GI Pathophys Flashcards
what is a inlet patch
most common type of ectopic tissue. It is a patch of gastric mucosa in the upper 1/3 of esophagus. Can result in dysphagia, esophagitis, Barrett esophagus or rarely adenocarcinoma
what is ectopic pancreatic tissue
Found in esophagus or stomach.
Asymptomatic
what is gastric heterotopia
ectopic gastric mucosa in small bowel or colon
Can results in peptic ulceration of adjacent mucosa
why causes Barrett esophagus and why does it need to be monitored
GERD causes acid in esophagus= metaplasia into gastromucosal cells to protect the esophagus by secreting mucos. The metaplasia can transform it into adenocarcinoma.
how does gastric heterotopia cause peptic ulceration
acid is secreted into the colon or duodenum which do not have mucus producing cells to protect it
what are congenital duplication cysts and where are they usually located
they form double smooth muscle layers by replicating normal anatomy of affected tissue.
Usually located in small bowel(50%), esophagus, and colon
what are bronchogenic cysts
fluid filled lung tissue often present as mediastinal masses lined by bronchial tissue.
what is the treatment for duplication and bronchogenic cysts
they usually need to be surgically removed and closed off
what is associated with increased risk of esophageal atresia
polyhydramnios (excessive amniotic fluid)
if a child has esophageal atresia, what other conditions is this child at inc risk for?
VATER(vertebral defects, anal atresia, tracheoesophageal fistula, and renal dysplasia) along with congenital heart defects, genitourinary malformations and neurologic disease
are esophageal webs and rings congenital or acquired
can be either (can be acquired from GERD creating fibrotic tissue)
what is the histology of esophageal webs/rings
Core of fibrovascular tissue lined with normal esophageal epithelium
what is the manifestation of esoph webs/rings
episodic dysphagia
where are schatzki rings located
Type A: above the GE junction
Type B: at the squamocolumnar junction
esophageal webs/rings Tx?
dilation or excision
What is Plummer-Vinson Syndrome and what can be a severe complication from it
Occurs mainly in females causing iron deficiency anemia, esophageal web, mucosal lesions of mouth and pharynx. Can cause carcinoma of oropharynx and upper esophagus
what is the most common manifestation of esophageal stenosis and why is it caused
progressive dysphagia from atrophy of the muscularis propria
what causes diaphragmatic hernia and what is its effect
Incomplete formation of diaphragm causing
- Abdominal viscera herniating into thoracic cavity
- Webs and rings
what is a Omphalocele
Closure of abdominal musculature is incomplete
Abdominal viscera herniates into ventral membranous sac
if a baby has a omphalocele, what else are they likely to have
40% have other birth defects (diaphragmatic hernia, cardiac abnormalities)
what is gastroschisis
bentral wall defect involving all layers of abdominal wall allowing the organs to move out of body w/o any type of membranous casing
what is a Meckel diverticulum
Blind outpouching Communicates with lumen All three layers of bowel wall Rule of 2s 2 feet from iliocecal valve 2% of population Approx. 2 inches long Twice as common in males Symptomatic by age 2 years 2 types of common ectopic tissue: gastric and pancreatic
what is a true diverticulum
blind outpouching of the alimentary tract that is lined by mucosa, communicates with the lumen, and includes all three layers of the bowel wall.
is a pyloric stenosis more common in men or women
4:1 men:women
when does pyloric stenosis begin its manifestatioins
2nd-3rd weeks of life
what is the genetic etiology of pyloric stenosis
nitric oxide synthetase deficiency= hyperplasia of pyloric muscularis propia
what are the Sx of pyloric stenosis
New onset regurgitation(vomiting) Persistant, projectile, nonbilious Hypochloremic alkalosis Physical Exam Hyperperistalsis Firm ovoid abdominal mass
how does regurgitation of SBO differ from pyloric stenosis
SBO will have bile in it
what does a firm acorn-like mass at the end of the xiphoid indicate
pyloric stenosis
what is Hirschsprung Dz (cause and effect)
Either normal migration of neural crest cells from cecum to rectum is arrested or ganglion cells undergo premature death= the distal intestinal segment to lacks both Meissner submucosal and Auerbach myenteric plexus= No peristalsis= distended colon
what is the two types of smooth muscle in the esophagus
longitudinal
circular
what is the role of the submucosa in the esophagus
contains glands that secrete mucus to prevent the esophagus from drying out
what is the role of the connective tissue around the esophagus
protection
what is the order of layers in the esophageal wall from inside out
squamous epithelium, muscularis mucosa, submucosa, muscularis propria
what are the two main enzymes in saliva and what do they break down
Alpha-amylase: break down sugars
lingual lipase: break down fats
what nerve controls chewing and where does it originate from
trigeminal- originates at the pons
what is trigeminal neuralgia
hyperactive afferent= inc pain with mastication
what are the 3 stages of swallowing
1-Voluntary - initiates swallowing process
2-Pharyngeal - passage of food through pharynx into esophagus
3-Esophageal - passage of food from pharynx to stomach
what nerves are involved in swallowing
Mainly CN 9 and 10. Some trigeminal in mouth
how do you test if there is damage to the medullary region of the brain stem
CN 9 and 10 can be tested by the gag reflex
what is the neural pathway when a bolus of food reaches the pharynx
it is sensed in the pharynx by CN 9/10 afferent. This is transmitted to the swallowing center in the medulla. Efferent n then go out to contract/relax the glottis/ epiglottis
what inhibitory effect does the swallowing center have
inhibits the respiratory center when swallowing
what is primary peristalsis
it is cordinated by the swallowing center and is a continuation of pharyngeal peristalsis moving bolus downward
what is secondary peristalsis
it only occurs when needed and is induced by distention of the esophagus. It repeats until the bolus is cleared
what is unique about the striated muscle in the upper esophagus
The striated and smooth muscle of the esophagus are both innervated by the vagus nerve. Striated muscle is normally innervated by motor neurons
can primary and secondary peristalsis occur after a vagotomy or stroke damage to the vagus nerve
primary cant, secondary can
when is a vagotomy indicated
not used often but it can dec acid production and dec spasms
what are the esophageal pressure measurements between swallows
High pressure at sphincters
Pressure in esophageal body = intrapleural pressure
what are the esophageal pressure measurements during swallowing
UES relaxes - (low pressure)
Peristaltic wave - (high pressure)
LES and fundus relax - receptive relaxation (low pressure).
to continue a peristaltic wave, what is released at the level of the bolus
Ach and SP (substance P) to initiate contraction
to continue a peristaltic wave, what is released inferior to the bolus. Also what nerve causes this
NO/ VIP/ATP to cause relaxation distal to the bolus. This is caused by vagal input to the nonadrenergic/ noncholenergic receptors
What is the purpose of high resting pressures in the UES and LES
UES - keeps air from entering esophagus
LES - prevents acid reflux into esophagus
how can a stroke cause aspiration
UES and pharyngeal contractions are not coordinated
how do myasthenia gravis and polio affect swallowing
both destroy Ach receptors= diff swallowing
how does botulism affect swallowing
blocks Ach release= diff swallowing
what is the nutcracker esophagus
“steakhouse esophagus”
Lack of coordination between longitudinal and circular smooth muscle contraction which can lead to obstruction from bolus
what is a diffuse esophageal spasm and what can it lead to
Functional obstruction
Can lead to diverticulae in esophagus
what is Zenker diverticulum
located above the UES
what is a traction diverticulum
located near the midpoint of esoph
what is a epiphrenic diverticulum
immediatly above LES
what is patterson brown kelly syndrome
AKA Plummer-Vinson syndrome
assoicated with iron deficiency anemia, glossitis, and cheilosis
what is the size of the protrusions from esophageal webs
protrude less than 5mm with thickness of 2-4 mm
what are schatzki rings
circumferential esophageal rings
what are type A and B schatzki rings
A rings: distal esophagus above gastroesophageal junction
Covered by squamous mucosa
B rings: located at squamocolumnar junction of lower esophagus. Have gastric type mucosa
achalasia is caused by what triad
Incomplete LES relaxation
Increased LES tone
Aperistalsis of esophagus
causing Food retained in esophagus and Organ hypertrophies and dilates
what causes primary achalasia
failure of distal inhibitory neurons
Other causes: degenerative changes(DM, ETOH) in neural innervation(vagus)
what is Chagas Dz
Trypanosoma cruzi infection which destroys myenteric plexus= dec parastolsis
what are complications of hiatal hernias
ulcerations, obstruction
what is the Mallory-Weiss syndrome
Longitudinal tears at GE junction due to severe retching or vomiting
May involve only mucosa or may penetrate deeply and perforate the wall
what type of pts is Mallory-Weiss syndrome more often seen in
bolemic, ETOH abuse
where are the lacerations from Mallory-Weiss syndrome usually located
Usually cross gastroesophageal junction and in proximal gastric mucosa
what is Boerhaave syndrome:
distal esophageal rupture
rare but catastrophic
what are the Sx of esophagitis
Retrosternal pain, dysphagia, odynophagia
what causes esophagits
Reactive: GERD
Infectious: Candida, Herpes, CMV
Toxic: Pill, Ulcer, Alkali or Acid Ingestion
Other: radiation, GVH
what is the pathology causing esophagitis
Inflammatory cells (eosinophils, neutrophils or lymphocytes) within the epithelium and lamina propria
what cells are likely to be the cause of esophagitis in 1)acute infection 2)allergic/ parasitic 3)chronic infection 4)yeast/ viral
1) acute infection = inc neutrophils
2) allergic/ parasitic =inc eosinophils
3) chronic infection = inc lymphocytes
4) yeast/ viral = inc lymphocytes
what are likely findings on a pathology report from acute esophagitis
Numerous neutrophils in the epithelium
Reactive squamous cells
what are likely findings on a pathology report from chronic esophagitis
Inflamed lamina propria with inc lymphocytes and inc monocytes
what are punched out ulcers seen with
herpes esophagitits
what is the pathophysiology causing GERD
dec in LES tone or inc abd pressure(ETOH, smoking, obesity, Pg) causing…
Inflammatory response (eosinophils and lymphocytes within the mucosa)
Basal zone hyperplasia
Elongation of lamina propria papillae into the top 1/3 of the epithelium with capillary congestion
Squamous cells react – mucosa may ulcerate and bleed – may undergo metaplasia
what is eosinophilic esophagitis
“Increased intraepithelial eosinophils in the esophagus”
First described in children; incidence appears to be increasing in adults (especially in young men)
what are the Sx of eosinophilic esophagitis
Longstanding dysphagia with solid foods
Food impaction
GERD Sx without improvement on therapy(proton pump inhibitors, etc)
what will endoscopy show if eosinophilic esophagitis is present
Small caliber esophagus
Corrugated (ringed) esophagus
Proximal esophageal stenosis
eosinophilic esophagitis
Dietary change
Steroids
Montelukast
what will a micro report show if eosinophilic esophagitis
Numerous intraepithelial eosinophils, often forming eosinophilic “microabscesses”
what differentiates eosinophilic esophagitis from GERD
Failure of proton pump inhibitor treatment and absence of acid reflux is necessary for diagnosis.
Also, EE is Present in proximal and distal esophagus (a biopsy from the proximal esophagus is needed to exclude GERD)
who is most likely to get Barrett’s Esophagus
middle aged to older white men
what is a complication of longstanding GERD
Chronic mucosal injury causes the squamous mucosa to change into intestinal-type mucosa with goblet cells (“intestinal metaplasia” / “specialized metaplasia”)
what is the management for Barretts esophagus
BE without dysplasia: 1yr then at 3yr intervals
BE with low grade dysplasia: 1 yr intervals until negative for dysplasia
BE with high grade dysplasia: Although HGD is not cancer, there is a high likelihood that there may be cancer elsewhere in the Barrett’s segment
Aggressive surveillance every 3 months
Resection (Esophagectomy)
Ablation/Endomucosal resection
what is the Tx for Barretts esophagus with “intramucosal adenocarcinoma”
Since lymphatics are present within the mucosa, treat aggressively: esophagectomy or Ablation/Endomucosal resection
what do esophageal varices result from
Dilated submucosal veins due to portal hypertension(Fibrotic liver) and shunting of blood from the portal to systemic venous system (collateral circulation)
esophageal varices buldge inward, what risk does this present
tearing from food, ulceration
how severe is ruptured esophageal varices
50% die from 1st bleeding episode
what are the three types of cells esophageal tumors are derived from and what type of tumors are they
squamous epithelium (squamous cell carcinoma and squamous papiloma)
glandular epithelium (adenocarcinoma)
the muscular wall (leiomyoma)
what is the most common benign tumor of the esophagus
leiomyoma
can leiomyomas be visualized
they can be visualized by endoscopy in the esophageal wall
what functional problem can occure with leiomyomas
they can form a obstruction so they can be removed (do risk reoccurring)
what causes squamous papilloma in the esoph
HPV
what is characteristic of squamous papillomas
Hyperplastic papilliform squamous mucosa overlying a fibrovascular core
why is the incidence of adenocarcinoma increasing
increasing barretts
what mutation is associated with SCC
p53 tumor suppressor gene
where is the most common location of SCC in esoph
middle most common but can occur in upper or lower (but lower more likely to be adenocarcinoma
what treatment has been known to inc risk for SCC in esoph
thoracic cavity radiation
what factors are associated with SCC
Alcohol Tobacco: increases risk 5 to 10 fold HPV Nitrosamines in food (China, S. Africa) Chemical injury Polycyclic hydrocarbons-Burnt food Chronic Fungus= constant inflam
what is the lifetime risk of developing adenocarcinoma from barretts
around 10% depending on the severity of dysplasia in Barretts
what is the process from Barretts becoming adenocarcinoma
Normal-inflamed and reactive- low grade dysplasia- high grade dysplasia- invasive adenocarcinoma
where does adenocarcinoma typically appear
distal esoph
what part of the stomach mainly produces mucus
fundus and the antrum
what types of cells are mainly located in the body of the stomach and what do they secrete
chief and parietal cells secrete acid and pepsinogen
what effect does increased vagus tone have on the stomach
inc motility inc secretions(HCl, mucus, pepsinogen)
what effect does increased sympathetic tone have on the stomach
dec acid
dec motility
dec vascular supply
what is the vascular supply of the stomach
many different arteries supply the different parts of the stomach. All drain into the portal system which goes to the liver
what are characteristic of gastric pits
they are shallow pits that rapidly reproduce for replacement. mucus does extend into these for protection
where is the lamina propria located and what does it do
located under the mucosal muscularis and epithelial cells. It acts as the loose connective tissue of the mucosa
what is a oxyntic
another term for parietal cells
what is the function of parietal cells
secrete HCL and intrinsic factor
what is the function of intrinsic factor
it is produced by the parietal cells and is necessary for the absorption of vit B12
what is the function of chief cells(Zymogen)
produces pepsiongen 1 which is a zymogen(activated by acid) that digests proteins
what are the enteroendocrine cells AKA
G cells
what is the function of the enteroendocrine cells
release Gastrin into the blood stream(endocrine). Not released into the stomach.
what is the function of mucus cells
secrete mucus and pepsinogen II
what is the function of pepsinogen II
function not exactly known. They are starting to test pep I/pep II ratio for some GI Dz
what is the pathway of stimulating and releasing HCl from the parietal cells
1) CO2 combines with H20 with carbonic anhydrase to make carbonic acid.
2) carbonic acid dissociates freely into bicarb and H+.
3) H+ is excreted by a energy dependent proton pump
4) Cl- follows the charge of the H+ leaving
are PPIs reversible or irreversible
irreversible so the parietal cells will need to create more proton pumps to release the acid
what stimulates parietal cells to release HCl
ACh- inc carbonic anhydrase and inc production of proton pumps
what effect does the vagus nerve have on parietal cells
inc Ach release = inc carbonic anhydrase and inc production of proton pumps
what stimulates the vagus nerve at the stomach
stomach distention
what stimulates the parietal cells to release HCl and what meds prevent this.
Vagus (Anticholenergics), Gastrin in bloodstream, Histamine (H2 blockers)
how do digested proteins inc HCl release
gastrin releasing peptides(protein in stomach) activate G cells= inc gastrin in blood stream= directly stimulates parietal cells to release HCl and indirectly stimulate H2 release
what is Zollinger ellsion syndrome
gastrin releasing tumor= inc HCl release= inc ulcers
where are the D cells located
antrum and duodenum
what is the function of D cells
They get stimulated as bolus moves into intestines and release somatostin which inhibit G cells= dec acid release
what type of receptor in the parietal cells do anticholenergic meds block so they do not affect the heart
muscarinic type 3 (M3)
what type of receptors does gastrin bind in the parietal cells
cholecyctokinin type 2 receptor (CCK-B)
what pathway do ACh and Gastrin both activate in the parietal cells
both activate PLC to inc Ca and phosphokinase= provides more energy for the parietal cell to inc HCl release
what receptor does Histamine bind on the parietal cells and what is its effect
binds H2 receptor= actives the G protein system= inc Camp= activation of protein kinases= physphorylation and inc energy
what is prostaglandins effect on the stomach
inc mucus production
dec acid production
what is somatostatins effect on the stomach
binds parietal cells which inhibit G cells= dec acid release
