NURS 350 patho GI Word Scramble
|
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
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. |
Created by:
lorrelaws
Popular Nursing sets