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
- Tumors Carcinoma
high in japan/korea
Risk fx- hpylori, chronic gstritis, gastric resection, smoking, nitrate diet, low SES.
Patho: related to hpylori
Tcell activation by B cells
metaplasia=carcinoma
Poor prognosis
s/s: abd pain, n/v, wt loss, changed bowels.
- Small intestine mechanism
Neural - sympathetic (celiac, sup and inf mesenteric ganglion) constrict sphincter, inhibit gi activity
parasympathetic (vagus/pelvic nerve) stimulates gi activity, relaxes sphincter
Enetric control myenteric plexus (Auerbach), submucosal plexus (Meissner)
Humoral - motilin stimulates duodenal motility
- Small intestine - structure
3: duodenum, jejeunum, ileum.
2 sphincters: pyloric and ileocecal.
Sturcture:
Villi
Enterocytes (epi cells) face lumen and facilitate absorption, life span 4-7 days. Affected by malnutrition,vb12 def, drugs, irradiation.
Crypts of Lieberkuhn - cells differentiate to enterocytes, goblet cells, enteroendocrine, paneth cells, contain fluid and elyte secretions.
- Small bowel secretions
From duo/jej sensory cells:
Secretin - HCO3 secretion, regulates gastric activity
GIP - stimulates insulin
Gastrin - stimulates acid secretion in peptides/AA
Cholecystokinin - acid secretion in presence of lipids, stim bicarb secretion
- Small bowel secretions
From Villi and Crypts of Lieberkuhn: Goblet cells - mucus Enterocytes - secrete water and lytes Paneth - antimicrobial peptides Enzymes
- Large bowel secretions
Mucin - secreted by goblet cells, has bicarb, lubricates, protects mucosa
- Zollinger-Ellison syndrome
Pancreatic or duo tumor which increases gastrin production.
Leads to increased acid secretion, parietal cell hyperplasia, ulceration of stomach/small bowel.
- Megacolon
Colonic dilation close to affected segment in conditions such as:
Hirschprung - absence of enteric NS
Obstruction - tumor
Secondary to crohn’s or ulcerative colitis
Functional disorder
- Diarrhea
Contain 70-95% water up to 250gm
Clinical manif Dehydration malnutrition vitamin deficiency muscle wasting wt loss shed bacteria/virus particles (if viral or bacterial)
- Diarrhea - osmotic abates with fasting
high osmolality of luminal solutes drawing water into lumen. multiple causes p 359
- Diarrhea - secretory persists with fasting
Excessive fluid/lyte secretion.
Etio:
anything that injures enterocytes (altering absorption)
tumors
I.e:
Rotavirus - age 5 common,
enterocyte function compromised
crypt cells stimulated > lyte fluid secretions
nutrients not absorbed
2. Cdiff - drug resistant anerobic bacilli
Antib decrease normal flora
enetrocyte injury & stimulates water water and lytes
Inflamm cells debris prevent absorption > osmotic diarrhea
3. E coli.
- Diarrhea - Exudative persists with fasting
Purulent, frequent, bloody stools.
Etio: destruction of epithelial layer and ibd
ie. Salmonella - infected food transmission. Adhere and destroy to epi cells altering absorption, initiate neutro/cytokine release
- Diarrhea - Malabsoprtion abates with fasting
Defective ability to digest/ absorb nutrients > bulky stools.
Due to :
enzyme deficiency (pancreatic enzyme def)
Mucosal cell abn (lactace deficiency undigested lactose ^ osmotic gradient)
epi cell ability to absorb,
reduced surface area (enterocyte loss or atrophy like celiac/gluten sensitive cases atrophy),
infection,
lymphatic obsturction.
Clinic manif:
same as diarrhea, predominate is steatorrhea
diarrhea - deranged motility
improper gut function producing variable stool patterns
Etio:
decreased retention time due to dec gut length,
IBS
- Inflammatory bowel disease
Idiopathic/genetic predisp.
Patho:
Unregulated immune/inflamm response to antigens or self antigens.
Epi tight junction alterations increases permeability
Microbia factors
Inflamm respnse (major role), up reg of cytokine release (TNF) causing loss of absorp and mucosal epi impairment.
- Crohns disease
Inflammatory disease transmural with fissures and granulomas.
Patho - common site ileum, discontinuous “skip lesions”, intestinalwall fibrotic> narrowed lumen.
Clinic Manif:
diarrhea (bloody/mucousy), fever, pain, malabsorp/malnutrition, anorexia, wt loss.
fibrotic strictures can form fistulas to adjacent organs.
- Ulcerative colitis
Patho:
Inflamm disease of colonic mucosa/submucosa, nongranulomtous, segmental
Erosions rarely extend past submucosa.
Crypt of liberkuhn abscess
Clinic manif: intemittent exacerbations/remissons bloody diarhhea pain, dhd, n/v risk for CA
Patho:
- Diverticular disease- outpouching of mucosa and submuc through muscularis.
Etio:
diet low fiber, refined foods
constipation
connective tissue d/o
patho:
focal weakness (where nerves and arteries penetrate inner muscle coat)
exaggerated peristaltic contractions increase luminal pressure and muscle hypertrophy
Diverticulitis - inflamm changes of mucosa of herniation
Clinic manif: painful spasms blood stools systems infections abd guarding diarrhea constip
- IBS
Main characteristic: altered bowel function with abd pain
Patho:
dysfunction of int and ext NS
altered bowel motility (decreased or increased frequency of peristaltic contractions or stress
- Ischemic bowel disease
Patho: poor/absent circulation > alterations in absorp, digestion, permeability & motility mucosal dysfunction
Injury: mucosal - mural - transmural infarcation
- Colon Polyps
colonic mucosa protruding from colonic wall.
Non-neoplastic- hyperplastic or inflamm polyps increasing with age.
Neoplastic -
Result from prolileriation and dysplasia (over age 60, genetic predisp)
Three forms - pedunculated, sessile or mixture.
Precursor for invasive colorectal adenocarcinoma.
(Risk - adenoma size increase > 4cm, ^ dysplasia.)
Asymptomatic (anemia/occult bleeding)
