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