GI histology and pathophys Flashcards
major functions of the GI tract
ingestion fragmentation digestion absorption elimination of waste defense - big one
4 major layers of GI tract
mucosa
submucosa
muscular propria
adventitia
layers of mucosa in GI tract
epithelium lamina propria (defense) muscularis mucosae (smooth muscle)
things found in submucosa
collagenous tissue blood vessels glands lymphatics nerves
role of submucosa
- binds mucosa to muscular wall
- secretion
- supply
- control
layers of muscularis propria
inner circular muscle layer
outer longitudinal muscle layer
role of muscularis propria
provide peristaltic contraction
4 types of mucosa in GI
protective
secretory
absorptive
lubricative
protective mucosa feature/location
- epithelium is squamous cells
- oral cavity, pharynx, esophagus, anus
secretory mucosa feature/location
- closely packed tubular glands
- stomach
absorptive mucosa feature/location
- finger-like projections
- small intestine
lubricative mucosa feature/location
- closely packed straight tubular glands (elongated)
- large intestine
air pressure level in esophogus
low (-5mmHg)
anti reflux barriers
- lower esophageal sphincter
- diaphragmatic sphincter
- acute angle of stomach and esophagus connection
functions of stomach
fragmentation
digestion
parts of stomach
fundus
body
pylorus
cell types found in stomach
mucus
parietal
chief
mucus cell function
mucus secretion in stomach
parietal cell function
acid secretion
chief cell function
pepsin secretion
3 segments of small intestine
duodenum
jejunum
ileum
length of small intestine
23 feet
ways small intestine increases surface area
- plicae circulares are folds of mucosa/submucosa
- numerous villi and crypts on the mucosal surface
- microvilli on the villi
amylase role
convert poly-, di- or mono-saccharides to glucose and maltose
role of disaccharidase and oigosaccaridase
convert maltose to monosaccharides
carbohydrate digestion sequence
- poly, di, and mono saccharides broken down to glucose/maltose
- maltose broken down to monosaccharidrd that are then absorbed
pepsin role
protease - breaks proteins down to poly peptides
where do amino acids go after the breakdown of peptides
liver
what needs to happen to digest fats
emulsification and then lipases can break them down
stomach absorbs what
water
alcohol
aspirin
duodenum absorbs what
iron, calcium, magnesium, sodium fats monosaccharides water AA's
jejunum absorbs what
monosaccharides
AA’s
Ileum absorbs what
bile salts
Vit B12
chloride
colon absorbs what
water
electrolytes
functions of colon
absorb water
store stool
propel stool
primary reservoir for stool
ascending colon
cellular components of large intestine
large glands goblet cells - secretion absorptive cells blood vessels lymphatic
mucosa-associated lymphoid tissues (MALT)
- defense mechanism
- T and B cells
- most active during childhood
GERD
symptoms/complications due to reflux of gastric contents into esophagus or beyond
-may or may not have erosions
GERD prevalence
10-20%
no difference between males/females
males may have more erosive esophagits
potential causes of GERD
- decreased lower esophageal sphincter pressure
- decreased mucosal resistance to acid
- decreased esophageal or gastric motility
- decreased salivary buffering of acid
drugs that may reduce LES pressure
anticholinergics
barbiturates
amlodipine
estrogen/progesterone
drugs that irritate esophageal mucosa
nsaids
aspirin
bisphophonates
potassium
main symptoms of GERD
heartburn
regurgitation
chest pain
dysphagia
ALARMD symptoms
- anemia
- loss of weight
- anorexia
- recent onset
- melena or hematemesis
- dysphagia
GERD diagnosis
-if heartburn/regurgitation you may presume GERD and treat with PPI
when to do endoscopy in GERD patients
if they have ALARMD symptoms
H.pylori screening in GERD
not recommended
ambulatory reflux monitor
catheter that goes through the nose and down the esophagus to monitor pH
complications of GERD
erosive esophagitis
esophageal strictures
Barrett’s esophagus (>50 y/o)
esophageal adenocarcinoma
peptic ulcer disease
- injury to digestive tract resulting in mucosal break
- usually in stomach or proximal duodenum
aggressive factors in PUD development
gastric acid
pepsin
protective factors against PUD
mucus secretion
bicarbonate secretion
prostaglandins
causes of PUD
H.pylori
NSAID induced
stress-related (ICU patients)
H.pylori PUD is usually where
duodenum
NSAID induced PUD is usually where
stomach
symptoms of H.pylori PUD
epigastric pain
symptoms of NSAID induced PUD
usually asymptomatic
PUD that is acute
stress-related
symptoms of PUD
non-specific*
abdominal burning
fullness
cramping
symptoms of duodenal ulcers
pain 1-3 hours after meals or at night and is relieved by eating
symptoms of gastric ulcer
postprandial pain, n/v
weight loss
PUD symptoms in elderly
usually asymptomatic
complications of PUD
bleeding - due to erosion into an artery
perforation - sudden sharp pain
gastric outlet obstruction
h.pylori transmission
usually fecal-oral
h.pylori risk factors
low socioeconomic status
many siblings
infected parent
contaminated water
where does h.pylori infect
between gastric mucus layer and surface epithelial cells
how does h.pylori protect itself
produces urease which converts urea in gastric juice to ammonia and CO2 to alkalinize the environment
complications of h.pylori
chronic gastritis
gastric and duodenal ulcers
malignancy
indications for h.pylori testing
- active or past PUD with no reported cure
- initiation of chronic NSAID
- unexplained iron deficiency anemia
- idopathic thrombocytopenic purpura
- low grade gastric MALT lymphoma
- Hx of endoscopic resection of early gastric cancer
when to consider non-endoscopic testing of h.pylori
< 60 with uninvestigated dyspepsia and no alarm symptoms
when is testing for h.pylori unnecessary
typical symptoms of GERD
no PUD history
endoscopic tests for h.pylori
histology
culture of biopsy
biopsy rapid urease test
non-invasive h.pylori tests
antibody detection in serum (ELISA)
urea breath test
fecal antigen
h.pylori test of choice during active bleed or EGD
biopsy rapid urease test
most convenient h.pylori test
urea breath test
risk factors for NSAID induced ulcers or upper GI bleed
>65 hx of PUD high does of NSAID alcohol cigarettes bisphosphonates, SSRIs, corticosteroids, anticoags, antiplatelets
inflammatory bowel disease
chronic inflammatory disease of GI tract with alternating remission and recurrence
features of Crohns disease
- all segments can be affected (ileum and colon most common)
- transmural inflammation
- discontinuous distribution
features of ulcerative colitis
- limited to colon and rectum
- inflammation is mucosal only
- continuous distribution
crohns disease onset
usually 20-40s
ulcerative colitis onset
usually 30s
inflammatory bowel disease greatest incidence poplulation
developed countries and urban areas
Jewish
risk factors for inflammatory bowel disease
- altered GI bacteria composition
- genetics
- cytokine dysregulation
- smoking (for crohns disease)
- nsaid and OC use
inflammatory bowel disease symptoms
abdominal pain diarrhea blood in stools weight loss fever extraintestinal manifestations
gold standard for inflammatory bowel disease diagnosis
endoscopy with biopsies
labs to do when diagnosing IBD
cmp cbc crp esr fecal calprotectin c.diff stool culture
complications of crohn’s disease
small bowel stricture and obstruction
fistulas
abscesses
intestinal cancer
complications of ulcerative colitis
- hemorrhoids, anal fissures
- perirectal abscesses
- toxic megacolon
- colonic stricture
- colorectal cancer
most commonly diagnosed GI condition
irritable bowel syndrome
Rome IV criteria for IBS
-recurrently abdominal pain (at least once weekly) with two or more of following
o related to defecation
o associated with change in stool frequency
o associated with change in stool appearance
typical symptoms of IBS
- diarrhea or constipation*
- bloating
- straining during defecation
- feelings of incomplete evacuation
IBS diagnosis
Rome IV criteria started at least 6 months prior and been present in last 3 months
IBS may be triggered by
- gastroenteritis
- food intolerances
- chronic stress
- diverticulitis
- surgery
IBS and serotonin
associated with an increase after meals in IBS with diarrhea
