GI Flashcards
- GI defense mechanism
From acid: mucus production bicarb production PG prod(attenuates acid prod) Tight junctions (protects epi breach) Bicarb from pancreas
From Infection: Secretory immune sysytem Rapid epi cell turnover normal colonic microbiota stomach acid
Esophagus motility and neural control
- Parasympathetic innervation of striated and smooth muscle
- Peristalsis (Primary and Secondary - Primary – first time through, Secondary
follows if the food has not moved out of the esophagus)
a. Stimulus for peristalsis is food in the esophagus which stretches the wall of
the esophagus
b. Esophageal wall stretch relaxes muscle below (receptive relaxation) and
contracts the muscle above forcing food downward (wave of contraction).
c. Continued wall stretch stimulates secondary peristalsis
. - Lower Esophageal Sphincter
a. Alpha adrenergic sympathetic stimulation increases constriction.
b. Parasympathetic stimulation and enteric system -> causes relaxation of the LES
- Achalasia
Definition: A disorder of the esophagus in which the LES fails to relax properly during swallowing
o Etiology
Primary - Unknown
Secondary – Disease states that affect the neuronal system
Pathogenesis:
1. Primary – Loss of intrinsic inhibitory innervation of the lower
esophageal sphincter
o Also, the smooth muscle of the lower half to two-thirds of the
body of the esophagus does not contract normally
2. Secondary - Myenteric plexus damage from disease
Produces:
o Aperistalsis (of the esophagus)
o Overly contracted LES
o Partial or incomplete relaxation of the LES with swallowing
o Progressive dilation of the esophagus (PPT8)
o Clinical manifestations
o Dysphasia
o Diffuse Esophageal Spasm
o Noncardiac chest pain
o Regurgitation and aspiration of undigested food through UES
o The risk of esophageal carcinoma is 2 -7%.
GERD - reflux esophagitis
KNOW Mcphee 351,&fig13.17
Gastroesophageal Reflux Disease (GERD)
a. Etiology - (5 major factors) (McPhee, Figure 13-17, p. 351, KNOW)
o Inefficient/slowed gastric emptying.
o Increased frequency of transient LES relaxations. (McPhee, Table 13-5, p.
368-Decrease).
o Increased acidity
o Loss of secondary peristalsis
o Decreased LES tone /incompetent LES
o Usually pressure is –30 cm, In GERD, pressure is less
b. Patho
o Persistant and repetitive acid exposure to the esophageal mucosa
o Occasionally reflux of pepsin or bile
o Causes mucosal damage and inflammatory response - esophagitis
o Continued injury results in epithelial hyperplasia and ulcerations
o Continued inflammation results in scar formation and further sphincter incompetence
o Prolonged injury results in the eventual replacement of distal esophageal squamous epithelium with a metaplastic columnar epithelium containing goblet cells - Barrett’s esophagus (PPT9) (K, Fig. 14-10, p. 561)
Rate of occurrence - 5-15 %
In 2-7% of cases, Barrett’s esophagus leads to adenocarcinoma
o Esophogeal stricture/perforation
c. Clinical Manifestations
o Heartburn typically worsening when lying prone
o Hoarseness, coughing, wheezing and pneumonia
o Endoscopy – reddened mucosa
- Hiatal Hernias
o Herniation of the upper part of the stomach through the diaphragm into the
thorax.
o Two patterns (PPT10)
o Sliding (axial) (95% of cases – protrusion of the stomach above the diaphragm creates a bell-shaped dilation) The gastroesophageal junction is above the diaphragm. May have reflex esophagitis from incompetent LES
o Paraesophageal (nonaxial) - Herniation of the greater curvature of the stomach through the opening in the diaphragm. The gastroesophageal junction lies below the diaphragm
o Can ulcerate, become strangulated or obstructed
o Reflux less common
- Mallory Weiss Syndrome and varices
a. longitudinal tears in the esophagus at the esophagogastric junction (PPT11)
b. Etiology: - severe retching
c. Pathogenesis
o inadequate relaxation of the LES at the moment of propulsive expulsion of gastric contents
o causes stretching and tearing of the esophagogastric junction
- Varices
a. Etiology
o Portal Hypertension
b. Dilated veins that are primarily within submucosa of distal esophagus and proximal stomach. (K. Figure 14-7, p. 559)(PPT12).
c. Pathogenesis
o Collateral bypass channels develop in the lower esophagus when portal HTN diverts blood flow through coronary veins of the stomach into esophageal subepithelial and submucosal veins
o Vessels become dilated and tortuous - varices
o May rupture
40% mortality rate
- Gastric secretion HCL
- HCL - secreted by parietal cells. H within parietal cell pumped against HKATPase (proton pump) to go in GI lumen. Cl follows. pH 1-2
HCO3 elimination from PC prevents mucosal injury
Serves as bactericidal, digestion, vb12 extraction, activates pepsinogen.
Stimulated by: Histamine, Acetylcholine, Gastrin, eating
Antagonized by : somatostatin, GIP, secretin (duodenum contents regulates secretion)
- Gastric secretion Intrinsic factor
Absorp VB12, secreted along with HCL
- Gastric secretion Pepsinogen secretion
Secreted by chief cells
stimulated by acetylcholine
hcl converts to pepsin
Digests protein
- Gastric secretion Mucins/Bicarb
Mucus secreted by Mucus cells Forms coat et bicarb trapped on coat pH 7 Pg aument bicarb and mucus. Inhibited by nsaids/asa by pg suppression.
- Acid secretion phases
- Cephalic (senses) - Hag release from parasymp
- Gastric phase - stomach distention, coffee, alcohol, CA. Stimulates parasympathetic HAG
- Intestinal - nutrients reach duodoun modulates gastric secretions
- Acute gastritis
transient
Etio: heavy etoh/smoking, stress, uremia, trauma, Hpylori
Patho: acid secretion increased or defense mechanism compromised.
injury to cells (inflammation).
Erosion/hemorrhage
Clinic manif:
n/v
epigastric pain
bleeding
- Chronic gastritis
chronic mucosal inflamm leading to metaplasia or atrophy, loss of glands
- H Pylori - 50% popn, oral/fecal transmission
- compromises immune system, coloniz of epi cell
- inflamm reaction produces urease, which produced ammonia
- Urease damages mucosa - leakage of acid to epi cells
- metaplasia, high acid production continues
Clinic manif:
n/v, pain, Hpylori +, urea breath test, reddened mucosa, neutrophil infiltrates, atrophy, hp on mucous layer.
- Peptic ulcers
Etio:
mucosal cell injury
defense impairment
h,pylori common cause (70% gastric 98% duodenalulcers)
Patho:
damage to submucosa and possible muscularis
autodigestion
98% ulcer found in duodenum
Clinical manif: epigastric pain/burning n/v wt loss gi bleed/performation
- Gastroparesis
Partial or incomplete paralysis of stomach motility.
Etio:
autonomic diab neuropathy
Produces:
outlet obstruction
delayed emptying
release of large boluses of chyme
Clinic Manif: n/v bloating wt loss bezoars erratic glucose levels
