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NURS 350 patho GI

patho GI system and GI disorders

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