abdominal distention, loss of appetite, and nausea
- tx: avoidance of identified irritating substances (e.g., caffeine, nicotine, alcohol) combined with the use of proton pump inhibitors (PPIs), ant/acids, and/or H2 blocking agents to block or reduce gastric acid secretion and minimize stomach acidity; vitamin B12 is administered to correct pernicious anemia when it develops secondary to chronic gastritis
SIFTT for Gastritis
-half of all clients receiving NSAIDs on a chronic basis have acute gastritis (often asymptomatic)
Gastroesophageal Reflux Disease (GERD)
- inflammation of the esophagus
- ↑’d incidence with ↑’d age (markedly after age 40)
- wide range of foods and lifestyle factors can contribute
- backflow of gastric or duodenal contents or both causing acute epigastric pain, usually after a meal; may be reflux of infectious agents, chemical irritants, physical agents like radiation and nasogastric tubes, gastric juices
- patho: Anything that may alter the ability of the lower esophageal sphincter (LES) to control fluid movement
- food or alcohol ingestion or cigarette smoking (↓’s pressure of LES)
- ↑’d gastric pressure; ↑’d abdominal pressure (obesity and pregnancy)
- medications
- gastric contents located near the gastroesophageal junction
- subsequent granulation tissue causes scarring that frequently develops into esophageal strictures that narrow the esophagus causing dysphagia
- CM: heartburn, (30-60 min after meal), reflux, dysphagia may have serious consequences, recumbency and bending, severe reflux may reach pharynx and mouth and result in laryngitis and morning hoarseness, may contribute to asthma in some patients: When acid enters esophagus, nerve reflex is triggered causing airways to narrow in order to prevent acid from entering, leading to SOB
- relief with antacids, baking soda, standing and walking and fluids
- tx: PPI’s, fundoplication, lifestyle modifications: wear loose clothes, don’t eat reflux causing foods, avoid caffeine, nicotine, alcohol, salicylates, NSAIDs, remain upright 3 hrs after a meal, avoid eating near bedtime or naptime, elevation of head of bed to reduce nocturnal reflux and enhance esophageal acid clearance, weight loss is overweight, drink fluids between, not with, meals, chew sugarless gum
SIFTT for GERD
- exercise can induce GERD in anyone as it inhibits both gastric and small intestinal emptying
- avoid high-calorie meals or fatty foods immediately before exercising to avoid or minimize exercise-related GERD
- avoid interventions requiring a supine position just after meals