Peptic Ulcer Disease, Achalasia, and Scleroderma, Esophageal Disease Flashcards
Patho of PUD
Two major factors can alter
H/pylori and NSAIDs
Most commonly between fundus and antrum and are associated with normal rates of acid secretion
Deuodenla are within 3 cm of pylorus and associated with inc acid secretion
H .pylori infection
Disrutps normal gastric acid secretion and stimulates a local immune response
Leads to release of gastrin and supp of somatostatin so more H+
Elaborates urease which damages epithelial cells and stimulates inflamm
Stimulates Th1 med response and inc IL8, IFNG, and TNF alpha…recurit leukocytes and neutrophils into mucosa
Has a catalase that neutralizies oxygen metabolites of neutrophils
NSAIDs and PUD
COX 1 is active normally
PGs - stimulate epithelial cells to secrete mucous, bicarb and phospholipids…local vasodilation…epithelial cell migration to surfaces
Maybe more for duodenal than gastric
Gastrinoma
Zollinger-Ellsion syndrome
Secretion of gastrin from duodenal or pancreatic gastrinoma
Stimulates gastric parietal cells to secrete mor gastric acid and ECL cells to release histamine which inc even more
High gastrin concentrations inhibit abs or sodium and water so chronic watery diarrhea
CM of PUD
Dyspepsia is most common sx
Epigastric pain 2-5 worse after eating
Improves with food intake or worsening
Complicated dz if pain radiating or tarry stools/coffee-ground emesis
Epigastric tenderness with both types
Comps of PUD
GI bleeding is most common
Perofration is 2nd most…duodenal is most likely…tend to occur along post wall near pancreas and lead to pancreatitis
Gastric outlet obstruction can also occur
PUD dx
Suspect in all pts with dyspepsia
SHould have endoscopy if any alarm sx are present
Tx with PPI and text for H.pylori
Upper endoscophy is most accurate diagnostic procedure…repeat after 12 weeks
Iron def anemia maybe?
If multiple ulcers in gastric or distal to duodenum, suggest gastrinoma…esp if resting gastrin levels high
Path of PUD
Punched out mucosal defects
Base is necrotic and smooth with formation of granulation tissue and fibrous scar
Mg of PUD
Erad of H pylori, withdrawl, and acid supp
Triple therapy is 1st line - amox, clarithro and PPI
Clarithro, metro PPI
Bismuth, metro, tetra and PPI
PPIs are more effective of healing than H2 receptor antagonists
Achalasia path
Inflammation and loss of ganglion cells in the myenteric plexus
Causes could be Chagas or Trypanosoma
Loss of NO inhibitory neurons with sparing of cholinergic
Achalaisa CM, dx, and mg
Sx progress slowly and primarily with dysphagia of liquids
Suspect in pts with dysphagia to both liquids and solids
Should deomnstrate aperistalsis of the distal 2/3 and incomplete relaxation
GE jxn with pirdbek appearance
Botulinum toxin injections….pneumatic dilation or myotomy
Scleroderma path
Microvascular injury and cytokine med inflammation
Lower 2/3 of esoph and sphincter
Incompetent LES leads to severe GE reflux with weak peristalsis leading to dec clearing of food and acid
CM, dx, and mg of scelorderma
Esoph reflux sx
Predominately solid dysphagia
Any pt with characteristic skin finding or raynaud phenomenon
Upper endoscopy is the test of choice and may show reflux
Manometry can be performed and would demonstrater weak or absent peristalsis with weak lower sphibcter
Dilated esophagus on barium swallow may help
No therapy so tx with PPI
