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NURS 350 patho GI
patho GI system and GI disorders
| Question | Answer |
|---|---|
| esophagus | food from oropharynx to stomach. upper esophageal shincter, lower esophageal/cardiac sphincter. |
| musculature of esophagus | top 1/3 striated, middle 1/3 striated/smooth, lower 1/3 smooth |
| stomach fxns | stores food, secretes/mixes food with digestive joices (mucous, HCl, enzy, IF for B12 absorption, hormones, gastroferrin for FE absorp) |
| stomach anatomical regions from top to bottom | lower esphageal/cardiac sphincter - fundus-body-antrum - pyloric sphincter |
| small intestine - 5 m long structure/fxn | duodenum-jejunum-ileum. digestion/absorption |
| how does absorption occur in SI | columnar epithilial + goblet cells = brush border on villi |
| large intestine 1.5 meters long consists of | cecum-appendix-colon-rectum-anal canal |
| function of cecum | pouch that receives chyme from ileum |
| parts of colon | (SI empties into cecum -->) ascending-transverse-descending-sigmoid colon |
| function of colon | major = water absorption, minor fatty acid absorption |
| when do we call chyme/waste feces | when it reaches the sigmoid colon |
| nutrient absorption- stomach | water, alcohol |
| nutrient absorption duodenum | Fe, Ca, fat, sugars, H20, protein, vitamins, Mg, Na |
| nurtrient absorption jejunum | sugars, proteins |
| nutrient absorption ileum | bile salts, vit B12, Cl |
| nutrient absorption colon | water, electrolyes |
| accessor organs of digestion | liver (makes bile, largest solid organ), gallbladder (stores bile), exocrine pancreas (hydrolytic enzymes, alkaline secretions) |
| what is required for CHO digestion | begins in mouth, requires pepsin & insulin. REQUIRES A NA/K TRANSPORT MECHANISM |
| GI structural/neural problems effect | can slow, obstruct or accelerate movement of chyme at any level |
| GI inflamm or ulcerative conditions effect | alter secretion, motility, absorption |
| manifestations of GI disorders (6) | a/n/v/d/c and abdominal pain, GI bleed |
| anorexia | lack of desire to eat even though normal stimuli produce hunger. can accompany other problems - stress & CV disease |
| vomitting - reverse peristalis | forceful emptying of stomach or intestinal contents |
| vomitting activated by | CTZ = chemoreceptor trigger zone in medulla. SNS --> perspiration, inc. HR. Psymp--> salivation, gastric motility, relaxing of sphincters |
| is projectile vomitting preceded by nausea? | no, it is caused by direct stimulation of CTZ or by GI obstruction. not reverse perstalsis, just stomach contents empty |
| normal bowel movement range | 2-3 per day --> 1 per week |
| causes/contributors to constipation - 6 | neurogenic---low residue diets---sedentary---hypothyroidism---drugs (codiene/anticholinergics) ---dehydration |
| diarrhea | > 3 stools/day. increase in fluidity and volum, presence of unabsorbed food |
| how many liters of lumenal content/day is processed | 9 L per day - 2 from ingestion, 7 from intestinal secretions |
| what percent of lumenal contents are reabsorbed | 90% of volume reabsorbed --- of which 90% is reabsorbed in SI and 9% in colon |
| 3 mechanisms for diarrhea | *osmotic *secretory *motility |
| what is osmotic diarrhea | when nonabsorbable substances (synthetic, lactase deficiency) are in the intestine, osmotic draw of water in. get a loss (dilution?) of pancreatic enzyems |
| What is secretory diarrhea | large volume diarrhea caused by excessive mucosal secretion and electrolytes (Cl, Bicarb) |
| what causes secretory diarrhea | bacterial enterotoxins/exotoxins, diabetic neuropathy-->excess motility |
| what is small volume diarrhea caused by | usually inflamm disorders (Crohn's, ulcerative colitis) but can be due to fecal impaction, gastrinomas |
| what is motility-related diarrhea | when food is not properly mixes, digestion/absorption impaired-->increased motility |
| what causes motility-related diarrhea | small bowel resection, surgical bypass of intestinal area, intestinal fistual (tubular connection btw 2 organs) |
| what are the 3 mechanisms of abdominal pain | mechanical, inflammation, ischemia |
| how does abdominal pain manifest | acute/chronic or localized/general |
| mechanical abd pain MOA | stretching/distention --> traction on peritoneum-->adhesions-->common bile duct distention, forceful peristalsis. local swelling/stretching |
| types of abdominal pain | parietal/somatic, visceral, referred |
| parietal pain | from peritoneum & is more localized than visceral. lateral pain as peritoneum is innervated by only 1 side of NS |
| viscreal pain | from stimuli acting on abd organs. USUALLY FELT MIDLINE - diffuse/vague. nerve endings are sparse and multisegmented in abd organs |
| referred pain | well localized at distant site as it shares central afferent pathway. develops as intensity of visceral pain increases. gb pain refers btw shoulder blades |
| upper GI bleed locations | esophagus, stomach, duodenum |
| what characterizes upper GI bleed | bright red blood, or coffe ground material due to effects of acid on blood |
| know this - what causes upper GI bleed | *bleeding varicies (dilated veins) in esoph - can be lethal in minutes *peptic ulcers *tears in esoph-gastric jxn AKA Mallory-Weiss tear |
| lower GI bleed locations | jejunum, ilium, colon, rectum |
| what causes lower GI bleed | *polyps *inflamm dx *cancer *hemorrhoids |
| melana is more common in | lower GI bleeds. black tarry stool whose RBCs have been oxidized/digested |
| occult bleed | trace amount of blood in fecal matter |
| can GI bleeds be life threatening | yes, severe acute GI bleeds can be, depending on volume/rate of blood loss |
| name 5 types of GI motility disorders | *dysphagia *gastresophageal refux (and GERD) *hiatal hernia *pyloric obstruction *intestinal obstruction. |
| know dysphagia vs dysphasia | dysphagia - difficulty swallowing - mechanical obstruction or impaired esophageal motility. common in stroke patients *dysphasia is a speech problem, not GI associated |
| types of obstructions in dysphagia | *intrinsic obstructions -originate in esophageal wall (tumors, strictures=narrowoing, outpouchings *extrinsic - orginate outside esophagus - tumors, etc |
| what causes functional dysphagia | caused by nerual/musculature disorders where there are problems with striated/smooth muscle of upper esophagus. interefere with swallowing. |
| functional dysplasia associated with 2 diseases | associated with Parkinsons, CVAs |
| gastroesophageal reflux & GERD (more serious form) | lower esophageal sphincter transiently relaxes 1-2h after eating. chyme stomach contents regurgitate into esophagus |
| how do we treat GERD/gastroesophageal refulx | *PPIs, antacids *lose weight *surgery to tighten lower esophogeal sphincter |
| What is a hiatal hernia | protrusion of upper part of stomach through diaphragm into thorax |
| two types of hiatal hernia | *sliding *paraesophageal |
| Sliding hiatal hernia (direct hernia) | *most common type *stomach slides through esophageal hiatus (normal opening in diaphragm where esophagus penetrates) |
| what contributes to sliding hiatal hernia | contributors are: short esophagus, trauma/weakining of diaphragmatic muscles at gastroesophageal jxn |
| paraesophageal hiatal hernia AKA rolling hiatal hernia | greater curvatuare of stomach herniates through SECONDARY opening of diaphragm, lies along esophagus. whole stomach could move through. REFLUX UNCOMMON. however flood flow congested --> gastritis/ulcers |
| in what type of hiatal hernia do we see GERD | we see it in sliding hiatal hernia NOT in rolling |
| manifestations of hiatal hernia | may be asymptomatic *dysphagia *heartburn *epigastric pain *regurgitation, substernal discomfort after meals *GERD in sliding hiatal hernia |
| how do we treat hiatal hernia | *scope stomach *sliding tx = sm meals, lose weight, stay upright after meals, use antacids |
| what is pyloric obstruction | narrowing or blocking of the opening between stomach and duodenum |
| what causes pyloric obstruction | congital or acquired (peptic ulcer disease, cancer near pyloris) |
| how does pyloric obstruction manifest | severe gastric distention, lack of tone/motility, vague sense of fullness, worse after meals. n/a/pain/wt loss |
| how do we treat pyloric obstruction | NG tube to drain stomach, PPIs, IV/Lytes, stent for pyloric sphincter |
| what is intestinal obstruction | most common in SI, caused by any condition that prevents normal flow of chyme through the intestinal lumen |
| intenstinal obstruction can either be simple or functional. what are differences | *simple obstruction = mechanical blockage *functional obstruction = due to impaired motility like peralytic ilus post-op |
| in obstructions, when might metabolic alkalosis develop | when obstruction is at *pyloris or *high in small intestine |
| MOA of obstruction --> metabolic alkalosis | when obstruction is high (pyloric/duodenum) the H+ secreted in stomach is unable to pass to intestines. Therefore, they cannot be reabsorbed resulting in alkalotic condition |
| In obstructions, when might metabolic acidosis occur? | if the obstruction is long or a lower obstruction |
| MOA of lower obstruction, metabolic acidosis | Normally, bicarb is secreted from pancreas. Also bile is secreted from gb. lower obstruction prevents these basic secretions from being absorbed. result is acidotic condition |
| what electrolyte imbalance often presents with metabolic acidosis bwo lower obstruction | hypokalemia (not enough K absorbed due to obstruction?) |
| hypokalemia may be extreme in a lower obstruction, what does this promote? | This promotes acidosis -->loss of muscle tone in intestinal wall |
| what can worsen metabolic acidosis | starvation --> ketosis. Also if obstruction is severe, can occlude ciruculation -->anerobic metab -->lactic acidosis |
| how does a partial obstruction present | with cardial signs of pain/vomitting and also presents with diarrhea |
| how does a complete obstruction/strangulation present | cardinal signs of pain/vomitting (?) however we will have increased bowel sounds with constipation |
| what is gastritis | an inflammatory conditon of gastric mucosa |
| MOA of acute gastritis | suface epithelim have been eroded. results from injury to protective mucosoal barrier from drugs or chemicals |
| pathophys of acute gastritis | anti-inflammatory drugs, ETOH, digoxin and uremia contribute -->INHIBIT PROSTAGLANDINS that normally stimulate mucos secretions |
| MOA of chronic gastritis | generally in elderly --> thining and degenreation of stomach wall |
| 2 types of chronic gastritis | *Type A fundal - immune type - rare/severe *Type B antral - non-immune |
| MOA chronic gastritis Type A fundal-immune | autoimmune Abs attack *mucosal cells -->decreased HCl-->mucosa generation-->gastric atrophy *parietal cells --> dec IF-->dec VitB12 abs-->dec DNA/RBC synth -->pernicous anemia *chief cells -->dec pepsinogen |
| peptic ulcer locations, MOA | lower esophagus, stomach, duodenum. break in protective mucosa exposes to acid-->autodigestion |
| peptic ulcer erosions vs. true ulcerations | erosions only erode mucosa. Ulcerations penetrate muscularis, damage bvessels -->hemorrhage |
| duodeneal ulcers | most common type due to hypersecretion of acid, pepsin |
| what causes duodeneal ulcers | *feedback broke to antral parietal cells, they make too much acid, gastrin to erode mucosa *H. pylori erodes mucosa like in peptic ulcers *rapid gastric emptying overwhelms bicard from pancreas |
| s/s and tx of duodeneal ulcers | intermittent epigastric pain 2-3 hours after eating, relieved by food/antacids. *if not relieved, may be obstruction/perforation --> blood in vomit, stools |
| gastric ulcers similar to duodenal ulcers, but are usually confined to what area | confined to antral area of stomach, where acid producing cells are |
| MOA gastric ulcers | increased acid production --> increase H+ permeability which decreases mucous production. Visious cycle of inflammation/damaged mucosa. Pain that comes back after eating. |
| what is a stress ulcer | actute forms of peptic ulcers that occur through stomach/duodenum (decreased mucousal blood flow) |
| What is post-gastrectomy syndrome - and 3 syndromes | Motor and control changes in stomach/SI due to resection *dumping syndrome *alaline reflux gastritis *afferent loop obstruction (bile, panc juice back up) |
| GI malabsorption diseases | *pancreatic insufficiency (dec CHO enzymes) *lactase deficiency *bile salt deficiency (fat & fat soluble vitamin malabsorption |
| Ulerative colitis | may be genetic. anticolon antibodies/autoimmune chronic inflammation of colonic mucosa |
| where is ulcerative colitis most severe | most severe in sigmoid colon, rectum. |
| manifestations ulcerative colitis | mucosal destruction -->bleeding, cramping frequent diarrhea (bloody and/or purulent) |
| Crohn's Disease location | inflamm disease in large AND small intestine, runs in families, gene NOD2(CARD15) |
| Crohn's and ulcerative colitis hard to differentiate, but what type of stool most common to Crohn's | non-bloody diarrhea most common |
| diverticular disease - diverticulosis - diverticulitis | outpouchings of mucosa through muscularis of colon. *asymptomatic = diverticulosis *inflammation = diverticulitis, esp in elderly |
| what contributes to diverticular disease | refined foods. generally invvolves sigmoid colon. |
| appendicitis | most common emergency abd surgery, MOA not known (obstruction, high pressure, infection) |
| Obesity associated with 3 leading causes of death | *CV disease *Cancer *DM |
| other health problems associated with obesity | *CAD *females: breast, cervical, endometrial, liver cancers *males - prostate, colon, rectal cancers |
| child onset obesity MOA | hyperplastic, hypertrophic fat cells dispersed over body |
| adult onset obesity MOA | hypertrophic, more centrally located fat cells |
| is there a genetic component to obesity | yes, over 41 genes implicated |
| pulmonary function in obesity | fas exchanged, VC and expiratory volume decrease (low 02, high C02)-->sleep apnea, exercise intolerance |
| anorexia nervosa | distorted body image, body weight less than 15% of normal with refusal to eat, loss of 3 consecutive periods |
| What % of ideal weight loss leads to heart failure | loss of 20-30% of ideal weight |
| bulimia MOA | binges followed by purging (vomitting, laxatives, excessive exercise) |
| short term starvation | *glycogenolysis peaks 4-8 hours *gluconeogenesis begins *stored nutrients depeled, some proteins catabolized |
| long term starvation | *several days after abstinence-->death *decreased dependence gluconeogenesis *increased lipolysis/pyruvate-->ketones *once adipose depleted, muscle breakdown including cardiac occurs |
| what are the clinical manifestations of liver disorders? | *portal HTN *ascites *hepatic encephalopathy *jaundice *hepatorenal syndrome |
| what is portal HTN | when normal pressure of 3mm is increase to 10mmHg. most commonly caused by cirrhosis |
| other causes of portal HTN | anything that impedes/obstructs flow through portal system/vena cava *thrombosis, inflamm *impeded hepatic vein outflow |
| long term effects of portal HTN | *varicies (distended collateral veins) *splenomegaly *ascites *hepatic encephalopathy |
| cirrhosis | irreversible inflamm disease with decreased ablumin, portal hyptension, ascites. |
| cirrhosis means liver can't produce | *albumin (leads to edema, ascites) *hormones to regulate Na/H20 (angiotensinogen?) |
| chronic degenerative disease of liver | long term cirrhosis --> fibrous tissue, fat infiltrates lobules |
| Hepatitis | swelling and inflammation of liver, usually by viral infection |
| What is most common cause of Hepatitis | Hepatitis C, no vaccine, may be asymptomatic before chronic. 50-8-% of Hep C cases --> chronic hepatitis |
| is there a vaccine for Hepatitis C | Nope. Bummer. |
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lorrelaws
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