PUD Flashcards
Gastroc mucosal Defense 3 Level Barrier
- PREEPITHELIAL
mucus bicarbonate e phospholipid layer surface epithelial cell - EPITHELIAL
- SUBEPITHELIAL
- generates hest shock proteins, trefoil factor family peptides and cathelicidins
- restitution: EGF, TGF, FGF
- has microvascular system that is the key component of subepithelial defense
EPITHELIAL SURFACE
- 2 Principal gastric secretory products; capable of inducing injury
- plays a role on digestion, absorption of iron and Vit B12 as well as killing bacteria
- HCl
- pepsinogen
- occurs in basal and stimulated condition
- the basal acid production occur in circadian rhythm (highest level during night, lowest during morning)
Gastric Secretion
- influence by cholinergic input (vagus nerve) and histaminergic input (local gastric sources)
- somatostatin, cholecystokinin, gherlin, obestatin, secretin, serotonin- plays a role in counterbalancing gastric acid secretion
Basal acid production
3 Phases of Gastric Secretion
- sight, smell, taste of food
- cephalic phase
3 Phases of Gastric Secretion
- activated once food enters the stomach
gastic phase
3 Phases of Gastric Secretion
- initiated as food enters the intestine
intestinal phase
- located in oxyntic gland
- also important in gastric secretory proceess
- secretes intrinsic factor, IL11
- express several stimulants of acid secretions (histamine 2, gastrin, Ach:M3)
- express receptors for ligands that inhibit acid production (prostaglandins, somatostatin, EGF)
Parietal cell
- responsible for generating large conc of H+
- consist of alpha (active catalytic site) and beta subunit
- usses chemical energy of ATP to transfer H+ ions from parietal cell cytoplasm to the secretory canaliculi
H+, K+- ATPase
- found primarily in the gastric fundus
- synthesizes and secretes pepsinogen- inactive precursor of pesin
- pepsin activity significantly diminished at pH 4, irreversibly inactivated and denatured at pH >/=7
Chief cell
break in the mucosal surface >5mm in size w/ depth to the submucosa
Ulcer
most common risk factor
H. pylori & NSAIDs
- often occur in the 1st portion, w/ 90% located w/in 3cm of pylorus
- usually = to 1cm in diameter but occ’l can reach 3-6cm
- sharply demarcated w/ depth at times reaching the muscularis propia
- the base often consist of zone of eosinophilic necrosis w/ surrounding fibrosis
Duodenal Ulcer
account for the majority of DU
H.pylori and NSAID
- attributed to either H.pylori or NSAID induced mucosal damage
- gastric acid output tends to be normal or decreased
- abnormalities in resting and stimulated pyloric sphincter pressure w/ increase in duodenal gastric reflux
Gastric Ulcer
Classification of Gastric Ulcer
-Type I
-Type II
- TYpe III
- Type IV
- Type I: gastric body; ass w/ low gastric acid production
- Type II: antrum; gastric acid vary from low to normal
- Type III: occur w/in 3cm of pylorus; acccompanied by duodenal ulcerl normal -high gastric acid production
- Type IV: found in cardia; low gastric acid secretion
2 factors that predispose to high colonization rate
- poor socioeconomic status
- less education
MOT of PUD
- person-person
- oral-oral
- fecal-oral
Risk Factors for H.pylori Infection
- birth or residence in developing country
- domestic crowding
- unsanitary living condition
- unclean food or water
- exposure to gastric contents of an infected individual
Pathogenic Factors Unrelated to H.pylori and NSAID in Aic Peptic Disease
- cigarette smoking
- genetic
- diet
- systemic mastocytosis
Infection Causes of Ulcers
- CMV
- HSV
- H. heilmannii
Drug/Toxin Causes of Ulcers
- biphosphonates
- chemo
- clopidogrel
- crack cocaine
- glucocorticoids
- mycophenolate mofetil
- KCl
Clinical Features of PUD
- abdominal pain: epigastric (burning or gnowing)
- nausea & weight loss
- tarry stools or coffee ground emesis