Chap 17- GI Tract Flashcards
upper division of GIT
- oral cavity
- pharynx
- esophagus
- stomach
- responsible for food consumption and chemical digestion
lower division of GI tract
- small intestine
- large intestines
- anus
- where absorption of nutrients takes place
what is the accessory system to the GIT?
- hepatobiliary system
- liver
- gall bladder
- pancreas
what is the function of the hepatobiliary system?
secrete digestive enzymes required for food metabolism
what are the layers of the GI tract?
- mucosa
- submucosa
- muscle
- serosa
what is the peritoneum?
large serous outer membrane that lines abdominal cavity
what are the divisions of the peritoneum?
- parietal
- visceral
- peritoneal cavity= space between the two
mesentary
- double layer peritoneum
- has BV and nerves that supply intestinal wall
what layer of the GI wall comes in contact with food?
mucosa layer
what are the portions of the mucosa layer?
- epithelium
- lamina propria
- muscularis mucosa
epithelium in GI wall
- made of simple columnar or stratified squamous cells
- contains goblet cells and endocrine cells
- had depressions that store stem cells and immune cells
what do goblet cells secrete?
mucus that protects epithelium from digestion
paneth cells
- secrete antimicrobial peptides
- found in epithelium
what is the lamina propia?
layer of CT tissue
what is the role of the muscularis mucosal layer?
- contracts to make closer contact with food particles
what is found in the submucosa?
- blood vessels
- lymphatic vessels
- submucosal plexus
what is the function of the submucosal plexus?
- regulate secretions of GIT
- regulate blood supply
- aka meissner’s plexus
what makes up the muscularis externa layer?
- circular muscle fibers
- longitudinal muscle fibers
- myenteric plexus
what is the role of the myenteric plexus?
- regulate peristalsis
- help move digested material out of gut
- aka Auerbach’s plexus
what controls swallowing?
- swallowing center in medulla
- CN 5, 9, 10 and 12
digestive juices of salivary glands
- bicarbonate- moisten food
- salivary lipase- digest fat
digestive juices of stomach
- hydrochloric acid
- pepsin
- gastric lipase
- intrinsic factor
- mucus
hydrochloric acid
kill bacteria
pepsin
digest protein
gastric lipase
digest fat
intrinsic factor
aids in B12 absorption
mucus
protects stomach lining
agenesis
- absence of part of GIT
- extremely rare
atresia
- development of part of GIT is incomplete
- common
- most commonly occurs at tracheal bifurcation and associated with a fistula
- associated with other congenital malformations
what is the result of atresia and fistula at the tracheal bifurcation
- aspiration
- suffocation
- pneumonia
- severe flid and electrolyte imbalances
acquired stenosis causes
- inflammatory scarring
- GERD
- irradiation
- systemic sclerosis
- caustic injury
diaphragmatic hernia
- incomplete formation of diaphragm
- abdominal viscera herniate into thoracic cavity
omphalocele
- closure of abdominal musculature is incomplete
- abdominal viscera herniate into ventral membranous sac
meckel’s diverticulum
- true diverticulum
- outpouching of all four layers of GI wall
- due to failed involution of vitelline duct
what is the vitelline duct?
connects yolk sac to developing embryos digestive system
characteristics of meckel’s diverticulum
- 2% of population
- present within 2 ft of ileocecal valve
- 2X as common in males
- if have symptoms, symptomatic by age 2
what can also happen with meckel’s diverticulum?
- ectopic pancreatic tissue
- ectopic gastric tissue
- secretions from these can lead to peptic ulceration
symptoms of meckel’s diverticulum
- painless bright red blood per rectum (BRBPR)
- abdominal pain resembling apendicitis
- obstruction
pyloric stenosis
- 3/5 times more common in males
- present between 3-6 weeks of life
- hyperplasia of pyloric muscularis externa which obstructs gastric outflow
pyloric stenosis symptoms
- projectile non-bilious vomiting after feeding
- frequent demands of refeeding
- edema and inflammatory changes in mucosa/ submucosa which can aggravate narrowing
who is at an increased risk for developing pyloric stenosis?
- monozygotic twins
- dizygotic twins
- siblings
- turner syndrome
- trisomy 18
- erythromycin or azithromycin exposure
causes of acquired pyloric stenosis
- antral gastritis
- peptic ulcers close to pyloris
- stomach cancer
hirschsprung disease
- aka congenital aganglionic megacolon
- associated with down syndrome
- no migration of neural crest cells leads to aganglionosis
clinical features of hirschsprung disease
- failure to pass meconium in immediate postnatal period
- obstruction/ constipation
- ineffective peristalsis
- abdominal distension
- bilious vomiting
what are major consequences of hirschsprung disease?
- enterocolitis
- fluid and electrolyte disturbances
- perforation
- peritonitis
achalasia
- occurs due to increased tone of lower esophageal sphincter
- low levels of NO and VIP
- high levels of ACh
triad of achalasia
- aperistalsis
- increased tone of lower esophageal sphincter
- incomplete relaxation of lower esophageal sphincter
primary cause of achalasia
ganglion cell degeneration
secondary causes of achalasia
- chagas disease
- diabetic neuropathy
- infiltrative disorders
- down syndrome
- alacrima
- adrenal insufficiency
symptoms of achalasia
- dysphagia for solids and liquids
- difficulty in belching
- regurgitation
- chest pain
- weight loss
reflux esophagitis
- aka GERD
- due to loose lower esophageal sphincter and increased abdominal pressure
- sensitive to acid
causes of GERD
- alcohol and tobacco
- obesity
- CNS depressants
- pregnancy
- hiatal hernia
- decreased gastric emptying
clinical features of GERD
- heart burn
- dysphagia
- regurgitation of gastric contents
complications of GERD
- ulceration
- hematemesis
- melena
- structure development
- barrett esophagus
what type of cells line the mouth to esophagus
stratified squamous epithelium
what type of cells line the stomach to terminal anus
ciliated columnar epithelium
esophageal varices
- abnormal dilation of veins at junction between portal vein and systemic venous system
- present in half of pts with cirrhosis
- is a medical emergency, can lead to severe bleeding and shock
varices
dilation of vein
how does portal HTN cause esophageal varices?
- increased pressure causes blood to flow from portal system to systemic system
- puts pressures on walls of veins (thin walls)
- increased pressure -> varices
barrett esophagus
- due to chronic GERD
- intestinal metaplasia
- replacement of normal stratified squamous epithelium with simple columnar epithelium
- increased risk of esophageal adenocarcinoma
how do you identify barrett esophagus
- endoscopy
- prompted by GERD sx
esophageal tumors
- 7th leading cause of cancer deaths
- mostly in elderly
what is the most common type of esophageal tumor world wide?
- squamous cell carcinoma
- mainly associated with alcohol and tobacco use
what is the most common type of esophageal tumor in the US?
- adenocarcinoma
- due to association with GERD, barrett esophagus, and obesity
clinical features of esophageal tumors
- dysphagia
- odynophagia (painful swallowing)
- progressively increasing obstruction
- weight loss
- hemorrhage
- lymph node metastasis= poor prognosis
anatomical regions of stomach
- cardia- continues with esophagus
- fundus
- body
- antrum
cells of cardia and antrum
- mucin secreting foveolar cells
- form small glands
- antral glands also have G cells that release gastrin
what is the role of gastrin
- stimulate acid secretion by parietal cells in fundus and body
chief cells
- found in body and fundus
- produce and secrete digestive enzymes like pepsin
acute gastritis causes
- NSAIDs
- alcohol
- bile
- stress
- mucosal erosion or hemorrhage
sx of acute gastritis
- variable
- epigastric pain, N/V
- mucosal erosion/ ulceration/ hemorrhage
- hematemesis
- melena
protective factors in stomach
- mucus secretion
- bicarbonate secretion
- mucosal BF
- epithelial barrier
- epithelial regeneration
- prostaglandins
pathogenesis of acute gastritis
- loss of protective mechanisms
- NSAIDS are cox inhibitors -> decreased PGE2/I2
- h. pylori -> decreased bicarb
- some chemicals/ alcohol can cause direct epithelial damage
- chemo decreases epithelial regeneration
what is the most common cause of chronic gastritis?
- h. pylori infection
- 2nd most common= autoimmune
how does chronic gastritis normally present
antral gastritis
pathophys of chronic gastritis infection
- h. pylori swims via flagella
- attaches to epithelium via proteins
- secretes urease and neutralizes acid
- injects exotoxin into host which causes epithelial death
- mucinase degrades mucus layer
- can extend from antrum to fundus
what does urease do
- neutralize gastric acid
- mechanism of h. pylori
peptic ulcer diease
- complication of chronic gastritis
- mucosal ulceration in duodenum or stomach
what is peptic ulcer disease associated with
- h pylori infection
- NSAIDs
- cigarette smoking
why is h. pylori associated with peptic ulcer disease?
- causes more gastrin to be secreted -> increased acid and decreased bicarb -> antral and duodenal uclers
- can progress to fundus and cause gastric atrophy increasing risk of stomach cancer
clinical features of peptic ulcer disease
- epigastric burning
- iron deficiency anemia
- hemorrhage
- perforation
- N/V, bloating
- weight loss
- complications= bleeding, perforation, obstruction
gastric polyps
- usually due to inflammatory and hyperplastic polyps
- generally are small
- if greater than 1.5 cm must be biopsied
- can be due to inflammatory response from h. pylori
fundic gland polyps
- in individuals with adenomatous polyposis
- increased prevalence due to PPIs
- asymp or have N/V and epigastric pain
why are PPIs associated with fundic gland polyps
- reduces acid secretion
- stimulates oxyntic gland growth (acid secreting glands)
gastric adenocarcinoma
- most common malignancy of stomach
- have intestinal or diffuse type
- early sx similar to chronic gastritis and PUD
intestinal type gastric adenocarcinoma
bulky mass
diffuse type gastric adenocarcinoma
spreads and invades walls of GIT early
precursors for gastric adenocarcinoma
- gastric dysplasia
- adenomas
- overall incidence has decreased due to decreased h pylori infections and decreased consumption of carcinogens
what is the most common cause of intestinal obstruction
adhesions
hernia
- weakness or defect in abdominal wall
- permits protrusion of serosa lined pouch of peritoneum
volvulus
twisting of bowel
intussusception
- segment of intestine is constricted by wave of peristalsis
- telescopes into immediately distal segment
- common in kids < 2
what are main arteries of GI T
- celiac a
- superior mesenteric a
- inferior mesenteric a
hyper coagulable states that can lead to ischemic bowel disease
- severe atherosclerosis
- aortic aneurysm
- oral contraceptives
- embolism
- hypoperfusion
result of ischemic bowel disease
- mucosal infarction
- mural infarction
- transmural infarction- across all four layers
pathogenesis of ischemic bowel disease
- phase 1= hypoxic injury
- phase 2= reperfusion injury
- most damage done in phase 2 due to ROS
clinical features of ischemic bowel disease
- common in elderly
- sudden cramping, lower left abdominal pain
- blood diarrhea
- can lead to shock
infectious enterocolitis
- major cause of death world wide especially in kids <5
- e. coli is major cause
symptoms of infectious enterocolitis
- diarrhea
- abdominal pain
- urgency
- perianal discomfort
- incontinence
- hemorrhage
cholera and enterocolitis
- spreads through contaminated drinking water
- causes rice water stools at a rate of 1 L/hour
- vomitting
- dehydration, hypotension, shock, death
pathophys of cholera infection
- enters in cell
- increases adenylate cyclase
- leads to increase in cAMP
- cAMP opens ion channel CTFR
- loss of chloride, water, Na
- results in severe secretory diarrhea
camylobacter enterocolitis
- most common bacterial enteric pathogen in developed countries
- impt cause of travelers diarrhea
- associated with undercooked chicken, unpasteurized milk
virulence factors of campylobacter
- motility
- adherence
- toxin production CDT
- invasion into lamina propia and lymph nodes
result of camylobacter infection
- watery diarrhea
- dysentery
- reactive arthritis
- GBS
shigellosis
- due to shigella flexneri
- secretes shiga toxin which decreases protein synthesis
- one of most common causes of dysentery
- fecal-oral or conatminated water transmission
clinical features of shigellosis
- most infections and deaths occur in kids <5
- 1 week incubation period
- diarrhea
- fever
- abdominal pain
pathophys of shigellosis
- invade m cells
- reaches basolateral side and enters macrophages
- macrophages release cytokines IL1 and IL8
- attracts PMN -> decreased absorption, increases permeability
how does shigella spread once in GIT
spreads horizontally from cell to cell
salmonella
- causes typhoid fever and salmonellosis
- over 1m cases each year in US
- peak incidence in summer and fall
type III secretion system
- found in salmonella
- transfers bacterial proteins into M cells and enterocytes
clinical features of salmonella
- indistinguishable from other enteric pathogens
- inflammatory diarrhea
- fever resolves in 2 days but diarrhea persists for a week
- organism can be shed in stool for several weeks
subtypes of typhoid fever
- typhi
- paratyphi
typhoid fever
- infects blood vessels and lymphatics
- can travel to other parts of body
- leads to typhoid nodules and typhoid ulcers
clinical features of typhoid fever
- N/V/D (bloody)
- anorexia
- abdominal pain
- rose spots
extraintestinal complications of typhoid fever
- encephalopathy
- meningitis
- seizures
- endocarditis
- myocarditis
- pneumonia
- cholecystitis
e. coli
- colonize healthy GIT
- most nonpathogenic
- some can cause diseases
classifications of e. coli
- enterohemorrhagic
- enterotoxigenic
- enteroinvasive
- enteropathogenic
enterohemorrhagic e. coli
- non-penetrating
- secretes shigella-like toxin which inactivates ribosomes
- assoc with inadequately cooked ground beef
- hemolytic uremic syndrome -> cytokine release -> RBC lysis, renal failure, thrombocytopenia
enterotoxigenic e. coli
- non-penetrating
- travelers diarrhea
- heat stable and heat labile toxin
- increase adenylate cyclase -> increase cAMP -> increased secretions
- secretory diarrhea, dehydration, shock
enterinvasive e. coli
- penetrating
- transm via food, water, person to person
- doesnt produce toxin
- invade epithelial cells -> dysentery
enteropathogenic e. coli
- non-penetrating
- impt cause of endemic diarrhea in kids <2
- attach to epithelium -> loss of microvilli -> mucus diarrhea
pseudomembranous colitis
- caused by c. diff
- highly related to antibiotic use
- recurrent infection
- forms a white membrane
risk factors for pseudomembranous colitis
- advanced age
- hospitalization
- antibiotic tx
clinical features of pseudomembranous colitis
- fever
- leukocytosis
- abdominal pain
- cramps
- watery diarrhea
- dehydration
- protein loss leading to hypoalbuminema
pathogenesis of pseudomembranous colitis
- disruption of bacterial flora
- colonization with c diff
- toxins released
- mucosal damage and inflammation
viral gastroenteritis
- most common causes are rotavirus and norovirus
- rotavirus most common in kids
- infections spread easily
- usually self limiting
- infective inoculum= 10 particles
pathophys of viral gastroenteritis
- release NSP4 -> increased Ca concentration and permeability
- release of peptide amines -> stimulate enteric NS -> secretary diarrhea
- when virus multiples cells die -> less nutrient absorption -> osmotic diarrhea
inflammatory bowel disease
- crohn’s and/or ulcerative colitis
- inappropriate mucosal immune acvtivation
- 2 diseases often coexist
crohn’s disease
- skip lesions in any part of GIT
- transmural inflammation
- hypoalbuminemia
- fibrosing strictures
- fistulae between bowel loops and can involve other areas
ulcerative colitis
- involves colon and rectum
- continuous involvement
- causes superficial ulcers and pseudopolyps
- bloody diarrhea
- 30% require colectomy
